Podiatry Institute Manual

PODIATRY INSTITUTE
THE P.I. MANUAL
A Handbook of
Podiatric Medicine and Surgery
2nd Edition
The Podiatry Institute

Decatur, Georgia
D. Scot Malay, DPM, MSCE, FACFAS, Editor
Podiatry Institute Publishing, Inc.

Decatur, Georgia
2006 by The Podiatry Institute, Inc. All rights reserved. This book is protected by
copyright. No part of it may be reproduced, stored in a retrieval system or transmitted
in any form or by any means electronic, mechanical, photocopy, recording, or otherwise
without the prior written consent of the publisher. For information write Podiatry
Institute Publishing, 2675 North Decatur Road, Suite 309, Decatur, GA 30033.
Care has been taken to confirm the accuracy of the information presented and to
describe generally accepted practices. However, the editor and publisher are not
responsible for errors or omissions, or for any consequences from application of the
information in this book, and make no warranty, express or implied, with respectto the
contents of the publication. The reader is urged to check the package insert of all drugs
for current recommendations regarding indications and dosage, and for added
warnings and precautions.
20<0811.08
Contents
Chapter 1. Selected Anatomy & Normal Physiology

Osteology 1
Arthrology 2
Myology 6
Tendons, Sheaths and Bursae 12
Neurology 13
Angiology 17
Chapter 2. Basic Pathophysiology

Skin Wounds and Healing 22
Bone Healing 24
Cartilage Healing 29
Tendon, Ligament and Joint Capsule Healing 29
Peripheral Nerve Wounds and Healing 30
Chapter 3. Selected Diseases and Pathological Conditions

Dermatoses and Common Skin Pathology 33
Bacterial Infection 40
Acquired Immunodeficiency Syndrome (AIDS) 51
Peripheral Vascular Diseases 52
Diabetes Mellitus 59
Thyroid Disease 60
Hepatitis 61
Arthritides 61
Neurological Disorders 68
Neoplasms 71
Selected Emergency Situations 81
Basic Cardiac Life Support 86
Chapter 4. Selected Diagnostic Techniques

History and Physical Examination 89
Diagnostic Imaging 89
Clinical Laboratory Testing 94
Neurological and Electroneurodiagnostic Evaluation 101
Vascular Examination 104
Biomechanics 106
Chapter 5. The Peri operative Patient

Preoperative Phase 116
Intra-operative Phase 116
Postoperative Phase 117
iv Contents
'.-,.
Chapter 6. Fundamental Techniques and Procedures
Suture Materials 123
Biopsy Techniques 124
Plastic Surgery Techniques 126
Bone Grafting and Orthobiological Agents 131
Selected Endoscopic Techniques 134
Laser Surgery 137
Microsurgery 140
Selected Tendon Lengthening and Transfer 140
Internal Skeletal Fixation 146
External Skeletal Fixation 152
Hemostasis 154
Anesthesia 157
Padding, Straping, Bracing and Prostheses 161
Chapter 7. Basic Reconstructive Foot and Ankle Surgery

Toenail Surgery 163
Sunbungual Exostosis 165
Hammertoes 166
Bunion Deformity and Hallux Abductovalgus 171
Hallux Limitus/Rigidus 184
Hallux Varus 191
Hallux Interphalangeal Arthrodesis 192
First Metatarsocuneiform Exostosis 193
Intermediate (Central) Metatarsalgia & Deformities 194
Fifth Metatarsal Surgery and the Tailor's Bunion 196
Heel Surgery 198
Ankle Equinus 204
Nerve Entrapments and Acquired Neuropathy 208
Amputations 213
Chapter 8. Major Reconstructive Foot and Ankle Surgery

Collapsing Pes Valgo Planus 214
Pes Cavus 219
Rheumatoid Foot and Pan Metatarsal Head Resection 223
Ankle and Pantalar Fusion 225
Total Ankle Replacement 228
Contents v
Chapter 9. Congenital Deformities and Juvenile Surgery

Macrodactyly 229
Syndactyly 229
Polydactyly 231
Congenital Hallux Varus 232
Congenital Hallux Abductus lnterphalangeus 232
Congenital Curly (Underlapping) Toe 232
Congenital Overlapping (Fifth) Toe 232
Cleft Foot 233
Brachymetatarsia 233
Metatarsus Adductus 234
Talipes Equinovarus 237
Congenital Calcaneovalgus 239
Congenital Vertical Talus 239
Tarsal Coalition 241
Pediatric In-Toe Deformity 242
Pediatric Toe-Walking Gait 242
Micromelia 242
Congenital Hemihypertrophy 242
Ostechondroses 243
Chapter 10. Management of Foot and Ankle Trauma

Selected Soft Tissue Injuries 244
~~ffis m
Chapter 11. Foot and Ankle Disability and Rehabilitation
Disability 282
Chapter 12. Evidence~ Based Medicine and Clinical Research

Levels of Clinical Evidence and Clinical Research Design Options 285
The Building Blocks of Clinical Evidence 286
Fundamental Elements of Scientific Publication 286
Appendices
Oral Exam TestTaking Algorithm 293
Informed Consent 294
Hospital Admission Orders 294
Hospital Postoperative Orders 295
Hospital Discharge Orders 295
Ch. 1 Selected Anatomy & Normal Physiology
Selected Anatomy & Normal Physiology

OSTEOLOGY
Table 1-1: LEG AND FOOT OSSIFICATION DATES
PRIMARY EPIPHYSIS OSSIFICATION

OSSICLE OSSIFICATION CENTER APPEARS CENTERS FUSE
APPEARS (YEARS) (YEARS) (YEARS)
Proximal phalanx Birth 2-3 (base) 15-21
Middle phalanx Birth 2-3 (base) 15-21
Distal phalanx Birth 2-3 (base) 15-21
1st metatarsal Birth 2-3 (base) 15-18
2nd metatarsal Birth 2-3 (head) 15-18
3rd metatarsal Birth 2-3 (head) 15-18
4th metatarsal Birth 2-3 (head) 15-18
5th metatarsal Birth 2-3 (head) 15-18
Medial cuneiform 3-4
Middle cuneiform 3-4
Lateral cuneiform Birth-1
Cuboid Birth-1
Talus Bith
Calcaneus Birth 5-12 (apophysis) 15-20
Navicular 3-4
Sesamoids 9-11
Fibula Birth (shaft) 2 (distal) 11-14
3-4 (proximal) 14-21
libia Birth (shaft) 2 (distal) 17-19
Birth (proximal) 19-21
ACCESSORY OSSICLES
These are developmental anomalies, often separations of normal processes or tubercles,
and need to be differentiated from avulsion fractures if there is a history of injury.
2 Pertinent Anatomy & Normal Physiology Ch. 1
Table1-2: ACCESSORY OSSICLES
ACCESSORY OSSICLE lOCATION

Os tibiale externum Posteromedial aspect tuberosity of navicular, within insertional
{accessory navicular) fibers of tibialis posterior.
Os Vesalianum Proximal to well-formed tip of the tuberosity of the 5th
metatarsal base; to be differentiated from fracture of the tip of the 5th
metatarsal base, or nonunited or fragmented apophysis.
Os peroneum Sesamoid bone within the peroneus brevis tendon insertion at
the 5th metatarsal base.
Os supranaviculare Dorsal apsect oftanlonavicular joint.
(talonavicular)
Os intermetatarseum Between the medial cuneiform and the 1st and 2nd metatarsal
bases.
Os sustentaculi Posterior aspect of sustentaculum tali.
Os calcaneus Dorsum anterior process of the calcaneus, at the junction of the
secondarius calcaneus, cuboid, head of the talus and the navicular.
Os trigonum The separated posterolateral tubercle of the talus; to be
distinguished from the intact trigonal process and fracture
thereof !Shepherd's fracture).
Os sublibulare Distal to the tip of the fibular malleolus; to be distinguished from
an avulsion fracture of lateral malleolus.
Os subtibiale Distal to the tip of the tibial malleolus; to be distinguished from
an avulsion fracture of the medial malleolus.
Os cuneo~ 1~ Plantar aspect of the 1stmetatarsal~medial cuneiform articulation.
metatarsale-1 ~p lantare
ARTHROLOGY
Interphalangeal Joints IIPJ) (Fig. 1.1)

Ginglymus (hinge) joints with capsule that is hooded dorsally by the fibrous extensor
expansion and the plantar ligament {flexor plate); reinforced with medial and lateral
collateral ligaments running obliquely from the head of one phalanx to the base ofthe next,
in a proximal~dorsal to distal~plantar direction. A plantar IPJ sesamoid may be present.
lesser Metatarsophalangeal Joints IMTPJ) (Fig. 1.2)

Spheroidal joints contained within a capsule that is contiguous with the extensor hood
expansion dorsally, and the thickened flexor (plantar) plate. The capsule is reinforced medially
and laterally by collateral and suspensory ligaments. The collateral ligament runs obliquely,
proximal~dorsal to distal~plantar, from the metatarsal head to the phalangeal base. The
suspensory ligament is a continuation of the extensor hood expansion that descends vertically
to the plantar plate, which is tethered to the adjacent MTPJ flexor plate by the deep transverse
intermetatarsalligament. A plantar sesamoid may be invested within the flexor plate of a
lesser MTPJ.
Ch. 1 Pertinent Anatomy & Normal Physiology 3
Figure 1.1
Figure 1.2
Slip from EHL or

ha!licus brevis Ant. Tib.
Tib. sesamoid lig.
Transverse
metatarsallig.
Plant. tib .. sesamoid lig.

lntersesamoidal Flexor
hallicus longus
Figure 1.3
Pattern of dorsal Pattern of dorsal Pattern of intermetatarsal

tarsometatarsal ligaments intermetatarsalligaments ligaments
Internal
cuneiform
Cuboid Navicular
Plantar tarsometatarsal Pattern of interosseous

ligaments tarsometatarsal ligaments
Figure 1.4
First Metatarsophalangeal Joint (1ST MTPJ) (Fig. 1.3)

The 1st MTPJ is of particular importance because of the sesamoid apparatus and its
relationship to the deformities of hallux valgus and varus. The tibial and fibular sesamoids are
tethered by the intersesamoidal and plantar sesamoidal ligaments, present medially and
laterally, running from each sesamoid to the proximal phalangeal base. The conjoined head of
adductorhallucis inserts plantarlateral intothefibularsesamoid, the 1stMTPJ lateral ligaments,
and the base ofthe proximal phalanx.
Tarsometatarsal Joints (TMTJ, USFRANC'S JOINT) (Fig. 1.4)

Complex consisting of arf1culations of the metatarsal bases with the cuneiforms and the
cuboid, stabilized by insertion of the base of the 2nd metatarsal (keystone) into the
intercuneiform recess. The complex Is arched dorsally in both the frontal and sagittal planes.
There are 3 capsular elements: medial, inveSting the interface between the 1st metatarsal
base and medial cuneiform; intermediate, investing the interface between the2nd and 3rd
metatarsal bases and the intermediate and lateral cuneiforms; and lateral, investing the
interface between the 4th and 5th metatarsal bases and the cuboid. The capsule is reinforced
by dorsal intercuneiform and cuneocuboid, tarsometatarsal, intermetatarsal base, and
plantar tarsometatarsal ligaments. Lisfranc's plantar ligament runs obliquely from the medial
cuneiform to the 2nd metatarsal base plantarly.
Calcaneocuboid Joint (CCJ)

Saddle-shaped interface invested in capsule reinforced with dorsal, lateral, and medial
ligaments. The medial ligament is actually the lateral, or calcaneocuboid, portion of the
bifurcate ligament. The joint is also supported by the extracapsular long plantar
calcaneocuboid ligament, which extends from the calcaneal tuberosity to the bases of the
2nd-5th metatarsal bases.
Talocalcaneonavicular Joint(TCNJ)
Commonly referred to as the talonavicular joint, an essentially condylar joint complex that
suspends the head of the talus in the midfoot's acetabulum pedis. The acetabulum pedis
consists ofthe concavity ofthe posterior surface of the navicular, the anterior and middle
facets ofthe sustentaculum tali of the calcaneus, and the plantar calcaneonavicular (spring)
ligament. The TCNJ's capsule is reinforced by the spring ligament, the calcaneonavicular
portion of the bifurcate ligament and dorsal talonavicular ligaments. The spring ligament is
crucial to arch support.
Midtarsal Joints (MTJ)

Complex consisting of the talonavicular and calcaneocuboid joints, and functions reciprocally
with the subtalar (talocalcaneal) joint. The STJ and MTJs are generally considered a
reciprocating complex. The transverse (Kite's angle) and sagittal plane radiographic cyma
lines are useful guides to subluxation of the MTJ.
Subtalar Joint (STJ)

A modified ginglymus \hinge) joint displaying triplanar motion that occurs primarily in the
frontal plane, as inversion and eversion. Anatomically, the STJ is defined as the interface
between the posterior facets of the calcaneus and the talus. Functionally, the STJ includes
the posteriorfacets of the calcaneus and talus, as well as the anterior and middle calcaneal
facets of the sustentaculum (an anatomical component of the talocalcaneonavicular joint),
and the sinus tarsi. The sinus tarsi consists ofthe dorsal concavity of the neck of the talus
and the plantar sulcus between the posterior facet and the sustentaculum tali of the
calcaneus. The sinus tarsi is widest laterally, and is reinforced posteriorly by the
talocalcaneal Y-ligament, which also envelops the FHL tendon between the posterior
processes ofthe body of the talus. The posterior facets are stabilized anteriorly, medially,
and laterally by ligaments. The interosseous talocalcaneal ligament is situated posteriorly
in the sinus Oust anterior to the posterior facet), and resists supination ofthe STJ. The
cervical ligament is located at the anterolateral aspect ofthe sinus tarsi, between the talus
and calcaneus, and resists supination of the STJ.
Talocrural (Ankle) Joint

A modified ginglymus (hinge) jointthat displays triplanar motion that occurs primarily in the
sagittal plane, as dorsiflexion and plantartlexion. The ankle mortise consists of the concave
distal tibial-bearing surface (plafond), the triangular facet of the lateral malleolus,
the comma-shaped facet of the medial malleolus, and the anterior portion of the distal
tibiofibular syndesmotic ligament The capsule may communicate with the peroneal tendon
sheath, and is reinforced by the deltoid ligament (medial collateral) and the lateral
collateral ligament. The deltoid ligament consists of the deep anteriortibiotalar component;
and superficial tibionavicular, tibiocalcaneal, and posterior tibiotalar components. The
lateral collateral ligament consists of the intra-capsular anteriortalofibular (ATFL), and the
extracapsular calcaneofibular (CFL) and posterior talofibular (PTFL)Iigaments. The ATFL
resists ankle plantarflexion, and anterior subluxation (anterior drawer stress) of the talus out
of the mortise. The CFL is deep to the peroneal tendons, and inversion injury often disrupts
both the CFL and the peroneal sheath. Clinically and radiographically, anterior drawer and
inversion stress manipulation ofthe latera! collateral ligaments, and more commonly MRJ,
are used to assess the injured ankle.
Tibiofibular Joints
The tibiofibular joints include the proximal, interosseous, and distal tibiofibular joints. The
proximal joint is planar, and supported by anterior and posterior ligaments. The interosseous
membrane (10) consists of obliquely oriented, dense fibrous connective tissue running from
proximal-medial to distal-lateral from the tibia to the fibula. The fibula is also situated slightly
posterior to the tibia, !important when transferring tendon through the 10 membrane). The
distal tibiofibular joint is supported by anterior, 10, and posterior ligaments. The tibiofibular
joints allow motion in frontal and transverse planes, and resists ankle dorsiflexion as the
wider anterior portion of the talar dome engages the mortise.
MYOLOGY
The intrinslc pedal muscles comprise 41ayers ln the plantar vault, innervated by the deep
peroneaiiEDB; 2nd, 3rd and 4th dorsal ID), medial plantar IFDB, FHB, abductor hallucis,
1st lumbrical), and lateral plantar lOP, abductor digiti minimi, flexor digiti minimi, aJIIO,
alllumbricals exceptthe 1st, and adductor hallucis) nerves.
Plantar layer I
Abductor Ha/lucis
origin------medial calcaneal wall.
insertion------tibial sesamoid and medial base of proximal phalanx of hallux (Fig. 1.5).
Flexor Digitorum Brevis

origin---calcaneal tuberosity, divides at base of proximal phalanx.
insertion-plantar surface of middle phalanx IFig. 1.6).
Abductor Digiti Quinti

origin---lateral calcaneal wall.
insertion---lateral aspect base of proximal phalanx (Fig. 1.7).
I I.
plantar
nerve
plantar
plantar artery
artery
Figure 1.5 Figure 1.6 Figure 1.7

Plantar Layer II
Quadratus Plantae
origin------2 calcaneal heads.
insertio{}-lateral aspect of FDL tendon before it divides IFig. 1.B).
Lumbricales
origin------1st, from medial aspect of FDL to 2nd toe; 2nd, from contiguous aspects of 1st and
2nd FDL tendons; 3rd, from contiguous aspects of 2nd and 3rd FDL tendons; 4th, from
contiguous aspects of 3rd and 4th FDL tendons.
insertion-media! aspect of mid-portion of proximal phalanges and fibrous expansion of
the dorsal hood of the 2nd-5th toes IFig. 1.9).
plantar
artery
Figure l.B Figure 1.9

Plantar layer Ill

Flexor Hallucis Brevis
origin--media[ arm from tendons oftibialis posterior inserting into the metatarsal bases, and
lateral arm from the cuboid, 3rd cuneiform, peroneus longus tendon, and long and short
plantar ligaments.
insertion-base of proximal phalanx on medial and lateral aspects, after investing 1st MTPJ
sesamoids and plantar plate !Fig. 1.10).
Adductor Hal/ucis
origin-oblique head arises from 2nd, 3rd, 4th metatarsal bases.
insertion-into fibular sesamoid, plantar plate, and lateral aspect base of proximal phalanx
origin-transverse head arises from plantar plates of 3rd, 4th, 5th MTPJs.
insertion-into fibular sesamoid, plantar plate, and lateral aspect base of proximal phalanx
!Fig. 1.11).
Flexor Digiti Minimi Brevis

origin-plantar aspect of cuboid and 5th metatarsal base.
insertion-plantar aspect base of proximal phalanx of 5th toe IFig. 1.12).
JIFl/--FiJs1 plantar
metatarsal
artery
Figure 1.10 Figure 1.11

Superficial
branch of lateral
plantar nerve
Lateral--j~
plantar
artery
Figure 1.12
Plantar layer IV
Dorsa/Interossei (10)
origin---1st, adjacent surfaces of 1st and 2nd metatarsals; 2nd, adjacent surfaces of 2nd
and 3rd metatarsals; 3rd, adjacent surfaces of 3rd and 4th metatarsals; 4th, adjacent
surfaces of 4th and 5th.
insertion-1st, base of proximal phalanx of 2nd toe medially; 2nd-4th, lateral aspect of bases
of proximal phalanges oftoes 2, 3, and 4(Fig. 1.13).
Plantar Interossei (10)

origin-medial aspect of 3rd, 4th, 5th metatarsal shafts and bases.
inseltion-medial aspect of bases of proximal phalanges of toes 3, 4, and 5(Fig. 1.14).
Dorsal
Plantar
metatarsal
metatarsal
arteries
arteries
Superficial-b/1it'&~~
branch of lateral Deep branch
plantar ne!Ve of lateral
plantar nerve
Dorsal Intrinsic Muscles

Extensor Digitorum et Hallucis Brevis
origin-lateral aspect of the calcaneal sulcus and the cervical ligament; forms four slips that
course distally.
insertio/'1------lateral aspect of EDL tendons to 2nd through 4th toes, and dorsal aspect of the
proximal phalanx otthe hallux or the lateral aspect ofthe EHLtendon. EDB is innervated by
the deep peroneal nerve.
EXTRINSIC PEDAL MUSCULATURE
Anterior Leg Compartment

The anterior leg compartment contains the muscles tibialis anterior \TA), extensor ha!lucis
longus (EHL), extensor digitorum longus (EDL), and peroneus tertius (PT). Each of these is
innervated by the deep peroneal nerve and supplied by the anterior tibial artery. The
tendons of these muscles traverse deep to the transverse and cruciate crural ligaments.
Tibialis Anterior (TAl

origin--most medial ofthe anterior crural muscles, from the lateral superior condyle and shaft
of the tibia, 10 membrane, deep crural fascia, and intermuscular septum adjacentto EDL
insettion-90% into the medial cuneiform,-10% into the base of the 1st metatarsal
Extensor Digitomm Longus (EDL)
origin-superior lateral condyle of the tibia and the proximal% of the fibula, 10 membrane,
crural fascia, and intermuscular septae common to TA and PL; the tendon divides into four
major slips that course distally
insertion-into each of the 4 lesser toes. In the digit, the tendon divides into a central slip
that inserts into the dorsal central aspect of the base of the middle phalanx~ and medial and
lateral collateral slips that course along the medial and lateral aspects of the middle
phalanx before they reunite and insert as a single tendon into the dorsal surface of the
distal phalanx. The tendons also yield medial and lateral fibrous expansions at the level
of the head of the metatarsal and MTPJ, creating the dorsal hood that also serves as an
insertion point for the dorsal and plantar 10 and the lumbricales.
Extensor Hal/ucis Longus (EHL)

origin--inferior to TA and EDL, from the fibula, 10 membrane, and adjacent intermuscular
septae.
insertion--dorsal aspect of base of the distal hallucial phalanx
Extensor Hallucis Accessorius

origin-medial aspect of EHL in the distal leg, ankle, or foot.
insertion-dorsa! and medial aspects of the base of the proximal hallucial phalanx.
Peroneus Terlius origin-inferior third ofthe anteromedial surface of the fibula and the 10
membrane.
insertion-base of the 5th metatarsal.
lateral Leg Compartment
The lateral leg (peroneal) compartment contains both the peroneus longus (PL) and
peroneus brevis IPB). The muscles are supplied by the peroneal artery and the superficial
peroneal nerve, and they traverse deep to the peroneal retinaculum distal to the lateral
malleolus.
Peroneus Longus (PL)

origin--head and proximal half of the fibula, deep crural fascia, and the anterior and
posterior peroneal septae. The muscle is superficial to the peroneus brevis at the
myotendinous junction proximal to the lateral malleolus, and must be retracted when
harvesting the underlying brevis for some lateral ankle stabilization. The tendon then
courses around the lateral malleolus, to the plantar-lateral aspect of the cuboid, where it
turns medially into the peroneal groove deep to the long plantar calcaneocuboid ligament.
inseJtion---plantar-latera! aspect of the base of the 1st metatarsal.
Peroneus Brevis (PB)

origin--anterior to PL from the distal 2/3 of the fibula, and the anterior and posterior peroneal
septae; just distal to the latera! malleolus, the PB tendon is superior and anterior to the
tendon of PL.
insertiof}-base of the 5th metatarsal.
Superficial Posterior leg Compartment

The superficial posterior leg compartment contains the triceps surae, which converge to
form the tendoAchillis that inserts into the posterior aspect of the calcaneus. The muscles
include gastrocnemius and soleus, and are innervated by branches of the tibial nerve, and
supplied by the posterior tibial artery. The triceps surae plantarflex the ankle, with some
inversion, and extend the knee by virtue of the femoral origin of gastrocnemius.
Gastrocnemius
origin------as two heads, larger medially, from the medial and lateral condyles of the femur
posteriorly.
insertion------as Achilles tendon into the central third of the posterior surface of the calaneus.
Soleus
origin-head and proximal third of the fibula and the middle third of the tibia above the
popliteal line.
insertiof}-----as Achilles tendon into the central third of the posterior surface of the calaneus.
Plantaris
origi(}-medial to the lateral head of the gastrocnemius at the lateral condyle of the femur,
coursing lateral to mediaL
inseraan---medial aspect of the tendoAchillis and, along with the Achilles, into the calcaneus.
Deep Posterior leg Compartment

The deep posterior leg compartment contains tibialis posterior ITP), flexor digitorum longus
IFDL), and flexor hallucis longus IFHL). The muscles are innervated by the tibial nerve, and
supplied by the posterior tibial artery. The tendons of these muscles traverse deep to the
flexor retinaculum \laciniate ligament) to enter the plantar vault.
Tibialis Posterior (TP)

origf(}-from the posteromedial aspect of the fibula, the posterior aspect of the tibia distal
to the popliteal line and lateral to the vertical line, the 10 membrane, and adjacent inter-
muscular septae; FHL and FDL both overlap the belly ofTP; and TP passes through the first
!medial) canal of the tarsal tunnel.
insertion----primarily into the tuberosity of the navicular, with additional slips inserting into
the plantar aspect of the intermediate 3 metatarsal bases and everytarsa! exceptthe talus.
Flexor Digitorum Longus (FDL)

origin--from the posterior aspect of the tibia distal to the solealline, and from fascia ofTP;
the tendon traverses the second canal of the tarsal tunnel to enter the foot where it first
crosses superficial to FHL, and then over TP, where it shares a vinculus {master knot of
Henry) with FDL; thereafter, FDL splits into 4 slips.
insertion----into the plantar aspect of the distal phalanx of the lesser 4 toes.
Flexor Hallucis Longus (FHL)

origin-from the distal2/3 ofthe posterior surface of the fibula, the posterior aspect of the
peroneal septum, the anterior surface of the deep transverse intermuscular septum
!separating the superficial and deep posterior groups), and the fascia aboutTP. The tendon
courses through the fourth canal of the tarsal tunnel.
insertion-into the plantar aspect of the base of the distal phalanx of the hallux.
TENDONS, SHEATHS liND BURSAE
Tendon Structure
Tendons consist of dense regular connective tissue made up oftropoco!lagen units, created
by fibroblasts, and organized to form collagen fibers. The fibers are supported within
endotenon, and grouped into fasciculi which are contained within an outer epitenon. The
epitenon defines the anatomical tendon. Go!gi tendon organs within tendon fibers inhibit
skeletal muscle contraction when excessive tension is registered. The organized tendon is
further surrounded, outside of the epitenon, by a loose, areolar and highly vascularized
paratenon, wherever the tendon courses a straight line. Paratenon is contained deep to,
and adherent to, the deep fascia \muscle fascia); or it is adherent to a neighboring inter-
muscular septum (fascia) betvveen intact skeletal muscle bellies; or it may be adherent to
deeper periosteum.
Tendon Sheath and the Gliding Mechanism

A tendon sheath exists where a tendon changes direction, such as about the ankle deep to
the extensor, peroneal, and flexor retinaculae. The sheath is distinct from paratenon and
Consists of a fibrous outer septum with a synovia! lining, much akin to joint capsule. Synovial
fluid bathes the tendon within the sheath. Within the sheath, on the tendon's deep
{non-friction) surface, a synovium lined fold of connective tissue called mesotenon, conveys
vascularity and further supports the tendon. Mesotenon attaches to the epitenon at the
hilus. At the proximal margin of the tendon sheath a double fold of paratenon, termed a
plicae duplicata, invaginates a short distance into the sheath and adheres to epitenon.
Similarly, at the distal margin of the sheath, a single fold of paratenon, termed a plica
simplex, protrudes into the sheath. As muscle contracts, the plicae unfold and elongate as
the tendon glides within the sheath as the tendon changes direction, or within paratenon
where the course is straight
Tendon Blood Supply

Tendon has three primary sources of blood supply: proximally, at the myotendinous junction
perimysial blood vessels from the muscle belly; centrally, from paratenon and/or mesotenon;
and distally, insertional periosteal vessels from bone. Synovial fluid within the sheath, and
local lymphatics within the paratenon, also nourish and drain metaboliTes from the tendon.
Occasionally, a condensed, highly organized fibrous connection, know as a vinculus, may
also convey vascularity between closely approximated tendons. The Master Knot of Henry,
between the tendons of FHL and the more superficial(plantar) FDL, at a level consistent
with the distal margin of the sustentaculum, is just such a vinculus. Vinculi also exist
between FHB and FDL near their phalangeal insertions.
Subfascial and Subcutaneous Bursae

A variety of bursae occur in the foot and ankle. Bursae protect tendon and muscle from
excessive friction or pressure caused by adjacent muscle, ligament or bone, or external
forces in the case of an adventitious bursa. Subfascia! bursae include the retrocalcaneaf
or pre-Achilles bursa, those at the insertions ofTA, TP, and the 10; and those between the
bellies of adductor digiti minimi and the 5th metatarsal, and the belly of FHB and the medial
cuneiform. Subcutaneous bursae are usually adventitious in origin, and may present at the
Cll. 1 Pertinent Anatomy & Normal Physiology 13
head of the 1st and 5th metatarsals, plantar to the tuberosity of the calcaneus (present in
about 50% of specimens), at the medial and lateral malleoli, and occasionally posterior to
tile insertion of tile Achilles tendon.
NEUROLOGY
The lower extremity nerve supply originates in the lumbosacral spine, and specifically
involves spinal nerve roots L4-S3. The spinal nerve roots traverse the lumbosacral plexus
to form the sciatic nerve, which divides into the tibial nerve and the common peroneal nerve
near the junction of the middle and distal thirds of tile thigh.
Table1.3. MOTOR INNERVATION TO THE LEG AND FOOT
MUSCLE PERIPHERAL NERVE SPINAL LEVEL

Tibialis anterior Deep peroneal u,5
Extensor digitorum longus Deep peroneal u,5
Extensor hallucis longus Deep peroneal u.5
Peroneus tertius Deep peroneal u,5
Gastrocnemius 1ibial S1,2
Soleus 1ibial Su
Plantaris 1ibial Su
Popliteus 1ibial u.5s,
Fexor ha!lucis longus 1ibial Sz,3
Flexor digitorum longus 1ibial s,
Tibialis posterior 1ibial u,5
Peroneus longus Superficial peroneal L5Su
Peroneus brevis Superficial peroneal L5Su
Extensor digitoum brevis Deep peroneal Su
Abductor hallucis Medial plantar S2.3
Flexor digitorum brevis Medial plantar s2.3
First lumbricalis Medial plantar S2,3
Flexor hallucis brevis Medial plantar S2,3
Abductor digiti quinti brevis lateral plantar S2,3
Quadratus plantae Lateral plantar S2,3
Second, third, fourth lumbricales Lateral plantar S2,3
Adductor hallucis lateral plantar S2.3
Flexor digiti quinti brevis lateral plantar Su
Plantar interossei lateral plantar S2,3
First, second dora! interossei Deep peroneal, lateral plantar Su,3
Third, fourth dorsal interossei Lateral plantar S2,3
COMMON PERONEAL NERVE

The common peroneal nerve trifurcates near the head of the fibula, forming the lateral sural
cutaneous nerve, the deep peroneal nerve, and the superficial peroneal nerve.
lateral Sural Cutaneous Nerve

This nerve ultimately anastomoses with the medial sural cutaneous branch of the tibial
nerve, to form the sural nerve.
The Deep Peroneal Nerve (Anterior Tibial) (Fig. 1.15)

This nerve begins atthe peroneal muscular hiatus between the fibula and peroneus longus,
then passes deep to EDL on the 10 membrane to innervate TA, EHL, EDL, and PT. At the
ankle, it divides into medial and lateral terminal branches.
The lateral terminal branch passes deep to, and innervates, EDB and then yields three
interosseous branches which supply the 2nd, 3rd, and 4th dorsaiiO.
The medial terminal branch runs parallel and lateral to the DP artery. The nerve divides at
the first interspace into two dorsal digital nerves supplying adjacent sides of the great and
second toes, and the first dorsal interosseous muscle {which is also innervated by the
lateral plantar nerve).
The muscular branches of deep peroneal nerve supply all anterior leg muscles, including
peroneus tertius.
The Superficial Peroneal Nerve

The superficial peroneal nerve supplies both the peroneus longus and brevis muscles, then
divides to form the medial and lateral dorsal cutaneous nerves.
The medial dorsal cutaneous nerve (Fig. 1.16) divides into two dorsal digital nerves, the
medial dorsal digital branch that communicates with the medial terminal branch from deep
peroneal nerve, to supply the medial aspect of the hallux.
The lateral dorsal digital branch supplies the adjacent aspects of the 2nd and 3rd toes
dorsally. The lateral dorsal cutaneous (Lemont's) nerve divides into a medial branch that
supplies the adjacent sides of the 3rd and 4th toes, and a lateral branch that supplies the
adjacent sides of the 4th and 5th toes.
,s
Dorsal proper ,I c
digital nerve ~ c [ \.
Saphenous
nerve Communicating
branch
dorsal~~~~~~r-.~:=~~o~~~~rve
Medial terminal
nerve branch Medial
of the deep cutaneous
peroneal nerve nerve Intermediate dorsal
digital
Medial plantar
nerve
Abductor hallucis

TIBIAL NERVE
The tibial nerve traverses the calf deep to the intermuscular septum between the superficial
and deep crural compartments, and in the distal third of leg runs parallel and medial to the
tendoAchillis. The tibial nerve yields the medial sural cutaneous nerve that unites with the
lateral sura! cutaneous branch of the common peroneal nerve, to form the sural nerve.
The Sural Nerve

The sural nerve courses distally through the leg, then posterior and inferior to the lateral
malleolus, en route to the lateral aspect of the foot and 5th toe. Just distal to the lateral
malleolus, the sural nerve sends a communicating branch dorsally to anastamose with the
intermediate dorsal cutaneous nerve. The tibial nerve also provides articular branches
that innervate the knee and ankle. In the calf, the tibial nerve innervates the popliteus,
gastrocnemius, soleus, plantaris, TP, FOL, and FHL muscles. Prior to bifurcation into the
medial and lateral plantar nerves, the tibial nerve yields the medial calcanean branch that
emerges through the laciniate ligament to innervate the skin of the heel medially and
plantarly.(Fig. 1.17)
The medial calcanean nerve can be injured or entrapped in scar tissue following
medial exposure (DuVries incision) of the heel, such as in plantar calcaneal spur surgery.
The division of the tibial nerve into the medial and lateral plantar nerves usually occurs near
the dorsal margin of the tarsal tunnel, however the bifurcation can occur at any level deep
to the laciniate ligament, and occasionally it occurs proximal to the ligament In many cases
oftarsal tunnel syndrome, operative inspection reveals a far distal bifurcation of the tibial
nerve at the porta pedis where the medial plantar nerve enters the anterior chamber, and
the lateral plantar nerve enters the posterior chamber, of the calcaneal tunnel which is the
distal continuation of the tarsal tunnel deep to abductor hallucis. The anterior and posterior
canals are separated by a fibrous septum coursing from the deep sutface of abductor
hallucis to the medial wall of the body of the calcaneus plantar to the sustentaculum tali.
PlANTAR NERVE SUPPLY
Medial Plantar Nerve(Fig. 1.18)

The medial plantar nerve is usually slightly larger than the lateral plantar nerve, and
traverses the 3rd canal of-the flexor retinaculum along with the medial plantar vessels. The
medial plantar nerve yields cutaneous branches innervating the medial aspect of sole;
muscular branches that supply FOB, FHB, abductor hallucis and the 1st lumbrical; the
proper digital branch to the plantar-medial aspect ofthe hallux; and three common digital
nerves that yield proper digital nerves to the contiguous surfaces of the 1st and 2nd, 2nd and
3rd, and 3rd and 4th toes. The 1st common or 2nd proper digital nerve yields a branch to
innervate the 1st lumbrical muscle. The 3rd common or 4th proper digital nerve yields a
branch that communicates with the lateral plantar nerve, and is often the site of Morton's
neuroma. The proper digital nerves supplythe digital pulp, and the tips and sides ofthe toe,
including the nail matrix.
The lateral Plantar Nerve

The lateral plantar nerve courses through the porta pedis deep to the plantar fascia, and
yields muscular branches to quadratus plantae and abductor digiti minimi; cutaneous
branches to the lateral aspect of the sole; a superficial branch that divides into common and
proper digital branches, and a deep branch. The proper digital branch supplies the lateral
aspect of the 5th toe; and the flexor digiti minimi brevis as well as the 3rd plantar and 4th
dorsa liD muscles. The common digital branch usually communicates with the digital branch
of the medial plantar nerve (often the site of Morton's neuromaL before dividing into proper
digital branches to the contiguous surfaces of the 4th and 5th toes. The deep branch of
the lateral plantar nerve supplies all of the 10 muscles except the 4th dorsal and 3rd
plantar in the 4th intermetatarsal space, all of the lumbricales except the 1st lumbrical, and
adductor hallucis.
Saphenous Nerve
The saphenous nerve is the terminal continuation of the femoral nerve, and courses through
the thigh to emerge from the adductor canal to become subcutaneous and continue distally
along the anteromedial aspect of the leg and foot It yields a branch to the skin over the
ankle, and a branch that courses distally to innervate the medial aspect of the tarsus and
greattoe.
ANGIOLOGY
ARTERIAL SYSTEM
The arterial supply to the lower extremities originates with the abdominal aorta, which
bifurcates into right and left common iliac arteries, which then further divides to form internal
and external iliac arteries. The external iliac artery becomes the femoral artery at the
distal margin of the inguinal ligament. The femoral artery is palpable in the groin, and
courses distally through the thigh to become the popliteal artery, which is palpable in the
popliteal fossa. The popliteal artery yields muscular, cutaneous, and articular (knee)
branches. The popliteal artery bifurcates to form the anterior and posterior tibial arteries at
the lower border of popliteus.
The anterior tibial artery courses through the crural 10 membrane to enter the
anterior compartment of the leg where it descends to the ankle, where it becomes the
dorsalis pedis artery. The anterior tibial artery courses between TA and EDLin the superior
third of the leg, between TA and EHL in the middle third, deep to the tendon of EHL just
proximal to the ankle and between the tendons of EHL and EDL atthe level of the ankle. The
branches of the anterior tibial artery include:
1. Posterior recurrent tibial artery, posterior to 10 membrane
2. Anterior recurrent tibial artery, which joins the circumpatellar network
3. Muscular branches to TA, EDL, EHL, and peroneus tertius
4. Anterior medial malleolar artery
5. Anterior lateral malleolar artery
The anterior leg muscles are supplied by muscular branches of the anterior tibial
artery. The anterior medial malleolar artery anastomoses with branches of the posterior
tibial and medial plantar arteries. The anterior lateral malleolar artery anastomoses with
the perforating branch of the peroneal and lateral tarsal arteries.
The dorsalis pedis artery, the second largest source supplying the foot, continues to
the 1st intermetatarsa1 space, where it courses as the deep plantar branch to join the plan-
tar arch IFig. 1.19). The branches of the dorsalis pedis artery include:
1. lateral tarsal artery; supplying EDB
2. medial tarsal artery
3. arcuate artery; yielding the 2nd, 3rd, and 4th dorsal metatarsal arteries
4. 1st dorsal metatarsal artery
5. deep plantar perforating branch
The dorsal metatarsal arteries lie in the corresponding intermetatarsal spaces, deep
to the extensor tendons and dorsal to the dorsal 10 muscles. Except the first dorsal
metatarsal artery, which yields the deep plantar perforating artery, the metatarsal arteries
yield posterior and anterior perforating branches at the Ieve! of the metatarsal base and
MTPJ, respectively. The arteries continue distally as common digital arteries, which divide
into proper dorsal digital arteries that are of smaller diameterthan the plantar digital arteries.
The posterior tibial artery, the largest source supplying the foot, is a terminal branch
of the popliteal artery and courses through the leg to the third canal of the flexor
retinaculum, then divides into medial and lateral plantar arteries deep to abductor hallucis
in the calcaneal canals IFig. 1.20). The branches ofthe posterior tibial artery include:
1. circumflex fibular artery, which supplies soleus
2. peroneal artery, which supplies soleus, TP, FHL, PL, PB, and the fibula; and the
perforating peroneal branch !third largest source supplying the foot) that pierces the
10 membrane proximal to the ankle to join with branches of the anterior tibial artery
3. nutrient artery to tibia, the largest nutrient artery in the body
4. muscular branches to soleus, TP, FHL, FDL
5. communicating artery that anastomoses with peroneal artery
6. medial malleolar branches
7. medial calcanean branches, which supply tendoAchillis and medial heel
8. medial plantar artery, medial to the medial plantar nerve
9. lateral plantar artery, which becomes the plantar arch and supplies all of the
muscles of the sole, except abductor hallucis, FOB, and 1st dorsaiiO muscle.
The plantar arch courses lateral to medial toward the first intermetatarsal space,
where it anastomoses with the deep plantar perforating branch of the dorsalis pedis
artery. The plantar arch separates the 3rd and 4th muscle layers, and yields anterior and
posterior perforating arteries that anastomoses with corresponding perforators from the
dorsum. The plantar arch yields 4 plantar metatarsal arteries, the first of which consists of
the union ofthe lateral plantar and deep plantar branches. The plantar metatarsal arteries
become common and then proper digital arteries to the corresponding toes. The plantar
digital arteries are larger than the dorsal digital arteries. In the hallux, the lateral plantar
digital artery is the largest, while in the lesser toes the medial plantar digital arteries are
largest In the hallux, the dorsal digital arteries extend to the toe tip, as do the plantar
digital arteries, the dorsal and plantar hallucial digital arteries supplying the hallux equally
distal to the interphalangeal joint In the lesser toes, dorsal digital arteries extend to the
level of the proximal ITPJ, while plantar digital arteries extend to the toe tip and then
retrograde to supply the dorsal aspect of the toe, including the nail bed (Fig. 1.21).
Proper dorsal
I
Lateral tarsal artery

artery
F"Latecall calcaneal
arteries
arteries
Figure 1.19
Figure 1.20
Proximal
nail fold
Lateral digital
artery Distal and
proximal arches
Figure 1.21
VENOUS SYSTEM
The dorsal venous system of the foot and ankle consists of superficial and deep networks.
The deep dorsal venous plexus converges to form the medial marginal vein. The superficial
dorsal venous plexus is immediately subcutaneous, and contains the dorsal venous arch.
The dorsal veins drain into the greater and lesser saphenous veins. On the plantar aspect,
a superficial venous plexus drains into the deep venous plexus, which ultimately converges
into the medial and lateral plantar veins, and communicates with the dorsal system via
perforating veins.
lYMPHATIC SYSTEM
Superficial lymphatics drain the skin of the toes, sole and heel, forming a medial system
that drains into the inguinal lymph nodes and a lateral (rays 3-5) system that drains into the
popliteal lymph nodes. The deep lymphatic system forms collecting ducts located dorsally,
laterally (peroneal), and plantarly, and drain into major lymphatics corresponding to the
adjacent anterior tibial, peroneal, and posterior tibia! vessels. The deep system drains
primarily into the popliteal lymph nodes.
CUTANEOUS ANATOMY
The skin consists of the epidermis and dermis (Fig. 1.22). The dermis consists of both
reticular and papillary layers, and contains microcirculatory elements (arterioles,
capillaries, venues, glom, and lymphatics), nerves and the annexed. Skin annexed include
echini sweat glands and ducts, hair follicles and arrestor pile muscles, sebaceous glands
at the base of the hair follicle (pilosebaceous gland), and the toenails and perionychium.
Near the nail bed, arterioles shuntdirectlyto venules via the Hoyer-Susquet canal, to effect
the glomus body important in temperature regulation. Eccrine glands are present on all
pedal skin surfaces, and are innervated by sympathetic nerves. Pilosebaceous glands are
only present on dorsal skin. Deep in the dermis, near the subcutaneous fat-superficial
fascia junction, lie the Pacinian (Pacini-Vater) corpuscles important in touch-pressure
sensation. The epidermis serves as a barrier, and contains five strata: basale, spinosum,
granulosum, lucid urn, and corneum. Melanocytes with dendritic processes exist amongst
the living cells of the stratum basale, and are responsible for melanin production
which serves to protect underlying living cells from the mutagenic effects of UV radiation.
langerhans immune cells, much like macrophages, as well as Merkel's sensory cells also
exist in the epidermis.
Relaxed Skin Tension lines (RSTl) (Fig. 1.23)

The skin's intrinsic tension is oriented such that maximum tension is directed parallel to the
long axis of the extremity. Intrinsic skin tension is generated by the forces of underlying
bone and soft tissue prominence, as well as joint motion and extrinsic forces upon the skin.
RSTLare oriented perpendicular to the long axis of the leg and foot, and can be clinically
identified with the pinch test As a rule, elective skin incisions should be made parallel to the
RSTL, as long as the exposure allows access to the underlying target structures and does
not unduly violate vital structures (vessel, nerve, tendon).
Epidermis
Papillary
layer granulosum
1:5''?.'1~'f);j";fi'i1f--St<-spinosum
IK.'P.Cf0 :l'9""!!l-- Str. bas ale
Subcutaneous
connective
tissue
Figure 1.22
j
___ _(
Plantar
Medial
Figure 1.23
22 Basic Pathophysiology Ch. 2
BASIC PATHOPHYSIOLOGY
WOUNDS ANIJ HEALING
This section will describe wounds and healing of a variety of tissues, including skin, bone,
cartilage, tendon, ligament joint capsule, and nerve. Wound healing relies upon an
adequate vascular supply and angiogenesis. Angiogenesis entails endothelial proliferation
with resultant capillary budding.
SKIN WOUNDS AND HEALING
Healing Phases
Dermal wounds include Punctures, Abrasions, Incisions, and Lacerations (PAIL); as well
as contusions, pressure injuries, mechanically or chemically induced and hypersensitivity
related bullae, burns and frostbite. The epidermis repairs by means of epithelial cell
mitosis that continues until contact inhibition occurs. The underlying dermis heals in three
phases: inflammatory, fibroproliferative, and maturation.
Inflammatory Phase
The inflammatory (substrate or lag) phase begins immediately upon wounding, comprises
approximately 10% of the healing process, and is also referred to as the substrate, or lag
phase because specialized blood cells and proteins necessary for healing are recruited
and migrate to the wound at this time. After initial vasoconstriction, usually lasting several
minutes, vasodilatation and erythema predominate during the inflammatory phase, which
lasts for 3 or 4 days. Angiogenesis and capillary budding occur while fibroblasts lay down
collagen in a random fashion, and tensile strength begins to return to the damaged skin.
Superficially, epidermal epithelialization occurs concomitantly with dermal inflammation,
and mitosis continues until contact inhibition occurs between epithelial cells, which
ultimately seal the wound surface.
Fibroproliferative Phase
The fibroproliferative (fibroblastic) phase comprises approximately 20% of the healing
process, and lasts from the 3rd to 4th day, until the 14 to 21 day. Granulation tissue, which
consists of new collagen and capillary buds, predominates and continues to form until the
wound contracts and epithelialization is complete. Collagenation rapidly increases during
this phase, and fibroblasts are the primary cell type present in the wound. The tensile
strength of the wound approaches only about 35% of the local skin's original strength after
14 days and, at this point, the wound's main source of tensile strength comes from suture
material used for primary closure.
Maturation Phase
The maturation (remodeling) phase comprises approximately 70% of the healing process
and lasts from approximately 3 weeks until one year post injury. During this phase,
randomly arranged collagen fibers that were laid down during the fibroproliferative phase
are microscopically debrided via macrophage enzymatic breakdown. New fibers are
produced and aligned in response to mechanical forces, and wound contraction occurs in
a centripetal direction (toward the center of the wound). Linear scar contraction occurs
Ch. 2 Basic Pathophysiology 23
from both ends of the scar toward the center. This is important when planning an elective
skin incision. The long axis of the anticipated scar should be oriented parallel to the axis of
motion of the underlying joint. A scar that is perpendicular to the joint axis may cause a joint
contracture due to scar contraction, often seen with a posterior longitudinal ankle or a
dorsal longitudinal MTP joint incision.
Skin Ulcers
Dermal wounds that develop secondary to pressure, (typically chronic, non- traumatic
weight-bearing or decubitus pressure), can result in ulceration. Technically, skin
ulceration is defined as an open wound where the full thickness of skin is violated.
The International Association for Enterostomal Therapy

(classifies pressure-induced cutaneous compromise)
Stage 1: Epidermis intact, however erythema remains longer than 30 minutes after
pressure relieved. Reversible with intervention.
Stage II: Partial thickness skin loss, including epidermis and perhaps superficial
dermis. There is surrounding induration, and local bullae or vesicles with erythema,
tenderness (if not insensitive), and the base of wound is moist and necrosis free.
Stage Ill: Full-thickness skin loss, through the dermis into subcutaneous fat and
superficial fascia, effecting a crater. Necrotic eschar filling the crater and covering
the base must be debrided in order to accurately stage the depth and properly
categorize the wound. The central wound base is generally nontender. There is often
undermining of the margin, sinus tract formation, local exudate, and a surrounding
halo of erythema. Ascending cellulitis and infection may also be present Underlying
osteomyelitis or, in the presence of an ischemic limb, subcutaneous gas or
necrotizing infection should also be ruled out
Stage IV: Deep crater with penetration through deep (muscle) fascia, with associated
involvement of musc!e, joint and/or bone. Again, the wound base is usually nontender.
Possible associated dissecting abscess, necrotizing infection, and osteomyelitis must
be ruled out
Wagner Classification of Neurotrophic Ulceration

(categorizes diabetic and neuropathic ulcers)
Grade 0: Skin intact, osseous deformity present, at risk.

Grade 1: Localized superficial ulcer.
Grade II: Deep ulcer extending to tendon, joint and bone.
Grade Ill: Deep abscess with osteomyelltis.
Grade IV: Gangrene of toes or forefoot.
Grade V: Gangrene of foot extending from forefoot to proximal to midfoot.
Keloids and Hypertrophic Scars

Keloids are reactive fibrous proliferations that develop at sites of cutaneous injury. They
occur more commonly in black individuals and the predilection is hereditary. Fibrous
proliferation extends beyond the area ofthe original skin injury and can be debilitating. The
lesion is thought to develop due to irregular wound granulation associated with abnormal
capillary endothelium, and the presence of excessive myofibroblasts. Excessive
col!agenation and decreased collagenase activity may also contribute to fibrous
proliferation. Hypertrophic scars are similar to keloids, however they remain within the area
of the original injury and tend to reduce in size over time. lntralesional injection of
glucocorticosteroid and surface compression, preferably with elasticized silicone polymer,
may reduce keloids and hypertrophic scars. Peptic ulcer, fibromatosis, and enostosis may
be present. Elective surgery should be considered cautiously in patients with a history of
hypertrophic scar or keloid formation.
Morphea and Systemic Sclerosis

Morphea is represented by one or more hardened, linear, plaques of atrophic skin.lt can
be idiopathic or posHraumatic and develops with an initial purple or pink margin. Morphea
responds to intralesional steroids. Systemic sclerosis (formerly Scleroderma) affects
cutaneous as well as multi~organ connective tissue hardening. In the skin, typically in the
extremities, there is sclerosis, stiffening of small joints, Raynaud's phenomenon, ulceration
and calcinosis (calcinosis cutis). Other findings include esophageal, Gl tract, pulmonary,
cardiac, and renal sclerosis.
BONE HEALING
Fractures
Fractures are described according to their location and orientation within the specific bone.
Incomplete fractures, wherein a portion of the bone's cortex remains intact are termed green
stick fractures, and generally develop secondary to flexural deformation of a long bone.
Similarly, a stress fracture results in bending without overt radiographic fragment separation.
A bone scan can be useful if diagnosis is in question. Incomplete fractures are diagnosed
primarily by clinical examination, and with subsequent radiographic evidence of secondary
bone callus. Complete fractures can be transverse, oblique, spiral, and comminuted, with
fracture stability and management varying with the fracture pattern. Fracture stability, in
descending order, is as follows:
Transverse> Oblique> Spiral> Comminuted

Ch.2 Basic Pathophysiology 25
Transverse and oblique fractures can be closed-reduced and immobilized, whereas

spiral and comminuted patterns are extremely difficult to adequately reduce and maintain
in a closed fashion. When a fracture violates a joint surface, open reduction and
stabilization is most often the besttreatmentoption. Growth plate injuries and open fractures
also deserve special consideration. Fracture repair is initiated with closed reduction and
immobilization.
Charnley's sequence of closed reduction is as follows: 1st) increase the
deformity, 2nd) distract, 3rd) reverse the deformity and realign, and 4th) maintain
correction with Immobilization.
Callus !Secondary) Bone Healing

Bone heals via either callus bone healing or primary bone healing, and requires an intact
vascular supply. Callus bone healing, which may also be referred to as secondary
bone healing, occurs in six phases: hematoma formation, hematoma organization,
fibrocartilaginous callus, primary bone callus, primary bone callus absorption, and
remodeling (maturation). The hematoma phase lasts 1to 3 days, and consists of hematoma
formation between fracture fragments. Hematoma organization lasts from 3to 10 days, and
entails inflammation with recruitment of osteoclasts and osteoblasts. The fibrocartilaginous
callus phase lasts from 10 days to 6 weeks, depending upon the degree of immobilization
and fragment stability; and consists of osteoclastic phagocytosis of necrotic bone,
chondroblastic and osteoblastic differentiation into cartilage (low oxygen tension) or bone
(high oxygen tension), and neovascularization derived primarily from endosteal, and to a
lesser degree periosteal, blood vessels. Fracture instability leads to progressive irritation
!fibrocartilaginous) callus formation, and delays the development of bone. The primary bone
callus phase lasts from 6 to 10 weeks, and includes condensation of the fibrocartilaginous
callus into bone that bridges the fracture interface. Primary bone callus absorption lasts
from 2.5 to 4 months, and includes new bone remodeling into secondary bone callus. The
remodeling, or maturation phase entails alteration of bone in response to applied forces in
accordance with Wolff's law, and continues from about 4 months post~injury.
Primary Bone Healing

Primary bone healing requires fracture reduction, rigid stabilization, and preservation
of fragment vascularity. When bone fragments are reduced and rigidly stabilized, the
fibrocartilaginous callus phase can be by-passed and new bone formation and remodeling
occur simultaneously via Haversian remodeling. Primary bone healing can occur via either
contact or gap healing. Contact healing involves stabilization of bone~to~ bone contact,
while gap healing involves stabilization of the fragments with maintenance of a small (up to
2mm) gap between the bone ends. Stabilization is enhanced by compression, which
increases friction between bone fragments and promotes rigidity. Fracture stability can be
achieved in a variety of ways (see Internal and External Fixation of Bone).
Haversian remodeling is the underlying process of normal bone healing. When
fracture fragments are reduced and stabilized, capillary budding from Haversian canals
occurs at points of contact and bridges the fracture interface by means of the cutting cone;
which consists of a leading tip of osteoclasts that phagocytose osteoid, a central capillary
emanating from the Haversian canal, and osteoblasts that are organized about capillary
margins and lay down lamellar new bone.
Avascular Necrosis
There are many causes of bone necrosis including trauma (accidental and surgical), steroid
therapy, occlusive vascular disease, venous thrombosis, collagen vascular disease
\rheumatoid, arteritis), status~post renal transplant, sickle~cell anemia, pancreatitis and
chronic alcohol abuse, radiation therapy, hyperuricemia and gout, hyperlipidemia,
barotrauma (Caisson's diseaselr osteoporosis and osteomalacia. The process involves
acute ischemia of bone, necrosis, then revascularization and new bone formation. Bone
scans, if used early and with fine localization, may show a cold spot due to ischemia.
Generally, however, bone scans are hot, which is consistent with new bone accretion
associated with healing. An MRl can be useful in establishing the diagnosis of AVN.
Radiographic Classification of AVN ofthe First Metatarsal Head (or Head of the Femur)
Stage 1: Pre-collapse
Early normal density, localized cold bone scan
Intermediate relative sclerosis of dead bone, due to surrounding
hyperemia and disuse osteoporosis
Late: true sclerosis due to new bone accretion,
hot bone scan
Stage II: Collapse
Early: mild step defect, loss of articular sphericity
late: fragmentation of articular surface and metaphysis
Stage Ill: Arthritis

Early: joint space narrowing, subchondral cysts and
sclerosis, osteophytosis
Late: sclerosis, ankylosis, articular erosion
Clinical Signs and Symptoms of AVN
Stage I : usually asymptomatic, or perhaps minimal pain and stiffness

Stage 11: usually significant pain and stiffness, occasionally asymptomatic
Stage Ill: pain and stiffness are most typical
The differential diagnosis of AVN includes arthrosis, RSOS, and infection. The ESR is
usually not elevated due to AVN and RSOS. The medical treatment of AVN consists of
protective or non-weight bearing, electrical bone growth stimulation, vasodilators, NSAIDs
to inhibit platelet aggregation, and avoidance of steroids. Surgical treatment of AVN
includes debridement of necrotic bone or core decompression and replacement with
autogenous bone graft, revascularization with a pedicle muscle graft, and resection with
endoprosthesis or arthrodesis. Rates of AVN of the first metatarsal head following distal
first metatarsal osteotomy have been reported to range from less than 1% to greater than
40%. Steps for the prevention of AVN include preservation of periosteal and capsular
attachments, accurate hemostasis, avoidance of immediately subchondral osteotomies, rigid
stabilization of metaphyseal osteotomies, protective or non-weight bearing, use of sharp
blades and osteotomes, and routine serial radiographs following osteotomy or fracture.
Delayed Union, Nonunion and Pseudoarthrosis

Following fracture, excessive motion and/or inadequate vascularity can lead to formation
of hypertrophic irritation callus, malunion, delayed union, nonunion, or pseudoarthrosis.
Conditions such as Puget's disease, osteitis fibrosa cystic a, rickets, hyperparathyroidism,
osteomalacia and osteoporosis, and debilitated or compromised host (immuno~
compromised, antimetabolite or steroid therapy, anemia, anticoagulation therapy, elderly
patient, chronic cigarette smoker) can also impede bone healing. The presence of irritation
callus rules out primary bone healing, and indicates instability between fragments.
Delayed union simply means the fracture has not healed within a reasonable period, and
can be identified radiographically by the presence of unchanged irritation callus and
persistence of a fracture cleft Causes of delayed union, and ultimately nonunion, include
inadequate fracture reduction and/or immobilization, overly-aggressive soft tissue
iperiosteal) stripping or injury, osteomyelitis, and local vascular compromise. Delayed unions
and non unions are determined primarily via serial radiographic inspection, combined with
clinical evidence of persistent edema and pain. Depending upon clinical needs and
indicators, a delayed union is treated with continued immobilization and non-weight
bearing, revisional surgery for callus channelization or bone grafting or re-fixation (internal
and external), and employment of electrical bone growth stimulation IEBGS).
A nonunion is classically defined as failure to achieve stable fracture healing after 8 to 9

months of management. It is not necessary to wait 8 or 9 months before intervening
surgically, either revisional or as an initial operation, when treating a delayed union,
however appropriate non-surgical intervention should be applied before deciding to go to
the operating room.
Non unions are classified as either atrophic or hypertrophic. The atrophic nonunion, also
termed non-reactive, displays radiographic evidence of bone ends rounding off and the
absence of bone callus. Atrophic nonunions are classified as comminuted, with multiple
fragments and gapping; torsion wedge, where a necrotic butterfly fragment impedes
healing; and simply atrophic, where the ends are wasted or markedly rounded. Devitalized
and/or septic bone requires surgical excision and often bone grafting for repair: Hypertrophic
nonunions display radiographic evidence of the bone ends flaring or mushrooming; and
are classified as elephant foot, where there is maximum widening at the interface; horse
hoof, where there is moderate callus flaring; and oligotrophic, where there is minimal
reactive callus.
A pseudoarthrosis is a nonunion with a fibrocartilaginous interface between the fracture

fragments. An articular fracture nonunion may develop into a synovial pseudoarthrosis.
A pseudoarthrosis can also be classified as infected, previously infected or non-infected;
as well as metaphyseal or diaphyseal. A bone scan or MRI can be useful in confirming
vascularity at the delayed or nonunion site. Diffuse increased uptake of radionuclide is seen
at the hypertrophic nonunion, and may display a biphasic pattern if elephant foot or horse
hoof hypertrophy are present. An lndium-1111abeled white-blood cell scan can also be
useful in the evaluation of suspected infected pseudoarthrosis or nonunion. If the fracture
cleft is large enough, or in the presence of a large-enough synovial pseudoarthrosis, a bone
scan may reveal a cold cleft. Otherwise, bone scans are not of much use in distinguishing
between delayed and nonunions. CT scans, linear tomography, MRI, stress fluoroscopy,
and intramedullary venography, can also be used to evaluate a delayed or nonunion of
bone. In regard to noninvasive measures, overall, MRI provides the most diagnostic and
anatomical information regarding a suspected nonunion or pseudoarthrosis. ACT scan is
particularly valuable when trying to identify intervening fracture fragments.
Treatment of a hypertrophic nonunion involves immobilization and non~weight bearing, bone

growth stimulation (BGS), and continued monitoring. The decision may also be made to
operate. An atrophic nonunion, or an infected or synovial pseudoarthrosis, requires
operative intervention for resection of necrotic or problematic tissue, bone grafting or
reapproximation of bone, followed by application of BGS and immobilization and non-weight
bearing. BGS is ineffective in the treatment of pseudoarthrosis, or, if the gap between
fragments is greater than 1/2 the diameter of the bone.
Bone Growth Stimulation (BGS)

Electrical bone growth stimulation (EBGS) and low-intesity ultrasound (LIUS) bone
growth stimulation can be used in the treatment of nonunion, failed fusion, congenital
pseudoarthrosis, and fresh fractures (see package insertforthe specific device, for precise
FDA-approved indications and contraindications). EBGS and UUS are not effective in the
presence of acquired synovial or infected pseudoarthroses, when the gap between bone
margins is greater than 1/2 the diameter ofthe bone, or when sepsis is advanced. BGS is
contraindicated in the presence of neoplastic bone disease. A "hot" bone scan or MRI
should be observed prior to use of BGS. BGS is founded on the fact that areas of bone
growth and fracture healing display electronegativity due to stress-generated (piezoelec-
tric) polarity in collagen. In the presence of electronegativity, low-intesity ultrasound,
and strain-generated potentials, bone forming growth factors are upregulated and new
bone formation induced. BGS can be achieved using any of a number of effective devices
(Table 2.1).
Table 2.1_ OPTIONS FOR STIMULATED OSTEOGENESIS
TYPE METHOD USE DEVICE

Invasive Direct current (20 uA) 24n* EBI OsteoGen
Noninvasive Pulse electroinagnetic 3-10 hrs/ EBI Bone Healing
fields IPEMF) (mV) day System, Orthofix
PhysioStimLite
Combined PEMF (mV) 30 min/day Don Joy Orthologic
Capacitative coupling 24n* EBI OrthoPak
19 volt dry cell,
skin patch electrodes)
Low energy ultrasound 20 min/day Smith &
(30 milliwatts/cm2) Nephew Exogen
* 24n = 24 hours/day, 7 days/week, or until power source is exhausted.
The precise method of BGS to be used is determined based on the surgeon's

experience and the patient's needs and abilityto properly use the device. The devices vary
in regard to size, weight, application, precision with which the energy is directed at the
target bone, and ease of use. Despite technical differences between the individual
stimulators, all of the devices have been clinically proven to work.
In regard to the surgically implantable direct current device, issues of compliance are
obviated by the fact that the stimulator, along with the hermetically sealed power supply,
stimulate bone growth constantly until the battery is exhausted 124-36 months).
Furthermore, with the implantable stimulator, cathode configuration can be varied
according to the specifics ofthe anatomical site, and the cathode and lead wire should not
contact any hardware used to stabilize the healing bone. The implantable EBGS requires
subsequent surgical retrieval of the power pack and lead wire.
In regard to the capacitative"coupled device, 2 electrodes are affixed (adhesive
patches like EKG leads) to the skin surface on either side of the nonunion, which may
require windowing the cast or using an external fixator to enable access to the target site.
The device runs constantly, as long as the batteries !supplied by EBI) are changed daily. Like
the capacitative-coupled EBGS, L!US requires access to the skin surface so that
u[traqsound gel can be applied driectly over the target bone, and this may warrant
windowing the cast or using an external fixator. PEMF devices only need to be secured in
close proximity to the target bone, and they induce electrical current in the bone by means
of a surrounding magnetice field. These devices can be worn outside of a bandage, cast or
immobilizing splint
CARTILAGE HEALING
Hyaline cartilage consists of chondrocytes within a glycosaminoglycan matrix, along with
type II collagen fibers. Fibrocartilage contains type I collagen. Cartilage does not have a
direct blood supply, however it requires synovial fluid for nutrition on its superficial
(articular) surface. Cartilage is viscoelastic due to canals through which synovial fluid flows,
allowing deformation in response to compression and shearing loads. Cartilage wounds
can be partial or full-thickness, and can be difficult to heal. Following articular fracture or
cartilage injury, necrotic cartilage is phagocytosed by macrophages arriving at the wound
via inflammation. Healing thereafter occurs by means of limited chondrocyte mitosis and,
for the most part, metaplasia of mesenchymal stem cells into fibrocartilage or near-hyaline
cartilage. Ideal joint repair increases the likelihood of hyaline-like Imore type II collagen)
cartilage repair. Undifferentiated stem cells arrive at the cartilage defect via disruption
of the subchondral cortical bone plate, whether via fracture or by means of surgical
perforation, from medullary sinusoids of adjacent epiphyseal and metaphyseal bone.
Healing requires restoration of joint capsule and ligaments, perforation and realignment of
the subchondral bone plate for support and vascularity, and motion under reduced pressure
(non-weight bearing motion). Partial thickness wounds require sculpting (saucerization) of
any jagged or elevated cartilage margins, and perforation of the subchondral plate. Necrotic
fragments should be excised.
TENDON, LIGAMENT AND JOINT CAPSULE HEALING

Tendon, ligament, and joint capsule heal by means of lag (substrate), fibroproliferative, and
maturation phases. The lag phase occurs during the first two weeks; is enhanced by
immobilization; and entails inflammation and fibroblastic splinting, with the majority of tissue
strength due to sutures. Fibroplasia and vascularization increase during the 2nd week,
30 Basic Pathophysiology Ch.2
and strength exists primarily due to sutures and immobilization is still required. The fibre pro-
liferative icollagenation) phase occurs during week 3, and consists of a marked increase in
fibroplasia. At this time, moderate collage nation strength can sustain gentle passive motion
or isometric (in cast or brace) exercises. The remodeling {maturation) phase begins after 4
weeks, with collagen realignment and remodeling yielding moderate (not full) strength.
Gradual, progressive strengthening occurs with subsequent passive and active exercises.
PERIPHERAL NERVE WOUNDS AND HEALING

Peripheral nerves respond to injury with inflammation, collagenation, and Wallerian
degeneration. Fibroblasts within the connective tissue sheaths respond to inflammation
with increased collagenation.
Seddon's Classification of Nerve Injury

Neuropraxia-the myelin sheath is disrupted by blunt trauma or compression, causing
physiologic blockade of saltatory conduction. Thickly myelinated, large diameter, rapidly
conducting nerve fibers are most susceptible. A differential paralysis can develop, wherein
deep tendon reflexes, skeletal muscle function, vibratory and two-point discrimination are
lost, while pain and temperature sensation, and autonomic function persist. Repair can take
days to months, and is usually perfect as the nerve sheaths and axons remain intact, and
only the myelin must regenerate.
Axonotmesis-involves disruption of axons, with maintenance of supporting connective

tissue sheaths. Causes include prolonged compression, traction, ischemia, and toxins.
Wallerian degeneration occurs with distal axon degradation via phagocytic Schwann cells,
while the proximal portion of the axon and nerve cell body convert from the production of
neurotransmitter to making macromolecules for axon regeneration. Axon.otmesis affects
heavily myelinated fibers equally as well as unmyelinated fibers. Nerve fiber regeneration
occurs at the rate of 1 mm per day from the point of injury. Because the endoneural
scaffold and supportive sheaths remain intact, the budding neurite (new axon) can grow
down its corresponding distal endoneural tube, en route to the nerve's end organ.
Functional recovery is generally good, but diminishes as the distance from the point of
injury to the end organ increases. The more proximal the lesion, the less likely it is that
normal function will return. An injury at the sciatic level is less likely to fully regenerate
compared to injury of the posterior tibial nerve at the level of the ankle. Proximal lesions
affect a wider distribution and convey a worse prognosis.
1\feurotmesis-involves disruption of nerve fibers as well as the supportive connective

tissue sheaths of the nerve trunk, and is therefore the most devastating form of injury.
Causes include sectioning injuries such as laceration, gunshot wound, open fracture,
severe traction or avulsion, punctures, and injection oftoxin. Because the di~al endoneura!
tubes are disrupted, it is difficult or impossible for budding neurites to bridge the defect and
grow into corresponding endoneural tubes and properly innervate end organs. Confused
reinnervation is often the case, as neurites that do manage to bridge the defect grow into
endoneural tubes that previously corresponded to other nerve fibers. Even with surgical
intervention to resect necrotic tissue and fibrosis, and to realign fasciculi, regeneration is
imperfect at best and almost impossible without surgical repair. For this reason, nerve-
suturing techniques are essentiaL Nerve fiber regeneration occurs at 1 mm per day, and
axon exhaustion can occur with far proximal lesions. In the case of nerve excision, such as
Ch.2 Basic Pathophysiology 31
in the treatment of Morton's neuroma, the distal segment of the nerve trunk is excised and
budding neurites have no chance of achieving reinnervation. A stump neuroma will always
form at the point where the nerve is sectioned, and can be minimized with epineuroplasty
(closure of the epineurial cuff).
Entrapment Neuropathy
Nerve entrapment involves impingement of a peripheral nerve trunk by neighboring
anatomic structures, typically where the nerve traverses a fibro-osseous tunnel. Classical
impingement sites include the posterior tibia! nerve and its branches in the tarsal and
calcaneal tunnels and the plantar common and proper digital nerves in the intermetatarsal
spaces {Morton's neuroma). Injury takes the form primarily of neuropraxia and, in severe
cases, axonotmesis. Prolonged entrapment leads to the development of a neuroma-in-
continuity. Inflammation of surrounding connective tissues can lead to perineural fibrosis.
Signs and symptoms include Tinel's sign, which is pain and paresthesia within the entrapped
nerve's distribution upon percussion or palpation of the nerve trunk at the point of
entrapment. Percussion or palpation of the entrapped nerve may also effect proximal
radiation of paresthesia along the nerves course (Val!eix sign). Generally, sensory
abnormalities occur before autonomic (sudomotor, vascular smooth muscle, arrector
pili) dysfunction, and skeletal motor dysfunction is usually lastto occur. Electroneuro-
diagnostic testing may show decreased nerve conduction velocity and electromyographic
evidence of fibrillation due to entrapment. It is important to note that electrical testing may
be normal despite functional entrapment with a great deal of symptomatology when the
patient is weight bearing or active. Differential diagnoses include radiculopathy, metabolic
or hereditary polyneuropathy, compartment syndrome, musculoskeletal pathology, and
complex regional pain syndrome (causalgia and RSDS).
Treatment includes protection of the nerve from external forces, anti-inflammatory

medication administered systemically as well as local corticosteroid infiltration about
the nerve trunk, ultrasound therapy, other pharmacological therapy, and surgical
decompression when non-surgical measures have failed to satisfactorily alleviate pain.
Pharmacological approaches are variable, and include:
CapsaiciiJ-topical, to diminish substance Pat C-type fiber terminals

Tricyclic antidepressants-oral, effect selective neurotransmitter blockade; watch
for anticholinergic effects such as dry mucus membranes, insomnia, palpitation,
lightheadedness, and cephalgia; available as: amitriptyline, imipramine, dsipramine,
nortriptyline, paroxetine, and trazodone
Anticonvulsants-oral, effect selective neurotransmitter blockade; with side effects
similar to those noted for tricyclics; available as: carbamazepine, diphenylhydantoin,
gabapentin, pregabalin, and cymbalta
Local anesthetics----such as mexiletine \oral administration) and lidocaine (IV
administration or via transcutaneous patch application)
Adrenergic agonists-such as clonidine transdermal patch
Aldose reductase inhibitors-these can be particularly useful for diabetic
neuropathy, and include: sorbinil, tolrestat, epalrestat
Other agents-including prostaglandin E1, and B-complexvitamins
The mainstay of surgical treatment involves external neurolysis, with subsequent nerve
repositioning or excision. Nerve ensheathing in silicone, or capping, is of questionable
benefit and usually effects symptoms of entrapment. External neurolysis alone is often
adequate for symptomatic relief, and is periormed using Ioupe magnification and fine-tipped
instruments. Specific entrapment neuropathies of the lower extremity include: saphenous
nerve where it emerges through the adductor canal, common peroneal nerve nearthe head
of the fibula {Fig. 2.1) {Maisonneuve fracture, constricting BK cast, lateral decubitus
position, traction injury with associated ankle sprain); superficial peroneal nerve where it
emerges through deep fascia proximal to the ankle (compartment syndrome, athlete or
jumper with peroneal muscle herniation through deep fascial hiatus [Henry's hiatus] at
emergence of superficial peroneal nerve (Fig. 2.2) [Henry's mononeuritis]), deep peroneal
nerve deep to the transverse or cruciate crural ligaments (anteriortarsa! tunnel}, sural nerve
near the lateral malleolus (any ankle sprain, or surgical approach to the lateral aspect
of ankle or heel, tendoAchillis surgery). tibial nerve and its branches deep to the flexor
retinaculum {tarsal tunnel syndrome), and the plantar nerves plantar to the deep transverse
intermetatarsalllgaments !Morton's neuroma).
\I
I
Saphenous
nerve and
vein
peroneal
nerve

Ch.3 Selected Diseases and Pathological Conditions 33
SELECTED DISEASES AND PATHOLOGICAL COII.IDITIOI\IS

DERMATOSES AND SKIN PATHOLOGY
The skin forms a barrier to the outside environment, serving as a protective layer from UV
radiation (melanocytes, dendrites and melanin), thermal and mechanical trauma, and
microbiological inoculation. It also retains moisture, participates in the immune response,
and regulates temperature. The epidermis consists of the following five strata, (listed from
deep to superficial): st. basale (the basal layer), st. spinosum, st. granulosum, st. lucidum,
and st. corneum. Melanocytes located in the basal layer expand via dendritic processes
that contain melanin, which absorbs UV-B and thereby protects underlying living cells
from radiation-induced mutation. Merkel cells in the epidermis serve as sensory neuro-
transducers, and Langerhans cells of the epidermis participate in the immune response.
The dermis is composed ofthe papillary and reticular layers. The papillary dermis and basal
layer of the epidermis adhere along an undulating interface of rete ridges and valleys. The
papillary dermis conveys capillaries (responsible for the pin-point hemorrhages noted upon
debridement of a verruca) and nerve endings; while the reticular dermis contains the skin
adnexae, microcirculatory vessels, and nerves. Deep in the dermis, near the subcutaneous
layer, are also found Pacinian corpuscles {Vater-Pacini units) that participate in deep touch-
pressure sensation. The skin adnexae include: eccrine sweat glands; pilosebaceous units
consisting of sebaceous gland, hair and follicle, and the arrector pili muscle, all of which are
under autonomic control; and the nail unit consisting of matrix, bed, folds and plate. The
glomus body is srtuated atthe toe tip, partially between the nail bed and distal phalanx, and
consists of an arteriole-to-venule capillary bypass (Susquet-Hoyer shunt) that participates
in thermoregulation, and may become tumorous.
Primary Skin Lesions

Macule-flat, discolored, well circumscribed, up to 1 em diameter
Patch--larger or coalesced macules, > 1 em diameter
Papule-slightly elevated Idue to inflammatory dermal infiltrate). well circumscribed,
up to 1 em diameter
Plaque-larger or coalesced papules,< 2 em diameter
Nodule-well circumscribed, firm elevations,> 2 em but< 3 em diameter
Tumor--well circumscribed elevation> 3 em diameter
Vesicle-serous fluid-filled, elevated,< 1 em diameter
Bulle-serous fluid-filled, elevated,> 1 em diameter Imay be hemorrhagic)
Cyst-sterile intradermal mass of fluid or other material, contained within a defined
wall, such as a mucus, epidermoid inclusion, or sebaceous cyst
Burrow-intra-epidermal tunnel formed by scabies or other insect/parasite
Secondary Skin Lesions

Scale-thin, plate-like, cornified compact epithelial cells
Excoriation---superficial loss of skin
Erosion-gradual epidermal breakdown, sometimes referred to as a superficial ulcer
that heals without scarring
Ulcer-local excavation or surface defect created by sloughing of inflamed
necrotic skin
Crust-a scab, caused by surface drying of exudate or secretions
34 Selected Diseases and Pathological Conditions Ch. 3
Fissure-abnormal cleft or deep groove, usually hyperkeratotic superficially with an

open or hemorrhagic dermal wound deep in the recess
Scar-cicatrix, or the mark remaining after a dermal, or deeper, defect or other
morbid process has healed (hypertrophic, keloid)
Pustule--visible accumulation of pus within or beneath the epidermis, frequently in
an eccrine duct or hair follicle (pus is a liquid inflammatory product consisting of
leukocytes and serous transudate, along with bacterial and other proteins)
Abscess-a collection of pus in a cavrtyformed by disintegration of surrounding tissue
Furuncle-an accumulation of pus in the skin and succutaneous tissue, also known
as a boil; typically caused by Staph. entering through a follicle, associated with a
painful, nodular inflammation of skin with corium erythema and subcutaneous edema
Carbuncle--a cluster of boils (furunc!es) affecting skin, associated with subcutaneous
necrosis and multiple draining sinuses
Sinus tract-a cavity or channel connecting an abscess to the skin surface or
adjacent tissue layers (a fistula generally refers to a channel or tract connecting a
deeper organ to another organ or tissue layer, or the skin surface)
Hyperkeratoses (HPKs)
Non~mechanically induced diffuse keratoses are usually bilateral, symmetrical, plantar
and palmar, and often inherited. Characteristics include 4:1 ratio of stratum (st.) corneum to
st Malplghil {germinative layers of the epidermis, st. basale and st spinosumL with the
granular layer, between the st. spinosum and st. lucidum of the epidermis. Common
non~mechanical diffuse HPKs include:
Psoriasis-maculopapulosquamous, silvery scales on erythematous base, Auspitz
sign (bleeds when scale removed), elbows and knees
Unna Thost disease--bilateral, symmetrical, palms and soles, dominant inheritance
Mal de Maleda-torme fruste (partial expression) of Unna Thost, recessive
inheritance, with nail, ocular and dental involvement.
Vohwinke/'s disease (keratoma mutilans hereditarium)--diffuse, honeycombed,
rippled keratosis of soles, star burst keratoma on knees. associated digital
contracture and pseudo ainhum
Keratosis pfantarum su/catum--status~post immersion toot with Dermatophilus
congolensis
Pachyderma periostosis-keratosis of soles, periosteal hyperostosis, associated
with alveolar cell carcinoma
Alcoholic keratosis-mosaic, honeycomb dystrophic keratosis with sympathetic
component
Hauxthausen's disease (keratosis climactericum)-commonly on heels, erythema-
tous base, in postmenopausal women, associated with hypertension and
hyperuricemia
Moccasin foot-chronic, dry, hyperkeratotic T. rub rum dermatophytosis
Hyperkeratosis traumaticum marginus os calcis (housewives heel)-secondary to
prolonged weight bearing barefoot or in an open back slipper failing to support the
heel (no counter)
Keratoderma blenorrhagica---chronic inflammatory maculopapular and scaly
dermatosis associated with Reiter's syndrome (urethritis, iritis, arthritis), usually
in young males, localized to palms, soles and digits
Mechanically induced diffuse keratoses can be unilateral or bilateral on the soles,

and show a 1:1 ratio of st. corneum to st. Malpighii with the granular layer intact. The
underlying dermis is usually fibrous, with dilated capillaries and eccrine sweat ducts, and
perineural fibrosis. There are typically about 400 eccrine ducts per cm 2 of plantar skin. This
is often observed in patients with global anterior pes cavus with callus extending across the
entire ball of the foot.
Non-mechanically induced punctate keratoses characteristically display increased st.

corneum, a normal st. Malpighii, an intact st. granulosum, and loose underlying dermis.
Genetically determined forms include keratosis punctata of Hallopeau, which is dominantly
inherited, and displays hundreds of evenly distributed punctate keratoses, bilateral and
symmetrical, with truncated, macular and verrucoid lesions. Acquired punctate keratoses are
generally few in number, asymmetrical, and localized to skin creases. Acquired forms include:
Arsenical keratoses--arsenic intoxication (Cruveiler~Baumgartener disease),
affecting palms/soles, with hepatic failure; associated in past with certain
asthma preparations, wines, and seen in coal miners
Secondary syphilis-palms/soles, maculopapular, evolves to punctate keratoses
Darier's disease-greasy, vegetative lesions, punctiform on palms/soles, external
auditory meatus, cheeks
Aigner's syndrome (form fruste of Albers-Schonberg disease}-----punctate keratoses
of palms/soles with osteopetrosis
Hanhart's syndrome-punctate keratoses of palms/soles, with multiple lipomas
Basal cell nevus syndrome-pink (ham colored) pits with ice pick, punctate keratoses
Non-mechanically induced punctate keratoses of unknown etiology include heloma

neurofibrosum, which displays keratinous filaments, typically about the perimeter of the heel,
resembling mosaic verruca, with banana~like projections, single or multiple, and very painful.
Mechanically induced punctate keratoses characteristically display a 1:1 ratio ofst corneum
to st. Malpighii, a parakeratotic plug with atrophy of underlying granular layer, dilated eccrine
sweat ducts, dermal fibrosis, capillary ectasia and perineural fibrosis. Included are:
Parakeratosis plantaris discretum of Steinberg---translucent keratinous plug with

surrounding white (macerated) rim of blocked eccrine duct
Vamp disease-typically overlying EHL, or another extensor, tendon, where shoe vamp
chronically irritates skin resulting in parakeratosis, loss of granular layer, and often a
sinus tract due to draining bursa or tendon sheath
Dermatitides
Dermatitis has many causes and forms, and is typically treated with topical or systemic
corticosteroid, local care, and protection.
Atopic dermatiti~a chronic pruritic eruption common in adolescents and adults,
attributed to allergic, genetic and psychogenic causes; common to flexor surfaces,
displaying crusts, lichenification, and excoriation
Nummular (coin~like} dermatitis-of unknown etiology, affects extensor surfaces,
buttocks and legs, and displays papulovesicular eruption, forming crusts
Lichen simplex chronicus (focalized neurodermatitis}-----due to repeated scratching,
most common in females and Asian individuals, with well~demarcated scaly erythema
36 Selected Diseases and Pathological Conditions Ch.3
Contact dermatitis-an acute inflammation caused by contact with an allergen

effecting delayed hypersensitivity, and usually well-demarcated with a raised margin
Dyshidrosis--any disorder of eccrine sweat ducts, such as pompholyx. Pompholyx
("bubbles") is a skin eruption, typically on the sides of fingers and toes, palms and
soles, consisting of discrete 1 to 2 mm intra-epidermal vesicles with surrounding
erythema, associated with intense itching, lasting 1to 2 weeks intermittently
ldreactian (id rash}-a remote rash associated with a primary lesion caused by
cutaneous sensitization resulting in a distant site allergic reaction to circulating
allergen, such as dermatophytid or syphilid
Stasis dermatitis-affects the distal leg, ankles and hindfoot, secondary to chronic
venous insufficiency (valvular incompetence due to dilation of vein) or lymphedema,
with cyanosis, erythema, pruritus; progressive over years, and may eventually ulcerate
Purpura and other Hemorrhagic Lesions

Purpura are a group of disorders characterized by brown, red or purple subepidermal
hemorrhages. Petechiae are pinpoint, macular, round, purple or red, intradermal or
submucous hemorrhages. Purpura are larger than petechiae{< 1 em), but smaller than
ecchymosis(> 1 em). Ecchymosis, are large hemorrhages causing black and blue marks or
bruises. Purpura are caused by thrombocytopenia, amyloid, steroids (capillary fragility),
rheumatic vasculitis (leukocytoclastic angiitis), polyarteritis nodosa, serum sickness, SLE,
Henoch-Schonlein disease, and hemorrhagic fever (Ebola virus). Splinter hemorrhages
occur in the nail bed, and may be indicative of subacute bacterial endocarditis.
Papulosquamous Eruptions
These are characterized by slightly elevated, erythematous and scaly lesions, and include:
linea pedis---dermatophyte or other fungal or yeast infection
Psoriasis---chronic, hereditary, recurrent papulosquamous eruption occurring on the
scalp and extensor surfaces, displaying a red macule, papule or plaque covered with
silvery scales, removal of which effects local bleeding (Auspitz sign)
Secondary syphHis-maculopapular and pustular eruption caused by T. pallldum
infection, a venereal disease; the primary stage being a hard chancre, from which the
bacteria spread systemically via lymphatics and blood. Secondary syphilis occurs 6-
12 weeks after initial infection, displays fever, copper-hued multiform papular skin
eruptions (syphilids), iritis, alopecia, mucous patches, and severe arthritis. Tertiary
syphilis is late stage generalized disease affecting the CNS, bones, joints, and
parenchymal organs
Lichen planus-wide, flat, violaceous, itchy skin papules with a characteristic sheen,
occurring in persistent patches, of unknown etiology (viral or psychogenic are
suspected). The scaling lesion of Lichen planus may demonstrate Wickham's striae
(network of white lines)
Pffyriasis rose.r---fine, branny, scaling pink oval maculas aligned with skin creases
Benign Pigmented Skin lesions

A nevus is a well-demarcated, stable, malformation of hereditary origin, involving
epidermal, skin adnexal or vascular elements. A nevus containing melanin is said to be
pigmented. Pigmented nevi include:
Junctional nevus---brownish, smooth, hairless, macular or slightly elevated, 1to 8 mm
diameter, occurring on any skin surface, histologically displaying nests of melanocytes
"dropping off" into the dermis
Compound nevus-raised, flesh~colored to brown, often papillomatous, may contain

hairs, with melanocytes in the epidermis (newly formed) and dermis (older)
Intradermal nevus-similar to compound, typically more papillomatous, with hairs,
and all melanocytes are in the dermis (older)
Nevi evolve from epidermis to dermis, associated with elevation and involvement of
skin appendages (hair). Nevus flammeus (port wine stain, or capillary hemangioma) is a
diffuse, poorly demarcated area of pink/red/blue/purple capillary dilation in otherwise normal
skin (not melanocytic). Livedo, or livedo reticularis, is vascular congestion causing mottled
cyanosis, often caused by cold exposure but may be permanent secondarytovenular dilation.
Vesicles and Bullae
Table 3.1. CAUSES OF BULLOUS ERUPTIONS
COMMON BUllOUS DISORDERS UNCOMMON BULLOUS DISORDERS

Physical (heat, friction, cold) Pemphigus
Excess sun or UV exposure Epidermolysis bullosa
Drug-induced photosensitivitv Dermatitis herpetiform is
Systemic drug reaction Bullous lichen planus
Infection (bacterial, fungal, viral) Toxic epidermal necrolysis
Contact dermatitis Diphtheria cutis
Eccrine dysfunction (pomphylox)
Erythema multiforme
Herpes infection--results in clusters of small vesicles, with H. simplex Type I

occurring on skin or perioral, and Type II affecting genitalia. There is often a
prodromal fever, and lesions can be recurrent Herpes zoster is caused by the same
virus that causes varicella (chicken pox), which resides in the dorsal root ganglion, and
erupts in a unilateral, tense vesicular, usuaHytruncal, inflammation in the dermatomal
distribution of the affected spinal nerve root, frequently painful, and occasionally
associated with post-herpetic neuralgia (shingles).
Erythema multiforme--an urticarial eruption of immune origin, displaying red to
purple, raised bullae, classically with target or iris lesions, severe forms of which are
termed Stevens-Johnson syndrome, and can be fatal.
Pemphigus-typically occurs in middle to older aged persons of Jewish descent,
considered autoimmune or viral, with vesicles and bullae On skin and mucus
membranes, treated with steroids, chronic, and often with high morbidity or death.
Epidermolysis bullosa-typically occurs early in life (1 to 2 years) at sites of previous
skin trauma, typically minor, can be fatal in an infant, and treated with supportive-
measures.
Dermatitis herpetiformis {Duhring's disease}-a chronic, systemic vesiculobullous
eruption on the extremities and torso, wrth associated enteritis, large concentrations of
lgA, and considered autoimmune.
Toxic epidermal necrolysis {scalded skin syndrome)-can affect all ages with
epidennal necrosis and slough or peeling, often caused by staphylococci, and treated
in a fashion similar to burns. Can also be a drug reaction, most notably with the use of
Allopurinol, NSAIDs, Sulfonamides and measles vaccine.
Nodular or Granulomatous Lesions

Necrobiosis lipoidica diabeticorum-------disp!ays dermal edema and collagen distortion,
yellow-brown pigmentation, loss of elasticity, well-circumscribed annular pretibial
patches in diabetics, histologically showing palisading granuloma.
Granuloma annulare---annular, hard, reddish, perimalleolar or dorsal. nodular lesion,
benign and. recurrent, occasionally related to diabetes, histologically showing
palisading granuloma.
Erythema nodosum----acute inflammatory skin disease with tender red, pretibial
nodules, successive patches over a few weeks, considered an allergic reaction,
frequently seen with tuberculotoxin, streptococcal infection, drug reaction,
coccidiomycosis and psittacosis.
Sarcoidosis-chronic, progressive, systemic granulomatous disease of unknown
etiology, affecting any organ system, a common cause of pulmonary hilar
adenopathy, histologically showing noncaseating epithelioid cell tubercles (tuberculin
negative usually).
Angiolipoma-we!l vascularized, benign tumor of mature fat cells, often localized
aboutthe tibial plateau and malleoli. Neurilemmoma is a peripheral nerve sheath tumor
of myelin.
Glomus tumor-reddish~blue nail bed lesion displaying myoepithelial cells and
dilation of the Sequet-Boyer canal in the subungual papillary dermis, rarely observed
beyond 25 years of age.
Eccrine spiradenoma---deep, benign, solitary nodule arising from the coil of an
eccrine gland, covered by normal appearing skin and associated with paroxysmal pain.
Leiomyoma---benign arrector pili smooth muscle tumor (more commonly, uterine
fibroid).
Leprosy (Hansen's disease}--due to Mycobacterium leprae infection, causing
asymmetrical, maculopapular, hypopigmented, circumscribed skin granulomas that
often progress to digital ainhum and spontaneous amputation. Leprosy is diagnosed
bacteriologically and histologically, and treatment entails diaminodiphenylsulfone
(Dapsone or DDS) combined with rifampin, or clarithromycin and clofazimine.
Ulcerative Skin lesions

Hypertensive ulcers-localize to the lateral malleolar, digital, and dorsal areas,
are punched-out secondary to occlusion or spasm of arterioles, and are very painful.
Treatment entails control of underlying HTN and local care.
Venous stasis ulcers-localize along the saphenous vein secondary to venous
hypertension caused by valvular incompetence, display stasis dermatitis with
surrounding hyperpigmentation and eczematous vesicles and crusts, and are
irregularly shaped with granular base and may become secondarily infected.
Treatment consists of venous compression, elevation, cleansing, and protection.
Decubitus ulcers-display a well-circumscribed, undermined margin; are
localized to bony prominences and are associated with immobility and pressure. They
are often tender, and respond well to cleansing and pressure relief.
Mal perforans ulcers-punched out, nontender (insensitive), undermined and
related to repetitive pressure. They respond well to supportive measures unless
underlying bone infection develops.
Sickle cell ulcerations-localize perimalleolar, are recurrent due to sludging of
sickled RBCs and infarction. They are associated with hyperpigmentation and
inflammatory infiltrate effecting induration, and are very painful.
Ch. 3 Selected Diseases and Pathological Conditions 39
Skin Lesions Predisposed to Malignant Transformation or Association

Actinic (solar) keratosis-sharply outlined, red or flesh colored macule, or slightly
raised, verrucous or squamous growth on sun exposed surfaces. It may develop into
a cutaneous horn, or evolve into squamous cell carcinoma. It is considered to be of
UV mutation origin and is seen in the middle aged to elderly, usually in light
skinned individuals (also called solar or senile keratosis).
Parakeratosis of Mibelli--rare chronic hereditary skin disease of the hands and feet,
with hypertrophy of the st. corneum about the eccrine sweat ducts. It may
become dysplastic and effect squamous carcinoma.
Xeroderma pigmentosu!TI---rare, familial recessive trait, that is often fatal,
affecting skin with atrophy and pigmentation. It is associated with skin and eye
photosensitivity has its onset in childhood with development of affiliates (freckles),
telangiectasia, papilloma, hyperkeratoses, melanoma and carcinoma.
Ataxia telangiectasia (Louis Bar syndrome)-hereditary progressive ataxia. It is
associated with oculocutaneous telangiectasia, pulmonary disease and respiratory
tract infection, and ocular muscle dysfunction.
Malignant Skin Lesions

See selected neoplasms.
Nail Disorders (Onychopathy)

Congenital Defects
Anonychia---------absence of one or more nail plates, associated with ichthyosis.
Macronychia-anomalously large nail plate, otherwise normal in appearance (may
also be acquired secondary to acromegaly, COPD or pulmonary hypertrophy
[clubbing ofthe digits]).
Micronychia-anomalously small nail plates, otherwise normal.
Onychoheterotopia--nail growth in abnormal location, such as the dorsal or
plantar skin of the toe or foot
Pachyonychi&-abnormallythick, heavily striated longitudinally, occasionally lytic nail
p!ates jean also be acquired secondary to repetitive microtrauma).
Polyonychia-extra or supernumerary nail plate on a single toe, with one or more
matrices.
Synonychia-a single nail shared by two or more syndacty!ized digits.
Traumatic Conditions
HangnaiJ.....-.periungual, filamentous epidermal spicule.
Subungual hematoma-damage to the nail bed causes hemorrhage that fills the
potential space between nail plate and bed, may be associated with simple or
complex bed laceration, open phalangeal fracture, and should be drained (hand
cautery perforation) if acute and painful or throbbing, or requires removal of the nail
plate for repair of the bed if more than 25% ofthe visible nail plate displays hematoma
or ifthe plate is substantially unstable.
Onychophagi&-nail biting.
Onychocryptosis-a late effect of matrix distortion due to acute trauma or
repetitive microtrauma, wherein the plate grows into the adjacent nail fold, or when the
nail is cut incorrectly and the adjacent fold is pushed by external forces into and over the
plate. Onychophosis represents nail fold hyperkeratosis prior to dermal violation and
paronychia.
Onychogryphosis-distal plantar curvature, with thickening or clubbing of the nail

plate, a late effect of matrix and/or bed disruption, either acute or chronic.
Leukonychia--white spots due to chronic microtrauma effecting plate
separation from the bed, with a change in the refractive index of light; to be
distinguished from white superficial onychomycosis.
Onychia or paronychia--nail fold inflammation, red and swollen, tender and often
with drainage, usually due to onychocryptosis.
Onycholysis--separation ofthe plate from the bed, can be traumatic or secondaryto bed
hypertrophy or accumulation of subungual debris, as in onychomycosis.
Metabolic and Systemic Conditions That Affect the Nails

Hyperthyroidism--koilonychia, onycholysis, fingernails more so than toenails.
Psoriatic arthritis-------pitting and onycholysis, discoloration, subungual hyperkeratosis,
splinter hemorrhages; usually treated with systemic control of arthritis, local
protection and palliative care.
Hypertrophic pulmonary asteodystrophy-<iigital clubbing due to periosteal new bone
formation, IPJ arthritis, distal and plantar curvature ofthe nail, paronychia, widening
of the distal digital tuft and phalanx. It is associated with COPD, lung CA, sarcoidosis.
Treatment locally is supportive in conjunction with identification and treatment of the
underlying systemic disease.
Non~mycotic yellow nail disease-usually due to pulmonary disease, such as chronic
bronchiectasis, pleural effusion, chronic sinusitis, or chronic lymphedema. It is
associated with slow nail growth, absence of the cuticle, nail plate hypertrophy,
increased transverse curvature and yellow discoloration, a variant of clubbed nail;
and may be treated with intradermal triamcinolone, oral vitamin E, and identification
and treatment of underlying systemic disease.
Vitamin 812 deficiency-black-gray discoloration due to melanin deposition in the
nail matrix and bed. Must rule-out melanoma.
INFECTION
local signs of infection are those of inflammation, and include rubor (redness), tumor
(swelling), calor (heat), and dolor (pain). The patient may display antalgic guarding of the
infected lower extremity. Wound drainage should undergo Gram's stain and culture and
sensitivity testing. Constitutional signs and symptoms of infection include fever, chills,
malaise, loss of appetite, and Gl distress. The CBC shows a "left shift" wherein the total
WBC count is elevated above 10,000, and granulocytes rise above 70%, and immature
leukocyte bands are identified in the peripheral smear. Blood cultures are indicated when
the oral temperature is 102 F(37 C) or greater, taken from three separate sites at30 minute
intervals, if chills and/or hypotension occurs, or whenever septicemia is suspected.
Blood cultures have been reported to be positive in up to 50% of septic arthritis and
osteomyelitis cases.
A variety of microorganisms can infect the lower extremity. Aerobic organisms
include gram-positive coagulase producing Staph aureus {the most common infecting
organism of skin and soft tissue). coagulase negative Staph epidermidis,beta-hemolytic group
A Strept. (usually nonsuppurative with intense cellulitis and lymphangitis); gram
negative aerobes E col Klebsiella, Pseudomonas, Enterobacter, and Serratia.
Anaerobic organisms include Bacteroides, Clostridium, and facultative Staph. and
Peptostreptococcus. Anaerobic infections develop when aerobic organisms metabolize 02,
thereby enhancing conditions for anaerobes. Common synergistic organisms include:
S. aureus, S. epidermidis, Peptostreptococcus, Corynebacterium, Bacteroides, and Clostridia.

Signs of anaerobic infection include foul smelling (fetid), brown, watery,. exudate; necrosis,
subcutaneous gas effecting soft tissue crepitus (readily observed on standard radiographs),
and there is great risk for tissue loss and permanent dysfunction, as well as limb loss.
Identification of infecting organisms requires culture and sensitivity testing (C&S). An
open or draining wound presents exudate that can be swabbed for aerobic and anaerobic
C&S. Clinical suspicion (immunocompromised, chronic or recurrent infection, sickle-cell
anemia, concomitant infection elsewhere in the patient) should guide the practitioner to
obtain special microbiological testing when indicated, including acid fast {mycobacteria)
chocolate agar (Neisseria), and fungal C&S. Specimens can also be obtained via joint or
abscess aspiration, aspiration of sterile saline infiltrated dermis and subcutaneous tissue
when frank pus is absent (rather unreliable), and excisional biopsy with deep swab of
infected bone or sinus tract base. Whenever aspirating for C&S, it is important to try to
obtain the specimen through noncellulftic overlying tissues if possible. This is particularly
true when aspirating a joint. Aspiration requires aseptic skin preparation, and may be
enhanced with fluoroscopy.
Sinus tract cultures are not reliable for identifying actual underlying causative organisms
in cases of osteomyelitis, where it has been reported that a sinus tract C&S growing
Staph. aureus correlates with the underlying causative organism only 50% of the time.
Identification of other organisms from a sinus tract C&S correlates <50% with underlying
causative organism in cases of osteomyelitis. Bone cultures are the most definitive
diagnostic tool in cases of suspected osteomyelitis, and should correlate with bone biopsy.
It is often useful to discuss the matter of biopsy and C&S directly with the pathologist and
infectious diseases specialist whenever a question arises regarding diagnosis.
There are several specific types of skin and soft tissue infections. Cellulitis displays
erythema, edema and pain, and is often caused by Strep. Cellulitis can exist as an isolated
infectious process, or in conjunction with deeper and more extensive types of infection.
Pure cellulitis is usually treated without incision and drainage (I&D). The patient can be
treated with appropriate oral or IV antibiotics depending on severity.
Common Cutaneous Bacterial Infections

Ecthyma- Group A streptococci (S. pyogenes)superficial infection due to minor trauma or poor
hygiene, with pustule formation, crusts and erythema, may ulcerate. The treatment is topical
mupirocin ointment (Bactroban) and 1st generation cephalosporin or erythromycin.
Impetigo- staphylococcus or streptococcus superficial infection, usually in children, pustules
with yellowish purulence, crusts. It is readily spread by contact with purulent lesions.
Usually treated with topical mupirocin ointment and oral lst generation cephalosporin
or erythromycin.
Erythrasma- intertriginous superficial infection caused by Corynebacterium minutissimus,
displaying maceration, scaling, fissuring, and erythema. Wood's lamp reveals coral red
fluorescence. It is treated with dilute povidone iodine soaks and oral erythromycin.
Necrotizing Fasciitis
Necrotizing Fasciitis involves infection dissecting along fascial planes, superficial to
muscle; and most often is caused by peptostreptococcus, S. aureus, Strept pyogenes,
Clostridium, and Bacteroides. Anaerobic muscle infection can cause myonecrosis with
subcutaneous gas, exotoxin release, myoglobinuria and renal failure, and bacteremia.
Myonecrosis (gas gangrene)

Myonecrosis is the most morbid and potentially lethal soft tissue infection of the lower
extremity. Necrotic muscle fails to display the four Cs: contractility (muscle stimulation with
the electrocoagulator causes visible contraction), capillary bleeding (bright red blood), color
(beefy red), and consistency (firm).
Osteomyelitis
Osteomyelitis is defined as infection of bone and marrow. Osteomyelitis is distinguished
from infectious osteitis, which is suppuration of cortex without marrow involvement; and
infectious periostitis, which is periosteal contamination and inflammation. Osteomyelitis is
confirmed primarily by bone culture and, to a lesser degree, by bone biopsy (inflammatory
biopsy may be false positive). As a rule, osteomyelitis requires surgical debridement
followed by at least six weeks of antibiotic therapy. In some cases, based on clinical
observation, a four week (or less) course of antibiotics may be sufficient following
definitive bone debridement. A variety of classification systems exists for osteomyelitis
including the Waldvogel, Cierny, and Buckholz systems.
Waldvogel Classification of Osteomyelitis Waldvogel described a classification based

loosely upon the pathogenesis of the disease. The categories are Hematogenous
Osteomyelitis, Contiguous Osteomyelitis, and Osteomyelitis associated with vascular
insufficiency.
Hematogenous Osteomyelitis ~ result of bloodstream dissemination of bacteria

emanating from an identifiable focus of infection or developing during transient
bacteremia unrelated to infection. This is most comrnon in patients between the ages
of 1 to 20 years,-and over 50 years. Blunt trauma to long bone (femur>tibia>humerus)
precedes this form of osteomyelitis in 33% of cases.
Acute Hematogenous Osteomyelitis (AHO)- can be effected by Streptococcal skin

infection, often associated with measles or chicken pox in childhood. Similarly, otitis
media due to Hemophilus, Staph.~ or pneumococcus can hematogenously spread
to bone. AHO localizes in metaphyseal bone due to the paucity of phagocytes and
sludging venous sinusoids. AHO in the infant (0 to 1 year) can involve the joint, as
capillaries traverse the epiphysis and effusion develops in 60~70% of cases. Group B
Strept, Staph. au reus, and E coli are the most common organisms in AHO in the
infant. In the child, AHO usually does not involve the joint space and most commonly
localizes around the hip, shoulder, and ankle (distal lateral tibial metaphysis is
intra-articular, and can lead to septic arthritis with osteomyelitis). Extensive cortical
damage and involucrum develop, rarely is there damage to the growth plate or joint,
and Staph. epidermidis is causative in 60~90% of cases of AHO. In patients with
sickle~cell anemia or Sc hemoglobinopathy, Salmonella is most common; and
Hemophilus influenza is most common in children less than two years old. In the adult,
AHO is usually seen in patients older than 50 years of age. Pseudomonas is common
in IV drug abusers developing AHO; and in adults using IV catheters, suffering urinary
tract and pulmonary infection, or within two .years following major surgery. Joint
infection may accompany AHO in the adult. Cases of AHO displaying purulence upon
aspiration, or failing to respond favorably within 36 hours of initiating antibiotic
therapy warrant operative intervention.
Contiguous Spread Osteomyelitis~ results from direct contamination of bone due to

spread of bacteria from contiguous tissue, is the most common form of osteomyelitis
observed in podiatric cases; generally involves patients over 40 years of age; and may
occurfollowing puncture, laceration, ulceration, or surgical intervention.
Postoperative Contiguous Spread Osteomyelitis- includes acute postoperative

osteomyelitis {observed within one month of surgery), delayed postoperative
osteomyelitis (observed between one month and two years of surgery), and late
postoperative osteomyelitis (not observed until at least 2 years after surgery). Most
commonly, postoperative osteomyelitis is ofthe delayed or late sort, usually growing
Staph. or mixed flora. In all forms of contiguous spread osteomyelitis, adjacent soft
tissue or bone infection must be identified. A thorough search for a nearby ulcer or
sinus tract is important
Direct Inoculation Osteomyelitis~ is caused by contamination of bone without

adjacent soft tissue infection, and is either traumatically or surgically induced. A
distinction between postoperative contiguous spread osteomyelitis should be made.
Vascular Insufficiency Osteomyelitis- occurs in patients with peripheral vascular

disease, wherein associated gangrene and ulceration are usually present. May
involve anaerobes, and myonecrosis should be considered. Has features similar to
contiguous spread osteomyelitis, however the overriding distinguishing factor is
peripheral vascular disease.
The Cierny-Mader classification of OM combines anatomic and physiologic categories in

an effort to direct therapy. Twelve different stages of osteomyelitis can be described by
combining the different categories (Table 3-2).
TABLE 3-2. THE CIERNY-MADER CLASSIFICATION OF OSTEOMYELITIS.

Anatomical category Physiological category
I. Medullary A. intact local vascularity and systemic immune competence
II. Superticial B. Compromised local vascularity and/
or systemic immune competence
Ill. Localized C. Host not a surgical candidate, as operative risks
IV. Diffuse outweigh potential benefits
Bucholtz classified osteomyelitis using 7 categories (Table 3-2).
TABLE 3-3. THE BUCHOLTZ CLASSIFICATION OF OSTEOMYELITIS.

Category Etiology, anatomical site, and physiological type
A Wound induced
B Mechanogenic
c Physeal OM
D Ischemic limb
E Combination of A-D
F Septic arthritis with adjacent OM
G Chromic OM with osteitis
Pus
Periosteum
Bone abscess
Dead and
dying bone
(sequestrum)
A B
Involucrum
c D
Figure 3.1
Diagnostic Imaging Of Infection-radiographic signs of infection inctude increased soft

tissue density and volume associated with inflammation and, in cases of OM, include
osteolysis, involucrum, cloaca, and sequestration (Fig. 3.1). Osteolysis is not visible as
radiolucency until 30-50% of osseous mineralization has been washed away by
inflammatory hyperemia. This generally takes 10-14 days after the onset of symptoms.
Thereafter sclerosis and periosteal new bone formation, known as involucrum, surrounds
necrotic and infected bone, known as sequestrum, and ultimately a channel, known as a
cloaca, forms in new bone as bacteria proliferate and exudate drains. Chronic OM involves
the presence of microbes living in dead bone (sequestrum), surrounded and contained
within new bone (Involucrum). Eventually, after trauma or some other instigating factor, an
ncute flare-up can develop with drainage, and signs and symptoms of acute infection.
Chronic osteomyelitis can lay dormant for many years (reportedly> 50 years) before a
flare-up occurs. In the presence of a chronic draining sinus due to OM (or other causes),
squamous cell carcinoma (SCC) can develop in the epithelium along the sinus tract as a
longterm seque!!um. Radionuclide studies can be useful in the evaluation of suspected OM,
and include WB'C scans labeled with Tc-99 or 1n-111.ln most cases, bone scintigrams
become positive within 48-72 hours. In patients with Charcot neuroarthropathy, or
suspected fibrous nonunion, bone and joint infection may be strongly suggested with
identification of a "hot" ln-111 or Tc-99 labeled WBC scan (Indium and Seratec scans,
respectively). MRI may be the most useful imaging method when considering OM,
however positron emission tomography {PET) scans have been shown to be even more
sensitive and specific for Charcot neuroarthorpathy, in comparison to MRI scans. None of
the imaging methods can be used to definitively ascertain OM, although alone and in
combination, they can be very helpful. Definitive diagnosis OM is made by means of biospy,
and bone gram stain and C&S.
Treatment of Infection-the treatment of any infection, including OM, entails adherence

to several general principles, including the 5 Ds: 1) decompression, 2) drainage,
3) debridement, 4) dressings, and 5) drugs. Decompression is achieved with incision and
drainage 0&0) or removal of operatively-placed sutures, following surgical preparation.
Drainage is achieved with copious lavage, debridement and excision of necrotic and/or
grossly infected tissue, removal of implanted materials or foreign bodies, removal of
unstable internal fixation devices, open packing with fine-mesh gauze, or partial or complete
closure with drain placement, and use of an appropriate dressing. Tourniquets are
generally not used when performing 1&0. The extent of infection is thoroughly explored and
drained, and definitive cultures and stains are obtained from the deep tissues. In cases
of OM, a small margin of apparently uninfected bone can be debrided and sent for
pathological inspection. In any infection, drainage is allowed to proceed as long as
necessary, usually a minimum of 48to 72 hours, with dressing changes consisting of lavage
and debridement as indicated by wound appearance.lf necessary, additional debridement
can be carried out by a return to the operating room, which is frequently necessary in cases
involving necrotizing infection. Care should be taken to avoid performing a delayed primary
closure too soon.
Antibiotic Therapy-antibiotics are the primary drugs used in the treatment of infection.
Consideration must be given to the spectrum of coverage, frequency of administration,
toxicity, duration of treatment and cost. Prior to ascertaining the microbiological results of
definitive culture specimens, empiric antibiotic therapy is initiated (Table 3-4). In cases of
OM, antibiotic therapy is usually continued for 6 weeks following final debridement A
Hickman, Broviac or PICC (peripherally inserted central catheter) can be used for longterm
IV therapy. Monitoring the course of treatment of infection requires attention to fever,
antibiotic levels, renal and hepatic function, wound appearance and pain, complete blood
count(CBC) and differential, erythrocyte sedimentation rate (ESR), insulin requirement in the
diabetic, and C&S results. Antibiotic impregnated calcium sulfate, or polymethyl-
methacrylate (PMMA), beads may be packed in the wound and used in conjunction with IV
antibiotics. Antibiotic beads are usually made in the OR, using gentamycin, vancomycin,
clindamycin, or another antibiotic, and packed in the debrided bone to increase local
concentration of antibiotic. The wound is closed over the beads and, after 10-20 days (or
sooner or later, depending upon wound appearance), the patient returns to the operating
room tor bead removal, further debridement, and placement of more antibiotic beads if
needed, or reconstruction and closure. A previously infected wound is ready for closure
after achieving at least one negative culture, and the wound looks clean with beefy red
granulations, no evidence of purulence or sinus tract, and resolution of marginal erythema.
In some cases, delayed primary closure can be undertaken without first ascertaining a
negative wound culture, as a wound that is clinically ready for closure usually has some
degree of surface contamination. Closure may be achieved by means of secondary
intention, or via delayed primary closure, skin graft, or flap. Previously infected wounds are
generally closed over a drain of some sort, or only partially closed. Depending upon the
specifics of the infection, use of the wound vacuum, as well as hyperbaric oxygen therapy,
should also be considered.
Diabetic Polymicrobial Infection-diabetic polymicrobial infection can be limb and life

threatening. Plantar space infection may develop, with abscess dissection along fascial
planes of the plantar vault into the posterior compartment of the leg, or through an
intermetatarsal space into the dorsum then into the anterior leg. The patient must be
evaluated for constitutional signs and symptoms of septic shock, including incoherence or
confusion, hypotension, tachycardia, and extreme hyperglycemia and ketoacidosis. Hospital
admission and inpatient management are usually in order. It is useful to obtain a serum
g!ucose level, CBC and differential, ESR, urinalysis, biochemical levels other than glucose,
EKG, foot/leg and chest X-rays, blood cultures x3 from 3 separate sites 30 minutes apart,
other labs and tests that may be warranted by the patient's individual condition, medical and
anesthesia consultation and co~management, and supportive therapy in preparation 'for
surgical debridement. Orders should also include NPO, wound and skin isolation, IV LR at
KVO via 18~gauge IV catheter, specific medications (chronic and acute), non~weight
bearing, on call to operating room for 1&0. The patient, and/or a family member, must be
informed of the emergent nature of the condition, and possible consequences. Empiric
antibiotic therapy should be initiated prior to identifying definitive culture results, and
coverage should include anaerobic, aerobic, gram(+) and gram(~) organisms. A useful
initial regimen consists of a combination of amoxicillin~clavulonate, clindamycin, and a
quinolone (see Table 3-4). Intravenous antibiotics, such as ticarcillin-clavulonate, could also
be used until definitive cultures are identified. It can be helpful to obtain an infectious
disease consultation, as well as consultation regarding the potential benefits of hyperbaric
oxygen therapy (HBOT).
Incision and Drainage (I&D}-once the patient is prepared for surgery, 1&0 is performed
in the operating room. The patient should be supine, without a tourniquet, and an orthope-
dic prep of the lower extremity performed. The wound or abscess is then probed to deter-
mine its extent and confines, after which a wide incision is made in order to allow drainage.
Exploration entails inspection of all undermined or abscessed areas. In cases of diabetic
plantar vault infection, decompression of the vault requires opening the deep fascia
adequately enough to drain the medial, central, lateral, and deep plantar spaces, as
necessary. Deep specimens are obtained for gram stain and C&S, necrotic and infected
tissues are excised and biopsied, and foreign bodies are removed. IV antibiotics may be
altered based upon the results ofthe gram stain, however empiric therapy usually does not
change until definitive culture results are known. Copious lavage, sometimes using a pulsed,
power-flushing system, is perfomed after initial sharp debridement. Close inspection is paid
to all tissues prior to open packing with fine mesh gauze, then application of sterile
dressing. Subsequent daily or BID dressing changes are performed with lavage and
curettage of the wound, and additional specimens obtained for C&S as indicated by the
appearance of the wound. If the patient and wound are not responding to the treatment,
then there is either persistent abscess or the choice of antibiotic is incorrect An MRI could
help detect an unrelieved abscess. A return to the operating room for additional
debridement is performed whenever indicated, based on the patient's progress. The goal is
to achieve a beefy red granular base, with no purulence or malodor, with decreased edema
and erythema and pain, and no residual undermining or tunneling. Closure occurs thereafter
via either continued secondary intention healing, or delayed primary closure, or the use of a
skin graft or flap. In some cases involving aerobic infection, especially those with deep or
large defects, as well as those with considerable drainage, vacuum-assisted wound closure
can be helpful. The wound vacuum can also be used over skin grafts and flaps.
Chronic Pedal Wound-when a patient presents with a chronic pedal wound, perhaps with
intermittent drainage that has lasted for months, consideration should be given to the
possibility of previous puncture wound or osteomyelitis. Common sites for chronic pedal
wounds include the digits, metatarsal ball, 5th metatarsal base, heel, and perimaHeolar areas.
Protective sensation should be determined, since chronic ulceration is very commonly
associated with the insensitive foot {mal perforans ulcer). Puncture wounds that have
penetrated the sole of the shoe are likely to involve Pseudomonas aeruginosa, although
Staph aureus remains the most common pathogen in barefoot punctures and in children.
As with a!I chronic wound, diagnostic images should be obtained, and consideration should
be given to the potential benefits of wound margin biospy and surgical debridement.
Radiographs are obtained, as are labs (as noted above for the diabetic infection), and
consideration given to a bone scan, or aCT or MAl scan. When indicated, the patient is
taken to the operating room for 1&0 and exploration. Do not dissect through the site of a
chronic draining sinus tract if possible, when exploring bone that may not be infected. A
dorsal approach can be useful in the case of a chronic plantar wound, as long as the nidus
of infection is not obscured from inspection. If there is any concern about compromising
drainage of the abscess, then simply excise the entire sinus tract The important point is to
explore the involved area and obtain appropriate samples for gram stain and C&S, as well
as soft tissue and bone biopsy. After obtaining specimens for C&S, then initiate IV antibiotics,
lavage, pack open, and initiate daily wound care.
Fungal infection-fungal infections are extremely common in the foot and !ower
extremities, and must be differentiated from other causes of papulosquamous eruption
\secondary syphilis, psoriasis, pityriasis rosea, contact dermatitis) when localized to the
glabrous skin. Fungi are eukaryotic and reproduce bv spore formation, grow as hyphae and
form a mycelium. Some organisms, such as Candida, are dimorphic and grow as either
yeast or fungal hyphae depending upon the host environment Fungi that infect humans are
categorized as either dermatophytes (superficial) or deep pathogens. The most common
pathogenic fungi affecting humans are the Fungi lmperfecti, although other groups can
infect the compromised host.
Identification of the infecting fungus is made via skin shaving or nail fragment exam
for hyphae or yeast using KOH (potassium hydroxide) to dissolve keratin from skin
scrapings, or periodic acid Schiffs (PAS) stain; and by means of fungal C&S using
Sabouraud's dextrose agar (SDA). Superficial mycoses include tinea pedis, candidiasis
(thrush), onychomycosis, tinea corporis, tinea cruris, tinea capitis, tinea axillaris, and tinea
versicolor. linea pedis is usually responsive to topical antifungal cream application for 2~6
weeks, with agents such asterbinafine and econazole proving to be effective. Patients are
encouraged to try oveHhe~counter antifungal preparations (tolnaftate, undecylenic acid,
miconazole, c!otrimazole) for minor conditions oftinea pedis, if they have not already done
so. Candida species often infectthe nail bed in compromised hosts, and cause paronychia
and pseudo-clubbing due to chronic digital inflammation. Onychomycosis typically
presents as either white superficial onychomycosis (WSO), which is usually caused by
Trichophyton mentagrophytes or yeast and is least common; distal subungual
onychomycosis (DSO), which is usually caused by T rubrum and is most common; and
proximal subungual onychomycosis IPSO), which is also usually caused by T rubrum and
is rare and usually associated with systemic disease or HIV. Onychomycosis must be
distinguished from mechanically induced nail dystrophy, psoriatic pitting and flaking, lichen
planus and pterygium, COPD induced clubbing, dystrophy due to peripheral vascular
disease, and subungual exostosis. When harvesting nail and nail bed fragments for fungal
tissue examination and C&S, it is imperative to obtain plenty of nail bed fragments from
deep to the nail plate. Palliative treatment of onychomycosis includes nail plate debridement
and regular application of topical antifungal (ciclopirox 8% lacquer or miconazole 2%
solution, or similar agents), however cure rates are usually< 75~80% with topical therapy,
although debridement alone is knownto improve foot~related quality of life. Cure is more
likely with oral administration of either terbinafine (250 mg PO QD x 3 months) or
itraconazole (200 mg PO QD x 3 months), or perhaps fluconazole (as an adjunct for the
treatment of yeast). it is prudent to check liver enzymes and CBC, current medications, and
past medical history, prior to initiating oral antifungal therapy. Chemically induced
hepatitis has been greatly diminished using the newer systemic antifungal agents, as
therapy is only administered for 3-4 months, generally. Drug interactions (certain
antihistamines, anti-lipid agents, and others) must also be considered prior to initiating oral
antifungal therapy. The active metabolite of the agent is maintained in the substance ofthe
nail for 6-9 months, and the ultimate appearance of the nail plate cannot be truly assessed
until 6-12 months following initiation of oral therapy. Prevention of recurrent
onychomycosis may require periodic maintenance use of topical therapy, and concurrent
debridement is a crucial part of any treatment plan. Deep mycoses include mycetoma and
madura foot, sporotrichosis, and blastomycosis; caused by Madurefla mycetoma, Sporothrix
schenkii, and Blastomycoses, respectively. Deep fungal infections are granulomatous, with
papular and nodular inflammation of the subcutaneous tissues and overlying skin, sinus
tract formation, foul odor, and secondary bacterial infection may ensue. Treatment may
require excision of infected tissue, including amputation, and systemic administration of
amphotericin-8 (sporotrichosis), sufonamide and other oral antifungal agents (mycetoma,
madura foot, blastomycosis).
Septic Arthritis (see Arthritides)
Antibiotic Therapy-antibiotic therapy varies from community to community, and the

clinician is encouraged to be familiar with the characteristics of the organisms in his/her
own community. The local hospital's antibiotic susceptibility and causative organism
prevalence report can be a useful guide to therapy, and the county health department also
monitors organisms responsible for reported infections. Although it is often necessary to
initiate therapy empirically, it is always adviseable to obtain a culture from the lesion if this
is possible. Once again, appropriate specimens should be obtained for isolation of the
causative organism and determination of its susceptibility to antibiotic therapy. Bacterial
cultures are particularly important in cases of severe infection, in diabetic or compromised
hosts, and for chronic or recurrent infection wherein previous culture and sensitivity has not
been performed. In all cases of infection, ongoing assessment of the response to therapy
must be undertaken. Therapy is generally continued for 10-14 days for soft tissue infections,
and 6 weeks for OM, and the treatment should be honed to the individual patients specific
local and systemic requirements. The following information is meantto serve as a general
guide to antibiotic therapy for infections involving the foot. ankle and leg. Since organisms
and antibiotcs evolve and change frequently, the reader is encouraged to check with
appropriate updated literature, such as the drug package insert, for specific indications
and dosages.
Methicillin-resistant Staphylococcus aureus(MRSA)-community acquired methicillin-

resistant Staphylococcus aureus (MRSA) represents an ever-increasing proportion of
wound infections, particularly in children. MRSA resists the cidal effects of beta lactam
antibiotics such as penicillin and cephalosporin, including cephalexin, ceftriaxone, and
amoxicillin-clavulanate; and the organism may also resist the static effects of
erythromycin, clarithromycin, and azithromycin. Potentially useful oral agents include
clindamycin, trimethoprim-sulfamethoxazole, doxycycline, and linezolid; IV agents include
vancomycin or daptomycin; and mupirocin can be used topically. Rifampin can also be used,
however not as a sole antibiotic. For limb- or life-threatening MRSA infection, high-dose IV
antibiotic therapy using vancomycin or daptomycin, perhaps combined with gentamicin,
should be considered. Some strains of MRSA display "inducible resistance" to agents such
as clindamycin, and these can oftern be identified using the "D test." A positive "D test" is
associated with an increased risk of antibiotic resistance, and careful clinical follow~up is
important. In an effort to prevent colonization and relapsing infection, 4~6 weeks of therapy
may be necessary.
Postoperative Infection------overall, the prevalence of postoperative infection ranges from

1~2% of clean, elective bone surgical cases, and most of these involve Staph. aureus. In
cases involving implant infection, Staph. epidermidis, with its glycocalyx, is also common.
Other causative species associated with postoperative infection include Proteus,
Pseudomonas, B-hemolytic Streptococcus, Klebsiella, Serratia, Enterobacter, E. coli, and
Bacteroides. In general, when stable osteosynthesis implants are present in cases of acute
postoperative infection, metallic fixation devices are left in place unless they are associated
with loose or necrotic bone (hence, loose or unstable). Chronically infected hardware should
be removed and osteomyelitis therapy instituted.
Puncture Wounds-the status of the patienfs tetanus prophylaxis should be ascertained

whenever a puncture wound is encountered. Appropriate diagnostic measures combined
with local wound care and antibiotic therapy are basic elements in the treatment of punc-
ture wounds. In general, antibiotic therapy should cover Staph. aureus, and other gram(+)
organisms, with appropriate attention to 1&0 if edema, cellulitis, induration, pain and Hx
suggest abscess. The use of cephalexin, dic!oxacillin, or amoxicillin/clavu!onate should be
considered. Punctures also convey the risk of anaerobic infection, and radiographs should
be inspected for the presence of subcutaneous gas, primarlly hydrogen sulfide. Gas~
forming infections are usually necrotizing and require timely 1&0, and hyperbaric oxygen
therapy may also be useful (see Necrotizing Infection, above). For punctures that involve
penetration through the sole of the shoe, coverage of Pseudomonas sp. should be
considered, and potentially useful agents include aztreonam + clindamycln, or imipenem +
ci!istatin, piperacillin +tazobactam, or ampicillin+ sulbactam (see Table 3~4).
Empiric Antibiotic Therapy-the following table (Table 3.4) is meant to provide guidelines
for empiric antibiotic therapy, and the reader is encouraged to obtain definitive specimens
for C&S, and to be familiar with the detailed information contained in the package insert for
the specific antibiotic used.
TABLE 3-4. EMPIRIC DRUGS OF CHOICE fOR PREDOMINANT BACTERIA SEEN IN

ADULT FOOT AND ANKLE SURGERY.*
Organism Therapy of Choice Alternate Therapy
Gram(+)
Staphylococcus cephalexin 1250 mg PO OlD) clindamycin (300 mg PO OlD)
(methicillin sensitive) cefazolin (1-2g IV q8h) vancomycin 115 mg/kg IV ql2h)
dicloxacillin 1250 mg PO OlD)
nafcillin 12 grams IV q4h)
azithromycin 1500 mg as a
single dose on day 1, followed
by 250 mg daily on days 2-5)
Streptococcus penicillin (penicillin clindamycin 1300 mg PO OlD)
V 0.25-0.5 grams PO TID-OlD,
or penicillin G 1.2-20 million
units IM/IV per day)
cephalexin (250 mg PO OlD) vancomycin 115 mg/kg ql2h IV)
cefazolin (1-2g IV q8h)
Staphylococcus vancomycin 115 mg/kg IV q12h) clindamycin (300 mg PO OlD)
\methicillin resistant) doxycycline (0.1 gram PO/IV q12h)
minocycline 10.1 gram PO ql2h)
linezolid (600 mg PO/IV q12h)
TMP/SMX 11 OS tab PO BID)
gentamicin 12 mg/kg load
followed by 1.7 mg/kg IV q8h) [if
limb- or life threatening]
enterococcus ampicillin (250 mg- amoxiclllin-clavulonate
1 gram PO TID) l875/125mg PO q12h x 14 days)
vancomycin (15 mg/kg IV q12h)
vancomycin resistant gentamicin (2 mg/kg IV load Streptomycin 115 mg/kg IM q24h)
enterococcus followed by 1.7 mg/kg IV q8h) piperacillin/tazobactam (3.375
grams IV q6h)
combination ciprof!oxacin i500-
750 mg PO BID), rifampin
(10 mg/kg/day up to 600 mg/day
PO single dose), gentamicin
12 mg/kg load fullowed by
1.7 mg/kg IV q8h) or ceftriaxone
(1-2 grams IV once daily)
chloramphenicol (0.25-1 gram
PO/IV q6h up to 4 grams/day)
! -
Gram(-)
Escherishia coli, Proteus cephalexin (250 mg PO QID) ciproftoxacin (500-750 mg PO BID)
cefazolin (1 gram IV qBh)
ECSM group ciprofloxacin 3rd generation cephalosporin
(500-750 mg PO BID) (such as ceftriaxone 1-2 grams
IV once daily)
aztreonam (1 gram qBh-
2 gram IV q6h)
TMP/SMX (1 DStab PO BID)
Pseudomonas ciprofloxacin (500-750 mg ceftazidime (2 grams IV q8h)
aeruginosis PO BID) aztreonam (2g IV q8h)
gentamicin (2 mg/kg load
followed by 1.7 mg/kg IV q8h)
Anaerobic infection
Bacteroides metronidazole clindamycin (300 mg PO GID)
(500 mg PO q6-8h)
Diabetic foot infection

polymicrobial amoxi cilli n-c Iavu Ion ate ampicillin sulbactam (1.5-3
(875/125mg PO q12h x 14days) grams IV q6h)
cefazolin (1-2 grams IV qBh) ticarcillin clavulonate (3.1
+metronidazole grams IV q6h)
(500mg PO/IV q6-8h) piperacillin tazobactam (3.375
grams IV q6h)
vancomycin lmipenem cilistatin
(15 mg/kg q12h IV)+ (500mg IV q6h)
aztreonam (2g IV q8h) +
metronidazole
(500mg PO/IV q6-8h)
*Specific dosages, serum drug level monitoring, creatinine and other appropriate serum laboratory tests, culture
and sensitivity, adjunct therapy, and clinical reassessments should be individualized to the specific patient The reader
is encouraged to consider the factthat recommended antibiotic therapy often varies overtime and geographic area.
ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)
AIDS is caused by infection with the cytopathic human immunodeficiency virus (HIV) retro-
virus (RNA virus), which causes cell death. The CD-4 surface glycoprotein is the essential
molecule recognized by the retrovirus, on the surfaces ofT41ymphocytes, monocytes, and
macrophages. T-helper lymphocytes also become infected and destroyed, which greatly
impairs the immune system. Natural killer lymphocytes are also destroyed, which impairs
immune surveillance against neoplasms and virus infected cells. Approximately 40% to
50% of patients infected with HI\/, and possessing less than 400T-helper cells, develop AIDS
within 2 years of HIV infection. Eighty-five percent of patients with T-helper cells less than
200, will develop AIDS within 2 years of infection.
Four Stages of Hl\llnlection

Stage 1- manifesting acute HIV, wherein the patient displays general malaise and
"mono-like" symptoms
Stage II - chronically infected wrth HIV, often asymptomatic while developing anti-
bodies to HIV
Stage Ill- persistent generalized lymphadenopathy
Stage IV- serious manifestations of immunodeficiency, frequent serious infections
and debilitation
Subgroups ol Manifestations of Hill Infection

Subgroup A- Constitutional symptoms
Subgroup B- Neurological syndromes
Subgroup C- Associated with infectious diseases
C(1)- Defect in cell mediated immunity (Pneumocystis pneumonia)
C(2)- Less profound infections
Subgroup D -Secondary cancers (e.g. Kaposi's sarcoma)
Subgroup E- Chronic lymphoid interstitial pneumonitis
The treatment of AIDS includes supportive measures, as well as suppressive and

disease modifying agents such as AZT. Therapeutic regimens have been shown to be most
effective when disease modifying agents are used in synergy. Maternal transmission of the
disease to the fetus has been controlled with AZT. Treatment regimens are very expensive.
Any patient suspected of being HlV positive should be counseled regarding the importance
of testing to confirm the presence of antibody, then appropriately referred for infectious
disease consultation. Social setvices consultation is also important as various agencies may
be able to assist with therapy. Regardless of whether or not you suspect a patient of being HIV
positive, univers.al precautions are the standard of care in ALL aspects of health care.
SElECTED PERIPHERAL VASCULAR DISEASES
Raynaud's Phenomenon
Raynaud's phenomenon is an episode of small arterial and arteriole constriction resulting
in acral pallor, cyanosis, or both color changes; with subsequent rubor due to hyperemia
after the vasospasm has subsided {white, blue, and red coloration pattern).ln severe cases,
prolonged vasospasm can effect cutaneous digital gangrene. The condition is usually
bilateral, however it may rarely be unilateral. It is more common in females. Serious organic
disease (atherosclerosis) is not usually present in the vessel in Raynaud's phenomenon.
When a specific cause for the vasospasm, such as trauma, connective tissue disease, or
neurogenic, cannot be identified after several years of suffering, then the condition can be
termed Raynaud's disease (also known as primary Raynaud's phenomenon). Secondary
Raynaud's phenomenon can be attributed to trauma, either acute or repetitive microtrauma;
neurogenic due to nerve entrapment such as thoracic outlet, carpal or tarsal tunnel
syndromes; occlusive arterial disease such as thromboangitis obliterans, arteriosclerosis
obliterans, or status-post arterial thrombosis or embolism; thermal injury such as trench
foot (cold and wet); or for miscellaneous conditions such as scleroderma, lupus
erythematosus, RA, dermatomyositis, Fabry's disease, cryoglobulinemia (as in multiple
myeloma or chronic leukemia), hemoglobinuria, myxedema, neoplastic disease, hepatitis B,
pheochromocytoma, and ergotism. Treatment consists of protection, maintaining warmth,
Ch.3 Sele~;ted Diseases and Pathological Conditions 53
use of vasodilators (Procardia, alpha~adrenerg.ic blocking prazosin, norepinephrine

depleting methyldopa, and reserpine), topical nitroglycerine and antibiotics.
Frostbite and Cold Injury

Frostbite implies freezing of the skin. Superficial frostbite is also termed chilblains, and is a
mild cold injury.
Classifications of frostbite
1st degree (chilblains)- skin frozen, no blisters
2nd degree -skin frozen, blisters formed
3rd degree- skin frozen and necrotic, ulceration, subcutaneous exposure
4th degree- skin and subcutaneous tissue frozen and necrotic.
The treatment of chilblains is re-warming in 105-108 Fwhirlpool for 30 minutes, and
administer analgesic (meperidine). Blisters are left intact unless they have ruptured, wherein
they are treated as burns with cleansing debridement, Silvadene and dry sterile dressing.
The treatment of more advanced or deep frostbite is rapid rewarming in 108~ 110 F water,
administer antibiotic (cefazolin), tetanus prophylaxis, and analgesic (meperidine). It is
important to protect the frozen part until proper thaw and care can be administered, and to
avoid thaw followed by refreeze. PosHreezing sequella include vasomotor instability and
cold hypersensitivity, paresthesia, depigmentation, hyperhidrosis, and atrophy.
Arteriosclerosis Obliterans (Atherosclerosis Obliterans, ASO~ASO is the primary cause

of occlusive lower extremity vascular disease, with the main lesion being atherosclerotic
plaque occlusion of the superficial femoral or femoral level arteries. It is most common in
males age 50-70 years, and more likely in patients with diabetes mellitus, hypertension,
cigarette smokers, and/or hyperlipidemia. Pathological findings include atheromatous
plaque formation, with secondary thrombosis. Symptoms include intermittent claudication,
rest pain, cold intolerance, ulceration and gangrene, ischemic neuropathy, disuse atrophy,
joint stiffness and contracture. Aorta or iliac artery occlusion causes buttock, hip and thigh
pain; occlusion of the femoral artery and its branches causes thigh and calf pain; and
popliteal and tibial artery occlusion causes calf, ankle and foot pain. Findings include
diminished peripheral pulsation, discoloration (dependent rubor, pallor, or cyanosis),
exaggerated distal cooling, edema, atrophy, cutaneous compromise, intrinsic atrophy,
ulceration, and gangrene. The ankle-brachial index (ABI, Table 3-51. toe pulse pressure and
amplitude, and TcPO, are diminished. Healing is generally anticipated if: ABI >.5, toe
pressure >40 mm Hg, TcP0,>30 mm Hg, and toe pulse amplitude >4 mm. Duplex Doppler ul-
trasound noninvasive vascular testing, magnetic resonance angiography, and perhaps an
arteriogram if surgical care warrants, can assist in the diagnosis. Treatment includes con~
trol of associated systemic disease (HTN, hyperlipidemia, anemia, arrhythmia).
avoiding cold exposure, exercise to tolerance, hemorheologic agent (pentoxifylline,
cilostazol), antiplatelettherapy (aspirin, clopidogrel, ticlopidine, dipyridamole), vasodilating
agents (a and ~~adrenergic blockers, calcium channel blockers), peripheral angioplasty or
vascular reconstruction, or amputation. Operative intervention is warranted whenever
claudication, rest pain, or non~helaing wound is present. Peripheral arterial disease is often
associated with carotid, coronary, and renal vascular insufficiency.
TABlE 3-5. ANKLE-BRACHIAL INDEX (ABI) CATEGORIES.*

Ratio Category
>0.96 Normal
0.81-0.95 Mild obstruction
0.051-0.8 Moderate obstruction
,0.05 Severe obstruction
*Misleading, elevated ratios may be observed in cases of noncompressible arteries.
Thromboangiitis Obliterans (TAO, Buerger's Disease)
TAO is a segmental inflammatory, obliterative disease of medium sized arteries and veins
(posterior tibial), most common in the lower extremities of males who smoke cigarettes, the
cause of which is unknown. TAO results in gangrene. Treatment involves arresting
progression of the disease by avoiding tobacco products, administering anticoagulants and
corticosteroids; followed by effecting vasodialation with Procardia or other agents; and
surgical management of gangrenous wounds.
Monckeberg's Medial Calcific Sclerosis

This is a form of non-atheromatous degenerative arterial disease observed in middle-age
to elderly males. There is fine calcification of the tunica media, which may lead to a
non-compressible vessel, and effect a misleadingly high ankle/arm index. This occurs in
the aorta and other large vessels.
Venous Thrombosis and Pulmonary Embolism-the deep veins of the lower extremity
include the plantar arch, posterior tibial, peroneal, anterior tibial, sura!, popliteal, superficial
femoral, and deep femoral. Venous thrombosis, particularly ofthe deep system at or above
the popliteal fossa, is associated with pulmonary embolism (PE), and for this reason can be
fatal or extremely morbid. Predisposing factors fOr venous thrombosis include congestive
heart failure, malignancy, trauma, surgery, pregnancy, and thrombocytosis. Other risk
factors include cigarette smoking, oral contraceptive use, obesity, advanced age, bed rest
or confinement, and paraplegia. Deep venous thrombosis prophylaxis should be instituted
in patients at risk (Tables 3-6 and 3-7).
Lower extremity deep vein thrombophlebitis {OVT, also known as venous thromboembolism,
or VTE) presents with deep, aching pain and tightness in the calf or thigh. Pain upon active
dorsiflexion ofthe ankle, or resistance to ankle dorsiflexion is known as Homan's sign, and
is a nonspecific and unreliable clinical diagnostic maneuver. Tenderness upon calf or thigh
muscle compression is a more specific test for DVT, when associated with edema and local
increase in skin temperature. Superficial thrombophlebitis, which conveys a lower likelihood
of PE, more commonly displays local heat, edema. erythema, and a palpable cord
consistent with the thrombosed vein. Application of a tourniquet above the suspected
thrombosis may cause pain at the level ofthrombosis within 30~45 seconds, and is strongly
suggestive of DVT. Comparison of calf circumference wiH often show enlargement of the
affected side. Constitutional findings may include temperature elevation 139.5'-40.5" C), chills,
and malaise. Arterial embolism is usually more painful early on, with less swelling,
exaggerated distal temperature decrease, and early sensory deficit. Severe venous
thrombosis effecting retrograde arterial flow decrease may result in phlegmasia cerulea
dolens, which can result in pedal ischemia and gangrene. Coagulation studies are usuarty
normal unless full blown disseminated intravascular coagulation (DIC), familial

antithrombin Ill deficiency, or lupus erythematosus clotting inhibitors exist The laboratory
diagnosis of DVT hinges on venous non-invasive duplex Doppler examination, and
magnetic resonance venography or contrast venography may be employed if ultrasound is
equivocal. Radioactive 125 1-fibrinogen scanning, in conjunction with occlusion impedance
plethysmography is also a sensitive combination for DVT of the calf. Use of the 0-dimertest
may also be useful, however combined clinical and venographic tests are more reliable. An
accurate diagnosis of DVT is made upon identification of predisposing factors and clinical
observation, combined with duplex Doppler ultrasound and, perhaps, magnetic resonance
venogram or contrast venography.
Prevention of DVT is recommended, and can be achieved in several different ways (Tables
3-6 and 3-7). Prophylactic therapy in the !ow-risk patient involves mini-dose subcutaneous
administration of 5000 units of heparin every 8 or 12 hours beginning about 60 minutes
preoperatively. Adjunct physical measures include support hose, intermittent sequential
pneumatic compression of the lower extremity, leg elevation with the knee flexed, and
out-of-bed activity at an early stage after surgery. In high-risk patients, DVT prophylaxis is
administered preoperatively with mini-dose heparinization, however in the postoperative
phase, the heparin dose is adjusted upward to keep the PTT within 4 seconds of high
norma!. Despite statistically more postoperative hemorrhage, this form of DVT prophylaxis
appears to be worthwhile in the high-risk patient A baseline platelet count is recommended
prior to mini-dose heparinization, and should be monitored periodically if it is observed to
be low. High-risk patients may also be prophylaxed with a combination of mini-dose
heparin and dihydroergotamine, which causes venular constriction and rapid venous return.
Other prophylactic combinations include heparin and antithrombin Ill administration, and the
use of low molecular weight heparin administered once daily has been shown to be
effective and popular (see risk stratification and guidelines for prophylaxis, below).
Coumadin, which inhibits the vitamin !<-dependent clotting factors II, VII, IX, X, and proteins
C and S, can also be administered preoperatively and during the postoperative phase to
effect DVT prophylaxis.
TABLE 3-6. DVT RISK STRATIFICATION (ASSIGN POINTS BASED ON PROCEDURE,

DISEASE, AND OTHER PATIENT-RELATED FACTORS).
Risk factors Risk factor points assigned
Operating room time> 105 min
Tourniquettime >90 min
Rearfoot or ankle surgery
Age 40-60 years
Pregnancy or postpartum <1 month
Varicose veins
Obesity (>20 lbs over ideal body weight)
Diabetes meHrt:us
Hypertension
Hyperlipidemia
Smoker
Polycystic ovary syndrome
Immobilized in BK or AK cast for> 1 week
Patient confined to bed for >72 hours
Central venous access
Age >60 years
Oral contraceptive use
Hormone replacement therapy
Inflammatory bowel disease 2
Congestive heart failure
Ankle, pi!on or tibial fracture
Severe sepsis/infection 3
Mu~iple trauma
Acute spinal cord injury
Cancer treatment
Currently treated or history of DVT or PE 5
TABLE 3-7. DVT RISK STRATIFICATION AND GUIDELINES FOR PROPHYLAXIS.

Risk Risk Clinical Prophylaxis
points stratum features
0 Low <40yearsold Patient education
Minor surgery Early ambulation
<30 minutes
1-2 Moderate 40-60 years old Patient education, early ambulatlon, elastic
+minor surgery stockings
General anesthesia Intermittent pneumatic compression (if
>30 minutes NWB)
Minor surgery Low dose unfractionated heparin
+ 1 or more other risks (5000 units sq), or low molecular weight
heparin (enoxaparin 30 mg sq q 12 hours or
40 mg sq qd)
Mechanical therapy starting 1-2 hours
before surgery, or 12-24 hours postop if
needed to achieve adequate hemostasis
Continue therapy while inpatient or during
initial recovery, then decide whether to
extend 7-14 days
3-4 High >60 years old+ Patient education, early ambulation, elastic
minor surgery+ stockings
no other risks Intermittent pneumatic compression
e >40 years old+ (ifNWB)
minor surgery+ ., Low dose unfractionated heparin
any other risk (5000 units sq), or low molecular weight
heparin (enoxaparin 30 mg sq q 12 hours or
40 mg sq qd)
Mechanical therapy starting 1-2 hours
before surgery, or 12-24 hours postop if
needed to achieve adequate hemostasis
Continue therapy throughout hospitalization
and up to 7-14 days, then decide duration
based on degree of immobilization, ROM
and WB status
Very high > Past PE, cancer Patient education, early ambulation,
or major trauma elastic stockings
>40yearsoldt Intermittent pneumatic compression
major surgery+ (ifNWB)
any other risk factor Low molecular weight heparin (enoxaparin
30 mg sq q 12 hours or 40 mg sq qd), or
fondaparinux, or adjusted dose heparin
Warfarin (therapeutic when INR 2-3)
Start therapy 1-2 hours preop, or 12-24
hours postop if needed to achieve
adequate hemostasis
Continue therapy 10-14 days or entire time
of immobilization
Encourage early ROM and/or WB
if indicated
Treatment of DVT involves assessment of the PT and PTT, followed immediately by IV

infusion of heparin 5000~ 10,000 units. Thereafter, heparin is infused continuously at a rate of
800-1500 units per hour, maintaining the PTI at2-2.5 times the baseline value, and the INR
at 2.0-3.0. The patient is maintained at bed rest with the lower extremities elevated at 15
degrees to 20 degrees above the level of the heart. It takes approximately one week for
thrombi to become firmly adherent to endothelium and thereby diminish the risk of PE.
Coumadin is started as soon as longterm anticoagulation is planned, and takes 3-5 days to
become therapeutic monitoring the PT. The patient is maintained in an anticoagulated state
for 4-6 weeks for the treatment of isolated calf DVT, and for 3-6 months for more proximal
vein thrombosis. Clinical and/or venographic evidence of clot propagation indicates the
need for vascular surgical consultation regarding the potential benefits of Greenfield filter
(umbrella) placement in the inferior vena cava. Moreover, thrombolytic therapy, or
phlebectomy in rare instances, may be indicated. Postphlebitic syndrome may ensue, and
involves venous insufficiency, chronic venous stasis dermatitis, permanent ca!f
enlargement and predisposition to recurrent superficial and deep thrombophlebitis,
postphlebitic neuritis, and the need for indefinite use of support hose and perhaps other
physical measures.
Chronic venous insufficiency(postphlebitic syndrome, chronic venous stasis) affects the

skin and subcutaneous tissues of the legs and ankles; and may occur secondary to DVT,
varicose veins, cavernous hemangioma, congenital A-V fistula, or pelvic neoplasm
obstructing venous outflow from the lower extremity. Findings include edema, stasis
dermatitis with hyperpigmentation, eczema, induration, pain, and ulceration. Ulcerations
are usually peri-malleolar, and display sharply demarcated or "punched-out" margins (local
tissue hypertension). Squamous cell carcinoma may develop. Treatment consists of
elevation, application of an Unna-paste bandage, antibiotics as indicated, diuresis, and
protection. Consideration should be given to the potentially beneficial effects of topical
corticosteroid on inflamed, non-ulcerated skin. Atypical skin lesions should be biopsied.
Skin grafting, often in combination with vein surgery wherein varicosities are ligated or
sclerosed, and incompetent perforating veins are bypassed via direct connection of
superticial veins to deeper veins, may also be usefuL
Pulmonary Embolism IPE}

PE is very common and a leading cause of death in the US. Lower extremity DVT accounts for
60-80% of PEs. Thrombi embo!ize from the lower extremities, traverse the pelvis and inferior
vena cava, then enter the right side of the heart, and subsequently obstruct the pulmonary
vessels. Pulmonary infarction ensues thereafter. Clinical signs and symptoms vary with the
degree of pulmonary occlusion and infarction, and include crushing chest pain, dyspnea,
tachypnea, tachycardia, low grade temperature elevation 138" C [101" F]}, neck vein
distension, ipsilateral diaphragm elevation on standard chest X-ray, a positive ventilation-
perfusion lung scan ("'I or 51Cr}, S-T segment depression (cardiac hypoxia} and other EKG
changes, arterial blood gas abnormalities such as decreased P02 and PC02 and Ph, increased
serum LDH and bilirubin in the presence of normal SGOT. The differential includes acute Ml
and pneumonia.
Treatment includes immediate anticoagulation with IV administration of 5,000-10,000 units

of heparin, followed by continuous infusion of 800-1500 units/hr while monitoring the PH
Supportive measures include administration of D2, bed rest, and analgesia; while
proceeding with definitive diagnostic measures. Thrombolytic therapy, or surgical

phlebectomy, may be indicated. Septic pulmonary emboli may be observed as a
complication of infected pelvic thrombosis, indwelling catheter, transvenous pacemaker,
arteriovenous or ventriculovenous shunts, or in cases of IV drug abuse.
Fat embolism is most common after long bone or pelvic fracture. Cerebral infarction
symptoms of restlessness, confusion, stupor and coma may accompany pulmonary
symptoms of dyspnea and tachypnea; in conjunction with fever, lipuria, and the
appearance of chest and conjunctival petechiae. The treatment of fat embolism includes
supportive measures identified previously for PE (heparin also activates lipase), in addition
to large doses of corticosteroid.
Catheter embolism is also possible when central venous catheterization is performed.

Surgical excision is usually indicated in patients that can sustain operative intervention.
lymphedema
Lymphedema is swelling of soft tissues due to an increased quantity of lymph, which is also
associated with increased tissue fluid found outside of the blood and lymphatic capillaries.
Primary (idiopathic) lymphedema is noted to be present at birth (congenital), seen early in life
(lymphedema praecox), or observed late in life (lymphedema forme tarde). Congenital
lymphedema can be hereditary (Milroy's disease) or non-familial (simple congenital).
Consideration should be given to congenital or acquired hemihypertrophy. Secondary
lymphedema is of either the obstructive or inflammatorytype. Obstructive lymphedema occurs
secondary to either malignant occlusion, or surgical radiation-induced disruption, of lymphatic
channels and/or nodes. Nontropical inflammatory lymphedema is highlighted by recurrent
lymphangitis and cellulitis, fever and chills, adenopathy, and is attributed most commonly to
streptococcus infection (although trichophytosis, and other microbes may be causative).
Tropical secondary lymphedema is attributed to filariasis. Chronic lymphedema may cause
fibrosis, verrucous dermatitis, ulceration, elephantiasis, and/or lymphangiosarcoma (rare).
The differential diagnosis for lymphedema includes hypothyroid myxedema, CHF, nephrotic
syndrome, and hypoproteinemia. Clinical acumen and historical interview are the mainstays
of diagnosis, and biopsy may be beneficial. Treatment should be instituted as early as
possible, and is primarily medical, although surgery may be indicated rarely. Medical treatment
consists of elevation of the edematous part, diuresis (furosemide), prophylactic
anticoagulation with subcutaneous heparin, and observation of serum potassium. Antibiotics
may also be indicated. After initial reduction of the extremity, customized support hose
measured and fabricated for regular wear, and longterm diuresis may be maintained. If
medical therapy fails, vascular consultation regarding surgical efforts aimed at improving
lymphatic drainage or excision of edematous tissues may be entertained.
DIABETES MELLITUS
Diabetes mellitus (OM) affects about 10 million people in the US. It is a leading cause of
blindness, renal disease, PVD, peripheral neuropathy, lower extremity ulceration and
amputation, and death. In DM, the ability to oxidize carbohydrates is diminished or lost,
usually due to pancreatic dysfunction, particularly of the islets of Langerhans, with resultant
disruption of insulin function. Classification includes insulin-dependent diabetes mellitus
(lOOM, Type 1, juvenile-onset [although it can develop in adulthood]), and non-insulin
dependent diabetes mellitus (NIDDM, Type 2, adult-onset}.IDDM is caused by autoimmune

destruction of pancreatic beta cells, and must be treated with insulin replacement NIDDM can
be divided into obese and non-obese groups, the obese group displaying the possibility of
returning to euglycemia associated with weight loss and dietary control. Gestational OM is
observed during pregnancy, and usually subsides postpartum. Findings include hyperglycemia,
polyuria, polydipsia, polyphagia, emaciation, weakness, acidosis due to dysfunctional fat
metabolism, dyspnea, ketonuria, and coma. lmmunopathy accompanies long-standing
hyperglycemia. Diabetic ketoacidosis or non ketotic hyperosmolar coma may result from
prolonged or severe hyperglycemia. Diabetic retinopathy and nephropathy are the result of
small vessel diseases associated with long-standing hyperglycemia. Diabetic peripheral
neuropathy produces pain and paresthesia, pedal insensitivity, anhidrosis, vasodialation,
brittle hyperkeratosis, mal perforans ulceration, and Charcot neuroarthropathy. All patients
suspected of having OM, or previously diagnosed with the disease, should undergo pedal
monofilament esthesiometer testing to determine whether protective sensation is present
Diabetic dermopathy creates thin, atrophlc, and friable skin in the pretibial region, wounding
of which results in post-inflammatory hyperpigmentation. Necrobiosis lipoidica diabeticorum
also affects the pretibial area as an atrophic plaque with telangiectasia, and microscopically
displays palisading granuloma formation.The laboratory diagnosis of DM hinges on an
abnormal glucose tolerance test, and/or repetitively high fasting blood glucose
measurements. C-peptide assay can be used to distinguish endogenous insulin, and Type 2
OM, from exogenous insulin (administered for therapy), since exogenous insulin doe not
contain C-peptide. The GAD 65 antibody assay can also be used to distinguish Type 1from Type
2OM. Therapy includes effortsto identify the cause, after which dietary controls and exercise
are instituted (as indicated). Patient education is a crucial partofthe management of DM. Oral
hypoglycemic agents may be used in conjunction with dietary control, and include
sulfonylureas (chlorpropamide, tolbutamide, tolazamide, and acetohexamide), as well as
metformin. Insulin preparations are indicated when the blood glucose level is not adequately
controlled with diet and oral medication, and in cases of Type 1 DM. Adjusting the
administration of insulin requires close communication between the internist and the patient,
and often entails lifestyle alteration. In the peri-operative period, a sliding scale of insulin,
based on the blood glucose value, can be useful until a regular regimen is resumed. The goal
of therapy in the perioperative phase is to maintain plasma glucose between 150-250 mg%.
Pancreas and islet cell transplantation can also be used in an effort to cure DM.
THYROID DISEASE
Hypothalamic thyrotropin-releasing hormone stimulates pituitary release of thyroid
stimulating .hormone, which activates thyroidal uptake of iodine and production of thyroxine
(T,} and triiodothyronine (T,}, which exert negative feedback inhibition of pituitary thyroid stim-
ulating hormone release. Thyroid hormones regulate metabolism. Enlargement of the
thyroid gland is referred to as a goiter, and may be associated with overactive or underactive
function. Hypothyroidism can occur due to surgical or medical (radioactive iodine) ablation,
or inflammation (Hashimoto's disease) of the thyroid gland; or secondary to hypothalamic or
pituitary dysfunction (tumor, CVA, trauma, other}. Hypothyroidism effects myxedema, which
specifically presents as non-pitting edema, associated with facial changes that include
swelling and a thickened nose, dry or hoarse voice, dry and waxy skin, and mucinous
deposition in tissues. Hypothyroid patients display fatigue, general malaise, weight gain,
bradycardia, and may become comatose (myxedema coma) in severe disease. Thyroid
supplementation with T (Synthroid) and T, (Cytomel), or natural preparations, as well as

supportive therapy are used as indicated. Hyperthyroidism, or Grave's disease, effects
exophthalmos (lid lag), tachycardia, profuse diaphoresis, nervousness, restlessness, fine
tremors, emaciation, and psychosis. Treatment involves supportive measures and drugs that
alter hormone metabolism or the end-organ effects of the hormone. Thyroid storm is a
medical emergency wherein severe hyperthyroidism effects organ damage and death. Drugs
that inhibit hormone formation and release include thiourea derivatives that block
organification of iodine, iodide which blocks thyroid hormone synthesis, and lithium which
blocks release of thyroid hormone. Propranolol controls the peripheral manifestations of
thyroid hormone. Radioactive iodine destroys thyroid tissue, thereby decreasing thyroid
function and possibly effecting hypothyroidism (which can be treated with thyroid
supplementation).
HEPATITIS
Inflammation of the liver can be caused by trauma, toxins, autoimmune disease, and viral
infection. Liver dysfunction results in inability to detoxify a wide range of substances,
failure to produce blood elements, such as platelets, and inadequate bile production,
resulting in faulty digestion. Acute hepatitis lasts< 6 months, and can result from trauma,
vascular insult, viral infection {cytomegalovirus, Epstein-Barr, Herpes simplex, adenovirus,
hepatitis A virus [infectious jaundice, due to picornavirus], hepatitis E viruses [common
during pregnancy]), bacterial or parasitic infection (Rocky Mountain spotted fever,
Leptospira, toxoplasmosis, and Q fever), toxicity (alcohol, carbon tetrachloride, APAP,
minocycline, isoniazide, ketoconazole, methyl-dopa, nitrofurantoin, ch!orambutol, penicillin,
anesthetics, mushroom toxin), collagen vascular disease (SLE), and metabolic or inherited
disorder (Wilson's disease, alpha 1-antitrypsin deficiency). Chronic hepatitis lasts
> 6 months, and can result from any of the conditions that cause acute hepatitis, if the
condition persists or treatment fails, or the most common forms are related to the hepatitis
viruses B, C, and D. Hepatitis B, due to hepadenovirus, results in chronic disease in
approximately 15% of those infected; is transmitted via blood transfusion, sexual intercourse
or exchange of body fluids, tattooing, needle sharing, and mother-to-child via breast feed-
ing; is successfully treated (remission) in about 45% of those infected, with alpha-
interferon, pegylated interferon adefovir, entecavir, telbivudine and lamivudine; causes
cirrhosis and hepatocellular carcinoma. A vaccine exists that conveys immunity to
hepatitis B virus. Hepatitis C(formerly non-A non-B), due to flavivirus, often results in chronic
hepatitis that evolves to cirrhosis. Hepatitis Cis transmitted through contact with blood,
and It crosses the placenta; and it may remain inactive for 10-20 years. Hepatitis C viral
loads can be made undetectable with a combination of interferon and ribavarin, and the
response to therapy has been shown to vary with viral genotype. There are other hepatitis
viruses, as well.
ARTHRITIDES
Rheumatoid Arthritis
Rheumatoid Arthritis IRA) is a constitutional disease with inflammatory changes through-
outthe connective tissues. It is generally a wasting disease with muscle and bone atrophy.
Chronic proliferative inflammation of the synovium exists and causes irreversible damage
to joint capsule and cartilage, which are replaced by granulation tissue. Radiographically
there is joint space narrowing, periarticular demineralization, bone erosion, "punched out"
periarticular lesions, subluxation, deformity (arthritis mutilans), and osteoporosis. RA
primarily affects the small joints of the hands and feet, most commonly the PIPJs and
MTPJs. It can also present in the hindfoot and ankle, with progressive metatarsal joint and
subtalar joint subluxation and ankle pes valgus. Frequentlythe posterosuperior process of
the calcaneus is involved.
Clinical manifestations include post~static dyskinesia (pain that is worse after periods of
immobility) and non-weight bearing, as well as stiffness. Post-static dyskinesia is a
hallmark of any type of arthritis. Pain and stiffness often subside somewhat after motion
has proceeded and the joint "warms up." Prolonged activity thereafter can lead to
worsening of pain. Constitutional symptoms of weight loss, fever, coldness, numbness,
tingling, fatigue and malaise are common. The cardinal objective findings are bilateral,
symmetrical sma!! joint swelling (fusiform, sausage fingers and toes), tenderness to
palpation (or even barometric pressure), and pain with motion. Swelling due to synovia!
hypertrophy is palpably spongy or rubbery, and often crepitant. Synovitis may lead to
effusion. Limited motion over a long period is associated with muscle wasting, contracture,
fibrosis, and ankylosis. Subcutaneous rheumatoid nodules {palisading granulomas) may
form in areas of bony prominence, weight bearing or contact.
Diagnosis ofRA is based on disease characteristics overtime. Classic RA displays 7 of the
fo!!owing symptoms, the first 5 presenting for at least 6 weeks: morning stiffness, painful
range of motion in at least one joint, swe!!ing in at least one joint, swe!!ing of at least one
other joint, symmetrical joint swelling wfth simultaneous involvement of the same joint on
both sides ofthe body (except PIPJs), subcutaneous nodules, X-ray changes typical of RA
{peri-articular osteopenia, joint narrowing, bone whittling), positive agglutination test
(rheumatoid factor), poor mucin clot precipitate, characteristic histologic changes in
synovial membrane, characteristic histologic granulomatous nodules. Five of these
findings in combination represent definitive RA, 3 represents probable RA. Possible RA is
represented by any 2 of the following tor3 weeks: tenderness or pain with motion, morning
stiffness, history of joint swelling, subcutaneous nodules, elevated ESR or CAP, or iritis.
Exclusions to RA include:
1. Malar rash typical of systemic lupus erythematosus ISLE)
2. Rash typical of drug reaction
3. High concentration of lupus erythematosus ILEI cells
4. Histologic evidence of polyarteritis nodosa
5. Trunk or neck or pharyngeal weakness or swelling or dermatomyositis
6. Definite scleroderma
7. Rheumatic fever
8. Tophi or gout
9. Septic arthritis
10. Reiter's syndrome
11. Tubercle bacilli in joint
12. Shoulder-hand syndrome
13. Hypertrophic pulmonary osteodystrophy
14. Clinical picture characteristic of neuropathy
15. Homogentisic acid in urine
16. Histological evidence of sarcoidosis
17. Positive Kveim {sarcoid antigen) test
18. Multiple myeloma

19. Characteristic skin lesions of erythema nodosum
20. Leukemia or lymphoma
21. Agammaglobulinemia
Lab Testing for RA includes CBC with slight to moderate normocytic hypochromic anemia,
white count decreased or, in acute cases, elevated (PMNs may be increased with left shift),
chronic normal to slight decrease ESR, moderate to marked increase rheumatoid factor
(RF) with this agglutination test positive 75% after several months to a year, normal uric
acid, altered plasma proteins (fibrinogen and globulin increased, albumin and total protein
and AJG ratio decreased), normal Ca++ and P04, and the synovial fluid is cloudy with
increased WBCs and decreased viscosity. The differential diagnosis includes any
po!yarthritic inflammatory disease with constitutional signs and symptoms.
Osteoarthritis
Osteoarthritis (OA) can be idiopathic and defined as primary OA; or the result of
repetitive mechanical strain, and defined as secondary OA. Secondary OA is also termed
degenerative joint disease or "wear and tear" arthritis, and is generally not inflammatory
beyond the confines of the joint Chronic subtalar joint and metatarsophalangeal joint
hyperpronation is a common cause of degenerative joint disease in the foot, with resultant
pes valgus, forefootsupinatus and hallux limitus/rigidus, plantar fascitis, flexor stabilization
induced hammertoes, and medial Lisfranc breakdown. Any joint can be subject to
degenerative joint disease, particularly when subjected to weight bearing or in the
post~traumatic phase. There are three cardinal roentgen signs of OA, including joint space
narrowing, subchondral sclerosis, and osteophytosis. The classic dorsal "flag" of hallux
rigidus (dorsal bunion), first metatarsal-cuneiform exostosis, and the anterior tibial
exostosis are examples of advanced osteophytosis. Clinical manifestations include PSD,
joint pain without acute inflammation, stiffness, fine and/or coarse crepitus, and symptoms
that worsen with weight-bearing activity. Although range of motion may be diminished,
there is rarely ankylosis. OA usually affects middle-aged or older individuals, with history
of insidious onset (unless post-traumatic), with gradual progression. The differential
diagnosis includes rheumatoid arthritis, gout, and Charcot neuroarthropathy.
GoutyArthritis
Chronic hyperuricemia can result in monosodium urate crystal deposition in joints and soft
tissues. The four main etiological forms of gout include:
1. primary metabolic gout- chronic over-production of uric acid, often dietary in origin
2. secondary metabolic gout- myeloproliferative disease with high rate of cellular
turnover causing over-production of uric acid
3. primary renal gout- under-excretion of uric acid due to primary kidney disease
4. secondary renal gout- under-excretion of uric acid due to renal disease other than
primary kidney lesion (certain diuretic medications).
Serum uric acid levels of7 mg/dl for males and 6 mg/dl for females indicate a super-
saturated state wherein crystals may precipitate In joints and the kidneys.
Clinical forms ofgouty arlhritisinclude acute gouty arthritis, intercritical or quiescent, and
chronic gouty arthritis. Acute gouty arthritis presents as monoarticular, sudden onset and
intensely painful inflammation (red, hot, swollen, excruciating pain), stiffness and antalgic
guarding, and overlying cutaneous desquamation. Chronic gouty arthritis presents
insidiously with gradual, progressive tophus formation; intermittent acute gouty attacks;
and is associated with indurated tophus formation (advanced monosodium urate
deposition) in subcutaneous and/or tendon, auricular helix, and the small joints of the hand
and foot; and advanced deformity (bunion, hammertoes, nodular lesions) effecting
cutaneous compromise. A draining tophus reveals a white, chalky exudate of monosodium
urate crystals. The diagnosis of gout is confirmed by the presence of strongly birefringent
monosodium urate crystals identified on joint aspiration. The presence of a phagocytosed
monosodium urate crystal within a granulocyte is pathognomonic, and termed the "martini
sign." Serum uric acid, which is chronically elevated in chronic gout is normally 8 mg%;
however the serum value can actually be within the normal range during an acute gouty
attack. Roentgen signs of acute gouty arthritis consist primarily of increased soft tissue
density and volume; while chronic gouty arthritis reveals punched out or "rat bite" defects
of bone at the capsular attachment. Overtime, chronic erosion and ankylosis may develop.
The most common locations of gouty arthritis are the first MTPJ, posterior heel at the
Achilles insertion, the plantar inferior calcaneus, other pedal articulations (lesser MTPJ,
MTJ), the ankle; the hand, wrist and elbow, and knee. The differential diagnosis includes
pseudogout; suppurative arthritis, acute bursitis, and rheumatoid arthritis.
Oral therapy consists of indomethacin 50 mg Q 6 hours x 24 hours, followed by 50 mg Q 8

hours x 24 hours, followed by 25 mg Q 8 hours x 24 hours. Alternatively, one may use
colchicine (inhibits PMN migration) 0.5 mg Q 1 hour or 1 mg Q 2 hours until the symptoms
subside, or Gl distress develops, or a total of 6 mg has been administered without relief.
Colchicine can also be administered intravenously as an inltia12 mg bolus followed by 1 mg
IV Q 6 hours for two additional doses. In surgical or traumatized patients with a history of
acute gouty arthritis, prophylactic therapy using colchicine can be administered as 0.5 mg
PO Q8 hour for one week, beginning two days preoperatively. Patients with hyperuricemia
require medical evaluation, including 24 hour urine uric acid analysis, and may benefit from
longterm anti-hyperuricemic therapy. ln such patients, if the uric acid excretion is less
than 700 mg/24 hour period, then probenecid sulfinpyrazone is used; and if the uric acid
excretion is over700 mg/24 hours, then Allopurinol is used regularly for an indefinite period
oftime.
1\nkylosing Spondylitis
The criteria for the diagnosis of ankylosing spondylitis include:
1. Limited motion of lumbar spine in anterior and lateral flexion and extension
2. History of pain or presence of pain in dorsolumbar junction or in lumbar spine
3. Limitation of chest expansion to one inch or less
Definite ankylosing spondylitis is confirmed by the presence of bilateral sacroiliitis

associated with at least one clinical criteria. Probable ankylosing spondylitis exists in the
presence of bilateral sacroiliitis associated with none of the clinical criteria. Common
symptoms include low back pain, prolonged back stiffness, ascending back pain, heel pain,
peripheral joint pain, fatigue, and diminished vision and/or eye pain. Roentgen signs vary
with duration of the disease. Early signs include sacroiliac joint blurring, joint space
narrowing and widening, subchondral sclerosis, diffuse osteoporosis of spine, apophyseal
joint sclerosis, and straightening of spine. Advanced ankylosing spondylitis reveals
apophyseal joint erosion, squaring of vertebrae, narrowed disc space, vertebral collapse,
pelvic whiskering, and pubic symphysis involvement Terminal roentgen signs include
intervertebral disc calcification, paravertebral ligament calcification, vertical syndesmo-

phytes, sacro-iliac joint fusion, and bamboo spine.
Reiter's Syndrome
This is a seronegative \no presence of rheumatoid factorL asymmetrical arthritis that
presents with one or more of the following: urethritis, cervicitis, dysentery, inflammatory
eye disease (iriditis), and mucocutaneous disease consisting of balanitis or oral ulceration
or keratoderma blenorrhagica. Characteristics include synovitis, symphysitis and
enthesitis; asymmetrical lower extremity arthritis with predilection for small joints of the
teet and the ankle, pericalcaneal enthesitis, knee and sacroiliac disease; bone erosion with
osteophytosls, and paravertebral. ossification. Diagnostic tests suggestive of Reiter's
syndrome include negative rheumatoid factor, demonstration of HLA 8~27 in the serum,
Pekin cells in synovial fluid and neutrophilia in prostatic fluid, and unilateral sacroiliitis.
Psoriatic Arthritis
Psoriatic Arthritis is an often severe polyarthropathy that is more common in females (3:2
M:F ratio), and can affect patients of any age. Patterns of psoriatic arthritis include
polyarthritis with DIPJ involvement and nail disease, symmetrical seronegative
polyarthritis simulating rheumatoid arthritis, monoarthritis or asymmetrical oligoarthritis,
sacroiliitis and spondylitis, and arthritis mutilans. Diagnostic features include papulosqua-
mous skin lesions and nail dystrophy (pitting, onycholysis, flaking, hypertrophy, non-
suppurative paronychia); DIPJ arthritis, fusiform digital swelling (sausage toes), unilateral
sacroiliitis, simultaneous exacerbation of cutaneous psoriasis and arthritis, absence of
subcutaneous nodules, and serum negative for rheumatoid factor. Roentgen signs include
bone resorption with "pencil-in~cup" IPJ osteolysis and mineral resorption (DIPJ
involvement with erosion and expansion of base of distal phalanx with proximal osteolysis),
oligoarthritis, sacroiliitis, and spinal column involvement.
Charcot Neuroarthropathy (Neuropathic Arthropathy)

Causes of Charcotneuroarthropathy include central nervous system defect, such as syphilis
(check fluorescent Treponema! antibody if suspect this with charcot foot), syringomyelia,
meningomyelocele, post-traumatic degeneration, multiple sclerosis, and spinal cord
compression. Peripheral nervous system disorders such as Charcot-Marie-Tooth disease,
diabetic peripheral neuropathy, alcoholic peripheral neuropathy, tuberculous or
lepromatous infection, amyloidosis, pernicious anemia, and steroid-induced neuropathy.
An unusual disorder known as congenital indifference to pain can also effect neuroarthro-
pathic joint disease. Pathologically, Charcot joints have been attributed to, primarily,
autonomic denervation with loss of vasomotor tone, hyperemia, increased bone perfusion
and loss of bone mineralization. The loss of proprioception, joint relaxation and hypotonia,
recurrent microtrauma, possible major injury, resultant malallgnment, cartilage fibrillation,
and subchondral plate fragmentation have also been sited as components of the
development of Charcot joint disease. Ankle equinus is a primary deforming influence in
many cases of pedal Charcot degeneration. The foot is usually warm, dry, and swollen.
Other effects of peripheral neuropathy, such as increased hyperkeratosis and keratin
stiffness, loss of sudomotortone (anhydrosis), protective touch-pressure sensation (5.1 0 or
red West-Foot monofilament esthesiometer), and intrinsic muscle atrophy (intrinsic minus
foot), also contribute to pedal breakdown. Increased blood flow results in abnormal venous
pooling and edema.
TABLE 3-8. HARRIS AND BRAND ClASSIFICATION OF INSENSITIVE FOOT DEFORMITY.

Pattern Anatomical apex of pedal breakdown
I Calcaneal
II Talar
Ill Midtarsal
IV Lateral hindfoot(calcaneocuboid)
v Usfranc (tarsometatarsal)
Harris and Brand have divided tarsal destruction in the insensitive foot into five
patterns. Pattern 1- Calcaneal, Pattern II - Talar, Pattern Ill - Midtarsal, Pattern IV- Lateral
hindfoot, and Pattern V - Lisfranc. As degeneration progresses, cartilage debris is
imbedded in synovium and detritic synovitis develops from deposition of cartilage and
bone fragments, and shards of bone and cartilage can migrate into soft tissue along
the extremity.
Other causes of detritic synovitis include silicone polymer degradation, osteonecrosis,
calcium pyrophosphate deposition {pseudogout), psoriatic arthritis, and osteoarthritis.
Microscopic evidence of shards of cartilage and bone in synovium is diagnostic of
Charcot joints. Extreme angular deformation of the joint leads to ligamentous and capsular
rupture, gross fracture, and progressive deformation. Treatment must encompass systemic
medical management in conjunction with local care. Nonwweight bearing using bedrest,
patellar tendon bearing bracing, and total contact casting; as well as antibiotic prophylaxis
or therapy, and surgical management of cutaneous wounds and bone and joint deformity,
are all components in the coordinated treatment of Charcot neuroarthropathy. Prior to
surgery for stabilization of deformed joints and fractured bone, it is necessary to achieve a
state of quiescence. Equinus deformity is addressed, and the mainstay of surgical
reconstruction is arthrodesis in conjunction with electrical bone growth stimulation.
Fixation methods for neuroarthropathic bone include internal fixation, external fixation, and
intramedullary nailing of the tibia. Careful perioperative management is critical.
Septic Arthritis
Septic arthritis usually presents as a monoarticu!ar, erythematous (unless vascular
compromised), lower extremity disease with the knee as the primary site of involvement.
Etiologies include contiguous spread, direct implantation, hematogenous sources, or
surgical contamination. Contiguous spread septic arthritis occurs when osteomyelitis
is present in metaphyseal or epiphyseal bone, with resultant bacterial spread into
subchondral bone leading to eventual joint infection. Hematogenous spread is common
in children, and often the result of otitis media or upper respiratory tract infections. Direct
implantation of bacteria into the joint may occur due to puncture wound. Postsurgical joint
infection is most likely when endoprosthesis are used.
Common infecting organisms include S. aureus, H. influenza, and others. Septic
arthritis correlates with patient age as follows: S. au reus is the most common organism in
all patient populations; Streptococcus and gram negative organisms are most common in
neonates, Hemophilus influenza is most common in children 6 months to 5 years of age,
Neisseria is most common in teenagers; and in adults, less than 5% of cases are caused by
E coli, Proteus mirabilis, and P aeruginosa. (P aeruginosa is common after puncture
injuries); while sickle cell anemia patients are predisposed to Salmonella; and the
compromised host (burn wounds, drug addict, HIV positive, chemotherapy, steroid
therapy) is susceptible to Serratia marcescens. Patients with pyarthrosis present with an
extremely painful, hot, and swollen joint that they will antalgically guard. The patient may
also exhibit varying signs of septicemia. The onset of symptoms and joint destruction are
frequently rapid and, therefore, timely diagnosis and treatment are necessary in order to
salvage the joint The differential diagnosis in children includes acute rheumatic fever and/or
a flare up of juvenile rheumatoid arthritis. In adults consideration should be given to the
possibility of joint trauma, gout, pseudogout, or foreign body synovitis.
Useful clinical lab findings include neutrophilia with left shift, elevated ESR, positive
CRP; and blood cultures are positive in 50% of cases. Roentgen signs include increased
soft tissue density and volume, effusion and juxta~articular osteopenia. A Tc-99 bone scan,
in combination with a Ga-67 scan, may be helpful in making an early diagnosis, despite the
lack of specificity. An ln-111 labeled leukocytes scan is both specific and sensitive for
infection, and may be used instead of Ga-67.
Joint aspiration should be performed when septic arthritis is considered, however
care should be taken to avoid aspiration through an area of distinct overlying cellulitis
or infection, as this technique may actually inoculate a sterile arthritic joint with bacteria.
A sterile surgical prep of the overlying skin is mandatory before joint aspiration is performed.
In order of importance, aspirate should undergo the following studies: C&S (aerobic and
anaerobic, and fungal), gram stain and acid-fast stain, examination for crystals, WBC count
and differential, glucose concentration. In a septic joint the WBC will usually be higher than
100,000, with the exception of gonococcal arthritis wherein the WBC count is usually less
than 50,000. In septic arthritis, the differential cell count consists of 90-95% neutrophils. In
additional to lab analysis, the aspirate is grossly inspected for color, consistency, and clarity.
In septic arthritis, the clarity and color will vary from cloudy yellow to creamy white or gray.
The treatment of septic arthritis is much the same as that for an abscess, wherein
incision and drainage, foreign body removal and debridement are performed. Controversy
exists as to whether or not adequate drainage and cleansing can be performed via
multiple repeated needle aspirations and lavage. This technique has also been criticized for
potential cartilage damage due to needle trauma as well as pain and anxiety related to
multiple aspirations (particularly in young patients). Open surgical joint drainage and
debridement allows for direct visualization, lysis of adhesion or scar tissue, removal of
necrotic and infected tissue, placement of drain tube, placement of antibiotic impregnated
PMMA beads if osteomyelitis is present, and thorough inspection of the joint confines.
The criticism of open drainage and debridement is that it promotes arthrofibrosis and
dysfunction due to scar formation. In a child, arthrotomy may be reserved in case of failed
drainage using multiple needle aspirations and lavage. Arthrotomy should be performed in
patients with suspected osteomyelitis, infected endoprosthesis, long-standing infection or
resistance to previous aspiration/lavage, or in the septicemic or endotoxic patient.
Following arthrotomy the wound is initially immobilized and packed open. It is
important to avoid dessication of the joint tissues, and BID wound lavage and fresh
dressing applications are used until the acute inflammatory episode subsides (24 to 48
hoursLafter which gentle passive range of motion should be initiated. Early motion is
critical in preventing significant arthrofibrosis and limited motion. Presumptive antibiotic
therapy should cover S. au reus (intravenous cefazo!in or nafcillin, or cl!ndamycin in
patients sensitive to PCN), and any other suspected organisms based on clinical history.
Antibiotic therapy is adjusted in accordance with definitive C&S results, and should be
continued IV for a minimum of two weeks. If the patient is responding well, then conversion
to oral antibiotics is made at approximately two weeks, and continued until a full antibiotic
course of four weeks is completed (oral antibiotic being administered from the second
through fourth weeks).
68 Selected Diseases and Pathological Conditions Gh. 3
SELECTED NEUROLOGICAL DISORDERS
Familial Sensorimotor Polyneuropathy (CharcotwMarie-Tooth Disease)

Familial Sensorimotor Polyneuropathy is also know as Gharcot-Marie-Tooth Disease (GMT)
and Peroneal Muscular Atrophy. GMT disease is a progressive, familial, symmetrical,
peripheral polyneuropathy that affects males five times more often than females, and
presents in varying degrees from mild to severe. Severe cases may display significant
cardiac dysrhythmia, Friedreich's Ataxia, and often do not survive beyond adolescence.
GMT involves distal muscle atrophy that begins in the feet and hands then legs and
arms. Lower extremity involvement is often more pronounced, and observed earlier, than is
upper extremity involvement Classically, the peronii, tibialis anterior, long extensors, pedal
lumbricals and interossei are gradually denervated as the disease progresses, leading to
muscular atrophy and the "stork leg" or "wine goblet" appearance of the legs. Muscle
wasting effects drop foot, pes cavus \more specifically, cavo-adductovarus), steppage gait,
recurrent lateral ankle ligamentous sprains that eventually develop into chronic instability,
claw toes and MTPJ subluxations, and mechanically induced cutaneous compromise.
Peripheral touch-pressure sensation, deep tendon reflexes, and voluntary muscle function
are diminished.
Electroneurodiagnostic testing will show markedly slowed conduction velocity
(normal conduction 45 to 55 m/sec), while EMG reveals increased fibrillation potentials.
Muscle biopsy reveals atrophy. Neurological consultation and genetic counseling are in
order. Conservative treatment is aimed at increasing stability, and includes cavus-mold
orthoses, digital retainers, ankle sleeve, drop foot bracing (MAFO or similar device), and
palliative skin and nail care.
ReconstrucTive surgical intervention addresses the pes cavus, digits, and drop foot; and
usually combines stabilization arthrodesis, or sometimes osteotomy, with tendon transfer.
Arthrodesis is generally preferred whenever progressive neuromuscular disease is treated.
Arthrodesis yields a stable bone mass upon which the transferred tendons can function. When
heel varus is mild, the Dwyer osteotomy combined with heel cord lengthening and Ste!nd!er
stripping \release of plantar intrinsics and fascia from calcaneus) may be adequate; however
triple arthrodesis and tendon transfer from the posterior or medial leg compartment to the
dorsum of the foot (tibialis posterior through the interosseous membrane) offers more
correction and longterm improvement Digftal stabilization, in the form of lesser toe PIPJ and
hallux IPJ arthrodesis, in conjunction with MTPJ relocation, is also very usefuL Consideration
may also be given to first metatarsal dorsiflexory base osteotomy.
Dejerine Sottas Disease (Hypertrophic Interstitial Polyneuropathy)

Clinically .this disease is similar to CMT, with distal muscle weakness of the lower
extremities with associated sensory deficit, and decreased deep tendon reflexes. Pedal
deformities include pes cavus and claw toes, and the patient may display kyphoscoliosis.
The most distinctive feature ofthis disorder is palpable and sometimes visible enlargement
of the peripheral nerves. Nerve biopsy (usually sural nerve) will confirm the diagnosis.
Roussy-Levy Syndrome
Patients with this disease have been compared to patients with CMT disease, with the
addition of an essential tremor that is most prominently expressed in the hands. This is a
familial, slowly progressive, symmetrical neuromuscular disease. Clinical findings include
areflexia, intrinsic pedal muscle atrophy, pes cavus and claw toes, clumsy gait and poor
equilibrium, and the presence of the previously noted essential tremor.
Refsum's Disease
This disease is the result of abnormal lipid metabolism wherein phytanic acid accumulates
in the serum, which results in elevation of serum phytanic acid to levels up to 50 times
greater than normal. Associated findings include ichthyosis, night blindness, and a
preceding febrile illness. Peripheral muscle paresis, areflexia, dropfoot, pes cavus, and
claw toes are also observed.
Friedreich's Ataxia
This is typically a more severe and disabling disease than CMT disease, and the onset is noted
early in life (childhood) and progresses until the patient is essentially incapacitated by
middle-age. Hallmarks ofthe disease are ataxia, unstable gait, and pes cavus with clawtoes.
Muscular Dystrophy I MDI

Muscle fibers atrophy and become necrotic, resulting in weakness, clinically evident
muscle atrophy (decreased girth), areflexia, and secondary muscle contracture. Mental
impairment may also be present
There are three types of MD:

1. Duchenne's pseudohypertrophic MD- most common, muscles appear large and
firm because of fatty conversion, affects only males, and the onset is between
1-3 years of age with subsequent rapid progression
2. Facioscapulohumeral MD
3. Limb girdle MD -Ankle equinus and equinovarus deformities are common foot
conditions seen in patients with MD, although pes valgus may also appear.
Classically individuals with MD display Gauer's sign when they raise themselves
from seated or recumbent position, where in they "climb up themselves" by
pushing their hands/arms against their knees and thighs, thereby pushing the
torso upward.
Myelodysplasia(Spina Bilida)
These disorders comprise a group of developmental deformities of the spinal cord and
vertebrae that most commonly affect the lumbar and sacral levels, and include:
1. spinal bifid a with meningocele
The meningeal sac protrudes through an open neural arch vertebral defect
and extends to the subcutaneous layer.
2. spina bifid a with myelomeningocele
Other elements ofthe spinal cord and nerve roots have also protruded
3. myelocele
Even the skin fails to enclose the cord protrusion, resulting in the most se-
vere form of spina bifida.
4. spina bifida occulta
The neural arches of the vertebra have not completely closed, however all
of the neural elements remain within the spinal canal.
Pathologically, the spinal cord defect effects motor, sensory and autonomic functional
deficits observed in the lower extremities. The dynamic muscle imbalance tends to worsen
over time, resulting in equinus, equinovarus, and equinovalgus, and marked rotary
deformities of the lower extremities. Associated findings include urinary bladder paralysis
(which requires catheterization during operative intervention) which may be associated

with chronic urinary tract infection; and profound anesthesia and lack of protective
sensation, often with mal perforans ulceration.
Poliomyelitis
The polio virus affects the anterior horn cells (!ower motor neuron) of the spinal cord,
resulting in some degree of lower extremity flaccid paralysis (areflexia, hypotonia, and
weakness). The central neJVous system defect in poliomyelitis is non~progressive,
however the disease can lead to contracture that changes overtime. Common deformities
include equinovalgus, and others, and tibiocalcaneal and pantalarfusion can be useful.
Cerebral Palsy (CP)

Classically, a congenital neuromuscular disorder caused by an intracranial brain lesion,
and identified early on in the patients life.
Three types of CP
1. Spastic CP
Upper motor neuron disease effects hyperreflexia, clonus, and extensor
plantar response, typically anterior leg compartment weakness, dropfoot,
pes cavus, clawtoes, and steppage gait with circumduction. This is the most
common form of spastic CP, and affects approximately 65% of CP patients.
2. Athetoid CP
This form affects approximately 20% of patients with CP, and is associated with
a slow, worm-like hypertonia due to upper motor neuron disease.
3. Ataxic CP
Ataxic affects about 15% of CP patients, and is associated with tremor and atonia.
UMN disease causes more spasticity in muscles that cross more than one joint, such
as gastrocnemius. Muscles of flexion, adduction, and internal rotation tend to overpower
those of extenslon, abduction, and external rotation. Talipes equinova!gus, or equinovarus,
is common.
Complex regional pain syndrome (CRPS)-This is a serious chronic pain condition, the
hallmark symptom being unrelenting, progressively worsening, intense pain out of
proportion to the severity of the injury or inciting event Patients with CRPS often display
allodynia, wherein they relate pain caused by what would have otherwise been a non-
oxious stimulus, and hyperpathia, wherein a stimulus that would typically be considered
painful is much more painful. CRPS usually affects an arm, leg, foot or hand, and the pain
may evolve to include the entire, dystonic extremity. Although CRPS affects men and
women, it is more common in young females. CRPS is thought to be the result of peripheral
and central nervous system dysfunction. CRPS I, often referred to as reflex sympathetic
dystrophy syndrome (RSDS), occurs with tissue injury that does not involve direct,
underlying nerve trauma. CRPS IJ, often referred to as causalgia, is associated with known
trauma involving a known anatomical nerve trunk. The clinical signs and symptoms of CRPS
1and II are the same. Characteristic signs and symptoms include color and teperature
changes involving the skin, associated with sharp and burning pain, swelling, and
sweating. Associated with these symptoms are exquisite skin sensitivity, vasomotor
instability that causes the affected part to be colder or warmer than the contralateral limb,
discoloration that includes mottled blue, pallor, purple; textural changes that include thin,
shiny skin; hypertrophy or atrophy of digital hair and nail growth; fusiform digital swelling and
stiffness, dystonia that affects the ipsilateral extremity and may extend to other
extremities; symptoms may be heightened by emotional stress, and depression secondary
to chronic pain is common. Although there is no definite cutoff between symptoms and
signs that define distinct stages of CRPS, many clinicians categorize Stage 1 as lasting from
1-3 months and characterized by sharp, burning pain, myalgia and dystonia, temperature
and color changes, and increased hair growth. Stage 2 extends from 3-6 months and is
associated with worsening pain, edema, nail dystrophy and diminished hair growth,
muscle atrophy and weakness. Stage 3 extends beyond 6 months and entails irrevesible skin
and bone atrophy (Sudek's atrophy of bone), and permanent pain and limb contracture. The
pathophysiology of CRPS is notfully understood, although it is believed that the sympathetic
nervous system plays an important role in maintianing the pain, as pain receptors in the
affected limb become sensitive to catecholamines. It has also been theorized that CRPS
represents disruption of the healing process secondary to an abnormal immune response
to injury. Due to the complexity of symptoms and similarities with other conditions, the
diagnosis of CRPS can be difficult to make, especially early in the course of the disease.
There is no single diagnostic test for CAPS, and it is important to rule out other conditions
so that the diagnosis can be made by exclusion. A triphasic bone scan may be useful, and
often shows a splotchy uptake of radiotracer in cases of CAPS. Supportive therapies
include the use of topical analgesics, anticonvulsant and antidepressant medications,
corticosteroids and opiate analgesics. Physical therapy and movement are encouraged.
Sympathetic nerve blockade, using phentoloamine or local anesthetic; sugical
sympathectomy, only if blockade afforded prolonged and marked relief; spinal cord
stimulation, using an implantable generator with a stimulating electrode along the spinal
cord; and spinal intrathecal local anesthetic and/or analgesic pumps, may be usefuL The
prognosis tor patients with CAPS varies from person to person, and outcomes range from
permanent pain and disability to spontaneous remision and revovery.
NEOPLASMS
Any enlargement oftissue, whether edematous, hypertrophic or neoplastic, can be referred
to as a tumor. Whenever dealing with neoplasm, a high index of suspicion should be
maintained tor potential malignancy. Malignancy of epidermal germ eel! origin is termed
carcinoma, whereas those of mesenchymal origin are referred to as sarcoma. Any lesion,
even what is thought to be persistent pyogenic granuloma, chronic onychocryptosis,
resistant verruca, or a diffuse subcutaneous mass that does not respond to reasonable
therapy should be more closely inspected. Closer inspection may involve radiographs or
MRI, lab testing, or biopsy. Consultation may also be helpful. In general, any lesion
suspected of being malignant warrants oncologkal consultation and systemic evaluation
for lymph node, lung, Gl, bone, and other sites of potential metastasis or regional
dissemination. Proper biopsy technique is crucial.
General considerations in the assessment of a neoplasm include coloration, change
in appearance, presence of symptoms such as pain or pruritus, hemorrhage, location
superticial(freely moveable below or within the skin) or deep (fixed) to the deep fascial
(muscle fascia), sensory or motor disturbance, vascularity or pulsatile nature of the lesion,
status of the popliteal and inguinal lymph nodes (tender and/or enlarged), and the presence
of metastatic disease elsewhere in the body.
Diagnostic imaging, such as standard radiographs, MRI and CT scans may be helpful,
and a chest X-ray should be obtained whenever cancer is considered, as the lungs are the
primary site of sarcoma (and many carcinoma) metastasis. Clinical lab testing, including CBC
and differential, biochemical profile, tumor antigen testing, and ESR may be helpfuL
Needle biopsy (not fine needle) can be helpful if multiple core specimens are obtained
from different sites within the lesion, and incisional biopsy through the mid portion of the
soft tissue mass is routinely performed. Whenever performing an incisiona! biopsy for
suspected sarcoma (or carcinoma), the biopsy channel to the lesion should be oriented
longitudinally in line with the suspicious mass and within a region to be fully excised with
subsequent definitive surgical excision of the lesion. Moreover, it is important to avoid
dissection into adjacent fascial compartments, in an effort to maintain natural anatomical
barriers to spread of malignant cells. The oncological surgeon can, in many cases of
sarcoma, preserve adjacent intact muscle compartments protected by intact deep fascia,
when appropriate biopsy technique has been used. Attention to such detail may be the
difference between muscle compartment resection from the foot into the leg, versus BK or
AK amputation.
Selected Neoplasms
Epidermal (epidermoid)inclusion cyst~ precipitated by skin trauma, wherein e-pidermis is
forced into underlying dermis and continues to desquamate and build up degenerating
keratin within the dermis. This leads to slow development of a firm, round, subcutaneous
nodule that is often seen on the sole or toes. Pilar and sebaceous cysts are inclusion cysts
around the hair follicle.
Eccrine poroma ~ a sweat gland tumor that is nodular and may drain serous fluid.
Squamous cell carcinoma {SCC)- a malignant epithelial neoplasm with predilection for skin
and mucous membranes. The lesions display erythematous margin, nodules or shallow
ulceration. There are several variations, including verrucous carcinoma, prickle cell
carcinoma, epidermoid carcinoma, and epithelioma cuniculatum. SCC is more common in
light-skinned individuals than in African-Americans, usually localizes to sun-exposed
surface or previously scarred, burned, or irradiated skin; is usually seen in patients over
the age of 40 years, 5% affect the foot and leg, rarely invade deep to bone and rarely
metastasize, and there is a 95% cure rate with adequate excision. sec can develop in
a chronic, non-healing wound or ulcer, Oncological consultation and possibly adjunct
radiation or chemotherapy may be in order.
Basal cell carcinoma (BCC)- the most common skin cancer, usually observed on sun-
exposed surfaces in the 30to 50 year-old patient, more common in women, lighter- skinned
individuals, involving basal cells of the epidermis, very slow growing and unlikely to
metastasize unless ignored or neglected.lt is also referred to as basal cell epithelioma due
to its failure to metastasize. Four types include superficial, pigmented, nodular, and
morpheaform. BCC has been known to form in scar tissue. Appears as a shiny nodule with
surface telangiectasia. There is a 99% cure rate with adequate excision or ablation via
cryogen, electrodesiccation, or radiotherapy. Routine follow~up is required after
eradication, and there is a 35% recurrence rate within 5 years.
Bowen's Disease (carcinoma in situ)- an in situ squamous cell carcinoma involving skin
and mucocutaneous junctions; appearing as a crusty, nodular looking plaque. When the
superficial crust is curettaged, the lesion appears dull red and moist It may appear as a
keratotic lesion on the plantar surface, and pathologically the basement membrane is
intact (CAin situ). Proper excision is curative. Bowen's disease is often associated with
internal malignancy, and oncological consultation is in order.
Dermatofibroma this fibrous skin tumor rarely occurs in the foot, appears flesh-colored,
and may be observed as a periungual angiofibroma which is also referred to as Koenen's
fibroma and associated with tuberous sclerosis, cafe au !a it spots and mental retardation.
Plantar fibromatosis- this is a benign and reactive lesion of fibrous tissue (plantar fascia)
affecting the plantar aspect of the foot. The lesions are firm and nodular, and may
resemble a low grade fibrosarcoma due to its fixed nature. Isolated excision is associated
with a 65% recurrence rate, and total excision of the affected band of plantar fascia is
indicated if padding and accommodative insole has failed to yield pain relief when weight
bearing. There is no distinct benefit to injection therapy. Plantar fibromatosis is also known
as Lederhaus disease, and associated with people of a Germanic heritage. These
individuals may also have Dupuytren's palmar contracture or Peronies penile fibromatosis.
Fibrosarcoma- these are firm, fixed small nodular to expansive irregular lesions that
may occur in the lower extremity. Fibrosarcoma may metastasize, and radical excision,
amputation, and oncological management are required.
Lipoma- these are composed of mature fat cells with thin capsular structures, and may
lead to adjacent nerve entrapment They are commOnly observed about the malleoli and
knee, and are amenable to excision.
Liposarcoma- a malignant lesion, often with vascular infiltration and termed angiolipoma.
Treatment is excision and oncological management
Ganglion cyst- the most frequently encountered tumor affecting jointtissue, and may also
affect the tendon sheath or nerve connective tissue (usually epineurium). These are
generally of traumatic etiology (perhaps distant incidental trauma), with myxoid
degeneration of connective tissue effecting gelatinous fluid that gels over time. A history
consistent with size change and aggravation by activity is common. The ganglion may
entrap adjacent vital structures and tendon. When in the popliteal fossa, a ganglion is
referred to as a Baker's cyst Conservative treatment consists of padding and gentle
compression, aspiration of cyst contents and local infiltration of acetate corticosteroid. Lesion
may recur after reduction in size and symptoms, and additional injection therapy or surgical
excision may be effective. Ganglions are seen in a!l age groups, even in the very young.
Digital mucous cysts~ a small cystic lesion overlying a digitaiiPJ, resembling a ganglion
cyst, and observed in the 30 to 80 year age group Inot typical in young individuals). The
lesion stems from myxoid degeneration of the underlying joint capsule, and treatment may
require IP arthroplasty.
Leiomyoma- a well-encapsulated, firm, rubbery-textured smooth muscle tumor arising from

erector pili or vascular smooth muscle. The treatment is usually excision or obseJVation
overtime.
Rhabdomyoma- a benign tumor of skeletal muscle that occurs usually in young patients.
The treatment is excision.
Rhabdomyosarcoma- a malignant tumor of skeletal muscle that occurs usually in the 5th
to 6th decade of life. The treatment is oncological consultation, adjunct radiation and/or
chemotherapy, and appropriate excision or amputation.
Giant cell tumor of tendon sheath- a true benign neoplasm of synovial structure which is
actually a variation of pigmented villonodular synovitis (PVS). It is usually seen in the 30 to
50 year age group, and is the second most common tumor oftendon after the ganglion cyst.
Observation or excision is the recommended treatmen~ and it is importantto note thatthere
is a high rate (25%) of recurrence following excision.
Synovial sarcoma- this malignancy arises from joint capsule, tendon, or bursa; and is
usually seen in youngsters and adolescents, aged 10 to 40 years. The knee and ankle
predominate, and radical excision, or perhaps amputation, is indicated after oncological
consultation and consideration to adjunct radiation and/or chemotherapy. The ankle is
frequently involved with a periarticular synovial sarcoma in the periarticular soft tissues.
Unlike piezogenic papules, synovial sarcoma is present as a subcutaneous nodule even in
the non-weight bearing attitude. The tumor can be of a fibroblastic (spindle cell) or
epithelioid cell type, and tissue specific antigens can aid the pathological diagnosis. Wide
excision, sometimes in conjunction with radiation or chemotherapy, is usually indicated
after biological staging is determined.
Schwannoma- a slow-growing benign, encapsulated tumor that develops within the nerve
sheath, often of traumatic origin. The tumor causes axon compression and nerve fiber
dysfunction. Microsurgical excision under Ioupe magnification is the indicated treatment
Neurofibroma- a benign, circumscribed, but not encapsulated neoplasm originating in the

nerve trunk, also of Schwann cell origin. The lesions are often multiple, pedunculated, and
nontender. Consideration must be given to von Recklinghausen's disease. Neurofibromas
may undergo malignant transformation.
Hemangioma- the most common benign vascular tumor observed in the feet There are
several distinct types of hemangioma. As with most vascular lesions, they are diascopy
positive (blanch when pressure is applied to the skin surface encompassing the lesion).
The capillary, or strawberry, hemangioma is the most common form. It is observed in the
newborn and may resolve as the child matures. The cavernous hemangioma is a large
lesion consisting of a thick, extensive proliferation of vessels which may involve a large
portion of the foot, and thereby pose serious surgical problems relative to excision.
Arteriography is useful in the evaluation of a suspected hemangioma.
Kaposi's sarcoma~ is a vascular malignancy comprised of a proliferation of capillaries and

connective tissue, seen traditionally in males over the age of 50 years, and of Mediterranean
descent There is also a high incidence in patients suffering with AIDS. The lesions are
bluish, or purple nodules or plaques. Treatment is observation (pending general medical
status) or excision.
Glomus Tumor- a benign, neuro-arterial neoplasm that is usually localized to the periungual
(nail bed) region, the hallmark of which is extreme pain, and a reddish or bluish color.
Treatment is excision.
Malignant Melanoma
Melanocytes have dendritic processes and are of epidermal germ cell origin. They function
to produce "sun~protective" melanin pigmentthatguardsthe underlying living cells of the
basal layer of the epidermis from the mutagenic effects of UV radiation. Lower extremity
melanoma is more common in women, while men more commonly display melanoma on the
torso. Melanoma is most commonly seen in the 30 to 60 year age group. Sun exposed
surfaces are most susceptible, however the palms and soles, particularly in individuals with
dark skin, can be affected. Anatomic sites prone to sun exposure include: "BANS" (back,
arms, neck, scalp). Diagnostic signs focus.on the size, shape, color, location, and duration
of the pigmented lesion. Benign pigmented skin lesions of the lower extremity should be
less than 5 mm in diameter, homogenous in color, smooth or regular in contour, and
present for as long as the patient can remember. Plantar and periungual pigmented lesions
warrant an especially high index of suspicion. Any lesion on the foot that is greater than 5
mm in diameter, heterogenous in color, or displaying an irregular or notched border should
be biopsied if it has not been present since birth.
Melanoma grows in a radial phase and an invasive or vertical phase. The vertical
growth phase correlates with metastasis. Melanoma in the horizontal or radial growth phase
appear macular, while the vertical growth phase is associated with a more aggressive
tumor. Poor prognostic indicators include lesions displaying a whitish or amelanotic co! or,
tumor regression (notched border), progressive nodu!arity (consistent with deeper
invasion of the dermis), change in size or shape, ulceration, hemorrhage, pain, or pruritus,
should be considered malignant and treated after accurate identification.
Four Main Clincohisto/gic Types

1. Superticial spreading melanoma (SSM) may develop on any portion ofthe body
with peak incidence around the 5th decade. Comprises about 70% of cutaneous
melanomas. Classic SSM displays the "red, white, and blue" of advanced malig-
nancy showing tumor regression. These are very common on the trunk of males.
2. Lentigo mallgna malignant melanoma (LMM) is the slowest growing lesion, seen
on sun exposed surfaces. LMM comprises about 15% of MM, and is most common
in the elderly (mean age 70 years). The lesion is macular with color variegation.
3. Nodular melanoma (NM) is highly malignantwith primarily a vertical growth phase
only. NM comprises about 12% of cutaneous melanoma, and is seen most
commonly in males approximately 50 years of age. The appearance is uniformly
blue, black, or dark brown, with a nodular appearance. Ulceration is rare with NM.
4. Acrallentiginous melanoma (ALM) shows predilection for plantar, palmar, and
nail bed or grooves. Hutchinson's sign (pigment changes in the eponychium of
subungual melanomas), whereas melanotic whitlow involves subungual
melanoma. The peak incidence of ALM is the 7th decade. ALM accounts for
about 3.5% of cutaneous melanomas.
Staging
Stage I malignant melanoma involves a primary lesion, or one with local satellite
within 5 em
Stage II malignant melanoma entails in transit metastasis and regional lymph node
involvement (identified by palpable adenopathy or node biopsy)
Stage Ill malignant melanoma entails distant metastasis. Melanoma can go any-
where in the body including the choroid of the eye and internal parenchyma.
The most important determinant of survival rate for malignant melanoma is clinical
staging. Survival of a clinical Stage !lesion is far more likely than survival of a clinical Stage
II lesion, whereas clinical Stage Ill lesions are usually lethaL
Clark's Levels and Breslow's Thickness Pathological staging systems of malignant

melanoma include Clark's levels and Breslow's thickness (Tables 3-9 and 3-10). The deeper
the level, or thicker the lesion, the more likely is there to be metastasis, and therefore the
prognosis worsens as the lesion thickens or progresses deeper into or through the skin.
Identification of the Breslow thickness has been shown to correlate better with survival
rate.
TABLE 3-9. CLARK'S LEVELS.

level Microscopic appearance of melanoma
I Involvement of epidermis with no involvement
deep to the basement membrane
II Penetrates the basement membrane
and enters the papillary dermis
Ill Fills the papi!lary dermis and cancer cells line
up against, but do not penetrate into the reticular dermis
IV Penetrates into the reticular dermis
v Fills the reticular dermis and enters
the subcutaneous fat layer
TABLE 3-10. BRESLOW MELANOMA THICKNESS AND CORRESPONDING SURVIVAL

Thickness (mm) 5-year survival rate(%)
0-0.75 83-100
0.76-1.5 37-90
1.51-2.25 37-83
2.26-3.0 44-72
>3.0 9-55
The most important service the podiatrist can provide in regard to malignant melanoma
is timely and accurate recognition and biopsy, thereafter followed by appropriate
consultation and/or definitive surgery or referral to an oncological surgeon. Clinical Stage
I lesions can be definitively excised by the podiatric surgeon, whereas Clinical Stage II
lesions, with regional lymph node involvement, require node dissection and the expertise
of a general or vascular surgeon familiar with melanoma.
Biopsy of a suspected malignant melanoma should be performed, when possible, using an

excisional technique that provides 1to 3 mm of norma! appearing skin about the lesion, and
the biopsy must include subcutaneous fat (full-thickness skin).
For small lesions, local anesthesia is infiltrated in a proximal V-b!ock fashion in normal
appearing tissue. Two semi-elliptical incisions are made about the lesion from proximal to
distal, the resultant dimension of the lesion being about 3:1 length:width. The proximal
normal margin of skin should be marked with a suture for pathological orientation.
For larger lesions, where complete excision is not possible without creating a large
defect, incisional or punch biopsy should be employed. The incisional or punch biopsy
should be oriented in a faShion that will allow the biopsy wound to be excised in toto when
subsequent definitive surgery is performed. The incision a! or punch biopsy must still be
ful!~thickness skin and include underlying subcutaneous fat. Select the most clinically
malignant appearing site of the lesion, and get enough of the lesion for pathological
inspection. As with any biopsy of suspected malignancy, timely diagnosis and appropriate
follow-up are mandatory. It is proper to perform an incisional biopsy when indicated, as
long as definitive care is subsequently administered.
Definitive treatment, based on clinical and pathological assessment, always includes
oncological consultation prior to definitive surgical ablation of the lesion. Malignant
melanoma can be a systemic disease, therefore chest X-ray and constitutional evaluation
are needed. In many cases, it is best to administer chemotherapy prior to definitive
surgical excision, in an effort to decrease the tumor and minimize the risk of metastasis.
Survival rates may increase with adjunct preoperative radiation or chemotherapy. Guide-
lines for definitive excision are depicted in Table 3-11.
TABLE 3-11. GUIDELINES FOR DEFINITIVE EXCISION OF MELANOMA.*

Melanoma depth (mm) Recommended margin of normal
appearing skin {em) about definitive excision
< 0.76 2
0.76- 4.0 3
>4.0 5 (with excision of underlying deep fascia)
*Closure may require use of a skin flap or graft
The definitive treatment of a subungual melanoma is digital amputation at the level of

the metatarsophalangeal joint Therapeutic lymph node dissection remains somewt"lat
controversial for clinical Stage II melanoma, particularly with lesions of Clark's Levell! and
Ill, however it has been recommended for lesions of Clark's Ieveii I - V, and the decision
has to be made by the oncological surgeon after discussion of adjunct chemotherapy,
prognosis and morbidity related to inguinal node dissection.
Bone Tumors
Radiographic Characteristics
Three common radiographic patterns of bone destruction
1. Geographic bone destruction represents the least destructive, slowly develop-
ing and usually benign process. There is a zone oftransition that separates the
lesion from normal appearing bone.
2. Moth-eaten bone destruction represents a more rapidly destructive, malignant

process such as sarcoma or osteomyelitis. The transition between the lesion
and normal bone is wide and less well-defined.
3. Permeative bone destruction represents the most aggressive and rapidly
progressive, malignant process. The zone of transition between tumor and
normal bone .is very wide and almost imperceptible radiographically.
Other important radiographic characteristics of bone tumors include the type of

trabecular pattern, the periosteal reaction, position of the lesion both relative to anatomic
location as well as.the transverse plane (cross sectional) location within the bone.
Trabecular patterns of some bone tumors

giant cell tumor of bone~ delicate, and thin trabeculae
chondromyxoid fibroma- coarse, and thick trabeculae
aneurysmal bone cyst~ delicate, and horizontal, parallel trabeculae
non~assifying fibroma- loculated trabeculae
intramedu!fary hemangioma~ striated, or radiating trabeculae
Periosteal patterns of new bone formation

solitary bone cyst- a monolayer of new bone formation adjacent to the tumor and
separated from pre-existing cortex
osteogenic and Ewing's sarcoma- multiple, concentric layers ("onion skin") of new
bone growth, sometimes creating a Cadman's triangle wherein periosteal
elevation adjacent to pre~existing cortex radiographically depicts an angle with
the apex pointing in the direction of normal bone (also seen in other expansile
lesions of bone cortex, such as osteomyelitis)
osteogenic sarcoma~ radiating spicules, or star burst pattern of new bone growth
multiple myeloma and Ewing's sarcoma~ hair~on-end radiating spicules of new
bone growth.
Transverse plane locations within the bone

enchondroma and solitary bone cyst- centrally located
giant cell tumor of bone, osteogenic sarcoma, chondrosarcoma, fibrosarcoma, and
chondromyxoid fibroma- eccentrically located within the medullary canal,
arising to one side of the central axis of a long bone;
non-ossifying fibroma and osteoid osteoma -located in the cortex periosteal sarcoma
osteochondroma~ lesions located in the periosteal region
Characteristic anatomic sites of tumor development

diaphyseal lesions- solitary and aneurysmal bone cysts, giant cell tumor of bone,
Ewing's sarcoma, enchondroma, non-ossifying fibroma, osteoblastoma,
eosinophilic granuloma, and fibrous dysplasia
metaphyseal lesions~ solitary bone cyst, osteogenic sarcoma, osteochondroma,
chondrosarcoma, non~ossitying fibroma, and chondromyxoid fibroma
epiphyseal lesions- chondroblastoma, intra osseous ganglion cyst, giant cell tumor
after epiphyseal plate closure, and hemangioma.
In general, malignant bone tumors radiographically display moth eaten or permeative

cortical destruction, periosteal new bone formation, and adjacent soft tissue swelling
(increased density and volume). CT scans and MRis can also be helpful in determining the
location, confines, and type of tissue involved in bone tumors. Arteriography can be useful
in determining vascular involvement, and aids in limb salvage planning when compartment
resection or amputation is considered. Laboratory findings consistent with bone tumor
formation and destruction include leukocytosis and anemia, elevated ESR, elevated serum
Cat+, elevated alkaline phosphatase (osteoblastic activity), and increased total serum
protein (multiple myeloma). Definitive diagnosis is made with appropriate bone biopsy, which
may involve fine needle aspiration or, more reliably trephine plug(s) or en bloc excision of
representative bone.
Treatment of benign bone tumors varies from observation to surgical resection and repair,
depending upon symptomatology, the presence of pathological fracture, and prognosis.
The treatment of malignant bone tumors always involves oncological consultation and
management, as adjunct radiation or chemotherapy may be used in conjunction with
appropriate resection or amputation. Longterm (life~long) follow-up is a required part ofthe
management of malignancy, regardless of tissue type.
Cartilaginous Tumors of Bone

Enchondroma usually a well-defined, asymptomatic, centrally located medullary lesion,
seen in the 3rd to 4th decade. This tumor often appears as a lytic lesion in fingers and toes,
and pathologic fracture may occur. If pain develops, consider chondrosarcoma. Multiple
enchondromatoses are associated with Oilier's disease.
Periosteal (juxtacortical) chondroma - usually observed in children, wherein the

juxtacortical soft tissue mass erodes or saucerizes the bony cortex.
Chondroblastoma ~ usually observed in 15 to 30 year-old age group, commonly localized to

the calcaneus or epiphysis of a long bone, with a well~defined osteolytic appearance.
Chondromyxoid fibroma- usually observed in 2nd to 3rd decade, this lesion appears as a
sharply-outlined, coarsely trabeculated, round, lytic lesion of the metaphysis.
Osteochondroma~ the most common benign growth of bone occurring anywhere in the
skeleton, typically in the 2nd to 4th decade, originating in the metaphysis, displaying a
cartilaginous cap over new bone proliferation, and rarely associated with malignant
transformation.
Chondrosarcoma~ a malignant cartilaginous tumor of bone. It can arise from malignant

transformation of an enchondroma, periosteal chondroma, or osteochondroma. It is rare in
children, and is usually observed in the 5th to 6th decade. lt is the second most common
malignant tumor of bone, following osteogenic sarcoma. Bone destruction appears moth
eaten, with speckled medullary and soft tissue calcification (in general, soft tissue
calcification in the presence of suspected tumor is an ominous radiographic sign), and
metastasis to the lungs is common. Treatment of this lesion involves oncological
management for radiation and/or chemotherapy, as well as appropriate resection or amputation.
Bone Forming Tumors

Osteoid osteoma- usually observed in children and young adults, marked by nocturnal pain
alleviated with aspirin, displaying a round osteolytic defect surrounding a central
radiodense (sometimes lucent) nidus that is usually no larger than 1 em in diameter. This
lesion is common in the foot.
Osteoblastoma- usually observed in 2nd to 3rd decade, larger than osteoid osteoma, more
common in males, rapidly growing, metaphyseal or diaphyseal lesion the pain of which is
not responsive to aspirin.
Osteogenic sarcoma- the most common malignant bone lesion, usually appearing in the 2nd
to 3rd decade, often affecting the metaphysis of the femur (40%) or tibia (16%). It is rapidly
expansile with a star burst pattern of periosteal new bone formation, cortical erosion, and
formation of Cod man's triangle. It can develop from Paget's disease of bone, which involves
haphazard new bone formation and bone resorption, effecting a "woven bone"
appearance, usually in males over the age of40 years, and is of unknown etiology (perhaps
viral). Very high levels of serum alkaline phosphatase and urinary hydroxyproline are
observed in Paget's disease.
Connective Tissue Tumors

Non-ossifying fibroma- usually observed in the lstto 2nd decade, eccentrically located in
the metaphysis, with a sharply demarcated, lobulated osteolytic lesion displaying a sclerotic
border.
Fibrosarcoma- usually observed in the medullary canal (67%) of a long bone in a young
male, displaying osteolysis with minimal new bone formation. Speckled soft tissue
calcification may be present
locally Aggressive Tumor

Giant cell tumor- usually obse!Ved in the 3rd to 4th decade well after growth plates have
closed (skeletally mature), localized to the diaphysis as well as metaphysis and epiphysis
Displays thin, delicate trabeculae that have a "soap bubble" appearance, expanding into
adjacent cortex, and known to undergo malignant transformation.
Tumors of Vascular Origin

Hemangioma- usually observed in the 4th to 5th decade, occurring in any bone. Displays a
cystic lesion surrounded by a "spoke wheel" appearance of periosteal new bone formation.
Glomus tumor- usually obse!Ved in the 4th-5th decade, often very painful, localized to the
distal phalanx, and may require IPJ disarticulation.
Tumor and Tumor-like Bone Lesions of Unknown Origin

Solitary bone cyst- these are simple, or unicameral; cystic lesions of bone, often observed
in the calcaneus or metaphyseal bone, in the 1st to 2nd decade, and contain a pinkish fluid
upon aspiration. This is the most common fluid filled cystic lesion of bone.
Epidennoid cyst- usually obse!Ved in the 2nd to 4th decade, it is an isolated lytic lesion,
usually of the distal phalanx.
Aneurysmal bone cyst a benign, blood-filled lesion that is usually observed in the 1stto 3rd
decade. It is expansile, with horizontal, parallel trabeculae that are readily observed on
MRI. The lesion is difficult to distinguish from malignancy.
Ewing's Sarcoma- usually observed in age group 5 to 25 years. It is a highly destructive

lesion of cortical bone, with both "onion skin" and "hair-on-end" appearance. It displays a
high rate of metastasis. It is the 4th most common malignant tumor of bone, and is rare in
African-Americans. Pathological fracture is common.
Metastatic Bone Disease

Breast and prostate cancer often metastasize to bone, including the bones of the feet.
Any musculoskeletal pain in an individual with history of previous malignancy warrants
a high index of suspicion and careful examination. Leukemia, although rarely arising
primarily in the foot, may effect secondary pedal osteolytic lesions, and is associated with
leukocytosis, anemia, fatigue and malaise, adenopathy and splenomegaly.
SELECTED EMERGENCY SITUATIONS
If a life-threatening event occurs in the office setting, the local emergency medical service
(EMS) should be notified (911) immediately so thattransportto the hospital can be achieved
in a timely fashion. The patient's vital signs should be monitored and recorded throughout
the event, and medications administered during the event should be recorded. Following
emergency treatment of any medical crisis, the patient must undergo immediate systemic
medical evaluation and ongoing treatment should be provided as indicated. Medical emer-
gencies occur, and the best treatment is prevention and preparation.
Syncope
Syncope is caused by temporary cerebral anoxia, often caused by bradycardia secondary
to parasympathetic overtone. lt is related to emotional stress and pain, often associated
with injection therapy. Trendelenburg positioning usually serves as adequate prevention.
Signs and symptoms include pallor, hypotension, tachycardia, mydriasis, and diaphoresis
(cool and clammy skin). Treatment consists of Trendelenburg positioning, loosening tight
clothing, cool compress to forehead, aromatic spirits of ammonia, oxygen administered at
4 to 6 !/min, and monitor vital signs.
Hypersensitivity Reactions
Hypersensitivity (allergic) reactions are caused by release of histamine, with resultant
vasodilatation and increased vascular permeability, and bronchospasm. If the reaction
progresses, airway constriction, hypotension and shock may ensue. There are four major
types urticarial rash, angioneurotic edema, asthma attack and anaphylaxis.
Utticarial rash presents with wheals, hives and pruritus. Treatment involves removal of the
allergen, and administration of 50-75 mg diphenhydramine (Benadryl) IM, followed by 50
mg PO q 6 h PRN.
Angioneurotic edema presents with marked mucous membrane edema resulting in swelling
of the eyelids, cheeks, lips, pharynx, and larynx. As the upper airway swetls, hoarseness
and stridor (laryngospasm), wheezing (bronchospasm) and cyanosis develop. Treatment
involves withdrawal ofthe allergen, and administration of 0.2-0.5 cc epinephrine SC q 15 min
as needed, in addition to 50-75 mg diphenhydramine IM, and 8 mg dexamethasone

(Decadron) IM for late effects.
Asthma attack presents with wheezing due to bronchospasm, effecting dyspnea, and
initial flush then cyanosis. Treatment involves administration of 2 puffs of aerosol
bronchodilator (Ventolln, Proventil), which asthmatic patients often carry themselves, or
0.3-0.5 cc epinephrine 1:1,000 SC q 15 min x3, in conjunction with aerosol bronchodilator.
Anaphylaxis results in rapid respiratory and cardiovascular collapse, and requires rapid
administration of epinephrine in order to avoid a severely morbid or fatal reaction. Signs
and symptoms include laryngospasm, bronchospasm, hypotension, nausea, diaphoresis,
pruritus, urticaria and angioedema, and unconsciousness. Treatment involves withdrawal
of the allergen, Trendelenburg position, maintain airway, 02, and administer epinephrine
1:1,000 SC or sublingual 0.3- 0.5 cc and repeated q 5-15 minutes until an adequate response
is observed, try to establish IV access. The sublingual route of administration is acceptable
when lV access is not attainable {inject into posterior ventral portion ofthe tongue where
it is vascularized with larger vessels). Inject .25 cc 1:1,000 epinephrine about site of
previous injection of allergen, or apply BP cuff proximal to site of allergen injection (release
every 10 to 15 minutes). If hypotension does not respond to epinephrine, administer
metaraminol (Aramine) 0.5- 5 mg IV. If bronchospasm persists, administer aminophylline
250 mg IV over 10 min.lf convulsion occurs, administer diazepam (Valium) up to 10 mg slow
IV infusion titrated until the seizure is controlled, or administer short-acting barbiturate
pentobarbitallOO mg IV. Be prepared to support and maintain respiration whenever IV
diazepam or pentobarbital are administered.
Toxic Reactions to Local Anesthetics

Toxic reaction to a local anesthetic involves initial central nervous system {CNS)
stimulation due to inhibition of inhibitory neurons, resulting hypertension, tachycardia, and
skeletal muscle twitching that may progress to convulsion. Treatment consists of
administration of Oz to counter hypoxia and resist convulsion, maintain airway and, in the
office, give diazepam (Valium) 10 mg slow IV titration. Following initial CNS excitation, CNS
depression may develop as the toxic level of local anesthetic proceeds to suppress CNS
function. Pathologic findings include hypotension, weak and rapid pulse, shallow, slow
respiration, loss of speech, confusion, delirium, and coma. Treatment involves airway
maintenance and administration of 02, ephedrine 0.5 cc IV or lM.Ifthe reaction proceeds
to cardiovascular collapse also administer atropine 0.4 mg IV, and commence BCLS and/or
ACLS.It is lmportantto know the toxic dose of the local anesthetic being administered. The
maximum allowable dose of local anesthetic varies with epinephrine co-administration
\Table 3-12), and readers are encouraged to be familiar with the toxic dosages of the agents
thatthey use.
TABLE 3-12. MAXIMUM LOCAL ANESTHETIC DOSAGES.*

local anesthetic Maximum dose (mg)
Plain W~h epinephrine
Lidocaine 300 500
Bupivacaine 175 225
"In order to calculate the proper volume of local anestheitc for injection, the following mass per volume proportions
are helpful: there are 2.5 mg/ml in a0.25% solution, 5 mg/ml in a 0.5% solution, 10 mg/ml in a 1% solution, and 20 mg/ml
in a 2% solution_
Hypertensive Crisis
Hypertensive crisis can develop as a result of progressive, neglected hypertension, head
injury or encephalitis, drug induced, pheochromocytoma, dissecting aortic aneurysm {will
rapidly drop if aneurysm ruptures), or associated with renal and/or heart failure. Diastolic
pressures of 130~140 mm Hg are considered emergent and require immediate treatment
with diazoxide (Hyperstat) 300 mg IV infused rapidly over 10 seconds. The patient is
transported to the hospital as soon as possible.
Hyperventilation
Hyperventilation is cased by anxiety and emotional stress, perhaps related to anticipation
of pain or injury, and results in blowing off C02 and development of respiratory alkalosis.
Signs and symptoms include rapid, shallow breathing, vertigo, confusion, paresthesia (often
affecting the forearms and hands), and carpopedal spasm. Treatment is to reassure and
have the patient rebreathe into a brown paper bag so that C02 is elevated. Sedation with 5-
10 mg of diazepam PO (or slow IV infusion) may be helpful in a prolonged event.
Seizure
Seizure can result from pre-existing seizure disorder, head trauma, encephalitis, or toxic
effect of medication, such as a local anesthetic. Signs and symptoms include aura, CNS
stimulation, and grand mal epilepsy with tonic-clonic spasms, coma, post-ictal aphasia, and
somnolence. Treatment focuses on protecting the patient from injury during the seizure and
allowing the seizure to run its course. Avoiding head injury as the patient convulses or falls is
important. If easily achieved, a padded tongue depressor may be placed in the mouth to
prevent laceration of the tongue due to jaw compression, however it is not advisable to force
anything into the mouth for fear of inducing injury (dental damage). If the patient becomes
cyanotic or the seizure fails to subside, or status epilepticus occurs (one seizure is
immediately followed by another), then administer diazepam 5-15 mg IV via slow infusion with
attention to respiratory support as indicated. Alternatively, 50 mg (2 ml of 2.5% solution) of IV
sodium thiopental may be administered. Phenytoin (Dilantin)300 mg IV slow push may also be
administered. 02should also be administered. The patient should thereafter be transported to
the hospital for neurological evaluation. It is important to know how well-controlled your
patients with epilepsy are, and when the patienfs last seizure took place.
Insulin (Hypoglycemic) Shock

Insulin shock is caused by an acute episode of hypoglycemia or hyperinsulinism. Signs and
symptoms include anxiety, confusion, diaphoresis, tachycardia, nausea, convulsion, and
coma. Treatment consists of administration of oral glucose either as an instant glucose
preparation or via fruit juice or a candy bar. An ampule of 050 may also be administered IV
if oral administration has not resolved the crisis. Most experienced diabetic individuals
know the warning signs of hypoglycemia, and take counter-actions in a timely fashion.
Hypoglycemia may occur in a patient who was running late for a morning appointment and
failed to eat breakfast after taking their insulin.
Acute Adrenal Crisis

Acute adrenal crisis can occur as a manifestation of insufficient corticosteroid administration
in a patient who regularly takes steroids for treatment of a steroid-responsive disease, or as
the initial presentation of previously undiagnosed adrenal insufficiency {Addison's disease).
Patients on chronic, regular corticosteroid supplementation or replacement therapy require
administration of exogenous corticosteroid in the perioperative period. These patients have

suppression or inadequate function of their hypothalamic-pituitary axis for any of a variety of
reasons, often due to the therapeutic use of corticosteroids for the treatment of rheumatoid
arthritis and other auto-immune diseases, asthma and other forms of COPD, or malignancy.
The body's own production of corticosteroid is suppressed after exogenous administration of
just 7.5 mg/day of prednisone over a 7 day period.
Symptoms of adrenal insufficiency include hypotension, syncope, nausea and
vomiting. Cardiovascular collapse can develop if corticosteroid is not administered in a
timely fashion. Serum cortisol level should be drawn as soon as possible, without delaying
administration of 100 mg hydrocortisone IV, followed by 100 mg, or 15 mg/kg, IV every 8
hours. The most common complicating effects of steroid therapy, in particular chronic
steroid use, are related to inhibition ofWBC function and diminished fibroplasia, both of
which negatively impact soft tissue and bone healing. In the acute postoperative period,
steroid supplementation can decrease the white count and mask infection, and also
diminish epithelialization and wound contraction. Consideration can be given to
supplementing with vitamin A to try to counter some of the detrimental affects of
corticosteroids on wound healing.
All patients requiring daily maintenance corticosteroid administration should continue
on their regular maintenance dose, and receive supplemental corticosteroid during the
peri operative period. For cases involving local anesthesia with or without lV sedation, IV
administration of 100 mg hydrocortisone 30 to 60 minutes preoperative, then again
postoperative in the recovery room for cases lasting greater than one hour, is generally
adequate. Alternatively, 15 mg prednisone can be administered orally at 0600 the day of
surgery, then again at 1600the day of surgery, and a final supplemental dose of 15 mg orally
at 1600 on postoperative day number one. For patients undergoing general anesthesia, 100
mg hydrocortisone can be administered HS the evening before surgery, then again
preoperative prior to starting the case, and then Q 8 hours over the first 24 hours
postoperative, and continued on a Q 8 hour basis up to the second -fourth postoperative
day, depending upon the physical and mental stress of the surgery. Steroid supplementation
should be tapered down to the regular maintenance level if supplemental steroid has been
administered for more than 3 days. Other supplementation regimens may be better suited for
an individual patient, and consultation with the patient's internist is helpful.
Alcohol Withdrawal
Alcohol withdrawal can occur in individuals of all walks of life, and is precipitated by
Illness or injury that precludes access to ethanol. Signs and symptoms include
tremulousness, irritability, nausea, anorexia, hallucination, and seizure. These can develop
as early as 3~5 hours or up to 48 hours after the last drink. Delirium tremens is
characterized by autonomic hyperactivity resulting in hyperpyrexia, diaphoresis, and
tachycardia; in conjunction with tremulousness, hallucination, agitation, and confusion.
Delirium tremens conveys serious risk of injury and/or death. Treatment of alcohol
withdrawal consists of chlordiazepoxide llibrium)25-100 mg PO q 6h or diazepam {Valium)
5~20 mg PO q6h; observation, protection, and reassurance. Adjuncttherapyfor malnutrition
and social service intervention is also indicated.
Airway Obstruction
Airway obstruction is caused by a foreign body in the airway, or angioedema- induced
oropharyngeal occlusion. Signs and symptoms include choking, gagging, violent inspiratory
effort, suprasternal notch retraction, cyanosis, respiratory arrest, and cardiac arrest.
Treatment involves establishing an airway via inspection and sweeping the oropharynx,
performance of the Heimlich maneuver, placement of an oral airway or endotracheal
intubation, or emergency cricothyrotomy. Once an airway is established, BCLS and/or ACLS
may be indicated. The patient is transported to the hospital as soon as possible.
Respiratory Arrest
Respiratory arrest is caused by airway obstruction or drug toxicity. Signs and symptoms
include apnea, cyanosis, and coma. The so-called "cardinal triad" of barbiturate toxicity or
narcotic overdose consists of apnea, miosis and coma (the patient is usually cyanotic as
well). Respiratory arrest that is not rapidly alleviated will be rapidly followed by cardiac
arrest Even a brief period of airway obstruction or respiratory arrest in an individual with
coronary artery disease can effect angina pectoris, myocardia! infarction, and/or cardiac
arrest Respiratory arrest is treated with BCLS wherein the airway is established and
artificial respiration (rescue breathing) administered. Transport the patient to the hospital
as soon as possible.
Pulmonary Embolism (PEl

PEcan cause acute, crushing chest pain and a sense of impending doom. See Venous
Thrombosis and PulmonaJY Embolism
Malignant Hyperthermia
Malignant hyperthermia is a severe, adverse reaction to general anesthesia (intra-
operative) that occurs in approximately 1:20,000 patients, and displays a familial tendency.
lfthere is a family history, the CPK should be assessed preoperatively for elevation (almost
80% correlation). Amide local anesthetics should be avoided in patients with a history of
malignant hyperthermia. The reaction occurs upon exposure to inhalant anesthetic agents,
and results in hypertonicity and skeletal muscle fasciculation, jaw clenching and rigidity,
hyperpyrexia, tachycardia, tachypnea, variable blood pressure, cardiac dysrhythmia,
hyperhidrosis, cyanotic mottling of the chest and extremities, and dark blood observed in
the surgical wound.
Treatment consists of immediate cessation of anesthetic agent, hyperventilation with
100% 02 at 810 liters per minute, and IV bolus administration of Dantrolene sodium at 1
mg/kg up to a maximum of 10 mg/kg. The EKG is monitored and procainamide may be
administered to stabilize the myocardium. Physical measures to cool the body are
instituted to counter braininjuring hyperpyrexia. Cooling efforts include IV administration
of cool saline, application of ice to the groin and axillae, ice water lavage of the stomach,
rectum, and bladder. Administration of sodium bicarbonate may be indicated to counter
acidosis and hyperkalemia. Kidney function is maintained at 2 ml/kg/hr using IV furosemide
or mannitoL Insulin may be administered to assist in providing the cells with glucose for
ongoing metabolism. Following control of the acute crisis, Dantrolene sodium is
administered orally over the next 23 days.
Angina Pectoris
Angina pectoris is caused by coronary artery disease or obstruction. The patient usually has
a family as well as personal history of such crushing chest pain, and may already be
medicated for their disease. Anxiety, emotional or physical stress usually precipitate angina
pectoris, and the characteristic crushing chest pain that lasts 3 to 5 minutes in the presence
of stable vital signs. The pain may radiate to the left arm and wrist The patient may also
display diaphoresis, dyspnea, nausea, and weakness. Treatment consists of administration
o,
of 100% at 61iters/minute, sublingual nitroglycerine INTG)1/150 tablets every 10 minutes
as needed. Loosen tight clothing, sitthe patient in semi-Fowler's position, and transport the
patient to the hospital as soon as possible.
Myocardiallnlarction IMI)
Ml is caused by respiratory arrest or coronary artery disease, and is usually preceded by
3to 5 minutes of angina pectoris with its associated signs and symptoms, as well as a sense
of impending doom. Cardiac dysrhythmia may also develop. Treatment consists of
administration of 100%02 at61iters/minute, morphine sulfate 5-10 mg IV push, or 10-15 mg
IM, while monitoring the BP and securing IV access and initiating infusion of 05W at KVO
IB hour) rate. Preparation is made to administer BCLS or ACLS, and to transportthe patient
to the hospital.
Cardiac Arrest
Cardiac arrest is caused by myocardial infarction and/or respiratory arrest. Signs and
symptoms include unresponsiveness, apnea, and absence of carotid artery pulse, and
clinical death with the pupils fixed and dilated, and facial, acral and chest cyanosis.
Treatment involves BCLS, ACLS, and transportation to the hospital as soon as the patient is
ready. The treatment protocol involves all of the interventions defined previously for MI.
BASIC CARDIAC LIFE SUPPORT
Basic Cardiac Life Support IBCLS) consists of establishment of the airway, rescue
breathing, and circulatory support with external chest compression (cardiopulmonary
resuscitation CPR).Table 3-13).
TABLE 3-13. CARDIOPULMONARY RESUSCITATION I CPR) PROTOCOLS.

Age of victim Number of rescuers Compression-to-ventilation ratio
Adult 1 15:2
Adult 2 5:1
Child 2 5:1
Infant 2 5:1
If the required equipment and medications are available, additional support can be
administered based on the recuers' level of training and experience. The EKG is observed
in a "quick-look" fashion via the defibrillator paddles, or an Automatic External
Defibrillator reads the rhythm without visual display, and identification of a lethal
dysrhythmia warrants defibrillation in the adult at200-360 joules delivered 12 joules /kg in a
child) for ventricular fibrillation.
ADVANCED CARDIAC LIFE SUPPORT
Advanced Cardiac Life Support IACLS) entails application of algorithms with a degree of
automaticity, however permutations of the algorithms may be helpful on an individualized
basis.
Statistics show that:

the majority of cardiac arrests occur in patients wfth pre~existing coronary artery
disease
20% of cardiac arrests are the first and last manifestation of the disease
30% of victims have a second arrest within one year if they survive resuscitation but
do not follow-up with treatment
50% suffer another arrest within the second year if left untreated the most common
cause of arrest is ventricular fibrillation {V-fib)
1-2% of all hospital admissions suffer cardiac arrest and 50% are resuscitated
33% survive at least 24 hours, but only 15% survive to leave the hospital
95% die if the resuscitation extends longer than 15 minutes most codes are called
\terminated) after 30 minutes if no significant positive response is noted
56% of out-of-hospital arrest victims survive if ACLS is administered within 4 minutes
the prognosis for survival worsens in ascending order as follows:
V-tachycardia > V-fib. >bradycardia/asystole;
CPR without appropriate drugs, such as epinephrine, is inadequate to sustain
adequate perfusion of the brain and heart.
The ABCs (Airway, Breathe, Circulate) of cardiopulmonary resuscitation (CPR):

1. Identify unresponsiveness
2. Call for help
3. Position and establish airway
4. Check breathing
5. Begin rescue breathing with 2 full breaths
6. Check circulation by palpa~ng the carotid pulse
7. Activate emergency medical service (EMS)
8. Begin chest compressions according to victim's size/age
9. Continue basic cardiac life support or implement advanced cardiac life support
(ACLS) and/or transport
Airway and ventilation protocol:

1. Heimlich maneuver--if obstruction is suspected, implement the Heimlich maneuver
2. Head back-jaw thrust-this is the standard approach to establish unobstructed
airway patency
3. Rescue breathing-"mouth-to-mouth" ventilation, using appropriate protective
shield \Pocket-mask or similar device)
4. Supplemental oxygen-administer 90% 02 at 10 liters/minute via line to mask or
nasal cannula
5. Ventilation-use an Ambu bag-valve-mask if airway remains patent
6. Endotracheal intubation or laryngeal mask airway (LMA) insertion-resortto more
secure airway management if head back-jaw thrust is insufficient; consider a
nasotracheal intubation if cases involving oral trauma
7. Spontaneous ventilation-if spontaneously ventilating, reduce to 20-40% 02 via
nasal cannula
Emergency IV access:
Line size-attempt to obtain z16 gauge access to facilitate administration of
emergency medications
Srte-a central line is preferable to peripheral access
Number of lines-as a rule, 2 sites may be useful, especially in a prolonged
resuscitation effort
Vein options-dorsal hand or antecubital, subclavian or internal jugular vein, and
femoral vein (keep in mind, during CPR there is decreased flow inferior to the
diaphragm)
Catheter methods-Seldinger guide wire and sheath dilator, typically the easiest;
catheter-over-needle (Angiocath), catheter-through-needle (lntracath)
Cut down-as a last resort, sharp dissection to expose and catheterize either the
saphenous or axillary vein can be undertaken
The EKG and cardiac dysrhythmia:

Conduction system-sinoatrial (SA) node, atrioventricular (AV) node, bundle of His, left
and right bundle branches
Electrocardiogram-P wave= atrial depolarization, PR interval= time between atrial
and ventricular depolarization, ORS complex= ventricular depolarization
EKG and cardiac rate-each small grid square= 0.04 seconds, there are 5 large
squares/second, 31arge squares approximates 90 beats per minute
EKG tracing-monitor quick-look paddles or lead-2to determine rate, rhythm, and axis
of the dominant pacer
Dysrhythmias and cardiac life support:

Normal sinus rhythm (NSR)----range 60-100 regular beats per minute
Sinus tachycardia-response to exercise, hypovolemia, fever, anxiety,
hyperthyroidism, sympathomimetic, etc.
Sinus bradycardia-response to vagal overtone or atropine, sinoatrial node defect
hypotension, ventricular ectopy, local anesthetic toxicity, etc. Premature atrial
contractions
{PACs)-ectopic atrial pacer cause irregular rate; response to sympathomimetic
stimulant or a-agonist hypoxia, etc.
Atrial tachycardia and fibrillation-atrium fails to effectively contract at 400-700 beats
per minute, as does ventricle at 150-200 beats per minute; due to myocardial infarct or
other disease; requires digitalis and/or cardioversion
Junctional rhythm-AV node acts as latent pacer after 1-1.5 second delay, typically
effects rate of 40~60 beats per minute
Premature ventricular contraction {PVC)-due to ectopic ventricular focus or foci,
runs of PVCs are ominous
Ventricular tachycardia-3 or more ventricular beats, rate> 100 beats per minute
Ventricular fibrillation-this results in no cardiac output and is lethal; coarse waveform
represents recent fibrillation, whereas fine waveform indicates late fibrillation
Ventricular asystole-flat line waveform due to cessation of ventricular contraction.
Atrioventricular block~conduction blockade between the AV node and the bundle
of His, effecting wide ORS segment and decreased cardiac output)
Ch.4 Selected Diagnostic Techniques 89
SELECTED !JIAGNOSTIC TECHNIQUES

HISTORY AND PHYSICAL EXAMINATION
The most importanttool in making an accurate diagnosis is a properly executed history and
physical examination (H&P). The astute practitioner listens to the patient See Oral Exam Test
Taking Format for a useful H&P form.
DIAGNOSTIC IMAGING
Radiation Safety
Radiation safety procedures and an understanding of the effects of ionizing radiation are
important matters tor all office personnel participating in preparation of diagnostic images.
X-rays are high energy electromagnetic radiation that can effect mutation of cellular genetic
material. There is no safe dose of ionizing radiation, and therefore exposure must be limited
while maximizing the diagnostic benefit of the image. Pregnant women should not
electively be radiographed, and alf subjects should wear protective lead apron, and the
examiner should use a similar apron, thyroid shield, cornea protection, and lead gloves
when manipulating the extremity under examination.
Variable factors in the imaging process include: kV (kilovoltage), mS (milliseconds),
collimation, distance between the foot (part), the film, and the X-ray source. Scatter
radiation must be minimized to reduce environmental radiation not used for creation of
diagnostic images. Fluorescent film screens are used with blue or green light sensitive films
to further decrease the amount of ionizing radiation required to obtain a useful diagnostic
image. Automatic or manual film processing requires exposure of the exposed film to
developer, fixer, and then a water rinse followed by drying. Poor quality images are
unacceptable practice, as useful diagnostic information is compromised at the expense of
patient and environmental radiation exposure. Use of a radiation dosimetry service enables
one to accurately monitor environmental and personal exposure.
Radiographic Views
Standard pedal radiographic views are taken with the patient weight bearing, with the feet
in the angle and base of gait. This allows reproducible and reliable images, from which
standard angles and relationships can be assessed. Variations can be useful, depending
upon specific needs. The primary views of the ankle include the mortise and lateral
projections. Ankle views do not necessitate positioning the foot in the angle and base of gait.
Contralateral radiographs can be obtained for comparison, particularly when evaluating
the skeletally immature, or when concerned about secondary centers of ossification.
Dorsoplantarfoot~ the patient standing on film cassette, beam angled 15 from vertical and
aimed atthe navicular.
Lateral foot~ the foot is posrtioned beside (against) the film cassette, which is vertical to the
substrate, beam angled 90 from vertical and aimed at the midfoot.
Lateral oblique foot- the patient standing on film cassette, beam angled 45 from vertical
and aimed at the lateral aspect of the foot. Useful in assessment of the calcaneus, cuboid,
fifth metatarsal and little toe.
90 Selected Diagnostic Techniques Ch. 4
Medial oblique foot- the patient standing on film cassette, beam angled 45 from vertical
and aimed at the medial aspect of the foot. An unconventional view, useful in assessment
of the medial aspect of the foot, the first metatarsal and hallux and, in particular, the
plantar medial border of the foot. It is also useful in evaluation of the tuberosity of the
calcaneus, as in the case of suspected plantar heel spur.
Calcaneal axial- the patient standing on film cassette, beam angled 45 to vertical and
aimed at posterior aspect of the heeL Modifications include Harris and Beath projections,
wherein the beam angle ranges from 10 above and 10c below the lateral view declination
angle ofthe posterior facet of the STJ las determined by a scout lateral view) or, more
simply, 30, 45 and 60 from vertical. Useful in assessment of the posterior aspect of the
calcaneus, suspected calcaneal fracture or inspection of the posterior facet of the STJ or
the sustentaculum.
Sesamoidal or metatarsal axial- the patient standing on orthoposer with the film vertical
to the substrate, and the toes dorsiflexed against the film. The hindfoot is supported with
enough radiolucent foam to elevate the heel above the substrate, with the beam angled
from posterior-to-anterior parallel to the substrate and aimed at the metatarsal heads.
Positioning devices are available to aid in stabilizing the patient for these views.
Isherwood views- a rarely used set of three non-weight-bearing views that display the
STJs. The lateral oblique view shows the anteriorfacet, the medial oblique view shows the
middle and posterior facets, and the lateral oblique axial view shows the posterior facet. CT
and linear tomography are more typically used, as positioning for Isherwood views is
difficult and time consuming. Other sets of radiographic views used to image the STJs,
and generally superseded by linear and axial tomography, include Anthansen and Broden
projections.
Mortise ankle- the heel is backed against the vertical film cassette, with the foot medially
rotated 15", the beam angled parallel to the substrate and aimed at the ankle. This is the
standard view for assessment of the tibiotalar and tibiofibular joints, and the dome of the
talus and tibial bearing surtace.
lateral ankle- the medial aspect of the foot is positioned against the vertical film, the beam
angled parallel to the substrate and aimed at the ankle.
Anterior-posterior ankle- the heel is backed against the vertical film cassette, with the toes
pointing straight ahead, the beam angled parallel to the substrate and aimed at the ankle.
The lateral malleolus is rotated posterior to and superimposed behind the tibia in this view,
and the distal tibiofibular syndesmosis is obscured. The mortise view is much more useful
for evaluation of the tibiotalar and tibiofibular joints.
Medial oblique ankle- oriented the same as in the AP or mortise of the ankle, however the
foot is medially rotated 45a, thereby further opening the tibiofibular syndesmosis.
Lateral oblique ankle- oriented the same as the AP or mortise of the ankle, however the
foot is laterally rotated 45. May be used to assess the medial malleolar cortex and the
media! aspect of the talus.
Stress Radiography
Stress radiography can be performed with static radiographs, or dynamically under
fluoroscopic image intensification. Stress radiographs are used to identify occult fractures
and ligamentous instability, and can be used to evaluate any bone or joint in the leg, foot
or ankle. The examiner should wear protective gloves, thyroid shield, and body apron
whenever stress fllms are made.
Anteriardrawerofthe ankle- with the patient supine, the lateral aspect of the foot is placed
against the film cassette and the heel is cupped with one hand while the opposite hand
stabilizes the anterior aspect of the tibia. The foot is rotated medially about 15, thereby
allowing visualization of the talar dome, while the talus is pulled forward out of the mortise.
The distance between the nearest point on the posterior aspect ofthe dome of the talus and
the most posterior margin of the distal tibial bearing surface is measured, and a distance of
> 4 mm is indicative of disruption of the anteriortalofibular ligament. A Telos apparatus can
be useful for applying anterior drawer in a reproducible fashion.
Inversion ankle stress (talartilt)~ with the patient supine, the ankle is oriented in a fashion
similar to that used in the mortise view, while the tibia is stabilized medially and the talus
lhindfoot with the STJ stabilized) forced into the tibial malleolus in an effort to stress the
lateral collateral ligaments. The angle created between the plane of the distal tibial
bearing surface and the dome ofthe talus is measured. Angles< 5 are considered normal,
between 5-20 may be normal or abnormal, and larger angles are suggestive of lateral
collateral ligament disruption. Loose bodies may be identified between the tibia and talus.
Stress ankle dorsiflexion (charger)- a weight-bearing lateral view of the ankle is taken
with the ipsilateral knee flexed and the ankle relatively dorsiflexed, This is used to depict
osseous ankle equinus.
Fluoroscopy
Fluoroscopy (image intensification) is used to obtain quick radiographic images of
operative maneuvers and stress manipulation, fracture reduction, fixation placement,
foreign body localization, and trocar or pin placement The C-arm must be used with a
radiolucent segment in the OR table.
Computerized Axial Tomography (CT)

And Magnetic Resonance Imaging (MRI)
CT and MRI are useful imaging techniques following review of standard radiographs.
Linear tomography {non-axial linear slices) can also be useful, however it is not readily
available currently. Computerized tomography (CT) or computerized axial tomography (CAT
scan) use high-energy ionizing radiation (X-rays), multiple projections, and a computer to
generate images, and is best suited to cortical bone imaging. Magnetic resonance
imaging (MRI) uses low energy radio waves traversing the body within a magnetic field,
and a computer to generate images. T1 ~weighted \fat) images are dependent on the fat
content of the tissue, while T2-weighted \water, inflammation) images are dependent on
the water content of the tissue and are especially useful in the presence of pathological
inflammation or fluid accumulation. Both CT and MRI can be enhanced when combined
with contrast medium.
Comparison of CT and MRI for Selected Pathological Conditions

Tarsal coalition- MRI is best, as not all coalitions are cortical bone
Arthritis, tendinitis, and other inflammatory processes- MRI is best, as it allows early
visualization of peri-articular and soft tissue changes
Avascular Necrosis- MRI is preferred, and the hallmark MRI sign is a well-defined
region of decreased intensity within medullary bone on both T1- and T2-weighted
images. CT could be used to show advanced AVN wherein joint space has collapsed
with cortical bone defect
Infection- MRI is sensitive, but not specific, tor imaging soft tissue abscess and
osteomyelitis (medullary). MRI does not image subcutaneous gas. CT is useful for
Imaging cortical defects, sequestrum, cloaca, involucrum, and intraosseous or
subcutaneous gas.
Neoplasm- MRI is superior for evaluating bone marrow and soft tissue; while CT is
best for cortical bone, calcification, endosteal thinning, and fine periosteal reactions.
Trauma- MRI is preferred for imaging soft tissue injury, in particular tendon, ligament
and cartilage. CT is superior for imaging cortical bone, especially when comminution
or growth plate (physeal) injury is suspected. Osteochondral lesions may warrant both
CT and MRI. When in doubt as to the preferred imaging technique, simply consult with
the radiologist.
Contrast Jmaging
Contrast imaging using radiopaque contrast dye injected into a joint space or tendon sheath
can be used to assess surface defects such as osteochondral fracture or tendon and sheath
disruption. Hypersensitivity (to the contrast medium), possible sepsis, and the invasive
nature of the procedure, the need for ionizing radiation and limitations related to patient
positioning, are all potential disadvantages of both arthrography and tenography. MRI as
well as CT scanning, despite their cost, offer excellent diagnostic images and have almost
replaced contrast imaging of the ankle and peroneal sheath. Arthroscopy and endoscopy
also offer diagnostic, and therapeutic, modalities applicable in the management of the foot
and ankle.
Ultrasonography
Ultrasonography can be used for localization of foreign bodies following puncture wound,
as well as identification of fluid or solid mass in the subcutaneous tissues.
Radionuclide Scans
Radionuclide scans are used to image bone physiology, and are usually performed using
technetlum-99, ga!lium-67, or indium-111. Most scans show increased scintigraphy within
48-72 hours after the infection or other osteitis has begun. Tc-99 has a half-life of about 6
hours. Only the technetium scan labels hydroxyapatite crystals in living bone, and is
therefore termed "a bone scan." Ga-67 is used to label white blood cells and plasma
proteins, and is used to identifyWBC accumulation (pus, infection) in bone or other tissues.
Gallium is not used as an isolated study, and is usually combined with a Tc-99 scan
performed about 24-72 hours earlier. An increased uptake of Tc-99 without increased
uptake of Ga-67, correlates 85% with the absence of osteomyelitis. If both Tc-99 and Ga-67
scans show increased uptake, then there is about a 70% correlation with osteomyelitis
being present. ln-111 is used to tag the patienfs neutrophils, after first drawing blood and
separating the PMNs. The labeled neutrophils are then infused back into the patient, and
the scan performed 18 to 24 hours later. ln-111 scans are positive in cases of osteomyelitis
and .negative in cases of osteoarthropathy. Since ln-111 is tagged to neutrophils chronic
osteomyelitis, which is primarily an accumulation of lymphocytes, may present as a false
negative indium scan (infection present despite a negative scan). An ln-111 scan may be
useful in trying to distinguish postoperative infection from pseudoarthrosis or nonunion.
Bone Scans
Bone scans (Tc-99) are imaged in atriphasic fashion, wherein a scintigram is made atthree
specified times following administration of the radioisotope. The radio angiogram (first or
immediate phase, blood flow images), is measured immediately following infusion of
radionuclide and shows dynamic flow to the area. The blood pool image (second phase) is
measured about 20 minutes after infusion, and shows increased scintigraphy in the
presence of hyperemia.
The first two phases are "hot" in both bone and soft tissue infection, or other causes
of inflammation and hyperemia. The blood flow image correlates with perfusion of the part,
and would not show uptake of radionuclide in the presence of ischemia. The delayed image
(third phase) is measured about three hours after infusion of radionuc!ide, and correlates
with skeletal uptake of the isotope. The delayed image often identifies activity related to
infection or other persistent bone pathology, such as pseudoarthrosis or hypertrophic
nonunion. Moreover, longer term delayed TC-99 bone scans, imaged at 24 hours !fourth
phase), may be used to image infection in patients with PVD, diabetes mellitus and Charcot
neuroarthropathy. Neuroarthropathy may present "hot" scans in all four phases. Soft tissue
infections are usually "hot" in only the first two phases. Furthermore, a Tc-99labeled WBC
scan (Seratec) can also be used to image bone infection, particularly in patients with
diabetes mellitus or suffering postoperative infection. In any case, a scan is a sensitive but
nonspecific imaging technique that must be combined with other diagnostic imaging
techniques and clinical, as well as surgical, diagnostic measures.
Standard Radionuclide Bone Imaging Combinations
Acute Osteomyelitis
Tc - 99m Scan Phase I +
Phase II ++
Phase Ill +++
Ga- 67 Scan Positive focal uptake
In -111 Scan Positive focal uptake
Inactive Chronic Osteomyelitis

Tc - 99m Scan Phase I +/-
Phase II +
Phase Ill +++!persists in longer delayed imaging)
Ga- 67 Scan Negative
In- 111 Scan Negative
Acute Cellulitis
Tc- 99m Scan Phase I +++
Phase II ++
Phase Ill +
Ga- 67 Scan Positive diffuse uptake
In -111 Scan Positive
Septic Arthritis
Tc- 99m Scan Phase I +++
Phase II +++
Phase Ill +/-
Ga- 67 Scan Positive focal uptake
ln-111Scan Positive
CARTILAGE IMAGING
Contrast arthrography-contrast agent (iodine for X-ray or CT, or gadopentetate

dimeglumine for MRI); direct, pseudo-direct (via peroneal sheath to ankle joint), indirect
methods; enhances visualization of articular cartilage margins and small cortical
abnormalities; entails need trauma, possible infection and hypersensitivity to local
anesthetic and contrast agent. High resolution delayed gadolinium~enhanced MRI of
cartilage (HR-MRI-dGEMRIC) with fat suppression is currently the best method of cartilage
imaging short of arthroscopy. The following methods are under development for clinical
use, and are currently experimental research tools that show superb cartilage detail: high
frequency ultrasound, diffraction enhanced imaging (MRI), gradient MRI, T1 rho time
relaxation MRI, T2 time relaxation MRI, optical coherence IR tomography, and positron
emission tomography (PET).
CliNICAl lABORATORY TESTING
Complete Blood Count

Complete blood count (CBC) with differential cell count is a general screening for a variety
of conditions. CBC includes:
Hemoglobin (Hgb)- normal range is 13.5-17 gm/1 00 ml for males and 12.5-16 gm/100 ml for
females. Values below 11 gm/100 ml are considered to represent anemia, and should be
evaluated. Elevation above 18 gm/100 ml may represent polycythemia, and increases blood
viscosity and increases risk of thrombosis.
Hematocrit(Hct)- normal range is 40-54% for males and 37-47% for females. Varies with the
Hgb.
fled blood cell count- normal range is 5.4 0.8x 106 /mm 3 for males and 4.8 0.6 x 106/mm'
for females. The RBC count increases in individuals living at high altitudes, in environmen-
tally hot work places, and in athletically fit individuals.
Corpuscular indices and anemia

normocytic macrocytic microcytic/
hypochromic
Mean corpuscular
volume 82-92 95-150 50-80
Mean corpuscular Hgb 25-30 30-50 12-25
Mean corpuscular 32-36 32-36 25-30

Hgb concentration
Remember the phrase "90, 30, 30," for normal MCV, MCH, and MCHC values.
Normocytic anemia can be observed with acute hemorrhage, hemolytic anemia, and
abnormal hemopoiesis. Macrocytic anemia occurs with pernicious anemia, sprue,
pregnancy, antimetabolic therapy, and other megaloblastic conditions. Microcytic anemia
occurs with iron deficiency or malabsorption, hemorrhage, and increased iron metabolism.
White blood cell count- normal range 5,000 -10,000/ mm3. Causes of leukocytosis include:
acute infection, metabolic acidosis, gout, uremia, heavy metal toxicity, tissue necrosis or
injury (burns, gangrene, tumor, myocardial infarction, pulmonary embolism), secondary to
hemorrhage or menstruation, and myeloproliferative diseases. Causes of leukopenia
include: adverse drug reactions to Thorazine, phenylbutazone, various antifungals and
antibiotics; pernicious anemia, aplastic anemia, and certain severe infections (septic shock).
Differential white cell count- segmented neutrophils 40-60%, band neutrophils 0-5%,
lymphocytes 20-40%, monocytes 4-8%, eosinophils 1-5%, basophils 0-1%. Some causes of
neutrophilia include acute infection, necrosis, pain, exercise or post-convulsion, anoxia,
hemorrhage, sunburn. Some causes of neutropenia include overwhelming infection,
marrow depression, antimetabolite therapy, and autoimmunity. Lymphocytosis may
indicate viral syndrome, hepatitis, chronic TB, and measles. Monocytosis occurs with
leukemia, Hodgkin's disease, collagen vascular diseases and arthritides, sarcoidosis,
subacute bacterial endocarditis, and other infections and wounds. Eosinophilia is
indicative of allergy, asthma, eczema and urticaria; parasitic infection; scarlet fever;
pemphigus and dermatitis herpetiformis; leukemia and pernicious anemia. Eosinopenia is
seen in Cushing's disease, excess ACTH, chronic steroid therapy, postoperative state,
shock, and labor. Basophilia occurs in polycythemia, chronic myelogenous leukemia,
chicken-pox, small-pox, hypothyroid myxedema, and renal disease.
Platelet count- normal range is 140,000-340,000/ mm1 Platelets are elevated in collagen
vascular disease, iron deficiency anemia, acute infection or injury, hepatic disease,
cardiac disease, malignancy and polycythemia Vera.
Important Labs in Rheumatoid Disease

Erythrocyte sedimentation rate (ESR)- normal anticoagulated blood shows very little
settling, however, elevated globulin and fibrinogen associated with inflammation leads to
Rouleaux formation and the clumped red cells settle rapidly. An elevated ESR is indicative
of a measurably higher column of red cells settled at the bottom of the tube wrthin a set
time. The ESR can be used to distinguish inflammatory from non-inflammatory conditions,
and is used to monitor resolution of inflammation during the course of therapy.
The ESR is very sensitive, however, nonspecific. The ESR is elevated in acute
infection, rheumatoid arthritis, polyarteritis, ankylosing spondylitis, septic arthritis, acute
gout, metastasis, and other connective tissue diseases.
C~reactive protein {CRP)- is a glycoprotein that reacts with C-mucopolysaccharide of many

pneumococci. It is commonly produced during the acute phase of inflammation. It rises
before the ESR, and normalizes in the presence of NSAIDs, aspirin and steroids. It rises in
acute flare of rheumatoid arthrftis, Strep. infection, in the last half of pregnancy, and in
females using an IUD and/or oral contraceptives.
Antinuclear antibody (ANA)- appears months after onset of connective tissue disease,
and may have its greatest value in monitoring SLE. It is more accurate than the LE cell test
because it is unaffected by steroids. The significance of ANA titers less than 16 is
uncertain, as healthy persons may display titers in this range. Elevated ANA titers suggest
connective tissue disease, while absent or low titers do not rule out connective tissue
disorders. High titers are common in SLE, scleroderma, and mixed connective tissue
disorders, and Raynaud's phenomenon.
Pattern Associated Antigens Clinical Conditions

Homogenous Deoxyribonucleoprotein Collagen-Vascular OS
?articulated Extractable Nuclear Mixed C.T. OS., scleroderma,

Antigen SLE, Malignancy
Peripheral Native DNA and Histones Active SLE with Nephritis
Nucleolar Nucleolar RNA Scleroderma, Raynaud's
Positive ANA is found in the following percentages in the following diseases
Systemic lupus erythematosus (100%, high titer)

Rheumatoid arthritis I< 60%, very low titer)
Sjogren syndrome (75%, low titer)
Systemic sclerosis 138%, low titer)
Liver cirrhosis (45%, low titer)
Polymyositis 120%, low titer)
Dermatomyositis (20%, low titer)
Malignancy (18%, low titer)
Bullous pemphigus (rare, low titer)
Polyarteritis nodosa or ulcerative colitis (rare, low titer)
Waldenstrom's macroglobulinemia (rare, low titer)
Drug reaction (rare, low to high titer)
Myasthenia gravis (rare, very low titer)
Rheumatoid factor (RF)- lgM or lgG auto-antibodies that react with the Fe portion of
denatured human lgG. There are two methods of measurement: latex fixation {75%
sensitive and 75% specific for RA at 1:80 dilution), and sheep cell agglutination (75%
sensitive and 95% specific for RA at 1:160 dilution). RF is found in the following
Ch. 4 Selected Diagnostic Techniques 97
percentages: Sjogren syndrome (75-100%), adult RA (70-80%), juvenile RA (10%), SLE

(20-40%), scleroderma 15-10%1, polyarteritis nodosa and dermatomyositis I0-5%).
Lupus erythematosus (LEI cell - mature polymorphonuclear neutrophil that has

phagocytosed a spherical, homogenous inclusion derived from another neutrophil.
Characteristic of SLE, and observed in the following percentages : SLE (70-80%),
Sjogren syndrome 110-20%), RA 15-10%1, scleroderma and polyarteritis nodosa and
dermatomyositis I0-5%).
Serum complement series of enzymatic proteins that combine with antigen-antibody

w
complexes and effect lysis when the antigen is an intact cell. Complement remains normal
in Sjogren syndrome, scleroderma, polyarteritis nodosa, and dermatomyositis; is normal or
decreased in SLE; and normal or slightly elevated in acute phase of RA.
Anti-streptolysin 0 (ASO)- antibody against streptolysin "0" of group A streptococci

{Strept. pyogenes). It is present in 80-85% of patients with acute rheumatic fever or other
streptococcal infection.
HL-A 827- histocompatability antigen found in the following percentages in the following
diseases: ankylosing spondylitis (90%), Reiter's syndrome (75%), psoriatic arthritis and
juvenile RA (high concentration).
HL-A 815- histocompatability antigen found in 33% of patients with SLE.
Uric acid (UA)- elevated in gout, malignancy, renal disease, and familial hyperuricemia.
Normal is 7-9 mg% in males, and slightly less in females. UA may be normal in the acute
stage (first 10 days) of gouty arthritis, as much has precipitated out ofthe serum into the af-
fected joint. Monosodium urate (gouty) crystals are needle-shaped, and form the "martini
sign" when phagocytosed by a neutrophil.
Calcium pyrophosphate~ crystals are rhomboid, and observed in pseudogout
Joint Fluid Analysis
Joint Fluid Normal Group-1 Group-11 Group-Ill

Volume Increase Increase Increase
Clarity Clear Clear Cloudy Opaque
Color Clear Yellow Yellow Yellow
Opalescent Green
Viscosity High High Low Variable
WBC/mm3< 200 200-2000 2000-100,000 > 100,000
% PMNs <25% <25% >50% > 75%
Culture 1-1 1-) 1-1 1+1
Mucin Clot Firm Firm Friable Friable
Glucose lmg%) =Serum =Serum <Serum <Serum
Differential Diagnosis Based on the Joint Fluid Analysis Chart
Group~!: Non-inflammatory conditions such as DJD, trauma, osteochondritis

dissecans, osteochondromatosis, neuropathic hypertrophic osteo-
arthropathy {Charcot), resolving or early inflammation, hypertrophic
pulmonary arthropathy, and pigmented villonodular synovitis.
Group-11: Inflammatory conditions such as RA, gout, pseudogout, Reiter's syndrome,

ankylosing spondylitis, psoriatic arthritis, arthritis associated with ulcerative
colitis or Grahn's regional enteritis, rheumatic fever, SLE, and progressive
systemic sclerosis.
Group-Ill: Septic arthritis due to bacterial infection.
Hemarthrosis results in a hemorrhagic joint fluid specimen, and can be caused by

hemophilia and other bleeding diatheses, ligamentous trauma with or without fracture,
neuropathic arthropathy, pigmented vfllonodular synovitis, synovioma, hemangioma, and
other neoplasms.
Coagulation Studies
Partial thromboplastin time (PTT)- normal range is 25-35 seconds. Used as a reliable
screening test however may not detect subtle defects. Also used to monitor heparin
anticoagulation therapy. The PTI can be used to evaluate the three stages of coagulation,
with the exception of factor VII or platelet factors. The PTI remains normal in von
Willebrand's disease, platelet dysfunction, and thrombocytopenia. The PTT is prolonged by
defects in clotting factors I, II, V, VIII, IX, X, XI, and XII.
Prothrombin time (PT)- normal range is 11-16 seconds. The PT is used to monitor longterm
Coumadin !Warfarin) anticoagulation therapy. The PT is prolonged with defects in factors
I, II, V, VII, and X; as well as in vitamin-K deficiency, fat malabsorption \steatorrhea, colitis,
jaundice), salicylate orwatfarin therapy, and advanced hepatic disease.
Bleeding time- normal range {Duke) is 1-4 minutes. The bleeding time is prolonged in
thrombocytopenia, abnormal platelet function, and von Willebrand's disease.
Clotting time- normal range (Lee-White) is 3-6 minutes in a capillary tube, and 6-17 minutes
in a test tube. This is a routine, nonspecific screening test used to determine the presence
of major clotting deficiencies.
Urinalysis
It is preferable to evaluate the first morning specimen. Physical and chemical properties are
assessed.
Color- normal is amber to pale yellow. Black urine is noted in alkaptonuria, malignant
melanoma, and malaria. Red urine is noted in hematuria, hemoglobinuria, methemoglobinuria,
and myoglobinuria. Blue urine may be noted in porphyria. Brown to green urine may occur with
bilirubinuria. Dark brown urine occurs in sickle cell anemia. Acidic urine appears orange.
Odor- normal urine smells like ammonia. A putrid odor may indicate bacteria. Mousy urine
occurs with phenylketonuria (PKU). Asparagus effects a peculiar urine odor.
Clarity- generally the urine is relatively clear, with some sediments. Cloudy urine may
represent infection, crystaluria, hemorrhage, or cellular debris.
Specific gravity- normal range is 1.003- 1.026.
pH- normal is 4.6- 8.0
Urine chemistries- glucose, ketones, protein, and drug by-products and metabolites can
a!! be measured.
Microscopic findings- blood and epithelia cells, casts, crystals, and bacteria can be
identified.
Serum Chemistries
Calcium- normal is 8.5-10.5 mg%. Elevated in primary hyperparathyroidism or secondary
to chronic renal failure, metastatic bone disease, lymphoma or multiple myeloma,
sarcoidosis; or lung or renal carcinoma that produce parathormone; or hypervitaminosis
D (excessive intake of cod liver oil), diuretic use, or acidosis. Decreased in
hypoparathyroidism, chronic renal failure (perhaps postoperative, and classically seen with
simultaneous elevation of phosphorous), malabsorption or steatorrhea, alkalosis,
pancreatitis, and when EDTA used to anticoagulate the blood specimen.
Phosphorus ~ normal is 2.5-4.5 mg%. Elevated in chronic renal failure, diabetic

ketoacidosis, fracture healing, acromegaly, growing children (physiological), and
hypervitaminosis D. Decreased in negative nitrogen balance (simultaneous decreased BUN
and alkaline phosphatase), hepatic disease, Fanconi syndrome, osteomalacia, and with
longterm IV glucose infusion in a non-diabetic patient.
Glucose~ normal is 65-110 mg%. Elevated in diabetes mellitus (serum phosphorous remains
normal), Cushing's disease, corticosteroid administration, pheochromocytoma, and brain
injury or tumor. Decreased in hyperinsulinism, pancreatic islet cell tumor, Addison's
disease, bacterial septicemia, and advanced hepatic necrosis.
Blood urea nitrogen (BUN)- normal is 10-20 mg%. Elevated in renal failure (with or without
obstructive uropathy}, dehydration, G.l. bleed. Decreased in hepatic failure (urea
production reduced), carbon tetrachloride toxicity, and associated with a negative
nitrogen balance.
Uric acid- normal is 2.5~8 mg%. Uric acid is the end-product of purine metabolism, and
may precipitate out of serum into the tissues as monosodium urate crystals, which is
responsible tor acute gouty arthritis as well as chronic tophaceous gout. Elevated in
conditions where there is excessive purine intake (tyramine, cheese, dark beer, game
meats), over-production of uric acid (rapid cell proliferation as in neoplasms such as
lymphoma or leukemia; extensive tissue necrosis), or under excretion of uric acid (renal
disease), eclampsia, starvation, thiazide diuretics, lead poisoning, and metabolic acidosis.
Decreased with use of uricosuric agents, Fanconi syndrome or Wilson's disease.
100 Selected Diagnostic Techniques Ch.4
Cholesterol- normal is 150-275 mg% (this is controversial). Elevated in obstructive

jaundice, hypothyroidism, nephrosis, uncontrolled diabetes, endotoxic shock or gram
negative septicemia, and pregnancy. Decreased in malabsorption syndromes, hepatic
disease (about 2/3 of the cholesterol is esterified in the liver), hyperthyroidism, anemia,
septicemia, and chronic stress.
Albumin - normal is 3.5-5 gm%. Hyperalbuminemia iS rare. Decreased in protein

malnutrition, hepatic failure, renal disease (nephrosis), Gl wasting (diarrhea) or
mal-absorption, burn wounds, or extensive exfoliative dermatitis.
Total protein - normal range is 6-8 gm%. Hyperproteinemia is typically caused by an

elevation of globulin, as in collagen vascular disease, chronic infection, or malignancy such
as multiple myeloma. Hypoproteinemia results from the same causes of hypoalbuminemia.
Note the following general formula for total protein:
3 gm% globulin+ 4 gm% albumin= 7 gm% total protein
Lactate dehydrogenase- normal is 90-200 mU/mL Lactate dehydrogenase catalyzes lactic

acid t pyruvic acid in the citric acid cycle (glycolytic cycle). Increased in cytolysis and
cytonecrosis (acute myocardial, pulmonary, renal, hepatic, skeletal muscle, and major organ
infarction); pernicious anemia, malignant neoplasm, and sprue. Decreased with radiation
therapy.
Bilirubin- normal is 0,1-1 mg%. Elevated in jaundice (hepatic, obstructive, or hemolytic),

Crigler~Najjar
syndrome and Gilbert's disease. Hemolysis and hemorrhagic or hematoma
due to pulmonary injury or other major trauma will elevate serum bilirubin.
Alkaline phosphatase - normal is 30-85 mU/mL Elevated in the growing individual; bone
diseases such as sarcoma, fracture healing, Paget's disease, metastatic carcinoma to bone
(usually norma! in osteomalacia}; other metastatic disease, histiocytosis, pulmonary
embolism, and congestive heart failure. Decreased hypophosphatasia, an inherited
condition similar to rickets however, the alkaline phosphatase and leukocyte counts are
decreased. Also decreased in magnesium deficiency, chronic diarrhea, malabsorption,
uncontrolled diabetes mellitus with magnesium deficient parenteral fluid administration,
malnutrition, and pernicious anemia.
Serum glutamic-oxa/oacetic transaminase(SGOT)- normal is 10-50 mU/ml. SGOT is found

in liver> heart> skeletal muscle> kidney, pancreas, red blood cells, and lung. Elevated in
cardiac and hepatic disease {myocardial infarction, liver cancer or injury or hepatitis), acute
tubular necrosis, acute pancreatitis, hemolytic anemia, leukemia, myonecrosis or injury,
pulmonary injury or riecrosis, and dermatomyositis. Decreased in conditions with elevated
serum lactate or pyruvate such as beriberi, thiamin deficiency, diabetic ketoacidosis, and
liver disease.
Serum glutamic-pyruvic transaminase (SGPT)- normal is 5-35 mU/mL SGPT is found

primarily in the liver, and is elevated in liver disease.
Microbiological Testing
Culture and sensitivity (C&S) ~ used to identify micro-organisms involved in an infectious
process. Standard C&S involves aerobic and anaerobic testing. Acid fast, chocolate agar,
sheep's blood, fungal culture, and other specific test media may be indicated based on
individual case requirements. Sensitivity of an organism to a particular antibiotic is
determined by Kirby-Bauer disk sensitivity, wherein antibiotic impregnated disks are placed
on the culture medium surface and areas of "no growth" are observed surrounding disks
containing antibiotic that kill the bacteria. Minimal inhibitory concentration (MIC) and
minimal bactericidal concentration (MBC) are also used to test sensitivity to specific
antibiotics, wherein the inhibitory concentration stops cell growth and the cidal
concentration kills the organism.
Gram's stain- used to identify the presence of bacteria, their morphology, and staining
characteristics. Wound exudate suspected of infection should be stained as follows:
1. Gentian violet~ H20 rinse
2. Alcohol- H20 rinse
3. Gram's iodine - HzO rinse
4. Safranin - HzO rinse.
Microscopic observation should reveal granulocytes indicative of inflammation, and
the presence of bacteria. The combination of granulocytes and bacteria is indicative of
infection. Antibiotic selection is made based upon bacterial morphology and staining.
Gram-positive bacteria appear violet-purple (gentian violet), while gram-negative bacteria
appear red (Safranin). Interpretation of the Gram's stain is particularly important when
considering anaerobic bacteria, as it can be difficult to grow such organisms in the micro-
biology lab.
KOH prep- squamous epithelial cells are dissolved in keratinolytic potassium hydroxide,
leaving microscopically evident fungal hyphae and/or spores and yeast Also known as a
tissue exam for fungus.
PAS- periodic acid Schiff stain forfungal hyphae/spores and yeast
Acid fast staining- for suspected tuberculin infection (Mycobacterium tuberculi).
Blood agar culture medium- for certain fastidious microbes, such as Neisseria.
Chocolate agar- predisposes to growth of Neisseria.
NEUROLOGICAL AND
ELECTRO-NEURODIAGNOSTIC EVALUATION
The basic clinical neurological examination involves sensory, motor, and autonomic testing
and observation. The exam involves touch-pressure (anterior spinothalamic tract and
peripheral sensory organs) monofilament esthesiometer testing of the skin surfaces,
wherein absence of the ability to appreciate touch-pressure of 10 kg/cm 2 is indicative of
lost protective sensation. Testing lighttouch with cotton or brush stroke is less reliable in
comparison to the use of the monofilaments.(Fig. 4.1)
Posftion sensation, proprioception, is tested at the first MTPJ and ankle levels, wherein
the patient notes the position of the joint without looking atthe part. Vibratory sensation is
tested with the 128 cycles/second tuning fork. Proprioception and vibratory sensation test
the dorsal column-medial lemniscus pathway. Pain and temperature assessment with pin
prick and a warm or cold water-filled test tube, respectively, tests the lateral spinothalamic
1. Medial and intem1ediate femoral cutaneous nerves

2. Posterior femoral cutaneous nerve
3. Lateral sural cutaneous nerve
4. Saphenous nerve
5. Superficial peroneal nerve 6
6. Sural nerve
7. Medial calcaneal branch of tibial nerve
8. Medial plantar nerve
9. Lateral plantar nerve
10. Deep peroneal nerve
Figure 4.1
pathway. Deep tendon reflexes are tested at the patellar (L2-4) and Achilles (S1-2)1evels.
The reflexes are graded as
silent or absent (0)
hyporeflexic 1+1
normoreflexic (++}
hyperreflexic but not necessarily pathological (3+)
multiple clonic contractions (4+)
sustained tonic contraction {5+)
Deep tendon reflexes test the integrity of the spinal reflex and the muscle spindle. The
plantar stroking superficial reflex should effect mild down going contraction of the toes,
whereas hallux dorsiflexion and lesser digital fanning represents the Babinski sign which
is indicative of upper motor neuron immaturity or lesion.
Skin temperature may be increased due to vasodilatation, in conjunction with dryness
due to sudomotor denervation, in the presence of peripheral neuropathy. Generally, sensory
dysfunction is noted before autonomic dysfunction, both of which precede motor
dysfunction, secondary to peripheral neuropathy, injury or nerve entrapment
The clinical assessment of muscle strength involves inspection for atrophy or hyper-
trophy, and placing the joint acted upon by the muscle4endon complex in the end range of
motion position, thereby providing the tendon maximum mechanical advantage and
yielding the most accurate clinical test of muscle strength. The grading system for gross
(clinical) manual muscle testing is:
Grade 5 "normal" strength, full resistance at end range of motion.
Grade 4 "good" strength, mild-moderate resistance at end range of motion, often

graded 4+ or 4-
Grade 3 "fair" strength, able to move against gravity only
Grade 2 "poor" strength, able to move only after gravity eliminated
Grade 1 "trace" strength, can visualize or palpate contraction without joint motion
Grade 0 "zero" strength, no clinical evidence of muscle contraction
Muscle strength testing is important when considering tendon transfer. Other

techniques useful in the assessment of muscle strength include biometric testing using
machines such as Cybex or Biodex, which yield information detailing povver, endurance, and
strength. Resting muscle tone is idealized to optimize synergistic muscle contractions to
effect movement.
Abnormal, Involuntary Movements

Myoclonus- rapid, abrupt, often cyclic, skeletal muscle contractions resulting in major
movement of the part.
Tremor- more refined, smooth, rhythmic movement, generally of the fingers or toes.
Athetoid movement- slow, worm-like writhing and twisting movement associated with rest
and intentional motion.
Choreiform movement- rapid, jerking movement associated with rest and intentional
motion.
Fasciculation- overt twitching of bundles of muscle fiber within a 1arger muscle belly,
nonpathologic when associated with fatigue.
During the gait cycle, biphasic contract'10ns of TA, EHL, EDL, and Peroneus Tertius
occur during the first 10% of contact at heel strike to decelerate, t::hen again at push
off through propulsion and into swing. The peroneii fire at about 15-20% of stance and
throughout propulsion. The FDL, TP, and FHL similarly fire at about 15-20% of stance and
throughout propulsion. A variety of abnormal gait patterns also exist, and are often
associated with specific pathological conditions, including:
Equinus -ankle plantarflexion in swing and, when advanced, stance; associated with
dropfoot, pes cavus, and extensor substitution.
Spastic/Circumducted- the lower extremity is adducted, medially rota1:ed, and flexed atthe
hip and knee, with ankle plantarflexion; associated with cerebra! palsy, cerebral vascular
accident, spinal cord lesion, familial diplegia, and other upper motor neuron lesions.
Ataxic- unstable, widened base of gait to enhance stability, with the single limb widely
swung and then crossing the midline in stance; associated with cerebellar disease,
Friedreich's ataxia, tabes dorsalis, syringomyelia, multiple scler()sis, and diabetic
polyneuropathy.
Steppage- swing phase dropfoot requires high elevation of the thigh and leg, with hip
flexion, in order to have the forefoot c!ear the ground: associated VI./ ith CVA, CP, familial
sensorimotor neuropathy (CMT), Landry~Guillain-Barre syndrome, and other paralytic

dropfoot conditions.
Waddling -widened base of stance, lumbar lordosis, external hip rotation, and imbalance;
associated with muscular dystrophy (Duchenne's, Becker's, and limb-girdle), and
congenital dislocated hip.
Trendelenburg- pelvic tilt toward the swing phase side with scoliosis pointing (convexity)
toward the affected side (weight bearing); associated with gluteus medius injury or
paralysis, or dislocated hip.
Festinating- shuffling, shortened and rapid stride, seemingly falling forward, uncoordinated
arm swing, actually moving slowly; associated with Parkinson's disease and similar
conditions.
Major Patterns of Neurological Deficit

Upper motor neuron disease- (above the anterior horn cell of the spinal cord) hyperreflexia,
clonus, superficial plantar response is upward with Babinski's sign, resting skeletal muscle
hypertonicity or rigidity; gait is steppage with spasticity and circumduction.
Lower motor neuron disease -I at or below the anterior horn cell) deep tendon reflexes are
absent or hyporeflexic, muscle tone is decreased, superficial plantar response is silent; gait
is flaccid.
Ataxia -loss of coordinated skeletal muscle synergy, "drunk" appearance in gait or stance,
or inability to move the contralateral heel along the tibial crest voluntarily.
Neurological consultation, EMG, and NCV testing is usually indicated when a

neurological defect is suspected or identified. Nerve conduction velocity can be measured
for sensory nerves !e.g. sural, saphenous, lateral femoral cutaneous) in an antidromic
fashion; while motor nerves (common peroneal, posterior tibial, medial and lateral plantar)
are measured from proximal to distal and tend to conduct impulses at about40 meter/
second. Nerve injury, entrapment, or demyelinating disease can decrease nerve
conduction velocity. Electromyography depicts on an oscilloscope skeletal muscle
electrical activity associated with needle electrode insertion. Denervated muscle shows
increased fibrillation potentials. Results in the intrinsic foot musculature are variable.
VASCULAR EXAMINATION
The basic clinical vascular evaluation involves inspection ofthe skin color, temperature,
turgor, and digital trichosis; as well as palpation of the arterial pulse at the popliteal,
posterior tibial and dorsalis pedis levels. If indicated, arterial pulSe at the perforating
peroneal, femoral, and abdominal aortic levels are also assessed. Edema is noted to be
either pitting, brawny or spongy. The skin barrier is inspected for areas of open compromise
or gangrene. Vasospastic instability may elicit livedo reticularis, while arterial insufficiency
may elicit dependent rubor associated with intermittent claudication or even rest pain.
Non~lnvasive Vascular Examination

The non-invasive vascular examination is performed with the duplex Doppler ultrasound
machine, and correlated with the clinical findings. The non-invasive arterial exam measures
segmental arterial pressures and waveform analysis. Ipsilateral segmental pressure
differences indicative of a 20-30 mmHg pressure drop from the proximal to the distal
segment, are strongly suggestive of occlusive disease. Moreover, arterial pulsation wave-
forms should be triphasic with a dicrotic notch, or at least biphasic. Monophasic Doppler
tracings and sounds are indicative of arterial occlusive disease with decreased flow.
Determining the ankle systOlic pressure involves pneumatic cuff placement above the
ankle and elevated until no arterial pulsation can be identified with the Doppler ultrasound
over the PT artery. The cuff is then deflated until the ultrasound identifies flow in the PT
artery, and the pressure recorded. The maneuver is repeated while measuring the opening
pressure in the DP artery, and then again for the peroneal artery. The highest of the three
values is used as the "ankle" systolic pressure. Forefoot and digital systolic pressures, as
well as pulse volume recordings using infrared sensors on the toe pulps can also be
determined.
Transcutaneous oxygen tension and thermography also offer tools for assessment of
pedal perfusion. The ankle/arm ratio (also know as ankle/brachial index or ischemic index)
is calculated by dividing the ankle systolic opening pressure by the arm systolic opening
pressure. Deceptively high opening pressures can be measured in the presence of medial
calcific sclerosis.
Ankle/Arm Ratio Guidelines in the Non-Diabetic Patient
Ankle/Arm Ratio Clinical Finding

>0.96 Normal
0.31 - 0.95 Intermittent claudication
0.25 -0 .3 Rest Pain
0- 0.3 Impending gangrene
Ischemic Index Guidelines for Reconstructive Surgery
Foot If ankle/arm index< 0.75, then generally do not operate.

If ankle/arm index> 0.75, then check toe/arm index.
If ankle/arm index> 0.75 and 1De/arm index< 0.65, then generally do not operate.
If ankle/arm index> 0.75 and toe/arm index> 0.65, then may operate.
If can't get measurement on toe because of deformity, use forefoot/arm index.
If ankle/arm index> 0.75 and forefoo1/arm index> 0.65, then check Doppler
flow of digital arteries.
Hallux: If ankle/arm index> 0.75, and toe/arm or forefoo1/arm index> 0.65 and two of
four digital arteries identified with Doppler, then Qenerally may operate.
Lesser Toe: If ankle/arm index> 0.75 and toe/arm or forefoo1/arm index> 0.65 and either
both dorsal arteries and one plantar or both plantar arteries identified with
Doppler, then generally may operate.
Invasive arterial testing, in the form of angiography with radiopaque contrast media,
is usually obtained only if reconstructive vascular surgery is being entertained. Infusion of
contrast medium is not a risk-free undertaking, and conveys the risk of hypersensitivity
reaction, as well as renal failure in dehydrated or predisposed individuals. Digital
subtraction angiography can further enhance identification of patent and occluded
vessels. Although noninvasive, MRI can also be used to evaluate blood vessels and yields
considerably accurate images.
Venous non-invasive Doppler assessment is used when deep vein thrombophlebitis is
suspected, and a venogram may further enhance identification of a thrombosis,
particularly one that is propagating or associated with embolism and consideration is given
to surgical intervention.
BIOMECHANICS
Biomechanics is the study of mechanical laws as they pertain to the human musculoskeletal
system and, in particular, bipedal locomotion.
Basic terms include:
1. Cardinal body planes sagittal (SP), frontal (FP), and transverse (TP)
2. Axes- frontotransverse, allowing motion in the SP frontosagiltal,

allowing motion in the TP sagittotransverse, allowing
motion in the FP
3. Motions- pronation and supin8.tion (triplanar)

inversion and eversion (FP)
adduction and abduction (TPI
internal rotation and external rotation (TP)
dorsiflexion and plantarflexion (SP)
flexion and extension (SP)
4. Positions- pronated, supinated, inverted, everted, abducted, adducted,

externally rotated, internally rotated, dorsiflexed,
plantarflexed. When a position is fixed, it is referred to as
flexion, extensus or extension, adductus, abductus, varus,
valgus, elevatus, supinatus, equinus, calcaneus.
Motion is described as occurring in the cardinal planes of the body or foot, in a plane
90 to the axis of motion. Single plane motion occurs in the plane perpendicular to the axis
that lies at the intersection of the remaining two planes. Triplanar motion occurs in a plane
perpendicular to an axis that courses through all three cardinal planes (oblique to all planes).
Triplanar motion of the foot is said to be pronatory/supinatory (pronatory), and the axis is
directed from posterior-lateral-plantar to anterior-medial-dorsa!. Pure SP motions include
dorsiflexion and plantarflexion, while pure transverse plane motions include adduction and
abduction, and pure frontal plane motions include inversion and eversion.
Biomechanical Examination
The examination begins with open chain visual inspection, then patient active motion,
followed by manipulation and palpation, followed by gait analysis. Special testing, such as
pedobarographic, kinematic, and other motion analysis methods may also be used. Visual
inspection is used to identify gross positional and structural features. Examination may
proceed as follows: hip, knee, ankle, subtalar joint, metatarsal joint, 1st ray, 1st
metatarsophalangeal joint, forefoot-to-hindfoot relationship, then on to other assessments
of specific concern.
Hip -is a diarthrosis that allows enarthrous gliding, rotation, angulation, and circumduction.
Motion occurs in all three body planes:

TP (sagittal-frontal axis): Internal and external ROM
FP (sagittal-transverse axis): Abduction/adduction ROM
SP (frontal-transverse axis): Flexion/extension ROM (including hyperextension).
The mechanical axis of the hip runs from the center of hip to knee, with the mechan-
ical axis of the femoral shaft running from a line between greater and lesser trochanters,
relative to the plane of femoral condyles.
Examination of the hip should reveal the following:
Adult Hip Range of Motion - Int. Rot. " Ext. Rot., with hip flexed or extended. The
neutral hip should align femoral condyles on the FP. Normal SP hip flex./ ext. at birth is
150, and about 100 after puberty. If limited in extension, then hamstrings are likely
tight; if limited in flexion, then Iliopsoas is likely tight; excessive internal to external
range of motion indicates tight adductors; excessive external to internal range of
motion indicates tight abductors; and asymmetrical limitation of motion may indicate
congenital or neglected hip dysplasia or limb length inequity. Total range of motion
decreases with age.
Knee- motion occurs aboutthls ginglymus jo.mtwith only two degrees of freedom \axes) of
motion: SP flexion-extension, and TP internal and external rotation. 5-6o of TP motion
occurs with SP flexion-extension of the knee. Motion occurs predominantly in the SP about
a frontal- transverse axis, and to a lesser degree about the frontal-sagittal. FP motion is
indicative of collateral ligament damage. The patella enhances quadriceps leverage.
In non-weight bearing (open kinetic chain) rotation of the knee, the tibia rotates on
the femur. In weight bearing \closed kinetic chain), the femur rotates on the tibia. The
lateral femoral condyle rotates around the medial condyle, with motion occurring between
the tibia and meniscus. Therefore, for internal rotation, the lateral tibial condyle moves
anteriorly on the lateral meniscus. For external rotation, the lateral tibial condyle moves
,j
posteriorly on the lateral meniscus. The greatest degree of rotation is available when the
knee is flexed at 90. Examination of the knee should reveal the following:
1. Knee position on the FP when hip and STJ neutral, with end range of motion 180',
and fixed
2. Flexion or hyperextension may indicate compensation for ankle equinus.
3. Genu valgum may effect compensatory hindfoot supination, but generally over
time acts as
4. A strong pronatory influence on the hindfoot
5. Genu varum must be distinguished from tibial varum, and pro nates the hindfoot.
6. Genu recurvatum may be due to cruciate ligamentous laxity or compensation for
ankle equinus. Thigh hamstrings or gastrocnemius can effect genu flexion deformity.
Ankle- range of motion occurs about a pronatory axis running from the latera! to medial
malleolus, normal range being 20-30 dorsiflexion OF and 30-50 PF. The axis is primarily at
the junction ofthe FP and TP. deviated in the TP by about 12'-15" of malleolartorsion, thereby
allowing primarily SP OF Iflexion) and PF !extension). The articulation represents a mortise
(medial malleolus, distal tibial bearing surface, lateral malleolus) and tenon (talar body) joint.
Range of motion is assessed by asking the patient to actively take the ankle joint through
OF/PF range of motion in the sagittal plane, followed by circumduction of the ankle or
figure-of-eight motion.
Examination of the ankle should reveal the following: Ankle range of motion should
allow 25-30 PF, and lOa or more dorsiflexion with the knee extended. Increased ankle
dorsiflexion when the knee is flexed is indicative of limitation by gastrocnemius (equinus if
< 10). The Silfverskiold test is then performed, and the presence or absence of gastrocne-
mius or gastro soleus equinus, or bony (talotibial exostosis) equinus, is determined. Pseudo
equinus, due to plantarflexed forefoot results in functional ankle equinus due to retrograde
ankle dorsiflexion in weight bearing. Compensation for ankle equinus may result in normal
heel-off due to adequate subtalar joint/metatarsal joint hyperpronation, early heel-off if only
partially compensated by hindfoot pronation, or no heel-off whatsoever (no heel contact) if
uncompensated in the foot (usually associated with genu recurvatum or fixed flexion).
Subtalar Joint- range of motion occurs about a pronatory axis deviated 42 from the TP
I nearly equidistant from the horizontal TP and the vertical FP), and 16o from the SP. STJ is
minimal in the SP, as the axis almost lies in this plane. Inversion/eversion and adduction/
abduction motion is greatest and almost equidistant in both the FP and TP, respectively.
A higher pitched subtalar joint axis would allow more TP motion, while a lower pitched
subtalar joint would allow more FP motion. The subtalar joint is an oblique hinge
diarthrosis with trip!anar motion. Motion from maximum pronation to maximum supination
defines an arc, with 2/3 of the arc supinated from the neutral position, and 1/3 pronated
from the neutral position.
Normal subtalar joint range of motion is 30-35, with about 10-15 eversion and
20- 30 inversion. Pronation of the subtalar joint in open kinetic chain (non-weight
bearing) entails abduction, eversion, and dorsiflexion of the calcaneus on the talus; whereas
pronation in the closed kinetic chain (weight bearing) attitude entails adduction, inversion,
and plantarflexion of the talus on the calcaneus. Range of motion is assessed by observing
normal excursion of 2/3 inversion to<< eversion with the ankle joint DF and the metatarsal
joint maximally pronated and locked on the hindfoot It has been estimated that a minimum
subta!ar joint range of motion of 8-12 is required for normal ambu!ation. The neutral
position of the subtalar joint, as determined by a posterior bisector of the calcaneus, is the
point 1/3 of the way from maximum subtalar joint pronation, and 2/3 of the way from
maximum inversion.
Calculation of subtalar jointISTJ) neutral position INP) is as follows:
NP STJ" eversion ROM -!total ROM/3).

A positive value indicates a valgus or neutral position
A negative value indicates a varus or neutral position.
Ch.4 Selected Dlagnost'1c Techniques 109
Example
If there is a maximum of 12 STJ eversion, and 18 maximum inversion, then the
tROM = 30".
NP STJ = 12'- 30"/3= 12'-10"= NP STJ of2'varus
To identify STJ NP, we need to know the point from which there is twice as much
supination as there is pronation:
total (STJ ROM /3) x 2 =inversion from NP, and (inv. from leg)-( inversion from
neutral)= NP
Example
If the calcaneus can evert 1Oo from the leg bisection and invert ZOo from the leg
bisection, what is the NP of the STJ?
total STJ ROM= 10" t 20" = 30", 30"/3 x 2 = 20" inversion from NP,
so (inv. from leg)- (inv. from neutral)= 20"- 20" = 0" = NP
Examination of the subta!ar joint should reveal:

Subtalar joint motion, as described previously, ideally 20 inversion (supination) and 10
eversion (pronationL with subtalar neutral being 1/3 the range from maximum eversion and
2/3 the range from maximum inversion. The posterior bisector of the heel should be
perpendicular to the ground with the subtalar joint neutral. In a subtalar joint varus
deformity, there is more than 2/3 of the range of motion in the direction of varus {example
25 inversion with supination, 5 eversion with pronation, so inversion of calcaneus to
ground), resulting in excessive compensatory subtalar joint/metatarsal joint pronation in
stance {compensated rearfoot varus). Compensated rearfoot varus can also effect
excessive subtalar joint pronation in a subtalar joint varus combined with tibial varum
deformity {eg. 25 inversion with sup-ination, 5 eversion with pronation, in presence of 5
tibial varum). if the calcaneus is perpendicular to the ground when the subtalar joint is
maximally pronated. A partially compensated rearfoot varus {eg. 30 inversion with
supination, oo eversion with pronation, so tibial varum), when the subtalar joint cannot fully
evert to perpendicular (remains in 5 varus, in this particular example).
Metatarsal joint (MTJ)- range of motion occurs about oblique (OMTJ) and longitudinal
(LMTJ) pronatory axes. The OMTJ axis lies 52" from the TP and 57' from the SP, coursing
from the mid-lateral aspect of the calcaneus to the TNJ. Primary motions are abduction/
adduction and DF/PF, with minimal inversion/eversion. The oblique MTJ (OMTJ) axis allows
predominantly OF/PF and adduction/abduction, with minimal inversion/eversion. The
longitudinal MTJ axis allows predominantly inversion/eversion with minimal DF/PF and
abduction/adduction. Both the OMTJ axis and LMTJ axis allow triplanar motion. Range of
motion is assessed with the forefoot loaded in OF and eversion at the 5th metatarsal head,
and the subtalar joint in neutral position. The plantar tangent to the hindfoot should be
perpendiculartothe posterior bisector of the calcaneus, while allowing the medial column
to seek its own level. Pronation of the STJ will unlock the MTJ and allow hypermobility of
the first ray (forefoot supinatus). The LMTJ (Hicks' axis)lies 9" from the SP and 15" from the
TP, coursing from the posterolateral aspect of the calcaneus to the 1st metatarsal-cuneiform
joint. Being so close to the SP and TP, the axis provides a primarily inversion/eversion in
the FP. Normal metatarsal joint range of motion is 4-6. Forefoot supinatus occurs primarily
around Hicks' LMTJ axis. When the STJ is pronated, the MTJs become parallel, allowing
the head of the talus to decline plantarly relative to the navicular.
Examination of the MTJ should reveal: MTJ motion with STJ pronation, the plantar
aspect of the forefoot everts relative to the hindfoot as the MTJ unlocks and becomes more
mobile. With STJ supination, the plantar aspect of the forefoot inverts relative to the
hindfoot, and MTJ motion is limi!Bd. lithe forefoot remains inverted to the rearfoot, forefoot
varus exists.lfthe forefoot remains everted to the reartoot, forefoot valgus exists. Forefoot
valgus may be rigid or flexible. Forefootsupinatus describes the compensatory inversion of
the forefoot on the rearfoot associated with hyperpronation olthe STJ and OMTJ, the
inversion of the forefoot occurring around the LMTJ axis.
1st ray- range of motion occurs about an axis coursing 45 from the SP and 45 from the FP
in a posterior-dorsal-medial to anterior-plantar-lateral direction, allowing motion aboutthe
medial cuneiform-navicular and 1st metatarsal-cuneiform joints. 1st ray range of motion is
assessed with the subtalar joint in neutral position, while manipulating the head of the 1st
metatarsal through its OF/PF SP excursion.
Examination of the 1st ray reveals: normal 1st ray motion is 5 mm (10) in both dorsal and
plantar directions, as compared to a normal second ray. As the 1st ray dorsiflexes, it
inverts; and when it plantarflexes, it everts, in a 1:1 ratio. This motion is important in
determining hypermobility of the 1st ray. McGiamry has noted that transverse plane
mobility of the 1st ray is comparable to sagittal plane mobility of the 1st ray, and is
indicative of the ability to reverse buckle the 1st MTPJ and thereby reduce the 1st IMA via
Reverdin osteotomy. Moreover, hypermobility of the 1st ray, with resultant forefoot
supinatus, may indicate the need for 1st metatarsal-cuneiform arthrodesis as compared to
1st metatarsal base wedge osteotomy in the correction of metatarsus primus varus and
hallux abducto valgus or other deformities.
A plantartlexed 1st ray reveals maximum dorsiflexion below, or plantar to, the level of
the 2nd metatarsal, resulting in a valgus attitude of the forefoot to the rearfoot. It is
important to assess the relation of the 1stthrough 5th, and 2nd through 5th, relative to the
reartoot. The forefoot valgus may be rigid or flexible. A rigid plantarflexed 1st ray effects
forefoot valgus, with retrograde supination of the metatarsal joint and, if severe enough,
even supination of the subtalar joint. Associated deformities include hallux malleus (hallux
hammertoe). with EHL and FHL mechanically advantaged relative to EHB and FHB; as well
as sesamoiditis (usuaHy tibial), lateral ankle and knee strain, symptomatic Haglund's
deformity (pump bump), and children may display an intoe gait This also results if a 1st
metatarsal-cuneiform fusion or 1st metatarsal base osteotomy effects too much
plantartlexion.
A flexible plantarflexed 1st ray effects a flexible forefoot valgus, which does not
function plantartlexed when the 1st ray is loaded. The 1st ray may function at the level of
the lesser metatarsals if the MTJ unlocks with hindfootpronation. Associated findings may
include submetatarsa\1 and 5 hyperkeratosis, tibial sesamoiditis, and flexor stabilizing lesser
hammertoes.
Metatarsus prim us elevatus exists when the 1st ray is positioned above, dorsal to, the
level of the lesser metatarsals, specifically the 2nd metatarsal, and is associated with
hallux limitus/rigidus, hallux equinus, dorsal bunion, lateral dumping of late midstance and
propulsive phase weight bearing and sub-second metatarsalgia and hyperkeratosis, as
well as 5th toe dorsolateral HO and perhaps 4th interspace HM or HO. The 1st met. may be
elevated relative to the 2nd, even in the presence of overall forefoot varus. An elevated 1st
ray may be congenital, or acquired secondary to longstanding hyperpronation of the

STJ/MTJ (hindfoot), or iatrogenic following fracture or base osteotomy. Hallux limitus may
also be caused by an excessively elongated 1st metatarsal, 1st MTPJ injury, metabolic
arthritis, or sesamoid adhesion. Prolonged metatarsus primus elevatus effects medial
column collapse and pes valgus over time.
5th ray- axis of motion is oblique to all three body planes and is therefore pronatory/supina-
tory, run'ning from proximal-plantar-lateral to distal-dorsal-medial, 20 from the TP and 35
from the SP, and predominately allows SP and FP motion. The 5th ray everts with dorsiflex-
ion and inverts with plantartlexion.
Intermediate rays- consist of the 2nd through 4th rays, which have frontal-transverse axes
and therefore allow motion only in the SP. MTPJ function is divided into 1st and lesser
groups, all of the MTPJs functioning primarily, or initially, as ginglymus joints with
predominantly SP dorsiflexion/plantarflexion although TP rotation is also allowed about a
vertical axis. The 1st MTPJ range of motion should display 65 {as measured from a
position parallel to the substrate, or 20-21 o from the long axis of the 1st metatarsal which is
declined relative to the substrate, in essence making a full range of motion from the long axis
of the metatarsal being 65" + 20-21" = 85-86") for normal propulsion, and firm plantarflexion
stabilization of the metatarsal (relative plantarflexion) is required in propulsion otherwise 1st
ray hypermobility and lesser digital flexor stabilization will result. The initial25" of 1st MTPJ
dorsiflexion occur with the joint acting strictly ginglymus, however reciprocal 1st metatarsal
plantart!exion is required for dorsiflexion> 25, which causes the frontal-transverse axis to
move proximally and dorsally Ipath of the evolute) as the joint behaves arthrodial in late
midstance and propulsion.
Lesser IVITPJs- should achieve 15 dorsiflexion in propulsion with good plantarflexion

stabilization against the substrate, and similarly require reciprocal metatarsal p!antatilexion
and proximal~dorsal migration of the transverse axis (evolute) for greater dorsiflexion.
Ontogeny as it Relates to Biomechanics of the Lower Extremity

The femoral segment displays a FP angle of inclination relating the head and neck of the
femur to the long axis of the femoral shaft birth, 150-160"; 6 years to adult, 125". The TP angle
of declination relates torsion within the shaft of the femur from the head and neck to the
distal condyles.
Femoral antetorsion refers to twisting of the femur such thatthe condyles of the femur
are internally rotated relative to the frontal plane and the head and neck. The angle
between the head and neck of the femur and the femoral condyles is normally 30 - 40" of
anteversion at birth and 8-12 in the adult, representing a gradual retrotorsion as the femur
untwists with maturation. Concomitant with the retrotorsion is femoral anteversion, or
inward twisting to the thigh segment to counter the more proximal retrotorsion, thereby
keeping the femoral condyles on the FP.
Delayed derotation can effect in-toe, and is often seen in the older female child and
clinical presentation of the "reverse tailor's" sitting position, increased medial femoral range
of motion, and knock-knee. Treatment includes proper sitting habits, Ganley femoral
de rotation splint (4 to 8 years), and femoral de rotation osteotomy in the older child. Knee
flexion diminishes the therapeutic influence of any pedal splinting directed at the femur,
and appropriate pediatric orthopedic consultation is in order whenever significant deformity
exists. The angle between the head and neck ofthe femur and the FP is normally60 external
at birth, and 80-100" external in the adult.
Terminology pertaining to the femur includes: antetorsion- internal femoral torsion,
anteversion - internal femoral position, retrotorsion - external femoral torsion, and retro-
version- external femoral position.
The knee alignment- varies with age as follows: birth, genu varum; 1-3 years, straight; 3-6
years, genu valgum; 7-13 years, stralght; 13-18 years, genu valgum, > 18 years, straight>
60 years genu valgum.1ibial varum is a FP inverted angulation of the lower leg to the ground
in static stance. Tibial valgum is a FP everted angulation of the lower leg to the ground in
static stance.
The malleoli- form a 0" angular relation to the FP at birth, followed by an external growth
torque of 18-23true tibial torsion or 13~18 of malleolar position, malleolar position being
about 5 less than true tibial torsion, occurring in the transverse plane. We measure
malleolar position because we can not actually measure tibial torsion clinically. As a guide,
external malleolar position should be as follows 0-10" from birth to 1 year, 8-13" frorn 1-5
years, and 13-18" from 6 years to adulthood.
The hindfoot relationship~ of talus to the calcaneus during fetal development reveals a FP
movement of the talus over the calcaneus from a parallel position (clubfoot TEV represents
cessation or limitation of the movement away from parallel). The talar head becomes less
plantatflexed relative to body of calcaneus, which is importantfor development of normal
TP TCA, cyma line, talar declination angle, CIA, and MTJ position.
Growth in length and width of metatarsals and phalanges- is ongoing from fetal to adult
stages, and includes FP eversion torsion of metatarsals lw5, and TP abduction of 1st
metatarsal to lesser metatarsals: fetal- 1st metatarsal adducted 50, birth~ adducted 6, by
4 years to adult~ 7-9 (if> 7~9, get metatarsal prim us adductus or varus with juvenile HAV).
The TP relation of the lesser metatarsals to the tarsus reveals: birth ~ 25 adducted,
adult -15-18" adducted. Metatarsus adductus is 15-35" at birth, and 15-22" in the adult.
Structural and Positional Deformities of the Lower Extremities

Forefoot varus ~ is a structural deformity of the forefoot in which the plantar plane of the
forefoot is inverted relative to the supporting sutface and the vertical posterior bisector of
the calcaneus when the subtalarjointls neutral and the metatarsal joint maximally pronated
and locked. It is associated with compensatory hyperpronation of the STJ/MTJ;
submetatarsal 2~5, especially 4~5, hyperkeratosis; tailor's bunionette, flexor stabilization
induced hammertoes, adductovarus 4th and 5th toes, HAV, metatarsus primus elevatus,
plantar fascitis, and heel spur syndrome, and hallux limitus, medial knee strain and internal
rotation secondary to compensatory hyperpronation of the hindfoot. Biomechanical
treatment generally entails supporting the deformity, thereby nullifying the need for
compensation in the foot, while posting the reatfootto allow 2~4 of motion.
Flexible forefoot valgus~ is a structural deformity wherein the plantar plane of the forefoot
is everted relative to the supporting sutface and the vertical posterior bisector of the cal-
caneus when the subtalar joint is neutral and the MTJ maximally pronated and locked. It is
associated with compensation via supination about the LMTJ axis (forefoot supinatus); sub~
metatarsal1 and 5 hyperkeratosis; tibial sesamoiditis, flexor stabilization hammertoes, and

adductovarus 4th and 5th toes. Biomechanical treatment generally entails supporting the
deformity, thereby nullifying the need for compensation in the foot, while posting the
rearfoot to allow 2 to 4n of motion.
Rigid forefoot valgus~ is a structural deformity wherein the plantar plane of the forefoot is
everted relative to the supporting surface and the vertical posterior bisector of the
calcaneus when the subtalar joint is neutral and the MTJ maximally pronated and locked.
lt is associated with compensation via supination about the OMTJ axis and subtalar joint
axis; hallux malleus, tibial sesamoiditis, lateral ankle and knee strain, symptomatic Haglund's
deformity (pump bump), and children may display an intoe gait Biomechanical treatment
generally entails supporting the deformity and using a 1st ray cut out, thereby nullifying the
need for compensation in the foot, while posting the rearfootto allow 2-4 of motion.
Reatfoot varus- is a structural deformity wherein the calcaneus is inverted relative to the
substrate when the subtalar joint is neutral and the MTJ maximally pronated and locked. It
is associated with lateral ankle sprain, compensatory pronation of the hindfoot only to
vertical (not a profound degree of pronation), submetatarsal 4-5 hyperkeratosis,
adductovarus 4th and 5th toes, tailor's bunionette, Haglund's deformity, and HAV.
Reatfootvalgus- is a structural deformity wherein the calcaneus is everted relative to the

substrate when the subtalar joint is neutral and the MTJ maximally pronated and locked. It
is associated with submetatarsal2 hyperkeratosis, HAV, plantarfascitis, flexor stabilization.
Metatarsus prim us elevatus- is a structural deformity wherein the 1st metatarsal displays
a resting position dorsal to the 2nd metatarsal and plane of the lesser metatarsals. It is
associated with hallux limitus/rigidus, hallux equinus, dorsal bunion, lateral dumping of late
midstance and propulsive phase weight bearing and sub-second metatarsalgia and
hyperkeratosis, as well as 5th toe dorsolateral HD and perhaps 4th interspace HM or HO.
Forefoot supinatus- is a fixed position of supination of the forefoot about the LMTJ axis,
when the subtalar joint is neutral and the MTJ maximally pronated and locked. It is
associated with plantar fascitis, and limited MTJ available range of motion.
Ankle equinus- is the condition of inadequate dorsiflexion range of motion ofthe foot on
the leg. It is considered present when < 10 of ankle dorsiflexion is available, and the
Si!fverskiold test is used to determine the influence of the Achilles tendon as a whole and
the gastrocnemius muscle and aponeurosis separately. Osseous talotibial blockade
may also be present Equinus deformity is associated with early heel off, knee flexion
throughout stance (unless damaging hyperextension-genu recurvatum occurs),
compensatory hyperpronation of the hindfoot with plantar fascitis, flexor stabilization,
adductovarus 4th and 5th toes, HAV, and extensor substitution ifthe equinus persists as a
dropfootthrough swing phase.
Tibial torsion- is measured as malleolar position with the malleoli forming< 13-18 of
external malleolar position, malleolar position being about 5 leSs than true tibial torsion, in
the transverse plane. External malleolar position is as follows 0-1 0" from birth to 1 year,
8-13 from 1-5 years, and 13~ 18 from 6 years to adulthood. Internal tibial torsion often
affects the left lower extremity (in utero pressure from maternal vertebral column) in males,
and treatment involves serial casting to above the knee, taking care to stabilize the hindfoot
and ankle in neutral position.
Genu valgum (knock knee)- is an angular deformity of the knee usually observed in obese
female children, and may be associated with coxa vara or uncompensated medial or
compensated lateral femoral torsion, tibial torsion, pes valgus, deformation (depression) of
the lateral tibial plateau with hamstring or quadriceps or calf pain and DJD in the adult.
Genu varum (bowleg)- is an angular deformity of the knee usually observed in cases of
Rickets due to vita min-D deficiency and abnormal Ca and Ph metabolism, or due to Blount's
osteochondrosis deformans wherein the medial tibial condyle is flattened and fragmented
(present at birth to 24-30 months).
Femoral anteversion- refers to positioning of the femur such that the condyles of the femur
are internally rotated relative to the frontal plane and the head and neck of the femur. The
angle between the head and neck of the femur and the femoral condyles is normally 30- 40"
of anteversion at birth and 8-12 in the adult, representing a gradual retrotorsion as the
femur untwists with maturation. Delayed de rotation can effect in-toe, and is often seen in
the older female child with the clinical presentation of the "reverse tailor's" sitting position,
increased medial femoral range of motion, and knock-knee. Treatment includes proper
sitting habits, Ganley femoral derotation splint (4 to 8 years), and femoral derotation
osteotomy in the older child. Knee flexion diminishes the therapeutic influence of any pedal
splinting directed at the femur, and appropriate pediatric orthopedic consultation is in order
whenever significant deformity exists.
Unequal limb length- may be structural within the thigh, leg or both femoral and tibial/
fibular segments; or functional secondary to scoliosis induced pelvic tilt with lower side of
pelvis effecting functionally longer limb, unilateral supination or pronation of the foot.
Compensation for limb inequity involves pedal pronation on the longer side, along with
ipsilateral inferior pelvic tilt (tilts downward) due to hyperpronating hindfoot, ipsilateral
shoulder tilt downward, scoliosis, ipsilateral head tilt toward longer limb, increased stance
phase on the longer side. On the short side, the hindfoot supinates, pelvis rises, shoulder
rises, and there is less stance phase weight bearing.
Radiographic Findings Related to Biomechanics

Radiographic signs of hyperpronation of the foot include: increased TP and SP
talocalcaneal angles, increased talar declination, decreased calcaneal inclination,
decreased forefoot adductus and increased abductus due to unlocked MTJ, anterior break
in the midtarsal cyma line, decreased (<70%) talonavicular articulation congruity, and
medial column breach in sever pes valgus. Radiographic signs of a supinated foot are
opposite to those seen with pronation, and include a bullet sinus tarsi, and a more parallel
relation of the talus and calcaneus. An acquired rocker bottom foot, due to equinus or
severe pes valgus, displays plantar articular gapping and dorsal jamming.
Basic Gait Analysis

Phases of the gait cycle include stance 162%) and swing (38%1.
The stance phase is subdivided into:
contact- which occurs from heel contact to forefoot contact and entails 27% of the
stance phase and 17% of the entire gait cycle, and is associated with the foot serving
as a pronating mobile adapter, with initial vertical force being about 125% of body
weight
midstance- (entails 40% of the stance phase) wherein the foot conve rtsto a rigid !ever
for push-off, and the vertical force decreases to about 75% of body vveight;
propulsion- (33% of stance) which consists of heel off and toe off, wherein the
vertical force again reaches about 125% of body weight and the foot is a rigid
supinated, tight-packed lever.
Swing phase- requires external leg rotation and ankle dorsiflexion, and hip and knee
flexion.
At heel contact, we note hip extending, knee flexing, ankle pi a ntatflexing, and
STJ neutral and pronating.
At midstance, we note hip flexing, knee extending, ankle d orsiflexing, STJ

supinating and MTJ pronating.
Double support occurs atthe beginning and end of each stance phase in walk-
ing gait, wherein both feet are on the ground, and this occurs at t:he 1st 0-12% and
again at50-62% of the gait cycle, or 25% of the entire cycle.
Double float, or an airborne phase, occurs in running gait
The phasic activity of the lower extremity musculature is as follows, rei ative to the gait
cycle:
hip adductors fire from heel contact to midstance and again from heel off to midswing
hip abductors fire through late swing to prior to heel off
hamstrings fire from late swing to 25% of stance; quadriceps femoris fire from hee
contact to 25% of stance and again from toe off through early swing
triceps surae fire from 15-20% of stance to toe off
peroneal musculature fires from 15-20% of stance to toe off; and the anterior leg
musculature fires from swing to midstance
116 The Perioperative Patient Ch. 5
THE PERIOPEilATIVE PATIENT

The perioperative period is divided into preoperative, intraoperative and postoperative
phases. Planning a safe and efficacious course for the patient requires that attention be paid
to many details. Open and frank discussion with the patient and their family, and consult-
ants, is important relative to achieving a smooth operative cOurse.
PREOPERATIVE PHASE
Considerations in the preoperative phase include the history and physical IH&PI, accurate
diagnosis and treatment protocol, the decision to operate, and informed consent.
Informed Consent Contains:

Review of the diagnosis
Planned surgery or procedure
The possibility of other intervention based upon operative findings
Potential risks and complications
Alternatives to the surgery or procedure
Postoperative course and expectations
Permission for observers in the operating room and for photography
Safe Medical Device Act
Identification that no guarantees have been made
Signature by the patient, a witness, and the surgeon
Appropriate systemic medical evaluation should also be obtained preoperatively, and

discussion with the patient's physician should be undertaken as indicated. PreOperative
consultation, physical therapy, attainment of postoperative medications and/or special
equipment, such as a bone growth stimulator for home use, notification of social services
if home wound care or lV antibiotic administnition and testing are anticipated, should also
be considered.
Special medical considerations include thrombophlebitis prophylaxis, corticosteroid
supplementation, prevention of gout, and infection prophylaxis with preoperative
administration of antibiotics. If the procedure is anticipated to last more than 2-3 hours,
urinary catheterization may be performed.
The preferred anesthesia should be discussed with the patient and, if there is a
question, the anesthesiologist. The operating room personnel should be notified ofthe need
for special equipment and studies, such as the C-arm and diagnostic imaging, specific
instruments or implants, power lavage, tubes for aerobic and anaerobic C&S, frozen
section, drains, bandages, and splinting/casting materials. The patient should fully under-
stand the planned postoperative course, analgesia, weight-bearing status, rehabilitation
schedule, time off from work, and prognosis.
INTRA-OPERATIVE PHASE
The intra-operative phase entails those activities that take place once the patient is in the
operating room. The details ofthis period are documented in the operative report, the record
of anesthesia, and the circulating nurses notes. Attention is paid to achieving surgical
Ch. 5 The Perioperative Patient 117
anesthesia, patient positioning, hemostasis, extensile exposure, wound exploration and

inspection of pathological anatomy, alteration of planned procedure if indicated,
intraoperative imaging to assess correction and fixation, wound closure and bandag-
ing/splinting, and control of any complications (hemorrhage, break of sterile field, malig-
nant hyperthermia, ischemia) that may have arisen during the course ofthe procedure.
POSTOPERATIVE PHASE
The postoperative phase entails the period commencing in the recovery room until the
patient is discharged from your care. Obviously the early postoperative period \first 1 to 3
days) is most critical relative to the possibility of systemic complications. The surgeon's
postoperative orders detail planned care of the patient once the anesthesiologist has
transferred the patient from the recovery room. The surgeon must also document the
procedure and findings of the surgery in the operative report
Standard Postoperative Orders Can Include
1. Vital signs (VS Q shift after return to floor)

2. Activity (CBR with side rails up; absolute NWB operated foot at all times; BRP
NWB operated foot with assistance; PT for gait and transfer training NWB
operated foot).
3. IV fluids (maintain IV D% LR at KVD until fully reactive/stable. Convert to Heparin
lock after D/C IV).
4. Medications, including antibiotics, analgesics for moderate and severe pain,
anti~inflammatory, anti-emetic, stool softener/bowel stimulant, hypnotic, and the
patient's regular medications.
5. Respiratorytherapy
6. Drain management
7. Diet
8. Discharge planning
9. Other orders specific to the case
Postoperative Complications
Postoperative complications are variable, and range from mild problems to life- threatening
crises. Complications can occur despite the best planning and technique. It is the surgeon's
responsibility to point out, within reason, the possible complications related to a specific
procedure, and to be on the look-outforthe development thereof in the postoperative phase.
The best approach to the management of a postoperative complication is straight-forward
identification of the problem, notification of the patient and documentation in the medical
record, and treatment. Consultation may certainly be in order.
A postoperative complication is defined as any untoward event occurring within thirty
days after the surgery. Complications may affect the surgical wound and various organ
systems, including pulmonary, gastrointestinal, cardiovascular, and urinary systems. The
phrase "wind, water, wound, walk, wonder," reminds the surgeon ofthe most common post-
operative complications and the postoperative day during which the specific complication
usually occurs.
118 The Perloperative Patient Ch.5
Postoperative Day Complication

first day pulmonary
second day urinary
third day wound
fourth day calf DVT
fifth day anything is possible
Pulmonary complications- include atelectasis, aspiration, and pulmonary embolism.

Pulmonary complications are more likely following general anesthesia, and in patients who
are obese or those with a history of COPD or regular cigarette smoking. Such patients should
undergo preoperative pulmonary function testing, and the anesthesiologist should be
notified of the results. Postoperative pulmonary assessment notes respiratory rate and
effort, in conjunction with auscultation ofthe lung fields.
Atelectasis is the condition of collapse of the adult lung, and is usually due to bronchial
occlusion (secretions) and subsequent absorption of air as alveolar perfusion
continues. Atelectasis may occur during or after general anesthetic.
Aspiration occurs when gastric c.ontents are admitted into the trachea, bronchial
passages, and lung, resulting in airway inflammation and pneumonitis. Aspiration may
occur in relation to administration of a general anesthetic, when the patient's gag
reflex is muted. Atelectasis and aspiration pneumonitis effect localized pain, dyspnea,
and fever. Auscultation may reveal abnormal breath sounds. A chest X-ray should be
obtained. Respiratory therapy to enhance ventilation is indicated for mild atelectasis,
and will usually suffice. Therapy ranges from simple incentive spirometry lTriflow) to
medicated breathing treatments. Aspiration pneumonitis is treated with appropriate
respiratory therapy, corticosteroids, and antibiotics.
Pulmonary embolism associated with lower extremity DVT, is the most devastating-
postoperative pulmonary complication. See Chapter 3.
Urinary complications- include retention and urinary tract infection. Postoperative

assessment involves observation of fluid input and output, blood pressure and heart rate,
and suprapubic palpation and percussion.
Retention is common in elderly males at bed rest, particularly if there is concomitant

benign prostatic hypertrophy or history of urinary stricture secondary to previous
traumatic urethral catheterization, infection or surgery. Atropine or other anti~
cholinergic in high doses associated with general anesthesia can cause urinary
retention. Similarly, prolonged surgery and anesthesia, with administration of IV fluids
may lead to bladder distention (average bladder volume is about 500 cc). Cases
anticipated to last 3 or more hours should entail placement of a Foley catheter after
general or spinal anesthesia has been achieved. If the patient has not voided by six
hours postoperative, examine for bladder distention (palpation and percussion) and
initiate treatment by encouraging the patient to stand (works we!! in males). If patient
remains unable to void, then pass a straight catheter once to evacuate the bladder and
measure the volume. If the urine volume is< 300 cc, discontinue catheterization. If the
urine volume is 500 cc or more, consider placement of an indwelling catheter until the
patient is more ambulatory and comfortable.
Ch.5 The Peri operative Patient 119
Urinary tract infection can be caused by prolonged urinary retention, or urinary

catheterization. Care should be taken to employ aseptic technique whenever passing a
urinary catheter. Females are more likely to develop urinary tract infection, and many have
previous history of urinary tract infection. Treatment entails adequate hydration, and
antibiotic therapy after obtaining a clean catch, midstream urine specimen for C&S.
Wound complications
Fixation failure or loss of surgical correction usually requires a return to the operating
room to rectify anything but the minimal deformity.
Circumferential bandage or cast compression. An excessively snug or tight

circumferential bandage or cast can induce pain that is unresponsive to analgesia,
cutaneous compromise and pressure ulceration, neuropraxia; and requires cast and
bandage replacement in order to effect relief.
Hemorrhage will usually cease with protection, rest, ice, compression, and elevation.
If hemorrhage persists beyond one or two bandage reinforcements, then
consideration should be given to a return to the operating room for exploration and
hemostasis. Hemoglobin and hematocrit levels will decline secondary to significant
hemorrhage, and preparation for transfusion should be considered if the hemoglobin
drops below 9 grams. (It is rare and quite problematic for a patient to require
transfusion following foot and/or ankle surgery.) Observation of the patienfs vital signs
may indicate the need to increase IV fluid administration above the KVO rate.
Dehiscence may be superficial or deep, and can usually be managed wfth local wound
care and secondary intention healing, as long as hematoma or infection does not
warrant intervention that is more aggressive.
Hematoma and infection warrant, at the least, selected suture removal, swab
specimen of any exudate or drainage for Gram's stain and C&S, CBC with differential,
observation of systemic temperature and blood glucose, close wound monitoring, and
possibly oral antibiotic therapy, for minimal or equivocal findings. If the signs of
inflammation associated with suspected hematoma and/or infection are significantly
advanced, or not responding within 24-48 hours to initial intervention, then a return to
the OR for wound inspection and cleansing debridement may be warranted. Actual
therapy will depend upon the local and systemic merits of the individual case. It is
better to error on the side of over-aggressiveness, rather than miss the diagnosis and
place the patient at more risk.
Infection is highlighted by unusual amounts of pain, often unresponsive to analgesic

medication, on or about the 2nd to 3rd postoperative day. Hemolytic Streptococcus
may cause fever and wound infection within 24 to 48 hours of the surgery.
Consideration should be given to an acute gouty attack in the hyperuricemic patient
with history of gout, and to an excessively tight bandage or cast. Excessive pain at
the operative site always warrants inspection. Nonsuppurative wound infection can
be difficultto identify, even with close observation of the surface of the well-coapted
incision, and a high index of suspicion should be maintained. Systemic signs of
120 The Perioperative Patient Ch. 5
endotoxin release and/or septicemia should be suspected, and include Gl distress,

general malaise, cutaneous rash and/or desquamation (toxic shock syndrome),
myalgia, cephalgia, and pyrexia.
Postoperative ischemia~ usually identified in the digits as a "blue toe." Other common
areas of postoperative ischemia include skin islands (actually isthmuses or bipedicle flaps)
situated between two long, parallel skin incisions. Causes of blue toes include venous
congestion, dissecting hematoma, and arterial occlusion or microcirculatory vasospasm.
Venous congestion effects a cyanotic, often warm, diascopy positive toe that may
respond well to eleVation and perhaps loosening of constriction bandages and
flexion of the knee. Ice, nicotine, and caffeine should be avoided whenever dealing
with a blue toe.
The term dissecting hematoma may be a misnomer, however it refers to the condition
wherein hematoma has separated and filled the potential space between intact and
viable dermis and overlying epidermis. The condition has also been described with
intradermal dissection. In this condition, the epidermis displays a dark appearance
consistent with hematoma observed through the thin, translucent epidermis. The basal
layer of the epidermis may also become necrotic, and the epidermis will eventually
slough. The digit may be anesthetic, cool, and stiff. The important clinical distinction,
related to dissecting hematoma, is the possibility of misconstruing the toe as being
gangrenous throughout. It is prudent to carefully inspect and debride the superficial
layers of the skin to ascertain whether deeper tissues are viable. Arterial Doppler
assessment of the digital vessels may also be useful when considering the possibility
of dissecting hematoma.
Occlusive vascular ischemia due either to functional vasospasm or organic disruption

of the flow (thrombus, embolism, impingement or laceration), effects a cold toe that
initially displays pallor followed by cyanosis and then gangrene. The ischemic toe
will usually blanch upon application of pressure {diascopy positive), however
subpapillary venous plexus refill time will be greatly delayed. If blood flow is restored
prior to the development of necrosis (3~6 hours), pink or red cutaneous hyperemia will
be observed. Vasospasm can be effected by surgical manipulation, often noted with
vessel traction and pin stabilization across the MTPJ; or seen in patients with a
history of Raynaud's phenomenon and subjected to a cool operating room and lavage
fluids; or due to the local use of dilute epinephrine in a patient with Raynaud's
phenomenon or treated with tricyclic antidepressant or MAO inhibitor.
Counter measures include dependency, loosening tight bandages, avoidance of

nicotine and caffeine and ice, adjustment or removal of a pin positioned across the MTPJ,
reflex heat(K-pad) applied to the abdomen and or thigh, posteriortibial nerve or ankle block
with plain bupivacaine, and oral (Procardia) and/or intra-arterial (Priscoline} vasodilator
following vascular consultation.
Postoperative OVT
See Chapter 3
Ch. 5 The Perioperative Patient 121
Gastrointestinal complications- include nausea and vomiting, constipation, gastritis and

reflux esophagitis, fecal impaction, and postoperative jaundice. Severe bowel obstruction
or postoperative paralytic ileus usually only occurs following abdominal surgery.
Postoperative assessment of the belly entails observation, auscultation for bowel sounds,
and palpation for tenderness, guarding, and rebound.
Postoperative nausea and vomiting may be the result of anesthetic or narcotic

influence on the central chemoreceptor trigger zone, or due to peptic ulcer disease or
gastritis in predisposed patients or those medicated with anti-inflammatory drugs.
Excessive emesis can effect dehydration, and IV fluids should be administered. Drugs
such as Compazine, Tnlafon, Phenergan, Dramamine, Tigan, and Emeticon can be
used to control postoperative nausea, and may be administered in suppository form.
Drug interaction with analgesics, sedative/hypnotic, and antidepressants should be

considered whenever administering centrally~acting antiemetics.
Constipation often results from inactivity, and commonly occurs in elderly patients
who are immobilized in bed. Bulk laxatives such as bran Metamucil or Senokot or
stool softeners such as Co/ace, Doxinate and DDS, are preferred over bowel stimulants
such as Milk of Magnesia or Dulcolax. Encouraging fluids and out of bed activity are
indicated. Rarely is an enema necessary.
Fecal impaction is rare following foot and ankle surgery and may present as
postoperative diarrhea.lfthe digital rectal examination reveals hard stool, then an oil
retention enema may be helpful. Digital disimpaction may also be necessary.
Gastritis and/or reflux esophagitis is common in patients maintained NPO and

positioned supine with the legs elevated, especially in those with hiatal hernia and/or
previous PUD. Treatment is elevation of the head and oral administration of antacid
(Riopan, Rolaids, TUMS)and/or H2 receptor antagonist such as Pepcid. Diarrhea can
often be controlled with bismuth (Pepto-bismol).
Postoperative jaundice usually associated with nausea, warrants assessment of

hepatic enzymes and review ofthe anesthetic record. If right upper quadrant pain is
marked (colic), then general surgical consultation and cholecystogram or ultrasound
is indicated.
Cardiac complications - uncommon in association with elective foot and ankle

reconstructive surgery, and are most likely to occur in patients with pre-existing coronary
artery disease, dysrhythmia, congestive heart failure, or patients with significant pulmonary
disease. Postoperative cardiac evaluation involves vital sign assessment, and
auscultation. Rarely fluid overload can precipitate congestive heart failure, and pretibial,
perimalleolar, and pedal pitting edema should be observed. Arrhythmias are most
commonly observed during general anesthesia and are usually related to periods of
hypoxia or myocardial sensitivity to the anesthetic agent (halothane, enflurane).
Consultation with the anesthesiologist is in order in patients with a history of significant
cardiac disease, and a recent chest X-ray and EKG are in order. In patients with a cardiac
murmur, prophylactic antibiotics are indicated, and an updated echocardiogram may be
122 The Perioperative Patient Ch.5
useful pending cardiology consultation. ln patients with a history of coronary artery

disease or CVA, elective surgery is avoided for at least six months following a documented
myocardial infarction.
Postoperative nerve entrapment- can occur even after strict attention has been paid to
avoidance and protection of peripheral nerve, secondary to norma! wound healing and
fibrosis effecting scar entrapment of the nerve trunk. This generally takes three weeks or
more to become symptomatic, as wound healing and fibroplasia progress. Sharp, burning,
shooting pain and paresthesia noted earlier in the postoperative phase may indicate
specific nerve trunk trauma due to sectioning, traction, or heavy-handed retraction
causing neuropraxia or intraneural hemorrhage.
Postoperative fever- is anticipated early on, especially following general anesthesia.

Fever is defined as a core (rectal) temperature of 37.8 C(100 F), or greater. Temperatures
of 38J C (101 F), or higher, indicate a major constitutional problem, and can result in
severe central nervous system damage. In searching for the cause of postoperative
systemic temperature elevation, considerations include: recent general anesthesia;
possibility of pulmonary atelectasis or aspiration, UTI, constipation; catheter sepsis {IV,
urinary); 0\IT and PE; wound infection or injury; drug reaction or serum sickness.
The physical examination should identify sites of inflammation and potential cause of
the febrile state. In addition to the clinical examination and discussion with the patient,
testing should include CBC with differential; urinalysis; C&S of wound drainage or exudates,
urine, blood, oropharynx and sputum; and a chest X-ray.
The treatment of hyperpyrexia (fever> 38.5 C) involves administration of antipyretic
such as acetaminophen or aspirin (600 mg PO Q 6 h PRN), and use of a cooling blanket If
the patient remains hyperpyrexic and symptomatic, then consider discontinuing all
medication, consult infectious disease specialist, and re-evaluate the patient.
Chronological Sequence of Postoperative Temperature Alteration
Intraoperative & Elevated temperature due to malignant hyperthermia,

first 12 to 24 hours postop or typically postoperative hypothermia.
1st postop day Postoperative hypothermia, postanesthesia

overshoot, atelectasis I pneumonitis
2nd postop day Benign postoperative fever, urinary tract infection,

pulmonary, DVT
3rd postop day Wound infection, benign postoperative fever, and

constipation.
Any time in the postop phase Drug fever, catheter sepsis, transfusion reaction,
cold, or flu.
Ch. 6 Fundamental Techniques and Procedures 123
FUNDAMENTAL TECHNIIJ.UES AND PROCEDURES
SUTURE MATERIALS and WOUND CLOSURE

Sutures are used to reapproximate sectioned tissue, whether it is skin, superficial or deep
fascia, muscle, tendon or ligament, nerve sheath, blood vessel, or bone (stainless steel wire
[SSW]). The ideal suture material is strong enough to resist disruptive tensile forces, non-
allergenic and non-toxic, pliable enough to handle easily and to stay fixed once tied. Sutures
that communicate between the external surface of the skin, and the subcutaneous and/or
intradermal layers should also be inert, non-wicking, and easily removable after the tissues
have healed. The decision to use an absorbable or nonabsorbable suture material varies
with the specific requirements of the operative procedure.
Absorbable sutures-these are made of materials that break down in the tissues over
varying time periods, ranging from 1~ 10 weeks. Since most soft tissues, excepttendon, heal
in 3~4 weeks, sutures that degrade at a rate that provides tensile strength up to 3~4 weeks
are commonly used in foot and ankle surgery. Classically, absorbable sutures were made
from sheep or beef intestine, and known as catgut. Plain gut can be strengthened by the
addition of chromium salts that slow down degradation by collagenase, or it can be
heat~treated to Increase the rate of degradation (rapid gut). Although it is not likely, disease
transmission, such as bovine spongiform encephalopathy (mad cow disease), is possible
with catgut, which is a xenogeneic materiaL Although many surgeons prefer the behavior
of gut suture, monofilament or braided multifilament synthetic polymers comprise the
majority of absorbable sutures used nowadays. Synthetic polymers, such as polyglycolic
acid, lactic acid and caprolactone, are relatively inexpensive, non~reactive due to
hydrolysis rather than collagenase degradation, nontoxic and nonallergenic, and they
handle very well. Immunological reaction to synthetic absorbable suture is rare, however
when it occurs a sterile abscess can form, and the material may not rapidly orfu!ly absorb.
Monofilament absorbable sutures are often used in the deep tissues during delayed
primary closure of previously infected or contaminated tissues. Sutures range in size
(gauge), as defined by the US Pharmacopeia (USP), from #11-0 (smallest) monofilament
nylon used for ophthalmologic and neurosurgery, to #5 (largest) braided polyester used for
ligament repair. Some suture materials are also coated or impregnated with antimicrobial
agents, to minimize risk of infection.
Non-absorbable sutures-these are made of materials that are not degraded by the body,
such as silk, polypropylene, polyester and nylon, and are often used for skin closure (where
they can readily be removed after the skin has healed), or in tissues where prolonged
strength is require, such as tendon or ligament, or myocardium and blood vessel. Due to the
inert nature of many of these materials, there is less inflammation and less scar formation,
so they are often preferred for skin closure. Stainless steel wire can be used for
intra osseous suture, cerclage, and tension banding.
Suture needles-needles used for suturing are available in a number of shapes, namely:
half curved, quarter circle, 3/8 circle, 5/8 circle, compound curvature, and straight (Keith
needle). Separate needles with eyelets for threading suture are known as traumatic
needles. Atraumatic needles have the suture material swaged to the needle by the
manufacturer. Needles can also be smooth and round or oval, or they may have a cutting
edge on the concave surface ofthe curve, or on the convex surface of the curve (reverse
124 Fundamental Techniques and Procedures Ch.6
cutting needle). The body of the needle maytapertoward the tip, or retain the dimension of
the body and form a blunt tip (forfriable tissue). The tip ofthe needle can be round, oval, or
diamond-shaped. Generally, a non-cutting, atraumatic needle is used for reapproximation
of friable tissues, whereas a cutting needle is often used for dense and durable tissues
such as fascia and joint capsule.
Suture (stitching) techniques and remova~some of the most common suture techniques
include the simple interrupted stitch (almost always applicable). horizontal and vertical
mattress stitches {excellent margin eversion, however can strangulate), running and
running lock stitches, figure-of-8 stitch, baseball stitch, and the running subcuticular stitch.
Running subcuticular skin closures are usually reinforced with adhesive skin strips. Skin
sutures that are designed to be removed, are generally taken out according to the
following schedule: face 3-5 days, scalp or trunk 7-10 days, limbs 10-14 days, over a joint
14-20 days, plantar 20-22 days. Care of the operative site varies with anatomical location,
and wound healing progress. Stitch maneuvers suitable for tendon include the Bunnell,
Kessler, and other lateral trapping methods. Nonabsorbable multifilament sutures are often
used to reap proximate tendon to bone, and a variety of tendon anchors are available forth is
(see section on tendon transfers).
Tissue adhesive---cyanoacrylate ("liquid suture" or tissue glue) can be used as an

alternative. to suture material for wound margin reapproximation where there is minimal
tendency toward margin disruption. Cyanoacrylate polymerizes when it comes in contact
with tissue fluid, forming a flexible adhesive bond between the wound margins. When used
for skin closure, cyanoacrylate is reinforced with adhesive skin strips.
BIOPSY TECHNIQUES
lncisional Biopsy---incisional biopsy removes only a selected portion of the lesion in

question, while an excisional biopsy removes the entire lesion (theoretically). Obviously, a
margin of supposedly "normal" tissue is excised around the lesion in question when an
excisional biopsy is performed. Actual pathological assessment of the margins of the biopsy
is necessary to determine whether a "clean" margin was created. When performing an
incisional biopsy, it is important to select representative portions of the lesion, and more
than one sample may be harvested. It is important to accurately identify the samples
relative to position about the lesion, and a diagram is helpful in this regard. The pathologist
would also benefit from review of the diagram when dealing with a difficult lesion. The
surgeon should not struggle to procure a margin of normal appearing tissue in the
incisional specimen at the risk of missing representative lesion. Scabs, crusts, and
vesicles should be preserved in the specimen, and not destroyed in the surgical
preparation of the skin. Most skin biopsies can be performed under !a cal anesthesia, and
dilute epinephrine (1:100,000 or 1:200,000 dilution) may aid hemostasis, if it is not
contraindicated in the particular patient. The local anesthesia should not be infiltrated
directly into the lesion, for fear of spreading potential malignancy or infection, although it
has been shown that direct injection below or through a lesion appears to cause no
significant microscopic alteration. The area is then prepped and draped in the usual s
terile fashion, priOr to biopsy.
Ch.6 Fundamental Techniques and Procedures 125
Punch Biopsy--the punch biopsy is a convenient and effective method of tissue extraction
and may be either incisiona! (usually), or excisional when dealing with a large punch and a
smaller lesion. In the lower extremity, the 4-mm punch is typically employed, and standard
punch sets include punches ranging from 2-8 mm. It should be noted that removal of a
specimen <4 mm in diameter might allow the histological confirmation of a tumor, however
it is generally considered inadequate for the accurate diagnosis of an inflammatory process.
When using the punch, the skin surrounding the lesion/s should be stretched taut,
perpendicular to the wrinkle lines before the circular punch is inserted. The punch is firmly
pressed downward into the lesion with a rotary back and forth cutting motion until it is well
into the subcutaneous tissue, thereby providing a full-thickness skin biopsy. To remove the
cylindrical specimen from the skin, gently grasp the biopsy plug with forceps, or a 27-gauge
needle, and cut the base with scissors or scalpel and then place the sample into 10%
formalin. Simple pressure is adequate for hemostasis. A punch biopsy defect of :24 mm
diameter may require suture closure, whereas a defect <4 mm will heal via secondary
intention with adhesive skin strips and a sterile dressing. A linear defect usually heals more
readily than a round defect.
Shave biopsy---the shave biopsy is used to remove that portion ofthe lesion elevated above
the plane of surrounding tissue and is useful for biopsy or removing many benign
epidermal growths. It is not indicated for biopsies of suspected melanoma, although it can
be used to identify the presence of malignancy without providing adequate tissue for
microstaging of a melanoma. However, it can be used as a convenient procedure for
I ' diagnosis of basal cell epithelioma !basal cellcarcinoma). The preparation is as noted
previously for biopsy, and a #15 blade is used to shave the lesion/sand a margin of
apparently normal surrounding tissue. The specimen is retained in 10% formalin. Pressure
is applied to effect hemostasis.
Curettage-curettage is a useful technique, distinguishable from the shave biopsy, for

removal of cutaneous lesions such as warts, seborrheic keratosis, and even malignancies
such as basal and squamous cell carcinomas. The curette is a spoon-like instrument with
a sharp rim. Typically, the 4-mm curette is used. A variation on this technique is
excochleation using a blunt instrument, such as a Freer elevator, when removing a lesion
that has a clear and separable margin with the adjacent normal tissue. An isolated verruca
is ideal for excochleation, as this provides an excellent specimen for biopsy and prepares
the base for ablative surgery (acid, cryogen, or laser).
Surgical excision------excisional biopsy should be considered whenever the lesion displays

active (spreading) margins and the border with normal appearing skin is to be surveyed, or
if the lesion is friable or very sclerotic, or whenever it is necessary to include full-thickness
skin to the level of, and including a portion of, the subcutaneous fat layer {e.g. in suspected
panniculitis, erythema nodosum, or melanoma). In theory, excisional biopsy is curative, and
may be used whenever excision of a lesion is desired. Local anesthesia is achieved as
described previously for incisional biopsy. With the exception of the smallest lesions (<4
mm), the planned incisions should be marked on the skin. The most common technique
involves the use of two semi- elliptical incisions to create a wedge of intervening tissue to
be excised. The length of the ellipse should be three to four times the width, with the long
axis of the wedge parallel to crease lines and, therefore, RSTL. Surrounding margins may
be undermined in order to decrease tension with closure, and weight bearing on the
126 Fundamental Techniques and Procedures Ch. 6
plantar skin should be avoided for 23 weeks, varying with the size of the wound and
progress of healing. When malignancy is suspected, it is importan~to avoid contamination
of surrounding tissue planes with cellular elements of the lesion in question. A sarcoma
can often be adequately eradicated with wide excision, compartment resection, or
amputation. Violation of adjacent soft tissue barriers at the time of biopsy may make
subsequent definitive therapy more ablative than it originally need to have been. A frozen
section may be used to identify the presence or absence of tumor in a particular specimen,
and perhaps yield identification ofthe specific 1ype of tumor present It is often difficult to
accurately identify the specific tumor from a frozen section specimen only, however the
presence of dysplasia and anaplasia can usually be determined. A frozen section must be
planned with the pathologist and OR team. If a local excisional biopsy is performed, and the
frozen section pathology report yields a diagnosis of malignancy, then an adequately wide
excision should only be attempted for very small and well-defined lesions. By definition,
sarcomas are usually invasive and not differentiated from adjacentsofttissues. Carcinomas
localized to the skin may be more readily isolated and amenable to definitive excision and
eradication at the time of excision aI biopsy. Definitive treatment such as wide excision and
coverage with a muscle flap, or amputation, is determined by oncological consultation and
additional testing to ascertain tumor staging. Additional radiographs and CT scans of the
part as well as the lungs, MRl, and other tumor specific tests are often warranted. Adjuvant
radiation and/or chemotherapy may be administered both before and after definitive
excision, and is determined by the oncologist. Definitive surgery is planned and carried out
in a timely fashion. Plastic surgical consultation and co-management is often needed in
order to effectively cover the defect created by wide excision, and a free muscle flap
(serratus, or other suitable donor site) in conjunction with skin grafting may be indicated.
PlASTIC SURGERY TECHNIQUES
Elective skin incision planning and execution--elective skin incisions should take into
consideration exposure of underlying target tissues, preservation of vital structures, and
relaxed skin tension lines (RSTL). As long as adequate exposure is not compromised, the
incision should be made parallel to RSTL An incision made parallel to RSTL will be
subjected to less gapping tendency, and should therefore form less scar. RSTL run
perpendicular to the long axis of the extremity and vital structures. When a transverse
incision fails to yield adequate exposure, an incision that is oblique to RSTL is considered
better than one perpendicular to RSTL, wfth respect to gapping and scar formation. Difficulty
may arise when RSTL are in a transverse direction and the exposure needs to be
longitudinal, as in the case of excision of the plantar fascia for treatment of fibromatosis. In
such a case, a zigzag incision can be used to effect longitudinal exposure while remaining
oblique to RSTL over the short segments of the zigzag.
Primary intention closure--involves direct wound margin reapproximation secured with

skin sutures. It results in immediate closure that seals with epithelium after 24-48 hours,
and usually results in a fine-line scar. Primary skin closure requires wound margin mobility
that allows approximation ofthe edges.
Secondary intention closure--involves wound granulation, contraction and epithelializa-

tion, and slowly progresses over several days to weeks, depending upon local and
systemic factors. This is often the preferred method of closure following incision and
drainage of an abscess or osteomyelitis, or when the wound presents chronic contamina-

tion and necrosis, such as ulceration in a debilitated patient
Tertiary intention (delayed primary) closure----involves an initial period of secondary

intention healing, followed by additional surgical wound debridement and primary
intention suture closure. Primary, secondary or tertiary intention healing are the preferred
methods of wound closure, and should be attempted whenever clinically indicated.
Indications include a clean wound with beefy red granulations and resolution of
surrounding cellulitis and edema. Generally, other methods of closure, such as skin plasty,
grafts, and flaps, entail a greater risk of dehiscence, dysvascularity, slough or other
complication, and should be reserved for those cases where simpler methods are
deemed inadequate.
Skin Graftintrskin grafts consist of epidermis and varying thicknesses of dermis. The graft
is said to "take" when it has successfully revascularized and effectively covered the
recipient site. The thicker the graft, the more difficult it is to achieve" graft take." Contrarily,
a thinner graft usually takes more rapidly. Moreover, thicker grafts are more durable and
contract less while healing, whereas thinner grafts are less durable and contract
considerably more. Skin grafts are most frequently autogenous, with the patient serving as
his/her own donor. For foot and ankle reconstruction, ipsi- or contralateral leg, thigh,
buttock, or the anterior aspect of the abdomen, can serve as donor skin graft procurement
sites. Donor skin can be meshed to provide for larger surface coverage at the recipient site.
Skin grafts can also be allogeneic {from another individual ofthe same species), xenogeneic
(the donor is of a different species, commonly porcine), or isogeneic (the donor is an
identical twin). By definition, a graft is detached completelywhen transferred from the donor
site to the recipient bed. There are 3 phases of skin graft healing (Table 6-1).
TABLE 6-1. PHASES OF SKIN GRAFT HEALING.

Phase Time period Key events
Plasmatic 24-48 hours Fibrin adhesion between
graft and recipient site
Inosculation 48-72 hours Microvasculature
traverses fibrin layer
Remodel/reinnervate 3 days to several months Collagenation, collagen
remodeling, reinnervation
Split-t/Jickness skingraft(STSG}--these can be thin, intermediate thickness, orthick. A thin

STSG measures 0.008-0.012 inches in thickness, while an intermediate graft measures
0.012-0.016 inches, and a thick graft measures 0.016-0.020 inches. Thin STSGs contract as
much 50-70%, and are often used as temporary coverage for large wounds. Intermediate
STSGs are most versatile and frequently used in coverage of foot and ankle wounds. Thick
STSGs only contract about 10~ 15%, however demand markedly increased recipient bed
vascularity, and have a higher risk offailure.lntermediate and thick STSGs can be used to
cover weight bearing and contact areas.
Full-thickness skin graft (fTSG)-these contains the entire epidermis and dermis,
including dermal appendages such as sweat glands and hair follicles. The subcutaneous
128 Fundamental Techniques and Procedures Ch.B
fat and superficial fascia are not included in a FTSG. FTSGs are very durable and contract
minimally, however take rather poorly in comparison to STSGs. A FTSG can be considered
for coverage of a weight- bearing surface, and can be harvested from a pinch of skin over
the sinus tarsi, anterior anlde, or medial arch. The inguinal region and popliteal fossa are also
potential donor sites. Full-thickness pinch grafts consisting of skin from the sirius tarsi are
useful for coverage of small defects in plantar and contact areas of the foot.
The recipient site must be prepared in order to increase the rate of skin graft take,
and this should be done prior to harvesting the graft. The recipient site must be free of
fibrosis, necrosis, infection, and active hemorrhage. A beefy red, confluent granulation
tissue base is the ideal recipientsutiace. Bare tendon, bone, and cartilage are inadequately
vascularized for graft support, and a period of secondary intention healing is required to
allow for the formation of a granulation tissue surface. In cases involving large or deep
wounds, temporary coverage may be achieved with a skin substitute (see below), prior to
subsequent autogenous skin grafting. After the recipient site is prepared, the autogenous
skin graft is harvested (procured) from the donor site manually using a Goulain or Hum by
knife, or via use of a pneumatic powered Brown or Pagget dermatome. Although the graft
can be stored for up to 21 days in lactated Ringer's solution at 0-5 C. After procurement,
attention should focus on getting the graft to the recipient site in a rapid (immediate) and
efficientfashion. The graft may be incised in a fashion similar to pie crusting, wherein small
incisions are made to allow expansion and seroma drainage. For large recipient sites, the
graft may also be meshed, in a 1:1.5 ratio using_ the graft masher, in order to increase the area
of coverage and enhance drainage of wound transudate through the mesh incisions. Mesh
ratios of 1:3, 1:6, and 1:9 can also be achieved, however these ratios make for sparse
coverage of the recipient site and are only used when a large surtace requires coverage.
After meshing, the graft is placed in contact with the recipient bed, maximizing contact and
eliminating dead space. The graft is then secured with several simple interrupted sutures
of 4-0 or 5-0 chromic gut at the margins. A small amount of excess graft may overlap
adjacent intact skin margins. The graft-recipient intertace is then secured with a tie~over
stent dressing. The tie-over stent dressing employs fine-mesh nonadherent gauze placed
directly over the skin graft, followed by coverage with fluffed gauze or mineral oil
impregnated cotton balls, then covered with a flat gauze barrier secured with evenly-spaced
silk sutures that convey gentle pressure over the graft In many cases, immobilization and
non-weight bearing are indicated, and the graft is typically not disturbed until 5-7 days. The
graft donor site is dressed with nonadherent gauze, after assuring hemostasis (topical
thrombin spray can be used), and redressed when the recipient site is inspected.
Application of a wound dressing consisting of porcine-derived extracellular collagen,
elastin, glycosaminogtycan, and glycoprotein (such as Oasislr can enhance donor site
healing. Complications related to skin graft healing usually develop secondary to disruption
of the grafHecipient interface with resultant failure to achieve revascularization. Causes
include seroma formation, infection, and inadequate immobilization. A dysvascular
recipient site is doomed to failure. Failure to achieve inosculation results in graft necrosis,
and this usually leads to contamination and subsequent infection if appropriate treatment
(debridement, antibiotic therapy, and revision) is not initiated. Reverse dermal grafts are
sometimes used for nail bed reconstruction, and require inverting an intermediate STSG
prior to application to the recipient bed.
Skin substitutes-----a number of options exist for skin coverage that do not involve
harvesting autogenous skin. These materials typically employ combinations of collagen,
glycosaminog!ycan (GAG), silicon elastomer, and water. One such option (Integra) is a
bilayer skin substitute that consists of a biodegradable type I collagen-GAG co-polymer
dermal analog combined with an epidermal analog consisting of a thin silicone polymer
that behaves in a fashion similar to normal skin. The cross-linked collagen and GAG matrix
maximizes ce!!ular in growth and degrades in a predictable fashion. After neodermis
formation, the silicone epidermal analog is removed and replaced with a thin STSG.In some
cases, use of the bilayer skin substitute obviates the need for subsequent use of an
autogenous skin graft. Other skin substitutes include combinations of keratinocytes and
fibroblasts, harvested from neonatal foreskin orxenogenic sources, in a collagen matrix, and
these are often used In the treatment of large cutaneous wounds such as those due to
burn injuries.
Skin flaps----flaps differ from grafts in that a vascular pedicle is maintained or, via micro~
surgical reanastomosis, reconstructed. Flaps are defined as either local or distant. In the
foot and ankle, defects larger than 2.5 cm 2 are generally covered with a skin graft, while
smaller defects are amenable to use of a local skin flap. Flaps are advantageous for full
thickness defects, poorly vascularized recipient wounds, and coverage of bony prominence
or contact areas. Sensation can also be restored when an innervated flap is used. Skin
flaps are classified according to their blood supply. Random pattern skin flaps are perfused
by the random dermal-subdermal plexus of vessels, and require a pedicle width equal to the
length of the flap. The Z-plasty and V-Y pia sty are techniques that create random pattern,
local, rotational or advancement skin flaps. Axial pattern skin flaps are supplied by an
identifiable (Doppler) cutaneous artery, such as the lateral calcaneal artery flap used to
cover heel defects, or the sural artery flap used to cover Achilles tendon defects, and can
be rather long in comparison to the pedicle width. Axial pattern flaps can be of the island
design, or actually distant flaps when the vascular origin is sectioned and later
reanastamosed atthe recipient site.
Local flaps----these are mobilized from adjacent skin, and are of either the rotational
or advancementtype. Rotational flaps are semicircular and are mobilized about a pivot
point where the flap is attached to its pedicle. A larger semicircle imparts less tension
on the pivot, and tension can be alleviated at the pivot by means of a back cut or
creation of a Burrow's triangle. The single and bilobed rotation flaps are commonly
used for coverage of smaff pedal skin defects. Advancement flaps are mobilized via
direct extension without rotation, and include the Y~V, V~Y, single, and bipedic!e flaJJs.
Distant flaps----these originate from a vascular pedicle in one area of the body and,
via maintenance of the pedicle or sectioning with subsequent microvascular
reanastomosis, are used to cover a remote defect. For example, a crossed leg flap
uses skin mobilized from the contralateral calfto cover a pedal defect; or a section of
latissimus dorsi, complete with its arterial supply and overlying fascia and skin may be
harvested to cover a pedal defect. In the crossed leg technique, the calf donor skin
remains attached at its pedicle while the legs are skeletally fixated and the flap sutured
to the contralateral pedal recipient site. Once the ftap has healed and attached to the
recipient bed, the donor side pedicle is sectioned and the skeletal fixation removed.
Currently, it is more common to use the microvascular free flap, ratherthan the crossed
leg method. The serratus free flap is commonly used by plastic reconstructive
surgeons to cover large pedal defects, and requires microvascular reanastomosis
and coverage of the muscle with a STSG.
Skin plasties-these employ !ocal flaps and are used to redirect skin, and alter skin tension
and volume. Scar tissue and contracture can be redirected and lengthened with the
Zplasty !Figure 6-1). The arms of the Z are of equal length, with the apices forming a 60'
angle, in order to achieve approximately 75% increase in skin length with resultant
decreased tension. Multiple Z-plasties, resulting in a W-plasty, can be used to further
elongate skin and relieve tension. The V-Y plasty results in skin lengthening after flap
mobilization. The skin defined by the V-incision is mobilized and elongated, and the
resultant wound is sutured closed in the shape of a Y. As a rule, the wider the V's base, the
greater the vascular pedicle. Skin can also be shortened or reduced by means of a Y~V
plasty. Redundant skin can be excised via the creation of an elliptical wedge using two
semi~elliptical skin incisions. This is often useful in digital surgery, in particular when
derotation of a frontal plant deformity is desired {Figure 6-2). Fasciocutaneous flaps are
useful in the leg, in particular for coverage of defects about the Achilles tendon. Muscle
flaps are useful for coverage of weight bearing or contact areas of the foot and ankle, and
convey excellent vascularity and provide a robust base over which skin can grow.
Identification and preservation of the muscle's vascular supply is critical to the success of
the flap. The heel and first metatarsal head area are amenable to coverage with FOB and/or
FHB (Figure 6-3), the medial and lateral malleoli with abductor hallucis and abductor digiti
minimi, respectively.
A_______
------~ .A!fr..
'?'__
Figure 6.1
Figure 6.2
Figure 6.3
BONE GRAFTING AND ORTHOBIOLOGICAL AGENTS
Bone grafting may involve transplantation of viable bone that is expected to remain viable
in the recipient host, whereas implantation implies transfer of non-living bone or tissue
i, (freeze-dried bone) to the host recipient bed. An autograft originates in the recipient host;
an isograft originates in an identical twin; an allograft or homograft is viable bone
originating in a donor of the same species, while an alloimplant or homoimplant is non-
living bone from the. same species; and xenograft or heterograft (or implant) implies bone
from a donor of another species (and are not recommended for general use). Autogenous
bone grafts are advantageous because of immunocompatabi!ity and transfer of
osteoconductive (trabeculae and porous channels), osteoinductive (chemotactic and
transformation factors), and osteogenic (viable cells) properties. Disadvantages
associated with autogenous bone grafts pertain to creation of stress risers at the donor
site with potential for fracture, as well as creation of another surgical wound that is
subject to potential hematoma, infection, or other wound complication. Moreover, the host
may not have adequate bone to donate, and the osteogenic quality varies with site and
age. Autogenous bone is favored for use in the repair of failed unions, previous infection,
or donor site/host morbidity. Allogeneic bone is suitable for orthotopic use, backfill of donor
site void, and in cases wherein donor bone is limited or harvestthereof is contraindicated.
There are 3 physiological elements critical to bone graft healing, including:
1) osteoconduction, 2) osteoinduction, and 3) osteogenesis !Table 6-2). Osteoconduction
pertains to the porous nature of trabecular bone, which provides the scaffold upon which
cells migrate and reside. Osteoinduction pertains to the chemotactic and differentiating
influence that bone morphogenetic protein, and other growth factors, has on belie growth.
Osteogenesis pertains to the bone generating properties of undifferentiated stem cells,
osteocytes and chondrocytes (via enchondral bone formation). Autogenous bone grafts
can take the form of cancellous, cortical, or corticocancellous bone Table 6~3. More
specifically, bone grafts function in the treatment of delayed union, nonunion and
pseudoarthrosis; to augment skeletal defects created by trauma or surgery, such as to fill
a void after cancellous bone biopsy or cyst evacuation; to facilitate arthrodesis and to
effect bone block limitation of motion; and to enhance reconstruction by means of
osteotomy, as with the Evan's latera! calcanea! (column) lengthening, or in the repair of
brachymetatarsia. To a certain degree, restoration of segmental bone defects using
autogenous bone grafts has been replaced by means of callus distraction, and the use of
bone graft substitutes.
TABLE 6-2. PHYSIOLOGIC PROCESSES OF BONE GRAFT HEALING.

Process Elements and function Source
Osteoconduction Pores (10-1000 microns) that Cancellous bone, bioceramics
mimic cancellous bone; (CaP04, CaS041, hydroxyapatite
scaffold for bone growth (coralline and natural coral grafts),
extracellular matrix scaffolds
(collagen or GAG+ HA + TCP),
polymers IPGA), alloys (1i)
Osteoinduction Bone morphogenetic Autogenous bone, allogeneic
proteins 2 & 7, platelet- stem cells or recombinant
and fibroblast-derived demineralized bone matrix,
transforming growth autogenous platelet rich
factors; recruit and plasma or bone marrow aspirate
transform mesenchymal
Osteogenesis Living osteocytes, AutOgenous bone, fresh
osteoblasts, chondrocytes, marrow or cloned cells
chondroblasts, and undifferentiated
mesenchymal stem cells
TABLE 6-3. STRUCTURAL TYPES OF BONE GRAFTS.

Structure Graft characteristics
Cortical Dense, compact bone containing few viable cells; provides stable
graft that can be secured to surrounding bone with fixation devices
Cancellous Spongy bone containing viable cells to stimulate
osteogenesis and rapid incorporation; no structural strength;
excellent back-fill
Corticocancellous Provides stability and osteogenesis; includes grafts such as
those harvested from the calcaneal body and iliac crest;
excellent reconstructive graft
Harvesting bone graft-when harvesting an autogenous bone graft, plenty of irrigation is

used for coo!ing during osteotomy in an effort to preserve viable cells. A sharp osteotome
is ideal for harvesting autogenous bone graft. The graft is procured and placed in a sterile
container and covered with a sa!lne moistened sponge. The graft should not be submerged
in saline solution. Prophylactic antibiotic therapy should be used whenever bone grafting
is planned. The graft is usually harvested from the ipsilateral lower extremity. Suitable sites
for harvesting autogenous bone graft material include the iliac crest, greater trochanter,
proximal and distal tibia, calcaneus, fibula (midshaft is almost all cortical), and rib. Donor site
morbidity is a notorious complication, and occurs in up to 25-45% of cases wherein the iliac
crest is used to procure autogenous corticocancellous bone, and pain at the donor site has
been reported to last up to 5 years postoperative. Furthermore, the use of autogenous bone
increases operative blood loss, duration of anesthesia and surgery, wound complications
related to a second operative site, including nerve entrapment
Healing of bone grafts.--bone graft healing requires mechanical stability, vascularity, and
close contact between the graft and recipient site. Incorporation takes place by means of
creeping substitution between viable bone and graft. Chondrogenesis and angiogenesis
take place by 5-7 days, and calcification occurs by 10-14 days, and osteoblasts lay down
osteoid from 15~50 days. Vascular in growth occurs over an approximately 2 em distance
by 6-10 weeks, while mineralization occurs over approximately 1 em in that same time
period, and it takes about 3-4 months to fully mineralize. Non~weight bearing may be
required for 3~4 months, and electrical or low-intensity ultrasonic bone growth stimulation
may be helpful. Complications of bone grafting include a failure rate reported to be 15-20%.
Failure to incorporate is usually due to inappropriate application or graft selection, and
mechanical instability. Whenever grafting a nonunion site, or in cases involving prior wound
sepsis, an autogenous graft is preferred. Allografts and alloimplants function best as a
spacer for in growth of vessels and new bone. Allografts and alloimplants may convey
immune incompatibility in rare cases, however they are sterile and readlly avallable with-
out creating another wound in the host tissues. Composite bone grafting employs both
autogenous and allogeneic graft materials.
Bone graft substitutes------alternatives to autogenous bone alone include: 1) extenders, which

consist ofosteoconductorthat serves to increase the volume of graft in addition to the usual
autogenous graft (osteoconduction); 2) enhancers, which consist of osteoconductor and
osteoinductor, and serve to expand volume and recruit stem cells; and 3) substitutes, which
convey osteoconduction, osteoinduction, and osteogenesis, and replace bone.
Osteoconductors serve to mimic trabecular bone, with pore sizes that range from 100-1000
microns. These are available in different forms, and vary in strength ranging from weak
tricalcium phosphate and calcium sulfate {more porous, rapidly incorporation) to stronger
(more dense, slower incorporation) coral hydroxyapatite and calcium carbonate. The pores
serve as a scaffold upon which stem cells and blast cells adhere, and capillary in growth
is promoted. These are often sterile and noninfectious and nonimmunogenic, if totally
synthetic. However, they are usually combined with allogeneic material to induce bone
healing. Osteoinductors include demineralized bone matrix (DBM), which contains
chemotactic BMP 7 (osteogenic protein 1) and BMP 3 (osteogenin); as well as
transforming growth factor B, which converts undifferentiated stem cells to chondro- and
osteoblasts; as well as other growth factors (insulin-like GF, fibroblast GFs, platelet-derived
GF, granulocyte colony stimulating factor, and others). These are antigen~extracted
allogeneic, and treated with either electron beam or gamma ray sterilization. Combinations
of osteoconductor with osteoinductor come in different forms, including crunch (DBM +
cancellous chips), flexible gel strips and sheets, paste, and putty. Osteogenesis requires
mesenchymal stem cells, chondroblasts (enchondral bone formation), fibroblasts

(collagen), and osteocytes. A bone marrow aspirate, preferably from the proximal tibia,
femur or ilium, can be obtained by aspirating with a Jansheedy needle in 4 cc increments,
with sequential advancement across the metaphysis; or aspirate 2 or more separate sites
and centrifuge to concentrate the MSCs.
SELECTED ENDOSCOPIC TECHNIQUES
Endoscopy involves the use of fiberoptic cameras and small surgical instruments to
evaluate and treat the intra-articular and periarticular compOnents of a joint, as well as
other corporeal spaces. Endoscopy has been shown useful in the ankle, however subtalar
and metatarsophalangeal arthroscopy can also be undertaken. Moreover, endoscopic
plantar fasciotomy has been shown to be useful is certain cases of recalcitrant plantar
fasciitis and heel spur syndrome, and it has been experimentally used for sectioning of the
deep transverse ~ntermetatarsalligament in the treatment of intermetatarsal neuroma, as
well as neurectomy and tarsal tunnel decompression. The value of endoscopy in making an
accurate diagnosis of joint (ankle) pathology is well-established. Arthroscopy is indicated
when CT and MR imaging remain equivocal, or when these studies indicate the need to
biopsy or manipulate intra-articular structures. Endoscopic techniques have advanced a
great deal in the past 35 years, and the application of Tiber optics, smaller systems, and
intra-articular laser ablation have contributed to newer approaches to long recognized
pathologies such as joint instability and cartilage degeneration.
Ankle atthroscopy--this can be used in both acute and chronic conditions of the joint. As
with any surgical intervention, proper patient evaluation (H&P) is prerequisite to
arthroscopy. Clinicallabtesting, including CBC and differential, ESR, rheumatoid factor, and
other indicators of arthritis may be indicated. Non-invasive imaging and testing includes
standard and stress radiographs (anterior drawer, inversion stress) radiographs, CT scan,
MRI, bone scan and/or other radionuclide imaging, and possibly an arthrogram ortenogram,
may be indicated prior to making the decision to intervene arthroscopically. The potential
benefits of arthroscopic intervention must be weighed against the potential complications,
and the potential benefits of open arthrotomy should be considered. In general,
arthroscopic indications increase with thE) ski!! ofthe surgeon, however adequate exposure
and completion of the job at hand should not be compromised by the decision not to open
the joint in a traditional fashion. Complications related to arthroscopy are the same as those
of open surgery, however there is potentially less likelihood of infection and damage to
surrounding vital and connective structures. This, in turn, implies the potential tor less joint
fibrosis and a faster rehabilitation. Infection, nerve injury and RSDS, excessive joint
distraction, hematoma, phlebitis, recurrent deformity and/or pain, and painful scar have
been encountered following arthroscopic surgery.
Instrumentation for ankle arthroscopy-small joint arthroscopic instruments have improved

a great deal since their introduction in the late 1970s. The arthroscope consists of an
eyepiece and a lens that is introduced into the joint. Fiberoptic systems enable the confines
of the joint to be explored and viewed videographically. Cannulas serve as portals through
which instruments, the video camera, and a light source are passed. Power instruments
include osteotomes, shavers and abraders; and more recently the laser and radiosurgical
instruments. Hand instruments include osteotomes, probes, curettes, knives, punches,
rasps, forceps, staplers, suture drivers, and magnetized rods. Adjunct instruments include
distractors, both invasive and noninvasive, and the pressurized distention system.
Arthroscopic ankle anatomy------anatomic considerations pertinent to ankle arthroscopy

include topographical landmarks and internal joint structures. Vital structures, including
vessels and nerves, as well as the tendons and ligaments about the ankle are marked on
the skin surface. Portals of entry for the ankle include: anteromedial, anterolateral,
anterocentral, posterocentral, posterolateral, and accessory portals (Figure 6-4). The
posteromedial portal is avoided for fear of neurovascular injury. The posterocentral portal
perforates the Achilles tendon. Ankle anatomy is subdivided into anterior and posterior joint
pouches. The anterior joint pouch contains the medial, anterior, and lateral gutters. The
medial gutter contains the medial malleolus, medial margin of the talus, anterior talotibial
ligament !the floor of the medial gutter), and the posterior talotibial ligament Iseen upon
application of valgus stress). The anterior gutter (anterior ankle) contains the anterior
tibial margin !lip), medial ankle bend, medial talar shoulder, tibial synovial recess, tibial
plafond, tibial capsular reflection, talar sagittal groove, lateral talar shoulder, tibiofibular
synovial recess and synovial fringe, and the anterior-inferior tibiofibular ligament The
lateral gutter contains the lateral talar articular surface, medial fibular articular surface,
anterior tibiofibular ligament IATFL), and the posterior talofibular ligament (seen upon
application of varus stress). The posterior joint pouch, when viewed through the sagittal
groove, contains the posteriortibiofibular ligament, posterior capsular surface, medial ankle
bend, medial gutter, and the posterior talar dome. When viewed through the posterolateral
portal, the posterior joint pouch contains the posterior tibial margin (lip), posterior talar
dome, talar sagittal groove, posteriortibiofibular syndesmotic ligament, labrum media ankle
bend, medial malleolus, and the posteriortibiotalar ligament
Ankle arthroscopy allows the surgeon to address a wide range of joint pathology (Table
6-4). Soft tissue maladies amenable to arthroscopic inspection and manipulation include
meniscoid ligaments (Collin's lesion), capsular adhesions, fibrous bands, and synovitis. It is
possible to do an adequate ankle synovectomy in patients with rheumatoid arthritis,
entirely via the arthroscope. The articular surtace may be treated for chondromalacia,
subchondral erosion, and other chondral defects. Amenable bone pathologies include
Posteromedial
Figure 6.4
osteochondral lesions and subchondral bone cysts. Other pathological ankle conditions
amenable to arthroscopic intervention include transchondral talar dome injuries, avulsion
fractures of the medial, posterior, and lateral malleoli; ligamentous and capsular repair;
talotibial exostosis, fractures of the tibial bearing surface and margin (lip); foreign body
retrieval, joint biopsy, and ankle arthrodesis (perhaps in conjunction with a trans-Achilles
portal, medial malleolar osteotomy, and cannulated screw fixation), can be undertaken by
means of arthroscopy. Although applicable to the treatment of many conditions ofthe ankle,
arthroscopy is particularly useful in the treatment of osteochondral defects and torn
cartilage. Because small portals are used to access the joint, recovery after arthroscopy is
often more rapid than that following open arthrotomy, and complications are generally
considered to be less likely. It may be possible to repair ta!ar dome and tibial bearing
surface fractures without osteotomlzing the malleoli. Despite the use of smaller incisions,
ankle arthroscopy still conveys a risk of infection, hematoma, nerve injury, and damage to
intact articular structures, and there are associated risks related to anesthesia and
tourniquet use. The postoperative course may involve non-weight bearing and
immobilization, depending upon the specific reconstruction undertaken, however early
return to weight bearing and ROM rehabilitation exercises are the norm.
TABLE 6-4. ClASSIFICATION SYSTEMS FOR CHONDROMALACIA.

System Subcategories Description of cartilage defect
Collins Grade I Fraying
Grade II Fibrillation and fissure
Grade Ill Deep, extensive fissure
Grade IV Full thickness defect
Goodfellow Superficial Type I Shallow erosion
Type II loss of superficial layer
Type Ill Exposed subchondral bone
Type IV Exposed deep matrix
Deep Type I Cartilage softening
Type II Blister formation
Type Ill Exposed matrix
Type IV Exposed bone
Bauer & Jackson Type 1 linear crack
Type 2 Stellate fracture
Type 3 Flap defect
Type4 Avulsion with exposed bone
Type 5 Fibrillation
Type6 Fibrillation & subchondral erosion
like most surgical maneuvers, arthroscopy requires training and repetition to become
fluent and successful in its application. After achieving satisfactory surgical anesthesia,
instrumentation is delivered into the joint via tubes placed through the small incisions, at
various locations about the ankle. Typically, the arthroscope, various instruments, and
suction are employed simultaneously. Specific operative interventions include joint
inspection, chondroplasty, synovectomy, biopsy, fragment excision, subchondral bone plate
perforation or microfracture, instillation of medications, graft and suture placement,
application of fixation devices, and other maneuvers as indicated by the pathology at hand.
Specific procedures amenable to arthroscopic application include: debridement and

fragment removal' for repair of anterior ankle impingement, excision of ost8ochondral
fragments, abrasion chondroplasty, excision and repair of anterolateral gutter meniscoid
ligament, and release of posttraumatic arthrofibrosis.
Most of the time, patients are positioned supine, with the ipsilateral knee flexed at90,
for ankle arthroscopy, although the specific position can vary with the needs of the
procedure and anesthesia. The joint is usually distracted (.... 1.5 mm) using the sterile
noninvasive foot strap and approximately 25 pounds of tension. Distraction forces >30
pounds, or for periods >1 hours, may cause dorsal cutaneous and/or anterior ankle
neuropraxia, although this can result from even lesser force and duration, and each patient
should be assessed forth is in follow-up after the anesthesia has subsided. An ingress pump,
set to 45-50 mm Hg pressure, and egress suction can be used to maintain a continuous flow
of saline through the articular cavity. The egress line may be fitted with a filter to procure
particulate matter flushed from the joint during the arthroscopic procedure. The 2.7 mm
arthroscope is ideal, however a 4 mm arthroscope can also be used. The 3.5 mm shaver
works well in most cases of ankle arthroscopy. The instruments are introduced to the
articular cavity by means of a transdermal incision made with a #15 blade scalpel. The
scope is usually positioned, initially, through an anteromedial portal situated medial to the
tendon of tibialis anterior at the level of the tibiotalar interface. Care should be taken to
avoid injury to the large saphenous vein and nerve. After penetration of the skin, an
18-gauge needle is used enter the joint, and saline is infused through this cannula. After
instilling saline into the joint, an anterolateral portal, situated immediately lateral to the
intermediate dorsal cutaneous branch of the superficial peroneal nerve and the tendon of
peroneus tertius, is made using the scalpel and 18-gauge needle. It is helpful to tent the
soft tissues and to transilluminate the skin and subcutaneous tissues wh:h the arthroscope,
in order to inspect for the course of any nerve in the area of the planned placement of the
anterolateral portal. After making the standard anterior portals, a systematic inspection of
the articular cavity includes identification of the deltoid ligament and medial malleolus, the
joint space between the talar dome and the medial malleolus !medial gutterL the dome of
the talus, the distal tibial bearing surface, the anterior joint cavity (anterior gutter), and the
syndesmosis between the distal tibia and fibula (anterior talofibular ligament, anterior and
posterior tibiofibular ligaments, and the associated talar and fibular articular surfaces).
The endoscope (small arthroscope) can also be used to inspect and manipulate other
joints and cavities in the foot, including the STJs, first metatarsophalangeal joint,
pre-Achilles space, intermetatarsal spaces (sectioning of the deep transverse
intermetatarsalligament), proxima! plantar fascia (endoscopic plantar fasciotomy), and
other areas depending upon the surgeon's skills and the patient's needs. Generally, the
diagnostic and therapeutic benefits related to implementation of the endoscope diminish as
the joint or cavity decreases in size, primarily due to technical limitations related to the size
ofthe instrumentation and the surgeon's skills.
LASER SURGERY
A variety of surgical lasers are used today, however the C02 laser remains the mainstay in
cutaneous and musculoskeletal surgery in the foot and ankle. Fundamental physical
properties of laser surgery are based on Planck's quantum mechanics and Einstein's
stimulated emission theories. LASER stands for Light Amplified Stimulated Emission
Radiation. Laser light is monochromatic and coherent, wherein all of the light waves line up
so that the peaks and troughs are equidistant in space and time. The laser beam
\electromagnetic radiation) is characterized by its frequency (Hz, or cycles per second),
wavelength (nanometers), time of application (milliseconds to picoseconds), power density
(watts per cm 2), and amount of energy delivered to the tissues (joules, or watts per
second). The coherent light is collimated by the flberoptic or articulated arm delivery
system, and can be aimed by the operator. The time of exposure to the laser beam is
controlled by gating the delivery system to allow passage of light as a continuous beam, a
single pulse, or repetitive pulses varying from milliseconds to picoseconds. The interval
between pulses allows the tissue to dissipate energy as heat, with the minimal thermal
relaxation ratio being 1:10 on:off. Ttssue absorption varies primarily with the wavelength
and tissue type, wherein light with a shorter wavelength has higher energy, and therefore
penetrates deeper or creates more heat in the same tissue. The specific wavelength is
determined by the specific element or elements used in the "active lasing media." The
lasing, or active media may be co, (with helium and nitrogen), or Nd-YAG (neodymium with
yttrium, aluminum and garnet), or other elemental gases. Tissue interaction with laser light
varies from one tissue type to another. For instance, skin and soft tissue may readily
vaporize, while bone and cartilage heat up and their protein content denatures with
resultant necrosis, in response to the same laser beam. lt is therefore important to select
the proper laser and settings for the tissue being manipulated. In foot and ankle surgery, the
a variety of lasers may be useful (Table 6-5).
TABLE 6-5. TYPES Of LASERS USED IN FOOT AND ANKLE SURGERY.

Laser Characteristics and applications
C02 Far infrared wavelength, readily absorbed by water and
therefore only used for superficial (0.1 mm) penetration such
as cutting, ablation, and coagulation of skin and nail lesions
Holmium-VAG Middle infrared wavelength, absorbed by bone and
non-contact tip cartilage, penetrates 0.4-0.6 mm, and used for lesion
ablation in more dense tissue
Nd-YAG noncontacttip Near infrared wavelength, poorly absorbed, penetrates
6-8 mm, deep lesion ablation and coagulation
Nd-YAG contacttip Near infrared wavelength, penetrateS 5~200 microns,
superficial cutting or incision
KTP (potassium, 532 micron wavelength, absorbed by dermal vessels and
titanium, phosphate) superficial lesions such as verrucae, penetrates 0.5 mm in
non-contact tip pigmented skin and up to 4 mm in nonpigmented skin,
used for ablation
KTP contact tip Penetrates 1-2 mm, used for incising skin
Argon non-contacttip 488-514 micron wavelength, penetrates 0.5-1 mm, absorbed
by dermal vessels and superficial skin lesions such as
verrucae, used for ablation of dermal lesions
Cu vapor, non-contact tip 478 micron wavelength, penetrates 0.5-1 mm, absorbed by
dermal vessels and superficial skin lesions, used for ablation
of dermal lesions
Safety with lasers-------laser safety entails special attention to instrumentation, eye protection
and personal shielding, vapor evacuation and filtration, and aiming technique. ANSI
publication 136.3 serves as a standard reference for laser safety. Specific eye safety
precautions vary with the wavelength of the laser beam as follows:
Class !-direct visualization of the beam does not cause ocular damage
Class 11-prolonged direct visualization will cause ocular damage
Class Ill-direct visualization causes immediate ocular damage
Class IV-directvisualization causes immediate, severe ocular damage ranging from
corneal burn to retinal ablation and blindness
All medical lasers are categorized as Class IV. They pose a fire hazard, damage the
unprotected eye, and are harmful to unprotected skin. Damaging effects can be caused by
director reflective laser exposure. Smoke plume evacuation systems should entail vacuum
suction atthe point of creation, and 0.2 micron dual filtration with carbon. Personnel in the
OR should wear proper body and eye protection, and a filtration mask. The door to the OR
must indicate the presence ofthe medical laser potential hazard.
Specific /aserprocedure~surgicallasertechniques are used primarily for lesion ablation

and soft tissue dissection (Table 6~6). As with any other form of dissection or tissue ablation
(scalpel, radiosurgery, cryotherapy, coblation), violation of the dermis results in tissue
repair with scar formation. Incisions are made with a focused beam directed in a repetitive,
linear fashion. Lesion ablation is achieved with a defocused beam directed in a
cross-hatched linear or back-and-forth fashion, or in an ever-increasing radial circle
fashion beginning centrally in the lesion. Periodic curettage may assist lesion ablation, as
non~vaporized eschar may accrue. It should be noted that, with the exception of skin lesions,
lasers are generally used to assist with dissection and lesion ablation, while standard
techniques of dissection and arthroscopy are employed to expose lesions and underlying
target structures. Patients should understand this concept of "laser assisted" surgery.
Appropriate lesion biopsy should be obtained prior to laser ablation. Appropriate sterile
bandage, with topical application of silver sulfadiazine cream, and follow-up are part of
the aftercare.
TABLE 6-6. COMMON LESIONS AND PROCEDURES AND APPLICABLE lASERS.

Lesion Laser
Verruca CO,, Argon, Nd-Yag, KTP
Cavernous hemangioma Nd-YAG bare fiber
Hypertrophic scar or keloid co,
Tattoo removal co,
Cutaneous granulomatous lesion co,
Nail matrix ablation C02, Argon, Nd-YAG
Synovitis, scar, chondromalacia, osteophyte Holmium-VAG
MICROSURGERY
Microsurgical techniques are valuable when manipulating peripheral nerves, veins and
arteries. These techniques can be used in cases of trauma, peripheral neurosurgery
(neuroma, tarsal tunnel, nerve entrapment), plastic reconstructive surgery (flaps), or
whenever magnification ofthe surgical field is desired. Magnification can be achieved with
the operating microscope (4-30x) or, more typically, by means of Ioupe magnification
(2.5-16x). Loupes also enhance inspection of the surgical field when foreign body
exploration is undertaken. Microsurgical instruments, namely forceps, scissors, and
needle holders, enhance the surgeon's ability to manipulate structures under magnification.
Typical suture gauges include 7-0 to 9-0 nylon. Specific vascular and neurological repair
techniques are learned and practiced in residency and fellowship training, and
microsurgical techniques courses.
SELECTED TENDON LENGTHENING AND TRANSFER PROCEDURES
Balance of muscle power-all of the joints of the foot and ankle are influenced by the
muscle~tendon units that cross each joint. The ultimate position of a functional joint, both
at rest and during function, is determined primarily by the forces created by the muscle~
tendon units acting upon the faint An accurate clinical assessment of the strength of the
muscle(s) in question must be documented. Every time a muscle~tendon unit is
manipulated (transferred), there is a change in the overall balance of the joint. To
effectively restore function, deforming influences must be removed and it may be
necessary to stabilize (arthrodesis) deformed or dysfunctional joints upon which the
transferred tendons can work (e.g. it is common to combine triple arthrodesis with major
tendon transfers crossing the ankle). Furthermore, there is only a fixed amount of power
available to influence a joint, and the total amount of power cannot be increased via
transfer. One can expect at least 1/2 grade decrease in strength following tendon transfer
{see manual muscle strength testing, in the section describing diagnostic techniques).
Rarely would a muscle weaker than grade 4 be considered for transfer, unless another
tendon transfer augments it. Only a muscle~tendon unit of satisfactory strength and range
of contraction is suitable for transfer.
Muscle and tendon anatomic and physiologic factors~see Chapter 1
Atraumatic tendon surgical technique-specific methods exist for handling tendon, all of
which are meant to enhance healing and ultimate function. These include:
A. Maintain tendon moisture (avoid desiccation)

B. Prepare the recipient site for transfer prior to harvesting the tendon;
C. Establish physiological tension in the transferred tendon (See Blix curve);
D. Use available, naturally occurring tendon sheaths and retinaculae to direct and
maintain the course of the transferred tendon;
E. Preserve the vascular supply to the transferred tendon by avoiding excessive
traction on the muscle belly, or overcrowding tendons within a sheath or fibro-
osseous tunnel or hiatus in the interosseous membrane of the leg; and
F. Enhanced rehabilitation based upon an understanding of tendon healing.
Blix Curve---depicts the relationship between muscle length and strength of contraction,
and shows that physiologically a muscle's ideal resting length allows for optimum strength
of contraction (Figure 6-5).1n Blix's contractile force curve, the actual contractile force of
muscle is greatest at about 120% of its resting length. Tension falls off markedly in both
directions, indicating that muscle must have optimum length for function, and deviations
from this length will reduce the contractile force of the muscle. A muscle subjected to
excessive resting tension will undergo fiber degeneration, while inadequate tension
predisposes to muscle weakness. Muscle tensile strength is approximately 75 psi, while
tendon tensile strength is 8,600-18,00 psi. Comparing tension versus length, as the length
increases beyond resting length, tension increases up to a point after which tension
decreases as the muscle belly fails to sustain force. Thereafter, tension actually rises as the
strength of the tendon, not the muscle, sustains the load. In some cases, it may be desirable
to use the transferred tendon as a sling or suspensory ligament, and not a gliding,
functional tendon.
Direction of pu/.1-:-the direction of pull determines the influence of the transferred tendon
on affected joints. The effect of various tendons on the foot and ankle can be
schematically summarized in Figure 6-6. Tendon anchors and reattachment techniques
include the hole and button, hole and bone plug, 3-hole intra osseous, 2-hole intra osseous,
side-to-side, Bunnell, lateral trap, and various commercially available anchors (Statak'M,
Mytek, Permanent Bone Anchor, and Tenodesis"" Screw System Ontetference screw), to
name a few).
Complications-complications of tendon transfer may include muscle spasm (diazepam is

useful in the early postoperative phase), stenosing tenosynovitis and adhesion,
overcorrection, under- correction or weakness, loss of correction, bowstringing, and neNe
entrapment.
Inversion )Eversion
'""':::- EHL EDL

'
TA
0 0 . /
' .$;'Y
'' Dorsiflexion ''
AJ\ ' AJ
Total ' ----. I
_/ TP
tension
t
c
' "
'6, 1:' Contractile ~I I

I Plantartlexion
0
-~ ~ i force 1
1
~ ;::,1 Passive /\ /
~:
.,
CI:I
strength)'
_ _......-
/
Length~

Tendon lengthening procedures-these include the open Z-tenotomy, which is commonly

used on the long digital extensor when correcting a hammertoe with a significant MTPJ
contracture. Ankle equinus is corrected using the gastrocnemius recession or lengthening
of the entire tendoAchlllis. The Baker tongue-in-groove gastrocnemius recession is used
when the Silverskiold test reveals limited dorsiflexion only when the knee is extended,
indicative of gastrocnemius tightness. The tendoAchillis lengthening (TAL) is used when
the Silverskiold test reveals limitation of ankle dorsiflexion with the knee extended and
flexed, indicative of gastrosoleus equinus. The TAL is commonly performed as an open
frontal plane Z-lengthening.
Common Tendon Transfers
Jones Suspension (figure 6-7)

Goals-eliminate cock-up hallux, enhance ankle dorsiflexion
Indications-cock-up hallux, weak tibialis anterior, loss of sesamoid function
Adjunct procedures--hallux IP arthrodesis, Heyman-Janes panmetatarsal
suspension
Complications-recurrence of deformity due to tendon regeneration
Attercare-BK weight bearing cast 2-3 weeks
Hibbs Suspension (Figure 6-8}

Goals-decrease MTPJ buckling and increase ankle dorsiflexion
Indications-anterior weakness (mild), flexible anterior cavus with extensor
substitution, claw toes often with associated IPK
Contraindications-posteriorweakness, weak interossei, gross EDL weakness,
structural rigidity, osseous instability
Aftercare-BK weight bearing cast 4-6 weeks
Tibialis Anterior Tendon Transfer (TATT) (figure 6-9)

Goals-decrease forefoot supinatory twist, increase true ankle dorsiflexion
Indications-recurrent clubfoot, flexible anterior cavus, dropfoot (GMT)
Contraindications-excessively weak TA (<4), pes valgus, weak PL, severe
anterior cavus with clawtoes
Aftercare-BK weight bearing cast 3-4 weeks
Sp/it1ibialis Anterior Tendon Transfer (STATT) (Figure 6-10)

Goals-increase true ankle dorsiflexion, decrease long extensor swing phase
overload, and decrease adductocavovarus forefoot deformity
Indications-flexible anterior cavus, extensor substitution, c!awtoes; spastic
posterior ankle equinus, equlnovarus (CP), anterior weakness dropfoot, flexible
cavovarus, overpowering inverters
Contraindications-excessively weak TA (<4), pes valgus, weak PL, severe
anterior cavus with c!awtoes
Aftercare-BK weight bearing cast3-4weeks
Figure 6.9
------------------~ ------------------~
1. Suitable case
10. Atraumatic
I
technique
2. Understanding
the anatomy
3. Supple local-11:1);1'5' I
tissue
necessary
c
11. Preserve blood supply
and innervation
12. Adequate <en,,on'-.:i.J.\1111

upon fixation
6. Select
suitable
tendon
9. Preserve the
1
14. Careful
gliding mechanism postoperative
management
D E
Figure 6.10
Tibialis Posterior Tendon Transfer (TPTT) (Figure 6-11I

Goals-eliminate dropfoot, eliminate flexor substitution (triceps surae weakness)
Indications-anterior muscle weakness, dropfoot, non-spastic equinovarus,
recurrent clubfoot peroneal nerve palsy (CMT), and triceps surae weakness
Contraindications-spastic TP, pes valgus, rigid clubfoot
Technical considerations-interosseous window aperture, phase conversion,
often combined with arthrodesis
Aftercare-BK cast3weeks non-weight bearing, then additional3 weeks weight
bearing, begin ROM at4weeks
Peroneus Longus Tendon Transfer (PLTT) (Figure 6-12)

Goals----increase ankle dorsiflexion, eliminate PL cavus influence
Indications-anterior muscle weakness, dropfoot, and flexible cavus
Technical considerations-easy phase conversion, caution sural and
intermediate dorsal cutaneous nerves
Contraindications-posterior weakness, pes valgus
Aftercare-same as forTPTI (above)
c E F
Figure 6.11
Figure 6.12
Peroneus Brevis into Talus Tendon Transfer (PBIT)

Goals-suspend talar neck, eliminate flexible vertical talus
Indications-type I vertical talus, severe pes valgoplanus
Contraindications-rigid pes valgoplanus, immature talus, or compromised talar
neck circulation
Technical considerations-may be combined with closing adductory wedge
osteotomy oftalar neck, medial arch tendosuspension (McGiamry-Young), and
Evans lateral column lengthening
Aftercare-up to 8 weeks, BK cast, non~weight bearing
Murphy Anterior Advancement ot the TendoAchil/is (Figure 6-13)

Goals-eliminate spastic posterior ankle equinus, shortens ankle lever arm 48%
and MTPJ lever arm only 15%
lndications-CP induced dropfootwith triceps surae contracture ankle equinus
Contraindications-osseous ankle equinus
Technical considerations-heel prominence, routing deep to FHL, McGiamry
modification involves medial-to-lateral intra osseous suture through calcaneus,
recurrent deformity, and weak propulsion
Aftercare-up to 5-6 weeks, BK non-weight bearing cast with ankle and STJ
neutral
Figure 6.13
INTERNAL SKELETAL FIXATION
Fracture, or osteotomy stability is determined by intrinsic and extrinsic factors. Intrinsic

factors include fracture configuration, and bone composition and quality. Certain fracture
configurations are intrinsically more stable than others. A transverse fracture is said to be
intrinsically stable, whereas a greenstick or torus fracture is said to be potentially stable, and
a spiral or comminuted fracture is said to be unstable. Unstable fractures tend to
displace when subjected to an axial load, resulting in shortening. Metaphyseal cancellous
bone fractures are generally more stable than cortical diaphyseal fractures due to the
composition of metaphyseal bone yielding more friction between the fragments. Healthy
bone stock without osteoporosis, provides intrinsic bone quality that enhances internal
fixation device.purchase and fragment stability.
Extrinsic factors that affect stability relate to surrounding soft tissues, including:
1) tendons, ligaments and periosteum-which either aid manipulation and reduction of a
fracture, or prevent successful reduction due to interposition between fragments; 2) when
multiple fractures exist, soft tissue attachments between larger fragments can be
instrumental in providing satisfactory realignment and stabilization; 3) vassal rule
(phenomenon)-fixation of the dominant fracture affords stabilization of the subordinate
fracture, as classically depicted with reduction and stabilization of the lateral malleolus and
subsequent spontaneous reduction of the posterior malleolus in certain ankle fractures;
and 4) extrinsic mechanical forces that affect fracture stability include bending, torsion,
shear, and axial tension and compression. Cortical bone tends to fail {fracture) on its
tension surface. The goals of internal fixation include anatomic reduction, stable internal
fixation, atraumatic technique with vascular preservation, and active mobilization in the
postoperative phase in an effort to avoid cast disease and fibrosis. Internal fixation devices
do not effect faster bone healing, however they create compression between fracture
fragments which, in turn, increases friction and enhances stability, the result of which is
improved healing without complication {less likely not to heal).
Biomaterials used for skeletal fixatio~a number of biomaterials are suitable for skeletal
fixation. Key features of metallic biomaterial alloys include strength, ductility and malleability,
and corrosion resistance. The basic composition of surgical stainless steel (316L [low
vacuum] or 316 LVM [low vacuum remelt]) consists of iron, with carbon added for hardness
(carbon steel), and molybdenum, nickel, and chromium added to enhance workability and
application to bone fixation {these elements make the alloy less brittle), and to impart
resistance to corrosion. Chromium oxide forms the surface passive layer that resists loss
of metallic ions in the aqueous environment of the tissues. Specifically, most of the
implantable fixation metals come in the form of Austenitic stainless steel. Cutting edges and
some wear surfaces are composed of Martensitic stainless steel, which is harder and less
malleable and less ductile. Cobalt-chromium alloys are. also particularly resistant to
compression and shearing wear and, as such, are often used in the fabrication of he wear
surfaces of joint endoprostheses. Titanium (99% pure) also serves as a useful metallic
implant, due to its ductility and malleability, a Young's modulus that is suitable for skeletal
fixation, and a passive tiTanium oxide passive layer that readily forms and resists corrosion.
Although surgical stainless steel and titanium implants are both considered appropriate for
permanent implantation, titanium is generally considered more appropriate for such use
due to its inert nature. As a rule, dissimilar metals should not be placed in direct contact, due
to the risk of galvanic corrosion. Other forms of corrosion include fretting between hardware
components that are in direct contact, such as the interface between the land at a screw
head and screw hole of a metal plate. Resorbable forms of fixation are often composed of
poly ILIactide) acid IPLLA) or polyp-dioxanone IPDS).
Splintage-----this is commonly used to effect fracture or osteotomy stability. Splintage

generally does not create rigidity, an.d secondary or callus healing is usually noted. K-wires
and Steinmann pins, as well as stainless steel wire suture and staples are usually used for
splintage. K-wires range in diameter from 0.035-0.062 inches, with the 0.045 and 0.062 inch
wires being used most commonly in the forefoot Steinmann pins are larger, with the most
frequent sizes used in the hindfoot and ankle being 0.078 inches or larger. Advantages of
single pin fixation include application when dealing with small fragments and physeal plates.
Disadvantages include poor resistance to distraction and rotary forces, however this can
be diminished by using additional pins in divergent directions; and the tendencyfor smooth
pins to migrate upon weight bearing or motion. Pin stability can be enhanced with proper
bending and burying, or with bandaging when the pin exits the skin. Threaded K-wires offer
resistance to distraction and pull out, but care must be taken to prevent separation of the
fracture fragments as the far fragment is penetrated. This is accomplished by compress-
ing the fragments together (preloading) prior to positioning the wire across the fracture or
osteotomy. Repetitive three-point bending, or pin flexure, can cause metal fatigue and wire
failure. This is more likely in narrower and threaded K-wires. Use of a built-up surgical shoe,
or non-weight bearing, may be needed to prevent pin failure.
Stainless steel wire suture can also be used to effect splintage. Wire size is
measured in gauges from 18 to 30 l!arger numbers" smaller gauges). with 18 and 24 gauge
wire being commonly used in foot and ankle surgery. Wire fatigue and failure can occur with
repetitive or excessive twisting or bending. Proper instrumentation, including use of a wire
twister, decreases the likelihood of inadvertent wire breakage. Application of an
intra osseous wire loop can be used to stabilize small fracture fragments in bones with thick
cortical walls Ito prevent pull through). Wire loops should be placed perpendicularto the
fracture and at 90 to each other for maximum stability (double box wire loops). Cerclage
wire is used to prevent telescoping of an oblique diaphyseal fracture, or as a gathering
influence to control small fragments when used with other forms of fixation (plates and
screws). Stainless steel wire suture can be used for: 1) intraosseous wire fixation, 2)
cerclage wiring (circumferential placement around a diaphysis), and 3) tension banding.
Staple fixation can also be used to effect splintage. Staples are designed to be used
almost exclusively in cancellous bone, and cortical bone should be predrilled to avoid
fracture during staple placement. Staples resist distraction forces across the osteotomy or
fracture, but do not withstand shearing or bending forces very well. Two staples oriented
at 90 apart provide excellent stability. During staple insertion, the surgeon should use a
minimum of mallet strikes in an effort to prevent loss of contact between the bone and
staple. A staple extractor set is needed to remove a staple that has been properly seated
against the cortex.
Absorbable fixation pins can also be used to achieve splintage. Bioabsorbable fixation
devices have become popular and they are particularly useful for treatment of
osteochondritis and chondral fragments, as well as for use in metatarsal osteotomy fixation.
Poly-p-dioxanone IPDS), and poly IL-Iactide) acid (PLLA). are useful bioabsorbable
materials that come in a variety of forms for bone fixation in the foot and ankle. These
materials have been shown to be biocompatible and safe, even in the phalanges when used
for arthrodesis and fracture stabilization. They are radiolucent and can be used in
diameters that yield an elastic modulus similar to that of bone IPLLAI, enable loading in
standard wire drivers, allow for cutting with a bone sectioning forceps or scalpel, and
degrade in a predictable fashion with creeping bone substitution. OrthoSorb pins (DePuy
division of Johnson & Johnson, New Brunswick, NJ) are made of PDS, and they are
available as straight pins in 1.3 mm and 2.0 mm diameters, as wei! as a tapered pin that is
swaged to a metallic guide pin. The.ArthrexTrim-lt Pin"' and Trim-It Drill Pin'" IArthrex, Inc.,
Naples, Florida) are made of PLLA and are available as a 1.5 mm pin, and a 2.0 mm pin with
a metal cutting tip.
Rigid internal fixation-rigid fixation provides absolute stability and promotes primary
(non-callus) bone healing. Rigid internal fixation can be achieved with interfragmental
compression screws, plates, and tension band wires.lnterfragmental compression is either
static or dynamic. Static interfragmental compression is achieved when tension is placed
upon a prestressed implant that in turn converts the tension to compression at the
osteotomy or fracture interface, and is best represented by the interfragmental
compression screw. Contact of the screw head with the near cortex, and purchase of the
distal cortex with the screw threads, places tension along the screw shaft as the threads
try to pull (!a g) the head into the bone. The screw resists this axial tensile force and, in turn,
imparts compression across the bone interface. Dynamic interfragmental compression
employs a combination of static force in conjunction with physiologic loads that naturally
occur about the part in question, thereby effecting compression across the fracture
interface. The classic example of this is the fractured patella, wherein a tension band wire
is place across the transverse fracture on the anterior (tension) surface and the knee slightly
flexed to convert the tension in the wire to compression between the fracture fragments.
Lag screw---this fixation device is used to achieve static interfragmental compression. A

lagged screw is one that engages only the far fragment with its threads. Compression
occurs as the head of the screw contacts the near cortex and the threads purchasing the
far fragment pull the fragments together. The screw itself then sustains tension throughout
its mass, as the thread end and head are relatively pushed apart by the bone cortices. The
tension within the screw is, in turn, converted to compression between the fragments. There
are different types of lag screws, including partially and fully threaded cortical screws and
cancellous screws. Cortical screws have a finer thread pitch, thereby increasing the
number of threads purchasing bone per unit length of screw. Increased thread purchase
increases friction between the screw and bone and, in turn, between the bone fragments.
Increased friction enhances rigidity, and promotes primary bone healing. In order to create
the lag effect using a fully threaded screw, it is necessary to overdrill the near cortex to
create a gliding hole.
The Swiss AD (Arbeitsgemeinschaft fUr Osteosynthesefragen, or Association for
Osteosynthesis) screws display an asymmetrical (buttress) thread design, which increases
purchase and minimizes pullout A screw's size is determined by the diameter of its threads,
with the core diameter actually being less than that of the threads. Cortical screws are
available in 1.5 mm,2.0 mm,2.7 mm,3.5 mm, and 4.5 mm sizes. Cancellous bone screws are
only partially threaded so that overdri!ling of the near cortex is not necessary to produce
interfragmental compression. The first rule of fixation states that all of the purchasing
threads of a lag screw must purchase only bone of the distallfar) fragment. Threads that
cross the osteotomy or fracture line can distract the fragments and maintain a gap.
Cancellous screws display a wider pitch and a thinner core diameter, and sizes include 4.0
mm, 4.5 mm, and 6.5 mm long and short thread pattern screws. Various companies make
both cortical and cancellous bone screws that are cannulated, which makes for ease of
placement and obviates the need to place temporary stabilization pins that can often impede
placement of permanent fixation.
Screw placement-this should ideally be perpendicular to the fracture or osteotomy

interface. In reality, this orientation is not always practical. When a lag screw is placed
perpendicular to an oblique fracture line, axial loading can cause telescoping and
shortening (Figure 6-14). When a single screw is used, it is often helpful to orientthe screw
midway between perpendicular to the long axis of the shaft of the bone and perpendicular
to the fracture/osteotomy interface. Long oblique or spiral fractures, wherein the fracture
length is 2~3timesthe width of the bone, are amenable to multiple screw fixation with each
screw being placed perpendicularto the fracture interface at each level along the shaft The
first screw should be placed centrally and perpendicular to the long axis of the bone.
Secondary screws are placed on each side of the initial screw and perpendicular to the
fracture line (Figure 6-15).
Screw insertion-this proceeds in a specific fashion that, as a rule, should not be altered.
To achieve the lag effect with a fully threaded screw, the following sequence is used:
1. Guide hole is drilled through botlt fragments with a K-wire or a drill bit.
2. The near cortex is then overdri!!ed to the diameter of the screw to be inserted, which
allows the threads to pass through the near cortex without purchasing.
3. The far cortex thread hole is then enlarged to a diameter that is less than that of the
threads, and just slightly larger than the core diameter of the screw's shaft. This
requires use of the concentric drill guide {T-sleeve).
4. Countersink the near cortex to fitthe undersurface of the screw head and minimize
the development of a stress riser.
5. Depth gauge measurement to determine proper screw size, and add 1-2 mm to
assure at least 1-2 thread purchase of the far cortex.
6. Tap (cut) the thread pattern into the far cortex to enhance buttress thread purchase,
using an alternating method of 3 clockwise rotations followed by 1/2 counterclock-
wise rotation to periodically clear the tap flutes of cortical bone. Appropriate drill
guides and tap sleeves should be used to assure proper orientation and prevent soft
tissue injury ithe tap has a predilection to becoming wrapped with adjacent soft
tissues).
7.1nsertscrewto 2-fingertightness.

When inserting a partially threaded screw, the sequence is the same as just described
for the fully threaded screw, with the exception of not overdrilling. Variations on the
sequence of instrumentation can be effective, however the surgeon is cautioned against
this, as each step in the sequence is meant to maximize stability.
Plates-these offer another means of

achieving rigid internal fixation and, in certain
applications, can be used to achieve axial
compression. In most cases, plates are used
-
to effect splintage and to provide protection of ~
a reduced and fixated fracture/osteotomy 1

that is already stabilized with interfragmental t
compression provided by lag screws. In this
way, the plate acts as a neutralization shield
that sustains forces and protects the reduced
and stabilized fracture from bending, torque,
axial tension and compression, and shear Figure 6.16
-- --
forces. Axial interfragmental compression
can only be achieved with a plate if the plate is prestressed, and the fracture is relatively
transverse in orientation. An oblique fracture will shorten and displace under axial
compression. In order to effect axial compression using the plate, standard 1/3 tubular
plates must be eccentrically drilled \load screw principle), so that when the undersurface
!countersink) of the screw head engages the plate, the plate is pushed away from the
osteotomy/fracture as the screw seats into the bone and through the plate. A 1/3 tubular
plate must be pre-bent prior to achieving axial compression via load screw placement
Pre-bending involves bending the plate away from the bone cortex, so that as the screws
seat and lag the plate to the bone, there is no tendency to gap the far cortex as the near
cortex is placed under greater axial load !Figure 6-16).
Dynamic compression plate-this is thick and wi!l not allow gapping of the far cortex, and the
hole/slots in the plate are designed to allow the creation of axial compression as the screws
seat Whenever possible, the plate should be applied to the Tension side of tlle bone. When
using the load screw technique, the first plate hole away from the fracture, after lagging the
plate to the bone on the other side of the fracture, is offset drilled away from the fracture
interface. Once this screw is seated, axial compression is achieved, and the remaining dri!l
holes may be concentrically drilled. It may be possible to get a bit more axial compression by
offset drilling the next distal screw, however it is necessaryto first loosen the first load screw
prior to securing final purchase with the distal load screws. Neutralization is a method by
which a relatively unstable fracture can be afforded more stability while subjected to axial
compression, despite the long oblique or spiral fracture orientation. Some fractures, such as
long spiral, oblique, or comminuted fractures, are simply not amenable to axial compression.
lnterfragmental compression can be obtained between certain fragments using Jag screws.
Once lag screw interfragmental compression is achieved, the fixation is protected from shear,
flexure, and torsion about the fracture with the use of a plate to neutralize force applied to the
bone. A neutralization plate can be applied using any size plate, as long as the plate is well
molded. Tubular plates work best for this application. When applying a neutralization plate, all
screw holes are drilled concentrically. You can use a separate interfragmental screw and you
can use a lag screw through the neutralization plate.
152 Fundamental Techniques and Procedures Ch.B
Buttress plating-this is used in the fixation of unstable fractures, wherein the strong (thick)
buttress plate is used to maintain alignment of the fragments despite the lack of intrinsic
stabilityieither tensile or compressive) within the injured bone. Buttressing precludes the
use of interfragmental compression, and gap healing may occur. The buttress plate
essentially serves as a bridge between larger fragments with intervening small fragments
"leaning againsrthe plate. Devitalized bone fragments should be removed and replaced by
cancellous bone graft under protection of a buttress plate.
Tension band wire fixation---this usually combines the splintage afforded by two smooth
K-wires with stainless steel wire tension, to effect dynamic interfragmental compression.
The tension in the stainless steel wire is converted to compression at the fracture
interface. This is useful at the fifth metatarsal base, malleolar fractures, and the patella.
Classically, dynamic interfragmental compression is created with an eccentrically
positioned tension wire used in conjunction with a load beam that converts the tension Jn
the eccentric wire to compression across the fracture interface, usually requiring joint
positioning that effects wire tension (Figure 6-17). A plate placed on the tension side of a
fracture also acts as a tension band.
Figure 6.17
EXTERNAL SKELETAl FIXATION
External skeletalfixatio~an external fixator can be used to achieve static interfragmental

compression, as long as the fracture/osteotomy/arthrodesis interface is relatively
transverse. A variety of external fixators are available tor use in the leg, ankle and foot. In
oeneral, these devices are of uniplanar, mu!tiplanar or circular designs. They can also be
miniaturized for use in the metatarsus and toes, or for focal use in the tarsus. Hybrid
systems, combining uniplanar and multiplanar elements are also ava1lab!e. The devices can
be used to distract and elongate bone, and to correct deformity. External fixation (EXFX)
devices yie!d a great deal of stability, while allowing periodic adjustment of the
compressive or distraction load. EXFX can be useful in the acutely injured patient when
temporary skeletal stabilization of the traumatized extremity is required while other injuries,
including head trauma, are managed. The external fixator can be used to provide
interfragmenta! compression, or it can be used to splint or maintain distraction of an open,
comminuted fracture. EXFX can also be used to span a joint or osseous segment that has
been debrided or resected for the treatment of infection or neoplasm. These devices are
also used for limb-lengthening by means of corticotomy and callus distraction and other
reconstructive interventions for deformity correction, and have been shown is some case
series to be useful in cases of Charcot reconstruction. EXFX can be achieved with
unilateral ieccentric), and multiplane and circular frames. In some cases, such as those
involving pilon fracture repair, EXFX can be combined with limited dissection internal
fixation to effect satisfactory results.
The frame is applied to the bones via pins or wires, or half pins (pin-screws), that are
positioned proximal and distal to, and as close to the fracture/osteotomy/fusion interface as
is possible. EXFX stability can be enhanced, and pin/wire loosening at the metal-bone
interface can be reduced, by maximizing pin diameter and radial preload, avoiding
overdrilling of the pin tract, and using pins coated with hydroxyapatite. Pin diameters
ranging from 4.5-6 mm are uSually sufficient for fixation of the adult tibia, and the diameter
of the bone should be >2/3 the diameter of the pin in order to minimize the risk of fracture.
Most tibial segments can be adequately stabilized with 2-3 pins separated as far as
possible within the segment, with one pin being placed as close as possible to the
fracture/nonunion, bone graft interface. As a rule, 3 pins provide more stability to an
osseous segmentthan do 2 pins; and, pins oriented in different planes maximize stability. The
distance of the extremity to the frame should also be minimized, without compromising the
adjacent cutaneous barrier. External fixators are also used to effect dynamization, wherein
cyclic micromovement is produced with a lever arm at 3-6 weeks after initial stabilization,
thereby stimulating callus formation (secondary bone healing) while maintaining alignment
When dynamization is desired, consideration should be given to the optimal length of the
frame at the time of initial application, so that shortening can be achieved when adequate
bone healing has occurred.
Disadvantages of EXFX include the bulky size of the devices, and the rather high rate
of pin tract infection. It can also be difficultto properly place the fixation pins, or pin-screws
(halfpins), so that they do not span adjacent joints or violate neurovascular structures. As
a rule, it is important to use safe zones for pin placement so that neurovascular structures
are not damaged. It is also importantto try and minimize placementthrough muscle bellies,
although this becomes necessary at certain locations. Pin and wire placement can be
enhanced with the use of intraoperative image intensification fluoroscopy.
In the tibia, proximal to the tibial tubercle and> 1 em distal to the knee joint, a safe zone
extends from the posteromedial to posterolateral border of the proximal tibia. Care should
be taken to avoid violation of the space immediately adjacent and posterior to the head of
the fibula, wherein lies the common peroneal nerve, and the space posterior to the tibia,
wherein lies the posterior tibial nerve, artery and vein. Transfixation wires can be inserted
through the anterior portion of the fibular head, aiming approximately 30 lateral-to-
medial into the proximal tibia to exit just medial to the patellar tendon. A second
transfixation wire can then be placed from lateral-to-medial in the frontal plane, anterior to
the head of the fibula and the medial collateral ligament. When halfpins are used, they can
be positioned obliquely through the medial or lateral portions of the anterior half of the
proximal tibia, or through the head ofthe fibula into the proximal tibia.
Immediately inferior to the tibial tubercle, the anterior and posterior tibial arteries are
vulnerable to impalement if placement of medial-to-lateral transfixation pins is attempted,
or if a pin is directed into the distal aspect of the popliteal fossa or the posterior leg,
therefore these methods are not recommended at this level. A transfixation wire can be
directed through tibialis anterior and the anterolateral aspect of the tibia, taking care to
avoid injuring the saphenous vein and nerve. Halfpins can also be positioned obliquely
through the medial portion of the proximal tibial metaphysis.
At the midshaft level of the tibia, to the junction of the middle and distal thirds of the
tibia, care should be taken to avoid injuring the tibial artery, venae commitans, and nerve
located medial to the midline along the posterior surface of the tibia. Here, a transfixation
pin can be directed posteromedia!lythrough the crest of the tibia, avoiding violation ofthe
posterior surface of the tibia. Again, it is important to avoid violating the saphenous vein
and nerve medial to the crest of the tibia. It is also safe to place an additional wire through
the anterior muscle compartment from lateral-to-medial, just posterior to the tibial crest. It
is best to align these pins carefully, so as not to redirect and repetitively perforate skeletal
musculature.
Just proximal to the ankle, care should be taken to avoid injuring the deep peroneal
nerve and the anterior tibial artery, adjacent to the lateral surface of the tibia. Placement of
tran;fixation pins through the fibula should be limited to the anterior portion of the fibula, and
avoid the perforating peroneal nerve lateral to the tibia, and the saphenous nerve and vein
medial to the tibia. At this level, it is also useful to position a tibiofibulartransfixation halfpin
through the tibia into the fibula, once again taking into consideration the position of the
petiorating peroneal artery.
It can also be helpful to stabilize the relationship of the foot to the leg, particularly
when fracture/dislocations warrant stabilization of the foot, or when reconstructive efforts
require immobilization of the ankle or protection of the foot from plantar weight bearing.
Purchase of the talus can be achieved with halfpins or transfixation pins, and it is best to
position these through the neck of the talus, between the talonavicular joint and the
anterior margin of the posterior facet of the talus. Purchase of the calcaneus, either with
halfpins or transfixation pins, should be localized to the tuberosity and take into
consideration the contents of the tarsal tunnel, the STJs, and the insertion of the Achilles
tendon, all of which should be avoided.
When using the llizarov technique, pins/wires are positioned obliquely, and this
requires elongation of the half ring with a footplate, or plates, and the addition of a distal half
ring oriented perpendicular to the substrate. The foot frame can be constructed of 2 half
rings that can be stabilized with a transtarsal fixation pin situated dorsa! to the plantar vault
and plantar to the dorsal neurovascular bundle; or, the first and fifth metatarsals can be
purchased with 2-3 halfpins.
Pin (or wire) tract infections are not uncommon when many pins/wires are used, and
the EXFX frame is left in place for >3-4 weeks. If the pin remains stable, and there is no
radiographic evidence of radiolucency about the pin, then the pin is usually left in place
and local pin tract care and, at the surgeon's discretion, oral antibiotic therapy can be
useful. If the pins/wires display loosening and radiolucency, then removal and bone
curettage, and implantation of vancomycin- or gentamicin-impregnated calcium sulfate (or
PM MAl beads, as well as IV antibiotic therapy, may be useful therapies.
HEMOSTASIS
Anatomic dissectiort--anatomic dissection is the foundation upon which target structures

and pathological anatomy are identified, tissues manipulated, and hemostasis achieved in
foot and ankle surgery. Anatomic dissection enables the surgeon to avoid tourniquet
application in almost any forefoot surgical case. The majority of bleeders are identified in
the subcutaneous layer, superficial to the deep fascia. The process involves skin incision,
transdermal dissection, separation of the superficial fascia and subcutaneous fat layer,
deep fasdal incision, then joint capsular and/or periosteal incision. Specific capsular and
deep muscular vessels are generally few and well known, and attention should be focused
upon these vessels when necessary. Hemostasis is achieved via ligature application
using a hand tie or instrument tie, when the lumen of the vessel is grossly visible.
Electrocoagulation can be readily used for vessels with a smaller lumen diameter. Anatomic
dissection is usually performed using the scalpel, however limited sectioning can be
achieved with the radiosurgical electro-sectioning unit
Dilute vasoconstrictor (epinephrine~dilute epinephrine can be used to enhance

hemostasis in certain cases when indicated. Epinephrine diluted 1:200,00-1: 400,000 in the
local anesthetic solution can be infiltrated in the subcutaneous tissues aboutthe surgical
site. Contraindications include any evidence of ischemia or PVD, organic occlusive or
vasospastic (Raynaud's phenomenon), connective tissue disease such as scleroderma,
vasculitis, concomitant use of MAO inhibitor or tricyclic antidepressant agent, pregnancy
(which usually contraindicates any elective surgical intervention), or distal tissue injury.
Tourniquets-these can be used, in conjunction with anatomic dissection, to achieve

hemostasis. Application of the pneumatic cuff is performed in a smooth and even fashion,
over a well-padded limb, after exsanguination via three minutes of elevation at 45, or
distal-to-proximal application of an Esmarch bandage. The cuff is applied at the ankle
isupramalleolar) or thigh !junction of proximal and middle thirds) level tor foot and
hindfoot/ankle surgery, respectively. Sterile tourniquets are available, although proper
draping will allow application of a nonsterile ankle cuff for forefoot surgery.
Inflation pressure-there are 3 variables used to determine tourniquet inflation

pressure: patient age, systolic blood pressure, and the size of the extremity. The usual
pressure range for a thigh tourniquet is 300-375 mmHg. The usual pressure range for
an ankle tourniquet is 70-100 mm Hg above the preoperative systolic blood pressure,
or approximately 225-250 mm Hg tor the average size adult, or approximately 125-150
mm Hg for children. Insufficient pressure may effect a "venous tourniquet" that only
inhibits venous return, while allowing arterial perfusion, congestion and stagnation of
the blood in the extremity, which can be problematic. The pneumatic tourniquet
pressure register should be checked regularly with the mercury manometer to assure
proper pressure measurement The tourniquet should remain inflated no longer than
90 minutes on the ankle, or 120 minutes on the thigh. The tourniquet can be re-inflated
after a 20 minute "breathing period/' however for most foot and ankle surgery, this is
usually not necessary. The "breathing period" enables hyperemic limb perfusion and
restoration of norma! pH, pC02, and p02. If it becomes necessary to deflate the
tourniquet additional times during a prolonged case, each tourniquet inflation period
should be shorter and each "breathing period" should be longer 115 minute
increments). Potential complications of tourniquet application include paralysis,
ischemia, clotting dysfunction, thrombophlebitis, and cutaneous compromise.
Paralysis may result from neuropraxia induced by excessive pressure or prolonged
inflation, inadequate pressure allowing creation of a venous tourniquet that allows
perfusion of the vasonervorum and intraneural hemorrhage; or prolonged ischemia.
Limb ischemia lasting greater than three hours effects some degree of sublethal
muscle damage. Tourniquet induced alteration ofthe clotting mechanism hinges on the
llberation of plasminogen activators secondary to non~physio!ogical pressure applied

to venous walls and limb hypoxia that, in turn, results in fibrinolysis. Increased
fibrinolytic activfty peaks at approximately 15 minutes post-deflation, and normalizes
at approximately 30 minutes post-deflation. The combination of post-deflation
hyperemia and increased fibrinolytic activity effects increased hemorrhage in the first
30 minutes following tourniquet deflation. Thrombophlebitis is rarely seen following
proper use of the pneumatic cuff in patients with no previous history of
thrombophlebitis or venous stasis. Chemical irritation of the skin can occur if the
tourniquet padding becomes soaked with povidone iodine or any other antiseptic
solution used to prepare the skin for surgery.
Topical hemostatic agents-these topical agents, when placed in contact with blood,
effect clotting.
Topical thrombin---bovine~derived prothrombin that is activated by tissue

thromboplastin. It catalyzes conversion of fribrinogen to fibrin monomers and
polymers and, ultimately, a fibrin clot Can induce hypersensitivity due to bovine origin.
Used to cause rapid, direct coagulation of capillaries and small vessel {minor)
bleeding. Available in a spray bottle, or blotted on bleeding surfaces. Not for
intravascular use.
Absorbable gelatin (Gelfoam"}-sterile, purified porcine skin collagen gelatin that is
H20 soluble, pliable, and non~antigenic. It is not intrinsically hemostatic, however
absorbs many times its weight in blood, providing tamponade and pressure, thereby
slowing bleeding. Once clot forms, the gelatin serves as a framework for granulation.
The gelatin is absorbed in 4-6 weeks. Used for small vessellminor), capillary, and
venous bleeding. It is deal for small dead space control, however it can interfere with
bone and dermal healing.
Oxidized cellulose (Surgicef}-when impregnated on a knitted fabric, oxidized
cellulose can be used to rapidly clot capillary, venous, and small arterial bleeding
impregnated knitted fabric. It is removed after the clot forms, and any residue left in
the tissues is absorbed via liquefaction in about2 weeks. It is non~antigenic, non~toxic,
and also antibacterial. It will inhibit bone healing if placed interfragmental.
Microfibrillar collagen (Avitene}-this is the dry, sterile, HCI acid salt of purified
bovine corium collagen, and it rapidly causes clot formation via the extrinsic clotting
pathway. It can be antigenic due to bovine origin. It can be used to stop brisk
bleeding, and is applied with gentle compression. It is more expensive than the other
topical hemostats described, above. It is notto be used between bone fragments, as
it will inhibit osteosynthesis.
Drains and dressing~itis advisable to use an appropriate wound drain, whenever closure
entails reapproximation of deep layers, in particular those layers deep to the deep fascia.
Drains are of 2 basic types: gravity and c1osed~suction. Gravity drains include fine~mesh
gauze and latex or non~latex, or silicone, rubber drains in various sizes and shapes. These
are typically pulled from the wound after several days, usually at the time of the first
dressing change, and may be appropriate following delayed primary closure. Closed
suction drains, using either a vacutainer or bellows chamber, are appropriate for deep
wounds with considerable muscle oozing, or when larger volumes of drainage are expected.
Negative pressure wound closure (Wound VAC) is often useful in achieving closure of
open wounds, and is not indicated for use in wounds closed by primary intention.
Wound dressings should also serve to absorb any drainage, serous or hemorrhagic,
that exude from the closed wound. To this end, the bandage should splint the healing tissues,
absorb drainage, and avoid excessive pressure or strangulation of circumferentially
wrapped tissues. For almost every tendon or osseous surgery performed on pedal
structures, bringing the bandage materials above the ankle can help to stabilize the tissues,
as well as prevent the bandage from coming loose.
ANESTHESIA
Local Anesthetics--these agents are either esters or am ides. Esters are formed from an
alcohol and acid by removal of water, and am ides are formed from an acid by replacing the
hydroxide group with the amide group (NH3). Amides are detoxified in the liver and
consequently their effects last longer. Esters are metabolized in the blood stream by
pseudocholinesterase and are more quickly detoxified, and they display a high potential
for hypersensitivity. When using local anesthesia, it is important to convert the
concentration of the solution(% solution) to milligrams of local anesthetic agent (Table 6-7).
TABLE 6-7. CONVERTING CONCENTRATION(% SOLUTION) TO MASS (MilliGRAMS)

OF LOCAL ANESTHETIC.
Percent(%) solution Milligrams (mg) ollocalanesthetic
0.25% 2.5
0.5% 5
1% 10
2% 20
General guidelines for the use of local anesthesia include: 1) having knowledge of the
patient's medical and allergy history, 2) knowledge of the toxic dose of the particular local
anesthetic being used, 3) use the smallest concentration of local anesthetic necessary to
effect anesthesia (a higher concentration does not last longer), 4) a larger volume of local
anesthetic may be necessary to anesthetize a larger diameter nerve, 5) allow enough time
for the anesthetic to take effect (each anesthetic agent has an intrinsic time lag before
anesthesia sets in), G) concomitant use of dilute epinephrine is helpful when a large volume
of local anesthetic would otherwise be necessary (when epinephrine is not contraindi-
cated), 7) infiltration should be done with frequent aspiration to assure avoidance of in-
travascular infusion ofthe local anesthetic, 8) patients who are scheduled for procedures
using local anesthesia should be maintained NPO preoperatively so that conversion to se-
dation or general anesthesia can be undertaken if deemed necessary, 9) avoid local infil-
tration into an infected or traumatized area since local anesthetic onset is delayed by lower
pH !inflammation and/or infection), and 10) each foot should be injected separately when
long duration bilateral cases are planned. Local anesthesia used in conjunction with IV se-
dation is usually adequate for many forefoot surgeries. The local anesthetic dose can be ad-
justed under certain circumstances, including: 1) use half of the standard adult dose for
debilitated or elderly patients, 2) use Clark"s rule for children, where the child"s weight in
pounds is divided by 150 and multiplied by the adult dose, and 3) use Fried's rule for infants,
where the infant's age in months is divided by 15 and multiplied by the adult dose. Standard
local anesthetic dosages are depicted in Table 6-8.
TABLE 6-8. STANDARD LOCAL ANESTHETIC DOSAGES FOR USE IN AN AVERAGE

ADULT(> 25 YEARS OF AGE, 70 KG MALE OR 60 KG FEMALE).
Local Proprietary Duration Class Maximum single dose (mg)
anesthetic name of action Plain With epinephrine
Procaine Novocaine 0.75-1 hour Ester 750 1000
Tetracaine Ponto caine 23 hours Ester 75 100
Lidocaine Xylocaine 1-Zhours Amide 300-350 500
Mepivacaine Carbocaine 1-3hours Amide 400 500
Bupivacaine Marcaine 3-12 hours Amide 175 225
General Anesthesia
General anesthesia causes reversible unconsciousness via CNS depression starting at the
cerebral cortex, and proceeding through the basal ganglia, cerebellum, medulla oblongata,
and finally, the spinal cord. The anesthesiologist must look for several potentially
complicating factors in patients anticipating general or IV sedation anesthetics, in
particular cardiovascular disease such as hypertension, coronary artery disease, valve
dysfunction or arrhythmia; endocrine disorders such as diabetes me!litus, adrenal
insufficiency, or thyroid disease; pulmonary disorders such as COPD, regular cigarette
smoking, or chronic cough; Gl concerns such as the last time the patient ate or drank, or
whether or not denture plates are present; history of hepatitis; and history of personal or
familia! neuromuscular disorder or anesthesia-related adverse reactions, such as malignant
hyperthermia. The stages of anesthesia are depicted in Table 6-9.
TABLE6-9. STAGES OF ANESTHESIA.

Stage Plane Physiological effects
1-amnesia 1 Preanalgesia, memory and sensation intact
and analgesia 2 Partial amnesia and analgesia
3 Total amnesia and analgesia
2-delerium 1 Unconscious, mydriasis, irregular breathing,
involuntary skeletal muscle movement
3-surgical anesthesia Sleeping, residual lid reflex, eyes fixed centrally,
regular breathing
2 Pupils dilating, full analgesia, heart rate and BP
stable
3 Partial intercostal paralysis, tachycardia and hy
potension, hypotonia
4 Complete intercostal paralysis and respiratory
arrest, requires artificial ventilation
4-medullary paralysis Reversible respiratory paralysis
2 Irreversible cardiovascular and respiratory
arrest
Anesthetic agents are used with such frequency that they are improved upon
regularly, and new agents become available with regularity. lnhalational agents used to
achieve general anesthesia historically include diethylether, methoxyflurane, and

chloroform. More recently, the following agents have been used:
Enflurane-supports the cardiovascular system, can be used with epinephrine, does

not induce emesis, however can be hepatotoxic.
lsoflurane----maintains heart rate, allows rapid induction and emergence, can be used
with epinephrine, does not induce emesis, may be hepatotoxic, however often induces
shivering.
Halothane--allows rapid induction, acts as a bronchodilator, is nonemetic, however

can be negative inotropic, arrhythmogenic and it sensitizes the myocardium to
catecholamines, can be hepatotoxic, often induces postoperative shivering, and is
associated with malignant hyperthermia.
Sevoflurane---very fast onset and offset, minimal mucus membrane irritation,

excellent cardiovascular stability, an agentthat replacing isoflurane and halothane in
everyday general anesthesia.
Desflurane--extreme!y fast onset and offset due to very high volatility, however may
be associated with tachycardia, limited potency, and relatively high cost.
Nitrous oxide--a low-potency inhalant gaseous anesthetic that has little effect on the heart,
liver, kidneys, and lungs, as long as hypoxia does not develop. Nitrous oxide provides
profound analgesia, without sensitizing the myocardium, and allows rapid induction and
emergence. There is, however, no muscle relaxation and nitrous oxide has been associated
with fatal agranulocytosis and spontaneous abortion after prolonged administration. The
patient receiving nitrous oxide should be ventilated with 100% 02 during emergence, in
order to prevent postanesthetic delayed-diffusion hypoxia.
Sedative and hypnotic agents are usually administered as induction and maintenance
agents before or in addition to an inhalational anesthetic, in an effort to diminish anxiety,
initiate, and maintain CNS depression. Traditionally used agents include barbiturates,
benzodiazepines, and narcotics. Neuroleptanalgesia effects somnolence, psychological
indifference, amnesia, analgesia, and loss of voluntary movement. As with all IV sedative-
hypnotic agents, careful assessment at the patient's respiration is mandatory, and
supportive measures are often necessary.
fentanyl-a short-acting narcotic that depresses respiration, effects analgesia, and

is reversed by naloxone. Fentanyl is administered 0.05-0.1 mg IM 30-60 minutes
pre-procedure, then titrated as indicated.
Droperidol-a sedative-tranquilizer that effects peripheral vasodilatation,

somnolence, mental dissociation (perhaps dysphoria), and serves as a strong
antiemetic. The sedative dose of droperidol is 2.5-10 mg IM 30-60 minutes pre-
procedure. The combination of droperidol and fentanyl combines the analgesic
effects of fentanyl wiTh the tranquilizing and antiemetic effects of droperidol in a 1:50
(fentanyl: droperidol) ratio.
Propofo~an IV sedative hypnotic agent used for induction and maintenance of

anesthesia or sedation, and can be used in conjunction with local anesthesia.
Midazola~a short-acting benzodiazepine CNS depressant often used in

conjunction with analgesia to achieve IV conscious sedation. Midazolam is titrated
IV starting with 1 mg, then increasing up to 2.5 mg over at least two minutes, then via
small increments (not to exceed 5 mg) while monitoring the degree of sedation.
Other medications used in a balanced anesthesia protocol may include phenothiazine

tranquilizers such as promethazine and prochlorperazine. Atropine (atropa belladonna) and
scopolamine are premedications used to minimize respiratory secretions and to counter
parasympathetic overtone by blocking the vagus nerve whenever a positive chronotropic
cardiac effect is desired. Ondansetron is a selective 5-HT3 receptor antagonist with strong
antiemetic properties, originally used in patients undergoing cancer chemotherapy, and
now regularly used following general anesthesia. Ondansetron is administered 4 mg IV slow
infusion over 3-5 minutes, in the treatment of postoperative nausea and vomiting. Paralytic
agents such as succinylcholine are used to paralyze the body and facilitate endotracheal
intubation, cause a fast onset and short duration depolarizing skeletal muscle blockade.
Depolarization can be associated with marked increase intragastric and intraocular
pressures, and a rise in serum K+. The rise in K+ can be arrhythmogenic in patients
predisposed to high serum K+, such as patients with burn, tetanus, trauma, uremia, or lower
motor neuron disease (paraplegia, quadriplegia, and muscular dystrophy, Landry-Guillain-
Barre syndrome). Depolarization may be associated with rhabdomyolysis, masseter spasm,
malignant hyperthermia, and dysrhythmia. Atracurium-besylate is a non-depolarizing
neuromuscular blocker that competitively binds with the cholinergic receptor sites on the
motor end plate, and is often used when depolarization is contraindicated. Muscle relaxants
not only facilitate intubation of the trachea, but aid in ventilation and abdominal dissection
by diminishing muscle tone. Skeletal muscle paralysis does not cause amnesia or
analgesia, and these conditions must first be achieved via administration of rapid onset IV
agents before paralyzing the patient.
Spinal and Epidural Anesthesia--these methods should be considered whenever general

anesthesia poses greater risk. Spinal anesthesia should not be attempted in the presence
of hypovolemia, anticoagulanttherapy or bleeding diathesis (peridural hematoma and spinal
compression), asthma or other GOPD, obesity, pre-existing neuromuscular disease (MS,
myasthenia gravis, poliomyelitis, spinal metastasist pre-existing lumbosacral disk disease
or DJD, local or systemic sepsis, or in the debilitated host Lumbar epidural anesthesia is
achieved by injecting local anesthesia into the spinal epidural space, usually below b.
Epidural anesthesia prevents spinal headache, can be maintained 24-48 hours for ongoing
anesthesia, rapidly resolves after discontinuing anesthetic, is not associated with
hypotension and allows segmental blockade. Spinal anesthesia may propagate proximally
and effect spinal headache or anesthetize a broader-than-desired area; however the
technique uses less local anesthetic than does an epidural block, and is generally easierto
perform than an epidural block. The most common acute complication of spinal
anesthesia is hypotension caused by sympathectomy. Late complications include postural
headache, lumbago, meningitis, spinal neuralgia, cauda equina syndrome (very rare and due
to fibrosis), and epidural hematoma.
Intravenous Block (Bier Block}-Bier block is commonly used for hand surgery, however
it is applicable to the lower extremity, as long as the surgeon and anesthesiologist are
prepared to handle a possible toxic reaction to local anesthesia. Two pneumatic
tourniquets are placed side-by-side proximal to the operative site after obtaining IV access
in the upper extremity. A butterfly needle is then introduced to the dorsal venous arch,
secured, and connected to a 10 ml syringe. The extremity is exsanguinated to the distal
tourniquet, and the proximal cuff inflated. Lidocaine, or carbocaine, is then infused using 3
ml/kg of body weight of a 0.5% solution 15 mg/ml), through the butterfly catheter. This effects
surgical anesthesia regionally in about 5 minutes, and lasts for 60~90 minutes. When the
patient begins to complain of proximal cuff tenderness, inflate the distal cuff over the now
anesthetized portion of the extremity, and deflate the proximal cuff only after the distal cuff
is inflated. Do not deflate both cuffs at the same time. At about 30~40 minutes after infusion
of the local anesthetic agent, slow deflation of the tourniquets can be safely performed as
enough of the anesthetic has been bound by local tissues and metabolized to avoid a toxic
dose in the systemic circulation. Even if the surgical procedure is finished before 30-40
minutes of elapsed time, the tourniquet must remain inflated at least this long before
deflation. Patient positioning and safety in the OR are the responsibility of the anesthesia!~
agist and surgeon, and care must be taken to avoid traction nerve palsy, neuropraxia,
injury secondary to pinching or crushing small parts (fingers, skin and other appendages)
in equipment and the operating room table.
PADDING, STRAPING, BRACING AND PROSTHESES
Padding with the use of felt, rolled cotton, felted-foam, various foams and sponge
materials, can be very useful whenever mechanical pressure is associated with pain or
skin compromise Hichenification, hyperkeratosis, or wound). Standard pads include the
metatarsal projection, toe crest medial longitudinal arch pad, heel cobra pad, heel counter
pad, heel lift, aperture or pontoon pads, and bunion and bunionette flange padding.
Strapping can be used to support musculoskeletal and ligamentous structures, and include
standard applications such as the low Dye strap, digital sling-down strap, the Gibney ankle
boot, and variations that combine different methods. A number of arch binders, and bunion
and hammertoe shields can be customized or obtained commercially. Similarly, a variety of
ankle and Achilles braces (McDavid-type lace~up, AircasfM stirrup, Malleotrain and
Achllliotrain) can be obtained from surgical supply services or via online services.
A wide range of braces is available for support and substitution of lost function. The
use of accommodative foot orthoses, an extra depth shoe that is anatomically fitted with a
roller sole or metatarsal bar can be used for many conditions, in particular the rheumatoid
or insensitive foot Simple adjustments for limb length and gait imbalance can be readily
applied. Reverse, adduction and straight shoe last, and custom~made shoes are also
available. Surgical shoes, forefoot~relief and heel~relief orthoses, healing sandals,
removable cast boots (fixed and adjustable, low- and high-top), ankle-foot orthoses IAFOs),
Charcot Restraining Orthotic Walkers (CROW), and total contact casts can be used in the
post-traumatic, postoperative and chronic settings. Of particular use in cases of dropfoot
are molded ankle foot orthoses that fit into the shoes, and the heavier double upright brace
with metal stays that are affixed directly to the shoe. The double upright (contoured
aluminum) brace is preferable when ankle edema or deformation prohibits the use of a
hinged AFO !Richie brace, or similar device), a gauntlet-style brace (Arizona AFO"'), or a
polypropylene molded AFO. The patellar tendon bearing brace, usually of a clamshell
design, can also be used to diminish weight-bearing load transfer through the foot Of
course, off~loading can be achieved using appropriately fitted crutches or a walker to aid
ambulation. Off-loading of the lower extremity can be enhanced with the use of a
wheelchair, a Roi!-A-BoufiD or Turning Leg Caddy"'', or, as a last resort, bed rest Braces and
shoe gear need to be periodically inspected, along with the patienfs lower extremities, in
order to monitor for the possibility of cutaneous compromise, especially in those with
neuropathy and/or vasculopathy, immunocompromise or steroid dependence, and
collagen disorders.
Ch. 7 Reconstructive Surgery of Basic Conditions and Deformities 163
RECONSTRUCTIVE SURGERY:
BASIC CONDITIONS AND DEFORMITIES
NAIL SURGERY
The ingrown toenail (onychocryptosis) involves nail pathology wherein the nail plate has
grown into the ungual labia, with or without concomitant infection. Paronychia (also termed
whitlow or run-around) consists of nail fold erythema, edema, and pain. Ingrown toenails
are commonly classified as self-inflicted or iatrogenic. Self-inflicted is where the patient
chronically cuts the nail too short or incorrectly angulates the nail nipper deep to the nail
fold. Other causes of ingrown toenails include congenital abnormalities where the matrix
is maligned and produces an incutvated plate; primary soft tissue hypertrophy wherein the
primary pathology involves the adjacent nail fold, which is enlarged and overlaps the plate;
and combinations of incurvated nail plate and nail fold hypertrophy. Nail fold hypertrophy
can also develop secondary to chronic plate incurvation and repetitive wound irritation
with the formation of a pyogenic granuloma. Treatment options include:
Avulsion~ treatment should involve education as to proper nail trimming technique, as well
as acute intervention to alleviate paronychia and allow the wound to heal. No amount of
antibiotic will cure an infected ingrown toenail until the offending nail border is
satisfactorily removed. The mainstay of treatment for onychocryptosis is avulsion of the
offending nail border. This effects temporary removal of the margin, and allows subsequent
regeneration over the ensuing months. Avulsion can be performed with, or without, local
anesthetic digital blockade, depending upon the extent of plate removal necessary to
alleviate the condition and other factors, such as peripheral sensory status. Avulsion is
followed by local wound care, perhaps concomitant use of oral antibiotics if paronychia
and/or systemic factors warrant doing so. Re~evaluation should be performed between 2
and 3 weeks after avulsion, at which time proper nail trimming technique is reviewed with
the patient Temporary removal of the offending border is generally recommended in a
firsHime case of ingrown toenail, whereas recurrent onychocryptosis may be best treated
with permanent matrix ablation via either chemical or surgical matrixectomy.
Phenol and Alcohol (P & A) and Sodium Hydroxide (NaOH) matrix ablatiot>-these
techniques of permanent partial or total nail matrix ablation are rather simple, and inflict
minimal pain. The P & A involves three 30Hsecond applications (causing the nail bed and
matrix to appear ashen gray) of 90% phenol followed by rinsing with alcohol (70-90%
isopropyl or ethyl), then copious saline lavage and application of silver sulfadiazine cream
and a sterile bandage. The NaOH procedure involves application of 10% NaOH until the
matrix and nail bed tissues appear ashen gray-brown (about 20-30 seconds); followed by
acetic acid (vinegar) rinse, then copious saline lavage, silver sulfadiazine cream, and a
sterile bandage. It is important to avoid excessive hemorrhage during application of either
chemical cauterant, as dilution could inactivate the chemical agent. A digital tourniquet
can be useful in this regard, and must be removed after applying the chemical. The main
disadvantage to both the P&A and NaOH procedures is the creation of a chemical injury that
denatures proteins much as a thermal burn would do. The wound remains open and
draining for 3-4 weeks. Chemical matrixectomy is generally not performed in the presence
of advanced paronychia, and it is recommended that the patient undergo avulsion of the
offending border/s followed by local wound care, and perhaps oral antibiotic therapy
164 Reconstructive Surgery of Basic Conditions and Deformities Ch. 7
(cephalexin), with planned matrix ablation to be performed anytime after resolution of the
paronychia and before recurrence of onychocryptosis. It is also advisable to have the
patient initiate oral antibiotic therapy 24 hours before the planned matrixectomy.
Matrixectomy techniques (true "open" matrix excisions) employing eponychial and nail
fold incision are numerous, and include:
Modified Steindler Matrixectomy-a useful technique for incurvated or iatrogenic

chronically ingrown toenails. This is often employed afterfai!ed chemical matricectomy, or
when an "open" excision is desired. The procedure is used to excise the matrix, and does
not address nail fold hypertrophy.
Frost Partial MatnXectomy-employs a right angle incision into the nail fold allowing
reflection of the fold and exposure of the underlying corner of the matrix, following nail plate
avulsion (Figure 7-1. The involved area of nail bed is also excised. The right angle incision is
actually rounded gently to avoid slough of the apex.
Winograd Partial Matricectomy--uses 2 incisions, one longitudinal through the nail bed,
and a second semi-elliptical incision through the adjacent nail fold, to create a wedge of nail
fold and bed that are excised after avulsion of the nail plate (Figure 7-2). Hypertrophic un-
gual labium is readily excised.
Ungual Labioplasty-involves a wedge-shaped excision ofthe hypertrophic labium, and is

useful only for reduction of nail fold hypertrophy.
Suppan Panhypertrophy Matrixectomy-uses a fish mouth incision through the nail folds
surrounding the entire nail plate, allowing excision of surrounding hypertrophic folds and
underlying matrix and bed.
I~ I
(
Figure 7.1
Figure 7.2
D
( ''~--J..'
:~~
Figure 7.3
Zadik (Quenu) Matrixectomy-an H-shaped incision is made with the two vertical arms
through the nail medial and lateral folds, and the transverse arm through the proximal nail
fold (Figure 7-3). The proximal nail fold is then reflected proximally and the underlying
matrix and proximal bed excised. The exposure a!lows removal of subungual exostosis if
necessary. Closure involves proximal advance of the distal nail bed flap, allowing closure
without shortening of the distal phalanx.
SUBUNGUAL EXOSTOSIS
Dorsal proliferation of the distal phalanx into the overlying nail plate can effect plate
deformation, often described as a pincer nail, with or without associated onychocryptosis
(Figure 7-4). Subungual exostosis can be of traumatic origin or, when capped with
fibrocartilage, congenital due to osteochondroma. Osteochondroma is usually observed
early in life, between 10-25 years of age, onset on or before puberty, and most commonly is
observed in females (F: M ratio 2:1 ). Eradication of a symptomatic subungual exostosis or
osteochondroma is via nail plate avulsion, and exposure of the phalangeal lesion with a
distal fish mouth incision, or via longitudinal or semi-elliptical nail bed incision or excision,
respectively. The semi-elliptical incisions are used to create a wedge excision of associated
nail bed, when the pathology has caused nailed scar or other lesion. It may not be
necessary to perform nail plate avulsion when the exostosis is small, however exposure of
the exostosis should not be compromised by trying to preserve nail plate attachment.
Osteotripsy may be a useful method for reduction of the osseous prominence. The excised
lesion should be submitted en bloc for pathological inspection, and specimens should be
obtained for bacterial C&S, as well.
Figure 7.4
HAMMERTOES
Digital contraction deformities include hammertoes, clawtoes, and mallet toes. The
deformities can be flexible or rigid, and the Kelikian push-up test is used to assess the
degree of flexibility. Anatomic considerations include extrinsic and intrinsic muscufature,
with emphasis on the MTPJ extensor hood expansion (Figure 7-5).
Extensor sling
Metatarsal head
Capsule
Plantar interosseous Dorsal interosseous
. ~ransverse metatarsal
Lumbncal~ ~ ligament
Flexor tendons
Figure 7.5
Dynamic etiologies of digital contracture include:
Flexor Stabilization-the most common cause of pathological digital contracture (>70%},

itself caused by late stance and propulsion phase hyperpronation; the FDL and FOB fire
earlier and longer to stabilize the hypermobile forefoot, thereby overpowering the
interossei with resultant dorsal subluxation of the MTPJ; associated with adductovarus
fourth and fifth digital deformities.
Extensor Substitution-this is associated with pes cavus, foot drop, and anterior
compartmentweakness, wherein the EDL overpowers the lumbricales during swing phase,
and causes dorsiflexion of the MTPJs; results in a high degree of MTPJ subluxation and
retrograde plantar buckling ofthe metatarsus.
Flexor Substitution-this is the least common cause of digital contracture, and occurs due
to weakness of the triceps surae wherein the deep posterior leg muscles compensate and
thereby overpower the interossei during stance phase, particularly during propulsion; the
digits are seen primarily in the sagittal plane, with minimal varus rotation; a calcaneus gait
may develop and this may be observed following over-lengthening (TAL) of the heel cord.
A mallettoe involves sagittal plane plantarflexion of the DIPJ, and may be associated with
a long toe. A congenital curly (varus) toe involves adduction contracture and varus rotation
of the DIPJ, usually toes 3-5, and radiographs (upon reaching skeletal maturity) may show
a delta-shaped middle phalanx. Hammertoes involve dorsiflexion of the proximal phalanx
and plantartlexion of the middle phalanx, perhaps with transverse plane deviation in the
direction of flexor plate subluxation. The clawtoe involves plantarflexion of both the PIPJ and
the DIPJ, and is often seen in cases of extensor substitution (Figure 7-6).
MPJ extension MPJ extension
DIPJ
flexion
Figure 7.6
Symptoms associated with advanced digital contracture deformity include painful PIPJ
motion, painful hyperkeratotic lesion(s), inability to wear regular shoes, contracted painful
toe that is short and possibly dorsiflexion deformity of the DIPJ. Radiographic findings
include joint narrowing and superimposition at the contracted joint levels, gun-barrel sign
on the AP view due to long axis imaging of the phalanx in either dorsiflexion (proximal) or
plantarflexion (middle), shortened contracted toe, DJD of the PIPJ and MTPJ, and
periarticular osteoporosis. Biomechanica! signs of digital contraction deformity include the
presence of hypermobile first ray and other hyperpronation findings (flexor stabilization), or
Stage I pes cavus as seen in anterior cavus and dropfoot related extensor substitution.
Postoperative management involves the use of a wooden or stiff-soled surgical shoe,
perhaps with build-up when the pins cross the MTPJ, and may involve casting depending
upon other procedures performed.
A variety of nonsurgical options are availablefortreatmentof symptomatic digital contractu res,

including the use of larger shoes with an extra-depth toe box, digital retainers such as dorsal
(early, flexible deformity) and/or plantar (advanced, rigid deformities) toe crests, sling-down
toe-MTPJ splints (Budin splint), sling-down or predislocation taping, pads and shields, and
periodic debridement of hyperkeratoses. The use of a supportive insole with a metatarsal
projection pad can also help to realign the MTPJs, and enhance nonsurgical treatment of
hammertoes. When nonsurgical efforts fail to effect satisfactory relief, then a variety of
surgical Interventions can be considered. Like the nonsurgical interventions, operative
measures also take into consideration the alignment of the MTPJ as well as that of the IPJs.
Surgical procedures for repair of contracted digital deformities include:
Flexor tenotomy-operative procedures for correction of digital deformities will vary

depending on the degree of toe and MTPJ flexibility. The reducible lesser digital
deformity may be responsive to flexor tenotomy, both long and short (flexor set),
however the use of this as an isolated procedure is rarely indicated and does not
provide a long lasting correction in most cases. Indications include plantarilexion
deformity at the PIPJ or DIPJ that is completely reducible with manipulation. Attention may
only be required at the long flexor and the IPJ capsule proximally and distally. Generally a
plantar stab incision is indicated, however a mild contracture may be approachable through
a medial or lateral exposure. This procedure can be useful in conjunction with PIPJ
arthrodesis in the presence of persistent mallet toe, when the toe is pin-stabilized in a
position ofslightDIPJ dorsiflexion.
Extensor tenotomy and capsulotomy--these are also rarely indicated as isolated

procedures, and are commonly useful in conjunction with PIPJ stabilization and MTPJ re-
location (see sequential release).
Resection arthroplasty--a variety of hammertoe procedures can be used, including the

Post arthroplasty wherein the head of the proximal phalanx is resected
transversely at the level of the metaphyseal flare. Resection of the base of the
proximal phalanx (Gotch and Kreuz) is wrought with complications due to destruction of
the intrinsic muscle attachments to the base, and must be combined with adjacent digital
stabilization and syndactyly in order to avoid floating or flail toe.
Digital stabilization---in general, multiple digital stabilizations, consisting of PIPJ fusion

and MTPJ relocation, are indicated for correction of advanced, dynamically induced digi-
tal deformities. Such deformities are usually associated with lesser metatarsalgia, con-
comitant plantar hyperkeratosis (intractable plantar keratoma [IPK] or diffuse plantar
tyloma), dorsal PIPJ and distal digital tip and hyponychium hyperkeratosis, mechanical ony-
cholysis and nail dystrophy that predisposes to fugal infection, and rigidity or incomplete re-
location with push-up loading. Transverse plane deformity may also be present, in particular
when the second toe crosses over or, less commonly, under the hallux in the presence of
associated HAV and bunion deformity. The crossover second toe is particularly hard to
completely realign. Isolated interphalangeal arthroplasty can be useful in the presence of
an unusually long digit that is contracted secondary to shoe crowding, however it is rarely
indicated for the treatment of multiple, dynamically-induced hammertoes. Moreover,
multiple adjacent PIPJ arthroplasty may IBBd to digital instability and recurrent deformity,
in the postoperative phase. It can be useful to approach the deformity by means of
sequential release. The sequential release for advanced hammertoe deformity (Figure 7-7)
includes the following steps:
1. Long extensor hood recession,

2. Long extensor tenotomy (open Z-tenotomy or transverse),
3. PIPJ capsulotomy and arthroplasty or arthrodesis,
4. MTPJ capsulotomy, and
5. MTPJ flexor plate release (made easy using the McGiamry metatarsal
elevator) and repair.
The Kelikian push-up test (apply a dorsally-directed force to the plantar surface of the
metatarsal head, to simulate ground reactive force) is performed between each step in the
sequential release, and progression to the next level of release is not necessary if the digit
and MTPJ properly align in a relaxed attitude with simple push-up loading. Full sequential
release is used in the correction of advanced clawtoe or hammertoe deformities. It is
necessary to perform the Z-tenotomy when advanced dorsal contracture is corrected,
otherwise it may be difficult to reapproximate the tendon upon closure. Medial or lateral
EDL
8
A
Phalangeal head
~cted
c
D
Figure 7.7
Figure 7.8
dislocation of the flexor plate will cause a medial or lateral deviation of the digit upon
push-up loading, and is usually related to chronic synovitis and subluxation of the flexor
plate to the side of deviation. Flexor plate subluxation must be addressed at the time of
sequential release, and an anchor suture may be necessary in order to maintain correct,
balance alignment. In some cases, persistent deformity may require MTPJ capsulorrhaphy
with wedge excision of redundant capsule, or metatarsal osteotomy lmedia! or lateral
transpositional and/or shortening) for satisfactory correction.
Interphalangeal arthrodesis-this entails several modifications, including end-to-end

(non-fixated, described by Soule; K-wire stabilization, described by Taylor and Selig); and
peg-in-hole (pike, described by Higgs; or rounded, described by Young) techniques.
Arthrodesis is generally indicated in cases of multiple lesser digital deformities, which is the
typical presentation when treating dynamically induced (flexor stabilization, extensor
substitution, or flexor substitution) contractu res of the toes and MTPJs. Either peg-in-hole
or end-to-end fusion can be used, based on surgeon's preference. If shortening is a
concern, then the end-to-end fusion may be used, as less shortening is encountered. The
peg-in hole may more reliably achieve radiographic fusion mass consolidation, however, the
functional result of a fibrous pseudoarthrosis of an end-to-end arthrodesis has been shown
to function as well as the radiographically solid fusion in many cases. After resection of the
articular surfaces, arthrodesis is completed with pin stabilization, starting the 0.045" (or
0.062" if desired) K-wire at the base of, or hole in, the middle phalanx and driving it distally
across the dorsiflexed and straightened DIPJ, then out the tip of the digit centrally. Care is
taken to avoid perforation of the nail bed. The K-wire is then retrograded
proximally across the PIPJ to the base of the proximal phalanx, then across the
realigned MTPJ if indicated by persistent upon push-up loading. Stabilization of the MTPJ
is performed with the toe situated half way between the horizontal substrate (parallel to
the bottom of the foot), and in line with the metatarsal declination angle.
Digital alignment is slightly over-corrected in plantartlexion, and the pin crossing the MTPJ
maintained for 3-6 weeks. The PIPJ fusion is stabilized for 5-6 weeks, or until
radiographic and clinical evidence of fusion is observed. Placing the pin across the MTPJ
requires use of a built-up surgical shoe postoperatively, in order to avoid
repetitive mechanical flexure and pin breakage in the MTPJ (Figure 7-8). Interphalangeal
arthrodesis can also be achieved using bioabsorbable fixation pins or screws, and other
devices made to press-fit or snap-fit once seated in either the proxima! and/or middle
phalanges. It is important to keep in mind that if absorbable fixation, or a device that is
limited to just the interphalangeal joint/s, is used to achieve digital fusion, attention to the
alignment of the corresponding MTPJ may require separate fixation or metatarsal
osteotomy, if the push-up test fails to display satisfactory MTPJ realignment After
realignment of the toe and MTPJ, the long extensor tendon is re-approximated in corrected
alignment, followed by subcutaneous and then skin closure.
Flexor tendon transfer (Girdlestone, Foerster and Brown)-can also be useful for the
correction of hammertoes and clawtoes, however care must be taken to transfer the
sectioned flexor tendon slips from plantar to dorsal on the phalanx in a subperiosteal
fashion (to avoid constriction of digftal vessels), or through a drill hole in the phalanx, and it
is possible to effect a PIPJ rocker-bottom deformity unless arthrodesis is performed
(obviating the need for flexor tendon transfer). Sgarlato's modification of the Girdlestone
procedure can be used for the correction of hammertoes and clavvtoes with MTPJ
subluxation, and serves to redirect the long extensor tendon's pull to that of a stabilizing
influence on the toe and MTPJ. Two incisions are used, 1 medial or lateral aspect at the
proximal phalanx, and an adjunct dorsal incision more to the side opposfte the medial or
lateral incision. The long flexor tendon is split and transferred dorsally in a subfascial
fashion and sutured to itself and the dorsal hood expansion as a sling dorsally atthe level
of the proximal phalangeal shaft. Care must be taken to transfer the splittendon segments
in a subfascial (deep fascia) fashion, in order to avoid circumferential constriction of the
subcutaneous neurovascular elements coursing to the toe tip. The transfer results in
decreased PIPJ range of motion. Dockery and Kuwada modified the transfer by use of a
dorsal-to-plantar drill hole in the anatomic neck ofthe proximal phalanx. Moreover, a rocker
bottom PIPJ or swan-neck deformity can be created if too much tension is placed within the
transferred long flexor. PIPJ arthrodesis is generally considered a more effective and
lasting method to stabilize the digit and convert the long flexor to a stabilizing influence on
the MTPJ, particularly for the intermediate lesser digits. A flexor tendon transfer may be
applicable to the fifth toe, or in the presence of congenital absence of the middle phalanx.
BUNION DEFORMITY AND HALLUX ABDUCTO VALGUS
First metatarsal anatomy pertinentto the bunion deformity and hallux abductovalgus (HAV,
hallux valgus) surgery includes the proximal physeal plate, which closes at about 15-18
years of age, the primary nutrient artery situated laterally about 2 em proximal to the
articular surface, and the peri-articular soft tissue sleeve and sesamoid apparatus. When
the hallux abducts and the first metatarsal adducts (metatarsus prlmus varus), the
dorsomedial eminence of the first metatarsal head becomes clinically prominent, and is
termed a "bunion." The term bunion basically refers to a bump, traditionally, from the old
French buignon, from buigne or "bump on the head." (Similarly, a prominent fifth metatarsal
head is often referred to as a bunionette.)
Radiographic Angular and Anatomic Relationships Related to HAV~there are a number

of angular relationships useful in the assessment of HAV, including:
HalluxAbductusAngle(HAA}--me angle formed by the intersection of the bisection ofthe

shaft of proximal phalanx and the bisection of the shaft of first metatarsal,
normally 15, and representative of the relative position of the hallux to the first metatarsal
(Fig 7-9).
Distal Articular Set Angle (OASA}--the angle formed by the intersection of a line
perpendicular to the effective cartilage of the base of the proximal phalanx and the
bisection of the shaft of the proximal phalanx, normally 7.5, and representative of the
relative position of the effective cartilage to the shaft of the proximal phalanx. An increase
in DASA may indicate lateral deviation in me shaft of the proximal phalanx (Fig 7-10).
Proximal Articular Sol Angle (PASA}--the angle formed by the intersection of a line
perpendicular to the effective articular cartilage of the metatarsal head and the
bisection of the shaft of the first metatarsal, normally 7.5, and representative of the
relative position of the effective cartilage to the shaft of the metatarsaL An increase in PASA
indicates lateral deviation (adaptation) ofthe cartilage surface (Fig 7-11).
Figure 7.9 Figure 7.10 Figure 7.11 Figure 7.12
Metatarsus Primus Adductus or First lntennetatarsal Angle (first IMA)--the angle formed
by the intersection of the bisection of the shaft of the first metatarsal and the bisection
of the shaft of the second metatarsal, normally 8, and representative of the angular
relationship between the first and second metatarsals. An increase in the first IMA makes
the head of the first metatarsal more prominent medially, and predisposes to HAV (Rg 7-12).
Hallux lnterphalangeusAngle (HIA)--the angle formed by the intersection of the bisection

of the shaft of the proximal phalanx and the bisection of the distal phalanx, normally 10",
and representative of hallux interphalangeal joint (HIPJ) or phalangeal deformily (Fig 7-13).
Metatarsal Protrusion Distance-the distance between two arcs which, respectively,

represent the lengths of the first and second metatarsals. A line representing the
bisection of the first metatarsal is extended to intersect with a line representing the
bisection of the second metatarsaL A compass is placed at the point of intersection and an
arc drawn from the distal portion of the first metatarsal and another arc is drawn from the
distal portion ofthe second metatarsaL A positive millimeter distance is used to indicate a
longer first metatarsal. A negative distance is used to indicate the second metatarsal being
longer than the first Normal is 2 mm, and represents the relative length between the first
and second metatarsals. A longer first metatarsal may be associated with hallux limitus,
whi!e shortening may correlate with lesser metatarsalgia (Fig 7-14).
Metatarsus Adductus Angle (MAA)--the angle formed by the intersection of the

bisection of the lesser tarsus and the bisection of the second metatarsaL The lesser tarsus
is bisected by obtaining the midpoint between the anterior-medial corner of the first
cuneiform and the posterior-medial corner of the navicular, and the midpoint between the
anterior-lateral corner ofthe cuboid and the posterior-lateral corner ofthe cuboid. The
midpoints are then connected and a perpendicular is drawn to this line. The MAA is
normally 10-20"; and represents the degree of adduction of the metatarsus. As the MAA
increases, the foot becomes more adducted and there is greater chance for development
of HAV. Moreover, the first IMA becomes pathologically significant at a lower degree in the
presence of increased MAA (Fig 7-15).
Tibial Sesamoid Position (TSP)--the position the tibial sesamoid is compared to the
bisection of the first metatarsal shaft, and designated as position 1-7; normally 1-3, and
traditionally representative of the need to remove the fibular sesamoid. TSP 4
predicts erosion of the tibial sesamoid against the plantar central crista of the metatarsal
~\ dl
,,1\ ,fJ
,,
2
'
''I
l-
(!.1, "'
Figure 7.13 Figure 7.14 Figure 7.15 Figure 7.16
head, and relative deviation of the metatarsal head medially so that the fibular sesamoid is
positioned in the first intermetatarsal space. When the first metatarsal plantarflexes, a
relative distal position of the sesamoids may appear, whereas dorsiflexion causes relative
proximal positioning (Fig 7-16).
Shape ollhe Metatarsal Head-the intrinsic stability ofthe MTPJ varies with the shape of
the metatarsal head. A round head is theoretically most unstable and likely to deviate into
HAV; a square head is considered stable, and a square head with a central ridge is
considered most stable and may be seen in cases of hallux rigidus (Fig 7-17).
First MTPJ Position (Congruous, Deviated or Subluxated)-first MTPJ alignment can be

congruous, deviated or subluxated. In the congruous joint, a parallel relationship exists
between the effective articular cartilage of the metatarsal head and the phalangeal base.
The deviated joint displays extra-articular intersection of the lines representing the
effective articular surfaces of the metatarsal head and phalangeal base. The sub luxated
(subluxed) joint displays intra-articular intersection of the lines representing the effective
articular suliaces of the metatarsal head and phalangeal base (Fig 7-18).
~ ./Ji
j '"~ ''': '
I I;
I I I
'II
Figure 7.17
~ =-
A- ./i
~ II\~ """;(~ '
( __.,/fl.
\ f
Figure 7.17
II l I
'
I.
I II
'I j
I
II
I
Figure 7.18 Congruous Deviated Subluxated
Structural, Positional, and Combined HAV Delormilies-HAV can be classified as to

whether or not the first MTPJ deformity is structural, positional, or a combined deformity
based on the formulae depicted in Table 71.
Table 7-1. FORMULAE FOR STRUCTURAl, POSITIONAl, AND COMBINED FIRST MTPJ
DEFORMITIES.
TYPE OF ANGLE PASAAND/ FIRSTMTPJ

DEFORMITY FORMULA ORDASA ALIGNMENT
Structural PASA + DASA ~ HAA PASAorDASA Abnormal, congruent

Positional PASA + DASA < HAA PASA and DASA Normal, deviated
or subluxed
Combined PASA + DASA < HAA PASAorDASA Abnormal, deviated

or subluxed
Example 1:
HAA ~ 35", DASA ~ 3", PASA ~ 5" (3 + 5 < 35, so MTPJ displays positional deviation or
subluxation, as PASA and DASA are normal).
Example 2:
HAA ~ 35", DASA ~ 7", PASA ~ 28" (7 + 28 ~ 35, so MTPJ displays a congruous structural
deformity, and PASA is abnormal).
Example 3:
HAA ~ 35", DASA ~ 1", PASA ~ 18" (1 + 18 <35, so MTPJ displays a combined deviated or
subluxated deformity, and PASA is abnormal).
Bunionectomies-specific procedures for bunion repair vary a great deal, and it is the
surgeon's responsibility to select the best procedure for the patient in question. Procedure
selection varies with patient expectations, bone stock, local and systemic tissue status, the
degree of deformity relative to the anatomic relationships, and the surgeon's skills. Repair
options are categorized as soft tissue manipulations, hallux osteotomies, and distal, shaft
and base metatarsal osteotomies, and combinations thereof.
Soft tissue manipulations used for correction of HAV include:
McBride Bunionectomy-this is a versatile and powerful

component of many bunion repairs, and focuses on muscleM
tendon balance that addresses the underlying pathologic
influences in the development of HAV. Preoperative criteria include
mild to moderate pain associated with the sesamoid apparatus, first
MTPJ range of motion that is essentially free of crepitus or
significant articular degeneration, mild-moderate axial rotation
(valgus) of the hallux, prominent dorsomedial bunion, medial
bursitis; and radiographic signs such as relative hypertrophy of the
medial eminence, deviated to subluxated first MTPJ, and a tibial
sesamoid position of 4 or greater. Specific surgical maneuvers used
in the true McBride bunionectomy include medial exostectomy, Figure 7.19
excision of the fibular sesamoid, medial capsulorrhaphy, and
transfer of the adductor hallucis tendon to the deep surface of the
medial capsular flap (Figure 7-19). The modified McBride procedure involves preservation
of the fibular sesamoid, with adductor tendon transfer following complete plantarlateral
soft tissue release (Figure 7M20). The primary limitation of the McBride procedure is an
inability to correct a structural deformity of the metatarsal head. The modified McBride
procedure serves as the foundation for many bunionectomies, and is usually combined with
f1rst metatarsal osteotomy for the correction of HAV with metatarsus prim us varus. OverM
aggressive manipulation ofthe soft tissues using the McBride procedure can overMcorrect
and predispose the patient to the development of hallux varus. Proper execution of soft
tissue release and realignment about the first MTPJ, in conjunction wtth distal metatarsal
osteotomy, can be carried out safely and without the development of capital fragmentAVN.
Figure 7.20
Keller Bunionectomy-this joint destructive procedure is a time~honored technique for

alleviation of debilitating pain related to severe, advanced HAV, usually with concomitant
DJD and/or hallux rigid us. Indications include apropulsive gait, pain in the first ray and lesser
metatarsalgia (lateral dumping) that presents a constant impediment to ambulation,
stiffness, and inhibition of weight bearing or motion. The Keller procedure classically
involves resection of the base of the proximal phalanx of the hallux. A number of
modifications of the Keller procedure have come to be appreciated in order to prevent
complication, including: re-attachment of the flexor apparatus to the phalangeal shaft, use
of a long medial capsular flap that serves as a sling to resist hallux abduction, and
lengthening of the EHL (and brevis). Other variations include use ofthe medial capsularflap
as a biological trellis over the metatarsal head (Ganley modification), K-wire nailing for
temporary stabilization, and purse string capsular interposition. The main complications
related to the Keller procedure are shortening of the hallux, recurrent hallux abductus,
hallux elevatus, lesser metatarsalgia secondary to proximal retraction of the sesamoid
apparatus, and sub-second metatarsal head IPK. The development of complications is
reduced with implementation of the modifications.
Silver (Simple} Bunionectomy--may be used in cases where bump pain and medial
cutaneous compromise predominate, especially in the elderly or debilitated host. It does not
address sesamoid pain, deep joint pain, or dynamic MTPJ imbalance. Preoperative
criteria include a satisfactory first MTPJ range of motion, no crepitus, and often a medial
adventitious bursa is present Surgery focuses on simple resection of the dorsomedial
eminence of the first metatarsal head while preserving the plantar sesamoidal shelf.
Caution should be taken to use a digital retainer postoperatively, so that rapid advance of
hallux abductus due to loss at medial capsular-ligamentous tethering of the hallux, is
countered. The procedure may convey poor long-term results, and recurrence may occur
because the etiology of the deformity is not addressed. The combination of first metatarsal
head medial exostectomy and Akin osteotomy for correction of significant HAV,
particularly in a young or active patient wherein systematic disarticulation and first MTPJ
reconstruction are not addressed, can convey a high rate of recurrent deformity.
Hallux osteotomies used for correction of HAV include:
Standard Akin Osteotomy-a closing adductory osteotomy of the

proximal metaphysis of the proximal phalanx of the hallux,
indicated for correction of true hallux interphalangeus or an
increased DASA. The Akin osteotomy is rarely indicated as an
isolated procedure, and is usually used in conjunction with more
proximal intervention that addresses first MTPJ muscle-tendon
balance and/or structural deformity. The Akin osteotomy itself does
not directly address a bunion deformity or HAV. Inadequate
correction of the first MTPJ cannot be adequately corrected with a
'cheater Akin," which creates the clinical appearance of a
straightened hallux even in the presence of a deviated or sub luxated
first MTPJ. The Akin procedure employs a wedge osteotomy in the
proximal phalangeal proximal metaphysis, the distal arm of the
osteotomy being perpendicular to the long axis of the phalanx and
the proximal arm being parallel to the articular surtace of the phalanx Figure
721
(Figure 7-21). Caution should be practiced if the proximal phalanx is
short, and the physis should be closed in a young patient The
osteotomy is stabilized using a nonabsorbable suture, wire suture, a K-wire, an
absorbable pin, or a staple. The Akin is an adjunct procedure to MTPJ realignment
Cylindrical Akin Osteotomy-a cylindrical resection of the proximal

phalanx, usually at the junction of the diaphysis and proximal
metaphysis, to correct abnormally high DASA and/or HIA in a very
long proximal phalanx. The epiphysis should be closed, and delayed
diaphyseal healing is a risk. The Akin is an adjunct procedure to MTPJ
realignment(Figure 722).
Distal Akin Osteotomy-a closing adductory proximal phalangeal

osteotomy positioned in the distal metaphysis, and indicated for the
correction of HIA >10-12, in the presence of a congruous first MTPJ
(corrected), and an adequately long phalanx. It can be used even when Figure 7.22
the proximal physis is open. The Akin is an adjunct procedure to MTPJ
realignment (Figure 723).
Distal first metatarsal osteotomies used for correction of HAV:
Reverdin Osteotomy-a useful technique for correction of high PASA,

when used in conjunction with appropriate muscle-tendon balancing
of the first MTPJ. The Reverdin can be performed in young patients,
however it is most frequently used in conjunction with a true McBride
procedure in an elderly patient with an advanced, yet
flexible HAV. The osteotomy is an intra-articular closing adductory
wedge osteotomy, at the level of the sesamoid apparatus, that
preserves an intact lateral cortical hinge. The distal cut is made
proximal and parallel to the residual articular cartilage of the
metatarsal head, and the proximal cut is made perpendicular to the
long axis of the first metatarsal (Figure 7-24). The osteotomy is
oriented perpendicular to the substrate {weight-bearing surface), and
Figure 7.23
positioning the osteotomy distal to the sesamoid apparatus may
theoretically decrease weight bearing load on the capital fragment.
Removal of the medially based wedge of bone decreases articular
cubic content, and may enhance range of motion in cases involving
hallux limitus. Placement of the osteotomy distal to the weight
bearing level of the sesamoids increases the risk of capital fragment
AVN. The osteotomy is ideally fixated with 1 or 2 diverging segments
of bioabsorbable pin. Alternative fixations include stainless steel wire
suture or 20 absorbable suture. A Kwire may also be used. The main
complications of the Reverdin osteotomy include AVN, sesamoiditis,
I
and first MTPJ stiffness. The Reverdin osteotomy enables first IMA
\1
reduction via reverse buckling, wherein the hallux applies an I\ II
1n- --,If
abductory force on the head of the flexible first metatarsal when
lk-. -~~
bandaged in slight overcorrection.
Figure 7.24
Green-Modified Reverdin Osteotomy (distai-L}-a useful
modification ofthe classical Reverdin osteotomy, wherein a horizontal
plantar osteotomy is made through the metatarsal head, dorsal to the
sesamoid, so that the Reverdin cuts do not penetrate the plantar
cortex and violate the sesamoidal articular surfaces (Figure 7-25).
Laird~Modified Reverdin Osteotomy--combines the Green-modified Reverdin with

completion of the osteotomy through the lateral cortex, eliminating the intact cortical hinge
and allowing transverse plane translocation of the capital fragment toward the second
metatarsal in an effort to decrease the first IMA. A K-wire or otherfixator is required to
stabilize the capital [ragmen~ and AVN is a risk (Figure 7-26).
Todd-Modified Reverdin Osteotomy-combines the Laird-modified Reverdin with

penetration of the plantar cortex to enable sagittal plane correction in addition to
transverse plane correction.
Peabody Osteotomy-addresses a high PASA using the same osteotomy as described for
the traditional Reverdin, however the osteotomy is positioned at the anatomic neck of the
first metatarsaL Bone healing is traditionally slower due to a higher degree of cortical bone
at the more proximal location.
Wilson Osteotomy-an oblique, through-and-through osteotomy at the surgical neck of

the metatarsal, usually oriented from distal~medial to proximaHateral to allow reduction of
the first IMA with shortening of the metatarsal. The orientation of the osteotomy can be
reversed to elongate the metatarsal, or oriented perpendicular to the long axis of the
second ray to avoid shortening or lengthening. The Wilson osteotomy, in the past, was often
employed in minimal-incision surgery, and conveys a high risk of malunion, delayed
union, and. recurrent deformity or transfer metatarsalgia when not adequately controlled
and stabilized.
Mitchell Osteotomy-a popular distal metaphyseal, step-down osteotomy wherein the

distal arm of 2 parallel cuts does not penetrate the lateral cortex while the proximal arm does.
Completion of the osteotomy allows both transposition and angulationa! correction of the
capital fragment lt is used for correction of mildly increased first IMA, and dorsal
displacement of the osteotomy can be problematic (Figure 7-27) .
. . /1

Austin Osteotomy-perhaps the single most commonly used osteotomy for correction of
moderate HAV, wherein the first IMA is usually no more than 16, and the joint is not
degenerated. The procedure consists of a through-and-through, sagittal plane
V-osteotomy (chevron), with base proximal and apex distal, situated at the first metatarsal
metaphysis. The osteotomy allows triplanar correction. The apex of the osteotomy is
positioned at the center of the imaginary circle of the metatarsal head, and application of
a smooth K-wire as an apical axis guide, for many surgeons, enhances control of the saw
and predetermines the direction of displacement of the capital fragment. The arms of the
V-cut usually intersect to form a 60 angle, however an offset-V, such as the Vogler and
Kalish modifications, with the dorsal arm extending proximally to the proximal (Vogler
osteotomy) or midshaft (Kalish osteotomy) level of the metatarsal can be used to achieve
interfragmental screw fixation and, perhaps correct a higher degree of metatarsus primus
adductus by virtue of additional angular correction made available by swiveling the distal
fragment upon the proximal portion of the metatarsal. An offset-V osteotomy positioned
through the shaft, with the dorsal arm exiting near mid-diaphysis, namley Kalish's
modification of the Austin, is readily stabilized with 2 interfragmental compression screws.
An offset-V osteotomy positioned through the shaft, with the dorsal arm exiting near the
proximal metaphysis, nam!ey Vogler's shaft osteotomy, is ideally suited to enable a
significant amount of transverse plane swivel of the dorsal fragment to reduce PASA
(Figure 7-28), and may be used to correct rather large degrees of HAA and first IMA. The
degree of displacement of the capital fragment in the Austin procedure, and ITs variations,
is dependent upon the width of the metatarsal and orientation of the osteotomy. The
plantar arm of the osteotomy creates a shelf that resists weight bearing, and the
osteotomy is very stable when soft tissues are properly preserved. Fixation of the
traditional Austin osteotomy is via buried or percutaneous K-wires, absorbable pins, or lag
screws. Although originally described as an unfixated osteotomy, the addition of fixation
decreases the likelihood of delayed union, loss of correction, and AVN of the capital
fragment. Postoperative care involves weight bearing in a surgical shoe and early return
(3-4 weeks) to a soft shoe or sneaker.
Figure 7.28
Oerotational Abductory Transpositional Osteotomy (ORATO}-a relatively difficult and

infrequently used osteotomy of the metatarsal head that addresses valgus rotation, PASA,
metatarsus prim us varus, and sagittal plane (usually elevatus) deformity. The DRATO
osteotomy is performed through the cortical bone of the anatomic neck, and requires cast
immobilization and K-wire stabilization. Complications, including AVN and delayed union, as
well as technical difficulties which have limited the use of this procedure.
Shaft osteotomies of the first metatarsal used for correction of HAV:
Off-set V Osteotomy (Vogler}-a weight bearing,

sagittal plane V-osteotomy !described above in the
discussion of the Austin osteotomy) that extends
through the shaft of the metatarsaiiFig 7-29), allowing
correction of a moderate to high first IMA, PASA via
swiveling of the dorsal fragment, and application of lag
screws or a K~wire or Steinmann pin for stabilization. Figure 7.29
Gudas-scarf Osteotomy-this Z-plasty osteotomy

accomplishes the same goals as does the Vogler
off-set V osteotomy, however it employs 3 bone cuts
whereas the V-osteotomy employs just 2 cuts
!Fig 7-30). The osteotomy, and its shortened variation,
the short Z-osteotomy, is amenable to lag screw or
pin fixation. Figure 7.30
Ludlof!Osteotomy-this osteotomy involves a straight oblique transection of the metatarsal

shaft from dorsal-proximal to plantar-distal, and is typically fixated wlth lag screws and
maintained for 6-8 weeks non-weight bearing. The Ludloff design can be used to elongate
the metatarsall-2 mm when indicated IFigure 7-31).
Mau Osteotomy--this osteotomy involves a straight oblique transection of the metatarsal

similar to the Ludloff, however the orientation of the osteotomy is reversed \dorsal-distal to
plantar-proximal) (Figure 7-32).
B
Proximal osteotomies of the first metatarsal and medial cuneiform, and metatarso-
cuneiform arthrodesis, for correction of HAV:
Juvara Oblique Base Wedge Osteotomy-employs the hinge axis concept (Figure
7-33) to create an oblique, closing abductory base wedge osteotomy that enables
correction in the transverse and sagittal planes. The osteotomy is oblique and
measures about twice the width of the metatarsal base. The Juvara is suitable for
correction of a first IMA of> 16, as long as the bone stock is satisfactory and the metatarsal
base not too narrow. It can be used in the presence of an open proximal physis, as long as
the osteotomy is positioned distal to the growth plate. A dorsomedial hinge allows
reduction of the first IMA with plantar declination of the distal fragment. Use of a pure
medial (vertical) hinge only allows reduction of the first IMA, whereas a plantarmedial hinge
allows dorsal excursion along with reduction of the first IMA, and a dorsomedial hinge
allows plantar excursion along with reduction of the first IMA. The osteotomy is ideally
suited forfixation using an anchor and lag, 2-screw arrangement. Potential complications
include delayed or nonunion,shortening and/or elevatus with transfer metatarsalgia, and
medial dorsal cutaneous neuritis (Figure 7-34). There are 3 variations of the Juvara oblique
base osteotomy:
Type A-oblique osteotomy directed from distal-lateral to proximal-medial,

with an intact medial cortical hinge, the arms of the osteotomy creating an
approximately 15 wedge resection.
Type 8-proceeds as described for Type A, however the medial hinge is sectioned
after wedge resection and a greater degree of sagittal plane manipulation can be
achieved, as well as shortening or lengthening by means of swiveling or sliding the
fragments upon one another.
Type C-an oblique osteotomy without wedge resection, completing the hinge thereby
allowing swiveling and sliding manipulations as in Type B.

Transverse Base Wedge (Louisan-Balacescu) Osteotomy--involves a transverse, closing

abductory, base wedge osteotomy of the proximal metaphysis, and maintains an intact
medial cortical hinge. The osteotomy is not amenable to lag screw fixation, and crossed
K-wires or stainless steel wire suture are applicable, in conjunction with immobilization and
non-weight bearing up to 6-8 weeks.
Crescentic Base Osteotomy-uses a crescent shaped saw blade

to create a crescentic osteotomy in primarily the transverse plane
(TP), offering easy manipulation ol the distal segment into a
corrected alignment in the TP. Sagittal plane (SP) correction must
be addressed via orientation of the osteotomyto include motion in
the SP. Minimal shortening occurs with this osteotomy if stabiliTy is
maintained. Delayed union is the most likely complication, and
crossed K-wire, lag screw and stainless steel wire suture fixation
can be used in conjunction with immobilization and non-weight
bearing for 6-8 weeks (Figure 7-35).
Figure 7.35
Proximal Chevron Osteotomy-a chevron osteotomy can be
positioned at the base of the metatarsal, and may be useful in regard to correction of the
first IMA and a small to moderate amount of angulational correction can also be achieved
by means of swiveling. The osteotomy can be fixated in a nuber of ways, including
interfragmental compression screw or screws, or splintage methods, and non-weight
bearing and immobilization for up to 6-8 weeks are indicated.
Ope11ing Wedge (Trethoan) Osteotomy and Bone Graff----this

repair can be performed on a short metatarsat and
traditionally packs a medial base cortical osteotomy with the
resected bone of the medial eminence (autogenous bone graft)
to lengthen the medial cortex of the metatarsaL Consideration
should be given to harvesting autogenous corticocancellous graft
from the calcanean body, as the medial exostectomy may not
provide adequate graft material. Alternatively, the use of a suit-
able bone graft substitute can work well. A staple or K-wire may
be used to stabilize (non-compressive splintage) the graft, and
immobilization and non~weight bearing up to 6-8 weeks are in
order (Figure 7-36). Specialized locking fixation plates (Darco'"
Figure 7.36
plates) are ideally suited to this procedure.
Lapidus Procedure (First MetatarsafwCuneiform Arlhrodesis)-applicable when there is

DJD, pain and/or instability at the first metatarsal cuneiform articulation in conjunction with
a high first IMA and bunion deformity, often observed with a round first metatarsal head. The
Lapidus procedure may shorten the first ray, and it is combined with a bone graft for this
reason. Fixation is usually via lag screws and a neutralization or load-screw plate applied
to the medial-plantar aspect of the metatarsal and, as with the opening wedge procedure,
specialized locking fixation plates (Darcor"' plates) are also suited to this procedure. Care
must be takentto accurately manipulate the intercuneiform and intermetatarsal articulations
as desired, and avoidance of excessive shortening is also important. Immobilization and
non-weight bearing lor up to 10-12weeks may be in order (Figure 7-37).
A s~
Cotton Procedure (Medial Cuneiform Opening Wedge Osteotomy and Gralt)-this

procedure addresses excessive first metatarsal-cuneiform adductus, and employs
application of the resected medial exostosis of the first metatarsal head or, more
typically a bone graft substitute perhaps combined with ipsilateral calcaneal or distal tibial
donor bone, as an autogenous graft placed into the opening medial cuneiform
osteotomy. The osteotomy preserves the lateral cortex of the medial cuneiform. Pin or
staple splintage, or locking fixation plates, along with immobilization and non-weight
bearing are also employed. Complications include cuneiform AVN, medial dorsal cutaneous
neuritis, and TA tendinitis. This procedure may be applicable in the correction of
metatarsus adductus, when combined with a closing wedge osteotomy of the cuboid.
Epiphysiodesis for Juvenile HAV-this may be applicable for correction of mild

juvenile HAV, wherein the first IMA is not greatly increased. Epiphysiodesis represents an
effort to control the final position of the first metatarsal by either staple fixation or bone graft
interposition at the lateral aspect of the first metatarsal base physis (Figure 7-38). The
staple can be removed at a later date, however bone graft consolidation of the physis is
permanent. Attention must be paid to standard growth charts, so that adaptation and
subsequent growth can be anticipated.
Combination Procedures for Correction of HAV:
Logroscino Procedure-application of a closing abductory base wedge osteotomy with

the Reverdin osteotomy, for correction of a high first IMA and PASA, comprises the
logroscino procedure. Use of an Austin-type chevron osteotomy has also been described
in conjunction with a base wedge osteotomy. Obviously, double osteotomy is associated
with extensive disruption of periosteal and epiphyseal blood supplies, and conveys a
higher risk of bone healing complications. There have been cases reported of AVN of
the intervening segment of first metatarsal, usually associated with loss of osteotomy
stability proximally.
Stamm Procedure-this procudure involves application of an opening base wedge

osteotomy and graft with the Keller procedure, and may be of historical importance only.
go
Dorsal and proximal
migration of instant
center of motion of
1st MPJ as hallux
dorsiflexes.
Neutral
A 8
Figure 7.39
HALLUX LIMITUS AND HALLUX RIGIDUS
Hallux limitus/rigidus (HUHR)traditionally implies limitation of first MTPJ motion to less than
65 of dorsiflexfon, with excessive compressive load of the proximal phalangeal base upon
the dorsal aspect of the first metatarsal head as the end range of motion is approached
(Figure 7-39). More recently, it has been appreciated that at least 35" of first MTPJ
dorsiflexion is typically needed for normal walking, and less motion will usually result in
pain and inhibited ambulation. Some surgeons refer to any limitation of 1st MTPJ
dorsiflexion, in general, as hallux rigidus. Others distinguish between limitus and rigidus,
wherein rigid us is reserved for those cases that display minimal to no dorsiflexion. In this
manual, we will referto the condition as hallux limitus/rigidus (HUHR). Etiologies of HUHR
include metatarsus prim us elevatus related to hypermobile first ray, forefoot supinatus, or
iatrogenic metatarsal elevatus following base wedge osteotomy; a long first metatarsal,
which may be associated with a distal metaphyseal epiphysis (pseudoepiphysis);
immobility of the first ray due to Lisfranc DJD or tarsal coalition; first MTPJ DJD due to
osteoarthritis, longstanding HAV, or systemic arthritic involvement of the joint status-post
trauma or iatrogenic deformity; and even a short first metatarsal wherein the hallux
vigorously plantartlexes {hallux equinus) to stabilize the first ray in stance. Signs and
symptoms include pain and swelling, stiffness and crepitus, dorsal bony prominence
(dorsal bunion) and HIPJ overload with plantar hyperkeratosis, and lateral metatarsalgia due
to antalgic guarding of the painful first ray, apropulsive gait, and fifth toe heloma durum
formation. Radiographic signs include subchondral sclerosis, joint space narrowing,
flattening of the metatarsal head, and osteophytosis with exostosis (dorsal flag sign)
formation. In some cases, the metatarsal head displays a central ridge. It is important to
ascertain the status and function of the sesamoids by loading the plantar aspect of the joint
while dorsiflexing the hallux. Nonsurgical treatment of HUHR involves use of a metatarsal
bar or tapered rocker-sole, orthosis control of hypermobility, and range of motion physical
therapy; and these measures are combined with anti-inflammatory intervention, intra-
articular chondroprotective agent (chondroitin sulfate and glycosaminoglycan
preparations), and alteration of activities. The surgical treatment of HUHR is founded upon
adequate chie!ectomy in conjunction with reconstructive osteotomy. Procedures include:
First MTPJ Chielectomy---involves removal of osteophytic proliferation via a

dorsomedial, longitudinal capsulotomy. It is necessary to remove osteophytes and spur for-
mation from the dorsal, medial and lateral aspects of the joint including the metatarsal head
and the phalangeal base. The metatarsal elevator can be used to release capsular and
sesamoidal adhesion plantarly at the flexor plate. loose or degenerated cartilage should be
debrided and sculpted to an intact and smooth surface, and exposed subchondral cortical
bone should be perforated with multiple 1.5 mm or 0.045" K-wire holes. Fenestration of the
cortex enables mesenchymal stem cells from the medullary sinusoids to cover the
articular surface and, under conditions of motion with reduced compression, convert to
functional fibrocartilage. It is important to understand that chielectomy does not address
structural deformity or the etiology that may have contributed to the condition in the first
place. First MTJ range of motion is initiated early in the postoperative phase. Chielectomy
is usually used in conjunction with metatarsal osteotomy and MTB, and serves as the
foundation upon which almost all repairs of HUHR are based.
Watermann Osteotom~a dorsally based trapezoidal wedge resection at the surgical neck
of the metatarsal, designed to rotate plantar cartilage dorsally and decrease first MTPJ
cubic content. Complications associated with the Watermann osteotomy include capital
fragment instability, loss of correction, sesamoiditis, delayed and/or nonunion, AVN, and
inability to truly rotate the articular surface without creating a transverse angular ridge at
the apex of rotation. Excessive shortening of the first metatarsal may also predispose to
lesser metatarsalgia. The McGiamry-modified Watermann osteotomy preserves a plantar
cortical hinge, while resecting a dorsally based, pie-shaped wedge of metatarsal head that
also rotates plantar cartilage dorsally and decreases internal cubic content of the joint
\Figure 7-40). Fixation is via absorbable pins or suture, or metallic splintage wires or screws.
The hallux may initially be splinted in dOrsiflexion for a few days, however early passive and
active range of motion is desirable. The Watermann and McGiamry-modified Watermann
are used in conjunction with chielectomy.
Modified Green-Watermann Osteotomy-this involves chielectomy, and osteotomy of the

metatarsal neck wherein a rectangular section of bone is excised from the dorsal aspect
of the surgical neck, while a plantar arm (much like that used for the Austin osteotomy) exits
the joint parallel to the substrate posterior to the articular surface IFig 7-41). An axis guide

can be used to orient the arms of the osteotomy, and the first IMA can be reduced if
necessary. This procedure enables shortening of the metatarsal while simultaneously
allowing plantar declination ofthe capita! fragment, thereby decreasing the risk of lesser
metatarsalgia. The osteotomy also avoids violation of the articular sutface with the
osteotomy, decreasing both the risks of sesamoiditis and AVN. Fixation of the osteotomy is
performed with lag screws, smooth or threaded K-wires, or absorbable pins. When threaded
K-wires are used, they are cut flush to the cmlica! surface and retained indefinitely.
Austin Osteotomy and Variations-this osteotomy has been described above, and is
applicable for correction of certain cases of H/HR. The apical axis guide is oriented
to effect primarily plantar declination of the capital fragment, which also limits
reduction of the first IMA. In the presence of concomitant HAV and HUHR, the Green
Watermann and Austin osteotomies enable simultaneous reduction of the first lMA,
although the Green-Watermann osteotomy generally enables greater plantar declination
without excessive shortening. The Youngswick modification of the Austin osteotomy
entails removal of a trapezoidal wedge of bone from the dorsal arm of the proximal segment
of the metatarsal, thereaby allowing plantar declination and some shortening of the first
metatarsal. This procedure is versatile and readily stabilized with tapered absorbable pins,
a K-wire, or an interfragmental compression screw.
Lambrinudi and Other First Metatarsal Plantarflexory Osteotomies---this employs an

oblique wedge osteotomy directed from plantar~distal to dOrsal-proximal in the metatarsal
base, with the base distal and the apex proximal, and is designed to correct structural
metatarsus prim us elevatus (Figure 7-42). Instability of the first metatarsal-cuneiform joint
contraindicates efforts at structural correction distal to the joint, and medial column
lisfranc arthrodesis (such as the Lapidus) may be indicated. The osteotomy is fixated with
lag screws. Excessive shortening of the first ray may complicate the Lambrinudi, however
concomitant over-aggressive plantar declination usually results in weight bearing
sesamoiditis. Various modifications of oblique base wedge osteotomy, abductory if
reduction ofthe first IMA is indicated, can also be used to achieve plantar declination of the
distal segment of the first metatarsal. Furthermore, osteotomy through the cortical hinge
allows plantar displacement ofthe distal segment via swiveling in the sagittal plane (Figure
7-43). Oblique and step-down (Giannestras) shaft osteotomies can also be used to effect
shortening and plantar declination of the distal segment of the first metatarsal
(Figure 744).
Opening Plantarflexory First Metatarsal Osteotomy--this can be used to correct

metatarsus primus elevatus, and involves a dorsally based wedge graft of bone placed into
an osteotomy of the dorsal portion of the proximal metaphysis of the first metatarsal base.
Autogenous corticocancellous bone graft, or a suitable substitute, is used.
Mayo Procedure and Stone Procedure--these involve varying degrees of first metatarsal
head resection. The Mayo procedure involves oblique resection, from dorsal~proximal to
plantar-distal in the sagittal plane, of the dorsal aspect of the metatarsal head. The
osteotomy penetrates the articular surface centrally in the sagittal plane, and includes
resection of any medial osteophytosis. The Stone procedure more aggressively resects the
dorsal portion of the metatarsal head, and penetrates the articular surface just distal to the
Ch. 7 Reconstructive Surgery of Basic- Conditions and Deformities 187
Figure 7.43
Figure 7.42
Figure 7.44
sesamoids. In effect, the Stone procedure attempts to preserve the plantar cortical surface
of the metatarsal head, while eliminating dorsal blockade to hallux dorsiflexion.
Heuter Procedure--this involves complete excision of the first metatarsal head, and may
be useful tor the treatment of osteomyelitis, or as a component of pan metatarsal head
resection. This procedure irreversibly destroys the weight bearing function of the first ray,
and is of historical interest only in regard to the treatment of HL/HR.
Bonney~Kessel Osteotomy-this procedure involves resection of a dorsally based wedge

of bone from the proximal metaphysis of the proximal phalanx of the hallux, however there
is very little indication for this procedure as it does not address metatarsus prim us
elevatus, degenerative changes of the first MTPJ, or length of the first metatarsaL It has
been said thatthis procedure may be indicated in young patients without DJD, however it
must be stressed thatfailure to definitively address the biomechanical and structural causes
of HUHR may result in progressive first MTPJ degeneration even after apparently correct-
ing lack of hallux dorsiflexion with a hallucial osteotomy. This criticism is analogous to that
of the isolated Akin osteotomy in the treatment of HAV.
Base enclavement (Regnauld procedure}-employs creation of a hat-shaped

osteocartilaginous proximal phalangeal base graft, in an effort to, theoretically decrease first
MTPJ tension and enhance range of motion (Figure 7-45). The hat-shaped graft is harvested,
and the proximal phalanx shortened via cylindrical resection of cortical bone, after which
the graft is implanted into the residual medullary canal of the phalanx. Care must be taken
to avoid proximal retraction of the sesamoids, which are the true weight-bearing level ofthe
first ray, and to this end actual relaxation of tension through the first MTPJ may be
compromised. The procedure has been shown most useful in repair of the traumatically or
iatrogenically deformed first ray with metatarsus prim us varus aggravated by concomitant
proximal phalangeal elevatus. Fixation Of the graft, despite its peg-in-hole arrangement
can be tenuous, and crossed K-wires may be used.
Figure 7.45
Keller Arthroplasty-the Keller procedure, which has been described above, can also be
used to treat HUHR.
first Metatarsophalangeal Arthrodesis (McKeever Fusion)-arthrodesis of the first MTPJ

is a versatile and time-honored method of achieving a stable, pain-free alignment in the
treatment of painful, inhibiting arthrosis (pain, decreased function, and deformity).
Indications for arthrodesis include apropulsive gait, flail toe, neuromuscular disease
(spastic or flaccid), failed implant, failed Keller, previous bone and/or joint sepsis, and
previous intra~articular fracture. The technique is also applicable for rheumatoid forefoot
reconstruction when combined with lesser metatarsal head resections and digital
stabl!izations, and it can also be used to repair longstanding hallux varus or severe HAV, or
Charcot degeneration of the first MTPJ. Contraindications include limited and/or painful
HIPJ motion, and inadequate bone stock. It may be combined with HIPJ fusion when the IPJ
is already arthritic or deformed. The optimum position affusion is parallel to the second toe
in the transverse plane, approximately 15-20 of sagittal plane dorsiflexion (varies with
anticipated heel height of shoes/boots), and a neutral frontal plane position.
McKeever originally described a peg-in-hole technique, and modifications of this can be
employed based on operative findings. However, effort should be made to
minimize bone resection and shortening, and the technique of cartilage removal via
curettage and perforation of the subchondral plate to expose cancellous bone works well,
as long as adequate trabecular bone is exposed. Stabilization of the arthrodesis can be
achieved with crossed K-wires (0.045 and/or 0.062"), a single axial retrograded 3/32" or 5/64"
Steinmann pin, lag screws, Herbert screws, tension band wire, cerclage wire, or a plate and
screws, and there are specialized locking plates available for this procedure, as well.
Immobilization and non-weight bearing may be helpful postoperatively, however it may be
necessary to use a removable, modified walking cast or brace that floats the hallux, in
patients with rheumatoid arthritis or neuroarthropathy. Advantages of first MTPJ
arthrodesis include preservation of intrinsic attachments to the phalanx, stability, good
cosmesis, improved weight bearing function of the first ray, and spontaneous reduction of
the first IMA. Disadvantages include technical difficulties that relate to achieving the
optimal position affusion; and post-fusion difficulty kneeling, potential HIPJ overload and
degeneration, and potential delayed or nonunion. A bone growth stimulator may be helpful
in cases of delayed union or anticipated bone healing difficulties.
First Metatarsophalangeal Endoprosthesis (Implant Atthrop/asty)-patients suitable for

first MTPJ end aprosthesis implantation should display adequate neurovascular status, skin
coverage, bone stock, and adequate capsular and tendinous structures, as well as an
understanding and acceptance of the procedure. Indications also include apropulsive gait,
previous joint trauma, stiffness, and pain that inhibit weight bearing. Contraindications to
endoprosthesis implantation include dense peripheral neuropathy, advanced
osteoporosis, excessively short proximal phalanx, inadequate joint and/or cutaneous
coverage, and allergy to implant materials. Relative contra indications include previous
septic arthritis, or a young and active patient. The goals of endoprosthesis implantation
include the classic triad of reconstructive surgical goals: 1) decrease pain, 2) increase
function, and 3) reduce deformity. Patients undergoing endoprosthesis placement should
be informed of the subsequent need for prophylactic antibiotic therapy wheneverthey are
subjected to invasive procedures and dental work. Implant design has improved greatly
over the past 10~ 15 years, and use of a silicone polymer (Silastic) joint spacer has given
way to functional designs that enhance motion and bear weight during propulsion.
Technical refinements related to endoprosthesis of the first MTPJ include reattachment of
FHB and the sesamoid apparatus to the proximal phalanx, lengthening of EHL, sectioning
FHL, and proper angulation of bone resection. Alternatives to joint implantation for the
treatment of HUHR with DJD include Keller arthroplasty and first MTPJ arthrodesis.
Complications associated with implants include stress~induced plastic deformation,
osseous and implant stress fracture, and microscopic shard production (wear debris) that
causes detritic synovitis with marked synovia! thickening. Softer implant materials,
especially silicone polymer, are subject to wear~induced shard formation, although all
biomaterials will eventually show microscopic wear~and~tear breakdown. Implant
arthropathy consists of detritic synovitis, subchondral bone cyst formation, ectopic new
bone proliferation, and aseptic necrosis. Host soft tissue inflammatory reactions are of the
foreign body granuloma type, as shards are phagocytosed with resultant capsular
fibroplasia and encapsulation. (Silicone polymer has also been used in the production of
interphalangeal implants and as metatarsal caps following head resection.) Basic implant
designs include hemi~implant endoprostheses and total joint replacement models.
Hemiimplant arthroplasty-silicone polymer hemi~implant functions as a spacer

(not an endoprosthesis) and is rarely used in the first MTPJ. Indications for the
hemHmplant included joint space narrowing, osteophytosis, joint subluxation, and
preservation of a satisfactory first metatarsal articular surface, if the subchondral
bone plate has good contour and direction and if resection of metatarsal head
exostosis will not destroy functional articulating surface. The technique of hemi~
implantation involved dissection of the first MTPJ in a fashion consistent with that
described for the Keller bunionectomy. lt is possible to perform a Reverdin or Austin
osteotomy when hemi-implanting. The proximal phalangeal base is transacted
perpendicular to the long axis of proximal phalanx (5 -10 degrees of abductus is
physiologic), and the hub ofthe implant should be wider than the cortical width ofthe
phalanx. An excessively wide implant may limit range of motion. The medial capsular
flap, which is made long via a vertical incision at aboutthe mid~diaphyseal level (as is
done when performing the Keller) of the proximal phalanx, is reattached following
implant sizing and placement. The capsular flap is attached via drill holes in the
phalanx positioned dorsomedial and plantar medial, while a central plantar drill hole
is used to reattach the intersesamoidal ligament or the FHB directly, using 2~0
nonabsorbable suture. The Weil angulated hemi-!mplant incorporates a 15 lateral

deviation of the phalangeal base surface, designed to compensate for
deviation of the first metatarsal articular surface (increased PASA).
Total implant arthroplasty (total replacement arthroplasty}-the total implant is

applicable, in limited situations, where severe DJD of both articular surfaces has
caused hallux rigidus. The Swanson-designed total implant, manufactured by
Dow-Corning Wright is made of Silastic silicone polymer. Contraindications
include a high first IMA and excessive HAA, as the implant cannot stand up to
angular deforming forces over time. Prolonged angular deformation of the
implant will result in implant degradation, and/or osseous erosion and/or fracture.
Metatarsal length is preserved in an effort to avoid transfer metatarsalgia, and the
majority of bone is resected from the phalanx. Titanium grommets are
available to fltoverthe implant stems, and function to shield the silicone polymerfrom
wear at the bone interface. Sutter Biomedical's Lawrence~designed total
implant displays a proxima! stem that is angu!ated 15 dorsally, to correspond to first
metatarsal declination; and their La Porta-designed total implants display right, left,
and neutral transverse plane sided angulated stems. When performing total implant
arthroplasty, the first IMA is corrected via closing abductory base wedge osteotomy
when indicated, or via aggressive distal and dorsal first metatarsal resection using
the Mayo partial head resection. Complications of total joint implantation include
floating or non~purchasing hallux, if too much metatarsal head is removed dorsally;
limited dorsiflexion and transfer metatarsalgia, if too much metatarsal head is
removed plantarly.
Multicomponent First MTPJ Endoprosthesis-these are designed to resist

wear-induced degradation while providing a degree of functional weight
bearing and motion in the first ray. They combine high density polyethylene I HOP) and
cobalt-chromium ICoCr) and/or titanium alloy. Wear surfaces are made of HOP and
CoCr, while scintered stems of titanium provide a Young's modulus compatible with
bone. Polymethylmethacrylate bone cement may be used as a leuting agent to secure
the implant stems, however is usually not necessary when appropriate broaches are
used to seat the device. These systems also employ osteotomy jigs {guides) for
preparation of the metatarsal and phalangeal surtaces to assure proper fit without
excessive bone loss, and allow near~physiological range of motion while maintaining
the weight~bearing level of the sesamoid apparatus. Accumet's great toe implant
employs an extended dorsal flange thattheoretically allows anatomic range of motion
as the first metatarsal plantarflexes and the hallux glides dorsally. The Biomet two
component endoprosthesis combines HDP and CoCr at the wear surfaces. The
Bioaction total endoprosthesis is anothertwo~component system made of HOP, CoCr
and titanium. andemploys a plantar flange that articulates with the sesamoids and
theoretically enhances weight bearing through the first ray.
Autologous Cartilage Transplant Procedures (OATS and ACT}-osteoarticular

transfer system (OATS) is a surgical procedure used to treat focal cartilage defects. An
osteochondral graft is usually harvested as multiple plugs procured from a
non~weight bearing surface of the knee, or the head of the talus, or some other
non-contact articular site. Once procured, the plugs are transplanted to the recipeint site
in a mosaic fashion. Care must be taken to try and match subchondral cortical contour and
cartilage thickness between the donor and recipient sites. The donor site usually heals by
secondary intention, and the recipient site heals by means of graft incorporation and
fibrocartilage regeneration. It is important to maintain range of motion under reduced
pressure, during the healing phase. Another potentially useful method is that of autologous
chondrocyte transplant (ACT), which is a procedure that entails collection of normal
cartilage cells from, typically, inside the knee and are then sent to a laboratory to grow for
several weeks in tissue culture. Once they are grown in the laboratory, the chondrocytes
are then transplanted to the recipient site and secured by means of articular
reconstruction that will enable reduced weight bearing motion in the postoperative phase.
A summary olthe surgical options lor the treatment of H[jHR is depicted in Table 7-2.
TABlE 7-2. A STEPWISE APPROACH TO HAllUX LIMITUS/RIGIDUS.
Amount of first metatarsal head Surgical options to be used alone

articular degeneration or in combination
<50% of central third of distal surface Arthroplasty
Cheilectomy and cartilage sculpting
Subchondral drilling (or cultured,
autogenous cartilage cell transplant)
Arthrodiastasis
Reconstructive osteotomy
Plantar and proximal displacement
(decompression)
?:":50% of centra! third of distal surtace Arthrodesis

Keller-type arthroplasty
Endoprosthesis
Autologous cartilage transplant (OATS)
Cultured cartilage celt transplant
HALLUX VARUS
Hallux varus involves an adductus and/or varus deviation of the hallux at the first MTPJ, and
is usually observed as a complication of hallux valgus surgery. Contributing iatrogenic
influences include excessive resection of the medial eminence (staking the metatarsal
head), excision of the fibular sesamoid, overcorrection of the intermetatarsal angle,
over-tightening of the medial capsule, and overcorrection of the PASA. The condition can
also occur post-traumatically, congenitally or secondary to neuromuscular imbalance.
Symptoms include difficulty wearing conventional shoes, pain along the medial aspect of
the hallux secondary to shoe pressure, medial arch pain due to abductor ha!lucis spasm,
and pain and crepitus and !imitus due to first MTPJ OJO. Clinical signs include adduction
and/or varus of the hal!ux, plantart!exion contracture of the hallux IPJ, and EHL contracture
effecting dorsiflexion of the MTPJ. Radiographic signs include hallux adductus, a reduced
or negative first IMA, possibly staked first metatarsal head and/or absent fibular sesamoid,
the presence of a previous osteotomy of the first metatarsal, a negative PASA, and MTPJ
DJD (narrowing, sclerosis, irregular contour). Non-surgical treatment includes counter-
~
I
Figure 7.46
bandaging, padding, and shoe weac Not every hallux varus requires surgical repair,
however significant deformity should be corrected as early as possible to prevent
resultant DJD. There is no single surgical procedure, but rather the causative factor must
be determined and corrected along with any secondary deformities that may have
developed. Surgical repair entails complete soft tissue release, correction of structural
deformity (reverse negative IMA), tendon transfer about the first MTPJ (Figure 7-46), tibial
sesamoidectomy, and arthroplasty or fusion in severe or degenerative cases. Arthrodesis
is preferred in cases of neuromuscular imbalance or spasticity.
HALLUX INTERPHALANGEAL ARTHRODESIS

Hallux interphalangeal arthrodesis is usually used as an adjunct procedure in cavus foot
reconstruction, or following excision of the hallucial sesamoids. The deformity of hallux
malleolus, or cock~up hallux, can be repaired with hallux interphalangeal arthrodesis.
Indications for HIPJ arthrodesis include the presence of partially or nonreducible HIPJ
contracture, painful hyperkeratotic or ulcerative lesion overlying the IPJ, transverse or
frontal plane hallux deformity, hallux hammertoe, or an abnormally short or long hallux.
Signs and symptoms include painful and/or limited HIPJ motion; lichenification, keratoma,
or ulceration; and inability to wear regular shoes. Radiographic findings include the
contracted IPJ, joint space narrowing, osteophytosis, and subchondral sclerosis; abnormal
hallux interphalangeal abductus angle; abnormal hallux length; and adequate bone stock
should be present when arthrodesis is considered. Biomechanical observations
associated with the need to fuse the HIPJ include instability of first ray and/or MTPJ
causing an abnormal weight-bearing position of the hallux, and severe pronatory
imbalance effecting forefoot supinatus, or loss of sesamoid stabilization of the hallux.
Surgery should be considered if a digital retainer and balanced inlay with a roller sole
have not satisfactorily alleviated symptoms. The surgical approach to the HlPJ is via either
a lazy-S, L-shaped, or two semi-elliptical incisions. The joint is resected with attention paid
to angulation and length, and planned fixation method. A variety affixation methods can be
used, including stainless steel monofilament wire (single or double box loops of 20 or 22
gauge stainless steel wire), two crossed 0.045" K-wires, a single 4.0 mm cancellous lag
screw, a single 3.5 mm cortical lag screw, and a 2.7 mm cortical lag screw.
Advantages of the stainless steel wire suture technique include relatively easy
application and minimal instrumentation, no need for intraoperative radiographs, can be used
in conjunction with first MTPJ endoprosthesis, and it can be used when a sagittal plane
deformity of the hallux is maintained. Disadvantages of the stainless steel wire technique
include pull~through in osteoporotic bone, requires intact cortical bone adjacentto the fusion,
difficulty achieving uniform interfragmental compression, and the wire becomes a permanent
fixation device. Advantages of the K-wire technique include easy application and minimal
instrumentation, and affords effective splintage even in osteoporotic bone, and it need not be
permanent if placed percutaneously, and it can be used when a sagittal plane deformity of the
hallux is maintained. Disadvantages of the K-wire include frequent need to confirm alignment
radiographically, pin-tract infection, difficulty when used in conjunction with first MTPJ
endoprosthesis, and inability to generate interfragmenta! compression. Advantages of screw
fixation for HIPJ fusion include interfragmental compression, typically rapid primary bone
healing ensues, and earlier mobilization of the first MTPJ is possible. Disadvantages of the lag
screw technique include technical difficulties with screw purchase and instrumentation,
prominence of the screw head distally at the hyponychium, screw removal is usually
indicated (and quite easy), intra-operative radiographs should be taken, not amenable to
concomitant first MTPJ endoprosthesis placement with stem of the implant secured in the
proximal phalanx, and sagittal plane hallux deformity must be corrected in order to enable the
screw to seat properly in the phalanges. Postoperative management includes use of a
built-up surgical shoe, cast, and/or non-weight bearing for reduction of push-off loading of
the hallux for 6-8 weeks. Percutaneous pins can be removed at about 6-8 weeks pending
radiographic and clinical evidence of consolidation. A lag screw inserted from distal to
proximal should usually be removed at approximately 8weeks postoperative, unless the screw
head has not caused any distal irritation.
FIRST METATARSOCUNEIFORM EXOSTOSIS

This degenerative process generally accompanies chronic first ray hypermobility and
dorsal jamming atthe metatarsocuneiform joint (MCJ). It can be seen in anterior cavus, as
well as forefoot supinatus, and is overall a component of Usfranc DJD. Over time, the
dorsal aspect of the MCJ becomes prominent, while plantar gapping occurs. Signs and
symptoms include cutaneous erythema, difficulty fitting shoes, medial dorsal cutaneous
neuritis, MCJ bursitis, EHL tendinitis and/or vamp disease. Anatomic considerations
relating to surgical intervention include the EHL and TA tendons, and the neurovascular
bundle. First MCJ exostosis is categorized as depleted in Table 7-3.
TABLE 7-3. FIRST METATARSOCUNEIFORM EXOSTOSIS.
Type of metatarsocuneiform Clinical description of exostosis

exostosis
Localized dorsal exostosis
II Dorsal exostosis with MCJ arthritis
Ill Dorsal exostosis with angular deformity, such as
adduction of the cuneiform and first metatarsal
IV Hyperostosis that extends across the
entire Lisfranc joint complex
v Pseudoexostosis of anterior cavus,
wherein an actual exostosis is not present, although
the dorsum of the articulation is relatively prominent
194 Reconstructive Surgery of Basic Conditions and Defonnities Ch. 7
Exposure of the exostosis can be approached from the medial aspect via a curvilinear
incision situated between the EHL and TA tendons, and this will allow retraction of the dorsal
neurovascular elements while providing access to the dorsal exostosis. Exostectomy is
performed with osteotome and mallet or power instrumentation, followed by hand rasping.
The articular margins should be saucerized. lf articular degeneration is extensive, then
arthrodesis should be considered, and is usually achieved with a combination of lag screws
and a neutralization or load~screw plate situated on the medial~piantar aspect of the
metatarsocuneiform fusion interface. Specialized locking plates are also available for this
fusion. Postoperative care involves application of a compression dressing and mobilization and
weight bearing to tolerance following exostectomy, or immobilization and non-weight
bearing following arthrodesis.
INTERMEDIATE (CENTRAl, Second-through-Fourth RAYS} METATARSAlGIA and

DEFORMITIES
The primary causes of lesser ray pathology are dynamic in nature, and include retrograde
buckling of contracted digits (flexors stabilization, extensor substitution, and flexor
substitution}, hypermobile first ray and hallux limitus/rigidus effecting lateral dumping of
weight bearing, and various forms of ankle equinus and dropfoot Isolated structural
deformities affecting the intermediate rays are less common, but certainly exist and must
be considered when evaluating the patient with lesser metatarsalgia. Isolated structural
deformities may be congenitat post-traumatic" or iatrogenic; and include hypertrophic
plantar condyle, elongated metatarsal or adjacent brachymetatarsia, isolated metatarsal
equinus, or adjacent elevatus. Radiographic inspection of the intermediate lesser
metatarsals should include the lateral oblique projection, as this allows comparison of the
sagittal plane relationship of the central metatarsals. The metatarsal axial view, and
measurement of relative metatarsal protrusion on the weight bearing A~P view, may also be
helpful. Signs and symptoms include metatarsalgia, IPK, diffuse tyloma, and MTPJ
enthesitis. The differential diagnosis entails functional and structural etiologies, as well as
systemic arthritis, intermetatarsal neuroma, MTPJ enthesitis and/or bursitis, stress
fracture, thrombocytosis and erythromelalgia. Treatment involves attention to the dynamic
etiology, and conservative protection of the metatarsus, as well as anti-inflammatory
measures both systemic and local, and physical measures. Application of a metatarsal
projection pad to the insole proximal to the metatarsal heads, in conjunction with digital
retainers and supportive shoes, perhaps with a roller sole, can be helpful. A forefoot
extension with aperture padding may also be used. Surgical intervention usually entails
digital stabilization and MTPJ relocation via the sequential release. Isolated metatarsal
osteotomy may be used if digital surgery and supportive measures prove inadequate.
Caution is practiced when considering intermediate lesser metatarsal osteotomy, as the
incidence of recurrence, transfer lesion, floating toe, delayed and/or nonunion are
relatively high, especially when osteotomy fixation is notpursued.lntermetatarsal osseous
bridging may develop in cases wherein multiple adjacent metatarsal osteotomies are
performed, even when fixation, immobilization, and non-weight bearing are employed.
Selected lesser metatarsal surgical procedures include plantar condylectomy, distal and
proximal osteotomies, shaft osteotomies, and adjunct techniques such as syndactyly and
bone grafting. It is important to understand the need for appropriate digital stabilization and
MTPJ alignment when it comes to successful management of lesser metatarsalgia, and
the foundation role that digital stabilization plays relative to metatarsal surgery. A number
of surgical procedures are useful for treatment of intermediate metatarsalgia, and include:
Plantar condylectomy-used to reduce a hypertrophic or prominent plantarlateral

metatarsal head condyle, and is rarely indicated as an isolated procedure. The procedure
is usually performed via a dorsal longitudinal incision over the MTPJ and is often combined
with arthrodesis of the corresponding and adjacent central PIPJ and sequential release of
the MTPJs, and syndactyly of the corresponding toe to the adjacent stabilized digit.
Syndactyly is an important adjunct procedure, as condylectomy results in decreased MTPJ
cubic content that, in turn, allows the toe to float dorsally due to loss of plantar tethering.
The MTPJ capsulotomy enables plantar displacement of the toe and exposure of the
plantar condyles ofthe metatarsal head. Use of the metatarsal elevator may expedite this
exposure and delivery of the metatarsal head into view. The hypertrophic condyle is then
resected with the osteotome and mallet, and the remaining bone smoothed with the rasp.
A temporary K-wire may be used to stabilize the toe and MTPJ if necessary. Layer closure
ensues, with attention paid to avoiding excessive EDL tension. A built-up surgical shoe will
be necessary if the MTPJ is pinned.
Wei/ osteotomy-this is a powerful procedure for shortening and elevating the

capital fragment of the metatarsal by means of a dorsal-distal to plantar-proximal oblique
osteotomythatcan be fixated with a single 2.0 or2.7 mm interfragmental compression screw
from dorsal to plantar. Caution should be taken in regard to the prevention of a
postoperative floating toe, which can accompany any shortening or elevating metatarsal
osteotomy, or procedure that decreases the internal cubic content of the MTPJ, such as
plantar condylectomy.
Jacoby V-osteotomy-involves a transverse plane chevron osteotomy, through-and-

through from dorsal to plantar at the surgical neck, with base proximal and apex
distal. The approach entails dorsal dissection, digital stabilization, and MTPJ relocation.
This osteotomy can also be used to plantar declinate the capital fragment when indicated.
The osteotomy is stabilized with a K-wire, either from proximal to distal or through the
stabilized digit and MTPJ in an axial (medullary nail) fashion.
Dorsiflexory wedge osteotomy (DFWO}-there are several variations of dorsiflexory wedge

osteotomy (OFWO). including distal metaphyseal (surgical neck) osteotomies such as the
transverse tilt-up and oblique wedge osteotomies; and the oblique base wedge osteotomy.
Distal osteotomies are readily fixated with an axial K-wire used to simultaneously stabilize
the corresponding digital arthrodesis and MTPJ relocation. The dorsal-distal to
plantar-proximal oblique distal DFWO at the anatomic neck usually involves resection of
only a thin wedge !thickness ofthe saw blade) of bone, and can be fixated with a K-wire or
a lag screw (Figure 7-47). The same dorsal-distal to plantar-proximal oblique DFWO can be
placed atthe metatarsal base, and stabilized with K-wires or a lag screw.
Lesser metatarsal shah osteotomy-a variety of shaft osteotomies can be used, often in
conjunction with bone grafting. The Giannestras step~down osteotomy is classical!y used
to shorten a metatarsal, however it can also be used to elongate. The step-down osteotomy
isthrough~and-through, and involves complete exposure of the metatarsal. The osteotomy
consists of three cuts oriented in the transverse plane. The proximal and distal transverse
arms exit opposite sides (medial or lateral) of the cortex, and are united by a longitudinal
central arm. When shortening is desired, an additional proximal and distal transverse cut
is made from the shaft segments. The osteotomy can be oriented somewhat in the sagittal
Figure 7.47
plane, in an effort to facilitate !ag screw fixation. Variations on the Ludloff and Mau, Gudas-
scarf Z-p!asty, and offset V-osteotomy, oriented in both the transverse and sagittal planes,
have all been used for lesser metatarsal shaft reconstruction. The sliding osteotomies are
more suitable to interpositional bone grafting with lag screw fixation.
FIFTH METATARSAL SURGERY AND THE TAILOR'S BUNION

The tailor's bunion deformity is observed in the uncompensated or partially compensated
rearfoot or forefoot varus foot types, which predispose to hypermobility of the fifth ray in
response to ground reactive forces. The plantarflexed fifth metatarsal will adduct, evert
and dorsiflex in response to the ground reactive force; and may present with a plantar-
lateral bursitis, hyperkeratosis, and pain. A congenitally dorsiflexed fifth ray may also result
in tailor's bunion symptoms, usually with a dorsolateral or lateral lesion. Weight bearing
radiographic analysis of the tailor's bunion deformity will usually display rotation of the
plantarlateral tubercle to a more lateral position, consistent with pronatory eversion of the
metatarsal. There will often be an increase in both the fourth IMA above 6.5, and the
lateral deviation (bowing) angle above 2.JO. There is often a dumbell-shaped and enlarged
fifth metatarsal head, and arthritic changes with osteophytosis may be present. When the
foot clinically appears to be very wide, the combination offirst IMA >12" and a fourth IMA
>8 is consistent with splayfoot deformity, and the tailor's bunion is often the primary area
of patient concern. Surgical goals in the treatment of tailor's bunion focus on elimination of
prominent lateral exostosis, either dorsal or plantar; along with correction of structural
deviations such as excessive fourth IMA and/or lateral bowing. Adjunct procedures may
include correction of an adductovarusflfth hammertoe. Specific procedures for correction
oftailor's bunion deformity include:
Lateralexostectomy-this procedure (Fig 7-48), performed performed on mild tailor's bunions

as an isolated procedure, or in conjunction with other structural corrections and a variety of
fifth metatarsal osteotomies. If an over-aggressive lateral exostectomy is performed
(staking the metatarsal head) in the presence of structural bowing or a high fourth IMA,
excessive fifth MTPJ laxity will lead to adductovarus fifth toe contracture and retrograde
MTPJ buckling with recurrence and worsening of deformity.
fifth metatarsal head excisiotr-a radical procedure that involves head resection at the
anatomic neck and usually well tolerated in less ambulatory individuals due to the fifth ray's
independent axis of motion; it may be indicated too, in cases of fifth metatarsal head
osteomyelitis, tumor or avascular necrosis.
Hohmann Reverse Wilson

Mitchell Thomasen's
Figure 7.51A Figure 7.51 B
Hohmann osteotom~a transverse through-and-through osteotomy at the anatomic neck,

usually stabilized with a K-wire (Fig 7-49).
Reverse Wilson osteotomy---an oblique osteotomy from distal-lateral to proximal-

medial often floated but better to be stabilized with a K-wire (Fig 7-50).
Mitchell osteotomy---a variation of the first metatarsal osteotomy that may be limited by a
narrow fifth metatarsal neck; this osteotomy is at risk for dorsiflexion if subjected to early
weight bearing (Figure 7-51A).
Thomasen's osteotomy--a peg-in-hole variation of the Hohmann osteotomy, usually

stabilized with a K-wire (Fig 7-51 B).
Reverse Austin osteotomy-a sagittal plane chevron limited by the width of the metatarsal
neck and stabilized with a K-wire or absorbable pin (Fig 7-52).
Closing adductory osteotomy at neck (MercadoHistal transverse plane medially based

wedge osteotomy with an intact lateral cortical hinge, stabilized wH:h either a K-wire or
stainless steel wire suture, or both (Fig 7-53).
Closing adductory base wedge osteotomy (Gerbett}-a transverse plane medially based
wedge osteotomy with an intact lateral cortical hinge, fixated with a K-wire and or stainless
steel wire suture, or made oblique to facilitate lag screw fixation
Oblique wedge osteotomy-located at the apex of the bowing deformity, fixated with a K-
wire and or stainless steel wire suture, or lag screws (Fig 7-54).
HEEl SURGERY
Approximately 15% of all adult foot complaints are related to disorders of the heel. The
circulation to the heel entails the medial calcaneal branches of posterior tibial artery
medially, the communicating branches of the peroneal and lateral malleolar arteries
laterally and plantarly, and communicating branches posteriorly. The neutral or vascular
triangle, of the calcaneus is the radiolucent area observed in the lateral radiograph,
inferior to the sustentaculum tali within the body of the calcaneus, where the subtalar
pressure trabeculae combine with traction trabeculae formed in response to the pull ofthe
plantar fascia and Achilles tendon are seen under sustentaculum tali.
Plantar Fascitis and Heel Spur Syndrome---this condition results tram prolonged,
excessive tension in the plantar fascia, usual!ysecondaryto hyperpronation of the STJ/MTJ,
and eventually leads to fasciosis at or near the attachment of the plantar fascia to the
calcaneus. Overtime, an elongated plantar spur may also develop atthe attachment of the
fascia. Stress fracture may lead to development of a prominent plantar protrusion. Chronic
inflammation of the fascia, with or without spur formation, may also be associated with
distal tarsal (calcanea!) tunnel syndrome. The diagnosis is made based on localization of
focal, deep tenderness to the fascial attachment to the calcaneus, the presence of similar
pain upon activation of the plantar windlass (simultaneous dorsiflexion of the MTPJs and
ankle, with the knee extended); post-static dyskinesia, and radiographic evidence of a
plantar spur in about 75% of cases. A distinct plantar spur need not be present to effect
pain. Differential diagnostic considerations for plantar heel pain include lumbosacral
radiculopathy, systemic arthritis, tarsal tunnel syndrome, subcalcaneal bursitis, contusion
or local trauma, stress fracture, entrapment neuropathy of the lateral plantar nerve and its
muscular branch, diffuse idiopathic skeletal hyperostosis (DISH) syndrome, Paget's
disease, and heel neuroma. A bone scan may be helpful in resistant cases when stress
fracture is suspected. Conservative treatment combines biomechanical, pharmacological,
physical, and surgical therapies (Table 7-4).
TABLE 7-4. TREATMENT HIERARCHY FOR PLANTAR FASCIITIS AND HEEL SPUR
SYNDROME.
Intervention Slagel Stage II Stage Ill Stage IV
Pharmacological NSAID NSAID
Local steroid
Oral steroid
Biomechanical Low Dye strap Custom orthotic Immobilization
Prefabricated Roller sole
orthotic
Physical Ice Iontophoresis Night splint
Flexibility Dynamic splint
Surgical ESWT Cold ablation
microdebridement,
fa scioto my,
spur resection;
bursectomy
fxtracorporeal Shockwave Therapy(ESWT}-shockwaves consist of high amplitude, fast

rising, asymmetrical, low frequency (>500 bar in 33 nanoseconds) sound energy that
imparts intense pressure to the target tissues, namely the plantar fascia. Shockwaves can
be generated by means of piezoelectric crystals or ceramics, electromagnetic energy, and
electrohydraulic vaporization of water. Shockwaves have been used in the treatment of
tendinosis calcarea (shoulder), lateral epicondylitis (tennis elbow), cedial epicondylitis (golf
elbow), chronic calcifications (thigh, apophysis), patellar tendinitis, ossoue nonunions and
pseudarthrosis, nephrolithiasis, and microscopic studies into the potential use in the
treatment of cancer and CNS lesions are alos underway. In order to treat plantar fasciitis,
shockwaves must deliver 0.260.32 mJ/mm2 of energy to the target fascia. This causes
physical alteration of small axons, inhibiting impulse conduction, chemical alteration of pain
receptor neurotransmitter, and hyperstimulation analgesia (gate control); as well as
neovascularization. Resultant tissue absorption and deformation create a wound healing
response that, in 3-6 weeks, may relieve chronic pain related to plantar fasciitis. Weight
bearing is immediate following ESWT. Potential complications of ESWT include
subcutaneous hematoma, skin erosion, swelling, petecchial hemorrhage, pain and
paresthesia, and vasovagal syncope. Contraindications to ESWT include pregnancy,
children, nerve damage, tarsal tunnel syndrome, tarsal tunnel syndrome, osteoporosis,
rheumatoid arthritis, peripheral vascular disease, infection or tumor, bleeding diasthesis,
cardiac pacemaker, and healing fracture.
Radiofrequency cold ablation (Coblationm} microdebridement-the plantar fascia can be

debrided in an open fashion by means of a small incision over the proximal portion of the
fascia, and application of 15-20 high voltage radiofrequency impulses in a saline medium that
creates a plasma layer between the concentric electrodes at the tip of the probe, and
disrupt the molecular bonds in the target tissue, thereby effecting localized fascia
debridement with minimal collateral tissue destruction. Non~weight bearing, or partial
weight bearing is employed following cold ablation debridement of the plantar fascia,
varying with the nature of the plantar skin incision, surgeon's preference, and the amount
of debridement undertaken.
Plantar Fasciotomy and Calcaneal Spur Resection---exposure of the attachment of the

plantar fascia to the calcaneus, and the plantar spur, can be achieved through a plantar
transverse, longitudinal, or oblique incision. Of historical .interest is the distally-based
U~shaped pedicle flap Griffith incision, which can be used to expose the entire plantar
aspect of the calcaneus. The medial DuVries approach can also be used, however this
incision makes the medial calcanean nerves vulnerable to post-incisional entrapment. The
deep plantar fascia is identified and sectioned from the calcaneal tuberosity, and the
plantar spur resected. A small segment of the most proximal fibers of the plantar fascia is
retained for pathological inspection. It is important to re-establish a normal cortical contour
when the spur involves prominent plantar protrusion, even if fascitis has been essentially
resolved with conservative measures. Care must be taken to avoid injury to the lateral
plantar nerve and its branches, and over~aggressive resection of bone as this could weaken
the calcaneus and predispose it to fracture. Other complications include recurrence,
hematoma, scar pain, and chronic plantar enthesitis. A compressive dressing is applied,
and early ankle range of motion and 3 weeks non-weight bearing ensue. Non~weight
bearing is necessary in order to allow the plantar skin wound to heal. A wide range of
techniques have been used over the years for the treatment of recalcitrant plantar heel
pain, some of which are of historical interest only while others show useful application.
Variations on the general theme of fasciotomy and spur resection include minimal incision
or semi-closed approaches wherein the fascia is released and the spur remodeled under
fluoroscopic guidance, or via topographical guidance and identification of palpable
landmarks. Instep plantarfasciotomy, localized to the mid portion ofthe medial band of the
plantar fascia, and not addressing the calcaneus, can also be useful in some cases.
Historically, spur reduction has been addressed with a countersinking osteotomy, or a
rotational osteotomy combined with tendoAchillis lengthening.
Endoscopic Plantar Fasciotomy (EPF}-endoscopic plantar fasciotomy has been shown

to be a useful option for releasing the fascia, and is based on the theory that the spur need
not be remodeled in order to alleviate plantar heel pain. The procedure is performed under
local or general anesthesia, and uses a blunt obturator to channel from medial to lateral
across the heel after initially making an incision through which the obturator is passed. The
deep fascia is visualized by passing a slotted cannula with obturator from medial to lateral
and rotating the slot toward the fascia. An L~shaped blade is then inserted from lateral to
medial while viewing through the endoscope, which is inserted from medial to lateral. The
blade is turned dorsally at the medial margin of the fascia, and then pulled laterally.
Fasciotomy is directly viewed, and several passes of the blade are usually necessary to
adequately section the fascia. Care is taken when inserting and removing the L-shaped
blade through the lateral incision. The wound is Javaged and skin closure performed,
followed by application of a compressive dressing. It is also possible to reduce bony
prominence endoscopically with the rota-osteotome and shaver, however this is generally
not done.
External Neurolysis-if the cause of plantar heel pain is thought to be entrapment

neuropathy of the lateral plantar nerve and/or its muscular branch (inferior calcaneal nerve
and calcaneal tunnel syndromeL then external neurolysis of the nerve trunks may be in
order. External neurolysis, however, is usually performed in conjunction with fasciotomy
and spur reduction. External neurolysis is best performed with the use of fine-tipped
instrumentation and Ioupe magnification.
Calcaneal Decompression-decompression of calcaneal intramedullary pressure, via

multiple small drill or K-wire holes aligned obliquely from posterior-proximal to anterior-
distal (dorsal cortex to plantar cortex) through the cortex of the calcaneal body, has also
been espoused as a treatment for plantar calcaneal pain. Currently, this procedure is
primarily of historical interest only, although there is some basis to its use. In essence, the
decompression holes result in cortical fracture when subjected to the pull of the Achilles
tendon and plantarfascia, thereby reducing tension in these soft tissues after resumption
of weight bearing. Calcaneal joint depression fracture is an obvious risk of the
decompression technique.
Haglund's Deformity-this deformity consists of prominence of the posterosuperior aspect

(bursal projection) of the calcaneus. It can be structural or positional, or a combination of
both. A variety of radiographic observations (Figure 7-55) are used to assess the posterior
aspect of the calcaneus. The Fowler and Philip angle (FPA) normally ranges from 44"-69",
and an FPA >75 will often present with posterior swelling, cutaneous compromise and
prominence just superior to Achilles insertion. Prominence of the posterior aspect of the
calcaneus predisposes to the development of retrocalcaneal bursitis, as the constant
pre-Achilles bursa becomes repetitively irritated with anl<le dorsiflexion (Figure 7-56). Ruch
has pointed out that the total angle is a more reliable assessment of the likelihood of the
s
T
1) Angle of Fowler & Philip

2) Calcaneal inclination angle A
3) Total angle
posterior aspect of the heel to irritate the retrocalcaneal bursa, as this measurement takes
into accountthe calcaneal inclination angle (CIA) and posterior structural prominence (FPA).
A total angle> 90 correlates highly with retrocalcanea! bursitis and Haglund's deformity.
Parallel pitch lines IPPL) have also been used to assess the prominence of the
posterosuperior prominence of the body of the calcaneus. An adventitious superficial
calcaneal bursa may develop superficial to the Achilles tendon secondary to repetitive
mechanical irritation. Kager's triangle is demarcated by the long flexor tendons anteriorly,
the Achilles tendon posteriorly, and the superior surface of the calcaneus inferiorly, and Is
visualized in the lateral radiograph as a dark, radiolucent triangle with apex pointed dorsally.
Kager's triangle represents the pre-Achilles fat pad. Thickening of the Achilles, which is
usually about 9 mm wide in the lateral radiograph, due to retrocalcaneal bursitis and/or
tendinitis will encroach on Kager's triangle and blur the usually sharp interface with the
pre-Achilles fat pad. The calcaneal apophysis usually closes at 14-16 years of age.
Biomechanical foot types associated with increased motion between the posterior aspect
of the heel and the shoe counter, thereby aggravated by Haglund's deformity, include
compensated reatfootvarus, compensated forefoot valgus, and rigid plantatflexed first ray.
Symptomatic Haglund's deformity is most commonly observed in young to middle-
aged females; with pain and cutaneous irritation at the posterior aspect of the heel,
radiographic evidence of a cortically intact bursal projection, loss of the pre-Achilles recess
indicative of retrocalcaneal bursitis, Achilles tendon widening > 9 mm indicative of
tendinitis, and loss of distinction of the posterior margin of Kager's triangle. A tender
superficial Achilles bursitis may be present, and causes the classic "pump bump"
aggravated by shoes with a tight counter and elevated heel height. Treatment of the
symptomatic Haglund's deformity, due either to a prominent bursal projection, a normal
posterior contour with a high CIA, or a combination of both, involves initial use of a heel lift
inside the shoe and a heel counter pad to shield the tender posterior aspect of the heel. The
use of NSAIDs, calf and arch flexibility exercises, orthotic control of hyperpronation, and
local infiltration of corticosteroid combined with gel-cast or similar immobilization can be
useful for persistent cases. Recalcitrant cases may warrant surgical intervention for
excision of chronic superficial and/or retrocalcaneal bursitis, and remodeling of the
prominent bursal projection. The treatment of Haglund's deformity and posterior calcaneal
spur are summarized in Table7-5.
TABLE 7-5. TREATMENT HIERARCHY FOR HAGLUND'S DEFORMITY OR POSTERIOR

CALCANEAL EXOSTOSIS.
Intervention Stage I Stage II Stage Ill Stage IV
NSAID NSAID
Pharmacological Local steroid*
Oral steroid
Heel lift Custom orthotic Continued
Biomechanical Heel counter pad Roller sole immobilization
Prefabricated
orthotic Immobilization
Physical Ice Iontophoresis Night splint
Flexibility Dynamic splint
Surgical Remodel
posterosuperior
process or spur
resection; preserve
Achilles or detach;
bursectomy
*Support of the ankfe and partial immobilization (gel cast and surgical shoe, cast boot (cam walker}, BK cast} with
weight bearing are ad'Jised whenever corticosteroid is infiltrated about the Achilles tendon.
Surgical repair of Haglund's deformity of the heel involves a lateral paratendinous incision
with the patient prone or in the contralateral decubitus position. The procedure is readily
performed under local anesthesia with IV sedation, and anatomic dissection yields
adequate hemostasis. The sural nerve must be protected within its subcutaneous bed. The
deep fascia is incised in a paratendinous fashion, in line with the overlying skin incision. Care
should be taken to avoid excessive reflection of the fibrous expansion of the Achilles
tendon at its insertion. Plantarflexion ofthe ankle enhances retraction ofthe Achilles. The
prominent posterosuperolateral process is resected with an osteotome and mallet and the
remaining calcaneal surface is then rasped. "Chasing the bump" prevents creation of a
new prominence dUe to over aggressive resection. It is possible to remodel the entire
posterior aspect from the lateral approach, however a second medial paratendinous
incision can be used if necessary, however a distance of at least 2.5 em should be
maintained between the two parallel incisions. A curvilinear or lazy-S incision could also be
used. Generally, with Haglund's deformity the single lateral incision will suffice. In the
symptomatic, structural cavus foot with a pathologically high CIA, in the presence of a
normal posterior contour and bursal projection, the Kelly and Keck osteotomy may be used
to resect a dorsally based wedge from the calcaneal body. This procedure brings the
posterosuperior aspect of calcaneus anteriorly. The osteotomy is fixated with Steinmann
pins, staples or lag screws.
Retrocalcaneal Exostosis with Calcification in the Achilles--the retrocalcaneal

exostosis differs from the Haglund's deformity in that it is usually seen in older individuals,
is situated distal to the posterosuperior process, and it generally traverses the entire
posterior aspect from lateral to medial. The patient should be positioned prone or in the
contralateral decubitus position, and the procedure can be performed under local
anesthesia if desired. lncisional approaches are variable, including two paratendinous

incisions, a central longitudinal posterior or an oblique curvilinear (Dickinson) incision, and
it is often necessary to create a central longitudinal tendon-splitting incision in order to
remove intratendinous calcification {Figure 7-57). The tendon splitting incision enables
the surgeon to expose the posterior surtace of the calcaneus while preserving distal
attachments medially and laterally. After remodeling the posterior surface of the calcaneus
and debriding the Achilles, the tendon is reattached with multiple intraosseous tendon
anchors and nonabsorbable sutures. Following layered closure, a compressive dressing and
short leg cast are applied. The patient is maintained non-weight bearing for 2-4 weeks, and
immobiHzation is discontinued at 5-6 weeks followed by gradual rehabilitation. The duration
of non-weight bearing and immobilization is determined by individual factors and the extent
of tendon reflection. Downey has advocated the use of an inverted V-tenotomy for debride-
ment ofthe Achilles tendon and removal of a posterior calcaneal spur, noting that this method
enables the surgeon to readily access the calcaneus and easily reap proximate the tendon.
52%
Anterior
Medial@:::> Lateral
Posterior
35%
Medial~ Lateral
13%
Medial ) lateral
Calcaneus
ANKlE EOUINUS
The triceps surae consist of the medial and lateral heads of gastrocnemius, plantaris, and
soleus. The medial head of gastrocnemius is thicker and broader than the lateral head, and
it extends further distally and attaches to the lateral aspect of the tendoAchillis. Soleus
attaches to the medial2/3 ofthe deep surface of the tendoAchillis (Fig 7-58). Plantaris arises
from the lateral femoral condyle, and Is absent 7% of the time. Plantaris attaches medially
along the Achilles. The tendoAchillis averages 15 em in length and originates near the
middle of the leg. Gastrocnemius traverses three joints: knee, ankle, and STJ; while soleus
traverses two joints: ankle, and ST.J. The gastrosoleus complex functions in late contact
through midstance and into early propulsion, and causes knee flexion and heel lift via
ankle plantarflexion.
Muscular Forms of Ankle Equinus-the muscular forms are caused by skeletal muscle
spasm, congenital shortness, and acquired conditions. Spastic equinus is the oldest
recognized form of ankle equinus, and is caused by upper motor neuron disease such as
cerebral palsy, CVA, and head and spinal trauma. Spastic equinus presents with
hypertonicity, hyperreflexia, and steppage gait Congenital equinus usually presents with toe
walking until about 1518 months of age !usually the first36 months after initial walking), and
thereafter the equinus subsides. Acquired ankle equinus may develop in response to
prolonged casting in plantarflexion, such as following Achilles tendon repair, or due to
chronic use of high~heeled shoes. Chronic equinus contracture results in tightness of the
deep flexors and peroneal tendons, posterior ankle and subtalar ligaments and capsule.
The Silverskio!d test indicates gastrocnemius equinus if ankle dorsiflexion is <10with
the knee extended, but 2'10 with the knee flexed; or gastrosoleal equinus it <10 of
dorsiflexion with the knee extended or flexed. Gastrocnemius equinus can be addressed
with gastrocnemius recession, while gastrosoleus equinus warrants tendoAchil!is length~
ening !TAL). The end range of motion should be smooth and "soft tissue," as compared to
an abrupt, bony end range consistent with osseous equinus. The standard lateral ankle and
charger (stress dorsiflexion) radiographs should be checked for talotibial exostosis, which
could cause bony blockage to dorsiflexion. Distal tibiofibular synostosis following trauma
can inhibit the wider anterior portion of the dome of the talus from gliding through the ankle
mortise, thereby blocking ankle dorsiflexion without the presence of talotibial exostosis.
Hamstring tightness can also cause ankle equinus, and the knee should be checked for
flexion contracture while plantarflexing the ankle (eliminates pull of gastrocnemius on the
knee) and passively extending the knee to end range. Pseudoequinus may be present when
the cavus foot(anterior equinus) uses available dorsiflexion at the ankle, simply to stand with
the forefoot loaded, thereby limiting available dorsiflexion range of motion and functionally
inducing equinus deformity.
Combined forms of equinus may involve gastrocnemius or gastrosoleus equinus, with
bony blockade and/or pseudoequinus. Distal pedal compensation for ankle equinus occurs
as hyperpronation of the STJ and MTJ with associated forefoot supinatus, flexor
stabilization induce hammertoes and HAV, and serves as one of the most forceful and
common deforming influences acting on the foot Failure to compensate with pedal
hyperpronation results in genu recurvatum or overt toe walking/standing. Uncompensated
equinus also presents as pes cavus, with equinovarus, fixed STJ supination, extensor
substitution, and dropfoot In the neuropathic (insensitive, Charcot) patient, equinus
deformity leads to tremendous Lisfranc fracture and luxation. Neurological consultation is
in order whenever UMN or spastic equinus is noted. Nonsurgical efforts to manage
significant equinus deformity are generally not very successfuL Efforts include stretching
and flexibility tor nonspastic forms, and possible acceptance of the deformity and use of a
heel lift, orthosis, and roller sole.
Gastrocnemius Equinus-gastrocnemius equinus has been treated with selective

dennervation of the gastrocnemius muscle bellles, as well as proximal recession via
transection of the medial and lateral heads near their femoral origins. Vulpius and Stoffel
described a distal transverse recession of the gastrocnemius aponeurosis, and they later
converted the technique to an inverted V-shaped lengthening of the aponeurosis without
suturing to underlying soleus muscle. Strayer described a transverse aponeurotic incision
with suturing of proximal portion to underlying soleus. Baker described a distally based
tongue-in-groove recession of the aponeurosis (Fig 7~59), and sectioned the central soleus
aponeurosis deep to the gastrocnemius aponeurosis. Fulp and McGiamry modified the
tongue~in-groove distal recession by basing the tongue proximally (Fig 7~60), however
Downey and Banks later noted this to associate with atrophy of the medial head of
gastrocnemius due to the natural rotation of the gastrocnemius fibers. Gastrocnemius
recession is used most effectively in cases of nonspastic gastrocnemius ankle equinus.
Distal gastrocnemius recession (Baker) is carried out on the prone or lateral decubitus
patient using an approximately 6-7 em longitudinal incision, originating at the palpable
myotendinous junction, and positioned just medial to the midline on the posterior aspect of
the calf. The incision is deepened through the dermis into the subcutaneous fat, where the
sural nerve and Jesser saphenous vein are preserved in their soft tissue bed laterally. The
deep fascia and paratenon are incised in line with the overlying skin incision, and reflected
as a single layer. Plantaris is transacted on the medial aspect of the wound (originates
laterally and traverses from lateral to medial as it propagates distally), and a segment is
excised to assure release. The ankle is then slightly plantarflexed to enhance access to the
most distal fibers of the aponeurosis, and the tongue-in~groove aponeurotomy is initiated
by transacting the medial and lateral thirds of the aponeurosis distally. The ankle is then
slightly dorsiflexed to make the remaining intact fibers taut, and the central third of the
aponeurosis is transacted proximally. The aponeurosis is then lengthened (recession) by
dorsiflexing the ankle with the knee extended until 10o of motion is achieved with the
subtalar joint neutral. The central so leal aponeurosis is then sectioned. The wound is the
lavaged and the central tongue portion of the aponeurosis is sutured to the medial and
lateral thirds in the corrected length, using 2-0 nonabsorbable, buried knot sutures
reinforced with 2-0 absorbable sutures to reapproximate the medial and lateral thirds
centrally. Paratenon and deep fascia are closed with 3-0 absorbable running lock suture,
and smooth gliding function deep to the fascia/paratenon layer is assessed by moving the
ankle through its range of motion. The subcutaneous layer and skin are then closed. A BK
cast or immobilizing splint is then applied with the knee extended and STJ neutral, and
maintained for 3-4 weeks before rehabilitation is initiated.
Gastrosoleal Equinus-gastrosoleal equinus has been treated with a variety of

tendo-Achillis lengthening (TAL) procedures. The frontal plane Z-lengthening (Fig 7-61) is a
commonly used techn)que for TAL, and provides excellent control of length and avoidance
of suture irritation of the overlying deep fascia and skin posteriorly. The procedure is
performed on the prone or lateral decubitus patient via a 6~8 em longitudinal incision
medial to the posterior midline, terminating at the insertion of the Achilles. Deep fascia and
paratenon are then incised longitudinally, and the entire Achilles tendon isolated for a
distance of 57 em from its insertion. A #11 (bayonet) blade is then used to hemisectthe
tendon in the frontal p_lane, creating anterior and distal hemisections. The hemisection is
converted to a Z~tenotomy by sectioning the posterior hemisection proximally, and the
anterior hemisection distally. The plantaris tendon is sectioned at the medial aspect of the
Achilles (or alternatively it can be Z-lengthened itself). Attention is directed to residual
contracture, and posterior ankle and/or STJ capsulotomy or deep flexor or peroneal tendon
lengthening is performed as necessary. The ankle is placed in corrected position, with the
STJ neutral, and the tendon sections reapproximated with a combination of 1~0 and 2~0
nonabsorbable and absorbable sutures taking care to bury the knots. Paratenon and deep
fascia are then reapproximated with 3-0 running lock absorbable suture, followed by
closure of the subcutaneous layer and skin. A BK cast is then applied with the knee
extended and the STJ in neutral position.
Figure 7.61
Osseous Ankle Equinus-an anterior talotibial exostosis can be addressed via an open or
arthroscopic technique, and involves removal of impeding osteophytosis and spurring until
adequate range of motion is achieved. lftibiofibular synostosis inhibits ankle dorsiflexion,
then mortise reconstruction may be in order.
Murphy Anterior Advancement of the Achilles Tendon-this procedure has been described
in Chapter 6, and is indicated in the treatment of spastic triceps surae equinus.
Selected Peripheral Nerve Entrapments and Acquired Neuropathy

Kopel and Thompson have defined peripheral nerve entrapment as an area of nerve trunk
impingement due to the surrounding "stress anatomy" at a point where the nerve traverses
a fibro-osseous tunnet or constricting soft tissue hiatus. In the lower extremity, a number of
entrapment sites are commonly symptomatic, and any peripheral nerve can become
entrapped. Most notable among the common entrapments inferior to the knee are tarsal
tunnel syndrome (medial), Morton's intermetatarsal neuroma, and superficial peroneal nerve
entrapment at the deep fascial hiatus proximal to the ankle.
Tarsal Tunnel Syndrome (TIS)-tarsal tunnel syndrome is classically described as

entrapment or compression neuropathy of the posterior tibial nerve and/or its terminal
branches, the medial and lateral plantar and medial calcanean nerves. The surgical
anatomy of interest includes the flexor retinaculum (laciniate ligament) extending from the
medial malleolus to the medial process of the calcaneal tuberosity and the plantar
aponeurosis. The porta pedis at the distal aspect of the medial tarsal tunnel is the canal
created by the abductor hallucis muscle belly and its deep fibrous septal attachmentto the
periosteum of the medial wall of the calcaneus, through which the medial and lateral
plantar nerves pass and enter the plantar vault The division of posteriortibial nerve into its
three terminal branches most commonly occurs proximal to the laciniate ligament, however
it may divide deep to the laciniate ligament, or even at the distal margin of the tunnel. The
distal bifurcation into medial and lateral plantar nerves is often identified in cases of TIS,
as the subabductor fibrous septum encroaches on the crotch of the division, and is termed
distal tarsal tunnel, or calcaneal tunnel, syndrome. This is often associated with
longstanding, recalcitrant plantar fascitis and medial heel pain. The medial calcanean nerve
usually emerges through the laciniate ligament, and is primarily a sensory branch. The
medial plantar nerve provides sensory innervation to the plantar aspect of the hallux,
second and third toes, medial half ofthe fourth toe, and medial half of plantar aspect ofthe
foot. The lateral plantar nerve provides sensory innervation to the plantar-lateral half of the
fourth toe, plantar aspect of the f1fth toe, and the plantar-lateral aspect ofthe foot The
plantar nerves provide motor innervation to the intrinsic muscles, and autonomic
innervation to sweat glands and vascular smooth muscle.
The etiology of medial TTS is generally thought to be due to overuse or repetitive
microtrauma, consistent with impingement of the nerve by the surrounding "stress
anatomy." Operative inspection may reveal no particular gross abnormality of the
structures, unless a distal bifurcation, or tumor within the tunnel is identified. In the
typical case, longstanding hyperpronation of the STJ and MTJ has effected chronic
constriction of the contents of the tunnel. The existence of dilated and tortuous
posterior tibial veins within the tunnel may lead to engorgement and concomitant chronic
stasis, which can result in peripheral nerve compression and severe nocturnal discomfort
which is often associated with calf cramping. Traumatic causes of medial TTS include ankle,
talar or calcaneal fracture; recurrent ankle and/or subtalar sprain and subluxation; both of
which may lead to chronic, recurrent hemorrhage and fibrosis. Systemic diseases such as
rheumatoid arthritjs, hypothyroid myxedema, and even diabetes mellitus predispose to TTS.
Space occupying lesions such as lipoma, neurofibroma, neurilemmoma, ganglion, and
synovial cyst ioften associated with rheumatoid arthritis), have also been implicated as
causes of entrapment within the tunnel. Even hypertrophy of the abductor hallucis muscle
belly has been implicated as a cause of TIS. The clinical symptoms associated with medial
TTS include forefoot pain with symptoms localizing to the metatarsal ball and digits plantarly,
as well as medial and plantar heel pain and paresthesia. Early symptoms include intermittent
burning pain, numbness, and paresthesia over the medial side of the heel, the toes and the
plantar aspect of the foot As the condition worsens, late symptoms include paresis that
will develop into paralysis of the pedal intrinsic muscles (intrinsic minus foot). Proximal
radiation of pain (Valleix sign) may propagate up the posterior calf. Pain and paresthesia are
generally proportional to the amount of weight-bearing activity sustained during the day. The
diagnosis of TIS is not always sharply defined. Important aspects of the diagnosis include
history of progressive symptomatology, unless there is a traumatic event relevant to the
tunnel; the presence of unilaterallinel's (Hotfman-linel's) sign upon gentle percussion or
moderate-deep palpation of the tunnel's contents and, similarly, the presence of a
unilateral Valleix sign; application of a venous tourniquet proximal to the ankle will elicit
pain and paresthesia on the affected side secondary to venous occlusion with a
temporary passive congestion in the presence of intra-tunnel varix; forced eversion of the
STJ may elicit symptoms on the affected side in cases related to prolonged hyperpronation;
radiographs may provide evidence of previous injury; and appropriate lab testing may be
1, useful in establishing the presence of RA, myxedema, or DM. It is important to rule-out
lumbosacral radiculopathy or plexopathy, employing the straight leg raise, Achilles and
patellar deep tendon reflexes, and extrinsic muscle strength testing. EMG and NCV testing
may be helpful, however need not necessarily be positive for nerve entrapment at this level
even in the presence of overwhelmingly suggestive clinical findings. For this reason,
treatment decisions are not made solely on the results of electrodiagnostic testing.
Conservative treatment of medial TIS entails local anesthetic block of the posterior
tibial nerve and local infiltration of corticosteroid into the third canal of the tarsal
tunnel, followed by rest and gentle flexibility exercises of the ankle and foot. Support hose
may be indicated in case involving dependency-related venous congestion. Functional
orthotics may be useful for those patients displaying weight-bearing hyperpronation.
Surgical management of medial TIS can be enhanced by avoiding use of a tourniquet as
this allows visualization ofthe posteriortibial artery and the tortuous veins that may require
ligation. A tourniquet may be used if this is the surgeon's preference. Extensile esposure is
gained via a curvilinear incision extending posterior and plantar to the medial malleolus.
The incision should be placed at least 1 em posterior to the malleolus. The laciniate ligament
is identified, and vessels and nerves in the superficial fascia and subcutaneous fat are
observed and protected. The medial calcanean branch, which may pierce the flexor
retinaculum at this level and may display multiple branches, should be identified. The flexor
retinaculum is then incised and opened in line with the overlying skin incision and the
contents identified and documented; afterwhich external neurolysis of the posterior tibial
nerve and its branches is performed. Nerve retraction is maintained with a latex drain or
vessel loop. The nerve trunks are identified from proximal to distal through the tunnel,
including inspection of the porta pedis. Dilation of the porta pedis is enhanced with loupe
magnification and microsurgical instrumentation. Abductor hallucis is examined for
hypertrophy and hypertrophic tissue may be excised. The posterior tibial veins may reveal
varicosities that require ligation and excision. The wound is then flushed, and the laciniate
ligament is realigned but generally not sutured directly. The superficial fascia is then
reapproximated with absorbable suture of choice, followed by skin closure and
application of a gently compressive, sterile dressing. The foot and ankle are allowed to
move freely, however weight bearing is avoided for 2-3weeks, depending upon wound and
patient progress. A gradual resumption of activity is thereafter undertaken. Complications
of TIS treatment include recurrence of symptoms secondary to fibrosis, and consideration
should be given to burying the nerve in the calcaneus or tibia in cases of severe disability
due to recurrent nerve entrapment. This is obviously a serious undertaking, as plantar
insensitivity and loss of intrinsic muscle function ensues. Severing the posterior tibial artery,
which provides 80% of the arterial supply to the foot is a potential complication that would
require microsurgical repair. Other potential complications include nerve laceration,
tenosynovitis, hematoma, and possible infection, as well as dehiscence.
Figure 7.62
Morton's Neuroma-this condition is a common cause of metatarsalgia, and must be

considered in cases involving pain in the ball of the foot It is most frequently encountered
in the fourth to 6th decades of life and, although any intermetatarsal space can be affected,
it is usually localized to the third intermetatarsal sapce. The patient relates sharp, shooting
pain with associated aching, brought on by weight-bearing load of the forefoot, insidious in
onset, progressively worsening, and intermittent in nature, and seemingly relieved by sitting
and massaging the unshod foot for a brief time. Hyperpronating individuals, the obese, and
those that wear high-heeled or tight-fitting shoes are prone to entrapment irritation of the
common plantar nerve and/or its branches in the intermetatarsal space, just plantar to the
transverse intermetatarsalligament (Figure 7-62). The mechanism of nerve entrapment in
the intermetatarsal space involves repetitive irritation of the nerve by the neighboring
ligament. Identification entails focal tenderness and paresthesia to direct deep palpation,
a positive Mulder's strum-click sign, and localization of anesthesia to the contiguous sides
of the adjacent toes. Differential diagnoses include MTPJ enthesitis, intermetatarsal
bursitis, diabetic peripheral neuropathy, neoplasm, trauma, TIS, and radiculopathy.
Nonsurgical treatment measures involve the use of a metatarsal projection pad
{proximal to the metatarsal heads), orthoses, local infiltration of corticosteroid, ultrasound
with MTPJ range of motion exercises, use of a sneaker with roller sole, NSAIDs, ice after
strenuous activity, and rest. Surgical intervention evolves around adequate external
neurolysis ofthe involved plantar nerve and, traditionally, excision ofthe common plantar
nerve proximal to the proximal margin ofthe DTIL. Approaches include: 1) the plantar
longitudinal interspace incision, which yields optimal exposure of the plantar nerve without
disruption of the DTIL; 2) the transverse plantar incision, which yields exposure to adjacent
interspaces; 3) the web-splitting incision, 4) the dorsallongitudinat which is satisfactory
for an interspace into which no previous dissection has been undertaken; and 5) the
plantar zig-zag or lazy-S incision, which affords exposure of the plantar metatarsus and
vault whenever revisional neurectomy is necessary. Sectioning the DTIL readily exposes the
plantar nerve and its branches, and makes IT easy to excise the neuroma, which is typicaly
present at the distal margin of the DTIL After identification of the common plantar digital
nerve trunk and its proper digital branches to the contiguous surfaces of the adjacent toes,
the nerve is inspected for coloration and texture and, usually, resected proximal to the
proximal margin of the DTIL. Some surgeons do not excise the nerve, and limit the
procedure to sectioning the DTIL or, less commonly, translocating the nerve from plantar to
dorsal to the DTIL The latter intervention entails sectioning the ligament, transposing the
nerve, and then repairing the ligament It is also possible to section the DTIL by means of
endoscopic identification and sectioning using specialized instrumentation, however such
intervention neither excises the neuroma nor translocates the nerve trunk. If the nerve is
section and the neuroma excised, the proper branches are procured as far distal as
possible in each toe, and the common nerve trunk is sectioned as far proximal to the
proximal margin of the DTIL as possible. This can be difficult when the dorsal incisional
approach is used, however this method of surgical treatment is commonly used. After the
common trunk is sectioned, the proximal nerve stump is allowed to retract further proximally
in the intermetatarsal space, where it can reside amidst intact intrinsic skeletal muscle
bellies. In an effort to further diminish the potential risk of developing a symptomatic stump
neuroma, closure of the common trunk's epineurium with 8-0 nylon suture can be
undertaken, prior to allowing the stump to retract proximally. All plantar incisions require
approximately 3 weeks of non-weight bearing thereafter. Complications of plantar
neurectomy include hematoma in dead space, and this is most often associated with the
dorsal longitudinal incisional approach. Hematoma predisposes to infection, and may
require suture removal and drainage. Vascular ischemia may also develop after neurectomy,
and is particularly likely following adjacent interspace dissection. If postoperative ischemia
is noted, avoid ice and elevation, nicotine and caffeine, excessive weight bearing, loosen
bandage, and administer bupivacaine posterior tibial nerve block, and consider using reflex
abdominal or popliteal heat (K-pad), as well as isoxsuprine IV 5 mg- 10 mg with careful
assessment of vital signs. Venous congestion may cause cyanosis, and elevation in this
case would be helpful. Recurrent intermetatarsal neuroma, also known as amputation or
stump neuroma, occurs in all cases of nerve resection. A symptomatic stump neuroma,
however, occurs in only about 10~ 15% of cases following excision of an intermetatarsa!
neuroma. Efforts to minimize the risk of symptomatic stump neuroma formation include
sectioning the nerve proximal to the proximal margin of the DTIL, epineurial closure over a
clot of thrombin or cyanoacrylate (not FDA approved) using 8-0 nylon simple interrupted
sutures. One may also bury the nerve stump in an adjacent metatarsal shaft. Silicone
capping and entubulation have not proven to be reliably effective in preventing
symptomatic stump neuroma formation. The ideal location for a sectioned nerve stump is
within well-vascularized, protected, intact skeletal muscle bellies, as is the condition within
the intrinsics ofthe foot wherein the plantar nerve retracts proximal to the DTIL Permanent
numbness of the contiguous surfaces of the involved digits and plantar interspace, as well
as loss of sudomotor and vascular smooth muscle tone, are anticipated.
Terminal Syme operation

for total nail removal
Hallux amputation
Fourth and fifth
ray resection
Transmetatarsal Lisfranc's amputation Chopart's amputation

amputation
Syme's amputation
Figure 7.63
Superficial Peroneal Nerve Entrapment (Henry's Mononeuritis}--this is most frequently

seen in active individuals, often involved in jumping sports or physically strenuous
occupations, or in older individuals who were once regular participants in such activities.
The pathology is localized to the deep fascial hiatus proximal to the ankle where the
superficial peroneal nerve emerges to enter the subcutaneous layer. It is usually
aggravated by peroneal muscle herniation through the hiatus, thereby impinging the nerve
and causing localized pain and paresthesia over the ankle and pedal distribution of the
nerves. Treatment involves local corticosteroid and nerve block, attention to any potential
causes of compartment syndrome, and recalcitrant symptoms may require surgical repair
ofthe skeletal muscle herniation and transposition of the intact nerve trunk. The branches
of the superficial peroneal nerve, namely the intermediate dorsal cutaneous nerve (IDCN,
Lemont's nerve) and the medial dorsal cutaneous nerve (MDCN), can also become
entrapped and, being located on the anterior aspect of the ankle and the dorsum of the foot,
these are particularly vulnerable to direct contusion as well as traction injury associated
with ankle inversion. Morever, they are vulnerable to iatrogenic involvement in association
with surgical dissection of these areas.
Amputations
The essential element in determining amputation level is tissue viability. Clinical
assessment, duplex Doppler ultrasound, and transcutaneous oxygen tension (Tc-p02) are
primary methods used to assess tissue viability, perfusion, and predisposition to healing. The
skin is warmed to 44~ C, and a Clark electrode is used to measure Tc-p02. Amputations are
likely to heal if the Tc-p02 is at least 40 mmHg, are questionable if the Tc-p02 is between
26-40 mm Hg, and likely to fail if the Tc-p02 is <26 mmHg. Surgical principles specific to
amputations include gentle handling of the skin, adequately wide flap pedicle, and
avoidance of skin tension or bony prominence. Bone resection and remodeling can be
performed with both power and hand instrumentation. Moreover, muscle insertions should
be maintained or recreated to avoid contracture deformity and severe muscular imbalance.
Preservation of muscle balance usually requires intraoperative decision making on the part
of the surgeon. Preservation of TA and PB tendons prevents equinovarus deformity.
Isolated digital amputation predisposes to adjacent digital transverse plane drift, and HAV
is likely following second toe removal. Hallux amputation predisposes to apropulsive
(pedestal) gait. During amputation, stump (amputation) neuroma formation should be
prevented by sharp sectioning under tension, with subsequent retraction proximally into
well-vascularized and protective skeletal muscle bellies. Epineurial closure may be helpful
on large nerve trunks. Planning should include use of a robust, sensate flap to cover the
stump. Hemostasis is critical, and vessels with lumens large enough to grossly visualize
should be ligated as compared to electrocoagulated. In general, transtibial amputations
are regarded as major amputations, and those distal to the tibia are considered minor
amputations. Pedal amputations include the following techniques: terminal Syme's
amputation, digital amputation and disarticulation, ray resection, transmetatarsal
amputation (TMA), Lisfranc amputation, Chopart amputation, Pirogoff amputation,
and Symes (ankle) amputation (Figure 7-63). The Symes amputation entails ankle
disarticulation with removal of the malleoli and proximal rotation of the heel pad to cover the
distal surface of the tibia. The Pirogoff amputation entails sectioning the talus and
calcaneus in line with the anterior margin of the tibia, thereby preserving the posterior portion
of the calcaneus, heel weight bearing surface, and the insertion of the Achilles tendon.
214 Reconstructive Foot and Ankle Surgery Ch. 8
RECONSTRUCTIVE FOOT AND ANKLE SURGERY:

COMPLEX CONDITIONS AND MAJOR DEFORMITIES
Complex conditions requiring major foot and ankle reconstruction often require combination
surgery. Repair may require major hindfoot or midfoot, or ankle, arthrodesis and adjunct soft
tissue manipulations such as tendon lengthening and/or transfer. These procedures can be
used to correct acquired, degenerative, or post-traumatic conditions, as well as neurologically
induced and congenital defects. Selected deformities amenable to major pedal recon-
structive intervention include advanced pes valgus, pes cavus, degenerative arthrosis, and the
rheumatoid foot. Congenital deformities will be discussed elsewhere. Deformities may be rigid,
or flexible and unstable. Selected procedures include triple arthrodesis, ankle and pantalar
arthrodesis, and Usfranc arthrodesis. At times, it may be applicable to perform isolated
intertarsal arthrodesis, or variations on midtarsal and intercuneiform fusion, as well as partial
tarsometatarsal fusion, based upon the needs of the individual case.
Collapsing Pes Valgoplanus (CPVP, Flexible Flatloot)-it is important to note that not all
flatfeet are pathological. Isolated sagittal plane arch depression, in the presence of a
perpendicular or minimally everted resting calcaneal stance position, is usually
asymptomatc and well tolerated throughoutthe individual's life with the exception of post-
traumatic degeneration or neuropathy. On the other hand, the presence of hindfoot
eversion, or pes valgus, is a strong destructive force during weight bearing and is
associated with steadily progressive articular subluxation and degenerative joint disease,
TP dysfunction, abnormal shoe wear, and difficulty walking or standing. A variety of
etiologies exist for CPVP, including: tibialis posterior muscle weakness, accessory
navicular iKidner foot), and chronic TP dysfunction; ligament weakness and laxity;
prolonged FF supinatus secondary to hyperpronation ofthe STJ and MTJ IFF and RFvarus,
flexible FF valgus, ankle equinus, and other pronating biomechanical foot types);
congenital or acquired calcaneovalgus; lower extremity torsional abnormalities such as
femoral anteversion; and Charcot collapse in its early stages.
Radiographic findings Associated with CPVP-standard radiographs include: AP view

Kite's angle (Kite's talocalcaneal angle) 30-50" reducing to 17-21" by age 5 years, with 75%
articulation of TNJ; lateral view CIA 18-21", talar declination angle 21", and lateral
talocalcaneal angle of 35- 50". Plana I dominance of deformity in flatfoot: transverse plane
dominance with increased Kite's angle, increased cuboid abduction, decreased FF
adduction; frontal plane dominance with superimposition of metatarsals, decreased first
met declination, decreased height of sustentaculum tali, midtarsal and STJ; sagittal plane
dominance with increased talar declination, navicular-cuneiform breach, and increased
T-C angle on lateral view.
Clinical Signs of CPVP-these include evidence of the Hubscher maneuver Itoe test of
Jack). indicative of flexibility. The Hubscher maneuver should cause the flexible flatfoot to
reform a medial longitudinal arch when the hallux is dorsifiexed and the patient externally
rotates the ipsilateral hip and leg, causing the heel to go into varus. A lateral radiograph can
be taken with the heel elevated to see if the medial column reduces, if not, there is a need
for medial column work in addition to other reconstructive procedures. In the young child,
simply have them attempt raise up on the ball of the foot and observe the heel go into varus,
which indicates a flexible deformity that will often respond well to supportive therapy while
the skeleton matures.
Ch. 8 Reconstructive Foot and Ankle Surgery 215
Surgical Repair of CPVP-indications for flatfoot surgery include: midfoot and tarsal
instability with associated FF hypermobility (HAV, flexor stabilizing HTs, MTPJ subluxation),
metatarsalgia, and plantar fasciitis; postural symptoms extending from the foot to the low
back; midfoot and arch pain, especially along TP and TNJ, as well as sinus tarsi; tight heel
cord with calf pain and inability to stand for iong periods of time; difficulty walking/running,
or performing other weight bearing activities; decreased activity level of youngster due to
symptomatic feet; failed non-surgical treatment such as foot orthoses and calfflexibility and
TP exercises. Contraindications to flexible flatfoot reconstructive efforts include rigid
flatfoot\convex pes valgus, tarsal coalition, paralytic); osseous equinus and extreme obesity.
CongeniTal gastrocnemius or gastrosoleus equinus often accompanies CPVP, and may be
contributory in the development of the deformity, and must be addressed with either
gastrocnemius recession or TAL, respectively, when the flatfoot is reconstructed. Similarly,
metatarsus adductus must be considered whenever medial arch enhancement, with or
without lateral column lengthening, is undertaken. Repair of CPVP effects FF adductus as
the medial arch elevates and TP becomes more effective. Therefore, it may become
necessary to address metatarsus adductus deformity in addition to repair of the CPVP.
Reconstruction ofCPVPtypica!!y addresses the triad of deformities including the medial arch,
lateral column, ankle equinus, and usually combines osseous and soft tissue manipulations.
As a rule, isolated soft tissue manipulations in the medial arch are inadequate without
associated osseous stabilization or lateral column lengthening. Surgical options include:
Extra~Articular STJ Bone Block Procedures Useful in Young Patients-a variety of

extra-articular blocking procedures are available for patients wherein arthrodesis is
not desireable.
Chambers procedure-indicated for children <8 years of age, wherein bone graft is
placed in the calcaneal sulcus of the sinus tarsi to inhibit adduction and plantar-
flexion of the talus on the calcaneus (Figure 8.1).
Baker and Hill procedure-calcaneal osteotomy and elevating bone graft under
posterior facet, to decrease vertical alignment of STJ and minimize adduction and
plantarflexion of talus.
Selakovich procedure-opening osteotomy and graft of sustentaculum tali, inhibiting

talar declination and adduction.
Subtalar Arthroereisis-STJ arthroereisis is also useful in young patients 4-8 years of age,
with CPVP displaying a transverse plane (TP) TC angle >30" and 50% TN articular congruity,
heel eversion of 8-10, and-FF varus of> 10 with superimposition of the metatarsals on the
Figure 8.1
216 Reconstructive Foot and Ankle Surgery Ch.8
lateral radiograph. This procedure can also be used in adults with CPVP, and is often used
in conjunction with other reconstructive procedures addressing the medial columnn and
triceps sura e. Arthroereisis uses synthetic polymer or metallic implant, rather than bone
graft, to block STJ pronation by impinging on the anterior margin of the leading edge of
posterior talar facet The implanted blocking plug is usually removed after the child has
achieved skeletal maturity and avoided the destructive, adaptive changes related to patho-
logical STJ/MTJ hyperpronation during the formative years. Specific techniques include:
Lelevre------si!icone polymer (SIIastic) plug positioned from_lateral to medial in the sinus

tarsi, thereby elevating the floor of the sinus (calcaneal sulcus) and blocking talar
adduction~plantarflexion. The polymeric plug has been criticized for instability,
displacement, and implant degradation.
StaPeg"-polyethylene plug positioned in the sinus tarsi, and noted to be more

stable and durable in comparison to the LeLevre procedure.
Villadot-an hour glass-shaped Sllastic<K: implant, also considered by many to be more

stable than the Lelevre design.
Va/ente----polyethy!ene plug with screw thread surface that actually screws into the
sinus tarsi using appropriately sized guides, designed to allow just 4-5o of STJ
pronation thereafter.
Maxwe/1-Brancheau M8A"'1itanium Subta/arlmplant---one of several highly refined

arthroereisis implants, the MBA"' probably has the longest record of clinical
successfuL It is a barrel-shaped, slotted implant made of titanium alloy that is readily
implanted by means of limited dissection and accurate sizing. The instrumentation
and surgical technique are welldeveloped. The implant is also easily assessed on
standard radiographs. Weight bearing in an immobilizing cast-bootfor approximately
2-3 weeks is commonly undertaken in the early postoperative phase. The implant can
be removed at a later date, or it can be retained permanently, depending upon the
requirements of the clinical course.
Medial Column Procedures--these focus on restoring joint stability, TPfunction, and arch
height (eliminate TN or NC fault), and include:
Kidner-excise os tibiale externum and transpose TP to plantar aspect of the

navicular.
Young-used to correct TN and/or NC fault in a flexible flatfoot with FF supinatus,

wherein theTA is rerouted through a keyhole slot in the navicular. McGiamry and Ruch
(Figure 8-2) have enhanced this procedure by specifically including advancementofthe
spring ligament, TP, and combining lateral column lengthening using the Evans open
calcaneal graft.
Lowman--TN arthrodesis combined with rerouting TA under the navicular and

suturing it to the spring ligament.
Figure 8.2
Mil/er-navicular~medial cuneiform combined with cuneiform-first metatarsal

arthrodesis, further combined with soft tissue reefing. This procedure results in much
shortening and it is difficult to achieve satisfactory bone-to-bone apposition without
interposition of corticocance!lous bone graft
Hoke--navicular to first and second cuneiform arthrodesis.
Cotton--dorsally-based opening wedge osteotomy of medial cuneiform, packed with

truncated corticocancellous bone graft; used to plantarflex the medial column.
Lateral Column Lengthenin[rlateral column lengthening enhances the stability and

longevity of medial arch reconstruction, and has proven to be highly reliable, readily
achieved, and associated with low morbidity and complication. The Evan's calcaneal
osteotomy and bone graft, or bone lengthening using corticotomy and callus
distraction with an external fixator, are the mainstays of lateral column lengthening.
Bone graft extension calcaneocuboid arthrodesis can also be employed. The highly
trabecular anterior portion of the body of the calcaneus readily heals, accepts
allogeneic corticocance!lous bone graft and bone transport manipulation, and is
ideally positioned to influence forefoot adduction (correct forefoot abduction by
reducing the calcaneocuboid abductus angle). Once again, attention must be paid to
pre-existing metatarsus adductus skewfoot deformity, and the metatarsus adductus
may require concomitant correction.
Evans Calcaneal Osteotomy and Bone Graft--this is the primary osteotomy used to
reduce forefoot abduction in the transverse plane iFigure 8-3). The procedure invo!ves
an opening osteotomy approximately 1.5 em proximal to the calcaneocuboid joint
(CCJ), preserving the ligaments and capsule of this joint, and directed from lateral to
medial through-and-through the anterior portion of the body of the calcaneus. The
osteotomy is distal to the posterior facet of the STJ, and it is extra-articular. A
trapezoidal block of allogeneic corticocancellous bone graft is then wedged into the
osteotomy, advancing the distal aspect of the calcaneus and CCJ, and adducting the
forefoot Autogenous bone graft could also be used, however the site is amenable to
alogeneic graft, and a secondary donor site wound is not necessary. Alternatively,
corticotomy and gradual distal transport of the anterior portion ofthe calcaneus can
be achieved, after an initial10-14 days of stabilization, using an adjustable external
fixator employing the principles of callus distraction osteotaxis.
Figure 8.3
Varus-Prod,.acing Calcaneal Osteotomies-varus~producing calcaneal osteotomies are

performed in the posterior aspect of the calcaneus, in patients >3 years of age. Fixation of
calcaneal osteotomies, both with and without bone graft, can be achieved with staples,
interfragmental compression screws, or absorbable pins (preferably without bone graft);
and postoperative non-weight bearing and immobilization are cruciaL Lateral approaches
to the calcaneus require that attention be paid to the course of the sural nerve, lesser
saphenous vein, and the peroneal tendons .. Specific procedures include:
Gleich--an oblique calcaneal osteotomy anterior to the posterior cortex that allows
medial shift of the posterior segment and relative adduction of the tuberosity and
posterior os cal cis.
Dwyer-a lateral opening wedge oriented

obliquely from the dorsal-to-plantar margins of
the calcaneus, midway between the posterior
margin of the posterior STJ facet and the
Achilles attachment, incorporating allogeneic
or autogenous corticocance!lous bone graft
insertion. It has also been described as a
medial closing calcaneal osteotomy, however
the contents of the tarsal tunnel can complfcate Figure 8.4
the dissection, and the procedure is not
commonly done in this fashion. The lateral
closing Dwyer osteotomy is a mainstay of pes cavus reconstruction \Figure 8-4).
Silver-an opening wedge bone graft pertormed via a lateral approach, wherein the
posterior aspect of the calcaneus and tuberosity are shifted plantarly, and medially.
Koutsogiannis-a versatile, frontal plane osteotomythrough the body of the calcaneus

midway between the posterior lip of the STJ and the Achilles insertion, allowing
triplanar correction ofthe posterior calcaneus and tuberosity via primarily medial and
plantar displacement.
Ch.8 Reconstructive Foot and Ankle Surgery 219
Pes Cavus-the etiology of pes cavus includes:
1. Muscular diseases such as muscular dystrophy,

2. Peripheral or spinal nerve lesions, such as Dejerine Sottas, Charcot Marie Tooth
\familial sensorimotor neuropathy, peroneal muscular atrophy), and polyneuritis
and/or trauma to peripheral nerves,
3. Spinal cord defects such as poliomyelitis (often effects paralytic flatfoot, also).
spina bifid a with myelomeningocele, diastematomyelia, and spinal tumors,
4. Spino-cerebellar defects, which are usually hereditary, including Roussy-Levy
syndrome, and Friedreich's ataxia,
5. Pyramidal and extrapyramidal tract lesions effecting spastic and athetoid
cerebral palsy,
6. Supratentorial conditions such as hysteria,
7. Congenital defects such as talipes equinovarus, and
8. Idiopathic pes cavus.
Etiopathogenesis hinges on muscle imbalances, often with spastic triceps surae and
deep posterior musculature, and anterior and peroneal compartment weakness causing
dropfoot. The first ray is usually plantarflexed as peroneus longus is unopposed. Extensor
substituion results chronic MTPJ subluxation, clawtoes, metatarsalgia, and inability to get
the heel to the ground. It is postulated that the extrinsic digital extensors overpower the
lumbricales. TP overpowers and supinates the foot and plantarflexes the ankle.
Classification of Pes Cavus-the classification of pes cavus can be confusing and

cumbersome, and several systems exist, including:
Apex of the Cavus Deformity--a common classification involves identification of the

apex of the cavus deformity. Anterior pes cavus can be described by the Sagittal Plane
(SP) shape of the foot as it relates to the dorsal apex of the deformity, as follows:
metatarsal, tarsometatarsal. lesser tarsal, and forefoot or midtarsal cavus.
Subcategories of anterior cavus include isolated medial or lateral column cavus, first
and fifth ray respectively, or global cavus wherein all of the metatarsal rays bear
weight more or less equally due to transverse plane symmetry of the plantarly declined
structures distal to the apex. Combinations of anterior cavus can also exist. Lower
extremity compensation for anterior cavus includes digital and MTPJ contraction,
effecting hammer and clawtoes and associated subluxation of the MTPJs; dropfoot
that often catches or scuffs across the substrate, and metatarsalgia with or without
plantar keratoma forma1ion. If the deformity is flexible, then loading the forefoot results
in a certain degree of metatarsal and tarsal dorsiflexion that, over time, can become
degenerative. Moreover, a certain degree of ankle joint dorsiflexion will also be used
to compensate for residual anterior cavus, thereby limiting available dorsiflexion
required for late stance propulsion. This relative limitation of ankle dorsiflexion is
referred to as pseudoequlnus, and functions to further load pedal structures and lead
to symptomatology. Pseudoequinus is more pronounced in rigid forms of anterior
cavus. Posterior pes cavus results from structural increase in the calcaneal inclination
angle, usuallywith adduction and varus of the hindtoot. Combined pes cavus typically
entails fixed frontal plane varus and a non-reducible rearfoot.
220 Reconstructive Foot and Ankle Surgery Ch.B
Three~Stage Classification of Pes Cavus-perhaps the most useful classification involves

3 stages of pes cavus, and focuses on options for surgical repair after failed non-surgical
efforts. The system includes:
Stage I Pes Cavus-entails claV\1oes and subluxated or dislocated MTPJs. Repair

evolves around digital stabilization with PIPJ arthrodesis and MTPJ relocation with pin
fixation. Adjunct procedures involve the Hibbs and Jones tendosuspensions, and
perhaps tendon transfer (STATI) to enhance ankle dorsiflexion.
Stage II Pes Cavus---entails those deformities of Stage I cavus, as well as heel varus
and more significantcavoadductovarus localized primarily to the distal to the midfoot
Reconstructive options are determined by the degree of flexibility, as determined by
the Coleman block testfor heel varus and plantarflexed first ray. Failure to establish a
perpendicular relationship of the posterior bisector of the heel to the ground when
the lateral column is elevated on a block, to eliminate the varus influence of a rigid
plantarflexed first ray on the hindfoot, indicates the presence affixed heel varus that
will require corrective osteotomy. Corrective procedures include the Dwyer closing
lateral wedge osteotomy of the calcaneus, dorsiflexory wedge o::.teotomy (DFVVO) of
the first ray, Jones and/or Hibbs suspension, and tendon transfer to the dorsum of the
footto enhance straight ankle dorsiflexion.
Stage Ill Pes Cavus-entalls marked, rigid, cavoadductovarus deformation, often of

neurological etiology, associated with adaptive arthrosis and serious dropfoot, and
typically requires Cole midfoot osteotomy or triple arthrodesis for correction. The Cole
procedure involves a through-and-through, dorsally based wedge resection of bone
positioned through the tarsal navicular and cuneiforms, and the cuboid, thereby
elevating the forefoot out of an equinus alignment The osteotomy, after reduction, is
stabilized with Steinmann pins or staples, and maintained non-weight bearing for up
to three months. The triple arthrodesis is a versatile procedure for correction of the
most severe cavus deformities.
Assessment ofthe Patient with Pes Cavus-assessment of the patient with pes cavus
requires a thorough family history that includes inquiry about parents, siblings, and
other blood relatives. Neurological examination, typically with neurology consultation
prior to surgery, should identify the presence or absence of spasticity, flaccidity,
muscular dystrophy, spinal and other CNS defects; as well as familial diseases that
may require genetic and social counseling. Nerve conduction velocity and EMG may
be in order. Pedal and ankle, as well as spinal radiographs if spina bifida or other
defect is suspected, should be obtained. Radiographically, the apex of the cavus
deformity should be identified and the deformity classified in this regard. The
radiographic evaluation of pes cavus should be performed weight bearing, and
include AP, lateral and lateral oblique projections, with consideration given to ankle
films. The lateral radiograph will show increases CIA >30, norma! to posterior break
in the SP cyma line, accentuated or bullet-hole sinus tarsi, SP long axis of the neck of
the talus passes superior to the long axis of the first metatarsal, and dorsally based
wedge shaped cuneiform& An axial view of the calcaneus at 45 should be obtained
to rule out a structural heel varus.
Surgical Procedures for Correction of Pes Cavus~procedures for the correction of pes
cavus vary depending upon the degree of flexibility.
Flexible Pes Cavus-procedures useful for correction of flexible pes cavus include the
Steindler stripping, wherein the plantar fascia and intrinsic musculature is reflected from
the plantar calcaneal cortex, and may be useful only if the deformity is flexible and not of
bony rigidity. A Hibbs suspension may also be combined with the Steindler stripping in a
flexible deformity. Tendon transfers such as the STAn and PLH or TPH are often used to
balance inverter/everter imbalance in flexible deformity. Digital fusion and MTPJ relocation
are crucial to the treatment of both flexible and rigid pes cavus.
Rigid Pes Cavus-for rigid deformity, where the Coleman block test failed to eliminate heel
varus or the medial column is rigidly plantarflexed, a first metatarsal base DFWO combined
with a Dwyer lateral closing osteotomy of the calcaneus, perhaps with the STATT, is a
useful combination (Stage II pes cavus). It may also be useful to transfer TA dorsally into
the base of first metatarsal and perform a plantar opening wedge osteotomy with bone
graft of the medial cuneiform, along with a Jones suspension of the first ray. If fixed bony
equinus is localized to the lesser tarsus and midfoot, the Cole osteotomy is indicated
(Figure 8-5). The Cole osteotomy is performed as a dorsally based wedge resection of bone
and joint through the navicular-cuneiform and cuboid level. A first metatarsal OFWO may
also be necessary, and adductovarus deformity can be addressed by manipulating the
forefoot on the hindfoot at the level of the osteotomy. The Cole should only be performed
on a skeletally mature foot, as shortening will ensue. The Japas osteotomy can be used for
less severe, rigid pes cavus, and involves a transverse plane V-osteotomywith the apex in
the navicular and the wings diverging distally through the cuneiforms and cuboid on the
medial and lateral aspects, respectively {Figure 8-6). The Japas causes less shortening
than does the Cole, however it is difficult to address adducto varus deformity. In
youngsters with open growth physes, in the presence of pan metatarsal global equinus, first
metatarsakuneiform dorsal opening wedge osteotomy with bone graft, along with pan-lesser
metatarsal DFWD may be used.ln the adult, pan metatarsal DFWOs may be considered. The
triple arthrodesis remains the most versatile and powerful reconstructive procedure for
repair of severe pes cavus, which is often of neurological etiology (Figure 8-7).
Charcot Foot Reconstruction-Charcot deformity and treatment are described in Chapter 3.
Rheumatoid Foot Reconstruction and Panmetatarsal Head Resection---when treating the

patient with rheumatoid arthritis, it is necessary to consider the patient's physiologic age,
general medical status, immunocompromise status, bone stock, wound healing capacity,
systemic corticosteroid supplementation, and current as well as anticipated weight-
bearing activity level. The combination of deformities caused by rheumatoid arthritis
mutilans is generally referred to as the rheumatoid foot The rheumatoid foot will usually be
symptomatic in either the forefoot or hfndfoot/ankle. The majority of symptomatic
presentations involve the forefoot, which displays claw or hammertoes, subluxated to
dislocated MTPJs, plantar metatarsalgia with or without IPK and/or rheumatoid nodules.
Excessive mechanical overload can effect ulceration and underlying bone infection.
Hindfoot and ankle involvement usually entails TP synovitis and chronic dysfunction,
rheumatoid nodules of the plantar and posterior heel, retrocalcaneal enthesitis, and
severe pes and ankle valgus deformity. The patient often adapts a pedestal gait with antalgic
c
Figure 8.5
Figure 8.6
E~
Figure 8.7
guarding. Fundamental non~surgical treatments include periodic, palliative skin and nail
care, accommodative foot orthoses, extra-depth shoes with an external roller sole, and
other supportive measures that hinge upon adequate systemic disease modulation under
a rheumatologist's guidance.
Rheumatoid Foot Reconstructive Surgical Techniques-techniques useful for repair of the

rheumatoid foot include: synovectomy, excision of rheumatoid nodules, digital stabilization,
Keller arthroplasty, pan metatarsal head excision, first MTPJ fusion along with lesser
metatarsal head excision, MTPJ and/or IPJ endoprosthesis, and arthrodesis of the greater
and/or lesser tarsus and ankle. Systemic corticosteroid supplementation and prophylactic
antibiotics are in order. Postoperative non-weight bearing can be difficult, and
immobilization can be detrimental to subsequent joint movement. Occupational and
physical therapy should also be considered.(Note: digital arthrodesis, Keller arthroplasty,
endoprosthesis implantation, and first MTPJ fusion have been described elsewhere in this
manua!). In regard to the use of first MTPJ endoprosthesis in rheumatoid patients,
multicomponent total joint replacement is common, although the use of silicone polymer
total hinged implants can also be useful. In these patients, however, endoprosthesis
probably offers little more in comparison to Keller arthroplasty. Importantly, implantation
requires the presence of adequate bone stock, and perhaps metatarsal osteotomy to
correct angular deformity. Other useful procedures include:
Panmetatarsal Head Resection-this is performed to eliminate pain and cutaneous

compromise, and maintain a pedestal gait Hoffman described excision of all five metatarsal
heads, while Clayton recommended excison of a portion if not all ofthe proximal phalangeal
bases 1f they were large or osteophytic. Proximal phalangeal base resection is wrought
with subsequent digital instability and may require syndactylization to effect stability.
lncisional options include transverse plantar, orfive or three dorsal longitudinal incisions.
The more severely dislocated MTPJs and clavvtoes invite a transverse plantar incision with
an elliptical excision of redundant plantar skin and postoperative non-weight bearing. The
subcutaneous fat layer should remain attached to the skin, and intermetatarsal dissection
should be avoided. The five incision approach includes a wound over each metatarsal,
while three dorsal incisions are localized to the first ray, between the second and third and
between the fourth and fifth toes respectively. Separate dorsal incisions are used to
perform PIPJ arthrodesis of the second through fourth and arthroplasty of the fifth. The
preferred length pattern after metatarsal head resection is: 2 = 1> 3 >4 > 5. The metatarsals
are transacted distally from dorsal to plantar and the plantar cortex rasped smooth. The
first metatarsal is also angulated from distal lateral to proximal medial, while the third-fifth
metatarsals are angulated from distal medial to proximal lateraL Most commonly, fusion of
the PIPJs 2 through 4 and arthroplasty of the fifth toe are performed along with the
metatarsal head excision, and for added stability a K~wire is directed through the PlPJ
fusion and into the metatarsals. The combination of first MTPJ fusion with lesser
panmetatarsal head excisions can be very usefuL Postoperatively, a protective cast boot
works well. Some shortening of the foot can be expected, but the patient should maintain
an apropulsive gait
lislranc Arthrodesis-arthrodesis of all or part ofthe tarsometatarsal joint(TMJ, Lisfranc's

joint) is useful in the treatment of post-traumatic or degenerative arthritis, Charcot foot
associated with ankle equinus, and other maladies localized to this level (Figure 8-8).
Isolated first metatarsal-medial cuneiform arthrodesis (Lapidus procedure), as previously

noted, can be used to stabilize the medial column and may be used to correct severe HAV
deformity with associated metatarsal-cuneiform instability, hypermobility of the first ray and
long-standing forefoot supinatus. Arthrodesis of Lisfranc's joint complex usually involves 3
dorsal incisions, the first medially over the medial column, the second and third between the
second and third, and fourth and fifth metatarsals, respectively. Fixation is achieved with a
plate and interfragmental compression screw pia cement across the first metatarsal-medial
cuneiform fusion site, Steinmann pins or crossed K-wires or single interfragmental screws
across the lesser metatarsal-cuneiform and cuboid fusion, or perhaps a plate and screws
across the fifth metatarsal-cuboid site. Specialized locking plates may also be used at this
site. Furthermore, achieving primary rigid internal compression fixation of the medial
column, in conjunction with splintage ofthe lesserTMJs, is an example of the vassal rule
of internal fixation and serves as a common approach to Usfranc arthrodesis.
Triple Arthrodesis-this is a versatile procedure that is applicable in cases that include

collapsing pes val go planus, tarsal coalition, convex pes valgus, tarsal arthritis, pes cavus,
residual clubfoot, neuromuscular disease, and others. Triple arthrodesis enables the
surgeon to orientthe foot in relation to the leg and ankle, and to manipulate the relationship
of the forefoot to the hindfoot. It also affords a stable hindfoot upon which the tendons of
the extrinsic pedal musculature can function. The classic Oilier incision can be used for
the triple arthrodesis, and courses from the tip of the fibular malleolus, across the sinus
tarsi then on to the dorsal aspect of the talonavicular joint The Oilier incision is applicable
in the cavus foot, however predisposes to difficulty exposing the TNJ in the valgus foot In
the valgus foot, a 2-incision approach is preferred, and most surgeons use the 2-incision
approach even for pes valgus correction. The lateral incision extends from the tip of the
lateral malleolus to the dorsum of the junction between the fourth and fifth metatarsal bases,
and provides excellent exposure of the STJ and CCJ. The medial incision extends from the
anterior margin. of the medial malleolus longitudinally to the first metatarsal-medial
cuneiform joint, and provides excellent exposure of the TNJ and neck of the talus. The
lateral dissection proceeds through the superficial fascia to the deep fascia, which is incised
longitudinally between EDB and the PB tendon Care is taken to preserve the peroneal
sheath. EDB is reflected away from the CCJ, and the intertarsal talocalcaneal ligament and
sinus tarsi are evacuated. The lateral aspect ofthe head and neck of the talus are exposed,
and the peroneal tendons are retracted plantarly to expose the posterior facet of the STJ.
Medially the dissection should avoid the medial marginal vein, and the deep fascial incision
is made medial to the tendon ofTA. A medial periosteal and capsular incision exposes both
the TNJ and the anterior margin of the ankle. The technique of osseous resection is crucial
A B
Figure 8.8
when performing the triple arthrodesis {Figure 8~9). Preoperative assessment of the
relationship between the foot and leg enables the surgeon to take into consideration knee
and ankle positions so that proper placement of the hindfoot can be achieved. The hindfoot
should be positioned in slight valgus, and varus should be avoided at all costs. A varus
hindfoot fusion is destined to marked weight bearing difficulties, pain, and ankle instability
postoperatively. The foot should be positioned in about 12-15 of pes abductus, when the
knee is on the frontal plane. Less pes abductus is needed if the knee is externally rotated,
and more may be useful in the presence of medial knee position or tibial torsion.
Resection proceeds from the MTJs to the STJs, as MTJ resection enables easier
access to the STJ. The foot is held in a reduced attitude and the CCJ and TNJ are resected
with the blade parallel to the articulations in most cases. Severe adductus or abductus may
warrant transverse plane wedging, however a flush resection preserves bone mass and
correction can usually be satisfactorily achieved via translocation of the forefoot on the
hindfoot without the need for specific wedge resection. Similarly, a near~para!lel resection
ofthe STJs (posterior, medial and anterior facets) is usually adequate, as only slight valgus
positioning will suffice. STJ wedging may be more pronounced if the frontal plane deformity
is severe. The calcaneus is translocated medially for correction of pes valgus, and laterally
for correction of pes cavus. Sagittal plane correction is also corrected primarily via
translocation of the forefoot on the hindfoot, after achieving the desired talocalcaneal
alignment The calcaneus can also be shifted posteriorly to increase the lever arm for the
tendoAchillis and to increase sagittal plane talar declination and thereby increase arch
height. Contrari!y, sliding the calcaneus anteriorly relative to the talus dorsiflexes the talus
and decreases arch heightAchilles function. The desired alignment is temporarily stabilized
with cannulated screw guide pins, and intraoperative radiographs in the AP, lateral, and
calcaneal axial projections are obtained and reviewed. The order of stabilization generally
proceeds from STJ to TNJ to CCJ, and is usually achieved with three 6.5-7.0 mm
interfragmental compression screws (Figure 8-10). The TC fusion is achieved with a !ag
screw directed from the neck of the talus dorsally, into the body of the calcaneus. In a
similar fashion, the TNJ and CCJ are stabilized with distal to proximal lag screws.
Care is taken to avoid the following fixation hazards: violation of the medial cortex of
the body of the calcaneus and entrance of the fixation device into the tarsal tunnel when
fixating the TC interface, entrance of the TN fixation into the ankle, and fracture of the
dorsolateral cortex of the cuboid with the screw head. Additional intraoperative radiographs
should be used to reassess final fixation if any questions exist. The TC lag screw can also
be directed from the apex of the calcaneus posteroMplantarly into the body and neck of the
talus. The MTJs can also be satisfactorily stabilized, each with two staples oriented 90 to
each other. Closure proceeds in layers following placement of drains medially and laterally,
and the foot is secured in a BK Jones compression immobilizing dressing. Aftercare
involves drain removal after 24 to 72 hours, redressing between 3 to 5 days, and BK cast
immobilization without weight bearing for up to 3to 4 months. Mobilization of the ankle and
MTPJs can be undertaken in a non-weight-bearing attitude as soon as desired, and
immobilized partial weight bearing can be initiated by 10 to 12 weeks pending clinical
and radiographic findings. Full weight bearing ensues thereafter, as does conversion to
desired shoes.
Ankle and Pantalar Fusion-the most common indication for ankle fusion is post-traumatic
arthrosis following ankle fracture, wherein a small proximal and lateral shift of the lateral
malleolus has produced mortise incongruity resulting in articular cartilage degeneration. It
Figure 8.9
Figure 8.10
has been shown that a 1 mm shift can result in greater than a 40% decrease in tibiotalar
congruity. The most common predisposing causes of the need for pantalarfusion is severe
cava adducto varus deformity with chronic ankle instability, and avascular necrosis of the
talus for whatever reason. Other indications for ankle and pantalar fusion include
destructive bone tumors, infection, and failed ankle endoprosthesis. Evaluation of the
patient requires inspection ofthe knee, leg, ankle, STJ and MTJ, and the relationship of the
forefoot to the hindfoot and leg. The ideal position of fusion is 90' of the foot relative to the
leg, with slight ankle and/or hindfoot valgus, and approximately 10-12' of pes abductus. If
tibial varum is present, increase the amount of valgus to adjust for the added varus
deformity. The surgical approaches to ankle fusion include Charnley's transverse anterior
incision, extending from one malleolus to the other, which is rarely used currently because
of risk of injury to anterior neurovascular and tendinous structures. The lateral
transmalleolar hockey stick incision is most commonly used, and begins over the junction
of the middle and distal thirds of the fibula, then curves distally toward the sinus tarsi for the
ankle fusion, and onward toward the junction of the bases of the fourth and fifth metatarsals
for pantalarfusion. This approach yields anterior, lateral, and posterior exposure forfibufar
osteotomy. An accessory medial incision over the anterior margin of the medial malleolus
is usually combined with the transfibular incision to provide anteromedial exposure for
resection of the cartilage of the medial malleolus and enables hardware placement through
the tibial pilon. When performing ankle fusion, we are looking to position the large
cancellous mass of the tibial metaphysis in rigid apposition to the trabecular bone of the
body ofthe talus.
Techniques to Achieve Ankle Fusion
1. Curettage of cartilage with interposition aI bone graft;

2. Sliding inlay graft from the anterior surface of the tibial metaphysis into the talar
neck/body;
3. Modified Ga!lie fusion wherein allogeneic graft is inserted anterolaterally and
stabilized with a staple;
4. Transmalleolar (either fibular or tibial) with osteotomy to enhance visualization of
the tibiotalar interface;
5. The subtotal fusion for debilitated patients that cannot sustain extensive bone
resection and trephine plug joint resection with dowel graft fusion will suffice;
6. Compression arthrodesis using any of a variety of external fixation devices or
interfragmentallag screws; and
7. The Blair tibiocalcaneal fusion which can be useful post*polio or after collapse
of the talus.
As with all fusion procedures, Glissane's criteria must be met for successful arthrodesis:
1. Removal of cartilage, fibrous tissue, or other material hindering raw bone

contact;
2. Accurate and close fitting of surfaces;
3. Optimal position of fusion; and
4. Maintenance of apposition in undisturbed fashion until fusion is complete.
The Podiatry Institute technique of ankle and pantarlarfusions entail the use of:
1. A lateral hockey stick incision;

2. Preservation of the fibula (avoid osteotomy);
3. Cartilage resection with preservation of as much ofthe talar body as possible;
4. Ancillary medial approach for removal of medial malleolar and talar body
cartilage;
5. Temporary stabilization with cannulated screw guide pins;
6. Fusion alignment of 90" of the foot to the leg;
7. 10-12" pes abductus and slight ankle/hindfoot valgus;
8. Intraoperative radiographs in the AP, lateral, and calcaneal axial views;
9. lnterfragmental compression fixation wrth crossing 6.5~7.0 mm cancellous
screws;
10. Placement of the fibular on lay graft with interfragmenta! compression screws
purchasing the tibia and talus (and calcaneus in pantalar fusion);
11. Be sure to allow a gap between the proximal and distal segments of the
osteotomized fibula in order to avoid pseudoarthrosis or nonunion;
12. Repeat intraoperative radiographs to ascertain fixation and bone alignment;
13. Place and activate closed suction drains, bandage and immobilize;
14. Plan to leave hardware in indefinitely or at least6 to 12 months; and
15. Be sure not to penetrate the STJ with fixators if only ankle fusion is performed.
228 Reconstructive Foot and Ankle Surgery Ch.B
Complications of ankle and pantalar fusion include infection (reported as high as 20% in the
literature); nonunion, malunion, and pseudoarthrosis; malposition due to operative
misadventure (most often varus or calcaneus); stress transfer to MTJ and STJ (may need
triple later if only ankle fusion originally performed); and limb shortening if bone graft is
not used.
Total Ankle Replacement (TAR) Arthroplasty-chronic ankle pain that is not responsive to
other treatments, as well as the potential complications related to ankle arthrodesis, have
prompted the quest for a total ankle replacement (TAR) that is reliable and effective. Severe
ankle pain, deformity and dysfunction that serves as a constant impediment to weight
bearing ambulation, often due to arthritis secondary to rheumatoid disease, trauma, joint
sepsis, or osteoarthritis, can be treated by means of TAR. There are basically 2 types of
ankle endoprostheses: 1) 2-part prostheses that are either constrained, semiconstrained
or nonconstrained; and 2) multi-axial 3-part prostheses that include a free gliding
interposition aI core. These devices have been under development since the 1970s and have
yet to be perfected, and the long term results have not be promising for any particular
device, so far. Earlier models were secured with cement, however most surgeons prefer
cementless models. Common complications of TAR include loosening without the presence
of infection, and postoperative dehiscence. Ankle geometry and soft tibial metaphyseal
bone contribute to aseptic loosening, and this complication is most common when a
constrained system is used. Unconstrained systems, on the other hand, are associated with
instability, ankle deformation and subsequent loosening. Difficulties mimicking ankle
geometry stem from the factthatthe ankle is not a true ginglymus (hinge) joint, and the path
of the center of motion evolves as the ankle goes through its range of motion. Current goals
of ankle en do prosthesis design focus attention on the normal contours of the talar dome and
the distal tibial bearing surface, and minimization of the amount of bone resection required
to secure the implant. A number of options exist for TAR, including the Scandinavian
Total Ankle Replacement (STAR) (Waldemar Link GmbH & Co., Hamburg, Germany), a
3-component device; the Agility'" Total Ankle System (DePuy, Inc., Warsaw, IN), a
2-component device; the TNK Ankle (Kyocera Corporation, Kyoto, Japan), a 2-component
device; and the Buechel-Pappas Ultra Total Ankle Replacement (Endotec, South Orange,
New Jersey), a 3-component device. The main alternative to TAR is ankle fusion, and both
procedures aim to alleviate pain while TAR also aims to improve function. While both
procedures are designed to reduce pain, TAR is also intended to improve function. If TAR
fails, then consideration is given to arthrodesis, the standard therapy option for ankle
arthrosis and the mainstay of salvage following failed TAR. Salvage after failed TAR often
requires the use of substantia! amounts of bone grafting. To date, unlike the results of hip
and knee arthroplasty, the long-term results of TAR have not been as successful. Although
there are many case series describing the benefits and shortcomings of different types of
TAR, further investigation is necessary to determine the best options for patients with
recalcitrant anlde arthrosis.
Ch.9 Congenital Deformities and Juvenile Surgery 229
COIIIGEI\IITAL DEFORMITIES AN II JUVENILE SURGERY

Congenital deformities can be familial, inherited traits, or they may present without a known
family history. The condition may be idiopathic; or a known etiology such as an identified
genetic defect, intrauterine or birth trauma, hypoxia, teratogenic drug or toxin exposure,
tumor or other cause may exist Some defects present as a component of a known
syndrome and other defects, both physical and mental, may be identified.
Macrodactyly (Localized Gigantism)--this idiopathic, rare, usually unilateral, congenital

defect displays abnormal largeness of a single or multiple adjacent toes. It may be related
to or caused by hyperplastic lymphatiC or vascular elements, or neurofibromatosis; and
usually occurs as an isolated defect without familial inheritance. In static macrodactyly,
the giant digit(s) display a growth rate proportional to the remaining norma! parts. In
progressive macrodactyly, the giant digit(s) display a more rapid growth rate than normal
tissues. Treatment consists either of partial or total amputation of the giant part, or
sequential operations to reduce excess soft tissue and bone in a staged fashion (Figure
91 ). Reconstructive efforts can be difficult and convey a high rate of complication.
A~~v ~
D~
{)
B
Figure 9.1
c~
Syndactyly-this is the most common congenital deformity of the foot and hand, and is
marked by partial or complete persistence of the interdigital web. The condition is familial,
and can occur unilaterally or bilaterally. The defect occurs during the sixth to eighth
intrauterine week, and most commonly localizes to the second-third toes. Simple syndactyly
involves only fusion of the skin and soft tissues of the adjacent toes, while complex
syndactyly involves fusion of the soft tissues, nails, and bone. Single syndactyly involves two
toes and one web, double syndactyly involves three toes and two webs, and triple
syndactyly involves four toes and three webs. Treatment is usually based not on physical
dysfunction, but rather on psychological or emotional concerns ofthe older child or adult
Surgical desyndactylization can be difficult, and techniques involve creation of dorsal and
plantar skin flaps or use of dorsal and plantar W-plasties (Figure 9-2A), or application of a
FTSG (Figure 9-28) after incislonal separation. Osteotomy may be necessary in cases of
complex syndactyly.
230 _ _ _ ___':C:C,oll\ngl"ellin''ttaa".'lD~e'!'fo~rmm1ilti'e_s_an_d_J_u_ve~n~ile~S~u~rg~e~rv
_ , _ _ _ _~~
Ch. 8
A B c
Figure 9.2A
A B
c
Figure 9.28
Ch. 9 Congenital Deformities and Juvenile Surgery 231
Polydactyly-this is a common congenital anomaly consisting of an accessory

(supernumerary) digit or digits. The condition is idiopathic and an irregular autosomal
dominant inheritance has been suggested. Preaxial polydactyly involves duplication of the
hallux, while postaxial polydactyly involves duplication of the fifth toe. Postaxial polydactyly
occurs in approximately 80% of cases, preaxial in about 15% of cases, and central ray
duplication occurs in about 5% of cases. Mixed polydactyly involves pre- and postaxial
duplication, and is observed most often in black individuals. Duplication can be either of an
entire extra digit complete with bone (Type A), or of a rudimentary or vestigial toe (Type B).
Polydactyly occurs bilaterally in about 50% of cases. Six radiographic patterns are seen with
extra digits, including the short block metatarsal, Y-shaped metatarsal, T-shaped metatarsal,
normal metatarsal shaft with wide head, partial or complete ray duplication, and normal
metatarsal with distal phalangeal duplication (Figure 9-3). Syndactyly can occur in addition
to polydactyly (synpolydactyly). Surgical treatment entails identification of the digit that has
the most potential for normal growth and function, as duplication can involve bone, tendon,
vessels, and nerves. Amputation should allow the foot to assume the most normal contour
and facilitate wearing a shoe. Usually, the most medial digit is amputated in preaxial
polydactyly while the most lateral digit is amputated in the postaxial state. Amputation for
preaxial polydactyly, involving disarticulation of the extra medial toe is associated with the
development of postoperative hallux varus, and K-wire stabilization across the MTPJ with
recession of abductor hallucis are recommended. In cases of postaxial polydactyly,
preserve robust skin (usually plantar) for coverage and closure over the lateral aspect of the
new fifth ray. In case of an abnormal metatarsal configuration (Y or T), the prominent portion
of bone should be osteotomized flush with the metatarsal shaft, and a wide metatarsal head
should be made more narrow with osteotomy perpendicular to the growth physis in an
effort to avoid growth disturbance. Central ray duplication can be managed with a dorsal
racquet shaped incision at the base of the toe, and disarticulation and/or osteotomy at the
appropriate level
Block met
.,
1
i~ Nocmal mel w/
J1 digital duplication
Figure 9.3
232 Congenital Deformities and Juvenile Surgery Ch.B
Congenital Hallux Varus-this deformity involves an adductus and/or varus deviation of

the hallux at the first MTPJ, and is usually observed as a complication of hallux valgus
surgery. Congenital hallux varus can be observed as a consequence of neuromuscular
disease, and often accompanies metatarsus primus adductus/varus. The Thompson
procedure involves abductor halluc.is recession and tendon lengthening, or actual excision
of the muscle, and may be used in the infant or juvenile with congenital hallux varus due to
non-spastic contracture of this muscle. This technique conveys risk of overcorrection and
hallux valgus.
Congenital Hallux Abductus lnterphalangeus (Ungual Phalanx Valgusl-this rare

congenital anomaly displays abduction and valgus positioning of the hallux, with the apex
of the deformity at the hallux IPJ. Radiographically, the phalangeal primary centers
appear at birth, and the secondary center between 2-3 years. By 2-3 years of age,
enlargement of the medial aspect ofthe distal phalangeal base can be observed. Surgical
treatment entails excision of the medial aspect of the distal phalangeal base and growth
p!ate arrest, or Akin osteotomy.
Congenital Curly (Underlapping) Toe-this familial, idiopathic anomaly can involve any of
the lesser toes and occurs uni~ or bilaterally. Adductovarus underlapping of a lateral toe
beneath its medial neighbor is most common, however abduction and vaiQus can also occur.
Treatment entails interphalangeal arthroplasty and derotational skin wedge plasty (Figure
9-4 A, B, and Cl.
Congenital Overlapping Filth Toe-this anomaly usually affects the fifth toe overriding the
fourth, with adduction and varus, and dorsal soft tissue contracture in a proximal and
medial direction. The second toe overriding the first is the next most common form of
congenital overlapping toe. As the individual matures, IPJ plantar contracture and hammer
or claw toe ensues. Nonsurgical treatment includes taping or use of a digital retainer to try
to redirect the digit in the infant or youngster. Surgical options include amputation, (which
Figure 9.4A
A
~
w
)
B
A B '
''
Figure 9.48 Figure 9.4C
c~
A
B
Figure 9.5
is a rather undesirable approach), as well as sequential release of the deformity and

reconstruction. The Butler procedure entails use of racquet-shaped incision, EDL
lengthening, MTPJ capsulotomy (Figure 9-5). The McFarland procedure involves excision
of skin of the web between the fourth and fifth toes, EDL lengthening, MTPJ and PIPJ
capsulotomy, and syndactyly of the fifth-to-fourth toe. The Podiatry Institute technique
involves a dorsal Z-plasty, EDL lengthening, MTPJ capsulotomy, PIPJ arthroplasty,
excision of redundant plantar skin wedge, and K-wire stabilization.
Cleft Foot (lobster Foot , Claw Foot)-this rare, familial, congenital anomaly displays
absence of part or all of the central rays, effecting a claw-like foot The defect can present
either unilaterally or bilaterally. Associated defects include syndactyly, polydactyly, cleft
palate, deafness, and many others. Surgical treatment focuses on establishing a functional
limb, and a footthat can be shod. Each case is unique and no specific procedure is always
applicable. Surgery usually combines soft tissue and bone surgery, such as skin and bone
grafting, arthrodesis and osteotomy.
Brachyrnetatarsia-this hereditary anomaly is characterized by premature closure of the

epiphyseal plate of one or more metatarsals, and most commonly affects the fourth
metatarsal although any or multiple metatarsals can be affected. Associated maladies
include Down's syndrome, pseudohypoparathyroidism, and poliomyelitis. The defect is
usually not recognized at birth, however becomes evident between 4~15 years of age.
Although usually unilateral, brachymetatarsia can occur bilaterally. Surgical treatment has
traditionally hinged on one-stage autogenous bone graft elongation of the affected
metatarsaL This technique, as well as elongating osteotomy such as the Giannestras
step-down, and other sliding shaft designs, are limited by skin and neurovascular
compromise secondary to excess lengthening. Skin plasty and Z-lengthening of tendon, as
well as staging and soft tissue expansion techniques can be useful in this regard. More
recently, bone transport with the mini external fixation has proven to be most effective and
very safe as the soft tissues can gradually elongate along with the bone. Postoperative non-
weight bearing is used for up to 2~3 months pending radiographic evidence of bone healing.
Metatarsus Adductus-this transverse plane deformity displays medial deviation of the

metatarsals with the apex of the deformity at Usfranc's articulation. Metatarsus adductus
IMAdd) occurs in 1 out of every 1,000 live births, is familial, and the presence of the
deformity conveys a 1 in 20 chance that a sibling will also have the anomaly, and it occurs
bilaterally in 55% of cases. Clinical findings include a C-shaped foot with convex latera! and
concave medial borders in the transverse plane, adducted metatarsals with the more
medial metatarsals being more adducted (1>2>3>4>51. a high arch if there is no STJ
compensatory pronation, a skewfoot (toes abducted, metatarsals adducted, tarsus
abducted) with heel valgus if compensatory STJ pronation is available, separation between
the first and second digits, inability to abduct the metatarsals past midline of the foot,
hypertonicfty and spasm of tibialis anterior in gait or upon striking in open chain, and
possible hyperactivity of abductor hal!ucis.lfthe hindfoot is in rigid equinus and varus, rule
out clubfoot. Total MAdd involves all five metatarsals, whereas atavistic MAdd localizes to
the first ray, and is termed congenital metatarsus prim us adductus or varus. MPV displays
a first intermetatarsal angle of 10 or greater. Radiographic assessment of MAdd is
necessary to quantify the degree of deformity. The AP view is used, and the long axis of the
lesser tarsus or that of the second cuneiform can be compared to the long axis of the
second metatarsai(Fig 9-6). Using the long axis of the lesser tarsus, the normal met-add
angle is 15-21, and 25 when using the middle cuneiform reference. The Podiatry Institute
radiographic classification system employs the long axis of the lesser tarsus, and defines
met-add as follows: normal(rectus foot) 0-15", mild 16-25', moderate 26-35", and severe
>35. Jn the AP view, long-term compensation will show moderate~severe hallux abductus,
cuboid abduction, and digital abductus as toes align with reatfoot, and increased Kite's
talocalcaneal angle as the talus adducts medial to the navicular. ln the lateral view of
the compensated deformity, an anterior break in the cyma line indicates hyperpronation
and is usually associated with a decreased CIA. The uncompensated toot will display
characteristics of pes cavus.
LTAx
Lesser tarsal axis {LTAx) represents

perpendicular to bisector of lesser
Points plotted for deremination of tarsus. Line "EF" is bisector of
logitudinal bisection of lesser tarsus. lesser tarsus. Line "G" is bisection
of second cuneiform.
Figure 9.6
Conservative treatment can be effective if instituted in a timely fashion. For patients <3
months of age, manipulation, taping or casting, can be effective. For patients <3 years of age,
altering sleeping habits to avoid adduction, use of the Ganley splint or corrective casting are
useful. Cast therapy involves three point bending of the foot in the transverse plane (Figure
9-71, and should be maintained an additional period of time equal to half of the time that was
required to eliminate the deformity. If cuboid abduction increases, then over correction is
occurring and casting should be discontinued. The BK cast should entail limited padding,
and effect abductory force at the first metatarsal head and medial aspect of the heel, with
an adductory force applied to the cuboid-fifth metatarsal junction. The hindfoot and ankle
are maintained in neutral position. Medial tibial torsion, if present, can simultaneously be
addressed with an AK derotating cast The cast is changed every 1-2 weeks. Following
correction, a reverse last shoe may be useful for up to 6-12 months.
Surgical treatment is indicated in patients >2 years of age who have reached an
impasse with nonsurgical methods, and offer treatment options for patients up to 8 years
of age. The Heyman, Herndon and Strong (HHS) procedure is performed through either a
transverse or three longitudinal incisions, and entails sectioning of the medial 2/3 of the
capsule and ligaments of the tarsometatarsal joints, followed by K-wire stabilization and
casting. The Thompson procedure can be used in the infant or youngster to correct hallux
varus associated with metatarsus primus adductus or varus. Johnson's chondrotomy
technique entails laterally based (medial apex) wedge resection (2.5 mm) of the
cartilaginous metatarsal base of the lesser metatarsals and a closing abductory base
wedge, distal to the physis, on the first ray; in addition to lengthening abductor hallucis. The
Lange procedure involves first metatarsal-cuneiform capsulotomy with recession of
abductor hallucis, followed by serial casting. The Lichtblau procedure entails sectioning of
a hyperactive abductor hallucis, much !ike Thompson's procedure, and is indicated in the
equinovarus foot with metatarsus adductus Brown described transfer of tibialis posterior
into the navicular from anomalous insertion, combined with medial cuneiform-navicular
caps ulotomy. Ghali described an anterior-medial release of the first metatarsocuneiform
and naviculocuneiform joints with division of tibialis anterior at the medial aspect of medial
cuneiform. Osseous procedures are indicated in patients 8 years of age or older. McCormick
and Blount described arthrodesis of the first metatarsocuneiform joint with lateral closing
wedge osteotomy of the second, third, and fourth metatarsals and the cuboid. Peabody and
Muro described mobilization of the first metatarsocuneiform joint combined with excision
of the second, third, and fourth metatarsal bases and lateral closing wedge osteotomy of
the fifth metatarsaL Steytler & VanDerWall described pan metatarsal oblique laterally based
dosing wedge osteotomies. The Berman-Gartland procedure is a popular technique that
employs lateral closing base wedge osteotomies of a!I five metatarsals distal to the growth
plates (Figure 9-8). The lepird procedure (Figure 9-9) is a refinement on the Borman-
Gartland technique that varies with the use of through-and-through rotational osteotomies
ofthe intermediate metatarsals, combined with lateral closing base wedge osteotomies of
the first and fifth metatarsals. The through-and-through osteotomies are made parallel to the
substrate and are initially made with preservation of the dorsal-distal-media! cortex, which
is completed only after interfragmental screw placement has been positioned and prior to
achieving final screw purchase after swiveling the metatarsals into corrected alignment
Fowler described an opening wedge osteotomy of the medial cuneiform, and Ganley
refined the technique to address a deformed LASA (lisfranc articular set angle)that displays
a severely oblique first met-cuneiform articular interface directed from proximal-medial to
distal-lateral. Ganley performed a medial cuneiform opening wedge osteotomy with
Metatarsus adductus angle. Correction is gained by compressing

the reartoot. Metatarsals are then
abducted on stable resrfoot.
Figure 9.7
Figure 9.8
Figure 9.9
autogenous bone graft in conjunction with a laterally based closing wedge osteotomy of the
cuboid. The resected corticocancellous cuboid bone is harvested for transplant into the
medial cuneiform. The osseous work is combined with appropriate soft tissue releases and
subsequent casting. Bankhart described excision of the cuboid, and Tachdjian-Grice
described a combination of hindfoot extra-articular arthrodesis with forefoot soft tissue
release for correction of skewfoot.
Talipes Equinovarus (TEV, Clubfoot}-this is an idiopathic, triplanar deformity thattypically

includes ankle equinus, hindfootvarus, and forefoot adduction; in addition to subluxation of
the TNJ. Although TEVis the most common form of clubfoot, equinovalgus can also occur.
Clubfoot occurs in 1:1,000 live births, with a 2:1 male: female ratio. 50% of cases are
unilateral, with the right foot being more commonly involved. The condition is familial, and
siblings display 20-30times the chance of having clubfootthan the general public. Acquired
forms of clubfoot can be neuromuscular in origin and associated with CP, CVA, meningitis,
cord lesion, and post-polio; or post-traumatic following burns, ischemic contracture, and
fracture malunion or tendon injury. In clubfoot, the head and neck ofthe talus are adducted
60-90 to the body in the transverse plane, whereas the normal relationship is 15-20. In the
sagittal plane, the head and neck of the talus are plantarflexed 25-30' in clubfoot, whereas
the normal relationship is 45-65. Recenttheory embraces medial rotation of foot under the
talus, with the talus staying aligned with the leg (Ganley). The anterior aspect of the
calcaneus is observed to be rotated beneath the talus in a medial direction, while the
posterior aspect of the calcaneus is rotated laterally. There is associated tightness of the
anterior deltoid, tibialis posterior and long flexors, and medial TNJ and NCJ and first
metatarsocuneiform joint; as well as tightness of the CFL laterally. Tethering of the tibialis
posterior tendon pulls the navicular medially and forces articulation with the medial
malleolus. The cuboid, tethered to the navicular by ligament, follows the navicular. Equinus
in clubfoot affects the ankle, and is due to tightness of the heel cord, long flexors, and
posterior AJ and STJ capsules. The wider anterior portion of the talar dome does not reside
in ankle mortise, and may pose difficulty in late term realignment due to tightness of the
mortise. Contracted ligaments in clubfoot include: posteriorly, the calcaneofibular, posterior
talofibular ligament; and medially, the deltoid, tibionavicular, and calcaneonavicular. Tendon
contractures include: posteriorly, the Achilles; medially, TP, FDL, FHL, and abductor
hallucis; and laterally, the peroneal tendons. Radiographically, clubfoot displays, in the AP
view (Figure 9-10), Kites talocalcaneal angle reduced to 0-15' (normal20-30'), the !alar-first
metatarsal angle >15, which is indicative of TN subluxation. In the lateral view, the
sagittal plane TCA 0-35" (normal35-55") with decrease upon dorsiflexion stress (this angle
will increase in the normal foot).
The Ponsetti method of corrective casting is the mainstay of conservative treatment
Much like metatarsus adductus, initial efforts are directed at reducing adductus until the
cuboid is anterior to the calcaneus and the navicular is anterior to the talus. Secondly, the
varus is reduced until the calcaneus is no longer medial to and inverted in relationship to
the talus. Lastly, the equinus is reduced after satisfactory reduction of the adductus and
varus components. If a dorsiflexory force is applied before reduction of the adductus and
varus, the STJ and MTJ will hyperpronate and subluxation will effect a rocker bottom foot
If the equinus resists manipulative reduction, and a nutcracker compression of the midfoot
is likely, then posterior release should be performed before continuing to force dorsiflexion.
Serial cast therapy should be initiated as early as possible, even in the infant. Neonates
may respond to taping alone. Casting is ideal before 6~8 months of age, but can be attempted
238 Congenital Deformities and Juvenile Surgery Ch. 8
l
1
Normal foot Clubfoot

Talocalcaneal L 20-40 Talocalcaneal L 15
Figure 9.10
even in older children. Clubfoot becomes more resistantto corrective casting after the child
begins walking. The typical duration of cast therapy is 6 weeks to 3 months in patients
<1 year old, and from 3-5 months in older children. Casting can be continued as long as
progressive correction occurs, however surgical intervention should be entertained if
impasse is reached. Serial casts are changed approximately every two weeks. The
duration of casting is proportional to the degree of rigidity, and growth must occur for the
deformity to reduce.
Surgery entails soft tissue release in the infant and young child. Correction entails
release of those structures that are tight, and varies from patientto patient Goals include
restoration of the TN, TC, and CC relationships. Consideration should be given to staging the
repair in older children and adults, to avoid neurovascular compromise. Turco popularized
the one stage posteromedial and circumferential releases (Turco procedure) for clubfoot
repair. The Cincinnati incision, or a medial hockey stick approach can be used. The
Cincinnati incision may limit posterior exposure. The posteromedial release involves
release and/or lengthening of the following: Achilles tendon Z-plasty; posterior ankle and
STJ capsulotomy; section CFL and posterior syndesmotic ligament; TP, FDL and FHL
Z-lengthening; TN, NC, cuneiform-metatarsal capsufotomy; sectioning the interosseous
talocalcaneal (cervical) ligament; abductor hallucis recession; and smooth K-wire
stabilization of the relocated TN and TC joints. Circumferential release includes the
posteromedial release with additional release of plantar and lateral structures. The plantar
release involves reflection of the plantar fascia and intrinsic musculature from the plantar
cortex of the calcaneus. Lateral release involves sectioning the bifurcate ligament
(Y-Iigament, or calcaneonavicular-calcaneocuboid ligament), and perhaps Z-plasty of the
peroneal tendons if indicated. Transfer of tibialis anterior into the lateral cuneiform may
also be a useful adjunct. Osseous procedures, performed in conjunction with soft tissue
releases, include lateral column shortening techniques such as the Lichtblau anterior
calcaneal lateral closing wedge osteotomy, the Evans calcaneocuboid wedge resection
and fusion, and Ganley's closing abductory cuboid osteotomy. It may be necessary to
osteotomize the lateral cuneiform as wei!. In case of neglected clubfoot, triple or pantalar
arthrodesis may be useful, howevertalectomywith tibiocalcaneal-tarsal arthrodesis is the
most frequently used reconstruction.
Congenital Calcaneovalgus-this congenital anomaly presents the foot in an acutely

extended position with the dorsal surtace in contact with the anterolateral surface of the
leg. The entire foot, including the heel, is in complete valgus to the point that when the
neonatal foot is pulled into plantarflexion, the following are noted: flexion is limited to the
neutral position, or perhaps slightly beyond; skin and subcutaneous tissues are stretched
tightly due to contracture that reveals a prominent, tight band that blanches in comparison
to surrounding normal skin; the underlying tendons usually not contracted; the calcaneus
(heel) is in valgus with the rest of the foot, and there is no frontal plane deviation of the
forefoot in relation to the hindfoot; and the foot is fairly flexible so thatthe heel and midfoot
can be brought into a corrected varus posrtion (a nonrigid deformity). Normal neonatal ankle
dorsiflexion is approximately 45, unlike the calcaneovalgus foot that can dorsiflex to
become flush with the pretibial surface ofthe leg. Normal neonatal ankle plantarflexion is
about 50, whereas the calcaneovalgus foot only gets to neutral or a few degrees of
plantarflexion. Increased plantarflexion of talus will be visible on the lateral radiograph,
and Kite's angle will be >35" in the AP view.
TABLE 9-1. COMPARISON OF THE NORMAl FOOT VS. THE CALCANEOVALGUS FOOT.
Normal foot Calcaneovalgus foot
Talus sits on top of calcaneus Talus is plantarflexed and the talar head
without overlap of the anterior overlaps the anterior edge of the calcaneus
edges of the bones Bisection ofthe talus falls plantar to the
Bisection of the talus passes through cuboid on the lateral radiograph
the superior half of the cuboid, If the deformity is severe, the talus lies
on the lateral radiograph in a vertical position
As with many pedal misalignments, the parents usually do not seek an opinion or care
until the child is 6-8 months of age, when the child first stands. In weight bearing, a
complete absence of the arch and severe valgus are noted. Conservative treatment
employs corrective casting using two layers of cast padding after applying skin adherent
(tincture of benzoin). An assistant holds the foot by the toe tips and maintains as much of
an equinus position as possible, while maintaining a neutral relationship of the FF to the
hindfoot, and adduction ofthe FFto correctthe TN alignment The cast is then applied from
the toe tips to below-the-knee, molding into the arch and aboutthe heel. A lateral X-ray is
obtained to confirm reduction, and correction is maintained for 2-3weeks, changing the cast
every 3-4 days in the neonate.
Congenital Vertical Talus (Congenital Convex Pes Valgus, Rocker Bottom Foot)-this
idiopathic anomaly, a form of clubfoot, is characterized by a footthat may actually contact
the pretibial surface at birth. The plantar surface is convex (rocker bottom), and the talar
head can be identified on the medial plantar aspect of the longitudinal arch, with the
hindfoot in equinovalgus. Deforming muscfe groups displaying contracture include
240 Congenital Deformities and Juvenile Surgery Ch.S
gastrosoleus complex (ankle equinus); ankle dorsiflexors (TA, EDL, EHL,) and the peroneal
tendons; and the peroneii and tibialis posterior are relatively more anteriorly migrated than
normal. Ligamentous shortening involves the dorsal talonavicular, tibia-navicular,
calcaneofibular, calcaneal-cuboid, interosseous talocalcaneal ligaments; and the
posterior AJ and STJ capsules are tightened. The spring ligament conversely, is elongated.
Radiographic evaluation employs use of the AP, lateral and forced plantarflexion views
(Figure 9-11).1n the lateral view, the long axis ofthetalus appears vertical and parallel to that
ofthe tibia while the calcaneus is in equinus and the forefoot dorsiflexed. ln the AP view,
the TCA is increased to >40. The navicular cannot be radiographically evaluated until3-4
years of age, when it ossifies. When it has ossified, the navicular is identified in a dorsally
dislocated position. The stress plantarflexion lateral view allows comparison of the first
metatarsal on standard lateral and the stress view, so that rigidity of the deformity can be
determined. Normally, the talar and first metatarsal axes are parallel; however in the
presence of a rigid plantarflexed talus, the talar axis passes through sole of foot and the first
metatarsal axis passes dorsal to head of talus. In the forced p!antatflexion view, this
relationship will not be reduced. Convex pes valgus is categorized as either Type I or Type
II. Type I involves dislocation of the TNJ, subluxation of the TCJ, and a normal CCJ. Type II
is more rigid and involves dislocation of the TNJ, subluxation ofthe TCJ and CCJ, and ankle
equinus. The differential diagnosis for calcaneovalgus includes talipes calcaneovalgus,
severe pes valgoplanus with gastrosoleus equinus, paralytic pes valgoplanus,
myelomeningocele, polio, and rigid pes valgus due to tarsal coalition. Associated
deformities include cleft palate, arthrogryposis, and spastic equinus due to CP and others.
Treatment of congenital vertical talus focuses on restoring the normal TN, TC, and
CCJ relationship as soon as possible. This condition is notoriously resistant to nonsurgical
treatment. As with talipes equinovarus, manipulation and serial corrective casting
(Ponsetti method) are useful. At birth, gentle manipulation is used to stretch the contracted
soft tissues. Manipulation entails stretch oftriceps surae and ca!caneofibular ligament via
distal and medial traction, plantatf!exion and adduction of the FFto stretch dorsiflexors and
everters, and distal traction of the FF and TNJ to effect adductus and varus stretch of the
tibionavicular and talonavicular ligaments. The stretch is held for 15 seconds and then
released, and the exercise is continued for 15 minutes after which the cast is applied. The
cast is changed twice per week for six weeks. As correction ensues, focus more on TN
reduction by means of distal FF traction until the head of the talus dorsiflexes and the
calcaneus is pulled under the talus. It may become necessary to maintain the closed
reduction with percutaneous pin stabilization. If, after 4-6 months of closed reduction,
Figure 9.11
impasse is reached, then open reduction should be performed. The longer the TN
dislocation persists, the more the soft tissue contracture deforms bone and surrounding
joints. Surgical repair of congenital vertical talus employs a medial, curvilinear skin
incision extending from the medial aspect of the Achilles tendon at a point 4-6 em proximal
to the ankle, around the tip of the medial malleolus, and onward to the junction of the first
metatarsal and medial cuneiform. The neurovascular bundle is retracted, after which the
Achilles, TA, EHL, and peroneal tendons are Z-plasty lengthened. The tibionavicular, TN,
bifurcate, and dorsal calcaneocuboid, calcaneofibular and TC interosseous ligaments are
then sectioned, The talar head is manipulated dorsally and the navicular moved in a
plantar direction with inversion, A smooth 0,062" K-wire is then driven from the posterior
aspect of the talus across the reduced TNJ, and continued anteriorly across the NCJ. The
spring ligament is then reefed tightly, and an AK cast used to maintain the correction for
12-16 weeks. The K-wire can be removed around 6 weeks postop. Avascular necrosis of the
talus is a possible complication. Excision of the navicular has been effective in the treatment
of rigid arthrogryposis in patients 36 years of age. In children >6 years old, rigid bone and
joint adaptation may indicate the need for triple arthrodesis.
Tarsal Coalition-this condition occurs due to failure of differentiation and segmentation

of primitive mesenchyme with resultant lack of joint formation. Types of coalitions include:
syndesmosis or fibrous, synchondrosis or cartilaginous, and synostosis or osseous.
The middle facet talocalcaneal (TC) coalition occurs most frequently, followed by the
calcaneonavicular (CN barL and then by the talonavicluar (TN) coalition. The age of onset
of symptoms varies as follows with the site of the coalition: TN coalition, 3-5 years; CN bar,
812 years; TC coalition, 12-16 years. The 3 predominant symptoms include:
1. Tonic peroneal muscle spasm, hence the term peroneal spastic flatfoot, with
antalgic eversion guarding against STJ motion;
2. Limitation of STJ and possibly MTJ motion; and
3. Pain upon weight bearing or attempted hindfoot motion.
Classically, a rigid flatfoot deformity displays the combination of peroneal spasm,

stiffness, and pain. Radiographic evaluation of tarsal coalition, in the lateral view, reveals
talar beaking, increased halo effect or sclerotic appearance of sustentaculum tali and
crucial angle area of the calcaneus, broadening and flattening of lateral talar process, and
diminished or absent joint space of middle and posterior facets. The medial oblique view
Oateral projection) is the best view to visualize a CN bar. Isherwood views and the 60
medial oblique are best for visualization of the anterior facet of the STJ. A single 45
calcaneal axial or a set of Harris and Beath views will reveal the relationship of the middle
and posteriorfacets, which should be paralleL The presence of a TC coalition wlll make the
relationship oblique or obliterate the involved, usually middle or medial, facet space.
Secondary articular changes are those of joint space narrowing, osteophytosis, and
subchondral sclerosis. These are classically observed atthe dorsal aspect of the TNJ in the
form of dorsal exostosis, or talar beaking, in association with a TC coalition; or in the form
of the parrot beak sign (anteater sign, calcaneal beak) in association with a CN bar.
Wide-angle linear tomography, making images across the STJs at 5 mm intervals beginning
at the lateral malleolus, can also be useful. CT scanning and MRI can also be used to
identify coalitions, and MRI is particularly useful in cases of fibrous or cartilaginous
bridging. Conservative treatment of tarsal coalition entails stabilization of the STJ using
strapping, foot orthoses, and cast immobilization in acutely painful cases with marked
peroneal spasm. Corticosteroid infiltration into the sinus tarsi may also yield symptomatic
relief. Surgical intervention for persistently painful CN bar involves resection of the
coalition and is best performed before 14 years of age. The bar is excised via an Ollier or
similar approach to the sinus, and Bagley described transplantation of the EDB muscle
belly into the excision site in an effort to avoid the development of rigid fibrosis in the cleft
(Figure 9~ 12). Postoperative non-weight bearing and immobilization are used for 4-6 weeks.
In cases of TC coalition in a youngster with no secondary arthrosis, consideration can be
given to resection of the coalition, and arthrodesis may become necessary in the future. In
the adult without significant secondary arthrosis, isolated TC fusion is indicated. In any
patient with significant secondary arthrosis, triple arthrodesis is indicated.
Figure 9.12
Pediatric ln~toe Deformity~a variety of conditions can cause an in-toe, or medially

adducted gait The most common causes are femoral anteversion, which usually self-
corrects by 3 years of age, and metatarsus adductus. Talipes equinovarus, metatarsus
primus varus, juvenile hallux varus, and medial tibial torsion also display m-toe.
Asymmetry pronounced deformity, pain, or gait imbalance all warrant evaluation.
Treatment may range from simple observation to manipulation, reverse last shoe, casting,
night splints, or surgery depending upon the cause and degree of deformity.
Pediatric Toe~walking Gait~a variety of causes can lead to an equinus or toe-walking

stance and gait, including: CP, delayed myelinization of the corticospinal tracts, muscular
dystrophy, CMT and other peripheral neuropathies, disease of the basal ganglia such as
dystonia musculorum, spinal cord defects such as spina bifida, talipes equinovarus,
gastrocnemius or gastrosoleus equinus, prancer syndrome where the child mimics toe
walking seen in adults or older children, autism and conditions of mental retardation
Micromelia,-this rare congenital defect has been associated with hypoxia, maternal
thalidomide intqke during gestation, and involves pathological smallness of the limb. The
condition Is usually associated with other defects. No specific treatment is recommended
for the extremity.
Congenital Hemihypertrophy---this rare, idiopathic anomaly usually displays enlargement

of the ipsilateral upper and lower extremities or parts thereof. Possible causes include
neurofibromatosis, vascular or lymphatic hyperplasia, AV fistula, malignancy, or benign
tumor. When indicated, treatment is directed at the identified primary defect, or ablative
intervention on the involved limb. Shortening osteotomy, arthrodesis, and soft tissue
debulking techniques can be used in one stage or multi~staged procedures.
Osteochondroses-these acquired diseases affect grovvt:h centers, both primary and

secondary, and have been attributed to vascular disturbance and/or trauma. Systemic
arthritis, infection, certain medications and toxins, and tumors can also disturb the growth
center, however the osteochondroses are generally observed as idiopathic, insidious
conditions that occur in active youngsters and cause diffuse aching and guarded
ambulation. Radiographic inspection may reveal irregularity and fragmentation of the
growth center and adjacent physis, and increased soft tissue density and volume. Treatment
usually entails rest, ice, compression, and elevation, and appropriate oral anti-inflammatory
medication can be helpful. Gel casting and use of a surgical shoe, cast or splint
immobilization, protected weight-bearing and follow-up use of foot orthoses may also be
used. Specific osteochondroses include:
Freiberg's infraction-osteochondritis that usually affects the second metatarsal head,

more common in females :::13 years of age, resulting in flattening and widening of the
metatarsal head, and attributed to traumatic disruption of the physeal blood supply.
Lushke's disease-osteochondritis of the fifth metatarsal base, observed in children 5-11

years of age.
Kohler's disease--osteochondritis of the tarsal navicular, most common in boys 3-6 years
of age.
Sever's disease--osteochondritis ofthe calcaneal apophysis, observed in children 8-14

years of age and most common in boys.
Osgood-Schlatter's disease-osteochondritis of the tibial tuberosity, most common in

athletic boys aged 11-15 years. It is important to rule-out osteosarcoma in this age group
and location.
244 Management of Foot and Ankle Trauma Ch. 10
MANAGEMENT OF FOOT AND ANKLE TRAUMA

Basic principles ofthe management oftrauma include a thorough assessment otthe injured
patient, triage, and appropriate treatment of specific injuries. Priorities include basic and
advanced life support (described elsewhere in the manual), which entail maintenance of
an airway, CPR, identification and control of hemorrhage, monitoring vital signs lBP, pulse,
respiration, temperature, and level of consciousness), and fluid management Blood should
be obtained for typing and cross matching, if the potential for substantial volume depletion
exists. While waiting for compatible whole blood, an IV infusion of glucose and water,
plasma, plasma expanders, or lactated Ringer's solution may control shock temporarily.
Ideally, whole blood should be administered for severe blood loss. Specific injuries of soft
tissues and bone should then be determined. Injuries include punctures, abrasions,
incisions, and lacerations (PAIL), as well as burns, penetrating trauma, fractures, and
dislocations. Tetanus prophylaxis is a consideration in every form of trauma that results in
cutaneous compromise. ln general, the injured lower extremity should receive protection,
rest, ice, compression, and elevation (PRICE), after assessment of the neurovascular
status to the injured limb.
SELECTED SOFT TISSUE INJURIES
Cutaneous Wounds-After ascertaining the systemic status of the patient. local tissue
factors may be evaluated. Inspection enables identification of pathological anatomy and the
presence of foreign body. An open wound is considered "old" and contaminated if care
has not been administered within 6 hours after the onset ofthe injury. The status of the skin,
vessels and nerves, tendons, bones and joints must all be documented based on the
merits of each individual injury. local, regionat and even general anesthesia may be
necessary in order to thoroughly identify pathology. The procedure may take place in the
office, emergency department. or the operating room. Intravenous conscious sedation with
local or proximal field block often suffices for foot and ankle injuries. local anesthesia
should only be infiltrated after assessment of the peripheral neurovascular status, and then
only proximal to the injured tissues. A proximal tourniquet is usually preferred as compared
to dilute vasoconstrictor in the local block. Normal sterile saline, warm or room
temperature, a bulb syringe or 18-gauge needle with a 20-50 cc syringe, and aseptic
technique are used for lavage, inspection and local debridement Tissue forceps, scalpel,
curette, and other probes may be helpful. Adequate debridement entails removal of all
necrotic or heavily contaminated tissue, including small fragments of bone, and foreign
bodies. Skin viability is ascertained clinically by a pink dermal coloration, warmth, and
capillary bleeding. If necessary, IV administration of 10-15 mg/kg of fluorescein dye
followed by observation of the tissues under Wood's light will reveal dye uptake in the
tissues by means of fluorescence. Fascia is relatively expendable due to its diminished
vascularity compared with other tissues, and it is also prone to infection. For tendon to
remain or become viable, it must be covered with intact skin or graft, flap, muscle, or a
suitable skin substitute. Muscle viability is determined by the presence of the 4 Cs: color
(beefy red), contractility (upon electrical stimulation). capillary bleeding (bright red blood).
and consistency (firm, elastic). Specimens should be obtained for C&S, as well as for
histopathological inspection of appropriate tissues. Following initial debridement
definitive therapy can be determined, or additional debridement may be in order.
Specialized vascular and/or neurological consultation may be indicated following initial
Ch. 10 Management of Foot and Ankle Trauma 245
debridement, prior to definitive reconstructive efforts. Similarly, infectious disease, internal

medicine and any other appropriated consultation that is indicated, could be obtained.
Tetanus Prophylaxis-the specific action to be taken is determined by the patient's

immunization history, as follows:
1. If immunization was completed previously, and the last booster was within 1
year; then there is no need to administer tetanus toxoid or immune globulin.
2. If immunization was completed within the preceding 10years without subsequent
booster, then administer 0.5 ml tetanus and diphtheria toxoid (adultTd).
3. If immunization was completed >10 years ago, and the last booster was within
the preceding 10 years; then administer 0.5 ml ofTd.
4. If immunization was completed >10 years ago, and there has been no booster
within the previous 10years, and the wound is minor, relatively clean and treated
promptly; then administer 0.5 ml ofT d.
5. If immunization was completed >10 years ago, and there has been no booster
within the preceding 5 years, and the wound is dirty or >6-8 hours old; then
administer 0.5 ml ofTd and 250-500 units of human tetanus immune globulin (TIG
[h]). The 500-unit dosage is used if the wound is considered prone to clostridial
contamination, otherwise 250 units is sufficient. The Td and TIG[h] are
administered using separate syringes and needles, at distant sites (deltoid and
contralateral glutei).
6. If there is no history of immunization, and the wound is minor, clean, and
treatment is prompt; then initiate an immunization program with 0.5 ml ofTd and
schedule the follow-up booster series.
7. If there is no history of immunization and the wound is dirty or treatment is
delayed; then administer 0.5 ml Td and 250 units TIH[h] and follow-up with the
booster series. Give 500 units TIG[h] if the wound is clostridia-prone. In addition
to Td and TIG[h]. 10-20 million units of aqueous penicillin-G should be
administered IV for a tetanus- prone wound, and appropriate cleansing
debridement and wound care undertaken.
Nail Trauma-traumatic conditions that affect the nail and associated structures include
subungual hematoma, and hematoma with underlying phalangeal fracture; simple and
complex nail bed lacerations; and nail bed tissue loss injuries such as partial digital
amputation, degloving and avulsion. The majority of nail injuries result from blunt trauma,
either stubbing or dropping something heavy on the toe. Treatment can be enhanced by
digital or metatarsal ray block with local anesthetic infiltrated into normal-appearing skin
proximal to the defect. Subungual hematoma causes throbbing pain as hemorrhage through
the nail bed accumulates in the potential space between the plate and bed, and usually
requires no more treatment than reassurance and observation. Hematoma will slowly
migrate forward with nail growth, and takes 7-9 months in the adult for complete
regeneration of a toenail. Painful hematoma in the acute phase may benefit from drainage
by perforating the nail plate with a hand cautery, or a narrow rotary bur or#11 scalpel blade.
The toe is prepped with antiseptic before drainage, then antibiotic cream and a sterile
coverlet afterwards.lfthe subungual hematoma involves greater than 25% of the visible nail
plate, and the plate is unstable upon the nail bed, then serious consideration should be
given to avulsion ofthe nail plate and inspection ofthe damaged nail bed (Zook's rule). Nail
bed lacerations are either simple transverse, oblique or longitudinal lesions; or complex
(stellate, crushing), perhaps with apices that will eventually undergo necrosis.
Approximately 20% of subungual hematomas are associated with distal phalangeal
fracture, which can technically be considered an open fracture after either traumatic or
therapeutic nail plate avulsion in the presence of nail bed laceration . .After cleansing
debridement the nail bed is sutured with 4-0 or 5-0 absorbable suture in fresh, clean
wounds; or nonabsorbable suture in heavily contaminated or longstanding (>6 hours)
wounds. The nail bed is bandaged with nonadherent gauze preserving the cui de sac
nature of the proximal nail fold, and appropriate supportive measures are used. Nail bed
tissue loss injuries are defined by the Rosenthal classification system, which describes the
level of tissue loss as either distalto.the bony phalanx (zone 1), distal to the lunule (zone 2),
or proximal to the distal margin of the !unula (zone 3); and according to the direction of
tissue loss as either dorsal oblique, plantar oblique, transverse guillotine, tibial or fibular
axial, or central gouging (Fig 10-1). Treatment includes cleansing debridement, and
coveragewith local transport of adjacent skin by means ofthe Atasoy flap (plantar-to-tip
V-Y flap) or Kutler flap (medial and lateral V-Y plasties) after reduction of any prominent
distal phalanx. Split- and full-thickness skin grafts can also be used to cover broad defects.
Lesions proximal to the DIPJ may require disarticulation. Complications of nail bed injury
include delayed nail regeneration; matrix disturbance with Beau's transverse line or ridge,
II Ill
~c~
c E
figure 10.1
onychocryptosis, and nail dystrophy with onycholysis and secondary fungal infection,
canaliformis or split~nail deformity, and an unstable nail.
Burns and Frostbite--burns are caused bythermal injury, both hot and cold, and chemical
and electrical injury. The severity of a burn depends upon the extent of surface area and
depth of skin penetration. Tissue damage is caused by protein denaturation, fluid
extravasation, and edema. The extent of a burn is designated as a percent of total body
surface area (TBSA). and the rule of nines is applicable. The body is divided into multiples
of 9% (Fig. 10-2). Partial-thickness burns include first and second degree wounds.
Full-thickness burns are designated as third degree. First-degree burns involve only the
epidermis, show erythema and no blisters, and are painfuL The most common form is
sunburn. Second-degree burns are either superficial or deep. A superficial second-degree
burn involves injury to the epidermis and a portion of the dermis; and they are
erythematous, moist with blister formation and serous drainage, and are very painfuL
A deep second-degree burn injures the epidermis and most of the dermis, leaving skin
appendages intact It may or may not show blister formation and can be dry and it might
display scattered anesthesia. A third degree burn involves full-thickness skin and a portion
of the subcutaneous layer, destroying all skin appendages, thrombosing vessels, and
appearing dry, anesthetic, whitish and leathery (eschar). A third degree burn can extend to
bone. Fourth degree burns are caused by low voltage (<1000 volts) electrical injury, and
fifth degree burns are caused by high voltage electricity or radiation injury. Fourth and fifth
degree burns involve muscle and bone.
Minor burns can be treated outpatient and include all first-degree, second-degree
<15% total body surface area (TBSA), and third-degree <2% TBSAwounds. Moderate burns
may be treated either in or out of the hospital, based on specific merits of each case, and
include second-degree >15% TBSA and third-degree <10% TBSA. Severe burns require
inpatient treatment and entail any third-degree burn of the foot, hand or face; second-
degree >30% TBSA, third-degree >10% TBSA, or any burn with associated sepsis,
l) l)
I I
Figure 10.2
fracture, or systemic complication such as shock or cardiopulmonary disorder. The goals

of treatment are to stop the burn process, prevent infection, and enhance healing.
Fundamentals include airway management, fluid management (IV lactated Ringer's
solution or fresh frozen plasma, monitor urine output along with tetanus prophylaxis, IV
and topical antibiotic, analgesia, and escharotomy. Silver sulfadiazine and sulfamyalon
(anti-pseudomonal [nosacomia!]), sterile water lavage, and porcine heterograft or
biosynthetic skin substitutes may be used. First-degree burns respond weH to topical lotions
to moisturize and diphenhydramine and methylprednisolone in a dose pack may be helpful
in some cases. Second-degree burns are managed much like abrasions, cleansed,
blisters that are very large or already show drainage are debrided, followed by application
of topical antibiotic cream and sterile bandage. Third degree, or full-thickness burns
require excision of necrotic eschar followed by autogenous split-thickness skin graft(STSG)
or temporary coverage with porcine heterograft or skin substitute until the patient can be
prepared both locally and systemically for definitive skin grafting or other plastic
reconstruction. Compressive dressings, splints, and early physical therapy for range of
motion are crucial therapeutic measures that minimize contracture and edema.
Complications of burns include hypertrophic scar, contracture deformity, syndactylization,
ischemia, and vasomotor instability.
Frostbite is also categorized based on the depth of penetration. First-degree frostbite
displays freezing of the epidermis with subsequent pain, erythema and exfoliation, but no
blister formation. Second-degree frostbite involves freezing of the entire epidermis and a
portion of the dermis, and pain develops after thawing. Third-degree frostbite involves
freezing of the entire thickness of skin and displays localized ulceration. Fourth-degree
frostbite also involves full-thickness skin freezing, however the extent of injury is more
extensive in the extremity, encompassing an entire hand or foot, leg or arm. Superticial
frostbite, first- and second-degree, is also termed chilblains. Trench foot implies freezing or
near freezing in a wet environment, with vasospastic hypoxia, necrosis and subsequent
edema. Systemic hypothermia is described as a core body temperature <90 F, with
dehydration, and cardiogenic shock can ensue.
Treatment of frostbite entails protection of the part, avoiding friction rubbing to try to
stimulate warming frozen tissues, and getting to a place where rewarming and
assessment of the core body temperature can be achieved in a definitive fashion.
Refreezing is particularly destructive. Rewarming of the frozen part is done in a footbath wfth
water at 38A4 C in 15-20 minutes. Administration of IV dextran counters the osmotic
imbalance due to local tissue dehydration in the frozen part Tetanus and antibiotic
prophylaxis, analgesia, and subsequent sterile bandaging are also in order. Sequelae
include cold sensitiviTy, Raynaud's phenomenon, paresthesia and pain, and contracture.
Puncture Wounds (see Chapter 3)
Gunshot Wounds (GSW) and Penetrating Trauma--gunshot wounds are a form of

penetrating trauma associated with a wide range of defects, both local and systemic. In the
lower extremity, low velocity injuries are most common. The projectile creates a path and
cavity in the tissues, which varies with projectile mass, velocity, and tissue density and
volume. Kinetic energy is equal to half of the mass times its velocity (KE" 1/2 mv2),
therefore both velocity and mass greatly influence the amount of energy sustained by the
body part. A low velocity projectile, shot from most handguns, effects a straight and
narrow, or focused path and cavity; whereas a high velocity projectile, shot from a hunting
rifle or military weapon, will yaw, tumble and create a large cavity as it traverses the body
part Soft nose or hollow point, as well as jacketed bullets, are designed to deform and
fragment upon impact, thereby creating more projectiles that result in more damage. Low
velocity projectiles frequently do not create an exit wound, even when bone is not involved.
High velocity bullets create entry and exit wounds. Exit wounds are usually larger than the
entry defect, since the projectile deforms and fragments, along with the tissues, as it
penetrates and traverses the part. When a low velocity projectile encounters bone in the
foot, a typical "drill hole" defect can be observed radiographically where the bullet
traverses the bone. High velocity bullets shatter small bone into fragments that are often too
small to repair. Treatment of GSWs entails triage, identification of the systemic and local
tissue status, attention to neurovascular compromise, tetanus and antibiotic prophylaxis,
cleansing debridement and removal of necrotic soft tissue and bone, foreign body bullet
removal, skeletal stabilization and reconstruction, often requiring bone grafting. Definitive
reconstruction may be performed on a delayed basis. Completion of a police report is
usually required.
Knife wounds represent a form of low velocity penetrating trauma. The path and
cavity are very narrow and distinct. Identification of systemic and local pathology proceeds
in a fashion similar to that for gunshot wounds, and the management protocol is
essentially the same.
Animal and Human Bite Wounds~these are crushing injuries that convey special
microbiology related to a wide range of organisms and tissue necrosis. Anaerobes and
both gram-negative and posrtive organisms may be present. Cleansing debridement with
identification of pathological anatomy proceeds in the standard fashion.
Peroneal Tendon Dislocation, Stenosis, and Rupture-dislocating peroneal tendons can

be caused by forced eversion of the hindfoot with ankle dorsiflexion, a direct blow to the
lateral aspect of the hindfoot and/or ankle, or due to congenital absence or defect of the
peroneal groove in the lateral malleolus. Symptoms include hindfoot and ankle pain and
edema due to peroneal tendinitis, palpable crepitus, and a clicking sensation as the tendon
subluxates from behind the fibula and displaces anteriorly. Radiographs may show an
avulsion fracture fragment from the lateral malleolus or defect in the peroneal tubercle of
the calcaneus. MRI can also be useful, and may reveal a split-tear of the peroneal tendon,
tenosynovitis of the peroneal sheath, as well as any associated osseous lesion. Treatment
involves cast immobilization in the acute phase for 3-6 weeks, or ankle bracing during
strenuous activity in the chronic state. Surgical reconstruction of the peroneal retinaculum
IRg. 10-3) orofthe peroneal groove in the fibula IFig. 10-4) may be indicated in recalcorant cases.
Stenosing peroneal tenosynovitis can be caused by direct, acute trauma sustained
during fibular, talar, or calcaneal fracture; or by chronic microtrauma due to an enlarged
peroneal tubercle or constricting retinaculum. Symptoms include pain upon hindfoot/ankle
inversion, and stiffness. Signs include point tenderness along the tendon at the point of
entrapment, and thick, boggy edema. Diagnostic studies include lateral and calcaneal
axial radiographs, peroneal tenogram, or MRI. Treatment involves supportive bracing,
corticosteroid infiltration, and perhaps physical therapy; or surgical repair of bone, sheath,
and tendon. Postoperative physical therapy may also be in order.
Peroneal tendon rupture is uncommon, and may result from laceration, severe
hindfoot/ankle fracture/dislocation or, more typically, chronic degeneration. Signs and
symptoms include edema and pain in addition to associated injury, as well as absence of
Figure 10.5
eversion function and inability to plantarflex the first ray. MRI is essential to making the
diagnosis, and has replaced the use of the peroneal tenogram in most cases. Longitudinal
split-tears may be identified. Treatment entails surgical repair, perhaps with tendon graft,
postoperative immobilization, and gradual rehabilitation.
Ankle ligamentous Injury--collateral ligament injury involving the ankle is very common.
It should be noted that the calcaneofibular ligament (CFL) runs anterior to posterior in the
sagitta! plane and angulates 20A0 from the long axis of the fibula, while the anterior
talofibular ligament IATFL) courses lateral to medial in the frontal plane (Fig. 10-5). The
orientation of the ligaments can be difficultto recreate with secondary surgical repairs,
and non physiologic motion may follow such treatment. Causes of ankle instability include
post-traumatic ligamentous disruption, osteochondritis dissecans (OCD) of the talar dome,
DJD with ligamentous laxity, peroneal subluxation, muscle weakness or paralytic dropfoot,
talofibular meniscoid (defective ligament trapped between articulating surfaces),
tibiofibular diastasis, nonunion of previous ankle fracture or poorly reduced yet healed
fracture (shortened fibula), fixed calcaneal varus, tibial varum, rigid plantarflexed first ray,
pes cavoadductovarus, or femoral anteversion or tibial torsion effecting pronounced in toe.
Acute Ankle ligament Disruption (lnstabilityf-acute disruption of the lateral

collateral ligaments causes immediate ankle instability, and may lead to chronic
instability and arthrosis. Most cases of .acute disruption are treated with non-
operative functional thera pythat involves temporary immobilization for up to 4 weeks,
weight bearing ambulation, and gradual rehabilitation for strength and flexibility.
Aspiration of hematoma or hemarthrosis may be indicated. Acute ankle instabilfty is
determined by the presence of pain, edema, antalgic gait, and clinical and
radiographic evidence of anterior drawer and/or talar tilt In many cases, chronic
instability conveys minimal chronic pain despite frequent inversion sprain. Instability
can be identified with the stress lateral (anterior drawer) and stress AP (talar tilt)
radiographs. Classification of the acute injury is based on the presence or absence of
ligament disruption and resultant instability. A first-degree sprain correlates with ATFL
rupture, while a second-degree sprain correlates with ATFL and CFL rupture, and a
third degree-sprain correlates with ATFL, CFL and posteriortalofibular ligament (PTFL)
rupture, although this classification system can be confusing and difficult to
accurately determine. Crucial to the diagnosis, however, is the determination that
ankle instability is or is not present Anterior drawer of 5-8 mm suggests rupture of
the ATFL, 10-15 mm suggests rupture of the ATFL and CFL, and >15 mm suggests
rupture of the ATFL, CFL, and PTFL. Talar tilt of> 10" suggests of rupture of the CFL.
Surgical intervention may be considered after acute disruption in the patient with an
active/strenuous occupation/avocation, positive stress radiography indicative of at
least ATFL and CFL rupture, and adequate local and systemic findings to sustain
surgery. Primary collateral ligament repair, in the acute or delayed (months to years
after disruption) setting, involves a lateral curvilinear incision extending from the
posterior margin of the fibular malleolus to the lateral margin of the EDL anteriorly.
Dissection should occur between the sural and intermediate dorsal cutaneous nerve
trunks. Immediately upon penetration of deep fascia, capsule and ligament will be
evident Hematoma is evacuated in the acute phase, and scar dissected in the chronic
scenario. Ligament is repaired with suitable suture, and intra-osseous anchors or
fracture fragment repair in the case of ligament avulsion, may be indicated.
Intraoperative stress anterior drawer and talartilt should be negative. Postoperative
immobilization in a weight-bearing attitude, with the ankle in a neutral alignment, for
3-4 weeks followed by bracing and rehabilitation is undertaken.
Chronic Ankle Ligamentous Disruption (lnstability)--;;econdary ankle ligamentous

reconstruction can be useful in the treatment of chronic instability, and entails
reconstructive procedures that approximate rather than truly restore ligaments to
their native state. It is difficult to recreate ligaments that mimic the ankle's normal
orientation and physiologic motion, despite restoring stability. Traditionally, peroneus
brevis has been harvested for ligament reconstruction, however peroneus longus is
now more frequently used as the supinatory influence of the first ray on the ankle can
be diminished by eliminating the pu!t of peroneus longus while preserving the everter
function of peroneus brevis. There are many options, and the surgeon should pursue
a reconstruction that best suits the patient's needs. The use of intraosseous tendon
anchors and nonabsorbable suture materials are useful in these repairs. Procedures
that recreate 1ligament, namely the ATFL, include:
Watson-Jones (Fig. 10-6}----detach peroneus brevis (PB) proximally and suture

its belly to peroneus longus, then reroute the distal portion through 2 drill holes
that course transversely through the fibula and a single drll! hole in the neck/head
of the talus. The tendon is first directed from posterior to anterior through the
proximal fibular channel, then from superior to inferior through the talus, then
back through the distal fibular channel from anterior to posterior and sutured
upon itself and periosteum atthe posterior aspect of the lateral malleolus.
Lee (Fig. 10-7}-detach PB tendon as proximal as possible and suture its belly to
peroneus longus, then reroute the harvested distal portion of tile PB tendon from
posterior to anterior through a drill hole in the distal fibula, then suture the
tendon to itself distal to the lateral malleolus.
Nilsonne (Fig. 10-8}-detach PB proximally and suture its belly to peroneus

longus. Create a subcortical trough with a gouge in the lateral malleolus while
preserving an anterior cortical hinge, then place the tendon into the trough and
flap the cortex over the tendon and suture periosteum to stabilize both cortex
and tendon.
Evans (Fig. 70-9}-detach PB proximally and suture its belly to peroneus longus,
reroute the distal portion of the tendon through a drill hole in the fibula from
anterior-inferior to posterior-superior, then suture the tendon to periosteum at
both ends of the osseous tunnel.

Procedures that recreate 21igaments (ATFL and CFL), include:
Christman-Snook (Fig. 10-IOHetach a split portion of PB proximally IPS is deep

to peroneus longus IPL) at the proximal level of sectioning), then split PB to the
vicinity of the fifth metatarsal base, then reroute the split portion in a subperiosteal
and subcapsular fashion to the anterior surface of the lateral malleolus. Next,
route the tendon from anterior to posterior through a drill hole in the fibula, then
course inferiorly superficial to the peroneal tendons posterior to the lateral
malleolus toward the lateral wall of the calcaneus. Route the tendon through a
small channel created in the calcaneus from posterior to anterior and suture the
tendon to periosteum and the PB and PL tendons posterior to the fibula.
Split Peroneus Brevis Lateral Ankle Stabilization (SPBLAS) (Fig. 10-11)--this is

a modification of the Christman-Snook procedure that involves simply
transplanting the split portion of PB into a trephine hole in the lateral aspect of
the calcaneus and packing the site with the trephine bone plug rather than
suturing the tendon to PB and PL after channeling through the calcaneus.
Having converted to the use of PL, this technique is now referred to as the
SPLLAS, and proceeds as described previously with the only significant
variation being use of a split portion of PL.
E!mslie {Fig. 10-12)--tascia lata is harvested and used as a tree graft anchored
through a channel in the calcaneus and one in the talar neck, routed through a
drill hole in the fibula.
A variety of other secondary ankle ligament repairs have also been described,
including use of free tendon graft and synthetic ligament substitutes. Over time,
however, the delayed primary repair has offered the best physiologic result and should
be the surgeon's first choice if enough ligament can be identified and sutured.

Figure 10.12
Achilles Tendon Rupture-this injury is most commonly seen in males, aged 25-40
("weekend warrior"), and typically occurs in the least vascularized portion of the tendon
2-6 mm proximal to its insertion in adults >25 years of age. The Achilles tendon is surrounded
by a richly vascularized paratenon, however has no true tendon sheath (a sheath is only
present where tendon changes direction). The mechanism of acute rupture in a previously
asymptomatic heel cord is severe traction sustained during weight bearing push-off with
the knee extended, or less commonly secondary to severe ankle dorsiflexion (downhill
skiing). Chronic degenerative tendinitis, with a long history of pain and inflammation, can
predispose to rupture near the insertion and is often associated with calcification ot the
insertional fibers and a prominent posterior calcaneal step defect Acute rupture may
effect a popping sensation, or the sensation of being struck across the tendon. Pain, edema,
and an apropulsive gait with inability to stand on the toes with the heel elevated on the
affected side are common findings. Palpation otthe tendon reveals a defect or rent in the
tendon, surrounding tenderness and induration, loss of active open chain ankle
plantarflexion, and the presence at the Thompson-Dougherty sign. The Thompson-
Dougherty test involves squeezing the ipsilateral triceps surae and noting absence of
passive ankle plantarflexion. Even a small amount ot intact tendon, despite partial rupture,
is enough to make the Thompson-Dougherty test negative. Standard radiographs display
increased soft tissue density and volume obliterating Kager's triangle. MAl reveals tendon
disruption, and may be useful when partial rupture is suspected. Conservative treatment is
indicated tor cases of partial rupture, and in patients with limited function or inadequate
local tissue factors. Nonsurgical care entails application at a Jones compression dressing
to splintthe ankle for 24-72 hours, followed by AK cast applicalion with the knee slightly
flexed and the ankle in plantarf!exion for up to 4 weeks, then conversion to a less
plantarflexed cast for an additional 4 weeks. Additional cast or removable walking boot
therapy, in addition to physical therapy to improve flexibility is thereafter used as needed.
Functional therapy, which can be very effective, entails the use of a plantarflexed brace that
is gradually converted to a right ankle orientation of the foot to the leg, enabling weight
bearing as tolerated by the patient Many cases at complete rupture warrant operative
repair, preferably in the acute setting with end-to-end reapproximation or other methods
that permit reconstruction. Tendon reapproximation requires the use of a Bunnell or other
lateral trapping suture technique to substantially purchase longitudinal tendon fibers and
resist tension. Good results have also been obtained with functional recovery using
gradually decreasing degrees of weight bearing plantarflexion splinting. Dissection via a
posterior incision just medial to the midline, taking care to avoid the sural nerve, and
preserving the paratenon for reapproximation over the repaired tendon is standard. A
number of repair techniques are notable, including:
Lynn Achilles tendon repair-this technique involves reapproximation ofthe 2 ends re~
info reed with a flap of free plantaris graft harvested from the same wound and fanned
out over and around the repair for reinforcement Schuberth has
recommended lengthening the tendon at the time of repair, to avoid posttraumatic
equinus and to hasten rehabilitation. V-to-Yplasty atthe myotendinous junction eases
reapproximation and decreases traction across the repair.
Lindholm Achilles tendon repair-this technique of delayed primary Achilles repair

employs two proximal, longitudinal flaps from the aponeurosis that are rotated
distally and sutured to the distal segment, and themselves, to bridge a fibrotic gap.
Transfer of a portion of tibialis posterior and peroneus longus to the distal portion of
the Achilles, as wei! as techniques using free tendon grafts, fascia lata, and synthetic
tendon mesh have also been described.
Compartment Syndromes~increased intracompartmental pressure can cause local

muscular and neurovascular damage. The compartment is that area defined by overlying
deep muscle fascia, surrounding intermuscular septae, and/or underlying bone and
periosteum. The contents of the compartment are skeletal muscle bellies, tendons,
bursae, and neurovascular structures. A compartment syndrome develops when the
intracompartmental pressure increases to a pathological level, thereby damaging the
contents of the compartment and distal structures dependent on blood flow through the
compartment. In the foot, there are 3 main longitudinal compartments: 1) medial
compartment~containing abductor hallucis and FHB; 2) superficial compartment-which
is plantar central and contains FOB; and 3) !atera!~which contains abductor digiti minimi
and flexor digiti minimi brevis. The forefoot also houses 5 smaller compartments:
4 intermetatarsal \interosseous) spaces containing the interossei; and the adductor
hal!ucis compartment plantar!y. The hindfoot houses a single deep compartment, referred
to as the calcanean compartment, which contains the quadratus plantae. In the leg, the
peroneal, anterior, and posterior deep and superficial compartments are of concern
(Fig. 10-13). Compartment pressure increases due to enlargement of intracompartmental
volume, or external pressure that causes a decrease in the compartment volume. The nor-
ma! lower extremity intra compartmental pressure, in the normotensive patient, is 4 4
mmHg. During exercise, the intracompartmental pressure may exceed 50 mmHg.
Immediately post-exercise, the pressure should be <30 mmHg; and within 5 minutes after
cessation of exercise, the pressure should normalize. In the normotensive patient,
compartment pressures approaching 100 mm Hg are necessary to occlude arterial
pulsatile flow. Any condition resulting in sustained intracompartmental pressure of :::30
mmHg, in a patient who presents 28 hours after injury or the inciting event, and who
demonstrates clinical signs and symptoms, should undergo emergency fasciotomy to
alleviate compartment syndrome. Signs and symptoms include allodynia, exquisite pain,
paresthesia, and pulse!essness {the 3 "P's"). Soft tissue and osseous injury may be
present, along with edema, pallor or cyanosis, decreased skin temperature, and
sensorimotor deficit The neurological and vascular deficits must be documented prior to
Deep oo,;terior-.1.
neurovascular
structures
Tibialis anterior
Superficial
Extensor digitorum longus
posterior
hallucis longus
.,.l,enone"' longus
and brevis
Figure 10.13
surgical intervention. Distal arterial pulsation may be appreciated even when compartment
syndrome causes pain and paresthesia, as the initial vascular compromise occurs at the
microcirculatory \arteriolar) level distally. Predisposing injuries include comminuted
fracture or crush defect, contusion, Volkmann's ischemic contracture (post~ischemiaL
intracompartmental hemorrhage or hematoma, burn wounds, decubitus stasis secondary
to drug overdose and coma, circular bandages and/or casting, abscess and tumor.
Diagnosis is confirmed via transcutaneous wick catheter measurement of the
intra compartmental pressure, with values of ;::-30 mmHg. Pressure measurements <10 mmHg
are indicative of neuropraxia (pulses will usually be palpable). Values of 10-20 mmHg should
be remeasured 30-60 minutes after observation, and administration of analgesic, systemic
corticosteroid (methylprednisolone or prednisone), and rest If the condition is thoughtto be
related to circumferential bandaging or casting, remeasure the compartment pressure
30-60 minutes after cast and bandage removal. Fasciotomy is performed after sterile prep,
and may be done in the emergency room or OR, depending upon the merits of the specific
case. Compartment decompression in the foot is achieved using 2 dorsal longitudinal
incisions located over the second and fourth metatarsals. Dissection is carried through the
deep fascia to periosteum, then medially and laterally into the adjacent intermetatarsal
spaces where the interosseous musculature is reflected from the corresponding metatarsal.
In a similar fashion, other compartments in the foot and leg are opened via fasciotomy. The
wounds are then packed open and maintained with local care for 3-5 days, keeping the
extremity at bed level with slight knee flexion, after which delayed primary closure or skin
grafting is undertaken.
FRACTURES
The principles of fracture management include:
Reduction and Immobilization-fractures are described according to their location and

orientation within the specific bone. Fractures are caused by pathological bending,
twisting, and shearing forces that are applied either directly (direct blow) or indirectly
(twisting). Fractures are either closed or open injuries. Radiographic inspection requires at
least two or three (preferably), or more views, as well as comparison views of the
contralateral extremity in questionable cases involving sesamoids, growth plates, or
suspected supernumerary bones. Incomplete fractures, wherein a portion of the bone's
cortex remains intact, are termed greenstick fractures and generally occur secondary to
flexural deformation of a long bone. Similarly, a stress fracture results in bending without
overt radiographic fragment separation. A bone scan can be useful if diagnosis is in
question. Incomplete fractures are diagnosed primarily by clinical examination, and with
subsequent radiographic evidence of secondary bone callus. Complete fractures can be
transverse, oblique, spiral, and comminuted, with fracture stability and management
varying with orientation. Fracture stability, in descending order, is as follows:
transverse> oblique> spiral> comminuted
Transverse and oblique fractures may be amenable to closed reduction and

immobilization, whereas spiral and comminuted patterns are extremely difficult to
adequately reduce and maintain in a closed fashion. When a fracture violates a joint
surface, open reduction and stabilization is most often the best treatment option. Growth
plate injuries and open fractures deserve special consideration.
Fracture repair is initiated with closed reduction and immobilization, regardless of
whether the injury is open or closed. Closed reduction, as described by Charnley, entails the
following sequential maneuvers: 1) increase the deformity; 2) distract; 3) reverse the
deformity and realign; and 4) maintain correction with an immobilizing splintiFig. 10-14).
These general rules apply to all fractures, and may be used as definitive treatment in
amenable injuries, or as a temporary intervention to improve neurovascular status in
preparation for open reduction and fixation in the OR. Closed reduction can be impeded by
soft tissue interposition, such as the tibialis posterior tendon at the medial malleolus.
Maintenance ofthe reduction with a castor brace is indicated when closed reduction and
immobilization are the mainstays oftreatment.lf open reduction and internal fixation lORI F)
Convex
Figure 10.14
or use of external fixation is employed, the brace may be removable or nothing more than
a posterior, sugar tong (medial and lateral stirrup), or anterior splint. The usual
fracture-healing phase lasts at least 6-8 weeks, and protection should be maintained
during this period. As a rule, the bone should be stabilized with immobilization extended to
one joint above the fractured ossicle. If internal or external forms of skeletal fixation are
used, the "one joint above" rule becomes less important. Fractures sustained distal to the
MTPJs are usually satisfactorily stabilized with a rigid sole trauma/surgical shoe (such as
the Darco shoe). Stress fractures of the metatarsals respond well to a gel-cast and
surgical shoe, and digital fractures can be managed with gauze dressings and a surgical
shoe. Acute metatarsal fracture is best treated with below-the-knee iBK) immobilization.
Only very stable fractures, due either to fracture pattern, location, or surgical fixation, can
sustain weight bearing during the healing phase (compare the fracture to surgical
osteotomy design and fixation to help decide how to protect during healing). For this
reason, non-weight bearing immobilization is the general rule for foot and ankle fractures.
Ambulation with crutches, a walker, or wheel chair or another protective device are
standard. Follow-up radiographic inspection is required after initial reduction, and perhaps
a few days later (initial follow-upL based on clinical progress, to assure maintenance
of alignment, then at about 6-8 weeks, or any time as indicated based on clinical signs
and symptoms.
Open fracture Management--open fractures may be associated with severe limb and/or
life threatening injuries. Locally, the extent of soft tissue injury must be evaluated. Open
fractures convey a 60-70% incidence of bacterial contamination and grovvth atthe time of
initial inspection. Open fractures that have gone without treatment for 6-8 hours are
considered infected. The Gustilo classification of open fractures is depicted in Table 10-1.
TABLE 10-1. THE GUSTILO CLASSIFICATION OF OPEN FRACTURES.

Type Description of the fracture
I Fracture with open wound <1 em, clean, minimal soft tissue necrosis, and the
fracture is usually transverse or short oblique with minimal or no comminution
II Fracture with open wound >1 em, clean, minimal soft tissue necrosis, and
fractL,Jre is usually transverse or short oblique with minimal or no comminution,
commonly associated with crush injuries sustained in motor vehicle accidents,
farm or industrial machinery mishaps, and gunshot wounds
111 Fracture with extensive open wound, contamination, and/or necrosis of skin,
muscle, neurovascular and surrounding soft tissues; and the fracture is often
comminuted
The principles of open fracture treatment tallow those stated previously for wound
debridement, tetanus and antibiotic prophylaxis, in addition to skeletal stabilization.
Appropriate antibiotic therapy entails initial administration of cefazolin 1 or 2 grams IV,
followed by 1 gm IVPB Q 8 hr thereafter until definitive cultures are available, depending
upon the specifics of the case. If the injury occurred in a farm o'r similar tetanus-prone
environment, then cover for Clostridia by administering aqueous penicillfn-G 10~20 million
units IV daily in divided doses every 6 hours. Alter antibiotic therapy based on allergy
history, and other systemic factors. Use antibiotics for at !east 3 days, and continue
therapy for 3 additional days in the noninfected wound if management warrants delayed
primary closure, secondary intention closure, OR IF or in the event that internal or external
fixations require alteration. Skeletal stabilization in an anatomic alignment enhances
tissue viability, wound healing, and diminishes the risk of infection. Initial treatment varies
with fracture stability and neurovascular status, and focuses on manipulative (closed)
reduction as described above. Temporary and/or permanentfixation can be achieved with
K-wires and Steinmann pins, external fixation, and interfragmental compression screws as
deemed indicated based on the specific merits of each fracture. It is preferable to minimize
periosteal reflection. If bone grafting is indicated, this can be done immediately in a Type I
open fracture, however is best performed on a delayed basis after initial stabilization of the
wound. In Type II open fractures, the bone graft is best applied at the time of delayed
primary closure when there is no evidence of infection. Application of an external fixator
obviates the need to effect stability with a bone graft at the time of initial intervention. If
infection does occur after graft transplantation, the autogenous graft may still take. Gustilo
recommended autogenous cancellous bone grafting in type Ill open fractures at
approximately 3 months after initial therapy, when reactive bone callus formation has
diminished. The decision to close the wound is based on factors previously described.
Digital Fractures and Dislocations-digital fractures usually occur secondary to dropping

a heavy object on the toe, which usually damages the distal phalanx; or by stubbing the toe
into a rigid object. which usually fractures the distal phalanx of the hallux or the proximal
phalanx of a lesser toe. Hyperplantarflexion injuries often result in IPJ dorsal avulsion
fracture. The fifth toe is the most commonly fractured digit, followed by the hallux and then
the intermediate toes. Intermediate phalanx fractures are rare in the lesser toes. The
medial oblique projection is useful for evaluating the hallux, as is isolation of the toe by
elevating it on foam or similar material to eliminate superimposition of adjacent digits.
Digital fractures should be stabilized with gauze bandaging, stabilizing the injured toe/s to
adjacent healthy digits (buddy splint), and a surgical shoe, much as would be used
following digital arthroplasty. Displaced or unstable fragments that are large enough,
particularly if intra-articular, can be stabilized via OR IF with K-wires or small lag screws.
Distal phalangeal tuft fractures, particularly if comminuted, may require surgical nail plate
avulsion, repair of any nail bed defect, and excision of displaced fragments. Distal
phalangeal fractures that heal with hypertrophy may require subsequent reduction of
prominent bone to eliminate subungual exostosis. Proximal phalangeal base fractures,
particularly of the hallux, can predispose to digital floating, and transverse plane
misalignment. If hallux abductus develops, consideration should be given to surgical
treatment. Hallux interphalangeal joint (HIPJ) dislocation is the essential differential
diagnosis in cases of suspected phalangeal fracture, as ft can also result from the same
pathological force. In the lesser toes, IPJ dislocation rarely involves the DIPJ, and most
commonly affects the PIPJ of the fifth toe. Treatment is closed reduction and buddy splint-
ing usually, unless the reduction is unstable or prevented by protrusion of the phalanx
through the IPJ capsule. In this case, open reduction and capsular repair are required.
Metatarsophalangeal Joint Fractures and Dislocations-turf toe is a traumatic condition

of the hallux and first MTPJ, wherein repetitive hyperdorsiflexion, hyperplantarflexion,
hyperadduction, or hyperabduction results in MTPJ sprain without gross change in joint
alignment. The injury usually affects athletes, in particular those playing on artificial turf
surfaces, although tennis and basketball players can also be affected. Clinically the joint,
as well as the HlPJ, appears swollen, indurated, and tender to palpation and motion. Often
there is an associated subungual hematoma and/or digital ecchymosis. Radiographs should

be obtained to rule out dislocation, osteochondral or avulsion fracture, or sesamoid
fracture. Treatment consists of PRICE with use of a gauze bandage and surgical shoe.
Gradual resumption of strenuous activity is initiated in 7-10 days, and athletic shoes should
be evaluated for proper fit. Orthoses may be helpful. Oral anti-inflammatory agents are
generally indicated, and corticosteroid injection should be avoided.
First MTPJ dislocation-this occurs secondary to hyperdorsiflexion force, and is

categorized as depicted in Table 10-2.
TABLE 10-2. CLASSIFICATION Of FIRST METATARSOPHALANGEAL JOINT DISLOCATION.

Type Description
I A transverse capsular rupture plantar to the metatarsal head/neck with the
proximal phalanx, plantar capsule, and sesamoids displaced dorsally on
metatarsal head. The retrograde plantar directed force of the phalanx drives
the metatarsal head in a plantar direction, and the HIPJ becomes fixed in
plantarflexion. This injury is usually not amenable to closed reduction.
11 A Same as Type I except that rather than the entire plantar capsule and
sesamoid apparatus dislocating distally and dorsally, the intersesamoidal
ligament ruptures and the sesamoids sublux to each side of the metatarsal
head. Radiographs readily show the sesamoids medial and lateral to the
metatarsal head. This injury is amenable to closed reduction, however the
soft tissue disruption should be repaired with suture.
B This injury also displays the sesamoids displaced medial and lateral to the
metatarsal head, however rather than rupture of the intersesamoidal
ligament, there is avulsion fracture of one of the sesamoids. Closed
reduction of the first MTPJ dislocation entails Mayo block of the first ray, then
distraction, followed by pushing the proximal phalanx into a congruous
relation with the metatarsal head. Correction is maintained with a slipper or
BK cast for 3A weeks, then a surgical shoe for an additional 3 weeks.
Resistant deformity requires operative repair. The Type liB injury should be
casted BK for 6 weeks non-weight bearing. Late term sequelae include
sesamoid nonunion and/or sesamoiditis, and surgical excision of the painful
ossicle may be necessary.
Lesser MTPJ dislocation---this occurs less often than does first MTPJ dislocation,
and dorsal dislocation of the phalanx on the metatarsal head is the usual pattern.
Closed reduction is similar to that performed for Type I first MTPJ dislocations.
Osteochondral fractures of the firstMTPJ--these can affecteitherthe phalanx base or

metatarsal head. Phalangeal osteochondral fractures usually occur due to stubbing
with forced transverse plane motion that avulses the intrinsic attachments to the base.
Metatarsal head osteochondral fractures usually occur due to hyperdorsiflexion that
causes impaction with high shear strain at the dorsal aspect of the head. Treatment
entails closed reduction and 6 weeks of immobilization In a slipper or boot cast for small
fragments, or ORIF and immobilization for 6 weeks in a cast for larger fragments. Very
small fragments can be treated much like a dislocation, with earlier return to weight
bearing and motion. When the joint is opened, loose or torn cartilage should be
remodeled and the subchondral cortical bone fenestrated with a 0.035" K-wire. Late
term sequelae include post-traumatic DJD, and arthrodesis or multicomponent
endoprosthesis may be indicated.
Sesamoid fractures-these can occur after a fall from a height wherein direct dorsally
directed force pushes the sesamoids into the plantar surface of the metatarsal head
while the hallux forcefully dorsiflexes. Cumulative microtrauma can also cause
sesamoidal stress fracture, and is associated with dancing, basketball, tennis and
other strenuous activities. The condition is often misdiagnosed and mismanaged. The
tibial sesamoid is more commonly fractured, and rarely are both the tibial and fibular
fractured in the same joint Moreover, bilateral sesamoid fractures are rare.
Symptoms include pain upon direct palpation or first MTPJ range of motion, in
particular with dorsiflexion. The differential diagnosis is extensive, and includes:
Joplin's neuroma, sesamoiditis, osteochondritis dissecans of the sesamoid,
osteochondrosis ofthe sesamoid, bi- or multipartite sesamoid DJD or rupture, turf toe,
HAV with eroded crista, and prominent or hypertrophic sesamoid with plantarflexed
first ray painful plantar callus. Radiographic evaluation can be difficult, particularly
when a bipartite sesamoid is present, 75% of which occur unilaterally. Medial and
lateral oblique, sesamoidal axial views, and contralateral comparison views are often
helpfuL When in doubt, order a bone scan or MRI. Treatment entails a slipper or boot
cast or immobilizing splint and non-weight bearing for 6-8 weeks, followed by
transition back to a sneaker using a surgical shoe until asymptomatic. The prognosis
for complete healing is guarded, and primary as well as delayed excision of the
fracture fragment{s) should be considered. Remember that sesamoidectomy, even
partial, conveys the risk of valgus or varus deformiTy for the tibial and fibular ossicles,
respectively, especially in cases involving a round metatarsal head. Appropriate
muscle-tendon balancing should be performed whenever sesamoidectomy is
performed. Removal of both sesamoids will decrease intrinsic muscle strength and
hallux purchase, causing a hallux hammertoe or cock-up hallux. Prophylactic fusion
ofthe HIPJ should be performed whenever both sesamoids are excised.
Metatarsal Fractures-the principles for management of metatarsal fractures, whether of

the first or Jesser metatarsals, at the head, shaft or base, are the same as those stated
previously in the general management of fracture discussion. A few points of interest should
be noted. It is importantto try and restore the weight bearing balance of the metatarsus, and
attention should be paid to length and sagittal plane relations. Transverse and short oblique
metatarsal fractures, particularly of the shaft, are amenable to closed reduction and
immobilization, and difficult lesions can be pinned either percutaneously or via open
dissection. Multiple metatarsal fractures often display spontaneous reduction of those of
the intermediate rays upon ORIF of either or both of the first and fifth metatarsals, and
fixation of the intermediate metatarsals can be adequately achieved with a single K-wire or
no fixation other than casting. This is an example of the vassal rule. A number of different
types of metatarsal fractures can be incurred, including:
Fifth metatarsal fractures~these are very common injuries. Keep in mind that the
apophysis of the fifth metatarsal styloid appears at 914 years and fuses at 12-15 years
of age. The physis is oriented almost parallel to the long axis of the fifth metatarsal
shaft. The accessory ossicle, os Vesalianum, appears in the tendon of peroneus

brevis near the base. Of particular interest is the Jones fracture (Fig 10-15), which is
caused by medial or lateral cutting or pivoting movementthat produces a transverse
fracture distal to the junction of the fourth and fifth metatarsals. This is actually a
proximal diaphyseal fracture that is not produced by inversion of the foot and ankle.
The Jones fracture is notorious for nonunion, and meticulous fracture management is
crucial. In the patient without great physical demands, closed reduction and
immobilization for 6-8 week in a BK non-weight bearing cast is indicated. In the
athlete or individual that participates in strenuous daily activity, ORIF and BK
non-weight bearing cast 5-6 weeks followed by weight-bearing cast for an additional
2-3 weeks is indicated. If delayed union is suspected, maintain non-weight bearing
and immobilization and add electrical bone growth stimulation (EBGS).I! a nonunion
develops, repair with autogenous cancellous bone graft, electrical stimulation, and
cast non-weight bearing. The base of the fifth metatarsal can also fracture into the
metatarsal-cuboid joint secondary to forced inversion and traction applied through
the tendon of peroneus brevis or the lateral slip of the plantar fascia. The result is an
avulsion fracture that enters the tarsometatarsal joint (TMJ). If the fracture is
displaced, the ORIFfollowed by weight- bearing BK cast for 6 weeks. lithe fracture is
nondisplaced, then closed reduction and immobilize in a non-weight bearing cast for
6 weeks. The fifth metatarsal base can also fracture at the styloid process (Fig 10-16).
which is an extra-articular fracture caused by the same force described above for the
intra-articular fracture. Treatment is the same as that described above for the
articular fracture at the fifth metatarsal base.
Metatarsal stress fracture--this is also known as a march or fatigue fracture, and

develops secondary to cumulative that surpasses the bone's ability to respond to
repetitive load. This is frequently observed when a person initiates a new exercise
program, undergoes basic training in the military (march fracture), suffers with a
specific biomechanical abnormality wherein there is loss of adjacent metatarsal
support (hypermobile first ray dumping force on the second ray, or following adjacent
metatarsal fracture or osteotomy). The onset of pain is usually gradual, but

exacerbated by recent increased activity. The pain is localized to the affected

metatarsaL with associated edema and local heat. Stress fracture usually localizes to
the metatarsal neck, and most commonly involves one of the intermediate rays. The
differential diagnosis includes neuroma, MTPJ enthesitis, arthritis, and extensor
tenosynovitis. Charcot fractures, pathological fracture, and osteoporosis should also
be considered. Radiographic findings initially may reveal a small cortical break at site
of maximum clinical tenderness. Periosteal reaction usually develops at the stress
fracture site, and may become evident at about 10 days or longer from onset of pain.
Repeat radiographs at 2-3 weeks after the onset of pain may be needed to confirm
diagnosis. A bone scan or MRI should be obtained if standard films are equivocaL
Treatment of metatarsal stress fracture entails a gel-cast and surgical shoe or a
removable cast-boot for 3-5 weeks, and orthoses may be useful to address
biome chanica! abnormalities thereafter.
Lisfranc Fracture Dislocation-this injury constitutes 1% of all reported fractures,

however the diagnosis is missed in almost 20% of cases. Anatomical considerations
include the "keystone" nature of the second metatarsal base in the intercuneiform recess,
which provides a significant amount of stability to the midfoot complex. The tarsometatarsal
joint (TMJ) is bound together by a series of transverse dorsal and plantar ligaments, as well
as intermetatarsalligaments. There is a distinct absence of an intermetatarsal ligament
between the first and second metatarsals. The plantar ligaments are thicker, and dorsal
displacement is most common. The ligament attaching the medial cuneiform to the first
metatarsal is the largest ligament at this level. The most important ligament of the TMJ is
Lisfranc's interosseous ligament, which attaches the base of the second metatarsal
medially to the lateral aspect of first cuneiform. Usfranc's ligament is often involved in
avulsion fracture of the second metatarsal base. The Hardcastle classification {also know
as Oueno and Kuss) is the standard system for identifying TMJ fracture/dislocations
(Fig. 10-17), and categorizes these injuries as depicted in Table 10-3.
TABLE ID-3. THE HARDCASTLE CLASSIFICATION OHISFRANC FRACTURE DISLOCATIONS.

Type Description of injury
A (total, homolateral The most common TMJ fracture/dislocation, it
dislocation) displays disruption of the entire TMJ in the sagittal or
transverse plane. This injury usually involves lateral
displacement of all ofthe metatarsal
B (partial 1. Medial displacement of the first metatarsal alone
dislocation) or with metatarsals 2, 3, 4, not 5
2. Lateral displacement of one or more of the lesser
metatarsals (notthe first metatarsal)
C (divergent) Displays the first metatarsal dislocated medially and
the lesser metatarsals either partially or totally dislocated
laterally in the sagittal and/or transverse planes
Although the Hardcastle classification is most commonly used, Wilson also classified
Lisfranc joint fracture/dislocations, as depicted in Table 10-4.
Partial Incongruity
Dorsa plantar
Type A
Lateral dislocation
Figure 10.17
TABLE 10-4. THE WilSON ClASSIFICATION OF LIS FRANC FRACTURE DISLOCATIONS.

Class Stage Description of the fracture
Plantar-flexion-
supination-most common Dorsolateral dislocation of metatarsals 2-5
II Dorsolateral dislocation of metatarsals 1-5
Plantart!exion pronation I Medial dislocation of first metatarsal
II Medial dislocation of first metatarsal, dorsolateral
dislocation of metatarsals 2-5
Plantarflexion Dorsal dislocation of second metatarsal base and/or
fracture dislocation base of first metatarsal
The mechanism of TMJ injury is usually a crushing force applied to the forefoot with
the ankle plantarflexed. The second metatarsal must be dislocated first, either by
transverse base fracture or medial avulsion by Lisfranc's ligament, in order to disrupt the
TMJ. Clinical findings include localized signs and symptoms of fracture/dislocation, and it
is critical to assess the neurovascular status to the forefoot. The foot may appear grossly
shorter than the contralateral limb. Radiographs can be difficult to assess, and attention
should be directed at the first metatarsocuneiform interfaces, as well as the base of the
second metatarsal. One should also look for a compression fracture of the cuboid.
Transverse and sagittal plane stress views can add information, and the CT scan has
become a mainstay of diagnostic accuracy in regard to this injury. Treatment begins with
attempted closed reduction and immobilization, if indicated. Distal traction can be achieved
by suspending the foot above the table with Chinese finger traps until adequate soft tissue
relaxation ensues. Counterweights strapped around the ankle can be used to enhance
distraction. An external fixation frame can also be used to effect distraction and
stabilization. Attention is directed attrying to relocate the second metatarsal base into the
intercuneiform recess, then to reduction of the first metatarsal-medial cuneiform joint
depending on the fracture/dislocation pattern. Percutaneous pin stabilization may be
attempted after reduction, however this is notoriously difficult If closed reduction fails, it
may be due to tibialis anterior or peroneus longus interposition, or due to the avulsion
fragment of the second metatarsal base. OR IF may be performed via 3 dorsal incisions:
1) dorsomedial first met-cuneiform, 2) between second and third metatarsals and
corresponding cuneiforms, and 3) between fourth and fifth metatarsals and the cuboid. The
first metatarsal is generally fixed first, followed by the remaining metatarsals from medial
to lateral. Pin stabilization is recommended as follows:
Type A-1 wire stabilizing first metatarsal-cuneiform and a second stabilizing the fifth
metatarsal-cuboid joints.
Type B (medial type)-2 pins stabilizing the first metatarsal-cuneiform.
Type C-2 pins medial and one lateral.
A BK cast is then used for 8-12 weeks, the first6-8 weeks being non-weight bearing.
The pins are removed after 6-8 weeks.
Calcaneal Fractures-this injury is most commonly observed in men aged 35-45 years, and
the male to female ratio is 5:1. Calcaneal fractures are associated with spinal fractures 20%
of time, with Tl2- L2 the most common vertebral range and L1 the most common vertebra
fractured. The most common mechanism is a fall from a height, followed by motor vehicle
accident Clinical findings include Mondor's sign, which is plantar ecchymosis extending
from the heel into the plantar vault The heel also appears wide and shortened, and the
patient is antalgic and unable to bear weight on the injured foot. Bohler's angle is made by
the intersection of a line extending from the posterosuperior process of the calcaneus to the
posterior margin of the posterior facet of the STJ, and the line extending from the posterior
margin of the posterior facet of the STJ to the tip of the anterior beak of the calcaneus
(Fig. 10-18). Bohle(s angle is usually 25-40", and is depressed or even negative when the
posterior facet is depressed by the talus into the body of the calcaneus in a joint
depression fracture. Radiographic signs include disruption ofthe calcaneocuboid joint on
the AP view; depression of the posterior facet of the STJ and Bohler's angle on the lateral
view; disruption of the posterior facet and widening of the calcaneus with lateral wall blow
out on the calcaneal axial view; and fracture of the anterior process on the medial oblique
view. Radiographs of the ankle, legs, and vertebral column may also be indicated, and a
CT scan of the hindfoot can be very useful prior to operative intervention. The Rowe
classification (Table 10-5) deals primarily with extra-articular calcaneal fractures (Fig. 10-19).
Lateral talar process
Neutral triangle
Figure 10.18
Ia lb
~ Ill
~ lc
._) ef) IV
~lla
~fcactuce
,,_. Break
~
lib '
Avulsion
11 fracture
v
Figure 10.19
TABLE 10-5. THE ROWE CLASSIFICATION OF CALCANEAL FRACTURES.
Type Description Treatment

I A Fracture of the calcaneal tuberosity Closed reduction immobilization
sustained in afall with the heel everted with BK cast, 6 weeks, weight
or inverted; can result in splaying and bearing if non-displaced. ORIF if
widening that may interfere with the displaced or unstable
peroneal tendons
B Fracture of sustentaculum tali, sustained Closed reduction immobilization
from fall with twist on a supinated foot; with BK cast 6 weeks if non-
tenderness upon passive or active displaced. ORIF if displaced or
flexion and extension of the hallux due unstable
to FHL; axial calcaneal X-ray is the
best view.
C Fracture of anterior process (most Closed reduction and immobiliza-
common Type I fracture); only cal- tion with BK walking cast for
caneal fracture where females have 6 weeks. Excise or ORIF the
i higher incidence; this is an avulsion in~ fragment if symptoms persist
jury of bifurcate ligament; force is
plantarflexion on a supinated foot;
seen clearly on lateral or medial
oblique views; may need tomograms
to visualize if the fragment is small
Non-weight bearing BK cast for
II A Beak or avulsion fracture of calcaneus about 6 weeks in plantarflexion if
I that does not affect Achilles insertion non-displaced. Must reduce if
B Avulsion fracture with pull off at large and/or displaced; percuta-
Achilles attachment neous pin may work, or ORIF if
unstable
Ill Fracture of body without involvement of AK Non-weight bearing cast with

STJ (most common extra-articular frac- knee flexed. ORIF if displaced or
ture); results from fall with edge of talus unstable
going into calcaneus; lateral X-ray and
axial views most helpful; axial view deter-
mines STJ involvement
IV Fracture of body of calcaneus involving

STJ; this is actually an articular fracture,
however fractures in the Rowe
classification are still considered as
primarily extra~articu!ar Closed reduction, percutaneous
pinning, or OR IF
V Central depression fracture with a
degree of comminution (also, an
articular fracture)
The Essex-Lopresti classification (Table 10-6) describes intra-articular calcaneal

fractures (Fig. 10-20). The Essex-Lopresti system of intra-articular fractures describes
approximately 75% of all calcaneal fractures that usually result from a long fall from a high
place. When the victim hits the ground feet first, the talus is driven down into the
calcaneus, crushing the posterior facet into the body of the as cal cis and splitting the bone
like a wedge. Essex-Lopresti Types A and Bare differentiated by the secondary fracture line
and the shape of the resultant fragments.
Tongue Type Joint depression type
Figure 10.20
TABLE 10-6. THE ESSEX-LOPRESTI CLASSIFICATION OF CALCANEAL FRACTURES.

Type PrimaiV fra.cture line Secondary fracture line
A !tongue fracture) Courses from superior to Propagates from the primary,
inferior, extending from posteriorly to exit the
Gissane's critical angle at posterior cortex, usually
the junction of the posterior proximal to the Achilles
facet and the calcaneal insertion
sulcus, to the plantar
aspect of the calcaneus
B !joint depression) The same as described Surrounds the posterior facet

above for the tongue- that is driven like a column into
type fracture the cancellous bone of the body of
the calcaneus, exploding the
bone medially and laterally
into comminuted fragments
The Sanders classification of calcaneal fractures is probably the most useful in

regard to directing surgical intervention (Table 10-7). To classify the fracture using this
system, the frontal plane CT scan is used, and the posterior facet of the subtalar joint is
divided into 3 equal segments, from lateral to medial, with the final line collinear with the
vertical margin of the sustentaculum tali. The Type I fracture are nondisplaced and involve
a fracture of either the lateral, central, or medial segment of the posterior facet. Fractures
localized to the medial segment are most difficult to visualize and reduce primarily. Type II
fractures involve 2-part split fracture of the posterior facet, and Type Ill injuries
involve 3-part split fractures with depression of the posterior facet into the body of the
calcaneus. Type IV fractures involve severe comminution of the posterior facet and the
body of the calcaneus.
TABLE 10-7. THE SANDERS CLASSIFICATION OF CALCANEAL FRACTURES.

Type Description olthe frontal plane CT appearance of the fracture
I Nondisplaced fracture of the posterior facet
II 2-part (split) displaced fracture
Ill 3-part Isplit) displaced fracture with joint depression
IV Severely comminuted fracture with joint depression
Mechanically speaking, the calcaneal tuberosity is situated lateral to the center ofthe
talus. When a vertical compressive force is applied,2 primary fracture fragments develop:
1) superomedial or sustentacular fragment !sustentaculum tali), and 2) the tuberosity
fragment that contains the lateral1/3 to 1/2 of the posteriorfacet. lfthe pathological force
continues, the talus and sustentaculum tali are driven plantar and media!. If the force still
continues, then the posterolateral edge ofthe talus is driven into the superolateral aspect
of the posterior facet, which is supported by cancellous bone that is crushed and impacted.
A lateral wall blowout fracture may also occur, with possible extension into the
calcaneocuboid joint. Palmer's three constant components of intra-articular fracture
include: 1) vertical shearing fracture, 2) fracture of the lateral cortex, and, 3) depression
fracture of the posterolateral STJ. Pedal deformity related to calcaneal joint depression
fracture includes: increased calcaneal width making shoe wear difficult, decreased
calcaneal height and length adversely affecting limb length and gait, intra~articularfracture
of the STJ with resultant DJD, and sural nerve and peroneal tendon entrapment along the
lateral wall of the calcaneus. Initial management involves neurovascular assessment,
PRICE, and attempted closed reduction and immobilization if indicated. Simple
immobilization, often combined with early weight bearing, eliminates surgical risks and may
be indicated in certain patients who are less active and perhaps at high risk for surgical
complication. Limited weight be-aring after 1 week, progressing to ful! weight bearing at 6-
12 weeks can be undertaken. Essex-Lopresti described manipulation with skeletal fixation
using a pin that enters the body of the calcaneus from the posterior aspect that is then
pulled in a plantar direction to try and lift the posterior facet out of the body ofthe calcaneus.
This can also be undertaken with more than 1 pin. The pin or pins is/are then secured in the
surrounding plaster that is applied AK with the knee flexed. This method is applicable only
in tongue fractures, and is not used much because of inaccurate STJ realignment, and
subcutaneous compromise at the pin tract. Palmer described a clamp \Palmer clamp) used
to squeeze the medial and lateral cortices together, however this did very little to improve
the STJ. Palmer also described OR IF with elevation of the posterior facet under direct
visualization and manipulation, followed by packing beneath the raised facet with
autogenous bone graft, followed by pin stabilization and BK non-weight bearing cast for 12
weeks. Galie described early triple arthrodesis, and indeed this is often a last resort for
patients who have developed post-traumatic arthrosis following fracture.lffracture blisters
are present, then surgical intervention should be postponed until the skin barrier is healthy.
Operative intervention is ideally performed within the first 2-6 hours of injury. The Zwipp
incision preserves the peroneal tendons and the sural nerve in an intact soft tissue flap.
The Podiatry Institute technique entails a lateral approach with sectioning or preservation
of the peroneal tendons, reconstruction of the posterior facet with supporting bone graft,
and a combination of buttress plate and lag screw and cerclage wire fixation, as necessary.
A number of specialty locking and nonlocking plates are available for reconstruction of
the fractured calcaneus. Complications of calcaneal fracture, and its repair, include
post-traumatic STJ arthritis, ankle joint arthritis, tenosynovitis of peroneals, plantar heel
pain due to diminished cushioning effect of fat pad, sural or PT nerve entrapment, shuffling
gait with shortened stride, and stiffness. Late salvage of arthrosis following calcaneal
fracture often entails talocalcaneal fusion, triple arthrodesis, or extra-articular bone bloc
distraction arthrodesis to restore the height of the heel.
Talar Neck Fractures-anatomically, 2/3 of the talus is covered with articular cartilage,
therefore most fractures of the talus are intra-articular. No muscles or tendons originate
from or insert into the talus. The extended neck with its tenuous blood supply is vulnerable
to injury. The blood supply to the talus entails:
Body-artery of tarsal canal from the posterior tibial and deltoid branch.
Head and neck-artery of tarsal sinus from perforating peroneal and DP.
Posterior talus-calcaneal branches of PT.
Avascular necrosis \AVN) is likely to occur when 2/3 of the vascular channels are
disrupted. Hawkins noted that it takes until 6-8 weeks after the injury to recognize the
presence of AVN, and it may not appear until 1-4 months have passed. Signs and
symptoms oftalar AVN include intractable pain, relative radiographic sclerosis, or opacity
of the dead bone, best observed on the AP view of the ankle. Hawkins noted the presence
of subchondral bone revascularization as radiolucency in the dome of the talus on the AP
view, and this is referred to as Hawkins' sign and is indicative of healing. The treatment of
AVN is non-weight bearing in BK cast for 6-8 months until revascularization occurs, with
electrical bone growth stimulation. The Hawkins classification (Table 10-8) oftalar neck
fractures can be useful in regard to anticipating the development of avascular necrosis
(Fig. 10-21).
TABLE 10-8. THE HAWKINS CLASSIFICATION OF TALAR NECK FRACTURES.

Type Fracture Clinical characteristics
I Vertical non-displaced Occurrence is 20%, only the blood supply
fracture oftalar neck to the neck disrupted, 0-15% incidence of AVN
II Vertical fracture through Occurrence is 42%, with 2 areas of disrupted
neck with dislocation blood supply, neck and body; 15-50%
of STJ (not ankle) incidence of AVN
Ill Vertical fracture of neck Occurrence is 34%, and all3 sources of
with dislocation of talar blood supply are disrupted; 90-100%
STJ and ankle incidence of AVN
IV Vertical fracture of neck Occurrence is 4%, disrupts all3 areas of talar
with dislocation of blood supply; 90-100% incidence of AVN
STJ, ankle, and TNJ
Figure 10.21
The treatment of talar neck fractures is based on the degree of injury and blood
supply. Hawkins Type I fractures are managed in a BK non-weight bearing cast for 6-8
weeks. Alternatively, an AK cast with the foot plantarflexed for 3-4 weeks followed by a BK
cast neutral for an additional 4 weeks can be used. Weight bearing and motion are not
initiated until adequate signs of healing are observed radiographically. Hawkins Type II, Ill,
and IV fracture/dislocations are initially closed reduced, however OR IF with lag screw
fixation of the neck is most effective. Immobilization and WB status are the same as
described previously for non-surgical treatment. Complications of talar neck fractures
include AVN, degenerative arthritis of the ankle and STJ, nonunion or mal-union, and
infection related to open fracture or surgery.
Os trigonum Syndrome and Shepherd's Fracture-as trigonum syndrome and Shepherd's

fracture can be very painful and debilitating. The os trigonum is present in 10% of the
population. The posterior aspect of the talus displays 2 processes that form a groove through
which the FHL tendon courses. The lateral process, also known as Stieda's process or the
trigonal process, is the larger of the 2 and develops from a secondary center of ossification
atS-11 years of age. Ossification with closure of the physiswill usually occur within one year
thereafter. The os trigonum represents failure of the secondary center to unite with the
posterolateral process of the body. Fracture of Stieda's process is referred to as Shepherd's
fracture, and must be differentiated from a painful os trigonum. Both the os trigonum and
Stieda's process are injured by means afforced plantatflexion. The os trigonum may occur
bilaterally, so contralateral radiographs may be informative. A fractured posterior process
will be jagged with rough edges in the early phase, while the margins of the os trigonum
should be smooth. Ankle and first MTPJ range of motion may be painful in both cases.
Treatment for both as trigonum syndrome and Shepherd's fracture entails a local anesthetic
block, BK weight bearing cast immobilization for 6 weeks, followed by range of motion
physical therapy. Recalcitrant cases require surgical excision of the os trigonum or the
Shepherd's fracture fragment, via a posterolateral incision that parallels the peroneal and
is anterior to the Achilles tendon.
Tatar Dome Fractures-talar dome defects can develop secondary to ankle sprain or
fracture, and are known to be debilitating in all age groups. The Berndt and Harty
classification {Table 10-9) is the standard system for identification of talar dome lesions.
Talar dome osteochondral defects develop as a result of shearing under compressive load
between the distal tibial bearing sutface and the dome. The injury causes AVN of
the subchondral trabecular and cortical bone, which eventually heals with cortical
irregularity, and resultant development of post-traumatic arthritis.
TABLE 10-9. THE BERNDT AND HARTY CLASSIFICATION OF TALAR DOME lESIONS.
Stage Description of the injury
I A small area of subchondral bone compression
II A partially detached osteochondral fragment
Ill A completely detached fragment, remaining in its crater
IV A displaced osteochondral fragment
The incidence of posteromedial talar dome defect is 56%, while anterolateral defects
occur in 44% of cases. Medial lesions are caused by ankle inversion and plantatflexion,
while lateral lesions are caused by ankle inversion with dorsiflexion (Figs. 10-22 and 10-23).
Treatment for all Stage I, II, and medial Stage Ill lesions is 6-12 weeks of BK non-weight
bearing cast immobilization, with consideration to use of a patellartendon bearing brace and
partial weight bearing; and surgical intervention for recalcitrant pain. Stage IV and lateral
Stage Ill lesions are treated surgically by means offragment excision, saucerize the crater,
drill hole fenestration of the subchondral bone to aid revascularization and enhance
fibrocartilage production. Medial lesions may require medial malleolar osteotomy and
subsequent replacement with lag screw fixation. Lateral lesions may be combined with
secondary repair of chronic lateral ankle instability if this condition exists. Very large
fragments may be amenable to reduction and fixation with either absorbable pin or screw
fixation. The use of autogenous osteochondral plug grafts (OATS) harvested from non~
contact articular cartilage from the head of the talus, or the knee, as well as allogeneic
grafts, and/or autogenous cultured cartilage cells, provide other reconstructive options.
Early postoperative range of motion in a nonweight bearing fashion is indicated, with
resumption of weight bearing at about 2-3 weeks postop. Salvage by means of ankle fusion,
or total ankle replacement may also be considered {explained elsewhere in this manual).
Ankle Fractures-the anterior inferior tibiofibular ligament attaches to the tibia at the
tubercle of lillaux. Avulsion fracture of the tibia at this location is termed a lillaux-Chaput
fracture. Avulsion of the fibula at the attachment of this ligament is termed a Wagstaffe
fracture. The Lauge-Hansen classification (Table 10-10) of ankle fractures provides a
functional description of the mechanism of injury. The first word in the system describes the
position of the foot at the time of injury, and the second word denotes the pathological
motion of the foot relative to the ankle.
Stage I Stage II
Anterolateral
lesions
Key
Stage Ill Stage IV I Sites of osteochondral fractures

TABLE 10-10. THE LAUGE-HANSEN CLASSIFICATION OF ANKLE FRACTURES.
Class Mechanism Stage Description of the pathology

Supination~ Pure I Rupture of lateral collateral ligaments or trans-
adduction inversion of verse avulsion fracture of lateral malleolus
(Figure 10-24) foot in the II Talus impacts the medial malleolus causing a
ankle mortise vertical (oblique) fracture of the tibia; the
tibiofibular syndesmosis remains intact and
diastasis does not occur
Pronation- Pure eversion Rupture of the deltoid ligament (medial clear

abduclion of the foot in space), or transverse avulsion fracture ofthe
(Figure 10-25) the ankle mortise medial malleolus
II Rupture ofthe anterior and posterior inferior
tibiofibular ligaments, or Tillaux-Chaput or
Wagstaffe avulsion fracture from the tibia or
fibula, respeclively
Ill Short oblique fracture of the lateral malleolus
originating at the level of the ankle joint; on
the lateral view, the fibular fracture appears
transverse
Supination- The talus Disruption of the anterior-inferior tibiofibular

eversion externally ligament or avulsion fractures of Wagstaffe
(external rotates about (fibula) or Chaput-lillauxtibia)
rotation) an axis II Classic spiral fracture of the lateral malleolus,
(Figure 10-26) comprised of beginning at the joint line; the fracture line
the medial runs laterally from anterior-inferior to
malleolus and superior-posterior
deltoid ligament Ill Disruption of posterior-inferior tibiofibular
ligament or avulsion fracture of Volkmann's
posterior malleolus
IV Rupture of deltoid ligaments or transverse
fracture of medial malleolus
Pronation- External Disruption of deltoid ligament or transverse

eversion rotation of avulsion fracture of medial malleolus
(external the talus II rupture of anterior-inferior tibiofibular
rotation) about an axis ligament or Wagstaffe (fibula) or lillaux-
(Figure 10-27) consisting of Chaput (tibia) avulsion fracture
the lateral Ill Interosseous membrane torn above
malleolus and syndesmosis and below fibular head,
lateral collateral followed by high fibular fracture at any level
ligaments starting above joint line, all the way to the
proximal neck of the fibula (Maisonneuve
fracture)
IV Disruption of posterior-inferior tibiofibular
ligaments or avulsion fracture of tibia
(Volkmann) or fibula
Stage 4
Stage 1
4
The Danis Weber classification (Table 10-11) focuses on the level of the fibular
fracture line relative to the ankle joint, and serves as a guide to repair of the fibula. The
fibular fracture is considered dominant, and restoration of its anatomic length takes
precedence over repair of the inferior tibiofibular syndesmosis. The goals of ankle fracture
repair are realignment of the ankle mortise, inspection of the talar dome and tibial plafond,
and reapproximation of supporting soft tissue structures.
TABLE 10-11. TilE DANIS WEBER CLASSIFICATION OF ANKlE FRACTURES.

Type Fracture pattern Pathological anatomy Corresponding
lauge~Hansen
classification
A Fibular fracture Transverse avulsion fracture Supination-
distal to the joint line of fibula at or distal to level adduction
of ankle joint
Inferior tibiofibular ligaments
remain intact
May see associated medial
malleolar vertical fracture
B Fibular fracture Spiral or oblique fibularfracture Supination-
at the joint line beginning at inferior tibiofibular eversion or
syndesmosis pronation-
Tibiofibular ligaments are abduction
usually disrupted but interosseous
membrane remains intact
May have disruption of deltoid
ligament or transverse medial
malleolar fracture
c Fibular fracture Fibular fracture above the Pronation-
above the joint line level of the tibiofibular eversion
syndesmosis up to the fibular head
Rupture of tibiofibular syndesmosis
and interosseous membrane
Deltoid rupture or transverse
medial malleolar fracture
Treatment in all cases begins with attempted closed reduction and immobilization, and
certain fractures are amenable to closed reduction and immobilization as the mainstay of
management Patients with minimal displacement, debilitated hosts, and patients with
limited ambulatory capacity may do best with closed reduction and immobilization, and
supportive therapy for post-traumatic arthrosis afterwards. Conscious sedation usually aids
closed reduction and immobilization. After closed reduction, immobilization in a curved
plaster cast with 3-point pressure (minimal padding) is continued 6-8 weeks non-weight
bearing. The radiographic criteria for adequate reduction of displaced ankle fractures include:
1. No widening of medial clear space;

2. No displacement of malleoli on AP view;
3. <2 mm of posterior displacement at lateral malleolus on lateral view;
4. No angular deformity ofthe ankle; and
5. Posterior malleolar fracture involvement of less than 25-30% ofthe tibial plafond.
Open reduction and fixation is best performed as soon as possible after injury, before
severe edema and hematoma form, as long as the patient is medically able to sustain
operative intervention. After 6-8 hours, edema with hematoma may prevent wound closure,
and fracture blisters may form. In such cases, therapy entails protection and rest, ice,
compression and elevation (PRICE} with closed reduction and application of a Jones
immobilizing dressing, and waiting 4-14 days until the skin barrier is intact and edema
reduced.
Suggested techniques for OR IF of ankle fractures (there are other useful fixation methods,
and the following are time honored guidelines) include:
Supination-Adduction (Type A)
1. Use two 0.062 inch K-wires with 22-gauge tension band wire for transverse
fibular fracture.
2. Use two 4.0 mm cancellous screws perpendicular to fracture line and parallel to
each other to fix vertical medial malleolar fracture.
Pronation-Abduction (Type B)
1. Fix the short oblique lateral malleolar fracture with a 5- or 6-hole 1/3tubular axial
compression plate with 3.5 mm cortical screws to secure the plate above the
fracture line (through both fibular cortices) but not below the fracture line, as
this could damage the talus. Only purchase the lateral fibular cortex.
2. Repair inferior tibiofibular ligaments with 0-gauge non-absorbable suture. If
lillauxfracture is present, use 4.0 mm cancellous lag screw/s.
3. Transverse medial malleolar fracture is fixed with two 4.0 mm cancellous screws
perpendicular to fracture line and parallel to each other.
Supination-Eversion (Type B)
1. Spiral fracture of fibula is fixed with interfragmenta14.0 mm cancellous screws
or 3.5 mm cortical screws. Supplement with 1/3 tubular 5-6-hole neutralization
plate placed perpendicular to plane of the interfragmental screws. The plate is
anchored with 3.5 mm cortical screws laterally, or a posterior anti-glide plate is
used to both reduce and stabilize the lateral malleolar fragment.
2. Repair of anterior-inferior tibiofibular syndesmosis or avulsions, as noted above.
3. tf small posterior malleolar fracture fragment occurs, it should spontaneously
reduce with reduction of the fibula since the posterior inferiortibiofibu!ar ligament
is intact (vassal rule).
4. If there is a large tibia fragment posteriorly (greater than 25% of posterior
malleolus) it must be reduced. Use 4.0 cancellous screws posterior to anterior.
5. Two 4.0 mm cancellous screws perpendicular to transverse avulsion medial
malleolar fracture and parallel to each other.
Pronation-Eversion (Type C)
1. For fibular fractures mid-diaphyseal level or lower, use interfragmental
compression, with 4.0 mm cancellous or 3.5 mm cortical screws, then augment
with 1/3 tubular neutralization plate. Use tibiofibular transfixing screw through
or above the plate for fractured distal diaphysis. Alternatively, absorbable screws,
or a nonabsorbable tension suture (TightRope), could be used for tibiofibular
transfixation.
2. In Maisonneuve fractures, do not open reduce due to potential complication with
common peroneal nerve, and adequacy of tibiofibular transfixation.
3. First, fit distal fibula into fibular notch on tibia and temporarily transfix tibia and
fibula with 5/64 Steinmann pins and X-rayto visualize mortise and length offibula.
If satisfactory, suture interosseous membrane and then use final fixation with
two 3.5 mm cortical screws. Goal is to stabilize the tibiofibular relationship
without compression ofthe mortise.
4. Remove transfixing screws at 6-8 weeks and hardware at 4-6 months.
Tibial Pilon Fractures-the distal tibial metaphysis (pilon) can be seriously disrupted in a
variety of injury patterns, and repair of this structure is difficult and requires considerable
experience. Pilon fractures enter the ankle, and may be associated with fibular fracture as
well. Repair entails anatomic reduction, autogenous corticocancel!ous bone grafting, and
internal as well as external fixation. A high rate of post~traumatic arthrosis, osteomyelitis,
delayed and nonunion, limb angular and length misalignment, and difficulty walking can
ensue. Revisional surgery, bone transport, ankle and pantalar arthrodesis, and amputation
are not uncommon. Although several classification systems are available, the most
straightforward is that of Ruedi and Allgower (Table 10-12).
TABLE 10-12. THE RUEDI-AllGOWER CLASSIFICATION OF PILON FRACTURES.

Type Description of the pilon fracture
I Pilon fracture with minimal displacement
II Pilon fracture with significant displacement
Ill Pilon fracture with significant displacement and loss of cancellous bone
Epiphyseal Plate Fractures--the epiphyseal complex consists of the epiphysis, physis, and
the metaphysis. Epiphyses are either of the pressure or traction type. Pressure epiphyses
are located at the end of a long bone and provide rapid longitudinal growth. Traction
epiphyses are non-articular, and located where muscle or tendon attaches to bone, and do
not contribute to axial growth. Anatomically the physis displays three distinct zones
\Fig. 10-28). The zone of growth is closest to the epiphysis and contains resting chondrocytes
that progress to dividing cells that arrange in columns. The next component is the zone of
cartilage maturation, which is the weakest region due to loss of intracellular matrix. Finally,
Ossification
Zone of
Transformation

I'
the zone of cartilage transformation displays cartilage converting to bone. Periosteum is

more vascularized, thicker, and stronger in the child. The cartilage is strongly attached to
the metaphysis, and more loosely attached to the diaphysis. The periosteum also acts as a
checkrein to resist fracture displacement. The vascular supply to the growth plate
complex is as follows: metaphysis-supplied by the nutrient artery of the diaphysis, vessels
from periosteum and perichondrium, and these sources extend to the zone of
hypertrophied cells; epiphysis-supplied by nutrient epiphyseal vessels; physis-supplied
by nutrient arteries from both the metaphysis and the epiphysis, as well as direct
perichondrial vessels to the physis.lfthe metaphyseal supply is compromised or lost, there
is usually very little change in physeal perfusion. If, however, either the epiphyseal or
perichondrial supply is lost, the physis may die and premature partial or total closure may
ensue. The epiphyseal vessels supply the physeal zone of growth. Partial closure may cause
angular deformity. The osseous ring of Lacroix is an extension of metaphyseal cortical bone
that stabilizes the physis at the zone of Ranvier, where the physis interfaces with the
metaphysis (Fig. 10-29). Evaluation of physeal injury requires at leastthree radiographic
views and comparison with the uninjured extremity. Epiphyseal fractures are categorized
by Salter-Harris (Table 10-13) and Aiken-Mueller (Table 10-14).
TABLE 10-13. SALTER-HARRIS ISH) CLASSIFICATION OF EPIPHYSEAL PLATE FRACTURES.

Type Description
I (Fig. 10-30) 1. Separation of epiphysis from metaphysis between layers of
hypertrophy and calcification
2. Resting cells remain with the epiphysis
3. Minimal displacement usually due to strong periosteum
II(Fig. 10-31) 1. Most common acute physeal injury
2. Separation of epiphysis from metaphysis between layers of
hypertrophy and calcification
3. Fracture line runs through physis then through metaphysis
4. Thurston-Holland sign-metaphyseal fragment where the
periosteum is intact adjacentto the metaphyseal fragment
5. Werenskiold sign-small fragment of metaphyseal fragment on
X-ray
III(Fig. 10-32) 1. Fracture begins in joint, runs up to the physis then makes a 90
turn through the layer of hypertrophied cells to periphery
2. Area of concern for blood supply to free fragment as well as
congruity of joint surface
3. Most germinal cells remain intact
IV (Fig. 10-33) 1. Injury runs from joint, through epiphysis, through physis and out
through metaphysis
v 1. Crushing injury that destroys all layers of physis
2. Premature closure usually ensues
VI(Fig. 10-34) 1. Injury associated with removal of bone loss at the zone of
Ranvier, due to trauma such as a burn or degloving injury
VII(Fig. 10-35) 1. Avulsion fracture of the epiphysis, not involving the physis
u
Type lA fracture Type IB fracture Type IC fracture
Figure 10.30
g ~ g
Type IIA fracture Type liB fracture Type IIC fracture
Type liD fracture

Figure 10.31
Type lilA fracture Type 1118 fracture
Figure 10.32
Type IVA fracture
Figure 10.33
Type IVB fracture
~~
it
Type IVD fracture
Type VJ fracture Type VII fracture
A triplane fracture is special distal tibial epiphyseal fracture that usually occurs in
older children, about 1 year prior to closure of the epiphysis, and results from external
rotation. The 2-part triplane fracture occurs when the medial part of the distal tibial
epiphysis has already closed, and the lateral radiograph displays a SH IV fracture, and the
posterior tibial plafond fragment extends to the metaphysis, and may be comminuted. The
3-part triplane fracture consists of a combination of a SH II and a SH Ill fracture, and
occurs when the middle portion of the distal tibial epiphysis has closed. The lateral
radiograph displays aSH II fracture, while the mortise view shows aSH Ill fracture. The tibia
displays a large posterior fragment consisting of a large posterior fragment of posterior and
medial portions of the metaphysis, while the mediall/31/4 of the tibial plafond and medial
malleolus remains intact. The fibula is also usua!!yfractured. Treatment recommendations
for epiphyseal plate fractures entail the fo!!owing guidelines:
Types I and II
1. Usua!!y respond well to closed reduction, especia!!y if seen early.
2. If seen 7 days after injury, the attempt at closed reduction may do more
harm than good due to fast healing that occurs at this site.
Types Ill, IV, V, and VI
1. Should attempt closed reduction first, but usually requires ORIF. 2. Must
anatomica!!y reduce the physis and preserve joint congruity.
3. Try to keep threaded K-wires or screws out of physis.
4. Try and maintain fixation devlces in metaphysis.
TABLE 10-14.
THE AIKEN-MUELLER EPIPHYSEAL PLATE FRACTURE CLASSIFICATION SYSTEMS.
Aiken Mueller
1 ~Salter II A~ Salter I, II
2 ~Salter Ill B ~Salter Ill, IV, VI
3 ~Salter IV C~ SalterV
232 Foot and Ankle Disability and Rehabilitation Ch. 11
FOOT AND ANKLE DISABILITY AND REHABILITATION

WORKABiliTY, DISABiliTY, AND REHABiliTATION
Rehabilitation ott.he foot and ankle following injury or surgery, or as a part of the treatment of
disease, ranges from straightfmward and simple intervention such as walking and range of
motion (ROM) exercises, to complicated diagnostic and therapeutic regimens that require
specialized training and equipment Specialization has developed due to an ever-increasing
number of woriHelated injuries, workers' compensation and disability lawsuits, costs, and
regulatory agencies and the Americans with Disabilities Act. Occupational therapy or
industrial medicine consultation and referral can be helpful, in such cases.
Work is defined as any and all forms of productive activity, regardless of whether or
not there is reimbursement. Work levels, as defined by the US Department of Labor, are
depicted in Table 11-1. Cumulative trauma disorders often develop secondary to repetitive
strain, vibration or cold exposure, and include plantarfasclitis and heel spur syndrome,
tarsal tunnel syndrome, stress fracture, and chronic tendonitis and/or capuslitis. Physical
therapy entails exercise and other physical modalities used in primarily the acute and
subacute phases oftreatment. WorkabHITy may be determined using a functional capacity
assessment (FCA), which entails a standardized questionnaire to assess appropriate
behavior and symptom magnification; direct measurements of strength, power, endurance,
coordination, balance and mobility; and job simulation. Patients who have been out of work
or incapacitated for greater than 3-6 months, despite accurate diagnosis and treatment
including physical therapy, may benefit from functional capacity assessment.lndividuals
incapacitated >6 months may require work conditioning in an effort to reestablish strength,
flexibility, and aerobic capacity, with outwork simulation. Work hardening involves real and
simulated conditioning tasks, designed to enable productive, safe, and tolerable re~entryto
the work place after temporary Incapacitation. Job modification may be recommended
based on the functional capacity assessment and efforts at work hardening, and may
entail work aids (a stool to sit upon, a cushioned floor mat, special shoes, etcl alteration
of labor category (job description), and measures to assure safety and prevent rein jury. Not
all physical therapists are equipped to pertorm a FCA, or to undertake work conditioning or
work hardening programs.
TABLE 11-1. WORK lEVElS DEFINED BY THE US DEPARTMENT OF LABOR*

Work level Maximum lift Frequently lilts Ambulation
Sedentary 10 lb. None Infrequent walkin or standing
Light work 201b 10 lbs. Frequent walking and/or standing
Medium work 50 lb. 251bs. Frequent walking and/or standing
Heavy work 1001b. 50 lbs. Frequent walking and/or standing
Very heavy work >100 lb. >50 lbs. Frequent lifting and carrying
* http://www.d ol.gov/esa/regs/compliance/whd/fa irpay!fs17a_ overview. htm, website last visited 10/27/2007.
Such reports may also be useful in legal matters where disability determination is in
question. Occupational therapy and social service intervention will often enhance the
patient's progress and lifestyle. For patients with chronic pain, or suspected RSDS/CRPS,
referral to the pain clinic can also be helpful. Categories for the industrial rehabilitation pre-
scription are depicted in Table 11-2.
Ch. 11 Foot and Ankle Disability and Rehabilitation 283
TABLE 11-2. INDUSTRIAL REHABILITATION PRESCRIPTIONS.

Phase Prescription
acute and subacute (<3 months) Accurate diagnosis, protection of the injured part,
rest. ice, compression and elevation, medications
and physical therapy
;:;::3 months FCA and work hardening
Prolonged rehabilitation (>6 months) FCA, work conditioning, work hardening
An example of a prescription for physical therapy following an ankle sprain follows:
Rx Physical therapy for: 1) strengthening, 2) flexibility/range of motion, and 3)

proprioception, right ankle; 6-8 sessions over 3-4 weeks, evaluate and treat.
Diagnosis: status-post ankle sprain (ICD9 xxx.xx)
An example of a prescription for work hardening following an ankle fracture follows:
Rx Work hardening status-post OR IF ankle fracture (ICD9 xxx.xx), please

send report
Activities of daily living (ADLs) include feeding, grooming, dressing, toileting, bathing,
continence, transfers, and communication. Some examples of complex ADLs include:
cooking, cleaning, laundering, shopping, housekeeping, telephone, money management,
care giving, traveling, and taking medications. Functional capabilities include self~care
(fundamental and complex activities of daily living), work, play and leisure. Disability status
can be categorized using the Karnofsky scale (Table 11-3).
TABLE 11-3.
DISABILITY STATUS ACCORDING TO THE KAMOFSKY SCALE OF PERFORMANCE.
ScoreDisability
100 Normal, no complaint or apparent disease
90 Normal, minor signs and symptoms of disease
80 Normal with extra effort, moderate signs and symptoms of disease
70 Unable to carry on normal activities or actively work, can care for self; marked signs
and symptoms of disease
60 Requires occasional assistance, primarily cares for self; marked signs and symp-
toms of disease
50 Requires considerable assistance and frequent medical care; marked signs and
symptoms of disease
40 Disabled, requires special care and assistance; marked signs and symptoms of dis-
ease
30 Severe disability, hospitalized or institutional care indicated; marked signs and
symptoms of disease
20 Very sick, hospitalization with active supportive care is necessary
10 Moribund, fatal processes progressing
0 Death
284 Foot and Ankle Disability and Rehabilitation Ch. 11
Range 100-80--the patient is able to carry on normal activity, and no special care is needed.
Range 70-50-the patient is unable to work, but is able to live at home and care for most
personal needs, with a varying amount of assistance as needed.
Range 40-10--the patient is unable to care for self and requires equivalent of institutional,
or hospital care, and disease may be progressing rapidly.
Ch. 12 Evidence-Based Medicine (EBM) and Documentation 285
EVIDENCE-BASED MEDICINE (EBM) AND llllCUMENTATION

EVIDENCE-BASED MEDICINE (EBM)
Evidence-based medicine (EBM) entails the application of 3 elements of information used

to make clinical decisions. The 3 components of EBM are: 1) the clinician's experience, 2)
the individual patient's needs, and 3) the scientific evidence related to the clinical question
at hand. There is a hierarchy of evidence related to human clinical scientific knowledge
(Table 12-1).
TABLE 12-1. lEVELS OF HUMAN CLINICAl EVIDENCE.

ACFAS* Score level of Clinical Evidence
1a Systematic review of homogenous RCTst
1b Individual RCT with narrow confidence intervals
1c "Ali-or-none" observational stUdy
2a Systematic review of homogenous cohort studies
2b Single cohort study, or poor quality RCT
2c Outcomes research or ecological study
3a Systematic review of homogenous case-control studies
3b Single case-control study
4 Case report or series, or poor quality case-control study
5 Expert opinion, animal physiology, bench study
* ACFAS- American College of Foot and Ankle Surgeons (http://VIIWW.acfas.org)
t RCT =randomized controlled trial
Furthermore, human clinical research follows a hierarchy of research design options (Table
12-2).
TABLE 12-2. HUMAN CLINICAL RESEARCH DESIGN OPTIONS.

Research Design Options*
Analytical RCTt (interventional experiment)
hypothesis- Prospective cohort study (observational)
testing Retrospective cohort study (observational)
Case-control study (observational)
Descriptive Analysis of secular trends (group correlational)

hypothesis- Cross sectional (individual point-in-time)
forming Case series
Case report (rare disease, novel treatment)
Animal physiology, cadaver, synthetic or computer model study
*The table is arranged from top to bottom, beginning with the research design that is most likely to produce valid
results (and conclusions), that being the randomized controlled trial, to the research design that is considered to be
least likely to produce valid results in regard to human clinical outcomes, that being the animal or berJCh-top
investigation.
tRCT =randomized controlled trial
286 Evidence-Based Medicine IEBMI and Documentation Ch. 12
The elements of a scientific investigation that contribute to the validity of the conclusions
gleaned from the study are depicted in Table 12-3.
TABLE 12-3. THE BUILDING BLOCKS OF GOOD CliNICAl EVIDENCE.

Building Blocks of Clinical Evidence*
1. Explicitly defined research question, population, and end points
2. Randomized treatment allocation and intention-to-treat analysis
3. Participants and outcomes assessors blind to treatment allocation
4. Use of a valid health measurement (quality of life) instrument
5. Power and sample size determined a priori
6. Statistical analyses compatible with type and distribution ofthe data
7. Point estimate and 95% confidence interval reported
~Turlick MA, Kushner 0, Stock 0. JAm Podiatri Med Assoc 93:392-8,2003.
FUNDAMENTAL ElEMENTS OF SCIENTIFIC PUBliCATION
When reporting scientific information, or submitting a manuscript to a peer-reviewed

journal, the fo!!owing information can be used to develop the report.
Abstract: Submit an abstract of:::; 250 words summarizing the contents of the article. The
Abstract canbe no longer than 250 words, since the National library of Medicine (via
Pubmed) truncates longer abstracts at 250 words, resulting in loss of information. The
Abstract can be written as continuous prose, or with subheadings for each section of the
manuscript, depending on the specific journal's preference. The Abstract for a report of
research should reflect the format ofthe manuscript itself, describing pertinent information
for each section of the manuscript It should briefly introduce the research problem,
explain methods, summarize results, and provide a conclusion. The Abstract for a case
study should state the condition of interest, and include a brief summary of the specific
clinical situation, the uniqueness or rarity of the diagnosis or the novelty of the intervention,
and a statement regarding the clinical significance of the case. Do not use any
abbreviations or bibliographic reference citations in the Abstract, since electronic
searching rnay limit the space not all abbreviations will be recognizable to all readers. If
necessary, parts of the Abstract may be written as phrases, rather than as complete
sentences. The level of clinical evidence (Table 12-1) should be noted in the last sentence
of the Abstract
Key Words: Provide 3-5 key words or phrases for electronic indexing purposes. Keep in
mind that electronic searches of the biomedical literature depend to a large degree on key
words. Refer to the National Library of Medicine's (via Pubmed) Medical Subject Heading
IMeSH) webpage (http.//www.ncbi.nlm.nih.gov) lor help selecting key words. Key words
are to be spelled in small case letters, unless representative of a proper name, and listed
in alphabetical order separated by a comma between each word/term. Avoid abbreviations
in the keywords, unless a proprietary name uses an abbreviation. In general, proper names
are not used as key words.
Introduction: This section should provide a concise overview of the state of knowledge
regarding the specific problem being studied. It should begin with a statement of the
problem and its clinical/social importance, followed by an explanation of recent and

important research related to the topic, supported by reference citations. The importance
of the topic is best t;:onveyed by means of statistics that indicate the prevalence and/or
economic impact of the condition in the population/society. After an explanation of what is
known, and what remains unknown in regard to the focus of the study, the author should
concisely state the specific research question or hypothesis for the current investigation.
Generally, the last sentence of the introduction should include a statement that describes
the specific study design I see Table 12-2) and reiterates the research question.
Patients/Materials and Methods: If the study is a clinical investigation involving living,

human participants !patients, subjects), then the heading for this section should
be "Patients and Methods." ltthe investigation involves animals, cadavers, or in vitro
models of any sort, including computer models, then this section should be termed
"Materials and Methods." In general, the methods section should describe the following
elements of the investigation: aims, assessors and other members ofthe investigational
team, population or sample, intervention, endpoints \measured variables), and the
statistical methods used to determine the meaning o_f the results (see details below).
Ideally, this section should provide enough detail to allow subsequent researchers to
replicate the study. When reporting randomized controlled trials, a study flow diagram in
CONSORT format, as well as all of the information required by the CONSORT checklist,
should be provided. The CONSORT statement, checklist, and study flow diagram are
available at http.//\IIILIIIVv.consort-statement.org. For observational investigations, the STROBE
statement (http//wiiVWstrobe-statementorg) guidlelines and checklist can be used.
Aims: The primary aim of the investigation, as well as any secondary aims, should also be
clearly stated. A distinction should be made between primary and secondary aims. As a
rule, the sample size should be adequate to identify. a statistically significant difference in
regard to the primaJY aim, if such a difference exists. Power and sample size calculations
can be determined using any of a number of software programs, such as that found at:
http//biostatmc.vanderbiltedu/twiki/bin/view/Main/PowerSampleSize. In describing the
primary aim, many authors will restate, in some fashion, their hypothesis and research
question, emphasizing that they undertook to answer the question.
Assessors: Members of the investigational team should be described in regard to their

participation in the study; namely, ifthey served as outcome assessors or if they performed
an intervention or, in the case of a retrospective study, if they abstracted data from medical
records. For studies in which subjective measurements are determined, such as
measurements of radiographic angles, a method should be described for breaking ties and
determining an outcome when indecision or uncertainty exists. If outcomes assessors were
blind to treatment allocation, this must be stated. If outcomes assessors were participants
in the intervention, such as members of the surgical team or treating clinicians, this must
also be stated.
Study population: The methods section should provide readers with an explicit description
of the participant/patient population and the time period from which they were selected. The
time period should delineate the day, month and year that the period started; and the day,
month and yearthatthe period ended IMM/DD!YYYY-MM/DD!YYYY.Ifthe daythatthe time
period started is not known, then it is acceptable to state just the month and year that
288 Evidence-Based Medicine (EBM) and Documentation Ch. 12
initiated and ended the period (MM!YYYY-MM!YYYY). It is also important for the author to
state whether or nottreatment allocation was determined in a random fashion, and whether
or not participants in a clinical trial were blind to treatment allocation. The method of
randomization should be described {random number table, electronic random number
generator, sealed envelopes, other). For case series and cohort studies, the author should
state whether or not the participants were enrolled consecutively. The inclusion and
exclusion criteria must be clearly stated, and it is best to simply list these.
Intervention: In any investigation, the intervention needs to be explicitly described. If

participants were randomized to an active therapy that was compared to standard
therapy, or placebo, each treatment arm needs to be described. Authors are encouraged
to avoid presenting a detailed narrative report of an operative intervention for a standard
procedure that can be referenced in any of a number of textbooks. Reference can be made,
with an appropriate citation, to a standard procedure as it is described in a textbook; and
variations on the procedure should be described in detail. Nov.el interventions, notable
variations on standard procedures, decision points related to an intervention, and adjunct
procedures should be thoroughly described.
Endpoints (outcomes): Outcome measures should be explicitly defined in terms of how the
variable was measured, who made the measurement, and whether or notthe assessor was
blind to the intervention (for an intervention trial). Authors should clearly state if outcomes
were based on physical examination, chart review, telephone interview, questionnaire or
radiographic films. As a rule, any variable that a reasonable clinician would consider
important in regard the treatment of a patient, as it pertains to the investigation, should be
considered in the analysis. In addition to the intervention/s or outcome/s of interest, typical
independent variables include such things as age and age category, gender, activity level,
body mass index (BMI) or BMI category, comorbidities, medications, duration of treatment,
surgeon or clinical site, adjunct therapies, frequency and duration of follow-up, and
post-intervention management procedures (immobilization, physical therapy, etc.). ltems
such as those just listed above should be referred to as "variables" and not as
"parameters," since the term "parameter" should be reserved for statistical expressions
that describe the data, such as the mean and standard deviation, or beta coefficients
derived from a regression analysis. Whenever possible, it is preferable that "hard"
endpoints be used, such as analytical measurements, clinical or microbiology laboratory
results, and the like. Whenever "soft" endpoints, such as quality of life (QQL), are
considered, it is preferable to use health measurement instruments that have previously
been shown to be reliable and valid. QOL instruments should be specific to the foot and
ankle (ACFAS, AOFAS, Bristol Foot Score, Foot Function Index, etc.), as well as measures
of general health (SF-36, etc). Investigator derived questionnaires should be described in
terms of reliability and validity, if such testing was undertaken. For scales that rank
categories (mild, moderate, severe, for example) an aggregate score should be used. For
measurements of pain, the 10-cm Visual Analog Scale (VAS) is recommended.
Statistical Methods: The statistical plan should be clearly described, and every investigation
should include at least descriptive and inferential, as well as univariate and multiple variable,
statistical analyses. The descriptive statistical analysis should define parameters such as the
measure of central tendency (mean or median average), and measures of dispersion
\standard deviation or range). The parameter, as well as the statistical test, should be selected
based on the type and distribution of the data. In short, continuous numeric data that are
normally distributed are suitable for representation using the mean and standard
deviation, and may be analyzed using mean-based statistical tests (such as Student's
Hest). Categorical data, and data that are non-normally distributed, are suitable for
representation. using the median and range, and may be analyzed using median-based
methods such as the Wilcoxon matched-pairs signed-ranks test, sign test, Wilcoxon
rank-sum test, and the Kruskai-Wallis equality-of-populations rank test, and other null
hypothesis tests and methods of estimation. For categorical data, Fisher's exact method should
be used as much as possible. Univariate analyses should describe the association of
independent variables with the outcome of interest (dependent variable), whereas
multiple variable analyses should describe the association of all of the clinically important
variables with the outcome of interest.
Results should be presented with only as much precision as is of scientific value. For
example, measures of association (odds ratios, relative risks, risk differences, etc.) should
typically be reported to two significant digits. As a rule, the terms "significant" and
"significantly" should be reserved for use when describing statistical differences. The
statement "no significant difference was found" between two groups should not be made
unless a power analysis was done and the value of alpha (level of significance, typically 5%)
or beta (the power to detect a statistically significant difference, usually 80% or 90%) is
reported. Use of the word "significant" requires reporting of a P-value (probability), or the
95% confidence interval about a point estimate. It is preferable to report the 95%
confidence interval (CI) rather than the P-value, since the 95%CI describes whether or not
the result was statistically significant, while also showing just how precise the estimate
was. Except when 1-sided tests are required by study methodology, such as in
noninferiority trials, 2-sided P-values should be reported. By convention, P-values larger
than O.Ot should be reported to two decimal places, those between 0.01 and 0.001 to three
decimal places, and P-values smaller than 0.001 should be reported asP< 0.001. P-values
should not be reported as "P::::: O."Furthermore, use of the word "correlation" or the term
"correlates with" requires that a correlation coefficient (Cronbach's alpha) be calculated
and reported. The results of a sensitivity analysis, such as that described by Greenland
(Maldonado G, Greenland S: Simulation study of confounder-selection strategies. Amer J
Epidemiol. 1993; 138: 923-936.1, or that described by Rosenbaum (Rosenbaum PR.
Sensitivity analysis for matched case-control studies. Biometrics. 1991 Mar; 47(1): 87-100;
and, Rosenbaum PR Discussing hidden bias in observational studies. Ann Intern Med.1991
Dec 1; 115(11): 901-5.1, should be presented for retrospective studies where unmeasured
independent variables may have potentially influenced the results.
Additional references that may be useful in regard to the description of the methods
and the presentation of a statistical plan include:
Bailar JC Ill, Mosteller F. Guidelines for statistical reporting in articles for medical
journals: amplifications and explanations. Ann Intern Med 1988; 108: 266-73.
Altman DG, Machin D, Bryant TN, Gardner MJ (eds). Statistics with Confidence.
second edition. London: BMJ Books, 2000.
Malay OS. Some thoughts about data type, distribution, and statistical significance.
J Foot Ankle Surg 45: 57-9, 2006.
Malay OS. Levels of clinical evidence. J Foot Ankle Surg 46: 63-4, 2007.
290 Evidence-Based Medicine (EBM) and Documentation Ch. 12
Results: The results section should presents quantitative information on the data collected,
in the form of descriptive and inferential statistics. Relevant information on the study
population includes demographic information for each subgroup (control group and study
groupsL exclusions and attrition. Inferential statistics should be used to compare groups
using appropriate statistical tests based on the size of the study population, type of variables
under study {discrete vs. continuous), and the distribution of the data collected.
Quantitative information should be summarized in the text, and readers should be referred
to relevant tables for more detailed information. As a rule, three results tables should be
presented, and designated Tables 1, 2, and 3. Table 1 typically depicts the baseline
demographic characteristics of the sample population, often categorizing the patients/
participants by intervention or outcome, and showing whether or not statistically
significant differences existed between the groups. For randomized controlled trials, it is not
necessary to depict statistically significant differences at baseline, since randomization
distributes the characteristics by chance. Table 2 generally depicts the results of the
univariate analyses, and Table 3 generally depicts the results of the multiple variable
analyses. Additional tables can be helpful when the data warrant such detail.
Discussion: The discussion section should offer the authors' interpretation of the results of
their investigation, Authors should consider how their results fit into the general state of
knowledge on the subject, as well as their clinical relevance. In addition, authors should
acknowledge the limitations of their investigation that may have introduced bias, and they
should discuss how the results may have been affected by bias. It is advise able that authors
tell the readers all of the shortcomings that they (the authors) understand to have
influenced their results and conclusions, rather than leave this criticism solely up to the
readers. Investigations that show a statistically significant difference betvveen treatment
groups should not be criticized for having too small a sample, Finally, suggestions for
clinical applications and/or further research may be appropriate. Do not include a
separate "Conclusion" subsection, as the final paragraph of the discussion should describe
the authors' conclusions.
Acknowledgement: In genera!, acknowledgments should be made to those who have

informally contributed their expertise or assisted in the investigation, ratherthan to those who
have contributed to the manuscript while performing the role of their regular occupation.
References: References are cited in the body of the text by means of numeric citations
listed parenthetically in the appropriate sentence, prior to the end of the sentence (usually
just before the period ending the sentence). Reference citations are to appear in
sequential numeric order, beginning with the number 'T' and continuing in sequential
numeric order the first time that a particular reference is cited, until the last citation is noted.
In other words, supply references numbered in the exact order they appear in the text (not
alphabetically). Sources not identified in the text should be listed as Additional References.
Unpublished sources must be included in parentheses within the body of the text, not in
the Reference Section. Abbreviations for journal titles should conform to those used by
Medline (www.ncbi.nfm.nih.gov/sites/entrez?db=pubmed). If Medline does not index a
journal, then spell out the entire journal name in addition to listing the author name/s, title
of the article, volume number, page numbers, and year of publication. Always list all
authors, and do not use "eta!" when listing your references. The term "eta!" may be used
in the body of the text; however, it is generally reserved for mentioning papers written by
Ch. 12 Evidence-Based Medicine IEBM) and Documentation 291
more than 3 authors. Whenever a textbook is referenced, it is necessary to include the

specific page or pages used. Whenever a web reference is cited, it is necessary to include
the date when the site was last accessed.
Examples of reference citations include:
Journal article: 1. Mendicino RW, Orsini RC, Whitman SE, Cantanzariti AR. Fibular
grove deepening for recurrent peroneal subluxation. J Foot Ankle Surg 40:252-263,
2001.
Textbook: 2. Trevino SG. Disorders of the hallucal sesamoids. In Foot and Ankle
Disorders, pp 379-398, edited by MS Myerson, WB Saunders, Philadelphia, 2000.
Electronic version of a print journal: 3. Gardner MJ, Boraiah S, Hentel KD, Helfet DL,
Lorich DG. The hyperplantarflexion ankle fracture variant. J Foot Ankle Surg [serial on
the lnternet]46:256-60, 2007.Mvailable at http://www.jfas.org/issues/contents.
Web page: 4. Clinical Practice Guideline Heel Pain Panel. Diagnosis and Treatment of
Heel Pain. American College of Foot and Ankle Surgeons Web site. September/
October 2001. Available at: http://www.acfas.org/pubresearch/c pg/heelpain-cpg.htm.
Accessed mm/dd/yyyy.
Figures: Photographs and illustrations should be clear and support the specific points
mentioned in the text. Figures and their accompanying legends should be able to stand
alone, communicating the meaning of the information without reference to the main text. In
the text, figures should be cited using parentheses about the figure-reference being cited.
For example: "[Agure 1)". Each figure should be titled, and accompanied by a figure legend.
The figure title should be formatted as in the following example: "Figure 1. The
gastrocnemius recession." Do not use abbreviations in either the figure title or the figure
legend, unless the abbreviation is defined in the legend. Abbreviations or footnotes shou!d
be explained in lower case alphabetical superscripts beneath the figure.lfthe figure reports
a statistical result, such asaP-value, then the statistical test used to determine the P-va!ue
needs to be described in the legend or elsewhere in the figure. Rgure titles and legends must
be submitted for each figure, and should be typed in consecutive order, double-spaced, on
a separate page from the text. Each figure must be submitted as a separate page
[electronic file). Images should be provided in TIF, GIF or EPS format, per the specific
journal's instructions. Manuscripts that describe a pathological entity should be
accompanied by a photomicrograph, with the type of stain and magnification indicated.
Radographic images should be submitted in grayscale format. Black and white line
drawings are acceptable only it they are of professional-quality. All figures must be
original, unless indicated otherwise. A Jetter should accompany figures that have already
been published in other sources, indicating that the previous publisher and author have
granted permission for their use. Keep in mind that hardcopy llustrations and figures are
usually not returned to authors.
Tables: Tables should be clear and support the specific points mentioned in the text Black
and white lines and text are preferred, and the "inserttable" function ofthetoolbar of most
292 Evidence-Based Medicine IEBM) and Documentation Ch. 12
word processors works well for this. Tables and their accompanying legends should be
able to stand alone, communicating the meaning of the information without reference to the
main text. In the text, tables are cited using parentheses about the table-reference being
cited. For example: "(Table 1)." Each table should be titled, and accompanied by a table
legend. The table title should be formatted as in the following example: "Table 1. The
dataset." Do not use abbreviations in either the title or the table legend, unless the
abbreviation is defined in the legend. Abbreviations or footnotes should be explained in
lower case alphabetical superscripts beneath the table. If the table reports a statistical
result, such asaP-value, then the statistical test used to determine the P-value needs to be
described in the legend or elsewhere in the table. Table titles and legends must be
submitted for each figure, and should be typed in consecutive order, double-spaced, on a
separate page from the text Each table must be submitted as a separate page (electronic
file). Tables should be provided in either .doc, TIF, GIF or EPS format, per the journal's
instructions for online submission. All tables must be original, unless indicated otherwise.
A letter should accompany tables that have already been published in other sources,
indicating that the previous publisher and author have granted permission for their use.
Registered trademarks and copyrights: As a rule, generic terminology is preferred. Any and
every time that a proprietary substance (such as a medication), device, equipment, or
softvvare program is mentioned in the manuscript it must be accompanied by either of the
following symbols: "" or "'""', indicating that the substance or device is a registered
trademark; and the following information must be provided in parentheses, immediately
following mention ofthe proprietary item: proprietor's name (the name of the company that
owns the registered trademark), city and state wherein the proprietor's headquarters are
located, and the country if other than the United States. If copyrighted material is
mentioned, then the "" symbol should accompany the item. Furthermore, the use of
copyrighted material requires that the author obtain explicit permission from the owner of
the copyright (publisher). and the author, for such use. As a rule, proprietary names should
not be used in the manuscript's title, and once a proprietary name is used to describe an
intervention or diagnostic test, generic terminology should be used thereafter. In an effort
to remain scientific, and to avoid the appearance of proprietary bias, generic terminology
is generally preferred by peer reviewers and editors.
Abbreviations: Do not use abbreviations in the litle, Abstract, or Key Words section of the
manuscript, because information from these portions of the paper is used in the process of
electronically indexing biomedical literature. If a proper or proprietary name entails the use
of an abbreviation, only then can it be used in the Title, Abstract or Key Words sections.
Abbreviations can be used in the Introduction, as well as any area of the manuscript
thereafter. Abbreviations are not to be used unless the term has first been spelled in full, and
the abbreviation noted in parentheses immediately following the full term. For example:
" ... deep peroneal nerve \DPN)." Abbreviations that are part of a proprietary name are to
be used in accordance with the guidelines noted for registered trademarks and copyrights.
EBM websites: Much of the information described above can be found in greater
detail at a number of evidence-based medicine websites, such as the Centre for
Health Evidence (http://www.cche.net/), the Centre for Evidence-based Medicine
(http://www.cebm.utoronto.ca/!, and the Oxford Centre for Evidence-based Medicine
(http://www.cebm.net/).
Appendices 293
APPENDICES
ORAL EXAM TEST- TAKING AlGORITHM
Do not deviate from this algorithm unless prompted by the examiner. You may ask if a
specific segment has been adequately covered, however do not assume anything unless
the proctor indicates so. Start with the history and physicai(H&P) examination, then make
a diagnosis and describe a treatment plan and fotlow~up.
History and Physical

Chief complaint
Nature of sign and/ or symptom
Location of sign and/or symptom
Duration of sign and/or symptom
Onset of sign and/or symptom
Course of sign and/or symptom
Aggravated by (activities or circumstances)
Treatment (what has been tried, helpful or not)
Previous Medical History, Medications, Allergies
Surgical History
Social History, Occupation/Avocation, Fami!y History
Physical Exam
Vital Signs (Temp, Pulse, Respiration, BPI
Vascular
Neurological
Dermatological
Orthopedic
Biomechanical
X~ray, and other clinical or diagnostic testing
Differential diagnosis
Consider confirmatory consultation or other testing
Diagnosis
Treatment Options and Plan
Non-surgical treatment
Pharmacological
Biomechanical
Physical therapy
Surgical treatment
Preoperative preparation
Intra-operative plan
Postoperative plan
Altercare in accordance with clinical response
294 Appendices
INFORMED CONSENT
Informed consent is a crucial part of adequate patient preparation for any procedure or
operation, and should be written, signed by the surgeon or person explaining the case,
witnessed, dated, and timed. The components of informed consent include, but are not
limited to, an explanation, in layman's terms, of the following points:
1. Goals and objectives of the planned procedure or operation.

2. Diagnosis (what you are treating).
3. Planned procedure and anesthesia.
4. Potential risks and complications (such as infection, recurrence of pain &/or
deformity, new and/or permanent pain &/or deformity, overcorrection, stiffness,
weakness, instability, scar pain or disfigurement, nerve &/or tendon injury,
hematoma, phlebitis and pulmonary embolism, bone or hardware breakage,
prolonged swelling or slow wound healing, difficulty walking, and other concerns
pertinentto the individual's specific case (cardiac arrest, severe blood loss, etc.).
5. Postoperative course and rehabilitation \ambulatory status, bandages, casts,
shoes, time off from work or school, or driving).
6. Therapeutic alternatives and surgical options.
7. No guarantees are given regarding an outcome.
8. Other points may be made depending upon the specific merits of the case. When
using a new or experimental drug or technique {not FDA labeled for the
application), this fact should be noted in the written consent.
9. lntentto have observers in the operating room, or to image the case (photo, video)
should be noted.
HOSPITAL ADMISSION ORDERS
Standard admission orders may include:

1. AdmittoserviceofDr.
2. Dr. __ for medical management (admission to a specific service may vary
depending upon hospital bylaws, rules and regulations, and staff privilege
delineation).
3. Diagnosis: _ _.
4. Condition:_ (stable, guarded, critical or urgent emergent).
5. Resuscitation status: _ _ {full, or otherwise).
6. IV access and fluids ("IV 05LR at KVO [keep vein open] via 18 gauge venous
catheter [specify preferences]."
7. Shave and prep [specify] preop.
8. Activity and WB status [specify].
9. Diet [specify].
10. NPO after 2400 preop [coordinate with dietary].
11. Labs and ancillary testing [specify].
12. Medications [specify].
13. Consultations [specify].
14. Supplies to bedside [specify].
15. Social services for discharge planning [specify].
16. Other items specific to the case at hand [wound and skin isolation, etc.].
Appendices 295
HOSPITAL POSTOPERATIVE ORDERS
Standard initial postoperative orders may include:

1. Vital signs ("VS q shift after return to floor").
2. Activity ("CBR (complete bed rest) with side rails up"; "absolute Non-weight
bearing operated foot at all times";" BRP Non-weight bearing operated foot
with assistance" ; " PT for gait and transfer training Non-weight bearing
operated foot"; "Assist with first OOB (out of bed) activity"; Dangle feet over
bedside while seated 3-5 minutes before first OOB activity").
3. IV fluids ("maintain IV 05LR [or other IV fluid as indicated] at KVO [or faster rate
as indicated] until fully reactive/stable"; "convert to heparin lock after 0/C IV").
4. Medications, considerations include antibiotics, analgesics for moderate and
severe pain, anti-inflammatory, muscle relaxant, anti-emetic, stool softener/bowel
stimulant, sedative/hypnotic, other indicated meds. as well as the patient's regular
meds.
5. Respiratory therapy ("Triflow incentive spirometry q 1 hour while awake, instruct
and encourage").
6. Drain management ("monitor drain/s [TLS, Hemovac or Jackson-Pratt] and
record output, change when '}j3 full or at least q shift").
7. Diet (regular, diabetic, restricted calorie, low sodium, as indicated).
8. Discharge planning ("social services for home antibiotic [specify], lab testing
[specify], PT. [specify], and wound care [specify]").
9. Radiographs {specify views, weight bearing status and any special attention
items).
10. Other orders, such as supplies to bedside, consultations, physical therapy,
notification of the attending internist or general practitioner of the patient's
postoperative status, and any other items that are specific to the case at hand.
HOSPITAL DISCHARGE ORDERS
Standard discharge orders may include:
1. Discharge _ _ (specify when, or "at-the discretion of" whomever).

2. Dispense written and oral postoperative instructions (separate form detailing
activities, medications, home or special care, problems to be aware of or on the
look out for, follow-up appointments, home health care, etc.).
3. Dispense prescriptions (specify).
4. Ambulatory status (specify).
5. Other pertinent items.[AEDl]
296 Index
A Adjunct
Abdomen 120,127 procedures 176-7,192,195-6,220,288
Abduct 234 radiation 72, 74, 79
Abduction 70, 106-9, 112, 176, 214,217,232, ADLs (Activities of daily living) 283
234-5,174,276-7 Administration 31, 45, 55, 58, 60, 81-6, 88, 93,
Abductor 118, 122, 160, 244, 248, 256
digiti quinti 6, 13 Admission 46,294
hallocis 6, 13, 16, 18,130,191,208-9,231-2, Adnexae 33
234-5, 237-8,255 Adrenal 83-4,158
Abductor hallucis Adrenergic 31,53
muscle belly 208 Advanced cardiac life support (ACLS) 86-7
recession 231-2,235,238 Aerobic 40-1,46,67,100,116,282
Abductorha!lucis Medial 13 Aerosol bronchodilator 82
Abductus 106,114,171,176,189,192,217, Aftercare 139, 142, 144, 146, 225
225-7,232,234, 259 Age 37-8,42-3,56, 65-6,69,72,74-5,80, 107,
pes 225-7 112,131,158,165,171,202,205,214-5,213,
ABIIANKLE-BRACHIAL INDEX) 53-4 232-3, 235, 237, 239-43, 254, 261' 272, 288
Ablation 60, 72, 138 Agents 31,47-9,54, 82,157-60
Absorbable fixation 148,170 Agglutination 62-3, 96
Absorbable suture 123, 177,207, 209,246,277 Agranulocytosis 159
Absorption, primary bone callus 25 AHO (Acute Hematogenous Osteomyelitis) 42
Accommodative foot orthoses 161, 223 AIDS (Acquired Immunodeficiency Syndrome)
Achilles 11,102,202-4,207,209,237,241,255 51-2, 74
tendon 11, 13,113,129-30,135,154,198, Aigner's syndrome 35
201-5,207, 213, 238,241,254-5, 272 Aiken-Mueller Epiphyseal Plate Fracture
Acid Classification Systems 281
fast 41,100-1 Ainhum 34,38
uric acid 63-4,97,99 Airway 81-2,84-7,118,244,248
Acidosis 60, 85, 95, 99 obstruction 84-5
ACLS (Advanced Cardiac Life Support) 82, Akin
85-7 osteotomy 176-7, 187, 232
Acral lentiginous melanoma 75 procedure 176
Acrallentiginous melanoma (ALM) 75 Albumin 63, 100
Acromegaly 39, 99 Alcohol withdrawal 84
Actinic 39 Alcoholic keratosis 34
Activities of daily living (ADLs) 283 Alkaline phosphatase 79,80, 99,100
Acute adrenal crisis 83 Allergen 36,81-2
Acute gouty arthritis 63-4,99 Allergic 35-6,38, 81
Acute metatarsal fracture 258 Allergy 95,157,189,258
Addison's disease 83, 99 Allodynia 70, 255
Adduct 196 Allogeneic 127,131-3,217-8,227,273
Adduction 70,106-9,161,166,172,191,193, Allograft 131,133
214-9,232, 235, 237, 239-40, 274,276-7 Alloimplant 131
Adductor Alloimplants 131,133
canal 17,32 Allopurinol 37,64
halluc is 6, 8, 13, 17, 175,255 ALM (Acrallentiginous melanoma) 75
tendon 175 Alopecia 36
Adductovarus 112~3, 166,196 Ambu bag 87
Add actus 106,112,114,172,179,183,191,215, Ambulation, early 57
217, 225, 232, 234-7, 240, 242 American College of Foot and Ankle Surgeons
Adenopathy 38, 59, 76, 81 285, 291
Adherent 12,58 Amide 85,157-8
Adhesion 67,111,127,141,185 Aminophylline 82
Adhesive skin strips 124-5 Amphotericin-8 48
Adjacent metatarsal fracture 262 Ampicillin 49-51
Amputation, transmetatarsal 211,213

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PODIATRY INSTITUTE

THE P.I. MANUAL

The Podiatry Institute

D. Scot Malay, DPM, MSCE, FACFAS, Editor

Podiatry Institute Publishing, Inc.

Chapter 1. Selected Anatomy & Normal Physiology

Chapter 2. Basic Pathophysiology

Chapter 3. Selected Diseases and Pathological Conditions

Chapter 4. Selected Diagnostic Techniques

Chapter 5. The Peri operative Patient

Chapter 7. Basic Reconstructive Foot and Ankle Surgery

Chapter 8. Major Reconstructive Foot and Ankle Surgery

Chapter 9. Congenital Deformities and Juvenile Surgery

Chapter 10. Management of Foot and Ankle Trauma

Chapter 12. Evidence~ Based Medicine and Clinical Research

Selected Anatomy & Normal Physiology

Table 1-1: LEG AND FOOT OSSIFICATION DATES

PRIMARY EPIPHYSIS OSSIFICATION

Table1-2: ACCESSORY OSSICLES

ACCESSORY OSSICLE lOCATION

Interphalangeal Joints IIPJ) (Fig. 1.1)

lesser Metatarsophalangeal Joints IMTPJ) (Fig. 1.2)

Slip from EHL or

Tib. sesamoid lig.

Plant. tib .. sesamoid lig.

Pattern of dorsal Pattern of dorsal Pattern of intermetatarsal

Plantar tarsometatarsal Pattern of interosseous

First Metatarsophalangeal Joint (1ST MTPJ) (Fig. 1.3)

Tarsometatarsal Joints (TMTJ, USFRANC'S JOINT) (Fig. 1.4)

Calcaneocuboid Joint (CCJ)

Midtarsal Joints (MTJ)

Subtalar Joint (STJ)

Talocrural (Ankle) Joint

Flexor Digitorum Brevis

Abductor Digiti Quinti

Figure 1.5 Figure 1.6 Figure 1.7

Figure l.B Figure 1.9

Plantar layer Ill

Flexor Digiti Minimi Brevis

Figure 1.10 Figure 1.11

Plantar Interossei (10)

Figure 1.13 Figure 1.14

Dorsal Intrinsic Muscles

EXTRINSIC PEDAL MUSCULATURE

Anterior Leg Compartment

Tibialis Anterior (TAl

Extensor Hal/ucis Longus (EHL)

Extensor Hallucis Accessorius

Peroneus Longus (PL)

Peroneus Brevis (PB)

Superficial Posterior leg Compartment

Deep Posterior leg Compartment

Tibialis Posterior (TP)

Flexor Digitorum Longus (FDL)

Flexor Hallucis Longus (FHL)

TENDONS, SHEATHS liND BURSAE

Tendon Sheath and the Gliding Mechanism

Tendon Blood Supply

Subfascial and Subcutaneous Bursae

Table1.3. MOTOR INNERVATION TO THE LEG AND FOOT

MUSCLE PERIPHERAL NERVE SPINAL LEVEL

COMMON PERONEAL NERVE

lateral Sural Cutaneous Nerve

The Deep Peroneal Nerve (Anterior Tibial) (Fig. 1.15)