PEDIATRIC MUSCULOSKELETAL DISORDERS

Torticollis: shortening of SCM.

Eti: Congenital (birth trauma/intrauterine deform) & Acquired (2° infection, fracture).
Sx: head toward SCM, chin away. Mid-portion SCM mass poss palpable. Facial deformity if not treated.
Tx: Congenital (PT=passive stretching, collar; surgery) Acquired (PT=stretching, exercise, traction, collar, treat
underlying cause=minor trauma, retropharyngeal abscess, myositis)

Scoliosis: Curve in spine > 10 degrees.

Epi: 90% Idiopathic. 2-3% of population = genetic role. > incidence if have cerebal palsy, spinal bifida, muscular
dystrophy. Onset = anytime. More progressive in F. MC = R thoracic convexities.
Dx: clinical & X-ray.
Tx: need to find Cobb angle = take most tilted vertebra at top & bottom, draw line out & find angle (xray)
Curve < 20° = Observe ~ 80% every 4-6 mo (+5° progression = ortho referral)
Curve > 25° = Refer – Brace.
Curve > 40° or fast progression = Refer – surgical intervention
Goal = <50° curve by adult
(bracing: only affects progression, most useful in growing kids, 2 types (CTLSO & TLSO))
5 Warning signs of scoliosis (~10 -12 yo): 1) Uneven shoulders 2) Prominent shoulder blade or shoulder blades
3) Uneven waist 4) Elevated hips 5) Leaning to one side

Developmental Dysplasia of the Hip (DDH): abnormal growth/development/dislocation hip

Eti: femoral head/acetabulam probs; lax ligaments, breech, postnatal posturing (first 6 wk of life critical for hip develop!)
Epi: 1/1,000 live births, genes, 1st born girls, breech position.
Sx: PAINLESS Limp! Unstable = femur head pops out of acetabulum. Stable = not properly shaped, shakes in place.
*PE: Barlow maneuver = hip is currently IN place, examiner attempts to dislocate.
Ortolani maneuver = his is OUT of acetabulum, examiner attempts to reduce dislocated hip. “clunk” = + sign.
Dx: Age dependent, <6 mo = US, >4-6 mo = X-ray, +/- MRI
Tx: Age & severity dependent. Newborn = pavlik harness (hips in flex&abd) 1-6 mo = closed reduction + harness.
6-24mo = closed reduction+spica splint + anesthesia. +24mo = surgery (open&osteomoty)

Slipped Capital Femoral Epiphysis (SCFE) = displacement of femoral head, slip thru growth plate (med&post)
Epi: Adolescent, AA, Male Obese. Eti: ? multi-factorial.
Sx: Pain: thigh/medial knee. Nerve: femoral nerve (goes right by femoral neck area). Painful limp.
Dx: Clinical = limitation of int rotation of hip. X-ray (kline line). Tx: Surgery = internal fixation. (20%=AVN,  risk)

Legg-Calve-Perthes Disease
Eti: Idopathic AVN femoral head. Epi: 1/1200 kids, 4-8yo, short, Caucasian, Male
Sx: Persistant pain +/- limp. Dx: X-ray. Tx: Varies (none  abd brace  stretching  Arthroplasty)

Osgood-Schlatter Disease = Rupture of growth plate at tibial tuberosity, inflammation below patella (patellar tendon)
Epi: adolescents (playing sports) M>F. Sx: Persistent Pain, swelling (uni/bilateral), improves w/ rest (min-hrs).
Dx: clinical (can do X-ray if severe/atypical) Tx: self-limiting, rest/restrict activity, icing/NSAIDs/bracing. RICE.

Patellofemoral Syndrome
Eti: Dysfunction 2/t injury/overuse. Physio=underdeveloped VMO/excessive valgus. Large Q angle, Mal-track patella
Epi: adolescent females Sx: Peripatellar pain/swelling Dx: Q angle, sunrise view in X-ray
Tx: Rest & Ice, PT (VMO strengthening), +/- bracing

Patellar Dislocation. Female, lateral dislocation, reduces prior to presentation. Tx: immobilize 4 wks, PT, brace, Surg if repeats

Osteochondritis Dissecans (OCD) = AVN of focal area of subchondral bone.

Eti: genetics, trauma, repetitive stress. Epi: M=F, sports +10 yo, MC of loose body in peds.
MC Sites: Distal femur, radial head, talar dome. Sx: Joint pain & swelling Dx: MRI is best (for AVN), X-ray.
Tx: observation & limitation. Arthroscopic removal. +/- drilling/grafting.
Metatarsus Varus (adductus) MC congenital foot deformity. Flexible to rigid.
Medial deviation of forefoot: adducted & supinated. Tx: observation, stretching, casting, surgery.

Clubfoot (Talipses Equinovarus) Fixed (rigid) Disorder 50% bilateral 2xM:F.

Plantar flexion & Varus (inversion) deform heel & Forefoot Varus. Tx: ALWAYS (serial casting & surg release/reconstruct)

Pes Cavus = abnormally high arch (supinator). Sx: anterior ankle pain. Tx: mild = shoe inserts, severe = surgery
Eti: muscle imbalance in growing foot (8-10 yo). Marker for neuromuscular disease = CP, MD

Pes Planus = Flat feet (pronator). Longitudinal flattening of arch – weight bearing. Asx. Tx: orthotics/observation.

Genu Varum = bow-legged. nL: Infant = 15° varum, 1 yr = 10° varum 2 yr = straight legs

Genu Valgum = knock kneed. nL: 3-6 yr =  valgum (15°) > 6 yr =  valgum (5-7°)

Pediatric Fracture Principles:

Bones are more flexible, heal faster, younger = more remodeling, growth plates are a concern.
 osteoblastic response; bone may heal longer than it started. Weakest site = physeal plate. Strongest site = periosteum

Salter-Harris Classification of growth plate fractures

Type I – through growth plate
Type II – through growth plate & metaphysis (MC type!!!)
Type III – through growth plate & epiphysis
Type IV – through (everything) growth plate & metaphysis & epiphysis
Type V – compression fracture through growth plate

Torus Fracture = buckle fracture d/t longitudinal force, cortex defect. MC = radius & ulna. Tx: immobilize x 3 wks

Greenstick Fracture. One side cortical disruption, angulation w/o displacement. Breaks on opposite of fracture.
Tx: anatomical reduction & cast immobilize.

Child Abuse Fracture = Suspect: Age or severity of fx NOT consistent with injury hx & If fx is rotary in nature
Classic: XS healing fractures of various ages (normally see multiple fractures healing)
MC Sites: Ribs, Femur & Humerus **Long bone fx < 3 yo = Abuse until proven otherwise!!!

Clavicle Fracture MC & earliest fx bone. Eti: Birth, direct trauma or fall onto shoulder. Tx: sling/figure 8. Px: good

Osteogenesis Imperfecta = DDi for abuse. Rare connective tissue disorder. Freq fx bc weak bones.
Sx: Short stature. Blue sclera, joint laxity/flexible, muscle weakness, thin skin, wk skin, multiple fx. nL intelligence.

Primary Bone Tumors* pretty common. 6th MC neoplasm in children. 3rd MC in adolescent/young adults

Osteochondroma = MC bone tumor in children! Benign, outgrowth near physis. 70% Fhx. Incidental finding.

Osteosarcoma = MC bone malignancy in peds (75%)! MC in teens, Femur, Dx: X-ray.

Ewing Sarcoma = 2nd MC bone malignancy in peds! “moth eaten / onion peel”.

Bone Cyst = NOT A TUMOR. Lipid cyst in bone ONLY seen in kids, fills w/ bone with growth.
(Membrane lined cavity (serious fluid cyst) grows only during bone growth hence peds. Incidental finding, monitor)
 FRACTURES
Types of Fractures

4 Phases of Bone Healing

1) hematoma/ inflammation, 1-7 days. 2) fibrocartilage callus, 2-3 wks. 3) bony callus, 3-4 wks. 4) remodeling, mo-yrs

Complications w/ Fx (trauma)
Acute: Compartment syndrome, Neurovascular injury, Blood loss, Infection
Compartment Syndrome = Surg emergency. Trauma -> swelling ->  compartment pressure.
Eti: Compartment is constricted/strangulated by fascia =  BF to muscle => muscle death.
Tx: release muscle & strip dead muscle, otherwise infection! Fasciotomy to release pressure.
*S/ Sx: “5 P’s” Pain (sharp), Pallor/pale, Paresthesia, Pulselessness, Paralysis*

Long term: Delayed/nonunion, Malunion, Loss of function, Infectionosteomyelitis (long term, esp if hardware in place)
Mal-union: Fx that heals in less than optimal position.
D/t: poor alignment when immobilized (cast/surgical fixation), no medical care.
Px: may result in loss or  in function
Delayed union: no progression in healing around 3-6 mo after injury.
Tx: initiate Tx to aid in healing (bone graft, bone stimulator)
Dx: check Ca2+ & Vit D levels, addit. imaging.
Non-union: no progress toward fx healing around 6-9 mo after injury.
Tx: additional tx (fusion, revision surgery).
Dx: infection workup (inflammatory markers! CT scan!)

Sever’s Disease = inflammation of calcaneal growth plate (heal) in growing kids/adolescents.

Resolves as growth plate closes. Tx: Ice, elevation, steroids, limit mobility.

Osgood Schlatter Disease = painful inflammation where patellar tendon attaches at tibial tubercle. Tx: NSAIDS, R.I.

Sail/Fat Pad Sign (elbow) = Xray finding on lateral view of flexed elbow, as anterior/posterior lucency (or both).
Suggests elbow Fx. MC = supracondylar or radial head.

Shoulder/Arm

Clavicle Fx: MC shaft fx, young active pts. Mech: FOOSH / direct trauma.
Bump vs Scar: fix w/ plate & screws if open fx, large displacement, neurovascular injury (BF). (will scar & irritate)
Non-op tx: immobilize in sling. Px: great rate of healing, don’t need to be fixed bc SCM pulling proximal,

Proximal Humerus Fx: Epi: MC in elderly Mech: low energy fall, F>M, Bone quality.
Displace from muscular attachments: Pecpull shaft ant & med. Supra/Infra/TeresER tuberosity, SubscapIR lesser tub frag
Op Tx: sig displacement & many Fx fragments. If Fx @ humerus neck = AVN of head = watch out for.
Non-op Tx: MC. Cuff & colar allows for gravity traction, sarmiento fracture cuff.

Humeral Shaft Fx: E fall=young & E fall=old. *Radial Nerve = can become entrapped! (see if can extend wrist&fingers)
Op Tx: open, many frags, poly trauma, displacement. Nonop Tx: MC, splint w/ fracture cuff.
Elbow

Supracondylar Fx: MC in kids 5-8 yo. Mech: fall on outstretched hand.

PE: Anterior interosseous neuropraxia (anterior interosseous nerve), (2nd MC is radial nerve palsy)
Unable to flex IP of thumb and DIP of index = can’t make OK sign. 20% have vascular inj = cold/pale hand
Tx: if vascular insufficiency  surg. MC closed reduction percutaneous pinning. Splint in 30-40° flexion for  BF.
If well perfused  nonop tx: long arm cast for 3wk w/ <90° flexion.

Intercondylar Fx: MC in young males & older females (dif tx). Tx: operative.
Mech: young M,  energy fall = splits both condyles when flexed > 90°.
Fall >90° = intercondyle fx, Fall <90° = supracondylar fx.
PE: gross instability. Serial neurovascular/compartment checks. Px: stiff elbow. Goal ROM = 30-130°. (nL = 0-140)
Many associated injuries:
Terrible Triad: elbow dislocation, radial head & coronoid Fx.
Floating Elbow: Fractures to distal humerus, radius & ulna (really bad, nothing holding together = surgery)
Volkmanns Contracture: Missed compartment synd of forearm  claw hand = permanent flexion of wrist & hand

Olecranon Fx: Mech: fall on flexed elbow/direct blow.  E fall=young & E fall=old. Triceps pull frag proximally.
Dx: palpable defect. Tx: Nonop in elderly & low demand pts w/ immob. In 45-90° flexion. Op: stabilization.
Px: early motion w/in 1-2 wks.

Monteggia Fx: Proximal 1/3 ulna Fx w/ proximal radioulnar dislocation (PRUJ). Cause instability & PRUJ
Mech: FOOSH in pronation. Epi: MC in kids.
Tx: adults = Op stabilization w/ reduction of PRUJ. Kids = nonop mgmt. in long arm cast. (Op if >10yo or open Fx)
Sx: Freq injury to post. Interosseous nerve = weak wrist extension, radial hand deviation, thumb extension

Galeazzi Fx/dislocation: Distal 1/3 radius Fx w/ dislocation of distal radioulnar joint (DRUJ).
Mech: crush/direct trauma vs FOOSH. Tx: Op stabilization of ulna w/ plates&screws w/ reduction & fixation of DRUJ

Both Bone Forearm Fx = ulnar & radial shafts. MC males. Mech: direct blow or indirect trauma (MVA, fall, sports)
Associated injuries: Monteggia & Galeazzi Fx. PE: gross deformity & swelling ( risk for compartment syndrome!)
Tx: adults = open reduction & internal fixation (ORIF) w/ plates & screws. Kids = conservative w/ cast 8-10wks

Colles Fx = distal radius Fx w/ fragment displaced dorsally  dinner fork sign (extraarticular).
Mech: FOOSH w/ wrist in extension.  E fall=young & E fall=old. Tx: nonop in cast.
X-ray: dorsal angulation, apex volar, +/- ulnar styloid fragment (closed, extraarticular = outside of joint)

Smith’s Fx (reverse Colle’s) = distal radius Fx w/ distal Fx fragment displaced ventrally. (extraarticular).
Mech: FLEXED wrist fall. Epi: elderly F, osteoporosis. Tx: nonop bc most extraarticular. Spint in slight extension.

Chauffer Fx = intraarticular Fx at base of radial styloid. Mech: Direct impact to thenar wrist.
Tx: op stabilization & repair intraarticular surface. Ventricle Fx into joint, surg to close gap.

Hand

Boxer’s Fx = 5th metacarpal neck. Mech: hitting something hard. MC males.

PE: loss of metacarpal height, underlapping 5th digit.
Tx: nonop w/ ulnar gutter splint. Op tx: if open/sig rotational deformity of metacarpal.

Scaphoid Fx = in proximal row (radial most bone). Mech: FOOSH (&hyperextended outstretched). PE: snuffbox pain
Dx: if no evidence on x-ray, repeat in 2-3 wks or do CT. if missed, long term comp = scaphoid nonunion adv collapse
Tx: nonop = nondisplaced, put in thumb spica splint. Op = unstable/comminuted fx. @ risk of AVN!!.
Leg

Femur Fx = MC femoral neck. Elderly Caucasian F. Mech: fall from standing height in elderly,  E trauma in youth.
PE: complain of groin pain on affected side. Leg is externally rotated & shortened. + pain w/ logroll.
Tx: Op stabilize w/ screw+plate, cannulated screws/arthroplasty.
Px:  mortality rate (50%). Poss complication of AVN in femoral head.

Patellar Fx: M>F, 20-50 yo. PE: palpable defect, large hemearthrosis. (bipartite patella = normal, just didn’t fuse)
Extensor mechanism intact? Straight leg raise! Important to check (quadraceps tendon). If doesn’t work  surg
Nonop Tx: Nondisplaced, Intact extensor mechanism. Hinged knee brace.
Op Tx: Extensor mechanism failure Open fx, Significant displacement bc X extensor mech, Better outcome w/ surg.

Tibial Plateau Fx: periarticular injury to tibia, MC in M (40-50, E, MVA) and F (70s, E, Falls), varus / valgus load,
lateral condyle > bidondylar > medial condyle, PE: varus/valgus laxity, suspicion for compartment syndrome
Tx: nonop can be considered in nondisplaced insufficiency in old, MC Tx w/ plate & screw, asso w/ soft tissue injury

Pilon Fx (distal tibia) = through distal tibia & involve joint, Epi: M 30-40yo, Mech: E MVA, falls from height.
PE: deformity & impressive soft tissue swelling/fx blisters
Tx: temporary exterior fixation if poor soft tissue, Def Tx: plates & screws & Ilizarov frame (external ring fixator)
Px: poor w/ post-traumatic arthritis, may fuse ankle for pain control

Distal fibula Fx: lateral malleolus / lower fibula, Mech: varus stress ankle roll;
PE: gravity stress view on xray may reveal medial clear space widening = syndesmotic injury (Mortise view)
Mortise view = gravity stress view. allows look down joint = gives best view of ankle joint (distal fib fx)
Tx: non-op if isolated lateral malleolus w/out syndesmotic injury, surgical if ankle unstable or open fx

Maisonneuve Fx: Combo of a spiral fracture of the proximal fibula & unstable ankle injury which could manifest
radiographically by widening of the ankle joint d/t distal tibiofibular syndesmosis and/or deltoid ligament disruption,
or fracture of the medial malleolus. Caused by pronation external-rotation mech. It requires surg fixation

5th metatarsal Fx:

Zone 1: avulsion fx d/t ankle inversion, non-op Tx, low chance for non-union (proximal)
Zone 2: Jones fx, lateral force on forefoot (pivot shifting); nonop Tx w/ immobile in CAM boot & NWB, screw for athletes
Zone 3: stress fx; Tx w/ non-weightbearing and immobilization, fix in high-level athletes (distal)

Stress Fx: Repetitive stress to bone, Rapid  in physical activity. MC in Tibial Shaft & Metatarsals. MC in Females.
Dx: plain films, bone scan. Tx: Immobilization & rest. Possible IMN fixation in tibial shaft fractures
 UPPER EXTREMITIES
Shoulder
Shoulder: Most motion of any large joint but very susceptible to injury. Not built to fxn overhead continuously.
Shoulder pain DOES NOT go past elbow (otherwise = cervical spine issue). Glenohumeral & AC ligaments.
Rotator Cuff = SITS: Supraspinatus (MC injured, 1st 15° of abd), Infraspinatus, Teres minor, Subscapularis (2nd MC)
Dynamic Stabilizers: Deltoid, Pec Major, Trapezius, Rhomboid, Rotator Cuff (DPTRR)
Static Stabilizers: Labrum, Capsule, GH ligaments, Articular Cartilage (ACGA)

Impingement: (AKA rotator cuff syndrome): Supraspinatus tendon rubs & gets stuck under bursa, becomes inflamed,
 sub-acromial space; Shoulder bursitis, Shoulder tendinitis, Shoulder inflammation, Subacromial/subdeltoid bursitis
Epi: Extremely common! Mech:  w/ age & activity level (overhead lifting repeatedly). HPI: insidious onset/trauma
Sx: Pain= Aching, dull @ rest, difficulty sleeping. Location: antero-lateral acromion, deltoid insertion, lat upper arm.
Feels like punched arm, radiates down. pain w/ palpitation. Sharp w/ shoulder abd, ext rotation, elevation > 90°
TTP: antero-lateral acromion (sometimes) PROM/AROM: normal or near normal
Dx: Clinical. Strength: Full (pain mediated) Special Tests: + Hawkins-Kennedy, + Neer X-ray: +- “spur” (type 3)
MRI: No tear & Show bursitis/tendinitis (PT & cortisone shot b4 MRI!)
Tx: Conservative: PT, Subacromial Inj Surgical: Arthroscopy (Debridement, Subacromial decompress, Distal clavicle excision)

Rotator Cuff Tear: (SITS) = more striking than impingement. Special test: Empty Can test & Drop Arm
Dx: X-ray: +/- “spur”. MRI: Full thickness tear. Dx US (if can’t do MRI) Tx: Arthroscopy

Glenohumeral Dislocation/Instability: Epi/Mech: Adolescent: trauma / inherited laxity Adult: trauma

May become Chronic Instability  Repeat subluxations/dislocations. Anterior shoulder dislocation = MC
Sx: Pain – joint/general, Deformity, poss transient tingling & numbness
Dx: Clinical, X-ray
Tx: 1st time traumatic = Conservative: Reduce, Immobilize 2-3 weeks, Rehabilitation (PT > 4 wks.), poss surg.
Repeat dislocations: Surgical: arthroscopy w/ capsulorrhapy w/ poss labral repair (tighten up capsule)
Bankart lesion: Traumatic detachment of glenoid labrum Hill-Sachs Fx: Impact Fx of the postero-lateral aspect of humeral head

Adhesive Capsulitis (Frozen Shoulder): MC in Diabetics, Can be w/w.o injury

Mech: Scarring and adhesions limiting ROM of the shoulder, Sx: Very painful ROM
Dx: Clinical exam: Stiffness with a “hard” end point during shoulder ROM
Tx: Conservative: Cortisone inj/6 wks, Xtreme PT, can self resolve in mo. Miserable bc cant lift arm, wipe butt, brush
Tx Surgical:can perform a Manipulation under anesthesia (break scar tissue) / arthroscopy with lysis of adhesions

Acromioclavicular Sprain (shoulder separation). Type 5 thru trapezius. Epi: young, active adolescent, adult.
Mech: Always traumatic, Fall on the lateral shoulder, MVA from seat belt
Dx: Clinical, X-ray: AP bilateral AC joints weighted and unweighted
Tx: Conservative: MC Immobilize=Sling, PT (Type II +), pad. Open Surg reconstruct = rare. Put rope & hold joint
Elbow Sprains & Strains: Strains>Sprains. D/t overuse. Hard to tell from fracture (trauma/no trauma). LCL: Rare

(medial) Ulnar Collateral Ligament (UCL): baseball pitchers  Torque from throwing.
Sx: VALGUS force from repeat trauma, Medial elbow pain, Tenderness over the UCL & LAXITY = valgus stress test
Dx: X-ray- look for avulsion fracture, MRI arthrogram: dye into elbow joint
Tx: R.I.C.E., PT, Correct throwing mechanics, Surgery- “Tommy John” surgery

Medial & Lateral Epicondylitis: Medial = Golfer’s. Lateral = Tennis elbow, ECRB (extensor carpi radialis brevis).
Extremely common, overuse injuries. Sx: Pain w/ use & tender to touch over the tendon origin, Pain w/ grip strength,
Muscle testing: pain w/ resisted wrist extension/flexion, +/- weakness Tx: Injection, bracing, PT  Rarely = surgery

Biceps Rupture: Key: Identify location of injury. Have 2 long heads, can tear one but still have full function!
Sx: Cant use screw driver, can use hook sign, if not they need tx. Need to treat within 3 weeks!! = importance
Tx: Don’t need treatment (deformity, aesthetically can treat or if it cramps)
Proximal (shoulder): Patient will have a permanent deformity, No loss of function or strength
Distal (elbow): think activity level, needs tx w/in 3 wks OR Pt will have weakness w/ supination permanently
if they rupture at shoulder = not a big deal, rupture at elbow = BIG deal. Tendon attaches to radial head.

Olecranon Bursitis: Eti: Direct blow, Repetitive rubbing of the elbow, Infection (bug, bacteria gets in)
Sx: Effusion of the olecranon bursa, Erythema, +/- Pain, Stiffness, Warmth
Tx: Compression, Poss aspiration/cortisone inj, Surgery- rarely unless infected

Hand/Wrist

Carpal Tunnel Syndrome: Extremely common! d/t work setting.

Sx: Tingling & numbness = median nerve distribution, Sleeping is often worse (wake up & shake arm)
Dx: + Tinel’s Sign, + Phalen’s Test, EMG & Nerve conduction studies
Tx: Short-term: Injection, Cock-up wrist splint, Long-term & Advised: Surgery
Px: Longer it is going on the worse chance of full recovery, Atrophy in the thenar/ hypothenar atrophy- BAD

Dequervain’s Tenosynovitis: MC: Women (30-50y.o.) (d/t New mom pick up baby)
Sx: Pain, +/- mild edema, + Finkelstein Test (conclusive!!) Tx: Inj, +/- bracing=thumb stable. PT, Rare=surg release

Trigger Finger: Inflammation causes nodular enlargement of the tendon distal to the A1 pulley
Sx: “Catching”, “locking” and pain with PROM and AROM of finger flexion, +/- palpable nodule, can’t extend joint.
Tx: Cortisone Inj, NSAIDs (don’t really work), +/- immobilize, rare=surg (scrape off nodule, closet hem back up)
 LOWER EXTREMETIES

Strain: muscle / tendon injury. d/t overloading/overuse = disrupts muscle tendon/musculotendinous junction integrity
 risk: Rectus Femoris, Biceps Femoris, Semitendinosus, Adductor Muscles, Vastus Medialis, Gastrocnemius Medial Head
RF: Muscles: that cross 2 joints, made primarily of type II fibers, that perform eccentric contraction
Previous Injury,  Age (weekend warriers trying to get back to shape), Change to  Competition Level.
 Grade 1: minor microscopic tear, activity tolerated, NO visible swelling, no  in ROM, strength ~ norm
 Grade 2: incomplete disruptions of fibers, partial tear, activity discontinued, change in static/dynamic pressures,
acute pain  ache, localized pain, delayed discoloration, poss deformity.
 Grade 3: complete/near complete rupture. Audible/sensation of “pop” during injury, activity discontinued, poster
changes, obvious deformity, severe swelling, loss of function, acute pain  ache.

Sprain: ligament/capsule injury. d/t joint exceeding nL range of motion/new plan by force. Sudden force/twisting!
 Ligaments have poor BF thus slow healing, affects joint itself. Overuse sprains = rare & joint laxity change w/ age.
 Sprain RF: Previous sprain, joint lacking range of motion/strength, lig near joint w/ other probs.
 Grade 1: minor intrinsic/extrinsic force that exceeds normal joint ROM, activity as tolerated, minimal or no visible
swelling, no decrease in ROM, minimal px or discoloration
 Grade 2: intrinsic/extrinsic force that causes partial ligament disruption, d/c activity, moderate swelling/effusion,
increased joint mobility w/ solid endpoint, loss of some ligament fxn
 Grade 3: intrinsic/extrinsic force causes subluxation or complete ligament tear, audible/sensation of “pop”, d/c
activity, immediate px and severe effusion, discoloration, gross joint instability – no ligament fxn, loss of endpoint
during ROM testing, usually more than 1 ligament

RICE Protocol: If it is a truly minor sprain/strain, treat w/ RICE for 24-48 hrs.
Rest = rest injured area, can exercise other muscles to maintain conditioning during healing
Ice = apply ice immediately for 15-20 mins, 2-3x/hr to  pain/swelling/inflammation
Compression = wrap area w/ elastic bandage to  swelling, starting at point furthest from heart
Elevation = elevate area bove the level of the heart, esp at night, bc gravity further reduces swelling.

Herniation: Blunt trauma thru fascial covering. Seein in small area of muscle. nL @ rest, pain during contraction.
Hematoma/contusion: direct trauma to BV of muscle. Affecting 1 muscle/muscle group. Strength maintained.
(risk compartment syndrome if taking blood thiners)

HIP INJURIES (mech of injury, Sx, special test results, Tx)

Greater Trochanteric Bursitis = Inflammation of bursa. Eti: TFL/IT band/gluteus medius rubbing, Direct pressure
Sx: aching @ night, pain w/ walking, Groin Pain, Bursa irritation (bc IT band, Glut medius tendon on top of bursa)
PE: TTP = greater trochanter, Full PROM & AROM of hip. May have lateral pain w/ some Strength Test.
Dx: X-ray = normal. Spur of greater trochanter. Tx: Injection, NSAIDs, +/- PT, Surgery=rare

Muscle Strain: Hamstrings, Quadriceps, Hip Flexors, Groin. HPI: overuse/acute injury. 15 yo boy w/ back pain.
DDi: inguinal hernia, joint probs, Avulsion Fx: ASIS = MC in teens. (tight hamstring)
PE: Acute: ecchymosis, warmth, tenderness = lot of bleeding. AROM &/or PROM restriction. Strength testing
Dx: X-ray normal unless avulsion fracture (ASIS), wt barring X-ray. Tx: Rest (crutches) Ice, PT.

Acetabular Labral Tear/Femoroacetabular Impingement (FAI) See both on X-ray.

Slipped Capital Femoral Epiphysis,
 If have FAI = something we are born with,  risk of having hip replacement. Better to catch early.
 Get bone spur created. Space gets smaller d/t this.  start tearing labrum (ring inside of the hip!) = red&irritated.
ALT = Epi: younger (15-35) injury, older DJD. Eti: DDH, Trauma (MVA, xs twist/splits).
Sx: GROIN PAIN. Worse w/ activity (in/out of car), may hear/feel “pop/click”.
FAI & ALT = Special Test: Impingement sign, FABER test (Flex, Abd & Ext Rotation). MR Arthrogram.
Tx: Rest, PT, Surg
Developmental Dysplasia of the Hip (DDH): abnormal growth/development/dislocation hip
Eti: femoral head/acetabulam probs; lax ligaments, breech, postnatal posturing (first 6 wks critical for hip develop!)
Epi: 1/1,000 live births, genes, 1st born girls, breech position. NEWBORNS right after birth. (pain  w/ age)
Sx: PAINLESS Limp! Unstable = femur head pops out of acetabulum. Stable = not properly shaped, shakes in place.
*PE: Barlow maneuver = hip is currently IN place, examiner attempts to dislocate.
Ortolani maneuver = his is OUT of acetabulum, examiner attempts to reduce dislocated hip. “clunk” = + sign.
Dx: Age dependent, <6 mo = US, >4-6 mo = X-ray, +/- MRI (Asymmetric Hip) (US for all F Breech babies)
Tx: Age & severity dependent. Newborn = pavlik harness (hips in flex&abd) 1-6 mo = closed reduction + harness.
6-24mo = closed reduction+spica splint + anesthesia. +24mo = surgery (open&osteomoty)

Slipped Capital Femoral Epiphysis (SCFE) = displacement of femoral head, slip thru growth plate (med & post)
Epi: Adolescent, AA, Male Obese. Eti: ? multi-factorial.
Sx: Pain: thigh/medial knee. Nerve: femoral nerve (goes right by femoral neck area). PAINFUL limp.
Dx: Clinical = limitation of int rotation of hip. X-ray (kline line). Tx: Surgery = internal fixation. (20%=AVN,  risk)

Legg-Calve-Perthes Disease
Eti: Idiopathic AVN femoral head. Epi: 1/1200 kids, 4-8yo, short, Caucasian, Male Dx: X-ray.
Sx: Persistant PERMANANT pain +/- limp. Tx: Varies (none  abd brace/stretching  replace hip  Arthroplasty)

Knee Disorders
Knee Strain: Hamstrings, Quadriceps, Gastrocnemius, Patellar. Strain very common!. Key 2 dx: location, trigger, TTP
Tx: RICE, PT, slow return to activity
Knee Sprains: ACL, PCL, MCL, LCL, Patellar. Severe = debilitating for +mo.
Unhappy Triad: ACL, MCL, Medial Meniscus.

Anterior Cruciate Ligament (ACL): partial/complete tear. Don’t fix + 50yo.

Eti: sudden change/direction, pivot of locked knee, sudden deaccel. Direct blow.
Sx: pop, severe pain, inability to continue activity, large effusion w/in joint (few hrs), Loss of ROM. Instability w/ WB
Special test: + lachman’s, + anterior drawer, R/O meniscal/MCL involvement. MRI 4 severity.
Tx: RICE, prehab b4 surg, regain ROM/strength. ACL reconstruction surg. Functional ACL brace. 6-9 mo b4 activity.

PCL: MVA, fall on bent knee, extreme hyperextension. Dx: + drawer, + tibial sag, MRI. Tx: RICE, PT, Surg (rare)

MCL: Eti: Valgus stress, blow to outside of knee. PE: Medial joint line pain, effusion, pain w/ ambulation.
Dx: Valgus stress test @ 0-30 degrees. Tx: RICE, crutches, PT, hinged knee brace, Surg (rare)

LCL: Eti: Varus stress, w/ more severe knee inj, blow to inside of knee. PE: lateral join line pain, effusion
Dx: Varus stress test @ 0-30 degrees. Tx: RICE, crutches, PT, hinged knee brace.

Meniscus Tears: Medial > Lateral. Epi: young = trauma/twisting. Older = everyday activity, chronic/degen tears=age.
Sx: Effusion (hrs later), clicking, catching, joint-line pain w/ activity, tenderness over medial/lateral joint line.
Dx: McMurray’s test = +pain, +/- clunk. MRI. Tx: arthroscopy (debridment & repair). Meniscus don’t heal d/t BF.

Prepatellar Bursitis: Largest & MC knee bursa to be inflamed. Eti: trauma (fall onto anterior knee), repeat kneeling.
Sx: Ant knee swelling, +/- TTP, water ballon sensation. Dx: Clinical (r/u knee effusion & infection)
Tx: Aspiration & compression wrap, avoid irritation, steroid inj, surg (rare), protective work gear.

Osgood-Schlatter Disease = Rupture of growth plate at tibial tuberosity, inflammation below patella (patellar tendon)
Epi: adolescents (playing sports) M>F. Sx: Persistent Pain, swelling (uni/bilateral), improves w/ rest (min-hrs).
Dx: clinical (can do X-ray if severe/atypical) Tx: Heat b4 activity, Ice after. rest/restrict activity, NSAIDs/brace/RICE.

Patellofemoral Pain Syndrome

Eti: Dysfunction 2/t injury/overuse. Physio=underdeveloped VMO/excessive valgus. Large Q angle, Mal-track patella
Epi: adolescent females Sx: Peripatellar pain/swelling Dx: +20 Q angle, sunrise view in X-ray
Tx: Rest & Ice, PT (VMO strengthening), +/- bracing

Patellar Dislocation. Female, lateral dislocation, Eti: direct blow/awk twisting motion
Epi: Girls, XS Q angle, misalign patella, insufficient VMO. Sx: reduces prior to presentation.
Dx: Clinical, + Subluxation test. Tx: immobilize 4 wks, PT, brace, Surg if repeats.

Osteochondritis Dissecans (OCD) = AVN of focal area of subchondral bone.

Eti: genetics, trauma, repetitive stress. Epi: M=F, sports +10 yo, MC of loose body in peds.
MC Sites: Distal femur, radial head, talar dome. Sx: Joint pain & swelling Dx: MRI is best (for AVN), X-ray.
Tx: observation & limitation. Arthroscopic removal. +/- drilling/grafting.

Ankle Sprains
Lateral: MC! d/t Anterior Talo-Fibular Lig (ATFL), +- Calcaneofibular Mech: Inversion Dx: Anterior drawer & Talar tilt

Medial = Injured Lig: Deltoid ligament Mech: Forced eversion Dx: Valgus stress/eversion. Poss combo w/ Fx.

High ankle/Syndesmotic sprains = don’t want space there, rubs = arthritis. Mech: Forced dorsiflexion & rotation
Injured Ligs: Ant. & Post & Transverse Tib-fib &, Interosseus Membrane Special Test: Squeeze test
Sx: Sig swelling & pain. Rarely full WB. Tenderness, + pain w/ forced dorsiflex. Longer recovery time, Xray = widening.

Achilles tendonitis/bursitis: d/t overuse. Ask about shoes. Swelling & Inflammation.
Tx: Mild = RICE, PT, change footwear, NSAIDs. Severe = same as mild +heel lift, boot.

Achilles tendon rupture: MC tendon rupture, Men + 30 yo. Eti: Jumping & hear pop. Kicked back of leg. Pivoting.
Sx: Pain in heel, +/- TTP, obvious deformity. Dx: Clinical, THOMPSON test. Tx: Complete rupture = surgery. PT

Plantar Fasciitis: Eti: Bad footwear, tight calfs, wk foot muscles, gait&balance probs, flat fat pad, obese.
Sx: Pain on bottom of foot by heal, in AM when out of bed, walking/standing long distance
Tx: R.I. Calf stretching, massage, NSAIDs, change footwear, arch supports.

Morton’s Neuroma: MC mid-age Female (heels). Dx: clinical, X-ray=normal. Tx: wide-toe shoes, cortison inj. (surg)
Sx: sharp/stinging pain btween toes when standing/walking. Pain in forefoot (3rd & 4th toes). Swelling btween toes.
Tingling ("pins and needles") & numbness. Pebble/marble under the ball of the foot Dx: + Squeeze test

Osteoarthritis 75% of arthritis. Meniscus removal, can cause it. Previous injury. Wearing of the articular cartilage
Mech: Wear & tear Dx: Weight Bearing x-rays Tx: NSAIDs, Cortisone Inj, Total joint replacement (only thing that’ll Tx)

Total Joint Replacements

 3 views is best. AP, oblique & lateral of every joint. WB imaging.
 For fracture = NO ANTI-INFLAMM! Slow down healing process

Avascular Necrosis / Osteonecrosis MC = knee, hip, foot, hand & shoulder. Poss bilaterally.
No Sx in initial stages. Worsening of dz =  pain in joint. AVN in hip = pain in thigh, butt & groin.
 Spine Disorders
Introduction
 Spine disorders = MC Pt complaints. Sx = lumbar, cervical or thoracic spine
 Patho = degenerative changes, traumatic, tumoral, infectious and vascular disease
Disc: Outer fibrous: annulus fibrosus, inner: nucleus pulposus

Common terms:
 Spondylosis: arthritis of the spine
 Spondylolysis: crack or fracture of the pars interarticularis
 Kyphosis: outward curvature of the spine, normal in thoracic and sacral regions
 Lordosis: inward curvature of the spine, normal in cervical and lumbar regions
 Stenosis: narrowing of the “normal” spinal canal and foramina
 Radiculopathy: symptoms of pain, paresthesias, or weakness in dermatomal pattern
 Myopathy = weakness of the nerves (similar to above term)

Abnormal Curvatures
 Kyphosis & lordosis exist in normal spine, these pictures depict pathological exaggerations of these features.
- GI problems, heart may not pump as well, can’t intubate them
 Lordosis = lax ligaments / poor muscle tone. Or have large abdomen that pulls weight forward on lumbar spine.

Bone = facet joints sit on pedicle. Nerve roots exit = get pinched.
Can happen from herniated disk, overgrown ligaments, bone spurs (usually a combo). Aka lumbar stenosis

Physiology of the Spine

 Discs are not sensitive but these are:
- Ligaments, Facet joints, Vertebral periosteum, Outer layer of annulus, Spinal nerve roots
 Paraspinal muscles are pain sensitive and common source of back pain.
 In adults, spinal cord ends at the conus medularis at L1-L2 levels. Below that nerve roots constitute cauda equina
 The most commonly involved areas include: lumbar, then cervical and then thoracic regions
 Lumbar spine is very vulnerable because of the continuous stress and the heavy load
 Cervical spine is second and very prone to trauma as well as degenerative disc disease (DDD) with nerve and spinal
cord compression (family history, smoking, poor posture can risk of DDD)

Herniated Lumbar Disc

 Weak paravertebral muscles and ligaments
 Disc protrusion is postero-lateral
 Symptoms consist of low back pain (LBP), buttock, thigh, calve and at times foot symptoms

Part One: Lumbago & Lumbar Disc Disease

Epidemiology: Incidence/Prevalence
 Estimated that up to 84% of adults have lumbago at some time in their lives
 In 2010, accounted for 1.3% of all office visits in the United States
 In 2014, 28.1% of adults reported lumbago in the past 3 months

Epidemiology: Cost to Society

 Lumbago is the single greatest cause of disability worldwide **
- Will see people on disability for this. High cost.
 2010 cost ranged from $560 to $635 billion, with cost of care for pain ranging from $260 to $300 billion, and lost
productivity cost ranging from $299 to $335 billion for U.S. economy

Classic Nerve Root Symptoms Rare

 Only 1% with nerve root symptoms
 Only 1-3% have lumbar disc herniations
 Prognosis for LBP is good
 Most improve without medical intervention

Lumbar Spine Anatomy good to know dermatome patterns. Can be some overlap. Pain can radiate down.
Risk Factors: Age #1 risk factor. Most over age of 60yo*
- More than 90% of those older than 60 years of age demonstrate degenerative changes on imaging of the spine
 Obesity  Abnormal gait, posture, excess stressor on the body
 Smoking  Accelerates rate of degeneration of intervertebral discs
 MC in females, Lower educational level, Depression / Anxiety
 Strenuous work, physically & mentally
- Less than 50% of those disabled longer than 6 mo return to work, and almost 0 return when disabled for 2 yrs
 Job dissatisfaction (don’t want to go back), BWC (workers compensation), Secondary gains

Etiology: Non-Specific Etiology: Non-Mechanical

 >85% of those seen in PCP = no spp cause identifiable  Not related to structural deficiency,
 Myofacial Pain Syndrome: 95% of Pts. w/ chronic pain. an inflammatory process
- Direct/Indirect muscle trauma & overload
- Neoplasia, Infection, Autoimmune
Etiology: Mechanical
 Structural pathology Etiology: Non-Spine Related
- Degenerative Disc Disease (DDD)  Pelvic organ / visceral dysfunction  PID,
- Spondylosis, Spondylolysis Prostatitis, Endometriosis, Neprholithiasis,
- Spondylolisthesis Pyelonephritis, Pancreatitis.
- Herniated disc, Spinal stenosis  SIJ dysfunction (Dysfunction in the sacroiliac
- Fractures, Congenital disease joint gives leg pain)
 Piriformis syndrome (wearing wallet, pain in
HPI: Asking the appropriate questions butt)
 Where is the pain located?  Comorbidities  Depression, DM, etc.
 When is the pain present? Is it constant, or intermittent, or
does it vary? Is it predictable or spontaneous?
 How long has the pain been present? Is it acute, sub-acute, chronic?
 What exacerbates or relieves?
 Are there any associated symptoms? Paresthesias, weakness, incontinence, radicular pain?
 What have you tried to relieve the pain? NSAIDs, PT, Ice/Heat, Rest/Activity, Specialist consultation/ imaging?
 Have you had this type of pain before, or is there a family history of lumbago?
 What are your expectations? Goals of returning to activity?

Physical Exam:
 Any obvious signs that emergent referral needed? in distress, or sign of infection or deformity? incontinent?
 Generalized appearance. Posture/ Affect
 Thorough exam of the spinal contour and palpation along the paraspinal musculature
- Excessive kyphosis / lordosis / scoliosis, Trigger point: palpable bundle of muscle fibers that are TTP
 Thorough neurological exam: Strength, reflexes, sensation, proprioception, gait, etc. detertome pattern.
 Specific tests: Straight leg raise = 30 degrees = + result
- Clonus = neuro exam (low back pain), dorsiflex foot. Clonus + = foot bounces. (sign of pinch nerve, mylopathy,
abn neuro exam). FABER (pain in back, SIJ pain)
 Waddell’s Signs (multiple positives may indicate some psychological component)
- Overreaction during exam, out of proportion, Pain with axial loading
- Improved tests while distracted, example SLR, Non-dermatomal pattern for symptoms
Different Signs and Symptoms of Radiculopathy L4. L5 and S1 ** know chart
Diagnostic Imaging / Labs:
 No labs are specific, but can help when ruling out infectious cause
 Generally, no imaging recommended for acute lumbago (less than 4 weeks duration), unless there are signs of
neurologic deficits that are either severe or progressing or there is presence of significant risk factors such as cancer
diagnosis or recent history of trauma
- Imaging studies initially considered would be radiography or MRI depending on findings of HPI/PE
- MRI considerations should generally be performed by specialists
 If no improvement in pain after 12 weeks, a plain radiograph is generally considered with referral to specialist
- It is common for no serious underlying condition to be seen on imaging
- Incidental findings are common and can lead to further testing that is not needed
- Results are best interpreted by providers such as surgeons or pain management if they are involved in the patient’s
care
Nomenclature & Classification of Abnormal Discs

Degenerated Disc (MC) Deterioration of internal structure (MRI), disc height & no disk extrusion

Bulging Extension of disc beyond end plates, normal variant

Protruded Focal or asymmetric extension of the disc beyond interspace

Extruded Free fragment, may be sequestered behind the PLL (disk herniation)

Contained Herniation Outer margin of annulus is intact, more than a bulge

Different Stages in Herniation of Intervertebral Disc

a) tearing of rings of annulus fibrosis

b) protrusion of the disk against the nerve root

c) extrusion of part of the nucleus pulposus w/ further nerve root compression

Differential Diagnosis:
 Diagnosis will depend on a thorough HPI and PE but can most often fall into one of the following categories
- Musculoskeletal
- Structural defect  May, or may not, be related to spine
- Inflammatory process  May, or may not be related to spine
- Psychosocial process

Differential Diagnosis of Back and Leg Pain with Metabolic and Inflammatory Diseases
 Bony infection: pyogenic, fungal, parasitic, tuberculosis…
 Spinal epidural abscess
 Rheumatoid variants: ankylosing spondylitis, psoriatic arthritis, Reiter’s syndrome, intestinal arthropathies, Paget’s dz
 Gout, Pseudogout, Fibrosis, Ochronosis, Hemochromatosis
 Osteogenesis imperfecta, Diabetic amyotrophy, Hyperparathyroidism

Differential with Metabolic, Inflammatory Diseases, Psychogenic and Tumor Related Pain
 Metabolic: Bursitis, Osteoporosis, Osteoarthritis, Diffuse Idiopathic Skeletal Hyperostosis(DISH), Adhesive arachnoiditis
 Psychogenic pain
 Tumors: Intramedullary, extradural, intradural-extramedullary, metastatic tumors of the spine, primary benign and
malignant tumors to bone, sacral cysts, retroperitoneal tumors and fibrosis
- Intramedullary = in spinal cord itself.
- Extradural = outside the dura (tumor of ligament, bone or dura gone extradural)
- Intradural-extramedullary = inside the dura in spinal cord itself (compression) grow within the spinal canal but
outside of the nerves.
Referred Pain Syndrome
 Gastrointestinal: peptic ulcer, pancreatic disorders, gallbladder disorders
 Vascular: abdominal aortic aneurysm, arterial occlusion or insufficiency, other aneurysms
 Renal: nephrolithiasis, infections, prostatitis
 Gynecological-obstetrical: pregnancy, pelvic tumors, pelvic inflammatory disorders
 Orthopedic: hip disorders, knee disorders, sacroiliac disorders, coccygodinia
 Mechanical: segmental instability, trauma, spinal deformity, spinal stenosis, leg length inequality, iliac crest syndrome,
facet syndrome, herniated intervertebral disc

Red Flags
 Cancer or Infection: Age>50or<20, hx of cancer unexplained weight loss, immunosuppresion, UTI, iv drugs, fever or
chills, back pain not improved with rest
 Spinal Fractures: Hx of trauma, prolonged steroids, age>70
 **Cauda equina syndrome or severe neurological compromise
- acute onset of urinary retention or overflow incontinence
- fecal incontinence or loss of anal sphincter tone
- Saddle anesthesia (perineal region),
- global (whole genital region) or progressive weakness in LEs (sudden inability to walk)
-  rectal turn, urinary incontinence (order surgery before doing MRI. Surgery ASAP!). surgery is TX!

Treatment:
 Non-specific lumbago
- Stay active, return to normal activities as tolerated
- Avoid excessive bending or twisting
- Use Ice/Heat for comfort
- NSAIDs or Acetaminophen, maybe muscle relaxer, and with severe pain possible opioid for short-term relief
- PT or Chiropractic manipulation can bring relief and should be considered (NetCE, 2016)
- Consider referral to specialist if pain persists
 Mechanical lumbago
- PT with focus on addressing the structural deficit can bring relief
- Surgical referral could be sought after
o Herniated discs, spondylolisthesis, radiculopathy
- Referral to multidisciplinary pain program may offer more options
o Injections, procedures, medical management
 Non-Mechanical and Non-Spine related lumbago: Address the underlying dysfunction accordingly
 Ultimately, the primary goal of treatment is to restore function to as close to baseline status as possible
 Rehabilitation may be a life-long process, with continuous monitoring and adjustments to the treatment plan

Medications to consider:
 NSAIDs: Ibuprofen, Naproxen, Diclofenac, Meloxicam (Consider risks with GI / Renal impairment)
 SNRI: Duloxetine (FDA approved for depression, anxiety, fibromyalgia, neuropathy, & chronic musculoskeletal pain)
o  risk of suicidality, eliminated in urine but extensively metabolized w/ CYP450, generally well tolerated
 Opioids: Risks vs. Benefits need to be weighed heavily
 Topical lidocaine
 Muscle relaxants: Tizanidine, Cyclobenzaprine, Benzodiazepines
 TCAs (not FDA approved for pain): Amitriptyline

Non-Pharmacological Treatment:
 TENS unit = stimulate up dorsal aspect of spinal cord (dorsal is sensory)
 CBT (cognitive behavior therapy), Acupuncture. Yoga, Lifestyle changes (stop smoking, lose weight, be more active)

Education of PT: Explain in simple terms & positive reassurance, Proper posture, sleeping positions, lifting techniques, PT.

Prognosis:
 Excellent for acute lumbago, 70-90% improve within 7 weeks
 Recurrence present in up to 50% w/in 6 mo and 70% in 12 months. Estimated that 5-20% will develop chronic lumbago
- Predictors of transition to chronic lumbago include maladaptive coping behaviors, functional impairment, poor
general health, and presence of psychiatric comorbidities
 Part Two: Cervical Disc Disease
Increase in the geriatric population!
 Degenerative cervical and lumbar spine disease, need for early diagnosis and treatment, Surgical risk

Elderly are vulnerable to post traumatic central cord syndrome = hyperextension.

Central Cord Syndrome Is Common

 Patient slips on ice!
 Acute painless weakness of both upper extremities
 Relative preservation of both lower extremities function
 DTR depressed
 Loss of sensation to pain and temperature in upper
 May lose motor function of lower extremities and bladder function (urinary
retention) if severe
 Central cord syndrome: marked weakness in upper extremities, less in lower
extremities

Treatment of Central Cord Syndrome

 MRI to visualize the pathology
 If stable, observation, in neuro-unit
 IV Steroids
 Cervical collar may be OK, if not deteriorating
 If deteriorates, surgery may be indicated in selected cases...
 Surgery if unstable: either anterior or posterior approach…
 Prognosis: If limited contusion, may recover spontaneously (usually better for younger people), unable to predict

Brown-Sequard Syndrome
 Loss of motor function ipsilateral to the lesion
 Loss of pain and temperature contralateral to lesion
 Position and vibratory sense is preserved side opposite to lesion bc doesn’t cross till levels above.
 Has the best prognosis of any incomplete spinal injuries.
 Up to 90% will ambulate and have sphincter control

Spinal Cord Syndromes

 Complete Spinal Cord injury
- Paralysis of all sensory and motor function below the lesion
 Anterior spinal cord syndrome
- Spares sensation mediated by the dorsal columns. Thrombosis of the anterior spinal artery may occur due to central
HNP. Poor prognosis .

Injury to Anterior Spinal Artery Could Lead to Devastating Neurological Deficit

Anterior Spinal Cord Syndrome due to Thrombosis of Anterior Spinal Artery

Cervical Disc Herniation

 Unilateral soft disc herniation
- Pain in neck and arm in a radicular distribution
- Paresthesias are distal
- Extension/rotation of neck induces pain
- Radiculopathy: sensory loss or pain in radicular pattern
- DTR loss in particular myotome
 Central Disc with cord compression is an emergency
- If the symptoms are acute and the patient is paraparetic, hope for recovery post surg
o (refer to the previous cord syndromes)
Lateral View of Cervical Spine: C5-6 and C6-7 are most common sites for HNP
C6-7 is the most common, root involved is C7, middle finger! = cervical disk herniation Sx
Herniation of C56, affecting C6
Cervical Disc Syndromes** myelotomes & determatones & reflexes

Look for Hoffman sign, equivalent of Babinsky in the lower extremities

 The MRI and CTScan are complementary. Here MRI discloses soft tissue (cord) compression and CTScan demonstrates
disc and osteophyte(bony) impingement on the neural structures

Surgical Treatment
 Up to 90% may recover with appropriate anti-inflammatory meds, intermittent traction…
 In case of severe pain and progressive neurological deficit, surgery.
 ACDF, fusion controversial, (30% chance need to do further fusion of lower part of spine)
 But if myelopathy due to osteophytes, fusion recommended

Cervical Spondylosis Is Not Uncommon

 Low back pain but has also neck pain
 Intrinsic hand muscles, Numbness, weakness, Buttoning shirt
 Tandem gait, Stumble and fall, Urinary urgency

Consult for LBP...

 But presents with myelopathy!
 Which area treat first? LBP or Cervical Spine Disease!, LBP becomes secondary!

Cervical Spondylosis
 With Radiculopathy
 With Myelopathy
- Patient complains of neck pain - Unilateral or bilateral symptoms.
- Numbness of hands - Pain and weakness
- Difficulty with gait - Sensory loss, paresthesias in a radicular pattern
- Central cord syndrome if fall - Hyporefelexia
- Intrinsic hand muscle weakness - Intrinsic hand muscle weakness
- Difficulty with fine motor skills

Cervical Spondylosis with Myelopathy(CS) and Amyotrophic Lateral Sclerosis(ALS) (MC ? to compare the 2)
 No sensory involvement in ALS,
 No bulbar involvement in CS, No tongue fasciculations in CS

Surgical Indication
 Progressive myelopathy with radiological evidence of spondylosis, Pts w/ severe pain & in early stages of disease

Loss of Normal Lordotic Curve Multiple Levels of Severe Compression

Choice of approach
 Anterior approach if lesion (osteophytes) confined to one or two or even occasionally three levels
 It consists of either corpectomy, fusion using bone or bone and cage and plating or diskectomy, fusion and plating
Skin Incision for Anterior Exposure of C-spine Stabilization Post Corpectomy

Posterior Approach
 Standard laminectomy from C3-7, with or without plating and bone graft
 Possibly with microforaminotomy

Impressive Postoperative Outcome

Surgery
 ACDF with plating
 Halo is used in case of multiple corpectomies
 Intraoperative SSEP monitoring

Part Three:
Thoracic Disc Disease

Thoracic Disc Herniation:

 Comprises 0.25% of HNP
 <4% of surgeries for HNP
 T8 or below(more mobile aspect of the T- spine)
 Frequently calcified
 Surgery if refractory pain and myelopathy

Epidemiology:
 Between 3rd and 4th decade(80%)
 Below T8(75%)
 Peak at T11 and T12(26%)
 Symptoms of
- Pain(60%)
- Sensory changes(23%)
- Motor changes(18%)

Surgical Indications:
 Refractory pain, band like distribution
 Progressive myelopathy
 Syringomyelia at site of disc herniation

Surgical Approaches:
 Midline laminectomy outdated and dangerous
 Posterolateral:
- Laminectomy and pedicle removal
- Transpedicular approach
- Costotranversectomy
 Anterolateral transthoracic
 Lateral extracavitary
 SPINE DISORDERS
 Define: Annulus fibrosis, nucleus pulposis, spondylosis, spondylolysis, spondylolisthesis, spinal stenosis, cauda equina
syndrome, sacroiliitis, radiculopathy, sciatica, myelopathy, compression fracture
 Recognize the associations between weakness, sensory loss, hyporeflexia / hyperreflexia, and pain location regarding
specific lumbar (L1 – S1) and cervical (C5 – T1) spine levels
 Identify the normal spine curvatures and anatomy of the spine
 Recognize red flags in the history or physical examination of a patient with back pain
 Differentiate between common causes of low back pain (spinal stenosis vs. herniated disc vs. low back
strain/sprain/musculoskeletal pain vs. referred pain) based on: Epidemiology, Clinical Manifestations, Treatment
 Differentiate btwn common back pain special tests: straight leg raise (SLR) test, reverse SLR, Spurling’s test, FABER
 Identify the recommendations regarding imaging of a patient with low back pain
 Recognize common non-surgical treatment for back pain
 Regarding the cervical spine, identify central cord syndrome etiologies, clinical presentation, and treatment
 Identify the primary differences between Brown-Sequard Syndrome & Anterior cord syndrome, (Eti & Sx)
 Recognize difference between complete & incomplete spinal cord injuries based on clinical manifestations & prognosis

OSTEOPOROSIS
 Osteoporosis, osteopenia, osteoclast, osteoblast, DEXA scan, bone marker, Dowager’s hump, T & Z-score, kyphoplasty
 Recognize the epidemiology associated with osteopenia, osteoporosis and osteoporotic fractures
 Identify the importance of diagnosing and treating osteoporosis
 Identify common clinical manifestations of osteoporosis
 Identify key factors that affect a patient’s BMD
 Recognize features associated with bone remodeling
 Recognize osteoporosis risk factors
 Identify the laboratory results associated with osteoporosis
 Recognize disorders most commonly in the differential diagnosis of osteoporosis
 Interpret DEXA scan results given patient demographics, clinical history and the results
 Differentiate between the main forms of pharmacologic treatment of osteoporosis
 Identify common non-pharmacologic treatments of osteoporosis

OA & GOUT
 Osteoarthritis, gout, pseudogout, monsododium urate crystals, calcium pyrophosphate dihydrate crystals, & podagra
 Identify common etiologies, and clinical manifestations of arthritis
 Recognize the joints that are most commonly affected by arthritis
 Be able to recognize arthritic changes, as discussed in class and on lecture, on imaging studies for arthritis
 Know generalized Tx for arthritis, you do not need to know specific drugs or the dosing but do need to know the classes
 Differentiate between osteoarthritis ^ rheumatoid arthritis. identify key differences regarding the clinical manifestations
 Recognize key findings on synovial fluid analysis for gout
 Differentiate between gout and pseudogout based on diagnostic findings
 Recognize the epidemiology, etiology, and clinical manifestations of gout
 Know the treatment recommendations for gout, you will need to know colchicine by name, as well as the dosing
recommendations for this drug for treating acute flare of gout

MUSCULOSKELETAL ID
 Define: Rhabdomyolysis, sequestra, involucrum, nidus, acute osteomyelitis, chronic osteomyelitis
 Recognize the common etiologies of rhabdomyolysis, clinical manifestations, test results and general Tx
 Identify mechanisms of septic bursitis, risk factors, clinical manifestations, and diagnostic measures
 Recognize risk factors for developing osteomyelitis. Identify the epidemiology and common etiologies of osteomyelitis
 Recognize clinical manifestations and test results consistent with osteomyelitis
 Identify the general treatment for osteomyelitis
 Identify the etiologies, risk factors for and joints commonly affected by septic arthritis
 Recognize the clinical presentation and test findings consistent with septic arthritis
 Identify common differences between gonococcal vs. non-gonococcal vs. viral arthritis
 Recognize synovial fluid analysis consistent with septic arthritis
 Identify cancers which commonly metastasize to bone
 Identify the most frequent area of bone metastasis
 Differentiate between common benign vs. malignant bone tumors based on epidemiology, common locations, clinical
manifestations, and treatment
 OSTEOPOROSIS

The Basics
 Osteopenia –  bone density, mild.
 Osteoporosis – “Porous Bone,” severe.
- Not making enough, or losing too much.
 BMD – Bone Mineral Density. The strength of your bone.
- Bone: Collagen and calcium phosphate
- 99% of the body’s calcium is in the bone and teeth
 Bones turn over naturally about 10% per year
 Osteoclasts = Bone resorption
 Osteoblasts = Lay down/build new bone, Can become Osteocytes
 Osteocytes = Manufacture needed products for bone matrix, i.e. collagen
 These cells work together in a constant remodeling process
 Formation > Resorption until around age 30

Bone Remodeling
 Due to need for calcium in the extracellular fluid or external stress on the bone.
 RANK stands for Receptor Activator of Nuclear factor-Kappa B
 Hypercalciemia stimulates PTH to be released. Hits osteoblast. RANKL & ligands & RANK receptors = tells it to form
more osteoclast  differentiate. Osteoclast = have ruffle membrane.
Osteoclastogenesis

Epidemiology
 54 million Americans have  bone mass, 10 million Americans have Osteoporosis, 80% are women
 Up to 50% of women and up to 25% of men over 50 will have a broken bone due to Osteoporosis
 2 million broken bones per year, $19 billion in related costs per year

Etiology
 Autoimmune Disorders  RA, Lupus, Ankylosing Spondylosis
 Medical Procedures  Gastric bypass, Gastrectomy
 Hematologic/Bone Marrow  i.e. Leukemia, Lymphoma, MM, Sickle Cell Disease (SCD), Thalessemia
 Endocrine/Hormonal Disorders  DM, thyroid or parathyroid disease, early menopause,  testo in men,
Cushing Syndrome, CKD,  estrogen
 Digestive/GI Disorders  Celiac Disease, IBD
 Neurologic Disorders  CVA (stroke), Parkinson’s Disease, Multiple Sclerosis
 Cancer  Breast, prostate
 Mental Illness  Eating disorders, depression
 Many Other Causes (amenorrhea, aids, liver disease, transplants, athlete triad)

Etiology - Medications
 Glucocorticoids (>3 months) (pts w/ RA, OA = do a dexa 1x/year ! )
 Lithium, Anti-epileptics, Aluminum-containing antacids
 Aromatase inhibitors such as Arimidex®, Aromasin® and Femara®
 Cancer chemotherapeutic drugs, Cyclosporine A and FK506 (Tacrolimus)
 Gonadotropin releasing hormone (GnRH) such as Lupron® and Zoladex®
 Heparin, Medroxyprogesterone acetate for contraception (Depo-Provera®), Methotrexate
 Proton pump inhibitors (PPIs) such as Nexium®, Prevacid® and Prilosec®
 Selective serotonin reuptake inhibitors (SSRIs) such as Lexapro®, Prozac® and Zoloft®
 Tamoxifen® (premenopausal use), Thiazolidinediones such as Actos® and Avandia,
 Thyroid hormones in excess
Risk Factors = F, old, smoke,  ETOH,  activity,  127lbs, FHx osteoporosis, White/Mexican,  Ca2+,  Vit D
 Female, Advanced Age, Smoking, Excessive ETOH, Inactivity, Weighing less than 127 pounds
 Family history of Osteoporosis, Caucasian or Mexican-American, Low Calcium/Vitamin D Intake

Clinical Manifestations
 Often asymptomatic  “I don’t need that, I feel fine.”
 Fracture, Bone pain, Loss of stature  Hunched posture, Deformities of bony structures, bony growth / development
 Dentition complaints (broken teeth), “Silent Disease”

Screening
 FRAX Score* Fracture Risk Assessment Tool
- Age, Gender, Weight, Previous Fracture, Parental Fractures, Smoking History, ETOH Use, BMD
 Bone Markers
- Check to see if rate of formation/resorption is abnormal
- 2 MC: C-terminal telopeptide of type 1 collagen (CTx), and Procollagen type 1 N-terminal propeptide (P1NP)
 DDI: Osteoporosis, Rickets, Paget disease, Osteogenesis imperfecta
 DEXA Scan (dual-energy x-ray absorptiometry)
- Small dose of ionizing radiation (< 1/10 of standard chest x-ray)
- No calcium supplements in the 24 hours prior to the scan
- Test takes 10-30 minutes
- T-Score – amount of bone you have compared to young adult, same gender
o -1 or higher = Normal, -1 to -2.5 = Osteopenia, less than -2.5 = Osteoporosis
- Z-Score – amount of bone you have compared to others in your age/gender group
 Who needs one? >65 y/o, <65 y/o with significant risk factors

Treatment Options
 Bisphosphonates, Selective estrogen receptor modulators (SERMs)
 RANKL Inhibitor, Calcitonin, Hormone Replacement Therapy, Parathyroid Hormone Analog
 Adverse Reactions
Bisphosphonates
 Inhibit osteoclast activity, reducing bone resorption and turnover. - Osteonecrosis (jaw)
 Risedronate (Actonel, Atelvia) - Uveitis, Scleritis
-  35 mg po once a week, or 150 mg po once a month - Esophageal Issues
 Alendronate (Fosamax, Fosamax Plus D, Binosto) - Atypical Femur Fx, MSK Pain
-  70 mg po once a week - Hypocalcemia
 Ibandronate (Boniva)  150 mg po once a month - Steven Johnson Syndrome,
 Given on empty stomach 30-60 min b4 first food/drink/med, - Toxic Erythema Necrosis, N/V, Etc.
- No laying down - *make sure to keep pt upright!!*
 Typically 3-5 years of treatment (10 for high risk) - Not good for bedbound pts.
 Monitoring
 Zoledronic Acid (Reclast)  5 mg IV once a year
 Can consider discontinuing after 3-5 years if low risk. - Creatinine at baseline (renal fxn)
 Make sure to check creatinine before each infusion. - Perodically: Ca, Mg, PO4
 Contraindicated:
- If CrCl is <35 Reclast is contraindicated.
 Stress importance of hydration to your patients. - Unable to stay upright 30-60 min
 Takes about 15 minutes, $2,926.35 per infusion - CrCl <30 ( creatinine clearance)
- Esophageal Stricture
SERMS
 Selectively binds to estrogen receptors.
- Estrogen antagonist in breast cancer cells . Agonist for estrogen’s actions in bone, liver, and uterus .
 Raloxifene (Evista)  60 mg po daily
 Tamoxifen (Soltamox), Toremifene (Fareston),  Both indicated for breast CA Tx, NOT Osteoporosis
 Black Box: Thromboembolism Risk, Fatal CVA Risk
 Adverse Reactions: Hot flashes, infections, joint pain, edema, N/V etc.

RANKL Inhibitors
 Binds to RANKL, inhibits osteoclast formation, maintenance, and survival.
 Denosumab (Prolia).  60 mg SubQ every 6 mo. 1st line Tx option.
 S/E: Hypocalcemia, Malignancy, Osteonecrosis of jaw, MSK pain, Atypical femur fractures (groin pain!!), pancreatitis,
check for murmur bc = infective endocarditis. N/V etc.
 Before starting & before each injection: No fever, No groin pain, No murmur, & do an oral exam.
 Monitoring: Creatinine at baseline, dental/oral exam. Periodically Ca, Mg, PO4.
 Treatment is indefinitely = foreverrrr. Must switch to alternate agent after discontinuing or  lumbar fx risk.

Calcitonin
 Hormone that inhibits osteoclasts and may increase osteoblast activity.
 Helps regulate calcium via bone, renal, and GI effects.
 Calcitonin-salmon (Miacalcin)  100 units SC/IM every other day OR every day. Also nasal spray.
 Caution if elderly, or prior bisphosphonate use.
 Adverse Rxn: Bronchospasm, osteogenic sarcoma, hypocalcemia, malignancy risk. N/V. Pruritis of earlobe.

Hormone Replacement Therapy (lots of request for this)

 Estradiol (for prevention, post-menopausal)
- 0.5 mg po daily, cycle 21 days on, 7 days off. (If pt has uterus, add Progestin for 2 wks of each month.)
 Black Box Warnings:
- Endometrial cancer, cardiovascular risks.
- breast & ovarian cancer risk.
- risk of CVA, MI, and DVT.
 Potential Reactions: Migraines, depression, dementia, pancreatitis, GB disease, ischemic colitis, etc.
 Caution if DM, HTN, >65 y/o, Smoker ( risk of clots), Thyroid disease, Migraines, etc.
 Monitoring:
- Check thyroid function prior to starting.
- Breast exam yearly. Routine Mammograms.
 Women will ask for it frequently.
- Helps manage other symptoms of menopause.
- We need to remind them, not without risks.
- Prescribe at the lowest effective dose, for the least amount of time.

Parathyroid Hormone Analog

 Regulates bone metabolism, intestinal calcium absorption, & renal tubular calcium/phosphate absorption. Stimulates
remodeling. ( osteoblast activity, overfilling deficit and  bone density)
 Teriparatide (Forteo): 20 mcg SubQ daily (MC drug to use for this)
 Abaloparatide (Tymlos): 80 mcg SubQ daily (new drug)
 Black Box Warning: Osteosarcoma = proliferation of cells, if to quickly = cancer.
 Safety and efficacy past two years of treatment is not yet established.

 Contraindications:  Potential Reactions:

- Skeletal Malignancy - Orthostatic Hypotension
- Hypercalcemia - Depression
- Hyperparathyroidism - Pneumonia
- Hypercalciuria
- N/V, dizziness, etc.

Any Med, For Any Disease, Any Time  weigh risks & benefits
Complications
 Fractures. Most common:
- Hip  20% die within the first year following hip fracture
- Spine (compression) – wedge deformity
- Wrist
 Dowager’s Hump/Kyphosis
- Alters body’s center of gravity  Predisposing the spine to more Fx (compression)! ( pressure on spine!)
- Height loss

Kyphoplasty for Vertebral Fractures (takes 5-7 minutes)

 Pros
- Minimally Invasive
- Outpatient
- Pain Reduction  Often immediately post-op
- Improves center of gravity  Reduces risk of future fractures
- High success rate
 Cons
- Requires IV sedation
- Risk of infection
- Not indicated for chronic fractures

Prevention
 For Bone Health
- Routine Exercise  Weight bearing (yoga, tai-chi, gardening, wt training, need to move!)
- Calcium supplements
o 9–18 years: 1,300 mg per day
o 19–50 years: 1,000 mg per day
o 51 and older: 1,200 mg per day
- Vitamin D supplements (key! Helps body to absorb calcium)
o 10-15 mins in the sun 3 x’s a week
o 600 IU daily, >71 y/o 800 IU daily
- Avoid Tobacco Use
- Alcohol in moderation
 Fall Prevention (90% of house ladies)
- Get rid of rugs!
- Proper shoes
- Install grab bars/railings
- Assistive devices (use eyeglasses to convince patients to do this. Pts don’t like to admit they are old!)
- Alcohol in moderation

Calcium Rich Foods

 Dairy Products Milk, Cheese, Yogurt, Cottage Cheese
 Green leafy vegetable Brocolli, Kale, Mustard greens, Collard greens
 Calcium may also be found in: Some breakfast cereals, Orange juice, Tofu, Soymilk, Breads, Pastas

Vitamin D Rich Foods

 Salmon, Mackerel, Tuna fish, Egg yolks, Beef liver, Cheese
 Can also be found in: Breakfast cereals, Milk, Orange Juice, Soymilk, Yogurt, Fortified Margerine

67 y/o female comes into the office. Has h/o Diabetes & Hypertension, both well controlled on current meds. Denies any Hx of Fx within the
last decade. Just had a DEXA Scan done & came in to review. T-Score was -1.8
- What is her diagnosis based on T-Score? Osteopenia
- Treatment options at this time? Supplements (1200 Ca2+, 600 VitD)

70 y/o female comes into office for a Medicare Wellness Visit. Has Hx of Hyperlipidemia, COPD, & CVA 3 yo. She fell last week while
walking dog, had a few bruises she did not injure herself. Would also like to review DEXA Scan. T-Score was -2.7
- What is her diagnosis based on T-Score? Osteoporosis
- Treatment options at this time? Stop smoking, bisphosphates + prolia
- Any advise for her? Household = get rid of the rugs. Shower bar. Better shows. Dog trainer.
 OSTEOARTHRITIS
 Osteoarthritis: Joint failure, all structures within the joint have undergone pathological change

OA: Epidemiology  Most common type of arthritis

 Prevalence  w/ age, but uncommon in those over 40 years of age, very common in those over 60 years of age
 More common in women than men, particularly in middle age and elderly
*MC Joints affected: Cervical / lumbar spine, Hip, Knee (MC), 1st MTP joint, Hands (DIP & PIP & base of thumb)
 Symptomatic OA of knee prevalent in about 12% those over 60 and 6% those over 30
 Hip OA about 1/3rd the prevalence rate of the knee
 OA of hand present in about 10% of the elderly

OA: Risk Factors / Etiology

 Age: joints become more susceptible due to thinning of the articular cartilage, dehydration of the cartilage, increased
fragility of cartilage
 Gender: some evidence estrogen is protective, thus postmenopausal women more commonly present with OA
 Genetics: inheritance likely plays a role, also congenital defects such as congenital hip dysplasia
 Joint injury: often see w/in 10 years, injury can cause disruption of joint mechanics, as well as increased inflammation
 Obesity: load on weight bearing joints, may also see a metabolic component contributing to  inflammation
 Anatomy: varus (bow) & valgus (knock) cause  risk for medial tibial-femoral OA & lateral tibial-femoral OA, respectively

OA:Pathophysiology
 Articular cartilage: “Shock absorber” fibrillation forms in early stages, leads to swelling, of anabolic/catabolic
activity of chondrocytes,  collagen matrix d/t inflammation,  chondrocyte death occurs  leads to  cartilage
 Bone: Hypertrophy of subchondral bone due to improper collagen matrix, osteophytes form at joint margins, cysts can
occur, microstructural damage to bone that is accompanied by localized necrosis and fibrosis
 Synovium:
- Synovitis (inflammation) and hypertrophy takes place, this contributes to pain and progression of OA, further
mediates destruction of cartilage through inflammation
 Soft tissue: Ligaments, joint capsule, menisci (knee) experience disruption of extracellular matrix, thickening of joint
capsule ensues, common to see tears in ligaments w/o injury, local nerves can be affected = contribute to pain &wknss

OA: Clinical Manifestations

 Pain: Worse as joint activity increases, Tenderness
 ROM (passive & active)
-  2/2 osteophytes, hypertrophy, & effusions
 Bony swelling  Secondary to bone remodeling
 Joint deformities (not to be confused with RA)  Adv OA
 Instability
OA: Diagnostic Testing
 No lab tests really considered unless suspect inflammatory (not an inflammatory process)
 X-ray:
- Most widely used imaging modality, detect osteophytes,  joint space
cysts, but may also be incidental findings so need to correlate w/ symptoms
 CT: Great for assessing bone, but not for soft tissue
 MRI: Great for soft tissues, but not so good for bone
 Fluid aspiration: Noninflammatory

OA: Diagnosis
 Typically a clinical diagnosis can be made if:
- Joint pain is persistently related to usage in one or a few joints
- Age greater than 45 years
- Morning stiffness present for less than 30 minutes** (otherwise = rheumatoid, OA won’t be +30 mins)
 Consider imaging studies for:
- Younger patients with signs of OA
- Atypical symptoms such as unusual joints, inflammation, exaggerated pain, or rapidly progressive pain
- Presence of constitutional symptoms such as weight loss, fevers, systemic illness
- Physiological changes indicating an anatomical abnormality

OA: Differential Diagnosis

 RA, Psoriatic arthritis, Crystalline arthritis  Gout & Pseudogout
 Hemochromatosis, Infectious arthritis  Septic arthritis (gonorrhea)
 Other abnormalities  Avascular necrosis, hip dysplasia, bursitis, tendonitis

OA: Treatment
 Primary goal of treatment is to alleviate pain, minimize loss of physical function, and maximize quality of life
 Usually requires multidisciplinary approach w/ combo of pharmacologic & non-pharmacologic interventions
 Extent to which interventions are needed varies widely based on joint(s) involved, and severity of OA

Tx: Non-pharmacologic therapy:

 Physical therapy, Occupational therapy
 Periodic monitoring, Education
 Weight loss if obesity is present, at least 10% of body weight
 Therapeutic devices  Braces, walkers, splints

Tx: Pharmacologic therapy: (refer to table 394-1 in text)

 NSAIDs  Topical (emboterin = gel, these work well! Keksaken = topical cream) and oral (aleves, motrin)
 Duloxetine (Cymbalta) (FDA approved tx=5 pathologies, depression, anxiety, chronic pain, DM neuropathy, fibro)
 Capsaicin Topical cream
 Intraarticular steroids  Careful with diabetes
 Hyaluronic acid  Expensive and efficacy is questionable

Tx: Surgery
 Total joint arthroplasty
 May not eliminate all pain as about 20% of knee and 9% of hip replacements still have pain
 Often many factors involved in getting approval to have arthroplasty done
- Ex: weight loss, diabetes control, age, tried and failed other methods

OA: Prognosis
 Varies, Progression is typically slow
 Factors associated with worse outlook: Higher pain intensity at baseline, Depression, Bilateral joint involvement
 GOUT, AND PSEUDOGOUT

Gout: Metabolic disease d/t  [urate]. Deposition of monosodium urate (MSU) crystals into joints & connective tissue
Pseudogout: Ca2+ pyrophosphate deposition disease (CPPD), deposition of Ca2+ pyrophosphate crystals into articular tissue

Gout: Epidemiology
 “Disease of the kings” and “rich man’s disease”   Purines & ETOH
- Had a diet rich in purines (sea food, meats), High alcohol intake
 MC in men in 40’s to 50’s  Can be seen in men by age 30 and women by age 50, Usually idiopathic
 More common in Pacific Islanders than Caucasians
 Incidence and prevalence increasing worldwide  Estimated about 3% of U.S. population

Gout: Etiology
 Asymptomatic hyperuricemia is the initial state (classically)
 Elevated uric acid:
- Overproduction
- Underexcretion
- Excessive purine intake
- Accelerated ATP degradation
 High purine foods: Uric acid is an end-product of purine metabolism

Gout: Clinical Manifestations

 Maximal severity usually within 12 to 24 hours
- Complete resolution usually within a few days to weeks
 Most often occurs overnight
 80% of the time initial flare involves a single joint  MC is base of great toe (podagral) = really painful
 Typical gout flare:
- Severe pain
- Erythema
- Warmth
- Swelling
- Disability

Gout: Clinical Manifestations  Intercritical gout:

 Time period following resolution of gout flare
 Often asymptomatic period
 Very uncommon in other arthritic disorders
 Variable duration, most often a recurrent episode will take place within 2 years
- Timing of this period will typically get shorter as progressive flares occur
 Highly suggestive of crystalline arthritis
 Can continue to see deposition of tophaceous crystal material during this period

Gout: Clinical Manifestations  Tophaceous gout:

 Chronic stage
 Cauterized by collections of solid urate and chronic inflammatory
changes to surrounding tissue
 Tophi present
 Expansive and destructive changes
 Tophus: Latin for “stone”
 Renal complications may ensue:
- Nephrolithiasis – uric acid stones
- Nephropathy
 Tophi can be seen and palpated in soft tissues like articular structures,
tendons, bursa, or even on the ears. They typically are not painful or
tender to palpation, and have a yellow/white color
Gout: Diagnosis
 Clinically, classic presentation and medical history (big toe pain, podagral)
 Blood testing:
- Nonspecific changes,  ESR or  CRP, Serum urate can be  / nL / 
 Imaging:
- X-ray may see bone cysts, but not usually until chronic stages
- US useful in early detection and monitoring
 Need to do synovial fluid aspiration:
- Rule out septic arthritis, psoriatic arthritis, pseudogout. Gram stain, cell count, culture
 Synovial fluid analysis: “Gold Standard”
- Obtained from joints or bursas
- Inflammatory appearance with elevated WBC (10K to 100K)
- Compensated polarized light microscopy is used to identify MSU crystals = gold standard
o MSU crystals are negatively birefringent and needle shaped
o Differentiated from pseudogout (calcium pyrophosphate dihydrate crystals) by shape (CPP are
rhomboidal) and CPP crystals are less likely to be negatively birefringent
= Monosodium urate crystals (MSU) indicating gout

= Intracellular calcium pyrophosphate dihydrate crystale (CPP crystals indicating pseudogout)

Gout: Differential Diagnosis

 Septic arthritis, Trauma, Pseudogout (CPPD), Cellulitis, RA, Psoriatic arthritis, Osteomyelitis, Acute rheumatic fever

Gout: Treatment
 Acute:
- Relief of pain and disability *ASAP, earlier you start treatment better the outlook
- NSAIDs such as naproxen or indomethacin
o Naproxen dosing: 500mg BID for 5-7 days
o Indomethacin: 50mg TID for 5-7 days
- Glucocorticoids (oral or injection)
- *Colchicine (very specific dosing)
o Colchicine: initial dose of 1.2mg followed by 0.6mg 1 hour later (do not exceed 1.8mg in first 24 hours w/
initial dosing).  continue treatment for duration of attack (until it resolves) with 0.6mg daily or BID
- Symptomatic relief of pain/inflammation
 Chronic:
- Not much difference from acute, Prophylactic care
- Initiation of urate lowering therapy
o Allopurinol, febuxostat, probenecid
 Allopurinol / febuxostat: reduce production of uric acid
 Probenecid: increases excretion of uric acid

Gout: Prognosis
 Dependent on several factors
 Stage of gout patient is in
 Presence of joint destruction
 Presence of tophi
 Compliance with treatment plan
 Accompanying comorbidities
 Musculoskeletal Infectious Disease

Rhabdomyolysis (not on test)

 Syndrome of muscle necrosis & release of intracellular muscle constituents into the circulation
 Rapid breakdown of skeletal muscle
 Presentation: Wide Variation
- Asymptomatic  life-threatening
 Epidemiology: ~26,000 cases/year in US
- 30-40% will develop AKI

Rhabdomyolysis: Etiology
 Traumatic
- Multiple injuries
- Crush injuries
- Surgery
- Prolonged immobilization
 Nontraumatic Exertional
- Extreme exertion
- Seizures
- Malignant hyperthermia
- Metabolic myopathies
- Sickle cell
 Nontraumatic Nonexertional
- Alcoholism
- Drugs / toxins (remember statins)
- Electrolyte abnormalities
- Infections

Rhabdomyolysis: Pathophysiology
 Destruction of muscle cells
 Spilling of components out of muscle cells  Into blood or surrounding tissue
 Fluid shift toward damaged muscle  Swelling, hypovolemia
 Renal hypoperfusion and increase in damaging components in blood (myoglobin, lactic acid, etc.)

Rhabdomyolysis: Classic Clinical Presentation

 Myalgias – pain, tenderness, weakness, +/- edema
 Myoglobinuria - red to brown (Coca Cola urine)
 ↑ Serum Muscle Enzymes
- CK > 10,000 (normal = 55 – 170 units/L). Myoglobin
 Coca Cola urine

Rhabdomyolysis: Labs
 Lab Abnormalities:
- Laboratory findings are related to the degree of muscle involvement
- Early findings -  blood levels of CK, myoglobin, potassium, urea, and phosphorus
- Metabolic acidosis may develop because of release of organic acids from damaged muscle
 Urine Dipstick: Protein, blood (heme/myoglobin), casts
 Urinalysis: Coke color, protein, brown casts, myoglobin
 Renal Failure
- Renal ischemia, tubular obstruction & injury
-  BUN, Cr
 Brown Casts

Rhabdomyolysis: Management
 Find & Treat the cause
 In-patient management
 Plasma volume expansion
- IV isotonic solution
 Forced alkaline diuresis  Mannitol (?) & Sodium Bicarbonate
- Monitor urine output (target of 200mL/hour)
 Monitor electrolytes  Potassium, Calcium, Phosphate, Creatinine  May require dialysis
 Osteomyelitis = Infection of bone or bone marrow
 Sequestra: piece of dead bone surrounded by normal bone
 Involucrum: new bone being deposited near necrotic area
 Nidus: “nest” center/focus of infection – bacteria breeding ground
Acute vs. chronic = Acute ~ 4-6 weeks, Chronic = anything else, (smoldering)
Formation of a sequestrum: (A) sound bone; (B) new bone; (C) granulations lining involucrum; (D) cloaca; (E) sequestrum

Risk Factors
 DM, IV drug use, Recent orthopedic surgery
 Sickle cell disease, HIV / AIDS, Alcoholism, Chronic steroid use, Chronic joint disease
 Prosthetic orthopedic device, Open fracture

Epidemiology (diabetics, IV drugs, hx orthopedic surg)

 Bimodal Peaks: Children , Adult > 45 years of age, (overall incidence of 2/10,000 people) M>F

Etiology Introduced by 3 different means:

 1) Hematogenous: bacterial seeding  Common in children, near metaphysis
 2) Contiguous spread from local infection  Cellulitis, abscess
 3) Penetration into bone:  Joint replacement, ORIF, open fracture
 Bones Affected = Children: long bones – femur, humerus , Adults: vertebrae, mandible, pelvis
 Joint replacement, ORIF, open fracture
 Organisms: Often Polymicrobial **
- *Staph. Aureus (most common in acute & chronic)
- Aerobic gram negative bacilli  Pseudomonas & Enterobacter
- Streptococcus (gram positive)

Clinical Manifestations = Gradual onset

 Chronic: Fatigue, malaise, Sinus tract drainage, Non-healing skin ulcer
 Fever – Acute (very high), Chronic (persistent low-grade)
 Septic arthritis - acute
 Erythema, Edema, Tenderness, Fluctuance & induration, Pain, motion

Diagnosis
 CBC:  WBC (left shift) (acute), ESR, CRP (nonspecific & not diagnostic), Blood cultures
 X-ray, +/- MRI, +/- Bone Scan
 Gold standard  Bone Biopsy (open or needle) – culture

Treatment
 1) IV antibiotics (based on culture results)
- (broad spectrums, vanco & cefepime),
- Duration of IV treatment: ≥ 4 - 6 weeks
 2) Surgical debridement
 Occasionally = amputation, Other: wound vacuum, hyperbaric oxygen
 *Septic Bursitis
Septic Bursitis = Infectious inflammation of the bursa
 *Source of infection:
- Usually inoculation through the skin  Pt. may not realize injury at the time, Nearby structures, Hematogenous
 At risk: occupation, DM, alcoholism, inflammatory conditions (AI)
 Common locations: superficial bursa  Olecranon (most common) or prepatellar

*Clinical Presentation:
 Pain, +/- Pain with joint movement, Peribursal edema, Erythema, Warmth
 Systemic: +/- Fever, Usually normal CBC (or slight increase + left shift)

Dx: usually clinical

 Aspirate & send to lab (cell count, gram stain, cultures, crystals)
- Color – bloody, purulent, normal, ↑ WBC, Culture – 85% are *Staph. Aureus (MRSA)
 ? MRI: may delineate extent but not septic vs not septic
 DDi: Nonseptic bursitis, cellulitis, crystal-induced bursitis, monoarticular arthritis

Treatment:
 Olecranon: Aspirations, oral antibiotics, rarely surgery (bursal debridement)
 Peri-patellar: Often treated as non-gonococcal septic arthritis  see coming slides

Septic Arthritis
Septic Arthritis AKA: Infectious Arthritis of Joint
 Eti: Occurs thru same 3 pathways as osteomyelitis (hematogenous, contiguous, penetrations) MC  hematogenous
 Risk Factors: similar to osteomyelitis, Also: pre-existing arthritis
 Joints affected: Larger  smaller joint = Knee > hip > shoulder > ankle = wrist

Septic Arthritis: Clinical Presentation

 Monoarticular arthritis (usually) (one joint) => Severe joint pain, large effusion, warmth, +/- erythema
 Fever, malaise, chills, Leukocytosis, May have signs/symptoms of infection elsewhere (lungs, UTI, skin, etc.)

Septic Arthritis: DDx (anything affecting joint)

 Rheumatoid arthritis, Other Rheumatologic process, Crystal-induced arthritis, Lyme disease (common missed dx)
 Osteomyelitis, Intra-articular issue – meniscus tear, Fracture, Coagulation disorder, Tumor

Septic Arthritis: Organisms

 Organisms: similar to osteomyelitis, Bacteria >>> Virus > Fungal
- Staph. Aureus, Streptococcus
- H. Influenzae, N. Gonorrhea (MC)
- Pseudomonas
 Usually due to 1 organism: Unlike osteomyelitis, which is often polymicrobial

Work-up: X-ray, joint aspiration, CBC, Blood cultures, ESR, CRP

Help to know image,

knowing different synovial fluids (analysis would be)
Gonococcal Arthritis
 N. Gonorrhea – MC septic arthritis etiology
- Sexually active adult (female > male)
o May have mucosal symptoms first (STI)
 Becoming more common in elderly
 Can be mono- or polyarticular
 Treatment: IV Ceftriaxone (Rocephin®) – until 2 days after clinical improvement (~3-4 days), then PO 3rd
generation cephalosporin (ceftriaxone, cefotaxime, cefdinir)
 Also add single dose of azithromycin 1g PO to cover C. Trachomatis
- Rarely need surgical intervention
 Sexually active adult, with symptoms of STI and symptoms of septic arthritis, think this!

Non-gonococcal Arthritis
 Staph, Strep, etc.
 MORE severe than gonococcal
- Mortality (>10%)
- More joint/articular destruction (25-50%)
 Usually monoarticular
 Treatment: IV antibiotics 4-6 weeks & surgical debridement
 Don’t forget Lyme Disease
 Vancomycin & ceftriaxone broad spectrum, then dial in to specific coverage based on cultures

Viral Arthritis
 Usually self-limiting: 7-10 days
 Sudden Symmetric polyarticular arthritis
- Rash, smaller joints
 Common with many viruses (serology helpful)
- Rubella (and rubella vaccine)
- Hepatitis B & C
- Mumps, Mono, Hep A, Herpes
 Rarely destructive
 Do not typically require specific treatment
- Pain relief

Reactive Arthritis
 Arthritis that develops shortly after an infection elsewhere, but no microorganisms are found in joint
- All the other stuff
 AKA: Reiter’s Syndrome

Days – Weeks after infection elsewhere

 Diarrhea or urethritis
- Salmonella, shigella, C. diff., Campylobacter
- Chlamydia
 Asymmetric (mono-arthritis), Lower extremity
 Treatment: NSAIDs, Steroid injection
 Usually resolved by a few months
 Benign Bone Tumors
 Characteristics:
- Frequently asymptomatic
- X-Ray: well defined lesion with sclerotic margins
- MRI or bone scan not needed
 Staging: (determines tx pathway)
- I – Latent (asymptomatic, usually resolve)
- II – Active (less demarcated, require surgery)
- III – Aggressive (typically surgical resection)

Types of Benign Tumors

 Osteoid Osteoma: Stage I

 Most common osteoid-forming tumor
 10% of all bone tumors, male > female (20’s)
 Symptoms: dull, achy pain
 Common site: Proximal femur
 X-Ray finding: Central lytic nidus (up to 1 cm in diameter)
 Tx: NSAID’s

 Enchondroma: Stage I / II
 Centrally located chondroma of bone
 > 10% of benign bone tumors
 Symptoms: Asymptomatic, incidental finding
 Common Site: Small tubular bone of hands & feet (50%)
 X-Ray finding: Sharp margins & central calcification
 Tx: Watch

 Osteochondroma: Stage I **
 Most common benign tumor of bone* MC benign tumor
 Arises from defect in outer edge of growth plate metaphysis
 Symptoms: Asymptomatic*
 Common Site: Knee or proximal humerus*
 X-Ray finding: Pedunculated or sessile (no stalk)
 Tx: Watch, Surgical intervention if painful or enlarges in adulthood

 Simple Bone Cyst: Stage I, occasional II

 Common pseudotumor that most frequently causes pathologic fracture in children
 Epidemiology: 5 to 15 years of age (boys>girls)
 Common Sites: Proximal humerus (50%) & Upper Femur (25%)
 Symptoms: Asymptomatic
 X-Ray: Solitary cyst centally located in metaphyseal area
 Tx: Varies depending on location of cyst (injecting, curettage)

 Giant Cell Tumor: Stage II / III

 5-10% all benign tumors
 Female > Male (30’s)
 Symptoms: Painful prior to diagnosis
 1-2% chance of metastasizing to the lung
 Common Sites: About the knee (distal radius, sacrum)
 X-Ray: lytic in nature, located in the epiphyseal-metaphyseal end of long bone
 Tx: Aggressive curettage, burring, adjuvent phenol, hydrogen peroxide, packing defect w/ bone cement
 Close follow-up: Chest XRay 6-12m for first 2-3 years
 Malignant Bone Tumors
 Characteristics: Painful*, X-Ray: permeative lesion with lytic destruction and poorly defined margins
 Additional testing – MRI, Chest X-Ray, Bone/soft tissue biopsy

Types of Malignant Tumors

 Osteosarcoma: M>F
 Most common primary malignant tumor of bone (20%)
 Most common bone malignancy in peds (75%)
 Symptoms: Pain before tumor mass, dilated veins in overlying skin
 Common Site: Metaphyseal area of long bone (50% about the knee)
 X-Ray: Permeated lytic destruction of metaphyseal bone, expanding to cortical bone, then soft tissue
 Additional studies: MRI – soft tissue appreciated, Bone/Tissue biopsy
 Tx: Chemo and surgical intervention (previously radical amputation)
- Methotrexate, cisplatin, ifosfamide, doxorubicin Q 3-4 weeks x 15 weeks
 Prognosis: 5 year is 70%

 Chondrosarcoma: Absence of osteoid formation

 Male > Female (30-60 years old)
 Symptoms: Minimal pain over course of years
 Common Sites: Pelvis & femur (metaphysis)
 X-Ray: Permeative lysis in surrounding cortex
 Tx: Surgical (do not respond well to chemo/radiation)
 Prognosis: Low grade central chondrosarcoma very good (pulmonary metastasis), reoccurance possible

 Ewing Sarcoma: Round cell sarcoma (Ewing sarcoma gene)

 90% found in 5-25 years of age Male > Female (poor prognosis)
 Symptoms: Skin necrosis, systemic fever,  ESR & WBC (masks osteomyelitis)
 Common Sites: Pelvis*, Femur, Tibia, Humerus
 X-Ray: Central lytic tumor of diaphyseal-metaphyseal bone, destroys cortical bone,
“hair-on-end”, “moth eaten”, “onion peel” appearance
 Additional Tests – Bone biopsy
 Tx: Multi-drug chemo, radiation (radiosensitive), and resection
 Prognosis: Localized 5 year rate 70%, Nonlocalized – 15-25%

 Fibrosarcoma Spindle-cell tumor

 Affects older population (Peak in 40’s) 10X less frequent than osteosarcoma
 Sx: Pain (can lead to pathologic fracture)
 Common Sites: Distal femur*, proximal tibia, pelvis
 X-Ray: Osteolytic, permeative
 Tx:
- Low-grade – aggressive wide resection (chemo/radiation of little value)
- High-grade – chemotherapy and resection
 Prognosis: Low-grade better prognosis depends on histologic grade of tumor, high-grade similar to osteosarcoma

Metastasis to the Bone

 Metastasis to bone is 15x greater than primary bone tumors
 Common metastasis sites: Prostate, Breast, Kidney, Thyroid, Lung
 Less common metastasis: Skin, oral, esophagus, cervix, stomach, colon
- Spine is most frequent area of bone metastasis (pelvis, femur, rib, proximal humerus, skull)**
o Rarely found distal to elbow or knee (if so think lung)

Diagnosis:
 PE, Labs – CBC, BMP, ESR, renal and liver panels, CT chest, abdomen, pelvis
 Chest X-Ray followed by involved bones, Staging bone scan, Tissue/Bone Biopsy

Treatment:
 Nonsurgical: Chemotherapy Radiation – reserved for palliative treatment, Treatment of primary carcinoma
 Surgical: Must have life expectancy of 6 wks, Varies per site involved , Goals- relief of pain, prevent pathologic
fractures, enhance quality of life & mobility