THE DIABETIC FOOT

(PHYSICIAN’S OVERVIEW)

DR. FAIZ-UR-RAHMAN
ASSOCIATE PROF. (MED)
KMC/ KTH.
Magnitude of problem

 5—10% risk of developing Diabetes Mellitus.

 12—25% of Diabetics developing Diabetic Foot in
their lifetime.
 In USA, >10,00,000 amputations /year for DM
 Foot wound incidence: 2—7% diabetics/ yr.
10—30% undergo amputations.
 Foot wound recurrence: 20—80%.
 Global long term outcome of hospitalized
patients is Poor.
 H/O Foot ulcer increases risk of Mortality.
 Thus need to Prevent & Treat Diabetic Foot.
DFU Rx: Challenges
 Denial of disease by the patient.
 Maintaining Target glucose levels (FFG, PPG,
HbA1c).
 Implementing lifestyle changes.
 Availability of Tx & follow-up facilities for DF.
 Patient education about DM--- Management,
Prevention & complications.
 Patient empowerment for self-disease
management.
SECTION 1

 ETIOLOGY.
 PATHOGENESIS.
 RECURRENCE.
RISK FACTORS

 Poor glycemic control.

 Peripheral Neuropathy.
 Foot Deformity.
 PVD (Peripheral Vascular Disease).
 Past H/O Amputation.
 Past H/O Ulcer.
 Visual impairment.
 Diabetic Nephropathy.
 Cigarette Smoking.
ETIOPATHOGENESIS
(THE CRUCIAL TRIAD)

DEFORMITY

REPETITIVE
NEUROPATHY
TRAUMA

DF
ETIOPATHOGENESIS
 PRIMARY ETIOLOGY: NEUROPATHY

1. Sensory. 2. Motor . 3. Autonomic.

 ASSOCIATED ETIOLOGY:

1. Deformity. 2. Infection. 3. PAD (Peripheral Arterial

Disease).

 ASSOCIATED PATHOGENIC MECHANISMS:

1. Ulceration. 2. Decrease in neurokines including

Substance P.
ETIOPATHOGENESIS

Sensory Neuropathy

Loss of Protective sense

Unrecognized Foot Trauma

Ulceration.

Infection & Impaired Healing

ETIOPATHOGENESIS:
Impact of Motor Neuropathy

Muscle atrophy
• Foot Deformity Areas of High
Motor neuropathy
• Altered Biomechanics Pressure

Infection & Unrecognised Foot

Ulceration
impaired healing trauma
Etiopathogenesis:

AN PAD
• Autonomic
AN neuropathy

• Dry skin due to

Hypohidrosis

• Cracks & fissures

ULCER
ETIOPATHOGENESIS: SUMMARY

S.N
M.N.
A.N.

• FOOT ULCER
PAD
RECURRENCE OF FOOT ULCERS

Risk factors:
 Peripheral Arterial disease.
 Location of index ulcer
 Plantar hallux ulcers more likely to recur.
 Ulcers on Bottom of Foot more likely to recur.
 Ulcers of lesser toes usually dorsally located ;
less likely to recur.
SECTION 2

DIAGNOSIS:
Clinical presentations &
investigations
Early indicators & Clinical
Progression
 NEUROPATHY:
SENSORY: Numbness, Tingling, Paresthesias, “Stock &
Glove”, hyperalgesia progressing to Insensitivity (Loss of
sensations).

MOTOR: Can result in deformities (Claw toes, Achilles

contracture, Hammer Toe)…. Abnormally high pressure areas
(Plantar MT heads, Dorsal proximal IP joints).

AUTONOMIC: Dry skin …. Cracks & Fissures.

Early indicators & Clinical
Progression
 VASCULAR DISEASE:
LARGE VESSEL DISEASE:
Diminished peripheral pulses, Cool limbs, Dry
skin

MICROVASCULAR DISEASE:
Affects peripheral neural fibres, aggravating
Neuropathy.
Retards access of Antimicrobial agents to wound/ ulcer.
DIAGNOSIS: History: Special
focus on …
 PAST H/O:
Ulceration, Amputation, Charcot joint, Vascular
surgery, Angioplasty, Cigarette smoking.
 NEUROLOGICAL SYMPTOMS:
Positive symptoms: Burning, Shooting pain,
Sharp sensation, Electrical sensation.
Negative symptoms: Numbness, Feet feel dead
 OTHER DIABETIC COMPLICATIONS:
 Nephropathy, Retinopathy.
DIAGNOSIS: Physical exam: 1

INITIAL & FOLLOW-UP EXAMINATION

 Visual inspection.
 Foot examination:
1. Vascular assessment.
2. Neurological assessment.
3. Dermatological assessment.
4. Deformity.
5. Mobility assessment of Foot & Ankle.
DIAGNOSIS

1. VISUAL INSPECTION:
 INJURIES & BRUISING.
 DEFORMITIES: Bunions, Achilles contracture,
Hammer toes
 VASCULAR SKIN CHANGES: Stasis dermatitis, Skin atrophy, Hair
loss, Nail changes, Clear areas of decreased perfusion.
 SHOE’S FITTING

2. VASCULAR ASSESSMENT:
 Dorsalis Pedis, Post. Tibial Artery.
 Temperature of Foot relative to leg, Capillary refill,
Pallor, Ankle-Brachial index.
DIAGNOSIS
 3. NEUROLOGICAL ASSESSMENT:
I. Sensory (Pin-prick) assessment vs. contralateral leg & Proximal leg.
II. Deep reflexes (Achilles tendon reflex).
III. Semmes-Winstein 10 g monofilament (For protective sensations).
IV. Vibratory- Proprioception testing (128- Hz fork).

4. DERMATOLOGICAL & OTHER ASSESSMENT:

I. Dryness, Scaling, Swelling, Thickened tissues.
II. Capillary Refill, Pallor, Ankle- Brachial index.
III. Corns, Calluses, Web spaces for Tinea pedis, Maceration, Fissures,
Ulceration.
IV. Deformities.
DX: LAB. INVESTIGATIONS

 FBC: Hb is especially important.

 Glucose profile: FG, PP, HbA1c.
 Markers of inflammation: ESR, CRP.
 Nutritional status: Serum Albumin.
 Liver & Renal Function tests.
 Urinalysis.
 Blood C/S.
 Wound C/S.
 X-Ray both Feet, MRI.
 OTHER TESTS….

IF REQUIRED:
 Arterial Doppler.
 Toe Pressure measurement.
 Oxygen tensiometry.
 Arteriogram.
DX: OSTEOMYELITIS

In Ch: non-healing ulcer, search for Osteomyelitis:

1. Probe-to-Bone test.
2. Bone biopsy (The Gold Standard).
3. Appropriate Imaging technique:
 X-Ray both feet, Bone scan, US, CT, MRI (Most reliable).
4. Radiographic milestones:
Radiolucency: 5—7 days.
Sequestrum & Involucrum: 10—14 days (First sign).
Osseous demineralization, Periosteal elevation, Cortical
irregularity usually detected after 35—50% reduction in BMD.
5. Other Radiographic features:
Soft tissue edema, Gas in soft tissue, Foreign bodies.
DX: MUSCLE ATROPHY

Estimation of Muscle Mass of Small Foot Muscles

 MRI is the Gold standard.(High spatial resolution permits
identification of individual foot muscles).
 Limitations of MRI:
 Cannot be done at bed side.
 Time-consuming.
 Expensive.
 Ultrasonography is a good alternative for detecting
Atrophy.
 Electromyography (EMG).
Section 3

Risk stratification &

scoring system
Risk stratification
Farber DC & Farber JS, 2007.

• No H/O Ulcer, Pedal pulses present, No

Category
deformity, No H/o Amputation , No sensory loss.
0
• No H/O ulcer, Pedal pulses present, No
Deformity, No previous Amputation.
1 • Sensory loss

• No H/O Ulcer, Pedal pulses present, Sensory loss

• Moderate Deformity (Prelesion), Single lesser
2 Ray-amputation.
 • No H/O ulcer, Pedal pulses present or
Absent,
• Moderate Deformity (Prelesion), Single
lesser Ray amputation, Sensory loss.
3
Diabetic Foot Grading

NUMEROUS GRADING SYSTEMS

 UT: University of Texas.
 SINBAD: Site, Ischemia, Neuropathy, Bacterial
infection, ulcer Area, Depth.
 S(AD)SAD: Size (Area, Depth), Sepsis, Arthropathy,
Denervation.
 PEDIS: Perfusion, Extent, Depth, Infection, Sensation.
 WAGNER
 DUSS.
DUSS GRADING

 Palpable Pedal Pulses: Yes= 0, No= 1.

 Probing to Bone: No = 0, Yes = 1.
 Site of Location: Toe= 0, Foot = 1.
 No. of ulcers: Single=0, Multiple= 1.

 Maximum score Possible is 4.

 High Score correlates with Poor Healing, Hospitalization
& Amputation.
SINBAD (SITE, ISCHEMIA, NEUROPATHY,
BACTERIAL INFECTION, AREA OF ULCER, DEPTH)
 SITE: 0= Forefoot 1= Mid-/Hind-Foot.
 ISCHEMIA: 0= Pedal flow intact.
1= Pedal blood flow clinically reduced.
 NEUROPATHY: 0= Protective sensations intact.
1= Protective sensations lost.
 BACT. INF: 0= None 1= Present.
 ULCER AREA: 0= <1cm2, 1= >1cm2.ssss
 DEPTH: 0=Ulcer limited to Skin & S/C tissue
 1= Ulcer reaching Muscles, Tendon or Deeper.
TREATMENT

 GOALS AND MODALITIES

 (RX. OF PPG, NEUROPATHIC PAIN & DFU)
DFU RX: Therapeutic
objectives

• •
Tx & Tx other
Prevent Complic
DM ations

Preventive
Tx DF measures
against DF

•
TX DIABETES

 “Wide glycemic variability, especially in the postprandial

state….” induces a high oxidative stress which is
especially damaging to the risk of long- term diabetic
complications.
 (Farber DC, Farber JS. 2007).

Therefore, in light of the above and other abundant data…

 PPG should not be neglected during Follow-up.
 Normal FPG with untested PPG as an indicator of good
glycemic control is a PLACEBO.
 Control of PPG, in addition to FPG, is strongly
recommended.
RX OF DIABETES

HIGH PPG • HIGH PPG PEAKS

PEAKS

• Enhanced detrimental
Activates Protein Metabolic consequences
Kinase C

• MACROVASCULAR
• COMPLICATIONS
MICROVASCULAR
COMPLICATIONS
Modalities of PPG Control

 Diet control.
 Pharmacological:
 A) Meglitinides
 Nataglinide, Rapaglinide.
 Side Effects of Wt gain, Hypoglycemia.

B) Alpha-Glucosidase inhibitors:
More preffered.
Acarbose.
Voglibose (Better tolerated).
NEUROPATHIC PAIN TX

 DULOXETINE (FDA APPROVED)

 PREGABALIN (FDA APPROVED)
 AMITRIPTYLINE.
 CARBAMAZEPINE.
 GABAPENTIN.

 No option exists for restoration of sensory loss.

 Surgical nerve release is controversial and
evolving.
DFU TX: Treatment team

 Primary care Physician.

 Certified Diabetes Educator.
 Endocrinologist.
 Orthopedic (Foot & Ankle ) specialist.
 Vascular surgeon.
 Infectious diseases specialist.
 Podiatrist.
 Physical therapist.
 Social worker.
 Home Health care Service,
DFU TX OBJECTIVES

 Off-Loading:
Objective: Pressure normalization on affected areas.

 Wound Care:
 Objective: To maintain moist wound bed, absorb exudate,
prevent infection.

 Antibiotic Treatment:
 Objective: To treat polymicrobial infection.

 Vascular intervention:
Objective: To restore vascular flow.
DFU TX: Off-Loading Devices (OLD)

 Following are some of the OLD:

 Bed rest, Wheel chair, Crutch-assisted gait.
 Total Contact Cast (TCC)– is Gold standard.
 Felted Foam.
 Half –shoes.
 Therapeutic shoes.
 Removable Cast walkers.

TCC, though a gold standard, were used by Only 1.7% centers

in USA …. As reported in a survey in 2008.
Section 5

PREVENTION

Goals and Modalities

DFU: Preventive measures

 Motivate patient to “take over”.

 Patient-education about gravity of DFU & glucose control.
 Smoking cessation.
 Appropriate diet & exercise.
 Avoid excessive high temperature to foot.
 Avoid hot surfaces (Sandy beaches. Cement areas, etc).
 Avoid chemical for removal of corns.
 Check shoes for foreign bodies, that might exert pressure.
 Daily foot hygiene inspection.
 Care during nail trimming.
 Immediate treatment of fungal infections.
DFU: TX SUMMARY

 Patient empowerment for strict compliance &

implementation of Life-style changes.
 multi-speciality team work.
 Off-load ulcers.
 Debride, if needed.
 Antimicrobial Tx based on Deep tissue C/S.
 Vascular surgery, if needed.
 Control Plasma glucose – FPG & PPG.
ORIGINAL STUDY ON DIABETIC FOOT

 Carried out in Med C Unit, KTH.(2000-2001)

 Included 68 patients of Diabetic Foot.
 Deep tissue swab for C/S taken.
 Staph. Aureus was found to be the
commonest culprit (44 %).
 Others were:
 E.coli (14.7%), Pseudo. aereginosa (11.7%),
Enterobacter (8.8%), and others.
THANK YOU

FOR YOUR PATIENCE

& ATTENTION.