Diabetic foot

Ulcer and
soft tissue
infections
(nf)

Prepared By: CHE WAN NUR HAJAR BINTI

SAIMI
SUPERVISED BY: MR NAIK
PATHOPHYSIOLOGY

A. POLY (NEUROPATHY)
1) Sensory
 Most common in patient with poor metabolic control, maybe due to
- Vascular disease occluding vasa nervorum
- Deficiency of myoinositol ( reduced myelin synthesis)
- Chronic hyperosmolarity  edema of nerve trunks
- Effects of increase sorbitol and fructose
– Earliest change: loss of vibration sense, pain and temperature at feet (‘glove-
and-stocking’)  protective sense lost: cardinal event in ulceration
– Loss of sensation  repetitive stress, unnoticed injuries and fracture, structural
deformity (hammertoes, bunions, MT deformities, Charcoat foot)  further
stress  tissue breakdown
– Neuropathic paresthesia
2) Autonomic
- Reduced sweat and increased thermoregulation  dry & warm foot  reduced
pliability of plantar skin  callus  cracks become portal for infection

3) Motor
- May effect single major peripheral nerve (e.g common peroneal  foot drop)
- Interosseous wasting and dysfunction of instrinsic mucles  disrupt flexors –
extensors balance  high arc (pes cavus), hammertoe  callus, dorsal ulcers
B. Vasculopathy
1) PVD
- Abnormal lipoprotein metabolism+glycosylation  endothelial disruption 
platelet aggregation  reduced blood flow  infection
- Usually rapid and bilateral
- Severity: glycemic control and duration
- Characteristic: medial arterial calcification (Monckeberg’s sclerosis) of distal arteries
- Most common: superficial femoral artery at adductor canal, aortic bifurcation,
common iliac bifurcation, common femoral artery bifurcation
 Different between Ischemic and
Neuropathic foot

Ischemia Neuropathy
Symptoms Claudication Usually painless
Rest pain Sometimes painful
neuropathy
Inspection Dependent Rubor High Arch
Trophic changes Clawing of toes
No tropic changes
Palpation Cold Warm
Pulseless Bounding pulse
Ulceration Painful Painless
Heels and Toes Plantar
2) Diabetic Microangiopathy
- Increase vulnerability of skin and impaired wound healing
- Polyneuropathy  increased shunt blood flow + impaired vasodilatory response
- Type I DM: increase permeability + impaired vasoconstriction  edema
- Type II DM: unaltered permeability, but vasodilatation capacity

C. Immunopathy
Impaired wound healing
- Glycation of skin collagen  impaires matrix degradation
- Impaired leukocyte function
- Decreased fibroblast proliferation
- Malnutrition + hyperglycemia + decreased oxygen tension + insulin concentration 
inefficient anaerobic  favorable environment of bacterial growth
HISTORY

1. General and medical

- H/O presenting foot complaints: duration, onset, discharge
- Diabetes: duration, how diagnosed, medication, any increase in dose,
hypoglycaemic attacks, insulin injection site, average RBS, HbA1c
- Target organ complication and damage: angina (CVS), edema (nephro), TIA (CVA),
retino
- Social: tobacco, alcohol
- Current medication and antibiotics
- PMH, Surgical History
- Cultural habits: bare foot
2. H/O Foot Problems
- Daily activity and current diabetic foot status
- Footwear (enwuire type of shoes, socks)
- Foot- care
- Callus formation
- Deformities and previous foot surgery
- Neuropathy and ischemic symptoms
- Skin and nails problem
3. H/O Foot Ulcer
- Site, size, duration, odor, type of drainage
- Precipitating event or trauma
- Recurrences
- Associated infections
- Wound care/ measures to reduce plantar pressure
- Previous foot trauma or surgery
- Features of Charcot’s Joint
 Impairment of efferent sensory input from joint receptors  progressive
destruction of foot architecture characterized by pathological fracture, joint
dislocation and fragmentation of articular cartilage
 Mobile, short, and broad, boggy, swollen, warm, bine resorption in an insensate foot
 May be painful
PHYSICAL EXAMINATION

A. GENERAL
- Ill, toxic, well
- Acidotic breathing
- Mental state
- Sallow appearance ( renal failure)
- Pallor
- Dehydration
- Febrile
- v/s
B. EVALUATION OF ULCER
 Site:
 neuropathic: plantar side, areas of pressure (dorsal)
 Ishcemic: tips of toes/ lateral border of foot
 Depth:
 Covered by necrotic tissue, callus  difficult to evaluate
 Sterile stainess steel probe sinus tracts, until bone/ tendon
 Don’t probe before debridement  OM
 Size
 Irregular shape: draw
 Floor
 Usually + slough/ granulation tissue with or without tendon and bone
 Ischemic ulcer: usually no granulation tissue
 Redness of granulation tissue  underlying vascularity and ability to heal
 Discharge
 infective, always take swab
B. SKIN AND NAILS
- Appearance: color, texture, turgor, quality, dry skin
- Heel fissures, cracking of skin (reduced sweat)
- Presence of hair (always compare, or ask)
- Ulceration, gangrene, infection
- Interdigital
Inspection
- Color
- Ischemic changes

Palpation
– Temperature: warm/cold
– Tenderness of ulcer and the surrounding skin
– Base of ulcer:
– indurated, fluctuate, fixation (mobility)
– Pus oozing
– Contact bleeding

Neurovascular examination
– Peripheral pulses
– Capillary return
– Sensory
– Pin-prick, vibration, proprioception
– Power: foot drop
– Reflex: ankle reflex
INVESTIGATION
A. GENERAL
- Fbc
- Renal Profile (urea level- impaired healing)
- ESR (monitor) and CRP (Acute)
- VBG
- LFT (albumin level- healing potential)
- Urine: glycosuria, ketonuria, proteinuria
- ECG
- CXR
- Blood culture and sensitivity
- Bacteriological swab (tissue best)
B. SPECIFIC
 X ray of foot (AP/LAT): OM changes, soft tissue involvements
 Ankle Brachial Systolic Index (ABSI)
 Ankle (PTA)/ Brachial artery
 Doppler for ankle pressure
 Advantanges : non invasive, cheap
 Disadvantages : can be misleading due to calcified vessels, operator dependent
0.9 -1.2 Normal
0.5 -0.9 Intermittent claudication
0.3 – 0.5 Rest pain, severe arterial disease
< 0.3 Ischemia
> 1.2 Medial arterial Calcification
WAGNER CLASSIFICATION

– Grade 0 — No ulcer in a high risk foot.

– Grade 1 — Superficial ulcer involving the full skin thickness but not underlying
tissues
– Grade 2 — Deep ulcer, penetrating down to ligaments and muscle, but no
bone involvement or abscess formation
– Grade 3 — Deep ulcer with cellulitis or abscess formation, often with
osteomyelitis
– Grade 4 — Localized gangrene.
– Grade 5 — Extensive gangrene involving the whole foot.
MANAGEMENT

1. Control blood sugar

2. Debridement
3. Wound care
4. Reduction of plantar pressure: reduce trauma, allow ulcer to heal
5. Treat infection (antibibiotics)
- Mild Infection (> 2 signs of inflammation + cellulities les than 2cam from the ulcer,
no systemic toxicity) : Oral Cloxacillin 500mg QID/ Oral Amoxicillin/ Clavulanate
625mg BD
- Moderate Infection (Infection extend to bone wagner 2-3): IV Unasyn 1.5g TDS/ IV
Cefuroxime 750mg TDS/ IV Ceftriaxone 1-2g OD + IV Metronidazole 500mg TDS
- Severe Infection (Infection+systemic toxicity): IV Piperacillin/ Talzobactam 4.5g TDS/
IV Ceftazidime 2g TDS + Metronidazole 500mg TDS
Indications for Amputation

– Uncontrollable infection or sepsis

– Inability to obtain a plantar grade, dry foot that can tolerate weight bearing
– Non-ambulatory patient
– Decision not always straightforward
NECROTISING FASCITIS

 Definition  gas forming, fulminating, necrotic infection of superficial and deep

fascia, resulting in thrombosis in subcutaneous vessels and gangrene of
underlying tissue

 Co- morbidities: DM, PVD,

Chronic liver disease, cancer
CLINICAL PRESENTATION

 Triad of:
- Exquisite pain (out of proportion)
- Fever
- Swelling
 Tenderness, erythema, and warm skin (early stage)
 Small bullae, filled with (black) serous fluid (intermediate stage)
 Large hemorrhagic bullae, skin necrosis, fluctuant, crepitus, sensory and motor
disturbance (late)
 Systemic signs of sepsis: hypotension, acidosis, leukocytosis, tachycardia, hyper/
hypothermia
PATHOLOGY

 Angiothrombotic microbial invasion and liquefactive necrosis

 Necrosis of superficial fascia, PMN infiltration of deep and superficial fascia
 Gangrene of subcutaneous fat and dermis  bullae, skin necrosis, ulceration
Medical illustration of advanced necrotizing fasciitis with necrosis of skin, vascular thrombosis and involvement of
underlying muscle.
Classification

Classification Factor Comment

Anatomic location Fournier’s gangrene

perineum/scrotum
Depth of Infection Necrotizing adipositis (most
(correlates with mortality) common), fasciitis, myositis.

Microbial cause Type I: polymicrobial (most

common, 55-75%)
Type II: Monomicrobial: (staph,
strep, clostridia).
Type III: Vibrio vulnificus
Differential Diagnosis
Disorder Characteristic

Cellulitis/adipositis Erythematous edematous tissue

with normal subc. fat and fascia

Myonecrosis Noninfectious inflammation/

necrosis of muscle only

Noninfectious fasciitis Chronic disorder, Dx. biopsy,

Tx. Steroids

Myxedema Systemic manifestations of severe

hypothyroidism
LRINEC Criteria

Our patient's
score =

9
He has HIGH
(>75%)
probability of
Nec Fasc.
Yikes!!
MANAGEMENT

1. Prompt diagnosis
2. Immediate resuscitation
3. Aggressive debridement, fasciotomy, amputation if necessary
4. Repeated exploration
5. Skin grafting
6. Antibiotics:
 Type I: IV Cloxacillin 2g 4-6 hourly + IV Metronidazole 500mg TDS + IV Gentamicin
5mg/kg OD
 Type II: IV Benzylpenicillin 2-4 Mu OD + IV Metronidazole 500mg TDS
 CONCLUSION
Prevention through education

Proper risk assessment

Early and aggressive treatment