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Case Analysis: 65-year-old Diabetic with Foul-smelling, Putrified Left Foot
a) Most Likely Diagnosis (1 mark)
Diabetic Foot Infection with Wet (Moist) Gangrene
The combination of long-standing Type 2 Diabetes, fever (38.9°C), tachycardia (112 bpm), hypotension (90/60 mmHg), soft/swollen/putrified foot with purulent discharge and markedly elevated blood glucose (386 mg/dL) is classic for infected diabetic wet gangrene - a surgical emergency.
b) Pathophysiology (4 marks)
Diabetic foot infection and wet gangrene arise from a convergence of several mechanisms:
1. Macrovascular disease (large vessel athersclerosis)
- Chronic hyperglycaemia accelerates atherosclerosis of peripheral arteries (tibial, peroneal vessels), causing chronic ischaemia of the foot. Reduced perfusion means the tissues cannot mount an adequate inflammatory response to infection.
2. Microvascular disease
- Basement membrane thickening of capillaries, endothelial dysfunction, and shunting of blood away from capillary beds leads to local tissue hypoxia. This critically impairs wound healing and immune cell delivery.
3. Peripheral Sensory Neuropathy (PSN)
- Diabetic neuropathy abolishes protective sensation. Minor trauma, pressure ulcers, and puncture wounds go unnoticed. Once the skin barrier is broken, bacteria invade.
4. Autonomic Neuropathy
- Loss of sympathetic tone causes arteriovenous shunting (bypassing capillary beds), arterial calcification (Monckeberg's medial sclerosis), dry cracked skin (reduced sweating), and abnormal foot biomechanics - all predisposing to ulceration.
5. Impaired Immune Function
- Hyperglycaemia impairs neutrophil chemotaxis, phagocytosis, and intracellular killing. Complement activation and opsonisation are also defective. This allows bacteria - often polymicrobial - to proliferate unchecked.
6. Superadded Infection and Wet Gangrene
- Once bacteria invade the compromised tissue, they spread rapidly in subfascial planes. Gas-forming anaerobes (e.g., Clostridium spp.) and facultative anaerobes produce putrefaction, oedema, blebs, and crepitus. This is wet gangrene: ischaemia + superadded infection + putrefaction together. Unlike dry gangrene (gradual arterial occlusion, desiccation, no infection), wet gangrene spreads proximally, is life-threatening, and is a surgical emergency.
As Bailey & Love states: "Ischaemia and PSN act synergistically to increase the risk of diabetic foot ulceration. Superadded infection due to poor wound care can spread rapidly and proximally in subfascial planes, leading to fulminant foot sepsis, gangrene and death."
c) Differentiation from Buerger's Disease, Raynaud's Disease, and Trauma (6 marks)
This is the key distinguishing table (wet/moist vs. dry/shrunken dark black lesion):
| Feature | Diabetic Wet Gangrene (this case) | Buerger's Disease | Raynaud's Disease | Traumatic Gangrene |
|---|---|---|---|---|
| Type of gangrene | Wet, soft, swollen, foul-smelling, putrified, with pus | Dry, shrunken, dark black digits | Dry, superficial fingertip necrosis | Dry initially (ischaemia from vessel injury) |
| Affected area | Whole foot, spreading | Distal digits/toes, then foot; segmental | Fingertips (thumb spared); upper limbs predominantly | Site of trauma/injury |
| Age/Sex | Elderly (>50), either sex | Young men (<40 years) | Young women | Any age |
| Background | Long-standing Type 2 DM, hyperglycaemia | Heavy smokers; lower socioeconomic group | Episodic vasospasm triggered by cold/stress | Clear history of trauma |
| Discharge/odour | Foul-smelling purulent discharge, putrefaction | No pus; no foul smell (dry/mummified) | No pus; no foul smell | Usually no pus unless secondary infection |
| Temperature & swelling | Warm, soft, oedematous | Cold, no oedema | Cold during attack; no persistent swelling | Cold, variable |
| Peripheral pulses | Reduced/absent (macro + microvascular disease) | Absent below occlusion (tibial/pedal arteries) | Pulses preserved (arteriolar disease only) | Absent distal to arterial injury |
| Systemic signs | Fever, tachycardia, hypotension (sepsis) | Migratory superficial thrombophlebitis | No systemic sepsis | No systemic sepsis (unless infected) |
| Blood glucose | Very high (386 mg/dL here) | Normal | Normal | Normal |
| Crepitus | May be present (gas-forming organisms) | Absent | Absent | Absent |
| Raynaud's phenomenon | Absent | Absent | Present - triphasic colour change (white → blue → red) | Absent |
| Special features | Neuropathy (reduced sensation), autonomic dysfunction | Buerger's test positive; phlebitis | Precipitated by cold; thumb generally spared | History of trauma or vessel injury |
| Arteriography | Diffuse atheromatous disease | Smooth large vessels + segmental small vessel occlusion with "corkscrew" collaterals | Normal | Vessel disruption at injury site |
Key differentiating point for this case: The foot is soft, swollen, putrified, foul-smelling with purulent discharge - this is wet gangrene due to infection. In Buerger's, Raynaud's, and trauma, the foot/digit is typically shrunken, dark, mummified, dry without pus or foul odour. Additionally, no patient with Buerger's or Raynaud's presents with blood glucose of 386 mg/dL and signs of sepsis.
d) Expected Culture Results (1 mark)
Cultures will likely show a polymicrobial infection, characteristically including:
- Aerobic Gram-positive cocci: Staphylococcus aureus, β-haemolytic Streptococcus spp.
- Aerobic Gram-negative bacilli: Pseudomonas aeruginosa, Klebsiella, E. coli, Proteus
- Anaerobes: Bacteroides spp., Clostridium spp. (explaining the foul smell and putrefaction)
Pseudomonas is over-represented in diabetic foot infections, and empirical therapy should include cover for this organism. Anaerobic cover (e.g., metronidazole) should also be included given the devitalised tissue and foul odour.
e) Potential Complications if Not Managed Promptly (1 mark)
The most serious complication is:
- Septicaemia / Septic shock progressing to multi-organ failure and death - already suggested by this patient's hypotension (90/60 mmHg) and tachycardia (112 bpm), indicating early septic shock.
Additional potential complications include:
- Proximal spread of gangrene requiring above-knee or below-knee amputation
- Osteomyelitis
- Diabetic ketoacidosis / hyperosmolar hyperglycaemic state (blood glucose 386 mg/dL in the context of sepsis)
Sources: Bailey and Love's Short Practice of Surgery, 28th Ed., pp. 628, 1030-1031; S. Das Manual on Clinical Surgery, 13th Ed., pp. 96-97
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