29. Arteriosclerosis and diabetic gangrene of the extremities

Arteriosclerosis and diabetic gangrene of the extremities

DEFINITIONS & PATHOGENESIS

• Arteriosclerosis is a broad term for arterial wall thickening and loss of elasticity; atherosclerosis is the common intimal plaque disease causing PAD.
• Diabetes accelerates atherosclerosis and causes endothelial dysfunction, medial arterial calcification, neuropathy and impaired immune/wound healing.
• Diabetic foot disease is commonly multifactorial: neuropathy causes unrecognised trauma and deformity, ischaemia impairs healing, and infection can spread through deep tissue and bone.

TYPES OF GANGRENE

• Dry gangrene results from chronic ischaemia with tissue desiccation and mummification; a clear demarcation line may develop.
• n/wet gangrene is infected necrotic tissue with swelling, discharge and systemic toxicity; it can progress rapidly to sepsis.
• Gas gangrene is a rapidly progressive clostridial or other gas-forming soft-tissue infection with severe pain, systemic toxicity and tissue gas; it is a surgical emergency.
• Diabetic foot infection may involve cellulitis, abscess, necrotising infection or osteomyelitis. Do not assume all black tissue is infected, but urgently assess for infection and perfusion.

CLINICAL ASSESSMENT

• Assess ulcer site, depth, size, callus, necrosis, discharge, odour, surrounding erythema, fluctuance, exposed tendon/bone and systemic signs.
• Test protective sensation with a 10-g monofilament and assess vibration, reflexes and deformity. Examine pulses, capillary refill, temperature and Doppler signals.
• Look for sepsis, deep abscess, compartment involvement and rapidly spreading infection. Use a recognised diabetic foot classification and document wound dimensions.

INVESTIGATIONS

• Check full blood count, CRP/ESR, glucose, renal function and cultures when clinically infected. Obtain deep tissue or bone samples when appropriate; superficial swabs are less reliable.
• Plain radiographs assess gas, foreign body and bony destruction; MRI is sensitive for osteomyelitis and deep infection.
• ABPI may be falsely elevated due to medial calcification; toe pressure, toe-brachial index, Doppler waveforms and duplex/CT angiography help assess perfusion.
• Differentiate neuropathic, ischaemic and neuro-ischaemic ulcers; consider vasculitis, pressure injury, malignancy and other causes.

MANAGEMENT

• Urgent multidisciplinary diabetic foot care includes off-loading, wound care, glycaemic optimisation, nutrition, smoking cessation and treatment of infection/ischaemia.
• Severe infection, wet gangrene, abscess or sepsis requires admission, IV antibiotics and urgent surgical drainage/debridement. Do not delay source control for prolonged imaging.
• Revascularisation should be considered for significant ischaemia to promote healing and preserve the limb. Choice of endovascular or bypass approach depends on anatomy, conduit, patient risk and local expertise.
• Amputation level is selected to remove non-viable/infected tissue while preserving the greatest functional length with adequate perfusion. Dry stable gangrene may allow planned management, but wet/gas gangrene needs emergency assessment.