1. GANGRENE
- Macroscopic death of tissue caused by a lack of blood supply
Etiology
- Secondary to arterial occlusion – atherosclerosis, emboli, diabetes, TAO, Raynaud’s
- Infective – boil, carbuncle, gas gangrene, Fournier’s gangrene (gangrene of the perineum)
- Trauma – direct and indirect
- Physical – burns, scalds, frostbite, chemical, irradiation, electrical
- Venous gangrene
Clinical features
- Colour changes – palor, grayish, purple, brownish-black
- Due to disintegration of haemoglobin into sulphide
- Absence of pulse, loss of sensation and function
- Line of demarcation between viable and dead tissue – band of hyperaemia and hyperaesthesia
Dry gangrene
- Due to slow, gradual loss of blood supply – causes dry, wrinkles, mummified part
- There is minimum infection
- Has a clear line of demarcation – gangrene is usually limited and does not extend past the line
- Common causes – atherosclerosis, TAO
Wet gangrene
- Due to infection with putrefaction – causes edematous, swollen, discoloured part
- The gangrene spreads proximally and the line of demarcation is vague – leads to higher level of amputation
- Common causes are emboli and trauma
Investigations
- Hb%, blood sugar
- Arterial Doppler, angiogram
- US abdomen – find out status of aorta
Treatment
- Drugs
- Antibiotics
- Vasodilator
- Pentoxiphylline – xanthine derivative; inhibits PDE and reduces inflammation
- Aspirin
- Control underlying disease – e.g. statins for atherosclerosis
- Surgeries to improve perfusioin – lumbar sympathectomy, profundoplasty, arterial bypass graft
- Amputation
2. DIABETIC FOOT AND GANGRENE
Features of diabetic foot
- Callosities, ulceration
- Abscess and cellulitis of foot
- Osteomyelitis – metatarsals, cuneiforms, calcaneum
- Diabetic gangrene
- Arthritis of joints
Classification – Meggitt’s Classification of Diabetic Foot
- Grade 0 – lesion is completely epithelialised
- Grade 1 – superficial ulcer
- Grade 2 – deep ulcer
- Grade 3 – deep ulcer with osteomyelitis or abscess formation
- Grade 4 – forefoot gangrene
- Grade 5 – full foot gangrene
Pathogenesis
- High blood glucose level (BGL) in tissues acts good media for bacteria
- Diabetic microangiopathy – blockade of microcirculation leading to hypoxia
- Diabetic neuropathy
- Sensory neuropathy – minor injuries go unnoticed so infection more likely
- Motor neuropathy – dysfunction of muscles and arches of foot and joints
- Loss of reflexes
- Diabetic atherosclerosis – reduces blood supply and causes gangrene
- Thrombosis can be precipitated by infection
- Increased glyocsylated Hb leads to defective oxygen dissociation, leading to more hypoxia
Clinical features
- Pain in foot
- Ulceration
- Absence of sensation and pulsations in foot (posterior tibial and dorsalis pedis arteries)
- Loss of joint movements
- Abscess formation
- Change in temperature and colour when gangrene sets in
- Patient may succumb to ketoacidosis, septicaemia or myocardial infarction
Investigations
- Blood sugar, urine ketone bodies, glycosylated Hb
- Blood urea and serum creatinine
- XR – osteomyelitis
- Pus – culture and sensitivity
- Doppler of lower limb – to assess arterial patency
- Angiogram – to look for proximal blockage
Treatment
- Foot can be saved only if there is good blood supply
- Antibiotics – decided by pus C/S
- Regular dressing
- Drugs – vasodilators, pentoxiphylline, dipyridamole, low dose aspirin
- Insulin
- Diet and weight control
- Surgical debridement of wound
- Amputation of gangrenous area – level decided by skin/temperature changes and Doppler study
- Care of feet – avoid injury, keep the feet clean and dry, appropriate footwear