Management of Stage 5 Necrotic foot

Many cases of necrosis can be prevented if the feet are inspected regularly and infections are detected early and treated rapidly and appropriately. It is essential for the stage 5 foot (and all stages of diabetic foot disease) to catch the foot early, diagnose it correctly, and treat it aggressively. Necrosis is too frequently underestimated by inexperienced clinicians.  The stage 5 foot should never be taken lightly or put off until another day. Necrosis can involve skin, subcutaneous and fascial layers. In lightly pigmented skin it is easily evident but in the subcutaneous and fascial layers it is not so apparent. Furthermore, the extent of necrosis may be difficult to determine: often the blueish-black discolouration of skin is just the ‘tip of an iceberg’ of massive necrosis.

Early signs of necrosis

The signs that part of a foot is becoming necrotic may be subtle in the early stages

A careful search should be made for early signs:

  • A toe which is developing a blue or purple tinge, having been previously pink because of infection or ischaemia
  • Toes which have become very pale in comparison with their fellows
  • An ulcer which has changed its colour from healthy shiny pink granulations to grey, purple or black or its texture from a smooth to a matt surface.

Causes of necrosis

Necrosis can be due to infection, when it is usually wet, or due to occlusive macrovascular disease of the arteries of the leg, when it is usually dry. Necrosis is not, as previously thought, due to a microangiopathic arteriolar occlusive disease, or so-called small vessel disease. Digital necrosis is common in patients with renal impairment, particularly those with end-stage renal failure, even though they are treated with dialysis. Patients with severe renal impairment also have a propensity to develop dry necrosis, sometimes in the presence of palpable pedal pulses and in the absence of infection.

Wet necrosis

Wet necrosis is secondary to a septic vasculitis associated with severe soft tissue infection and ulceration, and is the commonest type of necrosis in the diabetic foot. Untreated infection can rapidly lead to necrosis.

Key points

  • Gram-negative organisms including Pseudomonas,Citrobacter, Serratia and Klebsiella can cause infectionand necrosis in the diabetic foot
  • It is important to detect such organisms by collecting a tissue specimen, if possible, or a deep ulcer swab
  • Spreading necrosis in the neuroischaemic foot may be due to infection and not to increasing ischaemia and should be treated with antibiotic therapy and, if indicated, surgical debridement.
  • Puncture wounds should be followed up very carefully as signs of infection will only become apparent when they have spread from the deep tissues to the superficial structures.
  • Bulging of the plantar surface indicates deep infection with collection of pus which needs drainage.
  • In the neuropathic foot, extensive necrosis can be successfully treated by surgical debridement with eventual complete healing.

Necrotic foot

Dry necrosis

Dry necrosis is secondary to a severe reduction in arterial perfusion and occurs in three circumstances:

  • Severe chronic ischaemia
  • Acute ischaemia
  • Emboli to the toes.


Severe chronic ischaemia

Peripheral arterial disease usually progresses slowly in the diabetic patient, but eventually a severe reduction in arterial perfusion results in vascular compromise of the skin. This is often precipitated by minor trauma, leading to a cold, blue toe which usually becomes necrotic unless the foot is revascularized. Many diabetic feet with a very low pressure index do well until the skin is breached by an injury. Inflammation and successful healing make increased vascular demands which the ischaemic foot is unable to fulfil.

Many diabetic neuroischaemic patients never complain of intermittent claudication or rest pain. If the patient has concurrent retinopathy with severe visual impairment he will frequently be unaware of ulcers or necrosis. The name ‘eye–foot syndrome’ has been attached to cases of middle-aged or elderly men who live alone, have undiagnosed diabetes leading to retinopathy and neuropathy, and present late with necrosis of the feet.

Acute ischaemia

Blue discolouration leading to necrosis of the toes is also seen in acute ischaemia, which is usually caused either by thrombosis complicating an atherosclerotic narrowing in the superficial femoral or popliteal artery or emboli from proximal atherosclerotic plaques to the femoral or popliteal arteries.

Acute ischaemia presents as a sudden onset of pain in the leg associated with pallor and coldness of the foot, quickly followed by mottling and slaty grey discolouration, and pallor of the nail beds. The diabetic patient may not experience paraesthesiae because of an existing sensory neuropathy, which also reduces the severity of ischaemic pain and may delay presentation. Some patients may complain of extreme weakness of the affected limb but not of pain.

Emboli to the toes

Another cause of necrosis, particularly to the toe, is the passage of emboli to the digital circulation often originating from atherosclerotic plaques in the aorta and leg arteries.

‘Showers of emboli’ may originate from plaques in the aortoiliac and the superficial femoral arteries. The plaques are usually irregular or ulcerated and covered with debris, particularly in the aorta. The emboli lead to cool, painful cyanotic toes and the development of areas of necrosis at the tips of the toes, which generally heal without the need for amputation . These patients may present with palpable pedal pulses. Emboli may also occur as a complication of invasive angiographic procedures, presenting as trash foot. Emboli may also originate from the heart. Cholesterol emboli may be related to warfarin therapy. The initial sign of emboli may be blueish or purple discolouration which is quite well emarcated but quickly proceeds to necrosis. If it escapes infection it will dry out and mummify. If patients with emboli have minimal or no neuropathy, the foot is extremely painful.

Necrosis and renal impairment

Patients with advanced diabetic nephropathy or endstage renal failure have an increased propensity to develop necrosis. Most have anaemia, neuropathy (which may be aggravated by uraemia) and arterial calcification. In addition, the atherosclerotic process is accelerated. The reasons for this propensity of diabetic renal patients to develop necrosis are not entirely clear.



Whether the stage 5 foot is neuropathic or neuroischaemic it should always be regarded as a clinical emergency.

In the neuropathic foot, wet gangrene due to infection can be treated with intravenous antibiotics and surgical debridement.  In the neuroischaemic foot, this approach may also be used, but revascularization should be performed if feasible. If vascular intervention cannot be carried out, then surgical debridement should be avoided if possible, and intravenous antibiotics may be used to convert wet necrosis to dry necrosis.

Dry necrosis in the neuroischaemic foot can be successfully managed with revascularization of the foot and amputation of the necrotic part. If vascular intervention is impossible, some cases of dry necrosis will do well and autoamputate with conservative care alone. Patients should be admitted immediately for urgent investigations and multidisciplinary management. It is important to achieve:

  • Wound control
  • Microbiological control
  • Vascular control
  • Mechanical control
  • Metabolic control
  • Educational control.


Wound control

Feet at stage 5 must always be classified as neuropathic or neuroischaemic because the treatment offered will differ according to the vascular status of the foot, and treatment decisions need to be made very quickly if the foot is to be saved.

Neuropathic foot

In the neuropathic foot, operative debridement is almost always indicated for wet gangrene. The main principle  of treatment is surgical removal of the necrotic tissue, which may include toe or ray amputation (removal of  toe together with part of the metatarsal) or, rarely, transmetatarsal amputation. Although necrosis in the diabetic foot may not be associated with a definite collection of pus, the necrotic tissue still needs to be removed.

Neuroischaemic foot

In the neuroischaemic foot, wet necrosis should also beremoved when it is associated with spreading sepsis. This should be done whether pus is present or not. However, where necrosis is limited to one or two toes in the neuro- ischaemic foot we avoid surgery where possible until vascular intervention has been achieved. If angioplasty or arterial bypass is not possible, then a decision must be made either to amputate the toes in the presence of ischaemia or allow the toes, as infection is controlled, to convert to dry necrosis and autoamputate. Sometimes this decision can be a difficult one. Surgical amputation leaves a large tissue defect which, in the neuroischaemic foot, may never heal. However, a transcutaneous oxygen tension of greater than 30 mmHg on the dorsum of the foot indicates a reasonable chance of healing and postoperative VAC therapy of the wound may be useful. Autoamputation is a process which takes many months and there is always a danger that the foot may become infected if the necrotic toe is left to autoamputate.

Techniques to treat necrosis

  • Outpatient sharp debridement
  • Operative surgical debridement
  • Facilitated autoamputation

Key points

  • VAC pump therapy is now useful in accelerating healing of wounds in the neuroischaemic foot
  • It is also useful in desloughing wounds which may not have been completely debrided
  • VAC therapy together with bedside podiatric debridement achieves very good results in the postoperative diabetic foot wound.
  • In cases when the limb is not immediately threatened,and the necrosis is limited to one or two toes, it may be possible to control infection with intravenous antibiotics and proceed to urgent angiography and revascularization.
  • Angioplasty may improve the arterial circulation to allow healing of a toe or ray amputation. If angioplasty is not possible then arterial bypass should be considered and the toe or ray amputation can be performed at the same time as bypass.

Ischaemic wounds are extremely slow to heal even after revascularization, and wound care needs to continue on an outpatient basis in the diabetic foot clinic. Some feet take many months, or even years, to heal, but with patience outcomes may be surprisingly good. Even if healing is never achieved many patients prefer to live with an ulcerated foot than to undergo amputation.

Microbiological control


Wet necrosis

The microbiological principles of managing wet necrosis are similar to those for the management of infection of the foot with extensive soft tissue infection or the foot with blue discolouration. When the patient initially presents, deep wound swabs and tissue specimens are sent off for microbiology. Deeptissue taken at operative debridement must also go for culture.

Intravenous antibiotic therapy

Both neuropathic and neuroischaemic patients need parenteral therapy. They are admitted to hospital and given intravenous antibiotic therapy as follows: amoxicillin 500 mg tds, flucloxacillin 500 mg qds, metronidazole 500 mg tds and ceftazidime 1 g tds. For patients who are allergic to penicillin we substitute vancomycin 1 g bd or clindamycin 600 mg qds for amoxicillin and flucloxacillin.

Other regimes are in use including:

  • Ciprofloxacin with clindamycin
  • Piperacillin/tazobactam
  • Ampicillin/sulbactam
  • Ticarcillin/clavulanate
  • Meropenem
  • Ertapenem.

Intravenous antibiotics can be replaced with oral therapy after operative debridement and when infection is controlled. On discharge from hospital, oral antibiotics are continued and reviewed regularly in the diabetic foot clinic. When the wound is granulating well and swabs are negative then the antibiotics are stopped. It is often difficult to have all wet necrosis removed surgically. The foot may be ischaemic, and the patient may not be fit for an operation. In these circumstances it is best to leave the necrosis and convert wet necrosis to dry necrosis using antibiotics and allow it to separate. The presence of necrosis will increase the risk of infection; however, these patients are under very close surveillance and early signs of the return or spread of wet necrosis are carefully searched for.

Dry necrosis

When dry necrosis develops secondary to severe ischaemia, antibiotics should be prescribed if discharge develops, or the deep wound swab or tissue culture is positive, and continued until there is no evidence of clinical or microbiological infection. When toes have gone from wet to dry necrosis and are allowed to autoamputate, antibiotics should only be stopped if the necrosis is dry and mummified, the foot is entirely pain free, there is no discharge exuding from the demarcation line, and swabs are negative. In severely ischaemic feet (pressure index < 0.5) antibiotics may sometimes be continued until healing. Daily inspection is essential. Regular deep swabs and tissue should be sent for culture and antibiotics should be restarted if the demarcation line becomes moist, the foot becomes painful, or swabs or tissue cultures grow bacteria.


Vascular control


All neuroischaemic feet that present with necrosis must have Doppler studies to confirm ischaemia.  The patient should initially have duplex angiography, which is optimal in showing stenoses or occlusions in the iliac, femoral or popliteal arteries. Tibial arteries are sometimes difficult to visualize with this technique because of excessive arterial calcification. However, if the Doppler sonograms show monophasic damped pattern at the ankle arteries this implies tibial disease. Magnetic resonance angiography may also be used to show stenoses or occlusions of the arteries of the leg, particularly in the tibial arteries . Having diagnosed the site of disease, then revascularization can be planned.

In wet necrosis, revascularization is necessary to heal the tissue deficit after operative debridement. In dry necrosis, which occurs in the background of severe arterial disease, revascularization is necessary to maintain the viability of the limb. Revascularization can be achieved by angioplasty or bypass. However, with increasingly sophisticated techniques a hybrid procedure is often carried out which consists of initial angioplasty to one part of the circulation and then bypass to another. Thus a patient with superficial femoral artery disease as well as tibial artery disease may well undergo angioplasty above the knee to the superficial femoral artery, and then a distal bypass below the knee to achieve straight-line arterial flow. These procedures are planned in joint consultation with the interventional radiologist, vascular surgeon.


In some patients, increased perfusion following angioplasty may be useful and this will result in an improvement in the ischaemic wound. Indeed, this is often the only interventional procedure that can be performed as the patient may be too frail to undergo peripheral vascular surgery. As an alternative procedure to angioplasty, arterial stenting is now carried out. This has been fully established as a useful treatment in the iliac arteries with good long-term patency of the stent. Recently, stents have also been inserted into the superficial femoral arteries and even the tibial arteries.

Arterial bypass

Angioplasty rarely restores pulsatile blood flow unless a very significant localized stenosis in iliac or femoral arteries has been successfully dilated. When the limb is severely ischaemic and there is considerable tissue deficit, it is  necessary to restore pulsatile blood flow. This is best achieved by arterial bypass.

Mechanical control


During the peri- and postoperative period, bed rest is essential with elevation of the limb to relieve oedema and afford heel protection. Prophylaxis of deep vein thrombosis should be carried out using a low molecular weight heparin subcutaneously daily. Low molecular weight heparin is as  effective and as safe as unfractionated heparin in the prevention of venous thromboembolism. However, the serum creatinine should be less than 150 µmol /L. The standard prophylactic regimen does not require monitoring.In the neuropathic foot, non-weightbearing is advisable initially and then off-loading of the healing postoperative wound may be achieved with appropriate footware. After operative debridement in the neuroischaemic foot,especially when revascularization has not been possible,non-weightbearing is advised until the wound is healed. If necrosis is to be treated conservatively, by autoamputation, which can take several months, then the patient needs a wide-fitting shoe to accommodate foot.

Metabolic control


When patients present with necrosis, in the background of severe infection or ischaemia, they may be very ill, and will need close metabolic and haemodynamic monitoring. Considerable metabolic decompensation may occur, and full resuscitation is required with intravenous fluids and intravenous insulin sliding scale, which is often necessary to achieve good blood glucose control whilst the patient is infected or the leg severely ischaemic. High glucose levels are associated with postoperative infections in the leg as well as infections of the urinary tract and the respiratory system.

Patients will often have cardiac and renal impairment,which will need careful monitoring to optimize the regulation of fluid balance, so as to avoid hypotension from underperfusion and hypertension and peripheral oedema from overperfusion. Oedema is a potent cause of impaired wound healing. Many patients have autonomic neuropathy which may contribute to impaired blood pressure control and more frequent cardiac arrhythmias.Nutritional impairment is denoted by a serum albumen of < 3.5 g/L and a total lymphocyte count of less than 1.5 × 109 /L. A high-calorie diet should be instituted. A minimum of 1800 calories per day should be ingested to avoid the negative nitrogen balance that could accompany the depletion of protein stores.