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THE DIABETIC FOOT

VS BEDI
Vascular Surgeon, INHS Asvini, Mumbai.

Diabetes is a fairly common disease seen in India with a prevalence of almost 17% in the Indian urban population as per a recent study with a prevalence of 2.5% in the rural population.

Problems of the diabetic foot are the most common cause for hospitalization in patients with diabetes, with an annual health care cost of more than $1 billion in USA. Diabetes is a contributing factor in half of all lower extremity amputations in the United States, and the relative risk for amputation is 40 times greater in people with diabetes. Diabetic foot ulceration will affect 15% of all individuals with diabetes during their lifetime and is clearly a significant risk factor in the pathway to limb loss. The principal pathogenetic mechanisms in diabetic foot disease are neuropathy, infection, microvascular dysfunction, and ischaemia; acting together, they contribute to the sequence of tissue necrosis, ulceration, and gangrene (Fig. 1).

Fig 1 : Underlying mechanisms of diabetic foot ulceration. Sensorimotor neuropathy leads to diminshed sensation and small muscle atrophy in foot, resulting in flexed metatarsalas, metatarsal head metatarsal prominence, and clawing of toes. Altered architecture of foot, coupled with ischemia and microvascular dysfunction, ultimately leads to ulcerartion

The cause of diabetic neuropathy is unknown and most likely multifactorial. Peripheral neuropathy is a common complication of diabetes, afflicting as many as 50% to 60% of all patients and is present in more than 80% of patients with diabetes with foot lesions, thus further emphasizing the direct relationship between neuropathy and foot ulceration. Broadly classified as focal and diffuse neuropathies, the latter is more common and includes the autonomic and chronic sensorimotor polyneuropathies, which both contribute to foot ulceration.

The spectrum of infection in diabetic foot disease ranges from superficial ulceration to extensive gangrene with fulminant sepsis. Classical signs of infection may not always be present in the infected diabetic foot because of the consequences of neuropathy, alterations in the foot microcirculation, and leucocyte abnormalities. Fever, chills, and leucocytosis may be absent in up to two thirds of patients with diabetes with extensive foot infections, and hyperglycaemia is often the sole presenting sign. Therefore, a complete examination of the infected areas is mandatory and the wound should be thoroughly inspected, including unroofing of all encrusted areas, to determine the extent of involvement.

Most infections are polymicrobic, the most common pathogens being staphylococci, streptococci, and enterococci; anaerobes and gram-negative bacilli are also commonly cultured. Cultures should be obtained from the base of an ulcer or abscess cavity after debridement. Osteomyelitis is common in diabetic foot ulceration, appearing in almost 70% of benign-appearing ulcers and should be presumed if the bone is palpated on probing in an open ulcer.

Ischaemia is a fundamental consideration to the vascular surgeon faced with the diabetic foot. The combination of motor and sensory neuropathy along with loss of the neurogenic inflammatory response and microcirculatory dysfunction results in a biologically compromised foot. Even moderate ischaemia may lead to ulceration under these circumstances, and thus the concept of ischaemia must be modified in making decisions about arterial reconstruction. The biologically compromised foot necessitates maximum circulation to heal an ulcer. This leads to three significant principles : 1) all diabetic foot ulcers should be evaluated for an ischaemic component; 2) correction of a moderate degree of ischaemia will improve healing in the biologically compromised diabetic foot; and 3) whenever possible, the arterial reconstruction should be designed to restore normal arterial pressure to the target area.

Treatment of the diabetic foot should be directed towards the pathogenic factors outlined previously. In general, this can be broken down into a few simple guidelines :

1.Prompt control of infection. This assumes first priority in the management of any diabetic foot problem.

2.Evaluation for ischaemia.

3.Prompt arterial reconstruction once active infection has resolved.

4.Secondary procedures, such as further debridement, toe amputations, local flaps, and even free flaps, may then be carried out separately in the fully vascularized foot.

DIABETES AND LOWER EXTREMITY VASCULAR DISEASE

Unlike microvascular disease, which is unique to diabetes and its metabolic alterations, the cause of lower extremity ischaemia is similar in both patients with and without diabetes and is the result of accelerated atherosclerosis. One notable difference between these populations is the pattern and location of the occlusive atherosclerotic lesion. As noted earlier, there is no evidence for an occlusive lesion at the arteriolar level ("small-vessel disease") in patients with diabetes. However, patients with diabetes are more likely to have atherosclerotic disease affecting the infrageniculate arteries, with sparing of the foot arteries, which allows for successful arterial reconstruction to these distal vessels.

Because the foot vessels are often patent in the patient with diabetes and because of the success of bypass grafting to these vessels, an appropriate evaluation for ischaemia is essential in patients with diabetes. Unless recognized and corrected, limb salvage efforts will fail even if infection and neuropathy have been appropriately treated. The most important observation is the presence or absence of a palpable foot pulse; in simplest terms, ifthe foot pulses are not palpable, it can be assumed that occlusive disease is present.

A variety of noninvasive arterial tests may be ordered. However, in the presence of diabetes, all of these tests have significant limitations. Medial arterial calcinosis occurs frequently and unpredictably in patients with diabetes, and its presence can result in noncompressible arteries with artifactually high segmental systolic pressures and ankle-brachial indices. Lower levels of calcification in the toe vessels support the use of toe systolic pressures, but their use is often limited by the proximity of the foot ulcer to the cuff site. Segmental Doppler wave forms and pulsed volume recordings are unaffected by medial calcification, but evaluation of these waveforms is primarily qualitative and not quantitative. In addition, the quality of the waveforms is affected by peripheral oedema, and the presence of ulceration precludes accurate cuff placement. Regional transcutaneous oximetry measurements are also unaffected by medial calcinosis, and recent studies have noted its reliability in predicting healing of ulcers and amputation levels. Limitations, including a lack of equipment standardization, user variability, and a large "gray area" of values, preclude its applicability. Furthermore, transcutaneous oximetry measurements are higher in patients with diabetes with foot ulcers when compared with the nondiabetic population, which further limits the ability of this test to predict ischaemia. Therefore, although they have been used to predict healing in patients without diabetes, a high value may not correlate with healing potential in the presence of diabetes.

PRINCIPLES OF ARTERIAL RECONSTRUCTION IN THE DIABETIC FOOT

The limitations of noninvasive vascular testing in patients with diabetes with foot ulceration emphasize the continued importance of a thorough bedside evaluation and clinical judgement. The status of the foot pulse is the most important aspect of the physical examination. An absent foot pulse is an indication for contrast arteriography in the clinical setting of tissue loss, poor healing, or gangrene, even if neuropathy may have been the antecedent cause of skin breakdown or ulceration. Importantly, because the foot vessels are often spread by the atherosclerotic occlusive processes, even when the tibial arteries are occluded, it is essential that arteriograms not be terminated at the midtibial level. The complete infrapopliteal circulation should be incorporated, including the foot vessels. The advent of digital subtraction angiography has greatly helped in the visualization of these distal vessels. Both anteroposterior and lateral foot views should be included. Excessive plantar flexion should be avoided because this may impede flow in the dorsalis pedis artery.

A complete arteriogram will facilitate choosing an outflow artery that will restore a palpable foot pulse. Proximal bypass grafting to the popliteal or tibioperoneal arteries may restore foot pulses. More often, however, because of the pattern of occlusive disease in the patient with diabetes, bypass grafting to the popliteal or even tibial arteries cannot accomplish this goal because of more distal obstruction. Similarly, although excellent results have been reported with peroneal artery bypass grafting, the peroneal artery is not in continuity with the foot vessels and may not achieve maximal flow, particularly to the forefoot, to achieve healing.

Restoration of the foot pulse is a fundamental goal of revascularization in the diabetic foot. Autogenous vein grafting to the dorsalis pedis artery represents a technical advance that provides durable and effective limb salvage. Fundamental to the success of the dorsalis pedis bypass graft is meticulous technique and its appropriate use. The principal indication for the pedal graft is when there is no other vessel that has continuity with the foot, particularly in cases with tissue loss. Although the dorsalis pedis bypass graft may be effectively used for salvage of ischaemic heel ulceration, preference should be given to the posterior tibial artery if it is in continuity with the foot. Dorsalis pedis bypass grafting is unnecessary when a more proximal bypass graft will restore foot pulses and should not be done if there is an inadequate length of autogenous vein. In addition, if the dorsum of the foot is extensively infected and the peroneal artery is of good quality on the preoperative arteriogram, preference should be given to peroneal artery bypass grafting.

The distal location of the dorsalis pedis artery theoretically necessitates a long venous conduit, which is often not attainable. However, with the use of the popliteal or distal superficial femoral artery as an inflow site, a shorter length of vein may be used, with excellent long-term patency. This is particularly true in the patient with diabetes, again because of the pattern of atherosclerotic disease. The vein graft to the dorsalis pedis artery can be prepared as an in situ, reversed, or non-reversed vein graft, without any significant difference in outcome. Concomitant angioscopic assessment of the harvested vein should be performed to detect any intraluminal abnormalities. In the absence of saphenous vein, autogenous arm vein grafts may be used and provide comparable limb salvage rates.

Because of the presence of medial arterial calcification in patients with diabetes, severe calcification of the outflow artery may be encountered, but this should not preclude attempts at arterial reconstruction. Moreover, active infection in the foot is not a contraindication to dorsalis pedis bypass grafting, as long as the infectious process is controlled and away from the proposed incision area.

Some workers have recently reported their experience with dorsalis pedis arterial bypass grafting in 367 patients during an eight year period, with a perioperative mortality rate of 1.8%. Tissue loss was an indication for surgery in almost 85% of the patients. Twenty nine grafts (7.5%) failed within the first 30 days, but 19 were successfully revised when a correctable technical problem was found at reoperation. The actuarial primary and secondary patency and limb salvage rates were 68%, 82%, and 87% respectively, at five years of follow-up.

After successful revascularization, secondary procedures may be performed for both limb and foot salvage. Chronic ulcerations may be treated with ulcer excision, arthroplasty, or hemiphalangectomy. In the patient with extensive tissue loss, both local flaps and free flaps may be used. Because of the architecture of the diabetic foot, underlying bony structural abnormalities are often the cause of ulceration and may be corrected with metatarsal head resection or osteotomy. Heel ulcers may be treated with partial calcanectomy and local (e.g., flexor tendon) or even free flap coverage.

SUMMARY

This aggressive and systematic approach to diabetic foot disease has resulted in improved limb salvage among patients with diabetes.

Concomitant with this decrease has been an increase in the number of patients who undergo arterial reconstruction and a greater application of the dorsalis pedis bypass graft. An awareness and understanding of the complex pathophysiology of diabetic microvascular and macrovascular disease will lead to further decreases in lower limb amputation and reduce the overall morbidity and mortality of diabetes in general.



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