Peripheral arterial disease (PAD) in the lower limb is often diffuse and distal, involving the tibioperoneal trunk and crural arteries, and vascular insufficiency may be overlooked until signs of critical ischaemia develop. Cutaneous trophic changes such as corns, calluses, ulcers or frank digital gangrene occur (Figure 21.7). Ulceration is typically painful and at the distal extremities of the toes. The ABPI is easily measured and useful (ABPI < 0.9 indicates PAD; critical ischaemia is often reflected by ABPI < 0.5), but it can be falsely elevated and underestimate the degree of arterial disease in patients with diabetes and calcified vessels. Measurements of toe pressure and transcutaneous oxygen pressure (TcPO2) are also helpful. The probability of an ulcer healing is determined by perfusion, as indicated by measurements of ABPI, toe pressure and TcPO2.
Charcot’s arthropathy is a rare complication of severe neuropathy in long-standing diabetes (Figure 21.8). The initiating event may be an injury (perhaps unnoticed) that causes bone fracture in the mid-foot. Repeated minor trauma in pain-insensitive feet and possibly enhanced blood flow caused by sympathetic denervation result in decreased bone density and bony destruction. Excessive osteoclast activity causes bone resorption, coalescence and remodelling, which lead to the characteristic deformity and instability. Over months, the patient may notice the foot changing shape or the sensation of the bones crunching on walking. In the later stages a large effusion may surround disrupted joints and bone fragments – often giving the ‘bag of bones’ appearance on plain X-ray (Figure 21.9). Total contact casting is the most effective treatment, until the hyperaemia and swelling have settled, and bisphosphonates (potent inhibitors of osteoclast activation) are used in the acute phase of Charcot’s neuroarthropathy.