Delayed presentation of infection masked by callus

A 72-year-old woman with type 2 diabetes of 20 years' duration and peripheral neuropathy developed 'a dark spot' on the apex of her right 3rd toe and applied sterile gauze which was replaced at weekly intervals. The toe did not improve and regular dressings were continued for several months until her daughter noticed that the toe had become pink, and brought her up to the diabetic foot clinic. Her pedal pulses were strong and bounding. A plaque of callus covered the entire apex of the pink toe adjacent to the nail, which was thickened and difficult to distinguish from the callus. The callus was debrided with a scalpel to reveal an abscess cavity extending to the nail bed and the proximal phalanx was exposed. A speci

Deep Extensive Cellulitis

Fig. 5.2 Ulceration at the apex of the hallux with cellulitis.

men of pus grew Staphylococcus aureus. She was admitted to hospital and given intravenously amoxicillin 500 mg tds, flucloxacillin 500 mg qds, metronidazole 500 mg tds and ceftazidime 1 g tds. When the result of the culture was available this was reduced to flucloxacillin only. The foot healed in 1 week. She was followed up by the diabetic foot service and the problem did not recur.

Key points

• Callus may conceal deep infection which is producing very few physical signs of inflammation

• The well-perfused infected neuropathic foot responds well to debridement and drainage, pressure relief and appropriate antibiotics

• Patients with a history of ulceration and infection developing under callus need follow-up care to prevent recurrence.

The most common manifestation of infection is cellulitis, usually secondary to an ulcer, and presenting as a redness or erythema.

However, this stage covers a spectrum of presentations under the general chapter heading of infection, ranging from local infection of the ulcer to spreading sepsis, sloughing of soft tissue and finally, vascular compromise of the skin secondary to sepsis, seen as a blue discolouration. This spectrum occurs in both neuropathic and neuroischaemic feet. In the presence of neuropathy and ischaemia, signs of inflammation are often diminished, yet the final pathway of infection is to overwhelming destruction of the foot. It is thus important to treat even the initial stages with considerable respect.

Infection in the diabetic foot is a protean entity, but may be classified as follows:

• Ulcer with local signs of infection

• Ulcer with surrounding erythema

• Ulcer with diffuse spreading erythema

• Ulcer with extensive deep soft tissue infection

• Ulcer with extensive erythema and with blue/purple/ black discolouration of surrounding tissues.

Any break in the skin can lead to cellulitis and occasionally cellulitis is found without an obvious break in the skin being present.

Any of these presentations may be complicated by underlying osteomyelitis. Clinically, osteomyelitis may be suspected when a sterile probe inserted into the base of the ulcer penetrates to bone. This may happen in an apparently clean, uninfected ulcer, but osteomyelitis must still be suspected. X-ray and magnetic resonance imaging (MRI) may be helpful in the diagnosis of osteomyelitis,

Fig. 5.4 The granulation tissue in this large ulcer has become friable and bleeds easily. This is an early sign of infection.
Bone Probe Ulcer
Fig. 5.5 Exudate is dripping out of this neuropathic ulcer.

which may be confirmed by bone biopsy and a positive bone culture.

Any of the above presentations may be accompanied by systemic signs.

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