Deep infection in the foot spaces must always be suspected whenever the patient does not respond to apparently appropriate therapy, when there are signs of systemic illness, or when signs of inflammation are present at some distance from the wound or ulcer
Gram-positive organisms including staphylococci and streptococci are usually responsible for superficial foot infections, whilst deeper infection maybe associated with more than one pathogen, including anaerobic and Gram-negative organisms (Figure 14.8). Treatment of deep foot infection will usually require surgical removal of infected tissue, and antibiotics alone are unlikely to be adequate. Identification of the responsible pathogen is important but will take time and this should not delay the commencement of antibiotic treatment. Ideally, the infected tissue itself should be cultured following debridement but by this time the patient will usually have started empirical therapy and swabs including actual pus if present
(rather than ulcer slough) should be sent for microbiological analysis at the first opportunity. Antibiotic therapy is adjusted according to culture results and may need to be continued until the ulcer has healed (Table 14.2 and Box 14.9).
Severity of infection
Non-severe (oral for entire course) No complicating features GPC Recent antibiotic therapy GPC ± GNR Drug allergies
S-S pen; 1 G Ceph FQ, ß-L-ase Clindamycin; FQ; T/S
Severe (intravenous until stable, then switch to oral equivalent) No complicating features GPC2 ± GNR p-L-ase; 2/3 G Ceph
Recent antibiotic/ necrosis
GPC + GNR/ anaerobes
3/4 G Ceph; FQ + Clindamycin
Life-threatening (prolonged intravenous) MRSA unlikely GPC + GNR +
Aminoglycoside Glycopeptide or linezolid + 3/4 G Ceph or FQ + metronidazole
Given at usual recommended doses for serious infections; modify for azotemia, etc., based on theoretical considerations and available clinical trials. A high local prevalence of methicillin resistance among staphylococci may require using vancomycin or other appropriate anti-staphylococcal agents active against these organisms.
1 G Ceph, first generation cephalosporins (e.g. cephalexin, cefazolin); 2/3/4 G Ceph, 2nd/3rd/4th generation cephalosporins (e.g. cefoxitin, ceftazidime, cefepime); p-L-ase, lactam- p lactamase-p inhibitor (e.g. amoxicillin/clavulanate, piperacillin/tazobactam); FQ, fluoroquinolones (e.g. ciprofloxacin, levofloxacin); GNR, gram-negative rod; GPC, gram-positive cocci; S-S pen, semi-synthetic (anti-staphylococcal) penicillin (e.g. flucloxacillin, oxacillin); T/S, trimethoprim/sulfamethoxazole. Carbapenem, e.g. imipenem/cilastatin, meropenem, ertapenem; aminoglycoside, e.g. gentamicin, tobramycin, amikacin; glycopeptides, e.g. vancomycin, teicoplanin.
Reproduced with permission from the IDF International Consensus of the Diabetic Foot, the Practical Guidelines (1999) and Supplements (2003).
Box 14.9 General principles of antimicrobial management
A. Prescribe for all clinically infected wounds immediately, but not for uninfected wounds.
B. Select the narrowest spectrum therapy possible for mild or moderate infections.
C. Choose initial therapy based on the commonest pathogens and known local antibiotic sensitivity data.
D. Adjust (broaden or constrain) empiric therapy based on the culture results and clinical response to the initial regimen
The finding of callus should lead to a referral to a chiropodist experienced in treating the feet of people with diabetes. In the absence of ulceration this can be done less urgently but the availability of this service is an essential component of the team management of diabetes.
Under the UK's National Health Service, podiatry and chiropody for diabetic feet (and other medical conditions) has become prioritised at the expense of general foot care in the older population without diabetes. This reflects the importance of professional treatment of early foot complications, including callus formation, which should never be 'self-managed'
Removal of the slough and debris at the base of a diabetic foot ulcer may be achieved using maggots (Figure 14.9). This may be more effective than other means of desloughing and leaves the ulcer in a clean state ready to start healing.
Ulcers often occur at the site of pressure, on the balls of the feet, the heel, or elsewhere on the sole. They are unlikely to heel if they continue to be exposed to this pressure. Scotchcast dressings with
Figure 14.9 Maggot therapy.
a hole over the ulcer are fitted to ensure that pressure is relieved in this area. It is essential that such casts are properly fitted to avoid new ulcers forming elsewhere on the foot. Bedrest may also be necessary to assist healing, but immobility carries its own risk.
Surgical debridement is often required to remove necrotic tissue. This in a sense is a 'conservative' measure in that it helps to reduce/ prevent the need for amputation. Necrotic tissue acts like a foreign body, delaying healing, harbouring infection and making extension of infection, osteomyelitis and systemic sepsis more likely. In addition to debridement, other surgical measures include drainage of foot abscesses (which may require access to the deep foot spaces) (Figure 14.10).
Osteomyelitis underlying infected, ulcerated skin is a common complication and should be actively excluded through plain radiography (Figure 14.11) in all cases of deep or resistant infection. It often requires surgical excision and its presence will influence the choice, route of administration and duration of antibiotic therapy.
Revascularisation should preferably occur prior to the development of an ulcer in a patient with peripheral vascular disease (Figure 14.12), but often ulceration is the first symptom of a silent background process. Where ulceration is established, angioplasty, bypass or reconstruction to the major vessels may greatly improve the chances of healing. Revascularisation is required urgently in the case of the critically ischaemic foot, requiring inpatient management.
Amputation is indicated when conservative management fails, when persistent deep infection threatens systemic sepsis or progressive gangrene (Figure 14.13), or when rest pain is poorly controlled.
When this is necessary, the limb must be assessed to determine the viability of proximal tissue. Adequate vascular supply is essential for healing, and if amputation is not extensive enough this healing may fail. Toe amputation is usually unsuccessful when there is significant ischaemia present, but may be an option in the purely neuropathic foot, or when revascularisation is successful (Figure 14.14). If so, conservation of the great toe may reduce the impact on limb function post-operatively. A dry, necrotic toe (Figure 14.15) may be left to 'auto-amputate' if infection is not an issue.
The patient must also be assessed in a more holistic way to determine the options for rehabilitation. Some younger, fitter patients may manage with a prosthetic limb and regain walking mobility following limb amputation (Figure 14.16). Older, frailer or obese patients may not have this option, and are more likely to become wheelchair-dependent. These social consequences should be discussed with the patient and family if there is time before the decisions are made, even if amputation is inevitable. The psychological response to amputation is complex. For some, it has been compared to a bereavement. Involvement of the patient and carers in management decisions helps in this adjustment. Apart from the human costs of amputation and resulting disability, the health economic effects justify an intensive, proactive approach to ulcer management and follow-up, even in countries with less developed resources.
Amputation often signifies the end stage ofadvanced complications, and amputees not only have a high risk of future amputation in the other limb but also a high all-cause mortality rate in the year following the operation.
International Diabetes Federation. International consensus on the diabetic foot, 2003.
Jeffcoate W, Lipsky BA, Berendt AR, et al. on behalf of the three systematic review working parties of the International Working Group on the Diabetic Foot. Unresolved issues in the management of ulcers of the foot in diabetes. Diabetic Med 2008;25:1380-9.
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Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...