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Practical Diabetes Care, 3rd Ed., Excerpt #11: Infections in Diabetes Part 3 of 3

David Levy, MD, FRCP

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Diabetic foot infections (see also Chapter 10)

Multidisciplinary teamwork with specialist podiatrists is crucial. Patients in primary care must be referred for specialist wound débridement and dressing, which are as important as antibiotic treatment. Worsening clinical features of infection are associated with increasing rates of hospitalization and eventual amputation (Table 7.2)….

 

 

 

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Clinically uninfected ulcers do not benefit from ‘prophylactic’ antibiotic treatment. Distinguishing non-infected ulcers from mild infections is therefore important, and a CRP of 17 mg/L has been suggested as a cut- off [5]. Where there is a clinical infection, antibiotic treatment (Table 7.3) should be guided by the following factors.

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  • Chronicity: the more chronic, the less likely treatment for Gram-positive pathogens alone will be sufficient.
  • Depth: superficial, deep, bone involvement.
  • Community or hospital-acquired infection, and associated probability of specific organisms, for example MRSA in hospitalized patients, sensitive streptococci in first community-acquired infection, mixed organisms in chronic infection, presence of anerobic/gas-forming organisms.
  • Presence of ischemia (anerobes) and osteomyelitis (staphylococci).
  • Recent antibiotic treatment and antibiotic sensitivities.

Deep cultures, especially of tissue, are important in guiding treatment and limiting the use of broad-spectrum antibiotics, but results will not be available for several days. Staphylococcus aureus and streptococci should always be covered. It is difficult to give guidance for individual cases, but consider the following.

  • Do not undertreat: symptoms and signs of infection can be attenuated or obscured in diabetic neuropathy, which always accompanies foot ulceration. If in doubt about the severity of the infection or whether it can be managed in the community, admit the patient for intravenous treatment.
  • Abscesses are difficult to detect clinically in oedematous feet, and often become evident only when surgical or podiatrist débridement has been performed, or on magnetic resonance imaging (MRI).
  • Infections can spread with alarming speed.
  • Surgical liaison is often needed, especially when there is peripheral vascular disease, and frequent discussion with the microbiology team is important.
  • No topical antibiotic preparation is currently licensed for ulcers.

Osteomyelitis
Osteomyelitis in the foot usually occurs adjacent to a neuropathic ulcer; it rarely occurs with completely intact skin, through small puncture wounds, especially in flexures of the toes and at their tips, can sometimes heal up after infection has entered. Clinically therefore it is difficult to exclude osteomyelitis, but an ulcer in excess of 2 cm2 and a positive ‘probe-to-bone’ test are the best clinical indicators of its presence (though there is continuing doubt about the reliability of the ‘probe-to-bone’ test; see Chapter 10) [6]. When there is radiological suspicion of osteomyelitis, especially of midfoot bones, but without clinical ulceration, then consider Charcot neuroarthropathy (see Chapter 10). The painless ‘sausage toe’ – with characteristic swelling and dusky skin, probably caused by local ischemia – usually conceals underlying distal osteomyelitis, though radiologically it can be difficult to detect, because normal distal phalanges vary in appearance. Heel osteomyelitis is also difficult to spot radiologically.

Osteomyelitis can progress very rapidly, and if it is suspected, repeat films every month to detect subtle cortical changes. MRI may show marrow oedema, but Charcot neuroarthropathy gives the same appearance.

Bone infection in diabetes is nearly always caused by Staphylococcus aureus. Open biopsy and culture will confirm, but this is rarely needed except when there is high suspicion of another organism, or failure to respond to prolonged high-dose anti-staphylococcal antibiotics.

Treatment
Surgery is often needed when there is infection proximal to the phalanges, especially in the presence of peripheral vascular disease. However, the common situation of distal infection involving the phalanges in a well-perfused neuropathic foot can often be managed with long (3–6 month) courses of anti-staphylococcal bone-penetrating antibiotics (flucloxacillin, quinolones and clindamycin), and up to 75% of cases of forefoot osteomyelitis complicating ulceration can be eradicated in the medium to long term with 3-monthly cycles of antibiotics guided by repeated MRI scans [7]. In the outpatient setting, the quinolones are often well tolerated, and can be given twice daily. Flucloxacillin is sometimes poorly tolerated, requires dosing four times daily, and can cause hepatitis. In the otherwise well patient, clindamycin is also a good choice, though there is a higher risk of antibiotic-associated diarrhoea and C. difficile infection. During treatment small pieces of bone (sequestra) are often spontaneously discharged through the tip of the toe, or can be picked out by the podiatrist. Ultimately sclerosis or resorption occurs. Closure of any local ulceration usually (but not always) signals healing.

Uncommon infections characteristic of diabetes
Malignant otitis externa
‘Malignant’ otitis externa is usually caused by Pseudomonas eruginosa. Disproportionate pain, discharge and hearing loss are the warning features, but diagnosis is often delayed. Involvement of the skull through osteomyelitis with secondary cerebral venous thrombosis are late manifestations. Joint surgical management with the ENT and microbiology/ infectious disease teams and prolonged systemic and topical anti-pseudomonal antibiotics are required.

Rhinocerebral mucormycosis
Extremely uncommon (I have never seen a case), though frequently quoted in the literature, and said to be associated with DKA. Beginning with face or eye pain, there is progressive ocular involvement: proptosis, ophthalmoplegia and severe constitutional upset. Venous and arterial thromboses of the head and neck are described.

Ophthalmic infections
Staphylococcal endophthalmitis after cataract surgery, though rare, is more common in diabetes. There are also sporadic reports of endogenous endophthalmitis resulting from septicemia originating from an infection elsewhere, especially diabetic foot lesions (Staphylococcus), liver abscess (Klebsiella) and UTI (E. coli). Always consider a potentially serious eye infection whenever a diabetic patient presents with a red eye.

Cardiac infections
Mitral annular calcification is more frequent in diabetes, and affected valves can become infected. Staphylococcal valve infection is more common than viridans streptococcal infection in diabetic patients, who are more likely to be on dialysis; mortality is much higher in diabetes.

Musculoskeletal infections
Many have been described, and they often present as pyrexia of unknown origin, as do many other infections in diabetes. They include:

  • septic arthritis (including the sternoclavicular joint)
  • epidural abscess
  • discitis
  • psoas abscess
  • vertebral osteomyelitis.

Staphylococcus is the most common organism, but Streptococcus and the pneumococcus are also encountered. These are often indolent infections resistant to early diagnosis, but should be considered in poorly controlled, complicated diabetic patients with focal, especially lower back pain. Always be alert to the possibility of ‘metastatic’ infection in patients with infected foot ulceration or osteomyelitis. MRI is valuable in delineating the anatomical extent of a known infection, but combined FDG- PET/CT scanning is becoming the investigation of choice in localizing obscure infections and in the investigation of pyrexia of unknown origin, common scenarios in people with diabetes.

For more information and to purchase this book, just follow this link:

http://www.wiley.com/WileyCDA/WileyTitle/productCd-1444333852.html

David Levy, MD, FRCP, Consultant Physician, Gillian Hanson Centre, Whipps Cross University Hospital; Honorary Senior Lecturer
Queen Mary University of London London, UK

This edition first published 2011, © 2011 by David Levy. 1st edition 1998 (Greenwich Medical Media/Cambridge University Press) 2nd edition 2006 (Altman Publications)