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Practical Diabetes Care, 3rd Ed., Excerpt #10: Infections in Diabetes Part 2 of 3

David Levy, MD, FRCP

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Urinary tract infections (British National Formulary, section 5.1.13)
Type 1 patients in the long-term EDIC study were no more likely to have cystitis than non-diabetic women. Poor glycemic control and vascular complications were not associated with increased risk of cystitis and pyelonephritis, but cystitis was strongly associated with sexual activity. Few of these patients had advanced neuropathy: bladder dysfunction caused by autonomic neuropathy is generally thought to be an important factor contributing to urinary tract infections (UTIs). Patients with heavy proteinuria are more likely to have asymptomatic bacteriuria, and the two may be linked via endothelial dysfunction….

 

 

Asymptomatic bacteriuria
In males asymptomatic bacteriuria does not occur more commonly in diabetes, but it is twice as common in women with diabetes compared with non-diabetic women. Evidence is contradictory on the benefits of treatment, one study suggesting there was no difference in the rate of development of subsequent definite UTI, the other the opposite. The preferred approach following a positive urine culture is vigilance but no immediate treatment, except in pregnancy.

Management of symptomatic UTI (Table 7.1)
In diabetic patients, 80% of UTIs involve the upper tract, and bilateral involvement is more frequent. Other complications are more frequent. Escherichia coli remains the usual organism, but Proteus spp., Enterobacter spp., Enterococcus fecalis, Klebsiella pneumonie and group B streptococci are also common.

Treat bacterial cystitis for at least 7 days, possibly 14 days, longer than in a non-diabetic patient, because of the tendency to involve the upper renal tract. Treat pyelonephritis as in non-diabetic patients, but always admit for blood and urine culture, intravenous antibiotic treatment and to intensify diabetes treatment where possible, as bacteremia is about four times more likely to occur. Be vigilant for the development of a perinephric abscess (occasionally caused by hematogenous spread of Staphylococcus aureus) and the rare but possibly fatal emphysematous pyelonephritis.

Choice of antibiotic

  • Uncomplicated cystitis: trimethoprim 200 mg b.d.
  • Pyelonephritis: gentamicin, followed by trimethoprim or amoxicillin.
  • In the very sick patient: ceftazidime 0.5–1 g every 12 hours, or cefuroxime 0.75–1.5 g every 6–8 hours.
  • Once fever and systemic symptoms have resolved, transfer to oral antibiotics and maintain for 14 days.

In practice all patients with symptomatic UTIs more severe than simple cystitis should have a renal tract ultrasound scan. Recurrent UTIs require urological involvement, but low-dose prophylaxis can be started with trimethoprim 100 mg daily. Unfortunately, cranberry products do not seem to be effective (and may be high in glucose).

Emphysematous pyelonephritis (and emphysematous cystitis) is almost specific to people with diabetes. The organism is either E. coli or another Gram-negative organism generating gas (carbon dioxide) through unclear mechanisms. Unilateral nephrectomy used to be the only option, but intensive medical treatment (including hyperbaric oxygen therapy where available) has improved the very poor prognosis. Emphysematous pyelonephritis and renal abscesses are best seen on CT; manage closely with the urologists. Consider them in patients slow to respond to standard intensive treatment for UTI.

 

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Abdominal infections
Signs and symptoms may be subtle and undramatic. Patients with autonomic neuropathy have reduced abdominal visceral sensitivity. The most common specific abdominal infection is peritonitis in patients undergoing peritoneal dialysis. Gram-positive organisms, especially Staphylococcus aureus, are usually responsible, but Gram-negative infections occur; those caused by Pseudomonas spp. and Serratia marcescens carry a poorer prognosis. Other abdominal infections include:

  • emphysematous cholecystitis, usually polymicrobial infections (Gram-negative organisms and anerobes);
  • gynecological infections (remember small occult pelvic abscesses);
  • hepatic abscess (most commonly Klebsiella spp.), uncommon in the UK;
  • retroperitoneal abscess;
  • psoas abscess (see below, musculoskeletal infections).

Soft-tissue infections
Cellulitis
A spreading infection of the epidermis, dermis and subcutaneous fat, common in diabetes, frequently recurrent and associated with infected foot ulcers. Where there is no coexisting foot ulceration (always check carefully for minor skin breaks and interdigital fungal infection), treat as in a person without diabetes, covering the most likely organisms (Staphylococus aureus and [3-hemolytic streptococci, usually group A). Blood cultures are usually negative, but culture any fluid from unruptured blisters. Exclude coexisting deep venous thrombosis, and give prophylactic anticoagulation in immobilized patients.

Treatment
Oral antibiotics are suitable if there is limited or no involvement of the legs and no foot ulceration. A 7- day course of co-amoxiclav (or ciprofloxacin where available) are suitable, but review frequently, as infections can spread rapidly. Oral macrolides (erythromycin, clarithromycin) are probably not potent enough in this situation, and metronidazole is not necessary. Always err on the side of caution: an initial course of 24–48 hours of intravenous antibiotics (if possible ambulatory) is often valuable. High-dose intravenous benzylpenicillin and flucloxacillin are currently recommended, clindamycin in the penicillin-allergic, vancomycin where MRSA is known or suspected. Systemically unwell patients who have had previous antibiotic treatment should be started on a third-generation cephalosporin (e.g. ceftazidime) until more specific advice and culture results are available. Where there is a large volume of infected tissue, especially in the presence of ischemia or oedema, 2–4 weeks of treatment is sometimes necessary; diuretics and elevating the feet reduce leg oedema and the risk of skin breaks. Widespread desquamation during recovery is characteristic of streptococcal infection.

Necrotizing fasciitis
This is fulminating gangrene of the skin caused by rapidly spreading microvascular thrombosis affecting subcutaneous fat, dermis and muscle. Diabetes is a risk factor in up to 30% of cases (other factors include chronic alcoholism, immunosuppression and recent surgery). It usually occurs in the limbs, but any skin surface can be involved, including the feet, face and neck (where it is often of dental origin). Mortality is 20–40% from sepsis and multiorgan failure. At the onset, cutaneous signs are usually unimpressive, but irregular dusky blue and black patches appear and extend rapidly. It is a surgical emergency requiring intensive medical support. Think of necrotizing fasciitis in any diabetic patient with severe cellulitis; confirm with immediate ultrasound or CT.

Microbiology

  • Predominantly Lancefield group A [3-hemolytic streptococci.
  • Less severe infections are seen with group C and G [3-hemolytic streptococci.
  • Fournier’s gangrene is a specific form of necrotizing fasciitis, involving the perineum, genitalia and perianal area: multiple organisms can be involved, for example Staphylococcus aureus, E. coli, anerobes (clostridia, Bacteroides or anerobic streptococci). It is also described in the feet, face and neck (often of dental origin).
  • Community-acquired MRSA-associated necrotizing fasciitis has been described and is usually associated with other underlying medical conditions, diabetes included.
  • Vibrio vulnificans, found in warm coastal waters of the southern hemisphere, is increasing.

Management
Obtain immediate surgical advice. High-dose intravenous benzylpenicillin (e.g. > 14 g/day) and clindamycin (900 mg t.d.s.) should be given for streptococcal infection, metronidazole and cephalosporin for suspected Fournier’s gangrene. Hyperbaric oxygen treatment probably reduces tissue loss, but is not usually available quickly enough.

 

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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)