Complications
HUS is characterised by haemolytic anaemia, thrombocytopenia, and acute renal failure. Patients should have close monitoring of their haemoglobin, platelet count, and renal function until evidence of clinical improvement. Shiga-like toxins cause direct damage to renal glomerular endothelial cells.
Generally, 10% of patients with Escherichia coli O157:H7 develop HUS, although in outbreaks this can rise to over 25%.[59] HUS typically develops 5-9 days after the onset of diarrhoea. Epidemiological studies have shown that young age (<15 years), older age (>65 years), long duration of diarrhoea, elevated leukocyte count, hypoalbuminaemia, and proteinuria are associated with an increased risk of HUS.[59][60]
HUS is often associated with thrombocytopenia and petechial haemorrhage. Haemolysis laboratory screening can be useful if haemolytic uraemic syndrome is suspected clinically, or based on laboratory findings.
Temporary dialysis is required in as many as 50% of cases of HUS associated with E coli O157:H7 infections. Efficacy for the use of hyperimmune serum in HUS related to E coli infection has not been substantiated.
HUS has a mortality of between 3% and 5%, with approximately 50% of patients suffering sequelae, most commonly chronic renal failure or neurological deficits.[61][62]
One Cochrane review investigated the use of therapies (including some investigational therapies) against Shiga toxin as forms of secondary prevention of HUS in patients with Shiga toxin-producing E coli (STEC). Additional clinical trials are recommended as the study was unable to draw conclusions.[63]
Toxic megacolon may rarely complicate HUS secondary to E coli infection.
An uncommon complication of Escherichia coli infection, generally due to enterohaemorrhagic E coli (EHEC).
Caused by bacterial translocation across the gastrointestinal tract to the mesenteric lymph nodes. Normally bacteria are cleared by hepatic Kupffer cells, but bacteraemia can develop when this system fails. Bacteraemia is more likely to occur in those who are immunocompromised, young children (aged <5 years), or older people (aged >60 years).
Diagnosis is based on signs of sepsis (i.e., fever, tachycardia, hypotension) and positive blood cultures.
Antibiotic treatment should be initiated early and guided by bacterial sensitivities. Empirical antibiotic treatment until blood culture sensitivity results are available. Microbiology advice should be sought early.
Alongside antibiotic therapy, patients should be fluid resuscitated and monitored closely for signs of renal impairment or haemodynamic instability consistent with toxic shock.
Occurs in 4% to 32% (mean 10%) of patients who experience bacterial gastrointestinal infections. Gastrointestinal infections increase the risk of irritable bowel syndrome 12-fold.[64]
Treatment involves dietary and lifestyle modifications, as well as symptomatic treatment individualised to the patient's predominant symptoms.
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