Hemolytic-uremic syndrome: Difference between revisions
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*Typical HUS is caused by Shiga toxin from enterohemorrhagic [[Escherichia coli]] (e.g. O157:H7) |
*Typical HUS is caused by Shiga toxin from enterohemorrhagic [[Escherichia coli]] (e.g. O157:H7) |
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*Shiga toxin is absorbed systemically |
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**Damages vascular endothelial cells leading to cytokine release and thrombus formation |
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**Actives complement and binds Factor H (a complement regulator) |
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===Risk Factors=== |
===Risk Factors=== |
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Revision as of 00:33, 23 August 2020
Background
- Typical HUS is a thrombotic microangiopathy with prominent renal failure traditionally associated with Shiga toxin-producing Escherichia coli infection, especially enterohemorrhagic E. coli O157:H7
- Difference pathophysiology and treatment from atypical hemolytic-uremic syndrome
Pathophysiology
- Typical HUS is caused by Shiga toxin from enterohemorrhagic Escherichia coli (e.g. O157:H7)
- Shiga toxin is absorbed systemically
- Damages vascular endothelial cells leading to cytokine release and thrombus formation
- Actives complement and binds Factor H (a complement regulator)
Risk Factors
- Younger age
- Exposure to antibiotics
- Increased WBC count
- Vomiting
- Prolonged diarrhea
- Presence of stx2a and eae genes
Clinical Manifestations
- Abdominal pain and watery diarrhea about 4 days after exposure to toxin, progressing to bloody diarrhea with or without vomiting
- Up to one third do not have bloody diarrhea
- Fever is mild or absent
- About 7 days after onset of diarrhea, HUS develops
- Progression of hemolytic anemia, thrombocytopenia, and severe AKI
- Other preceding infections can include UTI, SSTI, or other causes of gastroenteritis
Management
- Supportive
