Hemolytic-uremic syndrome: Difference between revisions
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==Background== |
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*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 |
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* Much more common in pediatric patients, followed by elderly patients |
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*Different pathophysiology and treatment from [[atypical hemolytic-uremic syndrome]] and [[secondary hemolytic-uremic syndrome]] |
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===Pathophysiology=== |
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*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=== |
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*Younger age |
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*Exposure to antibiotics |
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*Increased WBC count |
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*Vomiting |
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*Prolonged diarrhea |
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*Presence of ''stx2a'' and ''eae'' genes |
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==Clinical Manifestations== |
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*Abdominal pain and watery diarrhea about 4 days after exposure to toxin, progressing to bloody diarrhea with or without [[vomiting]] |
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**Up to one third do not have bloody diarrhea |
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**Fever is mild or absent |
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*About 7 days after onset of diarrhea, HUS develops |
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**Progression of [[hemolytic anemia]], [[thrombocytopenia]], and severe [[AKI]] |
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*Other preceding infections can include [[UTI]], [[SSTI]], or other causes of [[gastroenteritis]] |
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==Management== |
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*Supportive |
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[[Category:Hematology]] |
[[Category:Hematology]] |
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Latest revision as of 13:29, 20 April 2023
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
- Different pathophysiology and treatment from atypical hemolytic-uremic syndrome and secondary 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
