Hemolytic-uremic syndrome: Difference between revisions

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== Background ==
==Background==

* [[Thrombotic microangiopathy]] with prominent renal failure traditionally associated with Shiga toxin-producing [[Escherichia coli]] infection, especially enterohemorrhagic ''E. coli''
*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
* Much more common in pediatric patients, followed by elderly patients
*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)
* Toxin is absorbed systemically, causing platelet activation and aggregation

=== Risk Factors ===

* Younger age
* Exposure to antibiotics
* Increased WBC count
* Vomiting
* Prolonged diarrhea
* Presence of ''stx2a'' and ''eae'' genes

== Clinical Manifestations ==

* A few days of bloody diarrhea
* Progression of [[hemolytic anemia]], [[thrombocytopenia]], and severe [[AKI]]

== Management ==

* Supportive


[[Category:Hematology]]
[[Category:Hematology]]

Revision as of 11:28, 15 August 2020

Background

Pathophysiology

  • Typical HUS is caused by Shiga toxin from enterohemorrhagic Escherichia coli (e.g. O157:H7)
  • Toxin is absorbed systemically, causing platelet activation and aggregation

Risk Factors

  • Younger age
  • Exposure to antibiotics
  • Increased WBC count
  • Vomiting
  • Prolonged diarrhea
  • Presence of stx2a and eae genes

Clinical Manifestations

Management

  • Supportive