Hemolytic-uremic syndrome: Difference between revisions

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

@@ Line 1: / Line 1: @@
 ==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
+*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]]
+*Different pathophysiology and treatment from [[atypical hemolytic-uremic syndrome]] and [[secondary hemolytic-uremic syndrome]]
-=== Pathophysiology ===
+===Pathophysiology===
-* 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)
-* Toxin is absorbed systemically, causing platelet activation and aggregation
+*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 ===
+===Risk Factors===
-* Younger age
+*Younger age
-* Exposure to antibiotics
+*Exposure to antibiotics
-* Increased WBC count
+*Increased WBC count
-* Vomiting
+*Vomiting
-* Prolonged diarrhea
+*Prolonged diarrhea
-* Presence of ''stx2a'' and ''eae'' genes
+*Presence of ''stx2a'' and ''eae'' genes
-== Clinical Manifestations ==
+==Clinical Manifestations==
+*Abdominal pain and watery diarrhea about 4 days after exposure to toxin, progressing to bloody diarrhea with or without [[vomiting]]
-* A few days of bloody diarrhea
+**Up to one third do not have bloody diarrhea
-* Progression of [[hemolytic anemia]], [[thrombocytopenia]], and severe [[AKI]]
+**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 ==
+==Management==
-* Supportive
+*Supportive
 [[Category:Hematology]]