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MICROANGIOPATHIC
HEMOLYTIC
ANEMIA
MICROANGIOPATHIC
HEMOLYTIC ANEMIA
• Microangiopathic subgroup of hemolytic
anemia (loss of red blood cells through
destruction) caused by factors in the small
blood vessels.
• Occurs when red cells are forced to squeeze
through abnormally narrowed small vessels.
• Types of TMAs assd. with MAHA:
– Thrombotic thrombocytopenic purpura.
– Hemolytic uremic syndrome.
– DIC
• Other TMA syndromes can occur with:
– Pregnancy
– Malignant hypertension
– SLE
• Common Feature:
– Microvascular lesion that causes
mechanical injury to circulating red cells.
• Damage evident in peripheral blood
smears in the form of red cell
fragments- schistocytes, “burr cells”,
“helmet cells” and “triangle cells”.
HEMOLYTIC-UREMIC
SYNDROME
PATHOGENESIS
1) Endothelial injury and activation.
2) Platelet aggregation
Both cause vascular obstruction and vasoconstriction
=> Precipitate distal ischaemia.
ENDOTHELIAL INJURY &
ACTIVATION
• Triggers can be :
– Bacterial endotoxins
– Cytotoxins
– Cytokines
– Viruses
– Drugs
– Antiendothelial antibodies
– Abnormal multimers or inhibitors of vWF
• Endothelial denudation exposes a
potentially thrombogenic subendothelial
connective tissue.
• Reduced production of PgI2 and nitric
oxide enhances platelet aggregation and
causes vasoconstriction.
• Activation of endothelial cells increased
adhesivity to leukocytes thrombosis.
• Endothelial cells elaborate multimers of
vWF that remain abnormally large
platelet aggregation.
PLATELET AGGREGATION
• With congenital or acquired loss of ADAMTS-
13(a vWF cleaving metalloprotease) activity,
very large vWF multimers persist in circulation
and induce aggregation by activating platelet
surface glycoproteins.
• CLASSIC(CHILDHOOD) HUS
• ADULT HUS
CLASSIC HUS
• 75% in children after intestinal infection
with verocytotoxin-producing E.coli.
• Verocytotoxin similar to Shiga toxin.
• Most frequently assd. with bloody diarrhoea.
• Some traced to ingestion of infected ground meat.
• One of the main causes of acute renal failure in
children.
PATHOGENESIS
• Clearly related to Shiga-like toxin.
• Toxin causes:
– Increased adhesion of leukocytes.
– Increased endothelin production.
– Loss of endothelial nitric oxide.
– Endothelial lysis( in presence of cytokines
such as TNF).
• Enhancement of both thrombosis and
vasoconstriction- microangiopathy.
• Verocytotoxin also binds to platelets and
directly activate them.
CLINICAL FEATURES
• Sudden onset.
• Usually after a GI or influenza-like prodromal
episode.
• Bleeding manifestations(hematemesis & malena).
• Severe oliguria.
• Hematuria.
• Microangiopathic hemolytic anemia.
• Prominent neurological changes in some patients.
Fibrin stain showing platelet-fibrin thrombi (red) in
the glomerular capillaries, characteristic of
thrombotic microangiopathic disorders.
ADULT HUS
• In association with infection.
• In the antiphospholipid syndrome.
• As complications of pregnancy and
contraceptives.
• Assd. with vascular renal diseases.
• In patients treated with chemotherapeutic and
immunosuppressive drugs.
• In typical(epidemic,classic,diarrhoea positive)
HUS the trigger for endothelial injury and
activation usually is a Shiga toxin.
• In inherited forms of atypical HUS, the cause
of endothelial injury appears to be excessive,
inappropriate activation of components.
LAB FINDINGS
• CBC
– Anemia
– Thrombocytopenia
– Peripheral smear checking for schistocytes,
burr cells, helmet cells, spherocytes and
segmented red blood cells
• LDH (elevated)
• Haptoglobin (decreased)
• Reticulocyte count (appropriate)
• PT/PTT (normal; differentiates from DIC)
• Stool tests
– Shiga toxin, E. coli O157:H7 test
• Urine Analysis
– Hematuria, casts
• LFT
– Increased indirect bilirubin
• Chemistry
– Creatinine, hyperkalemia (renal failure)
THANK YOU

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Microangiopathic hemolytic Anemia & Hemolytic Uremic Syndrome

  • 2. MICROANGIOPATHIC HEMOLYTIC ANEMIA • Microangiopathic subgroup of hemolytic anemia (loss of red blood cells through destruction) caused by factors in the small blood vessels. • Occurs when red cells are forced to squeeze through abnormally narrowed small vessels.
  • 3. • Types of TMAs assd. with MAHA: – Thrombotic thrombocytopenic purpura. – Hemolytic uremic syndrome. – DIC • Other TMA syndromes can occur with: – Pregnancy – Malignant hypertension – SLE
  • 4. • Common Feature: – Microvascular lesion that causes mechanical injury to circulating red cells.
  • 5. • Damage evident in peripheral blood smears in the form of red cell fragments- schistocytes, “burr cells”, “helmet cells” and “triangle cells”.
  • 6.
  • 8. PATHOGENESIS 1) Endothelial injury and activation. 2) Platelet aggregation Both cause vascular obstruction and vasoconstriction => Precipitate distal ischaemia.
  • 9. ENDOTHELIAL INJURY & ACTIVATION • Triggers can be : – Bacterial endotoxins – Cytotoxins – Cytokines – Viruses – Drugs – Antiendothelial antibodies – Abnormal multimers or inhibitors of vWF
  • 10. • Endothelial denudation exposes a potentially thrombogenic subendothelial connective tissue. • Reduced production of PgI2 and nitric oxide enhances platelet aggregation and causes vasoconstriction.
  • 11. • Activation of endothelial cells increased adhesivity to leukocytes thrombosis. • Endothelial cells elaborate multimers of vWF that remain abnormally large platelet aggregation.
  • 12. PLATELET AGGREGATION • With congenital or acquired loss of ADAMTS- 13(a vWF cleaving metalloprotease) activity, very large vWF multimers persist in circulation and induce aggregation by activating platelet surface glycoproteins.
  • 14. CLASSIC HUS • 75% in children after intestinal infection with verocytotoxin-producing E.coli. • Verocytotoxin similar to Shiga toxin. • Most frequently assd. with bloody diarrhoea. • Some traced to ingestion of infected ground meat. • One of the main causes of acute renal failure in children.
  • 15. PATHOGENESIS • Clearly related to Shiga-like toxin. • Toxin causes: – Increased adhesion of leukocytes. – Increased endothelin production. – Loss of endothelial nitric oxide. – Endothelial lysis( in presence of cytokines such as TNF). • Enhancement of both thrombosis and vasoconstriction- microangiopathy.
  • 16. • Verocytotoxin also binds to platelets and directly activate them.
  • 17. CLINICAL FEATURES • Sudden onset. • Usually after a GI or influenza-like prodromal episode. • Bleeding manifestations(hematemesis & malena). • Severe oliguria. • Hematuria. • Microangiopathic hemolytic anemia. • Prominent neurological changes in some patients.
  • 18. Fibrin stain showing platelet-fibrin thrombi (red) in the glomerular capillaries, characteristic of thrombotic microangiopathic disorders.
  • 19. ADULT HUS • In association with infection. • In the antiphospholipid syndrome. • As complications of pregnancy and contraceptives. • Assd. with vascular renal diseases. • In patients treated with chemotherapeutic and immunosuppressive drugs.
  • 20. • In typical(epidemic,classic,diarrhoea positive) HUS the trigger for endothelial injury and activation usually is a Shiga toxin. • In inherited forms of atypical HUS, the cause of endothelial injury appears to be excessive, inappropriate activation of components.
  • 21. LAB FINDINGS • CBC – Anemia – Thrombocytopenia – Peripheral smear checking for schistocytes, burr cells, helmet cells, spherocytes and segmented red blood cells • LDH (elevated) • Haptoglobin (decreased) • Reticulocyte count (appropriate)
  • 22. • PT/PTT (normal; differentiates from DIC) • Stool tests – Shiga toxin, E. coli O157:H7 test • Urine Analysis – Hematuria, casts • LFT – Increased indirect bilirubin • Chemistry – Creatinine, hyperkalemia (renal failure)