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HELLP SYNDROME
PRESENTED BY ANKIT SHARMA
TO LELA TANDASHVILLI
DEFINITION
• A life-threatening form of preeclampsia characterized
• by Hemolysis, Elevated Liver enzymes, and Low Platelets
• May occur without hypertension or proteinuria
• Preeclampsia: new-
onset gestational hypertension with proteinuria or end-organ
dysfunction
Risk factors
• Diabetes mellitus or gestational diabetes
• Chronic hypertension
• Chronic renal disease (e.g., SLE)
• Obesity (BMI ≥ 30)
• Previous preeclampsia
•
Family history
•
Chromosomal anomalies or congenital structural anomalies
•
Pathophysiology
• Uterine spiral arteries normally develop into high-capacity blood vessels. This
process is defective in patients with preeclampsia, which leads to abnormal blood
flow (high pressure, pulsatile flow) of the placenta and fetus (see “Placenta” for
more information on normal placenta formation).
• Arterial hypertension with
systemic vasoconstriction causes placental hypoperfusion → release of
vasoactive substances → ↑ maternal blood pressure to ensure sufficient blood
supply of the fetus
• Systemic endothelial dysfunction causes placental hypoperfusion → ↑ placental
release of factors → endothelial lesions that lead to microthrombosis
• Abnormal placental (or trophoblast) implantation or development in the uterus
•
Clinical feature
• Nonspecific symptoms: nausea,
vomiting, diarrhea
• RUQ pain (liver capsule pain; liver
hematoma)
• Rapid clinical deterioration pulmonary
edema, acute renal
failure, stroke, abruptio placentae)
Diganostics
• CBC: ↓ Hb; ↓ platelets seen in severe preeclampsia or HELLP
• Liver chemistries: ↑ Transaminases are suggestive of severe
preeclampsia or HELLP.
• Renal function tests: Declining eGFR is indicative of severe preeclampsia.
• Lactate dehydrogenase: Levels elevated in HELLP
• Coagulation studies: ↑ D-dimer, ↑ PT/aPTT, ↓ fibrinogen, and ↓ antithrombin III
Diganostic criteria
• H = Hemolysis (e.g., ↓ hemoglobin, ↓
haptoglobin, ↑ LDH, and ↑ indirect
bilirubin)
• EL = Elevated Liver
enzymes (↑ AST, ↑ ALT)
• LP = Low Platelets (< 100,000 cells/mm3
Management
• Administer blood products (e.g., platelets, PRBCs, FFP)
as needed to manage hemorrhage and coagulopathy
• Initiate antihypertensives for urgent blood pressure
control in pregnancy.
• Administer magnesium sulfate for seizure prophylaxis.
Obstetric management
• Expedited delivery is indicated for all patients regardless of gestational
age.
• ≥ 34 weeks' gestation: Deliver immediately.
• 24–34 weeks' gestation: Administer corticosteroids for fetal lung
maturity
• Delivery may be delayed until 24–48
hours after corticosteroid administration if maternal and fetal status
remains stable.
COMPLICATION
• Maternal complications
• pulmonary edema, acute renal failure, stroke, abruptio placentae)
liver rapture
• Fetal complications
Fetal growth restriction ,preterm birth
,fetal hypoxia ,fetal death
HELLP SYNDROME.pptx

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HELLP SYNDROME.pptx

  • 1. HELLP SYNDROME PRESENTED BY ANKIT SHARMA TO LELA TANDASHVILLI
  • 2. DEFINITION • A life-threatening form of preeclampsia characterized • by Hemolysis, Elevated Liver enzymes, and Low Platelets • May occur without hypertension or proteinuria • Preeclampsia: new- onset gestational hypertension with proteinuria or end-organ dysfunction
  • 3. Risk factors • Diabetes mellitus or gestational diabetes • Chronic hypertension • Chronic renal disease (e.g., SLE) • Obesity (BMI ≥ 30) • Previous preeclampsia • Family history • Chromosomal anomalies or congenital structural anomalies •
  • 4. Pathophysiology • Uterine spiral arteries normally develop into high-capacity blood vessels. This process is defective in patients with preeclampsia, which leads to abnormal blood flow (high pressure, pulsatile flow) of the placenta and fetus (see “Placenta” for more information on normal placenta formation). • Arterial hypertension with systemic vasoconstriction causes placental hypoperfusion → release of vasoactive substances → ↑ maternal blood pressure to ensure sufficient blood supply of the fetus • Systemic endothelial dysfunction causes placental hypoperfusion → ↑ placental release of factors → endothelial lesions that lead to microthrombosis • Abnormal placental (or trophoblast) implantation or development in the uterus •
  • 5. Clinical feature • Nonspecific symptoms: nausea, vomiting, diarrhea • RUQ pain (liver capsule pain; liver hematoma) • Rapid clinical deterioration pulmonary edema, acute renal failure, stroke, abruptio placentae)
  • 6. Diganostics • CBC: ↓ Hb; ↓ platelets seen in severe preeclampsia or HELLP • Liver chemistries: ↑ Transaminases are suggestive of severe preeclampsia or HELLP. • Renal function tests: Declining eGFR is indicative of severe preeclampsia. • Lactate dehydrogenase: Levels elevated in HELLP • Coagulation studies: ↑ D-dimer, ↑ PT/aPTT, ↓ fibrinogen, and ↓ antithrombin III
  • 7. Diganostic criteria • H = Hemolysis (e.g., ↓ hemoglobin, ↓ haptoglobin, ↑ LDH, and ↑ indirect bilirubin) • EL = Elevated Liver enzymes (↑ AST, ↑ ALT) • LP = Low Platelets (< 100,000 cells/mm3
  • 8. Management • Administer blood products (e.g., platelets, PRBCs, FFP) as needed to manage hemorrhage and coagulopathy • Initiate antihypertensives for urgent blood pressure control in pregnancy. • Administer magnesium sulfate for seizure prophylaxis.
  • 9. Obstetric management • Expedited delivery is indicated for all patients regardless of gestational age. • ≥ 34 weeks' gestation: Deliver immediately. • 24–34 weeks' gestation: Administer corticosteroids for fetal lung maturity • Delivery may be delayed until 24–48 hours after corticosteroid administration if maternal and fetal status remains stable.
  • 10. COMPLICATION • Maternal complications • pulmonary edema, acute renal failure, stroke, abruptio placentae) liver rapture • Fetal complications Fetal growth restriction ,preterm birth ,fetal hypoxia ,fetal death