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Hepatic Dysfunction During Pregnancy

Hepatic Dysfunction During Pregnancy. Ayman Mokhtar Kamaly, MD Professor of Anesthesiology kamaly3@hotmail.com. Most pregnant women are young & healthy.

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Hepatic Dysfunction During Pregnancy

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  1. Hepatic Dysfunction During Pregnancy Ayman Mokhtar Kamaly, MD Professor of Anesthesiology kamaly3@hotmail.com

  2. Most pregnant women are young & healthy. • Liver disease is a rare complication of pregnancy, but when it occurs it may be so dramatic & in a tragic fashion for both mother & infant.

  3. Abnormal liver tests occur in 3%-5% of pregnancies, with many potential causes:

  4. Normal liver in pregnancy • Physiological changes in pregnancy: • 40% increase in plasma volume, • Increase in CO & HR (peaks at 32 wks), • Hepatic Bl flow remains the same or even decreases (35% of CO in non-pregnant Vs 28% in pregnants).

  5. Abnormal LFT During Pregnancy ‘normal for pregnancy’ • AST • ALT • GGT • BIL • ALP • Triglycerides • Cholesterol • Transferrin • α1, α2 globulins 20% ↓ ↑ ↓ • Alb • Urea • Uric acid

  6. (I) Liver Diseases Unique to Pregnancy

  7. Hyperemesis Gravidarum (HG) • Occurs in 0.3% of pregnancies (1st trimester), • Sever enough to indicate IV hydration, • Risk factors: • Hyperthyroidism, • Molar pregnancy, • Pre-existing DM, • Multiple pregnancies.

  8. LFT: • Mild ↑ Bil (< 4mg%), related to malnutrition & impaired excretion of Bil. • ALP ↑ twice N. • AST/ALT ↑ 20-fold • Biopsy:Histological normal. • Management: Rehydration, nutrition, antiemetics (± steroids).

  9. Intrahepatic Cholestasis of Pregnancy (ICP) • 3rd trimester disease (25-30 wks), • ↑bile acid [BA] (due to defective biliary transport)& Pruritus • Etiology: • Hormonal: Sex hormones have known cholestatic effects • Genetic: Certain ethnic groups (gene associated ICP) • Exogenous: seasonal, geographical, selenium deficiency

  10. Clinical Features and Diagnosis: • Pruritus: • Affects all parts of the body, • Worse @ night, • Severe cases→ patient may be suicidal. • ObstructiveJaundice: • 2-4 wks post pruritus (20-60% of pts.), • Pale stools & dark urine, • Diarrhea or steatorrhea, • Sudden fetal death, (due to ↑ fetal levels of BA).

  11. Labs (= Biliary obst): • ↑ Bil. (< 5 mg%) • ↑ ALP x 4 • ↑ ALT/AST: 2-10 fold • ↑ B.A.(most specific): 10-100 fold.

  12. Management: • Symptomatic therapy for mother + close monitoring & early delivery for the fetus. • Urso-deoxy-cholic acid (UDCA), 10-15 mg/kg (ttt of choice, completely safe) • Dexamethasone (12 mg/day for 1 wk) has the advantage of promoting fetal lung maturity • Cholestyramine, 10-12 g/day, • ProphylacticVitaminK.

  13. Outcome of pts. with ICP: • Pruritus & liver dysfunction resolveimmediately after delivery. • 45-70% recurrence in subsequent preg. or with oral contraceptives. • More liable to: • Gallstones, • Cholecystitis, • Hepatitis C, • Nonalcoholic pancreatitis, • Nonalcoholic cirrhosis.

  14. Preeclampsia and Eclampsia • Triad(hypertension + edema + proteinuria), • 5-10% of pregnancies in the 3rd trimester. • Liver involvement, always indicates severe preeclampsia. Etiology: • Placental hypoperfusion, with alteration of vasomotor tone, initiation of the coagulation cascade. • Nitric oxide has role, (upregulation of NO-synthase in normal pregnancy) • Imbalance of prostacyclin (PGI2) : thromboxane ratio increase systemic resistance.

  15. Hepatic Involvement: • Abnormal LFT in 20–30% of pts due to VC of hepatic vascular bed. • ALP (which is often elevated in pregnancy), may be further ↑, • Transaminases: 10-20 fold ↑, • Bilirubin < 5 mg%, • Complications: Subcapsular hematoma & rupture, infarction, & fulminant failure.

  16. Acute Hepatic Hemorrhage of the Rt Lobe with a Subcapsular Hematoma.

  17. Extensive necrosis throughout the Rt lobe with patchy necrosis in the Lt lobe

  18. Autopsy of a eclamptic woman shows multiple regions of hepatic infarction (pale zones).

  19. Unfortunately; No specific therapy for the hepatic involvement of preeclampsia, • It is only significant as an indicator of severity & need for immediate delivery to avoid eclampsia, hepatic rupture, or necrosis.

  20. HELLP Syndrome • HELLP is a complication of severe preeclampsia in 2-12% of cases (Hemolysis, Elevated Liver tests, & Low Platelet). • Key abnormalities: • V.C, platelet activation & consumption, • Thromboxane : Prostacyclin ratio alteration, • Activation of complement & coagulation cascade causing microangiopathic hemolytic anemia, • elevated liver enzymes with periportal and hepatic necrosis.

  21. Clinical Features & Diagnosis • There are no distinguished clinical features from preeclampsia (upper abdominal pain, nausea & vomiting, headache, edema, hypertension, and proteinuria). • Diagnosis requires the all 3 laboratory criteria: (1)Hemolysis (↑ indirect bil.), (2)↑Transaminases (10-20 fold + bil. < 5 mg%), (3) Thrombocytopenia(<150000).

  22. Classification of HELLP: • Tennessee System • Complete syndrome: • AST &/or ALT > 40 • Platelets <100000 • LDH > 600 IU/L • AST > 70 • Incomplete syndrome: • Any 1 or 2 of the above Mississippi Class System: • Class 1: Platelets < 50000 • Class 2: Platelets 50-100000 • Class 3: Platelets 100-150000 + Hemolysis + ↑liver enzymes (LDH>600)

  23. Differential Diagnoses of HELLP Thrombotic disorders • Thrombotic thrombocytopaenicpurpura, • Hemolytic uremic syndrome, • Sepsis & DIC, • Drug-induced hemolytic anemias. Consumptive disorders • Acute fatty liver of pregnancy, • Sepsis and DIC, • Hemorrhage. Others • Connective tissue disease, • SLE, • Antiphospholipid syndrome, • Procoagulant disorders.

  24. Management: • Hospitalization for stabilization (hypertension & DIC, seizure prophylaxis, fetal monitoring), • Delivery is the only definitive therapy (< 34 wk → steroids for lung & plt), • Outcome @ < 34 wk is better when steroids(dexamethasone, which cross the placenta) are used for 24-48 hr (main benefit is lung maturity & platelet count).

  25. Complications of HELLP • DIC, ARF, eclampsia, pulm edema, ARDS, • Indications for liver transplantation are very limited (persisting bleeding from a hepatic hematoma or hepatic rupture or liver failure - necrosis). • Hepatic hemorrhage or rupture due to exogenous trauma (abdominal palpation, convulsions, emesis & unnecessary transportation)

  26. Lt lobe Large subcapsular hematoma. Rt lobe has widespread necrosis a (heterogeneous, hypodense appearance), with “sparing” of Lt lobe.

  27. Acute Fatty Liver of Pregnancy (AFLP) • Rare fatal complication of preg. (3rd trimester). • ChCh: microvesicular fatty infiltration →encephalopathy & hepatic failure with up to 10% mortality. • Etiology: Enzyme mutation (mitochondria fatty acid oxidation) • 20% of babies for mothers with AFLP are +ve for the enzyme .

  28. Clinical Features and Diagnosis • 40%-50% of pts with AFLP are in their 1st preg, with twin. • Presentation: vary from asymptomatic, nonspecific symptoms, to fulminant liver failure. • Transaminases: 300-500, Bil. < 5 mg% • Presumptive diagnosis is made on compatible clinical and lab features. • Definitive diagnosis is histological.

  29. AFLP: Diffuse fatty infiltration (A): (low power), (B):(high power)

  30. Management: • Immediate termination of pregnancy, • Vaginal Vs CS according to INR (< 1.5) & plt (> 50000), Outcome: • before 1980, both maternal & fetal mortality were 85%, • With advance of supportive care, mortality went down to 7-18%.

  31. (II) Liver Diseases Occurring Coincidentally in a Pregnant Patient

  32. Viral Hepatitis • 40% of jaundice in pregnant women in USA. • Hepatitis A, B, C, D, E, Herpes, CMV, Epstein-Barr viruses. • Management of pt with acute viral hepatitis is supportive, • Viral hepatitis is NOTan indication for termination of pregnancy, caesarean section, or discouragement for breastfeeding

  33. Pregnants with -ve HBV antibodies, & @ high risk (e.g., +ve partner) can be vaccinated safely with little fetal risk. • HBV transmission is NOT transplacental, but only during delivery. • HCV mother to infant transmission is only 1-5%.

  34. Gallstones & Biliary Disease • Cholesterol secretion ↑ in the 2nd & 3rd trimesters > bile acids & phospholipids, → to supersaturated bile, • Surgery is indicated when not responding to conservative measure (1st trimester (risk of abortion), & in 3rd trimester (risk of prematurity) ideally: Laproscopic. • ERCP for impacted CBD stone (fluoroscopy minimization)

  35. (III) The Pregnant Patient with Chronic Liver Disease

  36. In HCV, aminotransferases may fall & viral RNA ↑ during pregnancy. • Unfortunately, the optimal management of pregnancy with cirrhosis and portal hypertension in the modern era of obstetrics is undefined. • Most patients with advanced cirrhosis are amenorrheic & infertile due to hypothalamic -pituitary dysfunction.

  37. B-blocker is indicated for Pts with large varices, despite fetal effects, • Acute variceal bleeding is managed endoscopically (as in non-preg), however; Vasopressin is contraindicated. • In Pts with known large varices, avoidance of CS is recommended to avoid ↑ in portal pressure.

  38. Conclusion

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