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Hepatic Dysfunction During Pregnancy. Ayman Mokhtar Kamaly, MD Professor of Anesthesiology [email protected] Most pregnant women are young & healthy.

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Hepatic Dysfunction During Pregnancy

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Hepatic dysfunction during pregnancy l.jpg

Hepatic Dysfunction During Pregnancy

Ayman Mokhtar Kamaly, MD

Professor of Anesthesiology

[email protected]


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  • 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.


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


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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).


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Abnormal LFT During Pregnancy ‘normal for pregnancy’

  • AST

  • ALT

  • GGT

  • BIL

  • ALP

  • Triglycerides

  • Cholesterol

  • Transferrin

  • α1, α2 globulins

20% ↓

  • Alb

  • Urea

  • Uric acid


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(I) Liver Diseases Unique to Pregnancy


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  • 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.


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  • 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).


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  • 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


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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).


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  • Labs (= Biliary obst):

    • ↑ Bil. (< 5 mg%)

    • ↑ ALP x 4

    • ↑ ALT/AST: 2-10 fold

    • ↑ B.A.(most specific): 10-100 fold.


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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.


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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.


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  • 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.


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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.


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


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


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


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  • 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.


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  • 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.


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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).


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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)


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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.


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  • 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).


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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)


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


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  • 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 .


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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.


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AFLP: Diffuse fatty infiltration

(A): (low power), (B):(high power)


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  • 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%.


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(II) Liver Diseases Occurring Coincidentally in

a Pregnant Patient


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  • 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


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  • 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%.


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  • 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)


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(III) The Pregnant Patient with Chronic Liver Disease


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  • 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.


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  • 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.


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Conclusion


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