Hepatic Disorders of Pregnancy PDF

Hepatic disorders of pregnancy Waleed abanumay 439026310 -Hepatic disorders not directly related to pregnancy: Acute & chronic hepatitis Hepatic disorders which are unique to pregnancy: Intrahepatic cholestasis of pregnancy (ICP) Acute fatty liver of pregnancy Hyperemesis gravidarum Hepatitis A Epid...

Hepatic disorders of pregnancy Waleed abanumay 439026310 -Hepatic disorders not directly related to pregnancy: Acute & chronic hepatitis Hepatic disorders which are unique to pregnancy: Intrahepatic cholestasis of pregnancy (ICP) Acute fatty liver of pregnancy Hyperemesis gravidarum Hepatitis A Epidemiology: Transmission:via fecal-oral route High risk:countries in which HAV is endemic (tropical or subtropical regions) Prevalence:1 in 1000 pregnancies Clinical manifestations: Prodromal phase 1-2 weeks: malaise,fatigue,anorexia,nasuea,vomiting,RUQ,tender hepatomegaly Icteric phase: 2 weeks:jaundice,dark urine or pale stools,prurits Diagnosis: History & physical examination Lab:elevated alanine aminotransferase andaspartate aminotransferase) and hyperbilirubinemia Igm antibody Management: HAV immune globulin (single IM dose) Offer supportive care Disease is usually self-limited Prevention: HAV vaccine (4 to 6 months) Hepatitis B: transmission: occurs most commonly via parenteral exposure or sexual contact Clinical manifestations: rash, arthralgia, myalgia, and occasionally frank arthritis and jaundice. In adults, around 90% to 95% acute infections resolve completely, and the patient develops protective levels of antibody. Congenital: Maternal-fetal transmission can occur at any time during pregnancy but most commonly occurs at the time of delivery In women who are seropositive for both HBsAg and HBeAg (indicating active replication),the vertical transmission rate approaches 90% (active) in a woman who is HBsAg positive and hepatitis B core antibody positive with an undetectable hepatitis B viral load (carrier state), the risk of transmission drops to 10% to 30%. Diagnosis: It is confirmed by serology Persistence of HBsAg for more than 6 months implies chronic infection. HBeAG is detected during active viral replication. Management: The disease is generally self-limited, and symptoms resolve within 1 to 2 weeks. HBV immunoglobulin (HBIG) Antiviral therapy starting at 28-32 weeks of gestation. universal screening of all pregnant women for HBV at the first prenatal visit. Prevention: Vaccination for hepatitis B is recommended Hepatitis C Transmission: parental exposure Clinical manifestations: Asymptomatic infection occurs in 70% of patients and at least 50% of infected individuals progress to chronic infection Diagnosis: Anti-hepatitis c antibody (may take up to 1 year) HCV viral RNA Prevention:no method to prevent transmission. If transmission occurs, increase risk for acute and chronic hepatitis of neonate. Intrahepatic cholestasis of pregnancy is the most common liver disease in pregnancy Onset is typically in third trimester. Risk factors: personal or family history of ICP (Recurrence risk in subsequent pregnancies is approximately 70%) multiple gestations in vitro fertilization advanced maternal age chronic hepatitis C infection Complications: preterm labor-neonatal respiratory distress syndrome-IUFD Antepartum fetal testing is recommended. This disease has no clear etiology. Diagnosis: Initial diagnosis of ICP is primarily clinical, with confirmation by laboratory testing to exclude other possible diagnoses. pruritus,especially of the palms and soles that worsens at night. Anorexia, malaise, steator-rhea, and dark urine. Jaundice(15%) Laboratory findings: Elevated total bilirubin, aminotransferase, fast serum total bile acids (>10-14) Treatment: Symptomatic relief Ursodiol is the best treatment Acute fatty liver of pregnancy: Rare life threatening-disorder Idiopathic , inability the liver to process fat. occurring in approximately 1 in 10 000 pregnancies It typically occurs in primigravid women in the third trimester associated with multiple gestations, low maternal weight with a fetal mitochondrial gene mutation causing (Lchad syndrome) long chain 3-hydroxylacyl-CoA dehydrogenase deficiency High maternal and fetal mortality and morbidity if this disease is not diagnosed early. Clinical features: Sudden onset of jaundice RUQ pain, nausea, and vomiting Coagulopathy with an increased risk of DIC Hypoalbuminemia → ascites Encephalopathy Polyuria and polydipsia Intra uterine bleeding Laboratory findings: Hypoglycemia Elevated liver enzymes. Leukocytosis Thrombocytopenia. Metabolic acidosis. Hyperuricemia Treatment: Maternal stabilization with intensive supportive care. Delivery, either with induction of labor with close maternal and fetal surveillance or cesarean delivery. Hyperemesis gravidarum Definition: Severe, persistent nausea and vomiting associated with a > 5% loss of prepregnancy weight and ketonuria with no other identifiable cause. Usually starts between 4-8 week of gestation and peaks at around 8-12th weeks of gestation and may last up to 16 weeks. Clinical Features: Nausea Vomiting physical signs of dehydration Hypersalivation Orthostatic hypotension Malnourishment Diagnosis Mainly Clinical diagnosis Laboratory analysis: Electrolyte disturbances (hypokalemia and hypochloremic metabolic alkalosis) Signs of dehydration (e.g.,↑ hematocrit) ketonuria Treatment Antiemetic therapy: for nausea and vomiting of pregnancy (pyrdoxine and doxylamine) For refractory symptoms add the following: Diphenhydramine, Dimenhydrinate, Prochlorperazine For refractory symptoms despite combination therapy above add: Metoclopramide, Ondansetron, Promethazine Last resort: Add chlorpromazine or methylprednisolone (do not use them in the first trimester of pregnancy!) IV fluid resuscitation/replacement Electrolyte and thiamine repletion Enteral feeding or TPN: - recommended in patients with persistent symptoms & weight loss despite antiemetic therapy. References Johns Hopkins of medicine AMBOSS