Intrahepatic Cholestasis of Pregnancy
A 31-year-old primigravida woman with a history of infertility underwent ovulation induction. She is now at 20 weeks’ gestation with dizygotic twins of different genders. She is of Swedish descent and complains of intense skin-itching. She has not experienced these symptoms previously. Her sister experienced similar complaints when she was pregnant, and delivered her baby prematurely. No identifiable rash is noted on physical examination. She states that her urine appears dark-colored.
Pathophysiology. Intrahepatic cholestasis is stimulated by estrogen in genetically predisposedwomen in the second half of pregnancy. Risk is increased with twins.
Bile acids are incompletely cleared by the liver and accumulate in the plasma. The overall preva-lence is 0.5% in North America and Europe. There is a high recurrence rate with subsequent pregnancies.
Findings. The most significant symptom is intractable pruritus on the palms and soles of thefeet, worse at night, without specific skin findings.
• Laboratory tests show a mild elevation of bilirubin but diagnostic findings are serum bile acids increased 10- to 100-fold.
Outcome. No adverse effect on maternal outcome, but preterm births and stillbirths areincreased
Management
• Oral antihistamines can be helpful in mild cases.
• Cholestyramine has been used to decrease enterohepatic circulation.
• Ursodeoxycholic acid is the treatment of choice. Antenatal fetal testing should be initi-ated at 34 weeks. Symptoms disappear after delivery.
• Induce labor at 38 weeks gestation.
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GI
USMLE Step 2 l Obstetrics
Acute Fatty Liver
A 29 year-old primagravida is at 33 weeks’ gestation. She is brought to the maternity unit by her husband who states she is becoming mentally confused. He reports she started experiencing nausea and vomiting 3 days ago which are becoming worse, associated with lack of appetite. Fundal height is 30 cm. Fetal heart rate is 145/min with non-reactive non-stress test. Her BP is 150/95 mm Hg. Random blood glucose is 52 mg/dL. Platelet count is 75,000. PTT is prolonged at 64.7 seconds. Creatinine is 2.1 mg/dL. Uric acid is 11.9 mg/dL, lactic dihydrogenase 1063 U/I, ALT 220 U/I, AST 350 U/I, total bilirubin 8.4 mg/dL. Serum ammonia is elevated. Urine protein dipstick is 3+.
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Description. This is a rare life-threatening complication of pregnancy that usually occurs inthe third trimester. Prevalence is 1 in 15,000. Maternal mortality rate is 20%. It is thought to be caused by a disordered metabolism of fatty acids by mitochondria in the fetus, caused by deficiency in the long-chain 3-hydroxyacyl-coenzyme A dehydrogenase (LCHAD) enzyme.
Findings. Symptom onset is gradual, with nonspecific flulike symptoms including nausea,vomiting, anorexia, and epigastric pain.
• Jaundice and fever may occur in as many as 70% of patients.
• Hypertension, proteinuria, and edema can mimic preeclampsia.
• This may progress to involvement of additional systems, including acute renal failure,
pancreatitis, hepatic encephalopathy, and coma. Laboratory findings may include: moderate elevation of liver enzymes (e.g., ALT, AST, GGT), hyperbilirubinemia, DIC.
• Hypoglycemia and increased serum ammonia are unique laboratory abnormalities.
Management. Intensive care unit stabilization with acute IV hydration and monitoring isessential.
• Prompt delivery is indicated.
• Resolution follows delivery if mother survives.
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