CASE › 38-year-old, previously healthy G2 P2 girl arrives at your office with sudden-onset epigastric pain, chills, and nausea, but no vomiting. She has got no fever, shortness of breath, or pruritis. Her hunger is good and her weight is stable. Three days previously, she gave birth to a healthy baby. The span of pregnancy have been easy, and delivery was genital at 35 weeks’ gestation without any complications.
Her blood pressure (BP) was normal throughout being pregnant, and she got no signs of preeclampsia. She will not smoke. Although she usually daily beverages 1 beverage, she avoided alcoholic beverages during her pregnancy. She does not use illicit drugs. She has received no blood transfusions and does not have any previous background of viral hepatitis. On examination she actually is alert and oriented.
She is afebrile and anicteric. Her essential signs are normal with a BP of 116/80 mm Hg and a pulse rate of 86/min. Respiratory rate is 20/min, and air saturation is 98% while breathing ambient air. On palpation, her abdominal is soft and nontender without organomegaly. There is absolutely no ascites and bowel noises are audible. What’s the differential diagnosis of abnormally elevated liver organ enzymes in the peripartum period?
Narrowing the field. HG usually presents between 4 to 13 weeks of the start of pregnancy and is seen as a severe nausea, vomiting, weight loss, and electrolyte disturbances, none of which can be found in this patient. The patient doesn’t have neuropsychiatric signs or symptoms typical of Wilson’s disease, and the high-normal ceruloplasmin level despite above-normal serum copper weighs in at against this medical diagnosis also.
Our patient was not taking any hepatotoxic drugs or over-the-counter medications that cause liver harm. With intrahepatic cholestasis of pregnancy, aminotransferase levels can be as high as 20 times top of the limit of normal. However, with this disorder, raised serum bile acids during the second half of being pregnant-cause pruritis.
Absence of pruritis, jaundice, and features of obstructive jaundice, including pale stools and dark urine, makes intrahepatic cholestasis of being pregnant unlikely. The absence of jaundice, ascites, and hepatic vein thrombosis on ultrasound excludes Budd-Chiari symptoms. Preeclampsia is seen as hypertension and proteinuria after 20 weeks of gestation or within 48 hours of delivery.
Absence of seizures differentiates it from eclampsia. Right upper quadrant pain, nausea, and vomiting may be the presenting features. Aminotransferase levels can depend on 10 times the top limit of normal. Bilirubin concentrations are normal usually. These abnormalities typically resolve within 2 weeks of delivery. Though atypical clinical presentations have been known with preeclampsia-particularly as extremes of maternal childbearing age have been associated with preeclampsia-the patient’s normal BP and an absence of proteinuria make both preeclampsia and eclampsia unlikely. HELLP syndrome usually comes up in the next or third trimester of being pregnant but can also develop after delivery.
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Right upper quadrant and epigastric pain, nausea, and vomiting are usual presenting symptoms. Hypertension and proteinuria are located in 85% of instances.3 Lack of hypertension and proteinuria and normal microangiopathic blood smear and platelet count number make HELLP symptoms unlikely in the individual. AFLP usually presents in the 3rd trimester of being pregnant with nausea, abdominal pain, jaundice, and hepatic encephalopathy.
The hypoglycemia, lactic acidosis, hyperammonemia, and disseminated intravascular coagulation might complicate the clinical picture. Leukocytosis occurs in 98% of patients.4 Elevated concentrations of bilirubin, aminotransferases, and uric acid are commonly found. The biochemical picture inside our patient does not match that of AFLP and makes this diagnosis unlikely. Remaining potential diagnoses. Hepatitis C and B are options and must be excluded by appropriate serologic exams. The hepatitis A viral infection usually follows a far more severe course in pregnancy. Pregnant women will acquire hepatitis E in the third or second trimester. Also, though it is rare for autoimmune hepatitis to first appear during pregnancy, it too must be ruled out.