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Toxemia of pregnancy Case 15.2 Chapter 15 1
Miscellaneous Hepatic Disorders 1 Toxemia of pregnancy Case 15.2
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Clinical Presentation
15 Miscellaneous Hepatic Disorders 2 Clinical Presentation A 29-year-old woman (gravida 3, Para 1, Ab 1) was in her 38th week of gestation when she developed epigastric pain and dyspnea for several hours duration. She was not in labor and had no signs of other problems. On admission her blood pressure was 260/160, and on physical exam there was bilateral papilledema, 1+ peripheral edema, a gravid uterus with no contractions, and a fetal heart beat of 104/min.
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Laboratory Values Course in Hospital AST: 1150 ALT: 185
Miscellaneous Hepatic Disorders 3 Laboratory Values AST: 1150 ALT: 185 Total Bilirubin: 2.5 Total Protein: 5.8 WBC: 25,000 with 84% neutrophils Course in Hospital About 15 min after admission the patient suffered seizures. Neurologic exam showed little brain function. A term stillborn infant was delivered. Post-operatively the patient had considerable bleeding. She remained comatose and expired. An autopsy was performed.
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Pathology 15 4 Miscellaneous Hepatic Disorders
Patchy predominantly periportal liver cell necrosis was present with variable periportal sinusoidal dilatation and abundant fibrin deposited within these periportal sinusoids and amongst the necrotic hepatocytes, without any definite lobular inflammation (a). Figure 15.2(a)
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15 Miscellaneous Hepatic Disorders 5 Diagnosis Toxemia of pregnancy (“eclampsia” due to the occurrence of seizures)
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15 Miscellaneous Hepatic Disorders 6 Comment Toxemia (pre-eclampsia) of pregnancy occurs during the third trimester of pregnancy and is manifested by hypertension, proteinuria, and peripheral edema, with the term eclampsia used when complications of seizures also occur (as in this case example). The liver shows hepatocellular necrosis, usually in the periportal zones, with little accompanying inflammation in the parenchyma or portal tracts; however, fibrin deposition within the periportal sinusoids is prominent and can best be appreciated with the PTAH stain for fibrin. The small arteries and arterioles may also show fibrin deposition. In the more severe cases, extensive confluent necrosis and even liver cell rupture can develop.
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