Indian Journal of Critical Care Case Report
Volume 2 | Issue 6 | Year 2023

Massive Hepatic Infarct in a Patient with Eclampsia: A Rare Case Report

Shivnath Dudala1, Shashidhar Pulgam2

1,2Department of Critical Care, Yashoda Hospitals, Hyderabad, Telangana, India

Corresponding Author: Shashidhar Pulgam, Department of Critical Care, Yashoda Hospitals, Hyderabad, Telangana, India, Phone: +919542594824, e-mail:

Received on: 26 April 2023; Accepted on: 06 October 2023; Published on: 01 December 2023


Hepatic infarction is rare due to the unique dual hepatic blood supply from the hepatic artery and the portal vein. Here, we report a case of massive hepatic infarction that occurred as a complication of eclampsia followed by hemolysis, elevated liver enzymes, and low platelets (HELLP). A 30-year-old G2P1D1 female patient of 32 weeks gestation with gestational hypertension (diagnosed at 24 weeks of gestation) presented to the ER with low backache, pedal edema, and generalized tonic-clonic seizure (GTCS) lasting for 30 seconds. This patient was diagnosed with eclampsia followed by HELLP, which was further complicated by massive hepatic infarction, and was diagnosed with computed tomography (CT) of the abdomen and pelvis.

How to cite this article: Dudala S, Pulgam S. Massive Hepatic Infarct in a Patient with Eclampsia: A Rare Case Report. Indian J Crit Care Case Rep 2023;2(6):165–167.

Source of support: Nil

Conflict of interest: None

Patient consent statement: The author(s) have obtained written informed consent from the patient for publication of the case report details and related images.

Keywords: Case report, Computed tomograph, Eclampsia, Gestational hypertension, Hemolysis, elevated liver enzymes, and low platelets syndrome, Massive hepatic infarction


Preeclampsia is a pregnancy disorder in which a person has hypertension and proteinuria with or without associated systemic abnormalities involving the kidneys, liver, or blood and/or unexplained coma during pregnancy or after delivery in a woman.1,2

Hemolysis syndrome with microangiopathic blood smear, elevated liver enzymes and low platelet count, commonly known as hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome in pregnant and postpartum patients, may represent a complication or progression of severe preeclampsia. Recent data shows increasing evidence indicating that HELLP syndrome is an acute inflammatory condition and an impaired immunological process induced by the placenta, which targets the liver.3 The systemic ligand cluster of differentiation (CD95) is a placental-derived humoral factor involved in the pathogenesis of HELLP syndrome. CD95 (apolipoprotein-1, Fas; tumor necrosis factor receptor superfamily member 6)-mediated apoptosis of hepatic cells is a major pathogenic mechanism for liver disease in general. Apoptosis in liver tissue and cytotoxic activity for primary human hepatocytes have been reported in the serum of patients with HELLP syndrome. Blocking CD95 signalling may reduce the hepatocytotoxic activity of HELLP syndrome.4

Massive liver infarction is a fatal condition which causes preeclampsia-eclampsia-related death in 11% of patients, but fortunately, it is a very rare complication due to the dual blood supply of the liver. Severe vasospasm associated with toxemic vasculopathy in the hepatic arterial circulation may play a major role in the pathophysiological features of hepatic infarction.5

Pregnancy-related liver diseases are often complex and confusing to physicians, leading to misdiagnoses and unwarranted or delayed treatment. An accurate diagnosis may not be possible based on clinical symptoms, signs and laboratory evaluation alone. Liver computed tomography (CT) is said to be the imaging modality of choice in the differential diagnosis of liver dysfunction in late pregnancy and postpartum. Characteristic imaging findings are: ”homogeneous areas of low attenuation, either wedge-shaped lesions peripherally or geographically or larger lesions with enhanced vessels passing through these hypodense areas.”6


A 30-year-old G2P1D1 patient with 32 weeks of gestation, history of previous lower segment cesarean section (LSCS) and gestational hypertension diagnosed at 24 weeks of pregnancy now presented to the hospital with complaints of low backache, pedal edema and an episode of generalized tonic-clonic seizures (GTCSs) lasting for 30 seconds. At arrival, the patient was irritable with vitals—pulse rate of 120/minute, blood pressure of 180/110 mm hg, and peripheral capillary oxygen saturation of 90% on room air. On examination, diffuse crepts were heard bilaterally, per abdomen fundal length corresponding to 32 weeks, relaxed uterus, and fetal heart sounds were heard. The patient had been treated with a loading dose of magnesium sulfate, labetalol, and furosemide. A nonstress test and reactive pediatric counseling were done, and the patient was taken up for emergency LSCS. The patient had another episode of GTCS lasting for 60 seconds on the operating table, followed by sudden cardiac arrest and was revived after one cycle of cardiopulmonary resuscitation. LSCS proceeded under general anesthesia—a female baby of birth weight of 1.2 kg delivered with APGAR scores of 5 and 9 at 1 and 5 minutes, respectively.

Labs on Day 1

Hemoglobin (Hb) of 15.1 gm/dL, total leukocyte count (TLC) of 21,200, a platelet count of 1.3 lakhs, creatinine of 1.0, bilirubin of 3.3 with direct bilirubin/indirect bilirubin of 1.9/1.4, serum glutamic pyruvic transaminase (SGPT) of 163, serum glutamic oxaloacetic transaminase (SGOT) of 361, alkaline phosphatase of 245, albumin/globulin of 1.8/1.9, magnesium of 3.0, and an international normalized ratio (INR) of 1.0.

On postoperative day (POD) 0, the patient had atonic postpartum hemorrhage, for which the patient was treated conservatively with intravenous tranexamic acid, misoprostol per rectal (P/R) tabs, and 4 units of fresh frozen plasma (FFP) transfusion.

On POD 1, she had a drop in urine output with repeat labs suggesting a drop in hemoglobin, platelets, and worsening creatinine and liver functions—Hb of 10.4, TLC of 29,110, platelet count of 59,000, serum creatinine of 2.1, worsening transaminitis (SGPT 371 and SGOT 714), an INR of 1.34, and fibrinogen 161. Drain output was 200 mL serosanguinous fluid. A total of 6 units of cryoprecipitate and 2 units of FFP were transfused and underwent the first session of dialysis.

Repeat labs on POD 3 are suggestive of a drop in hemoglobin platelets, worsening liver function tests with raised bilirubin, worsening transaminitis (SGOT 3870 and SGPT 2640), an ALP of 1575, lactate dehydrogenase 1812. In view of persistent low Glasgow Coma Scale, a magnetic resonance imaging brain was done, which showed areas of altered signal intensity with subtle restricted diffusion posteriorly in cerebral hemispheres in bilateral temporo-parieto-occipital regions (left > right suggestive of posterior reversible encephalopathy syndrome.

In view of persistent high serum bilirubin with transaminitis (total bilirubin of 23.8 with direct bilirubin of 19.3), high drain output and abdominal distension—contrast-enhanced CT (CECT) abdomen was done, which revealed hepatomegaly with multiple hepatic infarcts largest in the right lobe, few foci of pneumoperitoneum seen anterior to the liver, organizing hematoma seen in pelvis, predominantly on the right side (Fig. 1).

Figs 1A and B: Contrast-enhanced CT (CECT) abdomen—suggestive of (S/O) hepatomegaly with multiple hepatic infarcts, largest in the right lobe and organizing hematoma seen in the pelvis

The patient was managed conservatively with supportive treatment and dialysis support for acute kidney injury. In view of the anticipated prolonged ventilatory requirement, a tracheostomy was done, and the patient was weaned to a portable ventilator.

Periodically, all invasive lines have been screened and removed, as culture has grown XDR-Klebsiella pneumoniae from dialysis sheath. As per Carba’s report, antibiotics were optimized to ceftazidime-avibactam + aztreonam, which was given for 10 days after line removal. RT feeds initiated, titrated and fibre-based diet given in view of feed intolerance.

During the subsequent day, repeat labs showed an improving trend of hemoglobin, platelet and liver function tests—labs—Hb 8.4 gm/dL, platelets 3.32 lakhs, INR 1.4, liver function—total bilirubin of 14.7 with direct bilirubin of 12, SGOT 165, SGPT 59. The patient was tolerating thermovent during the daytime and on portable ventilator support at nighttime, and the patient was tolerating a fiber-based diet well. The patient was discharged in a hemodynamically stable state to a rehabilitation center for further continuation of tracheostomy care, physiotherapy, dialysis, and nutrition.


Extensive liver infarction is a fatal finding of pregnancy in patients with HELLP syndrome. It is difficult to diagnose because the findings and symptoms are nonspecific. Doctors should always pay attention to pregnant women with complaints of hypertension, epigastrium or shoulder pain. In conclusion, preeclamptic patients with HELLP syndrome who complain of severe epigastric or right upper quadrant pain should undergo liver imaging.


Shivnath Dudala


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