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Spontaneous rupture of subcapsular liver hematoma in sudden onset severe preeclampsia

Shikha Rani

Department of Obstetrics and Gynecology, Government Medical College and Hospital Chandigarh, India

E-mail : bhuvaneswari.bibleraaj@uhsm.nhs.uk

Reeti Mehra

Department of Obstetrics and Gynecology, Government Medical College and Hospital Chandigarh, India

Sunita Dubey

Department of Obstetrics and Gynecology, Government Medical College and Hospital Chandigarh, India

Shefali Wadhwani

Department of Obstetrics and Gynecology, Government Medical College and Hospital Chandigarh, India

Kumar Abhishek

Department of Obstetrics and Gynecology, Government Medical College and Hospital Chandigarh, India

DOI: 10.15761/CCRR.1000505

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Background: Rupture of subcapsular liver hematoma in pregnancy is a nightmare. It is associated with almost 50% maternal and fetal death. It should be kept as one of the differential diagnoses for the sudden antepartum collapse in pregnancy with hypertensive.

Case: We are reporting a case of 30 years primigravida at 30weeks who had a sudden onset of severe preeclampsia with severe epigastric pain. Within a few hours, she developed severe hypotension. Resuscitation was started and bed-side ultrasonography revealed massive hemo-peritoneum with a dead fetus. The patient was shifted for a laparotomy. Intra-operatively, uterine contour was maintained with massive hemoperitoneum. There was a rupture of subcapsular hematoma with pale liver and multiple petechiae.

Conclusion: A possibility of subcapsular hematoma must be kept in hypertension of pregnancy with severe epigastric pain and hypovolemic shock.

Key words

Liver hematoma, preeclampsia, subcapsular hematoma


Spontaneous rupture of subcapsular haematoma or liver rupture in pregnancy is a rare life-threatening condition. Its incidence is 1/40,000-1/250,000 in pregnancy but is seen more frequently in hypertensive disorders of pregnancy (1-2%) [1].

Case summary

A 30 years old primigravida at 30 weeks period of gestation with oligohydramnios was admitted in the Department of Obstetrics and Gynecology for maternal and fetal surveillance. Her antenatal period was uneventful. There was no history of pain abdomen or leakage per vaginum. On admission, her vitals were pulse rate 78 per minute and blood pressure 112/74 mm of Hg. On a per speculum examination, cervix and vagina were healthy and there was no abnormal discharge or leaking. Abdominal examination revealed non-tender uterus of 28 weeks size with normal fetal heart sound. Initial lab investigation showed Hb of 13.1 gm%, platelet count of 148x109 /L. Total leucocyte count of 9.9x109/L. INR-1.0, urea-16 mg/dL, creatinine-0.8mg/dL. Serum bilirubin 0.3 mg/dL, SGOT-104IU/L, SGPT-97 IU/L. Total protein 6.5g/dL, Albumin-3.3g/dL. Spot urine for albumin by dipstick-Traces. Ultrasonography showed single live fetus of 28 weeks gestation with absent liquor, placenta was grade 2 and no gross congenital malformation. On Doppler flow study umbilical artery S/D ratio was 3.1.A diagnosis of severe oligohydroamnios with cholestasis of pregnancy was made. Patient was given tablet ursodeoxycholic acid and antenatal corticosteroids were given to accelerate lung maturity. Maternal surveillance was done by vital monitoring and fetal surveillance by daily biophysical profile. On day 4 of admission, the patient complained of severe pain in the epigastric region which was not relieved by injection ranitidine and metoclopramide. Her blood pressure record was raised for the first time to 160/110 mmHg. Spot urine albumin by dipstick was 2+. On examination, the abdomen was soft, non-tender and the uterus was relaxed. Patient was given intravenous labetalol. Patient was planned to start on magnesium sulphate for eclampsia prophylaxis and termination of pregnancy. Subsequent lab investigation showed Hb of 12.8 g%, platelet count 199x109/L, total leucocyte count- 8.8x109/L, urea-26mg/dL, creatinine-0.9 mg/dL, SGOT- 2391 IU/L, SGPT-666 IU/L. Serum amylase- 63 U/L, lipase- 34U/L. INR 1.0

Patient suddenly developed tachycardia and respiratory distress. Her pulse rate was 88/min, feeble and blood pressure was 70/40 mmHg. Immediate resuscitative measures were taken. On examination the abdomen was tender, uterine contour was not made out and the fetal heart could not be localized. Ultrasound showed intrauterine fetal demise with massive haemoperitoneum which was confirmed by paracentesis. Right lateral wall of uterus could not be made out on USG. A provisional diagnosis of uterine rupture was made, keeping in mind the possibility of rupture of rudimentary horn of uterus. Patient was shifted for a laparotomy. Intra-operatively, massive hemoperitoneum was present, 2000ml of blood drained with 550 grams of blood clots removed. Uterine contour and adnexa were normal. A dead fetus of 1200gm was delivered by caesarean section. On exploring the abdomen for the cause of hemoperitoneum, liver was found to be pale with multiple petechial hemorrhage. Generalized ooze was present from anterior surface of right and left lobe of liver. As it was generalized ooze no stitches could be placed Pringle method was tried to control bleeding from liver but haemorrhage could not be controlled. Peri-hepatic and intra-abdominal packing and packing of pelvis was done with multiple gelatin sponges and mops for controlling the bleeding from liver surface. Intra-operatively blood component therapy in the form of packed red blood cell, fresh frozen plasma, cryoprecipitate, and single donor platelet concentrate was given. Abdomen was closed and patient shifted to ICU. Resuscitation and vital monitoring were continued in the ICU. She remained hypotensive despite blood component therapy and inotropic support and succumbed to death.


Rupture of subcapsular liver hematoma is usually seen in multiparous women, early thirties and third trimester of pregnancy, hypertensive disorder of pregnancy and in the background of liver pathology [2,3].

Most accepted etiology is ischemic infarction of the liver due to the plugging of the fibrin thrombi in hepatic sinusoids. This leads to intrahepatic hemorrhage and hematoma under the Glisson’s capsule. Sometimes, periportal necrosis can cause subcapsular hematoma which gets ruptured. Rupture of the subcapsular hematoma causes intraperitoneal hemorrhage [4].

Clinical presentation of patients depends on whether hematoma remains contained in the liver or ruptures in the peritoneal cavity. Patients with contained hepatic hematoma present with abdominal and right shoulder pain, nausea and vomiting and may have severe thrombocytopenia. Rupture frequently present with hypo-volemic shock, abdominal distension, massive haemoperitoneum, respiratory difficulty [1,5]. Diagnosis can be made by ultrasound, although CT scan is sensitive. MRI can be done in less urgent situations.

Management depends on the clinical profile of the patient. Conservative and supportive management is for an isolated hematoma with a hemodynamically stable patient. Blood replacement therapy is done in these patients, percutaneous embolization of hepatic arteries can also be considered [6].

Ruptured subcapsular liver hematoma with shock is a surgical emergency. Resuscitation with component blood therapy and control of bleeding liver surface is the aim of treatment. No gold standard surgical treatment is there for control of bleeding from liver surface, however various techniques have been used. Packing of bleeding liver surface with vicryl mesh, absorbable gelatin sponge or perihepatic packing with surgical mops and drain [4]. Aldemir et al. managed two cases of liver hemtoma and rupture in HELLP syndrome. In the first case they applied deep mattress suture in liver and omentoplasty. In the second case they closed the liver defect with hemostatic absorbable gelatin sponge [7]. A supportive treatment with recombinant factor VIIIa and Pringle's method to control bleeding have also been reported in literature [8].

Shrivastava et al in a case report described the successful use of an argon beam coagulator to obtain hemostasis from ruptured liver haematoma in a patient with HELLP syndrome [9].

Hunter et al performed total hepatectomy with the creation of an end-to-side portacaval shunt in a patient at 36 weeks of gestation with massive spontaneous liver rupture following severe pre-eclampsia. The patient underwent orthotopic liver transplantation after 13 hours. Partial or extended resection of liver lobe has also been tried. Patients with hepatic failure or uncontrollable hepatic haemorrhage, liver transplant as a last resort measure must be considered where facilities of same are existent [2].

Even with quick and appropriate treatment, maternal and fetal mortality is almost 50%. Mortality is mostly due to disseminated coagulopathy and sepsis [10].


Triad of epigastric or right upper quadrant pain, early manifestation of shock- hypotension, tachycardia and history of hypertensive disorder of pregnancy or HELLP syndrome should raise a suspicion of subcapsular liver rupture.


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  10. Wicke C, Pereira PL, Neeser E, Flesch I, Rodegerdts EA, et al. (2004) Subcapsular liver hematoma in HELLP syndrome: Evaluation of diagnostic and therapeutic options--a unicenter study. Am J Obstet Gynecol 190:106-112. [Crossref]

Editorial Information


Andy Goren
University of Rome, Italy

Article Type

Research Article

Publication history

Received date: March 13, 2021
Accepted date: May 03, 2021
Published date: April 10, 2021


©2021 Rani S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


©2021 Rani S, Mehra R, Dubey S, Wadhwani S and Abhishek K (2021) Spontaneous rupture of subcapsular liver hematoma in sudden onset severe preeclampsia. Clin Case Rep Rev, 7: DOI: 10.15761/CCRR.1000505.

Corresponding author

Shikha Rani

Department of Obstetrics and Gynecology, Government Medical College and Hospital Chandigarh, India

E-mail : bhuvaneswari.bibleraaj@uhsm.nhs.uk

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