Liver laceration presented as intraabdominal bleeding in a newborn with hypoxic-ischemic encephalopathy

Introduction

A birth injury is one of the main causes of newborn mortality and morbidity. It usually occurs with two different mechanisms: trauma due to mechanic stress during labor and hypoxic-ischemic injury [1]. Sometimes these two mechanisms can occur at the same time and present a complex clinical picture. In this report, we present a baby girl born after a difficult labor, diagnosed with hypoxic-ischemic encephalopathy (HIE), and presented with intraabdominal bleeding caused by the liver laceration. Abdominal bleeding secondary to mechanical laceration of the liver is hard to diagnose and our case shows that it may coexist with perinatal asphyxia [2].

Case presentation

The baby girl was born by vaginal delivery at 37^2/7 weeks to a 36-year-old gravida 2, para two mother with a prolonged second stage of labor and difficult birth, weighing 3,725 g. There was no use of vacuum extraction or forceps during labor. The mother was diagnosed with urinary tract infection and gestational diabetes mellitus. There was no consanguinity between the parents and no family history of hereditary coagulation disorder. The baby was intubated in the delivery room due to the absence of breathing. Apgar scores were 3, 3, and 5 at 1, 5 and, 10 min of life respectively. On physical examination the patient appeared lethargic, there was a 5 × 6 cm bruise on the right temporoparietal region and, right brachial plexus paralysis was identified. Sarnat score evaluated grade 2 and Thompson score was 12. Umbilical cord sampling revealed a pH of 6.68 and a base excess of −35 mmol/L. The patient was admitted to the Neonatal Intensive Care Unit with the diagnosis of HIE.

On admission, therapeutic hypothermia was started. In the second hour of life, the baby suffered a repeated myoclonic seizure and was started phenobarbital and levetiracetam respectively. Dopamine, dobutamine, and adrenalin infusion were initiated for hypotension and poor peripheral perfusion. An echocardiographic evaluation revealed 2 mm patent ductus arteriosus, ejection fraction 71%, and fractional shortening 44%. Liver function tests (aspartate transaminase (AST) 1592 U/L; alanine transaminase (ALT) 250 U/L) and kidney function tests (creatinine 2.35 mg/dL) were found to be severely elevated and she was diagnosed with multiorgan failure. During follow-up, coagulation parameters were impaired (prothrombin time (PT) 65.4 s; activated partial thromboplastin time (aPTT) 62.4 s), thrombocytopenia developed (platelet 45,000/mm³), and hematocrit decreased to 20.9%. Because of the hemodynamic instability and coagulopathy, therapeutic hypothermia stopped on the first postnatal day. Packed red blood cells, platelets, and fresh frozen plasma were transfused. Cephalohematoma was detected on the cranial computed tomography (CT) scan that was taken to identify the source of bleeding (Figure 1A). Abdominal ultrasonography revealed intra-abdominal fluid. Diffusion magnetic resonance imaging (MRI) showed hyperintense areas (Figure 1B, D and E) in the white matter of frontal and parietal lobes of cerebral hemispheres in T2 A sequences.

Figure 1:

(A) Cephalohematoma in cranial CT (arrow). (B, D, E) Diffusion MRI, showing hyperintense areas in the T2 A sequences in the white matter of frontal and parietal lobes of cerebral hemispheres (arrows). (C) Laceration in the liver capsule (arrow).

In the follow-up, at the 36th hour, the patient had no urine output, kidney function tests were impaired further and hyperuricemia (uric acid 15.3 mg/dl) was detected. The decision was made to start on peritoneal dialysis on the second postnatal day. While attempting the peritoneal dialysis catheter insertion, bleeding was detected in the peritoneal cavity and the procedure was canceled. 400 mL of blood was drained from the peritoneal cavity. A laparotomy was performed to find the source of the bleeding. Laceration in the liver capsule on the right lobe was detected and appeared to be the source of bleeding and was repaired (Figure 1C). Bleeding was controlled with coagulation and hemostatic agents. No injury was observed in the liver parenchyma.

On the fifth postnatal day, the baby had 2000 gr excess compared to birth weight, hypertension, and urine output was 0.3 mL/kg/h. Hemodialysis was started by inserting a central jugular catheter. After 5 days of hemodialysis treatment edema reduced, urine output increased, blood pressure measurements returned to normal and the patient was extubated. The findings in the neurological examination regressed. On the 65th postnatal day, the baby was discharged with a nasoduodenal feeding catheter.

During the fourth month of outpatient follow-up, the patient recovered physically and neurologically. Kidney function tests were improving (creatinine 0.65 mg/dl) and liver function tests were slightly elevated (AST 64 U/L; ALT 24 U/L). Coagulation factor values were found to be normal (PT 13.9 s; aPTT 30.2 s). The weight and height were under the third percentile and the head circumference was between the third and tenth percentile.

Discussion

Although birth-related traumas tend to decrease gradually in the last years, they remain one of the important causes of neonatal morbidity and mortality. Macrosomia, prematurity, use of vacuum or forceps, prolonged or rapid delivery are among the most important known risk factors [1, 3]. Neonatal liver injury is one of the serious birth traumas presenting with nonspecific findings. Its soft and vascular structure makes the newborn liver very sensitive to trauma. Liver trauma causes subcapsular hematoma and rupture of hematoma results in abdominal bleeding [3]. It is difficult to detect since initial symptoms may be nonspecific and it is not frequent. In autopsies of 783 babies lost in the neonatal period, 15% hepatic hematoma was detected [2]. Serious life-threatening liver bleeding has been reported in a newborn born at 36 gestational weeks with a history of early rupture of membranes, and in two newborns diagnosed with hemophilia A [4, 5]. Our case was born after the prolonged second stage of labor with low Apgar scores and acidemia needing resuscitation and was diagnosed as HIE.

Perinatal asphyxia could also be the reason for bleeding since it causes clotting disorders by disrupting the balance of hemostasis, both by increasing the tendency to bleeding and by being predisposed to thrombosis [6]. Jha et al. [7] evaluated coagulation parameters and platelet counts in 126 newborns with perinatal asphyxia and compared them with the control group consisting of 150 newborns. PT and aPTT values were found to be significantly higher and platelet counts significantly lower in babies with perinatal asphyxia.

When evaluating newborns with HIE and difficult birth history it should be considered that these patients may develop intraabdominal organ lacerations due to mechanical trauma as well. Timely diagnosis and treatment are imperative to decrease mortality and morbidity however the initial insidious presentation of liver laceration makes early diagnosis difficult. The liver laceration is hard to diagnose on physical examination and many cases are diagnosed at autopsy [2]. This prompted us to report a case with abdominal bleeding secondary to mechanical laceration of the liver that coexisted with perinatal asphyxia.