Hypoxic hepatitis as a complication of newly diagnosed type 1 diabetes in a teenager

Abstract

Hypoxic hepatitis is a rare complication of type 1 diabetes with unknown prevalence in Pediatrics. We present a case report of an 11-year-old boy admitted to the ER in the spring of 2020 (the beginning of the COVID19 pandemic in Poland) due to nausea, abdominal pain, and weight loss. A diagnosis of type 1 diabetes accompanied by severe ketoacidosis (pH 6.9, blood glucose 632mg/dl, ketone bodies in urine - 150mg/dl) was made. The hyperglycemia, ketoacidosis, and water-electrolyte disturbances were treated in the Pediatric Intensive Care Unit. On day 4, the boy developed fulminant septic shock with high aminotransferases (AST 9026 U/l, ALT 3559 U/l). CT scan revealed hepatic enlargement and steatosis. Acute viral hepatitis was suspected. The levels of anti-CMV IgM and IgG antibodies were slightly elevated. At autopsy, the liver was enlarged, with petechial bleedings on the surface. The liver parenchyma was congested, with signs of steatosis. Microscopically, there was extensive centrilobular necrosis, acute passive sinusoidal congestion, and steatosis of hepatocytes. There were no signs of CMV infection. Based on the entire clinicopathological picture, the patient was diagnosed with hypoxic hepatitis, complicated by septic shock and multiple organ failure.

Keywords: Autopsy; Diabetes Mellitus; Gastroenterology; Hepatitis; Pediatrics.

Figure 1. A – The abdominal CT scan shows unevenly distributed liver steatosis and hepatomegaly; B – CT scan of the lungs shows peribronchial parenchymal consolidation and a small amount of fluid in both pleural cavities.

Figure 2. Photomicrographs of: A – Liver – the areas of centrilobular necrosis and passive and passive sinusoidal congestion with relatively preserved periportal hepatocytes (H&E, 4X); B – Early hepatocyte necrosis and passive sinusoidal congestion (left side) and preserved hepatocytes with features of steatosis (right side) (H&E, 20X); C, D – The areas of petechial bleedings in liver parenchyma and the subcapsular area (H&E, 40X).

Figure 3. Photomicrographs of: A – Pancreas – pancreatic islet with disturbed architecture, surrounded by lymphocytic infiltrate (H&E, 40X); B – Pancreas - abnormal pancreatic islet structure highlighted by synaptophysin staining (20X); C – Lungs – area of early bronchopneumonia (H&E, 20X); D – Lungs - signs of passive congestion with hyaline membranes formation (H&E, 40X).