Congenital absence of the pericardium, also known as pericardial agenesis, is an extremely rare anomaly. Although most cases are asymptomatic, some experience chest pain, dyspnea, dizziness, and syncope. A few sudden death cases have been reported. We report a case of congenital complete left-sided absence of the pericardium that is not related to the cause of death. In the autopsy of a skinny 45-year-old deceased man, there was no left pericardium, and the heart had direct contact with the left lung. Inflammation and adhesion around the heart, torsion of great vessels, structure abnormality of the heart, and histologic lesion of the myocardium were absent. Due to the chemical analysis result and morphology, we suspected that the cause of death was related to starvation. The congenital absence of the pericardium is usually accompanied by myocardial infarction, aortic dissection, and variable congenital anomalies in the heart and other organs. Additionally, both complete and partial defects can cause myocardial infarction. Therefore, we suggest that precise gross examination should be performed to determine the ischemic lesions in the heart and other anomalies if congenital absence of the pericardium is noted in the autopsy.

Ethylene glycol (EG), commonly used as antifreeze, is frequently ingested accidentally or in suicides, and causes acute renal failure. We report an unusual case of EG poisoning with acute liver injury. After vomiting and loss of consciousness, a 48-year-old male was admitted to the emergency room. Despite prompt conservative treatment for metabolic acidosis, kidney function deteriorated, necessitating the continuous renal replacement therapy. Blood toxicology results, showing EG levels of 510 mg/L, arrived 10 hours after admission. Oral ethyl alcohol therapy commenced 16 hours post-admission. By 36 hours, liver function tests indicated significant liver damage, and the patient died 45 hours upon admission. On autopsy, histological findings were hepatic centrilobular necrosis, cerebral perivascular neutrophilic and lymphocytic infiltration with calcium oxalate deposition, and renal tubular necrosis with calcium oxalate deposition. EG concentrations in the blood and gastric contents were 18.7 mg/L and 45.0 mg/L, respectively. Glycolic acid and oxalic acid, metabolites of EG produced by alcohol dehydrogenase in the liver, cause metabolic acidosis, renal tubular calcium oxalate deposition, and acute renal failure, leading to death. Generally, because fomepizole or ethyl alcohol block alcohol dehydrogenase in the liver, acute liver injury by EG poisoning is rare. To the best of authors’ knowledge, only one relevant report was found in the literature described a case in which EG caused centrilobular necrosis in liver. In the current case, delays in diagnosis and antidote therapy without gastric lavage allowed continued metabolism of EG which led to acute liver injury and acute renal failure.

Ethylene glycol (EG), commonly used as antifreeze, is frequently ingested accidentally or in suicides, and causes acute renal failure. We report an unusual case of EG poisoning with acute liver injury. After vomiting and loss of consciousness, a 48-year-old male was admitted to the emergency room. Despite prompt conservative treatment for metabolic acidosis, kidney function deteriorated, necessitating the continuous renal replacement therapy. Blood toxicology results, showing EG levels of 510 mg/L, arrived 10 hours after admission. Oral ethyl alcohol therapy commenced 16 hours post-admission. By 36 hours, liver function tests indicated significant liver damage, and the patient died 45 hours upon admission. On autopsy, histological findings were hepatic centrilobular necrosis, cerebral perivascular neutrophilic and lymphocytic infiltration with calcium oxalate deposition, and renal tubular necrosis with calcium oxalate deposition. EG concentrations in the blood and gastric contents were 18.7 mg/L and 45.0 mg/L, respectively. Glycolic acid and oxalic acid, metabolites of EG produced by alcohol dehydrogenase in the liver, cause metabolic acidosis, renal tubular calcium oxalate deposition, and acute renal failure, leading to death. Generally, because fomepizole or ethyl alcohol block alcohol dehydrogenase in the liver, acute liver injury by EG poisoning is rare. To the best of authors’ knowledge, only one relevant report was found in the literature described a case in which EG caused centrilobular necrosis in liver. In the current case, delays in diagnosis and antidote therapy without gastric lavage allowed continued metabolism of EG which led to acute liver injury and acute renal failure.

Ethylene glycol (EG), commonly used as antifreeze, is frequently ingested accidentally or in suicides, and causes acute renal failure. We report an unusual case of EG poisoning with acute liver injury. After vomiting and loss of consciousness, a 48-year-old male was admitted to the emergency room. Despite prompt conservative treatment for metabolic acidosis, kidney function deteriorated, necessitating the continuous renal replacement therapy. Blood toxicology results, showing EG levels of 510 mg/L, arrived 10 hours after admission. Oral ethyl alcohol therapy commenced 16 hours post-admission. By 36 hours, liver function tests indicated significant liver damage, and the patient died 45 hours upon admission. On autopsy, histological findings were hepatic centrilobular necrosis, cerebral perivascular neutrophilic and lymphocytic infiltration with calcium oxalate deposition, and renal tubular necrosis with calcium oxalate deposition. EG concentrations in the blood and gastric contents were 18.7 mg/L and 45.0 mg/L, respectively. Glycolic acid and oxalic acid, metabolites of EG produced by alcohol dehydrogenase in the liver, cause metabolic acidosis, renal tubular calcium oxalate deposition, and acute renal failure, leading to death. Generally, because fomepizole or ethyl alcohol block alcohol dehydrogenase in the liver, acute liver injury by EG poisoning is rare. To the best of authors’ knowledge, only one relevant report was found in the literature described a case in which EG caused centrilobular necrosis in liver. In the current case, delays in diagnosis and antidote therapy without gastric lavage allowed continued metabolism of EG which led to acute liver injury and acute renal failure.

Ethylene glycol (EG), commonly used as antifreeze, is frequently ingested accidentally or in suicides, and causes acute renal failure. We report an unusual case of EG poisoning with acute liver injury. After vomiting and loss of consciousness, a 48-year-old male was admitted to the emergency room. Despite prompt conservative treatment for metabolic acidosis, kidney function deteriorated, necessitating the continuous renal replacement therapy. Blood toxicology results, showing EG levels of 510 mg/L, arrived 10 hours after admission. Oral ethyl alcohol therapy commenced 16 hours post-admission. By 36 hours, liver function tests indicated significant liver damage, and the patient died 45 hours upon admission. On autopsy, histological findings were hepatic centrilobular necrosis, cerebral perivascular neutrophilic and lymphocytic infiltration with calcium oxalate deposition, and renal tubular necrosis with calcium oxalate deposition. EG concentrations in the blood and gastric contents were 18.7 mg/L and 45.0 mg/L, respectively. Glycolic acid and oxalic acid, metabolites of EG produced by alcohol dehydrogenase in the liver, cause metabolic acidosis, renal tubular calcium oxalate deposition, and acute renal failure, leading to death. Generally, because fomepizole or ethyl alcohol block alcohol dehydrogenase in the liver, acute liver injury by EG poisoning is rare. To the best of authors’ knowledge, only one relevant report was found in the literature described a case in which EG caused centrilobular necrosis in liver. In the current case, delays in diagnosis and antidote therapy without gastric lavage allowed continued metabolism of EG which led to acute liver injury and acute renal failure.

Mucinous borderline tumors (MBT) of the ovary with mild to moderately atypical epithelial cells that produce mucin rarely recur and very rarely become malignant after surgery. Due to their low malignant potential and large tumor size, most cases are diagnosed in stage I and have a good prognosis. The authors reported a case of MBT, which had been left untreated after diagnosis, progressed to stage IV, and caused massive pleural effusion (>3,000 mL) resulting in death. Grossly, severe abdominal swelling, a huge multiloculated cystic mass in the left ovary, and a metastatic mucinous mass in the pleura and peritoneum were observed. Histological findings include gastrointestinal type epithelial cells with mucin secretion, degenerative and autolytic nuclei, and occasional infiltration of inflammatory cells. Because sufficient sections cannot be made according to the clinical pathology criteria in forensic autopsy, efficient decisions are required during autopsy for diagnosis.