Background: Ischemic hepatitis (commonly referred to as shock liver and hypoxic hepa-titis) is an uncommon clinical condition associated with massive but transient elevation of liver enzymes up to more than 20 times the standard limit; without evidence of other causes of acute hepatitis such as viral, alcoholic, metabolic, and toxin-induced hepatitis. Clinically, it presents as an acute liver failure caused by decreased hepatic perfusion and oxygen delivery. It is often encountered in critically ill patients in intensive care units and can rarely be triggered by per-icardial tamponade. Case presentation: On hemodialysis, a 33-year-old end-stage renal disease male patient with hypertension and cardiomegaly presented with right upper quadrant pain. Examination revealed elevated jugular venous pressure, displaced apical beat, tender right upper quadrant and epigastric areas, and enlarged liver with a round border and soft surface. Electrocardiography revealed P mitral and electrical alternans but no ischemic changes. Chest radiography showed an increased cardiothoracic ratio and flask-shaped heart. Extensive la-boratory investigations showed elevated levels of aspartate aminotransferase (5000 U/L) and alanine aminotransferase (7000 U/L). Ultrasound showed passive congestion of the liver. Pericardial effusion was confirmed by echocardiography, and the diagnosis of cardiac tam-ponade was established. Pericardiocentesis was done, and 1200 ml of bloody fluid was aspi-rated. After pericardiocentesis, the patient demonstrated dramatic improvement. Conclusions: Ischemic hepatitis is an uncommon entity associated with a significant mortality rate, mainly when it develops on top of decreased cardiac output. Therefore, physicians must be familiar with the broad differential diagnosis for liver disease signs and symptoms and should always consider the possibility of ischemic hepatitis in such cases.

Background: Ischemic hepatitis (commonly referred to as shock liver and hypoxic hepa-titis) is an uncommon clinical condition associated with massive but transient elevation of liver enzymes up to more than 20 times the standard limit; without evidence of other causes of acute hepatitis such as viral, alcoholic, metabolic, and toxin-induced hepatitis. Clinically, it presents as an acute liver failure caused by decreased hepatic perfusion and oxygen delivery. It is often encountered in critically ill patients in intensive care units and can rarely be triggered by per-icardial tamponade. Case presentation: On hemodialysis, a 33-year-old end-stage renal disease male patient with hypertension and cardiomegaly presented with right upper quadrant pain. Examination revealed elevated jugular venous pressure, displaced apical beat, tender right upper quadrant and epigastric areas, and enlarged liver with a round border and soft surface. Electrocardiography revealed P mitral and electrical alternans but no ischemic changes. Chest radiography showed an increased cardiothoracic ratio and flask-shaped heart. Extensive la-boratory investigations showed elevated levels of aspartate aminotransferase (5000 U/L) and alanine aminotransferase (7000 U/L). Ultrasound showed passive congestion of the liver. Pericardial effusion was confirmed by echocardiography, and the diagnosis of cardiac tam-ponade was established. Pericardiocentesis was done, and 1200 ml of bloody fluid was aspi-rated. After pericardiocentesis, the patient demonstrated dramatic improvement. Conclusions: Ischemic hepatitis is an uncommon entity associated with a significant mortality rate, mainly when it develops on top of decreased cardiac output. Therefore, physicians must be familiar with the broad differential diagnosis for liver disease signs and symptoms and should always consider the possibility of ischemic hepatitis in such cases.