Posters
Academic Level (Author 1)
Resident
Discipline/Specialty (Author 1)
Internal Medicine
Discipline Track
Clinical Science
Abstract
Introduction: Hypoxic hepatitis (HH) also known as ischemic hepatitis is the result of a hypoperfusion state during diffuse hepatic injury1. The incidence of HH is 2:1000 of patients within any hospital care level. 94% of HH are related to chronic heart failure (HF). In this setting, hepatic dysfunction occurs as a result of passive venous congestion2. The most common predisposing factors are acute heart failure and shock states, however, more than half of the cases are not related to any hemodynamic change, thus, underrecognized.
Case description: A 77-year-old woman is admitted to the hospital for acute decompensated HF. She has a medical history of HF with reduced EF of 30%, paroxysmal atrial fibrillation, coronary artery disease with bypass grafting. Medication lists include sacubitril-valsartan, furosemide, metoprolol, and amiodarone. Upon admission, vital signs are within normal limits, she is in mild respiratory distress, with JVD at 3 cm, upper lobe crackles and wheezing on lung fields, and lower extremity non-pitting edema. Laboratory studies showed BUN/Cr 29/1.4 mg/dl, AST 377 IU/L, ALT 295 IU/L, BNP >4500, troponin 0.3, with unremarkable ECG. The patient was started on furosemide, and amiodarone and sacubitril-valsartan are suspended due to suspected hepatic toxicity and acute kidney injury, respectively. Echocardiogram reported EF 20-25% with severe diffuse hypokinesis, RVSP of 54 mmHg, tricuspid valve with moderate-severe regurgitation. The abdominal US with a prominence of the hepatic veins and inferior vena cava. Patient LFTs continued to trend up during hospitalization, with a peak in AST 2080 IU/L, ALT 1371IU/L, ALP 75IU/L, total bilirubin 1.1 mg/dL. Viral serologic markers were negative as well as a workup for autoimmune hepatitis, and primary biliary cholangitis. Gastroenterology is consulted, the patient is initiated on N-Acetylcysteine, and transaminases trended down.
Admission
Day 3
Day 8
AST
377
2080
69
ALT
295
1371
319
Discussion: The prevalence of hepatic dysfunction in acute HF is 20% to 30%. The mechanism of injury was previously thought to be solely related to HF, however, new studies suggest that patients with underlying liver conditions and even mild hemodynamic changes are predisposed to develop HH. The mechanism involves the liver’s high metabolic demands and oxygen requirements. The hepatocytes compensate for impaired blood flow by increasing oxygen extraction, which may lead to hepatocellular hypoxia and necrosis. HH is diagnosed clinically by three main criteria, 1. Presence of cardiac, circulatory, or pulmonary failure; 2. Severe and transient increase in aminotransferase levels >20 times the upper limit of normal and 3. Exclusion of other possible causes of liver damage. HH is usually self-limited, and aminotransferases trend down within 3-5 days, however fulminant hepatic failure can develop. Management involves treating underlying HF, as there is no specific treatment for HH. In our case, the progression of the HF was the cause that explained the acute increase in transaminases. It is important to keep in mind the gastrointestinal manifestation of HF, furthermore, that even with mild circulatory changes patients can develop HH.
Presentation Type
Poster
Recommended Citation
Pedraza Sanchez, Lina; Rivera, Jose; Rivas, Cynthia; Rapoport, Grigoriy; and Lopez, Michelle, "It takes a big heart to shape atrophic hepatocytes: Hypoxic hepatitis secondary to congestive heart failure" (2023). Research Colloquium. 21.
https://scholarworks.utrgv.edu/colloquium/presentation/poster/21
It takes a big heart to shape atrophic hepatocytes: Hypoxic hepatitis secondary to congestive heart failure
Introduction: Hypoxic hepatitis (HH) also known as ischemic hepatitis is the result of a hypoperfusion state during diffuse hepatic injury1. The incidence of HH is 2:1000 of patients within any hospital care level. 94% of HH are related to chronic heart failure (HF). In this setting, hepatic dysfunction occurs as a result of passive venous congestion2. The most common predisposing factors are acute heart failure and shock states, however, more than half of the cases are not related to any hemodynamic change, thus, underrecognized.
Case description: A 77-year-old woman is admitted to the hospital for acute decompensated HF. She has a medical history of HF with reduced EF of 30%, paroxysmal atrial fibrillation, coronary artery disease with bypass grafting. Medication lists include sacubitril-valsartan, furosemide, metoprolol, and amiodarone. Upon admission, vital signs are within normal limits, she is in mild respiratory distress, with JVD at 3 cm, upper lobe crackles and wheezing on lung fields, and lower extremity non-pitting edema. Laboratory studies showed BUN/Cr 29/1.4 mg/dl, AST 377 IU/L, ALT 295 IU/L, BNP >4500, troponin 0.3, with unremarkable ECG. The patient was started on furosemide, and amiodarone and sacubitril-valsartan are suspended due to suspected hepatic toxicity and acute kidney injury, respectively. Echocardiogram reported EF 20-25% with severe diffuse hypokinesis, RVSP of 54 mmHg, tricuspid valve with moderate-severe regurgitation. The abdominal US with a prominence of the hepatic veins and inferior vena cava. Patient LFTs continued to trend up during hospitalization, with a peak in AST 2080 IU/L, ALT 1371IU/L, ALP 75IU/L, total bilirubin 1.1 mg/dL. Viral serologic markers were negative as well as a workup for autoimmune hepatitis, and primary biliary cholangitis. Gastroenterology is consulted, the patient is initiated on N-Acetylcysteine, and transaminases trended down.
Admission
Day 3
Day 8
AST
377
2080
69
ALT
295
1371
319
Discussion: The prevalence of hepatic dysfunction in acute HF is 20% to 30%. The mechanism of injury was previously thought to be solely related to HF, however, new studies suggest that patients with underlying liver conditions and even mild hemodynamic changes are predisposed to develop HH. The mechanism involves the liver’s high metabolic demands and oxygen requirements. The hepatocytes compensate for impaired blood flow by increasing oxygen extraction, which may lead to hepatocellular hypoxia and necrosis. HH is diagnosed clinically by three main criteria, 1. Presence of cardiac, circulatory, or pulmonary failure; 2. Severe and transient increase in aminotransferase levels >20 times the upper limit of normal and 3. Exclusion of other possible causes of liver damage. HH is usually self-limited, and aminotransferases trend down within 3-5 days, however fulminant hepatic failure can develop. Management involves treating underlying HF, as there is no specific treatment for HH. In our case, the progression of the HF was the cause that explained the acute increase in transaminases. It is important to keep in mind the gastrointestinal manifestation of HF, furthermore, that even with mild circulatory changes patients can develop HH.