up transesophageal echocardiogram four days later showed a recovered ejection fraction (55-60%) without thrombus or vegetations. Cardiac monitoring revealed sinus tachycardia. CT angiography showed right-sided pleural effusion, bilateral cavitation, necrosis, and a pericardial effusion. Worsening right sided parapneumonic effusions required chest tube drainage with fibrinolytics. After minimal oxygen supplementation and continued care, she was discharged on amoxicillin-clavulanate, and GDMT was withheld as her cardiac function returned to baseline.
(IE). IE itself is a well-known precursor to heart failure due to structural heart damage. Although Streptococcus anginosus IE has been associated with heart failure with a reduced ejection fraction (HFrEF), HFrEF without IE due to this organism is uncommon. Similarly, Fusobacterium necrophorum is typically associated with Lemierre’s syndrome and other severe infections but is not commonly linked to IE. This patient’s acute decline in cardiac function was best explained as SIC, which likely exacerbated her symptoms and contributed to the rapid development of pleural effusions in the setting of underlying sepsis. This case adds to the growing literature on SIC.
Discussion: Streptococcus anginosus is often linked with abscess formation and infective endocarditis
SEVERE ACUTE LIVER INJURY IN THE SETTING OF CONGESTIVE HEPATOPATHY: A RARE CASE OF CARDIAC-INDUCED HEPATIC DYSFUNCTION. Sepehr Sadeghi, Allison Borst, Sanjay Kamboj; Louisiana State University, New Orleans, LA.
Introduction: Congestive hepatopathy can arise in the setting of right-sided heart failure and is generally associated with right upper quadrant abdominal pain, mild transaminitis, unconjugated hyperbilirubinemia, and rarely jaundice. Case: An 84-year-old female with heart failure (systolic and diastolic, HF), coronary artery disease (four drug-eluting stents), hypertension, hyperlipidemia, and stage 4 chronic kidney disease presented with two days of malaise and dyspnea on minimal exertion. She denied orthopnea, edema, or chest pain but reported poor appetite and a tea-and-toast diet for several days. Vitals showed blood pressure of 176/87 mmHg, pulse 75 bpm, and tachypnea at 22 bpm. Exam findings included dry mucous membranes, diffuse jaundice, scleral icterus, bibasilar crackles, and mild abdominal tenderness. Lung ultrasound showed bilateral B-lines, a dilated inferior vena cava with reduced respiratory variation, and decreased left ventricular contractility. Labs revealed sodium 121 mmol/L, creatinine 2.3 mg/dL (baseline 1.8 mg/dL), troponin-I 0.147 ng/mL (down- trended to 0.135 ng/mL), BNP >4900 ng/L, lactate 2.8 mmol/L (increased to 3.3 mmol/L), AST 903 units/L (peaked at 964units/L), ALT 944 units/L (peaked at
1213 units/L), INR 1.5, total bilirubin 2.3 mg/dL, and negative viral, COVID, and toxicology screens. Chest x-ray showed bilateral effusions, worse on the right, and abdominal ultrasound showed gallbladder wall thickening with mild pericholecystic fluid. The echocardiogram showed an ejection fraction of 26%, grade II diastolic dysfunction, and severe global hypokinesis. After significant diuresis with intravenous furosemide, the patient’s jaundice, transaminitis, hyperbilirubinemia, lactic acidosis, and acute kidney injury resolved. She was symptom-free at discharge. Discussion: This case exemplifies a significant acute liver injury (ALI) resulting from severe volume overload in acute-on-chronic HF. While elevated aminotransferases have been reported in similar cases, typical AST/ALT values are about 7.5-8 times the upper limit of normal (ULN), with median AST values reaching up to 30 times the ULN in cases of acute cardiac dysfunction without preexisting heart disease. In contrast, this case reports AST and ALT elevations, of approximately 29 and 48 times the ULN, respectively—levels more commonly observed in acute cardiac hepatopathy in individuals without preexisting cardiac conditions.
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