LAUSR

Learning Objectives: Left ventricular noncompaction (LVNC) is an anatomical diagnosis of prominent ventricular trabeculations in the LV cavity. Clinical presentations range from asymptomatic incidental findings to congestive heart failure (CHF), arrhythmia, and stroke. Methods: We describe a unique case of a 7-year-old male with chronic abdominal pain and acute liver injury secondary to LV failure and discuss the therapeutic considerations from associated coagulopathy and LV thrombus formation. One month prior to presentation, the patient was seen in the ED for suicidal ideation due to inability to play with his peers. He returned two weeks later with nausea, vomiting, anorexia, abdominal pain, and fatigue. An ultrasound ruled out appendicitis and choledocolithiasis. The pain and vomiting persisted, he returned one week later with pulmonary (tachypnea, CXR with cardiomegaly and pulmonary edema) and systemic (hepatomegaly, JVD, peripheral edema, and hepatovenous congestion) venous congestion and cardiogenic shock. Labs were significant for metabolic acidosis, lactate of 5.6, transaminitis with AST and ALT of 1224, 846 respectively, hyperbilirubinemia and elevated coagulation markers (PTT 38.9, INR 3.91). His liver enzymes were markedly elevated from his visit one week prior (AST/ALT 55/56). Echocardiogram showed LV apical hypertrabeculation with severe dilation, (LVEDDD Z score 7.9), global hypokinesis, and systolic dysfunction (LVEF 17%, SF 6%). Additionally, there was a well circumscribed echogenic mass (3x2cm) concerning for an LV thrombus. Therapy was initiated with furosemide, milrinone, and low molecular weight heparin despite the initial coagulopathy, out of concern for thromboembolic events. He underwent clot removal and BiVAD placement and is awaiting cardiac transplant. Results: In conclusion, pediatric presentations of cardiomyopathies vary. This case demonstrates that abdominal complaints are a common presenting symptom of CHF across all age groups. Abdominal pain as a sign of CHF can be easily missed. In addition, therapy in LVNC can be complicated by coexisting coagulopathy from liver injury and the hypercoagulable environment from stagnant blood flow in the LV.