CARDIAC TEMPONADE SECONDARY TO ENASIDENIB-INDUCED DIFFERENTIATION SYNDROME IN A PATIENT WITH ACUTE MYELOID LEUKEMIA

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Isocitrate dehydrogenase differentiation syndrome (IDH-DS) is a life-threatening complication that occurs in patients with acute myeloid leukemia (AML) receiving target mutant therapy IDH inhibitors. Here we will report case of IDH-DS patient AML Enasidenib presenting as cardiac tamponade, which rarely reported. CASE PRESENTATION: A 75 years old male diagnosed two months ago presented to the emergency for exertional shortness breath and cough started weeks after initiation therapy. On examination, blood pressure was 94/74 mm Hg, pulse 110/min, peripheral oxygen saturation 90% on room air, bilateral (b/l) mild expiratory wheezes, muffled heart sounds. Routine labs were abnormal white cell count 32x103/ul, serum creatinine 2.5 mg/dl, urea nitrogen 30 mg/dl. Chest X-ray unremarkable. computed tomography scan chest showed b/l ground-glass micronodules, subtle mosaic pattern lungs b/l, small right-sided pleural effusion, massive pericardial effusion. Echocardiography an ejection fraction 50-55%, moderately large anterior effusion evidence early right atrial ventricular diastolic collapse, suggesting tamponade. The intravenous dexamethasone based clinical suspicion IDH-DS. Pericardiocentesis performed 625 ml hemorrhagic fluid drained. During procedure, went into arrest successfully resuscitated. Pericardial analysis lymphocytic predominant total protein 5.3 g/dl, LDH 536 u/l. Bacteriological fungal cultures negative. Due high probability recurrence window procedure planned but refused desired be Hospice care. Later on, died DISCUSSION: diagnosis can challenging due lack diagnostic criteria. There are no randomized studies compare treated steroids compared those who not. Also, there definitive data prophylaxis. Given nature DS significant risk associated starting limited time course, empiric treatment recommended soon suspected. CONCLUSIONS: fatal adverse reaction inhibitors requires immediate recognition management. Despite being well described, several issues remain unresolved therefore well-controlled need done better understand disease. REFERENCE #1: Patel SA. Enasidenib-Induced Differentiation Syndrome IDH2-Mutant Acute Myeloid Leukemia. JAMA Oncol. 2018 Aug 1;4(8):1110-1111. doi: 10.1001/jamaoncol.2017.4724. PMID: 29346477 #2: Fathi AT, DiNardo CD, Kline I, Kenvin L, Gupta Attar EC, Stein EM, de Botton S; AG221-C-001 Study Investigators. Associated With Enasidenib, Selective Inhibitor Mutant Dehydrogenase 2: Analysis Phase 1/2 Study. 1;4(8):1106-1110. 10.1001/jamaoncol.2017.4695. 29346478; PMCID: PMC5885269. #3: Norsworthy KJ, Mulkey F, Scott Ward AF, Przepiorka D, Charlab R, Dorff SE, Deisseroth A, Kazandjian Sridhara Beaver JA, Farrell Claro RA, Pazdur R. Ivosidenib Treatment Patients Relapsed or Refractory IDH-Mutated AML: U.S. Food Drug Administration Systematic Analysis. Clin Cancer Res. 2020 15;26(16):4280-4288. 10.1158/1078-0432.CCR-20-0834. Epub May 11. 32393603; PMC7442588. DISCLOSURES: No relevant relationships by Raza Hussain, source=Web Response Pragna Janagam, Syed yousaf Shah, Akesh Thomas,