Severe Lactic Acidosis as a Fatal Presentation of Acute Myeloid Leukemia

Abstract

SESSION TITLE: Fellow Case Report Poster - Critical Care I SESSION TYPE: Affiliate Case Report Poster PRESENTED ON: Tuesday, October 25, 2016 at 01:30 PM - 02:30 PM INTRODUCTION: Often patients with acute myeloid leukemia (AML) present with fatigue, infections or bleeding due to cytopenias. Lactic acidosis as the presenting manifestation of acute myeloid leukemia is rare. CASE PRESENTATION: 75 year old female with a history of right stage III breast cancer (2013) with total mastectomy s/p chemotherapy and radiation therapy, presented to the emergency room with a one week history of flu like symptoms with increasing shortness of breath and altered mental status for 1 day. Vital signs showed a pulse rate100 bpm, BP 120/76 mmHg, respiratory rate 26 rpm with a saturation of 97% on room air. On exam she was ill appearing with diffuse abdominal tenderness and agitation. Lung and cardiac exam were unremarkable. Laboratory workup revealed a white blood cell count 194,000/uL, absolute monocyte count of 79,000/ uL (>20% blasts), hemoglobin 9.8 g/dL, platelet count 118 k/uL, serum creatinine was 1.98 mg/dL, liver enzymes were elevated (AST 1,486 U/L, ALT 2,404U/L, alkaline phosphatase 245 U/L). ABG revealed pH 6.73, pCO2 26 mmHg, pO2 91 mmHg, bicarbonate 8 mmol/L, anion gap 39 mmol/L and lactate 19.8 mmol/L. Chest X-Ray, CT brain and CT abdomen/pelvis showed no acute pathology. Blood cultures, urine cultures and urine toxicology screen were negative. She received IV fluid resuscitation, empiric broad-spectrum antibiotics and vasopressor support. The patient required intubation for worsening respiratory failure and mental status. Hematology oncology evaluated the patient due to the concern for acute leukemia with leukostasis. Peripheral smear showed acute numerous promonocytes consistent with an acute monocytic leukemia. Vasopressor requirements continued to increase and the patient expired within 24 hrs of presentation to the Emergency Department. DISCUSSION: The liver dysfunction alone in the absence of hypotension, hypoxia or infection would not explain the degree of lactic acidosis in our patient. Lactic acidosis is a rare but potentially fatal complication of AML. The pathogenesis of lactic acidosis in leukemia is unclear but is likely due to the anaerobic glycolysis by leukemic cells; tissue hypoxemia from leukostasis or thiamine and riboflavin deficiency. CONCLUSIONS: It is important to be cognizant that acute leukemia can present with lactic acidosis. Lactic acidosis in the presence of hematologic malignancy carries a poor prognosis. Reference #1: Udayakumar N, Rajendiran C, Muthuselvan R. A typical presentation of acute myeloid leukemia. J Cancer Res Ther. 2006;2(2):82-4. DISCLOSURE: The following authors have nothing to disclose: Shruti Gadre, Pulkit Chaudhury, Hariom Joshi, Adriano Tonelli No Product/Research Disclosure Information