SESSION TITLE: Critical Care Student/Resident Case Report Posters IV
SESSION TYPE: Medical Student/Resident Case Report
PRESENTED ON: Tuesday, October 29, 2013 at 01:30 PM - 02:30 PM
INTRODUCTION: Some sources of lactic acidosis, such as the one associated with lymphoma, may not be immediately obvious. When lymphoma infiltrates the liver the compounded effect may prove fatal.
CASE PRESENTATION: A 78-year-old man admitted for an elective carotid endarterectomy whose hospital course was complicated by increased transaminitis, acute renal failure, and Klebsiella pneumonia/UTI was transferred to our ICU. He had complained of left upper quadrant abdominal and left lower chest pain. He developed jaundice prompting transfer for ERCP to evaluate for possible ascending cholangitis. ERCP was unrevealing. Post procedure evaluation noted encephalopathy, shock and a suspicion of sepsis. Labs were congruent with presenting labs including persistently elevated transaminases AST/ALT 670/773 (U/L). Lactic acid was 14.3 (mmol/L) with a normal anion gap. He developed refractory shock and acidosis despite blood, fluids, vasopressors, increased minute ventilation and continuous renal replacement therapy. A new anion gap (increased from 11 to 23) and AST/ALT 7512/2642 (U/L) was noted 5 hours later followed by a gap of 25, lactic acid 19.9 (mmol/L), AST/ALT 18,903/5079 (U/L) five hours subsequently. He remained unresponsive to resuscitation efforts and died following the family’s request for withdrawal of life sustaining treatment. Autopsy revealed a splenic rupture and lymphoma with significant tumor burden in the liver.
DISCUSSION: Lactic Acidosis is dichotomized into two distinct categories. Type A is due to tissue hypoxia secondary to hypoperfusion or hypoxemia with resultant anaerobic metabolism and increased production of lactic acid. Type B encompasses a myriad of conditions in which lactate accumulates despite adequate perfusion and oxygenation. Lymphoma is rarely associated with Type B lactic acidosis and portends a poor prognosis.1 There are many purported mechanisms to explain this phenomenon, including decreased metabolism of lactate in patients with liver dysfunction.1 Patients with Type B lactic acidosis who subsequently acquire a superimposed Type A lactic acidosis are likely at a survival disadvantage due to excessive lactate burden and accompanying acidosis, with increased risk of being refractory to aggressive medical intervention. Clinicians should be aware of Type B lactic acidosis and, when possible, seek out reversible causes before these patients incur hemodynamic or hypoxic insult from which they may not be able to recover.
CONCLUSIONS: Type B lactic acidosis is a rare complication of hematologic malignancies. In atypical severe lactic acidosis situations, a high index of suspicion is needed to broaden the differential and may prompt a search for malignancy evaluation.
Reference #1: Friedenberg, Allison S., Douglas E. Brandoff, and Fred J. Schiffman. "Type B Lactic Acidosis As a Severe Metabolic Complication in Lymphoma and Leukemia." Medicine 86.4 (2007): 225-32.
DISCLOSURE: The following authors have nothing to disclose: Andrew Whiteley, Varsha Podduturi, Joseph Guileyardo, Adan Mora
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