SESSION TITLE: Critical Care Student/Resident Case Report Posters III
SESSION TYPE: Medical Student/Resident Case Report
PRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PM
INTRODUCTION: We present a rare and puzzling case of Type B lactic acidosis diagnosed in our ICU. After ruling out other sources, we eventually discovered that the patient's persistent lactic acidosis was caused by a high-grade B cell lymphoma.
CASE PRESENTATION: A 44-year-old African American female with AIDS, asthma, and alcohol and cocaine abuse was initially admitted to the detox program in our hospital. Despite having no significant complaints other than chronic abdominal pain, she was transferred to the ICU because routine labs revealed a very high lactic acid level of 14. The anion gap was 9, and the ABG showed a pH of 7.392, PCO2 of 32.5, and PO2 of 107 with an oxygen saturation of 99% on room air. Patient was not on any medications that would cause lactic acidosis, including HIV medications. Patient remained hemodynamically stable, but the lactic acid was trending up without any readily identifiable source and was not responding to IV fluids and bicarbonate injections. A CT-scan of the abdomen showed left adnexal, retroperitoneal, and bilateral inguinal masses. Biopsy of the masses showed high-grade B cell lymphoma, immunophenotypically concerning for Burkitt's lymphoma. It was confirmed that the patient had Type B lactic acidosis after ruling out other etiologies. Consequently, Patient was transferred to a higher institution for tumor management.
DISCUSSION: Type B lactic acidosis is a very rare condition with an unclear mechanism. The most common etiology is malignancy, especially lymphoma and leukemia. Probable pathogeneses include liver and kidney dysfunction, tumor cell overexpression of glycolytic enzymes and mitochondrial dysfunction, thiamine deficiency, tumor cell production of lactate, increased tumor necrosis factor α (TNF-α), and chemotherapy. Type A lactic acidosis, on the other hand, is more common and is usually caused by hypoperfusion or sepsis, in which case management would consist of aggressive fluid resuscitation, antibiotics, and close hemodynamic monitoring. Our patient’s unique presentation of hemodynamic stability with a very abnormal and worsening lactic acid level could be puzzling for many clinicians. Considering malignancy as a cause of Type B lactic acidosis is the key to clinching the diagnosis, and treating the malignancy is the mainstay of management. Additionally, hemodialysis and hemofiltration with a bicarbonate-based replacement fluid have been used as adjunct therapy. The prognosis of Type B lactic acidosis, nevertheless, remains very poor.
CONCLUSIONS: It is important to consider and identify Type B lactic acidosis in ICUs, especially in patients with persistent lactic acidosis without a clear etiology.
Reference #1: Type B Lactic Acidosis Associated With Multiple Myeloma Patrick Sia, Troy J. Plumb, Jennifer A. Fillaus Am J Kidney Dis. 2013
Reference #2: A Case of Type B Lactic Acidosis in Multiple Myeloma Patrick Tang, Anamarija M. Perry, Mojtaba Akhtari Clinical Lymphoma Myeloma and Leukemia, Vol. 13, Feb. 2013
DISCLOSURE: The following authors have nothing to disclose: Christopher Caesar Williams, Kaushal Sondarwa, Manohar Gajjela, Vanita Gupta
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