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Lactic Acidosis: It's Not Just Hypoxia Anymore FREE TO VIEW

Chandra Patel*, DO; James Anholm, MD
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Loma Linda University Medical Center, Loma Linda, CA

Chest. 2012;142(4_MeetingAbstracts):362A. doi:10.1378/chest.1390890
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SESSION TYPE: Critical Care Student/Resident Case Report Posters II

PRESENTED ON: Tuesday, October 23, 2012 at 01:30 PM - 02:30 PM

INTRODUCTION: Lactic acidosis is the most common cause of metabolic acidosis. Although generation of lactate is generally associated with hypoxia causing the body to shift towards anaerobic metabolism, the overproduction or underutilization of lactate is caused by more than just decreased tissue perfusion. We present a case of lactic acidosis with an ambiguous etiology.

CASE PRESENTATION: An 86 year-old male was admitted to the medicine service for lower extremity DVT and infection of unknown etiology. He had a history of hypertension. Pertinent positives from the review of systems included weight loss, anorexia, constipation and fatigue. In the emergency room,he was found to have a lactate of 12. On the second day of his hospital course, he developed rectal bleeding and was transferred to our intensive care unit for further management. Upon arrival in the ICU, he was tachypneic, tachycardic with a blood pressure of 98/64 mmHg. His physical exam was significant for somnolence, blood-tinged stool on rectal exam and bilateral lower extremity edema. Laboratory studies revealed a three-gram decrease in hemoglobin, normal white count, an anion gap metabolic acidosis and mild hypoglycemia. After aggressive resuscitation, his vital signs and urine output normalized. Interestingly, his lactate increased to 19.9 and he developed a significant leukocytosis of up to 32,000. Ultimately, a peripheral smear showed what was thought to be mantle cell lymphoma or diffuse large B cell lymphoma. Flow cytometry studies and bone marrow or lymph node biopsies were necessary for more specific diagnosis but the patient quickly deteriorated. His family requested a withdrawal of life support and he died less than 24 hours later.

DISCUSSION: The end product of glycolysis, pyruvate, reacts with NADH and lactate dehydrogenase to create lactate. Importantly, this process can occur despite ample supply of oxygen to the tissues. Epinephrine surges cause stimulation of the glycolytic pathway resulting in increased levels of blood lactate. Clearly, this process is at play in many ICU patients, albeit not necessarily in our patient. While insulin causes over-expression of glycolytic enzymes in healthy cells, IGF mimics insulin (with similar results) in malignant cells. Additionally, malignant cells often over-express insulin receptors, thereby creating two mechanisms for elevated lactate in some cancer states.

CONCLUSIONS: It is important for physicians to recognize that in addition to ischemia or shock, lactic acidosis may be a result of liver disease, medications, epinephrine surge or, as in our patient, hematalogic malignancy.

1) Sillos, E, et al. "Lactic Acidosis: A Metabolic Complication of Hematologic Malignancies." Cancer, 2001, 92: 2237-46.

2) James, J H et al. "Lactate is an Unreliable Indicator of Tissue Hypoxia in Injury or Sepsis." Lancet, 1999, 354: 505-08.

3) Madias, N. "Lactic Acidosis." Kidney International, 1986; 29: 752-74.

DISCLOSURE: The following authors have nothing to disclose: Chandra Patel, James Anholm

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Loma Linda University Medical Center, Loma Linda, CA




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