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Isolated Severe Lactic Acidosis as a Presenting Feature of Pheochromocytoma Crisis
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A3356 - Isolated Severe Lactic Acidosis as a Presenting Feature of Pheochromocytoma Crisis
Author Block: F. Shaikh1, S. J. De Cruz2, J. Ku3, S. Ahmadi3; 1UCLA Medical Center, Los Angeles, CA, United States, 2Pulmonary and Critical Care, UCLA, Los Angeles, CA, United States, 3UCLA, Santa Monica, CA, United States.
Pheochromocytoma crisis (PCC) is rare emergency characterized by hemodynamic instability and end organ dysfunction. PCC can present with various clinical syndromes including hypertensive crisis, cardiomyopathy, and hypotension with multi-organ failure. This case demonstrates an uncommon presentation of pheochromocytoma as an isolated severe lactic acidosis in the absence of hypotension, which presents unique diagnostic challenges.
A 55-year-old female presented to the Emergency Department (ED) with acute onset of chest and back pain with shortness of breath. On arrival, patient was oriented although in respiratory distress with cold extremities. Her presentation was notable for blood pressure (BP) of 153/121, heart rate 151, respiratory rate 33, oxygen saturation of 81% on 15L of oxygen, serum bicarbonate of 21mm/L, no anion gap, creatinine of 1.10mg/dL, glucose of 443 mg/dL, and a negative troponin. Computed tomography (CT) of the chest was negative for pulmonary emboli and aortic dissection but did note a large right adrenal mass. Her blood gas demonstrated severe metabolic acidosis (pH 7.14) and a lactate of 70mg/dL (5-25mg/dL). Her condition quickly deteriorated requiring endotracheal intubation and transfer to the medical intensive care unit where she was started on continuous renal replacement therapy (CRRT) for severe metabolic acidosis. TTE showed a Takotsubo cardiomyopathy with left ventricular ejection fraction of 15%. Subsequently, cardiac catheterization showed no obstructive coronary disease, cardiac index of 2.33L/min/m^2, and systemic vascular resistance of 2453 dynes*sec/cm^5. Her lactic acidosis peaked at 125mg/dL despite CRRT. Pheochromocytoma was suspected and patient was given phentolamine IV 5mg for persistent severe hypertension. Immediately following, she became hypotension not responsive to intravenous fluids, and pressors were initiated. Shortly afterwards, patient had a pulseless electrical activity (PEA) arrest. Pulse was eventually regained and patient was evaluated for extracorporeal membrane oxygenation but deemed to be a poor candidate. She was continued on maximal supportive care with 4 pressors but had another PEA arrest on hospital day 2 and expired. Serum plasma metanephrines collected on hospital day 1 returned with free metanephrine >50 nmol/L (0-0.49nmol/L), free normetanephrine >50nmol/L(0-0.89nmol/L), confirming the diagnosis of pheochromocytoma.
Lactic acidosis is rare and under-recognized complication of pheochromocytoma. High plasma catecholamines promote glycogenolysis, gluconeogenesis and insulin resistance with resultant excess production of pyruvate and subsequent metabolism to lactate. Additionally, catacholamines induce vasoconstriction which causes hypoxia and anabolic metabolism in the peripheral tissues. We show that severe lactic acidosis can be a presenting feature of pheochromocytoma crisis in absence of circulatory shock.
Author Block: F. Shaikh1, S. J. De Cruz2, J. Ku3, S. Ahmadi3; 1UCLA Medical Center, Los Angeles, CA, United States, 2Pulmonary and Critical Care, UCLA, Los Angeles, CA, United States, 3UCLA, Santa Monica, CA, United States.
Pheochromocytoma crisis (PCC) is rare emergency characterized by hemodynamic instability and end organ dysfunction. PCC can present with various clinical syndromes including hypertensive crisis, cardiomyopathy, and hypotension with multi-organ failure. This case demonstrates an uncommon presentation of pheochromocytoma as an isolated severe lactic acidosis in the absence of hypotension, which presents unique diagnostic challenges.
A 55-year-old female presented to the Emergency Department (ED) with acute onset of chest and back pain with shortness of breath. On arrival, patient was oriented although in respiratory distress with cold extremities. Her presentation was notable for blood pressure (BP) of 153/121, heart rate 151, respiratory rate 33, oxygen saturation of 81% on 15L of oxygen, serum bicarbonate of 21mm/L, no anion gap, creatinine of 1.10mg/dL, glucose of 443 mg/dL, and a negative troponin. Computed tomography (CT) of the chest was negative for pulmonary emboli and aortic dissection but did note a large right adrenal mass. Her blood gas demonstrated severe metabolic acidosis (pH 7.14) and a lactate of 70mg/dL (5-25mg/dL). Her condition quickly deteriorated requiring endotracheal intubation and transfer to the medical intensive care unit where she was started on continuous renal replacement therapy (CRRT) for severe metabolic acidosis. TTE showed a Takotsubo cardiomyopathy with left ventricular ejection fraction of 15%. Subsequently, cardiac catheterization showed no obstructive coronary disease, cardiac index of 2.33L/min/m^2, and systemic vascular resistance of 2453 dynes*sec/cm^5. Her lactic acidosis peaked at 125mg/dL despite CRRT. Pheochromocytoma was suspected and patient was given phentolamine IV 5mg for persistent severe hypertension. Immediately following, she became hypotension not responsive to intravenous fluids, and pressors were initiated. Shortly afterwards, patient had a pulseless electrical activity (PEA) arrest. Pulse was eventually regained and patient was evaluated for extracorporeal membrane oxygenation but deemed to be a poor candidate. She was continued on maximal supportive care with 4 pressors but had another PEA arrest on hospital day 2 and expired. Serum plasma metanephrines collected on hospital day 1 returned with free metanephrine >50 nmol/L (0-0.49nmol/L), free normetanephrine >50nmol/L(0-0.89nmol/L), confirming the diagnosis of pheochromocytoma.
Lactic acidosis is rare and under-recognized complication of pheochromocytoma. High plasma catecholamines promote glycogenolysis, gluconeogenesis and insulin resistance with resultant excess production of pyruvate and subsequent metabolism to lactate. Additionally, catacholamines induce vasoconstriction which causes hypoxia and anabolic metabolism in the peripheral tissues. We show that severe lactic acidosis can be a presenting feature of pheochromocytoma crisis in absence of circulatory shock.
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