P035: INTRAOPERATIVE MANAGEMENT OF SEVERE METABOLIC ALKALOSIS SECONDARY TO GASTRIC OUTLET OBSTRUCTION FROM PANCREATIC HEAD MASS.
Mrugesh Thakkar, MD; Vyshakh Shibu; Joanne Ramjohn; Amanda Frantz, MD; University of Florida
Introduction: Metabolic alkalosis in the setting of gastrointestinal losses is a common hospital admission diagnosis; however, the anesthetic management of severe electrolyte abnormalities associated with this condition are not frequently encountered. Metabolic alkalosis is defined by an elevation in the plasma concentration of bicarbonate, this leads to an increase in the arterial pH1. Excess vomiting can lead to hydrogen ion (H+) loss, which activates the H-K-ATPase pump in the renal collecting tubule increasing H+ ions in the extracellular fluid as a homeostasis mechanism resulting in severe intravascular hypokalemia2.
Case Presentation: An 86-year-old male with known CAD, HTN, COPD, and pulmonary fibrosis presented with food intolerance, abdominal pain, and emesis for three weeks prior to admission. Abdominal CT scan revealed irregular, lobulated mass in the pancreatic head measuring 4.9 x 5.5 cm. He was scheduled for a laparoscopic pancreaticoduodenectomy to remove the pancreatic head mass. The patient’s preoperative labs were remarkable for potassium of 2.4 mmol/L and creatinine of 0.65 mg/dL.
Intraoperative Management: General anesthesia was induced via rapid sequence induction due to his history of gastric outlet obstruction. Fasciculations were noted after succinylcholine administration and the patient was successfully intubated. Post-intubation nasogastric tube was placed with immediate removal of 1L of gastric contents. An arterial line was placed for frequent arterial blood gas (ABG) draws. The first ABG resulted: pH 7.74, pCO2 48mmHg, K 1.9mEq/L, and Ca 0.82mEq/L. His electrocardiogram lead II showed an atrioventricular escape rhythm with underlying sinus rhythm. He was immediately resuscitated with 25% albumin, calcium, and IV potassium. Intravenous fluids were changed from plasmalyte to normal saline with a decrease in respiratory rate for permissive hypercapnia. A follow-up ABG showed the following: pH 7.58, pCO2 56mmHg, K 2.7mEq/L, and Ca 1.01mEq/L. The patient remained intubated and was transferred to the ICU in stable condition.
Discussion: The patient’s severe metabolic alkalosis was likely due to his profound GI fluid loss. The resulting hypovolemia lead to an upregulation of the RAAS system and enhanced absorption of bicarbonate. H+ loss activated his H-K-ATPase in the collecting tubule and lead to his critically low potassium level. Treatment of metabolic alkalosis should be targeted at the source of bicarbonate generation3. The patient was treated with multiple liters of normal saline to assist with increasing intravascular volume, correcting the chloride deficit, and to drive the bicarbonate back intracellularly via chloride-bicarbonate exchange in the distal tubule. Infusion of hydrochloric acid was discussed due to the severity of his alkalosis and chloride depletion; however, this drug is not present at our institution. Calcium was given to facilitate stabilization of the cardiac membranes and permissive hypercapnia was allowed to create a respiratory acidosis to compensate for the severe alkalosis, this is why the patient remained intubated. The patient’s alkalosis resolved and he was extubated the following afternoon and discharged on post-operative day 6.