Abstract: SA-PO522
Acute Hypophosphatemia Due to Rapid Correction of Respiratory Acidosis
Session Information
- Acid-Base, Calcium, Potassium, and Magnesium Disorders: Clinical
October 26, 2024 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Sundaram, Sruthi, Emory University Woodruff Health Sciences Center, Atlanta, Georgia, United States
- Vasanth, Payaswini, Emory University Woodruff Health Sciences Center, Atlanta, Georgia, United States
- Fallahzadeh Abarghouei, Mohammad Kazem, Emory University Woodruff Health Sciences Center, Atlanta, Georgia, United States
Introduction
Acute respiratory alkalosis is a known cause of acute hypophosphatemia. Here we describe a case of acute hypophosphatemia due to rapid correction of respiratory acidosis in a patient with acute kidney injury (AKI) superimposed on chronic kidney disease (CKD).
Case Description
A 59-year-old male with end stage renal disease due to focal segmental glomerulosclerosis status post renal transplant 17 years prior, chronic kidney disease stage 3b of the allograft, scoliosis with restrictive airway disease, obstructive sleep apnea, and chronic hypercapnic respiratory failure, presented with encephalopathy and acute on chronic respiratory acidosis requiring intubation and mechanical ventilation. He was also noted to have an AKI. As expected in a patient with AKI on CKD, he had hyperphosphatemia on presentation, but did not require renal replacement therapy. However, after intubation and mechanical ventilation, which resulted in an acute decline in his pCO2 level from 88 mmHg to 31 mmHg and an acute rise in pH to 7.53, his phosphorus level acutely dropped to 1.0 mg/dL. His serum phosphorous levels rose to 3.0 mg/dL after being given 20 mmol of intravenous sodium phosphate, which was still within low-normal range despite remaining in an AKI state suggesting these values were true.
Discussion
Hypophosphatemia in acute respiratory alkalosis can occur from a rapid decline in pCO2 and an increase in intracellular pH which induces phosphofructokinase activity and glycolysis, leading to intracellular phosphorus consumption as phosphorylated glucose precursors are produced. As a result, extracellular phosphorus shifts intracellularly acutely dropping serum phosphorus levels. The correction of our patient's hypercapnic respiratory failure with intubation and mechanical ventilation induced a rapid decline in pCO2, which subsequently resulted in a similar decline in serum phosphorus levels likely through a similar mechanism. This case illustrates the importance of monitoring serum phosphorous levels in patients being treated for hypercapnic respiratory failure to avoid complications from acute hypophosphatemia.