Kidney Week

Abstract: SA-PO521

Rapid Correction of Chronic Respiratory Alkalosis Leading to Profound Hyperphosphatemia in a Patient in the Cardiac Intensive Care Unit (ICU)

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

• Eskander, Kirollos, UConn Health, Farmington, Connecticut, United States

Kirollos Eskander, MD

• Sahi, Akshita, UConn Health, Farmington, Connecticut, United States

Akshita Sahi, MD

• Siddique, Talha, UConn Health, Farmington, Connecticut, United States

Talha Siddique, MD

• Post, Jarrod B., Hartford HealthCare, Hartford, Connecticut, United States

Jarrod B. Post, MD, MBA

Introduction

In critically ill patients, changes in extracellular buffer (i.e. bicarbonate) concentrations are expected and usually trigger further work-up into the underlying acid-base disorder. However, hyperphosphatemia in a patient with acute renal failure is often thought to be in the setting of reduced creatinine clearance. But what about 'bone buffering'?

Case Description

Our patient is a 59-year-old female with mixed ischemic and nonischemic cardiomyopathy status post orthotopic heart transplant with a post-transplant course complicated by biopsy-negative rejection with subsequent cardiogenic shock. She developed acute kidney injury and respiratory failure in the setting of hypervolemia. She was initiated on pulse dose steroid and continuous veno-venous hemodialysis with improvement in her oxygenation.
The patient had been tachypneic for several months with mild respiratory alkalosis. In light of hypocapnia and normal oxygen saturation, we hypothesize this to be due to alveolar capillary J-receptor stimulation in the setting of chronic pulmonary edema secondary to decompensated heart failure. [1]
However, blood gas indicated worsening alkalemia and change in mentation. Labs showed pH 7.60, pCO2 23, bicarbonate 23, and an anion gap of 12.
She underwent serum electrolyte mass removal with normal saline replacement to induce therapeutic dilutional acidosis.
However, the patient developed concomitant steroid-induced diabetic ketoacidosis the following day with repeat labs showing pH 7.40, pCO2 19, bicarbonate 12, and an anion gap of 28. Within 24 hours, her phosphorus increased from 2.5 to 11.8 with a slight increase in serum calcium from 7.2 to 8.3. Her hyperphosphatemia improved with insulin therapy and with a subsequent increase in pH to 7.56.

Discussion

Our patient's pH, while within the acceptable range at 7.40, reflected a rapid increase in serum H⁺ concentration with a drop from 7.60 overnight. Our patient's respiratory compensation was already maximized due to her persistent tachypnea, and she was unable to renally excrete acid due to her AKI.
Therefore, we believe this case highlights bone resorption and intracellular buffers such as phosphate in strict control of serum hydrogen ion concentrations. This is congruent with the concomitant increase in serum calcium.