Abstract: SA-PO0529
Hyperventilation Causing Recurrent Hypophosphatemia
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 3
November 08, 2025 | 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
- Thiruvarudsothy, Srikanth, Virtua Health Inc, Marlton, New Jersey, United States
- Srikanth, Theesitha, Brown University, Providence, Rhode Island, United States
Introduction
There are many causes of hypophosphatemia including medications, refeeding etc. It is known that respiratory alkalosis can theoretically cause hypophosphatemia due to transcellular distribution. Here we present case of a young man who has a history of recurrent hypophosphatemia due to hyperventilation / respiratory alkalosis.
Case Description
28 y.o. with a history of recurrent Hypophosphatemia, hypermobile Ehlers Danlos syndrome, postural orthostatic tachycardic syndrome, anxiety presented to the hospital due to low phosphate levels. Initial phosphorus level was low at 0.5 mg/dL. Serum potassium was low at 3.2 mg/dL, bicarbonate was low at 12 mmol/L, Serum magnesium acceptable at 2 mg/dL and the calcium was acceptable at 10 mg/dL. He was previously on phosphorus supplementation along with calcitriol which were recently stopped due to good phosphorus levels. On exam, he was visibly very anxious and tachypneic. ABG showed a pH of 7.62 with pCO2 of 10. Was seen by pulmonary who recommended to breathe into a paper bag as needed. Unfortunately, he could not tolerate anxiolytic due to side effects. He did well with oral and IV supplementation of phosphorus and was discharged to follow up with nephrology as outpatient.
Discussion
Hypophosphatemia can be precipitated by diet, medications, disease entities, refeeding syndrome etc. Our patient had extensive work up for recurrent hypophosphatemia in the past. Workup included PTH, vitamin D, FGF which were unremarkable. Genetic studies have confirmed no genetic renal phosphate wasting disorder. 24-hour urine studies were not consistent with renal phosphate wasting. His clinical exam was dramatic and was significant for severe anxiety and hyperventilation. This in addition to the low serum bicarbonate level, prompted us to investigate further including getting an ABG which confirmed the respiratory alkalosis. Ideally an anxiolytic would have helped the patient but was declined due to side effects. He did try to breathe into a paper bag asper pulmonary recommendation. He is currently doing well on calcitriol and oral phosphate supplementation.