# Severe Hypophosphatemia Induced by Hyperventilation: A Case Report

## TL;DR

A 38-year-old man with severe low phosphate levels was found to have hyperventilation-induced respiratory alkalosis, highlighting the need for early electrolyte checks in similar cases.

## Contribution

This case report highlights hyperventilation as a rare cause of severe hypophosphatemia and emphasizes the importance of early diagnosis.

## Key findings

- Severe hypophosphatemia was linked to hyperventilation-induced respiratory alkalosis.
- Intravenous phosphate replacement resolved symptoms and normalized phosphate levels.
- Anxiety-related hyperventilation likely caused excessive CO2 loss and metabolic disturbances.

## Abstract

Hypophosphatemia is a clinically significant but often underrecognized electrolyte abnormality in acute medicine, arising from decreased intake, increased losses, or intracellular redistribution. One uncommon cause is hyperventilation-induced respiratory alkalosis, which promotes intracellular phosphate shifting and enhanced glycolysis, leading to depletion of serum phosphate. Severe hypophosphatemia may result in neuromuscular, cardiovascular, and metabolic complications, necessitating prompt recognition and management. We report a case of a 38-year-old male patient referred to the Accident and Emergency (A&E) department by his general practitioner with severe hypophosphatemia (serum phosphate <0.20 mmol/L) and an elevated lactate level (2.4 mmol/L). He presented with shortness of breath, paresthesias of the upper and lower limbs, near-collapse episodes, hunger, sugar cravings over four months, and recurrent diarrheal episodes (six to eight per month). His history included Crohn’s disease, anxiety disorder, muscle cramps, and recent weight gain (~6 kg). On examination, he demonstrated hyperventilation, with arterial blood gas showing respiratory alkalosis (pH 7.535). Investigations revealed normal calcium (2.6 mmol/L; reference range 2.1-2.6mmol/L) and ionized calcium on venous blood gas (1.27 mmol/L; reference range 0.8-1.5 mmol/L), normal thyroid function (thyroid-stimulating hormone (TSH) 1.5 mU/L), and no evidence of malabsorption or renal phosphate wasting. Differential diagnoses, including malabsorption syndromes, vomiting, hyperparathyroidism, Fanconi syndrome, and refeeding syndrome, were excluded. The patient received intravenous phosphate replacement with serial electrolyte monitoring to assess response and prevent hypocalcemia, followed by transition to oral phosphate supplementation. Symptoms resolved completely, and the serum phosphate level normalized. Hyperventilation related to anxiety likely caused excessive CO2 loss, triggering respiratory alkalosis, which increased intracellular phosphate utilization and lactate production. Although often overlooked, severe hypophosphatemia can cause muscle weakness, rhabdomyolysis, hemolysis, arrhythmias, and altered mental status if untreated. This case underscores the importance of recognizing metabolic disturbances in patients presenting with panic-like hyperventilation and supports early electrolyte assessment to prevent serious complications.