Severe Hypophosphatemia Induced by Hyperventilation: A Case Report.

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 CO