Endocrine Abstracts

Diabetic ketoacidosis (DKA) is a medical emergency that is associated with hyperglycaemia, metabolic acidosis, and electrolyte imbalances. Hypophosphatemia commonly occurs during DKA treatment but is typically mild and self-limiting. Current BSPED guidelines do not recommend routine phosphate replacement unless symptoms of severe deficiency develop. We present a case of severe symptomatic hypophosphatemia in an adolescent with DKA, highlighting the clinical impact and need for early recognition.

Case Summary: A 14-year-old previously healthy girl presented to paediatric ED in severe DKA with a pH of 6.83 and glucose of 37 mmol/l. She was tachycardic and drowsy (GCS 14/15) on arrival and managed as per BSPED guidelines. Her initial serum phosphate level was normal at 1.24 mmol/l (0.9-1.8 mmol/l). Despite ongoing management, over the next 24 hours, she developed worsening acidosis, acute kidney injury, and myocardial dysfunction, confirmed on echocardiography. By 16 hours post-admission, phosphate had fallen to <0.1 mmol/l, prompting oral replacement with phosphate Sandoz, however this was not tolerated due to ongoing nausea and dysphagia. Antiemetic therapy with ondansetron, cyclizine and pantoprazole was trialled but was ineffective. By day four, she remained on IV insulin with her symptoms persisting and additionally developed confusion, hallucinations and extreme weakness which were attributed to very low phosphate levels. Given ongoing symptoms and persistent hypophosphatemia, she was commenced on intravenous phosphate (Phosphate Polyfusor). By day six, serum phosphate had normalised, and her clinical condition had improved.

Discussion: Phosphate is lost during DKA due to osmotic diuresis and serum phosphate is often low during the recovery phase. Severe hypophosphatemia can lead to neurological symptoms, myocardial dysfunction, ileus, and myopathy. This case demonstrates that severe hypophosphatemia can cause significant morbidity in DKA and may not respond adequately to oral replacement alone. However, we considered whether her symptoms had been aggravated by the severity of dehydration at presentation.

Conclusion: This case highlights the need for phosphate monitoring in severe DKA and increased awareness of clinical signs of phosphate depletion. Current UK paediatric guidelines recommend replacement for symptomatic cases, however the lack of paediatric specific thresholds for treatment highlights the need for further research.