Phosphate enemas causing profound refractory hypocalcaemia: A case report

TY - JOUR

T1 - Phosphate enemas causing profound refractory hypocalcaemia

T2 - A case report

AU - Nobes, Jennifer

AU - Murphy, Michael J.

N1 - Publisher Copyright: © The Author(s) 2026

PY - 2026/5/20

Y1 - 2026/5/20

N2 - A 37-year-old woman attended hospital with melaena and coffee-ground vomiting on a background of alcohol-related liver disease (ALD). Following upper gastro-intestinal (GI) endoscopy she was admitted to the medical high dependency unit and commenced on multiple medications, in accordance with the decompensated cirrhosis care bundle of the British Association for the Study of the Liver (BASL).1 The patient was severely encephalopathic, prompting the addition of regular enemas to minimise colonic nitrogen production. On Day 4 post admission, the patient was noted to be hypocalcaemic (adjusted calcium 1.62 mmol/L) and intravenous calcium gluconate was prescribed. By Day 5, adjusted calcium had fallen to a nadir of 0.85 mmol/L; phosphate was 6.4 mmol/L. The rapidly developing inverse relation between calcium and phosphate strongly suggested a causal association. Since Day 3 the patient had received enemas three times daily for severe hepatic encephalopathy. We postulated that rectal absorption of phosphate in the enemas was occurring, contrary to the intended mechanism of action, and recommended they were stopped. Following discontinuation of the phosphate enemas, serum phosphate fell to within the reference range over 72 h. In total, over 70 mmol of calcium (infused as 280 mL of 10% calcium gluconate over a period of 5 days) was required to replace the sequestered calcium. By Day 11, calcium, phosphate and sodium were all within their respective reference ranges.

AB - A 37-year-old woman attended hospital with melaena and coffee-ground vomiting on a background of alcohol-related liver disease (ALD). Following upper gastro-intestinal (GI) endoscopy she was admitted to the medical high dependency unit and commenced on multiple medications, in accordance with the decompensated cirrhosis care bundle of the British Association for the Study of the Liver (BASL).1 The patient was severely encephalopathic, prompting the addition of regular enemas to minimise colonic nitrogen production. On Day 4 post admission, the patient was noted to be hypocalcaemic (adjusted calcium 1.62 mmol/L) and intravenous calcium gluconate was prescribed. By Day 5, adjusted calcium had fallen to a nadir of 0.85 mmol/L; phosphate was 6.4 mmol/L. The rapidly developing inverse relation between calcium and phosphate strongly suggested a causal association. Since Day 3 the patient had received enemas three times daily for severe hepatic encephalopathy. We postulated that rectal absorption of phosphate in the enemas was occurring, contrary to the intended mechanism of action, and recommended they were stopped. Following discontinuation of the phosphate enemas, serum phosphate fell to within the reference range over 72 h. In total, over 70 mmol of calcium (infused as 280 mL of 10% calcium gluconate over a period of 5 days) was required to replace the sequestered calcium. By Day 11, calcium, phosphate and sodium were all within their respective reference ranges.

KW - ALD

KW - Analytes

KW - Calcium

KW - Clinical studies

KW - Phosphate

UR - https://www.scopus.com/pages/publications/105039442619

U2 - 10.1177/00045632261453318

DO - 10.1177/00045632261453318

M3 - Article

C2 - 42163069

AN - SCOPUS:105039442619

SN - 0004-5632

JO - Annals of Clinical Biochemistry

JF - Annals of Clinical Biochemistry

ER -