Immobilisation is a recognised but rare cause of hypercalcaemia. Most reported cases are patients with spinal cord injury or trauma.
Case 1: A 26-year-old female experienced a 5½ months admission to the intensive care unit (ITU) with complications following small bowel resection for Crohns disease. At 16 weeks she developed hypercalcaemia. Investigations confirmed calcium 3.24 mmol/l, parathyroid hormone (PTH) <0.6 pmol/l (1.66.9), 24 h urinary calcium 17.64 mmol/24 h (<5), calcium:creatinine ratio 6.9, serum β-cross laps 1.55 μg/l (0.10.5), and normal renal function. Total parenteral nutrition was providing 3.8 mmol calcium/24 h. The calcium levels returned to normal with a reduction in the calcium content of her TPN and bisphosphonate treatment. She was later found to have multiple osteoporotic spinal wedge fractures. Her calcium levels have remained normal after mobilisation.
Case 2: A 60-year-old man with flaccid quadriplegia secondary to GuillainBarre syndrome developed hypercalcaemia four weeks into an ITU admission. Feeding was via a nasogastric tube with the feed delivering 35 mmol calcium/24 h. Investigations confirmed calcium 2.79 mmol/l, ionised calcium 1.348 mmol/l (1.121.32), PTH 1.4 pmol/l, urinary calcium 3.65 mmol/24 h, and β-cross laps 0.97 μg/l. I.v. pamidronate normalised calcium levels.
Immobilisation results in increased bone turnover with an imbalanced preponderance for osteoclastic bone resorption reflected by raised β-cross laps. This results in hypercalcaemia. These cases demonstrate that immobility of different aetiologies can result in the phenomenon at varying degrees of severity and duration of immobility. Also demonstrated is the impact of total parental nutrition on the severity of the hypercalcaemia which was less severe in enteral feeding, as the low PTH levels resulted in decreased calcium absorption. Pamidronate is confirmed as an effective treatment.