A 74-year-old woman was scheduled for colonoscopy due to positive fecal occult blood.
On admission, her serum levels of creatinine, adjusted calcium, and phosphate were
113 µmol/l, 2.24 mmol/l, and 1.17 mmol/l, respectively. She received 90 ml of oral
Fleet Phospho-Soda (C.B. Fleet Co. Inc., Lynchburg, Virginia, USA), from which she
developed profuse diarrhea. Six hours later, she complained of facial and limb numbness,
and appeared drowsy. Her serum phosphate level had risen to 7.29 mmol/l and her calcium
level had fallen to 1.82 mmol/l. During the next hour, muscle cramps and tetany developed
over her lower limbs, trunk, and face, with a positive Chvostek’s sign. Intravenous
administration of 9.0 mmol (40 ml 10 %) calcium gluconate was carried out over 6 h,
resulting in resolution of her tetany, while the numbness persisted over the distal
limbs. Further infusions totaling 24.75 mmol calcium gluconate were required over
the next 17 h to restore the calcium level to 2.32 mmol/l (Figure [1]). Extensive investigations excluded a secondary cause of the electrolyte disturbance.
Figure 1 Chart illustrating the evolving signs and symptoms, serum calcium and phosphate derangement,
and calcium replacement therapy given.
Most complications of sodium phosphate bowel preparation are the result of hyperphosphatemia
after rapid phosphate absorption and subsequent binding to serum calcium, causing
secondary hypocalcemia [1]. Patients usually present 6 - 12 h after ingestion, with abdominal pain, vomiting,
dizziness, muscle cramping, or seizures [2]. Other associated electrolyte disturbances include hypokalemia, hypernatremia, and
metabolic acidosis, with increased anion gap [3]. Excessive diarrhea can lead to significant potassium and bicarbonate loss, contributing
to hypokalemia and metabolic acidosis [2]. Hypernatremia is secondary to intestinal absorption of sodium from Phospho-Soda,
dehydration, and colonic shifting between sodium and potassium.
Factors exacerbating hyperphosphatemia are old age, impaired renal function with reduced
phosphate clearance, dehydration, bowel immotility, and repeated dosing. Symptomatic
hyperphosphatemia and hypocalcemia are very uncommon in patients with normal renal
function [4]. The aims of treatment are to reduce phosphate absorption by oral phosphate binders
(calcium acetate or Alusorb), to increase phosphate clearance, and to correct dehydration
and electrolyte disturbances. Care must be taken when giving calcium supplement, as
renal calcium-phosphate precipitation may further deteriorate renal function [2].
This unusual case is a dramatic reminder that patients with normal renal function
may rapidly develop symptomatic hypocalcemia and hyperphosphatemia after a single
dose of oral Phospho-Soda.
