Severe hyperphosphatemia and hypocalcemic tetany after oral laxative administration in a 3-month-old infant.

A 3-month-old infant presented to the pediatric emergency department with respiratory distress and tetany after ingestion of a phosphate-containing oral laxative. The initial phosphorus level was 38.3 mg/dL. With aggressive fluid resuscitation and intravenous calcium administration, the infant completely recovered. Although the risks of phosphate-containing enemas are well described, life-threatening hyperphosphatemia can also result from administration of phosphate-containing oral laxatives. Aggressive fluid hydration is the mainstay of treatment. Intravenous calcium administration may be necessary to avoid hemodynamic collapse despite the theoretical possibility of metastatic calcifications. Physicians should be alerted to the possibility of phosphate toxicity and hypocalcemic tetany in young children when treated with over-the-counter laxatives. Caregivers should be advised not to administer over-the-counter laxatives to infants without physician supervision.

Spurious hyperphosphatemia in a patient with alteplase-locked central venous catheter.

Alteplase has been shown to be effective in preventing central venous access clotting in patients on hemodialysis. Because of a high phosphorus content in its excipient, it can inadvertently contaminate blood samples, leading the physician in care of the patient to erroneously increase dialysis time or change diet in order to control the pseudo-hyperphosphatemia.

Life threatening hyperphosphataemia after administration of sodium phosphate in preparation for colonoscopy.

An elderly woman developed severe hyperphosphataemia, hypocalcaemia, and cardiac arrest after oral administration of sodium phosphate in preparation for colonoscopy. This is an unusual complication and is attributed to decreased phosphate excretion by the kidneys. At increased risk are patients with impaired renal function, age more than 65 years, and presenting with intestinal obstruction or decreased intestinal motility, increased intestinal permeability, liver cirrhosis, or congestive heart failure. Though there are no accepted guidelines for anticipation and prevention of this adverse effect, it may be desirable to check serum phosphate concentrations before choosing the method for colonic preparation and before giving the second oral dose of sodium phosphate in patients at risk. Hyperphosphataemia should be suspected if a patient develops hypotension or neuromuscular irritability after administration of sodium phosphate. Haemodialysis for direct removal of phosphate and intravenous calcium for treatment of symptomatic hypocalcaemia may be life saving.

[Acute hyperphosphatemia secondary to phosphate administration for bowel preparation]. / Hiperfosforemia aguda tras preparación para colonoscopia.

We report a 75-years-old woman, stable on a three-weekly hemodialysis program over a period of 3 years, who develop acute hyperphosphatemia secondary to phosphate administration for bowel preparation. The quick clinical diagnosis and the treatment with intensive hemodialysis resulted in a correction of hyperphosphatemia, hypocalcemia, acidemia and other electrolyte abnormalities. The phosphate cathartics are contraindicated in patients with severe renal insufficient or in dialysis program. Our case shows the severe side effects secondary to injudicious use of sodium phosphate cathartics.

Oral Fleet Phospho-Soda laxative-induced hyperphosphatemia and hypocalcemic tetany in an adult: report of a case.

PURPOSE: This study was undertaken to report an adverse outcome of the routine use of Fleets Phospho-Soda for bowel cleansing and to review the available literature. METHOD: Report of a case and review of the literature is presented. RESULT: Administration of Fleets Phospho-Soda for bowel preparation in an adult resulted in hyperphosphatemia and hypocalcemic tetany. Review of the literature shows this to be the first such report. Further evaluation suggests a role for partial bowel obstruction and renal failure in this complication. CONCLUSION: Although Fleet Phospho-Soda solution continues to be a safe bowel preparation, caution should be used in adults with bowel obstruction and renal failure.

Metabolic abnormalities associated with phosphoric acid ingestion.

A 64-year-old man ingested a phosphoric acid solution in a suicide attempt. He subsequently developed hyperphosphatemia, hypocalcemia, and systemic metabolic acidosis. Local caustic effects of the acid were mild. The patient recovered and was lost to follow-up.

[Acute anuric renal failure caused by hyperphosphoremia in acute lymphoblastic leukemia. 3 cases]. / Insuffisance rénale aiguë anurique par hyperphosphorémie au cours des leucémies aiguës lymphoblastiques. 3 observations.

Nephrocalcinosis due to hyperphosphataemia with hypocalcaemia is a rare cause of ARF during chemotherapy of ALL. Three cases are reported, one with renal anatomopathological studies and microanalysis of the intratubular calculi. All possible preventive measures should be taken against this complication which is related to acute tumoral lysis, especially in the hyperleukocytic and/or tumoral forms of ALL.

[Long-term anticonvulsant therapy and calcium and phosphorus metabolism]. / Terapia cronica anticomiziale e metabolismo calcio-fosforico.

The authors examined 114 epileptic patients who were taking anticonvulsant drugs from different periods of time. Serum and urinary calcium and phosphorus and serum alkaline phosphatase levels have been studied. Roentgenographic researches have been made in order to asses the bone mineral content. Urinary D-glucaric acid excretion as a quantitative index of hepatic enzyme induction has been determined in some subjects. The results show the presence of minor alterations both in calcium and phosphorus metabolism and in bone structure at a subclinical level. These findings suggest the importance of climatic and nutritional factors in the development of bone alterations pointed out by several authors in epileptic patients on long-term anticonvulsant therapy.

Distinction between the common symptoms of the phosphate-depletion syndrome and glucocorticoid-induced disease.

A phosphate depletion syndrome developed in a steroid-dependent asthmatic patient. Initially, the clinical picture was confused with steroid-associated myopathy rather than the phosphate depletion syndrome which has similar symptoms. The classic biochemical findings led to the correct diagnosis. Cessation of phosphate-binding antacids and phosphorus repletion rapidly corrected the biochemical findings and led to the patient's clinical improvement. Platelet phosphate metabolism was evaluated; it was found to correlate with the phosphorus-depleted state and clinical recovery with phosphate repletion. Attention is drawn to the clinical entity of phosphate depletion which may mimic steroid-induced side effects, both of which may occur in patients receiving steroids and antacids.