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Hypocalcemia, hyperphosphatemia, and dehydration following a single hypertonic phosphate enema
484
March 1977 TheJournalofPEDIATR1CS
Hypocalcemia, hyperphosphatemia, and dehydration following a single hypertonic phosphate enema Roy F. D a v i s , P h . D . , M . D . , J e r r o l d M . E i c h n e r , M . D . , W . Archie Bleyer, M . D . , and Gary Okamoto, M . D . , Seattle, Wash.
SEVERE HYPERPHOSPHATEMIA and hypocalcemia have been reported when sodium phosphate/biphosphate enemas (Fleet phospho-soda) are administered repeatedly or in the presence of renal failure. This communication reports the same adverse reaction following the use of a single enema in children with " n o r m a l " renal function.
CASE REPORTS Patient 1. A healthy, 4-month-old infant had had no bowel movement for five days and was given a one-half pediatric size Fleet enema on instruction from her physician. The infant vomited once following the enema and had four liquid bowel movements during the next ten hours. Mother described the infant as being "very stiff' while she was changing her diaper. Twelve hours after the enema, the infant was found to be lethargic and febrile and was admitted to the hospital. Rectal temperature was 38.6~ pulse, 156; respiration, 68: blood pressure, 90/50; weight, 3.96 kg. The infant was lethargic and hypertonic with a depressed fontanelle, poor skin turgot, and dry mucous membranes. Moderate nuchal rigidity, brisk deep tendon reflexes, and ankle clonus were noted. Chvostek and Trousseau signs were not present. The remainder of the physical examination was normal. Cerebrospinal fluid contained 10 white cells pe r mm:' (6 mononuclear and 4 polymorphonuclear cells), protein 15 mg/dl and glucose 47 mg/dl (concomitant blood glucose of 60 mg/dl). Serum sodium was 156 mEq/l; potassium, 3.5 mEq/1; chloride, 104 mEq/l: COs content, 15 mEq/1; blood urea nitrogen, 47 mg/dl; serum calcium, 4.6 mg/dl; phosphorus 28.6 mg/dl; magnesium. 1.7 mEq/1. QoTc interval by electrocardiogram was 0.24 second. The infant was treated with intravenous fluids and calcium gluconate. Four hours after admission her serum calcium had risen to 5.2 mg/dl (urine concentration 2.8 mg/dl; urinary phosphorus > 350 mg/dl). Eight hours after admission the cerebrospinal fluid contained only two white cells.
From the University of Washington School of Medicine, and Department of Pediatrics, The Children's Orthopedic Hospital and Medical Center.
VoL 90, No. 3, pp. 484-485
Twenty-four hours after admission serum calcium concentration was 9.3 mg/dl and phosphorus 6.3 mg/dl. Intravenous administration of calcium was discontinued, and normal feeding was slowly resumed. Patient 2, This 3-year-old white boy was seen by his pediatrician because of an upper respiratory infection of a week's duration and lethargy and decreased urination for one day. Because of constipation, he was given a single pediatric size Fleet enema with minimal return of fluid in the first few minutes. Over the next two to three hours the infant had three voIuminous stools and three emeses. He became lethargic and pate and was admitted to the hospital. Temperature was 38~ pulse, 144; respiration, 16; blood pressure, 96/68; weight 8.4 kg. Mucous membranes were dry and skin turgor poor. Deep tendon reflexes were brisk and muscle tone was increased. Hemoglobin was 13.4 gm/dl; hematocrit, 40%; serum sodium, 152 mEq/1; potassium, 3.4 mEq/1; chloride, 108 mEq/l; CO., content, 17 mEq/1; blood urea nitrogen. 11 mg/dl; calcium, 6.3 mg/dl; phosphorus, 21.0 mg/dl. He improved after administration of intravenous fluids for 12 hours. Repeat laboratory data included a serum calcium value of 7.8 mg/dl and phosphorus, 5.2 mg/dl (urine calcium, 2.7 mg/dl; urine phosphorus, 30 mg/dl). DISCUSSION The patients developed acute dehydration, hypocalcemia, and hyperphosphatemia following the use of a single proprietary sodium phosphate/biophosphate enema (Fleet). The use of oral phosphate therapy to lower serum calcium in hypercalcemia of different causes has been described.' Hypocalcemic tetany and coma have been reported in infants who have been given phosphate orally for the treatment of diaper rash.: :~ The repeated administration of phosphate enemas has also been shown to produce hypernatremia and hypocalcemia and has been associated with one death from acute renal failure. ~ :' Recently there have been two reports of tetany in
Volume 90 Number 3
patients with chronic renal disease following the use of one Fleet phospho-soda enema. ''~ Neither patient reported here had a history of renal disease. Each patient was dehydrated, however, and thus renal clearance of phosphate was retarded until hydration was instituted. The serum calcium concentration returned to normal in each patient over a 24- to 48-hour period, correlating well with the hypothesis that sequestered calcium has a short half-life and is returned to the circulation? SUMMARY Previous reports of hypocalcemia and hyperphosphatemia following use of phosphate enemas have either been in patients with renal disease or followed prolonged abuse of these products. The two patients described here had marked elevation of serum phosphate and concomitant lowering of serum calcium secondary to absorption of phosphate from a single administered enema. Associated moderate dehydration resulted in poor renal excretion of the absorbed phosphate and prolongation of hypocalcemia. Hydration was effective in permitting clearance of phosphate and restoration of normocalcemia.
Adverse reactions following phosphate enema
485
REFERENCES
1. Goldsmith RS, and lngbar SH: Inorganic phosphate treatment of hypercalcemia of diverse etiologies, N Engl J Med 274: I, 1966. 2. Levitt M, Gessert C, and Finberg L: Inorganic phosphate poisoning resulting in tetany in a child, J P~DIATR82:479, 1973. 3. Smith MS, Feldman KW, and Furakawa CT: Coma in an infant due to hypertonic sodium phosphate medication, J PEDIATR82:481, 1973. 4. Mosley PK, and Segar WE: Fluid and serum electrolyte disturbances as a complication of enemas in Hirschsprung's disease, Am J Dis Child 115:115, 1968. 5. McCortnel T: Fatal hypocalcemia from phosphate reabsorption from a laxative preparation, JAMA 216:147, 1971. 6. Chesney RW, and Haughton PB: Tetany following phosphate enemas in chronic renal disease, Am J Dis Child 127:584, 1974. 7. Osmond SC, O'Bell J, and Grupe WE: Severe tetany in an azotemic child related to a sodium phosphate enema, Pediatrics 53:105, 1974. 8. Chaudhuri TK, and Chaudhuri TK: Mechanism of hypocalcemic effect of inorganic phosphate, N Engl J Med 285:12:691, 1971.
March 1977 TheJournalofPEDIATR1CS
Hypocalcemia, hyperphosphatemia, and dehydration following a single hypertonic phosphate enema Roy F. D a v i s , P h . D . , M . D . , J e r r o l d M . E i c h n e r , M . D . , W . Archie Bleyer, M . D . , and Gary Okamoto, M . D . , Seattle, Wash.
SEVERE HYPERPHOSPHATEMIA and hypocalcemia have been reported when sodium phosphate/biphosphate enemas (Fleet phospho-soda) are administered repeatedly or in the presence of renal failure. This communication reports the same adverse reaction following the use of a single enema in children with " n o r m a l " renal function.
CASE REPORTS Patient 1. A healthy, 4-month-old infant had had no bowel movement for five days and was given a one-half pediatric size Fleet enema on instruction from her physician. The infant vomited once following the enema and had four liquid bowel movements during the next ten hours. Mother described the infant as being "very stiff' while she was changing her diaper. Twelve hours after the enema, the infant was found to be lethargic and febrile and was admitted to the hospital. Rectal temperature was 38.6~ pulse, 156; respiration, 68: blood pressure, 90/50; weight, 3.96 kg. The infant was lethargic and hypertonic with a depressed fontanelle, poor skin turgot, and dry mucous membranes. Moderate nuchal rigidity, brisk deep tendon reflexes, and ankle clonus were noted. Chvostek and Trousseau signs were not present. The remainder of the physical examination was normal. Cerebrospinal fluid contained 10 white cells pe r mm:' (6 mononuclear and 4 polymorphonuclear cells), protein 15 mg/dl and glucose 47 mg/dl (concomitant blood glucose of 60 mg/dl). Serum sodium was 156 mEq/l; potassium, 3.5 mEq/1; chloride, 104 mEq/l: COs content, 15 mEq/1; blood urea nitrogen, 47 mg/dl; serum calcium, 4.6 mg/dl; phosphorus 28.6 mg/dl; magnesium. 1.7 mEq/1. QoTc interval by electrocardiogram was 0.24 second. The infant was treated with intravenous fluids and calcium gluconate. Four hours after admission her serum calcium had risen to 5.2 mg/dl (urine concentration 2.8 mg/dl; urinary phosphorus > 350 mg/dl). Eight hours after admission the cerebrospinal fluid contained only two white cells.
From the University of Washington School of Medicine, and Department of Pediatrics, The Children's Orthopedic Hospital and Medical Center.
VoL 90, No. 3, pp. 484-485
Twenty-four hours after admission serum calcium concentration was 9.3 mg/dl and phosphorus 6.3 mg/dl. Intravenous administration of calcium was discontinued, and normal feeding was slowly resumed. Patient 2, This 3-year-old white boy was seen by his pediatrician because of an upper respiratory infection of a week's duration and lethargy and decreased urination for one day. Because of constipation, he was given a single pediatric size Fleet enema with minimal return of fluid in the first few minutes. Over the next two to three hours the infant had three voIuminous stools and three emeses. He became lethargic and pate and was admitted to the hospital. Temperature was 38~ pulse, 144; respiration, 16; blood pressure, 96/68; weight 8.4 kg. Mucous membranes were dry and skin turgor poor. Deep tendon reflexes were brisk and muscle tone was increased. Hemoglobin was 13.4 gm/dl; hematocrit, 40%; serum sodium, 152 mEq/1; potassium, 3.4 mEq/1; chloride, 108 mEq/l; CO., content, 17 mEq/1; blood urea nitrogen. 11 mg/dl; calcium, 6.3 mg/dl; phosphorus, 21.0 mg/dl. He improved after administration of intravenous fluids for 12 hours. Repeat laboratory data included a serum calcium value of 7.8 mg/dl and phosphorus, 5.2 mg/dl (urine calcium, 2.7 mg/dl; urine phosphorus, 30 mg/dl). DISCUSSION The patients developed acute dehydration, hypocalcemia, and hyperphosphatemia following the use of a single proprietary sodium phosphate/biophosphate enema (Fleet). The use of oral phosphate therapy to lower serum calcium in hypercalcemia of different causes has been described.' Hypocalcemic tetany and coma have been reported in infants who have been given phosphate orally for the treatment of diaper rash.: :~ The repeated administration of phosphate enemas has also been shown to produce hypernatremia and hypocalcemia and has been associated with one death from acute renal failure. ~ :' Recently there have been two reports of tetany in
Volume 90 Number 3
patients with chronic renal disease following the use of one Fleet phospho-soda enema. ''~ Neither patient reported here had a history of renal disease. Each patient was dehydrated, however, and thus renal clearance of phosphate was retarded until hydration was instituted. The serum calcium concentration returned to normal in each patient over a 24- to 48-hour period, correlating well with the hypothesis that sequestered calcium has a short half-life and is returned to the circulation? SUMMARY Previous reports of hypocalcemia and hyperphosphatemia following use of phosphate enemas have either been in patients with renal disease or followed prolonged abuse of these products. The two patients described here had marked elevation of serum phosphate and concomitant lowering of serum calcium secondary to absorption of phosphate from a single administered enema. Associated moderate dehydration resulted in poor renal excretion of the absorbed phosphate and prolongation of hypocalcemia. Hydration was effective in permitting clearance of phosphate and restoration of normocalcemia.
Adverse reactions following phosphate enema
485
REFERENCES
1. Goldsmith RS, and lngbar SH: Inorganic phosphate treatment of hypercalcemia of diverse etiologies, N Engl J Med 274: I, 1966. 2. Levitt M, Gessert C, and Finberg L: Inorganic phosphate poisoning resulting in tetany in a child, J P~DIATR82:479, 1973. 3. Smith MS, Feldman KW, and Furakawa CT: Coma in an infant due to hypertonic sodium phosphate medication, J PEDIATR82:481, 1973. 4. Mosley PK, and Segar WE: Fluid and serum electrolyte disturbances as a complication of enemas in Hirschsprung's disease, Am J Dis Child 115:115, 1968. 5. McCortnel T: Fatal hypocalcemia from phosphate reabsorption from a laxative preparation, JAMA 216:147, 1971. 6. Chesney RW, and Haughton PB: Tetany following phosphate enemas in chronic renal disease, Am J Dis Child 127:584, 1974. 7. Osmond SC, O'Bell J, and Grupe WE: Severe tetany in an azotemic child related to a sodium phosphate enema, Pediatrics 53:105, 1974. 8. Chaudhuri TK, and Chaudhuri TK: Mechanism of hypocalcemic effect of inorganic phosphate, N Engl J Med 285:12:691, 1971.