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Hyperphosphatemia during magnesium sulfate infusion
International Journal of Gynecology & Obstetrics 46 (1994) 329-330
Letter to the editor
Hyperphosphatemia
during magnesium sulfate infusion M.L. Elks
Department of Internal Medicine, Texas Technical University, Health Sciences Center, School of Medicine, Lubbock, TX, USA Received 24 February 1994; revision received 5 April 1994; accepted5 April 1994
Keyworcis: Magnesium;
Calcium;
Phosphate
Hypocalcemia is a well-recognized complication of magnesium sulfate infusion [ 1,2]. The mechanism for this appears to be multifactorial, including effects on renal handing of calcium as well as effects on parathyroid hormone secretion [ 1,2], The effects of magnesium infusion on serum phosphate appear to be more variable. Some studies have shown minimal or no effects on serum phosphate [2], while others have shown a rise. In two women receiving magnesium sulfate to suppress labor, we observed a markedly elevated serum phosphorus. The first case was a 16-year-old GlPO who presented at 26 weeks with premature rupture of membranes and mild labor. She was treated with oral terbutaline (5 mg every 3 h), magnesium sulfate (2 g/h in continuous intravenous infusion) and antibiotics. On the 3rd day of hospitalization, the blood calcium was 5.6 mg/dl (normal 8.4-10.2), phosphorus 8.4 mg/dl (2.5-4.9), albumin 3.0 g/d1 (3.5-5.0) and magnesium 7.3 mg/dl (1.8-2.4). Parathyroid hormone level (intact, by Nichols Institute, San Juan Capistrano, CA, USA) was inappropriately normal (for the hypocalcemia) at 58 pg/ml (normal range 50-330 pg/ml). The patient was asymptomatic, mildly hyporeflexic, and without tetany, Chvostek’s or
Trousseau’s signs. No specific treatment was given for the hyperphosphatemia/hypocalcemia. Classical cesarean section was performed 1 day later for amnionitis. A male child, Apgar scores 6 and 7, was delivered. Maternal calcium and phosphorus returned to normal after delivery and discontinuation of magnesium. The second case was a 33-year-old G3P2 who presented at 33 weeks with vasa previa and mild contractions. Fetal lung studies showed immaturity, and the patient was treated with oral terbutaline (5 mg every 3 h) and magnesium sulfate at 2 g/h in continuous infusion. After 3 weeks of therapy, calcium was 6.8 mg/dl, phosphorus 8.0 mg/dl, albumin 3.6 g/d1 and magnesium 5.8 mg/dl. Parathyroid hormone was inappropriately normal at 72 pg/ml. The patient was asymptomatic, normoreflexic, and without tetany, Trousseau’s or Chvostek’s signs. No specific treatment was started. Classical cesarean section was performed at 37 weeks and 4 days and a female child, Apgar scores 6 and 8, was delivered. Maternal calcium and phosphorus returned to normal after delivery and discontinuation of the magnesium. Hypocalcemia is a well-recognized phenomenon during magnesium therapy, but effects on serum phosphorus are more variable (normal or increas-
0020-7292/94/$07.00 0 1994 International Federation of Gynecology and Obstetrics SSDI 0020-7292(94)02 104-7
330
Letters
to the editor/Int.
ed) in studies and clinical observation [l-4]. In several studies, the initial hypocalcemic response to magnesium infusion appears to be due to increased calcium excretion due to competition for reabsorption within the tubule [2]. Magnesium can also suppress parathyroid hormone secretion, which, in turn, alters renal phosphate excretion [4]. Thus, while there are dual effects that lead to calcium suppression - direct renal effects as well as suppression of parathyroid hormone secretion, the phosphate effects are probably solely dependent on the effects on parathyroid hormone. In studies of magnesium administration, there is a decrease in renal phosphate clearance and subsequent elevation of serum phosphorus, consistent with a decreased parathyroid hormone effect. In one study, there was also evidence for a suppressive effect of magnesium on the renal phosphaturic response to parathyroid hormone, perhaps by suppressing renal CAMP generation in response to parathyroid hormone [3]. Thus, hypocalcemia is a relatively constant finding in magnesium administration. The more
J. Gynecol.
Obstet.
46 (1994)
329-330
variable finding of hyperphosphatemia perhaps results from the variable degree (and timing) and the parathyroid hormone suppression and renal handling of phosphate. Other than observation and appropriate adjustments of magnesium administration, no other action appears necessary in the asymptomatic patient. References
111Cruikshank DP, Pitkin RM, Donnelly E, Reynolds RM: Urinary magnesium, calcium and phosphate excretion during magnesium sulfate infusion. Obstet Gynecol 58: 430, 1981. 121Cholst IN, Steinberg SF, Tropper PJ, Fox HE, Segre GV, Bliezikian JP: The influence of hypermagnesemia on serum calcium and parathyroid hormone levels in human subjects. N Engl J Med 310: 1221, 1984. 131 Slatopolsky E, Morrison MA, Yates J, Kiahr S: Inhibitory effects of hypermagnesemia on the renal action of parathyroid hormone. J Clin Invest 58: 1273, 1976. 141 Massry SG, Coburn JW, Kleeman CR: Evidence for suppression of parathyroid gland activity by hypermagnesemia. J Chn Invest 49: 1619, 1970.
Letter to the editor
Hyperphosphatemia
during magnesium sulfate infusion M.L. Elks
Department of Internal Medicine, Texas Technical University, Health Sciences Center, School of Medicine, Lubbock, TX, USA Received 24 February 1994; revision received 5 April 1994; accepted5 April 1994
Keyworcis: Magnesium;
Calcium;
Phosphate
Hypocalcemia is a well-recognized complication of magnesium sulfate infusion [ 1,2]. The mechanism for this appears to be multifactorial, including effects on renal handing of calcium as well as effects on parathyroid hormone secretion [ 1,2], The effects of magnesium infusion on serum phosphate appear to be more variable. Some studies have shown minimal or no effects on serum phosphate [2], while others have shown a rise. In two women receiving magnesium sulfate to suppress labor, we observed a markedly elevated serum phosphorus. The first case was a 16-year-old GlPO who presented at 26 weeks with premature rupture of membranes and mild labor. She was treated with oral terbutaline (5 mg every 3 h), magnesium sulfate (2 g/h in continuous intravenous infusion) and antibiotics. On the 3rd day of hospitalization, the blood calcium was 5.6 mg/dl (normal 8.4-10.2), phosphorus 8.4 mg/dl (2.5-4.9), albumin 3.0 g/d1 (3.5-5.0) and magnesium 7.3 mg/dl (1.8-2.4). Parathyroid hormone level (intact, by Nichols Institute, San Juan Capistrano, CA, USA) was inappropriately normal (for the hypocalcemia) at 58 pg/ml (normal range 50-330 pg/ml). The patient was asymptomatic, mildly hyporeflexic, and without tetany, Chvostek’s or
Trousseau’s signs. No specific treatment was given for the hyperphosphatemia/hypocalcemia. Classical cesarean section was performed 1 day later for amnionitis. A male child, Apgar scores 6 and 7, was delivered. Maternal calcium and phosphorus returned to normal after delivery and discontinuation of magnesium. The second case was a 33-year-old G3P2 who presented at 33 weeks with vasa previa and mild contractions. Fetal lung studies showed immaturity, and the patient was treated with oral terbutaline (5 mg every 3 h) and magnesium sulfate at 2 g/h in continuous infusion. After 3 weeks of therapy, calcium was 6.8 mg/dl, phosphorus 8.0 mg/dl, albumin 3.6 g/d1 and magnesium 5.8 mg/dl. Parathyroid hormone was inappropriately normal at 72 pg/ml. The patient was asymptomatic, normoreflexic, and without tetany, Trousseau’s or Chvostek’s signs. No specific treatment was started. Classical cesarean section was performed at 37 weeks and 4 days and a female child, Apgar scores 6 and 8, was delivered. Maternal calcium and phosphorus returned to normal after delivery and discontinuation of the magnesium. Hypocalcemia is a well-recognized phenomenon during magnesium therapy, but effects on serum phosphorus are more variable (normal or increas-
0020-7292/94/$07.00 0 1994 International Federation of Gynecology and Obstetrics SSDI 0020-7292(94)02 104-7
330
Letters
to the editor/Int.
ed) in studies and clinical observation [l-4]. In several studies, the initial hypocalcemic response to magnesium infusion appears to be due to increased calcium excretion due to competition for reabsorption within the tubule [2]. Magnesium can also suppress parathyroid hormone secretion, which, in turn, alters renal phosphate excretion [4]. Thus, while there are dual effects that lead to calcium suppression - direct renal effects as well as suppression of parathyroid hormone secretion, the phosphate effects are probably solely dependent on the effects on parathyroid hormone. In studies of magnesium administration, there is a decrease in renal phosphate clearance and subsequent elevation of serum phosphorus, consistent with a decreased parathyroid hormone effect. In one study, there was also evidence for a suppressive effect of magnesium on the renal phosphaturic response to parathyroid hormone, perhaps by suppressing renal CAMP generation in response to parathyroid hormone [3]. Thus, hypocalcemia is a relatively constant finding in magnesium administration. The more
J. Gynecol.
Obstet.
46 (1994)
329-330
variable finding of hyperphosphatemia perhaps results from the variable degree (and timing) and the parathyroid hormone suppression and renal handling of phosphate. Other than observation and appropriate adjustments of magnesium administration, no other action appears necessary in the asymptomatic patient. References
111Cruikshank DP, Pitkin RM, Donnelly E, Reynolds RM: Urinary magnesium, calcium and phosphate excretion during magnesium sulfate infusion. Obstet Gynecol 58: 430, 1981. 121Cholst IN, Steinberg SF, Tropper PJ, Fox HE, Segre GV, Bliezikian JP: The influence of hypermagnesemia on serum calcium and parathyroid hormone levels in human subjects. N Engl J Med 310: 1221, 1984. 131 Slatopolsky E, Morrison MA, Yates J, Kiahr S: Inhibitory effects of hypermagnesemia on the renal action of parathyroid hormone. J Clin Invest 58: 1273, 1976. 141 Massry SG, Coburn JW, Kleeman CR: Evidence for suppression of parathyroid gland activity by hypermagnesemia. J Chn Invest 49: 1619, 1970.