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CASE REPORT
Year : 2021  |  Volume : 11  |  Issue : 1  |  Page : 43-45

Magnesium sulfate toxicity – Are serum levels infallible?


Department of Obstetrics and Gynaecology, Mahatma Gandhi Medical College & Research Institute, Pondicherry, India

Date of Submission17-May-2020
Date of Acceptance03-Jul-2020
Date of Web Publication16-Apr-2021

Correspondence Address:
Prof. Sendhil C Arumugam
Department of Obstetrics and Gynaecology, Mahatma Gandhi Medical College & Research Institute, Pondicherry
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/joacc.JOACC_41_20

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  Abstract 


Since a century, we have been using magnesium sulfate for prophylaxis and treatment of eclamptic seizures. There are various regimens followed throughout the world. Although the efficacy is of no doubt, side effects remain a problem. Here, we present a rare case of magnesium toxicity with normal serum magnesium levels.

Keywords: Magnesium sulfate, Hemodialysis, paralysis, toxicity


How to cite this article:
Arumugam SC, Takkellapati A, John LB. Magnesium sulfate toxicity – Are serum levels infallible?. J Obstet Anaesth Crit Care 2021;11:43-5

How to cite this URL:
Arumugam SC, Takkellapati A, John LB. Magnesium sulfate toxicity – Are serum levels infallible?. J Obstet Anaesth Crit Care [serial online] 2021 [cited 2021 Jun 15];11:43-5. Available from: https://www.joacc.com/text.asp?2021/11/1/43/313910




  Introduction Top


Magnesium sulfate was first used to prevent eclamptic seizures in 1906 by Horn in Germany, who injected it intrathecally. An intramuscular regimen was used in 1926 to prevent recurrent seizures in women with eclampsia. The drug was given intravenously in 1933 to women with pre-eclampsia and eclampsia.[1] Since then, many regimens have been developed by Pritchard, Zuspan, Dhaka, and Sibai. Of these, the most commonly used regimen in India is Pritchard's regimen, followed by Zuspan.[2] Although the use of magnesium sulfate is common in obstetrics, its dose-related side effects like hypermagnesemia-induced lethargy, decreased reflexes, muscle weakness, respiratory muscle paralysis, paralytic ileus, and even cardiac arrest have always been of concern. Clinically significant hypermagnesemia is usually uncommon with normal renal function.[1] This case report is interesting because it presents a woman with features of magnesium sulfate toxicity with normal serum magnesium levels.


  Case Report Top


A 32-years-old, gravida 3 para1 live 1 abortion 1 at 36 weeks gestation, post cesarean pregnancy, recently diagnosed to have gestational hypertension, was referred to us for high blood pressure (BP) readings. During her anomaly ultrasonography, she was diagnosed to have placenta previa. She was known hypothyroid on regular treatment. At admission, her BP was 160/90 mmHg. She had no imminent symptoms. The patient was started on labetalol, and all necessary investigations were sent. Her blood investigations and her fundus examination were normal. A day post admission, she complained of labor pains and was taken up for emergency lower-section Caesarean section. She delivered a stillborn male child. Per operatively, it was noticed that the liquor was bloody with uterus showing Couvelaire changes. She developed atonic postpartum hemorrhage, which was medically managed. Postoperatively, Pritchard's regimen was started. Eight hours postoperatively, she complained of blurring of vision. Urgent fundus examination showed bilateral exudative retinal detachment. Twelve hours postoperatively, she complained of breathlessness and inability to move all four limbs. Her temperature, pulse rate, and BP were normal, with a drop in oxygen saturation and a decrease in a respiratory effort to only eight cycles per minute. Her urine output was normal. Bilateral knee jerks were absent, plantar reflexes were upgoing, and power of 2/5 was present in all four limbs. Urgent physician and neurophysician input were sought. They suspected intracranial bleed or cerebral edema and advised urgent computed tomography (CT). It was decided that, if the CT scan is normal, then her symptoms can be attributed to magnesium toxicity though her magnesium levels were in the therapeutic range (6.2 Meq/ml). The CT scan was normal, so she was shifted to the intensive care, fearing respiratory paralysis. As a trial, 10 ml of calcium gluconate was given slowly over 5 min with cardiac monitoring. Within a while, the power increased, but the respiratory difficulty persisted. After the nephrology consult, the patient received two sittings of hemodialysis and improved markedly over the next 48 h. She was shifted out of intensive care and discharged uneventfully.


  Discussion Top


Magnesium is the fourth most common cation in humans and is the second most abundant intracellular cation. Total body magnesium in the human body averages 2000 mEq (24 gm). Approximately half of this is stored in the bone and the rest is divided among other intracellular compartments, with only 1% in the extracellular space. Approximately one-third of this extracellular magnesium is protein bound.[3] The excretion of magnesium is mainly through the kidneys. Reabsorption occurs mainly in the proximal tubules, with 3% to 5% of filtered magnesium excreted in the urine. Renal tubular reabsorption is by active transport with cotransport of calcium.[3]

The pathogenesis of eclampsia remains unclear to date. The treatment of eclampsia has been a controversy for many decades. Magnesium sulfate is now being used for almost a century. There has been no doubt in the efficacy of the drug. The Magpie trial in 2006 concluded that the use of magnesium sulfate halves the relative risk of eclampsia, without appearing to have a substantive harmful effect on either the mother or the baby in the short term and long term.[4] In these earlier dosing regimens, toxicity has always been a concern. The Dhaka regimen halved the standard dose of magnesium sulfate.[5] It appeared to be as effective as the usual dose, sufficient to control convulsions and serum levels of magnesium remained lower than levels that produce toxicity. The various magnesium sulfate regimens are as given in [Table 1].
Table 1: Regimens of magnesium sulfate

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Magnesium sulfate serves as an anticonvulsant by increasing the seizure threshold . It also decreases the intracellular calcium which would inactivate the calmodulin dependent myosin light chain kinase activity and decreased contraction of the vascular smooth muscle cells. A serum magnesium level of 4 mg/dl to 8 mg/dl is considered as a therapeutic range for the anticonvulsant property. Any value of more than 9 mg/dl is considered as toxicity. The first sign of magnesium toxicity is usually the loss of patellar reflexes that occur with serum magnesium levels of 9 mg/dl to 12 mg/dl, and early signs of toxicity include nausea, feeling of warmth, flushing, somnolence, double vision, slurred speech, and weakness. Muscle paralysis and respiratory arrest will develop at plasma levels of 15 mg/dl to 17 mg/dl. A cardiac arrest will develop at plasma levels of 30 mg/dl to 35 mg/dl. Hence, the respiratory rate, urine output, and deep tendon reflexes should be monitored very closely.

Hypermagnesemia is rare and is likely in patients with impaired kidney function, especially when exposed to exogenous magnesium sources. In this case report, the patient presented with hypotonia and difficulty in breathing. She was suspected to have magnesium toxicity, although her magnesium levels were within the therapeutic range, as all other reports turned normal. In addition, her partial response to calcium gluconate, the antidote for magnesium toxicity, gave us a clue. A single sitting of trial hemodialysis showed a marked difference in the clinical picture, however, magnesium levels continued to remain in the therapeutic range.

A case report by Donnell, et al. in 2009 reported a case of magnesium toxicity in a patient undergoing cesarean delivery under general anesthesia. She received 13 gm of magnesium intraoperatively over 40 min. In the immediate postoperative period, she was unable to move her limbs and her respiratory pattern became erratic. She was managed with calcium gluconate, forced diuresis, and dextrose-insulin infusion.[7]

Swartjes, et al. reported a case of magnesium sulfate toxicity presenting as cardiopulmonary arrest. The patient had accidentally received 25 gm of magnesium sulfate instead of 4 gm. Immediate resuscitation was done and calcium gluconate was given.[8] Kumar, et al. reported a case of magnesium toxicity because of inadvertent infusion of a large dose of magnesium, approximately of 40 gm. The patient was managed with Intravenous calcium, fluids, and forced diuresis.[9] Al-Shoha, et al. reported a case of magnesium toxicity-induced ileus in a postpartum patient. She was managed with calcium and forced diuresis.[10]


  Conclusion Top


Monitoring of patients on magnesium sulfate therapy in severe pre-eclampsia should be done both clinically and using blood parameters, as renal failure patients may manifest signs of toxicity even within the therapeutic range. Thus, the determination of serum magnesium levels is helpful, but we should not solely rely on this, as it may be misleading. In severe cases of magnesium toxicity, hemodialysis can be considered as an option of treatment.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Idama TO, Lindow SW. Magnesium sulphate: A review of clinical pharmacology applied to obstetrics. BJOG Int J Obstet Gynaecol 1998;105:260-8.  Back to cited text no. 1
    
2.
Pratt JJ, Niedle PS, Vogel JP, Oladapo OT, Bohren M, Tunçalp Ö, et al. Alternative regimens of magnesium sulfate for treatment of preeclampsia and eclampsia: A systematic review of non-randomized studies. Acta Obstet Gynecol Scand 2016;95:144-56.  Back to cited text no. 2
    
3.
Graber TW, Yee AS, Baker FJ. Magnesium: Physiology, clinical disorders, and therapy. Ann Emerg Med 1981;10:49-57.  Back to cited text no. 3
    
4.
Altman D, Carroli G, Duley L, Farrell B, Moodley J, Neilson J, et al. Do women with preeclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: A randomised placebo-controlled trial. Lancet 2002;359:1877-90.  Back to cited text no. 4
    
5.
Begum R, Begum A, Johanson R, Ali MN, Akhter S. A low dose (”Dhaka”) magnesium sulphate regimen for eclampsia. Acta Obstet Gynecol Scand 2001;80:998-1002.  Back to cited text no. 5
    
6.
Okusanya B, Oladapo O, Long Q, Lumbiganon P, Carroli G, Qureshi Z, et al. Clinical pharmacokinetic properties of magnesium sulphate in women with pre-eclampsia and eclampsia. BJOG Int J Obstet Gynaecol 2016;123:356-66.  Back to cited text no. 6
    
7.
McDonnell NJ, Muchatuta NA, Paech MJ. Acute magnesium toxicity in an obstetric patient undergoing general anaesthesia for caesarean delivery. Int J Obstet Anesth 2010;19:226-31.  Back to cited text no. 7
    
8.
Swartjes JM, Schutte MF, Bleker OP. Management of eclampsia: Cardiopulmonary arrest resulting from magnesium sulfate overdose. Eur J Obstet Gynecol Reprod Biol 1992;47:73-5.  Back to cited text no. 8
    
9.
Kumar K, Al Arebi A, Singh I. Accidental intravenous infusion of a large dose of magnesium sulphate during labor: A case report. J Anaesthesiol Clin Pharmacol 2013;29:377-9.  Back to cited text no. 9
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10.
Al-Shoha M, Klair JS, Girotra M, Garcia-Saenz-de-Sicilia M. Magnesium toxicity-induced ileus in a postpartum patient treated for preeclampsia with magnesium sulphate. ACG Case Rep J 2015;2:227-9.  Back to cited text no. 10
    



 
 
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