David H. Chestnut MD, in Chestnut's Obstetric Anesthesia, 2020 Most women with severe preeclampsia will present to the operating room while receiving magnesium
sulfate for seizure prophylaxis. The magnesium infusion should continue throughout surgery to minimize the risk for eclampsia.2 The primary anesthetic considerations for women receiving magnesium sulfate is the interaction with nondepolarizing muscle relaxants. Magnesium sulfate, when appropriately administered, is generally a safe drug, but systems should be in place to avoid inadvertent infusion of large boluses of the drug. Although magnesium sulfate has
been used for tocolysis, it is relatively ineffective, and uterine tone is unlikely to be altered significantly.300 Magnesium inhibits the presynaptic release of acetylcholine at the neuromuscular junction, decreases the sensitivity of the postsynaptic receptor to acetylcholine, and depresses the excitability of the muscle fiber membrane. Magnesium sulfate increases the potency and duration of vecuronium, rocuronium, and
mivacurium.301–303 Several case reports have described a requirement for overnight mechanical ventilation after administration of routine doses of vecuronium in women receiving magnesium sulfate.304 Thus, if nondepolarizing muscle relaxants are used, they should be administered in very small doses. Interpretation of responses to peripheral nerve stimulation may be difficult in this setting. Many practitioners avoid the use of nondepolarizing
neuromuscular blocking agents in women with preeclampsia because of concern regarding residual postoperative neuromuscular blockade. Airway guidelines discuss the use of sugammadex for the reversal of neuromuscular blockade when rocuronium has been used for rapid-sequence induction. Studies in nonpregnant populations showed that peri-induction administration of magnesium sulfate 40 to 60 mg/kg did not delay reversal of neuromuscular blockade with
sugammadex.305,306 No cases of recurarization were observed. Although these studies did not address the patient with preeclampsia who is receiving magnesium, several case reports of magnesium use in women with severe preeclampsia support the contention that magnesium does not influence reversal with sugammadex.307 Even though succinylcholine mimics acetylcholine at the nerve terminal, the onset and duration
of a single intubating dose is not prolonged when administered concurrently with a magnesium sulfate infusion308; a routine intubating dose of 1 to 1.5 mg/kg should be used during rapid-sequence induction of anesthesia. Although some reports have suggested that co-administration of a calcium entry–blocking agent and magnesium may cause hypotension and/or neuromuscular blockade,182–184,309 more recent
information suggests that these medications can be used safely together.184 Magnesium SulfateMark G. Papich DVM, MS, DACVCP, in Saunders Handbook of Veterinary Drugs (Fourth Edition), 2016 Indications and clinical usesMagnesium sulfate is used for constipation and bowel evacuation prior to certain procedures. An injectable solution of magnesium sulfate is used to treat magnesium deficiency and refractory arrhythmias in patients who are critically ill. (Magnesium chloride also has been used.) A dose of 1-2 mEq/kg of magnesium sulfate produced plasma concentrations of 8.5-12.2 mEq/L, and can increase heart rate, inotropy, and cardiac output. In horses, magnesium sulfate is administered for ventricular tachycardia that is not responsive to other drugs. In cattle, magnesium sulfate is used to treat hypomagnesemia, especially in dairy cattle. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B978032324485500351X Fetal and Neonatal Neurologic InjuryDavid H. Chestnut MD, in Chestnut's Obstetric Anesthesia, 2020 Magnesium Sulfate and Cerebral PalsyUntil recently there was considerable controversy regarding the role of magnesium sulfate in preventing or possibly exacerbating fetal brain injury. Some controversy remains, but the publication of several large randomized studies of the effect of antenatal maternal magnesium sulfate administration on offspring outcome has dramatically altered practice guidelines and clinical practice.206–208 Although none of these studies demonstrated significant improvement in the primary outcome, all showed reduced cognitive morbidity, and none showed any increase in pediatric morbidity or mortality associated with magnesium sulfate use for neuroprotection. In a placebo-controlled trial of women who were thought likely to deliver within 24 hours and before 30 weeks’ gestation in New Zealand and Australia, Crowther et al.206 reported a lower incidence of substantial gross motor dysfunction (3.4% vs. 6.6%; relative risk [RR], 0.51; 95% CI, 0.29 to 0.91) and combined death or substantial gross motor dysfunction (17% versus 22.7%; RR, 0.75; 95% CI, 0.59 to 0.96) in children whose mothers were randomized to receive antenatal magnesium sulfate treatment. In another large trial from France, which included women in preterm labor before 33 weeks’ gestation, a significant reduction in death and/or gross motor dysfunction was again identified in the children whose mothers received magnesium sulfate (25.6% versus 30.8%; OR, 0.62; 95% CI, 0.41 to 0.99).207 A reduction in death and/or motor or cognitive dysfunction (34.9% versus 40.5%; OR, 0.68; 95% CI, 0.47 to 0.99) was observed in the magnesium-exposed offspring at 2 years of age.207 Finally, a randomized, controlled multicenter trial in the United States found that fetal exposure to magnesium sulfate within 24 hours of preterm delivery (between 24 and 32 completed weeks’ gestational age) did not reduce the combined risk for moderate or severe cerebral palsy or death. However, fetal exposure to magnesium sulfate reduced the risk for moderate or severe cerebral palsy among survivors (1.9% versus 3.5%; RR, 0.55; 95% CI, 0.32 to 0.95) and was associated with a decreased overall rate of cerebral palsy (4.2% versus 7.3%;P = .004).208 Although the results are optimistic, it is difficult to compare these trials owing to differences in inclusion criteria, study interventions/dosages, and outcomes. Nonetheless, after the publications of these trials, it has been concluded from meta-analyses that fetal exposure to magnesium sulfate may reduce the risk for cerebral palsy without increasing the risk for neonatal death.209,210 In 2010, the ACOG and the SMFM released a joint committee opinion that supported antenatal maternal magnesium sulfate administration for fetal neuroprotection, stating that the available evidence suggests that magnesium sulfate administered before anticipated early preterm birth reduces the risk for cerebral palsy in surviving infants.211 Physicians electing to use magnesium sulfate for fetal neuroprotection should develop specific guidelines regarding inclusion criteria, treatment regimens, concurrent tocolysis, and monitoring. The ACOG and the SMFM have concluded that it is reasonable to use a protocol based on one of the large randomized trials206–208; magnesium sulfate should be offered to women at high risk for anticipated preterm delivery (< 28 to 32 weeks’ gestational age) within 24 hours. A loading dose of magnesium sulfate 4 to 6 g should be administered, followed by a maintenance infusion of 1 to 2 g/h for 12 to 24 hours, at which point the risk for impending preterm delivery should be reassessed. If there is no longer a concern for impending delivery, the magnesium sulfate should be discontinued and restarted with active labor or when delivery is again thought to be imminent. Cardiovascular medications in pregnancyAndrew Youmans, in Clinical Pharmacology During Pregnancy (Second Edition), 2022 16.5.7 Magnesium sulfateMagnesium sulfate is a unique medication in the obstetrical community. It is a vital medication for the treatment and management of preeclampsia, particularly the neurological effects [3]. Its primary mechanism of action is through cerebral vasodilation. If preeclampsia is suspected, magnesium sulfate should be started promptly [3]. Magnesium sulfate alone may not reduce blood pressure to safe levels. Medications like hydralazine may be used to quickly bring blood pressure to safe levels concurrently with the infusion of magnesium sulfate. For nonobstetric providers, it may seem counterintuitive to administer magnesium sulfate for seizure, where benzodiazepines are a first-line medication in nonpregnant patients and medications like levetiracetam (Keppra) are also used; magnesium sulfate is the primary medication for seizure in pregnant women as it is likely to be related to preeclampsia or eclampsia. Magnesium has several side effects and requires monitoring to ensure serum levels are not exceeding safe thresholds. High magnesium levels can lead to lethargy, decreased reflexes, hypotension, pulmonary edema, and respiratory issues. Most common is a general feeling of malaise. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780128189023000099 Obstetric Management of PrematurityRichard J. Martin MBBS, FRACP, in Fanaroff and Martin's Neonatal-Perinatal Medicine, 2020 Magnesium SulfateMagnesium sulfate has been one of the most commonly used tocolytic agents, especially since it has been shown to have fetal neuroprotective effects. Magnesium appears to have similar efficacy with fewer side effects than terbutaline. Magnesium has tocolytic properties by acting as a calcium competitor in the sarcoplasmic reticulum, diminishing the interaction of calcium with the actin-myosin complex and interfering with myometrial repolarization.72,98 Magnesium may also block influx of extracellular calcium and disrupt intracellular release of calcium via inositol triphosphate pathways. Ultimately, the release of acetylcholine at the neuromuscular junction is decreased, leading to decreased amplitude of motor endplate potential and leading to decreased sensitivity. Magnesium sulfate is administered intravenously and is normally given as an initial bolus of 4-6 g over 30 minutes, followed by a maintenance infusion of 1-4 g/hr. In contrast to intravenous magnesium sulfate for tocolysis, oral magnesium therapy is not effective for the treatment of preterm labor. Magnesium is a bivalent cation, and it is the second-most common intracellular cation.48 Less than 1% is found extracellularly. It is most commonly found in bone (53%), followed by myocytes (27%).185 Most extracellular magnesium is in ionized form and its serum level drops in pregnancy secondary to hemodilution of pregnancy.99,183 It is transported across the cell membrane through a sodium-ATP-dependent transporter. Magnesium is almost exclusively excreted by the kidneys. Approximately 75% of the infused dose of magnesium is excreted during the actual infusion, with 90% excretion by 24 hours. Magnesium is reabsorbed at the renal level by a transport-limited mechanism; therefore, the glomerular filtration rate significantly affects excretion. Serum magnesium levels of 5-8 mg/dL are considered therapeutic for inhibiting myometrial activity on the basis of in vitro studies. Once cessation of uterine activity is achieved, the patient is maintained at the lowest possible rate for 12-24 hours and then weaned off as tolerated. Maternal side effects caused by magnesium sulfate are typically dose related. Common side effects include flushing, heat intolerance, nausea, headache, drowsiness, and blurry vision. Constant monitoring of deep tendon reflexes is mandatory to avoid toxicity. Diminished deep tendon reflexes occur when serum magnesium levels reach or exceed 12 mg/dL (10 mEq/L). Significant respiratory depression can occur as serum levels reach 14-18 mg/dL (12-14 mEq/L), and cardiac arrest may occur with levels greater than 18 mg/dL (15 mEq/L). In general, respiratory depression does not occur before loss of deep tendon reflexes. The toxic effects of high magnesium levels can be rapidly reversed with the infusion of 1 g of calcium gluconate. Uterotonics and tocolyticsJeffrey S. Fouche-Camargo, in Clinical Pharmacology During Pregnancy (Second Edition), 2022 18.3.1 Magnesium sulfateMagnesium sulfate was first used as a tocolytic in the 1960s after it was shown to reduce uterine contractility both in vitro and in vivo [19]. Magnesium acts via extracellular and intracellular mechanisms to decrease intracellular calcium concentrations, thereby preventing the contractile response [20]. The most recent literature on the use of magnesium sulfate is highly variable on its efficacy and recommendations for use [21–25]. Even when different authors examined the same studies, different conclusions were reached. In the United States, the use of magnesium sulfate for acute tocolysis is still accepted [21]. Magnesium sulfate has an additional indication for threatened preterm birth at less than 32 weeks gestation: fetal neuroprotection [21]. When used for tocolysis, it is recommended not to exceed 48 h of administration [21]. Magnesium sulfate is usually administered with a loading dose of 4–6 g over 20–30 min, followed by a maintenance dose of 2 g/h. To prevent dosing errors, the loading dose should be administered from a separate premixed bag with the prescribed dose. Magnesium sulfate must be administered via an infusion pump and requires close observation, particularly during the loading dose. The most common side effects include flushing, nausea, headache, generalized muscle weakness, and diplopia. The patient must be monitored for signs of magnesium toxicity: absent deep tendon reflexes, respiratory depression, pulmonary edema, cardiac arrythmias, and cardiopulmonary arrest. Magnesium sulfate is excreted via the kidneys, so careful intake and output monitoring is indicated. In the presence of renal impairment, the likelihood of magnesium toxicity is increased. The antidote for magnesium toxicity is calcium gluconate, which should be readily available. Magnesium sulfate is contraindicated in patients with myasthenia gravis. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780128189023000038 Volume 2
Sam Mesiano, ... Louis J. Muglia, in Knobil and Neill's Physiology of Reproduction (Fourth Edition), 2015 Magnesium SulfateMagnesium sulfate was until recently the most frequently used tocolytic agent for treatment of preterm labor.645 Following harsh criticism in the obstetric literature regarding its lack of proven efficacy and concerns regarding its high risk of adverse side effects, many obstetric practitioners have begun to use calcium channel blockers rather than magnesium sulfate for first-line treatment of preterm labor.646 The mechanism of action of magnesium sulfate is not as well described as that of calcium channel blockers, but it appears to function in a similar manner by competitively blocking intracellular calcium channels, decreasing calcium availability and thus inhibiting smooth muscle contractility.647 It also competes with calcium at the motor end plate, where it reduces excitation by inhibiting acetyl choline release.648 Magnesium sulfate has poor patient tolerance when administered in adequate doses for tocolysis. Due to limited evidence of benefit, maternal risk of toxicity, and poor patient tolerance, the use of magnesium for the treatment of preterm labor is decreasing in recent years in favor of other tocolytic agents. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780123971753000429 SuxamethoniumIn Meyler's Side Effects of Drugs (Sixteenth Edition), 2016 Magnesium sulfateMagnesium sulfate is used mostly in the treatment of toxemia of pregnancy. Serum magnesium concentrations may be raised and, as magnesium inhibits the release of acetylcholine and reduces the sensitivity of the postjunctional membrane, the action of non-depolarizing agents will be prolonged. It is not so clear, however, why the action of suxamethonium is also prolonged [372–375]. Suxamethonium-induced fasciculation are reportedly prevented [376]. It has been suggested that the administration of intravenous magnesium sulfate should be stopped 20–30 minutes before muscle relaxants are given. Monitoring with a nerve stimulator is advisable. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780444537171014955 Prevention of Preeclampsia and EclampsiaAnne Cathrine Staff, ... F.Gary Cunningham, in Chesley's Hypertensive Disorders in Pregnancy (Fourth Edition), 2015 Treatment for Eclampsia (See Chapter 20)It is generally agreed that anticonvulsant treatment is necessary for the prevention of recurrent seizures in women with eclampsia. In the United States, magnesium sulfate has been used for this purpose for over 60 years. Until relatively recently, this was criticized as empirical and dogmatic because it had never been tested in randomized trials. The results of four large observational studies that address this are shown in Table 12.14.81–84 The overall rate of recurrent seizures among these studies is 11%. This in part stimulated the design of randomized trials to compare magnesium sulfate with traditional anticonvulsants. Table 12.14. Incidence of Recurrent Convulsions in Eclamptic Women Given Magnesium Sulfate
In apparently only one multicenter trial was there an adequate sample size to compute a significant difference between magnesium sulfate and the comparative drugs. The Collaborative Eclampsia Trial85 was conducted in several centers in South Africa and South America. The trial included 1680 eclamptic women who were randomized to magnesium sulfate, phenytoin, or diazepam in two different randomization schemes. As shown in Table 12.15, magnesium sulfate was superior to both phenytoin and diazepam to prevent recurrent seizures in eclamptic women. In addition, the data by Bhalla et al.88 indicate that magnesium sulfate is superior to lytic cocktail in this regard. Table 12.15. Randomized Trials Comparing Magnesium Sulfate with Other Anticonvulsants in Women with Eclampsia
The protective effects of magnesium sulfate to decrease maternal mortality with eclampsia are shown in Table 12.16. Overall, magnesium sulfate therapy was associated with significantly lower maternal mortality – 3.0% versus 4.8% compared with other anticonvulsants (p<0.05). Table 12.16. Maternal Deaths in Trials Comparing Magnesium Sulfate with Other Anticonvulsants in Women with Eclampsia
Side Effects and ToxicityMagnesium sulfate has a high rate of minor side effects such as an intense warm feeling, flushing, nausea or vomiting, muscle weakness, dizziness, and irritation at the injection site. The reported rates of these effects in randomized trials ranged from 15 to 67%.73,79,80,84 Side effects were the most common reason for discontinuation of treatment in the Magpie Trial.79 The most concerning major side effect of magnesium sulfate is respiratory depression.79,80 While postpartum hemorrhage has been reported,73 its incidence was not increased in the Magpie Trial.79 Life-threatening magnesium toxicity is rare with proper dosing, administration, and monitoring during therapy. That said, maternal deaths or “near misses” from magnesium overdose have been reported from the United States and require vigilance to prevent.83,90–92 Initiation, Dose, Duration, and Route of AdministrationRandomized trials vary widely regarding the optimal time to initiate magnesium sulfate, loading and maintenance dosing, route of administration, and duration of therapy. In all trials except in some women enrolled in the Magpie Trial,79 magnesium sulfate was started once the decision for delivery was made. In some trials, magnesium sulfate was given during labor and delivery, and for up to 24 hours postpartum.73,74,77,80 In contrast, in two of the trials,78,79 magnesium sulfate was only given for a maximum of 24 hours. In the Magpie Trial,79 some women did not receive the drug during labor, delivery, or postpartum.79 Among the trials utilizing the intravenous regimen, the loading dose ranged from 4 to 6 g, and the maintenance dose ranged from 1 to 2 g per hour. In most trials73,74,78,80 magnesium sulfate was given by continuous infusion. In the trial by Moodley and Moodley,77 the loading dose was given intravenously and the maintenance dose intramuscularly. In the Magpie Trial,79 several of these combinations were used and side effects with the intramuscular regimen were more common – 28% versus 5%, respectively – and as a result more women in this group stopped the medication early (28% versus 5%). This variation in the route of administration and the total amount of magnesium sulfate used in the various trials possibly explains the differences in seizure rates and side effects among those assigned to magnesium sulfate. Because of these protocol variations, investigators from the University of Mississippi Medical Center have suggested an individualized postpartum magnesium sulfate protocol based on clinical parameters in women with preeclampsia.93,94 Their first study93 included 103 women with mild and 55 with severe preeclampsia. Postpartum women with mild disease received a minimum of 6 hours of intravenous magnesium sulfate, and those with severe preeclampsia received a minimum of 12 hours infusion. This protocol was based on blood pressure levels, need for antihypertensive therapy, onset of diuresis, and presence of symptoms. Women with mild preeclampsia required an average duration of magnesium sulfate therapy of 9.5±4.2 hours, whereas those with severe disease required an average infusion of 16±5.9 hours. Those with HELLP syndrome required an average duration of therapy of 20±6.7 hours. Although there were no cases of eclampsia, the sample size is inadequate to evaluate efficacy for convulsions. In their second study, Isler et al.94 evaluated an individualized protocol for postpartum magnesium sulfate therapy in 284 women with mild preeclampsia and 105 with severe preeclampsia. Like the first study, this protocol also was based on blood pressure levels, onset of use of antihypertensive drugs, diuresis, and symptoms. Magnesium sulfate was given for 2 to 72 hours in those with mild disease and up to 77 hours postpartum in those with severe disease. Magnesium sulfate therapy which had been discontinued was reinstituted based on clinical parameters in 6.3% of women with mild or severe disease and in 18% of those with superimposed preeclampsia. Again, there were no cases of eclampsia, but the number of women included in this study – most had mild disease – is inadequate to draw any conclusions regarding efficacy. Because such a protocol requires intensive postpartum monitoring, it is impractical compared with an empirical protocol and is not used in the United States. Fontenot et al.95 reported a randomized trial of magnesium sulfate given postpartum to 98 women with severe preeclampsia. One group of 50 were given 24 hours of therapy, whereas the other group of 48 were given therapy until the onset of diuresis. Women in the latter group had a shorter duration of therapy compared with those treated empirically for 24 hours – 507±480 versus 1442±158 minutes, respectively. There were no cases of eclampsia, and the postpartum hospital stays were not significantly different – 3.1±1.1 versus 3.5±1.1 days, respectively. Ehrenberg and Mercer96 performed a randomized trial comparing a 12-hour to a 24-hour course of postpartum magnesium sulfate for women with mild preeclampsia. In the 107 women assigned to the 12-hour regimen, magnesium sulfate therapy was extended in seven for progression to severe disease compared with only one in the 24-hour group (p=0.07). There were no seizures, but women with chronic hypertension and insulin-requiring diabetes were at risk of progression to severe disease. Again, the small number of subjects in this study hampers the generaliziblity of these regimens. Dayicioglu et al.97 evaluated serum magnesium levels and efficacy of a standardized magnesium sulfate dose of 4.5 g loading over 15 minutes followed by 1.8 g/h in 183 women with preeclampsia. Serum magnesium levels were obtained within the first 2 hours, and every 6 hours in the subsequent 42 hours. In addition, serum creatinine levels and creatinine clearances were also studied to correlate with magnesium levels. They reported that most magnesium serum levels were<4.8 mg/dL in women whose BMI was≥36. Nine women developed postpartum convulsions while still receiving magnesium sulfate, and four of these were women with a low BMI. They found no association between eclampsia treatment failures and BMI or with serum magnesium levels. They also found no association between serum magnesium levels and serum creatinine or creatinine clearance. The effects of obesity on magnesium levels were further outlined in the study by Tudela et al.,98 who reported that 40% of women whose BMI was above 30 kg/m2 required a maintenance dose of 3 g/h of magnesium sulfate to achieve “therapeutic” levels. Thus, a review of randomized trials indicates that magnesium sulfate is the best available agent to use as prophylaxis in women with severe preeclampsia and for treatment of eclamptic convulsions. A Cochrane review in 2010 concluded that magnesium sulfate therapy more than halved the the risk of an eclamptic convulsion, and appeared to reduce maternal death.99 There is limited information regarding the efficacy of magnesium sulfate for prophylaxis in women with mild hypertension or preeclampsia, and there is a need for blinded placebo-controlled studies to address this. Questions remain regarding the optimal time to initiate magnesium sulfate as well as the dose and the duration of administration in the postpartum period. In sum, differences in approaches are used by practitioners regarding magnesium sulfate therapy, and this topic will be revisited in Chapter 20. At this time, magnesium prophylaxis for severe preeclampsia and treatment for eclampsia are recommended both by NICE guidelines15 as well as by the American College of Obstetricians and Gynecologists.37 Prevention of Long-Term Maternal Health Risks Following PreeclampsiaPreeclampsia identifies a group of women with increased risk of cardiovascular disease later in life. This is discussed in detail in Chapter 3. At present there is no agreement on how best to follow up this group of women after preeclampsia in order to prevent or reduce the severity of long-term health complications. In addition, whether prevention strategies for preeclampsia also reduce the risk of future cardiovascular disease is unknown. The general recommendation of combined physical activity and weight control is applicable to the group of women having had preeclampsia, but its efficacy is not well documented. A major challenge again is identifying the optimal target group among the heterogeneous preeclampsia group for follow-up and potential cardiovascular disease prevention studies.100 Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780124078666000122 Encephalopathy of PrematurityJeffrey J. Neil, Joseph J. Volpe, in Volpe's Neurology of the Newborn (Sixth Edition), 2018 Antenatal MagnesiumMagnesium sulfate has been used for many years in obstetrics as a tocolytic agent for preterm labor and as therapy for preeclampsia. The evidence of its effectiveness for the latter purpose is stronger than that concerning its role as a tocolytic (see Chapter 24). Particular interest for the maternal use of magnesium sulfate in the prevention of neurological deficits in infants born prematurely began with a report that only 7.1% of VLBW infants with later cerebral palsy were exposed to maternal magnesium sulfate versus 36% of a control group.213 In a subsequent study of approximately 1000 premature infants, those whose mothers received magnesium sulfate had a lower prevalence of cerebral palsy (0.9%) than those whose mothers did not receive this agent (7.7%).214 However, subsequent evidence regarding benefit for magnesium sulfate for prevention of cerebral palsy or associated brain lesions or both has not been consistently positive.215-231 Meta-analyses have shown that antenatal magnesium sulfate administered for neuroprotection in preterm infants is associated with a reduction of cerebral palsy at a corrected age of 18 to 24 months,232-234 but studies of longer-term outcomes have failed to show benefit.235,236 Experimental studies concerning a beneficial role for magnesium in prevention or amelioration of hypoxic-ischemic death also have yielded conflicting results. Thus, in perinatal hypoxic-ischemic models in the rat, piglet, and fetal lamb, magnesium sulfate treatment either during or immediately following the insult did not ameliorate adverse biochemical, neurophysiological, or neuropathological effects.237-239 Nevertheless, other experimental work supported the potential value of magnesium by several mechanisms (i.e., antiexcitatory amino acid [impairs release, blocks the N-methyl-d-aspartate (NMDA) receptor], antioxidant [essential for glutathione biosynthesis], anticytokine [decreases levels of inflammatory cytokines], and antiplatelet [decreases platelet aggregation] effects).240-246 Perhaps the most likely beneficial effect of magnesium relates to its strong vasodilatory properties, which can lead to an increase in uteroplacental blood flow and perhaps also to improved fetal perfusion.247-251 Such effects also could decrease the likelihood that the infant postnatally would experience a pressure-passive cerebral circulation and thereby cerebral ischemia and periventricular white matter injury (see Chapter 13). A recent large randomized trial suggests that the gestational age of the infant may be critical in determining whether antenatal magnesium sulfate is beneficial.252 Thus, in infants born at less than 32 weeks of gestation, 82% of the preterm infants in the study, magnesium sulfate was associated with a reduction in occurrence of echolucency or echodensity. Moreover, a reduced risk of cerebral palsy at 2 years of age (OR 0.63, 95%, CI 0.42 to 0.95) was observed and could be partially accounted for by the ultrasonographic findings. More data are needed on these issues. Read full chapter URL: https://www.sciencedirect.com/science/article/pii/B9780323428767000168 What are the risks to mother and fetus in condition of magnesium toxicity?In a baby, magnesium toxicity can cause low muscle tone. This is caused by poor muscle control and low bone density. These conditions can put a baby at greater risk for injuries, such as bone fractures, and even death.
How does magnesium sulfate affect the fetus?Administration of magnesium sulfate injection to pregnant women longer than 5-7 days may lead to low calcium levels and bone problems in the developing baby or fetus, including thin bones, called osteopenia, and bone breaks, called fractures.
What are the side effects of magnesium sulfate toxicity?What Are Side Effects of Magnesium Sulfate?. heart disturbances,. breathing difficulties,. poor reflexes,. confusion,. weakness,. flushing (warmth, redness, or tingly feeling),. sweating,. lowered blood pressure,. What pregnancy risk category is magnesium sulfate?Abstract. The U.S. Food and Drug Administration advises against the use of magnesium sulfate injections for more than 5-7 days to stop preterm labor in pregnant women. Based on this, the drug classification was changed from Category A to Category D, and the labeling was changed to include this new warning information.
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What are the risks to the mother and fetus in states of magnesium sulfate toxicity?
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