Magnesium Sulfate In Patients Research Articles

Role of magnesium sulphate in ischemic stroke

Objective: To evaluate the role of magnesium sulphate in patients presenting with ischaemic stroke. Methods: This experimental type of interventional study was carried out at Mayo Hospital, Lahore. Within 24 hours of onset of clinically diagnosed stroke, which was later confirmed by CT scan, patients were randomized to receive either magnesium sulphate (16mmol IV over 15 minutes and 65mmol over 24 hours) or placebo. Their disability was measured by Barthel score at presentation and outcome measured after three months by death and disability and the results were compared between the two groups. Those patients who had a Barthel score of = 12 at three months were considered independent and those with a score of < 12 were considered disabled. The results were analyzed by SPSS. Results: Fifty patients were recruited in the study. 25 patients were randomized to receive MgSO4 and 25 received placebo. The Barthel score improved from 5.13.3 at presentation to 13.53.4 after three months in all the patients so the re was improvement whether MgSO4 was given or not. Patients who were randomized to receive MgSO4 had a lower Barthel score of 4.22.9 as compared to controls 5.9 3.5, but after three months they improved more than the controls gaining a score of 15.71.9 versus 11.33.2 (p=0.000). The mortality rate was not statistically different in the two groups. 88% patients had a Barthel score of > 12 at three months in the MgSO4 and 30% in the control/placebo group. Combined death and disability was 8% in MgSO4 group and 60% in the control group. Moreover MgSO4 was well tolerated. Conclusion: Magnesium sulphate therapy was safe in patients presenting with ischaemic stroke irrespective of the site of infarct. It improves prognosis regarding Barthel score at three months as well as the difference in the Barthel score at presentation and at three months. A greater percentage of magnesium treated patients led independent lives after three months.

Prehospital Initiation of Magnesium Sulfate in Patients with Acute Intracerebral Hemorrhage (S39.003)

Prehospital Initiation of Magnesium Sulfate in Patients with Acute Intracerebral Hemorrhage (S39.003)

Prophylactic Magnesium Sulfate for Aneurysmal Subarachnoid Hemorrhage: A Systematic Review and Meta-analysis

Delayed cerebral ischemia following aneurysmal subarachnoid hemorrhage is a cause of considerable morbidity and mortality. Magnesium sulfate has been proposed as a prophylactic intervention for angiographic vasospasm and to improve clinical outcomes. A systematic review was conducted to determine the evidence for the prophylactic use of magnesium sulfate in aneurysmal subarachnoid hemorrhage. Medline, Embase, Cochrane library, clinicaltrials.gov, and controlled-trials.com were searched with a comprehensive search strategy. 2,035 records were identified in the initial search and 1,574 remained after removal of duplicates. Randomized, parallel group, controlled trials of magnesium sulfate in patients with aneurysmal subarachnoid hemorrhage were included. A total of ten studies were included. Review Manager and GRADE software were used to synthesize the results. The summary effect for Glasgow outcome scale and the modified Rankin scale is a risk ratio (RR) of 0.93 [95 % confidence interval (CI) 0.82-1.06]. The RR for mortality is 0.95 [95 % CI 0.76-1.17]. Delayed cerebral ischemia has a RR of 0.54 [95 % CI 0.38-0.75], which is the only outcome with a statistically significant summary effect measure favoring magnesium treatment. Delayed ischemic neurological deficit has a RR of 0.93 [95 % CI 0.62-1.39]. Transcranial doppler vasospasm has a RR of 0.72 [95 % CI 0.51-1.03]. Current evidence does not support the prophylactic use of magnesium sulfate in aneurysmal subarachnoid hemorrhage.

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Magnesium

Magnesium sulfate for aneurysmal subarachnoid hemorrhage: the end of the road or more trials?

Delayed cerebral ischemia (DCI) is a feared complication and an important cause of poor outcome after aneurysmal subarachnoid hemorrhage (SAH). In the current study, Wong and colleagues performed a systematic review and meta-analysis of randomized controlled trials that investigated the efficacy of magnesium sulfate in patients with aneurysmal SAH. Outcome measures were DCI, cerebral infarction, and functional outcome 3 and 6 months after SAH. Magnesium sulfate decreased the rate of cerebral infarction, but not of DCI or poor functional outcome. Regarding outcome, a beneficial effect of magnesium sulfate on outcome can not be ruled out because of sample size limitations. Even if this meta-analysis had shown an effect on outcome, the question remains which treatment protocol should be applied in daily practice, since the administration of magnesium sulfate differed between most included studies. The present meta-analysis also underlines the importance of defining clinically relevant endpoints in SAH trials. Clinical deterioration due to DCI is more subject to inter-observer bias compared to cerebral infarction, which represents the ultimate outcome of the ischemic event. The Magnesium in Aneurysmal Subarachnoid Hemorrhage-II (MASH-II: ISRCTN68742385) phase III clinical trial nears completion. It aims to include 1,200 patients, and its results are urgently awaited.

Magnesium Sulfate Treatment Improves Outcome in Patients with Subarachnoid Hemorrhage: A Meta-analysis Study

To elucidate the role of magnesium sulfate in patients with subarachnoid hemorrhagic (SAH) brain injury Studies for the meta-analysis were identified from PubMed (1966 to 2009), Embase (1980 to 2009), and two Chinese journals (1989 to 2009). Paper selection was based on randomized controlled trials comparing magnesium sulfate to placebo treatment in patients with SAH. Two independent review authors extracted the data and assessed trial quality. Meta-analysis was performed using the Cochrane Review Manger software. Five trials involving 482 patients were included in the review. Magnesium sulfate reduced the risk of poor outcome and reduced the occurrence of delayed cerebral ischemia. In the treatment groups, relative risk for poor outcome was 0.73 (CI 0.57-0.93) and 0.66 (CI 0.47-0.92) for delayed cerebral ischemia. Case fatality assessment at three to six months did not show statistically significant data (RR 0.88; CI 0.61-1.29). Magnesium sulfate appears to be an effective treatment option in the management of SAH. Further clinical trials are needed before magnesium sulfate can become a routine treatment for SAH.

Intravenous Magnesium Sulphate for Aneurysmal Subarachnoid Hemorrhage (IMASH)

Pilot clinical trials using magnesium sulfate in patients with acute aneurysmal subarachnoid hemorrhage have reported trends toward improvement in clinical outcomes. This Phase III study aimed to compare intravenous magnesium sulfate infusion with saline placebo among such patients. We recruited patients with aneurysmal subarachnoid hemorrhage within 48 hours of onset from 10 participating centers. The patients were randomly assigned to magnesium sulfate infusion titrated to a serum magnesium concentration twice the baseline concentration or saline placebo for 10 to 14 days. Patients and assessors were blinded to treatment allocation. The study is registered at www.strokecenter.org/trials (as Intravenous Magnesium Sulphate for Aneurysmal Subarachnoid Hemorrhage [IMASH]) and www.ClinicalTrials.gov (NCT00124150). Of the 327 patients recruited, 169 were randomized to receive treatment with intravenous magnesium sulfate and 158 to receive saline (placebo). The proportions of patients with a favorable outcome at 6 months (Extended Glasgow Outcome Scale 5 to 8) were similar, 64% in the magnesium sulfate group and 63% in the saline group (OR, 1.0; 95% CI, 0.7 to 1.6). Secondary outcome analyses (modified Rankin Scale, Barthel Index, Short Form 36, and clinical vasospasm) also showed no significant differences between the 2 groups. Predefined subgroups included age, admission World Federation of Neurological Surgeons grade, pre-existing hypertension, intracerebral hematoma, intraventricular hemorrhage, location of aneurysm, size of aneurysm, and mode of aneurysm treatment. In none of the subgroups did the magnesium sulfate group show a better outcome at 6 months. The results do not support a clinical benefit of intravenous magnesium sulfate infusion over placebo infusion in patients with acute aneurysmal subarachnoid hemorrhage.

Renal protection with magnesium subcarbonate and magnesium sulphate in patients with epithelial ovarian cancer after cisplatin and paclitaxel chemotherapy: A randomised phase II study

Background The aim of this study was to examine the effect of magnesium supplementation on nephrotoxicity accompanying standard cisplatin-based chemotherapy in patients with epithelial ovarian cancer (EOC). Patients and methods A double-blind, placebo-controlled, randomised study was conducted in which study arm magnesium sulphate (5 g) was administered before each course of standard chemotherapy with paclitaxel (135 mg/m 2/24 h) plus cisplatin (75 mg/m 2) every 3 weeks in patients with EOC. Magnesium subcarbonate (500 mg), three times per day orally, was administered during the treatment intervals. The control arm was administered a placebo instead of both magnesium salts. Magnesium serum levels (sMg) and GFR markers: serum levels of creatinine (sCr), Cockroft–Gault (ClCG) and Modification Diet of Renal Disease (MDRD) formulae were recorded before each cycle, and 3 weeks after the sixth course. Results 41 EOC patients were randomised and 40 were eligible. sMg varied significantly between the supplemented and placebo groups ( p<0.0001). The control group showed a significantly greater decrease of GFR assessed by: sCr ( p = 0.0069), ClCG ( p = 0.0077) and MDRD ( p = 0.032) formulae compared with the magnesium supplemented group. Conclusions These results demonstrate the nephroprotective effect of magnesium supplementation during chemotherapy with cisplatin.

Doppler das artérias umbilicais e cerebral média fetal após sulfato de magnésio na pré-eclâmpsia

To compare the ratio between the fetal middle cerebral artery and the umbilical artery using Doppler flow velocimetry indices (resistance index, pulsatility index and A/B relation) before and after administration of magnesium sulfate to pregnant women with severe preeclampsia (pure or superimposed). A prospective cohort study was conducted with each pregnant woman representing her own control. Forty severe preeclamptic women were included and underwent Doppler sonography before and 20 minutes after administration of 6g of magnesium sulfate. Analysis variables were the Doppler flow velocimetry indices evaluating the ratio of the fetal middle cerebral artery to the umbilical artery. To compare the mean indices before and after magnesium sulfate for the same patient, the "t-paired" Student test was used. The Stuart-Maxwell c(2) was applied to determine the difference of fetal diagnosis (normal, brain-sparing or reduced middle cerebral artery resistance) before and after magnesium sulfate. No significant difference of the mean ratio between the middle cerebral artery and the umbilical artery, before and after administration of magnesium sulfate was observed. After magnesium sulfate (25.0% x 47.5%; p= 0.01), there was an increased frequency of isolated lower Doppler flow velocimetry indices in the middle cerebral artery. Intravenous administration of magnesium sulfate in patients with severe preeclampsia is associated with increased frequency of fetal Doppler diagnosis of reduced resistance in the middle cerebral artery.

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A prospective randomized trial of magnesium sulfate in severe preeclampsia: Use of diuresis as a clinical parameter to determine the duration of postpartum therapy

The purpose of this study was to assess the use of the onset of diuresis in the determination of the duration of postpartum magnesium sulfate therapy among patients with severe preeclampsia. A prospective randomized trial of postpartum therapy with magnesium sulfate was conducted. The control group received 24 hours of therapy, and the study group received therapy until the onset of diuresis (urine output >100 mL/hr for 2 consecutive hours). The Student t test, chi 2 test, and Fisher's exact test were used for analysis of data; a probability value of <.05 was considered statistically significant. There were 50 patients in the control group and 48 patients in the study group. There was no difference in maternal demographic data, severe disease criteria, blood pressure, 24-hour postpartum urine output, or need for antihypertensive therapy. The study group had a significantly shorter duration of therapy, and no patient had eclampsia or required the re-initiation of therapy. The use of the onset of diuresis in the postpartum period as the determinant clinical parameter for the discontinuation of magnesium sulfate in patients with severe preeclampsia was associated with no untoward outcomes or need for the re-initiation of treatment.

The analgesic effect of magnesium sulfate and ketamine in patients undergoing laparoscopic cholecystectomy

In this randomized, double blind study, we investigated the analgesic effect of ketamine and magnesium sulfate in patients scheduled for laparoscopic cholecystectomy. Sixty patients were randomly assigned into three groups. Before the induction of anesthesia, Group 1 received a bolus of magnesium sulfate 50 mg/kg, and an infusion of 8 mg/kg/h for the next 4 h; Group 2 received a bolus of ketamine 0.5 mg/kg and an infusion of 0.15 mg/kg/h for the next 4 h; Group 3 received the same volume of saline solution. Intraoperative pain was treated with bolus alfentanil. Patient controlled analgesia (PCA) was used in all patients in the recovery room. Alfentanil consumptions of the Group 1 and 2 were lower than that of the Group 3 (p < 0.05). Postoperative morphine consumption of Group 2 was lower than that of the Group 3 two and three hours after surgery (p < 0.05) .W e conclude that addition of ketamine or magnesium sulfate to general anesthesia may decrease intraoperative analgesic requirements and administration of ketamine reduces postoperative morphine requirement. Our results indicate that a bolus of ketamine 0.5 mg/kg and subsequent infusion of 0.15 mg/kg/h is more efficient than a bolus of magnesium sulfate 50 mg/kg, and subsequent infusion of 8 mg/kg/h for postoperative pain management. summary

Room C, 10/17/2000 9: 00 AM - 11: 00 AM (PS) Cerebral Blood Flow Velocity Response to Intravenous Magnesium Sulfate in Patients Following Subarachnoid Hemorrhage

<b>Room C, 10/17/2000 9: 00 AM - 11: 00 AM (PS) Cerebral Blood Flow Velocity Response to Intravenous Magnesium Sulfate in Patients Following Subarachnoid Hemorrhage</b>

Magnesium sulfate for treating exacerbations of acute asthma in the emergency department.

Treatment of acute asthma is based on rapid reversal of bronchospasm and arresting airway inflammation. There is some evidence that intravenous magnesium can provide additional bronchodilation when given in conjunction with standard bronchodilating agents and corticosteroids. No systematic review of this literature has been completed on this topic. To examine the effect of additional intravenous magnesium sulfate in patients with acute asthma managed in the emergency department. Randomised controlled trials were identified from the Cochrane Airways Review Group register. Bibliographies from included studies, known reviews and texts were searched. Primary authors and content experts were contacted. Randomised controlled trials or quasi-randomised trials were eligible for inclusion. Studies were included if patients presented with acute asthma and were treated with IV magnesium sulfate vs placebo. Data were extracted and methodological quality was assessed independently by two reviewers. Missing data were obtained from authors. Seven trials were included (5 adult, 2 pediatric). A total of 665 patients were involved. Patients receiving magnesium sulfate demonstrated non-significant improvements in peak expiratory flow rates when all studies were pooled (weighted mean difference: 29.4 L/min; 95% confidence interval: -3.4 to 62). In studies of people with severe acute asthma, peak expiratory flow rate improved by 52.3 L/min (95% confidence interval: 27 to 77.5). The forced expiratory volume in one second also improved by 9.8 % predicted (95% confidence interval: 3.8 to 15.8). Overall, admission to hospital was not reduced, odds ratio: 0.31 (95% confidence interval: 0.09 to 1.02). In the severe subgroup, admissions were reduced in those receiving magnesium sulfate (odds ratio: 0.10, 95% confidence interval: 0.04 to 0.27). No clinically important changes in vital signs or adverse side effects were reported. Current evidence does not support routine use of intravenous magnesium sulfate in all patients with acute asthma presenting to the emergency department. Magnesium sulfate appears to be safe and beneficial in patients who present with severe acute asthma.

Protective effect of intravenous magnesium in acute myocardial infarction following thrombolytic therapy

The role of intravenous magnesium therapy in patients with acute myocardial infarction (AMI) who received thrombolytic therapy is controversial. The results from previous clinical trials were not in consonance. We therefore conducted a prospective, randomized, double-blind, placebo controlled study in 350 patients with confirmed AMI during the period January 1994 to December 1996. The role of intravenous magnesium sulphate therapy (2 g over 5 min followed by 16 g over 24 h) was evaluated in patients with AMI who received thrombolytic therapy. Study group consisted of 169 patients who were administered magnesium sulphate. Control group comprised of 181 patients who were given isotonic saline. Among those in the magnesium group, 70% received magnesium within 6 h after the onset of symptoms. All patients received magnesium immediately after the completion of thrombolytic therapy. Patients were followed up for 30 days after AMI. The number of deaths in the study group was 6 (3.5%) compared with control arm in which 18 patients (9.9%) died ( P value <0.01 95% Confidence intervals [CI] 1.2 to 11.6). Ventricular arrhythmias were also less in the magnesium arm; 27 patients [13%]) compared with 83 patients (48.6%) in the control arm ( P value 0.00001 95% Cl 26.7 to 44.5). In the magnesium group 15 patients (8.8%) had re-infarction compared with 23 patients (12.7%) in the placebo arm ( P value not significant). Post myocardial infarction angina was observed in 47 patients (27.8%) in the magnesium arm compared with 60 patients (33.1%) in the placebo arm ( P value not significant). The main side effect of intravenous magnesium was transient flushing observed in 152 (90%) patients. Intravenous magnesium sulphate in patients with AMI is a safe and useful adjunct to thrombolytic therapy in reducing the short-term mortality and ventricular arrhythmias after AMI.

Change in estimated cerebral perfusion pressure after treatment with nimodipine or magnesium sulfate in patients with preeclampsia

Objective: Data are accumulating to suggest that cerebral perfusion pressure may be either abnormally high or low in preeclampsia and eclampsia. Little is known of the cerebral perfusion pressure effects of magnesium sulfate or nimodipine. Our objective in this study was to compare the change in cerebral perfusion pressure in patients with severe preeclampsia randomly selected to receive nimodipine or magnesium sulfate. Study Design: Patients with severe preeclampsia were randomly selected to receive magnesium sulfate (6 g bolus and 2 g/hr intravenous infusion) or nimodipine (60 mg taken orally every 4 hours). Transcranial Doppler ultrasonography was used to measure flow velocities in the right and left middle cerebral arteries, and the results were averaged. Measurements were obtained before treatment (baseline) and 30 minutes after the magnesium sulfate bolus was completely infused or 30 minutes after the nimodipine was ingested. Studies were performed before any other intervention. The person performing the ultrasonography was unaware of the patient’s group assignment. Estimated cerebral perfusion pressure was calculated with the following formula: Estimated cerebral perfusion pressure = Velocity mean × [(Blood pressure mean – Blood pressure diastolic )/(Velocity mean – Velocity diastolic )]. The difference between estimated cerebral perfusion pressure at baseline and after treatment was compared between the 2 groups by means of the Mann-Whitney rank sum test. Results: Nine patients were randomly selected to receive nimodipine and 12 to receive magnesium sulfate. Patient demographics and severity of condition were not significantly different between the 2 groups. The change in estimated cerebral perfusion pressure was significantly different between the groups. Estimated cerebral pefusion pressure increased after nimodipine use and decreased after magnesium sulfate use. Conclusion: Shortly after administration to patients with severe preeclampsia, nimodipine resulted in increased cerebral perfusion pressure in comparison with magnesium sulfate. (Am J Obstet Gynecol 1999;181:402-7.)

Adjustment of magnesium sulfate infusion rate in patients with preterm labor

Objective: Our purpose was to investigate factors that might influence serum magnesium levels during intravenous magnesium sulfate tocolytic therapy. Study Design: Thirty-three women receiving magnesium sulfate for preterm labor participated in this prospective, observational study. Gestational ages were 24 to 34 weeks. Four groups of women were identified according to the maintenance magnesium infusion rate required for arresting preterm labor after 5 g of therapy induction: 1.5, 2, 2.5, and 3 g/h. Serum magnesium samples were drawn after a predefined period of at least 18 hours of arrested preterm labor, at a minimum of every 6 hours. Variables examined included serum albumin; serum protein; serum ionized calcium; serum creatinine; creatinine clearance; 24-hour urine output; maternal height, weight, body surface area; and body mass index. Results: By use of a multivariate stepwise regression model we identified four variables that independently and significantly contributed to the model: magnesium infusion rate (P < .001); total serum protein level (P < .001); serum creatinine level (P = .009); and maternal weight squared (P = .026). Seventy-two percent of the variance was accounted for by use of these parameters. A predictive linear model, developed to relate these factors, produced the following formula: Suggested magnesium infusion rate = 0.89 × Serum magnesium concentration (mg/dL) – 3.16 × Serum creatinine (mg/dL) – 0.66 × Serum total proteins (g/dL) + 0.0001 × (maternal weight)2 (kg) + 2.30. Conclusions: Serum creatinine, serum protein, and maternal weight can be used to adjust the dose of magnesium sulfate in patients with premature labor to achieve therapeutic serum levels of magnesium more rapidly and safely. (Am J Obstet Gynecol 1998;179:994-8.)

Magnesium therapy in acute myocardial infarction when patients are not candidates for thrombolytic therapy

Thrombolytic therapy reduces in-hospital mortality. However, 70% to 80% of patients do not receive thrombolysis and their in-hospital mortality is high. During the last decade some clinical trials demonstrated that magnesium sulfate reduced in-hospital mortality. The aim of this study was to evaluate the effects of magnesium sulfate in patients with acute myocardial infarction (AMI) who were considered unsuitable for thrombolytic therapy. Intravenous magnesium sulfate was evaluated in 194 patients with AMI ineligible for thrombolytic therapy in a randomized, double-blind, placebo-controlled study. Group I consisted of 96 patients who received 48-hour intravenous magnesium. Group II consisted of 98 patients who received isotonic glucose as a placebo. Magnesium reduced the incidence of arrhythmias, congestive heart failure, and conduction disturbances compared with placebo (27% vs 40%, p = 0.04; 18% vs 23%, p = 0.27; 10% vs 15%, p = 0.21, respectively). Left ventricular ejection fraction 72 hours and 1 to 2 months after admission was higher in patients who received magnesium sulfate than in those taking placebo (49% vs 43% and 52% vs 45%; p = 0.01, respectively). In-hospital mortality was significantly reduced in patients receiving magnesium sulfate than in those receiving placebo (4% vs 17%; p < 0.01), and also in the subgroup of elderly patients (>70 years) (9% vs 23%; p = 0.09). In conclusion, magnesium sulfate should be considered as an alternative therapy to thrombolysis in patients with AMI.

Phenyltoin versus magnesium sulfate in patients with eclampsia: Preliminary results from a randomized trial: [formula omitted], E. Schiff, L. Kao, B.M. Sibai. Dept. of OB/GYN, University of Tennessee, Memphis

Phenyltoin versus magnesium sulfate in patients with eclampsia: Preliminary results from a randomized trial: [formula omitted], E. Schiff, L. Kao, B.M. Sibai. Dept. of OB/GYN, University of Tennessee, Memphis

Abnormal QT intervals associated with negative T waves induced by antiarrhythmic drugs are rapidly reduced using magnesium sulfate as an antidote.

This study was undertaken to determine whether prolonged QTc interval as a consequence of abnormal repolarization induced by coronary disease or antiarrhythmic drugs could be shortened by intravenous administration of magnesium sulfate. A total of 21 patients with basal prolonged QTc intervals (QTc > 500 ms) were divided in two groups: 7 with ischemic coronary disease and negative T waves (Group A), and 14 treated with antiarrhythmic drugs (Group B). Nine of the latter had negative T waves (Subgroup B-1) and five had positive T waves (Subgroup B-2) recorded in precordial leads. Nine patients were taking amiodarone and six quinidine. Magnesium sulfate was given intravenously in a bolus of 3.75 g (25% solution) over 3 min. Patients had normal electrolyte serum levels. The prolonged QTc and JTc intervals were shortened after magnesium sulfate in patients of Subgroup B-1 from the basal values [QTc 20.7% and JTc 25.4%, (p = < 0.0001 and 0.02, respectively)]. None of the patients in Group A or Subgroup B-2 experienced altered QTc or JTc intervals. While some antiarrhythmic drugs are capable of altering the refractoriness of ventricular cells, probably by causing changes in the intracellular metabolic pathways, in patients with coronary disease gaps in the membrane induced by ischemic injury let calcium enter the cells parallel with dispersion of ventricular repolarization. When secondary negative T waves are present, magnesium sulfate as an antidote probably acts as a blocking agent at the sarcoplasmic reticulum, thus reducing both QTc and JTc intervals.