High-dose magnesium sulfate infusion protocol for status asthmaticus: a safety and pharmacokinetics cohort study

2012 ◽  
Vol 39 (1) ◽  
pp. 117-122 ◽  
Author(s):  
Tosha A. Egelund ◽  
Sarah K. Wassil ◽  
Elisa M. Edwards ◽  
Stephan Linden ◽  
Jose E. Irazuzta
1995 ◽  
Vol 21 (1) ◽  
pp. 94-95
Author(s):  
M. Sydow ◽  
T. A. Crozier ◽  
S. Zielmann ◽  
J. Radke ◽  
H. Burchardi

1993 ◽  
Vol 19 (8) ◽  
pp. 467-471 ◽  
Author(s):  
M. Sydow ◽  
T. A. Crozier ◽  
S. Zielmann ◽  
J. Radke ◽  
H. Burchardi

2012 ◽  
Vol 17 (2) ◽  
pp. 150-154 ◽  
Author(s):  
Jose Irazuzta ◽  
Tosha Egelund ◽  
Sarah K. Wassil ◽  
Christian Hampp

OBJECTIVE This report describes the feasibility of high-dose magnesium sulfate infusion in pediatric patients with status asthmaticus. METHODS Retrospective chart review over a 3-year period of all patients younger than 18 years of age with status asthmaticus who underwent a high-dose magnesium sulfate infusion for 4 hours. All patients were breathing spontaneously but were refractory to conventional therapy. The magnesium sulfate infusion regimen was 50 mg/kg (for patients weighing >30 kg) or 75 mg/kg (for those weighing ≤30 kg) over a period of 30 to 45 minutes, followed by a continuous infusion of 40 mg/kg/hr for 4 hours. Information regarding vital and clinical respiratory signs, serum magnesium (SrMg), ionized magnesium (iMg), electrocardiograms, and cardiac troponin levels were retrieved. We analyzed the relationship between SrMg and iMg by using linear regression analysis. RESULTS Nineteen patients were included. At the end of the infusion, SrMg levels were 4.4 ± 0.8 mg/dL, and iMg levels were 0.95 ± 0.2 mmol/L. SrMg levels only moderately predicted iMg (r2 = 0.541). There were no reports of hypotension, respiratory failure, neurological problems, or nausea. Discomfort at the site of infusion was reported in three cases. Troponin levels (n = 12) and electrocardiograms (n = 12), when available, were noted at the end of the infusion and were normal in all patients p=0.01. CONCLUSIONS In this case series, short-term high-dose administration of magnesium sulfate in the context of status asthmaticus was feasible, and we did not observe clinical complications with its use. Total SrMg was inadequate to reflect the active form of magnesium, iMg. The dose used achieved theoretical therapeutic levels of iMg.


2016 ◽  
Vol 21 (3) ◽  
pp. 233-238
Author(s):  
Danish Vaiyani ◽  
Jose E. Irazuzta

OBJECTIVES: To determine the feasibility and safety of a simplified high-dose magnesium sulfate infusion (sHDMI) for the treatment of status asthmaticus. METHODS: We retrospectively compared 2 different high-dose magnesium sulfate infusion regimens, as adjunctive treatment in status asthmatics, using data that were preciously collected. The initial high-dose, prolonged magnesium infusion (HDMI) regimen consisted of a loading dose of 75 mg/kg (weight ≤ 30 kg) or 50 mg/kg (weight > 30 kg) over a period of 30 to 45 minutes followed by a continuous infusion of 40 mg/kg/hr for an additional 4 hours. This was compared to the sHDMI regimen that consisted of 50 mg/kg/hr for 5 hours. No loading dose was given to the patients in the sHDMI arm. Obese patients were dosed by using ideal body weight. Physiologic parameters (i.e., heart rate, blood pressure, respiratory rate, oxygen saturation) and serum magnesium (SrMg) concentrations were monitored during administration of magnesium sulfate. RESULTS: Nineteen patients receiving the initial HDMI regimen were compared with 10 patients who received the sHDMI regimen. There was no significant difference in SrMg concentrations or physiologic parameters between the 2 dose regimens. CONCLUSIONS: The HDMI and sHDMI regimens both produced SrMg concentrations that are associated with bronchodilation. The safety profile was also similar for the 2 regimens. The unambiguity of sHDMI has the potential to reduce medication errors that are associated with calculation of the loading dose, product preparation, and ultimate administration.


2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Sanjay K. Agarwal ◽  
Warren G. Foster

The purpose of this study was to assess the impact of 3 months of aromatase inhibition together with progestin add-back on ovarian endometrioma size. This prospective cohort study was performed at University Medical Center (UC San Diego). Women trying to conceive were excluded. After informed consent, all women were treated with the aromatase inhibitor letrozole (5 mg/d) with norethindrone acetate (5 mg/d) add-back for 3 months. Pre- and posttreatment assessments of endometrioma sizes were performed by ultrasound. The impact of treatment on pain was determined using the patient assessed endpoints of the Biberoglu and Behrman scale. These included assessing dysmenorrhea, dyspareunia, and nonmenstrual pelvic pain each on a scale from 0 to 3. The primary endpoint of this study was the change in ultrasound documented endometrioma size. Fourteen endometriomas in 8 consecutive women were treated for 3 m. Mean endometrioma diameter decreased 50% from 4.6 ± 1.6 cm to 2.3 ± 1.6 cm (mean ± SD). This represents a 75% decrease in endometrioma volume. Endometriosis symptoms of dysmenorrhea, dyspareunia, and nonmenstrual pelvic pain also improved with treatment. In conclusion, a 3-month course of high dose aromatase inhibition with progestin add-back significantly reduces ovarian endometrioma size and warrants further investigation.


Critical Care ◽  
2019 ◽  
Vol 23 (1) ◽  
Author(s):  
Edgar Santos ◽  
Arturo Olivares-Rivera ◽  
Sebastian Major ◽  
Renán Sánchez-Porras ◽  
Lorenz Uhlmann ◽  
...  

Abstract Objective Spreading depolarizations (SD) are characterized by breakdown of transmembrane ion gradients and excitotoxicity. Experimentally, N-methyl-d-aspartate receptor (NMDAR) antagonists block a majority of SDs. In many hospitals, the NMDAR antagonist s-ketamine and the GABAA agonist midazolam represent the current second-line combination treatment to sedate patients with devastating cerebral injuries. A pressing clinical question is whether this option should become first-line in sedation-requiring individuals in whom SDs are detected, yet the s-ketamine dose necessary to adequately inhibit SDs is unknown. Moreover, use-dependent tolerance could be a problem for SD inhibition in the clinic. Methods We performed a retrospective cohort study of 66 patients with aneurysmal subarachnoid hemorrhage (aSAH) from a prospectively collected database. Thirty-three of 66 patients received s-ketamine during electrocorticographic neuromonitoring of SDs in neurointensive care. The decision to give s-ketamine was dependent on the need for stronger sedation, so it was expected that patients receiving s-ketamine would have a worse clinical outcome. Results S-ketamine application started 4.2 ± 3.5 days after aSAH. The mean dose was 2.8 ± 1.4 mg/kg body weight (BW)/h and thus higher than the dose recommended for sedation. First, patients were divided according to whether they received s-ketamine at any time or not. No significant difference in SD counts was found between groups (negative binomial model using the SD count per patient as outcome variable, p = 0.288). This most likely resulted from the fact that 368 SDs had already occurred in the s-ketamine group before s-ketamine was given. However, in patients receiving s-ketamine, we found a significant decrease in SD incidence when s-ketamine was started (Poisson model with a random intercept for patient, coefficient − 1.83 (95% confidence intervals − 2.17; − 1.50), p < 0.001; logistic regression model, odds ratio (OR) 0.13 (0.08; 0.19), p < 0.001). Thereafter, data was further divided into low-dose (0.1–2.0 mg/kg BW/h) and high-dose (2.1–7.0 mg/kg/h) segments. High-dose s-ketamine resulted in further significant decrease in SD incidence (Poisson model, − 1.10 (− 1.71; − 0.49), p < 0.001; logistic regression model, OR 0.33 (0.17; 0.63), p < 0.001). There was little evidence of SD tolerance to long-term s-ketamine sedation through 5 days. Conclusions These results provide a foundation for a multicenter, neuromonitoring-guided, proof-of-concept trial of ketamine and midazolam as a first-line sedative regime.


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