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M Jastremski

Publications and source records attributed to M Jastremski.

6 recordsLinked to original sources
PubMed1992

A comparison of standard-dose and high-dose epinephrine in cardiac arrest outside the hospital. The Multicenter High-Dose Epinephrine Study Group.

BACKGROUND: Experimental and uncontrolled clinical evidence suggests that intravenous epinephrine in doses higher than currently recommended may improve outcome after cardiac arrest. We conducted a prospective, multicenter study comparing standard-dose epinephrine with high-dose epinephrine in the management of cardiac arrest outside the hospital. METHODS: Adult patients were enrolled in the study if they remained in ventricular fibrillation, or if they had asystole or electromechanical dissociation, at the time the first drug was to be administered to treat the cardiac arrest. Patients were randomly assigned to receive either 0.02 mg of epinephrine per kilogram of body weight (standard-dose group, 632 patients) or 0.2 mg per kilogram (high-dose group, 648 patients), both given intravenously. RESULTS: In the standard-dose group 190 patients (30 percent) had a return of spontaneous circulation, as compared with 217 patients (33 percent) in the high-dose group; 136 patients (22 percent) in the standard-dose group and 145 patients (22 percent) in the high-dose group survived to be admitted to the hospital. Twenty-six patients (4 percent) in the standard-dose group and 31 (5 percent) in the high-dose group survived to discharge from the hospital. Ninety-two percent of the patients discharged in the standard-dose group and 94 percent in the high-dose group were conscious at the time of hospital discharge. None of the differences in outcome between the groups were statistically significant. CONCLUSIONS: In this study, we were unable to demonstrate any difference in the overall rate of return of spontaneous circulation, survival to hospital admission, survival to hospital discharge, or neurologic outcome between patients treated with a standard dose of epinephrine and those treated with a high dose.

Aged↗
PubMed1992

Effectiveness of a human monoclonal anti-endotoxin antibody (HA-1A) in gram-negative sepsis: relationship to endotoxin and cytokine levels.

Gram-negative sepsis is caused by endotoxin-induced release of tumor necrosis factor (TNF) and other cytokines. HA-1A is a human monoclonal antibody that binds specifically to endotoxin. HA-1A should prevent death in endotoxemic patients and reduce serum levels of TNF and interleukin-6 (IL-6). This hypothesis was tested in 82 septic patients who were randomly allocated to receive a single intravenous 100-mg dose of HA-1A or placebo. Pretreatment endotoxemia was detected in 27 patients (33%). Death occurred within 28 days of treatment in 8 (73%) of 11 placebo recipients and in 5 (31%) of 16 HA-1A recipients (P = .02). The median decrease in serum TNF level 24 h after treatment was 12 ng/L in patients given HA-1A and 0 ng/L in placebo recipients (n = 65; P = .04). For IL-6, this was 204 ng/L in patients given HA-1A and 44 ng/L in placebo recipients (n = 67; P = .4). Thus, HA-1A reduces mortality in septic patients with endotoxemia and lowers serum TNF levels.

Adult↗
PubMedDate not supplied

Problems in brain death determination.

During the last decade there has been philosophical acceptance of the concept that the state of brain death is equivalent to total patient death. The application of this concept to clinical medicine has been associated with major problems in both the diagnosis of brain death and the medical management of the brain dead patient. In our experience with 176 consecutive cases of suspected brain death over a seven-year period, we have found that a standardized protocol applied by experienced clinicians will minimize these problems.

Adolescent↗
PubMedDate not supplied

Glucocorticoid treatment does not improve neurological recovery following cardiac arrest. Brain Resuscitation Clinical Trial I Study Group.

Glucocorticoids are commonly given to patients with global brain ischemia, although their efficacy has not been proved. The database of the Brain Resuscitation Clinical Trial I, a multi-institutional study designed to evaluate the effect of thiopental sodium therapy on neurological outcome following brain ischemia, was used for a retrospective review of the effects of glucocorticoid treatment on neurological outcome after global brain ischemia. This study included 262 initially comatose cardiac arrest survivors who made no purposeful response to pain after restoration of spontaneous circulation. The standard treatment protocol left glucocorticoid therapy to the discretion of the hospital investigators. This resulted in four patient groups that received either no, low, medium, or high doses of glucocorticoids in the first 8 hours after arrest. Neurological outcome was scored using a modification of the Glasgow Cerebral Performance Category Scale. None of the steroid regimens statistically improved mean group survival rate or neurological recovery rate over that observed in the group that did not receive steroids. The routine clinical practice of administrating glucocorticoids after global brain ischemia may be associated with serious complications and is not justified.

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