Current concepts in brain resuscitation
Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore, Md 21205.JAMA The Journal of the American Medical Association (Impact Factor: 35.29). 07/1989; 261(21):3143-7. DOI: 10.1001/archinte.146.7.1413
The area of cerebral resuscitation has become an exciting area of research in critical care medicine. It is a complicated field, however, which has seen attempts to protect the brain using a single therapy such as barbiturates ultimately disappoint investigators in the field. It is likely that much more work needs to be done in understanding the intracellular metabolic and biochemical effects of ischemia before therapies can be designed that are likely to be effective. This work might ultimately require knowledge of how ischemia or hypoxia interrupt cellular RNA and DNA machinery before these effective therapies can be developed. Before we are discouraged by the difficulty of the task, however, it is useful to review how much progress has been made in understanding the pathophysiology of ischemic brain injury in the past decade, so that we may be challenged to continue our efforts in this exciting area of critical care medicine.
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ABSTRACT: The efficacy of CPR has been questioned. A major criticism is that neurologic outcomes have not been adequately studied. For a 26-month period, 138 patients from six major receiving hospitals were discharged alive following prehospital cardiac arrests. For 65/138 (47.1%) patients, either the patient or a direct family member was contacted for information concerning neurologic outcome. For 63/138 (45.7%) patients, contact with patient or family was unsuccessful, consequently neurologic outcome at time of discharge was obtained from the medical record. For 10/138 (7.2%) patients, no data on neurologic outcome was obtainable. Neurologic outcome was rated by a 5-point Cerebral Performance Categories Scale (CPC); (1) Minimal Disability; (2) Moderate; (3) Severe; (4) Vegetative; and (5) Brain Dead. The bystander/first responder CPR group had 55.1% CPC-1; 24.4% CPC-2; 16.7% CPC-3; and 3.8% CPC-4 outcomes. The bystander/first responder NO CPR group had 58.0% CPC-1; 18.0% CPC-2; 16.0% CPC-3; and 8.0% CPC-4 outcomes. There was no significant difference at any CPC level (P not significant). Furthermore, there was no statistical difference between either group when compared for age, response time, resuscitation time, witnessing of arrest or distribution of presenting rhythms. In conclusion, no significant effect in neurologic outcome among saved cardiac arrest victims was found between bystander/first responder CPR and bystander/first responder NO CPR groups in the paramedic program studied.Resuscitation 03/1989; 17(1):91-8. DOI:10.1016/0300-9572(89)90082-8 · 4.17 Impact Factor
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ABSTRACT: We reviewed the results of all pediatric patients undergoing intracranial pressure (ICP) monitoring in a 2-year period at our institution. The outcome of patients suffering hypoxia or ischemic injuries (HII) is compared to those suffering non-hypoxic or non-ischemic injuries (NHII). Thirty-four patients had ICP monitors placed during the study period. Incomplete patient information led to the exclusion of 5 patients. An additional 5 patients were excluded because no measures to control ICP were taken after the monitor was placed. Twenty-four patients required treatment for raised ICP (hyperventilation, 24; mannitol, 19; barbiturate coma, 6). Admission Glasgow Coma Score in patients suffering HII (median score 5) and NHII (median score 6) were not significantly different (Mann-Whitney U Test). Only 2 of 8 patients with HII were near-drowning victims. The remaining 6 had HII from other causes (5 survivors of various forms of asphyxia and 1 of cardiac arrest). All 8 patients had poor outcomes (1 severely disabled; 7 died). The 16 patients with NHII had a variety of diagnoses (6 trauma, 5 encephalitis, 4 bacterial meningitis, 1 diabetic ketoacidosis). Among these, 6 had good outcomes and 10 poor outcomes (2 severely disabled, 2 vegetative, and 6 died). The difference in outcome between patients with NHII and HII is significant at P = 0.059 (Fischer Exact test). Patients with NHII may benefit from ICP monitoring. Patients with HII from near-drowning and other causes did not appear to benefit from ICP monitoring and interventions directed at controlling ICP.Child s Nervous System 03/1991; 7(1):34-9. DOI:10.1007/BF00263831 · 1.11 Impact Factor
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ABSTRACT: An examination of the cellular and molecular mechanisms of neuronal cell damage may lead to the design of pharmacologic interventions during presumed or actual fetal asphyxia. Hypoxia-ischemia in its severest form results in insufficient adenosine 5'-triphosphate production. The most important effect of this is failure of adenosine 5'-triphosphate-dependent membrane functions, which maintain ionic homeostasis, that is, ionic pumping. There is K+ efflux and Na+ influx across the cell membrane, depolarization of the cell membrane, opening of the voltage-dependent calcium channels, and entrance of Ca++ into the cell. Cytosolic Ca++ is also increased by Ca++ efflux from the mitochondria and the sarcoplasmic reticulum. Ca++ is a toxin in high cytosolic concentrations; it activates phospholipases A and C, which cause membrane breakdown and release of free fatty acids, including arachidonic acid. The membrane is damaged, lysis occurs, and the neuron dies. High cytosolic Ca++ also causes release of excitatory amino acids (especially glutamate), which overwhelm the suppressant neurotransmitters, causing seizures, increased metabolism, and aggravation of the insufficient adenosine 5'-triphosphate availability. Thromboxane A2 is generated from arachidonic acid, increasing smooth muscle tone and thereby worsening the ischemia. Cyclooxygenase activity also results in formation of oxygen-free radicals that contribute to cell membrane damage, lysis, and death. Possibilities for pharmacologic interventions include (1) calcium channel blockers and antagonists, (2) excitatory neurotransmitter blockers, (3) oxygen-free radical scavengers (e.g., superoxide dismutase), (4) cyclooxygenase or prostaglandin synthesis inhibitors, and (5) seizure suppressants (e.g., phenobarbital). Some of these treatments have been shown experimentally to limit neuronal death in the adult and fetus, and after more investigative work they may be applicable to clinical practice.American Journal of Obstetrics and Gynecology 07/1991; 164(6 Pt 1):1582-9; discussion 1589-91. DOI:10.1016/0002-9378(91)91440-8 · 4.70 Impact Factor
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