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Delayed Death (delayed + death)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Early Death Due to Severe Organophosphate Poisoning Is a Centrally Mediated Process

ACADEMIC EMERGENCY MEDICINE, Issue 4 2003
Steven B. Bird MD
Objective: To distinguish whether early death from severe organophosphate (OP) poisoning with dichlorvos is mediated through peripheral or central nervous system (CNS) actions. Methods: Wistar rats (n= 72) were randomized to pretreatment with either: normal saline (controls), peripheral anticholinergics (glycopyrrolate [low, medium, or high dose] or nebulized ipratropium bromide), or CNS + peripherally acting anticholinergics (diphenhydramine, nebulized atropine, or injected atropine). All treatments were given prior to a subcutaneous injection of 25 mg/kg dichlorvos (n= 8 per group). Survival was assessed at 10 minutes (early death) and 24 hours (delayed death). Kaplan-Meier (95% confidence intervals [95% CIs]) and chi-squared analysis was then performed to determine differences between treatments. Results: Regardless of treatment, all animals exhibited profound nicotinic effects (fasciculations) without obvious seizures within 2 minutes of poisoning. In rats pretreated with peripherally acting agents, the fasciculations were rapidly followed by reduced motor activity, sedation, and death. Mortality at 10 minutes for saline controls, glycopyrrolate, and ipratropium was 88%, 96%, and 100%, respectively. The single control animal surviving beyond 10 minutes went on to develop peripheral cholinergic manifestations, including hypersalivation, urination, and defecation. Only one of 24 animals treated with injected atropine, nebulized atropine, or diphenhydramine died during the early phase of poisoning; all others survived to 24 hours (p < 0.01). Conclusions: Death in acute, severe OP poisoning is prevented by pretreatment with anticholinergic agents that cross the blood,brain barrier, but not by agents with only peripheral actions. Early death due to OP poisoning appears to be a centrally mediated process. [source]

Ischemia-induced modifications in hippocampal CA1 stratum radiatum excitatory synapses

HIPPOCAMPUS, Issue 10 2006
Tatiana Kovalenko
Abstract Relatively mild ischemic episode can initiate a chain of events resulting in delayed cell death and significant lesions in the affected brain regions. We studied early synaptic modifications after brief ischemia modeled in rats by transient vessels' occlusion in vivo or oxygen,glucose deprivation in vitro and resulting in delayed death of hippocampal CA1 pyramidal cells. Electron microscopic analysis of excitatory spine synapses in CA1 stratum radiatum revealed a rapid increase of the postsynaptic density (PSD) thickness and length, as well as formation of concave synapses with perforated PSD during the first 24 h after ischemic episode, followed at the long term by degeneration of 80% of synaptic contacts. In presynaptic terminals, ischemia induced a depletion of synaptic vesicles and changes in their spatial arrangement: they became more distant from active zones and had larger intervesicle spacing compared to controls. These rapid structural synaptic changes could be implicated in the mechanisms of cell death or adaptive plasticity. Comparison of the in vivo and in vitro model systems used in the study demonstrated a general similarity of these early morphological changes, confirming the validity of the in vitro model for studying synaptic structural plasticity. © 2006 Wiley-Liss, Inc. [source]

Salvaging The Ischaemic Penumbra: More Than Just Reperfusion?

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2002
Thanh G Phan
SUMMARY 1. The ischaemic penumbra is defined as a moderately hypoperfused region that retains structural integrity but has lost function. In animal models of ischaemic stroke, this region is prone to recurrent anoxic depolarization and will become infarcted if reperfusion does not occur. In the macaque model, an ischaemic penumbra has been identified for up to 3 h after ischaemic stroke onset, whereas in selected human patients it may exist for up to 48 h. 2. Although most definitions of the ischaemic penumbra stress a ,time,brain volume' concept, few incorporate the idea that selective and delayed neuronal injury plays an important role. Thus, in addition to necrotic cell death caused by acute injury, it is important to also consider delayed death mediated by caspase-dependent and -independent apoptotic pathways. 3. ,Salvage' of penumbral tissue is possible if reperfusion (e.g. after thrombolysis) occurs. However, neurons within this ,salvaged' region may be still at risk of further delayed neuronal injury. 4. In the present review, we aim to revisit the concept of the ischaemic penumbra and explore the role of selective and delayed neuronal injury in enlargement of the volume of infarction, as well as pathogenic mechanisms of white matter ischaemia. Both animal and human models of cerebral ischaemia imaged using magnetic resonance and positron emission tomography techniques will be discussed. [source]

Adverse Event Reporting: Lessons Learned from 4 Years of Florida Office Data

DERMATOLOGIC SURGERY, Issue 9 2005
Brett Coldiron MD, FACP
Background Patient safety regulations and medical error reporting systems have been at the forefront of current health care legislature. In 2000, Florida mandated that all physicians report, to a central collecting agency, all adverse events occurring in an office setting. Purpose To analyze the scope and incidence of adverse events and deaths resulting from office surgical procedures in Florida from 2000 to 2004. Methods We reviewed all reported adverse incidents (the death of a patient, serious injury, and subsequent hospital transfer) occurring in an office setting from March 1, 2000, through March 1, 2004, from the Florida Agency for Health Care Administration. We determined physician board certification status, hospital privileges, and office accreditation via telephone follow-up and Internet searches. Results Of 286 reported office adverse events, 77 occurred in association with an office surgical procedure (19 deaths and 58 hospital transfers). There were seven complications and five deaths associated with the use of intravenous sedation or general anesthesia. There were no adverse events associated with the use of dilute local (tumescent) anesthesia. Liposuction and/or abdominoplasty under general anesthesia or intravenous sedation were the most common surgical procedures associated with a death or complication. Fifty-three percent of offices reporting an adverse incident were accredited by the Joint Commission on Accreditation of Healthcare Organizations, American Association for Accreditation of Ambulatory Surgical Facilities, or American Association for Ambulatory Health Care. Ninety-four percent of the involved physicians were board certified, and 97% had hospital privileges. Forty-two percent of the reported deaths were delayed by several hours to weeks after uneventful discharge or after hospital transfer. Conclusions Requiring physician board certification, physician hospital privileges, or office accreditation is not likely to reduce office adverse events. Restrictions on dilute local (tumescent) anesthesia for liposuction would not reduce adverse events and could increase adverse events if patients are shifted to riskier approaches. State and/or national legislation establishing adverse event reporting systems should be supported and should require the reporting of delayed deaths. [source]