Neurocritical care
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Coagulopathy and platelet dysfunction commonly develop after traumatic brain injury (TBI). Thromboelastography (TEG) and platelet function assays (PFAs) are often performed at the time of admission; however, their roles in assessing post-TBI coagulopathy have not been investigated. We hypothesized that compared to blunt TBI, penetrating TBI would (1) demonstrate greater coagulopathy by TEG, (2) be associated with abnormal PFA results, and (3) require more blood product transfusions. ⋯ Patients presenting with penetrating TBI demonstrated increased coagulopathy compared to those with blunt TBI as measured by TEG and need for transfusion. PFA results did not correlate with TEG findings in this population.
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Mast cells are first responders to intracerebral hemorrhage. They release potent mediators that can disrupt the blood-brain barrier promoting injury, vasogenic edema formation, and hematoma exacerbation. Also, mast cells recruit other inflammatory cells that maintain and amplify brain damage. Given their early role in the cascade of events in intracerebral hemorrhage, mast cells may offer an alternative target for antichemotactic interventions.
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Hyperpyrexia is a severely elevated core body temperature secondary to an elevated hypothalamic set thermo-regulatory threshold. Hyperthermia is an elevated core body temperature beyond the normal hypothalamic set thermo-regulatory threshold. Intracranial hypotension can present with a wide variety of symptoms ranging from orthostatic headache up to coma. We report a rare case of hyperpyrexia associated with intracranial hypotension. ⋯ Hyperpyrexia might be a presenting symptom of intracranial hypotension, likely, secondary to hypothalamic dysfunction and compression. In our case, hyperpyrexia was reversible as the intracranial hypotension was emergently treated. Spontaneous intracranial hypotension might be difficult to diagnose, especially if it presented with non-classical symptoms like fever; thus, physicians should be aware of such association.
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Review
Cerebral Edema After Cardiopulmonary Resuscitation: A Therapeutic Target Following Cardiac Arrest?
We sought to review the role that cerebral edema plays in neurologic outcome following cardiac arrest, to understand whether cerebral edema might be an appropriate therapeutic target for neuroprotection in patients who survive cardiopulmonary resuscitation. Articles indexed in PubMed and written in English. Following cardiac arrest, cerebral edema is a cardinal feature of brain injury and is a powerful prognosticator of neurologic outcome. ⋯ Neuroprotection after cardiac arrest generally has focused on protecting neurons, not the microvascular endothelium or blood-brain barrier. Limited preclinical data suggest that strategies to reduce cerebral edema may improve neurologic outcome. Ongoing research will be necessary to determine whether targeting cerebral edema will improve patient outcomes after cardiac arrest.
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Status epilepticus (SE) has been identified as a predictor of morbidity and mortality in many acute brain injury patient populations. We aimed to assess the prevalence and impact of SE after intracerebral hemorrhage (ICH) in a large patient sample to overcome limitations in previous small patient sample studies. ⋯ SE is a significant, likely underdiagnosed, predictor of morbidity and mortality after ICH. Future studies are necessary to better identify which patients are at highest risk of SE to guide resource utilization.