Neurocritical care
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Anemia is common after subarachnoid hemorrhage (SAH) and may exacerbate the reduction in oxygen delivery that underlies delayed cerebral ischemia. Fall in hemoglobin may relate to blood loss as well as inflammatory suppression of erythropoiesis. Identifying factors associated with anemia may facilitate targeted interventions, such as the use of erythropoiesis-stimulating agents, which could minimize the burden of anemia and reduce red blood cell (RBC) transfusion requirements. ⋯ It may be possible to predict those most likely to develop anemia using simple baseline clinical variables. Anemia was strongly related to surgery, likely through greater blood loss, and greater systemic inflammatory response on admission, possibly explained by cytokine-mediated inhibition of RBC production.
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Aquaporin-4 (AQP4) plays an important role in the evolution of ischemia-evoked cerebral edema. Experimental studies have also demonstrated anti-edema effects of arginine-vasopressin (AVP) antagonists. In a well-characterized murine model of ischemic stroke, we tested the hypotheses that treatment with selective AVP V(1) but not V(2) receptor antagonist (1) attenuates injury volume and ischemia-evoked cerebral edema; and (2) modulates ischemia-evoked AQP4 expression. ⋯ These data demonstrate that following experimental stroke AVP V(1) receptor antagonism: (1) attenuates injury volume and ischemia-evoked cerebral edema; (2) modulates AQP4 expression; and (3) may serve as an important therapeutic target for neuroprotection and ischemia-evoked cerebral edema.
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The presence of pulmonary dysfunction after brain injury is well recognized. Acute lung injury (ALI) occurs in 20% of patients with isolated brain injury and is associated with a poor outcome. The "blast injury" theory, which proposes combined "hydrostatic" and "high permeability" mechanisms for the formation of neurogenic pulmonary edema, has been challenged recently by the observation that a systemic inflammatory response may play an integral role in the development of pulmonary dysfunction associated with brain injury. ⋯ Moreover, in patients with brain injury, hypoxemia represents a secondary insult associated with a poor outcome. Optimal oxygenation may be achieved by using an adequate FiO2 and by application of positive end-expiratory pressure (PEEP). PEEP may, however, affect the cerebral circulation by hemodynamic and CO2-mediated mechanisms and the effects of PEEP on cerebral hemodynamics should be monitored in these patients and used to titrate its application.
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Clinical Trial
Early EEG monitoring for detecting postanoxic status epilepticus during therapeutic hypothermia: a pilot study.
To determine whether routine electroencephalography (EEG) detected electrical status epilepticus (ESE), masked by neuromuscular blockade, in comatose cardiac-arrest survivors receiving therapeutic hypothermia. ⋯ These preliminary results indicate that postanoxic status epilepticus can be masked by neuromuscular blockade during our protocol of therapeutic hypothermia. Routine EEG monitoring might be helpful in cardiac-arrest survivors receiving therapeutic hypothermia. Further studies including continuous EEG monitoring are needed to determine whether early diagnosis and treatment of ESE during therapeutic hypothermia improves the outcome.
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The aim of our study is to confirm the reliability of optic nerve ultrasound as a method to detect intracranial hypertension in patients with spontaneous intracranial hemorrhage, to assess the reproducibility of the measurement of the optic nerve sheath diameter (ONSD), and to verify that ONSD changes concurrently with intracranial pressure (ICP) variations. ⋯ Our investigation confirms the reliability of optic nerve ultrasound as a non-invasive method to detect elevated ICP in intracranial hemorrhage patients. ONSD measurements proved to have a good reproducibility. ONSD changes almost concurrently with CSF pressure variations.