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BACKGROUND: Intracranial pressure (ICP) monitoring plays a key role in patients with traumatic brain injury (TBI), however, cerebral hypoxia can occur without intracranial hypertension. Aiming to improve neuroprotection in these patients, a possible alternative is the association of Brain Tissue Oxygen Pressure (PbtO2) monitoring, used to detect PbtO2 tension. METHOD: We systematically searched PubMed, Embase and Cochrane Central for RCTs comparing combined PbtO2 + ICP monitoring with ICP monitoring alone in patients with severe or moderate TBI. The outcomes analyzed were mortality at 6 months, favorable outcome (GOS ≥ 4 or GOSE ≥ 5) at 6 months, pulmonary events, cardiovascular events and sepsis rate. RESULTS: We included 4 RCTs in the analysis, totaling 505 patients. Combined PbtO2 + ICP monitoring was used in 241 (47.72%) patients. There was no significant difference between the groups in relation to favorable outcome at 6 months (RR 1.17; 95% CI 0.95-1.43; p = 0.134; I2 = 0%), mortality at 6 months (RR 0.82; 95% CI 0.57-1.18; p = 0.281; I2 = 34%), cardiovascular events (RR 1.75; 95% CI 0.86-3.52; p = 0.120; I2 = 0%) or sepsis (RR 0.75; 95% CI 0.25-2.22; p = 0.604; I2 = 0%). The risk of pulmonary events was significantly higher in the group with combined PbtO2 + ICP monitoring (RR 1.44; 95% CI 1.11-1.87; p = 0.006; I2 = 0%). CONCLUSIONS: Our findings suggest that combined PbtO2 + ICP monitoring does not change outcomes such as mortality, functional recovery, cardiovascular events or sepsis. Furthermore, we found a higher risk of pulmonary events in patients undergoing combined monitoring.

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BACKGROUND: Although the placement of an intraventricular catheter remains the gold standard technique for measuring intracranial pressure (ICP), the method has several limitations. Therefore, noninvasive alternatives to ICP (ICPni) measurement are of great interest. The main objective of this study was to compare the correlation and agreement of wave morphology between ICP (standard intraventricular ICP monitoring) and a new ICPni monitor in patients admitted with stroke. The second objective was to estimate the discrimination of the noninvasive method to detect intracranial hypertension. METHODS: We prospectively collected data of adults admitted to an intensive care unit with subarachnoid hemorrhage, intracerebral hemorrhage, or ischemic stroke in whom an invasive ICP monitor was placed. Measurements were simultaneously collected from two parameters [time-to-peak (TTP) and the ratio regarding the second and first peak of the ICP wave (P2/P1 ratio)] of ICP and ICPni wave morphology monitors (Brain4care). Intracranial hypertension was defined as an invasively measured sustained ICP > 20 mm Hg for at least 5 min. RESULTS: We studied 18 patients (subarachnoid hemorrhage = 14; intracerebral hemorrhage = 3; ischemic stroke = 1) on 60 occasions with a median age of 52 ± 14.3 years. A total of 197,400 waves (2495 min) from both ICP (standard ICP monitoring) and the ICPni monitor were sliced into 1-min-long segments, and we determined TTP and the P2/P1 ratio from the mean pulse. The median invasively measured ICP was 13 (9.8-16.2) mm Hg, and intracranial hypertension was present on 18 occasions (30%). The correlation and agreement between invasive and noninvasive methods for wave morphology were strong for the P2/P1 ratio and moderate for TTP using categoric (κ agreement 88.1% and 71.3%, respectively) and continuous (intraclass correlation coefficient 0.831 and 0.584, respectively) measures. There was a moderate but significant correlation with the mean ICP value (P2/P1 ratio r = 0.427; TTP r = 0.353; p < 0.001 for all) between noninvasive and invasive techniques. The areas under the curve to estimate intracranial hypertension were 0.786 [95% confidence interval (CI) 0.72-0.93] for the P2/P1 ratio and 0.694 (95% CI 0.60-0.74) for TTP. CONCLUSIONS: The new ICPni wave morphology monitor showed a good agreement with the standard invasive method and an acceptable discriminatory power to detect intracranial hypertension. Clinical trial registration Trial registration: NCT05121155.

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The goal of neurocritical care in patients with traumatic brain injury (TBI) is to prevent secondary brain damage. Pathophysiological mechanisms lead to loss of body mass, negative nitrogen balance, dysglycemia, and cerebral metabolic dysfunction. All of these complications have been shown to impact outcomes. Therapeutic options are available that prevent or mitigate their negative impact. Nutrition therapy, glucose control, and multimodality monitoring with cerebral microdialysis (CMD) can be applied as an integrated approach to optimize systemic immune and organ function as well as adequate substrate delivery to the brain. CMD allows real-time bedside monitoring of aspects of brain energy metabolism, by measuring specific metabolites in the extracellular fluid of brain tissue. Sequential monitoring of brain glucose and lactate/pyruvate ratio may reveal pathologic processes that lead to imbalances in supply and demand. Early recognition of these patterns may help individualize cerebral perfusion targets and systemic glucose control following TBI. In this direction, recent consensus statements have provided guidelines and recommendations for CMD applications in neurocritical care. In this review, we summarize data from clinical research on patients with severe TBI focused on a multimodal approach to evaluate aspects of nutrition therapy, such as timing and route; aspects of systemic glucose management, such as intensive vs. moderate control; and finally, aspects of cerebral metabolism. Research and clinical applications of CMD to better understand the interplay between substrate supply, glycemic variations, insulin therapy, and their effects on the brain metabolic profile were also reviewed. Novel mechanistic hypotheses in the interpretation of brain biomarkers were also discussed. Finally, we offer an integrated approach that includes nutritional and brain metabolic monitoring to manage severe TBI patients.

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INTRODUCCIÓN: Se denominan imitadores de ictus (falsos positivos, sobrediagnosticados) así como camaleones de ictus (falsos negativos, infradiagnosticados) a los casos que inducen a cometer errores en el diagnóstico y tratamiento del ictus. Los mismos deben ser considerados para aproximarse de una manera certera al diagnóstico y tratamiento más adecuados. El objetivo es relatar el caso de una paciente que se presenta con un imitador de ictus, afortunadamente con evolución favorable posterior. CASO CLÍNICO: Paciente de 17 años, procedente y residente de la ciudad de El Alto, segundigesta, sin antecedentes personales patológicos, cuadro clínico de 8 horas de evolución, caracterizado por alteración de la conciencia de manera progresiva así como crisis convulsivas tónico clónicas generalizadas; se realiza neuroprotección, tratamiento neurointensivo y se considera tratamiento trombolítico, el cual debido a una adecuada disquisición diagnóstica se decide evitar, orientándose el diagnóstico hacia epilepsia, realizándose el tratamiento respectivo con evolución favorable. DISCUSIÓN: El caso presenta varios datos importantes, tales como la edad de la paciente y la ausencia de crisis convulsivas con anterioridad, sin embargo debido a la urgencia del caso se consideró trombolisis, sin administrase la misma y decidiéndose por el tratamiento de epilepsia, evitando tanto el riesgo asociado a hemorragia intracerebral por la administración de trombolítico en un caso que no correspondía su utilización ya que como se pudo evidenciar la literatura cita como un importante imitador de ictus a las crisis convulsivas.

INTRODUCTION: Stroke mimics (false positives, over diagnosed) and stroke chameleons (false negative, underdiagnosed) are special cases that induce to commit mistakes on stroke diagnoses and treatment. They have to be considered to approximate an adequate treatment. The objective is report the case of a patient with stroke mimic, fortunately identified and treated with favorable evolution. CASE REPORT: Female 17 year-old patient, from El Alto city, without pathologic antecedents with 8 hours clinical manifestations with consciousness impairment and tonic-clonic seizures, neuroprotection is performed such as neurocritical care, thrombolysis is considered, but after an adequate diagnostic disquisition is avoided, the diagnoses of epilepsy is achieved and treatment is performed. DISCUSSION: Several important data are reviewed, such as the early age, lack of seizures antecedent, nevertheless thrombolysis is considered, throughout a careful literature review, epilepsy treatment is performed, avoiding intracraneal bleeding complications.

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Neurointensive care arose from the specific growth of the various therapeutic methods in neuroscience, similar to the formation of specific units in other specialties. The progress of the neurological intensive treatment is more recent and because of the high frequency of pathologies in this area it became necessary to structure this specialty in terms of theoretical and physical aspects. In this text, a commentary on the chronology of this development is set out briefly and objectively.

O neurointensivismo surgiu a partir do crescimento específico das diversas formas terapêuticas em neurociências, à semelhança da formação de unidades específicas em outras especialidades. O progresso do tratamento neurológico intensivo é mais recente e, em virtude da alta frequência das patologias nessa área, tornou-se necessária a estruturação dessa especialidade do ponto de vista teórico e físico. Neste texto, um comentário à cronologia desse desenvolvimento é exposto de maneira breve e objetiva.

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