Posts Tagged ‘traumatic brain injury’
Background: Cerebrovascular pressure reactivity is the principal mechanism of autoregulation of cerebral blood flow. Assessment of cerebral autoregulation can be performed using the mean flow index (Mx) based on transcranial Doppler (TCD) ultrasonography. Pressure reactivity can be monitored using the pressure reactivity index (PRx), which is based on intracranial pressure (ICP) monitoring. From a practical point of view, PRx can be monitored continuously, while Mx can only in short periods when TCD probes can be applied.
Objective: To assess to what degree impairment in pressure reactivity (PRx) is associated with impairment in cerebral autoregulation (Mx).
Methods: A database of 345 traumatic brain injury (TBI) patients was screened for data availability including simultaneous Mx and PRx monitoring. Absolute differences, temporal changes, and association with outcome of the two indices were analyzed.
Background: Monitoring brain tissue PO2 (PbtO2) is part of multimodality monitoring of patients with traumatic brain injury (TBI). However, PbtO2 measurement is a sampling of only a small area of tissue surrounding the sensor tip.
Objective: To examine the effect of catheter location on the relationship between PbtO2and neurological outcome.
Methods: A total of 405 patients who had PbtO2 monitoring as part of standard management of severe traumatic brain injury were studied. The relationships between probe location and resulting PbtO2 and outcome were examined.
Traumatic brain injury has long been associated with abnormal coagulation parameters, but the exact mechanisms underlying this phenomenon are poorly understood. Coagulopathy after traumatic brain injury includes hypercoagulable and hypocoagulable states that can lead to secondary injury by either the induction of microthrombosis or the progression of hemorrhagic brain lesions. Multiple hypotheses have been proposed to explain this phenomenon, including the release of tissue factor, disseminated intravascular coagulation, hyperfibrinolysis, hypoperfusion with protein C activation, and platelet dysfunction. The diagnosis and management of these complex patients are difficult given the lack of understanding of the underlying mechanisms. The goal of this review is to summarize the current knowledge regarding the mechanisms of coagulopathy after blunt traumatic brain injury. The current and emerging diagnostic tools, radiological findings, treatment options, and prognosis are discussed.
Background: Intracranial hypertension is the final pathway of many neurocritical entities, such as spontaneous intracerebral hemorrhage (sICH) and severe traumatic brain injury (sTBI).
Objective: To determine: (1) alterations in intracranial pressure (ICP) and cerebral hemodynamics following an Indomethacin (INDO) infusion test and the related association with survival in patients with refractory intracranial hypertension (RICH) secondary to sICH or sTBI; and (2) to assess the safety profile following INDO.
Methods: INDO was administered in a loading dose (.8 mg/kg/15 minutes), followed by a 2-hour continuous infusion (.5 mg/kg/h) in RICH patients with ICP>20 mmHg who did not respond to first line therapies. Changes in ICP, cerebral perfusion pressure (CPP) and cerebrovascular variables (assessed by transcranial Doppler and jugular bulb saturation) were observed. Clinical outcome was assessed at 1 and 6 months according to Glasgow Outcome Scale and correlated to INDO infusion test response. Analysis of INDO safety profile was conducted.
Background: Prediction of clinical course and outcome after severe traumatic brain injury (TBI) is important.
Objective: To examine whether clinical scales (Glasgow Coma Scale [GCS], Injury Severity Score [ISS], and Acute Physiology and Chronic Health Evaluation II [APACHE II]) or radiographic scales based on admission computed tomography (Marshall and Rotterdam) were associated with intensive care unit (ICU) physiology (intracranial pressure [ICP], brain tissue oxygen tension [PbtO2]), and clinical outcome after severe TBI.
Methods: One hundred one patients (median age, 41.0 years; interquartile range [26-55]) with severe TBI who had ICP and PbtO2 monitoring were identified. The relationship between admission GCS, ISS, APACHE II, Marshall and Rotterdam scores and ICP, PbtO2, and outcome was examined by using mixed-effects models and logistic regression.