Prediction of Discharge Outcome with the Full Outline of Unresponsiveness (FOUR) Score in Neurosurgical Patients

To identify the diagnostic properties of the Full Outline of Unresponsiveness (FOUR) score and the discharge outcome, 318 patients were studied. The evaluators rated the patients on admission or when they had mental status alteration with the FOUR score. The course of treatment was determined based on the clinical. The mortality rate and Glasgow Outcome Scale were recorded. Adjusted regression models and prognostic performance were tested by calculation of the receiver operating characteristic curve. One-hundred and twenty-two patients (40.1%) had a poor outcome defined as a Glasgow Outcome Scale score from 3-5, and 38 patients (12.5%) died. The area under the characteristic curve (AUC) for poor outcome and in-hospital mortality were 0.88 (95% CI, 0.83-0.92) and 0.92 (95% CI, 0.87-0.97). The cut-off point of 14 showed sensitivity and specificity of the total FOUR score predicting poor outcomes at 0.77 (95% CI, 0.69-0.84) and 0.95 (95% CI, 0.90-0.97), while the cut-off point of 10 showed the values for in-hospital mortality at 0.71 (95% CI, 0.55-0.83) and 0.93 (95% CI, 0.90-0.96). The total FOUR score showed satisfactory prognostic value for predicting outcome. The cut-off points for the poor outcome and in-hospital mortality are 14 and 10, respectively

The dosage of thiopental as pharmacological cerebral protection during non-shunt carotid endarterectomy: A retrospective study [version 3; peer review: 2 approved]

Background Thiopental has been used as a pharmacological cerebral protection strategy during carotid endarterectomy surgeries. However, the optimal dosage required to induce burst suppression on the electroencephalogram (EEG) remains unknown. This retrospective study aimed to determine the optimal dosage of thiopental required to induce burst suppression during non-shunt carotid endarterectomy. Methods The Neurological Institute of Thailand Review Board approved the study. Data were collected from 2009 to 2019 for all non-shunt carotid endarterectomy patients who received thiopental for pharmacological cerebral protection and had intraoperative EEG monitoring. Demographic information, carotid stenosis severity, intraoperative EEG parameters, thiopental dosage, carotid clamp time, intraoperative events, and patient outcomes were abstracted. Results The study included 57 patients. Among them, 24 patients (42%) achieved EEG burst suppression pattern with a thiopental dosage of 26.3±10.1 mg/kg/hr. There were no significant differences in perioperative events between patients who achieved burst suppression and those who did not. After surgery, 33.3% of patients who achieved burst suppression were extubated and awakened. One patient in the non-burst suppression group experienced mild neurological deficits. No deaths occurred within one month postoperative. Conclusions The optimal dosage of thiopental required to achieve burst suppression on intraoperative EEG during non-shunt carotid endarterectomy was 26.3±10.1 mg/kg/hr

Early cerebral perfusion pressure augmentation with phenylephrine after traumatic brain injury may be neuroprotective in a pediatric swine model*

Objective: Cerebral perfusion pressureage, and current guidelines recommend maintaining cerebral perfusion pressure between 40 mm Hg–60 mm Hg. Although adult traumatic brain injury studies have observed an increased risk of complications associated with targeting a cerebral perfusion pressure \u3e70, we hypothesize that targeting a cerebral perfusion pressure of 70 mm Hg with the use of phenylephrine early after injury in the immature brain will be neuroprotective. Design: Animals were randomly assigned to injury with a cerebral perfusion pressure of 70 mm Hg or 40 mm Hg. Diffuse traumatic brain injury was produced by a single rapid rotation of the head in the axial plane. Cerebral microdialysis, brain tissue oxygen, intracranial pressure, and cerebral blood flow were measured 30 min–6 hrs postinjury. One hour after injury, cerebral perfusion pressure was manipulated with the vasoconstrictor phenylephrine. Animals were euthanized 6 hrs posttraumatic brain injury, brains fixed, and stained to assess regions of cell injury and axonal dysfunction. Setting: University center. Subject: Twenty-one 4-wk-old female swine. Measurements and Main Results: Augmentation of cerebral perfusion pressure to 70 mm Hg resulted in no change in axonal dysfunction, but significantly smaller cell injury volumes at 6 hrs postinjury compared to cerebral perfusion pressure 40 (1.1% vs. 7.4%, p \u3c .05). Microdialysis lactate/pyruvate ratios were improved at cerebral perfusion pressure 70 compared to cerebral perfusion pressure 40. Cerebral blood flow was higher in the cerebral perfusion pressure 70 group but did not reach statistical significance. Phenylephrine was well tolerated and there were no observed increases in serum lactate or intracranial pressure in either group. Conclusions: Targeting a cerebral perfusion pressure of 70 mm Hg resulted in a greater reduction in metabolic crisis and cell injury volumes compared to a cerebral perfusion pressure of 40 mm Hg in an immature swine model. Early aggressive cerebral perfusion pressure augmentation to a cerebral perfusion pressure of 70 mm Hg in pediatric traumatic brain injury before severe intracranial hypertension has the potential to be neuroprotective, and further investigations are needed

Effect of phenylephrine and ephedrine bolus treatment on cerebral oxygenation in anaesthetized patients

BACKGROUND: How phenylephrine and ephedrine treatments affect global and regional haemodynamics is of major clinical relevance. Cerebral tissue oxygen saturation ([Image: see text])-guided management may improve postoperative outcome. The physiological variables responsible for [Image: see text] changes induced by phenylephrine and ephedrine bolus treatment in anaesthetized patients need to be defined. METHODS: A randomized two-treatment cross-over trial was conducted: one bolus dose of phenylephrine (100–200 µg) and one bolus dose of ephedrine (5–20 mg) were given to 29 ASA I–III patients anaesthetized with propofol and remifentanil. [Image: see text], mean arterial pressure (MAP), cardiac output (CO), and other physiological variables were recorded before and after treatments. The associations of changes were analysed using linear-mixed models. RESULTS: The CO decreased significantly after phenylephrine treatment [▵CO=−2.1 (1.4) litre min(−1), P<0.001], but was preserved after ephedrine treatment [▵CO=0.5 (1.4) litre min(−1), P>0.05]. The [Image: see text] was significantly decreased after phenylephrine treatment [▵[Image: see text]=−3.2 (3.0)%, P<0.01] but preserved after ephedrine treatment [▵[Image: see text]=0.04 (1.9)%, P>0.05]. CO was identified to have the most significant association with [Image: see text] (P<0.001). After taking CO into consideration, the other physiological variables, including MAP, were not significantly associated with [Image: see text] (P>0.05). CONCLUSIONS: Associated with changes in CO, [Image: see text] decreased after phenylephrine treatment, but remained unchanged after ephedrine treatment. The significant correlation between CO and [Image: see text] implies a cause–effect relationship between global and regional haemodynamics