Journal of neurosurgical anesthesiology最新文献

Background: Epidural opioids provide effective postoperative analgesia after lumbar spine surgery. Ketamine has been shown to reduce opioid-induced central sensitization and hyperalgesia. We hypothesized that adding ketamine to epidural opioids would prolong the duration of analgesia and enhance analgesic efficacy after lumbar spine surgery.

Methods: American Society of Anesthesiologists physical status class I to II patients aged between 18 and 70 years with normal renal function undergoing lumbar laminectomy were recruited into this single-center randomized trial. Patients were randomized to receive either single-dose epidural morphine (group A) or epidural morphine and ketamine (group B) for postoperative analgesia. The primary objective was to compare the duration of analgesia as measured by time to the first postoperative analgesic request. Secondary objectives were the comparison of pain scores at rest and movement, systemic hemodynamics, and the incidence of side effects during the first 24 hours after surgery.

Results: Fifty patients were recruited (25 in each group), of which data from 48 were available for analysis. The mean±SD duration of analgesia was 20±6 and 23±3 hours in group A and group B, respectively ( P =0.07). There were 12/24 (50%) patients in group A and 17/24 (71%) patients in group B who did not receive rescue analgesia during the first 24-hour postoperative period ( P =0.07). Pain scores at rest and movement, systemic hemodynamics, and postoperative complications were comparable between the groups.

Conclusions: The addition of ketamine to epidural morphine did not prolong the duration of analgesia after lumbar laminectomy.

Emergence delirium (ED) is delirium that occurs during or immediately after emergence from general anesthesia or sedation. Effective pharmacological treatments for ED are lacking, so preventive measures should be taken to minimize the risk of ED. However, the risk factors for ED in adults are unclear. In this systematic review and meta-analysis, we evaluated the evidence for risk factors for ED in adults. The PubMed, Scopus, Cochrane Library, Google Scholar, and Embase databases were searched for observational studies reporting the risk factors for ED in adults from inception to July 31, 2023. Twenty observational studies reporting 19,171 participants were included in this meta-analysis. Among the preoperative factors identified as risk factors for ED were age <40 or ≥65 years, male sex, smoking history, substance abuse, cognitive impairment, anxiety, and American Society of Anesthesiologists physical status score III or IV. Intraoperative risk factors for ED were the use of benzodiazepines, inhalational anesthetics, or etomidate, and surgical factors including abdominal surgery, frontal craniotomy (vs. other craniotomy approaches) for cerebral tumors, and the length of surgery. Postoperative risk factors were indwelling urinary catheters, the presence of a tracheal tube in the postanesthetic care unit or intensive care unit, the presence of a nasogastric tube, and pain. Knowledge of these risk factors may guide the implementation of stratified management and timely interventions for patients at high risk of ED. The majority of studies included in this review investigated only hyperactive ED and further research is required to determine risk factors for hypoactive and mixed ED types.

Background: This single-center, retrospective study investigated the outcome effect of the combined intensity and duration of differences between actual cerebral perfusion pressure (CPP) and optimal cerebral perfusion pressure (CPPopt), and also for absolute CPP, in patients with traumatic brain injury (TBI) and aneurysmal subarachnoid hemorrhage (aSAH).

Methods: A total of 378 TBI and 432 aSAH patients treated in a neurointensive care unit between 2008 and 2018 with at least 24 hours of CPPopt data during the first 10 days following injury, and with 6-month (TBI) or 12-month (aSAH) extended Glasgow Outcome Scale (GOS-E) scores, were included in the study. ∆CPPopt-insults (∆CPPopt=actual CPP-CPPopt) and CPP-insults were visualized as 2-dimensional plots to highlight the combined effect of insult intensity (mm Hg) and duration (min) on patient outcome.

Results: In TBI patients, a zone of ∆CPPopt ± 10 mm Hg was associated with more favorable outcome, with transitions towards unfavorable outcome above and below this zone. CPP in the range of 60 to 80 mm Hg was associated with higher GOS-E, whereas CPP outside this range was associated with lower GOS-E. In aSAH patients, there was no clear transition from higher to lower GOS-E for ∆CPPopt-insults; however, there was a transition from favorable to unfavorable outcome when CPP was <80 mm Hg.

Conclusions: TBI patients with CPP close to CPPopt exhibited better clinical outcomes, and absolute CPP within the 60 to 80 mm Hg range was also associated with favorable outcome. In aSAH patients, there was no clear transition for ∆CPPopt-insults in relation to outcome, whereas generally high absolute CPP values were associated overall with favorable recovery.

Introduction: Blood pressure (BP) management is common in patients with aneurysmal subarachnoid hemorrhage (SAH) admitted to an intensive care unit. However, the practice patterns of BP management (timing, dose, and duration) have not been studied locally.

Methods: This post hoc analysis explored BP management goals (defined as the setting of a minimum systolic BP target or application of induced hypertension) in patients enrolled into the PROMOTE-SAH study in eleven neurosurgical centers in Australia and New Zealand. The primary outcome was 'dead or disabled' (modified Rankin Score ≥4) at 6 months, with the hypothesis being that setting BP management goals would be associated with improved outcomes.

Results: BP management goals were recorded in 266 of 357 (75%) patients, of which 149 were recorded as receiving induced hypertension for delayed cerebral ischemia (DCI) or vasospasm on 738 (19%) study days. In patients with a minimum systolic BP goal recorded (on 2067 d), the indication for the BP management goal was vasospasm or DCI on 651 (32%) days; no indication for BP management goals was documented on 1416 (69%) days. Crude analysis demonstrated an association between setting BP management goals and reduced death or disability ( P =0.03), but this association was not significant after adjustment for the presence of DCI or vasospasm and clustered by the site.

Conclusions: BP management goals are commonly 'prescribed' to aSAH patients admitted to an intensive care unit in Australia and New Zealand, but BP management goal setting was not associated with improved outcomes in the adjusted analysis.

Enhanced Recovery After Surgery (ERAS) protocols have revolutionized the approach to perioperative care in various surgical specialties. They reduce complications, improve patient outcomes, and shorten hospital lengths of stay. Implementation of ERAS protocols for neurosurgical procedures has been relatively underexplored and underutilized due to the unique challenges and complexities of neurosurgery. This narrative review explores the barriers to, and pioneering strategies of, standardized procedure-specific ERAS protocols, and the importance of multidisciplinary collaboration in neurosurgery and neuroanesthsia, patient-centered approaches, and continuous quality improvement initiatives, to achieve better patient outcomes. It also discusses initiatives to guide future clinical practice, research, and guideline creation, to foster the development of tailored ERAS protocols in neurosurgery.

In 1932, Harvey Cushing described peptic ulceration secondary to raised intracranial pressure and attributed this to vagal overactivity, causing excess gastric acid secretion. Cushing ulcer remains a cause of morbidity in patients, albeit one that is preventable. This narrative review evaluates the evidence pertaining to the pathophysiology of neurogenic peptic ulceration. Review of the literature suggests that the pathophysiology of Cushing ulcer may extend beyond vagal mechanisms for several reasons: (1) clinical and experimental studies have shown only a modest increase in gastric acid secretion in head-injured patients; (2) increased vagal tone is found in only a minority of cases of intracranial hypertension, most of which are related to catastrophic, nonsurvivable brain injury; (3) direct stimulation of the vagus nerve does not cause peptic ulceration, and; (4) Cushing ulcer can occur after acute ischemic stroke, but only a minority of strokes are associated with raised intracranial pressure and/or increased vagal tone. The 2005 Nobel Prize in Medicine honored the discovery that bacteria play key roles in the pathogenesis of peptic ulcer disease. Brain injury results in widespread changes in the gut microbiome in addition to gastrointestinal inflammation, including systemic upregulation of proinflammatory cytokines. Alternations in the gut microbiome in patients with severe traumatic brain injury include colonization with commensal flora associated with peptic ulceration. The brain-gut-microbiome axis integrates the central nervous system, the enteric nervous system, and the immune system. Following the review of the literature, we propose a novel hypothesis that neurogenic peptic ulcer may be associated with alterations in the gut microbiome, resulting in gastrointestinal inflammation leading to ulceration.

Introduction: Cerebral infarction from delayed cerebral ischemia (DCI) is a leading cause of poor neurological outcome after aneurysmal subarachnoid hemorrhage (aSAH). We performed an international clinical practice survey to identify monitoring and management strategies for cerebral vasospasm associated with DCI in aSAH patients requiring intensive care unit admission.

Methods: The survey questionnaire was available on the European Society of Intensive Care Medicine (May 2021-June 2022) and Neurocritical Care Society (April - June 2022) websites following endorsement by these societies.

Results: There were 292 respondents from 240 centers in 38 countries. In conscious aSAH patients or those able to tolerate an interruption of sedation, neurological examination was the most frequently used diagnostic modality to detect delayed neurological deficits related to DCI caused by cerebral vasospasm (278 respondents, 95.2%), while in unconscious patients transcranial Doppler/cerebral ultrasound was most frequently used modality (200, 68.5%). Computed tomography angiography was mostly used to confirm the presence of vasospasm as a cause of DCI. Nimodipine was administered for DCI prophylaxis by the majority of the respondents (257, 88%), mostly by an enteral route (206, 71.3%). If there was a significant reduction in arterial blood pressure after nimodipine administration, a vasopressor was added and nimodipine dosage unchanged (131, 45.6%) or reduced (122, 42.5%). Induced hypertension was used by 244 (85%) respondents as first-line management of DCI related to vasospasm; 168 (59.6%) respondents used an intra-arterial procedure as second-line therapy.

Conclusions: This survey demonstrated variability in monitoring and management strategies for DCI related to vasospasm after aSAH. These findings may be helpful in promoting educational programs and future research.