Post-cardiac arrest syndrome (PCAS) is a multicomponent entity affecting many who survive an initial period of resuscitation following cardiac arrest. This focussed review explores some of the strategies for mitigating the effects of PCAS following the return of spontaneous circulation. We consider the current evidence for controlled oxygenation, strategies for blood-pressure targets, the timing of coronary reperfusion, and the evidence for temperature control and treatment of seizures. Despite several large trials investigating specific strategies to improve outcomes after cardiac arrest, many questions remain unanswered. Results of some studies suggest that interventions may benefit specific subgroups of cardiac arrest patients, but the optimal timing and duration of many interventions remain unknown. The role of intracranial pressure monitoring has been the subject of only a few studies, and its benefits remain unclear. Research aimed at improving the management of PCAS is ongoing.
Although sedative use is near-ubiquitous in the acute management of moderate to severe traumatic brain injury (m-sTBI), the evidence base for these agents is undefined. This review summarizes the evidence for analgosedative agent use in the intensive care unit management of m-sTBI. Clinical studies of sedative and analgosedative agents currently utilized in adult m-sTBI management (propofol, ketamine, benzodiazepines, opioids, and alpha-2 agonists) were identified and assessed for relevance and methodological quality. The primary outcome was the effect of the analgosedative agent on intracranial pressure (ICP). Secondary outcomes included intracranial hemodynamic and metabolic parameters, systemic hemodynamic parameters, measures of therapeutic intensity, and clinical outcomes. Of 594 articles identified, 61 met methodological review criteria, and 40 were included in the qualitative summary; of these, 33 were prospective studies, 18 were randomized controlled trials, and 8 were blinded. There was consistent evidence for the efficacy of sedative agents in the management of m-sTBI and raised ICP, but the overall quality of the evidence was poor, consisting of small studies (median sample size, 23.5) of variable methodological quality. Propofol and midazolam achieve the goals of sedation without notable differences in efficacy or safety, although high-dose propofol may disrupt cerebral autoregulation. Dexmedetomidine and propofol/ dexmedetomidine combination may cause clinically significant hypotension. Dexmedetomidine was effective to achieve a target sedation score. De novo opioid boluses were associated with increased ICP and reduced cerebral perfusion pressure. Ketamine bolus and infusions were not associated with increased ICP and may reduce the incidence of cortical spreading depolarization events. In conclusion, there is a paucity of high-quality evidence to inform the optimal use of analgosedative agents in the management of m-sTBI, inferring significant scope for further research.
There is continued controversy regarding the optimal anesthetic technique for endovascular therapy in patients with acute posterior circulation ischemic stroke. To compare the clinical outcomes general anesthesia (GA) and non-GA, we performed a systematic review and meta-analysis of randomized controlled trials and observational studies focused on the anesthetic management for endovascular therapy in patients with acute posterior circulation stroke, without language restriction. In addition, we compared clinical outcomes among the studies with different non-GA types (conscious sedation or local anesthesia). Outcome variables were functional independence, excellent outcomes, favorable outcomes, mortality, successful recanalization, hemodynamic instability, intracerebral hemorrhage, and respiratory or vascular complications. Eight studies including 1777 patients were identified. Although GA was associated with a lower odds of functional independence at 90 days (odds ratio [OR]: 0.55; 95% confidence interval [CI] 0.38 to 0.81; P =0.009), substantial heterogeneity was noted ( I2 =65%). Subgroup analysis showed that GA was associated with higher odds of mortality than conscious sedation (OR: 1.83; 95% CI, 1.30 to 2.57; I2 =0%), but there was no difference between GA and local anesthesia ( I2 =0%). Interestingly, subgroup analysis did not identify a relationship between functional independence and GA compared with local anesthesia (OR: 0.90; 95% CI, 0.64 to 1.25; P =0.919; I2 =0%). This meta-analysis demonstrates that GA is associated with worse outcomes in patients with acute posterior circulation stroke undergoing endovascular therapy based on current studies.
Background: Headache is the most common presenting symptom of spontaneous subarachnoid hemorrhage and managing this acute pain can be challenging. The aim of this study was to describe the course of headaches and factors associated with analgesic failure in patients with spontaneous subarachnoid hemorrhage.
Methods: We conducted a prospective observational study in patients admitted to a neurocritical care unit (between April 2016 and March 2017) within 48 hours of spontaneous subarachnoid hemorrhage. Headache intensity was assessed using a Numerical Pain Rating Scale (NPRS) ranging from 0 to 10. Analgesic failure was defined as any day average NPRS score >3 after 72 hours of hospitalization despite analgesic treatment.
Results: Sixty-three patients were included in the analysis. Thirty-six (56.25%) patients experienced at least 1 episode of severe headache (NPRS ≥7), and 40 (63.5%) patients still reported moderate to severe headache on the final day of the study (day 12). Forty-six (73.0%) patients required treatment with opioids and 37 (58.7%) experienced analgesic failure. Multivariable analysis showed that analgesic failure was associated with smoking history (odds ratio [OR]=4.31, 95% confidence interval [CI]: 1.23-17.07; P =0.027), subarachnoid blood load (OR=1.11, 95% CI: 1.01-1.24; P =0.032) and secondary complications, including rebleeding, hydrocephalus, delayed cerebral ischemia, hyponatremia, or death (OR=4.06, 95% CI: 1.17-15.77; P =0.032).
Conclusions: Headaches following spontaneous subarachnoid hemorrhage are severe and persist during hospitalization despite standard pain-reducing strategies. We identified risk factors for analgesic failure in this population.
Background: Studies have evaluated the effects of volatile and intravenous anesthetic agents on the cerebral vasculature with inconsistent results. We used digital subtraction angiography to compare the effects of propofol and sevoflurane on the luminal diameter of cerebral vessels and on cerebral transit time in patients with aneurysmal subarachnoid hemorrhage (aSAH).
Methods: This prospective preliminary study included adult patients with good-grade aSAH scheduled for endovascular coil embolization; patients were randomized to receive propofol or sevoflurane anesthesia during endovascular coiling. The primary outcome was the luminal diameter of 7 cerebral vessel segments measured on the diseased and nondiseased sides of the brain at 3 time points: awake, postinduction of anesthesia, and postcoiling. Cerebral transit time was also measured as a surrogate for cerebral blood flow.
Results: Eighteen patients were included in the analysis (9 per group). Baseline and intraoperative parameters were similar between the groups. Propofol increased the diameter of 1 vessel segment at postinduction and postcoiling on the diseased side and in 1 segment at postcoiling on the nondiseased side of the brain ( P <0.05). Sevoflurane increased vessel diameter in 3 segments at postinduction and in 2 segments at postcoiling on the diseased side, and in 4 segments at postcoiling on the nondiseased side ( P <0.05). Cerebral transit time did not change compared with baseline awake state in either group and was not different between the groups.
Conclusions: Sevoflurane has cerebral vasodilating properties compared with propofol in patients with good-grade aSAH. However, sevoflurane affects cerebral transit time comparably to propofol.
Background: Cardiopulmonary resuscitation (CPR) may not be sufficient to halt the progression of brain damage. Using extracellular glutamate concentration as a marker for neuronal damage, we quantitatively evaluated the degree of brain damage during resuscitation without return of spontaneous circulation.
Materials and methods: Extracellular cerebral glutamate concentration was measured with a microdialysis probe every 2 minutes for 40 minutes after electrical stimulation-induced cardiac arrest without return of spontaneous circulation in Sprague-Dawley rats. The rats were divided into 3 groups (7 per group) according to the treatment received during the 40 minutes observation period: mechanical ventilation without chest compression (group V); mechanical ventilation and chest compression (group VC) and; ventilation, chest compression and brain hypothermia (group VCH). Chest compression (20 min) and hypothermia (40 min) were initiated 6 minutes after the onset of cardiac arrest.
Results: Glutamate concentration increased in all groups after cardiac arrest. Although after the onset of chest compression, glutamate concentration showed a significant difference at 2 min and reached the maximum at 6 min (VC group; 284±48 μmol/L vs. V group 398±126 μmol/L, P =0.003), there was no difference toward the end of chest compression (513±61 μmol/L vs. 588±103 μmol/L, P =0.051). In the VCH group, the initial increase in glutamate concentration was suddenly suppressed 2 minutes after the onset of brain hypothermia.
Conclusions: CPR alone reduced the progression of brain damage for a limited period but CPR in combination with brain cooling strongly suppressed increases in glutamate levels.
Introduction: Standardized mortality ratios (SMRs), calculated using the Acute Physiology, Age, Chronic Health Evaluation II (APACHE II) and Intensive Care National Audit and Research Centre H-2018 (ICNARC H-2018 ) risk prediction models, are widely used in UK intensive care units (ICUs) to measure and compare the quality of critical care delivery. Both models incorporate an assumption of Glasgow Coma Score (GCS) if an actual GCS without sedation is not recordable in the first 24 hours after ICU admission. This study assesses the validity of the APACHE II and ICNARC H-2018 models to predict mortality in ICU patients with traumatic brain injury (TBI) or aneurysmal subarachnoid hemorrhage (aSAH) in whom GCS is related to outcomes.
Methods: In a retrospective analysis, the SMR calculated by the APACHE II and ICNARC H-2018 models for all UK ICU admissions in a 1-year period was compared with calculated SMRs in TBI/aSAH patients and at 3 GCS groups. Data for patients admitted to a single tertiary neurocritical care unit were similarly analyzed.
Results: Both models predicted mortality well for the overall TBI/aSAH population; SMR (95% confidence interval) was 1.00 (0.96-1.04) and 0.99 (0.95-1.03) for the APACHE II and ICNARC H-2018 models, respectively. When analyzed by GCS grouping, both models underpredicted mortality in TBI/aSAH patients with GCS ≤8 (SMR, 1.1 [1.05-1.15]) and "unrecordable" GCS (SMR, 1.88 [1.77-1.99]). Similar findings were identified in the local data analysis.
Discussion: The APACHE II and ICNARC H-2018 models predicted mortality well for the overall TBI/aSAH ICU population but underpredicted mortality when GCS was ≤8 or "unrecordable." This raises questions about the accuracy of these risk prediction models in TBI/aSAH patients and their use to evaluate treatments and compare outcomes between centers.
Background: Despite a renewed focus in recent years on pain management in the inpatient hospital setting, postoperative pain after elective craniotomy remains under investigated. This study aims to identify which perioperative factors associate most strongly with postoperative pain and opioid medication requirements after inpatient craniotomy.
Materials and methods: Using an existing dataset, we selected a restricted cohort of patients who underwent elective craniotomy surgery requiring an inpatient postoperative stay during a 7-year period at our institution (n=1832). We examined pain scores and opioid medication usage and analyzed the relative contribution of specific perioperative risk factors to postoperative pain and opioid medication intake (morphine milligram equivalents).
Results: Postoperative pain was found to be highest on postoperative day 1 and decreased thereafter (up to day 5). Factors associated with greater postoperative opioid medication requirement were preoperative opioid medication use, duration of anesthesia, degree of pain in the preoperative setting, and patient age. Notably, the most significant factor associated with a higher postoperative pain score and Morphine milligram equivalents requirement was the time elapsed between the end of general anesthesia and a patient's first intravenous opioid medication.
Conclusion: Postcraniotomy patients are at higher risk for requiring opioid pain medications if they have a history of preoperative opioid use, are of younger age, or undergo a longer surgery. Moreover, early requirement of intravenous opioid medications in the postoperative period should alert treating physicians that a patient's pain may require additional or alternative methods of pain control than routinely administered, to avoid over-reliance on opioid medications.
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