Lucia Rivera-Lara

Predictors of Outcome With Cerebral Autoregulation Monitoring: A Systematic Review and Meta-analysis

Objective: To compare cerebral autoregulation indices as predictors of patient outcome and their dependence on duration of monitoring. Data Sources: Systematic literature search and meta-analysis using PubMed, EMBASE, and the Cochrane Library from January 1990 to October 2015. Study Selection: We chose articles that assessed the association between cerebral autoregulation indices and dichotomized or continuous outcomes reported as standardized mean differences or correlation coefficients (R), respectively. Animal and validation studies were excluded. Data Extraction: Two authors collected and assessed the data independently. The studies were grouped into two sets according to the type of analysis used to assess the relationship between cerebral autoregulation indices and predictors of outcome (standardized mean differences or R). Data Synthesis: Thirty-three studies compared cerebral autoregulation indices and patient outcomes using standardized mean differences, and 20 used Rs. The only data available for meta-analysis were from patients with traumatic brain injury or subarachnoid hemorrhage. Based on z score analysis, the best three cerebral autoregulation index predictors of mortality or Glasgow Outcome Scale for patients with traumatic brain injury were the pressure reactivity index, transcranial Doppler-derived mean velocity index based on cerebral perfusion pressure, and autoregulation reactivity index (z scores: 8.97, 6.01, 3.94, respectively). Mean velocity index based on arterial blood pressure did not reach statistical significance for predicting outcome measured as a continuous variable (p = 0.07) for patients with traumatic brain injury. For patients with subarachnoid hemorrhage, autoregulation reactivity index was the only cerebral autoregulation index that predicted patient outcome measured with the Glasgow Outcome Scale as a continuous outcome (R = 0.82; p = 0.001; z score, 3.39). We found a significant correlation between the duration of monitoring and predictive value for mortality (R = 0.78; p < 0.001). Conclusions: Three cerebral autoregulation indices, pressure reactivity index, mean velocity index based on cerebral perfusion pressure, and autoregulation reactivity index were the best outcome predictors for patients with traumatic brain injury. For patients with subarachnoid hemorrhage, autoregulation reactivity index was the only cerebral autoregulation index predictor of Glasgow Outcome Scale. Continuous assessment of cerebral autoregulation predicted outcome better than intermittent monitoring.

Cerebral Autoregulation-oriented Therapy at the Bedside: A Comprehensive Review.

This comprehensive review summarizes the evidence regarding use of cerebral autoregulation-directed therapy at the bedside and provides an evaluation of its impact on optimizing cerebral perfusion and associated functional outcomes. Multiple studies in adults and several in children have shown the feasibility of individualizing mean arterial blood pressure and cerebral perfusion pressure goals by using cerebral autoregulation monitoring to calculate optimal levels. Nine of these studies examined the association between cerebral perfusion pressure or mean arterial blood pressure being above or below their optimal levels and functional outcomes. Six of these nine studies (66%) showed that patients for whom median cerebral perfusion pressure or mean arterial blood pressure differed significantly from the optimum, defined by cerebral autoregulation monitoring, were more likely to have an unfavorable outcome. The evidence indicates that monitoring of continuous cerebral autoregulation at the bedside is feasible and has the potential to be used to direct blood pressure management in acutely ill patients.

Cerebral Blood Flow Autoregulation in Sepsis for the Intensivist: Why Its Monitoring May Be the Future of Individualized Care

Cerebral blood flow (CBF) autoregulation maintains consistent blood flow across a range of blood pressures (BPs). Sepsis is a common cause of systemic hypotension and cerebral dysfunction. Guidelines for BP management in sepsis are based on historical concepts of CBF autoregulation that have now evolved with the availability of more precise technology for its measurement. In this article, we provide a narrative review of methods of monitoring CBF autoregulation, the cerebral effects of sepsis, and the current knowledge of CBF autoregulation in sepsis. Current guidelines for BP management in sepsis are based on a goal of maintaining mean arterial pressure (MAP) above the lower limit of CBF autoregulation. Bedside tools are now available to monitor CBF autoregulation continuously. These data reveal that individual BP goals determined from CBF autoregulation monitoring are more variable than previously expected. In patients undergoing cardiac surgery with cardiopulmonary bypass, for example, the lower limit of autoregulation varied between a MAP of 40 to 90 mm Hg. Studies of CBF autoregulation in sepsis suggest patients frequently manifest impaired CBF autoregulation, possibly a result of BP below the lower limit of autoregulation, particularly in early sepsis or with sepsis-associated encephalopathy. This suggests that the present consensus guidelines for BP management in sepsis may expose some patients to both cerebral hypoperfusion and cerebral hyperperfusion, potentially resulting in damage to brain parenchyma. The future use of novel techniques to study and clinically monitor CBF autoregulation could provide insight into the cerebral pathophysiology of sepsis and offer more precise treatments that may improve functional and cognitive outcomes for survivors of sepsis.

Acute Kidney Injury Following Acute Ischemic Stroke and Intracerebral Hemorrhage: A Meta-Analysis of Prevalence Rate and Mortality Risk

Background: The epidemiology of acute renal dysfunction after stroke is routinely overlooked following stroke events. Our aim in this meta-analysis is to report the prevalence of acute kidney injury (AKI) following acute stroke and its impact on mortality. Methods: A systematic literature search was performed on PubMed, EMBASE and Google Scholar for observational studies examining the prevalence and mortality risk of stroke patients with AKI as a complication. The pooled prevalence rates and odds ratios for mortality risk were calculated using subgroup analyses between the stroke subtypes: acute ischemic stroke (AIS) and intracerebral hemorrhage (ICH). Results: A total of 12 studies (4,532,181 AIS and 615,636 ICH) were included. The pooled prevalence rate of AKI after all stroke types was 11.6% (95% CI 10.6–12.7). Subgroup analyses revealed that the pooled prevalence rate of AKI after AIS was greater but not statistically significantly different than ICH (19.0%; 95% CI 8.2–29.7 vs. 12.9%; 95% CI 10.3–15.5, p = 0.5). AKI was found to be a significant risk factor of mortality in AIS (adjusted OR [aOR] 2.23; 95% CI 1.28–3.89; I2 = 98.8%), whereas this relationship did not reach statistical significance in ICH (aOR 1.20; 95% CI 0.68–2.12; I2 = 74.2%). Conclusions: This meta-analysis provides evidence that AKI is a common complication following both AIS and ICH and it is associated with increased mortality following AIS but not ICH. This highlights the need for early assessment of renal function in the acute phase of AIS, in particular, and avoidance of factors than may induce AKI in vulnerable patients.

Adult intestinal colonization botulism mimicking brain death

A 43-year-old woman, with a history of mild intellectual disability and no recent travel nor known toxic exposures, presented to another medical facility after awaking with nausea, lethargy, and unsteadiness. In the emergency room, she developed dysphagia, dysarthria, and hypercapnic respiratory failure requiring intubation. Laboratory studies showed a mild leukocytosis. Computed tomography of the head showed no acute abnormality. Lumbar puncture (LP) showed 2 white blood cells/mm and protein 29 mg/dl. Over several days, she developed sluggish pupils, impaired extraocular movements, and quadriparesis. On day 8, nerve conduction studies (NCS) showed normal sural sensory responses and absent motor responses. She received a 5-day course of intravenous immunoglobulin for treatment of suspected Guillain–Barr e syndrome (GBS), but her weakness worsened. She was transferred to our neuroscience intensive care unit on day 10. On admission, she was unresponsive to voice or painful stimuli, and pupils were fixed and dilated. Corneal, oculocephalic, cough, and gag reflexes were absent. Muscle tone was reduced with absent tendon reflexes and mute plantar responses. Her abdomen was distended with minimal bowel sounds. She demonstrated lability in blood pressure and heart rate. Laboratory studies showed normal creatine kinase. Electroencephalogram (EEG) showed low to medium voltage activity, no definite posterior basic rhythm, but intact sleep architecture. Transcranial Doppler studies (TCDs) demonstrated normal cerebral blood flow. Magnetic resonance imaging of the brain showed no acute abnormalities. On day 11, electrodiagnostic testing was repeated. NCS showed normal sensory nerve action potentials (SNAPs) and absent compound muscle action potentials (CMAPs) with stimulation of facial, musculocutaneous, median, ulnar, peroneal, and tibial nerves. CMAPs were unrecordable with 50-HZ repetitive stimulation. Needle electromyography (EMG) showed silence at rest. The patient was unable to generate volitional motor unit potentials. Repeat LP on day 12 showed 1 white blood cell/mm, protein 16 mg/dl, and negative West Nile virus (WNV) RNA and antibodies. Serum and stool botulism testing and ganglioside antibody testing for GM1, GD1 subtypes, myelin-associated glycoprotein, and sulfated glucuronyl paragloboside were sent. Plasma exchange was initiated for suspected GBS. On day 21, mouse bioassay, using serum collected 9 days earlier, was preliminarily positive for botulinum toxin. Endopeptidase–mass spectrometry (Endopep-MS) on serum from day 10 later confirmed botulinum toxin type A. Heptavalent botulinum antitoxin was administered on day 23 and, 10 days later, pupil reactivity and gut motility began to improve. By this time, ganglioside antibody testing returned negative and stool cultures grew Clostridium botulinum type A. Repeat serum and stool samples were collected on day 35. Because of delayed clinical improvement and concern for adult intestinal colonization, a second dose of antitoxin was administered on day 36. Follow-up nerve conduction studies were unchanged; however, EMG showed fibrillation potentials and positive sharp waves, consistent with an acute, ongoing process given silence on the previous EMG. Again, no volitional motor unit potentials were recruited. By day 38, slight muscle movements were observed. C. botulinum type A was identified by enzyme-linked immunoassay and polymerase chain reaction in stool, suggesting persistent gastrointestinal colonization. Botulinum toxin was not detected in serum drawn on day 36. A 14-day course of oral vancomycin was initiated. Upon discharge to a ventilator care facility on day 59, extraocular movements were improving but she was still quadraparetic. She eventually achieved independence from the ventilator during daytime hours, but died from an unwitnessed cardiopulmonary arrest 8 months after onset. This is a rare presentation of an adult with intestinal C. botulinum colonization who, on arrival to our institution, had a neurological examination indistinguishable from brain death. According to American Academy of Neurology guidelines, an irreversible cause of coma must be established for brain death diagnosis, which was lacking. Furthermore, EEG and TCDs were inconsistent with brain death. NCS demonstrated a profound motor VC 2017 Wiley Periodicals, Inc.

Elevated relative risk of aneurysmal subarachnoid hemorrhage with colder weather in the mid-Atlantic region

We have previously reported an increase of 0.6% in the relative risk of aneurysmal subarachnoid hemorrhage (aSAH) in response to every 1°F decrease in the maximum daily temperature (Tmax) in colder seasons from patients presenting to our regional tertiary care center. We hypothesized that this relationship would also be observed in the warmer summer months with ambient temperatures greater than 70°F. From prospectively collected incidence data for aSAH patients, we investigated absolute Tmax, average daily temperatures, intraday temperature ranges, and the variation of daily Tmax relative to 70°F to assess associations with aSAH incidence for patients admitted to our institution between 1991 and 2009 during the hottest months and days on which Tmax>70°F. For all days treated as a group, the mean Tmax (± standard deviation) was lower when aSAH occurred than when it did not (64.4±18.2°F versus 65.8±18.3°F; p=0.016). During summer months, the odds ratio (OR) of aSAH incidence increased with lower mean Tmax (OR 1.019; 95% confidence interval 1.001-1.037; p=0.043). The proportion of days with aSAH admissions was lower on hotter days than the proportion of days with no aSAH (96% versus 98%; p=0.006). aSAH were more likely to occur during the summer and on days with a temperature fluctuation less than 10°F (8% versus 4%; p=0.002). During the hottest months of the year in the mid-Atlantic region, colder maximum daily temperatures, a smaller heat burden above 70°F, and smaller intraday temperature fluctuations are associated with increased aSAH admissions in a similar manner to colder months. These findings support the hypothesis that aSAH incidence is more likely with drops in temperature, even in the warmer months.

Diploic arteriovenous fistulas—classification and endovascular management

BackgroundThe authors report on two cases of diploic arteriovenous fistulas (AVFs) in the left parieto-occipital region of a 20-year-old female and the right parietal region of a 68-year-old male. The clinical presentation, angiographic appearance, and endovascular management of these rare lesions are discussed.MethodsRetrospective data from two patients with diplopic AVFs are examined with a review of all published cases of diploic arteriovenous fistulas.ResultsWhere previously reported diploic AVFs showed venous drainage to be intracranial or combined, two case studies examined by the authors found exclusively extracranial drainage in the AVFs. In both case studies the lesions were primarily fed by the middle meningeal artery and treated via a transarterial endovascular approach using n-BCA glue.ConclusionsAfter reviewing all reported cases of AVF in the literature and combining our two new observations, we concluded that diploic AVFs can have three types of venous outflow: draining toward dural sinuses only, toward extracranial veins only, and combining the dural and extracranial pathways.

Cerebrovascular Events After Continuous-Flow Left Ventricular Assist Devices

AbstractBackgroundCerebrovascular events (CVE) are among the most common and serious complications after implantation of continuous-flow left ventricular assist devices (CF-LVAD). We studied the incidence, subtypes, anatomical distribution, and pre- and post-implantation risk factors of CVEs as well as the effect of CVEs on outcomes after CF-LVAD implantation at our institution. MethodsRetrospective analysis of clinical and neuroimaging data of 372 patients with CF-LVAD between May 2005 and December 2013 using standard statistical methods.ResultsCVEs occurred in 71 patients (19%), consisting of 35 ischemic (49%), 26 hemorrhagic (37%), and 10 ischemic+hemorrhagic (14%) events. History of coronary artery disease and female gender was associated with higher odds of ischemic CVE (OR 2.84 and 2.5, respectively), and diabetes mellitus was associated with higher odds of hemorrhagic CVE (OR 3.12). While we found a higher rate of ischemic CVEs in patients not taking any antithrombotic medications, no difference was found between patients with ischemic and hemorrhagic CVEs. Occurrence of CVEs was associated with increased mortality (HR 1.62). Heart transplantation was associated with improved survival (HR 0.02). In patients without heart transplantation, occurrence of CVE was associated with decreased survival.ConclusionsLVADs are associated with high rates of CVE, increased mortality, and lower rates of heart transplantation. Further investigations to identify the optimal primary and secondary stroke prevention measures in post-LVAD patients are warranted.

Epidemiology of septic meningitis associated with neuraxial anesthesia: A historical review and meta-analysis

INTRODUCTION Neuraxial anesthesia in the form of spinal and epidural are two of the most frequent forms of regional anesthesia. We aimed to describe and compare the relevant epidemiological, clinical and microbiological characteristics of all reported cases of septic meningitis associated with the use of spinal and epidural anesthetics. EVIDENCE ACQUISITION We performed a systematic review of septic meningitis associated with neuraxial anesthesia. We included all relevant case-reports and observational studies in which authors described septic meningitis in association with spinal, epidural or combined neuraxial anesthesia using local anesthetics. EVIDENCE SYNTHESIS A total of 234 cases of septic meningitis were reported following review of 71 case-report articles and 22 epidemiological studies. In total, there have been 199, 25 and 10 reported cases of septic meningitis associated to spinal, epidural and combined neuraxial anesthesia, respectively. The lack of use of surgical masks was the most common risk factor (41, 16.7%). Streptococcus salivarius was the most common bacteria (17.0%) related to spinal anesthesia and Staphylococcus aureus (26.7%) was the most common one related to epidural. The time to symptom onset was significantly reduced in spinal (median time, 24 hours IQR [8-72] vs. 96 hours IQR [84-240]; P=0.003) compared to epidural anesthesia. The overall mortality rate is 15.3% and 13.3% for reported cases related to spinal and epidural anesthesia, respectively. CONCLUSIONS While the true incidence remains speculative, this review suggests that given increasing indications for spinals and epidurals, septic meningitis remains an important associated with neuraxial anesthesia.

Comparison of intensive versus conventional insulin therapy in traumatic brain injury: a meta-analysis of randomized controlled trials

ABSTRACT Objective: To compare intensive insulin therapy (IIT) and conventional insulin therapy (CIT) on clinical outcomes of patients with traumatic brain injury (TBI). Methods: MEDLINE, EMBASE, Google Scholar, ISI Web of Science, and Cochrane Library were systematically searched for randomized controlled trials (RCTs) comparing IIT to CIT in patients with TBI. Study-level characteristics, intensive care unit (ICU) events, and long-term functional outcomes were extracted from the articles. Meta-analysis was performed with random-effect models. Results: Seven RCTs comprising 1070 patients were included. Although IIT was associated with better neurologic outcome (GOS > 3) (RR=0.87, 95% CI=0.78-0.97; P=0.01; I2=0%), sensitivity analysis revealed that one study influenced this overall estimate (RR=0.90, 95% CI=0.80–1.01, P=0.07; I2=0%). IIT was strongly associated with higher risk of hypoglycaemia (RR=5.79, 95% CI=3.27–10.26, P<0.01; I2=38%). IIT and CIT did not differ in terms of early or late mortality (RR=0.96, 95% CI=0.79–1.17, P=0.7; I2=0%), infection rate (RR=0.82, 95% CI=0.59–1.14, P=0.23; I2=68%), or ICU length of stay (SMD= –0.14, 95% CI=–0.35 to 0.07, P=0.18; I2=45%0.) Conclusions: IIT did not improve long-term neurologic outcome, mortality, or infection rate and was associated with increased risk of hypoglycaemia. Additional well-designed RCTs with defined TBI subgroups should be performed to generate more powerful conclusions.