Search

Cerebrovascular autoregulation (CA) is often impaired following traumatic brain injury. Established technologies and metrics used to assess CA are invasive and conducive for measurement, but not for continuous monitoring. We developed a trans-ocular brain impedance (TOBI) method that may provide non-invasive and continuous indices to assess CA. In this study, we monitored impedance metrics such as respiratory-induced impedance amplitude changes (dz) as well as a novel impedance index (DZx), which is a moving Pearson correlation between mean arterial pressure (MAP) and dz. Yorkshire swine were instrumented to continuously record ICP, MAP, and cerebral blood flow (CBF). TOBI was recorded by placement of standard ECG electrodes on closed eyelids and connected to a data acquisition system. MAP, ICP and CBF were manipulated utilizing an intravenous vasopressor challenge. TOBI indices (dz and DZx) were compared to the hemodynamic indicators as well as pressure reactivity index (PRx). During the vasopressor challenge, dz was highly correlated with ICP, CPP, and CBF (r =

Recent modeling and empirical studies support the hypothesis that large-scale brain networks function near a critical state. Similar functional connectivity patterns derived from resting state empirical data and brain network models at criticality provide further support. However, despite the strong implication of a relationship, there has been no principled explanation of how criticality shapes the characteristic functional connectivity in large-scale brain networks. Here, we hypothesized that the network science concept of partial phase locking is the underlying mechanism of optimal functional connectivity in the resting state. We further hypothesized that the characteristic connectivity of the critical state provides a theoretical boundary to quantify how far pharmacologically or pathologically perturbed brain connectivity deviates from its critical state, which could enable the differentiation of various states of consciousness with a theory-based metric. To test the hypothesis, we used a neuroanatomically informed brain network model with the resulting source signals projected to electroencephalogram (EEG)-like sensor signals with a forward model. Phase lag entropy (PLE), a measure of phase relation diversity, was estimated and the topography of PLE was analyzed. To measure the distance from criticality, the PLE topography at a critical state was compared with those of the EEG data from baseline consciousness, isoflurane anesthesia, ketamine anesthesia, vegetative state/unresponsive wakefulness syndrome, and minimally conscious state. We demonstrate that the partial phase locking at criticality shapes the functional connectivity and asymmetric anterior-posterior PLE topography, with low (high) PLE for high (low) degree nodes. The topographical similarity and the strength of PLE differentiates various pharmacologic and pathologic states of consciousness. Moreover, this model-based EEG network analysis provides a novel metric to quantify how far a pharmacologically or pathologically perturbed brain network is away from critical state, rather than merely determining whether it is in a critical or non-critical state.

Anesthetics are known to disrupt neural interactions in cortical and subcortical brain circuits. While the effect of anesthetic drugs on consciousness is reversible, the neural mechanism mediating induction and recovery may be different. Insight into these distinct mechanisms can be gained from a systematic comparison of neural dynamics during slow induction of and emergence from anesthesia. To this end, we used functional magnetic resonance imaging (fMRI) data obtained in healthy volunteers before, during, and after the administration of propofol at incrementally adjusted target concentrations. We analyzed functional connectivity of corticocortical and subcorticocortical networks and the temporal autocorrelation of fMRI signal as an index of neural processing timescales. We found that en route to unconsciousness, temporal autocorrelation across the entire brain gradually increased, whereas functional connectivity gradually decreased. In contrast, regaining consciousness was associated with an abrupt restoration of cortical but not subcortical temporal autocorrelation and an abrupt boost of subcorticocortical functional connectivity. Pharmacokinetic effects could not account for the difference in neural dynamics between induction and emergence. We conclude that the induction and recovery phases of anesthesia follow asymmetric neural dynamics. A rapid increase in the speed of cortical neural processing and subcorticocortical neural interactions may be a mechanism that reboots consciousness.

Background Severe hypocalcaemia is associated with increased transfusion in the trauma population. Furthermore, trauma patients developing severe hypocalcaemia have higher mortality and coagulopathy. Electrolyte abnormalities associated with massive transfusion have been less studied in the surgical population. Here, we tested the primary hypothesis that volume of packed red blood cells and fresh frozen plasma transfused intraoperatively is associated with lower nadir ionised calcium in the surgical population receiving massive resuscitation. Methods We performed a retrospective observational study at an academic quaternary care centre to characterise hypocalcaemia following large volume (4 or more units packed red blood cells) intraoperative transfusion. We used multivariable linear regression to assess if volume of transfusion with packed red blood cells and fresh frozen plasma were independently associated with a lower ionised calcium. We then used multivariable logistic regressions to assess the association between ionised calcium and transfusion with: (i) mortality, (ii) acute kidney injury, and (iii) postoperative coagulopathy. Results Hypocalcaemia following large volume resuscitation in the operating room is a very frequent occurrence (70% of cases). After controlling for demographic variables and intraoperative variables, the volume transfused intraoperative was independently associated with hypocalcaemia on multivariable linear regression. Hypocalcaemia, intraoperative transfusion of packed red blood cells, and intraoperative transfusion of fresh frozen plasma were not shown to be associated with clinical outcomes. Conclusions Hypocalcaemia was associated with increased transfusion volume in this single-centre study. Unlike the trauma population, hypocalcaemia was not associated with increased mortality during surgical care. Our findings suggest that despite improved practice patterns of calcium supplementation, intraoperative hypocalcaemia occurs with relatively high frequency following large volume intraoperative transfusion.

Understanding how the brain recovers from unconsciousness can inform neurobiological theories of consciousness and guide clinical investigation. To address this question, we conducted a multicenter study of 60 healthy humans, half of whom received general anesthesia for 3 hr and half of whom served as awake controls. We administered a battery of neurocognitive tests and recorded electroencephalography to assess cortical dynamics. We hypothesized that recovery of consciousness and cognition is an extended process, with differential recovery of cognitive functions that would commence with return of responsiveness and end with return of executive function, mediated by prefrontal cortex. We found that, just prior to the recovery of consciousness, frontal-parietal dynamics returned to baseline. Consistent with our hypothesis, cognitive reconstitution after anesthesia evolved over time. Contrary to our hypothesis, executive function returned first. Early engagement of prefrontal cortex in recovery of consciousness and cognition is consistent with global neuronal workspace theory., eLife digest Anesthesia is a state of reversable, controlled unconsciousness. It has enabled countless medical procedures. But it also serves as a tool for scientists to study how the brain regains consciousness after disruptions such as sleep, coma or medical procedures requiring general anesthesia. It is still unclear how exactly the brain regains consciousness, and less so, why some patients do not recover normally after general anesthesia or fail to recover from brain injury. To find out more, Mashour et al. studied the patterns of reemerging consciousness and cognitive function in 30 healthy adults who underwent general anesthesia for three hours. While the volunteers were under anesthesia, their brain activity was measured with an EEG; and their sleep-wake activity was measured before and after the experiment. Each participant took part in a series of cognitive tests designed to measure the reaction speed, memory and other functions before receiving anesthesia, right after the return of consciousness, and then every 30 minutes thereafter. Thirty healthy volunteers who did not have anesthesia also completed the scans and tests as a comparison group. The experiments showed that certain normal EEG patterns resumed just before a person wakes up from anesthesia. The return of thinking abilities was an extended, multistep process, but volunteers recovered their cognitive abilities to nearly the same level as the volunteers within three hours of being deeply anesthetized. Mashour et al. also unexpectedly found that abstract problem-solving resumes early in the process, while other functions such as reaction time and attention took longer to recover. This makes sense from an evolutionary perspective. Sleep leaves individuals vulnerable. Quick evaluation and decision-making skills would be key to respond to a threat upon waking. The experiments confirm that the front of the brain, which handles thinking and decision-making, was especially active around the time of recovery. This suggests that therapies targeting this part of the brain may help people who experience loss of consciousness after a brain injury or have difficulties waking up after anesthesia. Moreover, disorders of cognition, such as delirium, in the days following surgery may be caused by factors other than the lingering effects of anesthetic drugs on the brain.

The development of sophisticated computational tools to quantify changes in the brain's oscillatory dynamics across states of consciousness have included both envelope- and phase-based measures of functional connectivity (FC), but there are very few direct comparisons of these techniques using the same dataset. The goal of this study was to compare an envelope-based (i.e. Amplitude Envelope Correlation, AEC) and a phase-based (i.e. weighted Phase Lag Index, wPLI) measure of FC in their classification of states of consciousness. Nine healthy participants underwent a three-hour experimental anesthetic protocol with propofol induction and isoflurane maintenance, in which five minutes of 128-channel electroencephalography were recorded before, during, and after anesthetic-induced unconsciousness, at the following time points: Baseline; light sedation with propofol (Light Sedation); deep unconsciousness following three hours of surgical levels of anesthesia with isoflurane (Unconscious); five minutes prior to the recovery of consciousness (Pre-ROC); and three hours following the recovery of consciousness (Recovery). Support vector machine classification was applied to the source-localized EEG in the alpha (8–13 Hz) frequency band in order to investigate the ability of AEC and wPLI (separately and together) to discriminate i) the four states from Baseline; ii) Unconscious (“deep” unconsciousness) vs. Pre-ROC (“light” unconsciousness); and iii) responsiveness (Baseline, Light Sedation, Recovery) vs. unresponsiveness (Unconscious, Pre-ROC). AEC and wPLI yielded different patterns of global connectivity across states of consciousness, with AEC showing the strongest network connectivity during the Unconscious epoch, and wPLI showing the strongest connectivity during full consciousness (i.e., Baseline and Recovery). Both measures also demonstrated differential predictive contributions across participants and used different brain regions for classification. AEC showed higher classification accuracy overall, particularly for distinguishing anesthetic-induced unconsciousness from Baseline (83.7 ± 0.8%). AEC also showed stronger classification accuracy than wPLI when distinguishing Unconscious from Pre-ROC (i.e., “deep” from “light” unconsciousness) (AEC: 66.3 ± 1.2%; wPLI: 56.2 ± 1.3%), and when distinguishing between responsiveness and unresponsiveness (AEC: 76.0 ± 1.3%; wPLI: 63.6 ± 1.8%). Classification accuracy was not improved compared to AEC when both AEC and wPLI were combined. This analysis of source-localized EEG data demonstrates that envelope- and phase-based FC provide different information about states of consciousness but that, on a group level, AEC is better able to detect relative alterations in brain FC across levels of anesthetic-induced unconsciousness compared to wPLI.

Background: Motifs are patterns of inter-connections between nodes of a complex network, and have been investigated as the basic building blocks of directed networks. This study explored the re-organization of 3-node (i.e. 3-electrode) network motifs during anesthetic-induced loss and recovery of consciousness. We hypothesized that motif frequency and topography would change across states of consciousness, and that the frequency and topography associated with consciousness would recover prior to the return of behavioral responsiveness. Methods: Nine healthy subjects underwent a 3-hour controlled anesthetic protocol (propofol induction; isoflurane maintenance) in an operating room, while brain activity was recorded through 128-channel electroencephalography (EEG). In the alpha (8-13 Hz) frequency band, five-minute epochs of EEG were extracted for: baseline; induction; unconsciousness; 30-, 10- and 5-minutes pre-recovery of consciousness; 30- and 180-minutes post-recovery of consciousness. We constructed a functional brain network using the weighted phase lag index and the directed phase lag index, which were then used to calculate graph theoretical brain network properties and the frequency and topography of 3-node (i.e. 3-electrode) motifs. Results: Three motifs (motifs 1, 2 and 5) were significantly present across participants and epochs, when compared to random networks (p

The effect of neither transfusion guidelines nor decision support tools on intraoperative transfusion has been previously evaluated. The University of Michigan introduced a transfusion guideline in 2009, and in 2011, the Department of Anesthesiology developed a transfusion decision support tool. The primary aim of this study was to assess the associations of the transfusion guideline and the optional use of the software transfusion tool with intraoperative behaviors; pretransfusion hematocrit assessment (whether or not a hematocrit was checked before each red cell unit) and restrictive red cell use (withholding transfusion unless the hematocrit was ≤21%).This was a before-after retrospective study without a concurrent control group of patients transfused 1-3 units of red cells intraoperatively. Three phases were studied to provide data both before and after the implementation of the transfusion guideline and the intraoperative software tool. Within each phase, trends of checking hematocrits before transfusion and restrictive transfusion were charted against time. F tests were used to measure differences of slopes. The difference between means of each phase was measured using Mann-Whitney U tests. Independent associations were measured using mixed-effects multivariable logistic regression. A secondary outcome analysis was conducted for 30-day mortality, myocardial infarction, renal injury, and their combination.The transfusion guideline was associated with increased pretransfusion hematocrit evaluation (67.4%, standard deviation [SD] 3.9 vs 76.5%, SD 2.7; P.001) and restrictive transfusion practice (14.0%, SD 7.4 vs 33.3%, SD 4.4; P = .001). After adjustment for confounders, the guideline phase was independently associated with increased hematocrit checking (odds ratio, 1.72; 95% confidence interval, 1.46-2.03; P.001) and restrictive red cell transfusion (odds ratio, 2.95; 95% confidence interval, 2.46-3.54; P.001). The software tool was not associated with either transfusion behavior. There was no significant change in the rate of renal injury (16.06%), myocardial injury (4.93%), 30-day mortality (5.47%), or a composite (21.90%).The introduction of a transfusion guideline was independently associated with increased intraoperative pretransfusion hematocrit assessment and restrictive transfusion. The use of a software tool did not further influence either behavior.

BACKGROUND: Despite its designation as a ‘dissociative anaesthetic,’ the dissociative and psychoactive effects of ketamine remain incompletely understood. The goal of this study was to characterise the subjective experiences and accompanying EEG changes with subanaesthetic doses of ketamine. METHODS: High-density EEG was recorded in 15 human volunteers before, during, and after subanaesthetic ketamine infusion (0.5 mg kg(−1) over 40 min), with self-reported measures of altered states of consciousness obtained after ketamine exposure. Sensor- and source-level EEG changes were analysed with a focus on spectral power and regional changes. RESULTS: Ketamine-induced altered states were characterised predominantly by dissociative experiences such as disembodiment and ego transcendence; sensory disturbances were also common. Ketamine broadly decreased low-frequency power, with mean reductions largest at alpha (8–12 Hz) in parietal (−0.94 dB, P

Neurologic complications of surgery can be devastating. The authors review neurologic considerations and complications associated with liver transplantation and discuss strategies to prevent, identify, and treat such adverse outcomes in the perioperative period.

Background Previous studies have demonstrated inconsistent neurophysiologic effects of ketamine, although discrepant findings might relate to differences in doses studied, brain regions analyzed, coadministration of other anesthetic medications, and resolution of the electroencephalograph. The objective of this study was to characterize the dose-dependent effects of ketamine on cortical oscillations and functional connectivity. Methods Ten healthy human volunteers were recruited for study participation. The data were recorded using a 128-channel electroencephalograph during baseline consciousness, subanesthetic dosing (0.5 mg/kg over 40 min), anesthetic dosing (1.5 mg/kg bolus), and recovery. No other sedative or anesthetic medications were administered. Spectrograms, topomaps, and functional connectivity (weighted and directed phase lag index) were computed and analyzed. Results Frontal theta bandwidth power increased most dramatically during ketamine anesthesia (mean power ± SD, 4.25 ± 1.90 dB) compared to the baseline (0.64 ± 0.28 dB), subanesthetic (0.60 ± 0.30 dB), and recovery (0.68 ± 0.41 dB) states; P < 0.001. Gamma power also increased during ketamine anesthesia. Weighted phase lag index demonstrated theta phase locking within anterior regions (0.2349 ± 0.1170, P < 0.001) and between anterior and posterior regions (0.2159 ± 0.1538, P < 0.01) during ketamine anesthesia. Alpha power gradually decreased with subanesthetic ketamine, and anterior-to-posterior directed connectivity was maximally reduced (0.0282 ± 0.0772) during ketamine anesthesia compared to all other states (P < 0.05). Conclusions Ketamine anesthesia correlates most clearly with distinct changes in the theta bandwidth, including increased power and functional connectivity. Anterior-to-posterior connectivity in the alpha bandwidth becomes maximally depressed with anesthetic ketamine administration, suggesting a dose-dependent effect.

Background Burst suppression occurs in the EEG during coma and under general anaesthesia. It has been assumed that burst suppression represents a deeper state of anaesthesia from which it is more difficult to recover. This has not been directly demonstrated, however. Here, we test this hypothesis directly by assessing relationships between EEG suppression in human volunteers and recovery of consciousness. Methods We recorded the EEG of 27 healthy humans (nine women/18 men) anaesthetised with isoflurane 1.3 minimum alveolar concentration (MAC) for 3 h. Periods of EEG suppression and non-suppression were separated using principal component analysis of the spectrogram. After emergence, participants completed the digit symbol substitution test and the psychomotor vigilance test. Results Volunteers demonstrated marked variability in multiple features of the suppressed EEG. In order to test the hypothesis that, for an individual subject, inclusion of features of suppression would improve accuracy of a model built to predict time of emergence, two types of models were constructed: one with a suppression-related feature included and one without. Contrary to our hypothesis, Akaike information criterion demonstrated that the addition of a suppression-related feature did not improve the ability of the model to predict time to emergence. Furthermore, the amounts of EEG suppression and decrements in cognitive task performance relative to pre-anaesthesia baseline were not significantly correlated. Conclusions These findings suggest that, in contrast to current assumptions, EEG suppression in and of itself is not an important determinant of recovery time or the degree of cognitive impairment upon emergence from anaesthesia in healthy adults.

Background Perioperative hyperglycemia is associated with poor outcomes yet evidence to guide intraoperative goals and treatment modalities during non-cardiac surgery are lacking. End-stage liver disease is associated with altered glucose homeostasis; patients undergoing liver transplantation display huge fluctuations in blood glucose (BG) and represent a population of great interest. Here, we conduct a randomized trial to compare the effects of strict versus conventional glycemic control during orthotopic liver transplant (OLT). Methods Following approval by the Institutional Review Board of the University of Michigan Medical School and informed consent, 100 adult patients undergoing OLT were recruited. Patients were randomized to either strict (target BG 80–120 mg/dL) or conventional (target BG 180–200 mg/dL) BG control with block randomization for diabetic and nondiabetic patients. The primary outcomes measured were 1-year patient and graft survival assessed on an intention to treat basis. Graft survival is defined as death or needing re-transplant (www.unos.org). Three and 5-year patient and graft survival, infectious and biliary complications were measured as secondary outcomes. Data were examined using univariate methods and Kaplan-Meir survival analysis. A sensitivity analysis was performed to compare patients with a mean BG of ≤120 mg/dL and those > 120 mg/dL regardless of treatment group. Results There was no statistically significant difference in patient survival between conventional and strict control respectively;1 year, 88% vs 88% (p-0.99), 3 years, 86% vs 84% (p- 0.77), 5 years, 82% vs 78. % (p-0.36). Graft survival was not different between conventional and strict control groups at 1 year, 88% vs 84% (p-0.56), 3 years 82% vs 76% (p-0.46), 5 years 78% vs 70% (p-0.362). Conclusion There was no difference in patient or graft survival between intraoperative strict and conventional glycemic control during OLT. Trial registration Clinical trial number and registry: www.clinicaltrials.gov NCT00780026. This trial was retrospectively registered on 10/22/2008.

Background: Stroke is a devastating perioperative complication without effective methods for prevention or diagnosis. The objective of this study was to analyze evidence-based strategies for detecting cerebrovascular vulnerability and injury in a high-risk cohort of non-cardiac surgery patients.Methods: This was a single-center, prospective cohort study. Fifty patients undergoing non-cardiac surgery were recruited −25 with known cerebrovascular disease and 25 matched controls. Neurologic vulnerability was measured with intraoperative cerebral oximetry as the primary outcome. Perioperative neurocognitive testing and serum biomarker analysis (S-100β, neuron specific enolase, glial fibrillary acid protein, and matrix metalloproteinase-9) were measured as secondary outcomes.Results: Cerebral desaturation events (an oximetry decrease ≥20% from baseline or

SUMMARY Conscious access to sensory information is likely gated at an intermediate site between primary sensory and transmodal association cortices, but the structure responsible remains unknown. We perform functional neuroimaging to determine the neural correlates of conscious access using a volitional mental imagery task, a report paradigm not confounded by motor behavior. Titrating propofol to loss of behavioral responsiveness in healthy volunteers creates dysfunction of the anterior insular cortex (AIC) in association with an impairment of dynamic transitions of default-mode and dorsal attention networks. Candidate subcortical regions mediating sensory gating or arousal (thalamus, basal forebrain) fail to show this association. The gating role of the AIC is consistent with findings in awake participants, whose conscious access is predicted by pre-stimulus AIC activity near perceptual threshold. These data support the hypothesis that AIC, situated at an intermediate position of the cortical hierarchy, regulates brain network transitions that gate conscious access., Graphical abstract, In brief In a human neuroimaging study, Huang et al. manipulate the level and content of consciousness using independent experimental protocols to demonstrate that the anterior insula, situated between unimodal and transmodal cortical areas along the brain’s functional hierarchy, serves as a gate for conscious access of sensory information.

Detecting covert consciousness in behaviorally unresponsive patients by brain imaging is of great interest, but a reproducible model and evidence from independent sources is still lacking. Here we demonstrate the possibility of using general anesthetics in a within-subjects study design to test methods or statistical paradigms of assessing covert consciousness. Using noninvasive neuroimaging in healthy volunteers, we identified a healthy study participant who was able to exhibit the specific fMRI signatures of volitional mental imagery while behaviorally unresponsive due to sedation with propofol. Our findings reveal a novel model that may accelerate the development of new approaches to reproducibly detect covert consciousness, which is difficult to achieve in patients with heterogeneous and sometimes clinically unstable neuropathology.

The integrated information theory (IIT) proposes a quantitative measure, denoted as Φ, of the amount of integrated information in a physical system, which is postulated to have an identity relationship with consciousness. IIT predicts that the value of Φ estimated from brain activities represents the level of consciousness across phylogeny and functional states. Practical limitations, such as the explosive computational demands required to estimate Φ for real systems, have hindered its application to the brain and raised questions about the utility of IIT in general. To achieve practical relevance for studying the human brain, it will be beneficial to establish the reliable estimation of Φ from multichannel electroencephalogram (EEG) and define the relationship of Φ to EEG properties conventionally used to define states of consciousness. In this study, we introduce a practical method to estimate Φ from high-density (128-channel) EEG and determine the contribution of each channel to Φ. We examine the correlation of power, frequency, functional connectivity, and modularity of EEG with regional Φ in various states of consciousness as modulated by diverse anesthetics. We find that our approximation of Φ alone is insufficient to discriminate certain states of anesthesia. However, a multi-dimensional parameter space extended by four parameters related to Φ and EEG connectivity is able to differentiate all states of consciousness. The association of Φ with EEG connectivity during clinically defined anesthetic states represents a new practical approach to the application of IIT, which may be used to characterize various physiological (sleep), pharmacological (anesthesia), and pathological (coma) states of consciousness in the human brain.

Recent studies have investigated local oscillations, long-range connectivity, and global network patterns to identify neural changes associated with anesthetic-induced unconsciousness. These studies typically employ anesthetic protocols that either just cross the threshold of unconsciousness, or induce deep unconsciousness for a brief period of time-neither of which models general anesthesia for major surgery. To study neural patterns of unconsciousness and recovery in a clinically-relevant context, we used a realistic anesthetic regimen to induce and maintain unconsciousness in eight healthy participants for 3 h. High-density electroencephalogram (EEG) was acquired throughout and for another 3 h after emergence. Seven epochs of 5-min eyes-closed resting states were extracted from the data at baseline as well as 30, 60, 90, 120, 150, and 180-min post-emergence. Additionally, 5-min epochs were extracted during induction, unconsciousness, and immediately prior to recovery of consciousness, for a total of 10 analysis epochs. The EEG data in each epoch were analyzed using source-localized spectral analysis, phase-lag index, and graph theoretical techniques. Posterior alpha power was significantly depressed during unconsciousness, and gradually approached baseline levels over the 3 h recovery period. Phase-lag index did not distinguish between states of consciousness or stages of recovery. Network efficiency was significantly depressed and network clustering coefficient was significantly increased during unconsciousness; these graph theoretical measures returned to baseline during the 3 h recovery period. Posterior alpha power may be a potential biomarker for normal recovery of functional brain networks after general anesthesia.

Introduction. Almost all pediatric orthotopic liver transplant (OLT) recipients require mechanical ventilation in the early postoperative period. Prolonged postoperative mechanical ventilation (PPMV) may be a marker of severe disease and may be associated with morbidity and mortality. We determined the incidence and risk factors for PPMV in children who underwent OLT. Methods. This was a retrospective analysis of data collected on 128 pediatric OLT recipients. PPMV was defined as postoperative ventilation ≥ 4 days. Perioperative characteristics were compared between cases and control groups. Multivariable logistic regression analysis was used to calculate odds ratios for PPMV after controlling for relevant cofactors. Results. An estimated 25% (95% CI, 17.4%–32.6%) required PPMV. The overall incidence of PPMV varied significantly by age group with the highest incidence among infants. PPMV was associated with higher postoperative mortality (p=0.004) and longer intensive care unit (p<0.001) and hospital length of stay (p<0.001). Multivariable analysis identified young patient age, preoperative hypocalcemia, and increasing duration of surgery as independent predictors of PPMV following OLT. Conclusion. The incidence of PPMV is high and it was associated with prolonged ICU and hospital LOS and higher posttransplant mortality. Surgery duration appears to be the only modifiable predictor of PPMV.

THE USE OF echocardiography provides real-time, highyield information concerning valve and chamber function and allows intravascular volume assessment as well as an estimate of pulmonary and systemic vascular resistances. As such, the use of intraoperative transesophageal echocardiography (TEE) is recommended to facilitate the diagnosis for patients with hemodynamic instability undergoing noncardiac surgery. Pleural effusion is a common postoperative complication following cardiac surgery and mostly resolves with conservative management. Large pleural effusions can cause hemodynamic compromise, but this has not been reported previously in patients who display normal respiratory mechanics under positive-pressure ventilation. The authors present a case report of a known pleural effusion causing unanticipated hemodynamic compromise during general anesthesia. They postulate that the transition from negativeto positive-pressure mechanical ventilation was a pivotal contributing factor for the development of cardiac tamponade physiology. The emergent use of TEE provided for a rapid diagnosis and facilitated treatment of a pleural effusion with restoration of hemodynamic function.