Emergent Management of Severe Hypothermia, Acidemia, and Coagulopathy in Operative Penetrating Ballistic Cranial Trauma.

Hypothermia in a trauma patient has been associated with increased morbidity and mortality and is more frequently seen in those sustaining traumatic brain injuries (TBIs). Acidosis is an important consequence of hypothermia that leads to derangements across the spectrum of the coagulation cascade. Here, we present a case of a 31-year-old male presented after suffering a right parietal penetrating ballistic injury with an associated subdural hematoma and 7 mm midline shift requiring decompressive craniectomy and external ventricular drain (EVD) placement in the setting of severe hypothermia (28°C) and acidosis (pH 7.12). With aggressive rewarming intraoperatively, the use of full-body forced-air warming, warmed IV fluids, and increasing the ambient room temperature, the patient's acidosis and hypothermia improved to pH 7.20 and 34°C. Despite these aggressive attempts to rewarm the patient, he developed coagulopathy in the setting of concurrent hypothermia and acidosis. This case highlights the importance of prompt reversal of hypothermia due to its potentially fatal effects, particularly in the setting of severe TBIs. We discuss the critical aspects of surgical management of the injury and anesthetic management of hypothermia, acidosis, and coagulopathy perioperatively.

Intraoperative Fraction of Inspired Oxygen and Lung Injury in Coronary Artery Bypass Grafting: Study Protocol for a Randomised Controlled Trial.

OBJECTIVE: Postoperative pulmonary complications are a series of disorders that can contribute to respiratory distress and prolonged mechanical ventilation postoperatively. We hypothesise that a liberal oxygenation strategy during cardiac surgery leads to a higher incidence of postoperative pulmonary complications than a restrictive oxygenation strategy. METHODS: This study is a prospective, observer-blinded, centrally randomised and controlled, international multicentre clinical trial. RESULTS: After obtaining a written informed consent, 200 adult patients undergoing coronary artery bypass grafting will be enrolled and randomised to receive either restrictive or liberal oxygenation perioperatively. The liberal oxygenation group will receive 1.0 fraction of inspired oxygen throughout the intraoperative period, including during cardiopulmonary bypass. The restrictive oxygenation group will receive the lowest fraction of inspired oxygen required to maintain arterial partial pressure of oxygen between 100 and 150 mmHg during cardiopulmonary bypass and a pulse oximetry reading of 95% or greater intraoperatively, but no less than 0.3 and not higher than 0.80 (other than induction and when the oxygenation goals cannot be reached). When patients are transferred to the intensive care unit, all patients will receive an initial fraction of inspired oxygen of 0.5, and then fraction of inspired oxygen will be titrated to maintain a pulse oximetry reading of 95% or greater until extubation. The lowest postoperative arterial partial pressure of oxygen/fraction of inspired oxygen within 48 hours of intensive care unit admission will be the primary outcome. Postoperative pulmonary complications, length of mechanical ventilation, intensive care unit stay, hospital stay, and 7-day mortality after cardiac surgery will be analysed as secondary outcomes. CONCLUSION: This is one of the first randomised controlled observer-blinded trials that prospectively evaluates the influence of higher inspired oxygen fractions on early postoperative respiratory and oxygenation outcomes in cardiac surgery patients using cardiopulmonary bypass.

Validation of a Novel NeurOs Cerebral Oximetry Monitor Against the INVOS Monitor During Cardiac Surgery.

OBJECTIVES: To compare the performance of a novel NeurOs cerebral oximetry monitor against the INVOS monitor during the entire intraoperative phase of cardiac surgery, including periods of known fluctuation in brain oxygenation, such as preoxygenation, induction, cannulation, and cardiopulmonary bypass. DESIGN: This study was a prospective, nonrandomized, healthcare-provider and outcome-assessor blinded study. SETTING: Tertiary care university hospital; single institutional study. PARTICIPANTS: Twenty-three patients who underwent cardiac surgery with cardiopulmonary bypass. INTERVENTIONS: Both self-adhesive INVOS sensors and the assembled NeurOs sensors were placed accordingly when the patient arrived in the operating room. MEASUREMENTS AND MAIN RESULTS: Ten out of 13 cases under the normal mode and eight out of the 10 cases under the high- sensitivity mode showed significant correlations between the NeurOs and INVOS groups (p < 0.05, r value from 0.24-0.88). When all cases were combined, NeurOs demonstrated significant correlation with INVOS (r = 0.5, 95% confidence interval [CI] 0.44-0.56, p < 0.01 for normal mode; r = 0.69, 95% CI 0.64 to 0.74, p < 0.01 for high-sensitivity mode) in both modes. To evaluate the data diversity, the authors performed a cluster analysis and found much less variation existed in the NeurOs normal mode when compared with INVOS (standard deviation [SD] 16.6% in INVOS, 4% in NeurOs normal mode) but similar patterns in the high-sensitivity mode (SD 17.6% in INVOS, 15.2% in NeurOs high-sensitivity mode). Bland-Altman plot analysis showed that most of the data fell between ± 1.96 SD lines, which demonstrated good consistency between these two methods under both modes of NeurOs (-28.8 to 30.8 in the normal mode; -36.6 to 32.7 in high-sensitivity mode). In the normal mode of NeurOs monitoring, receiver operating characteristic analysis suggested a 2% cutoff point was most optimal from the baseline for detecting hyperoxia (sensitivity 73%; specificity 66%) and minus 1% (sensitivity 66%; specificity 67%) for detecting hypoxia. Whereas in the high-sensitivity mode, the optimal cutoff point was 3% from baseline for detecting hyperoxia (sensitivity 75%; specificity 68%), and minus 3% for detecting hypoxia (sensitivity 90%; specificity 45%). CONCLUSIONS: In conclusion, the novel NeurOs system was found to correlate with INVOS cerebral oximetry measurements during cardiac surgery.

Preventing Egregious Ethical Violations in Medical Practice: Evidence-Informed Recommendations from a Multidisciplinary Working Group.

This article reports the consensus recommendations of a working group that was convened at the end of a 4-year research project funded by the National Institutes of Health that examined 280 cases of egregious ethical violations in medical practice. The group reviewed data from the parent project, as well as other research on sexual abuse of patients, criminal prescribing of controlled substances, and unnecessary invasive procedures that were prosecuted as fraud. The working group embraced the goals of making such violations significantly less frequent and, when they do occur, identifying them sooner and taking necessary steps to ensure they are not repeated. Following review of data and previously published recommendations, the working group developed 10 recommendations that provide a starting point to meet these goals. Recommendations address leadership, oversight, tracking, disciplinary actions, education of patients, partnerships with law enforcement, further research and related matters. The working group recognized the need for further refinement of the recommendations to ensure feasibility and appropriate balance between protection of patients and fairness to physicians. While full implementation of appropriate measures will require time and study, we believe it is urgent to take visible actions to acknowledge and address the problem at hand.

Cutaneous tissue damage induces long-lasting nociceptive sensitization and regulation of cellular stress- and nerve injury-associated genes in sensory neurons.

Tissue damage is one of the major etiological factors in the emergence of chronic/persistent pain, although mechanisms remain enigmatic. Using incision of the back skin of adult rats as a model for tissue damage, we observed sensitization in a nociceptive reflex enduring to 28days post-incision (DPI). To determine if the enduring behavioral changes corresponded with a long-term impact of tissue damage on sensory neurons, we examined the temporal expression profile of injury-regulated genes and the electrophysiological properties of traced dorsal root ganglion (DRG) sensory neurons. The mRNA for the injury/stress-hub gene Activating Transcription Factor 3 (ATF3) was upregulated and peaked within 4 DPI, after which levels declined but remained significantly elevated out to 28 DPI, a time when the initial incision appears healed and tissue-inflammation largely resolved. Accordingly, stereological image analysis indicated that some neurons expressed ATF3 only transiently (mostly medium-large neurons), while in others it was sustained (mostly small neurons), suggesting cell-type-specific responses. In retrogradely-traced ATF3-expressing neurons, Calcium/calmodulin-dependent protein kinase type IV (CAMK4) protein levels and isolectin-B4 (IB4)-binding were suppressed whereas Growth Associated Protein-43 (GAP-43) and Neuropeptide Y (NPY) protein levels were enhanced. Electrophysiological recordings from DiI-traced sensory neurons 28 DPI showed a significant sensitization limited to ATF3-expressing neurons. Thus, ATF3 expression is revealed as a strong predictor of single cells displaying enduring pain-related electrophysiological properties. The cellular injury/stress response induced in sensory neurons by tissue damage and indicated by ATF3 expression is positioned to contribute to pain which can occur after tissue damage.

Clinical assessment of propofol-induced yawning with heart rate variability: a pilot study.

STUDY OBJECTIVES: To investigate the proportion of propofol-induced yawning and sympathovagal balance during propofol-induced yawning. DESIGN: Prospective, observational, clinical study. SETTING: University hospital and 2400-bed tertiary medical center. PATIENTS: 546 ASA physical status I and II patients undergoing elective surgery with general anesthesia. INTERVENTIONS: Standard induction of anesthesia was performed with intravenous (IV) propofol two to four mg/kg (group P), or pretreatment with atropine 0.1 mg/kg (group AP) or with fentanyl 1 to 3 microg/kg (group FP) before propofol. Continuous standard electrocardiogram for heart rate variability (HRV) was performed in another 20 patients to investigate sympathovagal balance during propofol-induced yawning. MEASUREMENTS AND MAIN RESULTS: The proportions of yawning were 53.5% (207/386), 61.1% (55/90), and 0% (0/50) in the P, AP, and FP groups, respectively. Propofol-induced yawning could be dramatically decreased by pretreatment with IV fentanyl (P < 0.001, chi2 test). Significant increased ratio of low-frequency/high-frequency power was detected during HRV monitoring in 9 patients with yawning in comparison with 11 patients without yawning (P < 0.05, Wilcoxon signed-rank test). CONCLUSIONS: Pretreatment with fentanyl may inhibit propofol-induced yawning. Fluctuations in autonomic function have been noted during propofol-induced yawning.

Unanticipated difficult endotracheal intubations in patients with cervical spine instrumentation.

We present two cases of unanticipated difficult airway in patients requiring reoperation after cervical spine instrumentation. In both cases, the upper airway examination was normal, and fiberoptic-guided intubation proceeded with the patient sedated and breathing spontaneously. Cord visualization was difficult, but the scope was eventually advanced into the trachea and the endotracheal tube placed safely. Later review of radiographs showed the previously unrecognized protrusion of cervical hardware into the meso- and hypopharynx. We recommend that anesthesiologists review recent radiographic studies for potential airway compromise before approaching the airway of patients presenting for revision of cervical instrumentation.

Recovery from paralysis with succinylcholine increased Response entropy and EMG but not State entropy.

OBJECTIVE: It is reported that the electromyogram is an indicator of patient arousal during pain stimulation if anesthesia is inadequate. This may not be true during recovery from succinylcholine induced paralysis. We evaluated State entropy of the electroencephalogram (EEG, 0.8-32 Hz) and Response entropy, a combined measure of the electromyogram (EMG) and EEG (0.8-47 Hz), during recovery from paralysis with succinylcholine. METHODS: Twenty patients were randomized to receive either 0.8% (n = 10) or 1.4% isoflurane (n = 10), with 2 mg/kg succinylcholine administered for paralysis in all patients. State entropy and Response entropy were evaluated using a Datex-Ohmeda Entropy module. Frontal EMG was measured separately by an EEG module. State entropy, Response entropy, and EMG were measured in awake patients, during isoflurane anesthesia and paralysis, and after 100% recovery to train of four stimulation. RESULTS: Response entropy and State entropy decreased from awake levels in a dose related manner during 0.8% or 1.4% isoflurane and succinylcholine. Recovery from succinylcholine significantly increased Response entropy and EMG in 5 of 10 patients with 0.8% isoflurane and 8 of 10 with 1.4% isoflurane without a change in State entropy. CONCLUSION: Although RE and EMG increased during recovery from paralysis with succinylcholine, SE, an indicator of EEG, was not stimulated. EMG activity may not be an indicator of patient arousal after succinylcholine treatment.

Jet injection of local anesthetic decreases pain of arterial cannulation in awake neurosurgical patients.

Arterial cannulation through the standard skin wheal of local anesthetic raised with a needle may be painful. The authors compared the efficacy of local anesthetic injected via a 25G needle versus a Bioject jet injector for arterial cannulation in awake neurosurgical patients. After institutional review board approval, 40 patients were randomized to receive 0.3 mL 1% lidocaine adjusted to pH 7.0 with NaHCO3 by Bioject with a 2-cm spacer between the syringe and skin or by 25G needle injection. Two pain assessments were used at the time of local anesthetic injection and at arterial cannulation. Patients rated their pain on a visual analog scale (VAS) (0 = no pain, 100 = worst pain). Observers scored patient response as 0 (no response), 1 (flinch), or 2 (withdrawal). The VAS at injection was 23 +/- 19 for the needle group and 3 +/- 6 for the Bioject group (P < 0.001). The VAS at arterial cannulation was 39 +/- 25 for the needle group and 15 +/- 22 for the Bioject group (P < 0.001). Median observer scores at injection and cannulation were 1 (range 0-2) for the needle group and 0 (range 0-2) for the Bioject group (P < 0.001). Patients in the Bioject group experienced significantly less pain during lidocaine administration and at the time of arterial cannulation by their own and by an observer's assessment than the needle injection group. Jet injection of local anesthetic should be considered prior to arterial cannulation in awake patients.

Loss of SSEP during sitting craniotomy.

A 54-year-old woman with a past medical history of asthma and depression presented with right side hearing loss and ataxia. She was scheduled for a sitting craniotomy for cerebellopontine angle tumor resection. Somatosensory evoked potential, brainstem auditory evoked response, and facial nerve EMG were monitored intraoperatively. Approximately 30 minutes into the case, there was an episode of air embolism, which resolved after the source was identified and treated. Near the conclusion of the case, there was an abrupt loss of the right cortical somatosensory evoked potential signal, which never returned to baseline. A postoperative CT scan showed a substantial amount of subarachnoid air and intraventricular air in the frontal and temporal regions. The patient awakened in the ICU with no new neurologic deficit besides preoperative hearing loss on the right side. Despite the high specificity of somatosensory evoked potential change associated with postoperative neurodeficit when the change never returns to the baseline, there was no postoperative neurologic deficit in this patient. This case indicates the false-positive somatosensory evoked potentials caused by pneumocephalus in the sitting position.

Estrogen inhibits NF kappa B-dependent inflammation in brain endothelium without interfering with I kappa B degradation.

The protective effects of 17beta-estradiol in cerebral ischemia may be partially due to the blockade of leukocyte adhesion in cerebral endothelial cells, although the molecular mechanisms are not well understood. We report that 17beta-estradiol (E(2)), but not the alpha-enantiomer, inhibited the basal and interleukin-1beta (IL-1beta)-mediated expression of the intercellular adhesion molecule type 1 (ICAM1) and NFkappaB activation, in cultured brain endothelial cells. However, the degradation of IkappaB-alpha, which is an essential requirement for the translocation of NFkappaB to the nucleus, and a common biological target to suppress NFkappaB activation, was not halted by E(2). These findings indicate that decreased expression of adhesion molecules may account for the capacity E(2) to reduce adhesion of leukocytes in cerebral endothelium in vivo, and suggest the existence of brain-specific, estrogen-sensitive pathways, other than IkappaB-alpha_-regulation, to modulate NFkappaB. The stereoselectivity of the E(2) effect is consistent with an estrogen receptor-mediated mechanism.