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Respiratory failure is a lethal complication of COVID-19 that has remained resistant to drug therapy. Vasoactive intestinal peptide (VIP) is shown in nonclinical studies to upregulate surfactant production, inhibit cytokine synthesis, prevent cytopathy, and block replication of the severe acute respiratory syndrome coronavirus 2 virus in pulmonary cells. The study aims to determine whether Aviptadil (synthetic VIP) can improve survival and recovery in patients with COVID-19 respiratory failure compared with placebo and demonstrate biological effects in such patients.A multicenter, placebo-controlled trial.Ten U.S. hospitals: six tertiary-care hospitals and four community hospitals.A total of 196 patients with COVID-19 respiratory failure.Participants were randomized 2:1 to receive 3 days of IV Aviptadil or placebo.The primary end point (alive and free from respiratory failure at day 60) did not reach statistical significance (odds ratio [OR], 1.6; 95% CI, 0.86-3.11) for patients treated with Aviptadil when controlling for baseline ventilation status as prespecified in the protocol. There was, however, a statistically significant two-fold odds of improved survival (OR, 2.0; 95% CI, 1.1-3.9) at 60 days ( p = 0.035). There was significant improvement in respiratory distress ratio and reduced interleukin 6 cytokine release ( p = 0.02) by day 3.Subgroup analysis identified a statistically significant likelihood of achieving primary end point among those treated with high-flow nasal oxygen at baseline ( p = 0.039). Subjects on mechanical ventilation also experienced a 10-fold increased odds of survival with drug versus placebo ( p = 0.031).The primary end point did not reach statistical significance, indicating that there was no difference between Aviptadil versus placebo. However, Aviptadil improves the likelihood of survival from respiratory failure at day 60 in critical COVID-19 across all sites of care. Given the absence of drug-related serious adverse events and acceptable safety profile, we believe the benefit versus risk for the use of Aviptadil is favorable for patient treatment.

Given the increased risk prevalence of coronary artery disease, inflammatory disease, and cancer, morbidly obese patients are frequently scheduled for various types of surgery. In addition, the number of bariatric surgeries has risen almost exponentially. Therefore, the anaesthesiologist is more frequently challenged with providing general anaesthesia for this patient population. General anaesthesia comes with increased risks of events such as perioperative morbid cardiac events and postoperative respiratory failure. Postoperative respiratory failure is particularly common after cardiac, thoracic, and major abdominal surgery. Anaesthesiologists have a range of support mechanisms at their disposal to reduce postoperative respiratory failure including emergent reintubation. Apart from simple oxygen delivery via nasal cannulas or face masks, Venturi masks, and Mapleson circuits, there are various positive pressure systems available. These systems are commonly referred to as non-invasive ventilation (NIV) systems. NIV can be non-invasive continuous positive airway pressure or non-invasive intermittent positive pressure ventilation. Both types of NIV have been shown to improve oxygenation and hypercapnia in morbidly obese patients in the perioperative environment. This chapter presents the physiology and pathophysiology of the respiratory system in the morbidly obese patient. In addition, it illustrates the impact and implications of NIV systems on this patient population in the perioperative setting.

The prevalence of obesity has tripled worldwide over the past four decades. The United States has the highest rates of obesity, with 88% of the population being overweight and 36% obese. The UK has the sixth highest prevalence of obesity. The problem of obesity is not isolated to the developed world and has increasingly become an issue in the developing world as well. Obesity carries an increased risk of many serious diseases and health conditions, including type 2 diabetes, heart disease, stroke, sleep apnea, and certain cancers. Our ability to take care of this population safely throughout the perioperative period begins with a thorough and in-depth preoperative assessment and meticulous preparation. The preoperative assessment begins with being able to identify patients who suffer from obesity by using diagnostic criteria and, furthermore, being able to identify patients whose obesity is causing pathologic and physiologic changes. A detailed and thorough anesthesia assessment should be performed, and the anesthesia plan individualized and tailored to the specific patient's risk factors and comorbidities. The important components of the preoperative anesthesia assessment and patient preparation in the patient suffering from obesity include history and physical examination, airway assessment, medical comorbidities evaluation, functional status determination, risk assessment, preoperative testing, current weight loss medication, and review of any prior weight loss surgeries and their implications on the upcoming anesthetic. The preoperative evaluation of this population should occur with sufficient time before the planned operation to allow for modifications of the preoperative management without needing to delay surgery as the perioperative management of patients suffering from obesity presents significant practical and organizational challenges.

Supplemental Digital Content is available in the text., Objectives: Acute stroke has a high morbidity and mortality in elderly population. Baseline confounding illnesses, initial clinical examination, and basic laboratory tests may impact prognostics. In this study, we aimed to establish a model for predicting in-hospital mortality based on clinical data available within 12 hours of hospital admission in elderly (≥ 65 age) patients who experienced stroke. Design: Retrospective observational cohort study. Setting: Academic comprehensive stroke center. Patients: Elderly acute stroke patients—2005–2009 (n = 462), 2010–2012 (n = 122), and 2016–2017 (n = 123). Interventions: None. Measurements and Main Results: After institutional review board approval, we retrospectively queried elderly stroke patients’ data from 2005 to 2009 (training dataset) to build a model to predict mortality. We designed a multivariable logistic regression model as a function of baseline severity of illness and laboratory tests, developed a nomogram, and applied it to patients from 2010 to 2012. Due to updated guidelines in 2013, we revalidated our model (2016–2017). The final model included stroke type (intracerebral hemorrhage vs ischemic stroke: odds ratio [95% CI] of 0.92 [0.50–1.68] and subarachnoid hemorrhage vs ischemic stroke: 1.0 [0.40–2.49]), year (1.01 [0.66–1.53]), age (1.78 [1.20–2.65] per 10 yr), smoking (8.0 [2.4–26.7]), mean arterial pressure less than 60 mm Hg (3.08 [1.67–5.67]), Glasgow Coma Scale (0.73 [0.66–0.80] per 1 point increment), WBC less than 11 K (0.31 [0.16–0.60]), creatinine (1.76 [1.17–2.64] for 2 vs 1), congestive heart failure (2.49 [1.06–5.82]), and warfarin (2.29 [1.17–4.47]). In summary, age, smoking, congestive heart failure, warfarin use, Glasgow Coma Scale, mean arterial pressure less than 60 mm Hg, admission WBC, and creatinine levels were independently associated with mortality in our training cohort. The model had internal area under the curve of 0.83 (0.79–0.89) after adjustment for over-fitting, indicating excellent discrimination. When applied to the test data from 2010 to 2012, the nomogram accurately predicted mortality with area under the curve of 0.79 (0.71–0.87) and scaled Brier’s score of 0.17. Revalidation of the same model in the recent dataset from 2016 to 2017 confirmed accurate prediction with area under the curve of 0.83 (0.75–0.91) and scaled Brier’s score of 0.27. Conclusions: Baseline medical problems, clinical severity, and basic laboratory tests available within the first 12 hours of admission provided strong independent predictors of in-hospital mortality in elderly acute stroke patients. Our nomogram may guide interventions to improve acute care of stroke.

Background Ischemic stroke is an emergency with elevated risk for morbidity and mortality. Hypoxia is harmful in acute ischemic stroke. Recent evidence raises concerns regarding hyperoxia as well in acute illness, and for supplemental oxygen therapy when SpO2greater than 92%. Current AHA/ASA guidelines recommend maintaining SpO2greater than 94%. In this study, we aimed to assess the relationship between the oxygenation levels within the first 6-hour of ischemic stroke admission and mortality. Methods With the approval of the Human Studies Committee (IRB #: 13.0396), we performed a retrospective cohort study of ischemic stroke patients consecutively admitted to our hospital in the years 2013-14 and 2017-18 (n = 1479). Relationship between the first 6 hours oxygenation status and in-house mortality was assessed. SpO2/FiO2 ratio was used as the oxygenation outcome parameter. Patients who were intubated at admission were excluded. Additionally, demographics, baseline confounding factors, neurological status, and laboratory values on admission were examined for their association with mortality in a multivariate logistic regression analysis. Results Mean age of patients was 64 ± 15 years. Time interval from last seen normal to hospital admission was 7 ± 5 hours (mean ± standard deviation). NIHSS on arrival was 4 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 (median-IQR). Fourteen percent of patients received IV alteplase and 6% were treated with mechanical thrombectomy. Baseline SpO2 was 97 ± 2%, and 47% of the patients required supplemental oxygen treatment per AHA/ASA guidelines. In hospital mortality rate of this cohort was 5.7%. Lower mean SpO2 /FiO2 levels were strongly correlated with increasing mortality rates (R2 = .973). Age (1.048 [1.028-1.068]), NIHSS (1.120 [1.088-1.154]), WBC (1.116 [1.061-1.175]) and Mean SpO2/FiO2 (.995 [.992-.999]) independently risk associated with mortality. Conclusions Baseline oxygenation varies within the acute ischemic stroke patient population. In this retrospective cohort study, we are reporting a strong association between lower SpO2/FiO2 levels in the first few hours of admission and mortality. In the light of these results, we plan to prospectively assess the role of oxygenation further in the context of recanalization status of stroke.

General anesthesia is the induction and maintenance of a state of unconsciousness with the absence of pain sensation. General anesthesia is accomplished by the administration of a combination of inhaled anesthetic gases and intravenous drugs. These medications eliminate behavioral thermoregulatory compensations, leaving only autonomic defenses to offset environmental perturbations. Anesthetics inhibit thermoregulatory control in a dose-dependent fashion over the entire clinical range. Impairment of thermoregulatory control is observed by a change in thermoregulatory thresholds with the vasoconstriction threshold being affected about three times as much as the sweating threshold. Consequently, the zone between sweating and vasoconstriction thresholds, called interthreshold range, is widened dose-dependently. Impairment of thermoregulation, triggered by general anesthesia, typically causes inadvertent hypothermia. In febrile patients, general anesthesia reduces the magnitude of perioperative fever.

Introduction: Ischemic stroke (IS) is a medical emergency with a high risk of morbidity, leading to disability, and mortality. IS’s impact on our patients’ lives and healthcare system make it essential to optimize its immediate management, triage requirements, and plans for transfer to comprehensive stroke centers. In this study, we hypothesized that it is possible to predict the mortality of IS patients within the first hour of hospital admission. Methods: With the approval of the Human Studies Committee (IRB #: 13.0396), we performed a retrospective analysis from the Stroke Quality Database. Patients who were admitted between 2007-2012 were included. In-hospital mortality was the main outcome of the study. Patients’ demographics, baseline illnesses, home medications, baseline neurological assessment scores, and basic laboratory values on admission were included in the analysis as potential factors. Multivariate analysis was performed to assess the independent contributing factors. Data is presented as odds ratio and 95% confidence intervals. Results: IS in-hospital mortality was about 10% in our study population. Multivariate analysis was performed in 2,131 patients. NIH Stroke Scale on admission, recurrent stroke, high WBC levels (>11K), elderly age, AHA Stage II hypertension, baseline use of Ca-channel blockers, and beta-blockers, admission glucose levels and albumin levels independently contributed to in-hospital mortality (Table). Conclusions: IS patients’ baseline characteristics, hospital admission assessment scales, and laboratory values on admission contributed to prediction of in-hospital mortality. Therefore, it is essential to rapidly initiate acute care for high-risk and complex stroke patients. Additionally, focusing on the modifiable factors such as blood pressure management, treating acute infections, and managing glucose levels may help to decrease acute IS mortality.

General anesthesia is the induction and maintenance of a state of unconsciousness with the absence of pain sensation. General anesthesia is accomplished by the administration of a combination of inhaled anesthetic gases and intravenous drugs. These medications eliminate behavioral thermoregulatory compensations, leaving only autonomic defenses to offset environmental perturbations. Anesthetics inhibit thermoregulatory control in a dose-dependent fashion over the entire clinical range. Impairment of thermoregulatory control is observed by a change in thermoregulatory thresholds with the vasoconstriction threshold being affected about three times as much as the sweating threshold. Consequently, the zone between sweating and vasoconstriction thresholds, called interthreshold range, is widened dose-dependently. Impairment of thermoregulation, triggered by general anesthesia, typically causes inadvertent hypothermia. In febrile patients, general anesthesia reduces the magnitude of perioperative fever.

Background Failed intubation may result in both increased morbidity and mortality. The combination of a video laryngoscope and a flexible tracheoscope used as a flexible video stylet may improve the success rate of securing a difficult airway. We tested the hypothesis that this combination is a feasible way to facilitate intubation in patients with a predicted difficult airway in that it will shorten intubation times and reduce the number of intubation attempts. Methods We conducted a randomized, prospective trial in 140 patients with anticipated difficult airways undergoing elective or urgent surgery. After insertion of video laryngoscope, patients were randomly assigned to either having their tube placed with the use of a preformed stylet (control group) or with a flexible tracheoscope (intervention group). The primary outcome measures were time to successful intubation and number of intubation attempts. Results The number of intubations requiring 2 or more intubation attempts was similar in the 2 groups (14% control vs 13% intervention, P = 1.0); the number of patients requiring 3 or more intubation attempts was not significantly different (8.6% control vs 1.4% intervention, P = 0.12). Distribution for time to intubation also did not differ between the control (median of 66 seconds, interquartile range 47-89) and the intervention group (median of 71 seconds, interquartile range 52-100; P = 0.35). In the control group, 4 patients, all with cervical spine pathology, had the trachea intubated successfully with the video laryngoscope plus flexible tracheoscope after 3 failed attempts with video laryngoscope and rigid stylet. For these 4 patients, time from the decision to change the intubation method to successful intubation with a flexible tracheoscope was 36 ± 14 seconds. Overall success probability for cervical spine patients was 100% (20/20) in the intervention group and 80% (16/20) in the control group, with an exact 95% confidence interval for the difference of 1.4% to 44%, P = 0.04. Conclusions Flexible tracheoscope-assisted video laryngoscopic intubation is a feasible alternative to video laryngoscope only intubation in patients with predicted difficult airways. A flexible tracheoscope used in combination with video laryngoscope may also further increase the success rate of intubation in select patients with a proven difficult airway, particularly when in-line stabilization is required.

BACKGROUND Both core and skin temperatures contribute to steady-state thermoregulatory control. Dynamic thermoregulatory responses trigger aggressive defenses against rapid thermal perturbations. These responses potentially complicate interpretation of thermoregulatory studies and could slow induction of therapeutic hypothermia. We thus tested the hypothesis that rapid external skin-cooling triggers vasoconstriction and shivering at higher mean skin temperatures than slow or moderate rates of skin cooling. METHODS Eleven healthy volunteers were cooled at 3 skin-cooling rates using forced air or/and conductive cooling in random order. One day volunteers received slow (≈2°C/h) skin cooling, and on another day, they received both medium (≈4°C/h) and fast (≈6°C/h) skin cooling. An endovascular heat-exchanging catheter maintained core temperature. Fingertip blood flow ≤0.25 mL/min defined onset of vasoconstriction; sustained ≥25% increase in oxygen consumption defined onset of shivering. Results were evaluated with repeated-measures analysis of variance, with P < 0.05 representing statistical significance. RESULTS Volunteers were 25 ± 5 years of age (mean ± SD), 175 ± 7 cm tall, and weighed 63 ± 10 kg. Core temperature remained constant (≈37°C) throughout each study day. At vasoconstriction, mean skin temperatures were 33.2°C (95% confidence interval [CI]: 32.0°C, 34.4°C), 33.5°C (95% CI: 32.3°C, 34.7°C), and 33.0°C (95% CI: 31.4°C, 34.6°C) at slow, medium, and fast skin-cooling rates, respectively. Mean skin temperatures at shivering were also comparable: 31.4°C (95% CI: 30.3°C, 32.5°C), 31.5°C (95% CI: 30.2°C, 32.8°C), and 30.7°C (95% CI: 28.9°C, 32.5°C), respectively. CONCLUSIONS Onset of vasoconstriction and shivering occurred at similar mean skin temperatures with all 3 cooling rates. Aggressive surface cooling can thus be used in thermoregulatory studies and for induction of therapeutic hypothermia without provoking dynamic thermoregulatory defenses.

Purpose Our main objective was to assess incidence, risk factors, and outcomes of ventilator-associated pneumonia (VAP) in stroke patients. Materials and Methods After obtaining approval from the Human Studies Committee, we reviewed the electronic records from our intensive care unit database of 111 stroke patients on mechanical ventilation for more than 48 hours. Thirty-six risk factors related to disease and general health status, and 8 related to care—all assigned a priori—were collected and analyzed. Selected factors with univariate statistical significance (P Results Thirty-one patients developed pneumonia (28%). Methicillin-resistant Staphylococcus aureus (n = 12) and methicillin-sensitive S aureus (n = 7) were the most common pathogenic bacteria. Chronic lung disease, neurological status at admission as assessed by the National Institutes of Health Stroke Scale, and hemorrhagic transformation were the independent risk factors contributing to VAP. Worsening oxygenation index (arterial partial pressure of oxygen/fraction of inspired oxygen) and proton pump inhibitor use for ulcer prophylaxis were other potentially important factors. Conclusions Pneumonia appears as a frequent problem in mechanically ventilated stroke patients. Chronic lung disease history, severity of stroke level at admission, and hemorrhagic transformation of stroke set the stage for developing VAP. The duration of both mechanical ventilation and intensive care unit stay gets significantly prolonged by VAP, but it does not affect mortality.

Background Hypothermia may be beneficial in stroke victims; however, it provokes vigorous shivering. Buspirone and dexmedetomidine each linearly reduce the shivering threshold with minimal sedation and no respiratory depression. This study tested the hypotheses that the combination of buspirone and dexmedetomidine would (1) synergistically reduce the shivering threshold, (2) synergistically reduce the gain and maximum intensity of shivering, and (3) produce sufficient inhibition to permit cooling to 34 degrees C without excessive hypotension or sedation. Methods Eight healthy men were randomly assigned on 4 days to (1) no drug, (2) buspirone (60 mg orally), (3) dexmedetomidine (intravenous infusion to target plasma concentration of 0.6 ng/ml), or (4) combination of buspirone and dexmedetomidine at same doses. Lactated Ringer's solution (approximately 3 degrees C) was infused intravenously to decrease tympanic membrane temperature by 1.5 degrees C/h. Shivering threshold was defined as an increase in oxygen consumption greater than 20%. Sedation was evaluated using the Observer's Assessment of Sedation/Alertness scale. Results Mean arterial pressure and heart rate were slightly lower on dexmedetomidine and combination days. Likewise, the level of sedation was statistically different on these 2 days but clinically unimportant. Buspirone reduced the shivering threshold from 36.6 degrees C +/- 0.4 degrees C to 35.9 degrees C +/- 0.4 degrees C, dexmedetomidine reduced it to 34.7 degrees C +/- 0.5 degrees C, and the combination to 34.1 +/- 0.4 degrees C. The interaction effect of 0.04 degrees C was not significant. The gain of shivering and maximum shivering intensity were similar on each day. Conclusions The combination of buspirone and dexmedetomidine additively reduced the shivering threshold. Thus, supplementing dexmedetomidine with buspirone blocks shivering and causes only minimal sedation.

Background Mean body temperature (MBT) is the mass-weighted average temperature of body tissues. Core temperature is easy to measure, but direct measurement of peripheral tissue temperature is painful and risky and requires complex calculations. Alternatively MBT can be estimated from core and mean skin temperatures with a formula proposed by Burton in 1935: MBT = 0.64 x TCore + 0.36 x TSkin. This formula remains widely used, but has not been validated in the perioperative period and seems unlikely to remain accurate in dynamic perioperative conditions such as cardiopulmonary bypass. Therefore, the authors tested the hypothesis that MBT, as estimated with Burton's formula, poorly estimates measured MBT at a temperature range between 18 degrees and 36.5 degrees C. Methods The authors reevaluated four of their previously published studies in which core and mass-weighted mean peripheral tissue temperatures were measured in patients undergoing substantial thermal perturbations. Peripheral compartment temperatures were estimated using fourth-order regression and integration over volume from 18 intramuscular needle thermocouples, 9 skin temperatures, and "deep" hand and foot temperature. MBT was determined from mass-weighted average of core and peripheral tissue temperatures and estimated from core temperature and mean skin temperature (15 area-weighted sites) using Burton's formula. Results Nine hundred thirteen data pairs from 44 study subjects were included in the analysis. Measured MBT ranged from 18 degrees to 36.5 degrees C. There was a remarkably good relation between measured and estimated MBT: MBTmeasured = 0.94 x MBTestimated + 2.15, r = 0.98. Differences between the estimated and measured values averaged -0.09 degrees +/- 0.42 degrees C. Conclusions The authors concluded that estimation of MBT from mean skin and core temperatures is generally accurate and precise.

Background. Hypothermia may be an effective treatment for stroke or acute myocardial infarction; however, it provokes vigorous shivering, which causes potentially dangerous haemodynamic responses and prevents further hypothermia. Magnesium is an attractive anti-shivering agent because it is used for treatment of postoperative shivering and provides protection against ischaemic injury in animal models. We tested the hypothesis that magnesium reduces the threshold (triggering core temperature) and gain of shivering without substantial sedation or muscle weakness. Methods. We studied nine healthy male volunteers (18–40 yr) on two randomly assigned treatment days: (1) control and (2) magnesium (80 mg kg � 1 followed by infusion at 2 g h � 1 ). Lactated Ringer’s solution (4 � C) was infused via a central venous catheter over a period of approximately 2 h to decrease tympanic membrane temperature by � 1.5 � Ch � 1 . A significant and persistent increase in oxygen consumption identified the threshold. The gain of shivering was determined by the slope of oxygen consumption vs core temperature regression. Sedation was evaluated using a verbal rating score (VRS) from 0 to 10 and bispectral index (BIS) of the EEG. Peripheral muscle strength was evaluated using dynamometry and spirometry. Data were analysed using repeated measures ANOVA; P

Background Resistance to cancer metastasis is mediated by host immunity, and mild perioperative hypothermia impairs immune function. We tested the hypothesis that mild perioperative hypothermia increases the risk of cancer recurrence and subsequent mortality Methods In a 5- to 9-year follow-up of 140 cancer patients enrolled in a study demonstrating that 2°C mild perioperative hypothermia triples wound infection risk, tumor characteristics likely to influence recurrence, patient outcome, and current health status were determined. Primary outcomes were tumor recurrence and all-cause mortality. Results Tumor status in the groups was similar and included Duke’s and TNM classifications, preoperative carcinoembryonic antigen concentration, histologic differentiation, numbers of nodes biopsied and positive nodes, blood vessel invasion, and adhesion of tumor to adjacent organs. Cancer-free and overall survival rates were similar in normothermic and hypothermic patients. These data provide 80% power for detecting a 25% difference between the groups. Conclusions Mild perioperative hypothermia did not increase recurrent tumors, cancer death, or all-cause mortality.

Studies suggest that acupuncture is more effective when induced before the induction of general anesthesia than afterwards. We tested the hypothesis that electro-acupuncture initiated 30 min before the induction reduces anesthetic requirement more than acupuncture initiated after the induction. Seven volunteers were each anesthetized with desflurane on 3 study days. Needles were inserted percutaneously at four acupuncture points thought to produce analgesia in the upper abdominal area and provide generalized sedative and analgesic effects: Zusanli (St36), Sanyinjiao (Sp6), Liangqiu (Sp34), and Hegu (LI4). Needles were stimulated at 2 Hz and 10 Hz, with frequencies alternating at 2-s intervals. On Preinduction day, electro-acupuncture was started 30 min before the induction of anesthesia and maintained throughout the study. On At-induction day, needles were positioned before the induction of anesthesia, but electro-acupuncture stimulation was not initiated until after the induction. On Control day, electrodes were positioned near the acupoints, but needles were not inserted. Noxious electrical stimulation was administered via 25-gauge needles on the upper abdomen (70 mA; 100 Hz; 10 s). The desflurane concentration was increased 0.5% when movement occurred and decreased 0.5% when it did not. These up-and-down sequences continued until volunteers crossed from movement to no movement four times. The P(50) of logistic regression identified desflurane requirement. Desflurane requirement was similar on the Control (mean +/- sd; 5.2% +/- 0.6%), Preinduction (5.0% +/- 0.8%), and At-induction (4.7% +/- 0.3%; P = 0.125) days. This type of acupuncture is thus unlikely to facilitate general anesthesia or decrease the requirement for anesthetic drugs.

Nitrous oxide has been used for more than 150 years and has been given to several billion patients. It justifiably remains a popular anaesthetic agent because it is inexpensive, analgesic, and extremely short acting. It reduces the need of maintenance anaesthetic, which has more significance when ventilators with larger fresh airflows are used. However, intestinal distension by nitrous oxide has been reported at least since the 1960’s (1), and it is well established that nitrous oxide inflates closed, gas-filled spaces (2). Nitrous oxide will move into air-filled cavities in the body that normally contain nitrogen; so as nitrous oxide transfers from the blood into the space, nitrogen transfers out. However, nitrous oxide is 34 times more soluble than nitrogen in blood. Thus, substantial quantities of nitrous oxide leave the blood and enter the bowel, but not much nitrogen can leave the bowel to enter the blood. The result is that during exposure to nitrous oxide, like in other compliant spaces, the volume of gas in the bowel increases. The amount of the increase depends on the alveolar partial pressure of nitrous oxide, the intestinal blood flow, and the duration of nitrous oxide administration. The evidence that nitrous oxide causes clinically important bowel distension is equivocal. Several studies have failed to identify any effect whatsoever of nitrous oxide on bowel distension(3–6) or postoperative intestinal function (6,7). In contrast, others have reported that nitrous oxide increases bowel distension in both animals (8) and humans (9). All of these studies were relatively small and some were seriously underpowered. We, therefore, tested the hypothesis that the use of nitrous oxide produces clinically important bowel distension in patients undergoing elective colon resection with isoflurane anaesthesia. We simultaneously quantified the magnitude of the effect by determining the number of patients in whom air must be substituted for nitrous oxide to avoid a single case of clinically important bowel distension (number-needed-to-harm).

The Laryngeal Mask Airway (LMA) is a frequently used efficient airway device, yet it sometimes seals poorly, thus reducing the efficacy of positive-pressure ventilation. The Perilaryngeal Airway (CobraPLA) is a novel airway device with a larger pharyngeal cuff (when inflated). We tested the hypothesis that the CobraPLA was superior to the LMA with regard to insertion time and airway sealing pressure and comparable to the LMA in airway adequacy and recovery characteristics. After midazolam and fentanyl administration, 81 ASA physical status I-II outpatients having elective surgery were randomized to receive an LMA or CobraPLA. Anesthesia was induced with propofol (2.5 mg/kg IV), and the airway was inserted. We measured 1) insertion time; 2) adequacy of the airway (no leak at 15-cm-H 2 O peak pressure or tidal volume of 5 mL/kg); 3) airway sealing pressure; 4) number of repositioning attempts; and 5) sealing quality (no leak at tidal volume of 8 mL/kg). At the end of surgery, gastric insufflation, postoperative sore throat, dysphonia, and dysphagia were evaluated. Data were compared with unpaired Student's t-tests, X 2 tests, or Fisher's exact tests; P < 0.05 was significant. Patient characteristics, insertion times, airway adequacy, number of repositioning attempts, and recovery were similar in each group. Airway sealing pressure was significantly greater with CobraPLA (23 ± 6 cm H 2 O) than LMA (18 ± 5 cm H 2 O, P < 0.001). The CobraPLA has insertion characteristics similar to the LMA but better airway sealing capabilities.

Fever occurs when pyrogenic stimulation activates thermal control centres. Fever is common during the perioperative period, but rare during anaesthesia. Although only a limited number of studies are available to explain how anaesthesia affects fever, general anaesthesia seems to inhibit fever by decreasing the thermoregulatory-response thresholds to cold. Opioids also inhibit fever; however, the effect is slightly less than that of general anaesthesia. In contrast, epidural anaesthesia does not affect fever. This suggests that hyperthermia, which is often associated with epidural infusions during labour or in the post-operative period, may be a true fever caused by inflammatory activation. Accordingly, this fever might be diminished in patients who receive opioids for pain treatment. Post-operative fever is a normal thermoregulatory response usually of non-infectious aetiology. Fever may be important in the host defence mechanisms and should not be routinely treated lest the associated risks exceed the benefits.

Anaesthesia alters normal thermoregulatory control of the body, usually leading to perioperative hypothermia. Hypothermia is associated with a large number of serious complications. To assess perianaesthetic hypothermia, core temperature should be monitored vigorously. Pulmonary artery, tympanic membrane, distal oesophageal or nasopharyngeal temperatures reflect core temperature reliably. Core temperatures can be often estimated with reasonable accuracy using oral, axillary and bladder temperatures, except during extreme thermal perturbations. The body site for measurements should be chosen according to the surgical procedure. Unless hypothermia is specifically indicated, efforts should be made to maintain intraoperative core temperatures above 36 degrees C. Forced air is the most effective, commonly available, non-invasive warming method. Resistive heating electrical blankets and circulating water garment systems are an equally effective alternative. Intravenous fluid warming is also helpful when large volumes are required. In some patients, induction of mild therapeutic hypothermia may become an issue for the future. Recent studies indicate that patients suffering from neurological disease may profit from rapid core cooling.

Background and Purpose— Hypothermia might prove to be therapeutically beneficial in stroke victims; however, even mild hypothermia provokes vigorous shivering. Meperidine and dexmedetomidine each linearly reduce the shivering threshold (triggering core temperature) with minimal sedation. We tested the hypothesis that meperidine and dexmedetomidine synergistically reduce the shivering threshold without producing substantial sedation or respiratory depression. Methods— We studied 10 healthy male volunteers (18 to 40 years) on 4 days: (1) control (no drug); (2) meperidine (target plasma level 0.3 μg/mL); (3) dexmedetomidine (target plasma level 0.4 ng/mL); and (4) meperidine plus dexmedetomidine (target plasma levels of 0.3 μg/mL and 0.4 ng/mL, respectively). Lactated Ringer’s solution (≈4°C) was infused through a central venous catheter to decrease tympanic membrane temperature by ≈2.5°C/h; mean skin temperature was maintained at 31°C. An increase in oxygen consumption >25% of baseline identified the shivering threshold. Sedation was evaluated by using the Observer’s Assessment of Sedation/Alertness scale. Two-way repeated-measures ANOVA was used to identify interactions between drugs. Data are presented as mean±SD; P Results— The shivering thresholds on the study days were as follows: control, 36.7±0.3°C; dexmedetomidine, 36.0±0.5°C ( P P P P =0.19). There was trivial sedation with either drug alone or in combination. Respiratory rate and end-tidal P co 2 were well preserved on all days. Conclusions— Dexmedetomidine and meperidine additively reduce the shivering threshold; in the small doses tested, the combination produced only mild sedation and no respiratory toxicity.

Background Tissue oxygenation is a strong predictor of surgical site infection. Improving tissue oxygenation should thus reduce wound infection risk. Supplemental inspired oxygen can improve tissue oxygenation, but whether it reduces infection risk remains controversial. Low-dose dexamethasone is often given to reduce the risk of postoperative nausea and vomiting, but steroid-induced immunosuppression can increase infection risk. We therefore tested the hypotheses that supplemental perioperative oxygen reduces infection risk and that dexamethasone increases it. Methods Using a factorial design, patients having colorectal resections expected to last ≥2 h were randomly assigned to 30% (n=270) or 80% (n=285) inspired oxygen during and for 1 h after surgery, and to 4 mg intraoperative dexamethasone (n=283) or placebo (n=272). Physicians blinded to group assignments evaluated wounds postoperatively, using US Centers for Disease Control criteria. Results Subject and surgical characteristics were similar among study groups. Surgical site infection incidence was similar among groups: 30% oxygen 15.6%, 80% oxygen 15.8% (P=1.00); dexamethasone 15.9%, placebo 15.4%, (P=0.91). Conclusions Supplemental oxygen did not reduce surgical site infection risk. The preponderance of clinical evidence suggests that administration of 80% supplemental inspired oxygen does not reduce infection risk. We did not observe an increased risk of surgical site infection with the use of a single low dose of dexamethasone, indicating that it can be used for nausea and vomiting prophylaxis without promoting wound infections. Clinical trial registration ClinicalTrials.gov number: NCT00273377.

Background Epidural analgesia is frequently associated with hyperthermia during labor and in the postoperative period. The conventional assumption is that hyperthermia is caused by the technique, although no convincing mechanism has been proposed. However, pain in the "control" patients is inevitably treated with opioids, which themselves attenuate fever. Fever associated with infection or tissue injury may then be suppressed by opioids in the "control" patients while being expressed normally in patients given epidural analgesia. The authors therefore tested the hypothesis that fever in humans is manifested normally during epidural analgesia, but is suppressed by low-dose intravenous opioid. Methods The authors studied eight volunteers, each on four study days. Fever was induced each day by 150 IU/g intravenous interleukin 2. Volunteers were randomly assigned to: (1) a control day when no opioid or epidural analgesia was given; (2) epidural analgesia using ropivacaine alone; (3) epidural analgesia using ropivacaine in combination with 2 microg/ml fentanyl; or (4) intravenous fentanyl at a target plasma concentration of 2.5 ng/ml. Results Fentanyl halved the febrile response to pyrogen, decreasing integrated core temperature from 7.0 +/- 3.2 degrees C. h on the control day, to 3.8 +/- 3.0 degrees C. h on the intravenous fentanyl day. In contrast, epidural ropivacaine and epidural ropivacaine-fentanyl did not inhibit fever. The fraction of core-temperature measurements that exceeded 38 degrees C was halved by intravenous fentanyl, and the fraction exceeding 38.5 degrees C was reduced more than fivefold. Conclusions These data support the authors' proposed mechanism for hyperthermia during epidural analgesia. Fever during epidural analgesia should thus not be considered a complication of the anesthetic technique per se.

OBJECTIVE Manifestation of intraoperative fever is impaired by volatile anesthetics and muscle relaxants. Opioids are common anesthetic adjuvants and remain the dominant treatment for postoperative surgical pain and sedation of critically ill patients. The effect of opioids on normal thermoregulatory control is well established. However, the extent to which these drugs might inhibit fever remains unknown. Accordingly, we tested the hypothesis that relatively low plasma concentrations of the mu-receptor agonist alfentanil reduce fever magnitude. DESIGN Prospective, randomized, crossover study. SETTING Outcomes Research Laboratory, at the Department of Anesthesia and Perioperative Care, University of California, San Francisco. PATIENTS Eight healthy male volunteers, aged 25-31 yrs, each studied on three separate days. INTERVENTION Each volunteer was given an intravenous injection of 30 IU/g interleukin (IL)-2, followed 2 hrs later by 70 IU/g. One hour after the second dose, the volunteers were randomly assigned to three doses of alfentanil: a) none (control); b) a target plasma concentration of 100 ng/mL; and c) a target concentration of 200 ng/mL. Opioid administration continued for 5 hrs. METHODS AND MAIN RESULTS Alfentanil significantly reduced the febrile response to pyrogen, decreasing integrated tympanic membrane temperatures from 7.5+/-2.2 degrees C x hr on the control day, to 4.9+/-1.5 degrees C x hr with 100 ng/mL alfentanil, and to 5.1+/-1.7 degrees C x hr with 200 ng/mL alfentanil (p = .011). Peak temperatures were also significantly reduced from 38.5+/-0.4 degrees C on the control day, to 38.0+/-0.4 degrees C on the 100 ng/mL-alfentanil day and 38.0+/-0.6 degrees C on the 200-ng/mL day (p = .019). Plasma cytokine concentrations increased after IL-2 administration, roughly in proportion to the elevation in core temperature. However, cytokine concentrations did not differ significantly among the treatment groups. CONCLUSION Alfentanil significantly reduced the febrile response to IL-2 administration. However, the reduction was comparable at plasma concentrations near 100 and 200 ng/mL. These data indicate that concentrations of opioids commonly observed in critical care patients significantly inhibit the manifestation of fever.

Background Thermoregulatory control is based on both skin and core temperatures. Skin temperature contributes approximately 20% to control of vasoconstriction and shivering in unanesthetized humans. However, this value has been used to arithmetically compensate for the cutaneous contribution to thermoregulatory control during anesthesia--although there was little basis for assuming that the relation was unchanged by anesthesia. It even remains unknown whether the relation between skin and core temperatures remains linear during anesthesia. We therefore tested the hypothesis that mean skin temperature contributes approximately 20% to control of vasoconstriction and shivering, and that the contribution is linear during general anesthesia. Methods Eight healthy male volunteers each participated on 3 separate days. On each day, they were anesthetized with 0.6 minimum alveolar concentrations of isoflurane. They then were assigned in random order to a mean skin temperature of 29, 31.5, or 34 degrees C. Their cores were subsequently cooled by central-venous administration of fluid at approximately 3 degrees C until vasoconstriction and shivering were detected. The relation between skin and core temperatures at the threshold for each response in each volunteer was determined by linear regression. The proportionality constant was then determined from the slope of this regression. These values were compared with those reported previously in similar but unanesthetized subjects. Results There was a linear relation between mean skin and core temperatures at the vasoconstriction and shivering thresholds in each volunteer: r2 = 0.98+/-0.02 for vasoconstriction, and 0.96+/-0.04 for shivering. The cutaneous contribution to thermoregulatory control, however, differed among the volunteers and was not necessarily the same for vasoconstriction and shivering in individual subjects. Overall, skin temperature contributed 21+/-8% to vasoconstriction, and 18+/-10% to shivering. These values did not differ significantly from those identified previously in unanesthetized volunteers: 20+/-6% and 19+/-8%, respectively. Conclusions The results in anesthetized volunteers were virtually identical to those reported previously in unanesthetized subjects. In both cases, the cutaneous contribution to control of vasoconstriction and shivering was linear and near 20%. These data indicate that a proportionality constant of approximately 20% can be used to compensate for experimentally induced skin-temperature manipulations in anesthetized as well as unanesthetized subjects.

UNLABELLED We measured afterdrop and peripheral tissue temperature distribution in eight patients cooled to approximately 17 degrees C during cardiopulmonary bypass and subsequently rewarmed to 36.5 degrees C. A nasopharyngeal probe evaluated trunk and head temperature and heat content. Peripheral tissue temperature (arm and leg temperature) and heat content were estimated using fourth-order regressions and integration over volume from 30 tissue and skin temperatures. Peripheral tissue temperature decreased to 19.7+/-0.9 degrees C during bypass and subsequently increased to 34.3+/-0.7 degrees C during 104+/-18 min of rewarming. The core-to-peripheral tissue temperature gradient was -5.9+/-0.9 degrees C at the end of cooling and 4.7+/-1.5 degrees C at the end of rewarming. The core-temperature afterdrop was 2.2+/-0.4 degrees C and lasted 89+/-15 min. It was associated with 1.1+/-0.7 degrees C peripheral warming. At the end of cooling, temperatures at the center of the upper and lower thigh were (respectively) 8.0+/-5.2 degrees C and 7.3+/-4.2 degrees C cooler than skin temperature. On completion of rewarming, tissue at the center of the upper and lower thigh were (respectively) 7.0+/-2.2 degrees C and 6.4+/-2.3 degrees C warmer than the skin. When estimated systemic heat loss was included in the calculation, redistribution accounted for 73% of the afterdrop, which is similar to the contribution observed previously in nonsurgical volunteers. IMPLICATIONS Temperature afterdrop after bypass at 17 degrees C was 2.2+/-0.4 degrees C, with approximately 73% of the decrease in core temperature resulting from core-to-peripheral redistribution of body heat. Cooling and rewarming were associated with large radial tissue temperature gradients in the thigh.

Background General anesthetics increase the sweating-to-vasoconstriction interthreshold range (temperatures not triggering thermoregulatory defenses), whereas fever is believed to only increase the setpoint (target core temperature). However, no data characterize thresholds (temperatures triggering thermoregulatory defenses) during combined anesthesia and fever. Most likely, the combination produces an expanded interthreshold range around an elevated setpoint. The authors therefore tested the hypothesis that thermoregulatory response thresholds during the combination of fever and anesthesia are simply the linear combination of the thresholds resulting from each intervention alone. Methods The authors studied eight healthy male volunteers. Fever was induced on the appropriate days by intravenous injection of 30 IU/g human recombinant interleukin 2 (IL-2), followed 2 h later by an additional 70 IU/g. General anesthesia consisted of desflurane 0.6 minimum alveolar concentration (MAC). The volunteers were randomly assigned to the following groups: (1) control (no desflurane, no IL-2); (2) IL-2 alone; (3) desflurane alone; and (4) desflurane plus IL-2. During the fever plateau, volunteers were warmed until sweating was observed and then cooled to vasoconstriction. Sweating was evaluated from a ventilated capsule and vasoconstriction was quantified by volume plethysmography. The tympanic membrane temperatures triggering significant sweating and vasoconstriction identified the respective response thresholds. Data are presented as the mean +/- SD; P < 0.05 was considered significant. Results The interthreshold range was near 0.40 degrees C on both the control day and during IL-2 administration alone. On the IL-2 alone day, however, the interthreshold range was shifted to higher temperatures. The interthreshold range increased significantly during desflurane anesthesia to 1.9+/-0.6 degrees C. The interthreshold range during the combination of desflurane and IL-2 was 1.2+/-0.6 degrees C, which was significantly greater than on the control and IL-2 alone days. However, it was also significantly less than during desflurane alone. Conclusion The combination of desflurane and IL-2 caused less thermoregulatory inhibition than would be expected based on the effects of either treatment alone. Fever-induced activation of the sympathetic nervous system may contribute by compensating for a fraction of the anesthetic-induced thermoregulatory impairment.

Initial treatments for fever include the amelioration of underlying causes and administration of antipyretic medications. However, patients who fail these treatments are often actively cooled, which may be counterproductive because decreasing skin temperature increases the thermoregulatory core target temperature. Cooling may also provoke metabolic and autonomic stress and thermal discomfort.We studied 9 subjects, each on 3 days. Fever was induced each day with 100,000 IU/kg of interleukin-2 administered intravenously (elapsed time zero). Randomly assigned treatments were 1) control (a cotton blanket), 2) cooling (forced air at 15 degrees C), or 3) self-adjust (forced-air warming adjusted to comfort). Treatments were maintained for 3 to 8 elapsed hours.Peak core temperatures (mean +/- SD) were 38.4 +/- 0.5 degrees C on the control day, 38.1 +/- 0.5 degrees C on the cooling day, and 38.5 +/- 0.4 degrees C on the self-adjust day. Integrated core temperatures were 6.0 +/- 1.6 degrees C x h on the control day, 5.7 +/- 2.2 degrees C x h on the cooling day, and 6.4 +/- 1.2 degrees C x h on the self-adjust day. Neither peak nor integrated core temperatures differed significantly on the 3 days. Shivering was common on the cooling day but otherwise rare. Oxygen consumption was normal on the control and self-adjust days but increased 35% to 40% during cooling (P = 0.0001). Mean arterial pressure and plasma norepinephrine and epinephrine concentrations were significantly greater during cooling (P0.05). On a self-reported thermal comfort scale, the subjects were miserable during cooling and significantly more comfortable on the self-adjust than control day (P0.05).We conclude that active cooling should be avoided in unsedated patients with moderate fever, because it does not reduce core temperature but does increase metabolic rate, activate the autonomic nervous system, and provoke thermal discomfort.

Background Nitrous oxide (N2O) is a commonly used sedative for painful diagnostic procedures and dental work. The authors sought to characterize the effects of N2O on quantitative electroencephalographic (EEG) variables including the bispectral index (BIS), a quantitative parameter developed to correlate with the level of sedation induced by a variety of agents. Methods Healthy young adult volunteers (n = 13) were given a randomized sequence of N2O/O2 combinations via face mask. Five concentrations of N2O (10, 20, 30, 40, and 50% atm) were administered for 15 min (20 min for the first step). EEG was recorded from bilateral frontal poles continuously. At the end of each exposure, level of sedation was assessed using primarily the Observer Assessment of Alertness/Sedation (OAA/S) scale. Results One subject withdrew from the study because of emesis at 50% N2O. N2O (50%) increased theta, beta, 40-50 Hz, and 70-110 Hz band powers. BIS and spectral edge frequency during 50% N2O/O2 did not differ significantly from baseline values. Abrupt decreases from higher to lower concentrations frequently evoked a profound, transient slowing of activity. No significant change in OAA/S was detected during the study. Conclusions Although the spectral content of the EEG changed during N2O administration, reflecting some pharmacologic effect, the subjects remained cooperative and responsive throughout, and therefore N2O can only be considered a weak sedative at the tested concentrations. Despite changes in the lower and higher frequency ranges of EEG activity, the BIS did not change, which is consistent with its design objective as a specific measure of hypnosis.

Background Fever sometimes occurs during anesthesia. However, it is rare considering how often pyrogenic causes are likely to be present and how common fever is after surgery. This low incidence results in part from dose-dependent inhibition of fever by volatile anesthetics. Paralysis, however, may contribute by preventing shivering and the associated increase in metabolic heat production. Therefore the authors tested the hypothesis that paralysis during anesthesia decreases the febrile response to pyrogen administration. Methods Seven volunteers each participated on two study days. They were given 30 IU/g intravenous interleukin-2, followed 90 min later by an additional 70 IU/g dose. Anesthesia was induced 30 min after the second dose and maintained for 6 h with 0.6 minimum alveolar concentration isoflurane. The volunteers were randomly assigned to (1) paralysis with vecuronium or (2) no muscle relaxants. Body heat content and distribution were determined from measured tissue and skin temperatures. Data are presented as mean +/- SD; P < 0.05 was considered significant. Results There was no clinically important difference in peak core (tympanic membrane) temperatures on the unparalyzed (37.6+/-0.9 degrees C) and paralyzed (37.2+/-0.6 degrees C) days. Core heat content increased 1.2+/-0.7 kcal/kg over the last 5 h of anesthesia on the unparalyzed day, but only by 0.9+/-0.4 kcal/kg when the volunteers were paralyzed. Peripheral tissue heat content increased 0.1+/-1.1 kcal/kg on the unparalyzed day but decreased 1.1+/-0.7 kcal/kg when the volunteers were paralyzed. Consequently, body heat content increased 1.3+/-1.3 kcal/kg on the unparalyzed day but decreased significantly by 0.2+/-0.8 kcal/kg when the volunteers were paralyzed. Conclusions Paralysis prevented shivering from increasing the metabolic rate. Consequently, body heat content decreased during paralysis, whereas otherwise it increased. Thermoregulatory vasoconstriction was nonetheless able to maintain similar peak and integrated core temperatures on each study day. Administration of muscle relaxants thus is not the primary explanation for the relative paucity of intraoperative fever.

Background Afterdrop following cardiopulmonary bypass results from redistribution of body heat to inadequately warmed peripheral tissues. However, the distribution of heat between the thermal compartments and the extent to which core-to-peripheral redistribution contributes to post-bypass hypothermia remains unknown. Methods Patients were cooled during cardiopulmonary bypass to nasopharyngeal temperatures near 31 degrees C (n=8) or 27 degrees C (n=8) and subsequently rewarmed by the bypass heat exchanger to approximately 37.5 degrees C. A nasopharyngeal probe evaluated core (trunk and head) temperature and heat content. Peripheral compartment (arm and leg) temperature and heat content were estimated using fourth-order regressions and integration over volume from 19 intramuscular needle thermocouples, 10 skin temperatures, and "deep" foot temperature. Results In the 31 degrees C group, the average peripheral tissue temperature decreased to 31.9+/-1.4 degrees C (means+/-SD) and subsequently increased to 34+/-1.4 degrees C at the end of bypass. The core-to-peripheral tissue temperature gradient was 3.5+/-1.8 degrees C at the end of rewarming, and the afterdrop was 1.5+/-0.4 degrees C. Total body heat content decreased 231+/-93 kcal. During pump rewarming, the peripheral heat content increased to 7+/-27 kcal below precooling values, whereas the core heat content increased to 94+/-33 kcal above precooling values. Body heat content at the end of rewarming was thus 87+/-42 kcal more than at the onset of cooling. In the 27 degrees C group, the average peripheral tissue temperature decreased to a minimum of 29.8 +/-1.7 degrees C and subsequently increased to 32.8+/-2.1 degrees C at the end of bypass. The core-to-peripheral tissue temperature gradient was 4.6+/-1.9 degrees C at the end of rewarming, and the afterdrop was 2.3+/-0.9 degrees C. Total body heat content decreased 419+/-49 kcal. During pump rewarming, core heat content increased to 66+/-23 kcal above precooling values, whereas peripheral heat content remained 70+/-42 kcal below precooling values. Body heat content at the end of rewarming was thus 4+/-52 kcal less than at the onset of cooling. Conclusions Peripheral tissues failed to fully rewarm by the end of bypass in the patients in the 27 degrees C group, and the afterdrop was 2.3+/-0.9 degrees C. Peripheral tissues rewarmed better in the patients in the 31 degrees C group, and the afterdrop was only 1.5+/-0.4 degrees C.

Case report A 58-year-old female was admitted to the hospital in a severely malnourished state. She was treated for Crohn's disease with total parental nutrition (TPN). The patient's blood glucose was monitored by point of care (POC) testing every 4 h, and a specimen is also drawn daily for metabolic assessment. The POC blood glucose values were consistently much higher than the lab values. Humalog insulin (5 U) was given to the patient to decrease high blood glucose levels that developed following administration of TPN. The patient then became hypoglycemic as a result of this insulin treatment. POC glucose testing, performed every 4 h, did not detect the iatrogenic hypoglycemia, while lab glucose results were not given close attention. The lab sample was always drawn 1–2 h after insulin was given to the patient and resulted in a lower blood glucose value. In addition, the symptoms of hypoglycemia such as shaking and dizziness were masked by the patient's poor health status, supine position, and the continuously given TPN. Conclusions These findings highlighted the importance of the correct sampling time following insulin administration and the consideration of the lab results in addition to POC. The patient's insulin regimen was modified to prevent further hypoglycemic events.

Background Mild perioperative hypothermia, which is common during major surgery, may promote surgical-wound infection by triggering thermoregulatory vasoconstriction, which decreases subcutaneous oxygen tension. Reduced levels of oxygen in tissue impair oxidative killing by neutrophils and decrease the strength of the healing wound by reducing the deposition of collagen. Hypothermia also directly impairs immune function. We tested the hypothesis that hypothermia both increases susceptibility to surgical-wound infection and lengthens hospitalization. Methods Two hundred patients undergoing colorectal surgery were randomly assigned to routine intraoperative thermal care (the hypothermia group) or additional warming (the normothermia group). The patients' anesthetic care was standardized, and they were all given cefamandole and metronidazole. In a double-blind protocol, their wounds were evaluated daily until discharge from the hospital and in the clinic after two weeks; wounds containing culture-positive pu...

Many neurosurgery patients may have unrecognized diabetes or may develop stress-related hyperglycemia in the perioperative period. Diabetes patients have a higher perioperative risk of complications and have longer hospital stays than individuals without diabetes. Maintenance of euglycemia using intensive insulin therapy (IIT) continues to be investigated as a therapeutic tool to decrease morbidity and mortality associated with derangements in glucose metabolism due to surgery. Suboptimal perioperative glucose control may contribute to increased morbidity, mortality, and aggravate concomitant illnesses. The challenge is to minimize the effects of metabolic derangements on surgical outcomes, reduce blood glucose excursions, and prevent hypoglycemia. Differences in cerebral versus systemic glucose metabolism, time course of cerebral response to injury, and heterogeneity of pathophysiology in the neurosurgical patient populations are important to consider in evaluating the risks and benefits of IIT. While extremes of glucose levels are to be avoided, there are little data to support an optimal blood glucose level or recommend a specific use of IIT for euglycemia maintenance in the perioperative management of neurosurgical patients. Individualized treatment should be based on the local level of blood glucose control, outpatient treatment regimen, presence of complications, nature of the surgical procedure, and type of anesthesia administered.

The human thermoregulatory system usually maintains core body temperature near 37 degrees C. This homeostasis is accomplished by thermoregulatory defense mechanisms such as vasoconstriction and shivering or sweating and vasodilatation. Thermoregulation is impaired during general anesthesia. Suppression of thermoregulatory defense mechanisms during general anesthesia is dose dependant and mostly results in perioperative hypothermia. Several adverse effects of hypothermia have been identified, including an increase in postoperative wound infection, perioperative coagulopathy and an increase of postoperative morbid cardiac events. Perioperative hypothermia can be avoided by warming patients actively during general anesthesia. Fever is a controlled increase of core body temperature. Various causes of perioperative fever are given. Fever is usually attenuated by general anesthesia. Typically, patients develop a fever of greater magnitude in the postoperative phase. Postoperative fever is fairly common. The incidence of fever varies with type and duration of surgery, patient's age, surgical site and preoperative inflammation.

Nosocomial hyperthermia (fever) occurs in about 30% of all medical patients at some time during their hospital stay. In patients admitted to the intensive care unit with severe sepsis the incidence of hyperthermia is greater than 90%, while in a specialized neurological critical care unit the incidence is reported as 47%. In contrast, hyperthermia during anaesthesia is rare owing to the impairment of thermoregulation by anaesthetic agents. This article is designed to give an overview on the various causes of hyperthermia with special emphasis on fever during general and regional anaesthesia in general and neurological critical care patients.

BACKGROUND Newer circulating-water systems supply more heat than forced-air, mainly because the heat capacity of water is much greater than for that of dry warm air and, in part, because they provide posterior as well as anterior heating. Several heating systems are available, but three major ones have yet to be compared directly. We therefore compared two circulating-water systems with a forced-air system during simulation of upper abdominal or chest surgery in volunteers. METHODS Seven healthy volunteers participated on three separate study days. Each day, they were anesthetized and cooled to a core temperature near 34 degrees C, which was maintained for 45-60 min. They were then rewarmed with one of three warming systems until distal esophageal core temperature reached 36 degrees C or anesthesia had lasted 8 h. The warming systems were 1) energy transfer pads (two split torso pads and two universal pads; Kimberly Clark, Roswell, GA); 2) circulating-water garment (Allon MTRE 3365 for cardiac surgery, Akiva, Israel); and 3) lower body forced-air warming (Bair Hugger #525, #750 blower, Eden Prairie, MN). Data are presented as mean +/- sd; P < 0.05 was statistically significant. RESULTS The rate of increase of core temperature from 34 degrees C to 36 degrees C was 1.2 degrees C +/- 0.2 degrees C/h with the Kimberly Clark system, 0.9 degrees C +/- 0.2 degrees C/h with the Allon system, and 0.6 degrees C +/- 0.1 degrees C/h with the Bair Hugger (P = 0.002). CONCLUSIONS The warming rate with the Kimberly Clark system was 25% faster than with the Allon system and twice as fast as with the Bair Hugger. Both circulating-water systems thus warmed hypothermic volunteers in significantly less time than the forced-air system.