Traumatic brain injury: integrated approaches to improve prevention, clinical care, and research

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Pharmacological methods for reducing coughing on emergence from elective surgery after general anesthesia with endotracheal intubation: protocol for a systematic review of common medications and network meta-analysis

Background: Emergence coughing and bucking, secondary to endotracheal tube stimulation of the tracheal mucosa, frequently occurs after the general anesthetic recedes. Besides general unpleasantness, coughing has important physiological sequelae that may be detrimental to the postoperative patient. Multiple pharmacological strategies have been published, but prior systematic reviews on this topic have neither been comprehensive enough in their literature or medication search, nor provided us the answer regarding what the best pharmacological method is to prevent or minimize peri-extubation coughing. Our systematic review and network meta-analysis’ primary objective is to determine the relative efficacies of different pharmacological methods on decreasing coughing (none to mild compared to moderate to severe, as defined by the modified Minogue scale) during emergence after a general anesthetic with endotracheal intubation in adult elective surgeries. Medications of interest are lidocaine or lignocaine (intravenous (IV), intracuff alkalinized, intracuff non-alkalinized, topical, endotracheal application), dexmedetomidine IV, remifentanil IV, and fentanyl IV. These medications were selected based on a preliminary review of the literature. Methods: Using a predefined search strategy, we will search MEDLINE, Cochrane Central Register of Controlled Trials, Embase, Cochrane Database of Systematic Reviews, ACP Journal Club, Database of Abstracts of Reviews of Effects, and the Cochrane Methodology Register, with no date or language restrictions. Gray literature search will encompass conference abstracts, Web of Science, and references from publications selected for full-text review. Two reviewers will independently screen the retrieved literature using predetermined inclusion criteria, process publications selected for full-text review, extract data from publications chosen for study inclusion, and evaluate for bias using the Cochrane risk of bias assessment. Risk ratios and 95% confidence intervals will be calculated for each study, and a surface under the cumulative ranking curve will determine the relative rank of each intervention in its ability to prevent coughing on emergence. Discussion: The proposed systematic review and network meta-analysis will not only provide a more thorough review of common medications used to decrease emergence coughing, but also inform clinicians which of these pharmacological strategies is the best approach. Systematic review registration: PROSPERO CRD42018102870Medicine, Faculty ofAnesthesiology, Pharmacology and Therapeutics, Department ofReviewedFacult

Therapeutic hypothermia attenuates physiologic, histologic, and metabolomic markers of injury in a porcine model of acute respiratory distress syndrome

Abstract Acute respiratory distress syndrome (ARDS) is a lung injury characterized by noncardiogenic pulmonary edema and hypoxic respiratory failure. The purpose of this study was to investigate the effects of therapeutic hypothermia on short‐term experimental ARDS. Twenty adult female Yorkshire pigs were divided into four groups (n = 5 each): normothermic control (C), normothermic injured (I), hypothermic control (HC), and hypothermic injured (HI). Acute respiratory distress syndrome was induced experimentally via intrapulmonary injection of oleic acid. Target core temperature was achieved in the HI group within 1 h of injury induction. Cardiorespiratory, histologic, cytokine, and metabolomic data were collected on all animals prior to and following injury/sham. All data were collected for approximately 12 h from the beginning of the study until euthanasia. Therapeutic hypothermia reduced injury in the HI compared to the I group (histological injury score = 0.51 ± 0.18 vs. 0.76 ± 0.06; p = 0.02) with no change in gas exchange. All groups expressed distinct phenotypes, with a reduction in pro‐inflammatory metabolites, an increase in anti‐inflammatory metabolites, and a reduction in inflammatory cytokines observed in the HI group compared to the I group. Changes to respiratory system mechanics in the injured groups were due to increases in lung elastance (E) and resistance (R) (ΔE from pre‐injury = 46 ± 14 cmH2O L−1, p < 0.0001; ΔR from pre‐injury: 3 ± 2 cmH2O L−1 s−, p = 0.30) rather than changes to the chest wall (ΔE from pre‐injury: 0.7 ± 1.6 cmH2O L−1, p = 0.99; ΔR from pre‐injury: 0.6 ± 0.1 cmH2O L−1 s−, p = 0.01). Both control groups had no change in respiratory mechanics. In conclusion, therapeutic hypothermia can reduce markers of injury and inflammation associated with experimentally induced short‐term ARDS