Outcomes after pancreaticoduodenectomy with or without preoperative hyperbaric oxygen therapy.

Background: Hyperbaric oxygen (HBO2) therapy is an alternative method against the deleterious effects of ischemic/reperfusion (I/R) injury and its inflammatory response. This study assessed the effect of preoperative HBO2 on patients undergoing pancreaticoduodenectomy. Study Design: Patients were randomized via a computer-generated algorithm. Patients in the HBO2 cohort received two sessions of HBO2 the evening before and the morning of surgery. Measurements of inflammatory mediators and self-assessed pain scales were determined pre-and postoperatively. In addition, perioperative variables and long-term survival were collected and analyzed. Data are presented as median (mean ± SD). Results: 33 patients were included; 17 received preoperative HBO2, and 16 did not. There were no intraoperative or postoperative statistical differences between patients with or without preoperative HBO2. Erythrocyte sedimentation rate (ESR), IL-6, and IL-10 increased slightly before returning to normal, while TGF-alpha decreased before increasing. However, there were no differences with or without HBO2. At postoperative day 30, the pain level measured with VAS score (Visual Analog Score) was lower after HBO2 (1 ± 1.3 vs. 3 ± 3.0, p=0.05). Eleven (76%) patients in the HBO2 cohort and 12 (75%) patients in the non- HBO2 had malignant pathology. The percentage of positive lymph nodes in the HBO2 was 7% compared to 14% in the non-HBO2 (p<0.001). Overall survival was inferior after HBO2 compared to the non- HBO2 (p=0.03). Conclusions: Preoperative HBO2 did not affect perioperative outcomes or significantly change the inflammatory mediators for patients undergoing robotic pancreaticoduodenectomy. Long-term survival was inferior after preoperative HBO2. Further randomized controlled studies are required to assess the full impact of this treatment on patients' prognosis.

Dopamine/BDNF loss underscores narcosis cognitive impairment in divers: a proof of concept in a dry condition.

PURPOSE: Divers can experience cognitive impairment due to inert gas narcosis (IGN) at depth. Brain-derived neurotrophic factor (BDNF) rules neuronal connectivity/metabolism to maintain cognitive function and protect tissues against oxidative stress (OxS). Dopamine and glutamate enhance BDNF bioavailability. Thus, we hypothesized that lower circulating BDNF levels (via lessened dopamine and/or glutamate release) underpin IGN in divers, while testing if BDNF loss is associated with increased OxS. METHODS: To mimic IGN, we administered a deep narcosis test via a dry dive test (DDT) at 48 msw in a multiplace hyperbaric chamber to six well-trained divers. We collected: (1) saliva samples before DDT (T0), 25 msw (descending, T1), 48 msw (depth, T2), 25 msw (ascending, T3), 10 min after decompression (T4) to dopamine and/or reactive oxygen species (ROS) levels; (2) blood and urine samples at T0 and T4 for OxS too. We administered cognitive tests at T0, T2, and re-evaluated the divers at T4. RESULTS: At 48 msw, all subjects experienced IGN, as revealed by the cognitive test failure. Dopamine and total antioxidant capacity (TAC) reached a nadir at T2 when ROS emission was maximal. At decompression (T4), a marked drop of BDNF/glutamate content was evidenced, coinciding with a persisting decline in dopamine and cognitive capacity. CONCLUSIONS: Divers encounter IGN at - 48 msw, exhibiting a marked loss in circulating dopamine levels, likely accounting for BDNF-dependent impairment of mental capacity and heightened OxS. The decline in dopamine and BDNF appears to persist at decompression; thus, boosting dopamine/BDNF signaling via pharmacological or other intervention types might attenuate IGN in deep dives.

Volume 50: The UHM Journal celebrates a milestone with the publication of this issue.

As the UHMS observes the distinguished anniversary of the publication of 50 volumes of the Undersea and Hyperbaric Medicine Journal, two of our past editors take a look at the evolution of our flagship publications.

Critical Review and Meta-Analysis of Postoperative Sedation after Adult Cardiac Surgery: Dexmedetomidine Versus Propofol.

OBJECTIVE: To evaluate reports from the published literature of all randomized clinical trials (RCT) comparing postoperative sedation with dexmedetomidine versus propofol in adult patients, after open cardiac surgery. DESIGN: A computerized search on Medline, EMBASE, Web of Science, and Agency for Healthcare Research and Quality databases was completed through June 2020. Meta-analysis of all published RCT comparing dexmedetomidine versus propofol utilization in the postoperative phase, using the standard Preferred Reporting Items for Systematic Reviews and Meta-Analyses checklist. SETTING: Assemblage and critical discussion of 11 RCTs comparing postoperative sedation from standard published reports from 2003 to 2019. PARTICIPANTS: The study comprised 1,184 patients and analyzed critical discussion of time-based parameters (time to extubation, intensive care unit length of stay, and hospital length of stay) and nontime-dependent factors (delirium, bradycardia, and hypotension). MEASUREMENTS AND MAIN RESULTS: Time to extubation was significantly reduced in the dexmedetomidine group (standardized mean difference [SMD] = -0.70, 95% confidence interval [CI] -0.98 to -0.42, p < 0.001); however, no difference in mechanical ventilation time was observed (SMD = -0.72, 95% CI -1.60 to 0.15, N.S.). Dexmedetomidine significantly reduced the intensive care unit length of stay (SMD = 0.23, 95% CI -1.06 to -0.16, p = 0.008), but this did not translate into a reduced hospital length of stay (SMD = -1.13, 95% CI -2.43 to 0.16, N.S). For nontime-dependent factors, incidence of delirium was unaffected between groups (odds ratio [OR]: 0.68, 95% CI 0.43-1.06, N.S), and higher rates of bradycardia (OR: 3.39, 95% CI: 1.20-9.55, p = 0.020) and hypotension (OR: 1.68, 95% CI 1.09-2.58, p = 0.017) were reported with propofol. CONCLUSIONS: Despite the ICU time advantages afforded by dexmedetomidine over propofol, the former did not seem to contribute to an overall reduction in hospital length of stay or improvement in postoperative outcomes of heart valve surgery and CABG patients.

The Role of Hyperbaric Oxygen Treatment for COVID-19: A Review.

The recent coronavirus disease 2019 (COVID-19) pandemic produced high and excessive demands for hospitalizations and equipment with depletion of critical care resources. The results of these extreme therapeutic efforts have been sobering. Further, we are months away from a robust vaccination effort, and current therapies provide limited clinical relief. Therefore, several empirical oxygenation support initiatives have been initiated with intermittent hyperbaric oxygen (HBO) therapy to overcome the unrelenting and progressive hypoxemia during maximum ventilator support in intubated patients, despite high FiO2. Overall, few patients have been successfully treated in different locations across the globe. More recently, less severe patients at the edge of impending hypoxemia were exposed to HBO preventing intubation and obtaining the rapid resolution of symptoms. The few case descriptions indicate large variability in protocols and exposure frequency. This summary illustrates the biological mechanisms of action of increased O2 pressure, hoping to clarify more appropriate protocols and more useful application of HBO in COVID-19 treatment.

Sugammadex Reduces PACU Recovery Time after Abdominal Surgery Compared with Neostigmine.

OBJECTIVE: This study blindly evaluated sugammadex compared with neostigmine on length of stay in the postanesthesia care unit (PACU). METHODS: Fifty patients undergoing elective laparoscopic cholecystectomy or abdominal wall hernia repair consented to receive either sugammadex (2 mg/kg) or neostigmine (0.07 mg/kg) for the reversal of rocuronium neuromuscular blockade. Reversal agents were administered during surgical closing, and the train of four was measured until a twitch ratio of T4:T1 ≥ 0.9 was obtained to signify a robust reversal. Postreversal outcomes also were measured during PACU stay. Aldrete scores, pain visual analog scale score, and nausea were measured during the PACU stay. RESULTS: Patients receiving sugammadex experienced a shorter PACU stay at the time of discharge than patients receiving neostigmine, by an average of 12 minutes (P < 0.05). CONCLUSIONS: Sugammadex patients had a significantly shorter PACU stay.

Arterial blood gases in divers at surface after prolonged breath-hold.

PURPOSE: Adaptations during voluntary breath-hold diving have been increasingly investigated since these athletes are exposed to critical hypoxia during the ascent. However, only a limited amount of literature explored the pathophysiological mechanisms underlying this phenomenon. This is the first study to measure arterial blood gases immediately before the end of a breath-hold in real conditions. METHODS: Six well-trained breath-hold divers were enrolled for the experiment held at the "Y-40 THE DEEP JOY" pool (Montegrotto Terme, Padova, Italy). Before the experiment, an arterial cannula was inserted in the radial artery of the non-dominant limb. All divers performed: a breath-hold while moving at the surface using a sea-bob; a sled-assisted breath-hold dive to 42 m; and a breath-hold dive to 42 m with fins. Arterial blood samples were obtained in four conditions: one at rest before submersion and one at the end of each breath-hold. RESULTS: No diving-related complications were observed. The arterial partial pressure of oxygen (96.2 ± 7.0 mmHg at rest, mean ± SD) decreased, particularly after the sled-assisted dive (39.8 ± 8.7 mmHg), and especially after the dive with fins (31.6 ± 17.0 mmHg). The arterial partial pressure of CO2 varied somewhat but after each study was close to normal (38.2 ± 3.0 mmHg at rest; 31.4 ± 3.7 mmHg after the sled-assisted dive; 36.1 ± 5.3 after the dive with fins). CONCLUSION: We confirmed that the arterial partial pressure of oxygen reaches hazardously low values at the end of breath-hold, especially after the dive performed with voluntary effort. Critical hypoxia can occur in breath-hold divers even without symptoms.

Association of Serum Albumin and Severity of Pulmonary Embolism.

Background and Objectives: Inflammation is considered a risk factor for venous thromboembolism. The association between inflammatory markers and the severity of acute pulmonary embolism (APE) has not been explored. Methods: We studied the association between two crude markers of inflammation, serum albumin, and red cell distribution width (RDW) and massive versus non-massive APE. Results: Among 552 consecutive cases of CT-angiogram-confirmed APE, a total of 46 cases (8.3%) had massive APE. Despite similar demographics and comorbidities, patients with massive APE had higher frequency of acute kidney injury (P = 0.005), higher lactic acid (P = 0.011), higher troponin (P = 0.001), higher BNP (P < 0.001), higher frequency of RV dilation (P = 0.017) and hypokinesis (P = 0.003), and higher in-hospital mortality (15.2% vs. 2%, P < 0.001). Patients with massive APE had significantly lower albumin level (median (IQR): 2.8 (2.2, 3.0) vs. 3.2 (2.8, 3.6) gm/dL, P < 0.001) and higher RDW (median (IQR): 14.7 (13.8, 17.1) vs. 14.2 (13.3, 15.6), P = 0.006) compared with non-massive APE. ROC curves showed that albumin and RDW had an AUC of 0.750 (P < 0.001) and 0.621 (P = 0.006) in predicting a massive APE, respectively. The optimal cutoff values for albumin and RDW that had the highest combined sensitivity and specificity for predicting APE was ≤3 gm/dL and >14, for albumin and RDW, respectively. Restricted cubic splines showed a significant association between albumin (P = 0.0002) and RDW (P = 0.0446) and the occurrence of massive APE. After adjustment for patients' age, body mass index, white blood cell count, the requirement of antibiotics during hospitalization, diabetes, RDW, and peak creatinine, serum albumin was independently associated with massive APE (OR 0.234, 95% CI 0.129-0.4242, P < 0.001). Conclusion: low serum albumin is associated with massive APE. This association is likely a proxy for higher inflammatory state in massive compared with non-massive APE.

Syncope on presentation is a surrogate for submassive and massive acute pulmonary embolism.

INTRODUCTION: There are conflicting data regarding the prognostic value of syncope in patients with acute pulmonary embolism (APE). METHODS: We retrospectively reviewed data of 552 consecutive adults with computed tomography pulmonary angiogram-confirmed APE to determine the correlates and outcome of the occurrence of syncope at the time of presentation. RESULTS: Among 552 subjects with APE (mean age 54years, 47% men), syncope occurred in 12.3% (68/552). Compared with subjects without syncope, those with syncope were more likely to have admission systolic blood pressure<90mmHg (odds ratio (OR) 5.788, P<0.001), and an oxygen saturation<88% on room air (OR 5.560, P<0.001), right ventricular dilation (OR 2.480, P=0.006), right ventricular hypokinesis (OR 2.288, P=0.018), require mechanical ventilation for respiratory failure (OR 3.152, P=0.014), and more likely to receive systemic thrombolysis (OR 4.722, P=0.008). On multivariate analysis, syncope on presentation was an independent predictor of a massive APE (OR 2.454, 95% CI 1.109-5.525, P=0.03) after adjusting for patients' age, sex, requirement of antibiotics throughout hospitalization, peak serum creatinine, admission oxygen saturation<88% and admission heart rate>100bpm. There was no difference in mortality in cases with APE with or without syncope (P=0.412). CONCLUSION: Syncope at the onset of pulmonary embolization is a surrogate for submassive and massive APE but is not associated with higher in-hospital mortality.

Lingual traction to facilitate fiber-optic intubation of difficult airways: a single-anesthesiologist randomized trial.

PURPOSE: Flexible fiber-optic bronchoscope-guided orotracheal intubation is a valuable technique with demonstrated benefits in the management of difficult airways. Despite its popularity with anesthesia providers, the technique is not fail-safe and airway-related complications secondary to failed intubation attempts remain an important problem. We sought to determine the effect of incorporating lingual traction on the success rate of fiber-optic bronchoscope-guided intubation in patients with anticipated difficult airways. METHODS: In this prospective, randomized, cohort study, we enrolled 91 adult patients with anticipated difficult airways scheduled for elective surgery to undergo fiber-optic bronchoscope-guided orotracheal intubation alone or with lingual traction by an individual anesthesiologist after induction of general anesthesia and neuromuscular blockade. A total of 78 patients were randomized: 39 patients to the fiber-optic bronchoscope-guided intubation with lingual traction group and 39 patients to the fiber-optic bronchoscope-guided intubation alone group. The primary endpoint was the rate of successful first attempt intubations. The secondary outcome was sore throat grade on post-operative day 1. RESULTS: Fiber-optic intubation with lingual traction compared to fiber-optic intubation alone resulted in a higher success rate (92.3 vs. 74.4 %, χ (2) = 4.523, p = 0.033) and greater odds for successful first attempt intubation (OR 4.138, 95 % CI 1.041-16.444, p = 0.044). Sore throat severity on post-operative day 1 was not significantly different but trended towards worsening grades with lingual traction. CONCLUSIONS: In this study, lingual traction was shown to be a valuable maneuver for facilitating fiber-optic bronchoscope-guided intubation in the management of patients with anticipated difficult airways.

The use of isoproterenol and phenytoin to reverse torsade de pointes.

Torsade de pointes is a form of polymorphic ventricular tachycardia that differs from other forms of ventricular tachycardia in its morphology, precipitating factors, and therapeutic approach. Its recognition is of utmost importance, as the standard anti-arrythmic drugs not only might be ineffective in its termination but also may aggravate it. Herein, we report a case of antipsychotic-induced torsade de pointes and describe the use of magnesium sulfate, isoproterenol, and phenytoin and their proposed mechanism of action.

Side effects of hyperbaric oxygen therapy.

Several side effects and complications from hyperbaric oxygen (HBO2) therapy have been described, with varying degrees of seriousness. By far, the two most frequent and benign side effects comprise middle ear barotrauma, which has been noted in up to 2% of treated patients, and can be prevented or minimized by teaching autoinflation techniques, or by inserting tympanostomy tubes. Another frequent complaint is claustrophobia, both during multiplace and monoplace chamber compression, requiring reassurance, coaching and, at times, sedation. Other more rare, but more severe side effects derive from oxygen (O2) toxicity, from the multiple exposures required for chronic treatments, especially progressive myopia, usually transient and reversible after stopping HBO2 sessions, or pulmonary dyspnea, with cough and inspiratory pain. More serious O2-induced seizures happen rarely, at higher O2 pressures, and often during acute treatments in acidotic patients (carbon monoxide poisoning).

Mechanisms of action of hyperbaric oxygen therapy.

Therapeutic mechanisms of action for hyperbaric oxygen (HBO2) therapy are based on elevation of both the partial pressure of inspired O2 and of the hydrostatic pressure. This last mechanism contributes to a compression of all gas-filled spaces in the body (Boyle's Law) and is relevant to treat conditions where gas bubbles are present in the body and cause the disease (e.g., intravascular embolism; decompression sickness with intravascular or intra-tissue bubbles). However, the majority of patients treated with HBO2 do not suffer from bubble-induced injuries, but derive clinical improvements from the elevated O2 partial pressures. High O2 partial pressures in various tissues increase the production of reactive O2 species (ROS) and also of reactive nitrogen species (RNS) because of hyperoxia. Most controlled studies have verified that the clinical efficacy from HBO2 derives from modulation of intracellular transduction cascades, leading to synthesis of growth factors and promoting wound healing and ameliorating post-ischemic and post-inflammatory injuries.

Hyperbaric oxygen pretreatment and preconditioning.

Exposure to hyperbaric oxygen (HBO2) before a crucial event, with the plan to create a preventing therapeutic situation, has been defined "preconditioning" and is emerging as a useful adjunct both in diving medicine as well before ischemic or inflammatory events. Oxygen pre-breathing before diving has been extensively documented in recreational, technical, commercial and military diving for tissue denitrogenation, resulting in reduced post-diving bubble loads, reduced decompression requirements and more rapid return to normal platelet function after a decompression. Preoxygenation at high atmospheric pressure has also been used in patients before exposure to clinical situations with beneficial effects, but the mechanisms of action have not yet been ascertained. During the reperfusion of ischemic tissue, oxygenated blood increases numbers and activities of oxidants generated in tissues. Previous reports showed that HBO2 preconditioning caused the activation of antioxidative enzymes and related genes in the central nervous system, including catalase (CAT), superoxide dismutase and heme oxygenase-1. Despite the increasing number of basic science publications on this issue, studies describing HBO2 preconditioning in the clinical practice remain scarce. To date, only a few studies have investigated the preconditioning effects of HBO2 in relation to the human brain and myocardium with robust and promising results.

Management of antithrombotic therapy before full-mouth extraction.

The management of antiplatelet and anticoagulant therapy before full-mouth extraction is a major concern for dentists. Approach should vary depending on the risk of bleeding and adverse cardiac events. We have adapted a more conservative approach with continuation of antiplatelet therapy in the majority of patients while implementing local hemostatic measures with good outcomes. Specific recommendations are provided for antiplatelet therapy before mouth extraction.

Relative hypoxemia at depth during breath-hold diving investigated through arterial blood gas analysis and lung ultrasound.

Pulmonary gas exchange in breath-hold diving (BHD) consists of a progressive increase in arterial partial pressures of oxygen ([Formula: see text]) and carbon dioxide ([Formula: see text]) during descent. However, recent findings have demonstrated that [Formula: see text] does not consistently rise in all subjects. This study aimed at verifying and explaining [Formula: see text] derangements during BHD analyzing arterial blood gases and searching for pulmonary alterations with lung ultrasound. After ethical approval, 14 fit breath-hold divers were included. Experiments were performed in warm water (temperature: 31°C). We analyzed arterial blood gases immediately before, at depth, and immediately after a breath-hold dive to -15 m of fresh water (mfw) and -42 mfw. Signs of lung interstitial edema and atelectasis were searched simultaneously with a marinized lung ultrasound. In five subjects (-15 mfw) and four subjects (-42 mfw), the [Formula: see text] at depth seems to decrease instead of increasing. [Formula: see text] and lactate showed slight variations. At depth, no lung ultrasound alterations were seen except in one subject (hypoxemia and B-lines at -15 mfw; B-lines at the surface). Lung interstitial edema was detected in 3 and 12 subjects after resurfacing from -15 to -42 mfw, respectively. Two subjects developed hypoxemia at depth and a small lung atelectasis (a focal pleural irregularity of triangular shape, surrounded by thickened B-lines) after resurfacing from -42 mfw. Current experiments confirmed that some BH divers can experience hypoxemia at depth. The hypothesized explanation for such a discrepancy is lung atelectasis, which could not be detected in all subjects probably due to limited time available at depth.NEW & NOTEWORTHY During breath-hold diving, arterial partial pressure of oxygen ([Formula: see text]) and arterial partial pressure of carbon dioxide ([Formula: see text]) are believed to increase progressively during descent, as explained by theory, previous end-tidal alveolar gas measurements, and arterial blood gas analysis in hyperbaric chambers. Recent experiments in real underwater environment found a paradoxical [Formula: see text] drop at depth in some divers. This work confirms that some breath-hold divers can experience hypoxemia at depth. The hypothesized explanation for such a discrepancy is lung atelectasis, as suggested by lung ultrasound findings.