Intrasplenic preconditioning: a model for the study of xenostimuli accommodation.

BACKGROUND: Discordant xenotransplantation, the grafting of organs from one phylogenic species to another, results in hyper-acute rejection (HAR). HAR is associated with the deposition of recipient preformed xenoreactive natural antibodies and complement on the endothelium of the donor organ, leading to activation and apoptosis of the endothelium, an event associated with xenograft rejection. Endothelial resistance to HAR, termed "accommodation," an active protection of graft endothelium, may be achieved by previous stimulation of endothelial cells by discordant xenoantibodies. MATERIALS AND METHODS: Forty-eight male Wistar rats were used to evaluate HAR induction in an isolated, dually perfused in-situ rat liver transfused with human blood. This ex-vivo model served to mimic rat-to-human liver xenotransplantation. Preconditioning of the liver endothelium was induced by rat intrasplenic injection of human blood (n=8) or effluent of previously xenotransfused rat liver (n=8), i.e., high versus low xenoantibody solution, each undertaken 1d before liver xenotransfusion. Two other groups were not preconditioned. Preconditioned and non-preconditioned rats were perfused directly with human blood, and eight rats were used as controls (non-preconditioned Krebs-perfused). Eight rats were perfused directly with human blood, and eight rats were used as controls. The effluent that exited these first-line livers was used to perfuse the second-line livers. RESULTS: Portal and hepatic artery perfusion pressures, resistances, rates of oxygen extraction, lactic acid and pH, and wet-to-dry weight ratio values were significantly increased in livers xenotransfused with blood indicating HAR, compared with unchanged values in livers perfused with Krebs solution. Portal pressure and resistance were best protected from HAR by the blood preconditioning in the blood perfused group, while the hepatic artery perfusion system was better protected by the perfusate precondition-blood perfused group. The physiologic effects of HAR were attenuated in most second-line livers. CONCLUSIONS: Attenuation of HAR in rats' livers is achieved by preconditioning with xenoantibodies and/or by "filtering out" xenoantibodies present in the circulation, and is suggestive of accommodation. This novel method may be useful in future studies aimed at refining methods for accommodating xenotransplantation.

Effects of methylene blue and volatile anesthetics on survival in a murine hemorrhage resuscitation model.

BACKGROUND: Hemorrhage is a frequent cause of morbidity and mortality, possibly complicated by volatile anesthetics administered during surgical emergencies. Because methylene blue (MB) was suggested to reduce bleeding, we reasoned that it may improve resuscitation. We used a rat model of controlled and uncontrolled hemorrhage with fluid resuscitation, aiming at high versus low mean arterial pressure (MAP) to assess the role of early MB injection on survival and the effects of different anesthetics on outcome. METHODS: Wistar male rats (n = 160) were subjected to 15-minute controlled and 60-minute uncontrolled hemorrhage and received lactated Ringer's solution replacement. Four sets (four groups per set, N = 10 per group) were anesthetized with halothane, isoflurane, sevoflurane, or ketamine (KET; control). Resuscitation-targeted MAP was 80 mm Hg in two groups per set and 40 mm Hg in two groups per set: one group received MB 25 mg/kg intravenously and the other one did not receive. RESULTS: All parameters were worse in the higher target groups compared with the lower MAP target groups. MB improved variable outcomes in the treated compared with the nontreated groups, independent of the MAP or anesthesia agent: the amount of replacement volume, lung tissue xanthine oxidase activity, and rats' survival rates. Outcomes with and without MB were worse in the halothane set, followed, in ascending order, by sevoflurane, isoflurane, and KET. CONCLUSIONS: MB improved parameters and survival rates after controlled and uncontrolled hemorrhage and fluid resuscitation, even in high MAP-resuscitated rats. KET seemed to be the best anesthetic choice among the four classic agents tested. The effects of balanced anesthesia and total intravenous anesthesia in similar conditions require additional studies.

Topical ophthalmic amethocaine alleviates trigeminal neuralgia pain.

BACKGROUND: Trigeminal neuralgia (TGN) is a challenging pain syndrome. AIM: To test the effectiveness of local instillation of ophthalmic solution of amethocaine in relieving the pain of TGN. METHODS: We performed an open-label prospective study in 40 consecutive currently treated patients suffering from TGN with a reported visual analog scale (VAS) >8 (severe pain). The patients received two drops of amethocaine 1% instilled on the cornea ipsilateral to the painful side. Pain score assessment using VAS was recorded pre- and post-treatment. RESULTS: A total of 32 (80%) patients reported a significant reduction in pain 10 minutes after drops instillation as compared with pre-treatment pain score. Pre-treatment VAS score was 8.53 ± 0.6 as compared with 4.78 ± 1.83 post-amethocaine treatments (P < 0.00001). CONCLUSION: Topical ophthalmic instillation of amethocaine 1% can be considered as an immediate effective method for pain paroxysm of TGN.

CobraPLA Insertion by anesthetists and non-anesthetists wearing unconventional protective gear: a prospective study in humans.

BACKGROUND: The threat of a mass casualty unconventional attack has challenged the medical community to devise means for providing rapid and reliable emergent airway control under chaotic conditions by inexperienced medical personnel dressed in self protective gear. Since endotracheal intubation may not be feasible under those conditions, other extraglottic devices should be considered. We assessed the performance of anesthesia and non-anesthesia residents in inserting the CobraPLA, a supraglottic airway device, on consecutive anesthetized patients, to assess its potential use under simulated conditions. MATERIAL/METHODS: Anesthesia and non-anesthesia residents wearing either surgical scrubs or complete anti-chemical gear inserted the CobraPLA in anesthetized patients. If post-trial positive pressure ventilation via the CobraPLA was unsuccessful, an LMA or endotracheal tube was inserted in its stead. RESULTS: It took anesthesia residents 57+/-23 sec and 43+/-13 sec (P<0.05) to place the CobraPLA while wearing anti-chemical gear and surgical scrubs, respectively. Non-anesthesia residents wearing anti-chemical gear performed worse than anesthetists in their first insertion (73+/-9 sec, P<0.05), but after the brief training period they performed as well as their colleagues anesthetists (58+/-10 sec, P=NS). Post-trial, twenty-one CobraPLA (42%) leaked, preventing adequate positive-pressure ventilation: 13 devices (26% of the total) required replacements. CONCLUSIONS: Anti-chemical protective gear slowed the insertion of the CobraPLA by anesthetists, and more so by other residents inexperienced in airway management. In 26% of the cases CobraPLA was inadequate for positive pressure ventilation.

Effect of small bowel perforation during laparoscopy on end-tidal carbon dioxide: observation in a small animal model.

INTRODUCTION: There are currently no reports in the literature regarding changes in end-tidal carbon dioxide (ETCO(2)) when the small bowel is deliberately or inadvertently perforated during laparoscopic surgery. The aim of this study was to assess the influence of small bowel perforation during laparoscopy on ETCO(2) in a rat model. MATERIALS AND METHODS: Two groups of Wistar rats (n = 8/group) were anesthetized, tracheostomized, and mechanically ventilated at a fixed tidal volume and respiratory rate. After a stabilization phase of 30 min, CO(2) pneumoperitoneum was established to 5 mmHg in one group and 12 mmHg in the other group, and maintained for 30 min. A small bowel perforation was then created and pneumoperitoneum was reestablished for another 30 min. Blood pressure, heart rate, peak ventilatory pressure, and ETCO(2) were recorded throughout the experiment. RESULTS: No significant changes in blood pressure throughout the experiment were noted in either group. The ventilatory pressure increased in both groups after the induction of pneumoperitoneum. In the 5 mmHg group, there was a modest increase in ETCO(2) following the induction of pneumoperitoneum (from 39.4 +/- 1.9 to 41.1 +/- 1.4, P = 0.014), and a further increase following the small bowel perforation (from 41.1 +/- 1.4 to 42 +/- 0.8, P = 0.007). In the 12 mmHg group, there was no change in ETCO(2) after the induction of pneumoperitoneum; however, there was a substantial increase in ETCO(2) following bowel perforation (35.0 +/- 2.0 to 49.8 +/- 7.1, P = 0.002). CONCLUSIONS: ETCO(2) increases when the small bowel is perforated during CO(2) pneumoperitoneum. This increase seems more substantial under higher pneumoperitoneal pressures. Small bowel injury may enable the diffusion of CO(2) through the bowel mucosa, causing ETCO(2) elevation. Therefore, an abrupt increase in ETCO(2) observed during laparoscopy may indicate small bowel injury.

ACC/AHA guidelines for preoperative cardiovascular evaluation for noncardiac surgery: a critical point of view.

This review examines the issue of preoperative cardiac evaluation from a critical point of view, based on recent medical literature. We reviewed the history of that field and focused on the American College of Cardiology and American Heart Association guidelines, which are a cornerstone in the field of cardiac patients undergoing noncardiac surgery. These guidelines synthesized the data into a comprehensive format and established the concept of integrating the patient's risk with the surgical risk. Nevertheless, there are some weaknesses in the guidelines. We believe that a better understanding of the guideline limitations will allow an improved and more educated practice of its recommendations.

Interaction between thiopental and fentanyl in mice is different between hypnotic and lethal doses.

Much is known about the interaction of intravenous anesthetics and opioids at the therapeutic level, but less is known regarding their combined lethal effect, leaving some uncertainty regarding the window of safety for their clinical use. We set out to document the type of interaction between thiopental and fentanyl for both the hypnotic effect (loss of righting reflex) and lethal effect in mice. Hypnotic and lethal dose-response curves were constructed for thiopenthal alone and in combination with fentanyl (0.8 microg/kg, each based on five to seven subgroups of six to ten ICR mice. The dose of fentanyl was that needed to double the lag time to tail flick following a noxious stimulus (the equivalent of human analgesia). While fentanyl did not change the median effective hypnotic dose of thiopental (8.9 mg/kg [95% confidence interval {CI} 8.0-9.9 mg/kg] alone versus 7.8 mg/kg [95% CI 6.7-8.7 mg/kg] in combination), it significantly reduced its median lethal dose from 71.8 mg/kg (95% CI 68.3-74.8 mg/kg) to 64.5 mg/kg (95% CI 63.7-65.2 mg/kg). Most remarkably, it increased the slope of the curve from 0.17 (95% CI 0.10-0.36) to 0.61 (95% CI 0.24-1.10), virtually eliminating the difference between the non-lethal and lethal ranges. We conclude that the type of interaction between thiopental and fentanyl is stronger for the lethal effect than for the hypnotic effect. This may become relevant to clinical situations in humans when higher doses of thiopental are used.

Beta1- or beta2-blockers to improve hemodynamics following endotracheal adrenaline administration.

BACKGROUND: The recommended dose for endotracheal adrenaline (0.02 mg/kg) causes a pronounced initial decrease in diastolic blood pressure which is detrimental at the initial phase of cardiopulmonary resuscitation. This effect was previously attributed to an early and preferential stimulation of the beta-adrenergic receptors causing vasodilatation unopposed by an alpha-adrenergic vasoconstriction. We hypothesized that inhibition of the beta2-adrenoreceptors is responsible for prevention of the deleterious initial decrease in blood pressure that takes place following endotracheal administration of adrenaline. METHODS: Adrenaline (0.02 mg/kg) diluted with normal saline (5 ml) was injected into the endobronchial tree of anesthetized dogs 3 min following pretreatment with the non-selective beta-blocker propranolol, selective beta1-blocker metoprolol (0.1 mg/kg, i.v.), or without pre-treatment. Heart rate, blood pressure and arterial blood gases were monitored. RESULTS: The selective beta-blocker metoprolol was almost as effective as the non-selective beta-blocker propranolol in attenuating the initial decrease in blood pressure following endotracheally administered adrenaline, a phenomenon that was previously attributed to inhibition of beta-adrenoreceptors. CONCLUSIONS: The outcome of this study might be explained by a dose-related loss of cardioselectivity of metoprolol. Further studies are warranted to refine the pharmacological means to abort the initial blood pressure-lowering effect of endotracheally administered adrenaline.

Involvement of nitric oxide in clonidine-induced spinal analgesia.

BACKGROUND: The chronic pain relieving effects following spinal administration of clonidine are probably connected to alpha2-adrenoreceptor-induced augmented synthesis of nitric oxide (NO) in the spinal cord. In contrast, when acute pain is considered, the possible role of NO is still speculative. The aim of the present study was to explore the role of NO in acute pain relief following intraspinal administration of clonidine. METHODS: We used the mouse tail-flick model of acute pain. Spinal injections of the following agents and their combinations were administered: clonidine, L-arginine (NO precursor), the NO production inhibitor nitro-L-arginine-methyl ester (L-NAME), the NO antagonist methylene blue (MB) and nitroglycerine (NO releasing agent). RESULTS: A 95% analgesic response was achieved with 2.0 microg clonidine. L-Arginine produced analgesia, and L-arginine administration followed by clonidine resulted in a pronounced synergistic analgesic effect. This synergistic effect was attenuated by L-NAME. Pre-treatment with MB decreased and nitroglycerine administration did not affect the clonidine-induced analgesia. CONCLUSIONS: NO may be involved in the mediation of the acute pain relieving effects of intraspinally administered clonidine. Further research is warranted to establish the potential benefits and possibility for incorporation of NO promoting agents in therapeutic regional pain regimens.

Cerebroventricular injection of clonidine causes analgesia mediated by a nitrogen pathway.

Whereas neuroaxially administered clonidine produces analgesia partially mediated by alpha2-adrenoceptor-induced augmented synthesis of nitric oxide (NO), the central mechanisms by which clonidine produces its antinociceptive effects are still speculative. We used the tail-flick model of acute pain in mice to further explore the role of NO in mediating clonidine-induced central analgesia. Cerebroventricular administration of the following agents was studied: clonidine, L-arginine (NO precursor), the NO production inhibitor nitro-L-arginine-methyl ester (L-NAME), the NO antagonist methylene blue (MB), and nitroglycerine (NO-releasing agent). Analgesic response was achieved with clonidine and L-arginine. Simultaneous administration of L-arginine and clonidine produced no additive analgesic effect. Prior administration of L-NAME or MB partially abolished the clonidine-induced analgesic effect, whereas nitroglycerine administration did not affect it. NO may be involved in the mediation of the central antinociceptive effects of clonidine. Further investigation is necessary to determine the possible role of NO-promoting agents in analgesia when co-administered with clonidine.

Atropine aborts bradycardic effect of endotracheally administered vasopressin.

BACKGROUND: Vasopressin is an alternative drug to adrenaline in intractable ventricular fibrillation. However, vasopressin can cause significant bradycardia, resulting in reduced cardiac output. We investigated whether pre-treatment with atropine abrogates vasopressin-induced bradycardia in a beating-heart canine model. MATERIAL/METHODS: Five adult mongrel dogs received endotracheal vasopressin (1.0 U/kg) with or without endotracheal atropine (0.02 mg/kg) or a placebo (10 ml saline) after being anesthetized and ventilated. Hemodynamic variables and arterial blood gases were determined. Each dog (studied 3 times, one week apart) served as its own control. RESULTS: Endotracheal vasopressin produced early and significant (p<0.05) bradycardia (from 55+/-7 mmHg to 35+/-5 beats/min) compared with controls, starting one minute post-injection and lasting one hour. In contrast, in atropine-pretreated animals the heart rate increased significantly (p<0.05) for as long as one hour post-atropine and vasopressin administration. In addition, animals treated with vasopressin with or without atropine exhibited a significant rise in diastolic blood pressure (from 83+/-5 to 160+/-15 and from 83+/-3 to 108+/-10 mmHg, respectively). Systolic and mean blood pressures also increased significantly compared with controls. Blood gases remained unchanged in all groups. CONCLUSIONS: Endotracheal administration of vasopressin can cause protracted bradycardia. Pretreatment with atropine can abrogate this effect. We suggest that atropine administration be considered when vasopressin is administered during cardio-pulmonary resuscitation. Further studies are warranted to evaluate the effect of vasopressin and atropine in a closed-chest model of cardio-pulmonary resuscitation.

Biphasic extrathoracic cuirass ventilation for resuscitation.

PURPOSES: The MRTX portable lightweight respirator (MRTX) provides noninvasive respiratory support using biphasic extrathoracic ventilation via a cuirass fitted around the patient's chest. METHODS: MRTX was applied with or without full protective gear, on adult volunteers simulating nerve agent (NA) victims by nonmedical caregivers. Assessment was made based on scores for correct positioning of the cuirass, quality of seal, and rapidness. RESULTS: For the unprotected and protected personnel, the respective median (+/-95% confidence interval) scores for correct positioning of the cuirass were 2 (1.4-1.9) and 1 (1.2-1.8) (n = 15 per group, P = NS); quality of seal scores were 2 (1.5-2.0) and 2 (1.3-1.8) ( P = NS); and mean (+/-SD) time required for instituting mechanical ventilation was 90.5 +/- 10.9 and 100.3 +/- 7.9 seconds ( P < .05). The respirator was activated at first attempt 11 times in the group of 15 without protective gear and 8 times in the group of 15 with protective gear ( P = NS). DISCUSSION: Biphasic cuirass ventilation is an easily learned and rapidly applied method suitable for use by nonmedical personnel, even when wearing cumbersome protective gear.

Single-dose ketamine administration induces apoptosis in neonatal mouse brain.

UNLABELLED: The activity of N-methyl-D-aspartate (NMDA) receptors is critical for neuronal survival in the immature brain. Studies have reported that chronic blockage of these receptors mediates apoptosis in neonatal animals. We investigated the apoptotic effect of a clinically relevant single dose of ketamine, an NMDA receptor antagonist, in the brain of neonatal mice. Seven-day-old ICR mice were injected with ketamine (1.25, 2.5, 5, 10, 20, and 40 mg/kg body weight, subcutaneously in 0.9% NaCl) or with 0.9% NaCl alone as control. Righting reflex testing was performed and mouse brains were examined at 24, 48, and 72 h and 7 days after injection. The number of degenerating neurons was measured using silver staining. Apoptosis was confirmed by DNA fragmentation (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling). We observed in the sensorimotor cortex and cerebellum of ketamine-treated mice extensive apoptosis, which was clearly dose-dependent and present even after a low dose of ketamine (5 mg/kg). The most prominent apoptotic damage was detected 72 h post-injection (P < 0.001 vs control), at doses ranging from 10 to 40 mg/kg. After 7 d the number of neurodegenerative neurons, at doses ranging from 5 to 40 mg/kg, remained significantly high. The brain weight was comparable to that of untreated control mice and no gross neurobehavioral effects in the righting reflex test or alteration in the pattern of behavior was observed. The results indicate that the administration of ketamine in a clinically relevant single dose triggers long-lasting neuronal apoptosis in certain brain areas of neonatal mice. IMPLICATIONS: The administration of ketamine in a clinically relevant single dose to 7-d-old mice induced apoptosis in the sensorimotor cortex and cerebellum. This effect was dose-dependent and long lasting.

Application of a cuirass and institution of biphasic extra-thoracic ventilation by gear-protected physicians.

OBJECTIVES: To evaluate the speed by which cuirass application, followed by biphasic extra-thoracic ventilation, can be instituted by full anti-chemical protective gear-wearing physicians. MATERIALS AND METHODS: Ten physicians of variable subspecialties applied a cuirass on an adult volunteer and instituted biphasic extra-thoracic ventilation, using the RTX respirator (Medivent, London, UK). Endotracheal (ET) intubation and manual ventilation of a mannequin and its ventilation was comparatively assessed. Performances were conducted in a prospective, crossover, randomized manner. Times to successful applications as well as failure rates were recorded. RESULTS: Cuirass application was performed more rapidly (102 +/- 9 s, 177 +/- 31 s, respectively, P <.01) and with a slightly lower failure rate than ET intubation. CONCLUSIONS: Physicians wearing full anti-chemical protective gear applied the cuirass and instituted biphasic extra-thoracic ventilation faster than ET intubation and manual positive pressure ventilation. Extra-thoracic ventilation should be further evaluated as an option for emergent respiratory support during toxic mass casualty events.

Attenuation of liver ischemia-reperfusion-induced atrial dysfunction by external pacing but not by isoproterenol.

Remote ischemia-reperfusion detrimentally affects myocardial function by initially interfering with the rate of contraction. We investigated the usefulness of isoproterenol versus external electrical pacing in attenuating secondary functional damage of isolated Wistar rat atria. Atrial strips (n = 10/group) were bathed within oxygenated Krebs-Henseleit solution that exited from isolated livers that had been either perfused normally (controls) or underwent no flow (ischemia) for 2 h. In addition to one noninterventional ischemia-exposed strip group, a second group was externally paced at a fixed rate (55 pulses.min-1, 6 V) and a third "ischemia" group was treated with isoproterenol (0.1 mM), both interventions commencing upon the strips' exposure to the hepatic effluents. Control strips displayed unaltered contraction rate and systolic-generated tension during the 2-h exposure. Nontreated strips exposed to ischemic reperfusate experienced bradycardia compared with baseline values (7 +/- 2 vs. 50 +/- 12 beats.min-1, p < 0.05), followed <1-min later by a fall in the generated tension (11 +/- 4 vs. 20 +/- 6 mmHg, p < 0.05). The paced-ischemic strips displayed unaltered rate and force of contraction, whereas the addition of isoproterenol did not prevent deterioration in the rate and force of contraction (8 +/- 3 beats.min-1, 12 +/- 4 mmHg, respectively; p < 0.05 vs. baseline control ischemia-paced strips). Thus, external electrical pacing prevented liver ischemia-reperfusion-induced atrial strips' bradycardia and loss of contractility, while isoproterenol did not.

Laryngeal mask airway control versus endotracheal intubation by medical personnel wearing protective gear.

The purpose of this study was to evaluate the rates of successful airway control using endotracheal tubes (ETs) or laryngeal mask airways (LMAs) and compare them between anesthetists and non-anesthetists wearing full antichemical protective gear. Anesthetists and non-anesthetists (n = 10 per group) twice attempted inserting ETs and LMAs on a mannequin model of airway management in a crossover, prospective manner. Times to successful insertion and failure rates were recorded. Non-anesthetists had a slightly higher failure rate inserting ETs compared with anesthetists (P = not significant). Respective mean times to successfully inserting ETs were 38 +/- 7.1 and 26.4 +/- 7.5 seconds (P < .05). Both groups inserted LMAs more rapidly than ETs (P < .05) and their failure rates in ET use were higher. In view of the relative rapidity by which LMAs were inserted as compared with ETs, by fully protected caregivers, the incorporation of LMA in algorithms dealing with emergency airway management in a nonconventional mass casualty scenario deserves further evaluation.

Antichemical protective gear prolongs time to successful airway management: a randomized, crossover study in humans.

BACKGROUND: Airway management is the first step in resuscitation. The extraordinary conditions in mass casualty situations impose special difficulties in airway management, even for experienced caregivers. The authors evaluated whether wearing surgical attire or antichemical protective gear made any difference in anesthetists' success of airway control with either an endotracheal tube or a laryngeal mask airway. METHODS: Fifteen anesthetists with 2-5 yr of residency and wearing either full antichemical protective gear or surgical attire intubated or inserted laryngeal masks in 60 anesthetized patients. The study was performed in a prospective, randomized, crossover manner. The duration of intubation/insertion was measured from the time the device was grasped to the time a normal capnography recording was obtained. RESULTS: Endotracheal tubes were introduced significantly (P < 0.01) faster when the anesthetist wore surgical attire (31 +/- 7 vs. 54 +/- 24 s for protective gear), but the mean times necessary to successfully insert laryngeal masks were similar (44 +/- 20 s for surgical attire vs. 39 +/- 11 s for protective gear). Neither performance failure nor incidences of hypoxemia were recorded. CONCLUSIONS: This first report in humans shows to what extent anesthetists' wearing of antichemical protective gear slows the time to intubate but not to insert a laryngeal mask airway compared with wearing surgical attire. Laryngeal mask airway insertion is faster than tracheal intubation when wearing protective gear, indicating its advantage for airway management when anesthetists wear antichemical protective gear. If chances for rapid and successful tracheal intubation under such chaotic conditions are poor, laryngeal mask airway insertion is a viable choice for airway management until a proper secured airway is obtainable.

Laryngeal mask airway insertion by anesthetists and nonanesthetists wearing unconventional protective gear: a prospective, randomized, crossover study in humans.

BACKGROUND: Mass casualty situations impose special difficulties in airway management, even for experienced caregivers. The laryngeal mask airway is part of the difficult airway algorithm. The authors evaluated the success rate and the time to secure airways by mask by anesthetists, surgeons, and novices when wearing either surgical attire or full antichemical protective gear that included butyl rubber gloves and a filtering antigas mask. METHODS: Twenty anesthetists and 22 surgeons with 2-5 yr of residency inserted a laryngeal mask airway in 84 anesthetized patients, and 6 novices repetitively inserted masks in 57 patients under both conditions in a prospective, randomized, crossover manner. The duration of insertion was measured from the time the device was first grasped until a normal capnography recording was obtained. RESULTS: Anesthetists needed 39 +/- 14 s to insert the masks when wearing surgical attire and 40 +/- 12 s with protective gear. In contrast, surgery residents needed 64 +/- 40 and 102 +/- 40 s (P = 0.0001), respectively. Anesthetists inserted masks in a single attempt, whereas the surgeons needed up to four attempts with no hypoxia or failure associated. The initial attire-wearing novices' insertions took as long as the surgeons'; three of them then reached the mean performance time of the anesthetists after four (protective gear) and two (surgical attire) trials, with only one occurrence of hypoxia and a failure rate similar to that of the surgeons. CONCLUSIONS: Anesthesia residents insert laryngeal mask airways at a similar speed when wearing surgical attire or limiting antichemical protective gear and two to three times faster than surgical residents or novices wearing either outfit. Novices initially perform at the level of surgical residents, but their learning curve was quick under both conditions.

Supraglottic devices: a possible role in prehospital toxic mass casualty event?

Rapidly progressive respiratory failure is the leading cause of death from inhalation of toxic chemical warfare agents. In an expected chaotic scenario, direct laryngoscopic tracheal intubation is unlikely to be easily and quickly performed due to shortage of medical personnel experienced with laryngoscopy and/or reduced dexterity imposed by the protective gear worn by the caregivers. Supraglottic devices have increasingly been used for emergent airway control in prehospital settings, thus avoiding the need for laryngoscopy. This review summarizes Medline English literature search on supraglottic devices and their use in the prehospital setting or in mass casualty event focusing on their potential role for emergent airway control in the setup of toxic inhalation.