Decreasing Time from Decision to Intubation in Premedicated Neonates: A Quality Improvement Initiative.

Endotracheal intubation carries the risk of discomfort, decompensation, oral trauma, and endotracheal tube malposition. Treatment with premedications reduces complications, increases overall intubation safety, improves pain control, and improves first-pass success. However, time is frequently a barrier to administration. We aimed to decrease the decision-to-intubation time interval from a baseline of 40 minutes to less than 35 minutes over 6 months. METHODS: We used the Model for Improvement with multiple plan-do-study-act cycles to reduce the time from decision to successful intubation in nonemergent neonatal intubations. Key drivers were timely administration of medications, availability of skilled personnel and equipment, and efficient use of time. RESULTS: During this project, time from the decision to successful intubation decreased from a historical mean of 40 minutes to a new baseline of 27 minutes. This change represents a 33% decrease, with 80% of intubations occurring within 35 minutes. During this time, success rates remained stable, and medication errors and side effects did not increase. CONCLUSIONS: Standard processes to prepare and administer premedications decreased the time from decision to intubation without significant adverse effects, allowing the benefit of premedication administration in a safe and timely manner in nonemergent neonatal intubations.

Acute pulmonary toxicity following inhalation exposure to aerosolized VX in anesthetized rats.

This study evaluated acute toxicity and pulmonary injury in rats at 3, 6 and 24 h after an inhalation exposure to aerosolized O-ethyl S-[2-(diisopropylamino)ethyl] methylphosphonothioate (VX). Anesthetized male Sprague-Dawley rats (250-300 g) were incubated with a glass endotracheal tube and exposed to saline or VX (171, 343 and 514 mg×min/m³ or 0.2, 0.5 and 0.8 LCt50, respectively) for 10 min. VX was delivered by a small animal ventilator at a volume of 2.5 ml × 70 breaths/minute. All VX-exposed animals experienced a significant loss in percentage body weight at 3, 6, and 24 h post-exposure. In comparison to controls, animals exposed to 514 mg×min/m³ of VX had significant increases in bronchoalveolar lavage (BAL) protein concentrations at 6 and 24 h post-exposure. Blood acetylcholinesterase (AChE) activity was inhibited dose dependently at each of the times points for all VX-exposed groups. AChE activity in lung homogenates was significantly inhibited in all VX-exposed groups at each time point. All VX-exposed animals assessed at 20 min and 3, 6 and 24 h post-exposure showed increases in lung resistance, which was prominent at 20 min and 3 h post-exposure. Histopathologic evaluation of lung tissue of the 514 mg×min/m³ VX-exposed animals at 3, 6 and 24 h indicated morphological changes, including perivascular inflammation, alveolar exudate and histiocytosis, alveolar septal inflammation and edema, alveolar epithelial necrosis, and bronchiolar inflammatory infiltrates, in comparison to controls. These results suggest that aerosolization of the highly toxic, persistent chemical warfare nerve agent VX results in acute pulmonary toxicity and lung injury in rats.

Development of a model for nerve agent inhalation in conscious rats.

This study characterizes the development of a head-out inhalation exposure system for assessing respiratory toxicity of vaporized chemical agents in untreated, non-anesthetized rats. The organophosphate diisopropyl fluorophosphate (DFP) induces classical cholinergic toxicity following inhalation exposure and was utilized to validate the effectiveness of this newly designed inhalation exposure system. A saturator cell apparatus was used to generate DFP vapor at 9750, 10,950, 12,200, 14,625 and 19,500 mg × min/m³ which was carried by filtered nitrogen into a glass mixing tube, where it combined with ambient air before being introduced to the custom-made glass exposure chamber. Male Sprague-Dawley rats (250-300 g) were restrained in individual head-out plethysmography chambers, which acquired respiratory parameters before, during and after agent exposure. All animals were acclimated to the exposure system prior to exposure to reduce novel environment-induced stress. The LCt50, as determined by probit analysis, was 12,014 mg × min/m³. Weight loss in exposed animals was dose-dependent and ranged from 8 to 28% of their body weight 24 h after exposure. Increased salivation, lacrimation, urination, defecation (SLUD) and mild muscular fasciculation were observed in all DFP-exposed animals during and immediately following exposure. In all exposed animals, DFP vapor produced significant inhibition of acetylcholinesterase (AChE) activity in cardiac blood, bronchoalveolar lavage fluid (BALF), whole brain and lung tissue as well as alterations in tidal volume and minute volume. These studies have provided valuable information leading to the initiation of studies evaluating inhalational toxicity and treatments following exposure to the more lethal and potent chemical warfare nerve agents.