Difficult or Impossible Ventilation after Sufentanil-induced Anesthesia Is Caused Primarily by Vocal Cord Closure

Introduction: Opioid-induced rigidity often makes bag-mask ventilation difficult or impossible during induction of anesthesia. Difficult ventilation may result from chest wall rigidity, upper airway closure, or both. This study further defines the contribution of vocal cord closure to this phenomenon.

Methods: With institutional review board approval, 30 patients undergoing elective cardiac surgery participated in the study. Morphine (0.1 mg/kg) and scopolamine (6 micro gram/kg) given intramuscularly provided sedation along with intravenous midazolam as needed. Lidocaine 10% spray provided topical anesthesia of the oropharynx. A fiberoptic bronchoscope positioned in the airway photographed the glottis before induction of anesthesia. A second photograph was obtained after induction with 3 micro gram/kg sufentanil administered during a period of 2 min. A mechanical ventilator provided 10 ml/kg breaths at 10/min via mask and oral airway with jaw thrust. A side-stream spirometer captured objective pulmonary compliance data. Subjective airway compliance was scored. Pancuronium (0.1 mg/kg) provided muscle relaxation. One minute after the muscle relaxant was given, a third photograph was taken and compliance measurements and scores were repeated. Photographs were scored in a random, blinded manner by one investigator. Wilcoxon signed rank tests compared groups, with Bonferroni correction. Differences were considered significant at P <0.05.

Results: Twenty-eight of 30 patients exhibited decreased pulmonary compliance and closed vocal cords after opioid induction. Two patients with neither objective nor subjective changes in pulmonary compliance had open vocal cords after opioid administration. Both subjective and objective compliances increased from severely compromised values after narcotic-induced anesthesia to normal values (P = 0.000002) after patients received a relaxant. Photo scores document open cords before induction, progressing to closed cords after the opioid (P = 0.00002), and opening again after a relaxant was administered (P = 0.00005).     

Nonoperative treatment ofacromioclavicular joint injuries

Nonoperative treatment is generally the choice for Type I and II acromioclavicular (AC) joint injuries. The situation issomewhat more controversial when Type III AC dislocations are considered, particularly with respect to athletes and heavy laborers. A number of recent studies have supported conservative treatment in these groups. There is general consensus as to the need for surgical intervention for Type IV, V, and VI AC injuries. Integral to any form of management, nonoperative or operative, is a rehabilitation program that addresses range of motion, strength, and neuromuscular control. We describe our program, which is divided into four phases: (1) Pain control and immediate protected range of motion and isometric exercises; (2) strengthening exercises using isotonic contractions and proprioceptive neuromuscular facilitation (PNF) exercises; (3) Unrestricted functional participation with the goal of increasing strength, power, endurance, and neuromuscular control; and (4) return to activity with sport specific functional drills. An athlete is ready to return to competitive sports once the following criteria are met: full range of motion (ROM), no pain or tenderness, satisfactory clinical exam, and demonstration of adequate strength on isokinetic testing. The unique considerations in a throwing athlete with an AC injury are also addressed. The primary goal of the nonoperative treatment protocol is to return the athlete to full activities as quickly and as safely as possible.     

Pulmonary aspiration of gastric contents after a priming dose of vecuronium

A case is presented of a 16-year-old girl with ectodermal dysplasia for whom dental surgery under general anaesthesia was planned. Following a priming dose of vecuronium, and immediately after injection of sodium thiopentone (5 mg·kg⁻¹) pulmonary aspiration of gastric contents occurred. It is hypothesized that, because of the rapid speed of onset of neuromuscular blocking agents on the laryngeal muscles, that partial laryngeal paralysis was present at the time of induction of anaesthesia and that this was responsible in part for the episode of pulmonary aspiration.