Magnus Wattwil

Scandinavian Clinical Practice Guidelines on the diagnosis, management and follow-up of anaphylaxis during anaesthesia*

The present approach to the diagnosis, management and follow‐up of anaphylaxis during anaesthesia varies in the Scandinavian countries. The main purpose of these Scandinavian Clinical Practice Guidelines is to increase the awareness about anaphylaxis during anaesthesia amongst anaesthesiologists. It is hoped that increased focus on the subject will lead to prompt diagnosis, rapid and correct treatment, and standardised management of patients with anaphylactic reactions during anaesthesia across Scandinavia.

Respiratory Depression After Epidural Morphine???An Experimental and Clinical Study

This study was comprised of an experimental part (20 volunteers) and a clinical part (10 surgical patients). In the experimental part, the effects of either 2-, 4-, or 10-mg doses of epidural morphine on ventilatory responses to a standardized CO2 challenge were studied in healthy volunteers. In the clinical part, ventilatory responses to CO2 were evaluated in patients receiving 4 mg of epidural morphine for pain relief after gall bladder surgery. Naloxone infusion was given to five volunteers to determine whether ventilatory changes due to epidural morphine could be prevented. Using a nonrebreathing method, end-tidal Pco2 (PETCO2) and minute ventilation (tidal volume × frequency) were measured before and 1, 5, 8, 13, and 22 hr after epidural morphine injection. Ventilation was stimulated by 4% CO2 in 21 % O2 and 75% N2. In the experimental study, a dose-related depression of ventilatory drive was seen after epidural morphine. After 2− and 4-mg doses, increases in PETCO2 were present up to 5 hr after injection with a corresponding reduction in minute ventilation. Ten mg of epidural morphine was followed by a significant reduction in minute ventilation and an increase in PETco2 that started 1 hr after injection, peaked at 5 hr, and then remained almost unchanged for the next 17 hr. PETco2 was higher and remained elevated longer in surgical patients than in volunteers given the same amount of epidural morphine (4 mg). Naloxone infusion (5 μg·kg−1·hr−1), prevented the reduction of minute volume and decreased the elevation of PETco2 due to epidural morphine. After larger doses (10 μg·kg−1·hr−1), minute volume and respiratory frequency were well above control levels, and PETco2 was restored to near control values. Thus infusion of naloxone could prevent the respiratory changes after 4 mg of epidural morphine.

Sugammadex Provides Faster Reversal of Vecuronium- Induced Neuromuscular Blockade Compared with Neostigmine: A Multicenter, Randomized, Controlled Trial

BACKGROUND: Sugammadex, a specifically designed &ggr;-cyclodextrin, is a selective relaxant binding drug that rapidly reverses rocuronium-induced and, to a lesser extent, vecuronium-induced neuromuscular blockade. In this study, we compared the efficacy of sugammadex and neostigmine for the reversal of vecuronium-induced neuromuscular blockade in patients scheduled for elective surgery. METHODS: Patients aged ≥18 yr, ASA Class I–III, and scheduled for a surgical procedure under sevoflurane/opioid anesthesia received an intubating dose of vecuronium (0.1 mg/kg) and maintenance doses of 0.02–0.03 mg/kg at reappearance of the second twitch (T2) of train-of-four (TOF) if required. Neuromuscular blockade was monitored using acceleromyography (TOF-Watch® SX, Schering-Plough Ireland, Dublin, Ireland). At end of surgery, at reappearance of T2 after the last dose of vecuronium, patients were randomized to receive either sugammadex (2 mg/kg) or neostigmine (50 &mgr;g/kg) plus glycopyrrolate (10 &mgr;g/kg) IV. The primary efficacy end-point was time from start of administration of sugammadex or neostigmine to recovery of TOF ratio to 0.9. RESULTS: The geometric mean time to recovery of the TOF ratio to 0.9 was significantly faster with sugammadex compared with neostigmine (2.7 min [95% confidence interval {CI}]: 2.2–3.3) versus 17.9 min [95% CI: 13.1–24.3], respectively; P < 0.0001). The mean recovery times to a TOF ratio of 0.8 and 0.7 were also significantly shorter with sugammadex. No serious adverse events or unexpected side effects were reported with either drug. CONCLUSION: Sugammadex provided significantly faster reversal of vecuronium-induced neuromuscular blockade compared with neostigmine.

Low-dose bupivacaine plus fentanyl for spinal anesthesia during ambulatory inguinal herniorrhaphy: a comparison between 6 mg and 7. 5 mg of bupivacaine

Background: Inguinal herniorrhaphy is commonly performed as an outpatient procedure. Spinal anesthesia offers some advantages over general anesthesia in this setting.

Systemic and central effects of morphine on gastroduodenal motility

Gastrointestinal side effects still constitute a major drawback in both acute and chronic use of opioids. The exact mechanism behind the gastrointestinal effects is not known, but experimental studies indicate both central and peripheral actions.

Superior prolonged antiemetic prophylaxis with a four-drug multimodal regimen: comparison with propofol or placebo

Background:  The purpose of this study was to compare the effects of a low‐dose propofol infusion with a four‐drug multimodal regimen for prophylaxis of postoperative nausea and vomiting (PONV).

Dexamethasone is as effective as ondansetron for the prevention of postoperative nausea and vomiting following breast surgery

Introduction:  Postoperative nausea and vomiting remain a common problem following breast surgery. This study assesses whether dexamethasone is as effective as ondansetron in the control of postoperative nausea and vomiting (PONV).

The influence of propofol on vomiting induced by apomorphine

It has been proposed that propofol has antiemetic effects even in nonsedative doses.The aim of this study was to investigate whether propofol influences vomiting induced by the dopamine agonist apomorphine. Ten healthy male volunteers received apomorphine infusion (1 mg/min) until vomiting was induced on four different occasions in a randomized order: a) during propofol infusion (2.4 +/- 0.7 mg centered dot kg (-1) centered dot h-1, mean +/- SD) at a sedation score of Grade 2-3 on a 5-grade scale; b) during midazolam infusion (0.13 +/- 0.04 mg centered dot kg-1 centered dot h-1) at a sedation score of Grade 2-3 on a 5-grade scale; c) after a single nonsedating bolus dose propofol 0.4 mg/kg; and d) during infusion of normal saline. The amount of apomorphine needed to induce vomiting was increased after sedation with propofol (P = 0.005) as well as midazolam (P = 0.001). There was no difference in the sensitivity to apomorphine between these sedative regimens. The nonsedating single bolus propofol did not change the sensitivity to apomorphine compared to the saline infusion. We conclude that propofol given in a nonsedative dose has no effect on apomorphine-induced vomiting. However, the total amount of apomorphine given to induce vomiting was significantly larger during propofol sedation than during saline infusion. This was probably an effect of sedation inasmuch as a similar result was achieved during midazolam sedation. (Anesth Analg 1995;80:967-9)

Long-term treatment of two patients with respiratory insufficiency with IPPV/PEEP and HFPPV/PEEP.

The respiratory centre is a multi‐input system and positive‐pressure ventilation is known to interfere with respiratory control mechanisms. Further, in intermittent positive‐pressure ventilation (IPPV) the ventilatory pattern produced by the ventilator and the lung systems is known to influence pulmonary and cardiovascular functions. High‐frequency positive‐pressure ventilation (HFPPV) has been shown to eliminate respiration‐synchronous variations in blood pressure and blood flow, and at frequencies of 60 per min or more spontaneous breathing ceases almost instantaneously if adequate alveolar ventilation and arterial oxygenation are achieved. However, activation of other inputs to the respiratory centre, e.g. chemo‐receptor inputs, can induce spontaneous respiration during HFPPV. Consequently the balance between excitatory and inhibitory afferents is decisive for the patients spontaneous respiratory efforts (discoordination) during artificial ventilation.

The effects of cricoid pressure, remifentanil, and propofol on esophageal motility and the lower esophageal sphincter.

Cricoid pressure is the gold standard during the induction of anesthesia when there is a risk of aspiration of gastric contents. However, the effect of cricoid pressure during the different steps of complete anesthesia induction has not been studied. The purpose of this study was to investigate the effects of cricoid pressure, remifentanil, and propofol on lower esophageal sphincter (LES) and esophageal motility. We recorded LES pressure (LESP) and calculated barrier pressure ([BrP] = LESP − gastric pressure) in 10 healthy volunteers using a Dent sleeve device. There was a significant decrease in LESP and BrP when a cricoid pressure of 30 N was performed in the awake volunteers (P < 0.05). However, this effect was not seen during the infusion of remifentanil 0.2 &mgr;g · kg−1 · min−1. Remifentanil per se or together with a bolus dose of propofol 1 mg/kg IV did not induce any statistical change in LESP or BrP. Remifentanil abolished spontaneous esophageal motility and completely eliminated the experience of discomfort induced by cricoid pressure. In conclusion, cricoid pressure of 30 N induced a decrease of LESP and BrP in awake volunteers. These effects were not seen during the remifentanil infusion. This shows the importance of when to apply cricoid pressure during rapid-sequence induction.