Anesthesia and analgesia
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Anesthesia and analgesia · May 2004
Trends in the practice of parental presence during induction of anesthesia and the use of preoperative sedative premedication in the United States, 1995-2002: results of a follow-up national survey.
Both parental presence during induction of anesthesia and sedative premedication are currently used to treat preoperative anxiety in children. A survey study conducted in 1995 demonstrated that most children are taken into the operating room without the benefit of either of these two interventions. In 2002 we conducted a follow-up survey study. Five thousand questionnaires were mailed to randomly selected physician members of the American Society of Anesthesiologists. Mailings were followed by a nonresponse bias assessment. Twenty-seven percent (n = 1362) returned the questionnaire after 3 mailings. We found that a significantly larger proportion of young children undergoing surgery in the United States were reported to receive sedative premedication in 2002 as compared with 1995 (50% vs 30%, P = 0.001). We also found that in 2002 there was significantly less geographical variability in the use of sedative premedication as compared with the 1995 survey (F = 8.31, P = 0.006). Similarly, we found that in 2002 parents of children undergoing surgery in the United States were allowed to be present more often during induction of anesthesia as compared with 1995 (chi(2) = 26.3, P = 0.0001). Finally, similar to our findings in the 1995 survey, midazolam was uniformly selected most often to premedicate patients before surgery. ⋯ Over the past 7 yr there have been significant increases in the number of anesthesiologists who use preoperative sedative premedication and parental presence for children undergoing surgery.
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Anesthesia and analgesia · May 2004
Case ReportsWater intoxication and symptomatic hyponatremia after outpatient surgery.
Severe hyponatremia is associated with a mortality rate of more than 50%, primarily from cerebral edema and central nervous system dysfunction. Water intoxication is an unusual but potentially lethal cause of perioperative hyponatremia. We report a patient with severe postoperative hyponatremia resulting from excessive perioperative water consumption. Anesthesiologists should maintain an index of suspicion for hyponatremia from water intoxication in patients with neurologic symptoms during the perioperative period. Routine preoperative instructions regarding maximum perioperative water intake and inquiry into any concurrent alternative medical therapies may help to avoid this preventable complication. ⋯ Water intoxication is an unusual but potentially lethal cause of perioperative hyponatremia. We report a patient with severe postoperative hyponatremia resulting from excess perioperative water consumption.
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Anesthesia and analgesia · May 2004
The effects of isoflurane on desensitized wild-type and alpha 1(S270H) gamma-aminobutyric acid type A receptors.
gamma-aminobutyric acid type A receptors (GABA(A)-R) mediate synaptic inhibition and meet many pharmacological criteria required of important general anesthetic targets. During synaptic transmission GABA release is sufficient to saturate, maximally activate, and transiently desensitize postsynaptic GABA(A)-Rs. The resulting inhibitory postsynaptic currents (IPSCs) are prolonged by volatile anesthetics like isoflurane. We investigated the effects of isoflurane on maximally activated and desensitized GABA(A)-R currents expressed in Xenopus oocytes. Wild-type alpha(1)beta(2) and alpha(1)beta(2)gamma(2s) receptors were exposed to 600 microM GABA until currents reached a steady-state desensitized level. At clinical concentrations (0.02-0.3 mM), isoflurane produced a dose-dependent enhancement of steady-state desensitized current in alpha(1)beta(2) receptors, an effect that was less apparent in receptors including a gamma(2s)-subunit. When serine at position 270 is mutated to histidine (alpha(1)(S270H)) in the second transmembrane segment of the alpha(1)-subunit, the currents evoked by sub-saturating concentrations of GABA became less sensitive to isoflurane enhancement. In addition, isoflurane enhancements of desensitized currents were greatly attenuated by this mutation and were undetectable in alpha(1)(S270H)beta(2)gamma(2s) receptors. In conclusion, isoflurane enhancement of GABA(A)-R currents evoked by saturating concentrations of agonist is subunit-dependent. The effects of isoflurane on desensitized receptors may be partly responsible for the prolongation of IPSCs during anesthesia. ⋯ Isoflurane enhances desensitized gamma-aminobutyric acid type A receptor (GABA(A)-R) currents, an effect that is subunit-dependent and attenuated by a mutation in an alpha(1)-subunit pore residue of the GABA(A)-R. As GABA release at inhibitory synapses is typically saturating, isoflurane modulation of desensitized receptors may be partly responsible for prolongation of inhibitory postsynaptic currents during anesthesia.
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Anesthesia and analgesia · May 2004
Case ReportsFailed obstetric tracheal intubation and postoperative respiratory support with the ProSeal laryngeal mask airway.
The ProSeal laryngeal mask airway (ProSeal LMA) provides a better seal and probably better airway protection than the classic laryngeal mask airway (classic LMA). We report the use of the ProSeal LMA in a 26-yr-old female with HELLP syndrome for failed obstetric intubation and postoperative respiratory support. Both laryngoscope-guided tracheal intubation and face mask ventilation failed, but a size 4 ProSeal LMA was easily inserted and high tidal volumes obtained. A gastric tube was inserted through the ProSeal LMA drain tube and 300 mL of clear fluid was removed from the stomach. There were no hemodynamic changes during ProSeal LMA insertion. Postoperatively, the patient was transferred to the intensive care unit, where she was ventilated via the ProSeal LMA for 8 h until the platelet count had increased and she was hemodynamically stable. Weaning and ProSeal LMA removal were uneventful. There is anecdotal evidence supporting the use of the LMA devices for failed obstetric intubation (19 cases) and for postoperative respiratory support (8 cases). In principle, the ProSeal LMA may offer some advantages over the classic LMA in both these situations. ⋯ We report the successful use of the ProSeal laryngeal mask airway for failed obstetric intubation and postoperative respiratory support in a patient with HELLP syndrome.
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Anesthesia and analgesia · May 2004
Intratracheal application of recombinant surfactant protein-C surfactant to rabbits attenuates acute lung injury induced by intratracheal acidified infant formula.
Our aim in the current study was to determine whether recombinant surfactant protein-C (rSP-C) surfactant improves acute lung injury (ALI) induced by intratracheal acidified milk products. Twenty-eight rabbits were randomly divided into four groups. ALI was induced with intratracheal acidified infant formula (0.8 mL/kg, pH 1.8) in 3 groups. The control group received intratracheal acidified saline. Therapy groups received 1 of 2 doses of intratracheal rSP-C surfactant (0.5 or 2 SP-C mg/kg) 30 min after the acidified infant formula. The lungs were ventilated with 100% oxygen for 4 h after induction of ALI. Acidified infant formula dramatically reduced oxygenation and lung compliance, and increased resistance. Both doses of rSP-C improved the variables [mean PaO(2) (mm Hg) and compliance (mL/cm H(2)O) at 4 h: 61 and 0.4 for infant formula, 162 and 1.0 for small-dose rSP-C, and 152 and 1.2 for large-dose rSP-C, respectively; P < 0.05]. Pulmonary leukosequestration and edema, and severe morphological changes were attenuated by rSP-C treatment (ALI score: 14, 7, 7 in infant formula, small-dose rSP-C, and large-dose rSP-C; P < 0.05). The efficacy was similar for the two doses of rSP-C. These findings suggest that intratracheal administration of rSP-C ameliorates ALI induced by aspiration of acidified milk products. ⋯ Small or large doses of recombinant surfactant protein-C surfactant given 30 min after intratracheal acidified infant formula attenuated physiological, biochemical, and morphological lung damage.