Anesthesia and analgesia
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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
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.
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Anesthesia and analgesia · May 2004
Ultrastructural findings in human spinal pia mater in relation to subarachnoid anesthesia.
We examined ultrastructural details such as the cellular component and membrane thickness of human spinal pia mater with the aim of determining whether fenestrations are present. We hypothesized that pia mater is not a continuous membrane but, instead, that there are fenestrations across the pial cellular membrane. The lumbar dural sac from 7 fresh human cadavers was removed, and samples from lumbar spinal pia mater were studied by special staining techniques, immunohistochemistry, and transmission and scanning electron microscopy. A pial layer made by flat overlapping cells and subpial tissue was identified. We found fenestrations in samples from human spinal pia mater at the thoracic-lumbar junction, conus medullaris, and nerve root levels, but these fenestrations did not appear at the thoracic level. We speculate whether the presence of fenestrations in human spinal pia mater at the level of the lumbar spinal cord and at the nerve root levels has any influence on the transfer of local anesthetics across this membrane. ⋯ The ultrastructural anatomy of the human pia mater, such as pial cells, membrane thickness, and subpial tissue at different levels of the thoracic and lumbar spinal cord and nerve roots, was studied by special staining techniques, immunohistochemistry, and transmission and scanning electron microscopy. Fenestrations were found in samples at the thoracic-lumbar junction, conus medullaris, and nerve root levels. No fenestrations were found in samples at the thoracic level. At present, we cannot determine the significance of these findings.
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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.