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PubMed2006

Down-regulation of norepinephrine transporter function induced by chronic administration of desipramine linking to the alteration of sensitivity of local-anesthetics-induced convulsions and the counteraction by co-administration with local anesthetics.

Alterations of norepinephrine transporter (NET) function by chronic inhibition of NET in relation to sensitization to seizures induce by cocaine and local anesthetics were studied in mice. Daily administration of desipramine, an inhibitor of the NET, for 5 days decreased [(3)H]norepinephrine uptake in the P2 fractions of hippocampus but not cortex, striatum or amygdalae. Co-administration of lidocaine, bupivacaine or tricaine with desipramine reversed this effect. Daily treatment of cocaine increased [(3)H]norepinephrine uptake into the hippocampus. Daily administration of desipramine increased the incidence of appearance of lidocaine-induced convulsions and decreased that of cocaine-induced convulsions. Co-administration of lidocaine with desipramine reversed the changes of convulsive activity of lidocaine and cocaine induced by repeated administration of desipramine. These results suggest that down-regulation of hippocampal NET induced by chronic administration of desipramine may be relevant to desipramine-induced sensitization of lidocaine convulsions. Inhibition of Na(+) channels by local anesthetics may regulate desipramine-induced down-regulation of NET function. Repeated administration of cocaine induces up-regulation of hippocampal NET function. Desipramine-induced sensitization of lidocaine seizures may have a mechanism distinct from kindling resulting from repeated administration of cocaine.

Adrenergic Uptake Inhibitors↗
PubMed1998

Effects of volatile anesthetics on vagal C-fiber activities and their reflexes in anesthetized dogs.

Effects of halothane, enflurane, isoflurane, and sevoflurane on vagal capsaicin (CAPS)-sensitive C-fibers were elucidated in anesthetized dogs. The CAPS-sensitive C-fibers were significantly stimulated by all volatile anesthetics with a significantly greater response to halothane than with sevoflurane. A significant increase in respiratory frequency (fR) and a significant decrease in tidal volume (VT) were observed with halothane and isoflurane, and a significant increase in fR was observed with sevoflurane. In contrast, a significant decrease in fR was induced by enflurane. The tachypnea induced by halothane, isoflurane, and sevoflurane was significantly reduced or no longer observed after perineural CAPS-treatment or bilateral vagotomy, whereas the slowing of respiration observed with enflurane was not affected by either of these treatments. These results suggest that vagal C-fibers play an important role in the reflex tachypnea that occurs with halothane, isoflurane, and sevoflurane.

Anesthesia↗
PubMed1996

Comparative electrophysiologic and hemodynamic effects of several amide local anesthetic drugs in anesthetized dogs.

Large and equipotent doses of several local anesthetics were administered in a cardiac electrophysiologic model on closed-chest dogs. Five groups of pentobarbital-anesthetized dogs were each given intravenously 16 mg/kg lidocaine, 12 mg/kg mepivacaine, 4 mg/kg or 8 mg/kg etidocaine, and 4 mg/kg bupivacaine. Lidocaine induced bradycardia, slowing of atrioventricular node conduction (AH), and marked hemodynamic depression, represented by a decrease in mean aortic pressure (MAoP), in the peak of first derivative of left ventricular pressure (LVdP/dt(max)) and by an increase in left ventricular end-diastolic pressure (LVEDP). Atrial pacing at pacing cycle length (PCL) of 298 ms did not enhance the alteration of variables of ventricular conduction (His ventricle [HV] interval and QRS duration). Mepivacaine induced slight alteration of electrophysiologic variables. Atrial pacing at PCL of 312 ms did not enhance the alteration of HV and QRS duration. Mepivacaine induced transient hemodynamic depression. Etidocaine (4 mg/kg) induced electrophysiologic and hemodynamic alterations similar to mepivacaine but artrial pacing at PCL of 330 ms enhanced HV lengthening and QRS widening (P < 0.05). Etidocaine (8 mg/kg) induced marked impairment of PR, HV, QRS, and QT, and dramatic hemodynamic depression represented by a decrease in MAoP from 123.5 +/- 16.2 at baseline to 36.5 +/- 8.3 mm Hg at 1 min (P < 0.001) and of LVdP/dtmax) from 1446 +/- 379 to 333 +/- 93 mm Hg/s (P < 0.001). Bupivacaine induced dramatic impairment of electrophysiologic variables. Bupivacaine also decreased LVDP/dtmax (from 1333 +/- 347 to 617 +/- 299,P < 0.001) and increased LVEDP. We conclude that mepivacaine induced moderate cardiotoxicity. In contrast, lidocaine induced dramatic hemodynamic depression while etidocaine and bupivacaine markedly impaired both electrophysiologic and hemodynamic variables. This double impairment could explain the great difficulty in resuscitating patients who have had cardiotoxic accidents induced by etidocaine or bupivacaine.

Amides↗
PubMed1998

Hypoxemia decreases the shivering threshold in rabbits anesthetized with 0.2 minimum alveolar anesthetic concentration isoflurane.

UNLABELLED: Shivering has been proposed as an etiology of postoperative hypoxemia. The difficulty with this theory is that hypoxemia inhibits shivering in unanesthetized cats, rats, and humans. However, anesthesia inhibits many protective reflexes, including the ventilatory response to hypoxemia. We therefore tested the hypothesis that arterial hypoxemia fails to inhibit shivering in lightly anesthetized rabbits. Rabbits were intubated and instrumented during exposure to surgical concentrations of anesthesia, and anesthesia was then maintained with 0.2 minimum alveolar anesthetic concentration isoflurane. The core was cooled at a rate of 2-3 degrees C/h by perfusing water at 10 degrees C through a colonic thermode. Core temperatures were recorded from the distal esophagus. Sustained, vigorous shivering was considered physiologically significant. The core temperature that triggering significant shivering identified the thermoregulatory threshold for this response. Arterial blood was sampled for gas analysis at the shivering threshold in each rabbit. Hypoxemia linearly reduced the shivering threshold from 36.7 degrees C at 130 mm Hg to 35.4 degrees C at 50 mm Hg (threshold = PaO2.0.019 + 34.3; r2 = 0.49). We failed to confirm our hypothesis: instead, even mild hypoxemia reduced the shivering threshold >1 C. A 1 C decrease in the shivering threshold is likely to prevent or stop most postoperative shivering because it exceeds the reduction produced by many effective anti-shivering drugs. These data do not support the theory that shivering causes postoperative hypoxemia. IMPLICATIONS: Shivering has been proposed as an etiology of postoperative hypoxemia. Our data, in contrast, show that mild hypoxemia inhibits shivering. Shivering is thus unlikely to be a cause of postoperative hypoxemia.

Anesthesia, Inhalation↗
PubMed2000

Neuroprotective, anesthetic, and cardiovascular effects of the NMDA antagonist, CNS 5161A, in isoflurane-anesthetized lambs.

BACKGROUND: N-methyl-d-aspartate (NMDA) receptor antagonists are neuroprotective in animal models of cerebral ischemia, but adverse cardiovascular and neurobehavioral effects have precluded their clinical use. The authors present the neuroprotective, anesthetic, and cardiovascular effects of a novel NMDA antagonist, CNS 5161A. METHODS: Lambs, 4.0-6.5 kg, were anesthetized with isoflurane, intubated, and ventilated and had thermodilution catheters placed in the pulmonary artery and 20-g catheters placed in the femoral artery. The minimum alveolar concentration (MAC) of isoflurane was determined using the "bracketing technique." CNS 5161A was given as a bolus and then as an infusion at three doses. Cardiovascular measurements were determined every 15 min. Other lambs (n = 25) were subjected to cardiopulmonary bypass (CPB) with hypothermic circulatory arrest (HCA) for 120 min. Eighteen received CNS 5161A, and seven received saline vehicle. One hour after CPB, brains were perfusion-fixed and removed for in situ hybridization and immunohistochemistry analysis in half of the animals. The other half survived 48 h before their brains were examined for neuronal degeneration. RESULTS: Isoflurane at MAC significantly decreased blood pressure, heart rate, cardiac output, and systemic vascular resistance by 30-48% (n = 16; P < 0.05). CNS 5161A (n = 12) had no significant cardiovascular effects. All concentrations of CNS 5161A caused a significant reduction (21-29%) of the MAC of isoflurane (n = 12; P < 0.05). CNS 5161A, at serum concentrations greater than 25 ng/ml, completely inhibited c-fosmRNA and c-FOS protein expression in hippocampal neurons after 120 min of HCA, attenuated neuronal degeneration, and improved functional outcome by 47% (P < 0.05). CONCLUSIONS: CNS 5161A at neuroprotective concentrations before CPB-HCA significantly reduces the MAC of isoflurane without cardiovascular effects.

Anesthesia, Inhalation↗
PubMed1994

Structure-selective anesthetic action of steroids: anesthetic potency and effects on lipid and protein.

Alphaxalone was a clinically used steroid anesthetic. Its analog delta 16-alphaxalone is nonanesthetic. The only difference between the two is the presence of a double bond at the hydrophobic end of the delta 16-alphaxalone molecule. This study determined the anesthetic potency of alphaxalone and delta 16-alphaxalone in goldfish and compared it with their effects on dipalmitoylphosphatidylcholine (DPPC) membranes and an alpha-helix polypeptide, poly(L-lysine). The goldfish EC50 values were: alphaxalone 5 mumol/L and delta 16-alphaxalone 80 mumol/L. Because these steroids are insoluble to water, the bulk of the steroid in water is absorbed by the fish. Larger containers hold more steroids than smaller containers at the same steroid concentrations. Then, EC50 values vary according to the size of the container. By assuming that the total amount of steroids in the container is distributed into the fish, the EC50 values expressed by the concentration in the fish body become 1.9 mmol/L for alphaxalone, and 30.5 mmol/L for delta 16-alphaxalone. A monoamino acid peptide, poly(L-lysine), can be formed into random-coil, alpha-helix, or beta-sheet. Addition of 0.07 mmol/L alphaxalone to the alpha-helix poly(L-lysine) partially transformed it to a beta-sheet structure. An equivalent change was observed with 3.0 mmol/L delta 16-alphaxalone. These values translate into 3.5 mmol/L for alphaxalone and 0.15 mol/L for delta 16-alphaxalone, when expressed by the concentration in the peptide. The change from alpha-helix to beta-sheet is accompanied by dehydration of the surface of poly(L-lysine). The steroids decreased the phase-transition temperature of DPPC membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

1,2-Dipalmitoylphosphatidylcholine↗
PubMed2003

Inhaled anesthetics and immobility: mechanisms, mysteries, and minimum alveolar anesthetic concentration.

Studies using molecular modeling, genetic engineering, neurophysiology/pharmacology, and whole animals have advanced our understanding of where and how inhaled anesthetics act to produce immobility (minimum alveolar anesthetic concentration; MAC) by actions on the spinal cord. Numerous ligand- and voltage-gated channels might plausibly mediate MAC, and specific amino acid sites in certain receptors present likely candidates for mediation. However, in vivo studies to date suggest that several channels or receptors may not be mediators (e.g., gamma-aminobutyric acid A, acetylcholine, potassium, 5-hydroxytryptamine-3, opioids, and alpha(2)-adrenergic), whereas other receptors/channels (e.g., glycine, N-methyl-D-aspartate, and sodium) remain credible candidates.

Anesthetics, Inhalation↗
PubMed2004

Intraoperative wake-up test and postoperative emergence in patients undergoing spinal surgery: a comparison of intravenous and inhaled anesthetic techniques using short-acting anesthetics.

Surgical procedures on the vertebral column may result in spinal cord damage, leading to neurological deficits that demand immediate therapeutical intervention. We designed this study to determine which anesthetic regimen allows a rapid wake-up test during and after surgery to detect neurological deficits. Fifty-four patients were randomly allocated to the following groups: group PR (propofol/remifentanil): target-controlled infusion with propofol (plasma concentration, 2-4 microg/mL) and remifentanil 0.2-0.5 microg . kg(-1) . min(-1); group PS (propofol/sufentanil): propofol (2-4 microg/mL) and repetitive boluses of 0.1-0.2 microg/kg of sufentanil adjusted to patients requirements; and group DR (desflurane/remifentanil): desflurane/air 3.0-4.0 vol% combined with remifentanil 0.2-0.5 microg . kg(-1) . min(-1). Group PS required significantly longer times for the onset of breathing (8.9 +/- 1.6 min), elevation of the head (17.0 +/- 3.8 min), and motion of the feet (17.0 +/- 7.4 min) than group PR (6.9 +/- 2.6 min, 9.3 +/- 2.2 min, and 9.4 +/- 2.4 min, respectively) or group DR (5.4 +/- 0.8 min, 6.1 +/- 1.0 min, and 6.2 +/- 1.0 min, respectively). The anesthetic regimen with desflurane and remifentanil allowed faster awakening during and after surgery that permitted immediate neurological examination after spinal surgery compared with propofol/remifentanil.

Aged↗
PubMed2003

Use of the bispectral index as a monitor of anesthetic depth in cats anesthetized with isoflurane.

OBJECTIVE: To determine whether the prestimulation bispectral index (BIS) value or relative change in BIS after noxious stimulation can be used to assess the depth of isoflurane anesthesia in cats. ANIMALS: 17 healthy female cats. PROCEDURE: Electroencephalogram (EEG) patterns and BIS values were examined in cats that received increasing end-tidal (ET) isoflurane concentrations. Subsequently, BIS values were determined before and after either a noxious somatic or visceral stimulus in cats that received ET isoflurane concentrations ranging from 1.8% to 2.4%. Electrical stimuli of the tail base and bladder distension to 50 cm of water were the somatic and visceral stimuli, respectively. RESULTS: The resting BIS at ET isoflurane concentrations from 1.4% to 1.9% steadily decreased concurrently with increasing degrees of EEG suppression. Prestimulation BIS values, however, were not related to 1.8% to 2.4% ET isoflurane concentrations and not useful for prediction of BIS values or hemodynamic and movement responses after a noxious stimulus. The poststimulation BIS value and the difference between mean BIS values before and after stimulation were inversely correlated with increasing ET isoflurane concentrations. Poststimulation BIS values > 60 were observed at ET isoflurane concentrations greater than those associated with a movement response after a stimulus. CONCLUSIONS AND CLINICAL RELEVANCE: The prestimulation BIS value has limited use in assessing anesthetic depth in cats during isoflurane anesthesia. The change in BIS values after a noxious somatic or visceral stimulus was a reliable measure of anesthetic depth and may be a useful measure of early arousal from the hypnotic state.

Analysis of Variance↗
PubMed1976

Study of local anesthetics. Part 46: Correlations between anesthetic activity and physico-chemical parameters of some alkoxy substituted esters of phenylcarbamic acids.

The partition in water-octanol and water-carbon tetrachloride systems and electronic spectra of three series of esters of phenylcarbamic acid and its m- and p-alkoxy derivatives were measured. The surface local anesthetic activity of these compounds as well as the infiltration anesthetic activity of some of them were correlated with combinations of partition coefficients, spectral parameters and sigma-coefficients.

Anesthetics, Local↗
PubMedDate not supplied

[Search for agents with prolonged anesthetizing action (the neurolytic type of local anesthetizing action)].

Compounds that possess long-term anesthetic effect have been found among phenylethylamine derivatives substituted by O-alkyl (position 4) or O-benzyl (positions 2, 3 and 4) radicals. It was shown that these compounds compare very favourably with novocain, since their anesthetic effect exceeds 54.8 - 66.9-fold that produced by novocain. Such an effect is a consequence of neurolytic properties of the compounds synthesized.

Anesthetics, Local↗
PubMed1996

Comparison of topical anesthetics without cocaine to tetracaine-adrenaline-cocaine and lidocaine infiltration during repair of lacerations: bupivacaine-norepinephrine is an effective new topical anesthetic agent.

OBJECTIVE: To compare the effectiveness of four topical anesthetics that do not contain cocaine with that of topical tetracaine-addrenaline-cocaine (TAC) and lidocaine infiltration during laceration repair in children. DESIGN: This was a randomized, blinded trial. SETTING: The study was conducted in the emergency department of a large children's hospital. PARTICIPANTS: Subjects were children 2 years of age or older with a laceration 5 cm or less in length that required sururing. INTERVENTIONS: Patients were randomly assigned to receive one of four noncocaine-containing topical anesthetics, topical TAC, or lidocaine infiltration anesthesia before laceration repair. OUTCOME MEASURES: Outcome measures assessed pain perceptions using a Visual Analogue Scale, Likert scale, and Anethetic Effectiveness scale. Distress behaviors of patients were measured with the Restrained Infants and Children Distress Rating Scale. RESULTS: Two hundred forty patients were enrolled in the study. Using alpha = 0.05 and beta = 0.2, there was statistical power to detect differences of 0.3 to 1.3 U for the outcome measures used. The bupivacaine-norepinephrine topical solution (Bupivanor) performed better than the other three new topical preparations. It provided effective wound anesthesia during lacertion repair, especially for lacerations of the face and scalp, where it was consistently rated as effective as TAC and 1% lidocaine infiltration by all observer groups for all outcome measures. There was a 4% overall wound complication, including one wound infection. CONCLUSION: Bupivanor is an effective alternative to TAC and lidocaine infiltration for local anesthesia during laceration repair, expecially on the face and scalp. The effectiveness of Bupivanor on the face is important, because it is here where TAC is most likely inadvertently to come into contact with mucous membranes and result in systemic toxicity. Because pain and distress scores did not take into consideration the pain associated with the initial injection of lidocaine, the findings of this study conservatively estimate Bupivanor's effectiveness, compared with lidocaine infiltration.

Administration, Cutaneous↗
PubMed1991

The effects of age and anesthetic solubility on anesthetic-induced opisthotonus in mice.

In our previous report which indicated volatile anesthetics-induced opisthotonus in mice, we hypothesized that opisthotonus might relate with the rapidity of anesthetic induction, i.e., the blood/gas partition coefficient of the agent. To confirm this, we determined the incidence of opisthotonus induced by four different halogenated ethers (2.0% sevoflurane, 1.3% isoflurane, 2.0% enflurane, and 0.5% methoxyflurane) and 1.0% halothane, a haloalkane, in male ddN mice. The effect of age on opisthotonus was also evaluated by using young (10 +/- 2 weeks), middle-aged (6 +/- 1 mouths), and elderly (12 +/- 1 months) groups of male ddN mice. In each age group, the incidence of opisthotonus occurred in the following order: sevoflurane > isoflurane > enflurane > methoxyflurane > halothane. This partly supports our hypothesis as far as halogenated ethers are concerned. Halothane rarely produced opisthotonus. In the sevoflurane, isoflurane, and methoxyflurane groups, incidence was lower in middle-aged than in young or elderly mice, while incidence increased with age in the enflurane group.

Journal Article↗
PubMed1991

Pulmonary vasoregulation by cyclooxygenase metabolites and angiotensin II after hypoperfusion in conscious, pentobarbital-anesthetized, and halothane-anesthetized dogs.

The authors investigated the extent to which endogenously produced metabolities of the cyclooxygenase pathway and angiotensin II modulate the pulmonary vascular response to increasing pulmonary blood flow after a period of systemic and pulmonary hypotension and hypoperfusion (defined as posthypoperfusion) in conscious, pentobarbital-anesthetized, and halothane-anesthetized dogs. The authors tested the hypothesis that vasodilator metabolites of the cyclooxygenase pathway offset the vasoconstrictor influence of angiotensin II to prevent pulmonary vasoconstriction posthypoperfusion. Baseline and posthypoperfusion pulmonary vascular pressure-cardiac index (P/Q) plots were constructed by stepwise inflation and deflation, respectively, of a hydraulic occluder implanted around the inferior vena cava to vary Q. In intact (no drug), conscious dogs, the pulmonary vascular P/Q relationship posthypoperfusion was not altered significantly compared with baseline. In contrast, after cyclooxygenase inhibition, active flow-independent pulmonary vasoconstriction (12-17%; P less than 0.01) was observed posthypoperfusion, and this response was abolished entirely by angiotensin converting-enzyme inhibition. During pentobarbital anesthesia, significant pulmonary vasoconstriction (27%; P less than 0.01) occurred posthypoperfusion in the no-drug condition. However, the magnitude of the posthypoperfusion vasoconstriction was not increased by cyclooxygenase inhibition, nor was it reduced by converting-enzyme inhibition. During halothane anesthesia, pulmonary vasoconstriction was not observed posthypoperfusion in the no-drug condition, but it was unmasked (8-13%; P less than 0.05) by cyclooxygenase inhibition and attenuated partially by converting-enzyme inhibition. These results indicate that cyclooxygenase metabolites and angiotensin II exert opposing vasodilator and vasoconstrictor effects, respectively, on the pulmonary circulation of conscious dogs posthypoperfusion. These competing mechanisms are active during halothane anesthesia but are abolished during pentobarbital anesthesia.

Anesthesia↗
PubMed1994

Pulmonary vasoregulation by arginine vasopressin in conscious, halothane-anesthetized, and pentobarbital-anesthetized dogs with increased vasomotor tone.

BACKGROUND: Arginine vasopressin (AVP) is an important "stress" hormone that is known to play a key role in cardiovascular homeostasis of the systemic circulation. In contrast, the effects of AVP on the pulmonary circulation have not been extensively investigated, and the extent to which general anesthesia alters the pulmonary vascular response to AVP is entirely unknown. Our first objective was to assess the effects of AVP on the pulmonary vascular pressure-flow relation in chronically instrumented conscious dogs in the setting of an acute elevation in pulmonary vasomotor tone. Our second objective was to investigate the effects of halothane and pentobarbital anesthesia on the pulmonary vascular response to AVP after inducing the same degree of pulmonary preconstriction achieved in the conscious state. METHODS: Conditioned, mongrel dogs were chronically instrumented to measure the left pulmonary vascular pressure-flow (LPQ) relation. LPQ plots were generated by continuously measuring the pulmonary vascular pressure gradient (pulmonary arterial pressure minus left atrial pressure) and left pulmonary blood flow during gradual (approximately 1 min) inflation of a hydraulic occluder around the right pulmonary artery, which directed total pulmonary blood flow through the left pulmonary circulation. LPQ plots were generated in conscious (n = 10), halothane-anesthetized (n = 9) and pentobarbital-anesthetized (n = 7) dogs. In each condition, LPQ plots were measured at baseline, during the intravenous administration of the thromboxane analog U46619 and during the cumulative administration of AVP (2-19 ng.kg-1.min-1, intravenous) in the presence of U46619 preconstriction. RESULTS: U46619 caused acute pulmonary vasoconstriction (P < 0.01) in conscious dogs. In this setting of U46619 preconstriction, AVP caused pulmonary vasodilation (P < 0.05) in the conscious state. In contrast, despite identical levels of U46619 preconstriction, the pulmonary vasodilator response to AVP was either reversed to vasoconstriction (P < 0.05) or abolished during halothane and pentobarbital anesthesia. CONCLUSIONS: These results indicate that AVP exerts a significant pulmonary vasodilator response in the setting of acute pulmonary vasoconstriction in conscious dogs. However, the pulmonary vascular response to this stress hormone is markedly altered during halothane and pentobarbital anesthesia.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1976

Cardiovascular effects of different anesthetics in man. Study of two volatile anesthetics: enflurane (ethrane), halothane (fluothane).

In the first part of this paper we report the effects of 4 short acting intravenous anesthetics (althesin, etomidate, epontol, brietal) on the cardiovascular effects due to ethrane. In the second part we learn with the same induction anesthetic (etomidate) the cardiovascular effects of ethrane and fluothane. We have proved that: 1 degree althesin least potentiates the variations in the cardiovascular parameters under the action of ethrane, 2 degrees halothane 2% decreases more the blood pressure than ethrane 1%.

Adolescent↗
PubMed2005

The Thai Anesthesia Incidents Study (THAI Study) of anesthetic outcomes: II. Anesthetic profiles and adverse events.

BACKGROUND AND RATIONALE: The purposes of the Thai Anesthesia Incidents Study (THAI Study) of anesthetic outcomes were to survey patients, surgical, anesthetic profiles and determine factors related to adverse events. MATERIAL AND METHOD: A prospective descriptive study of occurrence screening was conducted in 20 hospitals comprised of 7 university, 4 general and 4 district hospitals across Thailand. Anesthesia personnel were required to fill up patient-related, surgical-related, anesthesia-related variables and adverse outcomes on a structured data entry form. The data were collected during the preanesthetic evaluation, intraoperative period and 24 hr postoperative period. Adverse events specific forms were used to record when they occurred. All data were keyed at data management unit with double entry technique and descriptive statistics was used in the first phase of this study. RESULTS: A total of 163403 consecutive cases were recorded during first 12 months. MD. anesthesiologists involved with 82%, 89%, 45% and 0.2% of cases in university hospitals, regional hospitals, general hospitals and district hospitals respectively. Nurse anesthetists took a major involvement in hospitals run by the Ministry of Public Health. Two-thirds of cases did not receive any premedication (67%) and midazolam was most frequent premedication administered (20%). Common monitoring were non invasive blood pressure (NIBP) (97%), pulse oximetry (96%), electrocardiography (80%), urine output (33%), airway pressure (27%) and capnometry (19%) respectively. The choices of anesthesia were general anesthesia (62%), spinal anesthesia (23%), total intravenous anesthesia (6%), monitor anesthesia care (4%), brachial plexus block (3%) and epidural anesthesia (1%). The adverse events were oxygen desaturation (31.9:10000), cardiac arrest (30.8:10000), death within 24 hr. (28.3:10000), difficult intubation (22.5:10000),re-intubation (19.4:10000), unplanned ICU admission (7.2:10000), coma/cva/convulsion (4.8:10000), equipment malfunction/failure (3.4:10000), suspected myocardial ischemia or infarction (2.7:10000), awareness during anesthesia (3.8:10000), late detected esophageal intubation (4.1:10000), failed intubation (3.1:10000), anaphylaxis or anaphylactoid reaction (2.1:10000), nerve injury (2:10000), pulmonary aspiration (2.7:10000), drug error (1.3:10000), hazard to anesthesia personnel (1.5:10000), unplanned hospital admission (0.1:10000), total spinal block (1.3:10000) and mismatch blood transfusion (0.18:10000) CONCLUSION: Respiratory adverse events were common anesthesia direct related events. High incidence of cardiac arrest and death within 24 hr highlighted concerns for prevention strategies. Incidents of adverse events can be used for institutional quality improvement, educational quality assurance and further research for patient safety in anesthesia.

Adolescent↗