We experience a 1 day old female patient with congenital esophageal atresia and tracheoeso-phageal fistula combined with a subglottic laryngeal stenosis which was 2 mm in diamete. At the time of surgery, an attempt was made to intubate, but it was impossible to pass a tube beyond the vocal cord which was mormal in size and shape. Thus a gastrostomy was performed only under mask with pure oxygen and local anesthesia. The child died one day later due to respiratory failure. Congenital subglottic laryngeal stenosis combined with esophageal atresia and tracheoeso-phageal fistula is very rare, but it is a very critical anomaly to anesthesia and resuscitation. Therefore, in the case of esophageal atresia and tracheoesophageal fistula with signs of respiratory obstruction, the possible presence of subglottic laryngeal stenosis should be considered and accurately assessed.
Anesthesia* ; Anesthesia, Local ; Child ; Esophageal Atresia* ; Female ; Fistula ; Gastrostomy ; Humans ; Laryngostenosis* ; Masks ; Oxygen ; Respiratory Insufficiency ; Resuscitation ; Tracheoesophageal Fistula* ; Vocal Cords

Background: Esmolol is rapid hydrolyzed by plasma esterase but may inhibit plasma cholinesterase activity based on its structure. This study was designed to evaluate the interactions between esmolol and succinylcholine or mivacurium which are metabolized by plasma cholinesterase and to determine the inhibitory effect of esmolol on human plasma cholinesterase. Methods: Neuromuscular effects of succinylcholine (1.0 mg/kg) and mivacurium (0.15 mg/kg) with or without esmolol (0.5 mg/kg or 1.0 mg/kg) were compared in 57 adult patients (ASA class I) during O2-N2O-isoflurane anesthesia. Neuromuscular block was monitored by recording the compound electromyogram of the hypothenar muscle resulting from supramaximal train of four stimuli applied to the ulnar nerve. Also plasma cholinesterase activity was measured before and 5, 10 minutes after injection of esmolol. Results: Time from injection to onset of over 95% block, clinical duration from injection to 25% recovery of control twitch, and recovery index defined as from 25% to 75% twitch recovery of succinylcholine or mivacurium were not altered by pretreatment of esmolol. Plasma cholinesterase activity was not decreased after injection of esmolol 0.5 mg/kg, but decreased by 5% after injection of 1.0 mg/kg (p<0.05). Conclusions: It is unlikely that neuromuscular blocking effects of succinylcholine and mivacurium are prolonged by administration of clinical doses of esmolol (0.5~1.0 mg/kg) due to inhibition of plasma cholinesterase activity in human.
Adult ; Anesthesia ; Cholinesterases ; Humans ; Neuromuscular Agents ; Neuromuscular Blockade ; Plasma ; Succinylcholine* ; Ulnar Nerve

Severe bronchospasm after injection of succinylcholine iodide intravenously occurred in a 28 year old female during emergency Cesarean section. This was confirmed by repeated administration of the succinylcholine iodide and its symptoms with several referances are reviewed.
Adult ; Bronchial Spasm* ; Cesarean Section ; Emergencies ; Female ; Humans ; Pregnancy ; Succinylcholine*

Malignant hyperthermia is a recently described syndrome with rapid progress and extreme rise in body temperature of unknown etiology and high mortality rate. A case is presented of a 16 year old healthy male patient in whom a minor orthopedic operation was performed under O2-N2O-halothane anesthesia with induction by pentothal sodium and succiny- lcholine. This was complicated by an abrupt high rise of body temperature and rigid extremities when the operation was almost completed. He died 3 hours after cessation of anesthesia without any effective response to active fever therapy. The clinical features and management of malignant hyperthernia are described and possible etiologic factors are discussed.
Adolescent ; Anesthesia ; Body Temperature ; Extremities ; Humans ; Hyperthermia, Induced ; Male ; Malignant Hyperthermia* ; Mortality ; Muscle Rigidity* ; Orthopedics ; Sodium ; Thiopental

Diethyl ether was first described by Valerius Cordus in 1540, and it is generally agreed that Crawford Long used ether for 3 surgical patients in 1842, and Morton subsequently gave a definitive public demonstration in Boston in October, 1846, After this, ether use became widely published and the news spread to London, where Drs. Boot and Squires soon used it on surgical cases at University College Hospital. The importance and volume of diethyl ether in the anesthesia field grew day by day and year by year and it is widely used by various techniques. But, during the past rlecade, the frequency of usage of diethyl ether has declined and it is now hard to find new articles on diethyl ether. The reason is that. the experience of induction is most unpleasant and stormy with secretions, vomiting and laryngospasm; also, excessive depth is often produced and in the post operative course, headache, nausen, vomiting and fluid or electrolyte disorders may follow. Another reason is the production of various new inhalation anesthetics. Today, many serious complications of new anesthetics are reported; especislly halothane may have a hepato-sensitive effect (Burnap 1958, Virtue 1958, Barton 1959, Temple 1962 and Bunker 1963) and new recent articles were published by McArdle (1968), Oyama(1969) and Markello (1969). It should also be remembered that, although its use in clinical practice in Britain and other Western parts is now almost as limited as chloroform, ether is stil1 the main inhalational anesthetic in many parts of the world, because diethyl ether is still an excellent anesthetic safer and perhaps more inexpensive than any other. Since diethyl ether has recently been produced in Korea, objectives qf he study were mainly reevaluation of the effects of diethyl ether through experimental animal studies. Nine healthy normal dogs weighing appoximately 10 kg. body weight were employed in this experiment and 4 dogs (group 1) anesthetized with Squibb ether and 5 dogs (group 2) with Korean made ether, were used for the study. Endotracheal intubation was done under light sedation with pentobarbital sodium 30mg/kg I.V. and the tube connected with a Ruben valve; Nonrebreathing system which could be applied O2, 0.3 to 0.5 L/min. through the Heidbrink Ohio Chemical Anesthesia Apparatus without any anesthetics. Cannulations were applied into the right jugular vein for C.V.P. into the femoral artery for arterial pressure, the femoral vein for fluid infusion which contained Inulin and B.S.P. (priming doses were 50 mg/kg and 5 mg/kg and maintenance d were 0. 25 mg/kg/min. and, 0.05mg/kg/min) using the Harvard infusion pump (2 ml/min.), the other femoral artery for blood sampling, both ureters for urine collection, and the common bile duct for bile collection. A Polygraph Grass Type 4 Channel Machine was connected for E.E.G., E.C.G., C.V.P. and arterial pressure. During the whole of the study, E.E.G., E.C.G., arterial pressure, C.V.P. and arterial blood sampling for PaCO2,PaO2.pH and hemoglobin, and urine collection for Inulin clearance and bile collection for B.S.P. clearence was done every 20 minutes through a 4 hours (one hour for the pre-anesthetic period, two hours for the anesthesia period, and one hour for the post-anesthetic period.). Arterial blood gas, and pH were analyzed with a Radiometer, hemoglobin by the hemophotometer, Inulin clearance by the Schreiner method and B.S.P. clearance by the Pitt aceton method. After the post-anesthetic period, tissue specimens; the heart, lung, liver and kidney, were fixed in 10% formalin and stained with hematoxylin and eosin for histopathological study. RESULTS AND SUMMARY: An E.C.G. tracing with pulse rate, arterial pressure and C.V.P. were not changed significantly during ether anesthesia in dogs. Within the first 60 minutes during ether anesthesia, PaO2 were evaluated but after that gradually declined until post-anesthetic period. PaCO2,pH and hemoglobin values did not show any remarkable change in all experiments. B.S.P. and Inulin clearances during ether anesthesia were decreased but recovered slightly in the post-anesthetic period. Histopathologically, in a few dogs, a slight alveolar edema, capillary congestion, alveolar wall thickening, mucosal degeneration, destruction of bronchioles in the lung and glomerular ischemic changes in the kidney were observed. No other pathological findings in the heart and liver were found.
Anesthesia* ; Anesthetics ; Anesthetics, Inhalation ; Animals ; Arterial Pressure ; Bile ; Body Weight ; Bronchioles ; Capillaries ; Catheterization ; Chloroform ; Common Bile Duct ; Dogs ; Edema ; Eosine Yellowish-(YS) ; Estrogens, Conjugated (USP) ; Ether* ; Femoral Artery ; Femoral Vein ; Formaldehyde ; Halothane ; Headache ; Heart ; Heart Rate ; Hematoxylin ; Humans ; Hydrogen-Ion Concentration ; Infusion Pumps ; Intubation, Intratracheal ; Inulin ; Jugular Veins ; Kidney ; Korea ; Laryngismus ; Liver ; Lung ; Ohio ; Pentobarbital ; Poaceae ; Ureter ; Urine Specimen Collection ; Virtues ; Vomiting

No abstract available.
Anesthesia* ; Hyponatremia*

Pipecuronium bromide is a new biaquaternary steroid-type neuromuscular bloeking agent that is closely similar to pancuronium and vecuronium in chemical structure. The purpose of this study was to evaluate neuromuscular and cardiovascular effects of pipecuronium bromide in patients under enflurane anesthesia in comparison with those of pan- curonium and vecuronium bromide. 35 ASA class I or II adult patients were assigned to one of the following groups; pipecuro- nium 0.08mg/kg(n=15), vecuronium 0.08mg/kg(n=10), and pancuronium 0.1 mg/kg(n=10) as a bolus dose. To investigate cumulative effect of pipecuronium, an additional incremental doses (1 mg) of pipecuronium were given repeatedly to 5 patients in pipecuronium group at every 25% recovery of first twitch height(Ti) of train-of four(TOF) stimulation after administration of in- itial dose. Anesthesia was induced with iv thiopental 5-6 mg/kg and inhalation of 0 (21/min.)-NO(41/ min.)-enflurane(2%), and maintained with O(11/min.)-NA3(21/min.)-enflurane(1-2%). All pa- tients were intubated at 5 minutes after administration of one of these muscle relaxants fol- lowing T> of TOF was depressed more than 95% of control height. Neuromuscular blocking effect was assessed by electromyographic response of hypothenar muscles in response to TOF stimulation of ulnar nerve every 20 seconds at wrist throughout study. Heart rate, systolic and diastolic blood pressures, and mean arterial pressure were noninvasively measured for 20 minutes after adminisf,ration of muscle relaxant. The results obtained were as follows, 1) The onset times from administration of vecuronium, pipecuronium, and paneuronium to 95% depression of T, were 3.4k0.88, 3.8k0.21, and 4.3+/-0.86min. respectively. The onset time of pipecuronium was similar to that of vecuronium but significantly shorter than that of pancur- onium(p<0.05). 2) The duration of action from administration of pipecuronium to 25% reeovery of T was 92.9 +/-15.3min. which was significantly shorter than that of pancuronium(115.2 +/-17.04min., p< 0.05) and longer than that of vecuronium(27.5 +/-5.89 min., p<0.05). 3) Recovery index of pipecuronium was 39.5+7.53min. which was also shorter than that of pancuronium(46.2+/-3.52 min., p < 0.05) and longer than that of vecuronium(13.3+/-1.77 min., p < 0.05). 4) Durations from 10% to 25% recovery of T1 hy additional incremental doses of pipecuronium were not altered significantly by the repeated administration. 5) There were no significant changes on heart rate and blood pressure by 0.08 mg/kg of pipecuronium or vecuronium while heart rate was increased in 21% to 27% for 20 min. after administration of pancuronium. In conclusion, pipecuronium bromide appears to be a useful alternative to pancuronium or vecuronium in relatively long duration of muscular relaxation in patients in whom hemodynamic changes, especially tachycardia, must be avoided.
Adult ; Anesthesia ; Arterial Pressure ; Blood Pressure ; Cardiovascular System ; Depression ; Enflurane ; Heart Rate ; Hemodynamics ; Humans ; Inhalation ; Muscles ; Neuromuscular Blockade ; Pancuronium ; Pipecuronium* ; Relaxation ; Tachycardia ; Thiopental ; Ulnar Nerve ; Vecuronium Bromide ; Wrist

Halothane has become very popular in recent years and is an excellent agent in obstetric anesthesia (Bosomworth, 1962; Stoelting, 1964; Wilson and Vandewater, 1965) but the uterine depressant effect of halothane has been established from reports of numerous inveatigators(Vasicka and Kretchner, 1961; Miller et al., 1966; Munsoa et aL, 1969). Ahlquist (1966) reviewed the hypothesis which he introduced to explain the differing effects of adrenergic drugs in different body sites. He defined the adrenergic receptor as an entity in or on effector cells which interacts with adrenergic agonists to elicit the response characteristic of the cell. The alpha receptor is concerned with uterine contraction, and the beta receptor mediates inhibition of the uterine musculature. It was concluded that the myometrium in both the intact and isolated uterus is fully under neuro-humoral control(Shabanah et al., 1964a). On the other hand, some investigators concluded that halothane has a direct stimulant action on the adrenergic beta receptors in bronchial wall and pulmonary vessels. (Klide and Aviado, 1967; Price et al., 1970). The present investigation was undertaken to determine whether or not halothane depresses myometrium through the adrenergic mechanism. Female albino rabbits, weighing approximately 2.0 kg were employed. A uterine strip, about 2.0 cm in length, was carefully isolated from the non-pregnant rabbits and suspended in a muscle chamber containing 100 ml of Locke's aolution, maintained at a constant temperature of 38 ℃. A mixture of 95% oxygen and 5% carbon dioxide was bubbled through the bathing fluid by means of a sintered glass plate at the bottom of the muscle chamber. The uterine segment was attached to a Grass force displacement transducer, and the motility and tonus were recorded on a Grass model 7 polygraph. After being washed several times with fresh Locke's solution for a period of 30 minutes, the uterine segment attained a constant motility and tonus. Halothane then was added by diverting the mixed gas stream through a Fluotec® Mark II Vaporizer. RESULTS: 1. When the vaporizer was set at a concentration of 2% or less, halothane produced no appreciable effects on the spontaneous motility and tonus of the normal non-pregnant uterine segment. However, at a concentration of 2.5%, the motility and tonus were markedly depreased. Further increase of the concentration of halothane up to 3% by the Fluotec® Mark II vaporizer, depressed almost completely the motility of the uterine segment. After cessation of the perfusion of halothane, the uterine segment resumed its motility and tonua to the level just prior to the addition of this anesthetic. 2. Pretreatment of the uterine strip with dichloroisoproterenol(DCT) blocked completely the uterine inhihitory activity of isoproterenol but failed to alter the inhibitory action of halothane. MJ-1999[dl 4-(2-isopropylamino-I-hydroxylethyl) methanesulfonanilide HC1] or propranolol and dibenamine also produced no effects on the uterine inhibitory action of halothane. 3. Since the responsiveness of the uterine adrenergic receptors to cateeholamines is greatly influenced by ovarian hormones, effects of halothane on adrenergic receptors were examined on uterine strips isolated from oophorectomized, estrogen-treated and progesterone-treated rabbits. Halothane produced similar inhibitory effect, quantitatively as well as qualitatively, on these uterine strips to that on the non-pregnant uterus and the effect was found to be unrelated to adrenergic receptors. 4. Acetylcholine produced an appreciable stimulating effect on the spontaneous motility and tonus of the normal non-pregnant uterine segment, and atropine blocked completely the uterine contractile activity of acetylcholine but failed to alter the inhibitory action of halothane. 5. Oxytocin and ergot alkaloid produced some effects as stimulants on the uterine inhibitory activity of halothane but barium chloride (BaCl2) was found significantly to antagonize it. SUMMARY: A high concentration of halothane (above 2.5%) produced uterine inhibitory activity in vitro and these mechanisms were not concerned with adrenergic and cholinergic receptors, or ovarian hormones. It can be concluded that halothane depress the uterine contractility by direct action on smooth muscle.
Acetylcholine ; Adrenergic Agents ; Adrenergic Agonists ; Anesthesia, Obstetrical ; Animals ; Atropine ; Barium ; Baths ; Carbon Dioxide ; Dibenzylchlorethamine ; Female ; Glass ; Halothane* ; Hand ; Humans ; In Vitro Techniques ; Isoproterenol ; Mice ; Muscle, Smooth ; Myometrium ; Nebulizers and Vaporizers ; Oxygen ; Oxytocin ; Perfusion ; Poaceae ; Propranolol ; Rabbits ; Receptors, Adrenergic ; Receptors, Adrenergic, beta ; Receptors, Cholinergic ; Research Personnel ; Rivers ; Transducers ; Uterine Contraction ; Uterus

The onset time of the non-depolarizing muscle relaxants can be shortened significantly when small dose of the same or different non-depolarizing muscle relaxant is administered prior to single sufficient dose. Likewise, the hypothesis that administration of neostigmine in divided dose accelerate the antagonism of neuromuscular blockade from "priming priciple" is not known, but under this Phenomenon the Present study was investigated the reversal effects following administration of neostigmine in divided dories compared wish single bolus dose. All patients were ASA physical status class l or ll undergoing minor surgery, free from neuromusfular, renal or hepatic diseases and not taking any drugs known to interfere with neuromuscular function. In all patients, anesthesia was induced with thiopental sodium (5 mg/kg) and endotracheal intubation preceding by vecuronium(0.08 mg/kg) and was mainteined with 50% N2O in oxygen and enflurane (1.0~2.0%) with continuous vecuronium infusion (0.06 mg/kg/hr). The EK7, heart rate, mean arterial prssure and nasopharrngeal temperature by Datascope 2100, and Train of four(T1 and T4) sequence 2 Hz every 20 second and end tidal CO2 using Datex ABM were monitored continuously. At the end of operation, continuous vecuronium infusion was discontinued but N2O and enflurane was received until all measurements were complete. When T1 had returned to 10% of control value, anticholinesterase mixture (anti-chE : neostigmfne 0.04 mg/kg) was admini-stered as following; Anti-chE was administered in a single bolus dose(control group, n=10), in an initial dose 20% of anti-chE(group l , n=10), in an initial dose 50% of anti-chE(group ll , n=7) and in an initial dose toff of anti-chIn(group lll, n=8) followed three minutes later by remaining dose for antagonism of vecuronium induced blockade respectively. The recovery of T1 twitch height was faster from 8 minutes in group l, and 5 minutes in group ll and lll after anti-chE administration, compared with control group, but group If was statistically insignificant. The recovery of T4 twitch height was faster from 9 minutes in group 1, 6 minutes in group ll and 8 minutes in group B after anti-chE administration compared with control gro-up but in group ll it was statistically ignificant. T4 recovery (TOF artio, fade) which depend upon T1 in three divided group was faster than control group. After anti-ch E administration, in all groups, heart rate was increased following decreased, and the change of mean arterial pressure within+/-6% after anti-chE administration was observed. In conclusion, the administration of anti-chE mixture(neostigmine 0.04mg/kg and and atr-opine 0.02mg/kg) in divided dose accelerated a significantly more rapid reversal of vecuron-ium infusion induced neuromusculas blockade as compared to a single administration, especially in an priming dose as 20% of anti-chE mixture.
Anesthesia ; Arterial Pressure ; Enflurane ; Heart Rate ; Humans ; Intubation, Intratracheal ; Neostigmine* ; Neuromuscular Blockade ; Neuromuscular Nondepolarizing Agents ; Oxygen ; Surgical Procedures, Minor ; Thiopental ; Vecuronium Bromide*

To compare the rate of uptake and elimination of volatile anesthetics, we administered 2% Halothane, 2% Enflurane and 2% Isoflurane respectively for one hour to 90 healthy adult patients through a semicolsed circuit with controlled ventilation to maintain normocapnea for determining the rates of uptake, and the volatile anesthetics and nitrous oxide were discontinued to determine the rates of elimination for 30 minutes. The expired(Fe=Fa) and inspired(F1) vapor concentrations of volatile anethetics were measured using an infrared analyser and F(A)/ F(1) ratios were used to determine rates of uptake, and F(A)/F(AO)(Where F(AO) is the last end-tidal concentration during uptake) ratios were used to determine rates of elimination. And to evaluate the effects of gas flow pattern on the rate of uptake and elimination, the patients were divided into three groups: Control group inhaled three volatile anesthetics respectively with 3 liter of oxygen per minute, study group 1 inhaled three volatile anesthetics respectively with 6 liter of oxygen per minute and study group 2 inhaled three volatile anesthet- ics respectively with 1 liter of oxygen and 2 liter of nitrous oxide. The results obtained were as follows: l) To compare the rate of uptake(F(A)/F(1)) of the anesthetics, the pulmonary uptake was most rapid with isoflurane followed by enflurane and halothane in accord with their respective solubilities in blood 2) With increased fresh gas flow, the rates of uptake of anesthetics more rapidly augmented, especially significantly in halothane and enflurane 3) With gas mixture of 70% N2O, the rate of uptake of anesthetics more rapidly augmented, especially significantly in isoflurane and enflurane 4) To compare the rate of elimination of anesthetics, isoflurane and enflurane eliminated more rapidly than halothane but there are no difference in that of isoflurane with enflurane in control group. But there are no difference significantly between that of halothane, enflurane and isoflurane in study group 1 and 2. 5) With increased gas flow rate, the rate of elimination decreased more rapidly in halothane, enflurane and isoflurane significantly. 6) By the elimination of anesthetics with N2O simultaneously from the lung, the rate of elimination decreased more rapidly in halothane and isoflurane significantly. In conclusion, we have shown that we can obtained more rapid induction and recovery of inhalation anesthetics with lower solubility of anesthetics. In addition, with increased fresh gas flow and use of gas mixture af nitrous oxide, induction and recovery of anesthetics will be more rapidly.
Adult ; Anesthetics* ; Anesthetics, Inhalation ; Enflurane ; Halothane ; Humans ; Isoflurane ; Lung ; Nitrous Oxide ; Oxygen ; Solubility ; Ventilation