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We studied the effect of rapid sequence induction of anaesthesia on intraocular pressure in physically fit, ASA class I or II patients using combinations of sufentanil (1 microgram/kg), or fentanyl (5 micrograms/kg) and vecuronium (0.2 mg/kg) or atracurium (1.0 mg/kg). All patients received thiopentone (5 mg/kg), following which those in group 1 received sufentanil and vecuronium, group 2 sufentanil and atracurium, group 3 fentanyl and vecuronium, and group 4 fentanyl and atracurium. Laryngoscopy and intubation were performed 60 seconds after induction. Intraocular pressure was measured prior to induction, 30 and 60 seconds after induction, immediately after intubation, and postintubation for 5 minutes. Postinduction and postintubation intraocular pressure values in all four groups did not exceed baseline values. We conclude that in fit patients, the combination of thiopentone, moderate dose narcotics, and an appropriate dose of vecuronium or atracurium produces satisfactory conditions for intubation following rapid sequence induction without increases in intraocular pressure. This technique should not, however, be employed when multiple other injuries are present, along with an open eye.

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Patients given combinations of non-depolarizing neuromuscular blocking drugs have been reported to recover from neuromuscular block more rapidly than patients given a single drug. This study was designed to assess if this phenomenon occurred with the combination of atracurium and vecuronium. During nitrous oxide-fentanyl anaesthesia, 30 adult patients were allocated randomly to receive atracurium 0.5 mg kg-1, vecuronium 0.1 mg kg-1, or a combination of atracurium 0.125 mg kg-1 + vecuronium 0.025 mg kg-1. All patients had 100% neuromuscular block, and times to block onset did not differ significantly between the three groups. Recovery to 10, 25, 50 and 90% of control twitch height was significantly faster in the group receiving the combination of drugs.

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In order to determine whether a small, "defasciculating" dose of metocurine could prevent increases in intracranial pressure (ICP) induced by succinylcholine (Sch), the authors studied 12 patients (ages 25-79 yr) undergoing craniotomy for excision of malignant supratentorial gliomas. After insertion of a subarachnoid bolt for ICP monitoring and a radial arterial cannula for determination of blood pressure and blood gas tensions, six patients (group I) were randomly allocated to receive MTC 0.03 mg/kg 3 min before induction of general anesthesia with thiopental 4 mg/kg and nitrous oxide 70% in O2. Six other patients (group II) received saline 0.015 ml/kg instead of MTC, followed by the same induction sequence. After induction of anesthesia, ventilation was controlled by mask (PaCO2 = 40 mmHg +/- 2 SE), and arterial and intracranial pressures were allowed to stabilize. Four minutes after thiopental administration (7 min after MTC), after a 1-min period of relatively stable arterial pressure and ICP, Sch 1 mg/kg was administered as a bolus. ICP and blood pressure were recorded continuously until normal twitch tension was restored. In group I (MTC pretreatment), ICP did not change significantly from the mean value observed before Sch, 14 mmHg +/- 2 SE. In group II (saline pretreatment), ICP increased from 11 mmHg +/- 2 SE to 23 mmHg +/- 4 SE (P less than .05). This study not only confirms previous work showing that Sch may induce marked ICP increases in lightly anesthetized patients with intracranial mass lesions, but also indicates that pretreatment with a "defasciculating" dose of MTC can prevent these potentially deleterious ICP increases in patients known to be at risk.

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We studied 60 nonophthalmologic patients, allocated to six treatment groups, to assess the effects of atracurium and vecuronium on intraocular pressure (IOP). All patients had IOP measured while awake, using pneumotonometry. In group 1, anesthesia was induced with thiopental, 5 mg/kg, and maintained with N2O, 70% in O2, using controlled mask ventilation, for 5 min. These patients then received atracurium, 0.5 mg/kg. After 5 additional minutes of ventilation, the trachea was intubated. From 1 min after thiopental administration until 1 min after intubation, IOP was recorded every minute. Patients in groups 2, 3, and 4 were treated identically to those in group 1, except the muscle relaxant given was atracurium, 1.0 mg/kg, vecuronium, 0.1 mg/kg, or vecuronium, 0.2 mg/kg, respectively. Patients in groups 5 and 6 underwent rapid sequence induction with thiopental, 5 mg/kg, and atracurium, 1.0 mg/kg, or vecuronium, 0.2 mg/kg, respectively. IOP was measured 1 min later, followed by intubation and IOP measurements for the next 3 min. Intraocular pressure decreased significantly in groups 1, 2, 4, and 6 after thiopental and remained stable in all groups during ventilation with N2O. Neither atracurium nor vecuronium affected IOP, nor was there any correlation between IOP and degree of neuromuscular blockade. However, IOP increased significantly after intubation in all six groups. We conclude that atracurium or vecuronium alone has no adverse effects on IOP.

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Whether succinylcholine causes an increase in intracranial pressure (ICP) in patients with brain lesions is uncertain and, if increased ICP does occur, its pathophysiology remains unknown. The authors investigated both the effect of succinylcholine on ICP and its modification with prior neuromuscular blockade by measuring ICP (subarachnoid bolt) in 13 consecutive patients with brain tumors who received succinylcholine both before and after complete neuromuscular blockade with vecuronium. Anesthesia was induced with thiopental, 6 mg X kg-1 iv, and nitrous oxide, 70% in oxygen, while ventilation was controlled (PaCO2 = 37.2 mmHg +/- 1.7 SE). Succinylcholine, 1 mg X kg-1 iv, was administered and ICP, heart rate (HR), and blood pressure (BP) were recorded until normal twitch tension was restored. Complete neuromuscular blockade was then established with vecuronium, 0.14 mg X kg-1 iv; 3 min later, succinylcholine, 1 mg X kg-1 iv, was repeated. The resulting changes in ICP, HR, and BP were recorded for 3 min. Following the first dose of succinylcholine, mean ICP increased from 15.2 mmHg +/- 1.3 SE to 20.1 mmHg +/- 2.0 SE (P less than 0.05), with five of the patients sustaining increases in ICP of 9 mmHg or greater. In contrast, when succinylcholine was given after vecuronium-induced paralysis, no patient developed an increase in ICP greater than 3 mmHg (P less than 0.05 compared with the incidence of ICP greater than or equal to 9 mmHg observed after the first dose of succinylcholine). A second group of six patients received two doses of succinylcholine according to the same protocol but without an intervening dose of vecuronium.(ABSTRACT TRUNCATED AT 250 WORDS)

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Endotracheal tube "leak" is often estimated in children to judge the fit of uncuffed endotracheal tubes within the trachea. Twenty-five swine were intubated with uncuffed tracheal tubes to determine whether a more sensitive measurement of leaks could be devised and whether leak pressure estimates fit between tracheal tube and trachea. We compared leak pressure measurement using a stethoscope and aneroid manometer with a technique using a microphone, pressure transducer, and recorder, and found no differences between the two methods. The tracheas were then removed and slides prepared of tracheal cross-sectional specimens. Regression analysis revealed a linear relationship between tracheal lumen size and tracheal tube size for both low leak pressure (y = -0.4 + 0.79x, r = 0.88, P less than 0.05) and high leak pressure (y = -2.9 + 0.71x, r = 0.92, P less than 0.05) groups. We conclude that leak testing with a stethoscope and aneroid manometer is sensitive and accurate, and that tracheal tube leak pressure accurately portrays fit between tube and trachea.

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Serum potassium levels were measured in 15 patients with brain tumours between 3-7 cm diameter, during thiopentone/70 per cent N2O in O2 anaesthesia, with mask ventilation controlled to maintain a constant end-tidal CO2 concentration. Potassium levels were determined one minute before and one and ten minutes after administration of succinylcholine 1.0 mg X kg-1 IV. No statistically significant increase in serum potassium occurred following succinylcholine, nor were there any ECG changes associated with succinylcholine administration. Use of succinylcholine in patients with brain tumours does not appear to cause elevation of serum potassium levels or ECG changes.

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In spite of the increasing use of intravenous lidocaine in the operating room, no pharmacokinetic data exist for intravenous lidocaine in children. We studied ten children, ages 0.5-3 yr, and eight adults to determine lidocaine pharmacokinetics during anesthesia with halothane, nitrous oxide, and oxygen. After induction of anesthesia, tracheal intubation, and insertion of venous and arterial catheters, lidocaine, 1 mg/kg, was infused intravenously over 30 sec. Arterial samples were drawn at 0.5, 1, 2, 4, 5, 10, 15, 30, 60, 90, and 120 min. Plasma was separated and analyzed for lidocaine, using gas chromatography. Plasma concentration vs time data were fitted to a two-compartment model. Using standard formulas, we derived the following data: Children: distribution half-life (t 1/2 alpha) 3.2 min, elimination half-life (t 1/2 beta) 58 min, volume of the central compartment (V1) 0.22 L/kg, volume of distribution (Vd area) 1.1 L/kg, and total plasma clearance (Cl) 11.1 ml X kg-1 X min-1. Adults: t 1/2 alpha 3.6 min, t 1/2 beta 43 min, V1 0.16 L/kg, Vd area 0.71 L/kg, and Cl 9.8 ml X kg-1 X min-1. No significant differences were found between children and adults for all parameters analyzed. We conclude that children older than 6 months of age distribute and eliminate intravenous lidocaine in the same manner as adults.

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A two years, ten months old male with dermatomyositis was anaesthetized with enflurane, nitrous oxide and oxygen by mask followed by intravenous succinylcholine to facilitate endotracheal intubation. The evoked thumb twitch in response to succinylcholine demonstrated an abnormal, short-lived contracture. The depression, duration and return to control of muscle twitch tension and a transient rise in serum potassium concentration followed a normal pattern.

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In order to investigate the usefulness of atracurium for neurosurgical anesthesia, we studied its impact on intracranial pressure (subarachnoid bolt) mean arterial pressure (radial artery catheter) and cerebral perfusion pressure (mean arterial pressure-intracranial pressure) in 20 patients undergoing elective craniotomy for brain tumor excision. General anesthesia was induced with thiopental, 4 mg/kg intravenously, and maintained with 70 percent nitrous oxide in oxygen. Ventilation was controlled by face mask, with end-tidal CO2 held constant. Once intracranial pressure and mean arterial pressure had stabilized, the response to atracurium, 0.5 mg/kg intravenously, was continuously recorded for 5 min in 10 patients. An additional 10 patients received no atracurium and served as matched controls. Thiopental caused reductions in ICP in both groups of patients. Comparing the responses of the patients who received atracurium with those who did not, we found that atracurium had no significant effect on intracranial pressure, mean arterial pressure or cerebral perfusion pressure. Based on these data we conclude that atracurium appears to be preferable to the other available neuromuscular blocking agents that have been evaluated for neurosurgical anesthesia.

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A case of bronchospasm during general anesthesia is presented in which atropine appeared to reverse bronchoconstriction, after high halothane concentrations, intratracheal lidocaine, and isoproterenol i.v. had all proved ineffective. This case illustrates a rational approach to the treatment of bronchospasm during anesthesia, based on determination of the most likely site of origin of bronchoconstriction within the tracheobronchial tree.

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Unequal pupil size following anaesthesia is an unsettling finding, suggestive of acute, perioperative intracranial pathology. We report here an unusual cause of anisocoria after anaesthesia: unintended entrance of phenylephrine nasal vasoconstrictor solution into the eye.

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A 14-day-old infant received intravenous lidocaine (2 mg X kg-1) at the conclusion of cataract surgery to prevent coughing from tracheal tube stimulation. Within 30 seconds the infant developed high-grade AV heart block and a ventricular rate of 40. Following brief resuscitation efforts, the patient had a normal cardiac rhythm, blood pressure and respiratory pattern. Intravenous lidocaine may be followed by major disturbances in cardiac rhythm and rate. Cautious titration of small doses should decrease the potential for adverse effects.

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