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A comparison was made between atracurium and succinylcholine in 40 patients undergoing short gynaecological procedures of 30 minutes or less. Good intubating conditions were produced in 76.7 +/- 39.3 seconds (mean +/- S.D.) with succinylcholine 1 mg . kg-1 and 198 +/- 84 seconds with atracurium 400 micrograms . kg-1. Muscle relaxation was maintained with the initial dose of atracurium or with repeated boluses of succinylcholine. The mean time of surgery was 17.65 +/- 5.3 minutes in the atracurium group and 15.2 +/- 4.6 minutes in the succinylcholine group. Residual neuromuscular block with atracurium was reversed with neostigmine 0.036 mg . kg-1 and atropine 0.018 mg . kg-1. Recovery of neuromuscular function following reversal, assessed by return of all responses to train-of-four stimulation occurred in 5.05 +/- 4.6 minutes in the atracurium group but half the above doses of neostigmine and atropine were repeated in three patients. We conclude that a single dose of atracurium 400 micrograms . kg-1 is suitable for intubation and maintainance of muscle relaxation for short surgical procedures. However, the onset of action is slow, compared to succinylcholine. Residual neuromuscular block can be antagonised with standard doses of neostigmine, less than 20 minutes after the initial dose of relaxant. Atracurium appears to be a suitable alternative for short procedures where succinylcholine is unsuitable or contraindicated.

Inhalation anaesthetics For the inhalation anaesthetics there are age-related differences in uptake and distribution, in anaesthetic requirements as reflected by differences in MAC, in the effects on the four determinants of cardiac output (preload, afterload, heart rate and contractility), and in the sensitivity of protective cardiovascular reflexes (e.g., baroreceptor reflex). These differences limit the margin of safety of the potent agents in infants. Alveolar uptake of inhalation anaesthetics and hence whole-body uptake is more rapid in infants than in adults. J Lung washout is more rapid in infants than in adults because of the larger ratio between alveolar minute ventilation and lung volume (FRC) (3.5:1 in the infant vs. 1.3:1 in the adult). Increased brain size (ml.kg-J), limited muscle mass, limited fat content, and proportional differences in the distribution of cardiac output contribute to differences in uptake. Age-related differences in tissue partition coefficients also influence the equilibrium tissue concentration and the rate of change in the tissue concentration. Early in an anaesthetic induction (at equal inspired concentrations) the infant will have higher tissue concentrations in brain, heart, and muscle than will the adult. MAC, an estimate of anaesthetic requirement, is, in part, age related. 2 Neonates require 25 per cent less anaesthetic than infants; infants have a greater anesthetic requirement than older patients. MAC is dramatically lower in newly born animals than in their 12-hour-old counterparts. The response of the newborn to painful stimuli is attenuated even in the awake state. Most likely this is related to the immaturity of the central nervous system; elevated concentrations of progesterone and 13-endorphin and 13-1ipoproteins may also play a role in the decrease in MAC in neonates. Several investigators have studied the age-related cardiovascular effects of the potent inhalation anaesthetics at known multiples of MAC. At end-tidal concentrations of halothane bracketing MAC, Lerman er al . 2 noted no difference in the incidence of hypotension or bradycardia in neonates and in infants one to six months of age. Likewise, we 3 have noted no age-related differences in the determinants of cardiac output in developing piglets 1-20 days during either halothane or isoflurane anaesthesia. Halothane produced hypotension by a reduction in contractility and heart rate; in much older animals halothane also decreases peripheral vascular resistance. In piglets although blood pressure was equally depressed with isoflurane and halothane, cardiac output was better preserved during isoflurane anaesthesia. In awake man or animals decreases in blood pressure are compensated for by an increase in heart rate, myocardial contractility, and peripheral vascular resistance. Potent inhalation anaesthetics depress baroreceptor reactivity in a concentration dependent manner. In infants or newborn animals baroreceptor reflexes are more depressed (at equipotent anaesthetic concentrations) than in older animals. 4'5 This further limits the safety of potent anaesthetics in infants. Moreover, Cook et a l . 6 have demonstrated that the cardiovascular index for halothane is smaller in younger animals than in older animals. The cardiovascular index is a reflection of the therapeutic index (i.e., the ratio between the anaesthetic concentration at cardiovascular collapse to that of anaesthesia). Thus, potent inhalation anaesthetics must be used with caution in newborns and infants. Because of

The prophylactic effectiveness of a small "self-taming" dose of succinylcholine (0.1 mg X kg-1), of d-tubocurarine (0.05 mg X kg-1), and of pancuronium (0.02 mg X kg-1) on succinylcholine-induced fasciculations and myoglobinaemia was studied in 64 healthy children (ages two to nine years), anaesthetized with halothane, nitrous oxide and oxygen. Serum myoglobin was analyzed by radioimmunoassay and taken as a tracer of muscle damage. No correlation was found between the serum levels of myoglobin and the incidence of muscle fasciculations. Self-taming with succinylcholine decreased the incidence of fasciculations (p = 0.001) but did not decrease the succinylcholine-induced myoglobinaemia (p = 0.224). D-tubocurarine (0.05 mg X kg-1) and pancuronium (0.02 mg X kg-1) both significantly reduced the myoglobinaemia and the fasciculations produced by succinylcholine. The pancuronium pretreated group presented less variable values of serum myoglobin which, when compared to the control group, had a more significant p value (p less than 0.001) than for d-tubocurarine pretreated group (p = 0.003). Muscle fasciculations and increased myoglobin levels were observed in children less than four years old who received succinylcholine. The prophylaxis of acute rhabdomyolytic renal failure due to succinylcholine (seven cases reported in the medical literature) is considered.

In a prospective, double-blind placebo controlled trial, the effect of oral diazepam premedication on post-succinylcholine fasciculations and myalgia was studied. Forty patients undergoing septoplasty procedures received orally identical capsules containing either 10 mg of diazepam or a placebo 90 minutes preoperatively. A standardized anaesthetic regimen included induction with 5 mg X kg-1 of thiopental and 1 mg X kg-1 of succinylcholine. The diazepam and control groups did not differ significantly in extent of fasciculations or ease of intubation. However, only 15 per cent of the diazepam premedicated patients had myalgias postoperatively compared to 50 per cent of the control patients, a statistically significant difference (p = 0.04).

Tubocurarine 0.05 and 0.07 mg-kg-1, gallamine 0.1 and 0.2 mg-kg-1 and pancuronium 0.01 and 0.02 mg- kg-1 given three minutes before suxamethonium 1.0, 1.5 and 2 mg-kg-1 in groups of 10 patients each (total 210 patients) to compare ease of tracheal intubation and incidence of post-suxamethonium muscle pain. These were compared with a control group of suxamethonium 1.0, 1.5 and 2 mg-kg-1 given alone after thiopentone 5 mg-kg-1. On analysis, tubocurarine 0.07 mg-kg-1 and suxamethonium 2 mg-kg-1 was the ideal combination with the best intubation conditions and the lowest incidence of post-suxamethonium muscle pains. The second best combination was gallamine 0.2 mg-kg-1 and suxamethonium 2 mg-kg-1. Pancuronium 0.01 mg-kg-1 and 0.02 mg-kg-1 in combination with suxamethonium 2 mg-kg-1 were satisfactory, although less efficient than the combination with either tubocurarine or gallamine.

To determine whether intravenous atropine and glycopyrrolate are equally effective in preventing succinylcholine-induced heart rate changes, we studied the heart rate during the first 78 seconds of anaesthesia in 40 children anaesthetized with either thiopentone, atropine (0.02 mg X kg-1) and succinylcholine (2 mg X kg-1), or thiopentone, glycopyrrolate (0.01 mg X kg-1) and succinylcholine (2 mg X kg-1). Each treatment group was divided into four subgroups which differed only in the interval (6, 10, 15, 20 seconds) between injection of atropine or glycopyrrolate and succinylcholine. During the 54 seconds after succinylcholine, the mean heart rate of each subgroup decreased transiently and then returned to the pre-induction heart rate or higher. There was no difference in either the magnitude or the duration of the decrease in heart rate or the subsequent increase in heart rate between respective subgroups. Bradycardia occurred in only two patients, both of whom received glycopyrrolate. We conclude that atropine (0.02 mg X kg-1) and glycopyrrolate (0.01 mg X kg-1) are equally effective in attenuating succinylcholine-induced changes in heart rate in children.

The enzyme serum cholinesterase responsible for the hydrolysis of the muscle relaxant succinylcholine exists in the form of several variants. These may be identified in serum by using substances which inhibit their activity to different degrees. The heterozygote for the atypical and fluoride resistant enzymes (E1a E1f) is one of the phenotypes which has been reported to be sinsitive to succinylcholine. A case is described where succinylcholine given on two separate occasions did not induce apnoea in an individual phenotyped as E1a E1f by at least five methods of inhibition. This is the first reported example of such insensitivity to the drug in this phenotype. Temperature activities for the patient's serum over the range of 20 degrees C to 45 degrees C differed from that of an established E1a E1f phenotype used as a control. There was a progressive inactivation of the control serum at temperatures higher than 35 degrees C, as previously reported for this phenotype. Activity in the serum of the subject of this study did not exhibit the peak activity at 35 degrees C but continued to rise and probably reached a peak between 40 degrees C and 45 degrees C. The significance of these results in the context of current methods of phenotyping is discussed.

Thirty patients received general anaesthesia for forty intralaryngeal operations using a laser beam. The essential requirements for the anaesthetic management are: (1) Anaesthetic agents should be non-flammable. (2) Small diameter red rubber cuffed tracheal tubes provide maximum working space for the surgeon, facilitate controlled ventilation and minimize the explosion hazard of anaesthetic gases in the vicinity of the laser beam. (3) Continuous muscle relaxation of head and neck and of laryngeal muscles facilitates the instrumentation and lasing of lesions of vocal cords which are thus rendered fixed and immobile.

Succinylcholine-induced potassium efflux was studied in two groups of healthy adult patients presenting for elective surgery. One group (Group 1) of 12 patients received alfathesin induction followed by succinylcholine. The other group (Group 2) of 12 patients were pre-treated with fazadinium 0.075 mg . kg-1 about three minutes before administration of alfathesin and succinylcholine. Serial blood samples were taken pre-induction, post-induction and after succinylcholine for estimation of plasma potassium. The results show that pre-treatment with fazadinium 0.075 mg . kg-1 was effective in preventing succinylcholine-induced potassium efflux.

Urine concentrations and excretion rates of norepinephrine were measured in 28 patients anaesthetized with halothane or morphine before, during and for two hours after aortocoronary artery grafting procedures. All patients were paralyzed with d-tubocurarine, intubated and respiration was controlled. Urine was obtained for 90 minutes before induction, during induction, before, during and after bypass and postoperatively. In patients anaesthetized with halothane, urinary norepinephrine concentrations and excretion rates were not significantly different from preoperative values until the postoperative period. Patients anaesthetized with morphine did not have urine norepinephrine concentrations different from preoperative values until bypass, when they became significantly increased. All subsequent urine norepinephrine concentrations and excretion rates were significantly elevated when compared to preoperative values. These findings do not indicate a mechanism but they do demonstrate that morphine anaesthesia is associated with increased urinary and probably also increased plasma levels of norepinephrine during and after cardiopulmonary bypass in patients undergoing coronary artery operations.

Sixteen extremely obese patients were anaesthetized for intestinal short circuiting operations. Severe obesity may cause pathological cardio-pulmonary changes. Cardiovascular alterations include increased systemic, pulmonary artery and pulmonary capillary venous pressure. Cardiac output, total blood volume and left ventricular work increase. Expiratory reserve volume and consequently functional residual capacity decrease with gross obesity. Functional residual capacity falls below closing volume and inspired gas may be distributed to non-dependent lung zones, resulting in decreased ventilation/perfusion ratios and arterial hypoxaemia. Low total respiratory compliance increases the oxygen cost of the work of breathing. Obesity may change the dose requirements for regional anaesthesia and long-acting muscle relaxants. General anaesthesia may also reduce functional residual capacity. We used a technique of anaesthesia which consisted of epidural analgesia with intra-operative mechanical ventilation and which specifically avoided volatile inhalation agents and long-acting muscle relaxants. All patients were extubated immediately after operation and returned to the recovery room for an average duration of 26 hours. Post-operative treatment included humidified oxygen, chest physiotherapy and elevation of the head of the bed to 45 degrees. Each patient's respiratory progress was monitored by repeated determinations of arterial blood gases and vital capacity and by serial chest X-rays. None of the patients in this group required post-operative tracheal intubation and mechanical ventilation.

Precurarization with a protective dose of d-tubocurarine, 6 mg in the adult male, 4 mg in the female, was achieved in a series of 100 patients three minutes before the induction of anaesthesia. This procedure was well tolerated on both psychological and physiological bases. The patients displayed no modification of their respiratory mechanics and could exhibit normal coordinated movements of their hands, legs and head. Slight diplopia and a sensation of drowsiness occurred frequently.

The major factors controlling intraocular pressure during surgery are the dynamic balance between aqueous humour production in the ciliary body and its elimination via the canal of Schlemm; the auto-regulation and chemical control of choridal blood volume; the extraocular muscle tone and vitreous humour volume. Prior to surgical incision of the anterior chamber in open intraocular procedures, a low-normal intraocular pressure is mandatory to avoid the hazards of iris or lens prolapse and vitreous loss associated with sudden decompression. In general, the central nervous system depressant drugs, hypnotics, narcotics, major tranquillizers, volatile anaesthetic agents are associated with a reduction in intraocular pressure, with the exception of ketamine and possibly trichloroethylene. The mechanism of action of anaesthetic agents in reducing intraocular pressure may involve a direct effect on central diencephalic control centres, reduction of aqueous production, facilitation of aqueous drainage or relaxation of extraocular muscle tone. Succinylcholine administration is associated with a significant rise in intraocular pressure, with a peak increase between two to four minutes following administration and a return to base line values after six minutes. The intraocular hypertensive effect may be due to a tonic contraction of the extraocular muscles, choroidal vascular dilatation or relaxation of orbital smooth muscle. Despite many claims to the contrary, no reported method to date has been shown to consistently prevent the intraocular hypertensive response to intravenous succinylcholine administration. Because the non-depolarizing relaxants are associated with a reduced intraocular pressure, a barbiturate-non-depolarizing relaxant technique utilizing preoxygenation and cricoid pressure has evolved as the most commonly employed induction technique for the emergency repair of a penetrating eye injury. The alternative non-depolarizing relaxant pretreatment-barbiturate-succinylcholine technique may offer the advantages of more rapid onset of relaxation with only minor increases in intraocular pressure and in a carefully controlled rapid sequence induction technique may be the most acceptable method of handling emergency penetrating eye injuries.

The effects of pretreatment with both sub-paralyzing and paralyzing doses of pancuronium and d-tubocurarine, on the onset and duration of succinylcholine-induced neuromuscular blockade were evaluated and compared in 225 patients. D-tubocurarine antagonized both onset and duration of succinylcholine block, while pancuronium produced a dual effect, antagonizing the onset and potentiating the duration of succinylcholine block. Pretreatment with d-tubocurarine (0.07 mg/kg, 0.3 mg/kg and 0.6 mg/kg) increased the time to onset of succinylcholine paralysis from 28 to 118%, and decreased the duration from 16 to 37%. Pancuronium (0.02 mg/kg, 0.04 mg/kg and 0.08 mg/kg) also antagonized the onset of succinylcholine paralysis with increases of 32 to 114%, but potentiated its duration from 30 to 103% compared with succinylcholine alone in the same patients. Although pancuronium markedly inhibited serum cholinesterase in vitro (I50=5 X 10(-7) mol) there was only a 10% inhibition of cholinesterase in vivo after pancuronium 0.08 mg/kg.

The effects of atracurium 0.5 mg X kg-1 or succinylcholine 1.0 mg X kg-1 on intraocular pressure (IOP) were studied in ten patients during steady state nitrous oxide-oxygen-fentanyl anaesthesia. IOP was unchanged following atracurium but, one minute after succinylcholine, it had increased significantly (p less than 0.025) from 5.6 mmHg to 13.2 mmHg and remained significantly above control for 3 min. Twenty additional patients received either atracurium 0.75 mg X kg-1 or succinylcholine 1.0 mg X kg-1 as part of a rapid sequence induction, atracurium being administered prior to, and succinylcholine after, thiopentone. Intubating conditions were acceptable in all patients in both groups. Administration of thiopentone was associated with a significant (p less than 0.025) decrease in IOP. Although IOP increased in both groups as a result of laryngoscopy and intubation (from 8.0 mmHg to 12.1 mmHg in the atracurium Group and from 7.5 mmHg to 14.5 mmHg in the succinylcholine group) it did not exceed pre-induction IOP in the former. In the succinylcholine group, IOP after intubation exceeded pre-induction values for 2 min, although this increase was significant (p less than 0.05) only at the immediate post-intubation reading. It is concluded that atracurium in a dose of 0.75 mg X kg-1 is a suitable relaxant for use in rapid sequence induction.

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.

To compare the effectiveness of succinylcholine and pancuronium for rapid intubation in children, 49 healthy children ages two to eight years were studied. After induction of anaesthesia with thiopentone and atropine, and administration of droperidol, fentanyl, nitrous oxide, and oxygen, each child received one of the following muscle relaxants: succinylcholine 1.5 mg X kg-1 (n = 12), succinylcholine 1.0 mg X kg-1 (n = 13), pancuronium 0.15 mg X kg-1 (n = 11), or pancuronium 0.10 mg X kg-1 (n = 13). The force of thumb adduction was measured by stimulating the ulnar nerve with repetitive supramaximal single twitches (0.15 Hz). The time to 95 per cent twitch depression (mean +/- S.D.) was most rapid with succinylcholine 1.5 mg X kg-1 (40.8 +/- 3.0 seconds) and succinylcholine 1.0 mg X kg-1 (51.8 +/- 14.0 seconds), slowest with pancuronium 0.10 mg X kg-1 (150.9 +/- 38.0 seconds), and intermediate with pancuronium 0.15 mg X kg-1 (80.3 +/- 21.8 seconds) (p less than 0.005). The intubating conditions were excellent in 100% of the children who received succinylcholine 1.5 and 1.0 mg X kg-1, and pancuronium 0.15 mg X kg-1, but were excellent in only 69 per cent of those who received pancuronium 0.10 mg X kg-1. We conclude that succinylcholine 1.5 mg X kg-1 produces the most rapid onset of excellent intubating conditions in children. In children in whom succinylcholine is contra-indicated, pancuronium 0.15 mg X kg-1 provides excellent intubating conditions within 80 seconds.

Succinylcholine apnoea is usually the result of a delay in hydrolysis of the injected muscle relaxant due to the presence of an inherited defect in the enzyme cholinesterase. This report presents a Nova Scotia family in whom several members had "difficulty in breathing" following anaesthesia. Subsequent investigations revealed the presence of several phenotypes of the enzyme cholinesterase including individuals who were homozygous for the atypical cholinesterase genes. The frequency of occurrence and significance of the various phenotypes are discussed, together with their management and recommendations for family screening.

To test the possibility that individuals with and without plasma cholinesterase C5 isozyme have differences in neuromuscular sensitivity to succinylcholine chloride, we examined the effects of succinylcholine in these two groups of patients. Sera from 491 adult patients were examined for presence of the plasma cholinesterase C5 isozyme by use of electrophoresis with polyacrylamide; 24 were positive for the C5 isozyme. Plasma cholinesterase activity and duration of action of succinylcholine were measured in 12 C5 positive patients and 18 C5 negative patients, all of whom had the normal cholinesterase genotype. C5 positive patients had 30.1 per cent higher mean plasma cholinesterase activity than C5 negative patients. The duration of neuromuscular blockade, measured by the first twitch height evoked by train-of-four stimulation, was significantly shorter in C5 positive patients than C5 negative patients. The C5 positive individuals had shorter duration of action of succinylcholine than C5 negative individuals.

The neuromuscular effects of ORG NC45, used as the sole muscle relaxant, were compared with a succinylcholine-pancuronium sequence in patients during nitrous oxide-fentanyl anaesthesia. The subjects were divided into four groups with ten in each group. After induction of anaesthesia they received either succinylcholine, 1 mg . kg-1 or ORG NC45 in doses of 50, 70 or 90 micrograms . kg-1 and tracheal intubation was done 90 seconds later. Neuromuscular transmission was monitored using train-of-four stimulation. Succinylcholine produced 100 per cent block with uniformly excellent intubating conditions whereas the three doses of ORG NC45 were associated with blocks of 7.5, 18.7 and 30.7 per cent and acceptable conditions in only 30 per cent of subjects. Muscle relaxation was maintained in the NC45 groups with increments of 10 micrograms . kg-1 and in the succinylcholine group with pancuronium, initially as a bolus of 40 micrograms . kg-1, followed by increments of 5 mg . kg-1. All increments were given at 10 per cent recovery of twitch height. The overall requirement to maintain 90 per cent block with pancuronium was 1.1 microgram/kg-1 . min-1 compared with 1.28 microgram . kg-1 . min-1 with ORG NC45. No cumulative effects were seen with either drug during the first hour of neuromuscular blockade. At the end of the operation the neuromuscular block was antagonized with atropine 18 micrograms . kg-1, and neostigmine 36 micrograms . kg-1 and recovery was significantly more rapid with NC45 than pancuronium. We conclude that the lack of cumulation, easy reversibility and lack of cardiovascular effects suggest that NC45 has advantages over currently available non-depolarizing muscle relaxants but that its onset of action is too slow for rapid intubation.

Pretreatment with small (10 mg) doses of succinylcholine ("self-taming") decreases the incidence of muscle fasciculations following succinylcholine administration and may decrease the incidence of other unwanted effects. This study was designed to assess the cardiac effects of such self-taming and to assess the degree of protection afforded against bradydysrhythmias following subsequent succinylcholine administration. Sixty patients were studied and allocated randomly to three groups of twenty. Each group was assigned a different form of pretreatment. Patients in group I received 10 mg of succinylcholine immediately after induction. Patients in group II were treated with d-tubocurarine 0.04k mg . kg-1 three minutes before induction. Patients in group III received no pretreatment. All patients were induced with thiopentone 4 mg . kg-1 followed by succinylcholine 1 mg . kg-1 45 seconds later. A second dose of succinylcholine 1 mg . kg-1 was administered to the patients in the two pretreatment groups between four and five minutes after the first dose of succinylcholine. Following both the first and second doses of succinylcholine patients in the self-taming group showed a significantly greater incidence of bradydysrhythmias when compared to the other two groups. It is concluded that the use of a self-taming technique is potentially hazardous, and that it does not confer protection against repeated succinylcholine administration.

The present study evaluated possible contribution of succinylmonocholine in producing serious cardiovascular effects with or without succinyldicholine, using albino rabbits as the experimental animal. Forty-eight experiments were performed, 22 in vivo and 26 in vitro (Langendort heart). Succinyldicholine and succinylmonocholine administered separately or together produced an immediate bradycardia in vivo as well as in vitro. The combination of these drugs had a direct arhythmogenic effect as well as an indirect reflux mediated cardiac effect. When succinyldicholine was given within five minutes following a dose of succinylmonocholine there was significant nodal and ventricular ectopic beats, but no bradycardia. Dysrhythmias in in vivo hearts were abolished by cord trans-section, trimethaphan and reserpine pretreatment. There was no evidence in vivo that succinylmonocholine produced more serious bradycardia, dysrhythmias or hypotension than succinyldicholine

To assess the efficacy of neostigmine antagonism of succinylcholine phase II block, succinylcholine infusions were given to 17 patients for durations varying from 44 to 192 minutes. A control group (17 patients) received a pancuronium infusion for similar times. Ninety per cent neuromuscular block was maintained in these two groups by adjustment of the infusion rates and, in a third group, with intermittent doses of pancuronium. Neuromuscular transmission was monitored with train-of-four stimulation every 12 seconds and anaesthesia was maintained with N2O-O2-enflurane. Ten minutes after the infusion was stopped, atropine and neostigmine were given to all patients who received pancuronium and to 11 patients in the succinylcholine group whose train-of-four ratio (T4/T1) was less than 0.7. During the subsequent 15 minutes, recovery was more rapid in the succinylcholine group than in either the pancuronium-infusion or pancuronium-bolus groups. It is concluded that succinylcholine-induced phase II block can be safely and rapidly antagonized with neostigmine.

Focal muscle contracture in the limb following sytemic administration of depolarizing neuromuscular blocking agents have been demonstrated experimentally with transection or crush injury of the nerve, but has rarely been observed clinically in patients with partial peripheral nerve injury. Three cases of spastic response in the hand and wrist are described in patients with subclinical chronic, subacute, and acute nerve injury, to document the occurrence of this phenomenon under various circumstances.

The safety and efficacy of the jet injector (Sanders) technique for bronchoscopy in children was evaluated in a lung analogue and verified by clinical trial. Although the small internal diameters of paediatric bronchoscopes accommodate lower maximum flows, they also produce higher inflation pressures than adult bronchoscopes. It was found that even the smallest tapered bronchoscope (3 mm distal diameter) can compensate for flow limitations by producing high inflation pressures and can deliver tidal volumes of 6–9 ml kg-1 with a driving pressure of 276 kPa (40 PSI).

The effects of succinylcholine (1.5 mg X kg-1 IV) administered five minutes after a defasciculating dose of curare (0.05 mg X kg-1 IV), were compared with the effects of atracurium (0.5 mg X kg-1 IV) on intracranial pressure (ICP) in 13 cynomolgus monkeys with intracranial hypertension (ICP approximately 25 mmHg). Neither succinylcholine nor atracurium increased ICP during general anaesthesia with 60 per cent N2O/O2, 0.5-1 per cent halothane. During a rapid sequence induction and intubation with thiopentone 5 mg X kg-1 IV, ICP increased equally with intubation following both atracurium (25 +/- 1 to 32 +/- 2 mmHg) and succinylcholine (25 +/- 1 to 31 +/- 2 mmHg) (p less than 0.05). Intubation was also associated with significant increases in PaCO2, CVP and MAP. We conclude that in this primate model of intracranial hypertension, neither atracurium nor succinylcholine (when given following a defasciculating dose of curare) elevates ICP. In terms of the elevation of ICP associated with intubation, atracurium was found to offer no advantage over succinylcholine.

The case histories are presented including the anaesthetic and postoperative management, of two children, a two-year-old with undiagnosed Duchenne muscular dystrophy (DMD) and a three-year-old with known DMD. The child with undiagnosed DMD had no symptoms of DMD and had received halothane twice before, without succinylcholine, with no apparent difficulty. Following an uneventful induction of anaesthesia with halothane, nitrous oxide and O2, succinylcholine resulted in bilateral masseter muscle spasm and then, in rapid sequence, ventricular tachycardia and cardiac arrest. Resuscitation was difficult, prolonged and associated with hyperkalaemia (K+ = 12.57 mEq X L-1), severe metabolic and respiratory acidosis, high peripheral venous pressure and massive hepatosplenomegaly, but not hyperthermia. The patient was finally resuscitated but died two days later. Skeletal muscle biopsy results were consistent with malignant hyperthermia. The second patient was known to have DMD but did not receive prophylactic or intraoperative dantrolene nor have his anaesthetic machine flushed with oxygen for an extended period prior to induction of anaesthesia. This child was anaesthetized with fentanyl and N2O and, with the exception of a high intraoperative heart rate (155-160 beats X min-1), had an uncomplicated anaesthetic and operation (intraoperative axillary temperatures ranged between 36.8-37.9 degrees C). Postoperatively his temperature rapidly increased to 38.8 degrees C and then 40.3 degrees C and he became metabolically acidotic. Intravenous administration of dantrolene for 48 hours reduced the temperature and allowed normal recovery and discharge. A postoperative muscle biopsy was consistent with DMD.(ABSTRACT TRUNCATED AT 250 WORDS)

One hundred and eighteen patients undergoing surgical procedures not requiring immediate tracheal intubation, nor producing visceral reflexes, were pretreated with d-tubocurarine 6 mg, three minutes before the administration of a bolus of succinylcholine (2 mg/kg). Electrocardiographs changes, venous and arterial plasma potassium and calcium levels, CPK changes ( 12 patients ) and appearance of myoglobinuria ( 35 patients ) were followed. Pretreatment with a small dose of d-tubocurarine did not change the overall incidence and pattern of arrhythmias; it did, however, prevent increases in plasma potassium in 90.4 per cent of the patients, mean plasma potassium values remaining below pre-induction levels. The CPK level changed in only one of 12 patients (from 10 to 21I.U., the normal range being 0 to 34 I.U.). No myoglobinuria was detected in any of the patients tested. A rapid but short-lasting change in the K+/Ca++ ratio did not seem to influence the occurrence of arrhythmias. Pretreatment with a small dose of d-tubocurarine is effective in preventing or decreasing fasciculations, plasma potassium and CPK changes and myoglobinuria described after the intravenous administration of succinylcholine. The already useful role of succinylcholine in our armamentarium can be made safer by pretreatment with a small dose of d-tubocurarine.

A study was conducted to determine the optimal interval between the administration of d-tubocurarine (dTc) and succinylcholine (SCh) with regard to onset and duration of neuromuscular block and presence of fasciculations and postoperative myalgias. Forty female patients received dTc 3 mg X 70 kg-1 prior to SCh 1.5 mg X kg-1. The interval between drugs was 0, 1, 3, 5, or 7 minutes. Transduced thumb adduction recorded block onset and recovery. Fasciculations were visually detected. Myalgias were assessed on postoperative interview. Pretreatment interval did not affect the onset or recovery of neuromuscular block. Postoperative myalgias were also independent of pretreatment timing. Fasciculations were blocked with 3, 5, or 7 minute intervals, but not with 0 or 1 minute intervals. Therefore, three minutes appear to be the optimal time interval between administration of dTc and SCh since shorter intervals do not inhibit fasciculations and longer intervals do not afford any additional advantages.