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Biomedical subjects

B S Epstein

Publications and source records attributed to B S Epstein.

At least 19 recordsLinked to original sources

Changes in heart rate and rhythm after intramuscular succinylcholine with or without atropine in anesthetized children.

The effects of intramuscular injections of succinylcholine with or without atropine on heart rate and rhythm were studied in 50 unpremedicated children 6-18 months of age. All had anesthesia induced with N2O-O2 and halothane 2% by face mask. Sixty seconds later, one of four study drugs or drug combinations was injected into the deltoid muscle of patients in groups 1-4. Following injection, halothane concentration was reduced to 1%, and ventilation was controlled. Patients given atropine only (0.02 mg/kg), succinylcholine only (4 mg/kg), or a combination of both (4 mg/kg succinylcholine plus 0.02 mg/kg atropine) showed transient increases in heart rate to 106 +/- 7.5%, 113 +/- 11.8%, and 109 +/- 10.1% (mean +/- SD) of control, followed by a decrease to 78 +/- 6.7%, 79 +/- 9.4%, and 80 +/- 10.5%, respectively, in 2-3 min after injection. Patients given a combination of succinylcholine (4 mg/kg) plus a higher dose of atropine (0.03 mg/kg) also had a transient increase in heart rate to 107 +/- 7.5%, followed by a decrease to 82 +/- 11.8% 2 min after injection. However, this group differed from the other three groups in presenting a second, prolonged increase in heart rate to 115 +/- 9.0% of preinjection levels. Patients in group 5 (controls) received no injections. Their heart rate decreased to 76 +/- 10.78% of preinduction level within 90 sec of induction, and remained unchanged thereafter. We conclude that succinylcholine (4 mg/kg) can be used intramuscularly with or without atropine (0.02 mg/kg) in lightly anesthetized young children without producing severe bradycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗

Rectal methohexitone induction in pediatric outpatients: physostigmine does not enhance recovery.

Rectal methohexitone (25 mg X kg-1) was used to induce anaesthesia in 15 unpremedicated children scheduled to undergo bilateral myringotomies as outpatients. Induction time ranged from 4 to 11 minutes. In the recovery room, all children received a slow intravenous injection of physostigmine (60 micrograms X kg-1), or saline in a double blind randomized fashion. The use of physostigmine did not significantly decrease the recovery room stay as compared to placebo (34 vs. 43 minutes). Vomiting and soiling were two side-effects associated with the use of physostigmine.

Age Factors↗

Tracheal tube cuff pressure. Changes during nitrous oxide anaesthesia following inflation of cuffs with air and saline.

The volume and pressure of a tracheal tube cuff inflated with air increases during nitrous oxide anaesthesia. The study was designed to investigate the changes of tracheal tube cuff pressure during nitrous oxide anaesthesia following inflation of the cuff with air or saline in 10 mongrel dogs who were anaesthetised with nitrous oxide and their lungs artificially ventilated. At the end of 6 hours there was no change in cuff pressure when saline had been used for inflation, but was six times the initial pressure when air had been used. On microscopic examination of the trachea, only the air group had glandular inflammation, dilatation and destruction. Therefore, it appears that if saline is used to inflate tracheal tube cuffs, there will not be an increase in cuff volume and pressure during nitrous oxide anaesthesia.

Anesthesia↗

Nitrous oxide and air-filled balloon-tipped catheters.

The differential solubilities of gases permit nitrous oxide (N2O) diffusion into air-filled body cavities, increasing their size and/or pressure. An air-filled balloon-tipped catheter represents a body cavity that may be affected by the diffusion of N2O, and could account for the authors' clinical observation that more gas was aspirated than injected during insertion of Swan-Ganz (S-G) catheters in patients receiving N2O anesthesia. An accompanying increase in balloon diameter could conceivably account for difficulties in floating the tip into the pulmonary outflow tract. To help substantiate these observations, balloon volumes of three S-G catheters were measured at 0.5, 1, 2, 3, 4, 5, 10, 20, and 30 min in various N2O and oxygen mixtures, and the diameters of the balloon were compared with published diameters of pulmonary outflow tracts. The volume changes were near maximum between 5-10 min, increasing to 30 to 150 per cent depending on the N2O concentration. The increases in balloon diameter, when compared to pediatric pulmonary outflow tract diameters, could account for difficulties in passage of the catheter tip through the pulmonary outflow tract. These findings suggest that manipulation of S-G catheters under N2O anesthesia sould be done with intermittent deflation of the balloon every few minutes.

Anesthesia, Inhalation↗

Malignant hyperthermia and central core disease in a child with congenital dislocating hips.

We describe a development of a malignant hyperthermia (MH) syndrome, partially aborted by therapy, in a child with central core disease and congenital dislocating hips. Patients with central core disease appear to be more susceptible to MH; possibly those with elevated serum creatine phosphokinase levels, as in our patient, are especially susceptible. We review the clinical and pathologic aspects, possible pathogenesis, and treatment of the MH syndrome. An increased calcium level within the muscle fiber is suggested as the major cytodestructive factor, and that increase could be consequent to a plasmalemmal susceptibility to the provoking drugs hypothesized to be the basic defect in MH. Prevention of the full manifestations of MH is predicated on (1) a high index of suspicion in the search for history of anesthetic complications in the patient and his family, with or without evident neuromuscular disease, (2) recognition that there is a somewhat greater risk of MH developing in a patient who has certain "musculoskeletal" abnormalities or muscle weakness but that is not-except for central core disease-a classic clinicopathologically defined disease, (3) close monitoring of patients during anesthesia, and (4) if the syndrome develops, prompt therapeutic measures, including cessation of anesthesia.

Adult↗