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Biomedical subjects

A Ganendran

Publications and source records attributed to A Ganendran.

At least 19 recordsLinked to original sources
PubMed1987

Prolonged analgesia following preoperative bupivacaine neural blockade for oral surgery performed under general anesthesia.

The effectiveness of prolonged neural blockade following removal of impacted third molars under general anesthesia was evaluated in a controlled clinical study. There was a significant reduction in the amount of postoperative pain experienced, and no complications, either local or systemic, occurred. The technique has advantages, especially when general anesthesia is administered to outpatients.

Adult↗
PubMed1987

Attitudes and knowledge of nursing staff in relation to management of postoperative pain.

The effectiveness of pain control following surgery is notoriously difficult to assess, but objective assessment by nursing staff has been found to correlate reasonably well with subjective patient assessment. A study was designed to investigate the attitudes and knowledge of 86 qualified nursing staff in relation to postoperative pain management. Overall knowledge was sound to a point, but there were some obvious deficiencies in practical application; for example, 25% of staff would wait until a patient was in severe pain before using a prescribed (charted) analgesic. Additionally, almost three-quarters of staff felt that, in general, postoperative patients received adequate pain relief, while the great majority felt that prescription writing could be improved, mainly by improved legibility and clarity of actual instructions. The results suggest that the aim of postoperative pain management--that is, the provision of adequate analgesia--may need to be more strongly defined in nursing education.

Analgesics, Opioid↗
PubMed1981

The efficacy of potassium-induced cardioplegia and topical hypothermia in the correction of congenital cardiac lesions.

Myocardial metabolic, structural and functional preservation were evaluated in 44 patients who underwent open heart surgery under cardiopulmonary bypass, potassium cardioplegia and topical hypothermia. The duration of cardiac arrest varied from 14 to 87 minutes. Myocardial high-energy phosphates were not only adequately preserved but actually exceeded the control values during periods of cardiac arrest. Glycogen levels were decreased moderately and one to three fold increases in lactate/pyruvate ratios were detected. Myocardial ultrastructure was well preserved. Postoperative clinical recovery of the patients was excellent. The only patient who died from a low output syndrome showed no evidence of myocardial damage. The results of this study serve to illustrate the beneficial effects of potassium cardioplegia and topical hypothermia on myocardial preservation during prolonged periods of ischaemic cardiac arrest, as used for the correction of congenital cardiac lesions.

Adolescent↗
PubMed1980

Effect of potassium-induced cardioplegia in hypothermia on myocardial energy, ammonium, and intermediary metabolism in man.

Cardiac muscle biopsy specimens were obtained from 33 patients undergoing open-heart surgery under K+-induced ischemic arrest in hypothermia (cardioplegic right atrial and right ventricular muscles) or under hypothermic ischemic arrest without K+-cardioplegia (noncardioplegia right atrial muscle), and sequential patterns of changes in the myocardial metabolism were studied by standard enzymatic techniques. The concentrations of the high energy phosphates were not only adequately preserved but actually exceeded the initial values in the cardioplegic muscles during the 40-min period of the ischemic arrest. In addition, elevated ammonia levels were neutralized by these muscles, and excessive variations in the myocardial intermediary metabolism were prevented. The levels of ATP were also adequately preserved by the noncardioplegic right atrial muscle during the 12-min period of ischemic arrest. But this protection was achieved at the expense of a 20% reduction in the myocardial creatine phosphate levels and other associated severe intracellular metabolic derangements. Changes in the myocardial intermediary metabolism, at the end of 12 min of ischemic arrest and at the end of 40 min of K+-cardioplegic arrest, were almost identical. The results of these studies suggest that, in contrast to the hypothermic arrest alone, K+-cardioplegia in hypothermia offers a superior myocardial metabolic preservation over an extended period of time.

Ammonia↗
PubMed1979

Fogarty catheter extraction of foreign bodies from tracheobronchial trees of small children.

The inhalation of a foreign body into the tracheobronchial tree tree presents a life-threatening situation. A satisfactory outcome requires the timely and atraumatic removal of the offending agent. The morbidity associated with present methods of dealing with this problem is well documented. Four cases are described to illustrate the efficacy and simplicity of a new technique of endoscopic extraction with the aid of a Fogarty embolectomy catheter. The actual technique and anesthetic management are described.

Bronchi↗
PubMed1976

Reactivation studies on organophosphate inhibited human cholinesterases by pralidoxime (P-2-AM).

There is biochemical and clinical evidence that P-2-AM (Pyridine-2-Aldoxime Methiodide, Pralidoxime) does not reactive human acetylcholinesterase inhibited by either Malathion or Malaoxon. In vitro studies using Pralidoxime iodide up to ten times the recommended concentrations, produced insignificant reactivation of cholinesterases inhibited by Malathion or Malaoxon. This was observed inspite of prolonged exposure of the inhibited cholinesterases to the oxime. The value of Pralidoxime as a reactivator of phosphorylated cholinesterases is therefore in doubt, and should not be used in preference to large doses of atropine and other supportive treatment in poisoning by organophosphate pesticides.

Acetylcholinesterase↗
PubMed1976

Pralidoxime as an insignificant reactivator in severe anticholinesterase (organophosphate insecticide) poisoning.

In acute severe anticholinesterase poisoning by organophosphate compounds, pralidoxime (P-2-AM, pyridine-2-aldoxime methiodide) used in the recommended doses, intravenously, has not been shown to reactivate the inhibited cholinesterase, as evidenced both clinically and biochemically. In vitro studies using pralidoxime iodide up to ten times the recommended concentrations, produced insignificant reactivation of cholinesterases inhibited by the organophosphate insecticide Bidrin (di-methyl-3-hydroxyl-N, N-dimethyl-crotonamide phosphate). This was even so despite prolonged exposure of the inhibited cholinesterases to the oxime. The value of pralidoxime as a reactivator of phosphorylated cholinesterases is therefore in doubt, and should not be used in preference to large doses of atropine and other supportive treatment in poisoning by organophosphate insecticides.

Acetylthiocholine↗