Prevention of regurgitation during induction of anaesthesia with a cuffed oesophageal catheter.

Medical Memoranda MEDBYRNAL 545 Gardner (1953) and Kriss et al. (1955) reported certain side-effects after administration of cobalt even for short periods. These effects included nausea, vomiting, damage to the eighth cranial nerve nuclei, thyroid hyperplasia and myxoedema, and congestive heart failure (Goodman and Gillman, 1965). The case described above showed some of these toxic effects. The central nervous system was severely affected ; the vestibular and cochlear parts of the eighth nerve were damaged, as was shown by the abnormal caloric tests and audiometric curves. Paraesthesiae in the limbs, absent tendon jerks, and calf tenderness indicated that the patient also had a peripheral neuritis. The difficulty which she experienced in walking was probably due to a combination of vestibular damage and the peripheral neuritis. In the series published by Kriss et al. (1955) cobalt chloride was given to children with sickle-cell anaemia, and it was found that cobalt depressed the uptake of iodine by the thyroid gland and caused thyroid hyperplasia. In the above case the iodine uptake was greatly increased. This test, however, was carried out three weeks after withdrawal of cobalt chloride, during the rebound recovery phase after thyroid suppression. The exact lesion in the thyroid has not been elicited. However, Kriss et al. cite evidence that cobalt chloride inhibits the tyrosine iodinase system, which catalyses the iodinization of tyrosine to form monoiodotyrosine. This view is strengthened by the fact that in the case reported here potassium perchlorate caused an immediate discharge of radioactive iodine from the gland, indicating that much of the iodine was still in the inorganic form. Holly (1955) stated that cobalt is excreted primarily by the kidney, and he showed that rats receiving high doses of intra-peritoneal cobalt developed renal tubular necrosis, though no glomerular damage was noted. There appear to be no previous reports of renal toxicity in man. The above patient had evidence of tubular damage, as was shown by the temporary glycosuria and the amino-aciduria. The chromatographic pattern of the amino-acids wag very similar to that produced by other heavy metals-for example, copper in Kinnier Wilson's disease. There is no specific pattern of amino-aciduria caused by the different metals, and the basic lesion is again probably due to enzyme inhibition, perhaps the phosphorylation mechanism which is important in the active reabsorption of amino-acids. It was proved, by the disappearance of the tubular lesion three months after stopping the drug, that …