Clonidine for major vascular surgery in hypertensive patients: a double-blind, controlled, randomized study.

The utility of clonidine for hypertensive patients presenting for major vascular procedures remains debatable. Twenty-one hypertensive patients presenting for aortic surgery were given clonidine (n = 11) or placebo (n = 10) in a double-blind, randomized manner. Clonidine was administered 6 micrograms/kg per os 120 min before induction of anesthesia and 3 micrograms/kg intravenously (i.v.) over 60 min from aortic declamping to skin closure. Anesthesia was induced with alfentanil 20 micrograms/kg, midazolam, and atracurium and maintained with nitrous oxide 70%, an alfentanil infusion (0.25 microgram.kg-1. min-1), and isoflurane. Anesthetic requirements, circulatory variables, interventions, and isoproterenol dose-response curves (pre- and postoperatively) were determined. Plasma concentrations of clonidine, alfentanil, and vasoactive hormones were measured. When the clonidine group was compared with the placebo group, (a) isoflurane, alfentanil, and midazolam requirements were reduced by 38%, 42%, and 41%, respectively (P = 0.04, 0.03, 0.0002, respectively); (b) supplemental circulatory and anesthetic adjustments were reduced by 51% (P = 0.0006); (c) interventions with vasopressors were not significantly increased (placebo: two; clonidine: five); (d) systolic and mean arterial pressures and heart rate were reduced; (e) increases in norepinephrine, epinephrine, and plasma renin activity were suppressed, whereas vasopressin surge was attenuated; and (f) chronotropic response to isoproterenol was unaffected. Clonidine was effective in reducing anesthetic requirements and in improving circulatory stability in hypertensive patients presenting for major vascular procedures.

[Potassium cyanide poisoning treated with hydroxocobalamin]. / Intoxication au cyanure de potassium traitée par l'hydroxocobalamine.

A fifteen-year-old girl, with a clean medical history, was admitted to the intensive care unit 90 minutes after ingestion of 2.5 g potassium cyanide. She had typical signs of severe cyanide poisoning including deep coma, circulatory failure, and major metabolic acidosis. Gastric lavage and antidotal treatment with 4 g hydroxocobalamin and 8 g sodium hyposulfite was administered without delay together with supportive treatment consisting of mechanical ventilation with FIO2, blood alkalinisation and administration of beta-stimulants. These measures led to a rapid clinical improvement. The ventilatory support was discontinued after 24 hours and the patient left the intensive care unit on the fourth day with only slightly impaired mental status. She survived despite a very high blood cyanide concentration (494 mumol.l-1 on admission) probably because of the rapid symptomatic and antidotal treatment.