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PubMedDate not supplied

3,4-Diaminopyridine reverses respiratory paralysis induced by a presynaptically active snake venom and its major neurotoxin.

Presynaptically active snake venom neurotoxins induce a potentially fatal neuromuscular blockade which cannot be reliably overcome by current therapy. The drug 3,4-diaminopyridine (DAP) is effective in other presynaptic paralytic conditions and was therefore tried in anaesthetized rabbits with respiratory paralysis induced by krait (Bungarus fasciatus) venom. A strain gauge pneumograph measured rabbit chest circumference during the respiratory cycle to document objectively effects of toxins and treatments. DAP counteracted the effects of both whole krait venom and its purified presynaptically active component, beta-bungarotoxin. Respiratory excursions increased within 4-8 min after DAP injection in animals paralysed with beta-bungarotoxin and 4-10 min after the injection of DAP in animals paralysed with 1 mg/kg whole krait venom. The onset of complete respiratory paralysis after a lethal dose of whole krait venom (2 mg/kg) was delayed significantly by DAP. This is the first indication that presynaptic venom paralysis can be reversed and suggests that DAP merits further evaluation as treatment for this condition.

4-Aminopyridine↗
PubMed1979

Prolonged respiratory paralysis in wound botulism.

Two patients had wound botulism with longer duration of respiratory paralysis than previously described. Each sustained extensive trauma to soft tissues and grossly contaminated wounds when thrown from a vehicle in a rural area. Progressive muscular weakness and respiratory distress occurred 8 and 13 days after injury, in the presence of infected wounds and clinical and laboratory findings characteristic of botulism. Spontaneous vital capacity and inspiratory effort served as bedside indicators of ventilatory function throughout 11 weeks of ventilatory support in each case and paralleled other clinical assessments of progress and recovery. Wound botulism may result in neuromuscular paralysis for a prolonged period. These cases illustrate the primary role of scrupulous nursing and respiratory care throughout such a period of ventilatory insufficiency.

Adult↗
PubMed1979

Respiratory paralysis to improve oxygenation and mortality in large newborn infants with respiratory distress.

The nonsynchronous respiratory efforts of neonates with surgically correctable disorders may inhibit effective mechanical ventilation. The records of 25 infants treated with metocurine for muscular paralysis to improve mechanical ventilation were reviewed. All patients were greater than 35 (37.6 +/- 2.1) weeks gestation and 2.27 (2.98 +/- .47) kg. All required ventilatory support with an FiO2 of 100%. The mortality rate of this group of infants was 20% as compared with 73% (p < .001) in a similar group of 26 infants managed without paralysis. In 10 of the 25 infants treated with metocurine, pre- and 1 hr postparalysis paO2 values were available. The mean paO2 prior to paralysis was 62 (45--111) mm Hg and the mean post-paralysis paO2 was 144 (75--227) mm Hg, representing at 132% increase in paO2 (p < .001). The mean dosage for metocurine was 3.5 (1.45--6.79) mg/kg/day; however, those requiring paralysis for greater than 7 days showed a dramatically increasing requirement. These preliminary data suggest that respiratory paralysis reduces right-to-left shunting, improves paO2 and decreases mortality in large infants with severe respiratory distress requiring ventilatory support.

Diaphragm↗
PubMed2002

Hypokalemic respiratory paralysis in Bartter's syndrome.

Life threatening hypokalemia can be a mode of presentation in renal salt wasting (Group-1) patients of Bartter's syndrome causing hypokalemic respiratory paralysis. Treatment on an emergent basis is required. In the long run, such patients may require higher doses of supplementary potassium and potassium sparing diuretics.

Bartter Syndrome↗