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Heparin has been advocated for the treatment of poisoning by Echis carinatus, a snake whose venom causes disseminated intravascular coagulation. Fourteen patients with proven E. carinatus bite who had incoagulable blood were treated with specific Echis antivenom. Seven of them were also given low-dose heparin, initially 50 units/kg body weight by i.v. injection, followed by 10 units/kg/h by i.v. infusion for 22 h. Response to treatment was assessed clinically and by repeated tests of blood coagulation. All patients showed a rapid return to normal blood coagulability after treatment and the heparinized group were not significantly different in any respect from the group given antivenom alone. Heparin did not reduce the local effects of envenoming. There appears to be no place for heparin in the treatment of E. carinatus poisoning provided that potent antivenom is available. The in vivo results were supported by in vitro studies in which it was found that Echis-induced thrombin was less sensitive to the inhibitory effect of heparin than physiological thrombin.

1. Nineteen patients with louse-borne relapsing fever were studied in Addis Abeba (altitude 2285 m). 2. Following treatment with tetracycline a febrile Jarisch—Herxheimer-like reaction developed which showed the phases described in artificially-induced endotoxin fever. 3. During the chill phase body temperature, metabolic rate and pulmonary ventilation increased. Despite alveolar hyperventilation pulmonary venous admixture was high. Cardiac output, heart rate and systemic arterial pressure increased but pulmonary arterial pressure decreased. 4. During the flush phase systemic arterial pressure fell and remained low for many hours due to reduced vascular resistance, but pulmonary arterial pressure and inflow resistance increased. Small increases in glucose, lactate, and pyruvate concentrations were prevented by inhaling oxygen. 5. Stimulation of metabolic rate, ventilation and cardiac output during the reaction was not due simply to increased body temperature, hypoxia, or acidosis but was probably attributable to spirochaetal endotoxin. 6. Limitation of pulmonary oxygen diffusion may have been responsible for the impaired pulmonary oxygen uptake in these patients. 7. During the prolonged flush phase a greatly increased cardiac output is necessary to maintain systemic arterial pressure because of the very low vascular resistance. Prevention of extracellular fluid volume depletion, early detection and prompt treatment of cardiac failure and oxygen therapy may reduce fatalities during this critical period but hydrocortisone in large doses failed to reduce the severity of the reaction.