Renal involvement in Russell's viper bite patients without disseminated intravascular coagulation.

We measured urinary beta-N-acetylglucosaminidase (NAG: EC 3.2.1.30), blood urea, serum creatinine, albuminuria index and creatinine clearance in 16 patients bitten by Russell's viper (Daboia russelii siamensis) without disseminated intravascular coagulation (DIC) at the time of admission and then once daily for 5 d. Urinary NAG activity and the albuminuria index showed considerable variation whereas the other standard indicators of renal function revealed no abnormality. It is concluded that structural damage to the kidney occurred in these victims in the absence of DIC, indicating a direct toxic effect of Russell's viper venom on the kidney.

Clinical trial of intramuscular anti-snake venom administration as a first aid measure in the field in the management of Russell's viper bite patients.

Efficacy of intramuscular anti-snake venom administration immediately after bite as a first aid measure in the field followed by standard hospital management versus standard hospital management alone in the therapy of Russell's viper bite patients was studied. There was a definite reduction in the number of patients with systemic envenomation, complications following disseminated intravascular coagulation and in fatality rate of Russell's viper bite victims who had received first aid intramuscular anti-snake venom prior to hospitalization when compared with those who had not.

Local compression pads as a first-aid measure for victims of bites by Russell's viper (Daboia russelii siamensis) in Myanmar.

A prospective study of the efficacy of applying local pressure by compression pads in retarding spread of venom was carried out on 15 cases of bite by Russell's viper (Daboia russelii siamensis) in Myanmar. A firm rubber pad was applied with cotton bandaging over the site of bite and the limb was immobilized with a splint. Serial monitoring of venom levels by enzyme immunoassay (EIA) was carried out at 15 min intervals for 1h (2h in one case) while the pad was in place and at 15 and 30 min after its removal. A rise of 10-40ng/mL in serum venom antigen level was observed in most cases after removal of the pad. The central movement of venom antigen was retarded in 13 of the 15 cases. Mild haemostatic changes (factor V and X assays and screening tests) were observed in 10 pad-treated cases measured at the time of onset of incoagulability of blood. The side effects observed while the pads were in place were minimal, consisting of swelling, pain and tenderness, and were well tolerated by most patients (for up to 2h by one patient), except for 2 who had incisions or bruising at the site of the bite.

Heparin therapy in Russell's viper bite victims with impending dic (a controlled trial).

A controlled clinical trial of low-dose heparin was carried out in confirmed cases of Russell's viper bite. Twenty-eight patients with coagulable blood and serum FDP levels (more than 80 micrograms/ml) were included in the study. They were randomised to receive low-dose heparin in an initial dose of 50 units/kg body weight intravenously immediately after antivenom followed by a continuous infusion of 10 units/kg/hr in isotonic saline for 24 hours, or antivenom alone. Response to treatment was assessed clinically as well as by serial measurements of coagulation factors and biochemical variables. No features of systemic envenoming developed in any patient after treatment, but one patient in each group developed microscopic haematuria. No systemic bleeding or acute renal failure occurred in any patient. Recovery rate from the clotting defect was similar in the two groups, but in patients with initially very low fibrinogen levels there was a tendency for the heparin to restore fibrinogen faster than in comparable patients who did not receive heparin.