Specific antivenom for Bungarus candidus.

BACKGROUND: Bungarus candidus (Malayan krait) snake is a neurotoxin snake. Previous treatment after snakebite was mainly respiratory support until the patient had spontaneous breathing. Recently specific antivenom for the Bungarus candidus snake was produced by the Queen Saovabha Memorial Institute and distributed in June 2004. The present article is the first report on the clinical response to the specific antivenom for Bungarus candidus. OBJECTIVE: To analyze the signs and symptoms of patients after snakebite and the response of the patients after receiving specific antivenom for Bungarus candidus snake. STUDY DESIGN: Retrospective chart review. MATERIAL AND METHOD: Four cases of Bungarus candidus snakebite were identified and divided into two groups. Group I (Case 1, 2, and 3) had received specific antivenom for Bungarus candidus while group 2 (case 4) had not. Onset, signs and symptoms after snakebite, antivenom dosage, and response time after receiving antivenom were analyzed. RESULTS: The first three patients received specific antivenom for Bungarus candidus and the fourth patient did not receive any. All four patients developed neurological signs and symptoms from this neurotoxic venom. In case 1, 2, and 4, the first signs and symptoms were dyspnea, difficulty with speech, and opening the eyelids at 50 minutes (30-60 minutes). The onset ofother signs and symptoms included respiratory paralysis with intubation 3 hours (2-4 hours), full ptosis 3.66 hours (3-4 hours), mydriasis and fixedpupils 4.33 hours (4-5 hours), no response to stimuli 5.66 hours (4-10 hours), tachycardia 5.5 hours (47 hours), and hypertension 14 hours (4-24 hours). The first two patients received specific antivenom for Bungarus candidus after being bitten at 10 and 12 hours, respectively. The first clinical response in case 1, were 12 hours after receiving 16 vials, and in case 2, were 20 hours after receiving 16 vials. These were slight movement of feet phalanxes. At 40 hours after receiving specific antivenom 30 vials in case 1 and 32 vials in case 2, they were able to respond to commands, motor power changed from grade 0 to grade 1 and there was 50% elevated eyebrows. The motor power changedfrom grade I to grade 4 with 100% elevation of eyebrows from full ptosis was 65 hours after receiving specific antivenom 60 vials in case 1 and 70 hours after receiving specific antivenom 87 vials in case 2. The patients had spontaneous opening ofeyelids at 90 hours after receiving 80 vials for case I and 88 hours after receiving 87 vials for case 2. Case 2 was extubated on day 4 after the snakebite while case 1 was extubated later on day 10 because of superimposing pneumonia. The third case had delayed onset of signs and symptoms of neurotoxicity compared to the other three patients. Dyspnea, difficulty with speech, and opening eyelids occurred at 5 hours after the snakebite. No response to stimuli and respiratory paralysis occurred at 20 hours after the snakebite. His consciousness improved 10 hours after receiving 3 vials of specific antivenom. This was noted by being able to respond to commands and the motor power changed to grade 2 however, full ptosis was still present up to 24 hours. After receiving 23 vials ofspecific antivenom, he accidentally extubated himself however, he could breathe adequately using a mask with a bag. His motor power changed to grade 4 with 100% elevated eyebrows but full ptosis 34 hours after receiving 38 vials of specific antivenom. He could spontaneously open his eyelids 40 hours after receiving 38 vials specific antivenom. Cases 1, 2, and 3 had persistent mydriasis andfixed pupils until discharge. Case 4 did not receive specific antivenom for Bungarus candidus. He did not respond to stimuli 10 hours after snakebite and he was treated with respirator and symptomatic treatment. On day 2, his blood pressure dropped, he was on dopamine to raise his BP On day 3, he developed ventricular fibrillation. Defibrillation was administered and ECG returned to normal. He was given further supportive care. On day 7, he was discharged at the request of his relatives without any improvement. CONCLUSION: The patients who received specific antivenom had more rapid improvement ofsigns and symptoms comparing to the patient who did not receive the antivenon.

Serum diazepam levels after oral administration in children.

OBJECTIVE: To determine serum levels of diazepam after oral administration in children. PATIENTS AND METHOD: Forty six children admitted with febrile seizures were orally administered with 0.25 mg/kg/dose of diazepam six hourly for four doses. Trough (prior to the next dose) and peak (at 1 hour 20 minutes after the dose) serum levels of diazepam were analyzed. The patients were observed for adverse effects of the medication. RESULTS: The peak levels after 1st, 2nd, 3rd and 4th doses were above 0.15 microg/ml which is considered the therapeutic level in 93.5, 97.8, 97.7, and 100 per cent of the patients, respectively. The trough levels prior to the 2nd, 3nd, and 4th doses were greater than 0.15 microg/ml in 75.0, 84.0, and 91.3 per cent, respectively. Neither recurrent seizure nor serious adverse effects occurred in any of the patients. CONCLUSION: Serum concentrations above the therapeutic level were achieved after orally administered diazepam at 0.25 mg/kg/dose six hourly for four doses. Oral diazepam may be used as another method in the prevention of recurrent febrile seizures.