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Blood venom antigen levels after Malayan pit viper bite
548
‘I’a~~sac~~o~s OFTHEROYALSOCIETY OFTROPICAL
( Short
MEDICINE
Report 1
Blood venom antigen levels after Malayan pit viper bite
A. E. BROWN’ AND L. BROWN’ ‘Armed Forces Research Institute of Medical Sciences, Rajvithi Road, Bangkok 10400, Thailand; ‘Aranyaprathet District Hospital, Prachinburi, Thailand
Snakebitesleading to systemic envenoming are best treated with specific antivenom (WARRELL et al., 1986). Early treatment is recommended, but no delay is considered too long (WARRELL, 1984). Part of this recommendation is based on the classic studies by Reid and coworkers of bites by the Malayan pit viper (Calloselasma rhodostoma‘l. Thev rewrted 43 natients (for whom specific antivenom -was^unavailabie) with systemic poisoning who had “non-clotting blood” for up to 14 days, and “poor-clotting blood” up to 26 days (REID et al., 1963b). A defibrinating effect of the venom was demonstrated, but venom levels were not known (REID et al., 1963a). Recently, ELISA methods have been applied for detecting and auantitatina venom in various bodv fluids @IO et al., 1986bJ. Ho and colleagues in Thailand studied 46 Datients who had sienificant envenoming by the i&layan pit viper (H&itmmal., 1986a). 21 patients had non-clotting blood on admission, an average 9.6 h after being bitten, and a mean serum venom level of 175 &ml and a maximum of 595 r&ml; they received monospecific antivenom and all recovered. The absence of published data on the kinetics of viper venom in untreated humans is partially explained by obvious ethical problems. Thus, theraueuiic reconimendations remain imprecise.- We here report the case of a Thai farmer who oresented 22 h afier being bitten by a Malayan pit vip&; non-clotting blood was oozing from two puncture sites in the right foot, and he had ecchymosesand swelling of the lower leg and haemoptysis.-Venous blood did-not clot and the venom antigen level was 525 r&ml. For 56 h the patient receivea monospectic R&sell’s viper antivenom owing to initial misidentification of the snake. Venom levels, determined at 8 different times, were all in the 230-290 rig/ml range without a tendency to increase or decrease. By 60 h after admission, the patient’s foot had developed haemorrhagic bullae on a necrotic base, swelling extended to the groin, and chest X-ray revealed new infiltrates consistent with intra-alveolar haemorrhage. Venous blood still did not
AND HYGIENE (1987) 81, 548
clot. At that time monospecific antivenom against Malayan pit viper was borrowed from the Thai Red Cross and 5 ampoules were given. 6 h later, blood clotting was observed at 18 min with only a slight defect in quality (grade II of I&ID, 1963a), and no venom antigen was detected. Five more ampoules of antivenom were given and the patient recovered without further complication; 4 more serum samples collected over the next 40 h also contained no venom antigen. This man fortunately survived in spite of a calculated 82 h without specific antivenom. The persistently high serum venom levels found help to explain Reid’s findings, more than 20 years ago, of prolonged coagulopathy (REID 1963b). Whether this was due to slow catabolism or continued uptake of venom from the wound site cannot be determined. This is a unique glimpse of the persistence of viper venom in a human and also of the dramatic beneficial effect of swcif~c antivenom even when given more than 3 d after Hbite. We thank Dr Mav Ho of Mahidol Universitv for determining serum ;enom levels. The views of the authors do not purport to reflect’the position of the U.S. Department of the Army. References Ho, M., Warrell, D. A., Looareesuwan,S., Phillips, R. E., Chanthavanich,P., Karbwang,J., Supanaranond,W., Viravan, C., Hutton, R. A. & Vejcho, S. (1986a). Clinical significanceof venomantigenlevelsin patients envenomedby the Malayanpit FFr (C. rho@stomu). f,~~gn _,_
Journal of Tropscal Medscme and Hygme,
35,
_“,.
Ho, M., Warrell, M. J., Warrell, D. A., Bidwell, D. & Voller. A. (1986b).A critical reaooraisalof the use of enzyme&&ed inknosorbent ads’aysin the study of snake bite. Toxicon, 24, 211-221.
Reid, H. A., Ghan, K. E. & Thean, P. C. (1963a). Prolongedcoagulationdefect(defibrination syndrome) in Malayan viper bite. Lancet, i, 621-626. Reid, H. A., Thean,P. C., Ghan,K. E. & Baharom,A. R. (1963b). Clinical effects of bites by Malayan viper (Amistrodon rhodomma). Lance& i, 617-621. Warrell, D. A. (1984). Snakes. In: Hunter’s Tropical Medicine
(6th
edit.), Strickland, G. T. (editor), Phi-
ladelphia: W. B. Saunders, p. 800-812. Warrell, D. A., Looareesuwan, !i ., Theakston, R. D. G., Phillips, R. E., Chanthavanich, P., Viravan, C., Supanaranond, W., Karbwang, J., Ho, M., Hutton, R. A. & Vejcho, S. (1986). Randomized comparative trial of three monospecilic antivenoms for bites by the Malayan pit viper (Callaselasma rhodostoma) in southern Thailand: clinical and laboratory correlations. AmericanJournal of Tropical Medicine and Hygiene, 35, 1235-1247. Accepted
for publication 21 January 1987
‘I’a~~sac~~o~s OFTHEROYALSOCIETY OFTROPICAL
( Short
MEDICINE
Report 1
Blood venom antigen levels after Malayan pit viper bite
A. E. BROWN’ AND L. BROWN’ ‘Armed Forces Research Institute of Medical Sciences, Rajvithi Road, Bangkok 10400, Thailand; ‘Aranyaprathet District Hospital, Prachinburi, Thailand
Snakebitesleading to systemic envenoming are best treated with specific antivenom (WARRELL et al., 1986). Early treatment is recommended, but no delay is considered too long (WARRELL, 1984). Part of this recommendation is based on the classic studies by Reid and coworkers of bites by the Malayan pit viper (Calloselasma rhodostoma‘l. Thev rewrted 43 natients (for whom specific antivenom -was^unavailabie) with systemic poisoning who had “non-clotting blood” for up to 14 days, and “poor-clotting blood” up to 26 days (REID et al., 1963b). A defibrinating effect of the venom was demonstrated, but venom levels were not known (REID et al., 1963a). Recently, ELISA methods have been applied for detecting and auantitatina venom in various bodv fluids @IO et al., 1986bJ. Ho and colleagues in Thailand studied 46 Datients who had sienificant envenoming by the i&layan pit viper (H&itmmal., 1986a). 21 patients had non-clotting blood on admission, an average 9.6 h after being bitten, and a mean serum venom level of 175 &ml and a maximum of 595 r&ml; they received monospecific antivenom and all recovered. The absence of published data on the kinetics of viper venom in untreated humans is partially explained by obvious ethical problems. Thus, theraueuiic reconimendations remain imprecise.- We here report the case of a Thai farmer who oresented 22 h afier being bitten by a Malayan pit vip&; non-clotting blood was oozing from two puncture sites in the right foot, and he had ecchymosesand swelling of the lower leg and haemoptysis.-Venous blood did-not clot and the venom antigen level was 525 r&ml. For 56 h the patient receivea monospectic R&sell’s viper antivenom owing to initial misidentification of the snake. Venom levels, determined at 8 different times, were all in the 230-290 rig/ml range without a tendency to increase or decrease. By 60 h after admission, the patient’s foot had developed haemorrhagic bullae on a necrotic base, swelling extended to the groin, and chest X-ray revealed new infiltrates consistent with intra-alveolar haemorrhage. Venous blood still did not
AND HYGIENE (1987) 81, 548
clot. At that time monospecific antivenom against Malayan pit viper was borrowed from the Thai Red Cross and 5 ampoules were given. 6 h later, blood clotting was observed at 18 min with only a slight defect in quality (grade II of I&ID, 1963a), and no venom antigen was detected. Five more ampoules of antivenom were given and the patient recovered without further complication; 4 more serum samples collected over the next 40 h also contained no venom antigen. This man fortunately survived in spite of a calculated 82 h without specific antivenom. The persistently high serum venom levels found help to explain Reid’s findings, more than 20 years ago, of prolonged coagulopathy (REID 1963b). Whether this was due to slow catabolism or continued uptake of venom from the wound site cannot be determined. This is a unique glimpse of the persistence of viper venom in a human and also of the dramatic beneficial effect of swcif~c antivenom even when given more than 3 d after Hbite. We thank Dr Mav Ho of Mahidol Universitv for determining serum ;enom levels. The views of the authors do not purport to reflect’the position of the U.S. Department of the Army. References Ho, M., Warrell, D. A., Looareesuwan,S., Phillips, R. E., Chanthavanich,P., Karbwang,J., Supanaranond,W., Viravan, C., Hutton, R. A. & Vejcho, S. (1986a). Clinical significanceof venomantigenlevelsin patients envenomedby the Malayanpit FFr (C. rho@stomu). f,~~gn _,_
Journal of Tropscal Medscme and Hygme,
35,
_“,.
Ho, M., Warrell, M. J., Warrell, D. A., Bidwell, D. & Voller. A. (1986b).A critical reaooraisalof the use of enzyme&&ed inknosorbent ads’aysin the study of snake bite. Toxicon, 24, 211-221.
Reid, H. A., Ghan, K. E. & Thean, P. C. (1963a). Prolongedcoagulationdefect(defibrination syndrome) in Malayan viper bite. Lancet, i, 621-626. Reid, H. A., Thean,P. C., Ghan,K. E. & Baharom,A. R. (1963b). Clinical effects of bites by Malayan viper (Amistrodon rhodomma). Lance& i, 617-621. Warrell, D. A. (1984). Snakes. In: Hunter’s Tropical Medicine
(6th
edit.), Strickland, G. T. (editor), Phi-
ladelphia: W. B. Saunders, p. 800-812. Warrell, D. A., Looareesuwan, !i ., Theakston, R. D. G., Phillips, R. E., Chanthavanich, P., Viravan, C., Supanaranond, W., Karbwang, J., Ho, M., Hutton, R. A. & Vejcho, S. (1986). Randomized comparative trial of three monospecilic antivenoms for bites by the Malayan pit viper (Callaselasma rhodostoma) in southern Thailand: clinical and laboratory correlations. AmericanJournal of Tropical Medicine and Hygiene, 35, 1235-1247. Accepted
for publication 21 January 1987