Original Articles Management of Snake Bite in Saudi Arabia Michael E. Kingston, MD* * Chairman, Department of Medicine, King Faisal Specialist Hospital and Research Centre ABSTRACT A fatal case of snake bite due to Echis carinatus, the saw-scaled viper, is reported, and the distribution presented. Because of this case and the presence of both elapid and viperine snakes in Saudi Arabia and the controversy in management, a protocol for the management of snake bite is suggested and important principles discussed. Snake bite victims should be transported to a hospital without delay after immobilization of the bitten limb, but incision, suction, tourniquet application and on-site intramuscular injection of antivenin should usually be avoided. Observation for neurotoxicity and a simple, bed side test for blood incoagulability differentiates elapid from viperine toxicity and indicates the need for antivenin infusion. Replacement of clotting factors in viperine-poisoned patients and artificial ventilation in neurotoxic patients are important therapeutic adjuncts. Adrenaline should be given immediately for reactions to antivenin. Immobilization and early debridement, but not antivenin, are important in managing local tissue destruction. ME. Kingston, Management of Snake Bite in Saudi Arabia. 1981; 1(2): 87-94 KEYWORDS Snake bites Saudi Arabia Antivenins Introduction Poisonous snakes belong to three main groups: elapid, such as cobras, mambas, and krites, which have short, fixed fangs; viperine, which have very long, erectile fangs; and sea snakes which have flat tails and short fixed fangs. Table 1. A person who believes he has been bitten by a poisonous snake, particularly in the dark or in thick vegetation, may have been bitten by a non-poisonous snake, a scorpion, or injured by a thorn or piece of broken glass. Moreover, poisoning occurs in a minority of bites by poisonous snakes, and many persons survive envenomation without treatment. Thus, it is likely that only a small percentage of suspected snake bites result in envenomation, and fewer still in death. Severe reactions to antivenin occur in as many as 20 percent of treated patients. 1 These facts present a dilemma in treatment. Poisoning due to snake bite may be local or systemic. Elapid snakes mainly cause neurotoxicity and viperine, vasculotoxicity either by a direct effect on blood vessels or by causing a coagulopathy. The severe local manifestations of swelling, blistering, and necrosis are the most common consequences of viperine snake bites but, contrary to popular belief, commonly occur with some elapid snake bites. Neurotoxicity may result from scorpion sting as well as elapid snake bites. The diagnosis may be made difficult by failure to identify the cause of the snake bite and the facts described. The management of snake bite is plagued with uncertainty and controversy, a consequence of unsupported traditional beliefs and published recommendations based on uncontrolled observations. Although elapid and viperine snakes are present in Saudi Arabia and sea snakes in the Arabian Gulf, reports of snake bites are uncommon. This is one of the few, authenticated reports of fatal snake bite poisoning in Saudi Arabia due to Echis carinatus, the saw-scaled viper. Because of this tragic case and the confusion and uncertainty surrounding the management of snake bite poisoning, important principles are discussed and a protocol for management is suggested. Case Report A 40-year-old American man felt a sudden pain in his left foot while walking in the desert in sandals 60 miles west of Buraida in Saudi Arabia on the night of 10 April 1978. The cause was not identified. Within 15 minutes his foot became swollen and bruised, and headache, vomiting, and backache followed; he took two aspirins. The next morning he was driven approximately 500 kilometers to Riyadh, and during the journey he became confused, vomited, and had several brief convulsions. On admission to the King Faisal Specialist Hospital and Research Centre he was confused, restless, and inattentive. His pupils were briskly reactive to light, ptosis was absent, and
examination showed the neurological system was normal. The blood pressure was 120/80 mm Hg, and examination of the heart and lungs was normal. Blood was oozing from abrasions on the tongue; priapism was present. The left foot was moderately swollen and a blister between the second and third toes was surrounded by ecchymosis. Figure 1. Table 1. Some characteristics of poisonous snakes and bites Viperine Elapid (cobras, mamba, krites) Sea snake Fangs Hollow, erectile Short, fixed, not hollow Short, fixed (flat tail) Bite location Usually low Usually high Not identified Local poisoning + + + 0- + + + 0 Systemic poisoning (predominant effects) Vasculotoxic Coagulopathy Neurotoxic Hemostatic aberration Myotoxic Clinical signs of systemic poisoning Incoagulable blood, bleeding gums, bleeding puncture site, hemoptysis, hematemesis, hematuria, ecchymoses Ptosis, glosso-pharyngeal and respiratory paralysis, spontaneous hemorrhage with some species Myoglobinuria respiratory failure Onset systemic poisoning 1½-24 hours 1-12 hours Several hours Usual time of death 12-48 hours 6-12 hours 12-48 hours The hemoglobin was 16.0g/dl, the white cell count 17,700 with 93 percent neutrophils and the platelet count was normal. The prothrombin time and partial thromboplastin time were both abnormal, being greater than 120 seconds, plasma fibrinogen was undetectable and fibrin degradation products (FDP) were between 320 and 640 μg/ml. The arterial blood ph was 7.35, P0 2 94mm Hg PCO 2 26 mmhg and plasma bicarbonate 16 meq/l. The urine sediment, chest x-ray, and electrocardiogram were normal. Figure 1. Hemorrhagic blister and ecchymosis due to snake bite by Echis carinatus. A diagnosis of envenomation, probably due to Echis carinatus, was made based on the circumstantial evidence of the history, the presence of the local hemorrhagic blister on the foot, and incoagulable blood due to afibrinogenemia. Following a test dosage, 60 ml of polyvalent antivenin diluted in 200 ml normal saline was given over 30 minutes; subsequently 60 ml antivenin, eight units of cryoprecipitate, and three units of fresh, frozen plasma were infused over six hours. Following this, the prothrombin and partial thromboplastin time normalized and the plasma fibrinogen was 110mg/dl. However, during the infusion the patient became unresponsive, and respiratory arrest followed. He was placed on a ventilator, and 16mg dexamethasone was given every six hours intravenously to reduce possible cerebral edema. The pupils became fixed and dilated and re-examination showed bilateral, widespread fundai hemorrhage and absent occular-vestibular reflexes. A computerized tomographic (CT) scan carried out the next morning was normal but an electroencephalogram
was flat and remained so; brain death was confirmed by two independent neurologists. After three days, and following discussion with the family, respiratory support was discontinued. At autopsy, sections of the mid-brain showed extensive hemorrhage in the periaqueductal tissue, cerebellar hemorrhage, ante-mortum saggital and transverse sinus thrombosis, and congestion of the sub-arachnoid vessels. There was a left retroperitoneal hematoma. The fluid from the blister on the foot was sent to Dr H. A. Reid at the Liverpool School of Tropical Medicine. The enzyme-linked immunosorbent assay (ELISA) investigation was positive for the venom of Echis carinatus and negative for Cerestes cerestes. Figure 2a. Echis carinatus killed in Saudi Arabia. Dorsal and ventral view. Discussion The saw-scaled viper, Echis carinatus, probably bites and kills more people than any other species of snake. 1,2 Figure 2. Figure 3 shows its wide distribution in the Middle East. Echis carinatus sightings have been reported from many areas in Saudi Arabia; however, authentication of fatal bites is rare. Figure 4. Envenomation invariably produces local swelling, usually occurring within 60 minutes, and blistering and necrosis in severe cases. 1 Figure 5. Systemic poisoning, manifesting as hemorrhage, is due to incoagulable blood
depleted of fibrinogen and Factors V, VIII, II, and XIII. Vascular damage, perhaps partly due to complement activation, may possibly contribute to the poisoning. 1 Failure of the blood to coagulate occurs between 75 minutes and 27 hours following the bite and is due to consumptive coagulopathy, secondary to disseminated, intravascular coagulation initiated by a procoagulant in the snake venom. 1 Surprisingly, thrombocytopenia is rarely present. 1 Proteolysis of the fibrin follows and results in markedly elevated FDP greater than 160 μg/ml in all cases reported by Warrell. 1 Figure 2B. Artist's detailed drawing showing shape of head and pattern of scales. (With kind permission of John Gasparetti.) Characteristic pain in the lymph nodes draining the bite area usually occurs within 30 minutes to several hours after the bite. 1,3 Spontaneous gingival bleeding is the most common sign with hemoptysis, ecchymoses over pressure areas, hematuria, epistaxis, hematemesis, and melena occurring in about 60 percent of cases. 1 Although cerebral hemorrhage and hemorrhagic shock are uncommon, they are most often the cause of death. Diagnosis of systemic poisoning is suspected in all cases where swelling has resulted from snake bite and can be excluded if swelling is completely absent. The degree of swelling does not necessarily correlate with the severity of the systemic poisoning. 1 This diagnosis can be made by a simple test that can be used as a continuing guide for further dosages of antivenin. A few milliliters of blood is placed in a clean, dry, glass test tube and left undisturbed. After 20 minutes, it is tipped to see if clotting has occurred. The test is repeated in six hours to assess the need for further antivenin and, once the blood has clotted, is repeated daily for three days to detect recurrent incoagulability subsequent to further absorption of venom from the area of the bite. 1
Figure 3. Distribution of Echis carinatus in the Middle East. (With kind permission of John Gasparetti)
Figure 4. Sightings of Echis carinatus in Saudi Arabia. (With kind permission of John Gasparetti)
Figure 5. Severe blistering followed, in five days, by necrosis from an Echis carinatus bite in West Africa. The only, established indication for antivenin use is incoagulable blood, because there is little evidence that local swelling and necrosis are diminished. 3,4 However, recent use of antivenin for the common English viper (Viper berus) bite in experimental animals resulted in diminished local manifestation. 5 Antivenins vary greatly in effectiveness. Specific monovalent antivenin may be more effective than polyvalent antivenin but, because of antigenic variation, is unreliable if the venom used in its production comes from snakes in geographical areas remote from that of the biting snake. 1 A specific Echis antivenin, produced in Iran, was ineffective for use outside Iran for this reason. 1 Until the effective dosage of a particular antivenin has been established, between 40 and 100 ml of polyvalent antivenin should be used as the initial dose. Subsequent doses will depend on the response to treatment. Immediate reactions are common, 21 percent frequency in Warrell's series. 1 The patient should be treated with 0.5 ml 1/1000 strength epinephrine intramuscularly or five milliliters 1/10,000 by slow intravenous infusion, if he is in shock. A syringe with the appropriate dose of epinephrine should be kept at the bedside to minimize delay in its use. The values of hydrocortisone and antihistamines are unproven, and they are less important in treatment. Essential local treatment principles include immobilizing the limb in the most comfortable position, avoiding occlusive dressings, and early debridement of necrotic tissue followed by a skin graft. Tetanus toxoid should be given to
all snake bite victims and 1500 units of antitoxin to those with local necrosis. Pain should be treated with codeine and/or acetaminophen. Aspirin should be avoided because it interferes with hemostasis by its antiplatelet action. This may have been a contributing factor to our patient's bleeding. Elapid and viperine snakes and biting insects, such as scorpions, exist in Saudi Arabia. There is a dilemma in management because the cause of the bite is often, initially and especially at night, unidentified as in this case. A protocol for snake bite management that applies in this situation is, therefore, suggested. It is important to remember the following principles in snake bite management. Not all suspected snake bites are due to poisonous snakes. They may result from non-poisonous snakes, scorpions, or objects such as thorns or broken glass. A bite by a poisonous snake is not the same as snake bite poisoning. In many cases, only a small amount or no venom is injected either because the snake has bitten recently or because the bite is a warning and not a meal bite. In viperine bites, but not elapid bites, absence of local swelling excludes systemic poisoning. Contrary to popular belief, severe local swelling and necrosis, usually without systemic poisoning, are the predominant manifestations of many elapid snake bites, e.g., Naja nigricollis and Naja naja. 6,7 Popular, local measures such as incision over the bite, suction, ice application, and tourniquet are still of unproven practical value and are potentially harmful. 3,4,7,8 Antivenin has no proven value for use in man for local poisoning except, possibly, for the English adder. Immediate reactions to antivenin occur in 20 to 30 percent of patients. The majority of patients with systemic poisoning survive without antivenin. Death can occur between several hours to several days following the bite. Therefore, the routine intramuscular injection of antivenin at local dispensaries cannot be recommended. Neurotoxic poisoning is completely reversible within a few days, without antivenin, provided the patient is adequately ventilated and supported. 9 The algorithm in Figure 6 illustrates a practical method for managing snake bites. The use of protective footwear and extra caution at night are important preventative measures which cannot be overemphasized. Figure 6. Algorithm for management of snake bites. Immobilize the bitten limb in the most comfortable position and transport the victim to the hospital as soon as possible, avoiding all other local measures. If the snake has been killed, take it to the hospital along with anyone
who might have seen the attack. Codeine or acetaminophen, but not aspirin, can be given for pain. The two important and easily performed factors in management are observation for neurotoxicity and the blood coagulability test described. If the snake is positively identified as a viper, absence of local swelling excludes envenomation. If the blood coagulates normally and neurotoxicity and local necrosis are absent at 24 to 27 hours, then systemic poisoning can be excluded and the patient discharged. Antivenin is given, intravenously, at an initial dose of 40 to 100 ml at the first sign of neurotoxicity or blood incoagulability. The earliest sign of neurotoxicity is ptosis, followed by cranial nerve palsies, intercostal and finally diaphragmatic paralysis. 9 Even without antivenin, intubation and artificial ventilation will usually be sufficient for survival after several days. Indeed, antivenin, given late, may be ineffective. 9 In the case of viper bites, the clotting test should be repeated every six hours until the blood clots and, in cases of systemic poisoning, daily for three days. The dose of antivenin is repeated until the blood clots. Correction of hypovolemia, replacement of blood coagulation factors with infusions such as fresh frozen plasma and/or cryoprecipitate, and general supportive measures should be carried out as indicated. A tetanus toxoid booster is given routinely, and antitetanus serum is given in addition if necrosis occurs. Conclusion IMMOBILIZE THE LIMB IN A COMFORTABLE POSITION TRANSPORT THE VICTIM TO A HOSPITAL OBSERVE FOR NEUROTOXICITY AND BLOOD INCOAGULABILITY INFUSE ANTIVENIN FOR SYSTEMIC POISONING ONLY GIVE GOOD SUPPORTIVE CARE REFERENCES 1. Warrell DA, Davidson NMcD, Greenwood BM, et al: Poisoning by bites of the saw-scaled or carpet viper (Echis carinatus) in Nigeria. Q J Med 46(181):33-62 1977 2. Warrell DA, Arnett C: The importance of bites by the saw-scaled or carpet viper (Echis carinatus): epidemiological studies in Nigeria and a review of world literature. Acta Trop (Basel) 33(4):307-41 1976 3. Bhat RN: Viperine snake bite poisoning in Jammu. J Indian Med Assoc 63(12):383-92 1974 4. Reid HA: Abstract No. 166. Tropical Dis Bull 71:80-81 1974 5. Theakston RD, Reid HA: Effectiveness of Zagreb antivenom against envenoming by the adder, Vipera berus. Lancet 2(7977):121-23 1976 6. Warrell DA, Greenwood BM, Davidson NMcD, et al: Necrosis, haemorrhage and complement depletion following bites by the spitting cobra (Naja nigricollis). Q J Med 45(177): 1-22 1976 7. Reid HA: Cobra bites. Br Med J 4:540-45 1964 8. Reid HA, Thean PC, Martin WJ: Specific antivenene and prednisone in viper-bite poisoning: controlled trial. Br Med J 2:1378-80 1963 9. Campbell CH: Venomous snake bite in Papua and its treatment with tracheotomy, artificial respiration and antivenene. Trans R Soc Trop Med Hyg 58(3):263-73 1964 ACKNOWLEDGEMENTS The author wishes to acknowledge Dr David Barkham, Department of Medicine, King Faisal Specialist Hospital and Research Centre, for allowing him to use this case and D. A. Warrell upon whose work he has heavily relied.
Management of Snake Bite in Saudi Arabia