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ABSTRACT |
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONCASE REPORTDISCUSSIONREFERENCES |
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There are approximately 25 Vipera species throughout Europe. In Greece, three species are present: V. ammodytes, V. lebetina, and V. xanthina. Although these species are closely related, they may differ in size and appearance. However, their venom constituents and the treatment strategies for their bites used in field situations and hospitals are very similar. Envenomation by one of these three species is currently a rare occurrence in Greece. Although there are only a few such cases every year in this country, bites by these snakes constitute a serious problem for physicians who lack the necessary experience in diagnosing and treating them.
The case of a 65-year-old woman who was bitten by a viper snake is reported. She was admitted to the Department of Neurosurgery of Evangelismos General Hospital (Athens, Greece) with acute onset of right hemiplegia, confusion, and drowsiness. The importance of initial treatment and the necessity of monitoring coagulation status to prevent fatal cerebral hemorrhage are emphasized.
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CASE REPORT |
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On admission to this hospital, the patient was confused and drowsy, but could be aroused easily. Her pupils were symmetrical and the reaction to light was present. There was no evidence of cranial nerve dysfunction. Her fundus oculi was normal when examined by fundoscopy. Her vital signs were stable, with a blood pressure of 100/70 mm of Hg, slight tachycardia (110 beats per second), and tachypnea. There was 3/5-muscle power and increased tendon reflexes on the left side of her body. She had a positive Babinski sign on the left side and hemianopsia on the right side. Clinical examination revealed two hemorrhagic marks on the dorsal surface of her right foot, which was swollen and painful. The bite side was covered with a loose bandage instead of a pressure-immobilization bandage. The patient showed no signs of tetanus, but she received tetanus antitoxin as a prophylactic measure. We immediately started intravenous administration of a crystalloid solution, but since there were no obvious signs of shock or severe blood loss, colloid solutions, plasma, or packed red blood cells were not used. A computed tomography (CT) scan revealed multiple brain hemorrhagic infarcts located in the cerebral hemispheres, surrounded by edema (Figures 1
and 2).
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The patient was treated conservatively, with monitoring of her coagulation parameters (prothrombin time, partial thromboplastin time, fibrinogen levels, fibrin degeneration products), serum electrolytes, lactate dehydrogenase, hemoglobin, myoglobin, and urinalysis, both macroscopic and microscopic. The patient’s urine was also monitored for evidence of potentially nephrotoxic hemoglobinuria suggesting hemolysis. In addition, we monitored her urine output to exclude oliguria or anuria and her ECG. During the first week after the snakebite, CT scans were performed, but it was only two weeks later that the hemorrhagic infarcts started to show signs of resolution (Figure 3).
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DISCUSSION |
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The manifestations following viper bites depend on the severity of envenomation. In cases of minimal envenomation, only local signs at the bite site are observed, mainly swelling, erythema, and ecchymosis, while systemic manifestations are either insignificant or absent. If there is moderate envenomation, the local signs may also include the presence of blisters and may involve a larger part of the affected location. Systemic symptoms may be present, but are not life-threatening (mild hypotension, tachycardia, and tachypnea). In cases of severe envenomation, the local signs are profound, involving the entire affected location, spread rapidly, and include hemorrhagic edema and tissue necrosis. Systemic manifestations are also present and may include abdominal pain, nausea, vomiting, severe hypotension, tachypnea, dyspnea, tachycardia, and neurologic signs and symptoms. There may also be bleeding present, either from the bite site or from mucosal surfaces.
Snake envenomation may cause one or more major complications. Hemorrhagins and hemolysins destroy the walls of blood vessels and along with coagulation defects lead to blood loss severe enough to require a transfusion. Proteolysins result in cell and tissue destruction and tissue loss at the site of the bite. In addition, the necrotizing tissues are a good environment for anaerobic bacteria and may lead to abscess formation. The hemorrhagic activity of the venom causes widespread damage to the capillary walls and may result in pulmonary edema, tachypnea, or dyspnea. Moreover, hemorrhagin-induced hematuria, along with myoglobinuria from muscle destruction, affects renal function and may lead to renal failure. Cardiotoxins present in Viperidae venom may cause depolarization of cardiac muscles and lead to arrhythmias (supraventricular tachycardia). They may also alter heart contraction and in combination with hypotension cause cardiovascular collapse.2 Singh and others3 have reported a case of fatal, non-bacterial thrombotic endocarditis following a viperine bite.
Most of the viper venoms exhibit both anticoagulant and coagulant effects.4 The coagulant effect may be a result of arginine esterase hydrolase, an enzyme that is similar in action to thrombin, and which clots fibrinogen and aggregates platelets. These coagulant effects may also be due to the conversion of prothrombin to thrombin, a change catalyzed by proteinases.4 This triggering of the coagulation cascade in vivo results in the formation of microthrombi, the activation of fibrinolysis, and a bleeding tendency, which could lead to hemorrhagic complications.
Hypotension is a common and serious complication of Viperidae envenomation and should be treated aggressively. Direct action of toxins on the walls of blood vessels and the release of vasogenic agents such as bradykinin and histamine leads to vascular wall permeability deterioration, vasodilatation and lowering of peripheral vascular resistance, which results in pooling of blood in the pulmonary and splanchnic vascular beds. Subsequently, hemolysis and leakage of plasma and red blood cells through the damaged capillary endothelium can occur, along with fluid loss through sweating, vomiting, or diarrhea.
Hypotension was present at all times in the patient, from her initial examination at Argos District Hospital (blood pressure = 80/50 mm of Hg) to her transfer to Evangelismos General Hospital (100/70 mm of Hg). This patient had a known history of hypertension since the age of 45. There is a strong possibility that hypertension, if poorly regulated, had damaged the autoregulation mechanism of the cerebral blood supply. Thus, the sudden hypotension caused by the snake venom would place her at increased risk of central nervous system hemorrhage.
The neurologic features of viper snakebites include cranial and peripheral nerve symptoms, drowsiness, confusion, convulsions, fainting, dizziness, weakness, blurred vision, and loss of muscle coordination.4 Subarachnoid hemorrhage also may be present, along with systemic and neurologic hemorrhagic abnormalities.5,6 Tibballs and others7 reported a case of fatal cerebral hemorrhage following snake envenomation. However, nonhemorrhagic cerebral infraction is quite rare. This has been reported by Ameratunga,8 in which a Russel’s viper bite caused a middle cerebral artery occlusion. Bashir and Jinkins9 reported an infraction of the left supraclinoid part of the internal carotid artery after viper envenomation. However, the cause of cerebral arterial occlusion in both of these cases was not clear. These investigators suggested that the cerebral infarction could be related to the vessel-damaging toxin in the venom, possibly acting on a pre-existing abnormality in the blood vessel wall. Other possibilities they considered included low-grade dissemination of intravascular coagulopathy and hypotension.4
The patient in this study showed focal neurologic symptoms. However, the decrease in muscle strength, the increase in tendon reflexes, hemianopsia, and the positive Babinski sign were attributed to the cerebral pathology. The brain CT scan revealed multiple hemorrhagic infarcts. The pathogenesis of the infarcts was not clear. The hemorrhagins present in the venom are known to cause destruction of blood vessel walls and vasospasm, followed by vasodilatation of the microvessels and arterioles. It was assumed that the leakage of red blood cells through the damaged brain capillary walls, along with the coagulopathy present, resulted in small hemorrhages in the brain capillary bed.10
A second possible mechanism for the formation of multiple infarcts was an embolic infarction. The patient was hypotensive on her arrival at the local hospital, possibly as a result of the action of venom toxins on the blood vessel wall. Hypotension, along with the intravascular triggering of the coagulation cascade, may have resulted to formation of microthrombi that led to the multiple hemorrhagic infarcts. The multiplicity of the lesions and the gradual improvement of the patient’s clinical and laboratory status led to the decision for conservative treatment. Cerebral edema was controlled with the use of steroids.
Recognition of a snakebite is usually easy. The event as described by the patient, the fang marks, and the local pain are sufficient for diagnosis. However, some bites may be dry, with no envenomation following the injury. Another important issue is the snake species involved, since it is very rarely recognized or caught. This poses some clinical problems regarding the severity of the envenoming and the decision to administer antivenom. In these instances, an enzyme-linked immunosorbent assay may be helpful. This test can quantify some venoms in both blood and urine and, along with the increase in edema that appears within the first two hours of the bite and the presence of gastrointestinal and cardiovascular disorders, helps assess the severity of poisoning and decision making concerning specific treatment (antivenom).1
Snake envenomation is currently a rare event in Greece, with only a few cases reported every year. This leads to a lack of experience of physicians in treating cases of envenomation by snakebites. We believe this is one of the reasons for the high mortality and morbidity rates reported in the literature. In such cases, immediate medical treatment must be given without delay. This treatment should include six procedures.
First, the patient should be kept calm and remain as inactive as possible to limit the systemic spread of the venom. The patient should also be transferred in a horizontal position.
Second, the bite site should be washed thoroughly with soap and water or disinfecting solutions since snake venom may contain tetanus-causing bacteria or other anaerobes.
Third, the injured extremity should be immobilized and kept lower than the heart. Immobilization will reduce both the spread of venom and reduce pain. It is known that lymph will circulate slower in an immobilized extremity and help delay systemic poisoning.
Fourth, in cases in which the bite is located on a limb, a tourniquet should be applied proximal to the bite and tight enough to prevent venom absorption both by the superficial venous and the lymphatic system, which is responsible for systemic spread of most venoms. This should remain in place until the decision to administer antivenom is made at the hospital. The tourniquet should not be extremely tight since it will lead to interruption of arterial flow and deep vein venom absorption. Furthermore, a tightly applied tourniquet will encourage venom absorption by the products of tissue metabolism and after its removal may lead to rapid deterioration of the patient. Finally, in cases with rapidly increasing edema, the tourniquet should be loosened to avoid additional pressure-induced injury to the limb.
Fifth, making cuts over the fang marks should be avoided, especially in Viperidae envenomation, which is capable of producing significant local necrosis. These cuts are not as effective as previously thought and may result in severe damage if the bite has caused significant local tissue injury. A suction device, such as the Sawyer vacuum extractor (Sawyer Products, Safety Harbor, FL), which delivers one atmosphere of negative pressure to the wound, can be placed over the bite to help draw venom out of the wound. These devices are often included in commercial snakebite kits and can help remove up to 20% of the injected venom within 30 minutes of the bite. Negative pressure suction devices may mitigate the effect of envenoming and need for large doses of antivenom, but they should be applied immediately to be effective.
Sixth, vital signs should be monitored until the patient begins receiving medical care. It is also very important that all treatment measures under no circumstances delay the transport of the patient to the nearest hospital.
When the patient is transferred to the nearest medical facility, it is extremely important to obtain early intravenous access and begin fluid administration to aid in counteracting hypotension. Crystalloid solutions can be initially used, but in cases of severe bleeding or shock, colloid solutions, fresh frozen plasma, blood transfusions, and even vasopressors (e.g., dopamine) should also be used. Tetanus prophylaxis must be administered in all cases, since it has been observed that snake venom may contain tetanus-causing bacteria, and because there is a strong possibility of wound infection by dust or even clothes. Blood samples must be obtained for laboratory analysis that should include a complete blood count to evaluate the degree of hemorrhaging, a coagulation profile, studies of renal and hepatic function, and the determination of blood type and cross-matching. Urine should be tested for blood or myoglobin (which would suggest rhabdomyolysis) and a brisk urine output should be maintained. The patient must be closely monitored for renal and cardiac functions. Cardiotoxins may produce cardiac arrhythmias that may require a temporary pacemaker. Pulmonary function should also be closely monitored for pulmonary edema and dyspnea, and the patient may require supplemental oxygen or even intubation and mechanical ventilation with 100% oxygen.
The basic method for the treatment of envenomation is the use of one of the specific antivenoms available. An attempt to locate the appropriate antivenom should be done immediately, regardless if the envenomation is moderate or severe. The antivenoms available in Greece are gamma venin-P (Gerolymatos Pharmaceutical Company, Athens, Greece), viper snake antivenom (Greek Pasteur Institute), anti-snake venom serum OLGX21 (Aventis Behring, King of Prussia, PA), and serum antiviperin (Istituto Sieroterapico e Vaccinogeno Toscano Sclavo, Siena, Italy). Each of these antivenoms contains antibodies against the specific viper venom (e.g., the Sclavo antivenom contains antibodies against the venoms of V. ammodytes, V. aspis, V. erus, and V. ursini), but they should be administered only in a hospital because of possible complications, especially anaphylactic shock. Thus, before administration, a detailed history of the patient should be obtained regarding previous snakebites, antivenom administration, allergies to horses or goats, or previous serum sickness, followed by an initial sensitivity test.
The ischemic lesions caused by snake envenomation may occur more frequently than those reported in the literature. The possible pathogenic mechanism includes vasoconstriction and ischemia in the brain caused by the venom or the formation of microthrombi as a result of snake venom–induced hypotension and coagulopathy. We believe that the treatment of choice should be conservative in cases in which CT of the brain shows multiple lesions that do not cause serious medical problems. The small number of snake envenomations reported every year in Greece is responsible for the difficulties in diagnosis and treatment, since physicians lack the necessary experience in dealing with patients affected by snake-bites. Education of both public and private practitioners is essential to provide the knowledge needed to treat these patients.
Received July 22, 2002. Accepted for publication October 28, 2002.
Authors’ addresses: Efstathios J. Boviatsis (E-mail: eboviats{at} med.uoa.gr), Andreas T. Kouyialis (E-mail: Kouyialis{at}hotmail.com), Stefanos Korfias, and Damianos E. Sakas, Department of Neurosurgery, Evangelismos General Hospital, 45-47 Ipsilantou Street, Athens 106 76, Greece, Telephone: 30-10-729-1704, Fax: 30-10-721-5281. George Papatheodorou, Department of Radiology, Pireus General Hospital, 3 Petrou Ralli and Mantoubalou Streets, Pireus, Athens, Greece, Telephone: 30-10-4915281. Maro Gavra, Department of Radiology, Evgenidio Hospital, 10 Tzoumerkon Street, Papagou, Athens, Greece, Telephone: 30-10-6518138.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONCASE REPORTDISCUSSIONREFERENCES |
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