Acute Myocardial Infarction following a possible direct intravenous bite of Russell’s viper (Daboia russelli)
© Silva et al.; licensee BioMed Central Ltd. 2012
Received: 8 June 2012
Accepted: 3 September 2012
Published: 12 September 2012
Russell’s viper (Daboia russelli) bites lead to high morbidity and mortality in South Asia. Although variety of clinical manifestations is reported in viper bite victims, myocardial ischemic events are rare.
We report a unique case of inferior wall ST elevation myocardial infarction due to a Russell’s viper bite over a vein with possible direct intravenous envenoming, in a young male with no past history or family history suggestive of ischemic cardiac disease, from Sri Lanka. In addition, the possible mechanisms of myocardial ischemia in snake bite victims are also briefly discussed.
Importance of the awareness of physicians on the rare, yet fatal manifestations of snake envenoming is highlighted.
KeywordsMyocardial infarction Russell’s viper Intravenous Sri Lanka
Envenoming by Russell’s viper (Daboia russelli) is common in Sri Lanka, particularly in North Central Province where it leads to highest number of bites than any other snake , causing frequent systemic envenoming [2, 3]. Local swelling (92%), local necrosis (8.9%), coagulopathy (77%), neurotoxicity (78%), nephrotoxicity (18%), cardiac effects (3-12%) and myotoxicity (14%) is known to be associated with envenoming by Russell’s vipers . The available antivenom for this snake (Indian polyvalent antivenom), is known to be less effective in treating victims bitten by Sri Lankan Russell’s viper .
Ischemic cardiac events , arrhythmias  and cardiac tamponade  rarely occur after Russell’s viper bites. Although very rare, myocardial infarction following Russell’s viper bite has been previously reported from Sri Lanka . We report rapid development of inferior wall ST elevation myocardial infarction after Russell’s viper bite, probably due to direct intravenous venom injection.
Teaching Hospital - Anuradhapura is located in the North Central Province, where highest number of Russell’s viper bites is recorded from Sri Lanka . Of all the snakebite admissions to this hospital, 48% are due to Russell’s viper bites . In Sri Lanka, bites by these snakes are highest in months of March-April, and commonly occur at daytime on paddy fields and at dusk on footpaths and roads . Fang marks are almost always associated with Russell’s viper bites and 77% of victims develop prolonged WBCT . Although the assailant snake was not available for authentication, the victim identified the snake and told others accompanying him to the hospital, the geographical area, time and circumstance of the bite, prominent fang marks and prolonged WBCT all indicate to Russell’s viper bite.
Cardiac manifestations are relatively uncommon in snake bite victims, compared to more common systemic manifestations like coagulopathy, renal toxicity or neurotoxicity. Cardiac manifestations seem to be more rapid and life threatening than most of the other systemic manifestation of snake envenoming. Reported case of myocardial infarction had occurred within 1 hour following Russell’s viper bite, before other systemic manifestations .
Based on Troponin T levels and ECG of 13 victims of Sri Lankan Russell’s viper, Seneviratne et al.  opined that myocardial damage is not an important feature of Russell’s viper bites in Sri Lanka. Kularatne  observed ischemic EEG changes only in four of the 336 Russell’s viper bite victims from Sri Lanka. However in this case, ST elevations in LIII and aVF leads of the first ECG (Figures 1) and the changes in subsequent ECGs which were consistent with the first ECG suggests an inferior wall myocardial infarction, probably due to occlusion of the right coronary artery. The elevated Troponin I levels support the diagnosis of myocardial infarction, although this may be due to cardio- pulmonary resuscitation. The exact mechanism by which snake venom causes myocardial ischemia is unclear. However, hypovolemic shock, hypercoagulability , toxic myocarditis and coronary artery spasm have been proposed as possible mechanisms for myocardial infarction in snake bite victims, both humans and animals [9–13]. Hypovolemic shock and toxic myocarditis are unlikely in this patient as these lead to more extensive myocardial damage, and they take some time to develop in snake bite victims . In addition, toxic myocarditis as the cause of the ECG changes with elevated cardiac enzymes is unlikely due to lack of associated arrhythmias.
Russell’s viper venom contains components like factor V and Factor X activators, which create high procoagulant potential within the bite victim . Compared to small animals, this however, generally does not lead to thrombosis in humans because in usual snake bites venom injection is subcutaneous or intramuscular and the venom dose is small relative to the body weight . Therefore, rather than thrombosis, this give rise to venom induced consumption coagulopathy in humans . However, evidence for thrombosis in coronary, cerebral and pulmonary vasculature has been observed following viper bites in humans [11, 13, 17–20] and a possibility in this patient.
In most snake bites, the venom is being injected via intramuscular or subcutaneous route . However, intravenous route provides more rapid and efficient envenoming. Hence the ‘usual’ clinical picture may vary when the route of venom injection is intravenous. In this victim, gush of blood from the bite site, fang marks over a dilated vein and rapid bleeding through the fang marks with the rise of blood pressure following resuscitation indicate a direct intravenous venom injection. In addition, development of syncope within few minutes and the cardiac arrest, 45 minutes after the bite may also indicate rapid and severe envenoming, which could well be due to intravenous venom injection. Therefore, a high dose of venom entered via intravenous route leading to coronary thrombosis resulting in rapid development of myocardial infarction in this patient is a possibility.
Coronary artery spasm is also likely in cases of ischemic cardiac symptoms following the snake bite , Presence of normal coronary arteries in post myocardial infarction coronary angiograms of the viper bite induced myocardial infarction patients [9, 21] suggest coronary artery spasm as a possible cause of myocardial ischemia. Similar ST elevation myocardial infarctions have been observed in viper bite victims who had developed coronary artery spasm following Kounis syndrome , which is a concurrence of acute coronary syndromes associated with mast cell activation including allergic and anaphylactic insults . Clinically, we did not observe any evidence of above events in the victim on admission or following the recovery form the initial cardiac arrest, hence Kounis syndrome is less likely to have occurred in our patient. Hyperkalemia and cardiac arrest following Russell’s viper bites had been reported from Sri Lanka in two deaths . However, the serum potassium levels of our patient remained within normal range throughout, thus this is a remote possibility.
However, since the post mortem was not conducted in this patient, it is not possible to draw any firm conclusions on the aetio-pathogenesis of the myocardial infarction.
Neutrophil leukocytosis has been commonly observed among viper bite victims [3, 24], as similarly observed in this victim who had an on-admission count of 27.6 X 103 μl-1. Although a common phenomenon, extensive literature search failed to find studies investigating mechanism of leukocytosis following snake envenoming.
This unique case provides evidences for rapid development of ST elevation myocardial infarction following a possible intravenous envenoming by a Russell’s viper bite. Pathophysiology of myocardial ischemia in snakebites needs to be explored through careful documentation of clinical condition and thorough investigation of the snakebite victims.
Since the patient was unconscious throughout, the written informed consent was obtained from the spouse of the patient for publication of this case report and accompanying figure. A copy of the written consent is available for review by the Editor-in-Chief of this journal.
Whole blood clotting time.
Kalana Maduwage (Newcastle University, Australia) is acknowledged for providing valuable assistance in literature survey.
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