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| REVIEW ARTICLE |
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| Year : 2023 | Volume
: 22
| Issue : 3 | Page : 239-245 |
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Intravenous snake bite: A catastrophic snake envenomation
Sadananda B Naik
Senior Physician, Alva's Health Centre, Moodabidri, Karnataka, India
| Date of Submission | 21-Jan-2023 |
| Date of Decision | 02-Feb-2023 |
| Date of Acceptance | 09-Feb-2023 |
| Date of Web Publication | 4-Jul-2023 |
Correspondence Address:
Sadananda B Naik
Alva's Health Centre, Moodabidri - 574 227, Karnataka
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/aam.aam_9_23
 Abstract | | |
The rapid onset of life-threatening clinical manifestations in venomous snake bite could be due to an intravenous bite. This article seeks to review and consider the clinical implications, pathophysiology, and management of this rare route of snake envenomation broadly by venomous snakes which are little described in the available literature.
Résumé
L'apparition rapide des manifestations cliniques potentiellement mortelles dans la morsure de serpent venimeux pourrait être due à une morsure intraveineuse. Cet article vise à revoir et à considérer les implications cliniques, la physiopathologie et la gestion de cette rare itinéraire d'envenomations de serpents largement par des serpents venimeux qui sont peu décrits dans la littérature disponible.
Mots-clés: Effondrement cardiovasculaire, morsure de serpent intraveineuse, début rapide de la mort, envenimation de serpent
Keywords: Cardiovascular collapse, intravenous snake bite, rapid onset of death, snake envenomation
How to cite this article:
Naik SB. Intravenous snake bite: A catastrophic snake envenomation. Ann Afr Med 2023;22:239-45 |
| Introduction | |  |
Snake bite is a common public health problem in many tropical countries. According to the WHO, annually 4.5–5.4 million people get bitten by snakes, and the reported death after snake bite can range from 81,000 to 138,000. Many of the deaths are preventable as they are due to inadequate facilities available for the treatment in the rural areas and ignorance vitiated by myths surrounding the snake envenomation.[1] Whenever, a victim of snake bite succumbs within a very short span of time from the bite, clinicians may consider the possibility of an intravascular bite, as one among the several other possibilities. There is not a clear clinical definition of intravenous (IV) snake envenomation. Although it seems self-explanatory, actually not. However, this could be an important cause of rapid death following a venomous snake bite.[2],[3] The available literature on this aspect of venomous snake bite is scanty and this article aims to provide a possible overview of the incidence, pathophysiology, clinical features, and available management options of this life-threatening mode of snake envenomation. A search was done in PubMed with keywords – “snake envenomation,” “intravenous snake bite,” “rapid death,” and “intravenous snake venom injection/inoculation.” Relevant articles were reviewed along with the available cross-references and the manuscript was prepared.
| Background | | |
When a venomous snake bites, the venom gets injected into the dermis and subcutaneous tissues. Later, the venom gets absorbed slowly and steadily through the veins and lymphatics producing local, regional, and systemic manifestations of envenomation. Rarely one or both fangs could strike a superficial vein and inject an IV bolus dose of venom. In these cases, systemic symptoms evolve rapidly within 1 or 2 min and the result would be fatal if not treated on time.[4] Thus, when a victim of a venomous snake bite dies quickly following syncope or cardiovascular collapse, clinicians could contemplate the possibility of intravascular bite, though several other mechanisms for early deaths in different venomous snakes have been described.[5],[6],[7],[8]
Deaths occurring within hours of a venomous snake bite are usually attributed to the paralysis of respiratory muscles as seen in the bites due to kraits, cobras, mambas, or coral snakes. They may also occur due to unexplained cardiovascular collapse, anaphylaxis due to venom toxins, or rarely due to hypersensitization resulting from the previous bites. Whereas, the deaths occurring after 12 h of bite are generally thought to be due to the hemotoxicity as seen in viper bite,[2],[9] though there are reports of early deaths.[10] Very rapid death occurring in “a few minutes” has been reported following bite of the king cobra (Ophiophagus Hannah).[11]
| Incidence | | |
Direct IV venom injection can occur in venomous snake bites but it is difficult to prove. There are no methods available at present to estimate the actual incidence of IV envenomation and the same limitation is true for other variables such as mortality and morbidity.[12] Dr. Dana Atchley's paper describes probably the first reported case of IV snake bite where the patient was successfully treated with a large volume of IV saline following a rattlesnake bite in the vein presenting with shock. Subsequently, many other reports of IV bites were published.[13] However, there are no large-scale case studies/data available in the literature on the actual incidence of envenomation due to intravascular snake bites but for a few published case reports.[4],[14] Another source of information on intravascular envenomation in humans is by way of published literature on IV self-injection of snake venom with suicidal intention.[15] Animal experiments which have been carried out on regular basis by injection of various types of snake venom give some insight into IV envenomation.[3],[16],[17] Accidental IV injection while injecting the venom into the horses in preparation for antivenom has given vital scientific inputs.[13]
Any venomous snake bite over the superficial veins could result in IV injection of the venom. Details of such anatomical locations as reported in the literature are given below.
| Anatomical Sites and the Veins Bitten in the Reported Cases | | |
- Long saphenous vein at the medial malleolus, ankle[4],[14],[18]
- Antecubital vein used for suicidal venom injection[15]
- Branches of the cephalic vein which form the dorsal venous arch at the web space between the thumb and first finger[4]
- Superficial veins at the ulnar surface of wrist[4]
- Veins constituting dorsal venous arch on the dorsum of the foot.[4]
These are the anatomical sites described in the reported cases and IV snake bite could be seen any other anatomical sites where the veins lie superficial. In addition, there are increased chances of IV inoculations of venom if it involves snakes with relatively longer fangs. Almost all the reported cases of IV envenomation in this article are by crotaline viperids and could be assumed to support this hypothesis [Table 1].
| Pharmacokinetic Considerations of Intravenous Venom Injection | | |
The knowledge of venom pharmacokinetics is the very basis of the understanding of snake envenomation pathophysiology. The time taken for the venom to enter the bloodstream would decide the rapidity of the onset of functional effects of the toxins in the venom. However, the pharmacokinetics of the venom injected directly into a vein could only be studied in the experimental studies and can give us some insight into the envenomation by IV bite. However, results could vary in different species of snakes. In a study done by Tan et al.[16] found that in the case of hump-nosed pit viper (Hypnale hypnale), while injecting the venom intravenously into the rabbits, there was a rapid as well as a slow distribution phase which was followed by a long elimination phase to facilitate systemic clearance. They also found that the lethal dose of the venom significantly varied between IV and intramuscular and the former route induced a higher bioavailability of the venom.
A review of various other studies[17] on the pharmacokinetics of snake venom assessed by injecting the venom and toxins into the veins of animals such as rats and rabbits showed that the IV injections resulted in a reduced half-life of the venom and toxins irrespective of the type of snakes as compared to the subcutaneous and intramuscular injections. Another interesting observation which was clinically relevant was that not all the venom or the toxins there in would be absorbed into the circulation following subcutaneous or intramuscular injection unlike the IV injection. The unabsorbed components of snake venom retained at the bite site may possibly responsible for the local tissue damage. Hence, theoretically, the IV snake bite should in fact result in lesser or minimal local tissue damage. This fact was evident when the venom is directly injected into the vein as a suicidal attempt.[15] The IV injection practically avoids the issues related to bioavailability of venom.
| Pathophysiology | | |
Cardiotoxicity
Snake venom could result in cardiotoxicity due to the effect of several toxins and proteins in it, namely the phospholipases A2 which is basically cardiotoxic, elapid three-finger peptides (three-finger toxins), and snake venom serine-proteases.[19] There could be the occurrence of myocarditis due to the direct effect of the venom or coronary artery spasm and in some snakes in situ coronary thrombosis. All these pathological changes would eventually lead to clinical features of cardiotoxicity such as cardiovascular collapse, acute myocardial infarction, or cardiac arrhythmias.[14],[19] The cardiotoxins found in elapid and hydrophiid venoms because of their small molecular size and strong positive charge lead to their rapid absorption. The cardiotoxin found in the cobra venom acts directly on the cell membrane resulting in circulatory failure, respiratory paralysis, and cardiac asystole. The resulting, asystolic cardiac arrest or circulatory collapse could be attributed to the release of Ca++ or direct myocardial toxicity.[20] In situ coronary arterial thrombosis has been seen in Bothrops lanceolatus and Bothrops caribbaeus bites. The venom of B. lanceolatus has the unique ability to induce systemic thrombotic complication by way of causing direct endothelial injury resulting in local thrombosis.[21],[22],[23] All these cardiotoxic effects of snake venom would get amplified and occurs quickly because of a higher concentration of toxin if the venom reaches the heart directly following IV bite.
Some insights from animal studies and experiments
In an animal study in pigs which involved injecting rattlesnake venom intravenously, Fish et al.[3] found that the cardiovascular collapse resulted from reduced left ventricular filling rather than myocardial depression or arrhythmias as had generally been thought. Tungthanathanich et al.[24] found that IV injection of the minimal lethal dose of 0.1 mg/kg of Russell's viper venom in anesthetized mongrel dogs resulted in cardiovascular manifestation. These manifestations seem to occur in two phases.[24],[25]
- First phase: This is the initial postinjection period
- Second phase: Seen 2 h after the injection.
First phase
In this phase, there would be a decrease in mean arterial pressure along with decrease in the heart rate which sustains for about 30 min and changes return to normalcy within 2 h of injection of the venom. The hypotension and bradycardia are found to be independent of cholinergic origin as preatropinization did not prevent them. Vaso dilatation of capillaries in the splanchnic circulation or direct effect of venom fraction of PLA2 along with the kinins like histamine released by the victim results in peripheral vasodilatation and pulmonary vasoconstriction. Subsequent decreases of venous return to the left heart are the other possibilities.
Second phase
The release of catecholamines as compensatory mechanism seems to be responsible for the restoration of blood pressure in this phase. Any failure in this compensatory phenomenon would kill the victim. Renin–Angiotensin System activation was also found to contribute to this recovery.
Lu and Tsai[26] in their experiment on mice showed that the venom of different types of snakes shows variability in lethality when inoculated intravenously, intraperitoneal, and subcutaneous routes. In the case of hemorrhagic venom (Viperidae), it is the IV route which showed the highest lethality and in neurotropic venom (kraits and Cobras) it was intraperitoneal route. Oukkache et al.[27] in their experiment on the mice showed similar results and they attributed the difference to the rich composition of high molecular weight enzymes present in the viper venom. In physiological experiments on dogs and rabbits, it was found that IV inoculation of the venom of viper provoked fatal circulatory collapse but the cobra venom did not influence the blood pressure and in fact resulted in slow death by asphyxia resulting from respiratory muscle paralysis.[28]
The results of these snake venom experiments could be extrapolated to a clinical conclusion that, the Viperidae IV bite would results in rapid and fatal circulatory collapse and in the case of cobras and kraits bite results in relatively slow death due to asphyxiation.
Cardiovascular collapse
This is defined as a sudden drop in recordable blood pressure following the administration of venom, to a laboratory animal or after human envenomation.
Rahini Kakumanu et al[29] demonstrated two distinct patterns of cardiovascular effects in anaesthetized rats by injecting venoms of different snakes intravenously. Venom of Australian elapid, P. textilis[30], E. ocellatus showed 'rapid cardiovascular collapse' without recovery whereas venom of D. russelii, D. siamensis resulted in slower but prolonged hypotension with recovery seen in most of the cases. Both manifestations were found to be independent of the dosage and route of venom injection, hence proving that they are two separate cardiovascular manifestations of envenomation. The “rapid cardiovascular collapse” is typically sudden in onset and appears to be mediated by depletable endogenous mediators and the “prolonged hypotension” results from the peripheral vasodilatation. IV injections resulted in a cardiovascular collapse in around 2 min and it took 10 min for the intramuscular venom injection to produce a similar effect.
Pulmonary hemorrhage as the cause of rapid death
Benvenuti et al.[9] found in a case of Bothrops jararacussu snakebite, pulmonary hemorrhage causing rapid death. Over here, the victim died within 45 min of the bite over the ankle and the rapid onset of disseminated intravascular coagulation (DIC) and fatal pulmonary hemorrhage, an unusual occurrence in Viperidae bite was attributed to IV bite.
| Clinical Features | | |
Rapidly developing local and systemic features of snake envenomation occurring in a span of minutes of bite usually indicates the possibility of an IV venomous snake bite but not always. The IV route provides more rapid and efficient envenoming as it by passes the venom pharmacokinetics, which on other occasions, needs to be absorbed from the subcutaneous tissues and reach the circulation for it to act on various organs. Hence, the “usual” clinical picture may get amplified in terms of severity and the time required when the route of venom injection is IV.[14]
Local
The venom entering the vein directly without subcutaneous entry would not cause much signs of local envenoming.[15] However, there could be a situation where one fang puncturing the vein and the other one striking subcutaneous tissue resulting in local features of envenomation along with the rapidly occurring systemic envenomation. Blood gushing from the bite site, fang marks immediately following the bite or in some cases, immediately the following resuscitation of shock indicate a direct IV venom injection.[14] Fang puncturing the blood vessel could damage it which could explain the blood “gush.” However, it is scientifically very difficult to explain the phenomenon of blood gushing from a tiny punctured wall of the vein by the fangs as described in the published literature with no chance of local anti-hemostatic effects produced just by the fang contact. Ecchymosis seen all along the course of the vein starting from the bite site could be an indicator of IV venomous snakebite as described in the case report of fatal B. jararacussu snakebite where the postmortem study revealed ecchymosis along the great saphenous vein from the bite site in the ankle.[9]
Systemic
Systemic features appearing within minutes of snake bite could be thought occurring due to intravascular bite. The presentation could include severe nausea, vomiting, swelling of lips, tongue, altered sensorium delirium, or syncope occurring within minutes of bite. Neurological features such as extensive fasciculations of muscles of the tongue, face, limbs and hemodynamic collapse indicated by hypotension, tachycardia, and excessive sweating are seen within 15–20 min of bite in these patients. Early onset of bleeding tendencies like hematuria occurring within 15–20 min of bite could well be due to intravascular bite.[4] Patients presenting with cardiac arrest occurring within 45 min could also be an indicator of this kind of envenomation. There is also a report of acute myocardial infarction resulting from a possible direct IV Russell's viper bite.[14] However, it is possible to see a similar clinical picture in non-IV venomous snake bites as well.[31],[32] The victim dying within 45 min of bite and the rapid onset of DIC and fatal pulmonary hemorrhage as reported in the B. jararacussu snakebite could well be attributed to IV bite.[9] Whenever, a venomous snake bite which is otherwise known to produce a relatively benign features and no gross systemic response, results in severe life-threatening sequela as seen in the case report on copper head envenomation which resulted in shock, respiratory failure, and coagulopathy in the victim, one would contemplate the possibility of IV bite.[18] Another, a very surprising but reported feature of death occurring in a snake bite which is thought not to be nonvenomous could well be related to direct IV bite.[33] The fatality here could be more related to the vaso-vagal syncope occurring due to the bite as there is no venom sac connected to the snake teeth.[34]
| Hypotensive Peptides Overshadowing the Clinical Effects of Other Toxins | | |
The direct clinical effects of the prominent and specific snake venom toxins are obscured by the hypotensive peptides (bradykinin potentiating toxins) in some crotaline viperid venoms which causes sudden collapse of the patients due to rapid onset of hypotension. Hence, the rapid onset of classical clinical signs of specific envenomation fail to evolve.[35]
| Investigations | | |
There are no definitive investigations available as of now for the accurate diagnosis of IV venomous snake bite but the following laboratory abnormalities stood out in the case reports of IV bites.
- Patients with rapid reduction of platelet counts less 10,000/mm3 occurring within 1 h of bite could be an indicator of IV venomous snake bite[36],[37]
- Electrocardiography (ECG) showing acute myocardial infarction within 45 min of a venomous snake bite along with other clinical signs such as shock and cardiac arrest again may suggest an intravascular bite[14]
- Evidence of severe coagulopathy occurring less than an hour of bite[4] However, there are reports of early hemostatic defects following the non-IV bite of Echis romani (Carpet viper) in Nigeria.[38]
| Diagnosis | | |
The gold standard for diagnosis of IV snake bite would be the demonstration of a fang puncture wound on the vessel wall which is obviously a possibility postmortem rather than antemortem. Hence, as of now in clinical medicine the diagnosis of IV snake bite is essentially done with circumstantial evidence and clinical suspicion, based on the severity and rapidity with which features of snake envenomation sets in, in addition to the anatomical proximity of the bite the superficial veins.[4] Blood gushing from the bite site as described elaborately under local features, indicates a direct IV venom injection.[14] Ecchymosis seen all along the distribution of vein from the bite site in the case of Viperidae.[9] Thus, even though there are no conclusive tests, enough clinical indicators which could help the clinician to make a diagnosis of IV venomous snakebite and act accordingly.
| Differential Diagnosis | | |
Early death due to snake envenomation after non-intravenous -bite
There are several other mechanisms of early death other than IV bite following snake envenomation. They are as follows:
- Pseudonaja (Brown snakes) P. textilis in Australia by way of Procoagulant coagulopathy can cause acute cardiovascular collapse[6]
- There have been reports of early deaths attributed to cardiac arrest following brown snake (Pseudonaja spp.) non-IV envenomation in the Australian Snakebite Project (ASP-14). These early deaths were found to be due venom's cardiotoxicity[39]
- Hoffman et al. found venom-induced direct cardiotoxicity resulting in myocarditis in the horses during autopsy following injection of venom of Viper palaestinae and the cause of death in those horses was contemplated as uncontrolled hypotension[7]
- Weiser et al. in their experiments on the mice found that the venom components of the burrowing asp, Atractaspis engaddensis (Atractaspididae, Ophidia) caused rapid death due to prominent and direct action on the heart with or without artificial respiration. The ECG changes in these mice were similar to the changes seen in the human victims who presented with A-V block.[8]
Early fatalities and complications in venomous snake bites which are not due to envenomation
There are several acute complications in venomous snake bite which are not due to envenomation and would mimic intravascular envenomation by way of rapid onset of life-threatening clinical features or early death. Recognizing such problems and treating them could save life. Following are the possible causes of sudden death following venomous snake bite which are not due to envenomation.
- A nonimmune anaphylactic reaction to venom developing soon after the bite with angioedema characterized by swelling of lips, tongue, etc., urticaria, laryngeal edema, hypotension, and collapse.[5],[40],[41] In such fatal cases, the anaphylactic reaction is suspected and a postmortem measurement of serum mast cell tryptase will prove the diagnosis[42]
- Emotional shock: Mental shock of being bitten by a snake could make the victim get a neurogenic syncopal attack and lose consciousness. All the fatal complications occurring in an unconscious person due to venomous snake bite could be seen here as described in the case report by Norris et al.[43]
- Aspiration of food: Massive aspiration of food choking the airways could be the cause of sudden death in a venomous snake bite before the envenomation really sets in.[43]
| Management | | |
Intravascular snake venom injections result in rapid onset of systemic toxicity[16],[44] which is quite difficult to manage even if antivenom is freely available. It has been found that first aid measures are not of much use in these patients. However, advanced life support and supportive care have shown definite benefits.[3]
Symptomatic and supportive treatment
First aid measures which retard the venom absorption through the lymphatics by way of compression bandage (60 mmHg pressure) above the bite site and immobilization of the affected limbs are not relevant in the context of intravascular venom injection. However, if there is associated subcutaneous envenomation, these measures do help. Symptomatic treatments such as pain reduction using paracetamol infusion, hemodynamic stabilization using IV fluids with or without inotropes are to be initiated.
Specific measures
Antivenom treatment
A bolus dose of 10–15 vials of specific or polyvalent antivenom depending on the type of snake should be started as early as possible followed by continuous infusion. There is a possibility of concomitant subcutaneous injection of the venom along with intravascular when one fang pierces the vein and the other subcutaneous tissue. In these situations, the slow infusion of Anti snake venom will take care of the subcutaneously absorbed snake venom. Overall, a much higher dose of antivenom is needed and the need may go up as high as 30–40 vials.[4]
Prophylaxis and treatment of acute hypersensitivity reaction to antivenom
Although indeterminate value, use of high dose of corticosteroid in the form of Methylprednisolone (1 g) have been tried to protect against acute immunologic response while infusing a massive dose of anti-venom. However, if the patient develops anaphylaxis reaction, the use of antihistamines along with adrenaline is warranted.[4] However, the efficacy of antihistamines has not been proven as much as adrenaline.[45] Premedication with low-dose subcutaneous adrenaline has shown a reduction in the incidence of acute adverse reactions following the administration of antivenom therapy.[46]
Treatment of other life-threatening complications
Simultaneous management of complications like shock, coagulopathy and respiratory failure by way of inotropes, blood products and ventilatory support etc., is as important as the treatment with antivenom in saving the life.[18]
| Preventive Measures | | |
As the intravascular envenomation results in the rapid onset of symptoms with a high mortality rate despite timely and aggressive antivenom therapy, preventive measures are the best way forward. The routine preventive measures to avoid snake bite are applicable here as well. Avoid walking on bare feet or wearing only sandals, wearing gum boots with long pants will help to safeguard the ankle veins. The use of sticks to move rocks, stones instead of hands, the use of torch and stick while walking in the night, staying on trails while walking and hiking, etc., are the other preventive measures to be practiced.
| Limitations of the Article | | |
- Author was compelled to frequent extrapolation of experimental animal data due to relatively limited clinical data
- The exact definition of the IV snake bite is still illusive
- Limited by fewer literature on IV snake bites proved by way of autopsy.
| Suggestions | | |
Clinicians need to be encouraged to go for autopsy in cases of rapid onset of death to look for fang puncture of the superficial veins at the bite site which is the gold standard to confirm IV venomous snake bite.
| Conclusion | | |
Whenever there is a rapid onset of serious and life-threatening features of snake envenomation, a possibility of intravascular snake bite should be suspected and looked for. The diagnosis of IV snake bite is based on circumstantial clinical evidence along with the proximity of the bite to the superficial veins. We are yet to find any definitive method to diagnose this catastrophic manifestation of snake bite. In all the cases of suspected intravascular venomous snake bites, a relatively higher dose of antivenom should be started immediately as an IV bolus dose which should be followed by IV infusion after the initial recovery. The author hopes that this article would encourage venom researchers across the world to plan strategies to treat patients with rapidly evolving snake envenomation features as probable cases of IV snake bite. Until a definitive criterion is available, all those suspected cases could be labeled as “possible cases of IV snake bites.”
Acknowledgment
The author would like to thank Late Dr. Krishna Mohan Prabhu, Prabhu General Hospital, Moodabidri, India, for helping with the review of literature and typesetting the pages and also for being the digital backbone in preparing and submitting this manuscript.
The author is thankful to Mrs. Pooja Bhat, Chief Librarian, Kasturba Medical College, Mangalore, MAHE, INDIA for her wholehearted support and help in getting me the full text of some of the articles referred in the manuscript.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Table 1]
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