Cardiac Tamponade in Russell Viper (Daboia russelii) Bite: Case Report with Brief Review

doi:10.1016/j.jemermed.2010.11.052

The Journal of Emergency Medicine

Volume 42, Issue 3, March 2012, Pages 288-290

https://doi.org/10.1016/j.jemermed.2010.11.052 Get rights and content

Abstract

Background

Coagulopathy after snake bite is well known; however, cardiac tamponade as a manifestation of coagulopathy is rare.

Objective

To report a case of pericardial hemorrhage with cardiac tamponade after Russell viper bite.

Case Report

A 26-year-old man developed breathlessness after being bitten by a Russell viper. The clinical and laboratory follow-up of this case confirmed the clinical diagnosis of toxin-induced disseminated intravascular coagulation. Interestingly, pericardial hemorrhage with large pericardial effusion was evident clinically as well as on electrocardiogram and echocardiogram, as an initial presentation without any other bleeding manifestations. The patient developed cardiac arrest and was revived with cardiopulmonary resuscitation. Emergency pericardiocentesis was carried out. He was given fresh frozen plasma in addition to snake antivenin along with symptomatic management. On the third day of hospitalization, the patient’s clinical and laboratory profile returned to normal and he was discharged on the fifth day.

Conclusion

Pericardial hemorrhage may be due to toxin-induced myocardial damage or pericardial vessel injury coupled with coagulopathy, possibly in conjunction with vasculitis or endothelial damage. Practitioners and physicians should suspect and search for pericardial effusion in snake bite victims who develop breathlessness, and treat it vigorously in addition to antivenin therapy.

Introduction

Snake bites are common in rural India and many result in life-threatening medical emergencies. Every year, approximately 15,000 people die due to snake envenomation in India. Although coagulopathy after Viperidae snake bite has been well documented, the victims usually do not suffer from severe generalized bleeding 1, 2, 3, 4. Cardiac involvement is an infrequently recognized manifestation in the victims of viperine bites 4, 5, 6. We report a case of pericardial hemorrhage with cardiac tamponade after Russell viper bite that resulted in cardiac arrest; the patient was successfully revived with cardiopulmonary resuscitation.

With written informed consent from the patient and after institutional ethical clearance according to Helsinki Declaration guidelines, this case report was analyzed.

Section snippets

Case Report

A 26-year-old, healthy male farmer was brought to the Emergency Department after 6 h of progressive breathlessness after a snake bite. He kept a snake stone at the site of the bite and came to the hospital with the dead snake, identified as a viperine snake, Daboia russelii (Russell viper). A snake stone is a small, smooth-surfaced stone or piece of porous substance reputed in the native medical practice to cure snake bites. It is usually applied to the site of the snake bite and tied firmly.

Discussion

Daboia russeli, a monotypic genus, is found throughout the Indian subcontinent and Southeast Asia. Envenomation with Daboia has significant effects on the hemostatic system by producing coagulopathy and hemorrhage (1). Venom of Daboia is a mixture of various enzymes and peptides such as hemorrhagin, phospholipase A₂ (PLA₂), and procoagulants. These individually, or in association, lead to spontaneous activation of factors V, X, and fibrinogen, producing a fragile fibrin and bleeding (1).

Conclusion

In the present case of viper bite, hemorrhage may have occurred into the pericardium. In the treatment of hemotoxic snake envenomation, the treating physician should suspect and look for pericardial effusion at presentation or during the course of treatment, and confirm it by objective means, followed by appropriate management.

Acknowledgments

We would like to thank Dr. K. Arthanari, MS, for the logistical support and Dr. Sagar Galwankar, MBBS, DNB, MPH, and Dr. Praveen Aggarwal, MD, FICP, for their support.

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Envenoming by Russell's viper in Sri Lanka commonly leads to local envenoming, venom-induced consumptive coagulopathy, neurotoxicity, acute kidney injury and myotoxicity (Silva et al., 2016). Even though rare, cardiac ischaemic events (Silva et al., 2012), arrhythmias (Ventricular tachycardia, 1651) and the secondary effects of bleeding such as cardiac tamponade (Senthilkumaran et al., 2012) have been reported following Russell's viper bite. Kounis syndrome was first described in 1991, as the occurrence of acute coronary syndromes associated with mast-cell and platelet activation in the setting of allergic or anaphylactic insults (Kounis, 2016).
Kounis syndrome is the occurrence of acute coronary syndrome associated with mast cell and platelet activation in the setting of allergic or anaphylactic insults. Kounis syndrome has been previously reported following snake envenoming rarely, with or without antivenom therapy. We report a case of inferolateral ST elevation myocardial infarction 32 hours from a confirmed Russell's viper bite. He also had an anaphylactic reaction soon after antivenom. The absence of underlying atheromatous coronary artery disease during subsequent cardiac imaging was suggestive of a diagnosis of a type I variant of Kounis syndrome. Chest pain completely resolved by day 6 following initiation of standard treatment for acute coronary syndrome. Concurrence of allergic features and acute coronary syndrome in a snakebite patient following antivenom therapy should alert clinicians to the possibility of Kounis syndrome, which should be diagnosed with a high degree of clinical suspicion.
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RVV is also nephrotoxic in vitro. One of the most surprising histopathologic changes observed is the lysis of the vascular smooth muscule, which may also augment the action of the so-called hemorrhagins present in RVV.13 Vasolysis and mesangiolysis coupled with the action of hemorrhagins might lead to the leakage of blood into the adrenal glands of a susceptible individual.
Snakebite envenomation is an important public health problem in tropical countries. We report a case of bilateral adrenal hemorrhage in a 28-y-old man with Russell's viper bite that occurred in the Sathyamangalam forest range in the Indian state of Tamil Nadu. In this case, a combination of early bite recognition, hospital-based supportive care, corticosteroid therapy, and timely administration of polyvalent antivenom resulted in a favorable clinical outcome.
Problems and Paradoxes of Animal Toxins and the Heart
2015, Heart and Toxins
Animal poisons induce myocardial damage after envenomation. Those capable of producing toxins in their salivary gland and delivering them through biting or stinging are referred to as venomous animals. Snakes and arthropods, such as scorpions, spiders, and hymenoptera (e.g., bee, wasp), are common worldwide and envenomation of these species causes cardiac toxicity. This chapter focuses on the cardiac complications induced by the envenomation from snakes and arthropods.
Synergistically acting PLA<inf>2</inf>: Peptide hemorrhagic complex from Daboia russelii venom
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Among these, hemorrhage on the site of bite and unhealed wounds of the victim were severe and major manifestation of envenomation, though renal failure is considered as the primary cause of death (Kularatne et al., 2011) (Warrell, 1989). Recent studies and clinical observations have indicated higher case fatalities and more severe hemorrhagic manifestations in D. russelii envenoming in Eastern India, Myanmar and in other regions (Kumar and Gowda, 2006; Mukherje et al., 2000; Senthilkumaran et al., 2012) (Warrell, 1997). Although hemorrhage is a well-known phenomenon in the Daboia russelii bites, its mechanism of action needs to be elucidated.
Snake venoms are complex mixture of enzymatic and non-enzymatic proteins. Non-covalent protein–protein interaction leads to protein complexes, which bring about enhanced pharmacological injuries by their synergistic action. Here we report identification and characterization of a new Daboia russelii hemorrhagic complex I (DR–HC-I) containing phospholipase A₂ (PLA₂) and non-enzymatic peptide. DR–HC-I was isolated from the venom of D. russelii by CM-Shepadex-C25 and gel permeation chromatography. Individual components were purified and identified by RP-HPL chromatography, mass spectrometry and N-terminal amino acid sequencing. DR–HC-I complex was lethal to mice with the LD₅₀ dose of 0.7 mg/kg body weight with hemorrhagic and neurotoxic properties. DR–HC-I complex consists of non-hemorrhagic PLA₂ and neurotoxic non-enzymatic peptide. The non-enzymatic peptide quenched the intrinsic fluorescence of PLA₂ in a dose dependent manner, signifying the synergistic interaction between two proteins. PLA₂ and peptide toxin in a 5:2 M ratio induced skin hemorrhage in mice with MHD 20 μg. However, addition of ANS (1-Anilino-8-naphthalene sulfonate) to DR–HC–I complex inhibited skin hemorrhagic effect and also synergic interaction. But there was no impact on PLA₂ due to this synergistic interaction, and indirect hemolytic or plasma re-calcification activity. However, the synergistic interaction of PLA₂ and non-enzymatic peptide contributes to the enhanced venom-induced hemorrhage and toxicity of Daboia russellii venom.
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Selected Topics: ToxicologyCardiac Tamponade in Russell Viper (Daboia russelii) Bite: Case Report with Brief Review

Abstract

Background

Objective

Case Report

Conclusion

Introduction

Section snippets

Case Report

Discussion

Conclusion

Acknowledgments

Toxicon

Trends Pharmacol Sci

J Mol Cell Cardiol

Biochem Biophys Res Commun

Acute myocardial infarction complicating snake bite

J Assoc Physicians India

Selected Topics: Toxicology
Cardiac Tamponade in Russell Viper (Daboia russelii) Bite: Case Report with Brief Review