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| CASE REPORT |
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| Year : 2022 | Volume
: 17
| Issue : 4 | Page : 960-962 |
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Case report: Snakebite envenomation presenting with atrial fibrillation
Aditi Patni, Sourya Acharya, Vivek Lahane
Department of Internal Medicine, Acharya Vinobha Bhave Rural Hospital, Jawaharlal Nehru Medical College, DMIMS, Wardha, Maharashtra, India
| Date of Submission | 26-Aug-2022 |
| Date of Decision | 01-Oct-2022 |
| Date of Acceptance | 03-Oct-2022 |
| Date of Web Publication | 10-Feb-2023 |
Correspondence Address:
Dr. Aditi Patni
17061, ATS Advantage, Ahinsa Khand-1, Indirapuram, Ghaziabad - 201 014, Uttar Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jdmimsu.jdmimsu_380_22
Snakebite envenomation is a potentially life-threatening event which results due to the toxins present in the bite of venomous snakes. Snake bites commonly present with complications such as erythema, edema, bleeding, blistering, and tenderness at the bite site and autonomic symptoms such as nausea, vomiting, diarrhea, and increased salivation and sweating. Labored breathing and coagulopathy are among others. However, cardiac complications are not known to be a prominent feature of snakebites, although a few rare manifestations such as myocardial infarction and arrhythmias have been found in the literature. The case report that follows describes a patient of Snakebite who came with chief complaints of drowsiness, palpitation, nausea and vomiting. Blood investigation showed an abnormal coagulation profile. Electrocardiography revealed atrial fibrillation after which the patient was shifted to the intensive care unit and was treated with anti-snake venom. It eventually got resolved. Therefore, the case of snakebite warrants attentive cardiac monitoring.
Keywords: Anti-snake venom, atrial fibrillation, cardiotoxicity, snakebite
How to cite this article:
Patni A, Acharya S, Lahane V. Case report: Snakebite envenomation presenting with atrial fibrillation. J Datta Meghe Inst Med Sci Univ 2022;17:960-2 |
| Introduction | |  |
Snakebite is a life-threatening event caused due to the toxins in the bite of a venomous snake. Although it is widespread worldwide, South Asia and the Indian subcontinent have the highest prevalence rates. Rural agricultural workers, herders, and hunters are some of the high-risk groups. Although, Snakebite can occur in anyone. The outcome of the snakebite is determined by the variety of the snake, site of the bite, amount of snake venom administered, and the overall health of the victim. The toxin in snake venom has both local and systemic effects. Some viperid and elapid snakes can bite and inflict tissue damage, such as edema, pain, redness, and blistering. Venom can induce consumption coagulopathy, neuromuscular paralysis, and acute kidney injury. These are the most prevalent and significant systemic symptoms of snake envenoming.[1] Cardiac manifestation although uncommon includes myotoxicity and arrhythmias. The most common arrhythmias reported after viper snakebite includes ventricular tachycardia, torsades de pointes, and sinus arrest. Arrhythmia is a rare complication of snakebite.[2] Antivenom and supportive care are used as the initial treatments.[1] The treatment of bite wounds is the same as that of other puncture wounds. The area should be cleaned, and dressing should be done. The extremity is elevated and splinted in a functional position for limb bites. Daily inspection, cleaning, and sterile dressing application are required for wounds.[2]
| Case Report | | |
A 50-year-old male patient came to the casualty with the complaint of snakebite over his right foot at his home half an hour before the arrival. The relatives bought the snake with them on which diagnosis of Russell's viper envenomation was made.
The patient's relatives told, “He became drowsy and had difficulty opening his eyes soon after the bite. He also complained of palpitation and vomiting.”
On being inquired, no history of loss of consciousness, seizures, dysarthria, dysphoria, dysphagia, and diplopia was furnished.
Clinical findings
The patient's relatives confirmed that the patient is a known case of diabetes mellitus and hypertension for 5 years for which he is on tablet amlodipine and tablet atenolol for hypertension and tablet vildagliptin for diabetes mellitus.
On examination, the patient was afebrile and his pulse was 100 beats/min along with an irregular rhythm. All the peripheral pulses were palpable. Oxygen saturation at room air was 96%, respiratory rate was 18 cycles/min, and blood pressure was 130/80 mmHg. There were no abnormalities found during the systemic examination.
On local examination, two fang marks were seen on the right lateral aspect of the heel of the right foot. The marks were 1 cm away from each other and the blood was oozing from the site. Swelling of the surrounding area was also present [Figure 1].
Diagnostic focus and assessment
Blood investigation showed an abnormal coagulation profile with prothrombin time (PT) of 90 s, and activated partial thromboplastin time (APTT) of 120 s and decreased platelet count of 84000/mm3, hemoglobin 14.6 gm/dl, and total leukocyte counts of 6600/mm3. Both the liver function test and kidney function test came back normal. Cardiac enzymes creatine kinase-MB and Troponin-I levels were normal. Serum electrolyte levels were also within normal range.
Electrocardiography (ECG) was done in the emergency room and showed atrial fibrillation (AF) with a fast ventricular rate of 120 beats/min [Figure 2].
Treatment and its aftermath
The patient was shifted to the intensive care unit and was given 10 ampules of anti-snake venom along with ceftriaxone 1 g intravenously twice daily consecutively for 5 days. No adverse reaction to anti-snake venom was seen. Platelet count and coagulation profile gradually improved. With a ventricular rate of 90 beats/min, the ECG displayed a normal sinus rhythm. The patient's relatives told that his swelling subsided and his general health was improved. [Table 1] shows the timeline of events during the case.
Patient's perspective
On admission, the patient's relatives told, “He became drowsy and had difficulty in opening his eyes soon after the bite. He also complained of palpitation and vomiting.”
Posttreatment in the intensive care unit, the patient told, “I feel better, the swelling is reduced and there is amelioration in my general health.”
| Discussion | | |
Cardiac complications are not frequently recognized manifestations of venomous snakebites and are primarily linked to the genus Viperidae. Clinical presentation can differ following the different species of snake. The venoms of the cobra and krait are both cardiotoxic and neurotoxic. Cobra venom produces local effects, but krait venom does not. Rapid bloodstream absorption of the neurotoxins from sea snakes and elapids results in immediate systemic effects. The much larger molecules in viper venom, on the other hand, are absorbed through the lymphatics much more slowly, leading to severe local effects. The majority of venoms do not pass the blood–brain barrier.[3] The most specific sign indicating the involvement of the myocardium is the T-wave abnormalities on the ECG. Arrhythmia is one of the rare complications of snakebite. Arrhythmias which are less frequently reported following viper snakebite includes ventricular tachycardia, torsades de pointes, and sinus arrest. ECG alterations are typically transient, but when they last for a long time, they point toward the toxin causing direct myocardial damage.[4] It is unknown whether the venom, the ensuing systemic inflammatory response, or a combination of both causes cardiac complications. There are few reports of troponin elevation following snakebites in the literature.[5] Cardiotoxins primarily affect cell membranes directly, which has a wide range of outcomes on cardiac, skeletal, smooth muscles, and neuromuscular junctions. This results in the cessation of circulatory and respiratory function as well as cardiac asystole. It is demonstrated that the pharmacological effect of cardiotoxin is due to irreversible depolarization of the cell membrane transport mechanism and asystolic cardiac arrest, which may be brought on by the efflux of calcium from the surface membrane of the myocardial cells.[4] In our patient, it is seen that predisposing factors, toward arrhythmia, in the form of cardiovascular risk factors likely existed before envenomation. Established extracardiac predictors of AF include old age, hyperlipidemia, type 2 diabetes mellitus, and hypertension. AF may have been triggered by the activation of the autonomic nervous system (ANS), and subsequent adrenergic stimulation due to the activation of the ANS. Catecholamines have been demonstrated to influence the initiation of the AF, and or maintenance through various proposed electrophysiological mechanisms in the atrium.[2] Nevertheless, AF can result due to the direct toxic effects of the venom. It is thought that snake venom could potentially be toxic to the myocardial tissue and could change the electrophysiological characteristics of the cell membrane of cardiac tissue. This might affect the generation and conduction of cardiac impulses.[2] In various studies, cardiac manifestation was found in only 25% of patients with Russell's viper bite.
Seventy-six percent of the patients presented within 24 h of the bite. Seventy percent of patients had hemorrhagic manifestations, and 30% had cardiotoxicity.[6] 34.3% of patients had ECG changes, which made up the majority, and 21.9% of patients had a rise in troponin-I. SGOT levels were elevated in 10% of patients.[7]
| Conclusion | | |
The above report describes a case of a 50-year-old male patient who developed reversible AF following snakebite which was successfully treated with anti-snake venom. Although AF is an infrequently reported presentation of snakebite, it can frequently occur in patients who have certain risk factors. Therefore, the treating physician should foresee the possibility of developing AF following snakebite, and hence it warrants careful cardiac monitoring.
Takeaway points
- Presentation of cardiotoxicity should always be kept in mind while treating the patient of snakebite, especially in patients with certain risk factors such as hypertension and diabetes mellitus
- It demands attentive cardiac monitoring throughout the treatment course.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient (s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Waiddyanatha S, Silva A, Siribaddana S, Isbister GK. Long-term effects of snake envenoming. Toxins (Basel) 2019;11:193.  |
| 2. | Quan D, Zurcher K. Reversible atrial fibrillation following Crotalinae envenomation. J Venom Anim Toxins Incl Trop Dis 2017;23:16. |
| 3. | Mehta SR, Sashindran VK. Clinical features and management of snake bite. Med J Armed Forces India 2002;58:247-9. |
| 4. | Virmani SK. Cardiac involvement in snake bite. Med J Armed Forces India 2002;58:156-7. |
| 5. | Slade J, Baja A, Al Zaki A, Auerbach P, Rodriguez F. Wilderness cardiology: A case of envenomation-associated cardiotoxicity following a rattlesnake bite. Cardiol Ther 2021;10:271-6. |
| 6. | Nayak KC, Jain AK, Sharda DP, Mishra SN. Profile of cardiac complications of snake bite. Indian Heart J 1990;42:185-8. |
| 7. | Sunil KK, Joseph JK, Joseph S, Varghese AM, Jose MP. Cardiac involvement in vasculotoxic and neurotoxic snakebite – A not so uncommon complication. J Assoc Physicians India 2020;68:39-41. |
[Figure 1], [Figure 2]
[Table 1]
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