An 8.5-year-old sexually intact male mixed-breed (Labrador–Great Dane cross) dog was referred to the Small Animal Veterinary Clinic of Bern following a snakebite that occurred approximately 3 hours earlier. The owner saw and heard the snake (Vipera sp), but could not determine its species. The owner reported no knowledge of the dog having prior disease, and the dog had been adopted 1 year earlier. The dog weighed 33 kg (72.6 lb) and had a body condition score of 3/5. On initial evaluation, the dog's mucous membranes were pink and the capillary refill time was 1 second. The dog had been lethargic since being bitten by the snake. The upper lip was swollen (left side more so than the right side); the swelling extended to the right side of the neck without a visible bite site. On cardiac auscultation, tachycardia (144 beats/min) without arrhythmia was detected. The dog was panting with apparently mild dyspnea. Rectal temperature was 38.4°C (101.1°F).
A blood sample was collected for assessment. The Hct was 62% (reference interval, 39% to 57%), and anisocytosis, polychromasia, and a high hemolysis index (79; reference interval, < 15) were noted. Leukocytosis (14,570 cells/μL; reference interval, 6,000 to 12,000 cells/μL) was detected, defined by neutrophilia (13,260 cells/μL; reference interval, 3,000 to 11,500 cells/μL) and mild lymphopenia (800 cells/μL; reference interval, 1,000 to 1,250 cells/μL); the total solids concentration was 59.7 g/L (reference interval, 56 to 73 g/L). Coagulation status was considered normal (prothrombin time, activated partial thromboplastin time, thrombin time, and plasma fibrinogen concentration were within reference intervals). Serum biochemical analysis revealed mild hypokalemia (3.8 mmol/L; reference interval, 4.22 to 5.43 mmol/L); concentrations of other electrolytes were within reference intervals. The dog had high urea concentration (15.84 mmol/L; reference interval, 3.30 to 10.83 mmol/L), but serum creatinine concentration was 155 μmol/L (reference interval, 52 to 177 μmol/L). Fluid therapy with a balanced electrolyte fluida was initiated at a rate of 3 mL/kg/h (1.36 mL/lb/h). After allergy testing (0.1 mL of antitoxin diluted 1:10 with saline [0.9% NaCl] solution applied in the conjunctival sac) was performed during the first 3 hours after admission, snake antivenomb was administered IV (10 mL diluted 1:10 with saline solution) over a period of 30 minutes. The first ECG examination was performed on the fifth day of hospitalization, after an irregular heart rhythm was ausculted.
ECG Interpretation
For the initial ECG examination, the dog was placed in right lateral recumbency. The 3-lead ECG recording obtained revealed tachycardia with regular narrow QRS complexes and a ventricular rate of 360 beats/min. P waves were not recognizable (Figure 1). Two minutes later, without having changed the position of or having medicated the dog, another ECG recording was obtained (Figure 2). At this time, the heart rhythm and rate had changed to atrial flutter with second-degree atrioventricular (AV) block and a ventricular rate of 220 beats/min; P waves with a P wave-to-QRS complex ratio of 2:1 were visible. Treatment with diltiazem (1.98 mg/kg [0.9 mg/lb], PO, q 12 h) was started, and 6 hours later, the rhythm changed to atrial flutter with an atrial rate of 430 beats/min and a ventricular rate of 80 beats/min. The P wave-to-QRS complex ratio was 4:1 to 7:1 (Figure 3). Diltiazem treatment was continued; after 24 hours, an ECG examination revealed a sinus arrhythmia (80 beats/min).
Portion of an ECG tracing (leads I, II, and III) obtained from an 8.5-year-old mixed-breed (Labrador–Great Dane cross) dog that had been bitten by a snake. The tracing includes tachycardia with narrow QRS complexes and without recognizable P waves. The ventricular rate (360 beats/min) is regular. The ST segment has a decrement of 0.5 mV. The repolarization (T wave) is biphasic and therefore is seen as a negative T wave (arrow) that mimics a positive P wave (arrowhead). Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 251, 10; 10.2460/javma.251.10.1144
Portion of an ECG tracing (leads I, II, and III) obtained from the dog in Figure 1 two minutes after the initial tracing was recorded. The ST segment has a decrement of 0.3 mV. The ventricular rhythm is regular, and the rate has decreased to 220 beats/min. P waves are recognizable (arrow) at a rate of 440 beats/min (atrial flutter). A biphasic T wave is visible. Functional second-degree AV block (2:1) is present. Notching of the R wave (arrowhead) is visible on the lead III tracing. Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 251, 10; 10.2460/javma.251.10.1144
Portion of an ECG tracing (leads I, II, III, V1, V2, and V3) obtained from the dog in Figure 1 six hours after the initial tracing was recorded. Diltiazem was administered (90 mg, PO). The rhythm remains as atrial flutter with a rate of 430 beats/min (the P waves in lead I are denoted by asterisks) with a mean ventricular rhythm of 80 beats/min. The P wave-to-QRS complex ratio varies from 4:1 to 7:1. P waves are occasionally superimposed on QRS complexes, T waves, and ST segments. Paper speed = 50 mm/s; 5 mm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 251, 10; 10.2460/javma.251.10.1144
On the fifth day of the dog's hospitalization, tachycardia (160 beats/min) and an irregular heart rhythm were ausculted. Echocardiography revealed no abnormalities. Systolic arterial blood pressure was 118 mm Hg, and diastolic arterial blood pressure was 90 mm Hg. Serum cardiac troponin I (cTnI) concentration was 2.61 ng/mL (reference value, < 0.06 ng/mL).
The dog was discharged 8 days after the initial evaluation; the owner was to administer diltiazem (90 mg, PO, q 12 h) for 5 days at home. One month after discharge from the hospital, an ECG examination revealed sinus arrhythmia and serum cTnI concentration was apparently normal (0.05 ng/mL).
Discussion
Snakebites are known to induce a wide variety of clinical signs in humans, dogs, and other animals. Known constituents of snake venom include phospholipase, l-amino acid oxidase, hyaluronidase, aproteinase, ATP, phosphodiesterase, and metalloproteinases, all of which contribute to the pathological changes in affected dogs.1
The main clinical signs following snakebite observed in humans (listed in descending frequency of appearance) are pain, weakness, dizziness, nausea, severe hypotension, thrombocytopenia, fasciculations, regional lymphadenopathy, alterations in respiratory rate, prolonged clotting times, decreased hemoglobin concentration, arrhythmias, more profuse salivation, echinocytosis cyanosis, proteinuria, bleeding (melena, hematuria, or hematemesis), obtundation, and convulsions.2 Cardiac arrhythmias develop in up to 37% of dogs with Vipera envenomation.3,4 Reported ECG abnormalities in dogs during the first 36 hours after evaluation for a snakebite are ventricular premature complexes, left bundle branch block, idioventricular rhythm, sinus bradycardia,5 ST-segment depression or elevation, atrial premature complexes, and sinus tachycardia.6 In another report,7 sinus tachycardia, idioventricular rhythm, atrial premature complexes, ventricular premature complexes, and first- and second-degree AV blocks were the most frequent ECG abnormalities identified in dogs within 48 hours after envenomation. Ventricular tachycardia and ventricular premature complexes were detected 24 hours after the initial evaluation of 5 viper-bitten dogs that received interim glucocorticoid treatment.8 None of those dogs had cardiac abnormalities ausculted at the initial examination performed 3 to 7 hours after being bitten.
In dogs with snakebites, myocardial injury has been shown to be either induced by cardiotoxins or secondary to systemic inflammatory response.3 Cardiac troponin I is a highly specific marker for cardiac injury,9 and its serum concentration is an indicator for survival rate.10 Serum cTnI concentration increases within 2 to 3 hours after myocardial injury and reaches peak values at 18 to 24 hours.10,11 However, serum cTnI concentration can also be increased by tachyarrhythmias12 (eg, ventricular or supraventricular tachycardia) in humans. Ventricular tachycardia in dogs has been associated with increased serum cTnI concentration at 36 to 72 hours after envenomation.3 High serum cTnI concentration after a snakebite is associated with a higher resting heart rate as well as a higher occurrence of arrhythmias in dogs.7
In the dog of the present report, the initial ECG examination revealed supraventricular tachycardia without recognizable P waves. In a subsequent ECG tracing obtained prior to starting treatment, atrial flutter with functional second-degree AV block and a P wave-to-QRS complex ratio of 2:1 was detected. Such a spontaneous postenvenomation change in rhythm in the absence of anti-arrhythmic treatment in dogs has not been previously documented, to the authors' knowledge. Given that the dog did not receive any glucocorticoids and still developed tachycardia, we speculated that the tachycardia was most probably attributable to toxic myocarditis.
Six hours after the initial ECG and after diltiazem administration, atrial flutter was still present with a higher grade of second-degree AV block. Diltiazem, a calcium channel blocker, is known to slow conduction through and prolong the refractory period of the AV node. This results in a reduction in ventricular response to atrial flutter.
For the dog of the present report, it is not known whether the increase in serum cTnI concentration was due to toxic myocarditis, tachyarrhythmia, or both. Most likely, the envenomation caused toxic myocarditis that resulted in the atrial tachyarrhythmia, which further exacerbated the myocardial injury. Myocarditis can develop several days to weeks after snakebites in horses,13 and the case described in the present report has suggested that this can occur in dogs as well.
Footnotes
Plasma-Lyte A, Baxter SA, Volketswil, Switzerland.
Antitoksin za otrov europskih zmija, 10 mL, Institute of Immunology, Zagreb, Croatia.
References
1. Goddard A, Schoeman JP, Leisewitz AL, et al. Clinicopathologic abnormalities associated with snake envenomation in domestic animals. Vet Clin Pathol 2011; 40: 282–292.
2. Peterson ME. Snake bite: pit vipers. Clin Tech Small Anim Pract 2006; 21: 174–182.
3. Langhorn R, Persson F, Ablad B, et al. Myocardial injury in dogs with snake envenomation and its relation to systemic inflammation. J Vet Emerg Crit Care (San Antonio) 2014; 24: 174–181.
4. Segev G, Shipov A, Klement E, et al. Vipera palaestinae envenomation in 327 dogs: a retrospective cohort study and analysis of risk factors for mortality. Toxicon 2004; 43: 691–699.
5. Swindells KL, Russell NJ, Angles JM, et al. Four cases of snake envenomation responsive to death adder antivenom. Aust Vet J 2006; 84: 22–29.
6. Pelander L, Ljungvall I, Häggström J. Myocardial cell damage in 24 dogs bitten by the common European viper (Vipera berus). Vet Rec 2010; 166: 687–690.
7. Segev G, Ohad DG, Shipov A, et al. Cardiac arrhythmias and serum cardiac troponins in Vipera palaestinae envenomation in dogs. J Vet Intern Med 2008; 22: 106–113.
8. Lervik JB, Lilliehöök I, Frendin JHM. Clinical and biochemical changes in 53 Swedish dogs bitten by the European adder—Vipera berus. Acta Vet Scand 2010; 52: 26.
9. Adams JE, Bodor GS, Dávila-Román VG, et al. Cardiac troponin I. A marker with high specificity for cardiac injury. Circulation 1993; 88: 101–106.
10. Fonfara S, Loureiro J, Swift S, et al. Cardiac troponin I as a marker for severity and prognosis of cardiac disease in dogs. Vet J 2010; 184: 334–339.
11. Langhorn R, Willesen JL. Cardiac troponins in dogs and cats. J Vet Intern Med 2016; 30: 36–50.
12. De Gennaro L, Brunetti ND, Cuculo A, et al. Increased troponin levels in nonischemic cardiac conditions and noncardiac diseases. J Interv Cardiol 2008; 21: 129–139.
13. Hoffman A, Levi O, Orgad U, et al. Myocarditis following envenoming with Vipera palaestinae in two horses. Toxicon 1993; 31: 1623–1628.
