History

A 2-year-old 15.1-kg intact female Australian Cattle Dog was presented for left-sided facial swelling. The dog had a normal physical examination except for 2 small puncture wounds in the skin ventral to the left ear pinna and left sided subcutaneous edema of the face that was painful upon palpation. Neurologic examination was not performed as the dog was alert, responsive, and walking normally.

View Full Size

• Download Figure
• Download figure as PowerPoint slide

A snake had been seen and photographed next to the dog’s kennel earlier in the day, however, no one had witnessed the dog being bitten by the snake. The snake was identified as a timber rattlesnake (Crotalus horridus).

The dog was hospitalized overnight for observation and supportive care. The following morning, the physical examination was unchanged. Later in the afternoon, the dog was observed acting and walking normally. Prior to discharge (21 hours from time of admission), the dog was found in lateral recumbency and unable to walk. A neurologic examination was performed.

Assessment

Diagnostic Test Findings

On presentation, PCV and TS were 52% and 6.6 g/dL, respectively. Creatinine, BUN, liver enzymes, and glucose were normal. Venous blood gas analysis revealed a metabolic acidosis (pH, 7.345 [reference interval, 7.35 to 7.45]; anion gap, 23.0 mmol/L [reference interval, 8.5 to 19.0 mmol/L]; base excess, –13.5 mmol/L [reference interval, –9.5 to –2.9 mmol/L]; bicarbonate, 12.4 mmol/L [reference interval, 14.5 to 23.1 mmol/L]), a compensatory respiratory alkalosis (pCO2, 22.6 mm Hg [reference interval, 23.7 to 43.9 mm Hg]), hyponatremia (142.7 mmol/L [reference interval, 143.0 to 151.1 mmol/L]), hypokalemia (3.55 mmol/L [reference interval, 3.77 to 4.80 mmol/L]), and hyperlactatemia (2.6 mmol/ [reference interval < 2.5 mmol/L]). The combination of the diffuse LMN dysfunction, the puncture wounds and painful facial edema in conjunction with hypokalemia, metabolic acidosis, and the observation of a venomous snake in proximity to the affected dog provided a presumptive diagnosis of crotalid snake envenomation (Figure 1).

View Full Size

Photograph provided by the dog’s owner of the snake found in the proximity of the dog’s kennel shortly before identifying cutaneous puncture wounds and painful, facial edema. Although the image is blurry, the snake is identified as a timber rattlesnake (Crotalus horridus), based on the characteristic brown stripe running down the dorsal midline (red circle outlines the head), the solid black tail, and black chevron stripes (arrow).

Citation: Journal of the American Veterinary Medical Association 262, 4; 10.2460/javma.23.11.0642

• Download Figure
• Download figure as PowerPoint slide

Comments

Approximately 150,000 animals are bitten by snakes in the United States each year, and snakes of the family Crotalidae (rattlesnakes, cottonmouths, and copperheads) are responsible for the majority of those bites.¹ Clinical signs secondary to rattlesnake envenomation vary depending on the makeup of the venom and species bitten.¹ Moreover, intraspecies variations in venom composition exists depending on geographic location of the snake.² In general, components of rattlesnake venom can be divided based on their principle effects. Venom may be composed of a variety of metalloproteases, toxins, and peptide molecules resulting in hemorrhagic effects (Type I). Alternatively, venom may result in neurotoxic effects (Type II). Often venom contains a mixture of toxins and the predominant phenotypic effect of envenomation are subsequently classified as Type A (neurotoxic with little hemorrhagic effects) and Type B (hemorrhagic with little neurotoxic effects), Type A+B, and Type C. Type C venom has minimal hemorrhagic or neurotoxic effects.² Geographically, timber rattlesnakes from most US states most often have Type B venom while those with Type A venom have been identified mostly at the Georgia–Florida border.² The Type A neurotoxin is thought to work at the level of the neuromuscular junction by presynaptic blockade of calcium channels preventing the release of acetylcholine and resulting in failure of neuromuscular transmission and causing LMN weakness.¹ This toxin has its most serious effect on the diaphragm and can cause respiratory paralysis.^2,4 While it can lead to generalized flaccid paralysis, it is less commonly noted.¹ Clinical signs are rapidly progressive, and onset ranges from 30 minutes to 24 hours after envenomation.³ A rare consequence that is unique to timber rattlesnake envenomation is myokymia.¹ Myokymia is the clinical phenomenon of undulating ripples that appears as worms wriggling under the skin. It results from spontaneous, fine, involuntary, muscle fiber contractions that electromyographically are characterized by the firing of short bursts of single motor units that range from 5 to 150 Hz but may occur as doublets or triples. However, with timber rattlesnakes the frequency may vary from 91 to 250 Hz. Intravenous calcium administration may decrease the clinical signs.¹

Clinical signs of neurotoxic envenomation involve a variety of neurologic signs including abnormal mentation, diffuse weakness ranging from ambulatory tetraparesis to tetraplegia, postural reaction deficits, depressed spinal reflexes, muscle fasciculations, and rarely seizures.⁴ Abnormal clinicopathologic data include echinocytes, thrombocytopenia, hemoconcentration, coagulation abnormalities (prolonged prothrombin time [PT], activated partial thromboplastin time [aPTT], and clotting times), hypokalemia, and hypercapnia.⁴

Crotalidae envenomation treatment generally involves antivenom therapy, supportive care, analgesia, and monitoring of respiratory function.^1,5 In mild cases or those with localized tissue effects, antivenom administration may not be necessary. Indications for antivenom therapy include rapid progression of swelling, severe coagulopathy, defibrination, thrombocytopenia, neuromuscular dysfunction, and shock.¹ Antivenom therapy is most effective when administered immediately following envenomation, however benefit from antivenom therapy may be realized long after envenomation if circulating venom is present.¹ Overall mortality rates following Crotalidae envenomation range from 1% - 30%.^3–5 Mortality rates are among the highest for neurotoxic envenomation reaching up to 17.6%.⁴

The initial signs being limited to cutaneous punctures, bruising, and swelling were not considered severe enough to warrant antivenom administration. Therefore, initial supportive therapy included intravenous isotonic crystalloid fluids with potassium supplementation, hydromorphone 0.05mg/kg IV every 6 hours, maropitant 1mg/kg IV every 24 hours, and carprofen 4.4mg/kg subcutaneously once. Following development of diffuse LMN dysfunction, the dog was treated with 1 vial of antivenin (Crotalidae Polyvalent). Forty-eight hours following the onset of neurologic signs, the dog was discharged neurologically normal.

Antivenom dose varies depending on many factors. In 1 study, the typical dose was 1 to 2 vials; underdosing may result in recurrence of clinical signs necessitating additional antivenom administration.⁵ While the optimal dose of antivenom should be based on the volume of venom injected which is unknown, antivenom dosing may be based on clinical severity scoring. Dosing may also be impacted by potency of the antivenom product as well as financial constraints of the owner. Hypersensitivity to antivenom is infrequently reported and pretreatment with antihistamines or glucocorticoids may be unnecessary. Pretreatment skin testing in people is not recommended.⁵ As in the present case, resolution of clinical signs and reversal of metabolic and electrolyte derangements occurs rapidly.

In the present case, neurologic signs developed approximately 24 hours after envenomation while local tissue effects were more immediate. While a 10- to 18-hour delay in the onset of clinical signs following coral snake neurotoxin envenomation may occur, such delays are uncommon in rattlesnake envenomation. Rattlesnakes have the ability to inject variable amounts of venom per bite, ranging from no venom, so called “dry bites,” to large volumes based on physiological factors such as age and size of the snake and prey size.³ In part, the delay in this case may relate to injection of a small volume of venom as volume relates to clinical severity. In support of this, the patient presented here maintained adequate ventilatory capabilities despite severe, diffuse flaccid paralysis. Neurotoxic envenomation can result in respiratory paralysis.¹ Alternatively, delayed onset may have related to subcutaneous pocketing of venom from which absorption may have been slow or even delayed.

In the authors’ practice, neurotoxicity secondary to snake envenomation is uncommon. The occurrence of the present case may suggest a northern expansion of the habitat of the timber rattlesnakes with Type A venom from the Georgia–Florida border.

Ultimately, it is imperative for clinicians practicing in geographic regions inhabited by venomous snakes to be aware of the potential for neurologic sequalae from envenomation, and, based on clinicopathologic data, develop a raised index of suspicion for neurotoxic envenomation when evaluating animals with acute, diffuse LMN dysfunction. In the end, prompt recognition and early treatment with antivenom may provide for a good outcome.

Disclosures

Dr. Brainard is a member of the JAVMA Scientific Review Board, but was not involved in the editorial evaluation of or decision to accept this article for publication.

No AI-assisted technologies were used in the generation of this manuscript.

Funding

The authors have nothing to disclose.