Eastern Diamondback Rattlesnake (Crotalus adamanteus) Envenomation of Dogs: 31 Cases (1982–2002)
The medical records of 31 dogs treated for envenomation by the Eastern Diamondback Rattlesnake (Crotalus adamanteus) were reviewed. Twenty-four of 25 dogs that survived were hospitalized for an average of 4.3 days. The most common presenting signs were tachycardia, swelling/edema, depressed mentation, tachypnea, and bleeding puncture wounds. Thirteen (42%) of the 31 dogs were presented with or developed cardiac arrhythmias, predominantly ventricular premature contractions. Hematological disorders, including defibrination, elevated fibrin split products, hemolytic anemia, thrombocytopenia, and prolonged clotting times, were recorded in 81% of the dogs. Polyvalent crotalid antivenin was administered (mean of 4.0 vials per dog) to 88% of the surviving dogs and 50% of the nonsurviving dogs.
Introduction
Each year, approximately 20,000 people are treated in the United States for snakebites, with between 7000 and 8000 caused by venomous snakes.1 Although most practicing veterinarians have some familiarity with snakebites, there are no published data on the incidence of animal cases of envenomation. The southeastern United States is home to six native venomous snakes.2 The family Elapidae has short, fixed fangs and includes the Eastern Coral Snake (Micrurus fulvius). The family Crotalidae has larger, hinged fangs and includes the Eastern Diamondback Rattlesnake (Crotalus adamanteus), the Canebrake (Crotalus horridus atricaudatus, a subspecies of the Timber Rattlesnake), the Pygmy Rattlesnake (Sistrurus miliaris), the Copperhead (Agkistrodon contortrix), and the Cottonmouth or Water Moccasin (Agkistrodon piscivorus piscivorus).
Not all snakebites are true envenomations, because approximately 20% are “dry” bites with no venom inoculated.3 Various factors influencing the degree of envenomation include the species, age, and size of the snake; the time of year; the amount of venom regenerated during the period since the snake’s last strike; the number and depth of the strikes; and the nature of the strike (offensive, defensive, or agonal). The incidence of rattlesnake envenomations in animals is unknown. However, one study showed that the highest proportion of human cases of envenomation in the United States was caused by rattlesnakes, and another study attributed 74% of moderate to severe snake envenomations in Georgia to rattlesnakes.45 The Eastern Diamondback Rattlesnake causes more human fatalities annually than any other snake species.67 This is attributed to its high numbers in the southeast, an aggressive disposition, and a less reclusive nature than other species. Also, the Eastern Diamondback Rattlesnake is able to attain a much larger body size than other species, thereby allowing it to have the highest venom (dry weight) to body weight ratio of the native snake species.8
In the United States, the venom of the Eastern Diamondback Rattlesnake is second in relative potency to only the Eastern Coral Snake.89 The nature of the two venoms, however, is different. Traditionally, in the dog, crotalid venom has been considered to be vasculotoxic and necrogenic, while elapid venom has been considered to be neurotoxic and hemolytic. While this is an oversimplification, it helps explain the difference in potencies. Eastern Diamondback Rattlesnake venom immobilizes a victim and begins digesting its tissues soon after envenomation occurs.89 Chemically, the content of Eastern Diamondback Rattlesnake venom is divided into enzymes and nonenzymes. The enzymes include hyaluronidase and collagenase, which aid in the spread of venom through interstitial spaces; proteases that cause tissue necrosis and coagulopathies; and phospholipases, which produce direct cytotoxic effects, including endothelial damage and inflammation.1011 The nonenzymatic fraction of Eastern Diamondback Rattlesnake venom has direct effects on the cardiovascular and respiratory systems, causing ventricular arrhythmias, hypotension, and pooling of blood, especially in the splanchnic vascular beds. The nature of snake venom, including its toxicity, chemistry, and pathophysiological actions, has been reviewed elsewhere.212 The main purposes of this study were to evaluate and characterize this clinical syndrome and to contribute to the published database on this condition in the dog.
Materials and Methods
The case records of 31 dogs examined at the University of Florida College of Veterinary Medicine Teaching Hospital (UF-VTH) that were treated for Eastern Diamondback Rattlesnake envenomation during the period 1982 through 2002 were reviewed. Computer-generated searches of medical records from 1982 through 2002 coded as “envenomation” or “snakebite” were evaluated for inclusion in the study. Criteria for inclusion were confirmed identification of the snake as an Eastern Diamondback Rattlesnake by the owner, and clinical lesions compatible with envenomation by this particular species. These lesions included sudden occurrence of puncture wounds (with or without overt bleeding), severe regional swelling and dependent edema, shock, and petechial/ecchymotic hemorrhages. Each dog included in the study was also from a region known to be indigenous for the Eastern Diamondback Rattlesnake. The data reviewed included the clinical features, treatments, and outcome of each case. An earlier study has also been published from the UF-VTH that described 20 cases of envenomation from 1978 through 1983.13 Although there was a slight overlap of the years covered by each study, there was no overlap of the individual cases reviewed.
Results
Distribution of Cases
The number of envenomations per month varied from one to six. One envenomation per month occurred in January, November, and December; August, September, and October had two per month; February, April, May, and June had three per month; March had four; and June had six. The majority of envenomations occurred during the spring and summer months. The time of the envenomation was noted in 20 of the 31 cases, with 11 occurring between 10 am and 4 pm and seven occurring between 4 pm and 10 pm. Only two envenomations occurred between 10 pm and 10 am.
Case Data
Of the 31 cases, 17 were male (eight were castrated) and 14 were female (eight were spayed). The dogs’ ages ranged from 7 months to 11.5 years, with a mean age of 3.8 years and median age of 3 years. The dogs’ weights ranged from 5.0 to 45 kg, with a mean of 25.3 kg. Twenty-two of the dogs weighed at least 20 kg. Eleven were mixed-breed dogs. Purebred dogs were represented by 13 different breeds, with no breed including more than three dogs.
The location of the snakebite was determined in all cases. A total of 44 strikes were identified. Nine of the 31 dogs were struck two to four times. Twenty-eight (63.6%) strikes were to the head, including the ears and tongue; six (13.6%) were to the neck; five (11.4%) were to the forelimbs and prescapular regions; three (6.8%) were to the thorax or abdomen; and two (4.5%) were to the hind limbs [Figures 1A, 1B, 2A]. Six of the 31 dogs did not survive, with three being euthanized and three dying spontaneously [Table 1]. Five of the six deaths occurred within 9 hours of presentation. One dog was euthanized following an aborted surgical procedure to remove necrotic tissue, more than a week after its initial presentation. Twenty-four of the 25 surviving dogs required hospitalization, with the length of stay ranging from 14 hours to 23 days (mean 4.3 days; median 2.5 days) [Table 2]. The 23-day hospitalization of one dog was for treatment of renal failure, which was a very rare complication in this study population.
Elapsed time from envenomation to presentation at the referring veterinarian or the UF-VTH ranged from 15 minutes to >12 hours. Ten dogs were presented within 60 minutes (nine survived, one died); nine were presented between 60 minutes and 4 hours (seven survived, two died); and six were presented between 4 and 12 hours (all six survived). The interval from envenomation to presentation was unknown in the remaining six dogs (three survived, three died). Of the 25 with a known elapsed time until presentation, the mean was 3.5 hours.
Therapy
Three of the dogs that died received antivenin [Table 1], and three did not. Twenty-two of the 25 survivors received antivenin (from one to 10 vials; mean, four vials; median, four vials), and three did not. Each vial, when reconstituted, contained 10 mL of mixed crotalid antivenin.a One of the 25 dogs receiving antivenin had signs of a hypersensitivity reaction, as characterized by facial pruritus and additional facial swelling.
Twenty-seven dogs received antibiotics; two that did not died during initial presentation, and two survived [Table 1]. Twenty-eight (90%) dogs received intravenous fluids. Flow rates of administration were adjusted according to the needs of the animal. Blood products were administered at the individual clinician’s discretion to 11 (35%) dogs based on the degree of anemia and total plasma protein deficiency. Thirteen (42%) dogs were administered corticosteroids by the referring veterinarian at the time of initial presentation. One dog received corticosteroids on the second day of hospitalization. Two of the six dogs that did not survive received corticosteroids. Eleven (44%) of the 25 survivors received corticosteroids initially or early in the course of therapy.
Complications
Thirteen (42%) of the 31 dogs had pathological cardiac arrhythmias (ventricular premature contractions, ventricular tachycardia, ventricular fibrillation) either at presentation or during hospitalization. Of these, three died. Arrhythmias resolved in five dogs after administration of antiarrhythmic drugs, and arrhythmias resolved spontaneously in five dogs. Two of the 13 dogs with cardiac arrhythmias did not receive antivenin. One of these dogs died, and the other survived after its arrhythmia resolved spontaneously.
Twenty-five (81%) of 31 dogs had hematological disorders, including defibrination, elevated fibrin split products, hemolytic anemia (with hemoglobinuria), thrombocytopenia, prolonged clotting times, or combinations of these abnormalities [Tables 1, 2].
Discussion
In the previous study of Eastern Diamondback Rattlesnake envenomations, 75% of cases occurred from April to October, with 55% of the cases occurring in July or August.13 In the study reported here, 68% of the envenomations occurred from April to October, but only eight (26%) were in July or August. The cause and significance of this difference are not known. One study in people reported that 95% of snakebites throughout the United States occurred from April to October, and most happened between the hours of 8 am to noon or 4 pm to 10 pm, which correlated well with periods of human outdoor activity.14 In the authors’ study, 11 envenomations occurred between 10 am and 4 pm, seven occurred between 4 pm and 10 pm, and only two occurred after 10 pm but before 10 am. The milder fall and winter climate of the north central Florida region is less restrictive to both canine and human outdoor activity, and this may explain the more even monthly distribution of envenomations in this study.
The ages and sexes of the dogs in this study were similar to those in a prior study.13 The 19% mortality rate and the average number of days required for hospitalization were also similar. Overall, 71% of the dogs weighed at least 20 kg; however, three (50%) of the nonsurvivors weighed <15 kg. The high percentage of larger dogs envenomated could possibly be explained by breed popularity, the breeds generally favored for outdoor activities and sports, or the greater propensity for larger dogs to live entirely outdoors. The fact that smaller dogs had an increased representation in the nonsurvival group suggests that the prognosis is less optimistic for smaller dogs. All other things being equal, there is also a high likelihood of a greater venom-to-body weight ratio in smaller dogs.
Elapsed time from envenomation to presentation ranged from 15 minutes to >12 hours. Of the 25 cases with a known elapsed time until presentation, the mean was 3.5 hours. This was similar to the previous UF-VTH study, which documented a mean of 3.8 hours.13
The high proportion of bites to the head and neck was consistent with other reports of rattlesnake envenomations and was probably associated with the manner in which the dog confronts the snake.1315 An earlier study showed that 16 (80%) of 20 dogs were struck on the head region, with five (25%) of the 20 struck on the limbs.13 Interestingly, in spite of the profound swelling seen around the head and neck, airway obstruction was uncommon. Only one of the survivors received respiratory support via endotracheal intubation, while two of the nonsurviving dogs were intubated during efforts at cardiopulmonary resuscitation.13 In the experience of one of the authors (Schaer), most dogs are struck on the head or neck, while cats are struck more often on the thorax and abdomen. This phenomenon may be related to the confrontational posturing of cats and their faster evasive reactions, allowing them to spring away from the snakes and thereby exposing their lateral and ventral body surfaces to the striking snake.
As previously noted, 13 (42%) of the 31 dogs developed cardiac arrhythmias. Three of these dogs died, five resolved after administration of antiarrhythmic drugs, and five resolved spontaneously. Two of the 13 dogs did not receive antivenin; one died, and the other survived after its arrhythmia and illness resolved spontaneously. In the previous UF-VTH study, nine (47%) of 19 dogs evaluated had cardiac arrhythmias.13 It is interesting to note that in the previous study, three of the dogs that developed arrhythmias did not receive antivenin, and none of them survived.
Besides the three dogs that died from cardiac failure, three dogs in this study were euthanized. One was euthanized at presentation because of a total lack of brain-stem function, possibly caused by arterial envenomation and subsequent subdural bleeding. Another was euthanized owing to a combination of a guarded prognosis and financial constraints. The third dog was euthanized more than a week after presentation, from probable sepsis and multiple organ failure.
The rather high incidence of hematological disorders in the dogs of this study was consistent with the previous UF-VTH study, in which hematological disorders occurred in 12 (60%) of 20 dogs.13 Echinocytosis is a common finding (its presence occurred in 89% of rattlesnake-envenomated dogs in one study), but it is not pathognomonic because envenomation by the Eastern Coral Snake has also been reported to produce this same morphological red blood cell change.1617
The treatment goals for snake envenomation include (1) treatment or prevention of shock and associated arrhythmias, (2) neutralization of the venom with the hope of minimizing its local and systemic effects, (3) prevention of secondary bacterial infection, and (4) management of pain. Typical therapy entails the use of volume expansion with crystalloids and/or colloids, crotalid-specific antivenin, analgesia, and empirically chosen antibiotics. Cardiac antiarrhythmic drugs are used as indicated.
Twenty-eight (90%) dogs in the study reported here received intravenous fluids. Blood products (fresh whole blood, fresh frozen plasma) were given to 11 (35%) dogs. This was consistent with the previous UF-VTH study, in which 17 (85%) of 20 dogs received intravenous fluids while six (30%) of the 20 received blood products.13
Twenty-two of the 25 survivors received antivenin. Only one of the dogs receiving antivenin showed signs of hypersensitivity reaction, as characterized by facial pruritus and additional facial swelling. In the previous UF-VTH study, 12 (86%) of the 14 surviving dogs and three (50%) of the six dogs that did not survive received antivenin.13 None of the dogs in the previous study showed a reaction to the antivenin. Sixteen of the dogs that received antivenin received one to four vials, with the other nine dogs receiving five or more vials. This is similar to the previous UF-VTH study, in which 10 of 15 dogs received one to four vials, while five dogs with advanced clinical signs received five or more vials, based on the large amount of venom that can be injected by the Eastern Diamondback Rattlesnake.13
Analgesia may best be accomplished through the use of opioids like buprenorphine or fentanyl. However, the benefits of pharmacological pain management must be weighed against any depression of the animal’s mentation that might make clinical assessments more difficult. Only one (3%) dog in this study received analgesics, which were based on clinician preference. All of the dogs exhibited remarkable tolerance for their affliction, as based on their attitude, vocalization, and heart rates.
Thirteen (42%) dogs in the study reported here received corticosteroids at the initial presentation to the referring veterinarian, while 17 (54%) did not. The remaining animals received corticosteroids on the second day of hospitalization at UF-VTH. In the previous study, four (31%) of 13 of the surviving dogs received corticosteroids, along with five (83%) of the six nonsurviving dogs.13 The use of corticosteroids remains controversial for snake envenomation. Some studies have shown corticosteroids to be effective in treating envenomation, while others have shown the opposite effect.18–22 Although the literature does not describe the effects of glucocorticoid drugs in dogs, the human literature finds no rationale for their use except to combat anaphylaxis.23 Corticosteroids might even be detrimental to local tissues in the early stages of envenomation.2324 Some experts feel that glucocorticoids theoretically decrease the potency of the antivenin.22 Recommendations on the treatment of human cases of envenomation restrict the use of corticosteroids to treating hypersensitivity reactions from the antivenin.2425 In the study reported here, 48% of the surviving dogs and 33% of the nonsurviving dogs received corticosteroids, thus making it difficult to determine the benefits (if any) derived from glucocorticoids. The senior author (Schaer) reserves the use of corticosteroid drugs for treating antivenin-induced hypersensitivity reactions.
Twenty-seven (87%) of the 31 dogs received antibiotics. Two of the four that did not receive antibiotics died during initial presentation (one spontaneously, one was euthanized), and two survived. In the previous UF-VTH study, 18 (90%) of the 20 dogs received antibiotics, and it was unclear if antibiotics had been administered to the remaining two dogs.13 Bacteriological studies have shown that the most commonly isolated natural microflora of the crotalid mouth includes Pseudomonas aeruginosa, Proteus spp., coagulase-negative Staphylococcus spp., Clostridium spp., and Bacteroides fragilis.26 Additionally, the oral cavity of the snake may harbor coliforms introduced while ingesting prey. Because the fangs can disrupt tissue integrity, bacterial invasion is possible both in the local tissues and systemically. However, studies have questioned the use of prophylactic antibiotics during the treatment of envenomation and have recommended their use only for severely contaminated wounds.72728 Good topical wound management has been recommended instead. The decision to use antibiotics in the 27 dogs of this study was based on the preference of the primary clinician. It is entirely possible that antibiotics make no difference in the outcome of Eastern Diamondback Rattlesnake envenomation, because the necrogenic effects of the venom can cause considerable tissue damage.
One major difference between the routine medical management of human and canine envenomations is in the use of tetanus antitoxin in people.29 Because there have been no reported cases of tetanus associated with Eastern Diamondback Rattlesnake bites in the dog, none of the dogs in this study received tetanus antitoxin.13
Conclusion
Envenomation by the Eastern Diamondback Rattlesnake was a potentially life-threatening situation in the dog. Because the degree of envenomation varied, treatment and prognosis were based on the presence of shock (tachycardia, tachypnea, pale mucous membranes, weakness), the occurrence and character of cardiac arrhythmias, and the presence and degree of hematological disorders (hemolytic anemia, defibrination, prolonged clotting times, thrombocytopenia). Hypovolemic shock was managed aggressively with intravenous fluid therapy. Although death may occur in spite of the timely use of crotalid-specific antivenin, a higher survival rate was seen in dogs administered antivenin than in those not receiving antivenin. Hospitalization was required for affected dogs in order to provide intravenous fluid therapy, cardiac monitoring, nursing care, and certain emergency procedures. Controversy surrounding the use of corticosteroids and antibiotics still exists, and their use should be determined on an individual case basis.
Antivenin (Crotalidae) Polyvalent (equine origin); Fort Dodge Animal Health, Overland Park, KS 66225-5945
![Figures 1A, 1B—. A 4-year-old, castrated male Jack Russell terrier [case no. 10, Table 2] showing the typical facial swelling that occurs approximately 4 to 6 hours after being bitten by an Eastern Diamondback Rattlesnake (A). The swelling gradually resolved (B), leaving a focal area of skin sloughing on the ventral cervical region that resolved with conservative treatment.](/view/journals/aaha/41/1/p31fig1a.jpeg)
![Figures 1A, 1B—. A 4-year-old, castrated male Jack Russell terrier [case no. 10, Table 2] showing the typical facial swelling that occurs approximately 4 to 6 hours after being bitten by an Eastern Diamondback Rattlesnake (A). The swelling gradually resolved (B), leaving a focal area of skin sloughing on the ventral cervical region that resolved with conservative treatment.](/view/journals/aaha/41/1/full-p31fig1a.jpeg)
![Figures 1A, 1B—. A 4-year-old, castrated male Jack Russell terrier [case no. 10, Table 2] showing the typical facial swelling that occurs approximately 4 to 6 hours after being bitten by an Eastern Diamondback Rattlesnake (A). The swelling gradually resolved (B), leaving a focal area of skin sloughing on the ventral cervical region that resolved with conservative treatment.](/view/journals/aaha/41/1/inline-p31fig1a.jpeg)
![Figures 1A, 1B—. A 4-year-old, castrated male Jack Russell terrier [case no. 10, Table 2] showing the typical facial swelling that occurs approximately 4 to 6 hours after being bitten by an Eastern Diamondback Rattlesnake (A). The swelling gradually resolved (B), leaving a focal area of skin sloughing on the ventral cervical region that resolved with conservative treatment.](/view/journals/aaha/41/1/p31fig1b.jpeg)
![Figures 1A, 1B—. A 4-year-old, castrated male Jack Russell terrier [case no. 10, Table 2] showing the typical facial swelling that occurs approximately 4 to 6 hours after being bitten by an Eastern Diamondback Rattlesnake (A). The swelling gradually resolved (B), leaving a focal area of skin sloughing on the ventral cervical region that resolved with conservative treatment.](/view/journals/aaha/41/1/full-p31fig1b.jpeg)
![Figures 1A, 1B—. A 4-year-old, castrated male Jack Russell terrier [case no. 10, Table 2] showing the typical facial swelling that occurs approximately 4 to 6 hours after being bitten by an Eastern Diamondback Rattlesnake (A). The swelling gradually resolved (B), leaving a focal area of skin sloughing on the ventral cervical region that resolved with conservative treatment.](/view/journals/aaha/41/1/inline-p31fig1b.jpeg)
Citation: Journal of the American Animal Hospital Association 41, 1; 10.5326/0410022
Citation: Journal of the American Animal Hospital Association 41, 1; 10.5326/0410022
A 4-year-old, castrated male Jack Russell terrier [case no. 10, Table 2] showing the typical facial swelling that occurs approximately 4 to 6 hours after being bitten by an Eastern Diamondback Rattlesnake (A). The swelling gradually resolved (B), leaving a focal area of skin sloughing on the ventral cervical region that resolved with conservative treatment.
A mixed-breed puppy showing the typical head swelling (A) and inner lip hemorrhage (B) from blood extravasating into the soft tissues soon after envenomation by an Eastern Diamondback Rattlesnake. The oral pallor is from hypovolemic shock.
