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Basics ⬇

Outline

BASICS

Definition!!navigator!!

Condition associated with bite from a venomous snake.

Pathophysiology!!navigator!!

  • Pit viper venoms are complex mixtures of enzymes (including myotoxins, proteases, hyaluronidase, bradykinin-releasing enzyme, phospholipase A2, hemorrhagins) that are responsible for causing significant local tissue destruction, including myonecrosis, edema, hemorrhage, and inflammation. Systemically, venom enzymes and nonenzymatic peptides can alter capillary permeability with subsequent loss of plasma volume that can result in decreased cardiac output, hypoproteinemia, hypotension, and metabolic acidosis leading to respiratory and circulatory collapse. Other venom toxins induce hemolysis, platelet aggregation, thrombocytopenia, and alterations in the coagulation cascade. Mojave toxin, present in some rattlesnake subpopulations, is a neurotoxin that interrupts transmission at the neuromuscular junction, resulting in paralysis
  • Coral snake venom consists mostly of neurotoxins; phospholipase A, which causes hemolysis, may also be present

Systems Affected!!navigator!!

Pit Vipers

  • Skin, musculoskeletal—local skin and soft tissue necrosis and hemorrhage that advances outward from the bite; sloughing of skin and underlying tissue
  • Respiratory—upper airway obstruction (head and neck bites), direct damage to alveolar membranes, hemorrhage of pulmonary capillary bed
  • Hemic—alteration of vascular endothelial cell integrity, red blood cell lysis, vasodilation, stimulation of coagulation cascade via factor X activation, enhanced production of fibrin degradation products, enhanced platelet aggregation
  • Neuromuscular—neuromuscular junction dysfunction causing loss of skeletal muscle control
  • Cardiovascular—arrhythmia, myocardial necrosis ± fibrosis by unknown mechanism
  • Renal/urologic—nephrotoxic effects of myoglobinuria, hemoglobinuria, defibrination syndrome, disseminated intravascular coagulopathy, direct toxic effect, and hypovolemic shock

Coral Snakes

  • Nervous—neurotoxins cause irreversible decrease in neurotransmission at neuromuscular junctions. Possible sequelae include bulbar paralysis and respiratory arrest from diaphragmatic paralysis
  • Hemic—hemolysis
  • Musculoskeletal—rhabdomyolysis

Genetics!!navigator!!

N/A

Incidence/Prevalence!!navigator!!

  • Most bites occur from April to October
  • Several hundred horses are bitten each year by pit vipers, mostly by rattlesnakes in western USA; bites from coral snakes are rare

Geographic Distribution!!navigator!!

  • Pit vipers—widely dispersed throughout the USA
  • Coral snakes—restricted to southern edges of the USA

Signalment!!navigator!!

N/A

Signs!!navigator!!

General Comments

  • Most horses are bitten on or near the muzzle, fewer are bitten on the lower limbs, and bites to the trunk are uncommon
  • Less than 50% of bitten horses develop multiple or severe manifestations of envenomation
  • Most pit viper envenomations elicit local swelling within 60 min. Onset of systemic signs may be delayed for up to 6 h, so patients should be monitored for at least that duration. Lack of local signs does not indicate that life-threatening problems will not occur, particularly with bites from pit vipers with neurotoxic venom
  • Coral snake envenomations may have latent periods of up to 18 h between bite and onset of clinical signs

Physical Examination Findings

Pit Vipers

  • Marked skin discoloration and painful soft tissue swelling with hemorrhage at bite location. Fang marks may be obscured by tissue edema
  • Swelling of head/neck may lead to airway obstruction, causing dyspnea and tachypnea. With severe systemic toxicosis, dyspnea may occur owing to pulmonary edema or hemorrhage
  • Hemolysis and/or coagulopathy may develop
  • Cardiac abnormalities (tachycardia, dysrhythmias) may occur in severe cases
  • Neurotoxic envenomations may lead to muscle fasciculation, weakness, flaccid paralysis, and/or respiratory failure
  • Other possible signs include fever, epistaxis, lethargy, diarrhea, salivation, dysphagia, incontinence, laminitis, colic, shock, and coma

Coral Snakes

  • Fang wounds are usually small and without hemorrhage
  • Neurotoxic effects include dysphagia, salivation, muscle fasciculations, bulbar paralysis, flaccid paralysis, and respiratory paralysis

Causes!!navigator!!

  • In the USA 2 venomous snake families exist—Crotalidae (pit vipers), including Agkistrodon (copperheads and cottonmouth water moccasins), Crotalus (rattlesnakes), and Sistrurus (pygmy and massasauga rattlesnakes); and Elapidae, including eastern coral snakes (Micrurus fulvius fulvius) and Texas coral snakes (Micrurus fulvius tenere)
  • Pit vipers have bilateral pits between nostrils and eyes, elliptical pupils, and well-developed and retractable maxillary fangs that are hollow, hinged, and rotate forward for striking and delivering venom
  • Coral snakes have small heads, black snouts, round pupils, and banded red, yellow, and black color patterns. Coral snakes are shy, nocturnal, and have small, fixed, front maxillary fangs, all of which makes them less of a threat to large livestock

Risk Factors!!navigator!!

  • Because of their large body mass, adult horses have some innate protection from envenomations, but fatalities do occur
  • Severity of venomous snake bites is based on species of snake, age of the snake, circumstances of the bite, and venom composition
  • Snakes control the amount of venom delivered—defensive bites tend to be less severe than agonistic bites
  • Venom from young snakes tends to contain a high peptide fraction, causing less severe local injury, but more severe systemic effects. Additionally, venom in early spring may contain higher peptide fraction concentrations
  • Bite location, victim size, and activity level after envenomation influence the speed and extent of venom systemic circulation and severity of toxicosis

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Insect sting/bite
  • Trauma
  • Foreign body/abscess
  • Clostridial myositis
  • Purpura haemorrhagica
  • Botulism

CBC/Biochemistry/Urinalysis!!navigator!!

  • Echinocytosis
  • Elevated creatine phosphokinase, aspartate aminotransferase, sorbitol dehydrogenase, lactate
  • Initial hemoconcentration
  • Hemolysis, anemia
  • Leukocytosis, inflammatory leukogram
  • Hypoproteinemia
  • Thrombocytopenia

Other Laboratory Tests!!navigator!!

  • Coagulopathy—prolonged activated clotting time, prothrombin time, and partial thromboplastin time
  • High fibrin degradation products
  • Metabolic acidosis

Imaging!!navigator!!

N/A

Other Diagnostic Procedures!!navigator!!

ECG if dysrhythmias occur.

Pathologic Findings!!navigator!!

  • Extensive soft tissue edema, hemorrhage, and necrosis at/around bite
  • Generalized congestion, petechiation of major organs
  • ±Myocardial inflammation/fibrosis with effusion
  • Laminitis, pneumonia, secondary infections

Treatment ⬆ ⬇

Outline

TREATMENT

Appropriate Health Care!!navigator!!

  • Goals include maintaining patent airway, preventing/controlling shock, neutralizing venom, reducing swelling, and alleviating pain
  • Rigid tubing can be sutured into nostrils to maintain patent nasal passages. In 1 report, 57% of rattlesnake-envenomated horses required tracheotomy
  • IV crystalloids to enhance tissue perfusion, maintain hydration, and combat shock and hypotension

Nursing Care!!navigator!!

  • Whole blood or blood products to correct anemia, thrombocytopenia, and clotting abnormalities
  • Local wound management—continuous cleansing, hydrotherapy, and debridement
  • Administer tetanus antitoxin or toxoid as appropriate
  • Swelling may affect food prehension or drinking—ensure adequate intake

Activity!!navigator!!

Minimize activity to decrease distribution of venom.

Client Education!!navigator!!

  • Size and condition of the wound site may not correlate with severity of the systemic signs
  • Avoid first aid techniques such as tourniquets, cryotherapy, lancing, suction, and electroshock
  • Systemic signs may be delayed by several hours, so immediate treatment is essential
  • Delay in seeking medical intervention can significantly worsen prognosis

Surgical Considerations!!navigator!!

Rarely, fasciotomy may be indicated to manage compartment syndrome.

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • Specific antivenins:
    • M. fulvius—immune globulin, equine origin (Wyeth)
    • Crotalidae—polyvalent, equine origin (Boehringer Ingelheim); polyvalent F(ab), sheep origin (BTG International); polyvalent F(ab)2, horse origin (Bioveteria, Instituto Bioclon, and MT Venom Co.)
    • Most effective when administered shortly after envenomation, especially when combating local tissue necrosis and neurologic sequelae
    • Initial dose is 5 vials IV; however, clinical improvement has been seen when 1 or 2 vials were administered to horses
  • NSAIDs (e.g. flunixin meglumine) can be used 24 h after the bite for control of pain and swelling. Use caution when using NSAIDs in patients with coagulopathy or thrombocytopenia. Consider opioids in cases where NSAIDs are ineffective
  • Broad-spectrum antibiotic may be indicated, especially for horses with distal leg wounds
  • Tetanus toxoid administration as needed

Contraindications!!navigator!!

  • Heparin
  • DMSO

Precautions!!navigator!!

  • Corticosteroid use is controversial. Single dose dexamethasone administered within hours of envenomation may help reduce swelling, inflammation, and pain. Long-term, high-dose corticosteroids may depress immune responses against venom, foster secondary infection, or alter laboratory parameters used in monitoring disease progression
  • Antihistamines are of little benefit

Possible Interactions!!navigator!!

N/A

Alternative Drugs!!navigator!!

N/A

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

  • Assess CBC, serum chemistry panel, clotting panel, and fibrinogen at least every 12–24 h (more often if patient is deteriorating)
  • Close monitoring of respiratory and cardiovascular systems is recommended
  • Cardiac troponin levels in cases where cardiac dysfunction has occurred; peak troponin levels have occurred as late as 30 days post envenomation

Prevention/Avoidance!!navigator!!

N/A

Possible Complications!!navigator!!

Cardiac dysfunction, liver disease, serum sickness (from antivenin), pneumonia, colitis, laminitis, pharyngeal paralysis, various wound complications (slough, infection, etc.).

Expected Course and Prognosis!!navigator!!

  • Clinical signs may last up to 2 weeks
  • Use of a modified rattlesnake bite severity score similar to that used in humans and dogs may be helpful in determining prognosis
  • Equine mortality rate after rattlesnake bites in range 9–25%
  • Coral snake envenomations with neuromuscular signs warrant guarded prognosis

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

N/A

Age-Related Factors!!navigator!!

Young foals or ponies are at higher risk because of their small body mass.

See Also!!navigator!!

N/A

Abbreviations!!navigator!!

  • DMSO = dimethylsulfoxide
  • NSAID = nonsteroidal anti-inflammatory drug

Suggested Reading ⬆ ⬇

Fielding CL, Pusterla N, Magdesian KG, et al. Rattlesnake envenomation in horses: 58 cases (1992-2009). J Am Vet Med Assoc 2011;238:631–635.

Gilliam LL, Holbrook TC, Ownby CL, et al. Cardiotoxicity, inflammation, and immune response after rattlesnake envenomation in the horse. J Vet Intern Med 2012;26:1457–1563.

Author(s) ⬆

Author: Sharon Gwaltney-Brant

Consulting Editors: Wilson K. Rumbeiha and Steve Ensley

Acknowledgment: The author and editors acknowledge the prior contribution of Patricia A. Talcott and Michael Peterson.