Canis ISSN: 2398-2942

Rattlesnake bite

Synonym(s): Envenomation, pit viper, rattler

Contributor(s): Lyndi L Gilliam, Shane Lyon, Dawn Ruben, Melissa Wallace

Introduction

  • Most venomous snakebites in North America are due to Pit Vipers.
  • The Pit Vipers of North America include:
    • Species of rattlesnakes (genus Crotalus) Prairie rattlesnake (Crotalus viridis) Timber rattlesnake (Crotalus horridus).
    • Pygmy rattlesnakes (genus Sistrurus).
    • Massasauga (genus Sistrurus).
    • Cottonmouths (genus Agkistrodon).
    • Copperheads (genus AgkistrodonCopperhead rattlesnake (Agkistrodon contortrix).
  • Cause: snakebite by Pit Viper.
  • Signs: extensive swelling and bruising at the site of envenomation, persistent hemorrhage at site of envenomation. Patients are often agitated, excited, painful on presentation and occasionally the patient will present in shock.
  • Diagnosis: localized swelling and bruising, usually of the head or distal limbs. Scabbed-over or bleeding puncture wounds in the region of swelling from fang penetration.
  • Treatment: specific antivenom and supportive therapy.
  • Prognosis: mortality is low if appropriate therapy is initiated within the first 1-4 hours after envenomation, but will vary with venom dose and site of bite.
Follow the management tree for Snake envenomation.

Pathogenesis

Pathophysiology

  • Rattlesnakes have a pair of long, hollow fangs that lie in the rostral portion of the head, folded back against the roof of the mouth. These are connected to venom glands by small tubules or ducts.
  • When the rattlesnake strikes, the hollow fangs swing down from the roof of the mouth where they are positioned for biting.
  • Once the hollow fangs penetrate the skin, venom travels from the glands, on either side of the head, through the fangs and into the victim's subcutaneous tissues, muscles or blood vessels.
  • In general, rattlesnakes produce venom (type B venom) that CONTAINS various proteolytic enzymes including kininogenase, which activates bradykinins and stimulates the production of various inflammatory eiconsanoids, resulting in vasodilation, systemic inflammation and hypotension.
  • Other proteolytic enzymes disrupt the basal lamina of endothelial cells allowing the leakage of blood cells and plasma into the interstitial space resulting in edema, pain Pain , petechia, and ecchymosis formation.
  • Coagulopathies can be caused by many different venom components:
    • Venom may trigger platelet margination and activation resulting in activation of the coagulation cascade and disseminated intravascular coagulation Disseminated intravascular coagulation (DIC) with consumption of clotting factors; however, care should be taken not to mis-diagnose DIC. May also contain proteins that effect platelet function but not platelet number. Platelets may be present in normal numbers but may not be functional.
    • Defibrination can occur with fibrinolysins and an inability to clot.
    • Thrombin-like enzymes can result in an imperfect fibrin clot and a filaure to activate Factor XIII.
    • Phospholipase A2 is common in venoms and complexes with phospholipids making them unavailable for use in the activation of the coagulation cascade.
  • Some Mojave rattlesnakes (Crotalus scutulatus) possess a different type of venom (type A venom), which causes different clinical signs.
  • Type A venom populations of Mojave rattlesnakes produce the Mojave toxin, which is neurotoxic because it impairs the release of acetylcholine from pre-synaptic neuromuscular junctions.
  • Severe rhabdomyolysis and myoglobinuric renal failure has been reported with Mojave rattlesnake envenomation in people.
  • Type A venom also produces less proteolytic and hemorrhagic effects than other species of rattlesnakes.

Timecourse

  • The clinical signs associated with envenomation may appear immediately (hemorrhage from the fang marks) or be delayed for up to one hour.
  • If no swelling is apparent within one hour after presentation, it is unlikely that envenomation has occurred. If fang marks are present, it is likely that the dog received a dry bite.
  • The patient often becomes very painful in the region of the snakebite and resents palpation of the site beginning within the first hour after envenomation.
  • Some patients present in hypotensive shock due to vasodilation.
  • Beginning within three to four hours after envenomation, there is often significant petechia and ecchymosis associated with the bite site. At this point in time thrombocytopenia may be detected.
  • The swelling will gradually increase during the first 12 hours following envenomation.
  • After the first 24 hours, the tissue in the region of the bite site may become necrotic and begin to slough.
  • Often, after the first 24 hours, the swelling in the region of the bite site is mildly reduced while swelling and edema formation dependent to the bite site is significantly increased.
  • Disseminated intravascular coagulation Disseminated intravascular coagulation (DIC) may be followed by death if the patient is bitten several times, and suffers a severe envenomation. The quicker antivenom is administered, the more effective it will be. There may be benefits, however, up to 96 hours following envenomation due to the circulating half-life of some of the large venom proteins.
  • Although not a commonly reported complication of antivenin therapy in dogs, serum sickness (type II hypersensitivity reaction) is relatively common in humans following antivenin therapy.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Gilliam L L, Brunker K (2011) North American Snake envenomation in the dog and cat. Vet Clin North Am Small Anim Pract 41 (6), 1239-1259 PubMed.
  • Rosen P B, Leiva J L, Ross C P (2000) Delayed antivenom treatment for a patient after envenomation by Crotalus atroxAnnals Emerg Med 35 (1), 86-88 PubMed.
  • Boyer L V, Seifert S A & Clark R F (1999) Recurrent and persistent coagulopathy following pit viper envenomation. Arch Intern Med 159 (7), 706-710 PubMed.
  • Chippaux J P, Goyffon M (1998) Venoms, Antivenoms, and Immunotherapy. Toxicon 36 (6), 823-846 PubMed.
  • Bond G R & Burkhart K K (1997) Thrombocytopenia following timber rattlesnake envenomation. Ann Emerg Med 30 (1), 40-44 PubMed.
  • Dart R C, Seifert S A et al (1997) Affinity-purified, mixed monospecific crotalid antivenom ovine Fab for the treatment of crotalid venom poisoning. Ann Emerg Med 30 (1), 33-39 PubMed.
  • Bush S P & Jansen P W (1995) Severe rattlesnake envenomation with anaphylaxis and rhabdomyolysis. Ann Emerg Med 25 (6), 845-848 PubMed.
  • Consroe P, Egan N B et al (1995) Comparison of a new ovine antigen binding fragment (Fab) antivenin for United States Crotalidae with the commercial antivenin for protection against venom-induced lethality in mice. Am J Trop Med Hyg 53 (5), 507-510 PubMed.
  • Guisto J A (1995) Severe toxicity from crotalid envenomation after early resolution of symptoms. Ann Emerg Med 26 (3), 387-389 PubMed.
  • Clark R F, Selden B S & Furbee B (1993) The incidence of wound infection following crotalid envenomation. J Emerg Med 11 (5), 583-586 PubMed.
  • Burgess J L & Dart R C (1991) Snake venom coagulopathy - Use and abuse of blood products in the treatment of pit viper envenomation. Ann Emerg Med 20 (7), 795-801 PubMed.
  • Jurkovich G J, Luterman A et al (1988) Complications of Crotalidae antivenin therapy. J Trauma 28 (7), 1032-1037 PubMed.

Other sources of information

  • Carlson R W, Pineda-Roman M & Ramamrutham R (2000) Injuries by Venomous and Poisonous Animals.In: Shoemaker. 4th edn: Textbook of Critical Care. Philadelphia, W B Saunders Co. pp 226-232.
  • Hackett T & Winfield W E (1997) Rattlesnake Envenomation. In: Winfield: Veterinary Emergency Medicine Secrets. Philadelphia, Hanley & Belfus, Inc. pp 115-118.

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