Mojave Rattlesnake Envenomation

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Background

Envenomation by some rattlesnakes, such as the Mojave rattlesnake (formerly Mohave rattlesnake) (Crotalus scutulatus), may cause a different clinical presentation than that generally encountered after most rattlesnake bites. In addition, other species, such as the Southern Pacific rattlesnake Crotalus oreganus helleri, (formerly Crotalus viridis helleri), may cause signs and symptoms consistent with typical rattlesnake envenomation combined with signs and symptoms similar to Mojave rattlesnake envenomation.[1] (See Rattlesnake Envenomation for a more complete discussion of typical rattlesnake envenomation.)

Mojave rattlesnakes inhabit desert areas of the southwestern United States and central Mexico. Specimens with type A venom, which cause a different pattern of injury than other rattlesnakes, have been reported in southern California, Nevada, Utah, Arizona, Texas, and New Mexico.[2, 3, 4, 5] Populations with venom B and intergrades of types A and B venom have been found in south-central Arizona, around Phoenix and Tucson.[6]

The Mojave rattlesnake may be difficult to distinguish from the western diamondback rattlesnake (Crotalus atrox), which inhabits an overlapping geographical range. Some Mojave rattlesnakes are greenish, but they may have a similar color as western diamondbacks. In the Mojave rattlesnake, the diamond pattern fades into bands along the caudal third of the back, whereas the diamonds continue to the tail in the western diamondback.

The Mojave rattlesnake's white rings encircling the tail are much wider than the narrow black rings, whereas western diamondbacks have much more predominant black rings. The postocular stripe extends posteriorly above the mouth in the Mojave but intersects the corner of the mouth in the western diamondback. In Mojave rattlesnakes, supraocular scales are separated by fewer than 4 scales at their closest point. In western diamondbacks, at least 4 scales (usually >4) separate the supraocular scales.

See the image below.



View Image

This is a juvenile Mojave rattlesnake (postmortem). Note that the diamondback pattern fades into bands along the latter part of the snake's dorsum. Ph....

Other rattlesnakes in the Mojave rattlesnake's range and niche are distinguishable by the absence of a dorsal diamond pattern with light margins, black and white tail rings, facial stripes, or by the same criteria used to distinguish Mojave rattlesnakes from western diamondbacks.

Pathophysiology

Venom A populations of Mojave rattlesnakes possess Mojave toxin, which has been experimentally shown to induce neurotoxic effects. Mojave toxin or a similar toxin has been detected in the venom of other rattlesnake species. This toxin impairs presynaptic acetylcholine release. Mojave toxin may cause severe neurologic effects clinically, although this presentation has been reported only a few times in the literature. Envenomation by several other species of rattlesnakes has been reported to cause serious neurologic signs and symptoms (eg, severe motor weakness, respiratory difficulty).

Venom A Mojave rattlesnakes cause less local injury and less hemorrhagic/proteolytic effects than other rattlesnakes. In contrast, venom B specimens cause local, proteolytic, and hemorrhagic effects typical of other rattlesnakes. Severe rhabdomyolysis with myoglobinuric renal failure has been reported with Mojave rattlesnake envenomation.[7, 8, 9] This article focuses mainly on envenomation by venom A populations of Mojave rattlesnakes.

Etiology

A large percentage of bites occur when the snake is handled, kept as a pet, or abused. These bites are considered intentionally interactive.

Epidemiology

Sex

Males are bitten more commonly than females.

Age

Young adults are most commonly bitten.

Prognosis

Full recovery is usually anticipated. Before antivenom, estimates of mortality rates ranged from 5-25%. Because of the development of antivenom, rapid EMS transport, and emergency/intensive care, mortality rates have improved to 0.28% (or better) when antivenom is administered and to 2.6% when antivenom is not administered.

Mortality/morbidity

Mojave toxin is one of the most lethal venom components found in US snakes. Venom B populations are less lethal than venom A populations. At least one death has been attributed to a Mojave rattlesnake in the Annual Report of the American Association of Poison Control Centers, although a number of deaths have been documented.[10, 11]  Most documented deaths are associated with bites in which the bitten individual was intentionally interacting with the snake and when a delay occurred in seeking medical care.

Patient Education

Call professionals, such as animal control, to move snakes (if it is necessary to move the snake). Never attempt to handle, possess, or kill venomous reptiles. For patient education resources, see the patient education article Snakebite.

History

In some cases, it may be helpful to know where the bite occurred (geographically) and whether venom A populations are known to occur in the area.[12]  Findings may include the following:

Physical Examination

Findings may include the following:

Neurologic effects include the following:

Complications

Complications can include rhabdomyolysis, infection, respiratory difficulty, and death (rare).

Laboratory Studies

Rhabdomyolysis may occur from severe snake envenomations but is best described after canebrake (Crotalus horridus atricaudatus) and Mojave (C scutulatus) rattlesnake envenomations.[7, 8, 13] Rhabdomyolysis may lead to myoglobinuric renal failure and subsequent electrolyte abnormalities, such as hyper- or hypokalemia or hypocalcemia.

Mojave toxin has less effect on coagulation than other rattlesnake venoms. However, coagulopathies may occur. (See Rattlesnake Envenomation for suggested laboratory tests.)

For respiratory difficulty, consider arterial blood gas (ABG) measurements.

Obtain laboratory and other diagnostic data on a case-by-case basis. Factors to consider may include severity of envenomation, physician preference, and cost.

Imaging Studies

Radiographic findings may reveal teeth or fangs retained in the wound.

Other Tests

Obtain an electrocardiogram (ECG), if indicated. Although cardiac enzymes may rise with severe rhabdomyolysis, current literature suggests that this does not reflect cardiac injury.

Skin testing

Skin testing is not necessary before administering either the Crotalidae immune Fab ovine (CroFab) or equine (Anavip) antivenins. Sensitivity testing was previously required for the older polyvalent equine derived antivenin that is no longer on the U.S. market.

Procedures

Central venous or interosseous access may need to be obtained. However, avoid placing a central line in a noncompressible site (eg, subclavian) because of the risk of bleeding from venom-induced coagulopathy.

Fasciotomy probably is not indicated in Mojave (venom A) envenomation. If severe swelling is noted, suspect envenomation by a snake other than a venom A Mojave rattlesnake and treat accordingly (see Rattlesnake Envenomation).

Prehospital Care

Do nothing to injure the patient or impede travel to the ED.

Provide general support of airway, breathing, and circulation per advanced cardiac life support (ACLS) protocol; use oxygen, monitors, 2 large-bore intravenous lines (but minimize sticks when possible), and fluid challenge. In addition, minimize activity (if possible), remove jewelry or tight-fitting clothes in anticipation of swelling, and transport the patient to the ED as quickly and as safely as possible. Mark and time the border of advancing tenderness and edema often enough to gauge progression. No benefit was demonstrated when a negative pressure venom extraction device (eg, The Extractor from Sawyer Products) was evaluated in recent studies.[14, 15] Incision across fang marks is not recommended. Mouth suction is contraindicated.

Maintain the extremity in a neutral position of comfort.

Lymphatic constriction bands and pressure immobilization techniques may inhibit the spread of venom, but whether they improve outcome is not clear. These techniques may actually be deleterious for pit viper envenomation if they increase local necrosis or compartment pressure.[16] Special consideration of these techniques may be warranted for confirmed Venom A Mojave rattlesnake bites because local tissue injury is usually less. However, this application has not specifically been studied. Furthermore, it may not be possible to distinguish Venom A from Venom B snakes just by looking at the snake. The use of tourniquets is not recommended.

First aid techniques that lack therapeutic value or are potentially more harmful than the snakebite include electric shock, alcohol, stimulants, aspirin, ice application, and various folk and herbal remedies. Cost and risk of acute adverse reactions generally preclude field use of antivenom.

Although identification of the snake in suspected Mojave rattlesnake bites may be helpful, attempts to capture or kill the snake are not recommended because of the risk of additional injury.[17] If the venomousness of a particular snake is uncertain, consider taking photographs of the snake from a safe distance of at least 6 feet away using a digital or Polaroid camera.

Emergency Department Care

Adequate hydration with intravenous fluids is indicated. Patients with hypotension should be resuscitated first with 2 isotonic sodium chloride solution challenges (eg, 20 mL/kg). Treat persistent shock with colloids, followed by pressors as indicated.

Patients with Mojave rattlesnake envenomation may present with predominantly systemic and laboratory abnormalities, with only mild local and no hematological effects.

Administer antivenom for signs of envenomation progression or imminent risk of an acute complication of envenomation (see Complications).

Crotalidae Fab polyvalent immune FAB, ovine (CroFab) is a safe option and it is indicated even if the envenomation is minimal mild.[18]  An equine Crotalidae immune FAB (Anavip) was approved in the United States in 2015. An antivenin should be given as a preventative measure if there are any signs of envenomation at all. Do not wait for it to get worse—permanent injury could result.[19]

Grading envenomations is a dynamic process; administer additional antivenom as indicated by a worsening clinical course. When considering the use of antivenom, weigh the risk of adverse reaction to antivenom against the benefits of reducing venom toxicity.

Nonenvenomation, ie, dry bite (probably occurs in < 10% of rattlesnake bites), is characterized by the following:

Minimal or mild envenomation is characterized by the following:

Moderate envenomation is characterized by the following:

Severe envenomation is characterized by the following:

Further Care

Discharge instructions

Return immediately if swelling worsens or pain becomes severe.

Return immediately if any abnormal bleeding or bruising, dark tarry stools, or severe headache occur.

Return for signs of wound infection, such as swelling, excessive tenderness, redness or streaks, heat, or drainage (pus).

Return or follow up if a fever, itchy rash, joint pain, or swollen lymph nodes occur any time during the next few weeks.

Do not take nonsteroidal anti-inflammatory drugs (NSAIDs), such as aspirin, ibuprofen (Motrin, Advil), or naproxen (Naprosyn, Aleve) for 2 weeks after the snakebite. Acetaminophen (Tylenol) or a prescribed pain medication can be taken.

Do not participate in contact sports, undergo elective surgery, or have dental work for 2 weeks after the snakebite.

Drink plenty of liquids. Return if urine decreases in amount or becomes cola colored.

Referral to a physical therapist or surgeon may be indicated.

Wound check at the physician's discretion on a case-by-case basis. Return to the ED or follow up every 3 days for 2 weeks with repeat CBC, PT/INR, and fibrinogen. Laboratory studies may need to be rechecked more or less frequently or for a longer or shorter duration on a case-by-case basis.

Admit

Strongly consider admission for all Mojave rattlesnake envenomations. Because patients with severe Mojave envenomation may present with only minimal local tissue effects, underestimation of a significant injury can easily occur. Because of the relative infrequency of the injury, admitting all patients with suspected Mojave rattlesnake envenomations is probably prudent and cost effective.

Effects of Mojave rattlesnake envenomation may be prolonged and have been shown to improve with late administration of antivenom.

Transfer

All hospitals should have enough antivenom to treat at least one patient. However, antidote stocking varies and shortages do occur. Therefore, if antivenom is not available at the presenting hospital, patients should be transferred to a facility where antivenom may be administered. However, if it is available, antivenom may be necessary to optimize stabilization of a patient prior to transfer.

Consultations

The American Association of Poison Control Centers may assist in the management of envenomations. For assistance in treating snakebitten patients with crotaline Fab antivenom (CroFab), contact the CroFab hotline at 87-SERPDRUG (877-377-3784).

Complications

Antivenom-associated complications

Anaphylaxis is a type I (immediate) hypersensitivity reaction that may be life threatening. It is characterized by urticaria, wheezing laryngeal edema, and shock.[20]

Serum sickness is a type III (delayed) hypersensitivity reaction. It is characterized by fever, urticaria, lymphadenopathy, and arthritis and may occur 5 days to 3 weeks after antivenom treatment.

Prevention

Never handle a rattlesnake, even if it is believed to be dead. Serious, even fatal, envenomations have been documented to occur after handling the decapitated head of a rattlesnake up to 90 minutes after it was severed.

Do not reach or step into places outdoors that are not visible.

At home, remove debris in which snakes might hide (eg, log piles). Remove items, such as bird feeders, that might attract snakes—seeds that fall from bird feeders attract rodents, which attract snakes.

Heavy clothing (such as hiking boots) may retard some strikes.

Young children should be closely supervised, and older children should be educated to avoid snakes.

Keep garage doors closed to prevent rattlesnakes from seeking shelter in garages.

Medication Summary

Be prepared to support the patient's cardiovascular and respiratory systems after a Mojave rattlesnake or similar envenomation.

Crotalidae polyvalent immune FAB (ovine) (Copperhead Antivenom (Immune FAB), Cottonmouth Antivenom (Immune FAB), CroFab)

Clinical Context:  This antivenin appears to be more specific against rattlesnake venom and less allergenic than a previously available version of antivenin Crotalidae polyvalent that is no longer available. The usual starting dose is 4-6 vials. It is indicated for envenomation by North American Crotalidae rattlesnakes (eg, cottonmouths/water moccasins, copperheads, rattlesnakes).

 

Crotalidae immune FAB (equine) (Anavip)

Clinical Context:  Crotalidae immune FAB (equine) contains venom-specific F(ab’)2; fragments of immunoglobulin G (IgG) that bind and neutralize venom toxins, thereby facilitating redistribution away from target tissues and elimination from the body. It is indicated for management of adults and children with North American rattlesnake envenomation.

Class Summary

These agents neutralize toxins from snakebites caused by North American rattlesnakes.

Diphtheria-tetanus toxoid (dT)

Clinical Context:  Diphtheria-tetanus toxoid is used to induce active immunity against tetanus in selected patients. The immunizing agent of choice for most adults and children older than 7 years are tetanus and diphtheria toxoids. It is necessary to administer booster doses to maintain tetanus immunity throughout life.

Pregnant patients should receive only tetanus toxoid, not a diphtheria antigen–containing product. In children and adults, one may administer into the deltoid or midlateral thigh muscles. In infants, the preferred site of administration is the mid thigh laterally.

Class Summary

Patients should be immunized against tetanus.

Ceftriaxone (Rocephin)

Clinical Context:  Ceftriaxone is a third-generation cephalosporin with broad-spectrum gram-negative activity. It has lower efficacy against gram-positive organisms and higher efficacy against resistant organisms. Ceftriaxone arrests bacterial growth by binding to one or more penicillin-binding proteins.

Class Summary

Prophylactic antibiotics are probably not indicated routinely, although they are widely prescribed. Common etiologic bacteria suspected in snakebite wound infections include Pseudomonas aeruginosa species, Enterobacteriaceae species, Clostridium species, and Staphylococcus epidermidis. For infected wounds, empiric therapy may include ciprofloxacin (contraindicated in pediatric patients and pregnant women) as a single agent or a combination of ceftriaxone plus amoxicillin-clavulanate, pending wound culture and sensitivity results. Retained foreign bodies (eg, fang, other tooth) are a common cause of wound infection.

Morphine (Astramorph, Duramorph, MS Contin)

Clinical Context:  Morphine is the drug of choice for narcotic analgesia because of its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Morphine sulfate administered intravenously may be dosed in a number of ways and is commonly titrated until the desired effect is obtained

Class Summary

Pain control is essential to quality patient care. It ensures patient comfort and promotes pulmonary toilet. Most analgesics have sedating properties, which are beneficial for patients with painful skin lesions. Use opiates with caution in unintubated patients because Mojave rattlesnake envenomation may cause respiratory difficulties.

Diphenhydramine (Benadryl)

Clinical Context:  Diphenhydramine is used for symptomatic relief of allergic symptoms caused by histamine released in response to allergens.

Class Summary

These agents are used to treat minor allergic reactions and anaphylaxis to antivenom or venom. Diphenhydramine may be used to pretreat patients with prior documentation of minor allergic reactions. Antihistamines are used for premedication to antivenom administration to reduce acute adverse reactions (not for direct treatment of snakebite).

Author

Sean P Bush, MD, FACEP, Professor of Emergency Medicine, The Brody School of Medicine at East Carolina University

Disclosure: Nothing to disclose.

Specialty Editors

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

Disclosure: Nothing to disclose.

James Steven Walker, DO, MS, Clinical Professor of Surgery, Department of Surgery, University of Oklahoma College of Medicine

Disclosure: Nothing to disclose.

Chief Editor

Joe Alcock, MD, MS, Associate Professor, Department of Emergency Medicine, University of New Mexico Health Sciences Center

Disclosure: Nothing to disclose.

Additional Contributors

Robert L Norris, MD, Professor Emeritus, Department of Emergency Medicine, Stanford University Medical Center

Disclosure: Nothing to disclose.

References

  1. French WJ, Hayes WK, Bush SP, Cardwell MD, Bader JO, Rael ED. Mojave toxin in venom of Crotalus helleri (Southern Pacific Rattlesnake): molecular and geographic characterization. Toxicon. 2004 Dec 1. 44(7):781-91. [View Abstract]
  2. Farstad D, Thomas T, Chow T, Bush S, Stiegler P. Mojave rattlesnake envenomation in southern California: a review of suspected cases. Wilderness Environ Med. 1997 May. 8(2):89-93. [View Abstract]
  3. Hardy DL. Envenomation by the Mojave rattlesnake (Crotalus scutulatus scutulatus) in southern Arizona, U.S.A. Toxicon. 1983. 21(1):111-8. [View Abstract]
  4. Hardy DL. Fatal rattlesnake envenomation in Arizona: 1969-1984. J Toxicol Clin Toxicol. 1986. 24(1):1-10. [View Abstract]
  5. Wingert WA, Chan L. Rattlesnake bites in southern California and rationale for recommended treatment. West J Med. 1988 Jan. 148(1):37-44. [View Abstract]
  6. Glenn JL, Straight RC. Intergradation of two different venom populations of the Mojave rattlesnake (Crotalus scutulatus scutulatus) in Arizona. Toxicon. 1989. 27(4):411-8. [View Abstract]
  7. Bush SP, Jansen PW. Severe rattlesnake envenomation with anaphylaxis and rhabdomyolysis. Ann Emerg Med. 1995 Jun. 25(6):845-8. [View Abstract]
  8. Bush SP, Jansen PW. Severe rattlesnake envenomation with anaphylaxis and rhabdomyolysis. Ann Emerg Med. 1995 Jun. 25(6):845-8. [View Abstract]
  9. Jansen PW, Perkin RM, Van Stralen D. Mojave rattlesnake envenomation: prolonged neurotoxicity and rhabdomyolysis. Ann Emerg Med. 1992 Mar. 21(3):322-5. [View Abstract]
  10. Bronstein AC, Spyker DA, Cantilena LR Jr, Green J, Rumack BH, Heard SE. 2006 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS). Clin Toxicol (Phila). 2007 Dec. 45(8):815-917. [View Abstract]
  11. Gummin DD, Mowry JB, Spyker DA, Brooks DE, Fraser MO, Banner W. 2016 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 34th Annual Report. Clin Toxicol (Phila). 2017 Dec. 55 (10):1072-1252. [View Abstract]
  12. Massey DJ, Calvete JJ, Sánchez EE, Sanz L, Richards K, Curtis R, et al. Venom variability and envenoming severity outcomes of the Crotalus scutulatus scutulatus (Mojave rattlesnake) from Southern Arizona. J Proteomics. 2012 May 17. 75(9):2576-87. [View Abstract]
  13. Carroll RR, Hall EL, Kitchens CS. Canebrake rattlesnake envenomation. Ann Emerg Med. 1997 Jul. 30(1):45-8. [View Abstract]
  14. Bush SP. Snakebite suction devices don't remove venom: they just suck. Ann Emerg Med. 2004 Feb. 43(2):187-8. [View Abstract]
  15. Bush SP, Hegewald KG, Green SM, Cardwell MD, Hayes WK. Effects of a negative pressure venom extraction device (Extractor) on local tissue injury after artificial rattlesnake envenomation in a porcine model. Wilderness Environ Med. 2000 Fall. 11(3):180-8. [View Abstract]
  16. Bush SP, Green SM, Laack TA, Hayes WK, Cardwell MD, Tanen DA. Pressure immobilization delays mortality and increases intracompartmental pressure after artificial intramuscular rattlesnake envenomation in a porcine model. Ann Emerg Med. 2004 Dec. 44(6):599-604. [View Abstract]
  17. Bush SP, Cardwell MD. Mojave rattlesnake (Crotalus scutulatus scutulatus) identification. Wilderness Environ Med. 1999 Spring. 10(1):6-9. [View Abstract]
  18. Gerardo CJ, Quackenbush E, Lewis B, Rose SR, Greene S, Toschlog EA, et al. The Efficacy of Crotalidae Polyvalent Immune Fab (Ovine) Antivenom Versus Placebo Plus Optional Rescue Therapy on Recovery From Copperhead Snake Envenomation: A Randomized, Double-Blind, Placebo-Controlled, Clinical Trial. Ann Emerg Med. 2017 Aug. 70 (2):233-244.e3. [View Abstract]
  19. Carstairs SD, Kreshak AA, Tanen DA. Crotaline Fab antivenom reverses platelet dysfunction induced by Crotalus scutulatus venom: an in vitro study. Acad Emerg Med. 2013 May. 20(5):522-5. [View Abstract]
  20. León G, Segura A, Herrera M, Otero R, França FO, Barbaro KC, et al. Human heterophilic antibodies against equine immunoglobulins: assessment of their role in the early adverse reactions to antivenom administration. Trans R Soc Trop Med Hyg. 2008 Nov. 102 (11):1115-9. [View Abstract]

This is a juvenile Mojave rattlesnake (postmortem). Note that the diamondback pattern fades into bands along the latter part of the snake's dorsum. Photo by Sean Bush, MD.

This is the typical appearance of a southern California Mojave rattlesnake bite site. Photo by Sean Bush, MD.

Mojave rattlesnake (Crotalus scutulatus). Note the diamond pattern fades into bands along the caudal third of the back and the white tail rings are wider than the black. Photo by Sean Bush, MD.

This is the typical appearance of a southern California Mojave rattlesnake bite site. Photo by Sean Bush, MD.

Mojave rattlesnake (Crotalus scutulatus). Photo by Sean Bush, MD.

A red diamond rattlesnake (Crotalus ruber). The postocular light stripe extends above the angle of the mouth in Mojave rattlesnakes. Photo by Sean Bush, MD.

This is a juvenile Mojave rattlesnake (postmortem). Note that the diamondback pattern fades into bands along the latter part of the snake's dorsum. Photo by Sean Bush, MD.

A western diamondback rattlesnake (Crotalus atrox). Photo by Sean Bush, MD.