A 19-month-old male was bit by a rattlesnake on the face near his home in Montana. Family witnessed the bite. He was taken to a small local ED and had swelling around his forehead and eyes. He was treated with Crotalidae polyvalent immune fab (ovine), also known as CroFab, and transferred to a larger Montana hospital. There he received a dose of Crotalidae immune F(ab’)2 (equine), also known as Anavip. He was intubated for airway protection due to some stridor prior to transport. The swelling had progressed to his upper cheek but did not involve the airway. No abnormal movements or ventilatory compromise were noted. He was transferred to a tertiary care center.
He did not develop any coagulopathy with normal platelets, fibrinogen, and PTT throughout his course. He did not require any further antivenom to control swelling. He was extubated after 24 hours. About 36 hours after arrival, he developed diffuse twitching movements involving the entire body. He had normal respiratory effort and preserved consciousness. His CK was normal. He had no response to midazolam. He received additional maintenance doses of both types of antivenom without any change. His symptoms resolved spontaneously, and he was discharged home about 4 days after the envenomation.
The child was bitten by a Prairie rattlesnake, Crotalus viridis, the only rattlesnake species found near his home in Montana. While several rattlesnakes are known to cause various forms of neurotoxicity, there are no published reports in the literature of Prairie rattlesnakes causing such effects.
The Mojave rattlesnake, C. scutulatus, is well-known to cause myokymia (see video)1 or a rippling movement of the muscles and may cause respiratory paralysis.2 Other rattlesnake species known to produce neurotoxicity include the Timber (C. horridus), Southern Pacific (C. oreganus), Sidewinder (C. cerastes), and Midget faded (C. oreganus concolor).3 Neurotoxicity is not reported from the Great Basin rattlesnake (C. lotusus), the species most often responsible for bites in Northern Utah.
Mojave toxin, a phospholipase A2 presynaptic toxin which blocks neurotransmitter release, is the venom component responsible for neurotoxicity in Mojave, Timber, Southern Pacific, and Midget faded rattlesnakes.
Prairie rattlesnake venom contains Myotoxin A which opens muscle sodium channels. In animal models it is known to cause hindlimb paralysis.4 This toxin may compromise more than 50% of Prairie rattlesnake venom.5
Both rattlesnake antivenoms available in the United States have limited in vitro binding of these myotoxins. Case reports show mixed efficacy in reversing neuromuscular effects. Care is primarily supportive, with respiratory failure requiring intubation occurring in some cases.
For assistance in managing a suspected rattlesnake envenomation, call the Utah Poison Control Center at any time 24/7 at 1-800-222-1222.