Refer to Part 1 of the case posted here. Briefly, a 25y/o M was bitten on the right hand by a devenomated snake he purchased, becoming apneic and requiring intubation.
What common features allow snakes to be classified if the exact species is not known?
Certain physical features of indigenous crotaline andelapid species allow broad classification of US venomous snakes. The subfamily Crotalinae includes the rattlesnakes as well as copperheads and water moccasins. They have characteristically triangular heads with fangs and elliptical pupils that are vertical in orientation. Crotalines exhibit a single row of subcaudal scales, differentiating them from similar-appearing nonvenomous species that have two such rows. They also have a unique heat-sensing organ seen as a small depression behind their nostrils, earning them the moniker “pit-viper.” Species-specific features include the “rattle” of the rattlesnake (Figure 2), the white mouth of the cottonmouth (aka water moccasin), and the reddish brown coloration and hourglass markings of the northern copperhead (Figure 3). Brightly colored rings along their bodies easily identify native snakes of the family Elapidae, commonly known as coral snakes. One can distinguish these venomous species from the similar-appearing but benign scarlet king snakes by the sequence of the stripe colors. It is frequently taught: “Red on yellow kills a fellow; red on black, venom lack,” since coral snakes have red bands adjacent to yellow bands. Coral snakes also tend to have smaller fangs than those of the crotaline species. The identification of exotic (non-US) snakes can prove more challenging than that of native snakes. Al though there are online resources, consultation with a herpetologist via an academic institution, museum, or zoo may be helpful; this can usually be obtained through a regional poison center. In the absence of this luxury, certain unique traits might allow snake identification. For example, the snake in this case, a monocled cobra, also known as the Asiatic, Thai, or monocellate cobra, among other names, has a circular mark on the posterior aspect of its hood, surrounded by a pale ring, giving the appearance of a monocle.
Why did the patient become symptomatic if the snake was “devenomated”?
Venomous snakes that have been subjected to surgical procedures to make them nonvenomous are often termed venomoid in the lay literature. However, the reliability of such procedures is unknown. For example, the incomplete surgical removal of both exocrine venom glands may still allow venom production to occur. Similarly, ligation of the channel that connects the venom glands to the fang can fail if the channel recanalizes. These procedures may be attempted by nonveterinarian amateurs of dubious competence.
In the ED, the patient received 15 vials of antivenom over a period of 6 hours. Despite this intervention, he became increasingly tachycardic, with a heart rate of 150 beats/min, normal blood pressure, and an otherwise normal ECG. Normal saline was infused intravenously, and the patient maintained normal urine output. Initial lab values included a CBC that was notable for a mildly elevated white blood cell count, at 10.7 x 103/μL. Initial venous pH was 7.3 with an elevated lactate level of 2.77 mmol/L. The patient’s initial creatine phosphokinase (CPK) concentration was elevated, at 813 U/L, and his troponin level was slightly elevated, at 0.11 ng/mL. His right upper extremity became increasingly edematous, prompting evaluation by the plastic surgery hand con sultant and the initiation of IV antibiotics.
How is the correct antivenom chosen?
Currently, the only snake antivenom commercially available in the United States is Crotalidae polyvalent immune Fab (ovine) antivenom. This is FDA approved for the treatment of envenomations by rattlesnakes and other North American crotalines. An antivenom approved for treating coral snake envenomation currently does not exist. Treatment decisions for envenomations by nonnative snakes can be more challenging. In this case, a polyvalent equine antivenom produced in India for the treatment of cobra envenomations was administered. This antivenom is effective for the treatment of envenomation by a variety of elapids from Asia and the Indian subcontinent. Fortunately, this antivenom is often stocked by a zoo that houses a relevant species in its collection, and it was released by the zoo for administration to our patient. This drug is not FDA approved, and the purity and safety of imported antivenoms varies widely. Hospital rules regarding administration of such products vary; therefore, early involvement of the appropriate leadership is important. Unfortunately, there is no national system for distributing exotic antivenoms, though identification of potential antivenoms for exotic snake and other en- venomations is simplified by the Association of Zoos and Aquariums Antivenom Index (www.aza.org/antivenom-index). This nonpublic online resource, which was developed in 2006, helps guide the initial query but does not provide a mechanism for distributing the necessary drug.
Is there any antidote to prevent cobra envenomation–induced respiratory failure?
Cobra venom, a complex mixture of proteins and other macromolecules, produces its neurotoxic effects primarily at the neuromuscular junction. a-Neurotoxins, for example, block acetylcholine receptors at the motor end plate, while β-neurotoxins cause presynaptic inhibition of acetylcholine release. While these toxins affect the neuromuscular junction, phospholipase A2, another venom component, causes weakness through direct effects on muscle fibers. Early clinical signs and symptoms of the neurotoxic process include ptosis, dysphagia, and diffuse muscle weakness. This patient’s apnea, noted initially by EMS, resulted from paralysis of his respiratory musculature, the most consequential neurotoxic manifestation. A cardiotoxin is also present but is poorly characterized. In the case of Naja kaouthia envenomation, neurotoxicity results primarily from postsynaptic inhibition of the nicotinic acetylcholine receptor. The administration of neostigmine or another acetylcholinesterase inhibitor may sufficiently increase the amount of acetylcholine in the synapse to reverse the respiratory failure. In a series of Philippine cobra (Naja philippinensis) envenomations, neostigmine improved ptosis and respiratory function. One case report involving a monocled cobra envenomation describes a dramatic and complete reversal of all neurologic signs, including respiratory dysfunction, following administration of neostigmine 0.5 mg IV. The patient in this case report required three additional doses of neostigmine at approximately 20-minute intervals before ultimately receiving antivenom therapy. The antivenom is preferred, if available, as it would likely limit the degree of cardiotoxicity (elevated troponin) that was noted in our patient. Neostigmine is not expected to have any beneficial effect on this toxic effect.
The patient was transferred to the surgical ICU. He remained symptomatic and received an additional 10 vials of antivenom (a total of 25 vials). His lactate concentration peaked at 5.9 mmol/L; CPK, 1,653 U/L; and troponin, 0.38 ng/mL. Compartment pressures of the right hand and forearm were within normal range. Cellulitis with an abscess developed, which resolved with standard therapies. On follow-up 2 weeks after discharge, the hand wound had healed and the patient reported feeling well. The patient had purchased this and two other venomous snakes at a snake expo in western Pennsylvania, where the trade in venomous reptiles is unregulated. He then transported them to New Jersey, whereby he violated state law, which prohibits possession of these dangerous animals. The snakes were seized by the state authorities.
This above case is reproduced here with the permission of Drs. Touger & Ayala, and was published at www.emedmag.com in May 2011