1/316. Copperhead envenomations: clinical profiles of three different subspecies. Copperhead envenomation cases reported in the literature frequently lack identification of the subspecies of copperhead responsible for the envenomation. Whether subspecific identity would be useful in predicting possible different toxicity profiles may have clinical relevance. We report here the clinical profiles from envenomations involving 3 different subspecies of captive adult copperhead snakes--the southern copperhead (agkistrodon contortrix contortrix), the northern copperhead (agkistrodon contortrix mokasen), and the broad-banded copperhead (agkistrodon contortrix laticinctus). The bites occurred in the north-central region of the US where none of these subspecies are endemic and involved a professional and 2 amateur herpetologists. The victims were adult males with no previous history of venomous snake bite, and all bites were evidenced by fang puncture marks to their index finger or thumb. Envenomations from the broad-banded and northern copperhead subspecies caused localized symptoms of pain, edema and ecchymosis. In addition to these symptoms, southern copperhead envenomation resulted in a more severe clinical toxicity profile as evidenced by propulsive emesis, diarrhea and hematuria. Whether these differences in observed clinical toxicity were the result of unique subspecific venom pharmacological actions is an interesting question. However, independent of the copperhead subspecies involved, conservative medical management was effective in each case. ( info) |
2/316. A new monospecific ovine Fab fragment antivenom for treatment of envenoming by the Sri Lankan russell's viper (Daboia Russelii Russelii): a preliminary dose-finding and pharmacokinetic study. russell's viper is the most important cause of life-threatening snake bite and acute renal failure in sri lanka. Only equine polyspecific antivenoms imported from india are available. They have not proved effective clinically or in clearing venom antigenemia and they frequently cause reactions. In an attempt to reduce mortality and morbidity, a new monospecific ovine Fab fragment antivenom (PolongaTab; Therapeutic antibodies, Inc., london, United Kingdom) was raised against Sri Lankan russell's viper venom. In a preliminary dose-finding study in 35 patients, an initial dose of 3-4 g restored blood coagulability permanently and stopped systemic bleeding, even in severely envenomed patients. Venom antigenemia disappeared within 1 hr of antivenom treatment but recurred, probably as a result of continued absorption of venom from the site of the bite, after the rapid clearance of therapeutic antibody. Twelve patients (34%) experienced early reactions that were usually mild and always responded to epinephrine. ( info) |
3/316. Delayed antivenom treatment for a patient after envenomation by crotalus atrox. Bites by the Western diamondback rattlesnake (crotalus atrox) are the most common cause of envenomation in texas. We describe a patient who had delayed administration of antivenom after envenomation by C atrox. Because of an initial adverse response to a test dose, the patient had been unwilling to receive antivenom therapy. When compartment syndrome developed 52 hours after envenomation, however, the patient consented to antivenom therapy as an alternative to fasciotomy. We documented a decrease in compartment pressures and resolution of thrombocytopenia that was concomitant with antivenom administration. ( info) |
4/316. Neurotoxicity associated with suspected southern Pacific rattlesnake (crotalus viridis helleri) envenomation. An 18-year-old man was bitten on the hand by a snake he believed to be a Southern Pacific rattlesnake (crotalus viridis helleri). Within minutes he developed generalized weakness, difficulty breathing, diplopia, dysphagia, and dysphonia. Neurological examination revealed ptosis and decreased motor strength. These symptoms partially improved after administration of Antivenin (Crotalidae) Polyvalent, but the patient continued to have difficulty walking for several days due to weakness. In addition to neurological symptoms, the patient also experienced pain immediately after the bite occurred and rapid swelling of the entire extremity, which extended beyond the shoulder. He complained of a metallic taste in his mouth and developed intense muscle fasciculations of the face, tongue, and upper extremities, which lasted for 2 days and did not improve with antivenin treatment. He exhibited laboratory evidence of coagulopathy and rhabdomyolysis. Although neurotoxins are known to occur in the venom of certain populations of rattlesnakes, only a few clinical reports describing severe neurological symptoms appear in the literature. To our knowledge, this is the first reported case of neurotoxicity associated with a suspected Southern Pacific rattlesnake envenomation. ( info) |
5/316. Anaphylactoid reaction to rattlesnake envenomation. The clinical manifestations of an anaphylactoid reaction are identical to true anaphylaxis; however, a previous exposure to the offending agent is not needed to manifest these symptoms. We present a case of an anaphylactoid reaction in a 62-y-o female following a first-time envenomation by a rattlesnake. The patient required s.c. epinephrine and i.v. diphenhydramine, methylprednisolone, and ranitidine. She had not been envenomated by a rattlesnake previously or received any horse-derived antivenins in the past. ( info) |
| This study presents a case of severe disseminated intravascular coagulation (DIC) in a 3-year-old child following envenomation by the snake, Cerastes vipera. A literature search revealed very few similar cases. We describe a child who was bitten in his left foot by a snake identified as a C. vipera. Initial symptoms were relatively benign. Local signs included a hemorrhagic vesicle at the site of the bite with marked swelling of the entire leg. Twenty-four hours later, the child developed severe bleeding due to DIC, which lasted 5 days and required repeated administration of blood and blood products and total exchange transfusion. The patient was discharged from the hospital after 7 days in good condition. To the best of our knowledge, severe DIC following envenomation by a C. vipera has not been previously described in the literature. Treatment was essentially supportive. The case report indicates that a specific antivenin against this snake's venom should be made available in our area. ( info) |
7/316. morbidity after a bite from a 'non-venomous' pet snake. We report the first recorded case of morbidity from the bite of a red-neck keelback snake (Rhabdophis subminiatus) from South East asia. This is a species of the Colubrid family which originated from South East asia. Severe envenomation from this snake was reported as poisonous in the West as far back as 1978 but it is still being classified as non-venomous. This classification led our patient to keep this 'harmless' snake as a pet. We recommend that this snake be reclassified as 'venomous' or at least warnings be issued to the public not to keep it as a pet. ( info) |
8/316. The envenomation syndrome caused by the Australian Red-bellied Black Snake Pseudechis porphyriacus. The Australian elapids inject venom which is characteristic of each species; and which cause characteristic and specific envenomation syndromes in human victims of snakebite. Because many of the medically significant Australian elapids look similar, when glimpsed in the field by snakebite victims, defining human envenomation syndromes with secure species identification has been a slow process. Correlations between securely identified species and the human envenomation syndromes which they produce are still evolving. The genus Pseudechis is the most widespread in australia of the dangerous Australian elapid genera; and P. porphyriacus, the Red-bellied Black Snake, was the first terrestrial Australian elapid to be described and illustrated and the first to be the subject of experimental study. We present here five previously unreported cases of human envenomation in which the species diagnosis is secure. From these and with the perspective of a selected literature review, we describe the full envenomation syndrome of this species. Until the development of the Commonwealth serum laboratories' Venom Detection Kit in 1979 and the occasional case report of victims of securely identified species, envenomation syndromes for most Australian snake species have remained indeterminate, because of the lack of professional expertise in the identification of the species involved. Symptoms of the P. porphyriacus envenomation syndrome include those of bite-site pain, nausea and vomiting, generalised pruritis, chest pain, prostration and abnormalities of taste and smell. Signs include local necrosis and scarring of tissue at the bite-site, gross inflammation of surrounding tissues and, at least in one case, epilepsy. Although envenomation by the Red-bellied Black Snake is not lethal in adults, the correct therapy is Tiger Snake antivenom, administered with judgement, taking into account knowledge of the specific envenomation syndrome of this species and the clinical status of the victim. ( info) |
9/316. Cortical blindness: an unusual sequela of snake bite. Several ophthalmic effects may follow snake bite; this report describes an instance of cortical blindness that resulted from snake bite. ( info) |
10/316. Chronic ulceration of the leg following extensive scarring due to a snake bite complicated by squamous cell carcinoma. Chronic ulcers of the leg are common in brazil, perhaps more common than in the developed world. We report a case of a chronic ulcer of the leg following extensive scarring due to a bite by a venomous snake, which eventually led to a squamous cell carcinoma. ( info) |