Comparing cost of F(.ab')2AV vs FabAV in the treatment of copperhead envenomation-One center's experience.

The definitive treatment of North American crotalid snakebites is antivenin. In 2000, an FabAV antivenom (CroFab®) was introduced and in 2022, F(ab')2AV (Anavip®) was approved for treatment of copperhead bites. Our center that sees primarily copperhead snake bites added the recently approved treatment as a second option for the 2022 snake bite season. This brief report we describe our initial experience with the two antivenins via retrospective chart review: the cost, charge, laboratory differences, response to therapy, complications and duration of hospitalization of admitted patients with copperhead envenomation. Using three independent reviewers in this IRB exempt report we found 31 patients with copperhead bites (7 exclusions) leaving 19 adults and 7 children for analysis. We found there was no difference in age, sex, presence of lab abnormalities, total vials administered, or length of stay. There was significant differences in hospital costs and charges to the patient. Future research should include multi-center experiences comparing the two antivenins.

Retrospective chart review of substance abuse in patients with psychiatric emergencies in an emerging urban county.

Objectives: Substance abuse is common in patients with psychiatric emergencies. To further understand the connection between substance abuse and psychiatric disorders, a retrospective chart review was done that included positive drug screens among patients with psychiatric emergencies and to determine whether there was an association between substances used and the psychiatric diagnosis. Methods: A retrospective chart review of patients seen in an emergency department with psychiatric emergencies was conducted. The review comprised 1000 charts with diagnoses of anxiety, depression, schizophrenia, attention-deficit/hyperactivity disorder (ADHD), bipolar disorder, alcohol abuse, or schizoaffective disorder. Data collected included patient demographics, tobacco abuse, chief complaint, arrival mode, voluntary versus involuntary status, suicide attempt on presentation, psychiatric diagnoses, urine drug screen, and ethanol results. Chi-square statistical analysis was conducted to examine the relationship between substances of abuse and psychiatric diagnoses. Results: Approximately 58% of patients with a history of psychiatric illness had a positive urine drug screen. Of 245 patients with schizoaffective disorder, 69 (28%) were positive for tetrahydrocannabinol (THC) and 48 (20%) were positive for cocaine. Of 225 patients with depression, 59 (29%) were positive for THC and 33 (15%) were positive for cocaine. Cannabis was the most commonly reported substance used among patients with depression, schizophrenia, anxiety, schizoaffective disorder, and bipolar disorder, and ethanol was most common in patients with ADHD. No significant correlations were found between psychiatric diagnosis and positive drug screens. A statistically significant secondary end point was found that White people using cannabinoids were more likely to attempt suicide than were African American people (P = 0.02). Conclusions: Positive drug screens were common among patients presenting to an ED with psychiatric emergencies. Cannabis was the most commonly reported substance used among patients independent of diagnosis. Ethanol was the most common in patients with ADHD. Urine drug screens are unlikely to provide insights into relationships between specific substance use and psychiatric emergencies.

Failure of Computed Tomography (CT) in Detecting an Aspirin Pharmacobezoar: A Case Report.

BACKGROUND Prior studies suggest CT can identify bezoars under certain circumstances. Endoscopy provides diagnostic and therapeutic benefit in the setting of suspected aspirin bezoar. Does the absence of findings on CT scan exclude the presence of an aspirin bezoar? CASE REPORT A 64-year-old woman called the police and stated she ingested a bottle of aspirin to harm herself. Upon arrival to the Emergency Department, she was tachypneic with a GCS of 15. Initial laboratory results were: salicylate level of 1143 mcg/mL, respiratory alkalosis, bicarbonate of 9 meq/L, anion gap of 23, and normal renal function. Initial therapeutic intervention included infusions of glucose and bicarbonate, multiple doses of activated charcoal, intubation, and emergent hemodialysis. After hemodialysis, the salicylate level rebounded, and a Gastroenterology (GI) consultation was requested to rule out bezoar. On day 2, GI requested an abdominal CT scan with Gastrografin in place of endoscopy due to hemodynamic instability. A CT scan was negative for bezoar. After multiple hemodialysis sessions and whole-bowel irrigation with rebounding salicylate levels, GI was consulted again for reevaluation for endoscopy. On day 5, an endoscopy discovered a concretion containing pill fragments. Another endoscopy performed on day 7 removed further fragments. Salicylate levels began to consistently decline. Unfortunately, the patient's neurologic status did not improve, and on day 11 she was switched to palliative care and died. CONCLUSIONS Endoscopy with direct visualization is diagnostic and therapeutic in the setting of a possible bezoar. The absence of pharmacobezoar on imaging should not delay endoscopy in a clinical setting suggesting bezoar.

Trending of a falsely elevated serum creatinine after a pediatric nitromethane ingestion: A case report.

Introduction: Nitromethane is a primary nitroalkane used as a solvent and a fuel that may be toxic by ingestion, inhalation, or contact. Its presence can be detected in serum of exposed persons, but levels are not readily available to guide patient care. Nitromethane has been shown to falsely elevate serum creatinine when clinical laboratories use Jaffe assays to measure creatinine; enzymatic assays are not affected. Ex vivo experiments have demonstrated a linear relationship between serum nitromethane and the elevation in Jaffe assay creatinine. This case report demonstrates an elevation of creatinine measured by Jaffe assay with normal creatinine measurement by enzymatic assay after exposure to nitromethane. Case report: A 21-month-old girl ingested an unmeasured quantity of a hobby fuel, a fuel containing methanol, nitromethane (20%), and lubricants used in miniature internal combustion engines, such as remote-controlled cars. She was initially evaluated at a community hospital, treated empirically for methanol toxicity with fomepizole and folic acid, and transferred to a university hospital for further management. By 19 hours after ingestion, methanol was below detection, but a serum creatinine of 2.63 mg/dl raised concern for kidney injury. Toxicology consultation recognized that the creatinine had been measured using a Jaffe assay and recommended a repeat creatinine using an enzymatic assay, which was within normal limits. The patient remained an inpatient for further evaluation, which permitted trending of her Jaffe assay creatinine over a 3-day period. The Jaffe assay creatinine demonstrated a gradual decline; repeat enzymatic assay creatinine remained within normal limits. Discussion: The decline in this pediatric patient's Jaffe assay creatinine is consistent with first-order clearance of nitromethane, which has been previously described in adult exposures. This case demonstrates how Jaffe assay-derived serum creatinine may be useful in the pediatric population to establish, quantify, and trend nitromethane exposure with essential concurrent use of an enzymatic assay to determine actual creatinine.

Efficacy of methylene blue in a murine model of amlodipine overdose.

INTRODUCTION: Amlodipine overdoses have significant cardiac toxicity and are difficult to treat. Methylene blue has potential as a treatment for overdoses. METHODS: A randomized controlled study of methylene blue as a treatment for amlodipine toxicity was conducted in C57Bl/6 mice. A baseline echocardiography was followed by gavage administration of amlodipine (90 mg/kg). Five minutes after gavage, animals received either vehicle solution (controls) or methylene blue (20 mg/kg) by intra-peritoneal injection. Animals were continuously monitored, and cardiac parameters were acquired every 15 min up to two hours. RESULTS: Only 50% of control animals survived to the two-hour endpoint compared to 83% that received methylene blue. Amlodipine delivery induced significant reduction in left ventricular ejection fraction (EF), fractional shortening (FS), stroke volume (SV), and cardiac output (CO) in the vehicle treated animals relative to animals in the treatment group (p < 0.05 vehicle versus Methylene blue for EF, FS, SV, CO, and HR). DISCUSSION: The amlodipine dose induced cardiotoxicity that were effects were more pronounced in the untreated group. 50% vehicle controls quickly progressed into heart failure (within 90 min of exposure) and did not survive the two h observation endpoint. Distinctly, only one animal from the Methylene blue treatment group did not survive (83% survival) the study. Additionally, the surviving animals from the Methylene blue group displayed significantly higher ejection fraction, fractional shortening, stroke volume, and cardiac output compared to vehicle group, indicating that methylene blue preserved cardiac function. CONCLUSION: In this mouse model of amlodipine overdose, methylene blue decreased cardiac toxicity.

Wernicke encephalopathy associated with hyperemesis gravidarum.

Emergency physicians frequently treat hyperemesis gravidarum and should be aware of possible complications. Wernicke encephalopathy secondary to thiamine deficiency should be considered in the differential diagnosis of acute encephalopathy in pregnant women. A seventeen-week pregnant 27-year-old woman presented to the Emergency Department with nausea, emesis, and right upper quadrant abdominal pain. Ultrasound diagnosed gallbladder sludge. Surgical consultant offered cholecystectomy versus expectant management. She improved with IV hydration, ondansetron, and was discharged on hospital day 3 with a diagnosis of hyperemesis gravidarum and gallbladder sludge. Three days later she presented with continued emesis and altered mental status. She and family members denied alcohol or illicit drug use. Vital signs were pulse 99/min, blood pressure 115/70, temperature 36.4 °C, respiratory rate 18, and oxygen saturation 99%. Neurological examination was delirium, variable mentation, and inability to follow commands. She had internuclear opthalmoplegia with bilateral nystagmus. CT scan of brain was negative. MRI found abnormal T2-weighted signal in the central pons and medial thalami. Radiographic differential included central pontine myelinolysis, dysmyelinating conditions from malnutrition, toxic encephalopathy, and Wernicke encephalopathy. Thiamine level was below the limits of detection. Alcohol and urine drug screen were negative. Diagnosis was thiamine deficiency secondary to hyperemesis gravidarum with Wernicke encephalopathy. Emergency physicians frequently treat hyperemesis gravidarum. Nutritional status should be evaluated in patients who are unable to take neonatal vitamins. Awareness should exist of possible complications, including Wernicke encephalopathy secondary to thiamine deficiency.

First Aid and Pre-Hospital Management of Venomous Snakebites.

BACKGROUND: Antivenom is the definitive treatment for venomous snakebites, but is expensive and not available in many rural and poorly developed regions. Timely transportation to facilities that stock and administer antivenom may not be available in rural areas with poorly developed emergency medical services. These factors have led to consideration of measures to delay onset of toxicity or alternatives to antivenom therapy. METHODS: PubMed searches were conducted for articles on snakebite treatment, or that contained first aid, emergency medical services, tourniquets, pressure immobilization bandages, suction devices, and lymphatic flow inhibitors. RESULTS: The reviewed articles describe how venoms spread after a venomous snakebite on an extremity, list the proposed first aid measures for delaying the spread of venoms, and evaluate the scientific studies that support or refute methods of snakebite first aid. The recommendations for field treatment of venomous snakebites will be discussed. CONCLUSIONS: The evidence suggests that pressure immobilization bandages and related strategies are the best interventions to delay onset of systemic toxicity from venomous snakebites but may increase local toxicity for venoms that destroy tissue at the site of the bite, so their use should be individualized to the circumstances and nature of the venom.

Recent research on Gulf War illness and other health problems in veterans of the 1991 Gulf War: Effects of toxicant exposures during deployment.

Veterans of Operation Desert Storm/Desert Shield - the 1991 Gulf War (GW) - are a unique population who returned from theater with multiple health complaints and disorders. Studies in the U.S. and elsewhere have consistently concluded that approximately 25-32% of this population suffers from a disorder characterized by symptoms that vary somewhat among individuals and include fatigue, headaches, cognitive dysfunction, musculoskeletal pain, and respiratory, gastrointestinal and dermatologic complaints. Gulf War illness (GWI) is the term used to describe this disorder. In addition, brain cancer occurs at increased rates in subgroups of GW veterans, as do neuropsychological and brain imaging abnormalities. Chemical exposures have become the focus of etiologic GWI research because nervous system symptoms are prominent and many neurotoxicants were present in theater, including organophosphates (OPs), carbamates, and other pesticides; sarin/cyclosarin nerve agents, and pyridostigmine bromide (PB) medications used as prophylaxis against chemical warfare attacks. Psychiatric etiologies have been ruled out. This paper reviews the recent literature on the health of 1991 GW veterans, focusing particularly on the central nervous system and on effects of toxicant exposures. In addition, it emphasizes research published since 2008, following on an exhaustive review that was published in that year that summarizes the prior literature (RACGWI, 2008). We conclude that exposure to pesticides and/or to PB are causally associated with GWI and the neurological dysfunction in GW veterans. Exposure to sarin and cyclosarin and to oil well fire emissions are also associated with neurologically based health effects, though their contribution to development of the disorder known as GWI is less clear. Gene-environment interactions are likely to have contributed to development of GWI in deployed veterans. The health consequences of chemical exposures in the GW and other conflicts have been called "toxic wounds" by veterans. This type of injury requires further study and concentrated treatment research efforts that may also benefit other occupational groups with similar exposure-related illnesses.

Chronic Treatment with Naltrexone Prevents Memory Retention Deficits in Rats Poisoned with the Sarin Analog Diisopropylfluorophosphate (DFP) and Treated with Atropine and Pralidoxime.

Humans and rats poisoned with sarin develop chronic neurological disabilities that are not prevented with standardized antidotal therapy. We hypothesized that rats poisoned with the sarin analogue diisopropylfluorophosphate (DFP) and resuscitated with atropine and pralidoxime would have long-term memory deficits that were preventable with naltrexone treatment. Long Evans rats (250-275 g) were randomized to: DFP (N = 8): single subcutaneous (SC) injection of DFP (5 mg/kg). Treatment (N = 9): DFP (5 mg/kg) followed by chronic naltrexone (5 mg/kg/day × 12 weeks). Control (N = 12): single SC injection of isopropyl alcohol, (DFP vehicle) followed by chronic naltrexone (5 mg/kg/day). If toxicity developed after injection, antidotal therapy was initiated with atropine (2 mg/kg) and pralidoxime (25 mg/kg) and repeated as needed. After 12 weeks, rats underwent testing for place learning (acquisition) across 5 days of training using the Morris Water Maze. On day 6 a memory retention test was performed. Statistical analysis was performed using IBM SPSS Statistics. Rats receiving DFP rapidly developed toxicity requiring antidotal rescue. No differences in acquisition were seen between the DFP vs. DFP + naltrexone rats. During memory testing, DFP-poisoned rats spent significantly less time (29.4 ± 2.11 versus 38.5 ± 2.5 s, p < 0.05) and traveled less distance (267 ± 24.6 versus 370 ± 27.5 cm, p < 0.05) in the target quadrant compared to the treatment group. Treatment rats performed as well as control rats (p > 0.05) on the test for memory retention. Poisoning with DFP induced impaired memory retention. Deficits were not prevented by acute rescue with atropine and pralidoxime. Chronic naltrexone treatment led to preserved memory after DFP poisoning.

Efficacy of Trypsin in Treating Coral Snake Envenomation in the Porcine Model.

Antivenom is the definitive treatment for venomous snakebites. Alternative treatments warrant investigation because antivenom is sometimes unavailable, expensive, and can have deleterious side effects. This study assesses the efficacy of trypsin to treat coral snake envenomation in an in vivo porcine model. A randomized, blinded study was conducted. Subjects were 13 pigs injected subcutaneously with 1 mL of eastern coral snake venom (10 mg/mL) in the right distal hind limb. After 1 min, subjects were randomized to have the envenomation site injected with either 1 mL of saline or 1 mL of trypsin (100 mg/mL) by a blinded investigator. Clinical endpoint was survival for 72 h or respiratory depression defined as respiratory rate <15 breaths per minute, falling pulse oximetry, or agonal respirations. Fisher's exact t test was used for between group comparisons. Average time to toxicity for the saline control was 263 min (191-305 min). The development of respiratory depression occurred more frequently in control pigs than treated pigs (p = 0.009). Four of the six pigs that received trypsin survived to the end of the 3-day study. No control pigs survived. Two of the trypsin treatment pigs died with times to toxicity of 718 and 971 min. Survival to 12 and 24 h was significantly greater in the trypsin treatment group (p = 0.002, p = 0.009, respectively). Local injection of trypsin, a proteolytic enzyme, at the site of envenomation decreased the toxicity of eastern coral snake venom and increased survival significantly. Further investigation is required before these results can be extended to human snakebites.

Comparison of F(ab')2 versus Fab antivenom for pit viper envenomation: a prospective, blinded, multicenter, randomized clinical trial.

BACKGROUND: Crotalidae Polyvalent Immune Fab (Ovine) has been the only antivenom commercially available in the US since 2007 for treatment of Crotalinae envenomation. Late coagulopathy can occur or recur after clearance of Fab antivenom, often after hospital discharge, lasting in some cases more than 2 weeks. There have been serious, even fatal, bleeding complications associated with recurrence phenomena. Frequent follow-up is required, and additional intervention or hospitalization is often necessary. F(ab')2 immunoglobulin derivatives have longer plasma half life than do Fab. We hypothesized that F(ab')2 antivenom would be superior to Fab in the prevention of late coagulopathy following treatment of patients with Crotalinae envenomation. METHODS: We conducted a prospective, double-blind, randomized clinical trial, comparing late coagulopathy in snakebitten patients treated with F(ab')2 with maintenance doses [F(ab')2/F(ab')2], or F(ab')2 with placebo maintenance doses [F(ab')2/placebo], versus Fab with maintenance doses [Fab/Fab]. The primary efficacy endpoint was coagulopathy (platelet count < 150 K/mm(3), fibrinogen level < 150 mg/dL) between end of maintenance dosing and day 8. RESULTS: 121 patients were randomized at 18 clinical sites and received at least one dose of study drug. 114 completed the study. Of these, 11/37 (29.7%) in the Fab/Fab cohort experienced late coagulopathy versus 4/39 (10.3%, p < 0.05) in the F(ab')2/F(ab')2 cohort and 2/38 (5.3%, p < 0.05) in the F(ab')2/placebo cohort. The lowest heterologous protein exposure was with F(ab')2/placebo. No serious adverse events were related to study drug. In each study arm, one patient experienced an acute serum reaction and one experienced serum sickness. CONCLUSIONS: In this study, management of coagulopathic Crotalinae envenomation with longer-half-life F(ab')2 antivenom, with or without maintenance dosing, reduced the risk of subacute coagulopathy and bleeding following treatment of envenomation.

Long-term efficacy of pressure immobilization bandages in a porcine model of coral snake envenomation.

BACKGROUND: Pressure immobilization bandages delay mortality for 8 hours after coral snake envenomation, but long-term efficacy has not been established. OBJECTIVE: The objective of this study is to determine the long-term efficacy of pressure immobilization bandages after coral snake envenomation in the absence of antivenom therapy. METHODS: A randomized, observational pilot study was conducted. Ten pigs (17.3-25.6 kg) were sedated, intubated for 5 hours, and injected subcutaneously with 10 mg of lyophilized Micrurus fulvius venom resuspended in water. Pigs were randomly assigned to a control group (no treatment) or a treatment group (compression bandage and splint) approximately 1 minute after envenomation. Bandage pressure was not controlled. Pigs were monitored daily for 21 days for signs of respiratory depression, decreased oxygen saturations, and paralysis. In case of respiratory depression, pigs were humanely euthanized and time to death recorded. Statistical analysis was performed with Fisher exact test, Mann-Whitney U test, and Kaplan-Meier survival curve as appropriate. RESULTS: Median survival time of control animals was 307 minutes compared with 1172 minutes in treated animals (P = .10). Sixty percent of pigs in the treatment group survived to 24 hours vs 0% of control pigs (P = .08). Two of the treatment pigs survived to the end point of 21 days but showed necrosis of the distal lower extremity. CONCLUSIONS: Long-term survival after coral snake envenomation is possible in the absence of antivenom with the use of pressure immobilization bandages. The applied pressure of the bandage is critical to allowing survival without necrosis. Future studies should be designed to accurately monitor the pressures applied.

A randomized controlled trial of trypsin to treat brown recluse spider bites in Guinea pigs.

Brown recluse spider bites result in necrotic skin lesions for which there is no known antidote. Since venom toxins are proteins, a proteolytic enzyme like trypsin might be effective in reducing toxicity. The aim of this study was to conduct a randomized controlled trial of trypsin to treat brown recluse spider bites in guinea pigs. Subjects were 18 female guinea pigs. Anesthesia for injections was inhaled isoflurane. Analgesia was 0.05 mg/kg of buprenorphine twice a day as needed. Intervention was intradermal injection of 30 µg of brown recluse venom (Spider Pharm, Yarnell, AZ). Immediately after envenomation, subjects were randomized to two groups of nine: trypsin 10 µg in 1 mL normal saline and 1 mL of normal saline. The primary outcome was lesion area over a 10-day time period. Statistical analysis was performed with repeated measures ANOVA. Mean lesion area was smaller but not statistically different in the placebo group. Maximum lesion size occurred at day 4 in both groups, when lesion area was 76.1 ± 108.2 mm(2) in the placebo group and 149.7 ± 127.3 mm(2) in the treatment group. P value was 0.15 for placebo vs. treatment. This study did not establish a role for trypsin as a treatment for brown recluse spider bites in a guinea pig model.

Aldicarb: a case series of watermelon-borne carbamate toxicity.

Improper use of pesticides on food plants can result in significant toxicity. In spite of regulations, enforcement, and prior episodes of poisonings, poisonings from misapplication of pesticides continues to occur. The objective of this study was to present a case series of toxicity resulting from ingestion of watermelon inappropriately treated with the carbamate insecticide aldicarb. A restrospective review of medical records, impounding the suspected watermelons, and chemical analysis of the watermelon samples using liquid chromatography and mass spectroscopy were carried out. Seven farm workers shared a watermelon and presented to a rural emergency department with symptoms of cholinergic poisoning. They were treated empirically with atropine and pralidoxime. The farmer denied use of insecticides other than rat poison on the watermelon patch. Chemical analyst verified aldicarb in the watermelon samples from the field, but none in control samples. Despite government regulations, application of restricted pesticides such as aldicarb continues to occur and cause significant poisonings.

Naltrexone prevents delayed encephalopathy in rats poisoned with the sarin analogue diisopropylflurophosphate.

BACKGROUND: Acute poisoning with organophosphate compounds can cause chronic neuropsychological disabilities not prevented by standard antidotes of atropine and pralidoxime. We determine the efficacy of naltrexone in preventing delayed encephalopathy after poisoning with the sarin analogue diisofluorophosphate (DFP) in rats. METHODS: A randomized controlled experiment was conducted. Rats were randomly assigned to receive a single intraperitoneal (IP) injection of 5 mg/kg DFP (n = 12) or vehicle control (isopropyl alcohol, n = 5). Rats were observed for cholinesterase toxicity and treated with IP atropine (2 mg/kg) and pralidoxime (25 mg/kg) as needed. After resolution of acute toxicity, rats injected with DFP were again randomized to receive daily injections of naltrexone (5 mg/kg per day) or saline (vehicle control). Control animals also received daily injections of saline. For 4 weeks after acute poisoning, rats underwent neurologic testing with the Morris Water Maze for assessment of spatial learning and reference memory. Comparisons on each test day were made across groups using analysis of variance followed by Fisher's least significant difference. Comparisons of changes in performance between first and last test day within each group were made using a paired t test. Significance was determined at P < .05. RESULTS: All rats receiving DFP developed toxicity requiring rescue. Spatial learning was significantly worse in the DFP-only group compared with the naltrexone-treated and control groups at day 10 (P = .0078), day 13 (P = .01), day 24 (P = .034), and day 31 (P = .03). No significant differences in reference memory were detected at any time point. CONCLUSION: Naltrexone protected against impairment of spatial learning from acute poisoning with DFP in rats.

A localizing circumferential compression device increases survival after coral snake envenomation to the torso of an animal model.

BACKGROUND: Pressure immobilization bandages have been shown to delay onset of systemic toxicity after Eastern coral snake (Micrurus fulvius) envenomation to the distal extremity. OBJECTIVES: To assess the efficacy of a novel compression device in delaying onset of systemic toxicity after truncal envenomations with Eastern coral snake (Micrurus fulvius) venom in a porcine model. METHODS: With University approval, nine juvenile pigs (11 kg to 22 kg) were sedated, anesthetized, and intubated but not paralyzed to ensure continuous spontaneous respirations in a university animal laboratory. Each animal was injected subcutaneously with 10 mg of M. fulvius venom in a pre-selected area of the trunk. After 1 min, six animals had the application of a novel, localizing circumferential compression (LoCC) device applied to the bite site (treatment group) and three animals had no treatment (control group). The device was composed of a rigid polymer clay form molded into a hollow fusiform shape with an internal dimension of 8 × 5 × 3 cm and an elastic belt wrapped around the animal securing the device in place. Vital signs were recorded at 30-min intervals. End points included a respiratory rate below 3 breaths/min, oxygen saturation < 80%, or survival to 8 h. Survival to 8 h was analyzed using Fisher's exact test, with p < 0.05 indicating significance. Survival analysis was performed using the Mantel-Cox test to assess time to death with outcomes represented in a Kaplan-Meier Cumulative survival plot. RESULTS: Five of the six pigs in the treatment group survived 8 h (293-480 min). None of the control pigs survived to 8 h (Fisher's exact p = 0.04), with mean time of respiratory failure 322 min (272-382 min). Survival analysis showed a significant delay in time to event in the treatment group compared to the control group (p = 0.04). CONCLUSIONS: The LoCC device used in this study delayed the onset of systemic toxicity and significantly increased survival time after artificial truncal envenomation by Eastern coral snake venom.

A localizing circumferential compression device delayed death after artificial eastern diamondback rattlesnake envenomation to the torso of an animal model in a pilot study.

Nearly all prior studies to delay onset of systemic toxicity and death after snake bite use a model of distal extremity envenomation. In the first of a series of planned studies using snake venoms with different toxicity profiles, the application of a novel device in a new model of torso envenomation in the setting of Eastern Coral Snake (Micrurus fulvius) venom (a potent neurotoxin) envenomation showed promise by delaying systemic intoxication. In this pilot study, we investigated this novel localizing circumferential compression (LoCC) device's ability to delay onset of life threatening systemic toxicity after Eastern Diamondback Rattlesnake (Crotalus adamanteus) envenomation, a potent hemotoxic and myotoxic venom. With university approval, four juvenile female pigs (22-25 kg) were anesthetized, sedated, and intubated but not paralyzed to allow for spontaneous respirations. Each animal was injected subcutaneously with 50 mg of C. adamanteus venom in identical preselected areas of the trunk. After 1 min, two treatment animals had the LoCC device applied; two control animals had no intervention. Vital signs were recorded every 10 min for the first 2 h and every 30 min thereafter. Endpoints included cardiovascular collapse (fatal arrhythmia, loss of mean arterial pressure, or pulse) or respiratory arrest (<3 breaths/min, saturation < 80%) or survival to 7 h. The pigs in the treatment group reached an endpoint at an average time of 355 (+/-65) min compared with control 32 (+/-3.5) min (p < 0.04). In this pilot study, the LoCC device significantly delayed onset of systemic symptoms and death after torso envenomation with Eastern Diamondback Rattlesnake venom in this model.

Efficacy of North American crotalid antivenom against the African viper Bitis gabonica (Gaboon viper).

Envenomations by exotic snakes occur from zoological collections and private individual collectors. Antivenoms to these snakes may not be readily available. The objective of this study is to determine the efficacy of North American crotalid antivenin in treating mice envenomated with venom of the African viper Bitis gabonica (Gaboon viper). The subjects of the study were Swiss Webster mice weighing approximately 30 g. The study was conducted in the University research laboratory. B. gabonica venom was obtained from Venom Supplies Pty Ltd (Tanunda, South Australia) and reconstituted in sterile water. North American Crotalid Fab2 antivenin (Anavyp, Instituto Bioclon, Mexico) was donated by the manufacturer. The experimental groups were: Group I received two times an intraperitoneal LD(50) dose of venom, 2.58 mg/kg. Group II received the same dose after incubation for 1 h with 10 mg of antivenin. Time to onset of toxicity defined as respiratory rate <10/min or absence of response to prodding. t test and Chi square with p < 0.05 considered significant. Time to onset of toxicity was 7.040 +/- 4.334 h in group I, and 20.665 +/- 2.074 in group II (p = 0.0064, 95% confidence interval of difference of means -22.694 to -4.556). Antivenin was efficacious to statistical significance at 4, 8, 12, and 16 h (p values of 0.062, 0.0067, 0.0067, and 0.0253, respectively). Improvement at 20 and 24 h (p values of 0.0673 and 0.0673, respectively) did not achieve statistical significance. North American Crotalid antivenin (Anavyp, Instituto Bioclon, Mexico) demonstrated efficacy in increasing time to onset of distress in mice poisoned with B. gabonica (Gaboon viper) venom. Based on this result, treatment of humans envenomated with B. gabonica with North American Croatlid antivenin could be considered for severe envenomations if specific B. gabonica antivenin is unavailable.