pressure-immobilization bandages delay toxicity in a porcine model of eastern coral snake (micrurus...

TOXICOLOGY/ORIGINAL RESEARCH

Pressure-Immobilization Bandages Delay Toxicity in a PorcineModel of Eastern Coral Snake (Micrurus fulvius fulvius)

Envenomation

Benjamin T. German, MD

Jason B. Hack, MD

Kori Brewer, PhD

William J. Meggs, MD, PhD

From the Department of Emergency Medicine, Brody School of Medicine, East CarolinaUniversity, Greenville, NC.

Study objectives: Pressure-immobilization bandages are used in countries where neurotoxic snakeenvenomations are common. They impede lymphatic egress from the bite site and delay systemicvenom toxicity. The effectiveness of these devices has not been evaluated in coral snakeenvenomations. We investigated the efficacy of pressure-immobilization bandages in delaying theonset of systemic toxicity in a porcine model of coral snake envenomation.

Methods: A randomized controlled trial of pressure-immobilization bandages was conducted ina university animal care center. Subjects were 12 anesthetized, spontaneously breathing pigs, rangingfrom 9.1 to 11.4 kg. After injection with 10 mg of Micrurus fulvius fulvius venom in the subcutaneoustissue of the distal foreleg, subjects were randomized to receive no treatment or application ofa pressure-immobilization bandage at 1 minute after injection. Treated animals had elastic bandagesapplied to the extremity and splinting for immobilization. Vital signs and quality of respirations wererecorded. Outcome was the onset of respiratory failure or survival to 8 hours. Necropsies and histologicanalysis of the envenomation site was performed.

Results: One animal from each group was removed because of the discovery of pre-existing respiratorypathology. Four of 5 pigs in the treatment group survived to 8 hours, but none in the control groupsurvived. Mean time to onset of respiratory compromise was 170.4G33.3 minutes in the controlgroup. None of the pigs had histologic changes at the envenomation site consistent with ischemia orpressure-related injury.

Conclusion: Pressure-immobilization bandages delayed the onset of systemic toxicity in our porcinemodel of M fulvius envenomation. [Ann Emerg Med. 2005;45:603-608.]

0196-0644/$-see front matterCopyright ª 2005 by the American College of Emergency Physicians.doi:10.1016/j.annemergmed.2004.11.025

INTRODUCTIONThe North American coral snakes (Micrurus fulvius ssp.) are

elapid snakes endemic to the United States that cause fatalhuman envenomations. These snakes are found from Texas toNorth Carolina and as far north as Arkansas. An average of 70reports involving coral snake bites were received by UnitedStates poison control centers annually in the past 5 years.1-5 Theincidence of reported bites has been increasing, and in 2002there were 97, the most ever recorded.1-20 The mortality rate ofuntreated envenomations is reported to be near 10%, althoughno deaths have occurred in the United States since antivenomwas introduced in 1967.21,22

The venom of M fulvius contains low-molecular-weightpeptides that block postsynaptic acetylcholine receptors.23 Thevenom lacks significant proteolytic activity, and local effects are

Volume 45, no. 6 : June 2005

minimal to none. In severe, untreated envenomations, anasymptomatic period is followed by neuromuscular blockade andfatal respiratory muscle paralysis. Wyeth North American coralsnake antivenom has remained the definitive treatment forMicrurus envenomations but is less effective if administered afterthe onset of paralysis. Production ceased in 2001, and there is noalternative product licensed for use in the United States.24 Thecompany does retain limited emergency stocks of the product.24

Pressure-immobilization techniques, recommended forelapid bites in Australia, impede lymphatic return to the centralcirculation, thereby sequestering the venom near the bite siteand delaying systemic toxicity,25-27 which allows more time toaccess definitive care in the form of antivenom and advancedairway management. These devices are not tourniquets and aredesigned to preserve arterial and deep venous flow.

Annals of Emergency Medicine 603

Pressure-Immobilization Bandages and Delayed Toxicity German et al

Editor’s Capsule Summary

What is already known on this topic

Pressure-immobilization bandages are effective in thetreatment of snake bites found outside the United States.

What question this study addressed

Whether pressure-immobilization bandages would workwith envenomations from the Eastern coral snake(Micrurus fulvius fulvius) indigenous to the UnitedStates.

What this study adds to our knowledge

Assuming that the porcine model is appropriate, thisstudy provides compelling evidence that the pressure-immobilization bandages are effective.

How this might change clinical practice

Pressure-immobilization technique is a reasonableintervention for coral snake bites in the United States.

Three variations of this concept have been studied. The‘‘Commonwealth Serum Laboratories method’’(Commonwealth Serum Laboratories, Parkville, Victoria,Australia) consists of wrapping the bitten extremity witha bandage and then splinting the limb.25 The ‘‘Monash method’’(Monash University, Melbourne, Australia) places a firm clothpad directly over the bite site and then firmly secures it with clothstrips to apply direct pressure.26 The third method is theplacement of a full-limb air splint that is then inflated.27 Thesedevices have been evaluated in human studies with radiolabeledmock venoms and in animal studies with radiolabeled venomsfrom Russell viper (Daboia russellii) and the tiger snake (Notechisscutatus).25-30 In these studies, venom assays rather than clinicalparameters were measured. Both the Commonwealth SerumLaboratories and Monash methods have been effective inretarding systemic spread of real and mock venoms in studies,9-14

but the air splint has not been evaluated in this manner.Some sources in the United States advocate using pressure-

immobilization in the early management of coral snakeenvenomation.31-33 The pressure-immobilization technique hasnot been formally evaluated in coral snake envenomations.34

We tested the hypothesis that one of these methods, theCommonwealth Serum Laboratories method, would delay theonset of clinical systemic toxicity in a porcine model ofM fulvius envenomation.

MATERIALS AND METHODSA randomized, unblinded, controlled trial of pressure-

immobilization bandages in a porcine model of M fulviusenvenomation was undertaken. A porcine model was chosen byconsiderations of availability, cost, acceptability to theinstitutional animal review committee for experimental study,the expectation that venom toxicity is similar to that seen in

604 Annals of Emergency Medicine

humans, and literature supporting its use.35-38 The universityanimal care use committee approved the study. Subjects were 12pigs ranging from 9.1 kg to 11.4 kg. Subjects were initiallysedated with intramuscular tiletamine (5 mg/kg) and zolazepam(5 mg/kg), intubated, and then kept anesthetized with isofluranetitrated between 1% and 3%. A mixture of nitrous oxide (65%)and oxygen (35%) was also used. Animal care technicianstitrated anesthesia to ensure both animal comfort andspontaneous respirations.

Lyophilized M fulvius venom (Natural Toxins ResearchCenter, Kingsville, TX) was resuspended in pure water toa concentration of 10 mg/mL. This venom was obtained fromFlorida snakes, but no further geographic data are available.With a 27-gauge needle, pigs were injected with 10 mg ofvenom at a depth of 3 mm (near maximum length of adult Mfulvius fangs) in the subcutaneous tissue of the left distal foreleg.Injection site was midway between the distal and middleintraphalangeal joints. Before injection, negative pressure wasapplied to the syringe plunger to avoid intravascular injection.

The dose of 10 mg was chosen empirically to be lethal in thesubjects, given that the lethal adult human dose is 4 to 5 mg.39

A large M fulvius can yield more than 20 mg of venom ina single milking.40,41 All animals received the same dose. Thedose was approximately 1 mg/kg and reliably produced fatalrespiratory failure within 200 minutes.

After injection, subjects were randomized to either notreatment or a pressure-immobilization bandage 1 minute afterenvenomation. A forced randomization was accomplished byblindly drawing a card labeled to treat or not to treat. Six cardswere labeled ‘‘to treat’’ and 6 ‘‘not to treat.’’ A commerciallyavailable 2-inch-wide elastic bandage (Ace wrap) was applied totreated animals by a single operator, beginning at theenvenomation site, and then wrapped circumferentially, pro-ceeding proximally to the shoulder. The bandage was applied‘‘as tightly as one would wrap an acute sprain,’’ which is howmany authorities describe field placement of this device.40 Eachbandage was checked hourly to ensure that a finger could beeasily passed under; none required loosening. Aluminum andfoam splints were then loosely taped on either side toimmobilize the extremity (Figure 1).

Pulse rate, respiratory rate, pulse oximetry, and quality ofrespirations were recorded before envenomation and at sub-sequent 10-minute intervals. The endpoint was either the onsetof toxicity in the form of obvious respiratory distress or survivalto 8 hours. Respiratory distress was defined as a sustained,nonreversing change in the respiratory pattern marked bybradypnea, an apneic episode, agonal respirations, or fallingoxygen saturation. When any of these signs was observed, theanimal was checked to ensure proper endotracheal tubeplacement and patency. Anesthesia was lightened to watch forpossible recovery. The pig was then observed until it was clearthat severe, irreversible systemic toxicity was occurring, at whichpoint the animal was killed with pentobarbital per institutionalprotocol. The time to the first observation of sustainedrespiratory compromise was recorded. As a safeguard, when an


German et al Pressure-Immobilization Bandages and Delayed Toxicity

animal did experience respiratory difficulty, the isoflurane wasturned off, and the endotracheal tube was checked forplacement and patency. Animals that survived to 480 minuteswithout evidence of severe systemic toxicity were killed. Aveterinary pathologist performed necropsies on all subjects.

Statistical analysis was performed using c2 analysis andanalysis of variance as appropriate.

RESULTSTwo of the subjects, 1 from each group, developed fulminant

sanguinous bronchorrhea before the onset of respiratoryparalysis. Necropsy verified preexisting pulmonary infections inthese 2 animals, so they were removed from the study. None ofthe 10 remaining pigs demonstrated this finding or hadpulmonary abnormalities on necropsy.

Results for individual animals are given in the Table. Four of5 subjects in the treatment group survived to 8 hours, but nonein the control group did (P=.0036 using Fisher exact test forcategoric data). For the treatment group, the mean time todeath was 450 minutes (95% confidence interval [CI] 366.71 to533.29 minutes; median 480 minutes; interquartile range[IQR] 37.5). For the control group, mean time to death was182 minutes (95% CI 148.35 to 236.45 minutes; median 182minutes; IQR 70). For the difference of the mean time to death,

Figure 1. Pressure-immobilization bandage applied to forelegof pig.


the 95% CI was 179.34 to 335.86 minutes. The control animalsdeveloped severe toxicity at a mean time of 170G33 minutes,and none survived more than 200 minutes. The one animal inthe treatment group who did not survive the 8-hour period ofinvestigation developed respiratory difficulty at 310 minutes.When the statistical analysis was repeated including the 2animals who died of hemorrhagic bronchorrhea not related tocoral snake envenomation, with 4 of 6 animals in the treatmentgroup surviving to 8 hours and 0 of 6 animals in the controlgroup surviving to 8 hours, the P value was .06 (using Fisherexact test for categoric data). Effects of body weight on the timeto onset of toxicity was analyzed and found not to be a factor.

Mean values for respiratory rate, oxygen saturation, andpulse rate over time are shown in Figures 2A, 2B, and 2C,respectively. Respiratory rate predictably decreased as animalsbecame toxic, and pulse rate correspondingly increased. Oxygensaturation decreased rapidly when subjects became severelytoxic, but this was a late finding and a sign of imminentrespiratory failure. All endotracheal tubes were found to befunctioning properly at the endpoints, and no subject recoveredin the absence of isoflurane.

At death, the bandages were removed, and all animalswere subject to necropsy by a veterinary pathologist.Histologic examination revealed no evidence of pressure orischemic-induced injury at any of the envenomation sites.Minor localized hemorrhage was observed in allenvenomation sites, possibly because of venom effects.

LIMITATIONSThis study has several limitations. Investigators were not

blinded to which subjects received a pressure-immobilizationdressing. A relatively small number of animals were used.Animals were of necessity anesthetized and received supple-mental oxygen. Animals were not prescreened for respiratorypathology, which led to 2 pigs being removed from the study.

Table. Subjects, weights, and time to onset of systemic toxicityor survival to 480 minutes.*

Subject Weight, kg Bandage

Time to Toxicity or

Total Survival, min

1 10.9 N 942 9.1 Y 2333 11.0 N 1824 11.0 Y 4805 9.8 N 2006 10.6 N 2007 9.5 Y 4808 10.0 Y 4809 10.5 N 130

10 10.5 Y 48011 11.4 N 14012 9.1 Y 310

N, No; Y, yes.

*Pigs 1 and 2 developed hemorrhagic bronchorrhea before the onset of

respiratory paralysis, which is thought to be unrelated to coral snake

envenomation.



Figure 2. Comparison of A, pulse rate, B, respiratory rate, and C, oxygen saturation of pigs receiving pressure-immobilizationbandage to control pigs, versus time.

The alternative interpretation, that the pressure-immobilizationbandage failed in the pigs in the treatment group that developedhemorrhagic bronchorrhea, is inconsistent with the knowneffects of coral snake venom. Measurements of venom levelswere not performed and, if available, would have been helpful inconfirming results. This study applied pressure-immobilizationbandages under ‘‘field conditions,’’ in that we did not measurebandage pressures. The pressure-immobilization bandage wasapplied 1 minute after the injection of venom, and this rapiditymost likely will not be duplicated in the field.

The animals received supplemental oxygen mixed with theisoflurane through the ventilator circuit because this was theonly way to deliver the anesthetic with the equipment available.We would have preferred room air as the dissolving gas becausethe increased oxygen concentration could theoretically prolongsurvival. All subjects received the same mixture.

DISCUSSIONThis study is the first to evaluate pressure-immobilization

bandage efficacy in coral snake envenomation. Speculation andcontroversy over the usefulness of these devices in coral snakeenvenomations is found in the current emergency medicine,wilderness medicine, and toxicology literature. Most referencesmention that this technique could be useful but that it has notbeen formally studied. Some references state that the techniqueis not useful despite the previous lack of research. These sourcesstate that coral snake venom is absorbed by the venous system asopposed to the lymphatics,42 which is unlikely, considering thesnake’s very small fangs (1 to 3 mm), unsophisticated venomdelivery system, and the minute quantities of venom injected. Ifcoral snake venom were hematogenously spread, victims wouldbecome systemically toxic rapidly, when in fact the hallmark ofcoral snake envenomations is a period of delay of up to 12 hoursto the onset of systemic symptoms. In most snake envenoma-tions, coral included, venom is deposited in the subcutaneoustissue, where it is transported proximally by the lymphatics.27

The onset of toxicity was sudden and dramatic in all cases.After injection, most subjects experienced tremors in theaffected limb, which appeared to progress to full-limb jerks andapparent involuntary movements. Several appeared to havefasciculations. These movements would persist for several


minutes and then subside. These observations were much moreapparent in the control animals, although the range of motionwas restricted in the splinted animals. After the movementsceased, there was a period during which the animals wereasymptomatic, with normal respiratory patterns. At a mean timeof 170G33 minutes, control pigs developed signs of systemictoxicity that progressed to fatal respiratory distress.

The earliest sign of systemic poisoning was a noticeablechange in the respiratory mechanics of the animals. The pigsappeared to have more shallow respirations with increasedreliance on abdominal musculature. Respiratory rate would thendecrease. Two of the control pigs experienced apneic episodes asthe first sign of severe toxicity, and the other 3 went fromrespiring normally to agonal respirations within a 10-minuteperiod.

A significant challenge of the study was how to keep thesubjects anesthetized and immobile and breathing spontane-ously without compromising respiratory status. In consultationwith veterinary experts and animal care technicians, we chose toinitially sedate the animals with a single intramuscular injectionof tiletamine and zolazepam and then maintain anesthesia withisoflurane, which has minimal respiratory effects at usual doses.The agents worked well, and none of the animals experiencedrespiratory depression before envenomation. The animal caretechnicians and veterinarian witnessed the respiratory changesand did not think they were consistent with isoflurane effects.

One of the 5 treated animals exhibited severe toxicity anddied at 310 minutes, which could have occurred for severalreasons. Injection error could have placed venom in or very neara blood vessel, although precautions were taken to avoid this.An intravascular injection would result in death despiteplacement of the bandage because arterial and deep venousflows are preserved. Bandaging error is another possibility; if thebandage was placed too loosely, it may have been ineffective,although bandages were standardized as described. Finally, itmust be considered that pressure-immobilization bandages arenot perfect and have failures.

On the basis of the results of the study, we propose thatpressure-immobilization be considered in the management ofcoral snake envenomations until definitive care is available tothe patient. The device proved to be protective against systemic


German et al Pressure-Immobilization Bandages and Delayed Toxicity

venom toxicity and more than doubled average survival time.The pressure-immobilization technique is simple, uses commonmaterials, and should be taught to out-of-hospital providers andmedical personnel in areas where coral snakes are endemic.With remaining stocks of North American coral snakeantivenom in short supply and no immediate alternative,delaying toxicity will be essential in reducing the morbidity andmortality resulting from these envenomations. Use of pressure-immobilization devices should be also considered in LatinAmerican countries, where snakes bites are more frequent andaccess to medical care is often delayed.

We thank the veterinarians and staff at the ComparativeMedicine Center at East Carolina University for their help andsupport. John Bradfield, DVM, PhD, Kenneth Salleng, DVM, andDale Aycock, AAS, LATG, provided exceptional assistance.

Author contributions: BTG, KB, JBH, and WJM were involved inthe design of the study, working in the laboratory, andpreparation of the manuscript. BTG, WJM, and KB were involvedin ordering materials. KB was involved in the statisticalanalysis. WJM takes responsibility for the paper as a whole.

Funding and support: This study was funded by the EmergencyMedicine Residents Research Fund at the Brody School ofMedicine Medical Foundation.

Publication dates: Received for publication July 9, 2004.Revisions received September 16, 2004; and November 8,2004. Accepted for publication November 29, 2004. Availableonline April 14, 2005.

Reprints not available from the authors.

Address for correspondence: William J. Meggs, MD, PhD,Division of Toxicology, Department of Emergency Medicine,Brody School of Medicine at East Carolina University,600 Moye Boulevard, Greenville, NC 27858; 252-744-2954,fax 252-744-3589; E-mail [email protected].

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