Posts tagged #wilderness medicine

TPA in Frostbite

Written by: Patrick King, MD Edited by: Nery Porras, MD (NUEM ‘21) Expert Commentary by: Anne Lambert Wagner, MD

TPA in Frostbite

Figure 1. What we would like to avoid (Cline et al.)

It’s an early Saturday morning, and EMS brings in one of your ED’s regulars – a schizophrenic, undomiciled gentleman named Jack who finds occasional work as a day laborer. You walk to bed three to greet Jack who is uncomfortable and shivering while nursing collects vitals. His chief complaint is hand and foot pain. You listen to him speak, but you jump right into a cursory exam as he does – and your heart sinks when you see the icy hard, cyanotic, mottled digits across all four extremities. You wonder what else you might be able to offer in addition to the standard cold injury approach we are taught as emergency residents, and you recall that the What’s New in Emergency Medicine section of UpToDate just recognized growing evidence for yet another off-label use for tPA: severe frostbite.

As we head into the winter months, emergency physicians will continue to see frostbite wreck a significant level of morbidity on our most vulnerable patients – patients who are undomiciled, suffering from addictions or mental illness, and those with preexisting conditions that limit blood flow to extremities (Zafren and Crawford Mechem). This post will address the theory, evidence, and logistics behind tPA utilization in severe frostbite.

The proposed efficacy of tPA in frostbite is related to cold-induced thrombosis. Endothelial damage is sustained both as a direct result of cold-related injury and exacerbated by reperfusion injury during the period of rewarming. During rewarming, arachidonic acid cascades promote vasoconstriction, platelet aggregation, leukocyte sludging, and erythrostasis which further promote thrombosis throughout affected tissues. This process is compounded in instances of multiple freeze-thaw cycles (Cline et al).

Research on tPA in frostbite goes back years. In 2005, Twomey et al. demonstrated in an open-label study that technetium (Tc)-99m scintigraphy (i.e., nuclear bone scan) reliably predicts digits/limbs at risk for amputation. Historical control patients with no or minimal flow distal to radiographically identified “cutoff” points of ischemia on bone scans inevitably all required amputations. Untreated historical controls without flow cutoffs were more likely to retain digits. In contrast, 16 of 19 study patients with identified flow cutoffs responded to intra-arterial (IA) or intravenous (IV) tPA with an amputation rate of only 19% of at-risk digits. In 2017, Patel et al. showed a 15% amputation rate for severe frostbite in eight IA tPA patients compared to 77% in their control group.

Figure 2. Pre-tPA and Post-tPA using technetium (Tc)-99m scintigraphy bone scan (Twomey et al.)

While study results have been impressive in instances of small sample sizes such as the above, a paucity of evidence has prevented widespread utilization of tPA for frostbite use amongst emergency physicians. This year, however, What’s New In Emergency Medicine on UpToDate gave special attention to a 2020 systematic review of 16 studies by Lee and Higgins which wielded a sample size of 209 patients with 1109 digits at high amputation risk. The study, entitled “What Interventional Radiologists Need to Know About Managing Severe Frostbite”, ultimately demonstrated a 76% salvage rate amongst IA tPA (222 amputations amongst 926 digits) and 62% salvage rate in IV tPA (24 amputations amongst 63 patients). Importantly, the 16 studies are not randomized, though several such as Patel et al. and Twomey et al. utilize historical controls. There is also no direct comparison of IA vs. IV tPA, and for unclear reasons, the salvage rate for IA is in terms of digits salvaged out of those at risk while IV is expressed as a function of patients who required no amputations. Though there remains additional research to be done, UpToDate’s Frostbite authors Zafren and Crawford Mechem now give an overall grade 2C recommendation for tPA use in severe frostbite for patients otherwise at risk of life-altering amputations.

Figure 3. Grading severity of frostbite after rewarming (Cauchy et al.)

Figure 4. Grade 4 Frostbite, best seen in far right (Pandey et al.)

TPA utilization in frostbite is straightforward. UpToDate authors recommend tPA consideration for any patients with frostbite in multiple digits in a single limb, in multiple limbs, and/or in proximal limb segments who present within 24 hours of injury. The American Burn Association, which has its own guidelines (largely similar), recommends tPA for patients with cyanosis proximal to the distal phalanx after rewarming (i.e. grade 3 or 4). In more simple terms – injuries expected to be life-altering, as revealed following rapid rewarming, are likely to meet inclusion. Contraindications include general tPA contraindications as well as frostbite-specific considerations such as multiple freeze-thaw cycles which destroy tissue viability via repeated reperfusion injury as discussed previously. An additional frostbite-specific quandary with tPA use is the intoxicated frostbite patient, as substance abuse is a strong risk factor for frostbite, but intoxication can preclude tPA consent.

So you suspect you have a candidate – how do you proceed? Advice from UpToDate’s Zafren and Mechem is representative of many experts’ approaches. Early consultation with centers experienced in advanced frostbite therapeutics is recommended. General immediate frostbite care is undertaken on ED arrival, including 15-30 minutes rapid water bath rewarming at 37 to 39 degrees Celsius, at which point the tissue should change from hard and cold to more soft and pliable. Ensure adequate analgesia, as this rewarming process can be painful. Following rapid rewarming, the grade of frostbite can be assessed (fig. 2,3). Clinical suspicion is then confirmed via technetium (Tc)-99m scintigraphy (bone scan) or by angiography at centers with expertise in intra-arterial tPA use. Angiography is utilized only if IA administration is planned. UpToDate recommends IV tPA for most candidates given the ease of administration unless specific institutional protocol differs.

Specific UpToDate dosing regimen is as follows: “Give a bolus dose of 0.15 mg/kg over 15 minutes, followed by a continuous IV infusion of 0.15 mg/kg per hour for six hours. The maximum total dose is 100 mg. After tPA has been given, adjunct treatment can be started with IV heparin or subcutaneous (SC) enoxaparin. The dose of IV heparin is 500 to 1000 units/hour for six hours or targeted to maintain the partial thromboplastin time (PTT) at twice the control value. Enoxaparin can be given at the therapeutic dose (1 mg/kg SC).”

Additional research remains to be done on this topic. At this time, however, it is reasonable to give your patients – a hand – when it comes to severe frostbite. Consider tPA.

Expert Commentary

Background

Skin and soft tissue are readily susceptible to injury at either end of the temperature spectrum. With exposure to cold, unprotected tissues can readily become frostbitten and/or hypothermic (aka Frostnip); two distinct but often linked injuries. In the past, skin, limbs, and digits sustaining severe frostbite injury had predictable outcomes: sloughing or amputation. The only question was how long to wait to amputate. Essentially no progress was made in the treatment of frostbite until the early 1990’s when the development of a treatment protocol for frostbite patients was developed using thrombolytics to restore blood flow to damaged tissue.

Frostbite has two separate mechanisms to the injury itself. The initial insult is the cold injury that leads to direct cellular damage from the actual freezing of the tissues. Rewarming of the affected tissues leads to the second, a reperfusion injury resulting in patchy microvascular thrombosis and tissue death.

Frostbite Classification

First-degree frostbite: Superficial damage to the skin from tissue freezing with redness (erythema), some edema, hypersensitivity, and stinging pain.
Second-degree frostbite: Deeper damage to the skin with a hyperemic or pale appearance, significant edema with clear or serosanguinous fluid-filled blisters, and severe pain. Frostnip, first and second-degree frostbite will generally heal without significant tissue loss.
Third-degree frostbite: Deep damage to the skin and subcutaneous tissue. Cold, pale, and insensate without a lot of tissue edema. Shortly after rewarming, edema rapidly forms along with the presentation of hemorrhagic blisters. Significant pain often occurs after rewarming.
Fourth-degree frostbite: All the elements of a third-degree injury with evidence of damage extending to the muscle, tendon, and bone of the affected area.

Figure 2. 1st and 2nd degree frostbite (left), 3rd and 4th degree frostbite (right)

Pre-hospital or Emergency Department Management

Determining the extent of frostbite injury starts with a detailed history regarding how the affected area appeared on presentation.
The history of a cold, white, and insensate extremity on presentation is consistent with severe frostbite injury (3rd and/or 4th-degree frostbite).
A severe frostbite injury requires emergent therapy with thrombolytics unless the patient meets one of the exclusion criteria.
If in question regarding the depth of the injury, a clinical exam can be supported by a vascular study as indicated. A digital Doppler exam is a simple and quick modality to further Clarify the diagnosis of severe frostbite.
Complete a primary survey to rule out any traumatic injuries.
Correct hypothermia (warm room, remove wet clothing & jewelry, warmed fluids, etc.)
If there are areas of frozen tissue rapid rewarming is preferred (see next section, rapid rewarming is associated with the best outcomes and salvage rates. However, never thaw until the risk of re-freezing has been eliminated. Patients undergoing freeze-thaw cycles do not respond to thrombolytics and are treated with standard supportive frostbite therapy.
Protect affected areas from further trauma with padding, splinting, and immobilization while transporting.
Keep the patient non-weight bearing to avoid incurring additional injury to frozen tissue (ice crystals) and/or disrupting blisters.
Elevate the affected extremities when able to decrease tissue edema.
Obtain a large-bore peripheral IV & start warmed fluids. Most patients will present with dehydration secondary to hypothermia and/or intoxication.
Avoid direct radiant heat to prevent iatrogenic burns to the cold tissue.
Update the patient’s tetanus status
Expect the patient to have increasing pain as the involved tissue is rapidly rewarmed. Pain management should include scheduled Ibuprofen (800 mg if no contraindication) to block the arachidonic cascade, gabapentin (nerve pain), and narcotics as needed.

Figure 4. Rewarming — Figure 3. Rewarming

Rapid rewarming

Circulating water bath when able. Put each affected area in its own water bath to avoid the tissue “knocking” against each other.

Document start & completion time

Try to keep the water temp at 104 ºF (40º C)
It will take 30-45 min for a hand or foot
If the patient has boots, socks, gloves, etc frozen to the skin do not force off. Submerge the entire area as part of the rapid rewarming process
Continue until frostbitten limb becomes flushed red or purple, and tissue soft and pliable to gentle touch

Air Dry

Avoid any aggressive manipulation to decrease tissue loss and injury
Elevate the affected areas to decrease swelling
Dress the affected areas with bulky padded dressings for transfer to avoid trauma to the areas
Avoid rewarming with a direct heat source (heat lamp, warm IV bag, etc.). This will lead to a thermal injury secondary to the lack of blood flow.

Rewarming will be associated with:

A return of sensation, movement, and possible initial flushing of the skin. The vessels in the case of severe frostbite (3rd or 4th degree) quickly become thrombotic (<20 minutes) with mottling or demarcation, however, the demarcation may be subtle at first and requires careful observation.
In the case that the tissues return fully to a normal color and palpable pulses or Doppler digital signals are present, the patient may not need any further intervention other than close observation (inpatient or daily visits in the clinic) and pain management.
If any question exists, an urgent triple-phase bone scan can support perfusion to the affected area.

Figure 4. Early evidence of demarcation and patchy thrombosis

Indications for Thrombolytics

Patient presenting with frozen tissue (severe frostbite, 3rd and/or 4th degree)
Absent or weak Doppler pulses following rewarming
Clinical exam consistent with severe frostbite
< 24 hours of warm ischemia time (time from rewarming)
Time matters significantly. For each hour after rewarming delaying the start of thrombolytics decreased salvage rates even by 28.1%.
With correct training after discussion with a burn center that does a lot of frostbite care, thrombolytics can be safely started at the outside hospital prior to transfer to the center.

Frostbite Thrombolytic Protocol

Examine for any associated injuries or illnesses. If any question of injury the patient will require a head, chest, and abdominal CT to rule out any sources of bleeding.
The dosing of the thrombolytic requires an actual weight and while infusing the thrombolytic requires ICU status and monitoring for 24 hours.
Following completion of the therapy, the patient will immediately be started on treatment dose Enoxaparin for 1-2 weeks.

Figure 5. Patient before and after receiving thrombolytics

Contraindications to the Thrombolytic Protocol

Absolute contraindications:

> 24 hours of warm ischemia time
Repeated freeze/thaw cycles
Concurrent or recent (within 1 month) intracranial hemorrhage, subarachnoid hemorrhage or trauma with active bleeding
Inability to consistently follow a neurologic exam (eg. intubated and sedated, significant dementia)
Severe uncontrollable hypertension

Relative contraindications:

History of GI bleed or stroke within 6 mo.
Recent intracranial or intraspinal surgery or serious head trauma within 3 months
Pregnancy

Figure 6. Clinical guide for the management of frostbite

Frostbite Take-Home Points

Rapid rewarming of frozen tissue in a circulating water bath is the preferred method of rewarming.
Patients that have undergone trauma in conjunction with the frostbite injury are not an absolute contraindication to receiving tPA.
Starting tPA at the outside hospital, prior to transport, results in significantly improved outcomes even compared to those that receive it at UCH.
Frostbite patients, regardless of whether or not they get thrombolytics, do better at a center that has experience and protocols to take care of frostbite.

Anne Lambert Wagner, MD, FACS

Associate Professor

University of Colorado

Medical Director

Burn & Frostbite Center at UC Health

How To Cite This Post…

[Peer-Reviewed, Web Publication] King, P. Porras, N. (2021, Aug 16). TPA in Frostbite. [NUEM Blog. Expert Commentary by Lamber Wagner, A]. Retrieved from http://www.nuemblog.com/blog/TPA-in-frostbite.

Health Risks Imposed by the Beach

Written by: Alex Herndon, MD (NUEM ‘21) Edited by: Ashley Amick, MD, MS (NUEM ‘18) Expert Commentary by: Patrick Lank, MD — **Written by:** Alex Herndon, MD (NUEM ‘21) **Edited by:** Ashley Amick, MD, MS (NUEM ‘18) **Expert Commentary by**: Patrick Lank, MD

With warm weather fast approaching, it’s time to break out the sunscreen and beach gear. Besides protecting oneself from UV rays and heat exhaustion, there are other dangerous pathogens lurking in the sandy shores that are worth being aware of as patients begin to flood the Emergency Department during summer vacation. Here are a few dangerous diseases to consider that masquerade as common chief complaints.

1. More than just swimmer’s itch

A 17 year old female presents to the Emergency Department complaining of a patchy skin rash that developed only a couple days after her first swim of the summer. Freshwater lakes house trematode parasites that upon contact leads to cercarial dermatitis, otherwise known as “swimmer’s itch”. Symptoms typically develop 2 days after exposure and last a week. Relief can be easily obtained with antihistamines and corticosteroid cream. [1]

Now consider that same patient is returning from a trip from Key West, Florida for a Bachelorette Party. You notice that her legs are shaved and there are several small nicks around her ankles. She is presenting with a worsening red rash on her lower leg that is red, warm, blistering, and in some locations has formed superficial ulcers. While it can be easy to chalk this us to severe sunburn and possible superimposed cellulitis, it is important not to miss this deadly necrotizing skin infection caused by Vibrio vulnificus, commonly known as one of many “flesh-eating bacteria.” Unlike the more benign trematode, V vulnificus can be found in brackish or saltwater, and in North America most commonly in the Gulf of Mexico. [2] V vulnificus infects wounds and leads to skin breakdown and ulceration and if not treated immediately infection has a mortality rate of anywhere from 25-50%. [3] Given the virulence of the disease, it is important to treat early and aggressively. The mainstay treatment for V vulnificus includes intravenous 3rd generation cephalosporins along with a tetracycline such as doxycycline. Source control becomes prudent and may require surgical debridement. [4]

2. “It’s just a cough”

With the warm weather finally here, a 60 year-old retiree began breaking in his paddle board along the shores of Lake Michigan. To cool off afterwards, he would hit the public beach showers. One week later he shows up at the Emergency Department complaining of body aches, low grade fevers, and a cough that won’t quit. While the bacteria Legionella pneumophila is typically associated with hot tubs, don’t forget other warm freshwater places this microbe loves to grow, including beach showers, air-conditioning units, and outdoor misters like those seen at amusement parks and sporting events. [4] People fall ill after inhaling aerosolized droplets from the contaminated sources.

Pontiac fever is a mild form of Legionella infection, presenting as vague flu-like symptoms that typically resolve in 2 to 4 days without treatment. However, the more severe form of infection, commonly known as Legionnaires disease, presents as pneumonia with cough, fever and myalgias. Unlike other bacterial pneumonias, Legionnaires is also more commonly associated with gastrointestinal symptoms like nausea, vomiting, and diarrhea, and can also cause hyponatremia. On average 15% of cases per year have been fatal, thus never forget to start atypical coverage for pneumonia, such as azithromycin, which provides adequate coverage for Legionella infection. [5] And if Legionella is diagnosed or highly suspected, alerting local health authorities is important because early containment of possible sources, such as public showers, is imperative to preventing a deadly outbreak.

3. Beyond febrile seizures

A 10 year-old boy is sent to sailing camp in Wisconsin. While he was well upon arrival, after only 3 days his parents get a call that their son has been hospitalized. His camp counselors brought him to the ED after he became febrile and had a seizure a day after capsizing in the lake. They reported throughout the day the boy had been complaining of a headache and was increasingly lethargic. Typically the constellation fever, headache, altered mental status, and seizure heralds bacterial meningitis. However given this child’s unique summer camp experience, one must consider other environmental exposures that pose a risk.

While rare, warm freshwater lakes can house the deadly Naegleria fowleri, more commonly known as “the brain-eating amoeba.” [6] This amoeba enters via the swimmer’s olfactory nerve, reaching the brain where it causes primary amebic meningoencephalitis (PAM). Patients present within 1 day to 2 weeks after exposure, first with flu-like symptoms including fever, headache and vomiting, that eventually progress to involve hallucinations and seizures. Similar to any patient presenting with symptoms concerning for meningitis, performing a lumbar puncture is key in making the diagnosis. N fowleri can be identified within cerebral spinal fluid either via direct visualization, antigen detection or PCR. While the majority of cases have been fatal, with a fatality rate of nearly 98%, survival is possible if identified and treated early with miltefosine, an anti-leishmania drug. [7]

During these warm summer months it is vital to understand where your patients have been and what they have been doing because knowing those details can end up saving their lives.

Expert Commentary

Thank you Drs. Herndon and Amick for these wonderful reminders that there are more things to be afraid of at the beach than sharks (and/or Sharknados). While this blog post contains great tidbits on three diagnoses, I think these cases also highlight times when a careful focused clinical history changes the emergent work-up and treatment. These patients could have easily been diagnosed with another condition and had their definitive care delayed, so thank you for these reminders.

As a native Floridian who grew up within walking distance of the Atlantic Ocean, I think there are a few additional entities for the emergency physician to consider when treating beachgoers. My medical toxicology training is begging me to direct this commentary towards my wheelhouse, but I will resist and will be sure to mention some other diagnoses.

But to start, I have to bring up intoxication. For those readers who do not live in the Midwest of the United States, I want to make you aware that Chicago has a wonderful series of beaches. Having been working in an emergency department in Chicago for 15 years now, I also have to point out that the number one reason patients are brought to the ED from a beach is for alcohol intoxication. Higher temperatures, increased thirst, increased physical activity, prolonged drinking, and possible co-ingestion of other mind-altering substances all increase the chances that a day at the beach will end in the ED. So be careful, warn your teenage/twenty-something family members, and consider checking an ethanol concentration in altered beachgoers.

The geographic proximity our ED has to the beach and Lake Michigan also means we see a lot of drownings. Some are intentional, others accidental; some are associated with traumatic injuries, others with intoxication; some patients are pediatric, some are geriatric. Despite their variations, all drowning should be taken seriously and involve aspects of resuscitation that are worth reviewing when you get a chance. Although it is now a few years old, I recommend reading the review article “Drowning” by D Szpilman, et al. from NEJM in 2012 (DOI: 10.1056/NEJMra1013317). It’s a great review with some helpful references for people interested in reading more.

Finally I would recommend anyone working in a clinical environment where the weather is about to turn warmer should review the clinical features and resuscitation of patients with heat-related injuries and superficial burns. When I was a PGY-1 in Chicago and had my first patient check in with a sunburn, I was in complete shock. Why did this person not know homecare for a sunburn? Easy, I thought: lots of aloe, move like a mummy for a day, and bathe in self-loathing and regret. But years of experience in a northern clime have taught me that changes in seasons are particularly dangerous for these injuries – people are out of practice, they forget, or they simply don’t care. No matter the reason, these early parts of the season are when we see big upticks in significant presentations.

In summary, thank you again for bringing up these infectious complications of having fun at the beach. But if you want to scare some sense into your 15-year-old nephew, don’t only tell him about Naegleria fowleri – please also terrify him with stories of overdoses, drowning, and severe hyperthermia.

Patrick Lank, MD, MS

Assistant Professor of Emergency Medicine

Medical Toxicologist

Department of Emergency Medicine

How To Cite This Post:

[Peer-Reviewed, Web Publication] Herndon, A. Amick, A. (2021, Mar 15). Health Risks Imposed by the Beach. [NUEM Blog. Expert Commentary by Lank, P]. Retrieved from http://www.nuemblog.com/blog/health-risks-imposed-by-the-beach.

References

Parasites: Cercarial Dermatitis. Centers for Disease Control and Prevention. 2012 January. <https://www.cdc.gov/parasites/swimmersitch/faqs.html>
Thompson, H. Eight diseases to watch out for at the beach: “Flesh-Eating” bacteria. The Smithsonian. 2014 August. <https://www.smithsonianmag.com/science-nature/diseases-watch-out-beach-18095234 6/>
Horseman, M. Surani, S. A comprehensive review of Vibrio vulnificus: an important cause of severe sepsis and skin and soft-tissue infection. Int J Infectious Diseases. 2011 March: 15(3): 157-166.
Thompson, H. Eight diseases to watch out for at the beach: Pontiac Fever and Legionnaires Disease. 2014 August. <https://www.smithsonianmag.com/science-nature/diseases-watch-out-beach-180952346 /#mftUupdDj 5cwE00L.99>
Healthy Swimming: Respiratory Infections. Centers for Disease Control and Prevention. 2016 May. <https://www.cdc.gov/healthywater/swimming/swimmers/rwi/respiratory-infections.html>
Thompson, H. Eight diseases to watch out for at the beach: “Brain-Eating” Amoeba. The Smithsonian. 2014 August. <https://www.smithsonianmag.com/science-nature/diseases-watch-out-beach-180952346 /#mftUupdDj5cwE00L.99>
Parasites: Naegleria fowleri - Primary Amebic Meningoencephalitis - Amebic Encephalitis. Centers for Disease Control and Prevention. 2017 February. <https://www.cdc.gov/parasites/naegleria/pathogen.ht ml>

Posted on March 15, 2021 by NUEM Blog and filed under Environmental and tagged wilderness medicine envi infectious disease antibiotics.

Management of Snake Bite Injuries

Written by: Rafael Lima, MD (NUEM ‘23) Edited by: Mike Conrardy, MD (NUEM ‘21) Expert Commentary by: Sean Bryant, MD — **Written by:** Rafael Lima, MD (NUEM ‘23) **Edited by:** Mike Conrardy, MD (NUEM ‘21) **Expert Commentary by**: Sean Bryant, MD

An estimated 10,000 patients visit emergency departments for snake bite injuries each year in the United States [1]. The number of snake bite occurrences an emergency department sees depends largely on the geographic area of practice. While there are known remedies for these incidents, snake bites can be devastating if not promptly managed, meaning emergency physicians should be knowledgeable in the subject. In this article, we review the common management of snake bite injuries and envenomations for the two major snake groups in the United States.

Overview

There are about 20 known venomous species of snakes in the United States. While most envenomations occur in the Southwestern United States, every region is home to at least one species of venomous snake [2]. Not all snake bites result in envenomation. At least 25% of venomous snake bites are dry. You should still suspect envenomation upon the patient’s initial presentation and rule it out by monitoring their clinical symptoms and progression.

Identification of the snake is useful in guiding management of care, but it should not be attempted if doing so poses any additional risk to the patient or provider. In the United States, venomous snakes generally fall under two categories: Crotaline/pit vipers in the Viperidae family, and coral snakes in the Elapidae family.

Crotaline (Pit Vipers)

This group of snakes has historically been responsible for the more severe envenomations between the two groups [3]. The WHO classifies pit vipers in CAT 1 of their venom database, describing them as highly venomous with high rates of morbidity and mortality [4].

Pit vipers generally have a triangular shaped head with heat-sensing “pits” located on the face. They frequently have a rattle on their tail, but not all pit vipers are rattlesnakes. Copperheads and cottonmouth snakes are also included in this group.

Crotaline venom causes localized tissue necrosis and congestive coagulopathy. This can be identified by a prolonged INR, PT, PTT, and thrombocytopenia. Additionally, the viper venom can cause capillary and cellular membranes to increase in permeability. Large amounts of venom can cause diffuse vaso-extravasation and hemolysis that can lead to hypovolemic shock and DIC if untreated.

CroFab is the antivenom of choice for cotaline envenomation. It is a polyvalent antivenom, meaning it contains antibodies derived from the venom of multiple different species of snakes. Administration is titrated based on clinical and symptom response.

Elapidae

The venomous Elapidae snake in the United States is the coral snake. There are less severe envenomations from coral snakes compared to pit vipers. This is a result of how venom is administered between the two groups: pit vipers have venom glands that inject venom directly through the fangs, while coral snakes rely on passive seeping of venom through their glands while they chew.

Source: Tad Arensmeier from St. Louis, MO, USA

Coral snakes can be identified by their brightly colored rings extending along the length of the whole body. Usually, every other ring is yellow, separating the wider red or black rings in between. The common saying “red on yellow, kill a fellow; red on black, venom lack” has been been used to differentiate between venomous coral snakes and their harmless look-alikes in North America. A further level of differentiation is how far the rings extend circumferentially around the snake. Rings encircle the entire body in venomous coral snakes, while harmless look-alikes do not have the red coloration on the ventral side [5].

Venomous bites by coral snakes usually elicit little to no pain. This is because the Elapidae venom acts upon the neuromuscular junction and inhibits acetylcholine receptors. Clinical manifestations are predominantly neurological. Envenomation can cause lethargy, confusion, salivation, cranial nerve palsies, and respiratory paralysis. Symptoms are usually delayed, up to 12 hours from the initial bite. Coagulopathy and tissue necrosis does not happen with coral snake venom [2]. Unfortunately, the Elapidae antivenom is no longer manufactured in the United States and there is a limited supply available.

ED Work Up

As in all patients who present to the emergency department, first ensure that airway, breathing, and circulation are intact. All suspected snake bite injuries warrant a prompt toxicology or poison center consult.

Sometimes, patients will bring in a dead or decapitated snake for identification in the emergency department. DO NOT attempt to handle a snake the patient brought in for identification, even if it is dead. Many snakes have intact reflexes that are preserved even after death or decapitation and you can still be bitten and envenomated by a dead snake!

Examine the injury and look for clear fang marks or puncture wounds. Get a history focused on the timing of the injury, medication allergies, and description of the snake, if known. The borders of erythema should be measured and marked serially.

Laboratory work-up is focused on assessing coagulopathy and hemolysis, especially if the snake is a confirmed pit viper or is unknown. Obtain CBC with platelet count, PT, PTT, INR, fibrinogen, and D-dimer. It is also important to check a baseline set of electrolytes with a basic chem panel, assess the extent of myonecrosis with a CK, and assess for renal damage with a UA.

Manage the wound with copious irrigation and exploration for retained foreign bodies (ie. fangs or teeth). Inquire about the patient’s tetanus status and administer if they are not up to date. Do not attempt to tourniquet or suction venom out of the wound. There is no evidence for routine antibiotic use in snake injuries [6].

Crotaline Bite Management

Consider using CroFab antivenom if the local area of injury and erythema is expanding. If coagulopathy is detected, do not treat with heparin or FFP. Give antivenom first, as unneutralized venom will react with clotting factor replacements [2]. Patients with abnormal coagulation studies within 12 hours after CroFab administration are more likely to develop recurrent coagulopathy. In these patients, repeat coagulation studies should be obtained every 48 hours until resolved. If lab values are worsening, then antivenom retreatment should be reconsidered [7].

Observe the affected limb for compartment syndrome. If clinical suspicion is high for compartment syndrome, consider formally measuring compartment pressures. Elevate the affected limb, and administer extra vials of antivenom. Antivenom administration is preferred over fasciotomy in the treatment of compartment syndrome caused by Crotaline venom [8].

Crofab, the Crotaline antivenom, is typically administered in stepwise fashion and is titrated to clinical resolution of symptoms. Administer 4-6 vials of CroFab antivenom and watch for clinical improvement at the local site of injury. If no improvement seen, administer 4-6 more vials. Repeat until control is achieved, meaning a reversal of symptoms, such as erythema, swelling, pain. Then administer 2 vial doses 6 hours later, then 12 hours, then 18 hours. Envenomation patients should be monitored for at least 8 hours. Keep epinephrine and antihistamines nearby in case of anaphylaxis or allergy to antivenom [2].

Elapidae Bite Management

Because of their potential devastating neurologic effects, coral snake bites should be empirically treated with antivenom and monitored for respiratory deterioration. Provide good supportive care, including intubation and ventilation, if necessary. Avoid opioids for pain management as they may mask symptoms of impending neurologic manifestations. Patients with suspected coral snake envenomations should be monitored for 12 hours after the initial bite [2].

Expert Commentary

Thank you, Dr. Lima for bringing the important and timely topic of snakebites to the table by posting this excellent overview! Current poison center data (2018 National Poison Data System) indicate a total of 4,013 crotalid exposures with the majority being copperheads. While morbidity is worrisome, mortality was fortunately low in our country with only one fatality reportedly from a rattlesnake [1].

Prehospital snakebite management has been an area of deserved scrutiny. Limb immobilization, analgesia, and transport to a medical facility are critical actions. Tourniquets, pressure immobilization bandages, cryotherapy, electrotherapy, and incision/suction are not recommended and are likely harmful. One researcher discovered that venom extraction suction devices “just suck” [2]. Having a cell phone in the field is most important to prevent loss of limb or life!

In other regions of the world, capturing or killing the snake may be optimal in determining which species specific antivenom to administer. For North American crotalids, however, this practice is discouraged and exceedingly dangerous. Both CroFab and Anavip (recently approved and now marketed with the goal of reducing risks of late coagulopathy) are prepared from several species of North American crotalids and can be used to manage any crotalid envenomation. These contemporary antivenoms (Fab fragments) are safer than older polyvalent antivenom that resulted in high rates of anaphylaxis.

Consult your regional poison center (1-800-222-1222) or staff medical toxicologist when managing snakebites! For the number of snakebites that present to the emergency department, poison centers manage severalfold more each year. Making decisions regarding the management of a limb that resembles compartment syndrome (more antivenom vs. surgical consultation), the interpretation of laboratory results, redosing of antivenom to gain initial control of swelling, and the management of nonindigenous (e.g. cobras, gaboon vibers) pet snakebites are nuances your subspecialists would love to collaborate on!

References

1. Gummin DD, Mowry JB, Spyker DA, BrooksDE, Beuhler MC, RiversLJ, Hashem HA, & Ryan ML 2018 Annual Report of the American Association of Poison Control Centers’ National Poison Data System (NPDS): 36th Annual Report, Clinical Toxicology, 2019;57:1220-1413.

2. Bush SP. Snakebite Suction Devices Don’t Remove Venom: They Just Suck. Annals of Emergency Medicine, 2004;43:187-188.

Sean Bryant, MD

Assistant Director, Toxicology Fellowship Program, Department of Emergency Medicine, Cook County Health

Associate Professor, Department of Emergency Medicine, Rush Medical College

How To Cite This Post:

[Peer-Reviewed, Web Publication] Lima, R. Cornardy, M. (2020, Oct 26). Management of Snake Bite Injuries. [NUEM Blog. Expert Commentary by Bryant, S]. Retrieved from http://www.nuemblog.com/blog/snake-bites.

References

Snakebite Injuries Treated in United States Emergency Departments, 2001–2004. O’Neil, Mary Elizabeth et al. Wilderness & Environmental Medicine, Volume 18, Issue 4, 281 - 287
Gold, Barry S., et al. “Bites of Venomous Snakes.” New England Journal of Medicine, vol. 347, no. 5, 1 Aug. 2002, pp. 347–356., doi:10.1056/nejmra013477.
Seifert, Steven A., et al. “AAPCC Database Characterization of Native U.S. Venomous Snake Exposures, 2001–2005.” Clinical Toxicology, vol. 47, no. 4, 2009, pp. 327–335., doi:10.1080/15563650902870277.
“Venomous snakes distribution and species risk categories.” World Health Organization. 2010. http://apps.who.int/bloodproducts/snakeantivenoms/database/
Cardwell, Michael D. “Recognizing Dangerous Snakes in the United States and Canada: A Novel 3-Step Identification Method.” Wilderness & Environmental Medicine, vol. 22, no. 4, 1 Oct. 2011, pp. 304–308., doi:10.1016/j.wem.2011.07.001.
Prophylactic Antibiotics Are Not Needed Following Rattlesnake Bites. August, Jessica A. et al. The American Journal of Medicine, Volume 131, Issue 11, 1367 - 1371
Recurrence phenomena after immunoglobulin therapy for snake envenomations: Part 2. Guidelines for clinical management with crotaline Fab antivenom. Annals of Emergency Medicine, 2001, Vol.37(2), p.196-201., doi: 10.1067/mem.2001.113134
Hall, Edward L. “Role of Surgical Intervention in the Management of Crotaline Snake Envenomation.” Annals of Emergency Medicine, vol. 37, no. 2, Feb. 2001, pp. 175–180., doi:10.1067/mem.2001.113373.

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Posted on October 26, 2020 by NUEM Blog and filed under Toxicology and tagged toxicology Toxicology wilderness medicine.

SCUBA Diving Injuries and Treatments

Written by: Aaron Wibberly, MD (NUEM PGY-2) Edited by: Sarah Dhake MD (NUEM Alum ‘19 ) Expert commentary by: Justin Hensley, MD

Expert Commentary

Thanks for writing about one of the topics that isn’t frequently covered in emergency medicine. SCUBA isn’t terribly dangerous, but early recognition of the problems encountered in these patients can save lives.

First, barotrauma exists because of Boyle’s Law (P1V1=P2V2). There is no way to go around this law of nature, only ways to prevent negative outcomes.

Barotrauma mainly affects the ears but can also affect the sinuses or mask.

Mask squeeze is failure to maintain pressure in facemask as pressure increases. Signs include subconjunctival hemorrhages, lid edema, skin ecchymosis, hyphema, and orbital hemorrhage (1)

Both tympanic membrane ruptures and inner ear problems (round and oval window) can be very disorienting underwater, placing the patient in danger of ascending too quickly or not being able to find their way out.

In an unresponsive diver, the arterial gas embolism is assumed until proven otherwise. Alveolar barotrauma is a life threat that needs emergent treatment.

Decompression sickness is known as “the bends” because of caisson workers. It mainly affected the hips and knees, causing them to maintain a bent over stance. For reasons nobody has yet identified, SCUBA divers are affected in the shoulders and elbows.

The “chokes” are bubbles in the pulmonary and cardiac vasculature, and can cause a “mill wheel” murmur (splash, splash, splash).

Skin bends, known as cutis marmorata, may be related to bubbles in the vasculature, but there is some evidence that it may be centrally mediated and symptomatic of more severe DCS. It frequently causes itching. (2,3)

Neurologic DCS most commonly affects the spinal cord and causes 50-60% of sport diver casualties.

Knowing where your closest hyperbaric chamber exists is of utmost importance. Diver’s Alert Network (DAN) does not publish a database but maintains a referral network that you can speak to after emergency evaluation by calling their 24-hour DAN Emergency Hotline at +1-919-684-9111.

References:

1. Barron, E. (2018). The “Squeeze,” an Interesting Case of Mask Barotrauma. Air Medical Journal, 37(1), 74-75. doi: 10.1016/j.amj.2017.10.003

2. Germonpre, P., Balestra, C., Obeid, G. and Caers, D. (2015). Cutis Marmorata skin decompression sickness is a manifestation of brainstem bubble embolization, not of local skin bubbles. Medical Hypotheses, 85(6), pp.863-869.

3. Kemper TC, Rienks R, van Ooij PJ, and van Hulst RA. (2015). Cutis marmorata in decompression illness may be cerebrally mediated: a novel hypothesis on the aetiology of cutis marmorata. Diving Hyperb Med., 45(2), pp. 84-8.

Justin Hensley, MD

Founder and Editor of EBM Gone Wild

Quality Improvement/Assurance Director,

CHRISTUS Health-Texas A&M-Spohn Emergency Medicine Residency

How to Cite this Post

[Peer-Reviewed, Web Publication] Wibberly A, Dhake S. (2019, Aug 27). SCUBA Diving Injuries and Treatments. [NUEM Blog. Expert Commentary by Hensley J]. Retrieved from http://www.nuemblog.com/blog/scuba.

TPA in Frostbite

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Background

Frostbite Classification

Pre-hospital or Emergency Department Management

Rapid rewarming

Indications for Thrombolytics

Frostbite Thrombolytic Protocol

Contraindications to the Thrombolytic Protocol

Frostbite Take-Home Points

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1. More than just swimmer’s itch

2. “It’s just a cough”

3. Beyond febrile seizures

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