Posts tagged #environmental medicine

Marine Envenomations

Written by: Michael Tandlich, MD (NUEM ‘24) Edited by: Chloe Renshaw, MD (NUEM ‘22)
Expert Commentary by: Justin Seltzer, MD (NUEM ‘21)



Expert Commentary

An excellent post by Drs. Tandlich and Renshaw. Marine envenomations are common problems around the world. Like with land-based envenomations, the venomous organisms of note vary with geography; jellyfish encountered in Australia are different from those encountered in Florida, for example. As a result, we will focus on major envenomations in the United States. 


The invertebrates account for a large but ultimately unknown number of envenomations. Cnidaria includes jellyfish, hydrozoa, anemones, and fire coral. A majority of stings from this group result in painful dermatitis; tentacles create a “whip-like” pattern on the skin, whereas fire coral creates localized skin wheals. The sea nettle and Portuguese man-of-war are of greatest interest, given their potential to cause severe systemic symptoms. Box jellyfish are rare in US coastal waters but produce a life-threatening toxicity. 

Initial treatment is somewhat controversial. Many resources advocate for the use of seawater for the initial decontamination, given concern for vinegar triggering nematocyst release in some species common to US waters. However, further research is needed to determine which is best. At this time, seawater is recommended for empiric decontamination in the US unless a box jellyfish is strongly suspected, in which case vinegar is appropriate (a very rare circumstance). Systemically ill box jellyfish envenomations should be treated with pain and blood pressure control. The antivenom is not readily available in the US and is unlikely to be beneficial in the time course it would take to obtain it.

Echinodermata, which includes sea urchins, have mild venom on their spines that can cause local tissue irritation and pain. There are reports of severe envenomations with systemic symptoms, but this is ultimately quite rare. These injuries respond well to hot water immersion. Imaging and local wound exploration for retained spines are recommended. Soaking the wound in vinegar may help dissolve superficial spines.  

Of the vertebrates, stingrays and spiny fish are of primary concern. 

Stingrays stings are common and can cause serious penetrating trauma but envenomation mainly produces localized pain and swelling. The venom is heat-labile, so significant pain relief can be achieved with hot water immersion. Stingrays stings have the potential for both retained stinger and wound infections; evaluation for retained stinger with radiographs and local wound exploration is recommended along with prophylactic antibiotics. 


Spinyfish, in particular stonefish, lionfish, and scorpionfish, have venom located in their spines. Stonefish have the most potent venom of any known fish. Lionfish are not native to the US but have become an invasive species. Human contact with these fish occurs both in the wild and in aquariums. These fish also have heat-labile venom susceptible to hot water immersion. However, systemically ill stonefish envenomations should receive the antivenom as this envenomation can be life-threatening; the antivenom will likely work against other spiny fish too, however, these other envenomations are usually much less severe and rarely require more than hot water immersion and supportive care. 

So key learning points:

  • Most marine envenomations involve heat-labile venom. Hot water immersion is likely to help reduce local symptoms.

  • Systemic illness is rare but some marine envenomations can produce life-threatening toxicity. Be very wary of a systemically ill envenomation and try to figure out the source due to the limited availability of antivenoms.

  • Prophylactic antibiotics are recommended for stingray stings as they tend to get infected but otherwise are generally not necessary in most populations. Good wound care, evaluation for retained foreign bodies, and tetanus prophylaxis are the mainstays. 

  • For further information, see this review article 

Justin Seltzer, MD

UCSD Health Toxicology Fellow

Emergency Physician, UCSD Health


How To Cite This Post:

[Peer-Reviewed, Web Publication] Tandlich, M. Renshaw, C. (2022, Mar 7). Marine Envenomations. [NUEM Blog. Expert Commentary by Seltzer, J]. Retrieved from http://www.nuemblog.com/blog/marine-envenomations


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Posted on March 7, 2022 and filed under Environmental, Toxicology.

Stingray Stings

Written by: Mike Tandlich, MD (NUEM ‘24) Edited by: Peter Serina, MD, MPH (NUEM ‘22)
Expert Commentary by: Mike Macias, MD (NUEM ‘17)



Expert Commentary

Thank you Drs. Tandlich and Serina for this excellent infographic summarizing stingray envenomation! The good news is that the majority of stingray injuries are nonfatal and will heal without any complications! You hit all of the key points however I just wanted to highlight a few management tips below: 

Treat as a Trauma! 

While majority of the pain from stingray envenomation occurs as a result of its venom, it is important to remember that this is also a traumatic injury. Treat the injury just like you would any other penetrating trauma. Consider the location as well as surrounding structures and make sure to properly examine for tendon, nerve, and vascular injury. Injuries to the chest or abdominal regions should prompt advanced imaging and trauma consultation. 

Hot Water is Key! 

Stingray envenomation is noted to cause severe pain that is often out of proportion to your examination findings. While the exact mechanism is not clear, the venom can lead to not only pain but also local tissue necrosis. The good news is the venom is heat labile! The faster you can get the injured area into hot water the better. You want the water to be as hot as tolerable without causing a thermal burn. A good rule of thumb is to have the patient place their unaffected limb in the water first to see if it is tolerable. As this often occurs at a beach, lifeguards are often your best resource to get hot water fast! Oral analgesics can be administered if needed however often they are unnecessary as soon as the injured area is submerged in hot water. 

Retained Barb?

While uncommon, a retained barb from the envenomation can occur so be sure to consider this and evaluate appropriately. Traditionally, x-ray imaging of the affected area is performed to evaluate for a radio-opaque barb however some evidence suggests this to be a relatively low yield practice [1]. Ultrasound can also be considered if there is suspicion for retained barb or other material. In general ultrasound has been shown to be highly sensitive for identification of foreign body [2]. Not only can it be used to identify the barb but it can be used to facilitate removal [3]. 

Give Prophylactic Antibiotics 

Prophylactic antibiotics are recommended for stingray envenomation given that the limited data suggest a higher rate of wound infection in patients who were not initially treated with antibiotics [1]. Given these injuries often occur in the ocean make sure to cover for salt water species such as Vibro. Levofloxacin is my go to option.

Teach The Stingray Shuffle! 

Keeping these key management points in mind, the good news is that the majority of stingray injuries are nonfatal and will heal without any complications! Before your patient is discharged don’t forget to remind them that the next time they are going out for a surf to do the stingray shuffle!

References

  1. Clark RF, Girard RH, Rao D, Ly BT, Davis DP. Stingray envenomation: a retrospective review of clinical presentation and treatment in 119 cases. J Emerg Med. 2007 Jul;33(1):33-7

  2. Aras MH, Miloglu O, Barutcugil C, Kantarci M, Ozcan E, Harorli A. Comparison of the sensitivity for detecting foreign bodies among conventional plain radiography, computed tomography and ultrasonography. Dentomaxillofac Radiol. 2010;39(2):72-78. doi:10.1259/dmfr/68589458

  3. Nwawka OK, Kabutey NK, Locke CM, Castro-Aragon I, Kim D. Ultrasound-guided needle localization to aid foreign body removal in pediatric patients. J Foot Ankle Surg. 2014;53(1):67-70. doi:10.1053/j.jfas.2013.09.006

Michael Macias, MD

Systems Clinical Ultrasound Director,
Emergent Medical Associates

Ultrasound Director,
UHS SoCal MEC Residency Programs


How To Cite This Post:

[Peer-Reviewed, Web Publication] Tandlich, M. Serina, P. (2021, Nov 15). Stingray Stings. [NUEM Blog. Expert Commentary by Macias, M]. Retrieved from http://www.nuemblog.com/blog/stingray-stings


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Posted on November 15, 2021 and filed under Environmental.

Managing Minor Thermal Burns in the ED

Written by: Mitch Blenden, MD (NUEM ‘24) Edited by: Vytas Karalius, MD, MPH, MA (NUEM ‘22) Expert Commentary by: Matt Levine, MD

Written by: Mitch Blenden, MD (NUEM ‘24) Edited by: Vytas Karalius, MD, MPH, MA (NUEM ‘22) Expert Commentary by: Matt Levine, MD


Managing Minor Thermal Burns in the ED Final.png

Expert Commentary

Dr. Blenden and Dr. Karalius provided an excellent handy, high-yield, quick reference of thermal burn considerations in the ED.  There are some nuances of thermal burn care that I’d like to provide further commentary:

  • A pitfall is underestimating the severity of the burn when the patient presents within a few hours of the event.  Burn appearance evolves over 24-48 hours. What initially appears as erythematous skin can be covered in bullae the next day.  Consider a repeat examination in 24-48 hours, or at least discuss with the patient the possibility that this may occur and what to do if it does.  Otherwise, if you initially diagnosed the patient with superficial burns and provided only instructions for superficial burns, which require little treatment or follow-up, the patient can be set up for a worse outcome when these burns subsequently declare themselves to be partial thickness.

  • For years, most non-facial burns were sent home with instructions to use silver sulfadiazine (AKA Silvadene) cream. This would require teaching of how to apply and remove it. The cream needs to be removed daily before applying a new coat (I always sent the patient home with tongue blades to scrape it off).  The benefits of this are that it debrides some nonviable tissue when the cream is removed and provides a moist antimicrobial barrier.  The down sides are that removal can be painful and some patients have difficulty performing this procedure, which requires teaching.  Silver sulfadiazine can also cause skin staining.  There is scant evidence recommending one topical antimicrobial over another.  For these reasons, practice (including mine) has evolved in many places to simply prescribe whatever antibiotic ointment is on hand for ease of use and less painful and technically challenging application.

  • Another controversy is whether to debride blisters and bullae or leave them intact.  This is another area without definitive evidence and practice is often guided by gestalt, local custom, or prior teachings.  On one hand, intact bullae can be thought of as “sterile” coverings and may be less painful than dermal layers exposed to air and friction.  On the other hand, when bullae rupture, the patient is left with dead skin which can be a nidus for infection.  My practice has been to leave small blisters intact and debride large bullae if it seems like they will soon rupture and leave the patient with hanging skin fragments.  If the patient has reliable follow up burn care then I may choose a less aggressive approach in debriding.  Other clinicians are likely to give alternate approaches so ask your attendings what they do in these scenarios so you can develop a practice pattern that makes sense to you.

mattlevine.png

Matthew Levine, MD

Associate Professor of Emergency Medicine

Department of Emergency Medicine

Northwestern Memorial Hospital


How To Cite This Post:

[Peer-Reviewed, Web Publication] Blenden, M. Karalius, V. (2021, Oct 18). Managing Minor Thermal Burns in the ED. [NUEM Blog. Expert Commentary by Levine, M]. Retrieved from http://www.nuemblog.com/blog/managing-minor-thermal-burns


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Posted on October 11, 2021 and filed under Trauma.

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.)

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.)

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

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

Figure 1. Frostbite

Figure 1. Frostbite







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)

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

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

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

Figure 6. Clinical guide for the management of frostbite

Frostbite Take-Home Points

  1. Rapid rewarming of frozen tissue in a circulating water bath is the preferred method of rewarming.

  2. Patients that have undergone trauma in conjunction with the frostbite injury are not an absolute contraindication to receiving tPA.

  3. Starting tPA at the outside hospital, prior to transport, results in significantly improved outcomes even compared to those that receive it at UCH.

  4. 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 Wagner.png
 

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.


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References

Cauchy E, Davis CB, Pasquier M, Meyer EF, Hackett PH. A New Proposal for Management of Severe Frostbite in the Austere Environment. Wilderness & Environmental Medicine. 2016;27(1):92-99. doi:10.1016/j.wem.2015.11.014.

Cline D, Ma OJ, Meckler GD, et al. Cold Injuries. In: Tintinalli's Emergency Medicine: a Comprehensive Study Guide. New York: McGraw-Hill Education; 2020:1333-1337.

Grayzel J, Wiley J. What’s New in Emergency Medicine. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on November 3, 2020.)

Lee J, Higgins MCSS. What Interventional Radiologists Need to Know About Managing Severe Frostbite: A Meta-Analysis of Thrombolytic Therapy. American Journal of Roentgenology. 2020;214(4):930-937. doi:10.2214/ajr.19.21592.

Pandey P, Vadlamudi R, Pradhan R, Pandey KR, Kumar A, Hackett P. Case Report: Severe Frostbite in Extreme Altitude Climbers—The Kathmandu Iloprost Experience. Wilderness & Environmental Medicine. 2018;29(3):366-374. doi:10.1016/j.wem.2018.03.003.

Patel N, Srinivasa DR, Srinivasa RN, et al. Intra-arterial Thrombolysis for Extremity Frostbite Decreases Digital Amputation Rates and Hospital Length of Stay. Cardiovascular and Interventional Radiology. 2017;40(12):1824-1831. doi:10.1007/s00270-017-1729-7.

Twomey JA, Peltier GL, Zera RT. An Open-Label Study to Evaluate the Safety and Efficacy of Tissue Plasminogen Activator in Treatment of Severe Frostbite. The Journal of Trauma: Injury, Infection, and Critical Care. 2005;59(6):1350-1355. doi:10.1097/01.ta.0000195517.50778.2e.

Wagner A, Orman R. Frostbite, Asystole, Perfectionism, EQ, Middle Way, Flu. January 2019 - Frostbite - Frostbite, Asystole, Perfectionism, EQ, Middle Way, Flu | ERcast. https://www.hippoed.com/em/ercast/episode/frostbite/frostbite. Published 2019. Accessed November 3, 2020.

Zafren K, Crawford Mechem C. Frostbite: Emergency Care and Prevention. In: UpToDate, Post TW (Ed), UpToDate, Waltham, MA. (Accessed on November 3, 2020.)

Posted on August 16, 2021 and filed under Environmental.

Altitude Illness

Written by: Alex Herndon, MD (NUEM ‘21) Edited by: Danielle Miller, MD (NUEM ‘19) Expert Commentary by: Gabrielle Ahlzadeh, MD

Written by: Alex Herndon, MD (NUEM ‘21) Edited by: Danielle Miller, MD (NUEM ‘19) Expert Commentary by: Gabrielle Ahlzadeh, MD


Altitude Illness writing.png

Expert Commentary

During my four years of residency at sea level, I never treated a patient with altitude sickness. Now, living in Utah and working at a ski clinic where the peak is just over 11,000 feet, I see it almost weekly. Patients tend to be surprised when we diagnose them with acute mountain sickness, either because they are physically fit, otherwise healthy or have been to altitude before and never had symptoms. Educating patients that altitude sickness can affect anyone, regardless of how many marathons they’ve run, is important in ensuring that they follow directions to manage their symptoms. A lot of patients also don’t realize that it takes a few days to develop altitude sickness, and that days 2-3 are usually when symptoms develop. Oftentimes, not sleeping well may be the first symptom. If patients present with symptoms of poor sleep and headaches, it’s important to instruct patients to take it easy and take time to adjust, as well as the importance of staying hydrated and doing their best to get enough sleep. It’s helpful to frame this as days lost on the mountain so patients take their mild symptoms seriously.

Anecdotally, most patients improve pretty rapidly with oxygen administration so when any patient from out of town presents with vague symptoms, our first step in ski clinic is to put them on oxygen . Some patients look pale and ill while others don’t even look sick, and you’re often shocked by their low oxygen saturation. We’ve had fit young patients with oxygen saturations in the 70s who look completely fine, which again, just stresses the importance of obtaining vitals and not being fooled by healthy and fit patients. I’ve seen kids who present with fatigue, vomiting and headache who look sick and then after an hour of oxygen and some fluids, bounce right back to their normal selves.

Obviously it’s important to maintain a broad differential for patients who present with symptoms of altitude sickness, while recognizing that it is a diagnosis that can tie together multiple symptoms. This is especially true in pediatric patients who cannot articulate their symptoms clearly. Checking an initial blood sugar is part of our initial workup, especially in kids. But, if you don’t consider acute mountain sickness, then you won’t be able to make your patient feel better with oxygen, descent or other medications.

From the ski clinic, we often send patients home with portable oxygen tanks mainly to use while they are sleeping, since poor sleep often makes symptoms worse. We treat most patients with both acetazolamide and dexamethasone and frequently recommend they come back to clinic the next day for reassessment. We often recommend that patients sleep at lower altitude and just come up for skiing if possible. For patients with evidence of pulmonary edema, they must descend and are sent to the ER for closer monitoring and treatment. The same would be true with any patient with evidence of altered mental status.

Gabrielle Ahlzadeh, MD.PNG

Gabrielle Ahlzadeh, MD

Clinical Assistant Professor of Emergency Medicine

University of Southern California


How To Cite This Post:

[Peer-Reviewed, Web Publication] Herndon, A. Miller, D. (2020, Aug 31). Altitude Illness. [NUEM Blog. Expert Commentary by Ahlzadeh, A]. Retrieved from http://www.nuemblog.com/blog/altitude-illness


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Posted on August 31, 2020 and filed under Environmental.

Cold Injury Management in the ED

Written by:&nbsp;Sean Watts, MD (PGY-2)&nbsp; Edited by:&nbsp;David Kaltman, MD (PGY-4)&nbsp; Expert commentary by: Pinaki Mukherji, MD

Written by: Sean Watts, MD (PGY-2)  Edited by: David Kaltman, MD (PGY-4)  Expert commentary by: Pinaki Mukherji, MD

Learning Objectives:

Recognize the signs and symptoms of freezing injury 

Understand the pathophysiology of  freezing cold injury and how it manifests in the delineated signs and symptoms

Discuss the treatment practices for managing freezing injury in the emergency department 

• Discuss barriers to effective treatments for these conditions, and current research to improve outcomes

 Introduction 

As interests in outdoor activities and the rates of homelessness have increased over the past twenty years, so has the level of patients presenting with cold injuries. Due to this increasing prevalence, it is important for emergency physicians to understand the signs, symptoms, and management of these injuries. This is especially true for emergency physicians working in areas where mountaineering, skiing, ice-climbing and other outdoor activities are popular, or in areas with significant cold exposure and large populations of undomiciled patients.

Cold injuries get divided into two categories: non-freezing injuries and freezing injuries. Non-freezing injuries include trench foot, pernio, panniculitis, and cold urticaria and are generally due to prolonged exposure to damp, non- freezing conditions.  Freezing injuries include frostbite and its associated severity classifications. Of these categories frostbite remains the most severe and, and can present in a range of symptoms from clear blisters and cyanosis, to hard non-deforming necrotic skin.

Treatment of both non-freezing cold injuries and frostbite are similar, and co-presentation often occurs. However, if a patient presents with concomitant hypothermia, this should be treated first. The course of treatment for hypothermia should be guided by a patient's level of consciousness, shivering intensity, and cardiovascular stability in the field since accurate temperature readings cannot always be obtained. A rectal temperature should be obtained in the emergency department and active rewarming measures such as heat pads, or heated humidified oxygen should be utilized, and application of these rewarming devices should be applied to the areas of the body with the potential for greatest convective heat loss—back, axilla. While rewarming takes place, the practitioner should monitor vitals and provide CPR, AED, and intubation, as necessary.

Freezing Injury

The  mechanism that accounts for frostbite is due to direct cell death due cold exposure and further cell death due to ischemia. As water freezes in tissues it expands—poking holes in the cellular membrane—leading to hyperosmotic cell death. This cell death is further exacerbated by what is known as the hunting reaction—an alternating freeze/ thaw cycle due to local alternating vasoconstriction and vasodilation. Emboli form in the vasculature due to endothelial damage, resulting in ischemia, leading to destruction of the microvasculature and localized cell death.

Frostbite can occur anywhere on the body but generally occurs on the distal extremities, face, nose, and ears. The injured area often appears pale and feels stiff and cold, and patients endorse stinging and numbness. 

Now, frostbite gets divided into three zones: the zone of coagulation, the zone of hyperemia, and the zone of stasis. The zone of coagulation is distal and where the cellular damage is most severe. The zone of hyperemia is superficial, proximal, and has the least cellular damage. The zone of stasis is between the two and has the most potential for intervention to salvage tissue.

Frostbite also gets characterized into four different classifications  schemes based on severity of injury and prognosis of recovery. First-degree frostbite, also referred to as frostnip, is characterized by partial skin freezing with erythema, edema, and has excellent outcomes. Second-degree injury is defined by full-thickness skin freezing, formation of substantial edema, erythema, and the formation of clear blisters. Second degree injury has the most potential for intervention with modest outcomes. Third-degree injury is defined by damage that extends into the subdermis with associated hemorrhagic blisters  and necrosis of skin and necrosis of skin, appearing as a blue-gray discoloration. Fourth-degree injury is characterized by further extension into adipose tissue, muscle, and bone, with little edema that forms a dry black eschar. Fourth degree frostbite tends to have the “mummified” appearance of dry gangrene.

First Degree Frostbite

First Degree Frostbite

Second degree frostbite--note the clear filled blisters characteristic of this degree of frostbite

Second degree frostbite--note the clear filled blisters characteristic of this degree of frostbite

Third degree frostbite--note the areas of hemorrhagic blisters, characteristic of third degree frostbite

Third degree frostbite--note the areas of hemorrhagic blisters, characteristic of third degree frostbite

Fourth Degree Frostbite

Fourth Degree Frostbite

In the field and  the emergency department, treatment  should be focused on preventing refreezing injury.  It is imperative that active thawing measures not be initiated unless the thawed state can be maintained (remember the hunting reaction!). Preliminary measures to help thawing include hydration, administration of low molecular weight dextran (it has been shown to reduce blood viscosity and decrease thrombi), and NSAIDS that will reduce prostaglandin and thromboxane release. If it is possible to maintain a thawed state, active thawing can take place by submersion in a water bath maintained between 37 C and 39 C. The emergency physician will know the rewarming process is complete when the affected area becomes red or purple and is soft and pliable. If the affected area is an extremity, it should be elevated in order to prevent dependent edema from forming. When rewarming occurs patients will often note severe pain, and patients should be treated with parenteral opioid therapy. Other post-thaw therapy includes antithrombotic drugs—tPa has been used widely in addition to heparin, as well as vasodilating agents. When patients present within 24 hours, with multiple digits affected, or evidence of multiple limbs affected, intra- arterial tPA can be utilized along with intra arterial heparin. Iloprost has also been suggested for grade 2-4 frostbite when patients present <48 hours after injury.  If blisters form, they should be treated with topical aloe vera cream every 6 hours, and tetanus immunization status should be assessed and given if needed. 

One question that commonly arises in the emergency management of frostbite is does this injury need surgery? In general, early surgical intervention is not indicated for the management of frostbite. Studies have demonstrated that early surgery contributes to unnecessary tissue loss and poor cosmetic results. This stems from the inability to assess the depth of frostbite at its early stages and that tissue below blackened necrotic tissue is regenerating. Technetium (Tc)-99m scintigraphy often gets used after maximum rewarming therapy to predict long-term viability of affected tissue. Escharotomy is the only early surgical intervention indicated if the patient has range of motion or circulation abnormalities. Most patients with frostbite can be discharged from the emergency department with good follow up--barring a situation where the individual will simply be re exposed to cold temperatures or they require admission for pain management. 

Future Directions

While non-freezing and freezing injuries continue to become common occurrences in austere environments and amongst undomiciled patient populations, developmental therapies to improve  outcomes continue to be researched. For example, iloprost, as been gaining popularity, as it was recently used in Sweden with success. It is a prostacyclin analogue that mimic the effects of a sympathectomy and helps to prevent emboli from forming. In several studies it has proven more effective than tPA administration; however, it is not a currently approved FDA drug. More large scale clinical trials and cohort studies are needed, as many of these trials have low sample sizes.

Summary and Pearls

  • Suspect non-freezing or freezing injury in undomiciled patients or in patients with prolonged exposure in cold environments

  • Perform a thorough neurovascular exam of the afflicted digit/extremity, and attempt to grade if consistent with frostbite

  • Only begin rewarming if the warm state can be maintained

  • Frostbite, even when severe is not a surgical emergency

  • Consider iloprost or tPA for appropriate candidates


Expert Commentary

This is a nice overview of the spectrum of presentation of freezing injury. I would reinforce a few key points to give practical context in the treatment of these patients.

  • Systemic signs always take priority when resuscitating a cold injured patient. As such, the rewarming measures described will utilize dry heat, and target mental status and cardiovascular status. In contrast, in the rewarming of freezing injury, moist heat is always preferred.

  • As mentioned here, non-freezing and freezing injury coexist, and are not always easy to tell apart. While non-freezing injury may be outside of the scope of this blog post, severe cases of trench foot can appear similar to 2nd or 3rd degree frostbite injuries. Blister formation in non-freezing injury is rare, but can occur, and the sloughing of skin that occurs can be mistaken for ruptured blisters.

  • While the tissue damage of freezing injury can be severe, the deep necrosis that results is typically dry gangrene, whose natural course is auto-amputation. While a non-freezing injury like trench foot typically has better outcomes, severe cases can leave patients with circulatory compromise and non-intact skin, leading to wet gangrene and potentially sepsis.

  • Rapid rewarming of freezing injury (15 to 60 min.) is supported by animal models, with immersion being the preferred modality. The author above writes that rewarming should commence “if it is possible to maintain a thawed state.” For patients who have treatment initiated in the field, or en route to comprehensive care, this is a judgment not to be made lightly, as refreezing leads to much worse tissue destruction.

  • NSAIDs are indicated in the treatment of freezing injury, with an excellent safety to benefit ratio. The use of other agents aimed at improving consequences of thrombosis are less certain and should be reserved for more severe cases. Both tpa and iloprost have been associated with lower amputation rates in small studies and case series, along with PGE1 and isosorbide dinitrate as potential agents showing promise.

  • Low molecular weight dextran is recommended by Wilderness Medicine Society guidelines, with a minimal bleeding risk, but is often avoided if the patient is being considered for antithrombotic treatments such as tpa.

References

Sachs, C., Lehnhardt, M., Daigeler, A., Goertz, O. (2015). The Triaging and Treatment of Cold-Induced Injuries. Dtsch Arztebl Int., 112(44), 741-747. Doi:10.3238/arztebl.2015.0741

Petrone, P., Asensio, J., Marini, C. (2014). Management of accidental hypothermia and cold injury. Oct, 51(10):417-31. Doi: 10.1067/j.cpsurg.2014.07.004. 


Imray, C., Grieve, A., Dhillon, S. (2009). Cold damage to the extremities: frostbite and non-freezing cold injuries. Postgrad Med J., Sep; 85(1007):481-8. Doi: 10.1136/pgmj.2008.068635

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Pinaki Mukherji, MD

Assistant Professor

Department of Emergency Medicine

Department of Internal Medicine

Donald and Barbara Zucker School of Medicine at Hofstra/Northwell


References

Management of accidental hypothermia and cold injury. Petrone P, Asensio JA, Marini CP. Curr Probl Surg. 2014 Oct;51(10):417-31. doi: 10.1067/j.cpsurg.2014.07.004. Epub 2014 Jul 29.

Wilderness Medical Society practice guidelines for the out-of-hospital evaluation and treatment of accidental hypothermia: 2014 update.Zafren K1, Giesbrecht GG2, Danzl DF3, Brugger H4, Sagalyn EB5, Walpoth B6, Weiss EA7, Auerbach PS7, McIntosh SE8, Némethy M8,McDevitt M8, Dow J9, Schoene RB10, Rodway GW11, Hackett PH12, Bennett BL13, Grissom CK14.

Wilderness Environ Med. 2014 Dec;25(4 Suppl):S66-85. doi: 10.1016/j.wem.2014.10.010

Wilderness Medical Society Practice Guidelines for the acute treatment of Frostbite:2014 update. McIntosh SE1, Opacic M2, Freer L3, Grissom CK4, Auerbach PS5, Rodway GW6, Cochran A7, Giesbrecht GG8, McDevitt M9, Imray CH10, Johnson EL11, Dow J12, Hackett PH13. Wilderness Environ Med. 2014 Dec;25(4 Suppl):S43-54. doi: 10.1016/j.wem.2014.09.001.

Frostbite: a practical approach to hospital management. Handford C1, Buxton P2, Russell K3, Imray CE4, McIntosh SE5, Freer L6, Cochran A7, Imray CH8.Extrem Physiol Med. 2014 Apr 22;3:7. doi: 10.1186/2046-7648-3-7. eCollection 2014Gross, E., & Moore, J. (2012).

Using thrombolytics in frostbite injury. Journal of Emergencies, Trauma, and Shock, 5(3), 267. doi:10.4103/0974-2700.99709 

Tintinalli, J. E., & Stapczynski, J. S. (2016). Tintinalli's emergency medicine: A comprehensive study guide. New York: McGraw-Hill. 

Wrenn, K. (1991). Immersion foot. A problem of the homeless in the 1990s. Archives of Internal Medicine, 151(4), 785-788. doi:10.1001/archinte.151.4.785 

Petrone, P., Kuncir, E., & Asensio, J. A. (2003). Surgical management and strategies in the treatment of hypothermia and cold injury. Emergency Medicine Clinics of North America, 21(4), 1165-1178. doi:10.1016/s0733-8627(03)00074-9


Gonzaga, T., Jenabzadeh, K., Anderson, C. P., Mohr, W. J., Endorf, F. W., & Ahrenholz, D. H. (2016). Use of Intra-arterial Thrombolytic Therapy for Acute Treatment of Frostbite in 62 Patients with Review of Thrombolytic Therapy in Frostbite. Journal of Burn Care & Research, 37(4). doi:10.1097/bcr.0000000000000245


How to Cite this Post

[Peer-Reviewed, Web Publication] Watts, S, Kaltman, D. (2020, Mar 16). Cold Management in the ED. [NUEM Blog. Expert Commentary by Mukherji, P]. Retrieved from https://www.nuemblog.com/blog/cold-injury


Posted on March 16, 2020 and filed under Environmental.

SCUBA Diving Injuries and Treatments

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

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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.

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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.


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Posted on August 26, 2019 and filed under Environmental.