Questions of the Week for 10/17/2023: Outdoor Sim Edition
Author: Ly Cloessner, MD
Reviewed by: Jess Pelletier, DO
Case 1: Altitude
1) These past few months in residency have been busy, but you have a vacation coming up! You’re so excited about the time off; you and a few non-medical friends have finally been able to secure permits to summit Mt. Whitney (elevation ~4,421 m). Evidently, taking vacation to just “relax” isn’t in their plans. You are no big hiker, so you convince the group to make this a 2-day trip with an overnight at Trail Camp (elevation 3,658 m) on the ascent, giving you more time at the summit, and hopefully making this whole trip less tiring. Prior to the trip, one of your friends asks you how they can prevent getting sick from the altitude change. What do you tell him?
2) The hike up Mt. Whitney was hard, but the views at the top are incredible. As you and your friends are looking around the summit, you notice a group you saw last night at base camp—one of the members of their party, an older-looking gentleman, isn’t looking too well. In fact, he looks a little…blue? He’s coughing and seems to be aimlessly wandering around. His group is concerned, and one of them offers him an inhaler since he seems so short of breath. How can you help this guy?
Explanations:
Acute mountain sickness (AMS) happens in the setting of rapid ascent to altitude, generally over 2,000 m. Symptoms include headache, lightheadedness, gastrointestinal (GI) upset, and fatigue. It is extremely common, affecting over 40% of individuals who ascend over 10,000 ft (3,048 m, lower than the base camp at Mt. Whitney). AMS is actually just a mild form of high-altitude cerebral edema (HACE), which generally occurs at >3,000 m+.
The major risk factors for developing these symptoms are obesity, older age (>50), and rapid ascent. The only ways to prevent it are slowing the ascent (the Wilderness Medicine Society [WMS] recommends one day of travel for every 1,500 ft ascent above 10,000 ft above sea level and a day of rest every 3-4 days of travel), taking acetazolamide before you go, and non-steroidal anti-inflammatory drugs (NSAIDs) (question 1). Acetazolamide works to prevent AMS only if started a few days prior to the trip (125 mg PO q12 hours). It works to speed acclimatization by inducing a metabolic acidosis via bicarb diuresis, which will then trigger a compensatory hyperventilation, which helps hikers acclimatize more quickly. Unfortunately, acetazolamide IS a diuretic, so it can increase the risk of dehydration on a strenuous hike, and it may also trigger allergies in those allergic to sulfa drugs. If someone has a sulfa allergy, they can trial the acetazolamide to see if their symptoms are triggered, or they may try to prevent symptoms with dexamethasone 4 mg q12 hours instead (will need a steroid taper afterwards if used for longer than 10 total days).
Once mountain sickness has developed, the treatment is NSAIDs, acetazolamide (which works better as a preventative agent, but can help slow a progression AMS from HACE) and descending from altitude. Dexamethasone can slow the progression from AMS to HACE and should therefore be given to anyone with moderate AMS. The regimen for treatment is an initial dose of 8 mg PO followed by 4 mg every 6 hours thereafter. Dex is a steroid and a vasoconstrictor, which helps it counteract cerebral edema. If HACE develops, the patient needs immediate descent, as well as the steroid.
In addition to cerebral edema, hiking up to elevations like those on Mt. Whitney can also cause HAPE (high altitude pulmonary edema). Unfortunately for the patient above, he may have both HAPE and HACE, which can occur simultaneously. HAPE is the deadliest type of altitude sickness. The pathophysiology of both HACE and HAPE is rooted in our response to the decreased partial pressure of inspired oxygen found at higher altitudes. In brief, while the brain adapts to hypoxia by dilating its vessels, the pulmonary vasculature constricts. In the brain, this dilation causes vasogenic edema, resulting in the swelling seen in HACE. In the pulmonary arteries, the constriction causes an increase in pressures in the vessels, but the epithelial alveoli remain leaky, leading to a non-cardiogenic pulmonary edema. For those with HAPE, not only does the patient need descent, but they will also need oxygen, and a vasodilatory agent, like nifedipine 30 mg q12 or 20 mg q8 hours (most commonly used, but some other things have been trialed, like sildenafil).
For those who get HAPE and HACE, treatment becomes more complicated—a patient may have HAPE but not HACE and appear altered from the hypoxia without any underlying cerebral edema. If you suspect HAPE, and the patient isn’t improving with oxygen only, give dexamethasone. If a patient has both HAPE and HACE, giving nifedipine will decrease mean arterial pressure (MAP), which will also decrease cerebral perfusion pressure, potentially leading to cerebral ischemia if the patient also concomitant HACE. For this reason, treatment of HAPE with nifedipine is controversial in an altered patient. In any case, if you’re considering HAPE or HACE in the differential, this patient needs immediate descent (Question 2).
References:
1) For those who learn with visuals:
Image credit: Dr. Aaron Lacy, Washington University in St. Louis
https://foamcast.org/2016/09/12/episode-56-altitude/
2) For those who learn from podcasts (short!):
https://emergencymedicalminute.org/podcast-622-high-altitude-pulmonary-edema-hape/
https://emergencymedicalminute.org/podcast-625-high-altitude-cerebral-edema-hace/
3) For those who prefer to read:
https://pubmed.ncbi.nlm.nih.gov/20417343/
https://www.ncbi.nlm.nih.gov/books/NBK560677/
https://litfl.com/high-altitude-illness/
4) For those who like to do questions:
https://foamcast.org/2016/09/12/episode-56-altitude/
Case 2: Backboards
3) You’ve just taken the gentleman with HAPE back to base camp. He’s getting treatment; time to finish your own descent and get off this mountain. As you trudge back out, tired at the end of a long day, you see a bike…upside down…in a tree. “That’s not where that goes,” you think. And then you see him, limbs akimbo, blood everywhere, looking like a bad trauma bay drop-off here in the middle of the woods. You call back to camp for help and approach your newest patient. What exam findings would make you want to immobilize this man’s neck or spine when the park ranger arrives?
4) Despite how bad the scene looked, the man seems to have only suffered a lot of dirty lacerations. Ouch. He appears sober, GCS is 15, and he’s giving what appears to be a reliable history. The park rangers who arrive on scene have thankfully come with a large first aid kit, and you are ready to hand the patient off to them. They’ve got a backboard, c-collar, and straps, and they want to transport this man on the board. The patient insists he can walk out. The ranger insists the patient be on the board, but then they tell him, “Just ask the doctor. She’ll tell you we have to carry you out on this board.” What evidence would you present to change his mind??
Not every injured patient needs to be immobilized on a stretcher. Immobilization is uncomfortable. Moreover, there are multiple studies linking morbidity and mortality to spinal immobilization. Additionally, what we know from cadaver studies suggests that physiological movement is unlikely to result in further spinal cord injury (SCI) when a patient has suffered a vertebral or SCI. Given these findings, guidelines from multiple academic societies are moving away from strict spinal immobilization on a backboard and towards spinal motion restriction (SMR), which can be achieved with scoop stretchers, vacuum splints, cots, or similar devices. This restriction is only needed in certain instances (Question 4). There is NO ROLE for SMR in penetrating trauma. Physical exam findings that indicate a need for SMR after blunt trauma in adult patients include intoxication, GCS <15, midline spinal pain at any level or any spinal deformity, focal neurologic signs/symptoms (numbness/weakness), or any distracting injuries that impairs the patient’s ability to reliably contribute to your exam (Question 3). If any of these injuries is identified, then the entire spine needs to be in restricted motion, as the risk of noncontiguous injuries is high. SMR will therefore always include a c-collar. While SMR can be achieved with head elevation, the patient cannot be sitting up straight. For children, while they may have communication barriers, they should not be put in SMR due to age-appropriate communication skills. Children should be placed in a c-collar if any of the following are present: Neck pain, torticollis, neurologic deficits, altered mental status, high-impact diving injury, high-mechanism motor vehicle collision (MVC), or substantial torso injury. Children do NOT have the same risk of noncontiguous multilevel spinal injury as adults and so do not necessarily need whole SMR if their suspected injury is in the cervical spine.
Resources:
1) For those who learn with visuals:
https://limmereducation.com/wp-content/uploads/2019/03/SMR-flow-chart-LimmerEd.pdf https://handbook.bcehs.ca/clinical-resources/pediatrics/pediatric-spinal-motion-restriction-smr/
2) For those who learn from podcasts:
https://dustoffmedicpodcast.com/episode-32-spine/
3) For those who prefer to read:
https://doi.org/10.1080/10903127.2018.1481476
https://pubmed.ncbi.nlm.nih.gov/31780084/
https://www.ncbi.nlm.nih.gov/books/NBK557714/
4) For those who like to do questions:
https://quizlet.com/205946396/ce-spinal-motion-restriction-flash-cards/
https://www.quiz.biz/quizz-230249.html
Case 3: Heat
5) After you return from your strenuous mountain trip, you decide to spend the rest of your vacation relaxing and visiting extended family on the bayou in Louisiana. You are helping your mom prepare for tonight’s big family gumbo and your brother, who smokes like a chimney and is yet training for a marathon, comes in after his long run. He arrives home absolutely covered in sweat, is warm to the touch, and he just looks ill. Your mom panics, and she asks you to help her throw him under a cold shower. Will this help?
6) Your brother’s condition turns around after a few hours at the hospital, and everyone gets together for gumbo in the evening. It’s great to see the whole family together, even though it’s hot and humid as anything outside (it is Louisiana, after all). You go to catch up with your elderly auntie, who’s 96 and not in the best health. When you sit down with her, she tells you she’s not feeling well. Her skin looks dry, and she feels burning hot when you touch her hand. Her pulse is racing, and she seems confused, which is not normal for her at all. You’re worried. What’s the first thing you should do?
Explanations:
Your brother and your auntie both have what’s commonly called heat stroke. “Exertional” heat stroke is generally seen in younger athletes, like your brother. These patients present sweaty and profoundly dehydrated. For patients in this state, the cornerstone of treatment is rapid evaporative cooling. If the patient is young and healthy, and they aren’t somewhere where you can put them in an ice bath (which is the most effective method to physically cool someone—0.2°C /minute), you can spray them with lukewarm water (not cold—which actually slows cooling) and use fans to help evaporate off the sweat (so avoid the cold shower, Question 5). Evaporative cooling can cool patients about half as fast as the ice bath. Ice packs, if available, can also be placed in the axillae or groin; this is a method of conductive heat loss (which is faster than evaporative heat loss). Some sources recommend also adding a cooling blanket UNDER the patient if you have that available to aid in conductive heat loss. The goal is to get the patient actively cooled until their core temperature is 38-39°C (you don’t want to overshoot). The patient will need to be monitored for a few hours after cooling to watch for thermal instability. You need to call emergency medical services (EMS) for your brother, so that he can receive aggressive fluid resuscitation for his dehydration. The following laboratory testing is indicated to rule out end-organ damage from exertional heat stroke: Glucose monitoring, an electrocardiogram (ECG), liver enzymes (patients can actually get hepatitis from direct tissue injury and splanchnic blood flow diversion as the body tries to cool itself), creatine kinase and a urinalysis (to assess for rhabdomyolysis and renal failure), venous blood gas (VBG), and coagulation studies (a these patients can get disseminated intravascular coagulation [DIC]).
“Classic” heat stroke is seen more commonly in elderly patients, like your auntie. This type of heat stroke is caused by a combination of poor thermoregulation and being surrounded by ambient Louisiana summer swamp temperatures or similar environments. Usually, our bodies only have about a 1°C change in temperature for every 25-30°C change in ambient temperature, but our ability to thermoregulate begins to degrade around age 70. We can thermoregulate by increasing cardiac output and dilating our cutaneous blood vessels, but, as we age, the body has more difficulty increasing cardiac output. The elderly also produce less sweat to dissipate heat. Additionally, if humidity is >75%, our bodies’ ability to evaporatively cool via sweating is diminished, making an outdoor bayou summer cookout the perfect condition for auntie to develop heat stroke. Heat stroke has an extremely high mortality (30-80%) so you need to call EMS immediately (Question 6). You can help auntie while you wait for the ambulance by doing some evaporative cooling like you did for your brother (but no ice bath, which can be associated with INCREASED mortality in elderly patients). Once EMS brings Auntie to the hospital, she will need central temperature monitoring, in addition to the previously described diagnostic workup. Since this type of heat stroke is a non-exertional problem, and the patients generally aren’t very dehydrated, aggressive rehydration usually isn’t necessary, though a bolus and maintenance intravenous fluid (IVF) with chilled fluid is usually appropriate. However, care must be taken not to over-resuscitate these patients, as fluid overreplacement may result in cerebral edema. These patients must be monitored carefully as tachydysrhythmias can occur (but will respond to temperature management, so they don’t require cardioversion). If the patient is becoming agitated or shivering from the cooling process, they can be treated with IV benzodiazepines, which will help them to feel calm and reduce the shivering mechanism (which aids in cooling). In severe cases, the patient may need a definitive airway while you resuscitate. In these cases, use rocuronium (not succinylcholine, due to the risk of hyperkalemia with rhabdomyolysis) for your paralytic.
Resources:
1) For those who learn from podcasts:
https://gpnotebookpodcast.com/general-practice/ep-49-heat-exhaustion-and-heatstroke/
https://emergencymedicalminute.org/podcast-141-heat-stroke/
https://embasic.org/hyperthermia/
2) For those who prefer to read:
http://www.emdocs.net/em3am-heat-stroke/
https://emcrit.org/ibcc/hyperthermia/ (has a great section on evaporative cooling versus ice baths)
3) For those who like to do questions:
https://study.com/academy/practice/quiz-worksheet-comparing-heat-stroke-heat-exhaustion.html
Case 4: Drowning
7) The morning after the eventful gumbo cookout, you are on the back porch swing drinking your morning coffee with your mom. Finally, a chance to relax and have a quiet day. The moment the word “quiet” crosses your mind, you see the neighbor running towards the house. He is coming from the direction of the bayou, carrying his kid, hollering for help. It’s horrifying: His three-year-old young son was playing out on the dock where everyone goes fishing, and he must have fallen off when no one was looking. He wasn’t alone for more than a minute or two. His family pulled him out of the water. He is cold and not breathing. You don’t feel a pulse. You have three adults and no equipment available; how do you start resuscitation? How will this change when EMS arrives?
8) You get pulses back quickly (even though it felt like forever), but the child is still cold and barely breathing. Water is coming from his airway. He needs better resuscitation. EMS scoops the child up, and they are off to the big hospital not too far away. You’re lucky: They have extracorporeal membrane oxygenation (ECMO) there. When would it be appropriate to resuscitate this child using ECMO?
In the United States, drowning is the number one cause of unintentional injury-related death in children aged 1-4, and the second leading cause of unintentional injury-related death in children aged 5-14 (after MVCs). Not much water is needed to drown someone, as it’s not the volume of water swallowed that’s the problem; it’s that water washes away surfactant, which collapses the alveoli, causing a shunt, leading to hypoxia. Hypoxia leads to tachycardia followed by bradycardia, then pulseless electrical activity (PEA)/asystole, and subsequent death. In warm water, this whole process only takes a few minutes, but in ice water, the process of drowning followed by death can be prolonged to almost an hour.
Given that you have multiple adults available in this scenario but no equipment, you can provide compressions and breaths in a 15:2 ratio; dad can give breaths while you administer compressions. It is important to keep in mind that in pediatric AND adult cardiopulmonary resuscitation (CPR) in the setting of drowning, the breaths are ESSENTIAL. European resuscitation council guidelines for cardiac arrest in special circumstances current recommendations state that CPR for drowned victims should start with 5 rescue breaths. If you had equipment and could place an airway, then you could switch to continuous CPR with a breath every 2-3 seconds. When EMS arrives, the first steps will be clearing/suctioning/securing the airway, putting automated external defibrillator (AED) pads on the child, getting IV or intraosseous (IO) access, and getting the child warmed by removing cold, wet clothing and applying warm blankets on (Question 7). After placement on a ventilator, the child will need a high fraction of inspired oxygen (FiO2) and a high positive end expiratory pressure (PEEP) to help keep alveoli open, since water washes away surfactant. Suction will also be important, as the majority of these patient will regurgitate everything in their stomach, and aspiration will further worsen hypoxia.
Hypothermia is an incredibly common complication of drowning. Generally, any body of water is much cooler than average body temperature (even if it is a Louisiana swamp). The rapid cooling associated with drowning will slow cerebral metabolic rate, meaning that a quick drowning event may not in itself cause massive cerebral hypoxia (if you were curious: The rate of cerebral oxygen consumption is reduced by approximately 5% for each reduction of 1°C in temperature within the range of 37°C to 20°C, and this is also why children who drown in winter/very cold water have higher survival rates). There is some evidence that children may benefit from therapeutic hypothermia if they have suffered a massive brain injury with their drowning, but generally, if you do not also suspect major hypoxic injury from another cause and core temperature in your patient is less than 34°C, then you may start warming. Warmed blankets, warmed IVF, and other internal lavage methods are all methods in practice for rewarming, but ECMO has been shown to GREATLY increase rates of survival from hypothermic arrests and is usually considered when: 1) the child had a cardiac arrest, 2) the child had a temperature of less than 28°C with ventricular tachycardia (VT) or ventricular fibrillation (VF) on the monitor, or 3) the child was hypotensive (Question 8).
Resources:
1) For those who learn with visuals:
https://cpr.heart.org/en/resuscitation-science/cpr-and-ecc-guidelines/algorithms
Use of CPR in Drowning Victims
When to initiate
- Ventilate those with respiratory distress/respiratory arrest to prevent cardiac arrest
- Start CPR in those submerged for <60 minutes with no obvious physical signs of death (i.e. rigor mortis, body decomposition)
When to discontinue
- Continue BLS unless signs of life reappear, rescuers are exhausted, or ACLS team takes over
- Continue ACLS until patient has been rewarmed (if hypothermic) and has had asystole for >20 minutes
Table adapted from: Szpilman D, Bierens JJLM, Handley AJ, Orlowski JP. Drowning. N Engl J Med. 2012;366(22):2102-2110. doi:10.1056/NEJMra1013317
From NEJM, as listed below
Image credit: emDOCS.net (http://www.emdocs.net/em3am-hypothermia-2/)
2) For those who learn from podcasts:
https://litfl.com/drowning/ (video at the bottom)
http://www.emdocs.net/emdocs-podcast-episode-70-drowning/
https://www.emrap.org/episode/pedsem-enduring/drowning
3) For those who prefer to read:
A brief, clinical overview: https://www.rch.org.au/clinicalguide/guideline_index/Drowning/
A bit in the weeds: https://derangedphysiology.com/main/required-reading/trauma-burns-and-drowning/Chapter%20407/immersion-submersion-and-drowning
Definitely in the weeds: https://www.nejm.org/doi/full/10.1056/NEJMra1013317?rss=searchAndBrowse#t=article
4) For those who like to do questions:
https://www.merckmanuals.com/home/multimedia/quiz/drowning
Case 5: Lightning
9) You’ve given up on the idea of a relaxing vacation. Heck, you need a vacation to recover from this “vacation.” You head back to Saint Louis, where there are no mountains, the fall weather has arrived, and there’s no swamp in the backyard. It starts raining hard when you get back into town—the Midwest has thunderstorms like nowhere else, really. You’re passing by Barnes Jewish Hospital, and you see some people running towards a tree in Forest Park, trying to escape the rain. Then you see some flashes. You see people drop. You make the perhaps unwise decision to stop and help. You’ve already been seeing patients all week—might as well help these folks across the street to the emergency department (ED). You call 911. Who should your team of co-residents treat first?
· Patient with pulses, no corneal reflexes, not breathing
· The woman who is running around in circles screaming “I’M DEAD” repeatedly
· The unconscious man with intact pulses, mildly elevated respirations, and a major head lac—he appears to have been thrown against a sharp rock on the ground when he fell
10) Shortly after you’ve shipped the patients to the ED, you get a call from your classmate. “That pulseless patient you sent, her heart restarted almost immediately, but she just….won’t breathe on her own. Do you know more about what happened?” Explain why the cardiac activity has returned, but the respiratory function hasn’t.
Lightning strikes can affect people via multiple mechanisms. People can be directly struck by lightning (5%); get a “side flash” when a nearby (1-2 foot) object is struck and air conducts the current onto them (20-30%); get hit by ground current, when energy from the strike is transmitted into the ground around the struck object (40-50%); suffer from a conduction injury if they are touching a metal surface that has been struck (with ground current impacting 40-50%); or become a part of a streamer injury (10-15%), where one of the positive currents from the ground that did not complete the circuit of the main lightning strike goes through the patient. These strikes can cause multiple types of injury and injury to every organ system. The most common injuries encountered subsequent to lightning strikes include thermal burns (90% of patients will get a superficial skin burn), barotrauma-related (tympanic membrane [TM] perforations, organ contusions), or the result of blunt trauma from muscle contractions that can throw the patient to the ground or into a nearby object. We will cover the potential injuries by system here.
· Cardiac: Cardiac arrest is the most common cause of death in lightning strikes and is most commonly seen after a direct strike. Asystole is the most common dysrhythmia caused by a lightning strike, as the electricity of the strike depolarizes the entire myocardium immediately. However, ventricular dysrhythmias and QT prolongation are also frequently seen. VF is more common in electrical injuries than in lightning strikes. As time passes, cardiogenic shock may result from a stunned myocardium.
· Hematologic: Blood vessels are ideal conduits for electricity, so vessels are frequently injured. Patients can develop thrombosis and aneurysms immediately, and some patients will go on to develop coagulopathies like DIC.
· GI: GI insults tend to occur secondary to vascular ones, with ileus and organ ischemia resulting from injuries to the vessels supplying the GI tract. These symptoms generally occur later in the patient’s course after lightning strike.
· Pulmonary: The medullary respiratory center or respiratory muscles can be paralyzed by lightning, resulting in apnea that can cause a respiratory arrest. If this happens, the muscle recovery can be slow (patients with cardiac and pulmonary arrest will generally recover cardiac activity well before respiratory activity). If intracranial hemorrhage is present, the brainstem is commonly affected, so intracranial hemorrhage (ICH) in the respiratory center may also cause this presentation (Question 10). Barotrauma can also cause pneumothoraxes.
· Neurologic: Lightning strike to the head can cause immediate ICH, with the basal ganglia and brainstem most commonly affected. Be aware that fixed and dilated pupils may be present in lightning strike victims, but do not use this in your prognostication of a patient struck by lightning—these are actually caused by massive catecholamine release and are not necessarily suggestive of brain death. Additionally, the electrical overstimulation of the autonomic nervous system may lead to immediate but temporary hypertension, sensory loss, and vasospasm. This vasospasm can lead to transient tetraplegia, or paraplegia (called keraunoparalysis). Immediate but permanent findings may include peripheral neuropathies, strokes, and development of cerebral salt wasting syndromes. Parkinsonism and movement disorders have been seen as delayed effects of lightning injury.
· Ear/Nose/Throat: TM rupture is possible. Sensorineural damage to the auditory nerve can lead to hearing loss. Tinnitus and vertigo have also occurred after injury.
· Ophthalmologic: Damage to the eyes is common, with the classic effect being cataracts (which may develop weeks or years after injury). Optic neuritis, vitreous hemorrhage, retinal injury, optic nerve injury, and corneal ulceration maty also occur.
· Orthopedic: Immediate injuries of concern in lightning strike victims include posterior shoulder dislocations and deep burns. As bones are the part of the body with the greatest resistance to current, damage to muscle may be greatest nearest the bone (contrast tomography [CT] may be necessary to identify this damage, as deep burns may lack external manifestation). Subsequent effects may include compartment syndrome and rhabdomyolysis.
· Renal: The kidneys are at risk from injury due to rhabdomyolysis, and the most common electrolyte abnormalities see are elevated potassium and phosphate (elevated secondary to cell death caused by the lightning strike).
· Dermatologic: Lightning causes a burn as sweat is vaporized over the skin that lightning travels down. Full thickness burns remain rare. The Lichtenberg figures pathognomonic of lightning strikes usually last less than a day, and small punctate/circular burns indicate where current exited the body.
Since all organ systems can be affected, lightning strike victims need a thorough, head-to-toe examination. As a part of your laboratory workup, ECG is recommended (even though most dysrhythmias are transient), as well as CK, renal and liver function testing. CT head is not recommended as a part of the general workup unless the patient has signs of intracranial injury (refer to typical decision rules). IVF may be given, but there is no need to aggressively resuscitate as if this is a burn patient; let the clinical picture of the patient guide this management and titrate IVF administration to urine output. Amazingly, if you find nothing wrong with the patient on exam, and initial labs are reassuring, they can be discharged home without an extended monitoring period.
But who do you see FIRST? In most mass casualty incidents, patients who are not breathing or are pulseless are labeled “expectant”/black tagged and are not prioritized to receive limited medical resources. However, in a lightning strike, these patients are PRIORITIZED, as they have a decent chance for a positive outcome if they are tended to quickly (Question 9). It is rare that someone who survives the initial strike will later die, but those who initially die from the lightning strike can be revived. As stated earlier, in these patients, return of cardiac activity usually precedes return of respiratory activity, so attention must be paid to ongoing ventilatory support.
Resources:
1) For those who learn with visuals:
Image credit: https://aaemrsa.blogspot.com/2020/08/lightning-strike-emergencies-part-1.html
https://www.weather.gov/safety/lightning-struck
2) For those who learn from podcasts:
https://emergencymedicinecases.com/electrical-injuries/
https://coreem.net/tag/electrical-injuries/
3) For those who prefer to read:
http://www.emdocs.net/lightning-strike-injuries/
https://aaemrsa.blogspot.com/2020/08/lightning-strike-emergencies-part-1.html (also has a part 2)