Under the scorching sun – Heat Stroke Q&A

October 25, 2021September 4, 2021 ~ Sumaiya Hafiz, UAE ~ Leave a comment

Different parts of the world are experiencing extremes of temperature. Especially in the Middle East and Asia this time of the year, heatstroke is one of the commonest presentations in the emergency department (ED). Both developed and developing countries suffer from it.

Heatstroke can range from being mild to severe, and it can lead to multi-organ damage and eventually death, especially in cases not treated in time.

Heatstroke can present in various ways and may mimic other illnesses. In the ED, just like anything else, history is an essential part of management.

What is heatstroke and how does it occur?

The body functions well at a set temperature. When a person is present in extremes of temperature, dehydrated, or performs physical exertion in high temperatures, the thermoregulatory mechanism does not work effectively, causing overheating and body temperature to reach up to 40 degrees celsius. This change in body temperature, if not treated rapidly, causes different organs to deteriorate, as the organs function at the optimal temperature and a change from the normal causes their dysfunction.

Heatstroke is divided into two types – Classical or non-exertional heatstroke is common in children and the elderly who spend time outdoors in the heat and exertional heatstroke is seen in workers and soldiers who perform activities outdoors for long periods of time.

What are some risk factors that may increase the chances of developing a heat stroke?

Heatstroke can occur in almost anyone, but certain factors increase the risk, such as:

People of extremes of age and those who work outdoors during the daytime (eg – construction workers).
Dehydration and exposure to high temperature with inadequate ventilation.
Certain medications such as antipsychotics, antidepressants, and diuretics etc.

How do the patients present to the ED?

The presentation of heatstroke may mimic many illnesses and history is one of the most important factors in making a decision. Here is the various presentations that can be related to heatstroke:

High body temperature >40 degrees celsius
Changes in behaviour
Changes in perspiration – skin would be dry and warm to touch
Seizures
Symptoms of dehydration
Nausea and vomiting
Flushing of skin
Tachypnea and tachycardia
Headache
Coma

How to evaluate the patient?

The evaluation starts with taking a history from the patient or someone accompanying them. History of heat exposure increases the suspicion. You should also see:

Vitals signs and temperature monitoring, rectal if possible.
Cardiac monitoring – the monitor will show sinus tachycardia
Complete blood count (CBC), Reflo, Urea and Electrolytes, Liver and Kidney function, Lactate
Creatine phosphokinase (CPK) levels

Management in the ED

Start with ABC’s – patients may present in a coma and may require intubation
Remove any excessive materials of clothing
Cool the patient with a cooling blanket
Fluid resuscitation – cold IV Fluids
The target temperature is 38.5 degrees celsius

Cooling Techniques

Cold exposure – Several techniques can be used such as cold water splashes/spraying, placing a fan, immersion in an ice bath, or cold water packs
Dantrolene – A drug that reduces heat production in the body, has shown no effect in improving outcomes in patients with heatstroke and hence is not indicated.
Medications may be used for symptomatic relief. However, the gold standard management is rapid cooling using any of the above-mentioned methods.

689.3 - Figure 3. Waterproof matress and Cooling Unit

What complications can occur if the patient is not treated rapidly?

Coma
Seizures
Electrolyte imbalance
Bleeding
Multi-organ damage
Neurological dysfunction
ECG changes
Hypotension

What are some of the differential diagnoses of heatstroke?

Drug ingestion and overdose
Meningitis
Malaria
Serotonin syndrome

How can we prevent heat stroke?

Public education and occupational health initiatives to spread awareness amongst the public and workers to protect themselves, stay hydrated at all times, and set duty and break hours during peak daytime.
Availability of rapid cooling equipment in emergency departments

References and Further Reading

Abdulaziz Mulaik, Heat Illness – https://iem-student.org/heat-illness/
Heat Stroke – Wikem”. Org, 2021, https://wikem.org/wiki/Heat_stroke.
“Heatstroke – Symptoms And Causes”. Mayo Clinic, 2021, https://www.mayoclinic.org/diseases-conditions/heat-stroke/symptoms-causes/syc-20353581.
Nickson, Chris. “Heat Stroke”. Life In The Fast Lane • LITFL, 2021, https://litfl.com/heat-stroke/.
Morris A, Patel G. Heat Stroke. [Updated 2021 Jun 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK537135/
Bouchama A, Cafege A, Devol EB, Labdi O, el-Assil K, Seraj M. Ineffectiveness of dantrolene sodium in the treatment of heatstroke. Crit Care Med. 1991 Feb;19(2):176-80.
https://www.rcemlearning.co.uk/reference/heat-related-illness/#1625580396401-81a090d4-50b6

Cite this article as: Sumaiya Hafiz, UAE, "Under the scorching sun – Heat Stroke Q&A," in International Emergency Medicine Education Project, October 25, 2021, https://iem-student.org/2021/10/25/heat-stroke/, date accessed: September 27, 2023

Question Of The Day #46

July 16, 2021June 19, 2021 ~ Joseph Ciano, USA ~ Leave a comment

Which of the following is the most appropriate next step in management for this patient’s condition?

Explanation

This patient presents to the Emergency Department with altered mental status. This presenting symptom can be due to a large variety of etiologies, including hypoglycemia, sepsis, toxic ingestions, electrolyte abnormalities, stroke, and more. The management and evaluation of a patient with altered mental status depends on the primary assessment of the patient (“ABCs”, or Airway, Breathing, Circulation) to identify any acute life-threatening conditions that need to be managed emergently, the history, and the physical examination. One mnemonic that may help in remembering the many causes of altered mental status is “AEIOUTIPS”. The table below outlines this mnemonic.

ALTERED MENTAL STATUS

The serum chemistry results provided show elevated BUN and Creatinine with a BUN/Cr ratio of 21.3. A BUN/Cr ratio greater than 20 indicates decreased perfusion to the kidneys, also known as pre-renal azotemia, which can indicate dehydration, hypovolemia, or shock. The serum chemistry also shows a severely low sodium level. Hyponatremia can present with a variety of symptoms, including weakness, fatigue, myalgias, nausea, vomiting, headaches, altered mental status, focal neurologic deficits, seizures, or coma. Hyponatremia can be acute or chronic, asymptomatic or symptomatic, and mild or severe. Sodium levels below 120 mEq/L are severely low. Neurologic symptoms, such as seizures, altered mental status, and focal neurologic deficits, are also considered severe. Treatment should be based on patient symptoms, rather than the sodium level, as it can be difficult to assess how acute or chronic the hyponatremia state is on initial evaluation. The presence of any severe neurologic symptoms as is seen in this scenario should prompt administration of hypertonic saline (3% NaCl). This allows for rapid correction of serum sodium levels, which should in turn relieve the neurologic symptoms. A 100-150mL IV bolus of 3% NaCl can be given a second time if symptoms continue after 5-10 minutes.

Typically, hyponatremia should be corrected slowly to avoid central pontine myelinolysis. Increases in sodium greater than 8mEq/L per 24hours should be avoided for this reason. However, in the case of neurologic symptoms, rapid correction of sodium is opted for to prevent further damage.

Administration of “normal saline”, or 1000mL of IV 0.9% NaCl (Choice A), can increase the sodium level. However, normal saline is not concentrated enough to rapidly increase the serum sodium to terminate neurologic symptoms. A noncontrast CT scan of the head (Choice B) is a reasonable investigation for this altered patient, but hypertonic saline should be administered first if hyponatremia is known. Administration of 25mg IV dextrose (Choice C), also known as “D50”, would be helpful in a patient with hypoglycemia and altered mental status. However, this patient is not hypoglycemic.

Administration of hypertonic saline (Choice D) is the best next step in this patient with severe hyponatremia and neurologic symptoms.

Correct Answer: D

References

Alvarez, A & Sekhon, N. (2019). Altered Mental Status. Society of Academic Emergency Medicine. Retrieved from https://www.saem.org/cdem/education/online-education/m4-curriculum/group-m4-approach-to/approach-to-altered-mental-statu
Farkas, J. (2020). Hyperosmolar hyperglycemic state (HHS). EMCRIT: The Internet Book of Critical Care. Retrieved from https://emcrit.org/ibcc/hhs/
MDCalc. Sodium Correction for Hyperglycemia. Retrieved from https://www.mdcalc.com/sodium-correction-hyperglycemia#evidence

Cite this article as: Joseph Ciano, USA, "Question Of The Day #46," in International Emergency Medicine Education Project, July 16, 2021, https://iem-student.org/2021/07/16/question-of-the-day-46/, date accessed: September 27, 2023

Organophosphate poisoning

March 29, 2021February 27, 2021 ~ Temesgen Beyene, Ethiopia ~ Leave a comment

Introduction

Organophosphate compounds can be commonly found in insecticides and are associated with systemic illness.
Mortality is higher in developing countries where organophosphate pesticides are more commonly available.
Organophosphorus poisoning can result from occupational, accidental, or intentional exposure.
Its use as a suicidal agent is frequent.
The primary cause of death in acute organophosphate poisoning is bradyasystolic arrest from respiratory failure.

Pathophysiology

Organophosphate compounds bind irreversibly to acetylcholinesterase inactivating the enzyme through the process of phosphorylation and acetylcholine at nerve synapses and neuromuscular junctions. Thus, it results in overstimulation of acetylcholine receptors.

Clinical presentation

Here are a few mnemonics for the Muscarinic Effects of Cholinesterase Inhibition: SLUDGE, DUMBELS, and Killer B’s (Figure 1 & 2).

Out of four distinct syndromes that can occur from organophosphate poisoning, the first two are clinically important in emergency setting 1. Acute poisoning, 2.intermediate syndrome, 3.chronic toxicity, and 4.organophosphate induced delayed neuropathy. Of these syndromes, the intermediate syndrome is the most feared one as it presents with paralysis of the neck’s flexor muscles, muscles innervated by the cranial nerves, proximal limb muscles, and respiratory muscles. It occurs up to 40% of poisonings within 1 to 5 days of initial symptoms.
Acute organophosphate poisoning can present with differing severities. Mild poisonings generally present with symptoms like lightheadedness, nausea, headache, dyspnea, lacrimation, rhinorrhea, salivation, and diaphoresis while moderate poisonings cause autonomic instability, confusion, vomiting, muscle spasms, bronchorrhea and bronchospasm. Coma, seizures, flaccid paralysis, urinary and fecal incontinence, and respiratory arrest may occur in the course of severe poisonings.
Diagnosis is based on history (people may bring bottles/substance itself) in the presence of a suggestive toxidrome. Cholinesterase assays and reference laboratory testing for specific compounds may confirm the diagnosis but take time and have limitations. Treatment should be started without delay based on the clinical findings.
Miosis (papillary constriction) and muscle fasciculation are the most reliable signs of organophosphate toxicity and help in diagnosis.

Treatment

The first step of the treatment is decontamination. Healthcare workers must wear protective equipment to avoid secondary poisoning. The patient should be decontaminated with ample water and soap preferably before arriving in a hospital or once stable. Water should be disposed of as hazardous waste.
In addition to decontamination, treatment consists of airway control, intensive respiratory support, general supportive measures, prevention of absorption, and the administration of antidotes.
The patient should be monitored continuously and provided 100% oxygen. Gastric lavage and activated charcoal are not recommended.
A non-depolarizing agent should be used when the neuromuscular blockade is needed during intubation since succinylcholine is metabolized by plasma butyrylcholinesterase, and therefore, may prolong paralysis.
The specific agents are atropine and Atropine can be given repeatedly every 5 minutes until tracheobronchial secretions attenuate (1-3 mg IV in adults or 0.01-0.04 mg/kg IV in children – never <0.1 mg per dose). Then, a continuous infusion should be started to maintain the anticholinergic state (0.4-4 mg/h in adults).
Pralidoxime is the single most important treatment for the nicotinic effect of organophosphate poisoning and is life-saving for intermediate syndrome if used within 48 hours (First dose: 1-2 g in adults or 20-40 mg/kg – up to 1 g – in children, mixed with NS and infused over 5-10 min, continuous infusion: 500 mg/h in adults or 5-10 mg/kg/h in children)
Seizures can be treated with benzodiazepines.

Disposition and follow-up

Minimal exposures may require only decontamination and 6 to 8 hours of observation in the ED to detect delayed effects.
Admission to the intensive care unit is necessary for significant poisonings.
Most patients respond to pralidoxime therapy with an increase in acetylcholinesterase levels within 48 hours.
The endpoint of therapy is the absence of signs and symptoms after withholding pralidoxime therapy.
Death from organophosphate poisoning usually occurs in 24 hours in untreated patients, usually from respiratory failure secondary to paralysis of respiratory muscles, neurologic depression, or bronchorrhea.

References and Further Reading

Burillo-Putze, G. & Xarau S. N. “Pesticides. Tintinalli JE, Stapczynski JS, Ma OJ, Yealy DM, Meckler GD, Cline DM, editors. Tintinalli’s emergency medicine: a comprehensive study guide 8th ed.” (2016): 1318-25.
Katz K. D. & Brooks D. E. “Organophosphate Toxicity Treatment & Management” Medscape, Dec 31, 2020, https://emedicine.medscape.com/article/167726-treatment. Accessed Feb 05, 2021.

Cite this article as: Temesgen Beyene, Ethiopia, "Organophosphate poisoning," in International Emergency Medicine Education Project, March 29, 2021, https://iem-student.org/2021/03/29/organophosphate-poisoning/, date accessed: September 27, 2023

Snakebite: Two years and 200 cases later

February 1, 2021January 29, 2021 ~ Carmina Shrestha, Nepal ~ Leave a comment

We practice as independent doctors right after MBBS in Nepal. One of my professors used to say, “One day, you will sleep as a medical student and wake up as a doctor.” What that meant for me was, after I graduate from medical school, I’d pack my bags and head towards a rural village to “save lives.” Like any other life transitions, this one felt unchartered, unknown, and scary. I felt severely underprepared. As time passed by, I started appreciating my internship year. We have a year of internship after MBBS at the teaching hospital where we work as a junior doctor. At Beltar—my workplace, I’d remember how the patient with enteric fever was managed back home, brush up on the details with a quick read in UptoDate, and play doctor.

"One day, you will sleep as a medical student and wake up as a doctor." What that meant for me was, after I graduate from medical school, I'd pack my bags and head towards a rural village to "save lives." Like any other life transitions, this one felt unchartered, unknown, and scary. I felt severely underprepared.

Carmina Shrestha Tweet

The general structure of how I practiced medicine was; model what my professors used to do, read up on what is new/has changed, and treat patients. One day, some people carried a young child with droopy eyes, flappy tongue, and drowning in his saliva to the PHC. “He was bit by this snake!” The man with tearful eyes was holding on to a dead brown snake. Do you see a problem there? My go-to structure for practicing medicine crumbled. Underprepared would be an understatement. We were lucky that a team of trained armies helped set up the snake bite center in the PHC.

As some months passed by, I started feeling somewhat competent in managing snakebite cases. Any lesson you learn in medicine is a work in progress, but here are some I can recall:

The oversimplified version of snakebite treatment is–give antivenom and wait. In my experience, what we do while waiting, matters a lot. The neurotoxin that makes the patient paralyzed does not shut his brain down. He can listen and see, and we can use that to our advantage. Tell him what you are doing. Let him know what to expect. Talk to him. Open his eyes and make him see his loved ones are nearby. Make him believe that people are working hard to help him.

Amid scrutinized protocols, results of giant multi-center RCTs, and excellent well-formatted articles, it is easy to forget that what we do is taking care of a patient—the most basic of human skills. “LATERAL RECUMBENT!” I found myself shouting out of instinct. The patient was drowning in his saliva. My team tried hard to protect the patient’s airway as per protocol by extending his neck. But the patient was having a hard time breathing due to secretions. Sure we could not use the suction; unreliable electricity supply, broken suction machine, lack of funding, and whatnot, but we could still care. Use your mirror neurons; what would you want people to do if you were where the patient is?

Timely referral can be the difference between life and death. Understand the limitations of where you are working. Do you have a properly functioning suction? How reliable is your electricity? Do you have a ventilator? How far would you have to send the patient to get one? Manage your internal alarm accordingly. For us, the only respiratory support was a bag valve mask, and the transport to the nearest facility with a ventilator was at least 2 hours. Knowing that helps you be acceptably anxious and make informed decisions.

There is no substitution for empathetic yet informative communication with the patient and their loved ones. Clarify your assessment, plan, and signs that will prompt you to refer the patient. Talk to the anxious patient parties in a supportive tone but tell them that antivenom has ADRs, probably more than most drugs you use. When working in rural, especially in high-risk cases like snakebite, keeping the patient and their caretakers informed should be a priority.

Talk about ways to prevent snake bites. These beautiful creatures aren’t violent. Be interested in how the patient was bitten. After a while, you will start recognizing a pattern that you can use to educate the target population. Also, not everyone comes with the snake to the hospital. Have a poster of different types of snakes available. Identifying if the snake was venomous is one of the initial steps, after all. Print the local and national statistics about antivenom use and results and paste them in the waiting area. It will help patient parties calibrate their expectations accordingly.

Summer and rainy seasons are when the unfortunate encounters between humans and snakes happen. It is easy to forget the snakebite management protocol, equipment necessary, what workarounds were used to help us, and what drugs we have in stock. A small refresher session can go a long way in boosting your team’s confidence in treating snakebites.

Cite this article as: Carmina Shrestha, Nepal, "Snakebite: Two years and 200 cases later," in International Emergency Medicine Education Project, February 1, 2021, https://iem-student.org/2021/02/01/snakebite/, date accessed: September 27, 2023

Recent blog posts by Carmina Shrestha

Tired before the long journey

Snakebite: Two years and 200 cases later

Hypoglycemia – A Rural Perspective

The Rural Paradox

COVID-19 Pandemic: Rural Preparations

A case of decreasing resistance in ER

Can I Eat This? – A Helpful Guide To Plant Toxicology – Cardiac Glycosides

July 17, 2020July 10, 2020 ~ Mohammad Anzal Rehman, UAE ~ Leave a comment

Not only is the identification of toxic plants from their gross appearance a commonly tested topic in Emergency Medicine Board Exams, but it is also a necessary skill for doctors operating in institutions where an established Toxicology division does not exist or where the opinion of a specialist in the field is not immediately available.

This is the second part in a series of blog posts dedicated to providing you with original mnemonics and visual aids that serve to highlight a few classes of common toxic plants prominent for both their inclusion in the academic assessment as well as their prevalence in the community. These memory tools will attempt to highlight key features in the identification of well-known toxic plant species and are designed to aid clinicians from various regions of the globe as well as hone the skills of aspiring toxicologists.

Picture the Scene

A 21-year-old female is brought to your Emergency Department via ambulance due to persistent vomiting, abdominal pain, and some dizziness. She is visibly distressed, clutching her stomach, and reports having vomited at least six times over the past 3 hours. Her brother reports that she had been feeling ill with reported abdominal cramping and diarrhea for the past two days. Earlier that day, she had been given some herbal soup to help with her abdominal cramps by her grandmother, who had prepared it using leaves and flowers from the backyard garden. Soon after drinking the soup, the patient was reported to have multiple episodes of vomiting and began to experience some occasional dizziness, prompting contact of Emergency Medical Services and transfer to the hospital.

Upon initial examination, the patient’s vital signs were significant for a heart rate of 50 beats/minute with a Blood Pressure of 135/76 and spO2 of 95% on room air. No fever, abnormal breathing patterns, or signs of poor perfusion were noted. An Electrocardiogram (ECG) was done and revealed bradycardia, with a first-degree AV block, but no other T wave, QT, ST, or QRS segment abnormalities.

A laboratory workup was initiated, and the patient was given IV Atropine for her bradycardia. A Venous Blood Gas (VBG) was remarkable for hyperkalemia of 6.8 mEq/L with no acid/base disturbance. Therefore, treatment for hyperkalemia was initiated with IV Dextrose and Insulin as per standard management. When bradycardia persisted, a second dose of IV Atropine was given. The patient’s heart rate improved, but the blood pressure was noted to drop down to 95/68. After that, IV fluids were initiated, and the possibility of toxic ingestion explored by asking the patient’s brother for details of the ingredients present in the herbal soup.

The brother contacted the family at home and provided a picture of the plant used, as shown in Figure 1. The in-house Medical Toxicologist was shown the image and confirmed that the patient was suffering from Cardiac Glycoside toxicity secondary to the ingestion of an Oleander plant species.

Figure 1- Photograph of the flower used to make herbal soup. The flower was correctly identified as part of the toxic Oleander species.

Overview of Cardiac Glycoside Toxicity

Cardiac glycosides and related cardenolides represent a group of compounds that exhibit their effects primarily through their action on the Sodium-Potassium (Na+/K+) ATPase pump in cardiac myocytes and other tissues.[1] Inhibition of this pump, as outlined in Figure 2, causes an increase in intracellular Sodium (Na+), with subsequent activation of the Sodium-Calcium (Na+/Ca2+) exchanger, resulting in accumulation of intracellular calcium (Ca2+).

The increased intracellular Ca2+, along with direct stimulation of vagal tone, produces inotropic effects on the heart, increases ventricular ectopy, causes bradycardia, and impaired conduction through the atrioventricular (AV) node. At the same time, the inhibition of the Na+/K+ ATPase pump can lead to hyperkalemia.[2]

Cardiac glycosides are found in a variety of naturally occurring plant and animal species. Acute poisoning often presents with gastrointestinal manifestations (such as nausea, vomiting, abdominal pain or diarrhea), generalized body weakness, and dizziness. However, toxicity can also cause hyperkalemia and cardiotoxicity, represented by bradycardia, heart blocks, and various other dysrhythmias. Death is usually a result of ventricular fibrillation or tachycardia.[3]

Management involves addressing specific symptoms of severe disease. Atropine can be used to increase heart rate and reverse the effects on vagal tone in patients presenting with bradycardia. Reversal of toxicity can be achieved using Anti‐digoxin Fab as with Digoxin overdoses. Hyperkalemia can be managed using a combination of Insulin and dextrose solution to shift potassium back into cells. Activated charcoal may be used for initial decontamination, with Multidose activated charcoal for enhanced elimination.[4]

IV Calcium Chloride or Carbonate use in hyperkalemia was traditionally discouraged in patients suffering from cardiac glycoside poisoning. This was due to concerns that the additional calcium load would result in sustained cardiac contraction, termed as ‘the stone heart.’ However, several studies have since proven that such a phenomenon is unlikely to manifest in patients treated with IV Calcium.[5]

Figure 2- Mechanism of action of cardiac glycosides/digitalis drugs

Identifying Plants with Cardiac Glycoside toxicity

The most prominent species of plants known to contain cardiac glycosides include the foxglove plants Digitalis purpurea and Digitalis lanata, Oleander species (e.g., Nerium oleander and Thevetia peruviana), and Lily of the Valley (Convallaria majalis).[6] These plant species are commonly found in numerous tropical and subtropical countries around the world. Unfortunately, toxicity from accidental or intentional ingestion of their toxic leaves, roots, stems, and seeds is not uncommon and has, in several cases, lead to fatal outcomes for patients.[7-11]

References and Further Reading

Lingrel J. B. (2010). The physiological significance of the cardiotonic steroid/ouabain-binding site of the Na,K-ATPase. Annual review of physiology, 72, 395–412. https://doi.org/10.1146/annurev-physiol-021909-135725
Benowitz, N. (2012). ‘Chapter 61- Digoxin and Other Cardiac Glycosides’ Poisoning & drug overdose. New York, N.Y.: McGraw Hill Medical.
Kanji, S., & MacLean, R. D. (2012). Cardiac glycoside toxicity: more than 200 years and counting. Critical care clinics, 28(4), 527–535. https://doi.org/10.1016/j.ccc.2012.07.005
Roberts, D. M., Gallapatthy, G., Dunuwille, A., & Chan, B. S. (2016). Pharmacological treatment of cardiac glycoside poisoning. British journal of clinical pharmacology, 81(3), 488–495. https://doi.org/10.1111/bcp.12814
Levine, M., Nikkanen, H., & Pallin, D. J. (2011). The effects of intravenous calcium in patients with digoxin toxicity. The Journal of emergency medicine, 40(1), 41–46. https://doi.org/10.1016/j.jemermed.2008.09.027
Hollman A. (1985). Plants and cardiac glycosides. British heart journal, 54(3), 258–261. https://doi.org/10.1136/hrt.54.3.258
Bavunoğlu, I., Balta, M., & Türkmen, Z. (2016). Oleander Poisoning as an Example of Self-Medication Attempt. Balkan medical journal, 33(5), 559–562. https://doi.org/10.5152/balkanmedj.2016.150307
S, Lokesh & Arunkumar.R,. (2013). A clinical study of 30 cases of Acute Yellow Oleander Poisoning. Journal of Current Trends in Clinical Medicine and Laboratory Biochemistry. 1. 29-31.
Haynes, B. E., Bessen, H. A., & Wightman, W. D. (1985). Oleander tea: herbal draught of death. Annals of emergency medicine, 14(4), 350–353. https://doi.org/10.1016/s0196-0644(85)80103-7
Janssen, R. M., Berg, M., & Ovakim, D. H. (2016). Two cases of cardiac glycoside poisoning from accidental foxglove ingestion. CMAJ : Canadian Medical Association journal = journal de l’Association medicale canadienne, 188(10), 747–750. https://doi.org/10.1503/cmaj.150676
McVann, A., Havlik, I., Joubert, P. H., & Monteagudo, F. S. (1992). Cardiac glycoside poisoning involved in deaths from traditional medicines. South African medical journal = Suid-Afrikaanse tydskrif vir geneeskunde, 81(3), 139–141.

Cite this article as: Mohammad Anzal Rehman, UAE, "Can I Eat This? – A Helpful Guide To Plant Toxicology – Cardiac Glycosides," in International Emergency Medicine Education Project, July 17, 2020, https://iem-student.org/2020/07/17/cardiac-glycosides/, date accessed: September 27, 2023

A Song of Ice and Fire

December 25, 2019December 20, 2019 ~ Arthur Martins, Brasil ~ Leave a comment

As the year comes to an end, the holidays approach and, for lots of people, it means traveling to different places around the world. For those who live in the southern hemisphere, like me, the summer comes with al power, with temperatures as high as 35°C (95°F) or 40°C (104°F). For those who live in the northern hemisphere, “the winter is coming” and bring with him temperatures below 0°C (32°F) in some places. With these temperature extremes, we have some conditions to have in mind when working in the ED. How to treat a homeless patient who has slept on the streets on a freezing night? And how about an elderly person who lay on the beach sand under a blazing sun?

Hyperthermia

What is hyperthermia?

By definition, hyperthermia is a condition when there is a failure of the body’s thermoregulatory mechanisms to handle extrinsic and intrinsic heat. It’s common to see the expression “Heat-related Illness” to describe the conditions associated to the exposure to environmental heat.

Physiology

The heat-related illness (HRI) develops following a progressive pattern, divided in 3 phases [1].

ACUTE PHASE:
- Activation of inflammatory mediators, especially in the blood vessels;
- Gastrointestinal tract hypoperfusion, leading to bacterial translocation
- Respiratory alkalosis due to hyperventilation
ENZYMATIC PHASE:
- Coagulopathy, leading to a hypercoagulability state
- Endothelial injury and microvascular thrombosis
- All of this leading to disseminated intravascular coagulation (DIC)
LATE PHASE:
- Liver dysfunction secondary to DIC
- Kidney failure due to dehydration and hypotension
- CNS lesions leading to cerebral edema and hemorrhage
- Cardiovascular dysfunction, worsening hypotension and causing vasoconstriction

Risk Factors

Extremes of age
Obesity
Elevated humidity rate
Lack of acclimatization and/or fitness
Ambient temperature
Dehydration
Cardiovascular disease
Drugs/medication (i.e alcohol, diuretics, amphetamines)

Categories of heat illness

Minor Heat Illness:
- Heat cramps: Intermittent muscle cramps likely related to salt deficiency and muscular fatigue, although the exact mechanism is not well known.
- Heat Edema: Swelling of the feet and ankles typically in non-acclimatized people
- Heat Syncope: Similar to orthostatic hypotension, caused by the physiologic response to the heat: volume depletion, peripheral vasodilatation and a reduced vasomotor tonus. More common in elderly people.
- Prickly Heat: cutaneous rash caused by pores and sweat gland obstruction
Heat Exhaustion:
- Occurs with a moderate elevation in the body core temperature (<40°C or 104°F) – RECTAL temperature is the most reliable method (even though is a level C evidence)
- Usually accompanied by symptoms related to conditions described in the Minor Heat Illness and other nonspecific symptoms like nausea/vomiting, weakness and headache
- DOES NOT PRESENT WITH ALTERED MENTAL STATUS
Heat Stroke:
- Body temperature above 40° (104°F) WITH ALTERED MENTAL STATUS
- Target organ damage
- Usually dry and pale skin, however athletes can present with warm and wet skin

Management

Primary, we need to proceed with the basic measures: secure airway, monitorize and place IV fluids in order to maintain a mean arterial blood pressure > 60 mmHg [2].
The second step is to perform a rapid cooling, targeting a temperature <39°C (102°F) in the first 30 minutes. After reaching this goal, the active cooling should be stopped in order to avoid overshoot hypothermia
- Cold water immersion is the best method available (level C evidence) [3].
  - Treat shivering with benzodiazepines if needed (avoiding extra heat generation)
- DO NOT USE ANTIPYRETICS, they are not effective in this scenario [4].

Disposition

Patients with heat stroke should be admitted to a ICU to monitoring organ dysfunction, electrolytes disturbances and rebound hypothermia.
Young and otherwise healthy patients with heat exhaustion can be discharged home
Be aware for the risk of recurrent hyperthermia when considering discharge a patient (returning to the same ambient)

Hypothermia

What is hypothermia?

Condition in which the body loses heat at a higher rate than its capacity in maintain the core temperature or elevate the heat production
Clinically defined as unintentional decrease of body temperature below 35°C (95°F)
In other settings, we can talk about “secondary hypothermia”, when the patient has an impaired thermoregulation due to a clinical condition such as hypothyroidism, ketoacidosis, malnutrition etc – In this article we will focus on accidental hypothermia, related to environmental exposure

Physiology

Initially, the metabolic rate increases, peripheral blood flow is shunted towards vital structures, and shivering initiates to increase heat production
If these compensations are not enough, the body temperature continues to drop, with the CNS being affected when it reaches 35°C (95°F).
Cardiovascular: initial increase in heart rate and blood pressure; however, as core temperature declines, progressive bradycardia and hypotension occurs. In more severe hypothermia, myocardial irritability increases, leading to a high risk of arrhythmias.
Oxygen consumption: At a temperature of 28°C (82°F), the oxygen consumption is decreased by 50%, leading to a protective effect in CNS and other vital organs – but just if it develops before asphyxia (there are several studies trying to better understand the role of hypothermia as a protective measure in cardiac arrest) [5].

Risk Factors

Fatigue
Sleep deprivation
Rain, wind and water immersion
Burn
Extremes of age
Trauma
Alcohol
Hypoglycemia
Hypothyroidism
Hyperthermia treatment (rapid cooling)

Classification

Stage 1: Mild Hypothermia

Core temperature: 32 – 35°C (90 – 95°F)
Initially presenting with tachycardia, hypertension, shivering and vasoconstriction
Gradually develops ataxia, poor judgement, amnesia, apathy, dysarthria

Stage 2: Moderate Hypothermia

Core temperature 28 – 32°C (82 – 90°F)
Loss of shivering, lethargy, mydriasis, hyporeflexia, alterations in cardiac rhythm (Osborne J waves on EKG)

Stage 3: Severe Hypothermia

Core temperature: 24 – 28°C (75 – 82°F)
Hypoventilation, ventricular fibrillation, acid-basic disturbances, anesthesia, pulmonary edema

Stage 4: Profound Hypothermia

Core temperature: below 24°C (75°F)
Oliguria, fixed pupils, asystole, apnea, coma
Curiosity: 13,7°C (56,7°F) is the lowest temperature registered at which CPR was performed with satisfactory results [6].

Management

The first thing we need to do is to stop the cooling process
- Remove the environmental factor (take the patient out of the street, take off wet clothes etc.)
- Try stop heat loss, putting up barriers like warm clothes, blankets, sleep bags, etc

Second step, we should identify the degree of hypothermia to guide our approach:
- For Mild hypothermia, besides the strategies described before, we need to offer calories (food and warm drinks), monitoring for at least 30 minutes and warm the trunk

- [F]or Moderate hypothermia, we also need to keep the patient laid down and still, start volume reposition with warm fluids (40 – 42°C/104 – 107°F), Avoid food and beverage.

- For Severe hypothermia: All the above and check for pulse and breathing – of pulse/breathing is absent, START CPR. – Consider transferring to a facility where ECMO is available
  - ECMO is the best option for severely hypothermic patients without signs of life who do not respond to initial resuscitative efforts. It has been shown to improve neurologically intact survival (48% to 63% survival with ECMO, <37% without ECMO) [7].

“Nobody is dead until warm and dead”

Patients with core temperatures of <28°C have decreased electroencephalographic activity and loss of brainstem and pupillary reflexes, all of which may mimic death. Because of that, the patient can not be considered “dead” until his body temperature reaches at least 32°C.

Some conditions allow us to presume death even in patients with body temperature below 32°C and no vital signs: obvious lethal injury (i.e. decapitation), frozen body, potassium > 12, avalanche victims with burial > 35min or airway packed with snow.

References and Further Reading

The primary reference for this article was the recently launched book: “Medicina em Áreas Remotas no Brasil” (Wilderness Medicine in Brazil): JULIANA R. M. SCHLAAD e SASCHA W. SCHLAAD, Medicina em Áreas Remotas no Brasil, 1ed, Barueri (SP), Manole, 2020

Other sources of information as numbered and referred in the text:

Powers SK, Howley ET. Regulação de temperatura. In: Powers SK, Howley ET. Fisiologia do exercício: teoria e aplicação ao conhecimento e ao desempenho. 9ed. Barueri: Manole; 2017. p.261-281.
Tran TP. Heat emergencies. In: Ma OJ, Cline DM, ed. Emergency medicine manual. 6th ed. McGraw-Hill, NY: 2004:564-565
Becker J, Stewart L. Heat-related illness. Am Fam Physician. 2011;83(11):1325-1330
Lipman GS, Eifling KP, Ellis MA, Gaudio FG, Otten EM, Grissom CK. Wilderness medical society practice guidelines for the prevention and treatment of heat-related illness: 2014 update. Wilderness Environ Med. 2014; 25:S55-S65
Soar J, Perkins G, Abbas G, et al. European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution. Resuscitation. 2010;81(10):1400-1433.
M. Gilbert, R. Busund, A. Skagseth, Nilsen PÅ, J.P. Solbø Resuscitation from accidental hypothermia of 13.7 degrees C with circulatory arrest Lancet, 355 (2000), pp. 375-376
Brown DJ et al. Accidental hypothermia. NEJM 2012; 367(20): 1930-1938. PMID: 23150960

Cite this article as: Arthur Martins, Brasil, "A Song of Ice and Fire," in International Emergency Medicine Education Project, December 25, 2019, https://iem-student.org/2019/12/25/a-song-of-ice-and-fire/, date accessed: September 27, 2023

Death on the Roads

November 1, 2019October 31, 2019 ~ Ibrahim Sarbay, Turkey ~ Leave a comment

Save the date: 17th November 2019!

Why? Because road victims will be remembered that day. Starting from 2005, The World Day of Remembrance for Road Traffic Victims is held on the third Sunday of November each year to remember those who died or were injured from road crashes (1).

Road traffic injuries kill more than 1.35 million people every year and they are the number one cause of death among 15–29-year-olds. There are also over 50 million people who are injured in non-fatal crashes every year. These also cause a real economic burden. Total cost of injuries is as high as 5% of GDP in some low- and middle-income countries and cost 3% of gross domestic product (2). It is also important to note that there has been no reduction in the number of road traffic deaths in any low-income country since 2013.

Emergency care for injury has pivotal importance in improving the post-crash response. “Effective care of the injured requires a series of time-sensitive actions, beginning with the activation of the emergency care system, and continuing with care at the scene, transport, and facility-based emergency care” as outlined in detail in World Health Organization’s (WHO) Post-Crash Response Booklet.

As we know, the majority of deaths after road traffic injuries occur in the first hours following the accident. Interventions performed during these “golden hours” are considered to have the most significant impact on mortality and morbidity. Therefore, having an advanced emergency medical response system in order to make emergency care effective is highly essential for countries.

Various health components are used to assess the development of health systems by country. Where a country is placed in these parameters also shows the level of overall development of that country. WHO states that 93% of the world’s fatalities related to road injuries occur in low-income and middle-income countries, even though these countries have approximately 60% of the world’s vehicles. This statistic shows that road traffic injuries may be considered as one of the “barometer”s to assess the development of a country’s health system. If a country has a high rate of road traffic injuries, that may clearly demonstrate the country has deficiencies of health management as well as infrastructure, education and legal deficiencies.

WHO is monitoring progress on road safety through global status reports. Its’ global status report on road safety 2018 presents information on road safety from 175 countries (3).

We have studied the statistics presented in the report and made two maps (All countries and High-income countries) illustrating the road accident death rate by country (per 100,000 population). You can view these works below (click on images to view full size).

References and Further Reading

Official website of The World Day of Remembrance, https://worlddayofremembrance.org
WHO. Road traffic injuries – https://www.who.int/news-room/fact-sheets/detail/road-traffic-injuries
WHO. Global status report on road safety 2018 – https://www.who.int/violence_injury_prevention/road_safety_status/2018/en/

Cite this article as: Ibrahim Sarbay, Turkey, "Death on the Roads," in International Emergency Medicine Education Project, November 1, 2019, https://iem-student.org/2019/11/01/death-on-the-roads/, date accessed: September 27, 2023

ELECTRIC SHOCK; Injuries beyond what the eyes see.

October 2, 2019October 4, 2019 ~ Kilalo Mjema ~ Leave a comment

Authors: Dr. Nour Saleh and Dr. Kilalo Mjema

Case presentation

A 53-years-old male, sustained burn wounds on both hands 40 minutes prior presentation to the ED

Primary survey

Airway: patent and protected.
Breathing: bilateral equal air entry
Circulation: warm extremities, capillary refill time is 1 second
- Vitals on presentation
  - BP: 177/114mmHg
  - HR: 115
  - RR: 16
  - SPO2: 96% in room air
  - T: 36.4
Disability: alert and oriented, pupils 5mm bilateral equal light reaction, glucose: 7.3mmol
Exposure: holding his hands up in pain with some black discoloration

SAMPLE History

Sign and symptoms: pain, see pictures
Allergy: no known allergies
Medications: not on any medication
Past medical history: no known comorbid or any significant medical history
Last meal: he ate about 2.5 hours prior presentation
Event: pain on both hands after sustaining burn injury forty minutes prior presentation to the ED while trying to connect two circuits that sparked causing burn wounds on his hands and felt a jolt of electricity.

No history of heartbeat awareness or any loss of consciousness

Interventions and key steps in management

Make sure ABCD is checked and there is no critical intervention needed
IV access and fluid resuscitation may be considered depending on the case
Analgesics: depends on the severity of pain. Fentanyl 50mcg IV stat can be necessary for many patients.
Informed consent for procedural sedation for the dressing of the wounds.
Sedation: during the dressing of wounds
Point-of-care investigations: ECG, Urine dipstick
Blood samples for some labs should be taken; Creatinine, CK, Myoglobin, Electrolytes, Calcium, and Troponin
Imaging: X-ray if there is a worry for associated fracture
Monitor: input of fluids and output of urine to watch for acute kidney injury, compartment syndrome and rhabdomyolysis
Do not forget tetanus immunization

Associated injuries

Cardiac arrhythmias

Ventricular fibrillation is the most common. It occurs in 60% of patients with electrical current traveling from one hand to the other.
Renal - Rhabdomyolysis

Massive tissue necrosis may result in acute kidney injury. Labs to check includes; Creatinine, Blood Urea Nitrogen, Total CK, myoglobin.
Neurological

Damage to both central and peripheral nervous systems can occur. The presentation may include weakness or paralysis, respiratory depression, autonomic dysfunction, memory disturbances, loss of consciousness.
Skin

Degree of injury cannot determine the extent of internal damage especially with low voltage injuries. Minor surface burns may co-exist with massive muscle coagulation and necrosis.
Musculoskeletal

Bones have the highest resistance of any body tissues resulting in the greatest amount of heat when exposed to an electrical current. Results in surrounding tissue damage and potentially may lead to periosteal burns, destruction of bone matrix and osteonecrosis.
Vascular / Coagulation system

Due to electrical coagulation of small blood vessels or acute compartment syndrome.
Internal organs

The internal organ injury is not common but when it happens may result serious problems such as bowel perforations leading to polymicrobial infection, sepsis, and death.

Disposition

Admission and discharge decisions of burn patients depend on the patient’s current situation, burn percentage according to body surface area, location of the burn, and complications of burn. Low voltage electrocutions, if they are asymptomatic with normal physical examinations, can be discharged. Discharge precautions regarding burn care and complications should be clearly explained to the patient and relatives.

A Farmer’s Dilemma

July 19, 2019September 4, 2019 ~ Shaza Karrar, UAE ~ Leave a comment

Case Presentation

It was a rainy night preceding my morning shift as a year 3 EM resident at one of our training centers in Abu Dhabi. The paramedics barged in with an agitated patient, who was found soaking wet in a farm field.

According to brief history that we got from the paramedics, the patient works at a farm and his boss found him collapsed, cold to touch and confused in the early morning hours. Paramedics also reported a confused, hypothermic, and tachycardic patient. They brought him directly to the ED, with no accompanying friends or family.

As we proceeded to resuscitate the patient, we noted that his initial vital signs did confirm hypothermia of 32 Celsius measured rectally, tachycardia, hypertension, and normal O2 saturation. We hooked him to the monitor, removed his wet clothing, gained IV access, started him on warm IV fluids, and covered him with blankets and a warming Bair Hugger (a warming blanket system).

Physical Exam

The patient was confused, agitated and uttering incomprehensive words, with a GCS of 11 (E3 V3 M5). I proceeded to examine him looking for more clues of why he was laying semiconscious under the rain all night. Systematic physical examination revealed pinpoint pupils, frothing and excessive salivations. Furthermore, diffuse mild crackles were noted on chest auscultation, and he was tachycardic with a regular rate and rhythm. Remaining physical exam was unremarkable, and a complete neurological exam was challenging.

Differential Diagnosis and Workup

Thinking of a broad differential diagnosis of altered mental status, systematic consideration of all possible etiologies similar to our patient presentation was reviewed. We have considered metabolic derangements, head trauma, CNS causes such as seizures and post-ictal status, infectious causes such as pneumonia or meningitis, and toxicologic causes, such as alcohol withdrawal, or medications overdose.

You may find useful this mnemonic for altered mental status!

Further management plan included giving him benzodiazepines for the agitation and possible post-ictal status. We collected basic blood work and proceeded for a head CT to rule out traumatic or atraumatic intracranial pathologies. Blood workup was inclusive of an alcohol level, Aspirin, Acetaminophen level, and a urine toxicology screen.

As the patient returned from the CT, he apparently had passed the copious amount of loose stools, that smelled surprisingly like garlic that studded the ED with its smell.

The head CT was normal, and most of his blood workup came back unremarkable. But, he remained confused and agitated as the benzodiazepines were wearing off and despite all the warming measures. ECG showed only sinus tachycardia, and a chest X-Ray was unremarkable.

smells like garlic!

What do you think? What are the causes for this?

agents smells like garlic

phosphorus, tellurium, inorganic arsenicals and arsine gas, organophosphates, selenium, thallium, dimethyl sulfoxide

Learn More

The garlic smell did give us a lead though, we thought further of possible toxic agents that may give such a smell, along with a consistent similar clinical picture.

Case Management and Disposition

Collecting our clues once more, we had pinpoint pupils, frothing, salivation, wet lungs, vomiting and loose motions. Patient’s collective symptoms and signs indicated a Cholinergic Toxidrome, possibly due to Organophosphates ingestion.

The patient was already decontaminated with removal of all his clothes. All healthcare providers were equipped with personal protective equipment.

This was confirmed an hour later when his farm owner showed up with a Pesticides Bottle that he found near him in the early morning hours before calling an ambulance. Pesticide is shown in Figure. The content of the bottle is consistent with Organophosphates Toxicity, and hence his Cholinergic Toxidrome.

He was started on Atropine, and Pralidoxime, assessed and admitted to the ICU with arranged psychiatric consult to assess his suicidal ideations once he stabilizes.

Critical Thinking and Take-home Tips

What is Toxidrome?

A collection of symptoms and physical signs caused by a certain toxic agent.

What are the main Toxidromes I should be familiar with?

Cholinergic
Anticholinergic
Sedative/Hypnotic
Sympatholytic
Sympathomimetics

What is Cholinergic Toxidrome?

Cholinergic toxicity represents a cholinesterase inhibitor poisoning. It results from the accumulation of excessive levels of acetylcholine in synapses. Clinical picture resulting from the Acetylcholine build up depends on the type of receptors that it stimulates and where is it found in the body. It can stimulate the nicotinic and muscarinic receptors. The balance of these stimulations reflects such clinical presentations.

What are the clinical features of an Organophosphates toxicity? (1)

Think of the symptoms that can be caused depending on the type of receptors affected by the buildup of acetylcholine.

Muscarinic Receptors – SLUDGE(M)

Salivation
Lacrimation
Urination
Diarrhea
Gastrointestinal pain
Emesis
Miosis

Nicotinic Receptors (NMJ) – MTWThF

Mydriasis/Muscle cramps
Tachycardia
Weakness
Twitching
Hypertension
Hyperglycemia
Fasciculations

What are the common causes of mortality in such cases?

These are called the Killers B’s which consist of Bradycardia, Bronchorrhea and Bronchospasm.

How to Treat Cholinergic Toxicity?

Decontamination should always be considered first in all cases with possible hazardous exposure from the patient and his environment to all health care providers in contact with him. All caregivers should wear appropriate personal protective equipment’s and make sure to remove all clothing and possible objects with the suspected contaminant.

Supportive care is a cornerstone to all unstable patients, make sure that they are monitored, with proper IV access and supplemental oxygen as needed.

Furthermore, airway management is lifesaving in similar patients, as bronchorrhea is one of the killer B’s and can lead to high fatality.

Antidotes such as Atropine and Pralidoxime in Cholinergic toxicity are paramount, as they help reverse the etiology, and prevent further worsening of the toxicity.

Make sure that such patients are admitted under needed specialty care with proper observation and reassessment for the patient.

Consult a toxicologist if feasible in your center to provide you with further management details and interventions that can help your patients better.

Conclusion

Organophosphates can be found in pesticides, chemical weapons such as nerve gases, and few medications as well such as neostigmine or edrophonium. They are highly lipid soluble making them easily absorbed via breathing and skin contact as well. Encountering similar patients, it is quite important to always be systematic in your approach, resuscitate your patient first, and make sure to use your history taking as feasible and physical examination to collect all the clues needed to narrow down your differentials and find the most appropriate treatment needed for your patient.

References and Further Reading

Organophosphate toxicity on WikEM: https://www.wikem.org/wiki/Organophosphate_toxicity
Das RN, Parajuli S. Cypermethrin poisoning and anti-cholinergic medication- a case report. Internet J Med Update. 2006;1:42–4.
Aggarwal, Praveen et al. “Suicidal poisoning with cypermethrin: A clinical dilemma in the emergency department.” Journal of emergencies, trauma, and shock vol. 8,2 (2015): 123-5. doi:10.4103/0974-2700.145424
Lekei EE, Ngowi AV, London L. Farmers’ knowledge, practices and injuries associated with pesticide exposure in rural farming villages in Tanzania. BMC Public Health. 2014;14:389. Published 2014 Apr 23. doi:10.1186/1471-2458-14-389

Adventures on the Annapurna Circuit

July 12, 2019September 4, 2019 ~ Helene Morakis, Canada ~ Leave a comment

For this blog entry, I want to share two issues I encountered while traveling in Nepal, just shy of my graduation from medical school: acute mountain sickness (AMS) and responding to a wilderness medicine incident as a medical trainee.

There is nothing more glorious

There is nothing more glorious than the period just after finishing medical school and before residency! For me, the highlight was being able to hike in Nepal. With the long travel time from Canada, and the multi-day itineraries most hikes necessitate, the post-grad period seemed like the ideal opportunity to make my dream of visiting the Himalayas come true.

I wrote my medical licensing exam, hopped on a flight and got ready to soak up the change of pace. While traveling, I found time to relax, (tried my best to) practice mindfulness and experienced the incredible kindness of Nepali people. Traveling was the perfect recharge that now has me geared up and excited for residency.

Annapurna Circuit

A few weeks before leaving for my travels, I began researching the Annapurna Circuit (APC). Having grown up at a staggering 240m above sea level in the Canadian prairies, I felt threatened by the Thorong La pass, which at 5416m is the highest part of the trek. My highest previous experience at altitude was 4200 meters, where I (unfortunately) developed Acute Mountain Sickness (AMS). My history of having AMS and following a typical itinerary for the APC put me at moderate risk for AMS(1). I decided to heed the Wilderness Medicine Society’s recommendation to take acetazolamide 125mg every 12 hours as prophylaxis(1).

While on the trek, I overheard many myths about AMS and sensed a general reluctance to take acetazolamide as prophylaxis(2). Himalayan Rescue Association does free daily teaching about AMS on the APC in Manang and on the Everest Base Camp trek as well(3). As we moved to higher altitudes, many guest houses and Annapurna Conservation Area Project outposts had accurate information about AMS and its consequences (High Altitude Pulmonary Edema and High Altitude Cerebral Edema). Surprisingly, despite this teaching and the availability of acetazolamide on the trail for purchase, there are still hikers that routinely require evacuation due to AMS, some by helicopter.

On the day before crossing the Thorong La Pass, I stopped for lunch with some trekking mates at Thorong Phedi (4538m). A few minutes passed before someone came into the guesthouse, visibly worried, requesting help from a doctor. It took me a few seconds (and my friends practically lifting me off my seat) to register that I could help! I was thankful to be hiking with an experienced nurse and we went to see the hiker together.

We were asked to see a fit hiker in his 60’s whose foot had been the victim of a rockslide. I clarified my training as a fourth-year medical student before asking details about the mechanism of injury and his past medical history. The hiker and his family were concerned and asked me to “rule out” a fracture. With positive Ottawa Ankle Rules findings, I wished for an X-Ray machine to rule out a clinically significant fracture(4). Keeping in mind there was no road access – the nearest road before the camp was in Manang (3500m, 15km away) or in Muktinath (3800m, 16km away) after the pass – the only ways out were by donkey or helicopter.

From a wilderness medicine standpoint, the injury was by all measures considered stable and the patient did not require an evacuation [reproduced from Isaac & Johnson 2013](5):

No deformity or instability on exam
No sense of instability reported by patient
Able to move and weight bear after accident
Distal circulation, sensation, movement (CSM) intact
Slow onset of swelling
Pain proportional to apparent injury

After a discussion with the patient, we decided that treating the injury as “stable” was reasonable and accepted the risk of delaying healing of a potential fracture. I recommended 24 hours of rest, ice (which kept the patient’s family busy fetching snow!), and elevation. I gave them ibuprofen to be administered on a regular schedule and instructed them to monitor CSM and plan an evacuation if there were any signs of impairment. I told the patient to continue the hike the following day if the pain did not increase with activity and to obtain medical follow up once they had returned to the city.

In hindsight, I recognized that I should have documented the encounter. I had written down the dosing of ibuprofen for the family, but I did not write a detailed SOAP (subjective, objective, assessment and plan) note. Properly documenting wilderness medicine encounters was a skill I learned in Advanced Wilderness Life Support. When we met the patient, he was generally well other than his foot injury. What if the patient’s condition worsened? What if the family forgot the plan in the stress of the situation?

I also found myself wondering about this patient long after I had left them. Reflecting upon this, I recognized that it is easier to “discharge” someone from an urban Canadian ED, where I have had most of my clinical experience because I know they can access good care if things change. The huge potential on the trail for loss to follow up made documentation much more vital in this case.

Later on, I pondered about the potential legal ramifications of helping this hiker. In Ontario, Good Samaritan laws protect health care professionals who provide first aid(6). From my understanding, there are no similar laws in Nepal, and there have been calls to define the rights and duties of those who witness or are requested to aid with an injury in the country(7).

In Nepal, I had a much-needed change of pace from medical school and plenty of time for reflection. I was inspired to see many organizations work together to educate guides, locals and hikers about AMS and hope to spend some time volunteering at the Himalayan Rescue Association in the future. Even after wilderness medicine training, being asked to provide first aid on the trail as a soon to be medical graduate caught me by surprise. I was happy to help and be able to have an approach to the patient in a low resource setting – and now recognize the importance of documentation.

I would like to hear your comments on this article: any experiences dealing with AMS, tips and tricks for musculoskeletal injuries in the wilderness setting, advice for navigating giving medical treatment outside of a hospital as a trainee or anything you would have done differently.

References

Luks, A. M., Auerbach, P. S., Freer, L., Grissom, C. K., Keyes, L. E., McIntosh, S. E., … Hackett, P. H. (2019). Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Acute Altitude Illness: 2019 Update. Wilderness & Environmental Medicine. https://doi.org/10.1016/j.wem.2019.04.006
Kilner, T., & Mukerji, S. (2010). Acute mountain sickness prophylaxis: Knowledge, attitudes, & behaviours in the Everest region of Nepal. Travel Medicine and Infectious Disease, 8(6), 395–400. https://doi.org/https://doi.org/10.1016/j.tmaid.2010.09.004
Himalayan Rescue Association. (2019). [online] Available at https://himalayanrescue.org.np/ [Accessed 30 Jun. 2019].
Stiell IG, Greenberg GH, McKnight RD, Nair RC, McDowell I, Worthington JR. A study to develop clinical decision rules for the use of radiography in acute ankle injuries. Ann Emerg Med. 1992; 21:384–90.
Isaac, J. E., & Johnson, D. E. (2013). Chapter 13: Musculoskeletal Injury. In Wilderness and Rescue Medicine (pp. 84–85). Burlington, MA: Jones & Bartlett Learning.
Good Samaritan Act, Government of Ontario (2001). Retrieved from the Ontario e-Laws website: https://www.ontario.ca/laws/statute/01g02
Pandey, S. (2014). Good Samaritans. [online] The Kathmandu Post. Available at: https://kathmandupost.ekantipur.com/news/2014-07-13/good-samaritans.html [Accessed 30 Jun. 2019].