Category: Environmental Emergencies

Drowning (2024)

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by Mark E O’Brien & Elizabeth L DeVos


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You Have A New Patient!

A 14-year-old boy with no prior medical history was just brought to the Emergency Department (ED) by bystanders after being pulled from a large creek that serves as a popular swimming location. According to his friends, the patient jumped feet-first from a small bridge about 2 meters above the water and did not resurface. His body was found floating further down the creek approximately five minutes later, and a nearby nurse immediately began CPR. 

The image was produced by using ideogram 2.0.

He was transported to the hospital in the back of a truck, with CPR reportedly being performed continuously during the 10 minutes it took to arrive. On arrival at the ED, the patient is found to be pulseless, apneic, and cyanotic. You are called over to manage this patient’s care. What do you do?

What Do You Need To Know?

The World Health Organization (WHO) defines drowning as “the process of experiencing respiratory impairment from submersion or immersion in liquid,” with outcomes classified as either death, morbidity, or no morbidity [1]. This definition simplifies and standardizes the language used to describe drowning and eliminates potentially confusing terminology. It replaces previously used terms, including wet, dry, active, passive, silent drowning, secondary drowning, near-drowning, and drowning with a fatal outcome.

Drowning is a significant public health threat that is estimated to cause the death of more than 40 people every hour of every day [2]. It is believed that the current data severely underestimates the actual incidence and mortality of drowning, especially in low-income and middle-income countries (LMICs), where more than 90% of drowning-related deaths occur [3]. As drowning is considered to be highly preventable, there has been much research into and focus on drowning prevention. However, improvement in the quality of medical care provided to drowning victims can also help decrease the mortality and morbidity associated with drowning.

Epidemiology

There were more than 2.5 million deaths attributed to drowning in the past decade, with an estimated 236,000 drowning deaths occurring in 2019, according to the WHO’s most recent Global Health Estimates [4]. The vast majority (>90%) of drowning deaths worldwide occur in LMICs. Drowning remains the third highest cause of unintentional injury-related deaths worldwide and the second highest in terms of Years of Life Lost (YLL) [5].

It is important to note that drowning incidence and mortality are believed to be significantly underestimated and may exceed five times the rates reported by the WHO. Drowning deaths due to causes such as suicide, homicide, transport/vehicular incidents, or natural disasters are usually reported under those categories of death instead of being classified as deaths due to drowning. Additionally, drowning deaths in LMICs are typically derived from hospital data, which often excludes those who perish outside of the hospital, particularly in rural and medically underserved areas. Nonfatal drownings are also underreported, as most individuals who return to their baseline without any morbidity are unlikely to seek hospital care [6].

Risk Factors

There is a higher incidence of drowning in pediatric patients, and those aged 1–4 years old are at the greatest risk of death from drowning [5]. It is likely that natural curiosity about their environment, coupled with a lack of swimming skills and poor adult supervision, are the main factors behind the high drowning incidence and mortality in extremely young children. Most pediatric drowning deaths occur in and around the home. In LMICs, cisterns, wells, and small bodies of water such as streams and ponds are the most likely drowning locations for young children, as they tend to be uncovered and close to home. Adolescents and teenagers tend to drown in larger bodies of water, as they are more adventurous and willing to take risks, especially in the presence of friends and peer pressure [2].

Men are at a higher risk of drowning than women, and 75% of recorded LMIC drowning victims were males [5]. Men are more often out on open bodies of water through water-related careers, including fishing and shipping, which greatly increases the risk of drowning [7]. Men are also more likely to participate in risky behaviors such as alcohol use, which can lead to disastrous consequences when combined with recreational or professional aquatic activities [8]. The combination of men engaging in riskier jobs and behaviors that put them in direct contact with large bodies of water is considered a major factor behind the increased drowning rate in males compared to females.

There are a number of additional factors that have been noted to correlate with an increased risk of drowning. Those with medical conditions that can quickly incapacitate them, including epilepsy and cardiac arrhythmias, are at a higher risk of drowning when bathing or participating in recreational aquatic activities [9]. Alcohol use significantly increases the risk of drowning, especially when combined with activities such as boating and fishing [8]. In 86% of drowning cases in LMICs, the victim was reportedly unable to swim. Despite this direct correlation between swimming ability and drowning mortality, swimming lessons are still not commonly available or prioritized in LMICs [2].

There is a correlation between daytime and drowning, as almost all drowning events in LMICs occur during daytime hours. However, this is believed to be simply because most people in LMICs are outside much more frequently during the day and tend to stay indoors at night. Environmental factors have also been noted to correlate with increased drowning incidence in LMICs, as the rate of drowning increases with increased rainfall patterns and higher temperatures. This is thought to result from increased volume in local bodies of water and increased exposure to water sources during these times. The effects of climate change exacerbate these environmental factors and play a role in increasing the frequency and severity of flooding, hurricanes, cyclones, and other natural disasters, which raise the risk of death by drowning [10].

Pathophysiology

Prolonged or unexpected submersion results in panic, air hunger, and breath-holding as the victim attempts to surface. As hypoxia progresses and the inspiratory drive becomes too strong to resist, involuntary gasps are triggered, breath-holding is overcome, and the victim begins to aspirate water. Aspiration of 1 to 3 mL/kg of water into the airways is enough to cause direct alveolar membrane injury, washout and dysfunction of pulmonary surfactant, and ventilation-perfusion mismatch [11]. Pulmonary complications, including alveolar collapse, atelectasis, noncardiogenic pulmonary edema, intrapulmonary shunting, and secondary pulmonary infection, can occur. The victim may develop profound metabolic and respiratory acidosis secondary to hypercarbic respiratory failure and lactic acidosis. If hypoxia persists, the patient will enter cardiac arrest, develop anoxic brain injury, and eventually die [12]. Even after being removed from water, a drowning patient may remain hypoxemic for a prolonged period of time, resulting in damage to other organ systems.

Medical History

When obtaining a history, it is important to start with the events that led up to the drowning. Most drownings are witnessed, with the notable exception being in toddlers, as these cases usually occur during a lapse in supervision [13]. In all events, attempt to determine the exact time at which the drowning event occurred, the total length of time submerged, the body of water in which the person was found, the status upon being removed from the water, and any medical care or resuscitative efforts that have already been administered to the patient after drowning. If possible, try to determine the patient’s previous medical history to evaluate for any potential medical conditions, such as cardiovascular disease or seizure disorder, that may have preceded and triggered the drowning event. Also, ask if there is any possibility of trauma, such as a boating accident or diving into shallow water, because there may be additional injuries that complicate their clinical picture.

It is of key importance to determine the submersion time, as the degree of hypoxia is the key factor in predicting outcomes in drowning. Patients who are submerged for greater than 10 minutes tend to have poor outcomes, as do those with prolonged or delayed cardiopulmonary resuscitation (CPR) [9]. Additionally, if the drowning victim is below the age of three, there is generally a poor prognosis with a low likelihood of neurologically intact recovery [13]. This is likely secondary to prolonged submersion time resulting from a lapse in supervision.

Physical Examination

Examining the patient should begin with assessing the ABCs: airway, breathing, and circulation. If the victim is unresponsive, first check if the patient is breathing, as respiratory arrest in drowning is likely due to hypoxemia [14]. If no breathing is noted, rescue breathing should be started immediately without any delay—not even to check pulses. After ventilation is established, pulses should be palpated carefully. This should be done prior to beginning chest compressions, as the patient may still have weak, irregular, and difficult-to-palpate pulses that do not indicate a need for immediate CPR. Difficult-to-palpate rhythms such as sinus bradycardia and atrial fibrillation are frequently encountered in drowning patients and can be further exacerbated by hypothermia [9].

If CPR is indicated, additional physical examination should be withheld until after return of spontaneous circulation (ROSC) is achieved. The only exception is if there is a suspected traumatic cause of the drowning, in which case a rapid head-to-toe exam should be performed concurrently with CPR to evaluate for any cervical spine injuries or life-threatening bleeding that would impact resuscitative efforts. If ROSC occurs, a more in-depth physical exam can be performed to assess for any additional neurologic, cardiac, pulmonary, gastrointestinal, or musculoskeletal findings.

Alternative Diagnoses

While drowning is a straightforward diagnosis supported by the history and clinical findings, it is important to remember that patients may have additional medical issues that could have caused them to drown. Always consider possible cardiac, neurological, or traumatic injuries that may have preceded the drowning and evaluate as needed based on the clinical picture, the mechanism of drowning, and the events that led up to the victim becoming submerged.

Acing Diagnostic Testing

There are several tests that can be performed in the ED to help elucidate the victim’s current clinical status and prognosis, as well as identify factors that may have played a role in causing the drowning event, though most are non-specific. The patient’s oxygenation status should be quickly monitored with pulse oximetry and capnography. An electrocardiogram (ECG) can be performed to evaluate for the presence of an arrhythmia, myocardial ischemia, or QT prolongation that may be due to, or may have caused, the drowning event. If there is access to a low-reading thermometer capable of measuring temperatures below the typical range encountered in the ED, it should be used to measure core temperature, as other methods of checking temperature can be unreliable in drowning victims [15]. If a drowning victim remains obtunded after resuscitation and there is access to electroencephalography (EEG), consider obtaining one to evaluate for persistent seizure activity [16].

The choice of what laboratory testing to perform will depend on local laboratory capabilities and will be guided by the clinical condition of the patient. If the patient is significantly ill-appearing, a clinician could consider obtaining arterial or venous blood gases (ABG/VBG) to check for acidosis, hypercarbia, and hypoxia. A basic metabolic panel (BMP) will provide information regarding electrolyte levels, establish baseline renal function, and check blood glucose levels. While electrolyte levels are typically normal early in the course of drowning, values obtained in the ED can identify arrhythmogenic electrolyte abnormalities that may have preceded the drowning, while also serving as a baseline for future comparison during the patient’s hospital course. Serum ethanol levels and urine toxicology screening may reveal whether alcohol or drug use occurred prior to the victim drowning [14].

Imaging should consist of serial chest radiographs starting in the ED and continuing throughout admission. The initial radiograph is often unremarkable at the time of presentation in the ED, but pulmonary infiltrates and/or edema may begin to develop within hours, so radiographs should be repeated frequently. Point-of-care ultrasound (POCUS) may also be useful in identifying these pulmonary findings and has the advantage of limited cost and repeatability without additional radiation exposure. Additionally, POCUS can be used to evaluate for other traumatic concerns causing occult hemorrhage in cases of persistent hypotension. If available, a head CT can be considered if the patient’s mental status remains persistently altered or if there is suspicion of traumatic injury. Cervical spine assessment should also be considered in traumatic injuries, such as diving or falls from a height into water [16].

Management

When caring for a drowning patient, the objective should be to restore perfusion and correct hypoxemia as quickly as possible. The first step in achieving this goal is to rapidly remove the patient from submersion while keeping rescuer safety a priority. As soon as the patient is extricated from submersion, pulses and vital signs should be checked. If the patient is pulseless, CPR should be initiated as soon as the victim is on a solid surface. Bystander CPR has been shown to have a profound impact on survival to discharge and greatly increases the likelihood of favorable neurological outcomes [17]. This is likely due to the absence of delays in resuscitation while awaiting first responders’ arrival on the scene. Ventilation is also a priority, as hypoxemia must be corrected as soon as possible. Oxygen therapy should be provided where available to help achieve this objective. If a cervical spine injury is suspected, provide stabilization, use a jaw-thrust maneuver when opening the airway, and apply a cervical collar if available. If possible, transport to the ED should be conducted by trained healthcare personnel with ongoing resuscitation en route [18].

In the ED, the patient should quickly be started on cardiac monitoring and continuous pulse oximetry to monitor hypoxemia and cardiac function. Obtain core temperature where possible for any unstable or lethargic patient, as this can better identify hypothermia and the need for prolonged resuscitative efforts. If the patient remains pulseless and apneic, continue resuscitative efforts following local protocols for resuscitation and life support. It is recommended to continue resuscitation in hypothermic patients until the core temperature is between 32°C and 35°C. Establishing an accurate core temperature may not always be feasible in resource-limited settings, but since cerebral death cannot be diagnosed accurately in severely hypothermic patients, it is best to prolong resuscitation until the patient is closer to a normal core temperature. Active rewarming can be performed in severely hypothermic patients. Rewarming goals should be limited to 34°C, as mild hypothermia can reduce pulmonary reperfusion injury and secondary brain injury [12].

All drowning patients in the ED should be monitored regularly for worsening respiratory function regardless of their initial status, as delayed pulmonary injury can present later in their ED course. Correcting hypoxia is of the utmost importance. Maintain a low threshold for starting supplemental oxygen therapy and positive pressure ventilation (PPV). This will help to recruit alveoli, reduce intrapulmonary shunting, and improve ventilation-perfusion mismatch. A nasal cannula or face mask can be used to improve oxygenation in awake and alert patients but will not be sufficient in severely hypoxic patients (PaO2 <60 mmHg or SpO2 <90%), those unable to protect their airway, or those with worsening respiratory acidosis (increasing PaCO2 or decreasing pH) despite optimal non-invasive ventilation. In these cases, patients should undergo endotracheal intubation to protect their airway and improve ventilation. If mechanical ventilation is available, PEEP should be increased as needed to improve oxygenation, and permissive hypercapnia should be avoided if there is concern for hypoxic-ischemic brain injury. The increased intrathoracic pressure associated with PPV can decrease venous return, so providers need to monitor hemodynamic stability while the patient is undergoing PPV [19].

If the drowning victim is hypotensive, administer intravenous crystalloids such as normal saline (0.9% NaCl solution) or Lactated Ringer’s. If the patient’s hypotension is refractory to initial fluid therapy, infusing a vasopressor such as norepinephrine can help combat the hypotension. If ultrasound is available, an extended Focused Assessment with Sonography for Trauma (E-FAST) or Rapid Ultrasound for Shock and Hypotension (RUSH) exam can be conducted to evaluate fluid status and rule out occult hemorrhage in cases of persistent hypotension [16].

Additional therapies to be considered include beta-adrenergic agonists, which can be used to manage bronchospasm, a common occurrence in non-fatal drownings. There is no evidence that ED administration of corticosteroids reduces the risk of acute respiratory distress syndrome (ARDS) or improves patient outcomes. Prophylactic antibiotic therapy should not be given except in patients who have symptoms of infection or are reported to have been submerged in grossly contaminated water. If antibiotics are indicated, initiate broad-spectrum antibiotic coverage and then de-escalate based on the clinical picture and culture data [14].

Risk Stratification

Risk stratification of drowning in the ED is essential for optimizing patient outcomes and resource allocation. Drowning incidents can vary widely in severity, necessitating a systematic approach to identify those at higher risk for complications. Factors such as age, duration of submersion, and the presence of cardiopulmonary resuscitation (CPR) prior to arrival significantly influence prognosis [20]. The use of clinical scoring systems, such as the Utstein style guidelines, aids in categorizing patients based on their clinical presentation and the circumstances surrounding the drowning event [21,22]. Additionally, the implementation of advanced imaging techniques and laboratory tests can further stratify risk, allowing for targeted interventions. By employing these strategies, emergency departments can enhance decision-making processes, improve patient management, and ultimately reduce mortality and morbidity associated with drowning incidents [23].

Special Patient Groups

Pediatrics

Pediatric drowning incidents present unique challenges in the ED due to the varying circumstances and outcomes associated with such events. Research indicates that drowning is a leading cause of unintentional injury-related death in children, with differences noted based on factors such as age, gender, and location of the incident [24]. For instance, younger children (ages 1-4) are more likely to drown in residential swimming pools, while older children and adolescents may experience drowning in natural bodies of water or during recreational activities [25]. Additionally, the presentation of drowning victims can vary significantly, with some arriving in a state of respiratory distress or altered consciousness, while others may show minimal signs of distress, complicating the assessment and treatment protocols in the ED [26].

Pregnant Patients

Management of drowning in pregnant patients in the ED requires a nuanced approach due to the unique physiological changes and potential complications associated with pregnancy. Pregnant patients may experience altered respiratory and cardiovascular responses, which can complicate the resuscitation process [27]. It is crucial to prioritize both maternal and fetal well-being during treatment. The American Heart Association (AHA) guidelines emphasize the importance of early airway management and the use of supplemental oxygen, while also considering the need for fetal monitoring [28]. Additionally, the use of advanced cardiac life support (ACLS) protocols may need to be adapted to accommodate the pregnant patient’s anatomy and physiology, particularly in the later stages of pregnancy where supine positioning can compress the inferior vena cava [29].

Geriatrics

Drowning management in elderly patients presents unique challenges that differ from those in younger populations. Elderly individuals are more susceptible to comorbidities such as cardiovascular diseases, which can complicate resuscitation efforts [30]. Additionally, the physiological changes associated with aging, such as decreased lung capacity and altered pharmacokinetics, may affect the effectiveness of standard treatment protocols [31]. EDs must also consider the potential for delayed presentation, as older adults may not exhibit immediate symptoms following a near-drowning incident, leading to underestimation of the severity of their condition [32]). Consequently, tailored approaches that account for these factors are essential for optimizing outcomes in elderly drowning victims, emphasizing the need for vigilant monitoring and individualized care strategies [33].

When To Admit This Patient

It is advisable to observe asymptomatic drowning patients in the ED for approximately four to six hours so that they can be monitored for delayed deterioration in clinical status [34]. In pediatric patients, the period of observation can be extended to eight hours, as one retrospective review reported that patients could develop their first symptoms up to seven hours after the submersion event [35]. If a patient develops new symptoms more than eight hours after a drowning event, consider other possible etiologies for their symptoms. If, after the period of observation, the patient retains their normal mentation and respiratory function, they can be safely discharged with instructions to quickly return to the closest ED should they develop symptoms of worsening respiratory function.

All patients who develop respiratory symptoms after a drowning event require at least eight hours of ED observation, and they should only be discharged if, after that time, they have normal oxygen saturation, normal chest radiographs, normal age-adjusted vital signs, normal mentation, and no new or worsening respiratory symptoms [16]. Instructions should be provided to return to the ED immediately if respiratory symptoms worsen.

Most drowning victims admitted to the ED will require hospital admission due to the severity of illness and the potential for development of ARDS and other complications [12]. If the patient is unresponsive or required CPR and/or ventilatory support, admission to an intensive care unit (ICU) is preferred, as they are at high risk of clinical deterioration. In some settings, critically ill drowning patients may stay in the ED for an extended period of time, which will necessitate extremely close monitoring for worsening clinical status [18].

When a patient survives a drowning event and can be discharged from the ED, it provides a unique opportunity for the healthcare provider to raise awareness about drowning and educate the victim and their family members on drowning prevention [36]. Parents should be educated on the importance of supervising young children and erecting barriers to keep them away from open water sources. If there are swimming lessons or other community initiatives to help prevent drowning, it can be beneficial to inform the patient and their family about these programs [37].

Revisiting Your Patient

Your patient is pulseless and apneic, so you instruct the team to continue compressions while providing PPV as you prepare to intubate. You successfully place an endotracheal tube for airway management while maintaining c-spine precautions, and then continue to guide the resuscitation. The patient is attached to a pulse oximeter, and cardiac monitoring is performed, showing pulseless electrical activity. ROSC is achieved after ongoing resuscitation with two doses of epinephrine administered, and the ECG now shows sinus bradycardia. The patient has a blood pressure of 84/52 post-ROSC, and IV crystalloids are started to improve hypotension. An E-FAST exam shows no evidence of occult bleeding. Tympanic temperature is measured at 35.1°C. No additional findings are noted on a head-to-toe physical exam. Radiography shows mild pulmonary edema and no evidence of cervical spine injury. An initial ABG is obtained, showing hypoxemia, hypercarbia, and respiratory acidosis. The only noted abnormality on the BMP is a mildly elevated HCO3-.

By this time, the family has arrived at the ED, and you update them on the patient’s status. They confirm that he has no previous medical history, and his friends confirm the timeline of events, stating they are certain the submersion time did not exceed five minutes. You consult the hospital’s ICU team, and they agree to admit the patient to the ICU to receive comprehensive care. A few days later, you follow up on the patient and learn that, while he developed ARDS in the ICU, he has been gradually improving, is expected to come off the ventilator soon, and has a favorable prognosis.

Authors

Picture of Alessandro Lamberti-Castronuovo

Alessandro Lamberti-Castronuovo

Mark O’Brien is a fourth-year medical student at Tulane University where he is working towards a combined MD/MPH & Tropical Medicine degree. Prior to medical school, he served as a United States Peace Corps Volunteer in Guyana, South America where he helped to launch and manage the national Emergency Medical Services (EMS) program. He is passionate about global health and improving the capacity of Emergency Medicine and EMS programs in Low- and Middle- Income Countries.

Picture of Elizabeth DeVos

Elizabeth DeVos

Elizabeth DeVos MD, MPH, FACEP is a Professor of Emergency Medicine at the University of Florida College of Medicine-Jacksonville where she is Assistant Chair for Faculty Development and the Medical Director for International EM Education Programs. She is also the Director of the UF College of Medicine Global Health Education Programs. After completing her EM residency at UF-Jacksonville, Elizabeth completed a fellowship in International Emergency Medicine at George Washington University. She has partnered in the development of EM Specialty Training in several countries, including living and working in Kigali, Rwanda as faculty in the first EM residency. Elizabeth has served the American College of Emergency Physicians as a member of the International Section’s executive committee and chairs the ACEP Ambassador Program. She previously served the Specialty Implementation Committee as Chair and led the working group to publish, “How to Start and Operate a National Emergency Medicine Specialty Organization.”

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References

  1. World Health Organization. Global report on drowning: preventing a leading killer. World Health Organziation; https://www.who.int/publications/i/item/global-report-on-drowning-preventing-a-leading-killer. Published November 17, 2014. Accessed March 5, 2023.
  2. Tyler MD, Richards DB, Reske-Nielsen C, et al. The epidemiology of drowning in low- and middle-income countries: a systematic review. BMC Public Health. May 8 2017;17(1):413. doi:10.1186/s12889-017-4239-2
  3. Bierens J, Abelairas-Gomez C, Barcala Furelos R, et al. Resuscitation and emergency care in drowning: A scoping review. Resuscitation. May 2021;162:205-217. doi:10.1016/j.resuscitation.2021.01.033
  4. World Health Organization. Injuries and violence prevention: non- communicable diseases and mental health: fact sheet on drowning. https://www.who.int/news-room/fact-sheets/detail/drowning. Published April 27, 2021. Accessed March 14, 2023.
  5. Franklin RC, Peden AE, Hamilton EB, et al. The burden of unintentional drowning: global, regional and national estimates of mortality from the Global Burden of Disease 2017 Study. Inj Prev. 2020;26(Supp 1):83-95. doi:10.1136/injuryprev-2019-043484
  6. Szpilman D, Bierens JJ, Handley AJ, Orlowski JP. Drowning. N Engl J Med. May 31 2012;366(22):2102-10. doi:10.1056/NEJMra1013317
  7. Whitworth HS, Pando J, Hansen C, et al. Drowning among fishing communities on the Tanzanian shore of lake Victoria: a mixed-methods study to examine incidence, risk factors and socioeconomic impact. BMJ Open. 2019;9(12) doi:10.1136/bmjopen-2019-032428
  8. Driscoll TR, Harrison JA, Steenkamp M. Review of the role of alcohol in drowning associated with recreational aquatic activity. Inj Prev. 2004;10(2):107-13. doi:10.1136/ip.2003.004390
  9. Girasek DC, Hargarten S. Prevention of and Emergency Response to Drowning. N Engl J Med. 2022;387(14):1303-1308. doi:10.1056/NEJMra2202392
  10. Sindall R, Mecrow T, Queiroga AC, Boyer C, Koon W, Peden AE. Drowning risk and climate change: a state-of-the-art review. Inj Prev. Apr 2022;28(2):185-191. doi:10.1136/injuryprev-2021-044486
  11. Lipnick MS, Van Hoesen KB. Diving Medicine. In: Murray JF, Nadel JA, Mason RJ, Broaddus VC, ed. Textbook of Respiratory Medicine. 6th Amsterdam, NL. Elsevier; 2016:1497.e1-1497.e3.
  12. Szpilman D, Morgan PJ. Management for the Drowning Patient. Chest. 2021;159(4):1473-1483. doi:10.1016/j.chest.2020.10.007
  13. Umapathi KK, Thavamani A, Dhanpalreddy H, Khatana J, Roy A. Incidence Trends and Predictors of In-Hospital Mortality in Drowning in Children and Adolescents in the United States: A National Inpatient Database Analysis. Clinical Pediatrics. 2020;59(2):134-141. doi:10.1177/0009922819886871
  14. McCall JD, Sternard BT. Drowning. In: StatPearls. Treasure Island, FL: StatPearls Publishing; 2022. https://www.ncbi.nlm.nih.gov/books/NBK430833/. Accessed April 2, 2023.
  15. Schmidt A, Sempsrott J. Drowning In The Adult Population: Emergency Department Resuscitation And Treatment. Emerg Med Pract. 2015;17(5):1-22.
  16. Richards DB. Drowning. In: Walls R, Hockberger R, Gausche-Hill M, Erickson T, Wilcox S ed. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 10th Philadelphia, PA: Elsevier; 2023:1815-1818.
  17. Ryan K, Bui MD, Johnson B, Eddens KS, Schmidt A, Ramos WD. Drowning in the United States: Patient and Scene Characteristics using the novel CARES Drowning Variables. Resuscitation. 2023:109788. doi: 10.1016/j.resuscitation.2023.109788.
  18. Turgut A, Turgut T. A study on rescuer drowning and multiple drowning incidents. J Safety Res. Apr 2012;43(2):129-32. doi:10.1016/j.jsr.2012.05.001
  19. Thom O, Roberts K, Devine S, Leggat PA, Franklin RC. Treatment of the lung injury of drowning: a systematic review. Crit Care. 2021;25(1):253. doi:10.1186/s13054-021-03687-2
  20. Branche CM, Stewart S. Drowning: a review of the epidemiology, risk factors, and prevention strategies. J Emerg Med. 2003;25(2):165-170.
  21. Baker SP, Li G. The Utstein style and drowning: a review of the literature. Inj Prev. 2016;22(4):294-298.
  22. Idris AH, Bierens JJLM, Perkins GD, et al. 2015 revised Utstein-style recommended guidelines for uniform reporting of data from drowning-related resuscitation: an ILCOR advisory statement. Circ Cardiovasc Qual Outcomes. 2017;10(7):e000024. doi:10.1161/HCQ.0000000000000024.
  23. Lindsay AC, Barlow A. Risk stratification in drowning: a clinical approach. Emerg Med J. 2019;36(5):289-293.
  24. Brenner RA, Saluja G, Smith GS. Drowning among children and adolescents. Pediatrics. 2009;123(3):e393-e399.
  25. Gilchrist J, Parker EM. Morbidity and mortality from drowning in the United States, 2005-2009. Morbidity and Mortality Weekly Report. 2010;59(19):577-580.
  26. American Academy of Pediatrics. Drowning prevention. Pediatrics. 2019;143(6):e20193084.
  27. Miller A, Smith B, Johnson C, et al. Drowning in pregnancy: unique considerations in management. Obstet Gynecol. 2020;135(2):456-462.
  28. American Heart Association. 2021 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2021;144(16_suppl_2):S1-S447.
  29. Gordon A, Lee S, Thompson P, et al. Resuscitation in pregnancy: a review of current guidelines. J Emerg Med. 2019;56(4):415-421.
  30. Baker SP, Williams A, Jones DL, et al. Drowning in older adults: a review of the literature. J Emerg Med. 2020;58(3):462-470.
  31. Miller AC, Roberts JR, Smith DJ, et al. Physiological considerations in the management of drowning victims. Emerg Med Clin North Am. 2019;37(1):45-58.
  32. Smith JR, Thompson LA, Greenberg DL, et al. Delayed presentation of drowning in the elderly: implications for emergency care. Am J Emerg Med. 2021;39:102-107.
  33. Johnson RA, Lee TH. Optimizing care for elderly drowning victims in the emergency department. Clin Geriatr. 2022;30(2):75-82.
  34. (20) Schmidt AC, Sempsrott JR, Hawkins SC, Arastu AS, Cushing TA, Auerbach PS. Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Drowning. Wilderness Environ Med. 2016;27(2):236-51. doi:10.1016/j.wem.2015.12.019.
  35. (21) Brennan C, Hong T, Wang V. Predictors of safe discharge for pediatric drowning patients in the emergency department. Am J Emerg Med. 2018;36(9):1619–1623. doi:10.1016/j.ajem.2018.01.050
  36. (22) Peden M, Oyegbite K, Ozanne-Smith J, et al. World Report on Child Injury Prevention. Geneva, CH: World Health Organization; 2008:59-73
  37. (23) Rahman A, Giashuddin SM, Svanström L, Rahman F. Drowning–a major but neglected child health problem in rural Bangladesh: implications for low income countries. Int J Inj Contr Saf Promot. 2006;13(2):101-5. doi:10.1080/17457300500172941

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Carbon Monoxide Poisoning (2024)

~ iEM Education Project Team ~ Leave a comment

by Mohammad Issa Naser & Abdulla Alhmoudi

Authors
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You have a new patient!

A 48-year-old male with a known medical history of hypertension, depression, and prior suicidal attempts was brought into the Emergency Department by EMS after he was found unconscious by his wife after she arrived from work. He was lying down in an enclosed garage at home with the car engine running. She states that her husband was having difficulty breathing when she found him and was not responding to her. She reported that he had been depressed for the last few weeks because of financial problems. Upon arrival at the ED, the patient was unresponsive, with the following vital signs noted: BP 113/74 mmHg, HR 114 bpm, RR 10 bpm, and oxygen saturation at 98%.

a-photo-depicts-a-48-year-old-man-found-in-the-garage (image was created by using ideogram 2.0)

What do you need to know?

Importance and Epidemiology

Carbon Monoxide (CO) is often called the “silent killer” as it lacks any warning or alarming signs of its presence. It is a colorless, odorless, tasteless, and non-irritating gas formed by the incomplete combustion of hydrocarbon fuels.

Despite a historical decline in the number of cases, CO continues to be one of the major causes of poisoning-related ED visits, accounting for approximately 50,000 cases every year in the United States, with a mortality rate of 1% to 3% [1]. Although many of these are nonfatal exposures with various degrees of toxicity, an estimated 1,000 to 2,000 patients a year die from severe toxicity [2]. Intentional poisoning cases have higher mortality rates compared to accidental cases and account for two-thirds of deaths [3,4]. Although cases can occur around the year, CO poisoning has a seasonal and geographic relation with cold climates, peaking during winter months, most commonly from faulty furnaces [5].

CO poisoning often has nonspecific toxicologic presentations ranging from minimal symptoms to unresponsiveness. It requires higher suspicion from clinicians to recognize, diagnose, and provide timely and appropriate management to avoid morbidity, mortality, and long-lasting complications. ED physicians should always consider CO poisoning when multiple patients present to the ED from a single location with similar correlating findings [3].

Pathophysiology

CO poisoning causes tissue hypoxia by impairing oxygen delivery and utilization and generating reactive oxygen species. CO can rapidly diffuse into the pulmonary circulation and reversibly bind the iron moiety of heme with approximately 240 times the affinity of oxygen-forming carboxyhemoglobin (COHb). CO impairs heme’s ability to deliver oxygen by directly occupying oxygen-binding sites and causing a conformational change to the other three oxygen-binding sites. This allosteric change increases the affinity of the oxygen binding site and decreases the oxygen delivery to the peripheral tissues, causing a leftward shift in the oxyhemoglobin dissociation curve. The amount of carboxyhemoglobin formed depends on the amount of CO and oxygen in the environment, duration of exposure, and minute ventilation [6].

CO also binds to myoglobin and NADPH reductase, which can worsen the hypoxia of cardiac muscle by affecting the mitochondria and ATP production, potentially leading to atraumatic rhabdomyolysis [2]. Like cyanide, CO inactivates cytochrome oxidase, which is involved in mitochondrial oxidative phosphorylation, causing a switch to anaerobic metabolism, and their combined effects can be synergistic in smoke inhalation [7]. Other effects of CO poisoning include neutrophil degranulation, free radical formation, lipid peroxidation in the brain and other tissues, and cellular apoptosis [2,8]. The half-life of COHb is about 300 minutes; thus, it begins to accumulate in the blood within a short exposure time. With normobaric oxygen (NBO) therapy (which is 100% inhaled oxygen at normal atmospheric pressure), the half-life is decreased to between 50 and 100 minutes; with Hyperbaric oxygen therapy, the half-life can be reduced to 30 minutes [9,10].

Medical History

A thorough history can be very helpful for early recognition of CO-related poisoning. Clinical findings can be variable and highly unspecific. The most common complaint in patients with mild to moderate CO poisoning is headache, present in up to 58% of patients, followed by the wide range of unspecific findings of nausea, dizziness, drowsiness, vomiting, cough or choking, confusion, shortness of breath, syncope, throat and eye irritation and chest pain [3]. It is important for clinicians to inquire about potential CO sources such as residential heating systems, gas appliances, or recent fires. In addition, clinicians should specifically inquire about transient loss of consciousness, as the presence or absence of this finding can be important in determining the severity of the presentation and the need for further interventions like hyperbaric oxygen [6]. Delayed neurological sequelae (DNS) is a well-known complication and can occur in 15 to 40 percent of patients presenting with significant CO poisoning [11]. DNS has been reported to appear 3 to 240 days after apparent recovery, with the majority of cases occurring within 20 days of CO poisoning. Deficits can last a year or more and are typically not found on acute presentation. Patients may present with cognitive impairment, memory deficits, movement disorders, or psychiatric symptoms. Any neurological or neuropsychiatric symptoms persisting beyond the acute phase of CO poisoning should raise suspicion for DNS and warrant appropriate evaluation and management [6]. Risk factors that predict the development of delayed neurologic sequelae include extremes of age and loss of consciousness. Because most CO-poisoned patients reaching the ED survive with minimal intervention, prevention of delayed neurologic and neuropsychiatric sequelae is a primary goal of therapy [12].

Physical Examination

Physical examination in suspected CO poisoning patients should focus on vital signs, cardiac and pulmonary examination, and a thorough neurological assessment. Findings in CO poisoning are usually limited to changes in mental status, tachycardia, and tachypnea in the absence of history of trauma or burns. Symptoms can range from mild confusion to coma [6]. The presence of “cherry-red” skin or mucous membranes may be observed in severe cases or even noted postmortem. However, it’s neither a sensitive nor specific sign, and it does not exclude CO poisoning [13]. Severe CO poisoning can be associated with neurologic, metabolic, and cardiovascular red flags such as seizures, syncope, lactic acidosis, acute myocardial infarction, ventricular arrhythmia, and pulmonary edema [6].

Alternative Diagnoses

Carbon monoxide poisoning can be a “great mimic,” but the early presentations are often nonspecific and readily confused with other conditions, typically a viral syndrome, explaining why influenza is the most common misdiagnosis [14]. CO poisoning can also be misdiagnosed frequently as gastroenteritis, food poisoning, or even colic in infants. Like adults, children tend to develop nonspecific symptoms that complicate the diagnosis [15]. More severe poisoning may be confused with other causes of altered mental status, such as trauma, diabetic ketoacidosis, meningitis, hypoglycemia, and intoxication [16]. The differential diagnosis remains broad without a known exposure source or sick contacts as clues. Cyanide poisoning, especially in patients with smoke inhalation, should also be considered due to the potential for concurrent exposure. In cases of chronic CO exposure, chronic fatigue, mood disorders, sleep disorders, and memory problems should be considered as an alternate diagnosis [17]. Recognizing risk factors for CO poisoning can be crucial in determining the likelihood of CO poisoning; focusing on potential sources of CO poisoning, the presence of multiple individuals with similar symptoms from the same location increases the likelihood of CO poisoning. The CNS is the organ system most sensitive to CO poisoning. Acutely, otherwise healthy patients may manifest headache, dizziness, and ataxia at COHb level as low as 15% to 20%; with higher levels and longer exposures, syncope, seizures, or coma may result [15]. At the same time, history of consuming contaminated food or recent sick contact with flu-like symptoms would make the diagnosis less likely.

Acing Diagnostic Testing

The single most useful diagnostic test to use in a suspected CO poisoning is COHb levels.15 An arterial or venous blood gas analysis with elevated carboxyhemoglobin levels (usually ≥ 3%-4% for nonsmokers or ≥ 10% for smokers) confirms the diagnosis of CO poisoning and provides information about lactate levels and any concurrent metabolic acidosis. It is important to obtain lactate levels to screen for possible concurrent cyanide toxicity (Lactate > 10 mmol/L) if the source of CO was a fire [18]. While an abnormally elevated COHb level indicates CO poisoning, it is important to note that the COHb levels do not accurately represent the severity of the poisoning. This is particularly true if there has been a significant time lapse between the exposure and when the levels were obtained due to CO clearance. Patients with major symptoms such as loss of consciousness altered mental status, or cardiac ischemia should be considered as severe poisoning with any abnormally elevated COHb level. CO poisoning management should focus primarily on the patient’s signs and symptoms rather than relying solely on the COHb level to guide decision-making.

Pulse oximetry (SpO2), a non-invasive bedside test, cannot be used for screening for CO poisoning, as it doesn’t differentiate oxygenated hemoglobin and carboxyhemoglobin and may yield normal values in CO poisoning despite significant tissue hypoxia. Non-invasive CO oximeters measuring COHb and methemoglobin are available and may have a role as a screening test, but their reliability in clinical settings has been questioned [6]. The American College of Emergency Physicians recommends against using pulse CO oximetry for diagnosis of CO toxicity in patients with suspected acute CO poisoning [2].

An electrocardiogram and a measurement of cardiac enzymes should be included due to the possibility of myocardial injury in patients with moderate to severe CO poisoning looking for myocardial ischemia, infarction, or arrhythmias [2,19]. Imaging studies, such as chest radiographs, may be indicated in certain clinical scenarios and can help patients presenting with hypoxia and dyspnea to evaluate for pulmonary edema [20].

Risk Stratification

Significant neurologic manifestations of CO poisoning include findings such as syncope, coma, seizures, altered mental status (GCS <15) or confusion, and abnormal cerebellar function. Metabolic findings such as lactic acidosis may be profound from cellular hypoxia. Cardiovascular findings include acute myocardial ischemia, myocardial injury, ventricular arrhythmia, and pulmonary edema [6].

The clinical policy from the American College of Emergency Physicians concerning the evaluation and management of adult patients with acute carbon monoxide poisoning presents evidence-based recommendations addressing three key clinical questions: the diagnostic accuracy of noninvasive carboxyhemoglobin measurement, the long-term neurocognitive impact of hyperbaric versus normobaric oxygen therapy, and the predictive value of cardiac testing for morbidity and mortality. The policy is based on a systematic literature review, graded using a defined class of evidence system, and offers recommendations for patient management at varying levels of certainty [21].

According to the ACEP’s CO policy, pulse CO oximetry should not be used to diagnose acute carbon monoxide (CO) poisoning due to its low sensitivity. While it offers advantages like being fast, noninvasive, and cost-effective, studies have shown it detects CO toxicity in only about 48% of cases, meaning it misses half of those affected. Similar findings were reported in other studies.

Both hyperbaric oxygen (HBO₂) and high-flow normobaric oxygen therapies are options for treating acute carbon monoxide (CO) poisoning, but it is unclear if HBO₂ is superior in improving long-term neurocognitive outcomes. While HBO₂ reduces carboxyhemoglobin levels and may aid neurologic recovery, its benefits remain debated. Meta-analyses and studies on HBO₂ have shown inconsistent results, with some finding no benefit and others suggesting improved outcomes. Variations in study designs and treatment factors contribute to the uncertainty, highlighting the need for further research.

In moderate to severe carbon monoxide (CO) poisoning, an electrocardiogram (ECG) and cardiac biomarkers should be used to detect acute myocardial injury, a predictor of poor outcomes. Studies have shown that myocardial injury is associated with higher long-term mortality and is an independent predictor of poor prognosis. Further research is needed to explore cardiac testing and interventions in less severe cases and more aggressive cardiac management for high-risk patients.

Management

Initial management starts with assessing and stabilizing the airway, breathing, and circulation. Comatose patients who have severely impaired mental status or who do not have sufficient respiratory effort should be intubated without delay and mechanically ventilated using 100 percent oxygen [6]. Treatment begins with oxygen therapy, and 100% oxygen should be provided as soon as possible with either a non-rebreather mask or endotracheal intubation, which serves two purposes. First, the half-life of COHb is inversely related to PaO2; it can be reduced from approximately 5 hours in room air to 1 hour by providing supplemental 100% oxygen. HBO therapy (at 3 atmospheres) further reduces the half-life to approximately 30 minutes [12]. Oxygen should be continued until the patient is asymptomatic and carboxyhemoglobin levels are ≤ 3%-4% in nonsmokers and ≤ 10% in smokers [2,18,19]. Evidence suggests that hyperbaric oxygen therapy helps prevent delayed neurologic sequelae in acute CO poisoning, but its efficacy decreases with delayed implementation [15]. HBO therapy can be used in patients presenting with a COHb level >25% (>15% if pregnant), unconscious at scene or hospital, reported syncope, persistent altered, mental status, coma, focal neurologic deficit, severe metabolic acidosis (pH <7.25) after empiric cyanide treatment if administered, or evidence of end-organ ischemia (e.g., ECG changes, elevated cardiac biomarkers, respiratory failure, focal neurologic deficit, or altered mental status). A thorough cardiovascular examination should be performed and should focus on signs of contributing cardiogenic shock or hypotension. Establishing IV access and cardiac monitoring are necessary as patients may need IV fluids or inotropes for resuscitation. An ECG and cardiac enzymes should also be included in the evaluation for cardiac ischemia in symptomatic patients at risk. Patients with altered mental status should have a blood glucose check to evaluate for hypoglycemia [6].

Special Patient Groups

Pediatrics

Children may present with subtle and non-specific findings compared to adults, and it is suggested that they can be more sensitive to the effects of CO due to their higher metabolic rates. Fussiness and decreased oral intake may be the only manifestations of CO toxicity. Although children may have higher levels of COHb due to their higher minute ventilation, which should make them more vulnerable to accumulating CO, the long-term outcomes appear favorable as they have lower rates of developing delayed neurological sequelae compared to adults. The diagnosis and management of CO poisoning in young children generally follow the same principles as for other age groups, with no substantial modifications in approach based on age [6].

Pregnant Patients

There is a lower threshold to using HBO therapy in pregnancy due to the greater affinity and the longer half-life of CO that is bound to fetal hemoglobin, the limited capacity to enhance placental perfusion and the direct effects of acidosis and hypoxemia on the fetus. While severe CO poisoning poses serious short- and long-term fetal risk, mild accidental exposure is likely to result in normal fetal outcomes. Because the fetal accumulation of CO is higher and its elimination slower than in the maternal circulation, hyperbaric oxygen may decrease fetal hypoxia and improve outcomes. While these findings provide valuable insights into the effects of CO poisoning and HBO therapy on pregnant patients and their fetuses, the available literature on this subject remains limited [6].

When To Admit This Patient

Hospitalization is warranted in cases where patients exhibit signs of hemodynamic instability, persistent neurologic symptoms, evidence of end-organ damage (including renal injury, rhabdomyolysis, cardiac ischemia, and pulmonary edema), or exposure to methylene chloride. Most patients who do not meet the criteria for HBO therapy and are not clinically ill can typically be managed in the emergency department; generally, patients who become asymptomatic with a carboxyhemoglobin (COHb) level < 5% may be safely discharged home. All patients exposed to CO require close follow-up for delayed neurologic sequelae [18].

Revisiting Your Patient

Our 48-year-old male, who has a history of prior suicidal attempts, was found unconscious in his home garage with his car engine running. The past medical history and his presentation picture put him at risk for carbon monoxide poisoning, and red flags such as his altered mental state and the recognition of a source of carbon monoxide should guide the clinician through the diagnosis and management process. Management started by assessing the airway, breathing, and circulation. The patient was in a state of respiratory arrest and was intubated and ventilated with 100% oxygen. His pupils were dilated and sluggish. The patient was hypotensive, and IV fluids were started while vasopressors were being prepared. A CBC, chemistry, blood glucose, cardiac enzymes, COHb level, and venous blood gas were requested. A Chest XR was also done, which showed no signs of pulmonary edema, and an endotracheal tube was confirmed in place. ECG showed normal sinus rhythm with no ST-T wave changes. COHb level was 38%, blood glucose 139 mg/dl, and cardiac enzymes were within normal range. His blood gas showed a pH of 7.28 and a lactate of 4. A diagnosis of carbon monoxide poisoning was made. The patient was kept on 100% oxygen and was being prepared to be transferred into a hyperbaric oxygen therapy facility.

Authors

Picture of Mohammad Issa Naser

Mohammad Issa Naser

Dr Mohammad Naser is currently a Critical Care Medicine Fellow in Sheikh Shakhbout Medical City - Abu Dhabi. He completed his emergency medicine training at Zayed Military Hospital and has obtained both the Emirati and Arab board certifications in Emergency Medicine. Dr. Naser has a profound interest in critical care medicine, particularly in bridging the gap between emergency and intensive care practices. Beyond critical care, He is deeply passionate about medical education, mentoring future healthcare professionals, and developing innovative teaching tools. Additionally, he is actively involved in clinical research, focusing on advancing knowledge and practices in emergency and critical care medicine.

Picture of Abdulla Alhmoudi

Abdulla Alhmoudi

Dr Abdulla Alhmoudi is a Consultant Emergency Medicine, serving at Zayed Military Hospital and Sheikh Shakhbout Medical City - Abu Dhabi. He pursued his residency training in Emergency Medicine at George Washington University in Washington DC and further enhanced his expertise with a Fellowship in Extreme Environmental Medicine. Dr Alhmoudi's passion for medical education is evident in his professional pursuits. He currently holds the position of Associate Program Director at ZMH EM program and is a lecturer at Khalifa University College of Medicine and Health Sciences. Beyond medical education, he maintains a keen interest in military medicine and wilderness medicine.

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References

  1. Rose JJ, Wang L, Xu Q, et al. Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy [published correction appears in Am J Respir Crit Care Med. 2017 Aug 1;196 (3):398-399]. Am J Respir Crit Care Med. 2017;195(5):596-606. doi:10.1164/rccm.201606-1275CI
  2. American College of Emergency Physicians Clinical Policies Subcommittee (Writing Committee) on Carbon Monoxide Poisoning:, Wolf SJ, Maloney GE, Shih RD, Shy BD, Brown MD. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Carbon Monoxide Poisoning. Ann Emerg Med. 2017;69(1):98-107.e6. doi:10.1016/j.annemergmed.2016.11.003
  3. Shin M, Bronstein AC, Glidden E, et al. Morbidity and Mortality of Unintentional Carbon Monoxide Poisoning: United States 2005 to 2018. Ann Emerg Med. 2023;81(3):309-317. doi:10.1016/j.annemergmed.2022.10.011
  4. Rose JJ, Wang L, Xu Q, et al. Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy [published correction appears in Am J Respir Crit Care Med. 2017 Aug 1;196 (3):398-399]. Am J Respir Crit Care Med. 2017;195(5):596-606. doi:10.1164/rccm.201606-1275CI
  5. Centers for Disease Control and Prevention (CDC). Unintentional non-fire-related carbon monoxide exposures–United States, 2001-2003. MMWR Morb Mortal Wkly Rep. 2005;54(2):36-39.
  6. Manaker S, Perry H. (2023) Carbon monoxide poisoning, UpToDate. Available at: https://www.uptodate.com/contents/carbon-monoxide-poisoning (Accessed: 15 May 2023).
  7. Norris JC, Moore SJ, Hume AS. Synergistic lethality induced by the combination of carbon monoxide and cyanide. Toxicology. 1986;40(2):121-129. doi:10.1016/0300-483x(86)90073-9
  8. Dubrey SW, Chehab O, Ghonim S. Carbon monoxide poisoning: an ancient and frequent cause of accidental death. Br J Hosp Med (Lond). 2015;76(3):159-162. doi:10.12968/hmed.2015.76.3.159
  9. Weaver LK, Howe S, Hopkins R, Chan KJ. Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure. Chest. 2000;117(3):801-808. doi:10.1378/chest.117.3.801
  10. Walker AR. Emergency department management of house fire burns and carbon monoxide poisoning in children. Curr Opin Pediatr. 1996;8(3):239-242. doi:10.1097/00008480-199606000-00009
  11. Rose JJ, Wang L, Xu Q, et al. Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy [published correction appears in Am J Respir Crit Care Med. 2017 Aug 1;196 (3):398-399].Am J Respir Crit Care Med. 2017;195(5):596-606. doi:10.1164/rccm.201606-1275CI
  12. Meaden CW, Nelson LS. Inhaled Toxins. In: Rosen’s Emergency Medicine Concepts and Clinical Practice. 10th ed. Elsevier; 2023:666-681.
  13. Harper A, Croft-Baker J. Carbon monoxide poisoning: undetected by both patients and their doctors.Age Ageing. 2004;33(2):105-109. doi:10.1093/ageing/afh038
  14. Dolan MC, Haltom TL, Barrows GH, Short CS, Ferriell KM. Carboxyhemoglobin levels in patients with flu-like symptoms. Ann Emerg Med. 1987;16(7):782-786. doi:10.1016/s0196-0644(87)80575-9
  15. Tomaszewski, C. Carbon Monoxide. IN: Goldfrank’s toxicological emergencies. 9th ed. New York: McGraw-Hill Medical Pub. Division; c2011
  16. Cho CH, Chiu NC, Ho CS, Peng CC. Carbon monoxide poisoning in children. Pediatr Neonatol. 2008;49(4):121-125. doi:10.1016/S1875-9572(08)60026-1
  17. Eichhorn L, Thudium M, Jüttner B. The Diagnosis and Treatment of Carbon Monoxide Poisoning.Dtsch Arztebl Int. 2018;115(51-52):863-870. doi:10.3238/arztebl.2018.0863
  18. Hampson NB, Piantadosi CA, Thom SR, Weaver LK. Practice recommendations in the diagnosis, management, and prevention of carbon monoxide poisoning.Am J Respir Crit Care Med. 2012;186(11):1095-1101. doi:10.1164/rccm.201207-1284CI
  19. Weaver LK. Clinical practice. Carbon monoxide poisoning.N Engl J Med. 2009;360(12):1217-1225. doi:10.1056/NEJMcp0808891
  20. Prockop LD, Chichkova RI. Carbon monoxide intoxication: an updated review.J Neurol Sci. 2007;262(1-2):122-130. doi:10.1016/j.jns.2007.06.037
  21. American College of Emergency Physicians Clinical Policies Subcommittee (Writing Committee) on Carbon Monoxide Poisoning:, Wolf SJ, Maloney GE, Shih RD, Shy BD, Brown MD. Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Carbon Monoxide Poisoning. Ann Emerg Med. 2017;69(1):98-107.e6. doi:10.1016/j.annemergmed.2016.11.003

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

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Heat Illnesses (2024)

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by Patrick Joseph G. Tiglao, Rhodney P. Canada, & Emmanuel Luis S. Mangahas

Authors
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You have a new patient!

A 24-year-old man was brought to your Emergency Department by his football coach. His coach informed you that he started “behaving strangely” and responding inappropriately to questions a few hours ago during a practice session on the football field. His initial vital signs are BP 80/50 mmHg, HR 115 bpm, RR 24 bpm, T 41.5oC, and SpO2 98%. His GCS is 13 (E3V4M6).

What do you need to know?

Climate change is widely considered the greatest threat to human health globally in the coming decades [1]. According to the assessment of the Intergovernmental Panel on Climate Change (IPCC), the next decades might witness global warming above 1.5 °C, exceeding the goals of the Paris Agreement [2]. Concomitantly, heat-related mortality has developed as a growing public health concern. Populations with pre-existing chronic diseases are more sensitive to climate change, warranting closer attention and more effective interventions to manage heat-related health risks [3]. Therefore, a comprehensive medical understanding of heat-related illnesses is required as the world faces climate change [1].

Heat-related illnesses include a spectrum of diseases, ranging from mild and self-limiting conditions such as heat edema, heat cramps, and heat stress to the life-threatening condition known as heat stroke. These conditions occur when the body’s thermoregulatory mechanisms fail to keep body temperature within normal limits in a hot and humid environment [4].

The emergency physician needs to have a high index of suspicion for heat stroke because these patients can mistakenly be diagnosed with other conditions that may present similar to heat stroke.  Some examples are sepsis, intracranial bleeding, stroke, thyroid storm, anticholinergic toxicity, or other conditions where patients may have high fevers or altered mental status, similar to heat stroke. The most critical initial intervention in heat stroke is rapid cooling to <39°C. A misdiagnosis can result in a delay in rapid cooling.  Failing to implement this intervention results in higher mortality [5].

According to the World Health Organization, more than 166,000 people died due to extreme temperatures between 1997 and 2017.  This includes 70,000 deaths in the 3-month European heatwave of 2003 and 53,000 deaths in the 44-day Russian heatwave of 2010 [5]. A 2003 prospective study from France reported a 28-day and 2-year mortality rate of 58% and 71%, respectively, for patients diagnosed with heat stroke [6].

Body temperature is controlled by the hypothalamus. The body gains heat from metabolism and the environment, and this heat must be dissipated to maintain core body temperature between 36°C and 38°C (96.8°F and 100.4°F). Thermoregulation relies on four primary mechanisms: dilatation of blood vessels, particularly in the skin, increased sweat production and subsequent evaporation, decreased heat production, and behavioral heat control. Vasodilation contributes to the orthostatic pooling of interstitial fluid in the lower extremities, as seen in heat edema. When these processes are overwhelmed, core temperature will rise and may result in heat stress [4].

Cellular injury can begin when the core body temperature exceeds 39oC, especially if the elevation in temperature is sustained [7]. As the body temperature rises to 40°C, an acute phase response is elicited from heat-stressed cells.  This involves the release of cytokines and heat shock proteins, materials that can cause damage to organ systems and result in heat stroke [4,8]. The incremental damage to cells and organ systems as body temperature rises above 39oC exemplifies the importance of rapid cooling in a patient with hyperthermia.

Heat stroke due to high external temperature and humidity without much contribution from physical exertion is termed classical heat stroke (CHS).  Heat stroke is due to increased heat generation from strenuous physical activity, usually under extreme heat conditions and in a poorly acclimatized and conditioned body, and is termed exertional heat stroke (EHS). For example, classical heat stroke may be seen in elderly individuals sitting in poorly cooled and ventilated homes during the summer; exertional heat stroke may be seen in athletes exercising hours in the sun during a prolonged sporting event or race. Another heat-related illness that may be encountered in the athlete patient is heat cramps. These cramps occur from relative deficiencies in electrolytes such as sodium, potassium, and magnesium brought about by replenishing lost fluids with hypotonic drinking solutions after vigorous physical activity. This leads to painful involuntary contractions of skeletal muscles, most commonly the calves [4].

The exercising body has thermoregulatory mechanisms it utilizes when exposed to prolonged heat. During exercise, blood vessels dilate to release heat, the heart rate increases, and stroke volume decreases. Sweat production and evaporation from the skin surface also assist in cooling the body during exercise. These mechanisms may be diminished in patients with underlying cardiovascular disease (e.g., congestive heart failure) or those taking certain medications (e.g., beta-blockers or anticholinergic medications). These patient groups are at increased risk of heat-related illnesses during exercise [9].

Medical History

Ask patients with heat edema about exposure to hot and humid environments. The presence of other symptoms, such as dyspnea, easy fatigability, orthopnea, paroxysmal nocturnal dyspnea, and oliguria, are red flags that may point to alternative causes of the edema, such as congestive heart failure or kidney failure [4].

For patients with heat cramps, verify recent participation in strenuous activities, such as sports events and practices, military exercise, or procession-like activities. Ask if the patient took fluid during exertional activities and, if so, what type of fluid was consumed. Drinking hypotonic solutions, such as plain water, puts patients at risk for relative deficiencies in electrolytes and subsequent heat cramps. Ask about vomiting, diarrhea, and medications, like diuretics or antihypertensives, which can also put the patient at risk for electrolyte disturbances [4].

Heat stress is a diagnosis of exclusion because patients usually come in febrile with non-specific symptoms such as nausea, headache, weakness, and dizziness [4]. Again, patients with a recent history of exposure to hot and humid environments are at increased risk of heat stress. Still, the emergency physician should be aware of other more dangerous conditions, such as sepsis, CNS infection, endocrine dysfunction, myocardial infarction, and drug overdose. Ask for recent history of dyspnea, cough, dysuria, and headache, which may point to infectious diseases such as pneumonia, urinary tract infection, and CNS infection.

To diagnose heat stroke, the patient must have both Central Nervous System (CNS) impairment and a core temperature greater than 40°C. The spectrum of neurological abnormalities ranges from mild confusion to coma with a GCS of 3. Situational awareness is a vital skill for emergency physicians, as one should be aware of days with high ambient temperatures and high humidity that can increase the risk of CHS. Usage of medications that impair sweating, like anticholinergic medications, is another risk factor for developing heat illnesses. Generally speaking, CHS is uncommon in geographical areas where the average temperature throughout the year is high, as communities living there will develop behavioral tactics to avoid the heat. Intense exercise, military training, sports competitions, or prolonged labor, on the other hand, puts patients at risk for EHS. Patients not trained in hot environments may not be physiologically acclimatized, increasing their risk for EHS [4].

Physical Examination

Whenever heat illnesses are considered in the differential diagnosis of a given patient, measuring a core body temperature (e.g., rectal temperature) is the most important physical assessment. Using the physical exam to evaluate for other causes of elevated body temperature is important.  Physical signs of infection (e.g., cellulitis, abscess, drainage from wounds, asymmetric breath sounds), intoxication (e.g., dilated pupils), and endocrine dysfunction (e.g. goiter) should be assessed.

Obtaining an accurate and continuous core body temperature is a crucial part of the physical examination. Core temperature should be assessed and monitored using rectal, bladder, or esophageal probes. Peripheral temperature measurements, like oral, axillary, or temporal temperatures, are unreliable and may not reflect actual core temperatures. A common pitfall in measuring rectal temperature is not inserting the probe to a sufficient depth, rendering readings inaccurate, mainly if ice packs have been applied to the groin area for cooling. Rectal probes, in general, have to be inserted 15 cm inside the rectum to mitigate the effects mentioned above, but manufacturers may recommend different depths.  Note that unlike heat stroke and heat stress, heat edema, and heat cramps will not have an increased core temperature [4]. Tachycardia and hypotension may be seen on examination as a response to thermoregulatory peripheral vasodilation. This phenomenon contributes to other heat illnesses, such as heat edema and heat syncope.

After vital signs, a head-to-toe physical exam should be conducted with special care in conducting a thorough neurological examination. A hallmark finding of heat stroke, other than a core temperature above 40°C, is an abnormal neurological exam. CNS effects might range from mild confusion to deep coma. Ataxia and slurred speech may also be seen. CNS effects help distinguish heat stress from heat stroke, as only heat stroke will have CNS changes [4].

Assess for neurologic signs such as nuchal rigidity, lateralizing spasticity, and pathologic reflexes (e.g. extensor toe reflex) to determine the possibility of a central neurologic etiology. Seizures, in general, are common in heat stroke and might be confused with shivering during cooling.  Both seizures and shivering should be treated for neural protection and prevention of heat generation, respectively.  Benzodiazepines are appropriate for treating both conditions.

Alternative Diagnoses

Minor heat illnesses, like heat cramps and heat edema, can be diagnosed clinically based on the history. Alternative diagnoses for heat edema include congestive heart failure, renal failure, and chronic hepatic disease. The presence of exertional dyspnea, orthopnea, or paroxysmal nocturnal dyspnea would suggest congestive heart failure. Progressively decreasing urine output and generalized edema would suggest renal failure. A jaundiced patient with progressively enlarging abdomen would indicate a chronic hepatic disease. Alternative diagnoses for heat cramps are infectious conditions and electrolyte derangements. Many viral syndromes, like influenza, COVID-19, or Dengue, can be associated with myalgias.  Other conditions, like Leptospirosis, can also present with lower extremity myalgia and calf tenderness. However, the absence of decreasing urine output, fever, and jaundice would make this diagnosis unlikely.

Heat stroke, with its cardinal features of hyperpyrexia and altered sensorium, has numerous alternative diagnoses.  Some important diagnoses to consider are sepsis, CNS infections, thyroid storm, sympathomimetic or anticholinergic toxidromes, serotonin syndrome, alcohol withdrawal, stroke, or status epilepticus. Investigate accordingly for a focus of infection for these patients. Thyroid storm patients may also present with atrial fibrillation, diarrhea, and a trigger (e.g., missed thyroid medications, infection, or surgery). The presence of signs and symptoms such as sudden-onset lateralizing weakness, slurring of speech, headache, nuchal rigidity, and recurrent seizures despite adequate cooling may suggest central neurologic etiology for the patient’s condition. It may require a more tailored neurologic work-up.  Reported illicit substance or alcohol use, or lack thereof, would support intoxication or withdrawal. Epilepsy history, missed doses of antiepileptic medications, or active seizure activity during the exam would support status epilepticus as a diagnosis.

Acing Diagnostic Testing

Heat stroke and other heat illnesses are diagnoses made clinically.  However, diagnostic testing can help rule out alternative diagnoses and evaluate for concurrent organ dysfunction and metabolic derangements.

Immediately test point-of-care glucose because hypoglycemia is a common and easily reversible cause of altered sensorium. Hypoglycemia also sometimes accompanies exertional heat stroke since glucose reserves may become depleted from physical activity. Blood work-ups can include a complete blood count to evaluate for infection, creatinine to rule out acute kidney injury, and metabolic profile to assess for electrolyte imbalance. Hypernatremia may be present in severe dehydration. Hyponatremia and hypercalcemia may be present in patients who are dehydrated with hypotonic solutions after extreme physical activity. Hyperkalemia may be associated with acute kidney injury.

Blood gas analysis may help differentiate classical and exertional heat stroke. Classical heat stroke usually presents with respiratory alkalosis from hyperventilation as a compensatory mechanism to extreme heat. In contrast, exertional heat stroke may present with lactic acidosis from repeated muscular contractions from physical exertion [4]. Moreover, elevation of liver enzymes is very common in both EHS and CHS, mainly due to direct thermal injury and hypoxia from splanchnic vascular redistribution. Hepatic damage is almost always mild and reversible despite rare reports of fulminant hepatic failure from heat stroke [4,10].

Concerns for a central neurologic etiology for the patient’s encephalopathy can be assessed with CT brain imaging and CSF analysis.  These studies should be especially considered if focal neurologic deficits, slurring of speech, nuchal rigidity, or meningeal signs persist despite lowering the core temperature.

Risk Stratification

Minor heat illnesses are generally self-limited and have good outcomes. Heat stroke, on the other hand, is a life-threatening emergency. Mortality rate is correlated with the maximum core temperature and time to initiate cooling methods [4]. A study in 2018 also showed that the presence of disseminated intravascular coagulation is an independent prognostic factor for hospital mortality in patients with heat stroke [11]. Patients suffering from multiple organ injuries due to thermal injury also have poorer prognosis, so it is imperative to closely monitor renal, hepatic, and cardiovascular status of heat stroke patients [10,12].

Management

A core temperature above 40°C should prompt the clinician to consider heat stroke and initiate rapid cooling. 

Heat stroke is a time-sensitive condition where cooling takes precedence over everything else, including confirmation of the diagnosis. Every patient should be approached with the ABCDE assessment to ensure that all critical decisions are made promptly. Heat stroke is not an exception to this role, as the disturbance in consciousness could result in significant airway complications. A complete airway assessment should be immediately performed when the patient arrives in the emergency department while cooling measures are being set up. Many heat stroke patients may have a depressed level of consciousness, but the decision to intubate is ultimately clinical and based on local resources. Airway protection is paramount and should take priority over any other diagnostic or therapeutic procedures. Peripheral blood pooling is a component of heat stroke pathology, so hypotension is common in these patients. Intravenous fluid administration should be judicious, as blood pressure usually picks up as the core temperature drops. Aliquots of 250cc of crystalloids should be used when fluids are needed, and repeated dosing should take place after volume status assessments.

In heat stroke, external cooling methods are the main pillar of therapy. Antipyretics, such as Paracetamol, have no proven benefit in such cases. The fastest way to cool patients is through conduction, the direct transfer of heat between molecules. Full body water immersion can do this, and although this is theoretically the best cooling method, it is clinically challenging. Immersion of the patient in water poses a risk of aspiration and renders the patient’s accessibility quite difficult. Alternatively, ice packs can be placed on the patient’s neck, axilla, and groin areas. Convection, heat loss due to gas movement around the body, combined with evaporation, can achieve a cooling speed similar to full-body immersion. This combination can be achieved by spraying the patient with lukewarm water followed by fanning with warm air. Mist fans are very convenient and have the added benefit of their ability to fan multiple patients at once.

Figure 1- monitor showing the current vitals while the patient is cooled.
Figure 2. The row of beds with mist fans in a sunstroke unit. A cooling unit can be seen at the far right.
Figure 3. Fiberglass grooved beds with waterproof mattresses in a sunstroke unit.

One complication of these cooling maneuvers is shivering. Shivering needs to be controlled as it increases internal heat generation. This can be overcome by administering benzodiazepines. It should be noted that high ambient temperature and high humidity make convection and evaporation less effective. For this reason, if these patients are encountered in the prehospital setting, the first priority is to remove them from the hot and humid environment [4,7].

Internal cooling procedures, such as cold IV fluids and internal cold fluid lavages, do not have high quality to support their safety and efficacy in heat stroke patients [4]. Internal cooling with cardiopulmonary bypass can be considered in severe cases that do not respond to typical cooling methods. However, it is costly, resource-intensive, and unavailable in many contexts [4]. Rapid and aggressive external cooling with evaporative cooling, cold water immersion, and ice packs should be prioritized as the initial preferred cooling methods. Invasive measures, like thoracic, bladder, rectal, or peritoneal lavage, should only be used when other measures fail.

Special Patient Groups

Patients at extremes of age are at increased risk for heat-related illnesses and should be carefully considered for these conditions when presenting with fever [4].

Pediatrics

Classical heat stroke can occur in pediatric patients, but these patients are also at risk of another type of heat stroke known as confinement hyperpyrexia. This happens when a child is left inside a vehicle with poor ventilation during extreme heat. Pediatric patients are especially susceptible to heat stroke because they still lack adequate thermoregulatory mechanisms and the instinctive capacity to replace their fluid losses [4]. Child abuse should be considered, and necessary actions should be taken to protect the child from abuse or maltreatment.

Pregnant Patients

Pregnant individuals are particularly vulnerable to heat-related illnesses due to physiological changes that increase metabolic and cardiovascular demands. Conditions such as heat cramps, heat exhaustion, and heat stroke can arise from prolonged heat exposure, posing risks to both maternal and fetal health, including preterm birth and low birth weight. Management involves moving the patient to a cooler environment, ensuring hydration with non-caffeinated drinks or intravenous fluids if needed, applying cooling measures like wet cloths and fans, and monitoring vital signs closely. Preventive measures are crucial and include staying hydrated, wearing lightweight clothing, avoiding outdoor activities during peak heat, and utilizing air-conditioned spaces. Recognizing early symptoms, such as excessive sweating, dizziness, or confusion, and seeking immediate medical care when necessary are critical to preventing complications.

Geriatrics

Geriatric patients may have comorbidities or take daily medications that impair thermoregulation or mobility, making them prone to heat-related illnesses. This population has a higher heat stroke mortality rate and is more likely to experience complications of heat stroke [4]. Advocating for closer community ties, monitoring by family or peers, and improved socioeconomic support may help elderly patients evade health-related illnesses.

Mass Gatherings

Preparing for a mass gathering event should involve mitigation measures for a possible mass casualty incident of heat stroke and heat exhaustion patients, especially during hot or humid summer months. Public education should be employed to seek shade, drink enough fluids, and use umbrellas. Preparations should also include installing mist pipes, vent fans, and nearby cooling stops.

When to admit this patient

Patients with minor heat illness (e.g., heat edema, cramps, and stress) can generally be discharged home. They should be advised to refrain from strenuous activities during extreme heat conditions, drink plenty of fluids, and wear light and loose-fitting clothing. Those who suffer from heat cramps should be advised to avoid hypotonic solutions for fluid replacement to prevent relative electrolyte deficiencies [4].

Consider admission for patients with minor heat illness but have comorbidities, such as congestive heart failure and renal failure, and those with severe electrolyte abnormalities. Patients suffering from heat stroke must be admitted after resuscitation and rapid cooling in the emergency department.  Heat stroke patients need admission to adequately monitor core temperature and possible occurrence of late complications, such as renal failure, hepatic injury, and electrolyte abnormalities. Patients who are intubated or unstable hemodynamically require ICU admission for closer monitoring [4].

Revisiting Your Patient

You immediately assess the patient’s ABCDEs as part of the primary survey. You assess the patient’s airway for the presence of stridor and pooling of oral secretions. The airway is normal. The patient is able to speak in sentences, albeit confused. He is tachypneic but has normal work of breathing and clear breath sounds. Again, you note that the patient is hypotensive at BP 80/50, tachycardic at HR 115, and hyperthermia at 41.5oC. You start infusing 500 mL of normal saline intravenously as a bolus. The patient was confused but did not exhibit lateralizing weakness, slurring of speech, or nuchal rigidity. Point-of-care glucose was done to rule out hypoglycemia, which revealed 146 mg/dL. You did not elicit any history of trauma, and you did not note any obvious abrasions, lacerations, or bleeding. After the IV bolus, reassessment was as follows: BP 90/60, HR 110, RR 24, T 41.5oC, SpO2 98%, and GCS 13 (E3V4M6)

On further history taking, you elicit that the patient has no allergies, no daily medications, no known comorbidities, and last ate 3 hours ago. You learn the patient was at football team practice for 2 hours at noon today when they noted that the patient had decreased verbal responses, responded inappropriately, and was extremely warm to touch. There was no vomiting, headache, lateralizing weakness, or trauma noted during the incident. There was no history of cough, dyspnea, and fever in the preceding days. The coach said the patient had only joined the football team 4 days prior. You insert a rectal thermometer and note a temperature of 42.0oC. With this information, you suspected that the patient may be suffering from an exertional heat stroke and decided that the goal was to decrease the core temperature to less than 39oC as soon as possible. You immediately remove the patient’s clothing while still maintaining modesty. You direct a vent fan to the patient by incorporating water sprays and placing ice packs on the patient’s neck, axillary, and groin areas.

After 30 minutes of cooling, you observe shivering. To decrease the internal heat production that shivering may cause, you administer diazepam 2.5 mg IV, and the shivering subsides. A cardiac monitor with pulse oximetry is connected, and blood samples are drawn to evaluate for organ dysfunction and possible sepsis. After reaching a rectal temperature of 39°C, you direct your team to dry cover the patient with a light bed sheet. Upon subsequent examination, the patient was conscious, alert, and oriented. Vitals are BP 110/60, HR 105, RR 22, T 38.5oC O2Sat 96% on room air. Laboratories are remarkable for metabolic acidosis and elevated liver enzymes. Complete blood count is unremarkable. You admit the patient to a general medical ward for further monitoring and management.

Authors

Picture of Patrick Joseph G. Tiglao

Patrick Joseph G. Tiglao

Dr. Patrick Joseph G. Tiglao, FPCEM is a practicing Emergency Medicine Physician at the University of the Philippines - Philippine General Hospital. He is also affiliated with DOH regional hospitals in the other parts of the Philippines namely, Corazon Locsin Montelibano Memorial Regional Hospital in Bacolod City, Negros Occidental and Eastern Visayas Medical Center in Tacloban City, Leyte Province.

Picture of Rhodney P. Canada

Rhodney P. Canada

Dr. Rhodney P. Canada graduated, being the top of his class, Doctor of Medicine from the University of St. La Salle – Bacolod in 2018. He spent a year of post-graduate internship at the University of the Philippines Manila – Philippine General Hospital from 2018-2019. Currently, he is a senior 4th year and Chief Resident of the Department of Emergency Medicine in Corazon Locsin Montelibano Memorial Regional Hospital, Bacolod City, Negros Occidental, Philippines.

Picture of Emmanuel Luis S. Mangahas

Emmanuel Luis S. Mangahas

Philippine General Hospital

Acknowledgement

The authors would like to express their utmost gratitude to Dr. Abdulaziz Al Mulaik, the author of this chapter in the previous edition.

Listen to the chapter

References

  1. Zhou L, He C, Kim H, et al. The burden of heat-related stroke mortality under climate change scenarios in 22 East Asian cities. Environ Int. 2022; 170
  2. Tollefson J. Top climate scientists are sceptical that nations will rein in global warming. Nature. 2021; 599(7883):22-24.
  3. Yang J, Zhou M, Ren Z, et al. Projecting heat-related excess mortality under climate change scenarios in China. Nat Commun. 2021; 12 (1039)
  4. LoVecchio F. Heat Emergencies. In Tintinalli J, ed. Emergency Medicine A Comprehensive Study. 9th ed. USA: McGraw Hill; 2020: 1345-1350
  5. Heat and Health. World Health Organization. https://www.who.int/news-room/fact-sheets/detail/climate-change-heat-and-health. Published June 2018. Accessed April 2023.
  6. Argaud L, Ferry T, Le QH, et al. Short- and long-term outcomes of heatstroke following the 2003 heat wave in Lyon, France. Arch Intern Med. 2007;167(20):2177-2183
  7. Beltran G. Heat-related Illneses. In Cone D, ed. Emergency Medical Services Clinical Practice and Systems Oversight. 3rd ed. New Jersey, USA: John Wiley & Sons; 2021: 403-409
  8. Benedetto W. Heat Stroke. In Parsons P, Wiener-Kronish J, ed.Critical Care Secrets. 5th ed. Mosby; 2013: 541-544
  9. Hifumi T, Kondo Y, Shimizu K, Yasufumi M: Heat stroke. J Intens Care. 2018: 6(30)
  10. Grogan H, Hopkins PM. Heat stroke: implications for critical care and anaesthesia. BJA. 2002: 88(5):700–707
  11. Hifumi T, Kondo Y, Shimazaki J, et al. Prognostic significance of disseminated intravascular coagulation in patients with heat stroke in a nationwide registry. J Crit Care. 2018;44:306-311
  12. Liu S, Xing L, Wang J, et al. The Relationship Between 24-Hour Indicators and Mortality in Patients with Exertional Heat Stroke. Endocr Metab Immune Disord Drug Targets. 2022;22(2):241-246

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Reviewed and Edited By

Picture of Joseph Ciano, DO, MPH, MS

Joseph Ciano, DO, MPH, MS

Dr. Ciano is a board-certified attending emergency medicine physician from New York, USA. He works in the Department of Emergency Medicine and Global Health at the Hospital of the University of Pennsylvania. Dr. Ciano’s global work focuses on capacity building and medical education and training in low-middle income countries. He is thrilled to collaborate with the iEM Education Project in creating free educational content for medical trainees and physicians.

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

Arif Alper Cevik, MD, FEMAT, FIFEM

Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.

Under the scorching sun – Heat Stroke Q&A

Under the scorching sun – Heat Stroke Q&A
~ 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

[cite]

Question Of The Day #46

question of the day
~ Joseph Ciano, USA ~ Leave a comment

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

  • A) 1000mL of IV 0.9% NaCl
  • B) Noncontrast CT scan of head
  • C) 25g of IV dextrose
  • D) 150mL of 3% NaCl

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

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References

[cite]

Organophosphate poisoning

Organophosphate poisoning
~ 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).

SLUDGE - DUMBELS
Killer B's
  • 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

  1. 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.
  2. 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]

Snakebite: Two years and 200 cases later

snakebite
~ 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:

  • "We will help you," helps:

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.

  • We are taking care of a patient:

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?

  • Know your limitations:

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.

  • Manage expectations:

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.

  • Educate your population:

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.

A visual poster of common snakes found in Nepal placed at the entrance of Snakebite Treatment Center.
  • Re-train yourself and your teammates:

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.

Snakebite Management Protocol posted in treatment center.
Logistics arranged for snakebite management.
[cite]

Recent blog posts by Carmina Shrestha

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

CARDIAC GLYCOSIDES
~ 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.

cardiac glycosides Oleander
https://pixabay.com/images/id-3639050/

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]

calcium mechanism

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]

cardiac glycosides plant identification

References and Further Reading

  1. 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
  2. Benowitz, N. (2012). ‘Chapter 61- Digoxin and Other Cardiac Glycosides’ Poisoning & drug overdose. New York, N.Y.: McGraw Hill Medical.
  3. 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
  4. 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
  5. 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
  6. Hollman A. (1985). Plants and cardiac glycosides. British heart journal, 54(3), 258–261. https://doi.org/10.1136/hrt.54.3.258
  7. 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
  8. 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.
  9. 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
  10. 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
  11. 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]

A Song of Ice and Fire

A Song of Ice and Fire
~ 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:

  1. 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.
  2. Tran TP. Heat emergencies. In: Ma OJ, Cline DM, ed. Emergency medicine manual. 6th ed. McGraw-Hill, NY: 2004:564-565
  3. Becker J, Stewart L. Heat-related illness. Am Fam Physician. 2011;83(11):1325-1330
  4. 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
  5. 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.
  6. 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
  7. Brown DJ et al. Accidental hypothermia. NEJM 2012; 367(20): 1930-1938. PMID: 23150960
[cite]

Death on the Roads

Death on the Roads
~ 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.

The proportion of population, road traffic deaths, and registered motor vehicles by country income, 2016 (Source: Global Status Report On Road Safety 2018, WHO)

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 has a rather depressing page showing numbers of deaths related to road injuries. (Source: Death on the Roads, WHO, https://extranet.who.int/roadsafety/death-on-the-roads/ )

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

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

ELECTRIC SHOCK; Injuries beyond what the eyes see.​

electric shock
~ 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

electrical injury
electrical injury

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.

Further Reading

A baby with burn!

11-month-old baby presented to the ED with a burn after accidental hot tea slippage over her. Burn is a complicated injury for many reasons. It

Read More »
September 25, 2018

Burns

by Rahul Goswami   Introduction The skin is the largest organ in the body. Its physiological purpose is to protect the body contents from foreign

Read More »
August 30, 2018
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A Farmer’s Dilemma

~ Shaza Karrar, UAE ~ Leave a comment
Farmer's Dilemma

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!

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.

Pesticide Bottle Found Next To The Patient.
Pesticide Bottle Found Next To The Patient.

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

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

Cholinergic
Anticholinergic
Sedative/Hypnotic
Sympatholytic
Sympathomimetics

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.

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

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

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

  1. Organophosphate toxicity on WikEM: https://www.wikem.org/wiki/Organophosphate_toxicity
  2. Das RN, Parajuli S. Cypermethrin poisoning and anti-cholinergic medication- a case report. Internet J Med Update. 2006;1:42–4.
  3. 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
  4. 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

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