Neutropenic Fever Syndrome

Neutropenic Fever Syndrome

The story of Carl Wunderlich, his dedication to determine average body temperature, and his not so accurate thermometer is well known among the medical fraternity. Like any other physiological parameter, the average temperature should be looked at as a range and not a number. There are certain instances when a temperature above 0.5-degree centigrade of average is too hot for an ER doctor. Let us talk about one such condition today.

Cancer patients being treated with anti-neoplastics are at risk of neutropenic fever syndrome (NFS). An overly simplistic, and hence super helpful way of looking at NFS is: anti-neoplastics damage gastrointestinal mucosa, help bugs translocate into the bloodstream, and at the same time damage our white blood cells. All this happens in the background of malignancy, already an immunocompromised status.

Eighty percent of identified infections in NFS arise from endogenous flora. Well, that backs up my oversimplification. Now I can confidently tell you this statistic; infectious sources are only found in up to 30% of the cases.

NFS is a disease of acute leukemia patients. Up to 95% of leukemia patients, 25% of non-leukemic patients with hematologic malignancies, and 10 percent of patients with solid tumors get NFS after being started on cytotoxic therapy.

Fever in neutropenic [Absolute Neutrophil Count (ANC) <500] patients is a single temperature of 101F or a temperature of 100.4° F over one hour.

How would you calculate ANC?

Total leukocyte X (% of neutrophils + % of band neutrophils)

How do you measure temperature?

Neutropenia is one of the two common instances when a rectal temperature is wrong; the other is thrombocytopenic patients. Oral temperature is adequate; make sure they don’t have oral mucositis that can falsely increase the reading in the patient’s thermometer and your head at the same time.

To make it even more complicated, guess what most patients on cancer chemotherapy are taking? Glucocorticoids! Also, remember, they are neutropenic, meaning they don’t have an adequate inflammatory response. Infections in neutropenic can present without elevated temperature, so be aware of SIRS: tachycardia, tachypnea, hypotension.

There are scoring systems to stratify NFS patients in high and low risk; CISNE and MASCC scores are examples, but none are comprehensive and hence are underused.

The management’s holy grail is antibiotics, but with such diverse and elite targets, where do you shoot? Let us try and oversimplify this: If the bugs are coming from our gut, they better be gram-negative rods (Pseudomonas aeruginosa!) That was so very true back in the day. Now, with the introduction to long-term indwelling central venous catheters, the empiric antibiotics to cover P. aeruginosa, and other gram negatives (Ciprofloxacin)– Staphylococcus epidermidis is winning the race. The gram-negatives are catching up; 60:40 is the score currently.

Fungi are not frequently the cause of the first febrile episode, but candida from the gut (of course!) and aspergillus from the lungs are culprits in long-term invasive fungal infections.

Here is another one for those who like analogies; Remember how there is a time-dependent door to needle approach in treating STEMI or acute stroke? There is one for NFS, sort of; 60 mins, some agree, some don’t! The unanimous consensus is to do it fast!

The problems like time for confirmation of neutropenia, a protocol for what to cover, and where to start antibiotics are yet to be discussed and solved. Studies have been done to demonstrate that mortality increases with every hour delay in administering antibiotics. A good rule of thumb to follow is administering antibiotics right after you draw blood for culture and before you send it.
They pose one last problem while recovering from neutropenia. Myeloid reconstitution syndrome is fever and a new inflammatory focus while neutrophil numbers go up. That is vaguely reminiscent of immune reconstitution syndrome in newly started HAART patients.

Next time you see a patient being treated for leukemia with a temperature of 100.4° F being triaged to a green zone in your ER, know that green has different shades.

Cite this article as: Sajan Acharya, Nepal, "Neutropenic Fever Syndrome," in International Emergency Medicine Education Project, January 18, 2021,, date accessed: January 21, 2021

The Unspoken Damage of COVID-19 on Spanish-Speaking Patients

The Unspoken Damage of COVID-19 on Spanish-Speaking Patients

The COVID-19 pandemic has uncovered some ugly truths about the American healthcare system. One of the ugliest is discrimination against non-English-speaking patients. This form of discrimination particularly affects native Spanish-speaking only patients (defined in this article as “Spanish-speaking patients), who comprise not only a large proportion of America’s hospital patronage but also a majority of those suffering from COVID-19.

In May 2020, as part of my Emergency Medicine residency training, I worked at a small community hospital in northern Virginia, located in an agricultural area with a large number of Central American and Mexican migrant workers. The first few days of the rotation were relatively unremarkable until the COVID-19 cases began to pour in. Most of those suffering from severe COVID-19 were Spanish-speaking patients employed at a local plant nursery where an outbreak was occurring.

I intubated a COVID-19 patient almost every day I worked there. I speak Spanish fluently, and since I was able to communicate with Spanish-speaking patients and their families, I was able to obtain consent for the procedure. I will never forget one patient who had tears rolling down his face shortly after intubation as we titrated his post-intubation sedation medications. I spoke with his son over the phone, in Spanish, who thanked me profusely and cried, worried he would never see his father alive again. He asked if he could visit his father in the hospital. He cried more when I explained the no visitor policy for hospitalized COVID-19 patients. He still thanked me.

The ER staff also thanked me, because until I arrived, few in-person Spanish interpreters or fluent Spanish-speaking providers worked there. Therefore Spanish-speaking patients consented to intubations using a phone-based interpretation service. Though The Joint Commission states that telephone or video interpretation is sufficient to obtain informed consent (especially during the COVID-19 pandemic), in-person interpretation has proved superior. Unfortunately, at this small hospital, out of necessity and due to inundation by COVID-19 victims, Spanish-speaking patients had occasionally been intubated without true informed consent. For example, I remember a case when the overwhelmed nursing staff struggled to connect to and understand the phone-based interpreter while donning PPE and equipping a Spanish-speaking patient’s room for emergent intubation, only to be followed shortly thereafter by another critical COVID-19 patient.

Despite the large number of Spanish-speaking patients receiving care in the United States, a 2016 survey of 4,586 American hospitals showed that only 56 percent offered some sort of linguistic and translation services. As a former volunteer Spanish interpreter for a university hospital, the cost is cited as the primary reason, among many. Discrimination against undocumented people and xenophobia are unstated reasons. I remember distinctly a Grand Rounds presentation about native Spanish-speaking patients in hospitals and how a Latinx pediatrician emotionally expressed how often she witnessed Spanish-speaking families receive worse care than their English-speaking counterparts. Indeed, inadequate or inaccurate interpretation has resulted in serious legal, financial, and patient safety repercussions for hospitals.

In June, I worked in the COVID-19 ICU at my residency program’s hospital. Most of the COVID-19 ICU patients had been transferred from the same small hospital where I worked the previous May. After rounds, most of my afternoon was spent contacting Spanish-speaking family members and updating them on their loved one’s condition. It was heartbreaking to tell these families that they could not visit their loved ones in the hospital. Undoubtedly, the family is incredibly important to all cultures, and particularly to central and Mexican-Americans. Sadly, these strong family ties underscore an important reason Latinx people have been disproportionately affected by COVID-19: many live in large, multigenerational family homes, accelerating virus exposure and transmission. Furthermore, many are undocumented and work under substandard conditions, with few or no COVID-19 precautions. They may also be underinsured or have no insurance or benefits like sick leave, further fueling the virus’ devastation.

When you pull the bandage off a gangrenous wound to expose the decaying flesh below, you have two options: put the bandage back on and let someone else deal with it, or clean the wound and treat it so it can heal. The COVID-19 pandemic has pulled the bandage off and exposed certain disgusting realities of our health care system – how can we as Emergency Physicians heal this wound?

We must recognize that hospital under-investment in adequate Spanish interpreters is a form of racism. Medical Spanish should be required curriculum for medical students and residents. The knowledge of basic conversational Spanish goes a long way when communicating with patients and their families. Medical Spanish is not difficult, and there are enough cognates and Latin derivatives that most people, with minimal practice, can get through history and physical in Spanish. Most importantly, hospitals should invest in full-time in-person Spanish interpreters, at the very least for the Emergency Department.

The COVID-19 pandemic has ravaged our healthcare system in myriad ways. With destruction comes the opportunity to rebuild and improve. This is one area that needs it.

Cite this article as: Sarah Bridge, USA, "The Unspoken Damage of COVID-19 on Spanish-Speaking Patients," in International Emergency Medicine Education Project, January 11, 2021,, date accessed: January 21, 2021

Erythema Types in Medicine – Rapid Review For Medical Students

Our skin, the largest organ in the human body, is crucial for maintaining life and overall health. It serves as an airtight, watertight and flexible barrier with the outside world and helps with temperature regulation, immune defense, vitamin production and sensation.

However, the skin is unique in that no other organ demands as much attention in states of disease and health. Our skin’s quality and condition significantly contribute to health, wellness, youth, and beauty perceptions. Such a focus even causes self-esteem and mental health problems stemming from scars, acne, and inflammation to abnormal redness of the skin known as erythema.

Erythema stems from the dilation and irritation of the superficial capillaries and the augmented blood flow that imparts a reddish hue to the skin. Often presenting as a rash, erythema can be caused by environmental factors, infection, or overexposure to the sun.

Since exam season is here, this serves as a rapid review to recall the most common types of Erythema!

Erythema Ab Igne (EAI)

  • The skin reaction stems from chronic exposure to infrared radiation in the form of heat. Once considered a common condition of the elderly who stood or sat closely to open fires or electric space heaters. EAI has reduced significantly with the advent of central heating, although it is still found in individuals exposed to heat from other sources. In EAI, the skin and underlying tissue begin to atrophy, causing patients to complain of mild itchiness and a burning sensation.
  • To prevent the progression of EAI, discontinuing contact with the heat source is necessary.

By <a href=”//″ class=”mw-redirect” title=”User:Jmh649″>James Heilman, MD</a> – <span class=”int-own-work” lang=”en”>Own work</span>, CC BY-SA 3.0, Link

Erythema Chronicum Migrans

  • The primary manifestation of Lyme Disease, erythema chronicum migrans appears 7 to 14 days after the infected tick bite. As an expanding red patch of skin, the size of the rash can reach several centimetres in diameter. The central spot surrounded by clear skin ringed by an expanding red rash known as a bull’s-eye is the most typical appearance.
  • Successful treatment of erythema migrans may be accomplished with 20 days of oral doxycyclineamoxicillin, or cefuroxime axetil.

Bullseye Lyme Disease Rash.jpg
By Hannah Garrison – <a href=”; class=”extiw” title=”en:User:Jongarrison”>en:User:Jongarrison</a>, CC BY-SA 2.5, Link

Erythema Induratum

  • Erythema induratum from Bazin disease presents as recurring nodules or lumps on the back of the legs in mostly women that ulcerate and scar.
  • Drugs for treatment include isoniazid, rifampicin, and pyrazinamide, that may be administered orally or intravenously in combination.

An introduction to dermatology (1905) erythema induratum 2.jpg
By Norman Purvis Walker – Walker, Norman Purvis (<span style=”white-space:nowrap”>1905</span>) <a rel=”nofollow” class=”external text” href=””>An introduction to dermatology</a> (3rd ed.), William Wood and company Retrieved on 26 September 2010., Public Domain, Link

Erythema Infectiosum or Fifth Disease

  • Erythema infectiosum is also known as the Fifth disease. It is caused by Parvovirus B19 that affects mostly children. The main clinical feature is the “slapped face” appearance along with a sore throat, mild fever and malaise, and signs of Fifth Disease’s prodrome period. The confluent netlike rash begins on the cheeks and spreads to the trunk and extremities.
  • Children may be given NSAIDs to alleviate and relieve fever, headache and achiness.

Fifth disease.jpg
By Andrew Kerr – <span class=”int-own-work” lang=”en”>Own work</span>, Public Domain, Link

Erythema Marginatum

  • Erythema marginatum rheumaticum occurs in about 10% of first attacks of Acute Rheumatic Fever (ARF) in children appearing on their trunk, upper arms and legs as pink or red macules or papules spreading in a circular shape. As the lesions advance, the edges become raised, red, and persist intermittently for weeks to months, even after successful ARF treatment.
  • There is no treatment for erythema marginatum specifically as the rash fades on its own.

Erythema Multiforme

  • Erythema multiforme is a cell-mediated cytotoxic reaction in the skin and mucous membranes triggered by Mycoplasma Pneumoniae or Herpes Simplex Virus or even drugs as sulfonamides, penicillin, barbiturates, NSAIDs, & phenytoin. Vesicles and bullae on the soles, palms, and extensor surfaces with a “targetoid” appearance are characteristic of the rash. Without treatment and care by dermatologists, Steven Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) occur as they are severe forms of erythema multiforme.
  • Treatment includes oral antihistamines, analgesics, local skincare, and soothing mouthwashes.

Erythema multiforme minor of the hand.jpg
By <a href=”//″ class=”mw-redirect” title=”User:Jmh649″>James Heilman, MD</a> – <span class=”int-own-work” lang=”en”>Own work</span>, CC BY-SA 3.0, Link

Erythema Nodosum

  • Erythema nodosum is an acute inflammatory reaction involving the subcutaneous fat where the skin becomes red, raised and painful on the anterior portions of the shins and wrist. It is more common in women than men, and although the most identifiable cause is streptococcal pharyngitis, it is associated with coccidioidomycosis, histoplasmosis, tuberculosis, leprosy, sarcoidosis, ulcerative colitis, and pregnancy.
  • Anti-inflammatory drugs and corticosteroids by mouth or local injection may serve as treatment options. Colchicine is also administered to reduce inflammation.

By <a href=”//″ class=”mw-redirect” title=”User:Jmh649″>James Heilman, MD</a> – <span class=”int-own-work” lang=”en”>Own work</span>, CC BY-SA 3.0, Link

Erythema Toxicum Neonatorum

  • Erythema toxicum neonatorum is a self-limited skin eruption occurring in newborns due to an unknown cause. Erythematous papules, macules and plaques present in all sites except the soles and palms and may last approximately 2-3 weeks.
  • No treatment is necessary for erythema toxicum neonatorum as the lesions regress after 5 days to 2 weeks.

Erythema Elevatum Diutinum (EED)

  • Erythema elevatum diutinum (EED) is a type of necrotising vasculitis characterised by red, purple, or brown papules, plaques, or nodules. It is a rare form of erythema usually found on extensor surfaces overlying the joints, and the buttocks. It is a chronic and progressive skin disease that may last as long as 25 years.
  • The drug of choice for EED is Dapsone because of its rapid onset of action; however, it is possible for lesions to recur the following withdrawal promptly.

Erythema elevatum diutinum on hand.jpg
By <a href=”//;action=edit&amp;redlink=1″ class=”new” title=”User:Dswierc (page does not exist)”>D Swierczek</a> – <span class=”int-own-work” lang=”en”>Own work</span>, CC BY-SA 4.0, Link

Erythema Gyratum Repens

  • Erythema gyratum repens is a rare paraneoplastic type of annular erythema with a ‘wood-grain’ appearance associated with malignancy. Furthermore, almost half of the patients with erythema gyratum repens have lung cancer and less commonly, oesophageal, breast, and stomach cancer.
  • The rash usually resolves once the malignancy has been removed with surgical resection.

References and Further Reading

Cite this article as: Leah Sarah Peer, Canada, "Erythema Types in Medicine – Rapid Review For Medical Students," in International Emergency Medicine Education Project, January 4, 2021,, date accessed: January 21, 2021

Question Of The Day #24

question of the day
738.1 - Prior ECG before 738.2 - STEMI

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

This patient is suffering from severe bradycardia with signs of poor cardiac output, shock, and diminished perfusion to the brain. Bradycardia is defined as any heart rate under 60 beats/min. Many individuals may be bradycardic at rest with no danger to the patient (i.e. young patients or athletes). Bradycardia in these scenarios is physiologic and is not associated with difficulty in perfusing the brain and other organs. This patient’s 12-lead EKG shows sinus bradycardia since there is a P wave prior to every QRS complex. Sinus bradycardia is the most common type of bradycardia. Other types of bradycardia include conduction blocks (i.e. type 2 or type 3 AV blocks), junctional rhythms (lack of P waves with slow SA nodal conduction), idioventricular rhythms (wide QRS complex rhythms that originate from the ventricles, not atria), or slow atrial fibrillation or atrial flutter. About 80% of all bradycardias are caused by factors external to the cardiac conduction system, such as hypoxia, drug effects (i.e. beta block or calcium channel blocker use or overdose), or acute coronary syndromes.  

For any patient with a bradyarrhythmia or tachyarrhythmia, it is crucial to determine if the arrythmia is “stable” or “unstable”. Signs that an arrhythmia is unstable include altered mental status, hypotension with systolic blood pressure under 90mmHg, chest pain, or shortness of breath. Patients with a stable arrhythmia can be managed supportively with observation and less invasive medical management. Patients with unstable arrhythmia are managed more aggressively with the use of electricity, often in combination with other medical treatments. This patient has an unstable bradyarrhythmia, given her altered mental status and hypotension. Intravenous metoprolol (Choice D) would make the patient more bradycardic since this medication blocks beta-adrenergic receptors of the heart that control heart rate and contractility. Intravenous Amiodarone (Choice C) is an antiarrhythmic agent used often in wide complex tachyarrhythmias (i.e. Ventricular Tachycardia). Intravenous atropine or epinephrine are agents that can be used in this patient prior to preparing for electric pacing. Transcutaneous pacing (Choice A) should always be attempted prior to Transvenous pacing (Choice B), as Transcutaneous pacing is less invasive and quicker to set up. If Transcutaneous pacing does not result in electrical “capture” or change the heart rate, the next step is Transvenous pacing. Correct Answer: A 


  • Brady W.J., & Glass III G.F. (2020). Cardiac rhythm disturbances. Tintinalli J.E., Ma O, Yealy D.M., Meckler G.D., Stapczynski J, Cline D.M., & Thomas S.H.(Eds.), Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill.
  • Burns, E. (2020). Sinus Bradycardia. Life in the Fast Lane. Retrieved from
Cite this article as: Joseph Ciano, USA, "Question Of The Day #24," in International Emergency Medicine Education Project, December 11, 2020,, date accessed: January 21, 2021

Hypertrophic Cardiomyopathies

Hypertrophic Cardiomyopathies

Hypertrophic cardiomyopathy is an inherited cardiovascular disease [1]. The condition can lead to sudden death in young adults and other problems such as heart failure, arrhythmias and stroke. It is prevalent in the world, with cases reported in over 50 countries and in people of all sexes, ethnicities and races. In diverse regions including the USA, Europe and East Africa, the prevalence of hypertrophic cardiomyopathy is 1 in 500 in the general population [2]. While considered a common and possibly fatal disease, most affected individuals remain undiagnosed in their lifetime and do not experience symptoms or reduced life expectancy [1].

Hypertrophic cardiomyopathy is passed on by an autosomal dominant fashion through mutations in more than 12 genes that encode for thick and thin myofilament proteins. However, sporadic cases caused by de-novo mutations in the predisposing genes can also occur [3]. Genetic testing for the identification of causative mutations can be conducted via DNA sequencing; however, pathogenic mutations are identified in roughly fewer than 50% of clinically affected patients [1].

Clinical Presentation, Signs and Symptoms

Clinical diagnosis of hypertrophic cardiomyopathy entails a hypertrophied but non-dilated left ventricle without evidence of any other disorders, such as cardiac or systemic diseases that may cause cardiomyocyte hypertrophy [4]. Often, patients with hypertrophic cardiomyopathy do not have any symptoms, and diagnosis is made either incidentally or through familial genetic screening. However, symptomatic patients may experience chest pain with exertion and varying rates of dyspnoea on a daily basis. Chest pain may also present at rest and can be caused by large meals. Some patients can also experience syncope [5]. Dyspnoea, chest pain and syncope are common symptoms that we faced in the emergency department. Although there are more common and deadly presentations with those symptoms, hypertrophic cardiomyopathy should always be in our differential diagnoses, particularly in cases with additional findings explained below.

Clinical Exam and Investigations

Clinical examination of patients with hypertrophic cardiomyopathy often reveals little information. In patients with dynamic left ventricular outflow tract obstruction, a systolic murmur may be heard with auscultation at the left sternal edge, radiating to the aortic and mitral areas [5]. However, if hypertrophic cardiomyopathy is suspected, either due to familial screening, the presence of a murmur or an abnormal 12-lead electrocardiogram (ECG), its diagnosis needs to be confirmed with either echocardiography and/or cardiovascular MRI [1].

Natural History and Clinical Course of Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathies can present at any age from infancy to adulthood. Many patients with this cardiovascular disease are expected to have a normal life expectancy without any major complications or even therapeutic interventions [6]. However, complications may occur in some patients and can include a range of events. Sudden death may occur in patients who are mildly symptomatic or even asymptomatic. Progressive heart failure with possible obstructive outflow obstruction and normal systolic function can occur, which may slowly lead to systolic dysfunction [4]. Cardiac arrhythmias may also develop – most commonly atrial fibrillation. This can lead to symptoms of heart failure and embolic stroke in 20% of the patients [7].

Sudden Death

Sudden death is the most unpredictable and devastating consequence of hypertrophic cardiomyopathy and is the most common cause of sudden death in young patients (under the age of 30) and young athletes [1,4,8]. However, the risk of sudden death falls gradually with older age. Although sudden death from mild physical activity or even inactivity can occur, death due to vigorous exertion amongst this patient population is more common [1]. Sudden death from hypertrophic cardiomyopathy usually occurs due to ventricular fibrillation and tachycardia. Risk stratification of high-risk patients for sudden death is important and can lead to the prevention of sudden death using various approaches, such as an implantable defibrillator [1,9]. Additionally, young professional athletes should be screened to detect silent signs of cardiovascular disorders that may lead to sudden death. Unfortunately, if young athletes are found to have hypertrophic cardiomyopathy, implementation of a cardiovert-defibrillator is not sufficient to grant athletes to return to competing. Athletes are often advised to stop participating in competitive sports, unless it is of low intensity such as golf [8].

Heart Failure

Symptoms of heart failure associated with preserved left-ventricular systolic function most often occur in middle-aged patients but can occur at any age [13]. Functional limitations can occur at differing rates but are often gradual and involve day to day variability. Women with hypertrophic cardiomyopathy have been shown to experience more severe symptoms of heart failure later in life compared to male patients. Frequently, these symptoms experienced in women have been associated with left-ventricular outflow-tract obstruction [14]. Some causes of heart failure in hypertrophic cardiomyopathy patients include left-ventricular outflow-tract obstruction, atrial fibrillation and diastolic dysfunction [1,4]. Treatment strategies include drugs and surgical myectomy or alcohol septal ablation for relief of symptoms of heart failure and outflow obstruction, and pharmacological strategies to treat atrial fibrillation and prevent stroke (such as blood thinners).

Hypertrophic Cardiomyopathy Management in the ED

Patients with hypertrophic cardiomyopathy exacerbation may present to the ED with a range of symptoms including syncope, chest pain, dyspnea, cardiac arrhythmia and worst of all, sudden cardiac death [10]. Diagnosis of hypertrophic cardiomyopathy patients presenting with these symptoms to the ED may be difficult as most of these patients are not aware of their underlying cardiovascular disease. Therefore, ED staff should keep this differential in mind and should be aware of certain diagnostic tools and approaches for acute management of hypertrophic cardiomyopathy.

Primarily, ED staff should conduct a complete history of the patients, including family history of relatives with early cardiovascular disorders or sudden death at a young age. Physical examination of the patient may be inconclusive, as patients usually don’t present with any specific cardiovascular symptoms, unless their disease has progressed to having left-ventricular outflow obstruction tract. An electrocardiogram (EKG) should be conducted, as most patients with hypertrophic cardiomyopathy will have abnormal EKGs. Specifically, their EKGs will show signs of left ventricular hypertrophy through large amplitude QRS, and deep, narrow Q waves particularly in the lateral leads if the patient has septal hypertrophy [11]. Physical examination should be coupled with EKG to rule out other cardiac problems.

Adopted from - Ed Burns. Hypertrophic Cardiomyopathy (HCM).

Deep narrow Q waves in chest leads are typical ECG finding of the hypertrophic cardiomyopathy patients. For more ECG information please visit –

In managing hypertrophic cardiomyopathy patients, following the ACLS algorithm if the patient is hemodynamically unstable is first priority. Otherwise, the goal of acute treatment of hypertrophic cardiomyopathy is to restore normal sinus rhythm or control the ventricular rate. Appropriate vasopressors should be given if patients are experiencing volume fluctuations due to diarrhea or other consequences of their disease. If patients present with a new onset of atrial fibrillation, approach of rate versus rhythm control and thromboembolism risk management should be considered [10]. If acute pharmacological treatment of hypertrophic cardiomyopathy patients is required, caution should be taken considering the state of their disease. For example, caution must be exercised when giving diuretics to patients with severe heart failure, as reduction in left ventricular preload can exacerbate obstruction and lead to hypotension [12]. The same considerations must be applied to any other treatment and guidelines should be followed closely. In conclusion, quick identification of the patient’s underlying cardiovascular problem and acute pharmacological management in the ED is critical to help the patient until a specialist can see them.

References and Further Reading

  1. Maron, B. J., & Maron, M. S. (2013). Hypertrophic cardiomyopathy. The Lancet381(9862), 242-255.
  2. Maron, B. J., Gardin, J. M., Flack, J. M., Gidding, S. S., Kurosaki, T. T., & Bild, D. E. (1995). Prevalence of hypertrophic cardiomyopathy in a general population of young adults: echocardiographic analysis of 4111 subjects in the CARDIA study. Circulation92(4), 785-789.
  3. Alcalai, R., Seidman, J. G., & Seidman, C. E. (2008). Genetic basis of hypertrophic cardiomyopathy: from bench to the clinics. Journal of cardiovascular electrophysiology19(1), 104-110.
  4. Maron, B. J. (2002). Hypertrophic cardiomyopathy: a systematic review. Jama287(10), 1308-1320.
  5. Elliott, P., & McKenna, W. J. (2004). Hypertrophic cardiomyopathy. The Lancet363(9424), 1881-1891.
  6. Maron, B. J., Casey, S. A., Hauser, R. G., & Aeppli, D. M. (2003). Clinical course of hypertrophiccardiomyopathy with survival to advanced age. Journal of the American College of Cardiology42(5), 882-888.
  7. Olivotto, I., Cecchi, F., Casey, S. A., Dolara, A., Traverse, J. H., & Maron, B. J. (2001). Impact of atrial fibrillation on the clinical course of hypertrophic cardiomyopathy. Circulation104(21), 2517-2524.
  8. Maron, B. J. (2003). Sudden death in young athletes.New England Journal of Medicine349(11), 1064-1075.
  9. Maron, B. J., Shen, W. K., Link, M. S., Epstein, A. E., Almquist, A. K., Daubert, J. P., … & Estes, N. M. (2000). Efficacy of implantable cardioverter–defibrillators for the prevention of sudden death in patients with hypertrophic cardiomyopathy.New England Journal of Medicine342(6), 365-373.
  10. Gardner, M., Nair, V., Hu, D., & Derry, S. (2018). The evaluation and management of decompensated hypertrophic cardiomyopathy in the emergency department.The American journal of emergency medicine36(12), 2286-2288.
  11. Kelly, B. S., Mattu, A., & Brady, W. J. (2007). Hypertrophic cardiomyopathy: electrocardiographic manifestations and other important considerations for the emergency physician.The American journal of emergency medicine25(1), 72-79.
  12. Efthimiadis, G. K., Pagourelias, E., Zegkos, T., Parcharidou, D., Panagiotidis, T., Arvanitaki, A., … & Karvounis, H. (2016). An overview of pharmacotherapy in hypertrophic cardiomyopathy: current speculations and clinical perspectives.Reviews in Cardiovascular Medicine17(3-4), 115-123.
  13. Melacini, P., Basso, C., Angelini, A., Calore, C., Bobbo, F., Tokajuk, B., … & Thiene, G. (2010). Clinicopathological profiles of progressive heart failure in hypertrophic cardiomyopathy.European heart journal31(17), 2111-2123.
  14. Olivotto, I., Maron, M. S., Adabag, A. S., Casey, S. A., Vargiu, D., Link, M. S., … & Maron, B. J. (2005). Gender-related differences in the clinical presentation and outcome of hypertrophic cardiomyopathy.Journal of the American College of Cardiology46(3), 480-487.


Cite this article as: Maryam Bagherzadeh, Canada, "Hypertrophic Cardiomyopathies," in International Emergency Medicine Education Project, December 9, 2020,, date accessed: January 21, 2021

How To Present Your Case In The ED

how to present your case in the ED

As a medical student, presenting history and physical exam of a patient to the attending can be nerve-wracking. In the ED, physicians typically prefer an even more succinct presentation than usual, ideally less than 3 min. Case presentations are a great opportunity to show that you understand what the pertinent positives and negatives for the patient’s presenting complaint are and that you can summarize a large amount of information collected in an organized manner. Case presentations are your opportunity to impress your preceptor, so it is an important skill to master. It will also be the mode of communicating with the rest of the healthcare team throughout your career in medicine. Better communication = better patient care!


Before we get started, it is important to recognize that every physician may have their own preference for how they would like case presentations organized. Some prefer more details, and some prefer a specific order. Therefore, it is always a smart idea to ask your preceptor at the beginning of your ED shift if they have a preference for how they like cases to be presented.

The One Liner

State the patient’s name, age, sex, chief complaint, and any pertinent medical history. E.g., John Doe is a 16-year-old male with a history of eczema presenting with wheezing.

History of Presenting Illness (HPI)

include the details of the chief complaint, as well as any pertinent positives and negatives.
  1. Why did this patient present to the ED today?
  2. What are the details of the chief complaint? I.e. Onset, Duration, Progression, Alleviating and Aggravating Factors, Causes/Triggers, Changes with Position, etc.
    • For pain, it is helpful to describe OPQRSTU – Onset, Position, Quality, Radiation, Severity, Temporal, déjà vU (has it ever happened before).
  3. Any associated symptoms
  4. Any risk factors?
    • Any relevant past medical history (e.g. chronic conditions, hospitalizations, surgeries, etc.), family history, or social history (e.g. habits, living situation, alcohol consumption, smoking history, illicit drug usage)?

Review of Systems

Describe any other symptoms here.

  • Note that some ED physicians may not want a review of systems included in the oral case presentation if it does not include any additional pertinent information, but a review of systems should always be included in your written patient note. 



if the patient states that they do not have any allergies, this can be recorded and/or stated as “NKDA” which stands for No Known Drug Allergies.

Physical Exam Findings

  1. Start off by stating the most updated set of vitals.
  2. Next, state the patient’s general appearance as this helps decide between sick vs. not sick. E.g., patient is alert, oriented, and in no apparent respiratory distress.
  3. Then, delve into the pertinent details of the physical exam. E.g. for a cardiac complaint, it is important to include the specific details of the cardiovascular exam and respiratory exam, but not of all the other systems.
  4. A brief overview of the other systems that a physical exam was conducted for can be useful, but be as concise as possible, and organize information in a head-to-toe fashion if needed. If there were no other findings, you can state that the remainder of the physical exam was unremarkable. 


In 2-3 sentences, gather the main findings of your history and physical exam. Be sure to restate the initial one-liner sentence, other pertinent positives and negatives, and any important test results so far.


State your differential diagnosis for each problem.

  • Start off by stating what you think the most likely diagnosis is, and why you think it is the most likely.
  • Then, state any other likely diagnoses you are suspecting.
  • Lastly, state the deadly diagnoses that could be possible with this patient’s chief complaint. In some cases, this can be the first thing you may want to say. It is important to specify why you do or do not feel confident in ruling these out. E.g., in a baby presenting with fever of unknown origin, it is important to state why you are not (or are) suspecting meningitis, encephalitis, malignancy, or autoimmune conditions.
  • Many medical students will shy away from stating their impression of what could be going on in terms of differential diagnosis, but this is an important thing to attempt. Preceptors will appreciate your effort in synthesizing what could be going on and be impressed by it, even if your impression is incorrect. This is often what sets apart students that “meet expectations” vs. students that are considered “outstanding”.


What do you want to do next?

  • Plan includes anything from the tests you want to order (including repeat vitals, bloodwork, and imaging), immediate treatment (including analgesics and fluids), and referrals you want to make (including consults, admission/discharge plan, and referral to allied health professionals such as social work, speech-language pathology, occupational therapy, and physiotherapy).  
  • Do not forget to take the patient’s social history into account when deciding what to do next.

Congrats – you have now completed your oral case presentation! This is a skill you will continue to develop with practice, so do not worry and keep working at it. It is also a good idea to always ask your preceptor for feedback on your case presentation once it is complete, as that will help you identify your strengths and weaknesses.

References and Further Reading

Cite this article as: Sheza Qayyum, Canada, "How To Present Your Case In The ED," in International Emergency Medicine Education Project, December 7, 2020,, date accessed: January 21, 2021

More Blog Posts By Sheza Qayyum

Question Of The Day #23

question of the day
3. PEA

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

This patient presented to the emergency department with acute pleuritic chest pain, dyspnea, and experienced a cardiac arrest prior to a detailed physical examination. The cardiac monitor shows a narrow complex sinus rhythm morphology. In the setting of a cardiac arrest and pulselessness, this cardiac rhythm is known as pulseless electric activity (PEA). PEA includes any cardiac rhythm that is not asystole, ventricular fibrillation, or pulseless ventricular tachycardia. The ACLS algorithm divides the management of patients with pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) and patients with pulseless electric activity (PEA) or asystole. Assuming adequate staff and medical resources are present, patients with all of these rhythms receive high-quality CPR, IV epinephrine, and airway management. Patients with pVT or VF receive electrical cardioversion, while patients with PEA or asystole do not receive electrical cardioversion. Patients with PEA or asystole generally have a poorer prognosis than those with pVT or VF. Out of hospital cardiac arrests that present to the emergency department with PEA or asystole on initial rhythm have a survival rate of under 3%. The etiology of PEA in cardiac arrest includes a wide variety of causes. A traditional approach to remembering the reversible causes of PEA are the “Hs & Ts”. The list of the “Hs & Ts” along with their individual treatments are listed in the table below.

PEA treatments

Sodium bicarbonate (Choice A) would be the correct choice for a patient whose PEA arrest was caused by severe acidosis. This can occur in severe lactic acidosis (i.e. sepsis), diabetic ketoacidosis, certain toxic ingestions (i.e. iron, salicylates, tricyclic antidepressants), as well as other causes. Calcium gluconate (Choice B) would be the correct choice for a patient whose PEA arrest was caused by hyperkalemia. This can occur in renal failure, in the setting of certain medications, rhabdomyolysis (muscle tissue breakdown), and other causes. Blood products (Choice D) would be the correct choice for a patient whose PEA arrest was due to severe hemorrhage, such as gastrointestinal bleeding or in the setting of traumatic injuries. This patient has symptoms and risk factors for pulmonary embolism, including pleuritic chest pain, dyspnea, and a cancer history. These details make pulmonary embolism the most likely cause of PEA arrest in this scenario. The best treatment for this diagnosis would be thrombolysis (Choice C).


Cite this article as: Joseph Ciano, USA, "Question Of The Day #23," in International Emergency Medicine Education Project, December 4, 2020,, date accessed: January 21, 2021

Emergency Medicine Course Experience

It has been two years that the International Emergency Medicine (iEM) Education Project ( met with medical students. The project, which aims to promote emergency medicine and provide free, reusable education resources for medical students and educators, reached another important milestone during the COVID-19 pandemic.

iEM education project, which supported by United Arab Emirates University College of Medicine and Health Sciences and endorsed by the IFEM, announced a 4-week free open online emergency medicine core content course for medical students via IFEM newsletter and multiple emergency medicine platforms at the end of the April. In the first 24 hours, the course website ( was visited more than 3000 times from 57 countries. Syria (13%), Indonesia (10.6%), Thailand (8.1%), United States (7.3%), and Vietnam (6.5%) were the top five countries where registered students are coming from. The report of this social responsibility initiative shows a great collaboration of academic,  non-profit and commercial organisations during a pandemic. The background and the first 24 hours of this journey has now been published as an editorial in the African Journal of Emergency Medicine. 

You can read the editorial “From the pandemic’s front lines: A social responsibility initiative to develop an international free online emergency medicine course for medical students” from this link – (

Sleep and Shiftwork

sleep and shiftwork

The emergency department is open 24/7, meaning that most ED physicians experience shift work. Shift work means that service is provided around the clock, whether it be night or day. Though shift work is almost always part of the job description for an ED doctor, it may not always favour the wellbeing of the physician. Inspired by a classmate, who adopted the sleep cycle of an ED early on in his M1 year, I wanted to discuss the science of sleep, the impact of shift work and how can we improve sleep hygiene when shift work is part of our job.

Basic Science of Sleep?

Sleep is part of every human being’s existence, as we could not live without it. Even though we have limited recollection of what happens during sleep, the process is quite complex. First, sleep latency is the time needed to fall asleep. Second, sleep is broken down into four stages that we oscillate through 4-5 times a night. The time it takes to go through all stages in a sleep cycle is approximately 90-120 minutes. The four stages we must pass through are called stage 1, stage 2, stage 3 and rapid eye movement (REM) sleep, respectively. Stage 1 through 3 is collectively called non-rapid eye movement sleep (NREM).

Stage 1 is the lightest stage of sleep and the first one we enter from wakefulness and is characterized by theta waves (4-7 Hz) on an EEG. Stage 2 is a deeper sleep and the period where we spend most of our time sleeping. It is characterized by theta waves, sleep spindles and k-complexes. Finally, stage 3 is known as slow-wave sleep, where delta waves predominate the EEG (0-4 Hz). Finally, after the three NREM stages, we enter REM sleep. REM is the deepest stage of sleep, despite the EEG activity being the closest to waking state. It is during REM sleep that we experience vivid dreams and have low muscle tone.

So why is sleep important?

First, there is a growing body of evidence that slow-wave sleep is when we store memories. Therefore, through proper sleep, we can consolidate memories, increasing retention of what we had learned the previous day. Moreover, sleep is important in our ability to regulate our emotions and respond appropriately to different circumstances. In addition, when we get proper sleep, we are more like to be in a positive mood, which can impact our patient interactions. Furthermore, sleep is important in immune regulation and the ability to fight off infection. Finally, sleep helps with muscle recovery and favours protein anabolism (growth). I personally believe that muscle recovery is important given the time spent on one’s feet during an ER shift. This theory of sleep and muscle recovery has been supported in sports medicine literature, and I am intrigued to see if this evidence also existed for ED Physicians and other medical specialities that are more physically demanding.

Shift work in health care workers

So, what happens when we don’t sleep? First, shift work and lack of proper sleep increase levels of fatigue and errors made by health care workers. This can have profound implications on patients, especially in the ED, where the severity of presentation is often greater than in other clinical environments. This is also alarming, given that shift workers tend to have a reduced total amount of sleep. This reduced amount of sleep most commonly impacts stage 2 NREM sleep and REM sleep, thus reducing the quality of sleep, in addition to the duration of sleep. This reduced sleep quality is worse in shift workers on a rotating shift schedule, compared to a nighttime or daytime only worker.

Moreover, in some studies of ER workers, the duration of sleep, especially REM, is less during the day then at night. So even if one believes they are still getting sleep, it may be of reduced quality. Some explanations for this diminished REM sleep during the day is the body’s natural response to a light-dark schedule and the release of melatonin, the sleep hormone. Melatonin is the sleep hormone, which often rises at nighttime when it is time to go to bed. Sunlight inhibits the release of melatonin, signalling our bodies that it is time to be awake. So, even if one tries to sleep in a dark room, the walk home from a shift or exposure to hospital lights may confuse the circadian clock, diminishing sleep quality. Finally, other studies have reported that shiftwork could increase cardiovascular disease risk, blood pressure, increase levels of stress and cause gastrointestinal issues. In women, shiftwork can cause fertility problems, such as premature birth and low-birth-weight infants.

How to combat some of the negative effects of shiftwork

Individual Strategies

There are many things we can do to manage our sleep quality and scheduling. For example, our sleep environment can be adjusted to maximize our sleep quality. Strategies can include the use of earplugs and ensuring a dark room devoid of as much light as possible. Additionally, sunglasses can be worn to and from a night shift, to avoid daylight, which may signal to our body the biological start or end of a day.

Organizational Strategies

While some of the individual strategies may be useful to improve sleep hygiene with a shift work schedule, I also believe that some strategies should be implemented at the institutional level. For example, there is a body of literature which discusses that shifts longer than 12 hours are the most detrimental to sleep quality and a physician’s health. Moreover, the duration and timing of a break during a shift could help reduce some of the symptoms of shift work. Longer breaks during a shift are favoured, though the reasons why the longer breaks are better for sleep hygiene are unknown. Finally, scheduling strategies should be implemented. A paper by Burgess, has suggested that shifts be organized in a clockwise manner. For example, on performs a morning shift, then evening shift and a night shift etc. Moreover, morning shifts should not start earlier than 8:00 A.M. to favour our natural circadian rhythm. Issues with this approach are that multiple physicians work in an emergency department, many with families and different lives, which may prefer different schedules. Another issue is when a physician is sick, and another substitutes in. This could throw off the sleep schedule of both the physician cancelling and substituting the shift. Furthermore, is there an ideal number of days between shifts? Should this change with physician age knowing how melatonin levels decrease and the body becomes less resistant to stressors with ageing. While there are currently no gold standards with sleep regulation and shiftwork, we should at least be aware of why this is important and be mindful of our practices. It is easy to neglect our health in favour of our careers, something I have been all too familiar with and hope to improve.


I would like to end this article with a few comments about sleep. While the published literature may not tell a complete story due to the publication bias, there are a few things we can take away. Sleep is essential for our health and mental wellbeing. Shiftwork cannot be avoided, and, if self-care is not practiced, lack of sleep can have detrimental effects on our body and wellbeing. The impact of shiftwork on everyone can be different. Therefore, individual strategies to advocate for personal health is important. Organizations have a role in fostering an environment that supports good sleep habits and employee health. Finally, medical schools and residency programs should incorporate time to educate students on sleep hygiene and hopefully, inspire students to be agents of change in their own hospitals, thus fostering wellness practices. I look forward to joining you next time while I talk about imposter syndrome in medicine.

References and Further Reading

  • Burgess P. A. (2007). Optimal shift duration and sequence: recommended approach for short-term emergency response activations for public health and emergency management. American journal of public health, 97 Suppl 1(Suppl 1), S88–S92.
  • Dall’Ora C, Ball J, Recio-Saucedo A, Griffiths P. Characteristics of shift work and their impact on employee performance and wellbeing: A literature review. Int J Nurs Stud. 2016;57:12-27. doi:10.1016/j.ijnurstu.2016.01.007
  • Dattilo M, Antunes HK, Medeiros A, et al. Sleep and muscle recovery: endocrinological and molecular basis for a new and promising hypothesis. Med Hypotheses. 2011;77(2):220-222. doi:10.1016/j.mehy.2011.04.017
  • Gruber R, Cassoff J. The interplay between sleep and emotion regulation: conceptual framework empirical evidence and future directions. Curr Psychiatry Rep. 2014;16(11):500. doi:10.1007/s11920-014-0500-x
  • Halson SL, Juliff LE. Sleep, sport, and the brain. Prog Brain Res. 2017;234:13-31. doi:10.1016/bs.pbr.2017.06.006
  • Ibarra-Coronado EG, Pantaleón-Martínez AM, Velazquéz-Moctezuma J, et al. The Bidirectional Relationship between Sleep and Immunity against Infections. J Immunol Res. 2015;2015:678164. doi:10.1155/2015/678164
  • Kuhn G. Circadian rhythm, shift work, and emergency medicine. Ann Emerg Med. 2001;37(1):88-98. doi:10.1067/mem.2001.111571
  • Marshall L, Helgadóttir H, Mölle M, Born J. Boosting slow oscillations during sleep potentiates memory. Nature. 2006;444(7119):610-613. doi:10.1038/nature05278
  • Paller KA, Voss JL. Memory reactivation and consolidation during sleep. Learn Mem. 2004;11(6):664-670. doi:10.1101/lm.75704
  • Qureshi, S., Karrila, S., & Vanichayobon, S. (2018). Human sleep scoring based on K-Nearest Neighbors. Turkish Journal of Electrical Engineering & Computer Sciences, 26(6), 2802-2818.
  • Sack RL, Lewy AJ, Erb DL, Vollmer WM, Singer CM. Human melatonin production decreases with age. J Pineal Res. 1986;3(4):379-88. doi: 10.1111/j.1600-079x.1986.tb00760.x. PMID: 3783419.
Cite this article as: Brenda Varriano, Canada, "Sleep and Shiftwork," in International Emergency Medicine Education Project, November 30, 2020,, date accessed: January 21, 2021

More Blog Posts by Brenda Varriano

More Wellness Blog Posts

Question Of The Day #22

question of the day
1. VFib

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

This patient presents to the Emergency Department after a cardiac arrest with an unknown medical history. Important components of Basic Life Support (BLS) include early initiation of high-quality CPR at a rate of 100-120 compressions/minute, compressing the chest to a depth of 5 cm (5 inches), providing 2 rescue breaths after every 30 compressions (30:2 ratio), avoiding interruptions to CPR, and allowing for adequate chest recoil after each compression. In the Advanced Cardiovascular Life Support (ACLS) algorithm, intravenous epinephrine is administered every 3-5 minutes and a “pulse check” is performed after every 2 minutes of CPR. The patient’s cardiac rhythm, along with the clinical history, helps decide if the patient should receive additional medications or receive unsynchronized cardioversion (defibrillation, or “electrical shock. The ACLS algorithm divides management in patients with pulseless ventricular tachycardia (pVT) or ventricular fibrillation (VF) and patients with pulseless electric activity (PEA) or asystole.

The cardiac rhythm seen during the pulse check for this patient is ventricular fibrillation. The ACLS algorithm advises unsynchronized cardioversion at 150-200 Joules for patients with pVT or VF. Continuing chest compressions (Choice A) with minimal interruptions is a crucial component of BLS, however, this patient’s cardiac rhythm is shockable. Defibrillation (Choice B) takes precedence over CPR in this scenario. Amiodarone (Choice C) is an antiarrhythmic agent that is recommended in patients with pVT, in addition to unsynchronized cardioversion. This patient has VF, not pVT. Sodium bicarbonate (Choice D) is an alkaline medication that is helpful in cardiac arrests caused by severe acidosis or certain toxins (i.e. salicylates or tricyclic antidepressants). The next best step in this patient scenario would be defibrillation for the patient’s VF (Choice B).


Cite this article as: Joseph Ciano, USA, "Question Of The Day #22," in International Emergency Medicine Education Project, November 27, 2020,, date accessed: January 21, 2021

Physiologically Difficult Airway – Metabolic Acidosis

Physiologically Difficult Airway - Metabolic Acidosis

Case Presentation

A 32-year-old male with insulin-dependent diabetes mellitus came to your emergency department for shortness of breath. He was referred to the suspected COVID-19 area. His vitals were as follows: Blood pressure, 100/55 mmHg; pulse rate, 135 bpm; respiratory rate, 40/min; saturation on 10 liters of oxygen per minute, 91%; body temperature, 36.7 C. His finger-prick glucose was 350 mg/dl.

The patient reported that he had started to feel ill and had an episode of diarrhea 1 week ago. He developed a dry cough and fever in time. He started to feel shortness of breath for 2 days. He sought out the ER today because of the difficulty breathing and abdominal pain.

The patient seemed alert but mildly agitated. He was breathing effortfully and sweating excessively. On physical examination of the lungs, you noticed fine crackles on the right. Despite the patient reported abdominal pain, there were no signs of peritonitis on palpation.

An arterial blood gas analysis showed: pH 7.0, PCO2: 24, pO2: 56 HCO3: 8 Lactate: 3.

The point-of-care ultrasound of the lungs showed B lines and small foci of subpleural consolidations on the right.
At this point, what are your diagnostic hypotheses?

Two main diagnostic hypotheses here are:

  • Diabetic ketoacidosis (Hyperglycemia + metabolic acidosis)
  • SARS-CoV2 pneumonia

We avoid intubating patients with pure metabolic decompensation of DKA if possible, as they respond to hydration + insulin therapy + electrolyte replacement well and quickly. 

But in this scenario, the patient is extremely sick and has complicating medical issues, such as an acute lung disease decompensating the diabetic condition, probably COVID19. Considering these extra issues may complicate the recovery time and increase the risk of respiratory failure, you decide to intubate the patient in addition to the treatment of DKA.

You order lab tests and cultures. You start hydration and empirical antibiotics while starting preoxygenation and preparing for intubation.

Will this be a Difficult Airway?

Evaluating the patient for the predictors of a difficult airway is a part of the preparation for intubation. Based on your evaluation, you should create an intubation plan. 

This assessment is usually focused on anatomical changes that would make it difficult to manage the airway (visualization of the vocal cords, tube passage, ventilation, surgical airway), thereby placing the patient at risk.

“Does this patient have any changes that will hinder opening the mouth, mobilizing the cervical region, or cause any obstruction for laryngoscopy? Does this patient have any changes that hinder the use of Balloon-Valve-Mask properly, such as a large beard? What about the use of the supraglottic device? Does this patient have an anatomical alteration that would hinder emergency cricothyroidotomy or make it impossible, like a radiation scar? ”

So the anatomically difficult airway is when the patient is at risk if you are unable to intubate him due to anatomical problems.

The physiologically difficult airway, however, is when the patient has physiological changes that put him at risk of a bad outcome during or shortly after intubation. Despite intubation. Or because of intubation, because of its physiological changes due to positive pressure ventilation.

These changes need to be identified early and must be mitigated. You need to recognize the risks and stabilize the patient before proceeding to intubation or be prepared to deal with the potential complications immediately if they happen.

5 main physiological changes need attention before intubation are: hypoxemia, hypotension, severe metabolic acidosis, right ventricular failure, severe bronchospasm.

Back to our patient: Does he have physiologically difficult airway predictors?

  • SI (Shock Index): 1.35 (Normal <0.8) – signs of shock
  • P / F: 93 (Normal> 300) – Severe hypoxemia
  • pH: 7.0: Severe metabolic acidosis – expected pCO2: 20 (not compensating)
  • qSOFA: 2 + Lactate: 3 (severity predictor)

Physiologically Difficult Airway

"Severely critical patients with severe physiological changes who are at increased risk for cardiopulmonary collapse during or immediately after intubation."

Sakles JC, Pacheco GS, Kovacs G, Mosier JM. The difficult airway refocused.

Severe Metabolic Acidosis

In this post, we will focus only on the compensation of the metabolic part, but do not forget that this is a patient who needs attention on oxygenation and hemodynamics as well. That is, this is intubation with very difficult predictions.

What happens during the rapid sequence of intubation in severe metabolic acidosis?

To perform the procedure, the patient needs to be in apnea. During an apnea, pulmonary ventilation is decreased and the CO2 is not “washed” from the airway. These generate an accumulation of CO2, an acid, decreasing blood pH. In a patient with normal or slightly altered pH, this can be very well-tolerated, but in a patient with a pH of 7.0, an abrupt drop in this value can be ominous.

We know that the respiratory system is one of the most important compensation mechanisms for metabolic acidosis and it starts its action in seconds, increasing the pH by 50 to 75% in 2 to 3 minutes, guaranteeing the organism time to recover. So, even seconds without your proper actions can be risky for critical patients.

In addition, it must be remembered that increased RF is the very defense for the compensation of metabolic acidosis, and most of the time the organism does this very well. So if after the intubation the NORMAL FR and NORMAL minute volume are placed in the mechanical ventilator parameters, again there is an increase in CO2 and a further decrease in pH.

And what’s wrong? After all, a little bit of acidosis even facilitates the release of oxygen in the tissues because it deflects the oxyhemoglobin curve to the right, right?

Severe metabolic acidosis (pH <7.1) can have serious deleterious effects:

  • Arterial vasodilation (worsening shock)
  • Decreased myocardial contractility
  • Risks of arrhythmias
  • Resistance to the action of DVAs
  • Cellular dysfunction

What to do?

Always the primary initial treatment is: treating the underlying cause! In patients with severe metabolic acidosis, it is best to avoid intubation! Especially in metabolic ketoacidosis, which as hydration and insulin intake improves, there is a progressive improvement in blood pH.

Sodium bicarbonate

The use of sodium bicarbonate to treat metabolic acidosis is controversial, especially in non-critical acidosis values ​​(pH> 7.2). If you have acute renal failure associated, its use may be beneficial by postponing the need for renal replacement therapy (pH <7.2).

As for DKA, where sodium bicarbonate is used to the ketoacidosis formed by erratic metabolism due to the lack of insulin and no real deficiency is present, its use becomes limited to situations with pH <6.9.

The dose is empirical, and dilution requires a lot of attention (avoid performing HCO3 without diluting!)

NaHCO3 100mEq + AD 400ml

Run EV in 2h

If K <5.3: Associate KCl 10% 2amp

I would make this solution and leave it running while proceeding with the intubation preparations.

Attention: Remember, according to the formula below, that HCO3 is converted to CO2, and if done in excess, is associated with progressive improvement of the ketoacidosis and recovery of HCO3 from the buffering molecules. In a patient already with limited ventilation, its increase can cause deviation of the curve for the CO2 increase, which is also easily diffused to the cells and paradoxically decrease the intracellular pH, in addition to carrying K into the cell.

H + + HCO3 – = H2CO3 = CO2 + H2O

Mechanical ventilation

I think the most important part of the management of these patients is the respiratory part.

If you choose the Rapid Sequence Intubation: Prepare for the intubation to be performed as quickly as possible: Use your best material, choose the most experienced intubator, put the patient in ideal positioning, decide and apply medications skillfully, to ensure the shortest time possible apnea.

You will need personnel experienced in Mechanical Ventilation and you must remember to leave the ventilatory parameters adjusted to what the patient needs and not to what would be normal!

I found this practice very interesting: First, you calculate what the expected pCO2 should be for the patient, according to HCO3:

Winter’s Equation (Goal C02) = 1.5 X HCO3 + 8 (+/- 2)

And then, according to this table, you try to reach the VM Volume Minute value.
Goal CO2 Minute Ventilation
40 mmHg
6-8 L
30 mmHg
12-14 L
20 mmHg
18-20 L

These are just initial parameters. With each new blood gas analysis repeated in 30 minutes to an hour, you re-make fine adjustments using the formula below:

Minute volume = [PaCO2 x Minute volume (from VM)] / CO2 Desired

With the treatment of ketoacidosis, new parameters should be adjusted, hopefully for the better.

Another safer option for these patients would be to use the Awake Patient Intubation technique so that you would avoid the apnea period. However, Awake Patient Intubation Technique is contraindicated in suspected or confirmed COVID-19 cases due to the risk of contamination.

That’s it, folks, send your feedback, your experiences, and if you have other sources!

Further Reading

  1. Frank Lodeserto MD, “Simplifying Mechanical Ventilation – Part 3: Severe Metabolic Acidosis”, REBEL EM blog, June 18, 2018. Available at:
  2. Justin Morgenstern, “Emergency Airway Management Part 2: Is the patient ready for intubation?”, First10EM blog, November 6, 2017. Available at:
  3. Salim Rezaie, “How to Intubate the Critically Ill Like a Boss”, REBEL EM blog, May 3, 2019. Available at:
  4. Salim Rezaie, “RSI, Predictors of Cardiac Arrest Post-Intubation, and Critically Ill Adults”, REBEL EM blog, May 10, 2018. Available at:
  5. Salim Rezaie, “Critical Care Updates: Resuscitation Sequence Intubation – pH Kills (Part 3 of 3)”, REBEL EM blog, October 3, 2016. Available at:
  7. Scott Weingart. The HOP Mnemonic and Next Week. EMCrit Blog. Published on June 21, 2012. Accessed on July 15th 2020. Available at [ ].
  8. IG: @pocusjedi: “Pocus e Coronavirus: o que sabemos até agora?”


  1. Sakles JC, Pacheco GS, Kovacs G, Mosier JM. The difficult airway refocused. Br J Anaesth. 2020;125(1):e18-e21. doi:10.1016/j.bja.2020.04.008
  2. Mosier JM, Joshi R, Hypes C, Pacheco G, Valenzuela T, Sakles JC. The Physiologically Difficult Airway. West J Emerg Med. 2015;16(7):1109-1117. doi:10.5811/westjem.2015.8.27467
  3. Irl B Hirsch, MDMichael Emmett, MD. Diabetic ketoacidosis and hyperosmolar hyperglycemic state in adults: Treatment. Post TW, ed. UpToDate. Waltham, MA: UpToDate Inc. (Accessed on July 15, 2020.)
  4. Cabrera JL, Auerbach JS, Merelman AH, Levitan RM. The High-Risk Airway. Emerg Med Clin North Am. 2020;38(2):401-417. doi:10.1016/j.emc.2020.01.008
  5. Guyton AC, HALL JE. Tratado de fisiologia medica. 13a ed. Rio de Janeiro(RJ): Elsevier, 2017. 1176 p.
  6. Kraut JA, Madias NE. Metabolic acidosis: pathophysiology, diagnosis and management. Nat Rev Nephrol. 2010;6(5):274-285. doi:10.1038/nrneph.2010.33
  7. Calvin A. Brown III, John C. Sakles, Nathan W. Mick. Manual de Walls para o Manejo da Via Aérea na Emergência. 5. ed. – Porto Alegre: Artmed, 2019.
  8. Smith MJ, Hayward SA, Innes SM, Miller ASC. Point-of-care lung ultrasound in patients with COVID-19 – a narrative review [published online ahead of print, 2020 Apr 10]. Anaesthesia. 2020;10.1111/anae.15082. doi:10.1111/anae.15082
Cite this article as: Jule Santos, Brasil, "Physiologically Difficult Airway – Metabolic Acidosis," in International Emergency Medicine Education Project, November 25, 2020,, date accessed: January 21, 2021

More Posts by Dr. Santos

Local Anaesthetic Toxicity (LAST)

Local Anesthetic Toxicity (LAST)

Think about the number of times a month you use a local anaesthetic; maybe not every day, but I know there are a lot of emergency department shifts when I use a local anaesthetic. The uses and applications for local anaesthesia abound: wound care and laceration closure, pain control with painful procedures like a paracentesis or lumbar puncture, and targeted regional anaesthesia blocks after a broken hip. It is important to know and understand a bit more about this commonly used class of drug given how often we use them in emergency medicine, including the recommended dosing, signs of toxicity, and treatment of toxicity.

Local anaesthetics fall into two divisions, based on their chemical structure:

  • the Esters (have one i): procaine, cocaine, tetracaine, chloroprocaine, etc
  • the Amides (have two i’s): lidocaine, bupivacaine, mepivacaine, prilocaine, ropivacaine, etc


These drugs have their effect as sodium-channel blocking medications with variable durations of action. Interestingly, 1% diphenhydramine has also been used as a local anaesthetic since the 1930s, given its sodium channel blocking mechanism. Local anaesthetics can be administered with other drugs, namely epinephrine, to help increase the duration of action and minimize the spread of the anaesthetic from the site of injection.

Maximum Dose

The safe maximal dose for the local anaesthetics is based on patient weight and correlates to the risk of systemic toxicity. The maximally safe dose of two common local anaesthetics is detailed below, and as you can see, the use of epinephrine allows for an increased dose of local anaesthetic injection.

Max dose without Epi Max dose with Epi Duration of Action
4.5 mg/kg
7 mg/kg
0.5 - 1.5 hours
3 mg/kg
3 mg/kg
6-8 hours

Usage abd Absorbtion

Absorption into the bloodstream of a local anaesthetic can occur when the drug is injected directly into the bloodstream. Still, it can also occur in highly vascular areas or near neurovascular bundles in locations such as intracostal, epidural, and the brachial plexus. Local anaesthetic systemic toxicity (LAST) occurs when there are elevated circulating levels of local anaesthetic and occurs within minutes of injection. As you may know, lidocaine is used intravenously as an antiarrhythmic drug, and cocaine when used (or abused) systemically can cause numerous systemic effects and a sympathomimetic toxidrome. Bupivacaine is the most commonly discussed cause of LAST, and extra care should be taken when utilizing this for local anaesthesia.

Sign and Symptoms of LAST

Signs and symptoms of LAST predominate in the central nervous system and the cardiovascular system. CNS symptoms can include oral/perioral numbness, paresthesia, restlessness, tinnitus, fasciculations/tremors, seizures, decreased level of consciousness, and/or apnea. Cardiovascular symptoms can include: hypertension and tachycardia though more commonly vasodilation and hypotension, sinus bradycardia, AV blocs, conduction defects (notably: long PR and QRS), ventricular dysrhythmias, cardiovascular collapse, and/or cardiac arrest.

The differential diagnosis for LAST includes anaphylaxis (rare with amides), other sodium channel blockers (antihistamines, TCAs, cocaine, antimalarials), and anxiety. However, the timing nearly immediately following local anaesthetic administration should help one to hone in on the diagnosis.


If a patient develops LAST, ACLS protocols should be followed. Furthermore, lipid emulsion (Intralipid) is the treatment that will help bind the anaesthetic in the bloodstream. While this medication is not on the WHO essential medication list, in a patient with LAST, Intralipid should be administered if available. Dosing is a 1.5 mL/kg bolus (standard dose of 100mL for 70kg patient), followed by a 0.25-0.5 mL/kg/min infusion until the patient is hemodynamically stable (and for at least 10 minutes).

How To Decrease Risk of LAST

A few strategies to minimizing the risk of causing harm to your patients when using local anaesthetics: 
  • know the maximum dose your patient can receive
  • know the dose you’re giving by dose (milligrams) and how that correlates to drug volume (mg/mL)
  • aspirate prior to injection(s) to ensure you are not in a blood vessel
  • consider using point of care ultrasound to ensure needle location

References and Further Reading

Cite this article as: J. Austin Lee, USA, "Local Anaesthetic Toxicity (LAST)," in International Emergency Medicine Education Project, November 23, 2020,, date accessed: January 21, 2021

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