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, https://iem-student.org/2021/01/18/neutropenic-fever-syndrome/, date accessed: January 20, 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, https://iem-student.org/2021/01/11/covid-19-on-spanish-speaking-patients/, date accessed: January 20, 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.
  •  

Hotbottlerash.JPG
By <a href=”//commons.wikimedia.org/wiki/User:Jmh649″ 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=”https://en.wikipedia.org/wiki/User:Jongarrison&#8221; 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=”https://books.google.com/books?id=fnYoAAAAYAAJ”>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=”//commons.wikimedia.org/wiki/User:Jmh649″ 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.

ENlegs.JPG
By <a href=”//commons.wikimedia.org/wiki/User:Jmh649″ 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=”//commons.wikimedia.org/w/index.php?title=User:Dswierc&amp;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, https://iem-student.org/2021/01/04/erythema-review-for-medical-students/, date accessed: January 20, 2021

Emergency Medicine Course Experience

It has been two years that the International Emergency Medicine (iEM) Education Project (iem-student.org) 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 (iem-course.org) 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 – (https://www.sciencedirect.com/science/article/pii/S2211419X2030135X).

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: https://rebelem.com/simplifying-mechanical-ventilation-part-3-severe-metabolic-acidosis/.
  2. Justin Morgenstern, “Emergency Airway Management Part 2: Is the patient ready for intubation?”, First10EM blog, November 6, 2017. Available at: https://first10em.com/airway-is-the-patient-ready/.
  3. Salim Rezaie, “How to Intubate the Critically Ill Like a Boss”, REBEL EM blog, May 3, 2019. Available at: https://rebelem.com/how-to-intubate-the-critically-ill-like-a-boss/.
  4. Salim Rezaie, “RSI, Predictors of Cardiac Arrest Post-Intubation, and Critically Ill Adults”, REBEL EM blog, May 10, 2018. Available at: https://rebelem.com/rsi-predictors-of-cardiac-arrest-post-intubation-and-critically-ill-adults/.
  5. Salim Rezaie, “Critical Care Updates: Resuscitation Sequence Intubation – pH Kills (Part 3 of 3)”, REBEL EM blog, October 3, 2016. Available at: https://rebelem.com/critical-care-updates-resuscitation-sequence-intubation-ph-kills-part-3-of-3/.
  6. Lauren Lacroix, “APPROACH TO THE PHYSIOLOGICALLY DIFFICULT AIRWAY”, https://emottawablog.com/2017/09/approach-to-the-physiologically-difficult-airway/
  7. Scott Weingart. The HOP Mnemonic and AirwayWorld.com Next Week. EMCrit Blog. Published on June 21, 2012. Accessed on July 15th 2020. Available at [https://emcrit.org/emcrit/hop-mnemonic/ ].
  8. IG: @pocusjedi: “Pocus e Coronavirus: o que sabemos até agora?”https://www.instagram.com/p/B-NxhrqFPI1/?igshid=14gs224a4pbff

References

  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. https://www.uptodate.com (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, https://iem-student.org/2020/11/25/physiologically-difficult-airway-metabolic-acidosis/, date accessed: January 20, 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

Effect

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
Lidocaine
4.5 mg/kg
7 mg/kg
0.5 - 1.5 hours
Bupivacaine
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.

Management

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, https://iem-student.org/2020/11/23/local-anaesthetic-toxicity/, date accessed: January 20, 2021

More Posts By Dr. Lee

Pathological Brain CT Findings – Illustration

Pathological Brain CT Findings

In this post, we will share the traumatic (Epidural, subdural, cerebral contusion, subarachnoid hemorrhage, cerebral edema) and atraumatic (intracranial parenchymal hemorrhage, subarachnoid hemorrhage) brain computerized tomography (CT) findings. We will also provide GIF images and one final image, which includes all pathologies in one image.

ATRAUMATIC PATHOLOGICAL BRAIN CT FINDINGS

TRAUMATIC PATHOLOGICAL BRAIN CT FINDINGS

ATRAUMATIC PATHOLOGICAL BRAIN CT FINDINGS – GIF

TRAUMATIC PATHOLOGICAL BRAIN CT FINDINGS  – GIF

PATHOLOGICAL BRAIN CT FINDINGS  – ONE POST

References and Further Reading

  1. https://iem-student.org/2019/09/04/cranial-ct-anatomy-a-simple-image-guide-for-medical-students/
  2. The Atlas of Emergency Radiology
Cite this article as: Murat Yazici, Turkey, "Pathological Brain CT Findings – Illustration," in International Emergency Medicine Education Project, November 18, 2020, https://iem-student.org/2020/11/18/pathological-brain-ct-findings-illustration/, date accessed: January 20, 2021

Push Th(d)ose Vasopressors

Push Th(d)ose Vasopressors

Background

Since Scott Weingart first advocated for using push-dose pressors in the Emergency Department (ED) over a decade ago(1), push-dose vasopressors, also known as bolus-dose vasopressors have seemingly found their way into many EDs. However, recent studies have sought to ask more questions regarding its use and safety in the Emergency Department.

Vasopressors such as epinephrine and norepinephrine are commonly used for regulating and maintaining adequate blood pressure or mean arterial pressure (MAP). While these are usually administered as a continuous infusion via central access, administering them as a small bolus through peripheral access came to be known as push-dose vasopressor in practice.

Traditionally, this small bolus strategy was used in the operating room (OR) by anesthetists to treat transient hypotension due to sedating agents or spinal anesthesia. Multiple studies have supported the safety and efficacy of push-dose vasopressors in this clinical setting/patient population (2).

Swensen, et al. (3) studied the safety of bolus-dose phenylephrine for hypotension in the Emergency Department, however, data on the efficacy and safety of push-dose pressors remains sparse in ED and in-patient settings. Studies published in the past few years have questioned the lack of evidence regarding the safety and efficacy of push-dose pressor use in ED settings and highlighted some negative consequences of its use (4). To understand the concerns, it’s important we first understand the vasopressors, indications for use, and preparation in the ED.

Push-dose pressors in the Emergency Department

The two common vasopressors used as push-dose pressors in the Emergency Department are Epinephrine and Phenylephrine. Patients needing emergency airway, traumatic brain injury, and post-cardiac arrest with the return of spontaneous circulation may all experience hypotension which could lead to adverse outcomes. Push-does pressors have been proposed as a temporary measure to limit the hypotension while a vasopressor infusion/definitive treatment is being set up (5).

phenilephrine vs epinephrine
push dose epinephrine
push dose phenilephrine

Clinical settings in the ED where the use of push-dose pressor is proposed:

  1. Airway management: Hypotension prior, during, and post-intubation could be treated with bolus-dose vasopressors. Panchal et al. (6) did a retrospective chart review of intubated hypotensive patients in which phenylephrine was used. Bolus-dose phenylephrine demonstrated an increase in systolic blood pressure and the authors recommended further studies to understand the best use of phenylephrine for post-intubation hypotension.
  2. Return of spontaneous circulation (ROSC): In patients with ROSC, bolus-dose pressors may aid in the maintenance of end-organ perfusion, which is often impaired after ROSC (7).
  3. Traumatic brain injury: By rapidly increasing mean arterial pressure and thus cerebral perfusion pressure, bolus-dose vasopressors may help to prevent secondary brain injury.

What are the concerns regarding the use of push-dose pressors in the ED?

Acquisto and Bodkin (8) cited a few dosing errors while using push-dose pressors and highlighted that emergency physicians are less familiar with the practice of medication preparation/manipulation and hence dosing errors are expected, inadvertently causing patients more harm than benefit. They also emphasized on the lack of evidence in the literature regarding the efficacy and safety of push-dose pressors in a stressful environment like the ED.

Rotando and Picard et al. (9) in their prospective observational study of 146 patients receiving push-dose pressors in the ICU had thirteen (11.2%) patients have a dose-related medication error and seventeen (11.6%) adverse events. They concluded while push-dose pressors where efficacious, they were associated with adverse drug events and medication errors.

Cole et al (10). performed a retrospective analysis of 249 patients receiving push-dose pressors and found a higher incidence of adverse hemodynamic effects (39%) and human errors (19%). They emphasized the need for further studies to question whether push-dose pressors improve outcomes, and if so, how to safely implement them in practice.

Another concern raised is whether physicians may bypass standard resuscitation practices of fluid boluses in favor of using push-dose pressors. Schwartz et al. (11) found that only 34% of patients received an appropriate fluid challenge before using push-dose pressors in a retrospective chart review of 73 patients receiving push-dose pressors for acute hypotension in the ED. Furthermore, it appeared that patients who did not receive an appropriate fluid bolus needed more doses of bolus-dose pressors followed by the need for continuous vasopressor infusion within 30 minutes of bolus-dose pressor use.

Emergency physicians work in stressful environments which raises concerns on the ability of the physician to perform accurate dose calculations under duress (4). The prepared syringe also contains multiple individual doses, and using more concentrated solutions potentially increases the risk of overdose and extravasation injury (12).

Conclusion

While the practice of using push-dose pressors has found its way into the Emergency Department, it is crucial to acknowledge that evidence regarding its safety and benefits is limited. However, rather than disregarding the practice, high-quality research should be encouraged, which could potentially be practice-changing. Holden et al. (12) offer a framework of operational and safety considerations for the use of push-dose pressors in the ED and is a must-read for all using push-dose pressors in their current practice.

References

  1. Scott Weingart. EMCrit Podcast 6 – Push-Dose Pressors. EMCrit Blog. Published on July 10, 2009. Accessed on September 25th 2020. Available at [https://emcrit.org/emcrit/bolus-dose-pressors/ ].
  2. Lee A, Ngan Kee WD, Gin T. A quantitative, systematic review of randomized controlled trials of ephedrine versus phenylephrine for the management of hypotension during spinal anesthesia for cesarean delivery. Anesth Analg. 2002 Apr;94(4):920-6, table of contents. doi: 10.1097/00000539-200204000-00028. PMID: 11916798.
  3. Swenson K, Rankin S, Daconti L, Villarreal T, Langsjoen J, Braude D. Safety of bolus-dose phenylephrine for hypotensive emergency department patients. Am J Emerg Med. 2018 Oct;36(10):1802-1806. doi: 10.1016/j.ajem.2018.01.095. Epub 2018 Feb 19. PMID: 29472039.
  4. Cole JB. Bolus-Dose Vasopressors in the Emergency Department: First, Do No Harm; Second, More Evidence Is Needed. Ann Emerg Med. 2018 Jan;71(1):93-95. doi: 10.1016/j.annemergmed.2017.05.039. Epub 2017 Jul 26. PMID: 28754354.
  5. Weingart S. Push-dose pressors for immediate blood pressure control. Clin Exp Emerg Med. 2015;2(2):131-132. Published 2015 Jun 30. doi:10.15441/ceem.15.010
  6. Panchal AR, Satyanarayan A, Bahadir JD, Hays D, Mosier J. Efficacy of Bolus-dose Phenylephrine for Peri-intubation Hypotension. J Emerg Med. 2015 Oct;49(4):488-94. doi: 10.1016/j.jemermed.2015.04.033. Epub 2015 Jun 20. PMID: 26104846.
  7. Gottlieb M. Bolus dose of epinephrine for refractory post-arrest hypotension. CJEM. 2018 Oct;20(S2):S9-S13. doi: 10.1017/cem.2016.409. Epub 2017 Jan 10. PMID: 28069098.
  8. Acquisto NM, Bodkin RP, Johnstone C. Medication errors with push dose pressors in the emergency department and intensive care units. Am J Emerg Med. 2017 Dec;35(12):1964-1965. doi: 10.1016/j.ajem.2017.06.013. Epub 2017 Jun 7. PMID: 28625533.
  9. Rotando A, Picard L, Delibert S, Chase K, Jones CMC, Acquisto NM. Push dose pressors: Experience in critically ill patients outside of the operating room. Am J Emerg Med. 2019 Mar;37(3):494-498. doi: 10.1016/j.ajem.2018.12.001. Epub 2018 Dec 3. PMID: 30553634.
  10. Cole JB, Knack SK, Karl ER, Horton GB, Satpathy R, Driver BE. Human Errors and Adverse Hemodynamic Events Related to “Push Dose Pressors” in the Emergency Department. J Med Toxicol. 2019 Oct;15(4):276-286. doi: 10.1007/s13181-019-00716-z. Epub 2019 Jul 3. PMID: 31270748; PMCID: PMC6825064.
  11. Schwartz MB, Ferreira JA, Aaronson PM. The impact of push-dose phenylephrine use on subsequent preload expansion in the ED setting. Am J Emerg Med. 2016 Dec;34(12):2419-2422. doi: 10.1016/j.ajem.2016.09.041. Epub 2016 Sep 22. PMID: 27720568.
  12. Holden D, Ramich J, Timm E, Pauze D, Lesar T. Safety Considerations and Guideline-Based Safe Use Recommendations for “Bolus-Dose” Vasopressors in the Emergency Department. Ann Emerg Med. 2018 Jan;71(1):83-92. doi: 10.1016/j.annemergmed.2017.04.021. PMID: 28601272.
Cite this article as: Neha Hudlikar, UAE, "Push Th(d)ose Vasopressors," in International Emergency Medicine Education Project, November 11, 2020, https://iem-student.org/2020/11/11/push-thdose-vasopressors/, date accessed: January 20, 2021

More Posts From Dr. Hudlikar

Hypoglycemia – A Rural Perspective

hypoglycemia - a rural perspective

Waiting for patients is among some of the weird perks of working in a rural ER. “Too little isn’t fun as well”, said an enthusiastic new paramedic at Beltar PHC. Later that night, I’d find a funny connection between what he said and what followed.

A 56Y/M patient is brought to the ER on a particularly silent evening. Following the usual ER premise; I reach the department from upstairs. The patient was unconscious when I arrived. A paramedic was trying to open a peripheral line, and a nurse was taking a pulse oximeter reading while keeping the patient at 2L via nasal cannula. The bystanders who brought him had no clue of what had happened or if the patient had any comorbidity. As I grabbed the glucometer from the drawer, I could not help but remember how in med school exams all the hypoglycemic patients were medics who injected themselves with insulin. As I poked the patient with a lancet and measured his blood glucose, I realized the paramedic had already given up trying to get IV access. “I couldn’t get in”, he said. The glucometer beeped exactly then as if to confirm “this is trouble” – 37! “That is hypoglycemia”, I exclaimed!

Although there is no universally accepted definition of hypoglycemia (low blood glucose), a level below 60 rings the bell. As I tried to establish the line, I requested my nurse to prepare a thick paste of glucose powder. Of all the medicine I was taught, one thing I’ve found the most useful is the “available” medicine. Sure, start with a bolus of the glucose-containing solution: D50 or D10, if you cannot get IV access go for IM glucagon and so forth. But when you’re working in a setting where you second guess yourself for wasting a lancet while checking a patient’s blood glucose, IM glucagon becomes nothing more than a very good test question.

I could not get the line started either. Minutes after we applied the glucose paste on the buccal mucosa, the patient woke up. The sigh of relief was audible in the small ER of our PHC. Eventually, we were able to feed the patient per oral. The patient turned out to be diabetic who thought, “insulin is a medicine, hence should not be ignored, but the food is optional.”

Clinical hypoglycemia is sometimes defined as blood glucose low enough to cause symptoms. For most people, this occurs at 50-60 mg/dL. Clinically significant hypoglycemia is confirmed by the presence of the ‘Whipple triad’. Yap, that’s the same Allen Whipple, the American surgeon who also coined the Whipple procedure! The presence of symptoms consistent with hypoglycemia, a low serum glucose level, and resolution of the symptoms and signs of hypoglycemia with the administration of glucose is what confirms hypoglycemia.

Because diabetics are most prone to get hypoglycemic, in a diabetic patient, hypoglycemia is defined as a self-monitored blood glucose level ≤ 70mg/dL. Everyone else must have a documented experience of Whipple’s triad for the diagnosis. There is also something called relative hypoglycemia, it occurs when a patient with diabetes reports hypoglycemic symptoms, but the blood glucose remains above 70 mg/dL. This still requires treatment. Remember, we treat patients, not numbers.

The causes of hypoglycemia can be diverse, but the horses include missed meals or overnight fasting but still using hypoglycemic agents (sulphonylureas, insulin) in a person with diabetes. Be vigilant about recent exercise enthusiasts, alcohol ingestion, weight loss, and renal failure (which can reduce insulin clearance).

Signs and symptoms of hypoglycemia in non-diabetic patients are generally fairly obvious. Sympathetic autonomic nervous system activation symptoms like nervousness, anxiety, tremulousness, sweating, palpitations, shaking, dizziness, hunger, and symptoms due to decreased availability of glucose to the brain; confusion, weakness, drowsiness, speech difficulty, incoordination, odd behavior are seen below the commonly quoted glycemic values of 50-60. In severe cases, hypoglycemia may result in seizures, coma, or death.

A logical treatment flowchart should start with a glucose-containing solution: D50 or D10. In regards to D50, be aware that the bolus may cause rebound hypoglycemia, may overshoot glycemic targets and is hypertonic hence should be given slowly over 2-5 minutes. There has been extensive debate over D50 vs D10, here is what I try to keep in mind; If using D50, give 1 amp at a time over 2-5 mins. If D10, a 100ml bolus over 2 mins. Check the patients’ glucose levels often.

Remember both of those approaches require you to have IV access. Intramuscular glucagon (5mg) may be given to raise serum glucose levels. Keep in mind two things: the efficacy of glucagon is dependent upon hepatic glycogen stores. Patients with prolonged hypoglycemia may have a minimal response and repeating glucagon does not make much sense.

If the blood glucose goes back to > 60mg/dL in a non-diabetic patient, and >70mg/dL in a diabetic patient and/or there is an improvement in symptoms, patients who can eat should do so otherwise IV dextrose drip (D5W at 75-100 mL/hr) is the way to go.

Cite this article as: Carmina Shrestha, Nepal, "Hypoglycemia – A Rural Perspective," in International Emergency Medicine Education Project, November 9, 2020, https://iem-student.org/2020/11/09/hypoglycemia-a-rural-perspective/, date accessed: January 20, 2021

Read Other Posts from Dr. Shrestha

Approach to Acute Cough in Adults

Approach to Acute Cough in Adults

Cough is one of the most common complaints presenting to any emergency physician or primary care practitioner – whether it is the chief complaint or an associated symptom. An acute cough is one that has been present for less than three weeks. In the era of COVID-19, a patient presenting with an acute cough can be alarming and scary. So, now more than ever, it is important to develop a strong diagnostic approach to the acute cough, which is largely a clinical diagnosis.

Differential Diagnosis of Acute Cough

*Indicates the most common causes of acute cough.
Cause Example Symptoms / warning signs
Infectious (viral/bacterial) Upper respiratory tract infection aka common cold* Rhinorrhea, nasal obstruction, sneezing, scratchy/sore throat, malaise, headache, and no signs of consolidation
Acute bronchitis* Recent upper respiratory tract infection, and absence of COPD, and absence of high fever or other systemic signs
Influenza Fever, sore throat, nasal congestion, myalgia, headache, and no signs of consolidation
Pneumonia* Fever, tachycardia, tachypnea, consolidation signs on respiratory exam, and mental status change in patients >75y old
Pertussis Whooping cough and cough-emesis
COVID-19 Fever, non-productive cough, fatigue, dyspnea, and/or other less common symptoms such as sore throat, diarrhea, headache, skin rash, and anosmia
Post-nasal drip aka upper airway cough syndrome Post-nasal drainage sensation, need to clear throat, and rhinorrhea

Allergic rhinitis aka hay fever Itching and watering of eyes, rhinorrhea, pruritis
Exacerbation of a pre-existing chronic disease Exacerbation of Asthma   History of episodic wheezing, non-productive cough, dyspnea, reversible air-flow obstruction, allergen exposure or triggered by exercise
Exacerbation of COPD Smoking history, dyspnea, signs of obstruction on respiratory exam i.e. decreased breath sounds, and irreversible air-flow obstruction
Exacerbation of CHF Dyspnea, orthopnea, peripheral edema, gallop rhythm on cardiac exam, and elevated JVP
Drug-induced ACE inhibitor use Non-productive cough, tickling or scratchy sensation in throat typically arising within 1 week of starting medication
Gastroesophageal reflux disorder (GERD)

 

Heartburn, regurgitation, dysphagia, and cough is more prominent at night
Other pulmonary causes Pulmonary embolism Clinical signs and symptoms of DVT, dyspnea, tachypnea, tachycardia, pleuritic chest pain, immobilization for 3 or more days, surgery in the past 4 weeks, history of DVT/PE, hemoptysis, and malignancy with active treatment in the past 6 months
Lung cancer Smoking history, new change in cough, hemoptysis, dyspnea, night sweats, weight loss, and signs of focal obstruction on respiratory exam i.e. decreased breath sounds
Foreign body aspiration Dyspnea, inspiratory stridor, choking, and elevated risk in children
Acute inhalation injury History of exposure to smoke (e.g. in firefighters, thermal burn victims) or chemicals (e.g. chlorine, ammonia)
Bronchiectasis Large volumes of purulent sputum, dyspnea, wheezing, and chest pain
Interstitial lung disease Non-productive cough, dyspnea, fatigue, weight loss
         

Picture the scene: A 23-year-old female presents to the emergency department with a cough that has been ongoing for one week. What are your next steps?

History

  1. Confirm the duration and timing of cough
  2. Nature of cough, i.e. whooping, hemoptysis, and productive vs non-productive?
  3. Presence of the following associated symptoms: fever, dyspnea, sore throat, headache, chest pain, heartburn, rhinorrhea, facial pressure/pain, nasal congestion, or weight loss
  4. History of any chronic lung disease (i.e. asthma, COPD), allergies, CHF, or immunosuppression?
  5. Smoking history?
  6. Medication history, i.e. ACE inhibitor use?

Physical Exam

  1. Vitals
  2. HEENT exam (head, eyes, ears, nose, and throat)
  3. Respiratory exam
  4. Cardiac exam, including JVP

Laboratory Tests

  • Send for COVID-19 swab according to your hospital’s guidelines
  • Order CBC if suspecting infection
  • Order ABG if dyspnea present or life-threatening cause of acute cough suspected
  • Order sputum culture if suspecting bacterial pneumonia
  • Spirometry if need to differentiate between obstructive lung disease (e.g., asthma, COPD) and restrictive lung disease (e.g., interstitial lung disease)

Imaging

  • Consider starting with a Chest X-ray if red flags for serious pathology are present >> dyspnea, hemoptysis, chest pain, weight loss, immunosuppression, significant smoking history, elderly or at risk of aspiration, tachypnea or hypoxemia, abnormal cardiac or respiratory exam, or sepsis.
  • If suspecting foreign body aspiration, need to order bronchoscopy 

Please note that treatment of the conditions that may cause acute cough are not discussed in this blog post, but can be found through medical resources such as those in the references section. Treatment for acute cough often requires treating the underlying cause.

References

  1. Boujaoude ZC, Pratter MR. Clinical approach to acute cough. Lung. 2010;188 Suppl 1(Suppl 1):S41-S46. doi:10.1007/s00408-009-9170-6
  2. Holzinger F, Beck S, Dini L, Stöter C, Heintze C. The diagnosis and treatment of acute cough in adults. Dtsch Arztebl Int. 2014;111(20):356-363. doi:10.3238/arztebl.2014.0356
  3. Madison JM, Irwin RS. Cough: A worldwide problem. Otolarynogol Clin North Am. 2010 Feb;43(1):1-13, vii.
  4. Strong Medicine. An Approach to Cough. Published 25 March, 2018. https://www.youtube.com/watch?v=LDMEtNXik-A
  5. University of Toronto. Cough and Dyspnea. 2015. http://thehub.utoronto.ca/family/cough-and-dyspnea/ Accessed 17 August, 2020.

 

Cite this article as: Sheza Qayyum, Canada, "Approach to Acute Cough in Adults," in International Emergency Medicine Education Project, November 4, 2020, https://iem-student.org/2020/11/04/approach-to-acute-cough-in-adults/, date accessed: January 20, 2021

Triads in Medicine – Rapid Review for Medical Students

triads in medicine

One of the most convenient ways of learning and remembering the main components of disease and identifying a medical condition on an exam are Triads, and medical students/interns/residents swear by them.

Be it a question during rounds, a multiple-choice exam question to be solved, or even in medical practice, the famous triads help physicians recall important characteristics and clinical features of a disease or treatment in an instant.

Since exam season is here, this could serve as a rapid review to recall the most common medical conditions.

While there are a vast number of triads/pentads available online, I have listed the most important (high-yy) ones that every student would be asked about at least once in the duration of their course.

1) Lethal Triad also known as The Trauma Triad of Death
Hypothermia + Coagulopathy + Metabolic Acidosis

2) Beck’s Triad of Cardiac Tamponade
Muffled heart sounds + Distended neck veins + Hypotension

3) Virchow’s Triad – Venous Thrombosis
Hypercoagulability + stasis + endothelial damage

4) Charcot’s Triad – Ascending Cholangitis
Fever with rigors + Right upper quadrant pain + Jaundice

5) Cushing’s Triad – Raised Intracranial Pressure
Bradycardia + Irregular respiration + Hypertension

6) Triad of Ruptured Abdominal Aortic Aneurysm
Severe Abdominal/Back Pain + Hypotension + Pulsatile Abdominal mass

7) Reactive Arthritis
Can’t See (Conjunctivitis) + Can’t Pee (Urethritis) + Can’t Climb a Tree (Arthritis)

8) Triad of Opioid Overdose
Pinpoint pupils + Respiratory Depression + CNS Depression

9) Hakims Triad – Normal Pressure Hydrocephalus
Gait Disturbance + Dementia + Urinary Incontinence

10) Horner’s Syndrome Triad
Ptosis + Miosis + Anydrosis

11) Mackler’s Triad – Oesophageal Perforation (Boerhaave Syndrome)
Vomiting + Lower Thoracic Pain + Subcutaneous Emphysema

12) Pheochromocytoma
Palpitations + Headache + Perspiration (Diaphoresis)

13) Leriche Syndrome
Buttock claudication + Impotence + Symmetrical Atrophy of bilateral lower extremities

14) Rigler’s Triad – Gallstone ileus
Gallstones + Pneumobilia + Small bowel obstruction

15) Whipple’s Triad – Insulinoma
Hypoglycemic attack + Low glucose + Resolving of the attack on glucose administration

16) Meniere’s Disease
Tinnitus + Vertigo + Hearing loss

17) Wernicke’s Encephalopathy- Thiamine Deficiency
Confusion + Ophthalmoplegia + Ataxia

18) Unhappy Triad – Knee Injury
Injury to Anterior Cruciate Ligament + Medial collateral ligament + Medial or Lateral Meniscus

19) Henoch Schonlein Purpura
Purpura + Abdominal pain + Joint pain

20) Meigs Syndrome
Benign ovarian tumor + pleural effusion + ascites

21) Felty’s Syndrome
Rheumatoid Arthritis + Splenomegaly + Neutropenia

22) Cauda Equina Syndrome
Low back pain + Bowel/Bladder Dysfunction + Saddle Anesthesia

23) Meningitis
Fever + Headache + Neck Stiffness

24) Wolf Parkinson White Syndrome
Delta Waves + Short PR Interval + Wide QRS Complex

25) Neurogenic Shock
Bradycardia + Hypotension + Hypothermia

Further Reading

Cite this article as: Sumaiya Hafiz, UAE, "Triads in Medicine – Rapid Review for Medical Students," in International Emergency Medicine Education Project, June 12, 2020, https://iem-student.org/2020/06/12/triads-in-medicine/, date accessed: January 20, 2021

ACEM2019 and Incredible India

ACEM 2019 and increadible India

The 10th Asian Conference on Emergency Medicine was successfully completed in New Delhi, India, during the last couple of days. The conference hosted around 1700 attendees around the globe, mainly Asia. There were approximately 300 speakers from all continents. Dr. Tamorish Kole and Dr. Sirinath Kumar were the two Emergency Medicine professionals who behind the success of this conference. Both experts are also a member of the board of directors of the Asian Society for Emergency Medicine (ASEM). At the end of the conference, Dr. Kole took over the presidency from Prof.Dr. Yildiray Cete (Turkey) who served to ASEM for two years.

ASEM board
Asian Society for Emergency Medicine, Board of Directors

Vice-President of India, Venkaiah Naidu, opened the conference with promising support to the improvement of Emergency Medicine care in India as well as highlighting the implementation of Emergency Medicine into the undergraduate curriculum. As many countries in Asia, Indian medical graduates are working in acute care settings after graduation. Therefore, focusing on undergraduate education can help many countries in the same context. 

Venkaiah Naidu
Venkaiah Naidu, Vice-President of India

This topic one of the items discussed in the ASEM Board of Directors meeting. Creating a widely acceptable undergraduate curriculum is a necessity for Asian countries, especially those in the development stage of Emergency Medicine. ASEM board formed a sub-committee to work on this highly significant problem. Dr. Mohan Tiru (Singapore) and I will be leading board members to continue and finalize the process. Because the International Federation for Emergency Medicine (IFEM) currently working on a comprehensive update process for its’ undergraduate curriculum, there is no need to reinvent the wheel for ASEM. Taking the updated version of the IFEM undergraduate curriculum as the main framework and working on it to create a precise Asian undergraduate curriculum will be enough and probably the fastest way. However, there is a need to understand the current situation and needs in Asian countries. Therefore, the sub-committee of ASEM will work on learning needs assessment and current situation analysis until the IFEM undergraduate curriculum finalized. The expected time for the new updated version of the IFEM undergraduate curriculum is April-May 2020. Completing learning needs assessment and current situation analysis of Asia by March-April 2020 will give the Asian board a chance to move forward with updated IFEM undergraduate curriculum. Probably, developing the Asian curriculum will be possible in a short period of time until the end of 2020.

ASEM board meeting
Asian Society for Emergency Medicine, Board of Directors Meeting

While ACEM2019 continues, I was able to meet a couple of contributors to the International Emergency Medicine Education Project. I visited Rob Rogers’ well-known course, Medutopia, which aims to increase the quality of the teaching skills of educators. According to Dr. Rogers, this is the most enthusiastic and knowledgable group since the Medutopia journey has begun. Dr. Andy Little and Dr. Mike Giosondi were other two experts who gave the course with Dr. Rogers. You can read and listen to Dr. Rogers’ contributions to the International Emergency Medicine Education Project here.

I also came across to Dr. Simon Carley from Manchester, who is well-known for ST.EMLYN’s blog. He gave a couple of amazing talks during the conference, including one plenary presentation.

Simon Carley, plenary session
Simon Carley, plenary session
Arif Alper Cevik and Simon Carley
Arif Alper Cevik and Simon Carley

One of the surprising things was meeting with one of our blog authors Dr. Kaushila Thilakasiri (Sri Lanka) and her team. This energetic group was not only coming for ASEM to attend meetings, but they also came to compete in SimWars. And of course, they won the first prize.

Kaushila Thilakasiri and Sri Lanka team

Two days of workshops and three days of the busy scientific program passed like lightning. In addition to scientific activities, ACEM 2019 team prepared many social events for participants. I think, socially and scientifically, ACEM 2019 was a very busy conference. This created many networking opportunities.

One of the final event was graduation ceremony of 2018-2019 class of Emergency Medicine residents. Around 120 new graduated were appreciated with a nicely setted up ceremony with attendence of leaders of Emergency Medicine such as Prof. Lee Wallis (Past President of IFEM), Dr. Taj Hassan (Pas President of Royal College of Emergency Medicine) and Prof. James Ducharme (President of IFEM) as well as local leaders of Emergency Medicine of India.

2018-2019 Indian Emergency Medicine Graduates
2018-2019 Indian Emergency Medicine Graduates

As a summary, ACEM2019 was a successful gathering for international Emergency Medicine experts and Asian emergency physicians, residents and medical students.

ACEM 2021 will be in Hong Kong. ASEM board of directors decided to give ACEM2023 to Manila, Phillipines and ACEM2025 to Dubai, United Arab Emirates. We hope to see you all in these upcoming events.

Cite this article as: Arif Alper Cevik, "ACEM2019 and Incredible India," in International Emergency Medicine Education Project, November 13, 2019, https://iem-student.org/2019/11/13/acem2019-and-incredible-india/, date accessed: January 20, 2021