Question Of The Day #11

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod 11

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

  • A) IV antihypertensives and cardiothoracic consultation
  • B) IV heparin
  • C) Pericardiocentesis
  • D) IV Fluids, antibiotics, and surgical consultation

IV antihypertensives and CT surgery consultation (Choice A) would be the best treatment for a patient with aortic dissection. This diagnosis is characterized by severe tearing chest pain that radiates to the back, along with hypertension. Risk factors include tobacco smoking, uncontrolled hypertension, trauma (i.e. rapid deceleration), and connective tissue diseases (i.e. Marfan syndrome). Other than chest pain with radiation to the back, this patient lacks the other risk factors for aortic dissection, making Choice A less likely. IV heparin (Choice B) would be the correct choice for the treatment of pulmonary embolism and acute coronary syndrome (i.e. NSTEMI). Both of these diagnoses are possible, but a chest CT scan with PO water-soluble contrast is not the gold standard for diagnosing PE or ACS. A CT Pulmonary angiogram is ideal for PE diagnosis, and an EKG along with troponin levels are ideal for ACS diagnosis. Pericardiocentesis (Choice C) is the treatment for cardiac tamponade. The patient’s vitals show no evidence of obstructive shock, and there is no history of penetrating chest trauma, pericardial effusion, end-stage renal disease, HIV, lupus, cancer, or other risk factors for cardiac tamponade. Choice D outlines the best course of action to take in a patient with esophageal rupture, which is the disease described in the question stem. This condition can occur spontaneously after forceful vomiting causing high pressures in the esophagus (Boerhaave syndrome). In this situation, the chest pain typically begins after the onset of vomiting. Other etiologies of esophageal rupture include deceleration injuries and penetrating trauma (i.e. gunshot wounds, iatrogenic via esophagogastroduodenoscopy (EGD)). A “Hamman’s Crunch”, subcutaneous emphysema, fever, and signs of shock can be seen on exam. Diagnosis is confirmed by an esophagram or a CT scan of the chest with water-soluble oral contrast (i.e. Gastrograffin). Esophageal rupture is a life-threatening diagnosis as esophageal contents can spill into the mediastinum, causing mediastinitis and septic shock. The treatment is typically surgical with the repair of the perforated segment and drainage of fluid collections. Correct Answer: D  

References

Smith LM, Mahler SA. Chest Pain. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9e. McGraw-Hill; Accessed August 17, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=2353&sectionid=219641169

Nickson, C. (2019) Oesophageal Perforation. Life in the Fast Lane. Accessed August 17, 2020. https://litfl.com/oesophageal-perforation/

[cite]

The Rural Paradox

rural paradox
~ Carmina Shrestha, Nepal ~ Leave a comment

While trying to refrain from a complainer’s mindset, we often ignore discussing problems and hence seeking solutions.

Carmina Shrestha Tweet

The problem of having less time has existed from the day time and consciousness intersected. There are 24 hours in a day despite most of us wishing for more. I have been many things for many of those 24 hours: a student, an intern, a daughter, a friend, and a doctor. Most of the time, I’d be playing some combination of those roles. While an avid supporter of the make-time mentality, I have struggled with what one might call “Rural doctors paradox”. Simply put, the paradox is: there are supposedly fewer cases, and less severe cases in the rural, so few doctors are posted there which dramatically decreases doctor to patient ratio and has its multi-facet consequences.

What do you imagine when I say a rural doctor? How many patients a day does she look after? When does she wake up? How does her day go by? What does she reflect on while lying on the bed at the end of the day?

Carmina Shrestha Tweet

Not falling victim to the narrative fallacy, I would like to break this complex story into digestible chunks. Today I present you with challenges I as a rural doctor running a 24-hour emergency and a PHC can recall.

Beans again!

At the surface, it would seem like my mom’s lifetime of an attempt at hard-wiring my brain with negotiation skills failed when I agreed to buy potatoes at the offered price. The reason wasn’t my inattentiveness during those joyous negotiation classes I received, rather a phone call I used to dread the moment I stepped out of the PHC premise. “An unconscious middle-aged male is brought to the ER…”, said my health assistant. I was out buying vegetables for the week. I had to rush to the ER; 15 minutes of a run, tempo, hitchhiking, or teleportation.

Do hell with potatoes; I’ll make beans for dinner today, again!

Carmina Shrestha Tweet

Good but far.

“The view is serene, climate adequately cold and it is just 35 minutes away from here”. The picnic spot pitched by an office staff really stood out. Everyone was excited before we proceeded to choose, by lottery, the unfortunate souls who’d be in duty on the day. I was lucky enough to not have to stay, but that meant we would have to comply with the 30 minutes rule. Being 30 minutes far from the PHC would provoke anxiety of not reaching the PHC on time if need be. The consensus was it was not worth the risk.

Not me! The USG doctor!

“Why would the doctor make us wait for so long?”, said a patient to no one in particular. She has been waiting for her obstetric USG for an hour or so. After taking a quick shower to get rid of the stench and bacteria I accumulated from doing an autopsy on the days-old body, I rushed down to the USG room. “I hope no serious case arrives at the ER today!”, I find myself thinking. That day, while going to my bed, I reflected that the patient wasn’t mad at me for being late. Not the whole of me anyways. The me that was in the autopsy, she is fine. The patient was angry at the USG doctor. It just so happens to be me too.

Just another rainy day

Brinjals, Potatoes, Rice, and some medication: that is a typical to-get list of a villager who walks for quite some time to get to the marketplace on Thursdays. “My child often gets feverish! It was a market-day so I could not bring him with me”, says the 116th patient on a typical Thursday.

There are days when we literally wait for patients while enjoying the bright sun and delicious peanuts too. Busy-ness has a predictable spectrum in Beltar.

Carmina Shrestha Tweet

Like any other predictable spectrum, there are curve-balls once in a while. Those are the days that I remember the most when I look back.

[cite]

Giant Hogweed Burns

Giant Hogweed…and the Lesions it Causes.
~ Francesco Adami, Italy ~ Leave a comment

Summer is the time when outdoor work and leisure activities increase. It is also the season when plants like giant hogweed grow and bloom most. Direct contact with this beautiful umbrella plant, however, leads to serious skin lesions and skin burns[1] that often necessitates a visit to the emergency room.

MurielBendel / CC BY-SA (https://creativecommons.org/licenses/by-sa/4.0) - https://commons.wikimedia.org/wiki/File:Heracleum_mantegazzianum_Zinal.jpg

Have you ever heard of the giant hogweed?

The giant hogweed is an extremely toxic exotic plant particularly present in the British popular culture. It is also mentioned in the 1971 studio album entitled “Nursery Cryme” by the English rock band Genesis where the eternal struggle between this exotic plant and the English authorities trying to eradicate it is (humorously) narrated. Historically this plant was rediscovered in 1895 by two Italian doctors: Emile Levier and Carlo Pietro Stefano Sommier, to which they gave the botanical name of Heracleum mantegazzanium, in honour of their friend and physician Paolo Mantegazza, the first popularizer of Darwin’s scientific theories in Italy.

How can you recognize giant hogweed?

Giant hogweed, also known as Heracleum mantegazzianum, is considered to be the largest and most beautiful umbrella plant in the world[2]; it can reach a height of over 3 meters[3]. It is recognizable due to the colour of its leaves, which are a bright light green colour tending towards yellow with deep lobes and segmentations. The trunk is very thick and robust, similar to that of artichoke, with dark red streaks and surrounded by spiky hairs. The diameter of the umbrella makes it the largest among the umbrella plants. 

Petr Polívka / CC BY (https://creativecommons.org/licenses/by/3.0)

The fruits have an ovoid appearance, and at the moment of flowering, their envelopes remain attached to the base of the umbrella and subsequently tend to wither. Giant hogweed blooms from early spring until late summer, especially in the vicinity of wetlands (streams or canal banks). These characteristics differentiate it from the garden angelica (Angelica archangelica) and the common hogweed (Heracleum sphondylium).

Who is most at risk of coming across giant hogweed?

Gardeners, trekkers, forest workers, and people who work outdoors in wooded or undergrowth areas where giant hogweed is present are most at risk of injury caused by giant hogweed.

How is giant hogweed sap toxic?

The sap of giant hogweed contains different photoactive agents called furocoumarins, of which the most predominant is 5-MOP (5-methoxypsoralen). Injuries are caused when these photoactive agents are exposed to and activated by UV-A rays present in sunlight. This gives rise to a toxic process in which the furan ring of the photoactive agent is cross-linked with the pyrimidine bases of DNA in the patient’s skin, thus causing an increase in oxidative stress leading to cell membrane damage and subsequent inflammation and oedema. The culmination of these processes leads to the development of phytophotodermatitis (PPD)[4].

Similar to other plants capable of phototoxicity, skin damage is dependent on certain factors[5] such as:

  • The concentration of the phototoxic agent
    • During summer months, levels of phototoxic agents are higher. Moreover, they are more concentrated in fruit, present in intermediate levels in the leaves, and are minimally present in the stem.
  • The thickness of the skin
    • Damage is more extensive and deeper in the skin that is thinner.
  • Sun exposure
    • When sun exposure is prolonged, there is greater photoactivation and therefore greater damage.
  • Skin moisture
    • Sweat or dew that may be present on the skin can accelerate the toxicity process.

What are its symptoms?

Symptoms of giant hogweed exposure usually involve an erythematous lesion[6] accompanied by extremely intense pain. If not treated early, erythematous lesions evolve into burns[7] with the appearance of one or more liquid-filled vesicles. Generally, patients may have fatigue and slight tachycardia, but vital signs and laboratory test may be normal.

During the history and physical examination, staphylococcal infection, allergic dermatitis, purpura, impetigo, and fungal infection must be considered in the differential diagnosis.

Dragan Marjanovic / CC BY-SA (https://creativecommons.org/licenses/by-sa/3.0) - https://commons.wikimedia.org/wiki/File:Phytophotodermatitis-Severe-Case.jpg
Cosima Pferdeliebe / CC0 - https://commons.wikimedia.org/wiki/File:Heracleum_-_B%C3%A4renklau_-_Hautreaktion.png

Therapy

Upon contact, the subject should immediately wash the red area abundantly, dry it, and cover it to avoid sun exposure. Other recommendations would include avoiding to take baths and showers and apply high protection sunscreen to the lesion.

If erythema appears, the use of sulfadiazine cream and analgesic anti-inflammatory drugs should be considered. Moreover, the use of ice to reduce inflammation can also be useful. In the event of an injury characterized by one or more blisters or loss of tissue, a conservative treatment[8] consisting of cleansing with antiseptic solution (i.e. Clorexidine) and bandaging with synthetic microporous membranes[9] have proven effective. In cases where the phototoxicity process has been prolonged enough to cause extensive and deep burns, skin grafting and surgical debridement are necessary.

Take-home message

In conclusion, the message for our patients who operate or live in areas where giant hogweed is present is to “look but absolutely don’t touch” this beautiful plant. Secondarily, it is also important to subsequently report its presence to public authorities; in fact, many countries or regions follow a specific eradication program for this plant which can prove dangerous for humans and animals.

Look but absolutely don't touch this beautiful plant.

Francesco Adami, Italy Tweet

References and Further Reading

[1] https://www.plymouthherald.co.uk/news/plymouth-news/man-suffers-horror-burns-hogweed-4216136

[2] Heracleum mantegazzianum (giant hogweed) – Invasive Species Compendium – https://www.cabi.org/isc/datasheet/26911

[3] Derraik JG. Heracleum mantegazzianum and Toxicodendron succedaneum: plants of human health significance in New Zea-land and the National Pest Plant Accord. N Z Med J 2007;120: U2657.

[4] Marcos LA, Kahler R. Phytophotodermatitis. Int J Infect Dis 2015;9(July (38)):7–8.

[5] Pira E, Romano C, Sulotto F, et al. Heracleum mantegazzianum growth phases and furocoumarin content. Contact Derm 1989; 21:300e3.

[6] J Emerg Nurs. 2006 Jun;32(3):246-8. A 43-year-old woman with painful, vesicular lesions from giant hogweed photodermatitis. Langley DM(1), Criddle LM.

[7] Baker BG, Bedford J, Kanitkar S. Keeping pace with the media; Giant Hogweed burns – A case series and comprehensive review. Burns. 2017 Aug;43(5):933-938. DOI: 10.1016/j.burns.2016.10.018.

[8] Chan JC, Sullivan PJ, O’Sullivan MJ, Eadie PA. Full thickness burn caused by exposure to giant hogweed: delayed presentation, histological features and surgical management. J Plast Reconstr Aesthet Surg. 2011;64(1):128-130. doi:10.1016/j.bjps.2010.03.030

[9] Pfurtscheller K, Trop M. Phototoxic plant burns: report of a case and review of topical wound treatment in children. Pediatr Dermatol 2014;31:e156–9.

[cite]

Question Of The Day #10

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod10 palpitation

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

  • A) IV Adenosine 6mg
  • B) Synchronized cardioversion
  • C) IV Amiodarone 150mg
  • D) Vagal maneuvers

This patient has a narrow-complex tachycardia with a regular rhythm. A narrow QRS complex is defined as a QRS interval less than 120msec. This is a normal finding. The differential diagnoses for regular narrow complex tachycardia include sinus tachycardia, atrial tachycardia, atrial flutter, and supraventricular tachycardia (“SVT”). SVTs are typically associated with narrow QRS complexes, unless there is a concurrent bundle branch block, other aberrant conduction, or the existence of electrical accessory pathways as in Wolff Parkinson White (WPW) syndrome. The heart rate of an SVT can vary from 140-280 beats/min. Intravenous Adenosine (Choice A) is a hallmark of SVT treatment, however, Adenosine is given after vagal maneuvers have been attempted and have failed. Synchronized cardioversion (Choice B) is a last-ditch effort treatment in a patient with SVT. Vagal maneuvers and medications are attempted prior to using cardioversion. However, if the patient is hypotensive, cardioversion should be employed. Intravenous Amiodarone (Choice C), beta-blockers, calcium channel blockers, or other antiarrhythmics can be used to terminate SVTs if vagal maneuvers and adenosine are not effective. Vagal maneuvers (Choice D), such as the Valsalva maneuver (“bearing down”) or carotid massage, are the initial treatment for SVTs. Correct Answer: D 

References

Burns, E. (2019, March 30). Supraventricular Tachycardia (SVT). Life in the Fast Lane. https://litfl.com/supraventricular-tachycardia-svt-ecg-library/

Nickson, C. (2019, March 24). Narrow Complex Tachycardia. Life in the Fast Lane. https://litfl.com/narrow-complex-tachycardia/

[cite]

iEM Monthly – August 2020

~ iEM Education Project Team ~ Leave a comment

Welcome to the iEM Education Project Monthly Newsletter. We will share the achievements, information about top posts, chapters, activities and future plans of the project.

Recent News

Recent Posts

Top Countries

Top Reads

News

  • We have 3 new authors
Picture of Brenda Varriano

Brenda Varriano

Brenda has just completed her first year of medical school at Central Michigan University. She has an interest in Emergency Medicine, and participated in the 2020 STAR-EM (Summer Training and Research in Emergency Medicine) at Toronto Western Hospital. Aside from school she loves working out, drawing and listening to music. At school she volunteers with Special Olympics, designed a study that aims to develop a crisis preparedness toolkit for rural Older Adults Impacted by COVID-19 through CMU-CARES, and is working with a group of students to host Pre-Medical School Workshops. Brenda loves to see others succeed while keeping a healthy lifestyle and avoiding burnout.

Picture of Sheza Qayyum

Sheza Qayyum

My name is Sheza Qayyum, and I am a third-year medical student at the University of Toronto in Canada. My interests include medical education, FOAMed, and inner-city health. I am one of the podcast co-directors at the International Student Association of Emergency Medicine (ISAEM), which I enjoy greatly. I also love baking (and really all things food-related), chasing waterfalls with pretty hikes, and laughs with my friends and family.

Picture of Joseph Ciano

Joseph Ciano

Joey Ciano, DO is an Emergency Medicine Physician from New York, USA. He completed his Emergency Medicine Residency in Brooklyn, NY and is the current International Emergency Medicine Fellow in the Northwell-LIJ Health System. One of his main professional interests is building the educational infrastructure of EM in countries where EM is not yet recognized as a field and in countries that are in the early stages of this process. He has partnered with international NGOs in EM educational projects and works as a visiting EM faculty member in West Bengal, India. He is excited to collaborate with the other authors of the iEM Education Project to contribute to world of FOAM-ed.

Blog Posts of July

Top Countries

These countries viewed iEM content the most in July 2020. 

Top Three Chapters of May 2020

How to read chest x-rays, by Ozlem Koksal

336.3 - normal PA chest x-ray AIRWAY STRUCTURES

How to Read C-Spine X-Ray, by Dejvid Ahmetović and Gregor Prosen

626.4 - Figure 4 - c-spine lateral x-ray - alignement

How to read pelvic x-rays, by Sara Nikolić and Gregor Prosen

628.12 - femur neck fx

Top Four Post of June 2020

Doctor, My Head Hurts!

DOCTOR, MY HEAD HURTS
~ Arthur Martins, Brasil ~ Leave a comment

February was the last of my three months at Family Medicine clinical rotation. In addition to normal clinical consultations, we also had to take turns attending spontaneous demands coming “from the street”, in a primary care resource center that works similar to a green zone setting in the ED. During these three months, I’ve noticed that, sometimes, the easiest patient to manage is that one with a major complaint like chest pain, severe dyspnea, altered mental status, and so on. Things become more difficult, however, when you have a patient that has just a headache, a very common symptom, but one that could be related to an enormous variety of conditions, some of which life-threatening. Sometimes, you dig under the “green” patient and discover a secret “yellow” or even a “red” condition.

Next, I will try to put some light on the investigation of one of the most common complaints I’ve seen, and one of the symptoms that always put a bug in the ear: Headache.

Epidemiology

Headache is a very common complaint at the Emergency Department, being the fifth leading cause of ED visits¹. Alarmingly, about 0.5% of patients who had presented with a headache and discharged home have returned with a serious condition, of which 18% were acute ischemic stroke.²

Clinical Presentation

Patients can describe headache, a very nonspecific and hard to clarify complaint, in diverse ways, ranging from saying solely “my head hurts” to making a circular gesture around his/her head with. Therefore, identifying potential risk factors that can alert us to potential adverse outcomes. Here are a few decision rules for patients with headache:

SNNOOP10

The mnemonic SNNOOP10³ refers to the red flag symptom and findings to screen, which may point to related secondary headaches.

snnoop10

Ottawa Subarachnoid Hemorrhage Rule

Ottawa Subarachnoid Hemorrhage Rule fundamentally helps to rule out (Sensitivity: 100% Specificity: 15%) subarachnoid hemorrhage (SAH) in patients with headache. You can apply this rule ONLY IF:

  • The patient is alert and older than 15 years old with
  • New severe non-traumatic headache, reaching maximum intensity within 1 hour and
  • NO new neurological deficits, no history of intracranial tumors, previous SAH or aneurysms, and similar headaches (≥ 3 episodes over ≥ 6 months)

Risk factors are:

  1. Age ≥ 40
  2. Neck pain or stiffness
  3. Witnessed loss of consciousness
  4. Onset during exertion
  5. “Thunderclap headache” (defined as instantly and immediately peaked pain)
  6. Limited neck flexion on examination (defined as the inability to touch chin to chest or raise head 3 cm off the bed if supine)

If ANY of these factors is present, SAH can not be ruled out, and this patient needs further investigation. A recent study has assessed the performance of the Ottawa decision rule for patients presenting with headache in the ED, showing that it is a highly sensitive test (100%), making it useful in order to “not miss the disguised red patient.”5 Not by coincidence, Tintinalli’s book states with bold letters: “Acute onset of a severe headache is subarachnoid hemorrhage until proven otherwise.”

Acute onset of a severe headache is subarachnoid hemorrhage until proven otherwise.

Tintinalli's Comprehensive Study Guide Tweet

Investigation

Neuroimaging is a valuable diagnostic tool but is also an expensive one. Besides, it can be harmful due to radiation exposure or contrast use.

There is a lot of controversy in the literature regarding the question “When to image patients with a headache?”, but the consensus is to image when a patient presents with red flags, especially those related to vascular causes, raised intracranial pressure and focal signs.4

CT scan is the preferred method to investigate SAH, with excellent sensitivity and specificity (both bigger than 90%) in the first 6 hours of hemorrhage.6 However, if more time has passed, other diagnostic tools will probably be required in this case. Also, as said before, the costs are a major factor regarding neuroimaging, and sometimes you have to use what you have.

Lumbar Puncture

  • Indications7:
    • Suspected infectious disease of the CNS
    • Suspected SAH
    • Suspected idiopathic intracranial hypertension – as diagnostic and treatment
  • Contraindications7:
    • Coagulopathy (including anticoagulant drugs) or thrombocytopenia
    • Infection at the puncture site
    • Suspected epidural abscess
    • Findings on the CT scan to deferring LP
    • Brainstem herniation
    • Mass with signs of compression of the 4th ventricle
    • Signs of increased intracranial pressure or midline shift
    • Acute intracranial hematoma

Disposition and Follow-up(7,8)

  • Most patients can be discharged with a simple painkiller prescription. About 95% of patients presenting to the ED with headache have a benign etiology and don’t need further investigation in the ED.
  • The acute benign headache usually resolves with acetaminophen, NSAIDs, hydration, and rest.
  • An adequate follow-up plan is a good practice since most headaches are due to chronic conditions that may benefit from pharmacologic prophylaxis as well as lifestyle modifications.

This subject is open to discussion. Although it looks (and it is) a simple and easy-to-manage condition 90% of times, it has the potential to give the doctor some headache, too!

References and Further Reading

  1. American College of Emergency Physicians Clinical Policies Subcommittee (Writing Committee) on Acute Headache:, Godwin, S. A., Cherkas, D. S., Panagos, P. D., Shih, R. D., Byyny, R., & Wolf, S. J. (2019). Clinical Policy: Critical Issues in the Evaluation and Management of Adult Patients Presenting to the Emergency Department With Acute Headache. Annals of emergency medicine, 74(4), e41–e74. https://doi.org/10.1016/j.annemergmed.2019.07.009
  2. Dubosh, N. M., Edlow, J. A., Goto, T., Camargo, C. A., Jr, & Hasegawa, K. (2019). Missed Serious Neurologic Conditions in Emergency Department Patients Discharged With Nonspecific Diagnoses of Headache or Back Pain. Annals of emergency medicine, 74(4), 549–561. https://doi.org/10.1016/j.annemergmed.2019.01.020
  3. Do, T. P., Remmers, A., Schytz, H. W., Schankin, C., Nelson, S. E., Obermann, M., Hansen, J. M., Sinclair, A. J., Gantenbein, A. R., & Schoonman, G. G. (2019). Red and orange flags for secondary headaches in clinical practice: SNNOOP10 list. Neurology, 92(3), 134–144. https://doi.org/10.1212/WNL.0000000000006697
  4. Good C. (2019). British Society Of Neuroradiologists Guidelines for Headache. Retrieved July 23, 2020, from https://bsnr.org.uk/_userfiles/pages/files/standards_and_guidelines/bsnr_guidelines_for_imaging_in_headache_april_2019_final.pdf
  5. Wu, W. T., Pan, H. Y., Wu, K. H., Huang, Y. S., Wu, C. H., & Cheng, F. J. (2020). The Ottawa subarachnoid hemorrhage clinical decision rule for classifying emergency department headache patients. The American journal of emergency medicine, 38(2), 198–202. https://doi.org/10.1016/j.ajem.2019.02.003
  6. Kwiatkowski T. and Friedman B. W. (2018). Headache Disorders. In: R. M. Walls, R. S. Hockberger, M. Gausche-Hill, K. Bakes, J. M. Baren, T. B. Erickson, A. S. Jagoda, A. H. Kaji, M. VanRooyen, R. D. Zane, (Eds.) Rosen’s Emergency Medicine Concepts and Clinical Practice (9th ed. pp: 1265-1277). Philadelphia, PA: Elsevier.
  7. Perry, J. J., Stiell, I. G., Sivilotti, M. L., Bullard, M. J., Emond, M., Symington, C., Sutherland, J., Worster, A., Hohl, C., Lee, J. S., Eisenhauer, M. A., Mortensen, M., Mackey, D., Pauls, M., Lesiuk, H., & Wells, G. A. (2011). Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study. British Medical Journal (Clinical research ed.), 343, d4277. https://doi.org/10.1136/bmj.d4277
[cite]

Question Of The Day #9

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod9

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

  • A) Give sodium bicarbonate
  • B) Give diazepam
  • C) Give physostigmine
  • D) Give naloxone

This patient is suffering from sympathomimetic toxicity. Signs of a sympathomimetic toxidrome include agitation, psychosis, delirium, tachycardia, hypertension, diaphoresis, mydriatic (dilated) pupils, and decreased bowel sounds. The features of anticholinergic toxidromes overlap with many features of sympathomimetic toxidromes. A clinical finding that can be used to differentiate the two toxidromes is diaphoresis. Diaphoretic skin supports a sympathomimetic ingestion, while dry, warm skin supports anticholinergic ingestion. Examples of substances that can cause a sympathomimetic toxidrome ae cocaine, amphetamines, synthetic cannabinoids, ketamine, bath salts, and ecstasy (MDMA). The treatment for this toxidrome is mostly supportive care, such as benzodiazepines and cooling. Cocaine can cause coronary artery vasospasm along with sodium-channel blockade, which can predispose to cardiac arrhythmia. For this reason, a 12-lead EKG is important in any patient with possible cocaine toxicity. Sodium bicarbonate (Choice A) would be beneficial in salicylate toxicity, tricyclic antidepressant toxicity, or cocaine toxicity if the QRS was widened. The EKG for this patient has a normal QRS interval (<120msec). Physostigmine (Choice C) is an acetylcholinesterase inhibitor. This medication would likely worsen the patient’s tachycardia. Physostigmine is the antidote for anticholinergic toxicity. However, physostigmine should not be used in TCA overdose as it may increase the risk of cardiac arrhythmia. Naloxone (Choice D) is the antidote for opioid toxicity. Signs of opioid overdose include miotic (constricted) pupils, respiratory depression, and CNS depression. This patient does not possess these symptoms on exam. Diazepam (Choice B) is the best treatment. Correct Answer: B

References

Greene S. General Management of Poisoned Patients. “Chapter 176: General Management of Poisoned Patients”. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9th ed. McGraw-Hill.

Donaldson, R. (2019). Cocaine toxicity. WikEm. https://www.wikem.org/wiki/Cocaine_toxicity

[cite]

Troponin and nothing more

troponin and nothin more
~ Israa M Salih, UAE ~ Leave a comment

It’s almost impossible to have an ER shift without encountering a chest pain patient!

The first thing that always comes to mind is to rule out STEMI; well, unless the patient is having chest pain, and you see a knife stabbed in his chest!

It’s a no brainer situation; investigations wise, you will start with an EKG, and a set of labs, including cardiac markers.

Acute coronary syndrome (ACS) with its subcategories, ST-elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina, is responsible for one third of total mortality in individuals more than 35 years of age.(1)

The role of cardiac markers in diagnosis and management of ACS and cardiovascular problems is vital. In the United States cardiac biomarkers testing occurs in nearly 30 million emergency department visits nationwide each year.(2)

What is a biomarker?

The National Institutes of Health defined a biomarker as “a characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention.” (3)

Biomarkers utilization in cardiovascular medicine is a wide domain; it’s used in screening, diagnosis, prognosis and monitoring. (4)

What’s available?

Numerous cardiac markers are available today and can be classified as:

  1. Biomarkers of myocardial injury, which is further divided into:
    1. Biomarkers of myocardial necrosis: CK-MB fraction, myoglobin, cardiac troponins
    2. Biomarkers of myocardial ischemia: Ischemia-modified albumin (IMA), heart-type fatty acid-binding protein (H-FABP)
  2. Biomarkers of hemodynamic stress: Natriuretic peptides (NPs): atrial natriuretic peptide (ANP), N-terminal proBNP (NT-proBNP), B-type natriuretic peptide (BNP)
  3. Inflammatory and prognostic markers: hs C-reactive protein (CRP), sCD40L, homocysteine. (4)

What’s best?

Cardiac Troponin and the B type cardiac natriuretic peptides are the two markers recommended by ACEP and AHA in diagnosis of ACS and heart failure respectively.(5)

The ACS biomarker of choice

ACS is subcategorized based on ECG and cardiac troponin. The fourth universal consensus definition of Myocardial Infarction (MI); by the European Society of Cardiology (ESC) and American College of Cardiology (ACC), takes Troponin as a detrimental parameter in case definition, because of its high sensitivity and specificity.(6)

ACEP and AHA guidelines recommend the use of Troponin as level A class 1 in diagnosis of ACS. (7) It was practiced before to consider multiple markers dealing with ACS, more precisely in NSTEMI ruling out recommendation. However, this practice is now outdated with the use of hs cT solely.(7-9)

What’s troponin and why do we like it?

It’s a protein that regulates the interaction between actin and myosin filaments, found in skeletal and cardiac myocytes. Cardiac troponin (cTn) has three subunits troponin T, troponin C and troponin I. Troponin T and I are highly specific and sensitive.(10) The half-life of troponin T and troponin I in the blood is about 2 hours and last in serum for 4 to 10 days10

For ACS, the sensitivity of troponin is about 95%, and the specificity is about 80%, higher than any other marker available.(12)

However, many causes can elevate serum troponin which includes pericarditis, myocarditis, heart failure and chest trauma; non-cardiac conditions are sepsis, renal disease, pulmonary embolism, COPD, strenuous exercise and hypertension.(14)

High-sensitivity cardiac troponin (hs-cTn T and I) can detect troponin at concentrations much lower than the old cTn tests, and has replaced it.7 For ACS, hs cT substituted and limited the roles of other markers; it’s proven to be safe, cost effective, and a valuable prognostic factor. (7-9, 14)

For all of the above and the heart score… In ACS, use Troponin and nothing more!

References and Further Reading

  1. Anumeha Singh; Abdulrahman S. Museedi; Shamai A. Grossman. Acute Coronary Syndrome. StatPearls[Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan.
  2. Alvin MD, Jaffe AS, Ziegelstein RC, Trost JC. Eliminating Creatine Kinase–Myocardial Band Testing in Suspected Acute Coronary Syndrome: A Value-Based Quality Improvement. JAMA Intern Med. 2017;177(10):1508-1512. doi:10.1001/jamainternmed.2017.3597.
  3. Biomarkers and surrogate endpoints: preferred definitions and conceptual framework. Biomarkers Definitions Working Group. Clin Pharmacol Ther. 2001 Mar; 69(3):89-95. doi.org/10.1067/mcp.2001.113989.
  4. Jacob R, Khan M. Cardiac Biomarkers: What Is and What Can Be. Indian J Cardiovasc Dis Women WINCARS. 2018 Dec; 3(4): 240–244. doi: 10.1055/s-0039-1679104.
  5. Richards AM. Future biomarkers in cardiology: My favourites. European Heart Journal Supplements, Volume 20, Issue suppl_ G, 1 August 2018, Pages G37-G44. doi.org/10.1093/eurheartj/suy023.
  6. Thygesen K, Alpert JS, Jaffe AS, et al., on behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction. Fourth Universal Definition of Myocardial Infarction (2018). J Am Coll Cardiol. 2018. Volume 72 DOI: 10.1016/j.jacc.2018.08.1038. 
  7. Ezra A. Amsterdam, Nanette K Wenger, Ralph G. Brindis, Donald E. CaseyJr, Theodore G. Ganiats, David. HolmesJr, Allan S. Jaffe, Hani Jneid, Rosemary F. Kelly, Michael C. Kontos, Glenn N. Levine, Philip R. Liebson,Debabrata Mukherjee, Eric D. Peterson, Marc S. Sabatine, Richard W. Smalling, Susan J. Zieman. 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014; 130:e344–e426. 2014. doi.org/10.1161/CIR.0000000000000134.
  8. Edward W Carlton, Louise Cullen, Martin Than, James Gamble, Ahmed Khattab, Kim Greaves. A novel diagnostic protocol to identify patients suitable for discharge after a single high-sensitivity troponin. Heart. 2015 Jul 1; 101(13): 1041–1046. doi: 10.1136/heartjnl-2014-307288.
  9. Ron M. Walls, Robert S. Hockberger, Marianne Gausche-Hill, Katherine Bakes, Jill Marjorie Baren, Timothy B. Erickson, Andy S. Jagoda, Amy H. Kaji, Michael VanRooyen, Richard D. Zane. Rosen’s Emergency Medicine: Concepts and clinical practice. 9th edition. Elseivier; 2018.
  10. Ooi DS1, Isotalo PA, Veinot JP. Correlation of antemortem serum creatine kinase, creatine kinase-MB, troponin I, and troponin T with cardiac pathology. Clin Chem. 2000 Mar; 46(3):338-44.
  11. Harvey D. White, DSC. Pathobiology of Troponin Elevations: Do Elevations Occur With Myocardial Ischemia as Well as Necrosis?. Journal of the American College of Cardiology. Vol. 57, No. 24, ISSN 0735-1097/$36.00 Published by Elsevier Inc. doi:10.1016/j.jacc.2011.01.029.
  12. John E. Brush, Jr., Harlan M. Krumholz. A Brief Review of Troponin Testing for Clinicians. American College of Cardiology. 2017 Aug 7th. acc.org/latest-in-cardiology/articles/2017/08/07/07/46/a-brief-review-of-troponin-testing-for-clinicians.
  13. Asli Tanindi, Mustafa Cemri. Troponin elevation in conditions other than acute coronary syndromes. Vasc Health Risk Manag. 2011; 7: 597–603. PMID: 22102783. doi: 10.2147/VHRM.S24509.
  14. Donald Schreiber, Barry E Brenner. Cardiac Markers. emedicine.medscape.com/article/811905-overview [Accessed 2020 March 23rd].
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The Importance of Wellness in Medicine – My Story and Introduction to a Series of Blog Posts

wellness in medicine
~ Brenda Varriano, Canada ~ Leave a comment

Either be the light in the room or the mirror that reflects it

Unknown Tweet

I always believe that going to work means putting personal issues aside. As physicians, we have a role to make every patient feel welcome, cared for, and heard. However, being in the ER can be stressful. Not only can stress impact our job performance, but it can increase the burnout rate. So begs the questions; how you handle stress, why is it important and what happens when you lose your main source of stress reduction, is there a back-up plan. For my wellness series, I hope to discuss my own experience of losing my main outlet for stress so you know who I am and why I am writing about this topic, the importance of physical fitness, effective quick workouts for a busy ED lifestyle, and a favorite topic of mine, imposter syndrome. As medical students, aspiring ED physicians or an ED physician, I believe we have a role to protect our own health, so that we may best support our patients. 

As medical students, aspiring ED physicians or an ED physician, I believe we have a role to protect our own health, so that we may best support our patients.

Brenda Varriano Tweet
brenda - who I am

My name is Brenda-Maricela and I have just finished my first year of medical school at Central Michigan University as an international student, having done all prior education in Canada. While, academically, I had performed well in medical school, mentally, I was burnt out. It is not that I was not used to difficult schoolwork, I had graduated from the University of Toronto, where I was quite accustomed to immense workloads, working part-time jobs and juggling extra-curriculars. It was the fact that I had no outlet for my stress.

You see, prior to medical school, my outlet would be running. I was a modern-day Forest Gump. I craved the long runs that would allow me to shake off any stress I was holding onto. The longer the run the better. I was addicted. During my MSc, I was training with the University of Toronto Triathlon club, running road races and trying to win my age group and felt I could face any challenge that crossed my path. However, I would never have anticipated that I would not be able to run for 2 years. 

In the summer of 2018, I recall the moment where I was getting off of a chair at a conference. I felt a twinge in my right knee but thought nothing of it. I had a minor limp, but nothing too severe. A week later the pain grew, and before I knew it, I was in the ER. “I believe you have Patellar Femoral Pain Syndrome,” the doctor told me while reviewing my X-Rays. Patellar Femoral Pain Syndrome (PFPS) is a clinical term to define anterior knee pain, which often shows no structural damage in imaging.

brenda ER

It is most common in female athletes, and given the multifactorial nature, there is no single treatment. However, it often resolves with physical therapy and reducing activity. Reading about PFPS is one thing, experiencing it is a nightmare.

What would I do without running? The most common advice that I had received was to switch to biking and swimming, something which was a lower impact. These strategies worked, but as time had waned on, my knees became worse and soon, even the pool became a source of pain. I was in a rut. I would do anything to get the endorphins, but nothing would suffice. I would do anything to run again, let alone kneel in a yoga class. I saw multiple doctors, physical therapists, chiropractors and each time, I got the same diagnosis and was told it would resolve on its own.

Spring 2019, I got the phone call informing me of my acceptance to medical school. It was something I had dreamed of since I was a little girl. On one hand, I was ecstatic, but on the other hand, I was drained, depressed and couldn’t look at a jogger on the roads without feeling a sinking feeling in my stomach. How on earth was I going to get through medical school? During my undergraduate degree, I had exercising to sharpen my mind and combat stress. I knew medical school would be intense. How would I deal with the stress? What if my knee got worse? I would be in a new country, without friends and family. Would I draw too much attention if I limped, sat all the time, didn’t participate with social outings? I almost wanted to defer a year. However, my father and biggest mentor reminded me that I had managed to get through the application process without my exercises, perhaps studying would be a good distraction.

My father was right about studying being a distractor. At times, I would be so focused on learning the content, that I forgot about the pain. Other times, my brain would be so fried that I needed a distraction. But what could I do? Sitting for so long, my body craved movement, but my knees would be hesitant. During this time, I did educate myself on other exercise styles such as High-Intensity Interval Training (HIIT), or As Many Reps as Possible Workouts (AMRAP), both with weights, and both focusing on the upper body and core. I will discuss the concept of AMRAP and HIIT in my second article, where I talk about quick and effective workouts. I believe that a sound body and mind are critical to perform well and avoid burn out in, school, the ED and beyond. However, the busy lifestyle as a medical student or a physician may make the time a limiting factor. Therefore, short effective workouts may be of use, and I hope to share my research and experiences.

So, while AMRAP and HIIT didn’t replace running, it would provide some mental soundness on days when I felt particularly on edge. Over time my knees improved, and I owe thanks to some wonderful healthcare providers in Michigan. Unfortunately, while volunteering with Special Olympics in November 2019, I got a hockey-related injury to my knees, setting my progress back a few weeks. I was devastated. Mentally, I was fried, emotionally I was drained. However, the schoolwork was still there, and I had to study. So, what did I learn from November 2019 to present? I learned how important mental health and physical wellness is. This has been a topic among peers who lost their gyms due to COVID-19, thus experiencing a loss of an outlet for stress. Personally, I saw the difference that stress made in my productivity, wellbeing and ability to retain information. So, I started exploring different outlets, many of which will be discussed in upcoming articles.

Exercise is still my favorite outlet, and I think it should be a part of a daily regimen. So, for my next two articles, I will discuss different styles of exercises and free resources I discovered on the web, such as timers, YouTube Channels and websites. Following my articles on exercise and fitness, I would like to dive into the science of yoga. I remember being told about traditional meditation, however, I found that my mind was too busy, and ironically, meditation caused me stress. Many of my ED-oriented friends similarly need to keep mentally busy, and one had recommended yoga as an active meditation. This being said, traditional mediation is effective, and my ED mentor loves it. Therefore, meditation will be discussed, most likely through research and interviews with those who have benefited from it. Finally, I intend to write about imposter syndrome. A lack of self-love can be a mental stressor. If we can learn to love and appreciate all that we have accomplished, I believe that the stress will go down. To show some self-love sounds simple but is often something that so many medical students struggle with. I know I question my own acceptance into medical school, being my own worst critic.

To conclude this article, I want to say I am passionate about medicine, and in seeing my colleagues succeed. Given my enthusiasm for exercise, and having done some personal training in the past, I am eager to share all I know. Maybe I’ll be running when I write my next article. If not, I know there are alternatives, and I hope what I share can be of use to my colleagues around the world. As I tell my friends, even if life clips your wings, just know you have all it takes to fly.

References and Further Reading

LaDonna KA, Ginsburg S, Watling C. “Rising to the Level of Your Incompetence”: What Physicians’ Self-Assessment of Their Performance Reveals About the Imposter Syndrome in Medicine. Acad Med. 2018;93(5):763-768. doi:10.1097/ACM.0000000000002046

Moukarzel A, Michelet P, Durand AC, et al. Burnout Syndrome among Emergency Department Staff: Prevalence and Associated Factors. Biomed Res Int. 2019;2019:6462472. Published 2019 Jan 21. doi:10.1155/2019/6462472

Petersen W, Ellermann A, Gösele-Koppenburg A, et al. Patellofemoral pain syndrome. Knee Surg Sports Traumatol Arthrosc. 2014;22(10):2264-2274. doi:10.1007/s00167-013-2759-6

 

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Question Of The Day #8

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod 8 toxicology

Which of the following is the most likely cause of this patient’s condition?

  • A) Amitriptyline
  • B) Cocaine
  • D) Physostigmine
  • C) Diphenhydramine

This patient is suffering from an anticholinergic toxidrome. Symptoms of anticholinergic medication toxicity include altered mental status with agitation or delirium, tachycardia, hypertension, hyperthermia, mydriatic (dilated) pupils, hot and dry skin, decreased bowel sounds, and urinary retention. The sympathomimetic toxidrome is very similar to the anticholinergic toxidrome; however, patients with anticholinergic ingestions have dry skin while patients with sympathomimetic ingestions have diaphoretic skin. Some notable types of anticholinergics are atropine, antihistamines, Tricyclic antidepressants (TCAs), and Jimson weed. Amitriptyline (Choice A) is a TCA medication and can cause anticholinergic toxicity. When taken in high doses, a major adverse effect of TCAs is Na-channel blockade, resulting in QRS widening on EKG and cardiac arrhythmias. Therapy includes sodium bicarbonate and supportive care. This patient has a normal QRS interval on EKG, making this choice less likely. Cocaine (Choice B) is a sympathomimetic. Many features of the exam support sympathomimetic toxicity, but the presence of dry skin makes this choice less likely. Physostigmine (Choice C) is an acetylcholinesterase inhibitor which would have a cholinergic toxidrome if taken in excess. Features of this include bradycardia, bronchorrhea, bronchospasm, diarrhea, hypersalivation, sweating, and hyperactive bowel sounds. Treatment for cholinergic toxicity is atropine. Along with supportive care, physostigmine is the main treatment for anticholinergic toxicity. One exception is in TCA toxicity where physostigmine should be avoided. Diphenhydramine (Choice D) is an antihistamine with anticholinergic properties, and it is the most likely medication ingested in this case scenario. Correct Answer: D 

References

Greene S. General Management of Poisoned Patients. “Chapter 176: General Management of Poisoned Patients”. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9th ed. McGraw-Hill.

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Unmasking communication during COVID-19

Unmasking communication during COVID-19
~ Neha Hudlikar, UAE ~ Leave a comment

As face masks become ubiquitous in our health-care practice due to the COVID-19 pandemic, communication between the patient and health-care provider has become harder than ever before. The challenges posed by COVID-19 have highlighted various areas of deficiencies in the health care industry as well as heightened anxiety among health-care providers as well as patients. Communication with patients has become particularly challenging and ever so more important than before.

Imagine the plight of a patient struggling to breathe, being greeted by someone in full PPE, struggling to understand your muffled speech through the mask amidst the background noise of oxygen hissing through a breathing mask. Earlier, your smile would have worked to ease some of the anxiety by coming across as approachable and friendly; however, your face mask has cost you a brave soldier in your battle of gaining trust. The situation is worse in the elderly, frail, and cognitively impaired patients who may rely on lip-reading and facial expressions to communicate.

Health care workers are forced to have difficult conversations of do-not-resuscitate orders, advance care planning, and break bad news while wearing a face mask and PPE, creating a barrier for effective communication with patients and their family members.

If you have previously relied on a firm handshake and a smile to lessen the anxiety of patients but are now finding it challenging to have clear communication, here are few ways to improve communication with patients.

Unmasking communication during COVID-19
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Question Of The Day #7

question of the day
~ Joseph Ciano, USA ~ Leave a comment
qod7 - sepsis

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

  • A) Perform endotracheal intubation
  • B) Give more IV fluids
  • C) Start IV vasopressors
  • D) Give acetaminophen

This patient has a diagnosis of septic shock due to pneumonia. In all patients presenting to the Emergency Department, the initial assessment should involve the “ABCs” (assessment of Airway, Breathing, and Circulation). The patient is given supplemental oxygen for her hypoxemia with an improved oxygen saturation from 89% to 95%. Performing endotracheal intubation (Choice A) is too aggressive at this time as the patient is improving with non-invasive oxygenation techniques. The Centers for Medicare and Medicaid sepsis guidelines recommend a 30 mL/kg of isotonic crystalloid fluid bolus in patients with sepsis. However, there is limited data to support this recommendation, as some patients may benefit from less or more fluids than 30 mL/kg. The question stem indicates that an appropriate bolus of fluids has been given, so providing more IV fluids (Choice B) is not the best course of action. The use of passive leg raising or bedside ultrasonography to assess for Inferior Vena Cava (IVC) size may help a clinician discern if more or less fluids are required. For example, visualizing a flat, collapsible IVC on ultrasound indicates additional fluids may be helpful. An increase in blood pressure after a patient’s legs are raised above the level of the heart (“passive leg raise”) also supports the use of additional IV fluids. Giving acetaminophen (Choice D) will help reduce the patient’s fever and improve patient comfort. However, initiating vasopressor therapy (Choice C) is the more appropriate next course of action. Vasopressors (i.e. norepinephrine, epinephrine) are generally recommended after IV fluid boluses if a patient is persistently hypotensive with a MAP less than 65mmHg. Vasopressors help to maintain cerebral and organ perfusion in states of shock. They should be titrated to a dose that maintains a MAP of 65mmHg or above.  Correct Answer: C 

References

Nicks BA, Gaillard JP. Approach to Nontraumatic Shock. “Chapter 12: Approach to Nontraumatic Shock”. In: Tintinalli JE, Ma O, Yealy DM, Meckler GD, Stapczynski J, Cline DM, Thomas SH. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 9th ed. McGraw-Hill.

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