Question Of The Day #15

question of the day
qod 15 - pleuritic chest pain

Which of the following is the best course of action to further evaluate for a diagnosis of pulmonary embolism?

Pulmonary embolism (PE) is a potentially lethal diagnosis evaluated by a combination of a thorough history, physical exam, and the use of risk stratification scoring tools. The Wells criteria and the PE rule-out criteria (PERC) are two well-accepted risk stratification tools for PE. These criteria are each listed below (Wieters et al., 2020).

Wells’ Criteria for Pulmonary Embolism

CriteriaPoint Value
Clinical signs and symptoms of DVT+3
PE is #1 diagnosis, or equally likely+3
Heart rate > 100+1.5
Immobilization at least 3 days, or Surgery in the Previous 4 weeks+1.5
Previous, objectively diagnosed PE or DVT+1.5
Hemoptysis+1
Malignancy w/ Treatment within 6 mo, or palliative+1
Interpretation
Score >4 = High probability
Score 2–4 = Moderate probability
Score <2 = Low probability

Pulmonary Embolism Rule Out Criteria

All Variables Must Be Present for <2% Chance of PE
Pulse oximetry >94% (room air)
HR <100
No prior PE or DVT
No recent surgery or trauma within prior 4 wk
No hemoptysis
No estrogen use
No unilateral leg swelling
The patient in this clinical vignette would have a Wells score of 1.5 (low risk) due to her persistent tachycardia of unknown etiology. The PERC rule can not be applied to this patient as she is over 50-years-old and has tachycardia. If the patient was low risk on Wells score and meet all the PERC rule criteria, she would have a less than 2% likelihood of her symptoms being due to a PE. It is important to note that only patients with a low-risk Wells score (low pretest probability for PE) can be subjected to the PERC rule. A low-risk Wells score (<2) is investigated with a D-Dimer test (Choice B), while moderate to high-risk Wells scores are investigated with a CT Pulmonary Angiogram (CTPA) (Choice C). A V/Q Scan (Choice A) is not a first-line test for the diagnosis of PE as it is less sensitive than a CTPA scan. Unlike a CTPA scan, a V/Q scan may be nondiagnostic in the setting of lung consolidation, effusions, or other airspace diseases. V/Q scans are second-line tests to CTPA when there are contraindications to a CTPA (i.e., renal failure). Lorazepam (Choice D) is a benzodiazepine that may be helpful in reducing tachycardia, which is secondary to anxiety. However, this therapy does not help further discern if the patient may have a PE. Correct Answer: B 

References

Wieters J, McDonough J, Catral J. Chest Pain. In: Stone C, Humphries RL. eds. CURRENT Diagnosis & Treatment: Emergency Medicine, 8e. McGraw-Hill; Accessed August 17, 2020. https://accessmedicine.mhmedical.com/content.aspx?bookid=2172&sectionid=165059275

Nickson, C. (2019). Pulmonary Embolism. Life in the Fastlane. Accessed on August 17, 2020. https://litfl.com/pulmonary-embolism/

Cite this article as: Joseph Ciano, USA, "Question Of The Day #15," in International Emergency Medicine Education Project, October 2, 2020, https://iem-student.org/2020/10/02/question-of-the-day-15/, date accessed: July 2, 2022

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Hypokalemic Periodic Paralysis in the ED

Hypokalemic Periodic Paralysis in the ED

Case Presentation

A middle-aged man with a two days history of weakness in his legs. The patient works as a construction worker and is used to conducting heavy physical activity.

After a thorough history and examination, the weakness was reported in the lower extremities with a power of 2/5, whereas the power in upper extremities was 4.5/5, Achilles tendon reflex was reduced, plantar response and other reflexes were intact, with normal sensation. Rest of the examination is unremarkable.

The vitals are within normal ranges, Blood investigations include – Urea and electrolytes, liver and renal function, full blood count, thyroid function tests, creatine kinase, urine myoglobin, vitamin B12 and folic acid levels.

Potassium level was 1.7 mEq/L (normal 3.5-5.5), and all other parameters were within normal ranges.

The ECG showed inverted T waves and the presence of U waves. An Example of an ECG:

Hypokalemic periodic paralysis is a rare disorder that may be hereditary as the primary cause, or secondary due to thyroid disease, strenuous physical activity, a carbohydrate-rich meal and toxins. The patients are mostly of Asian origin.

The most common presentation is of symmetrical weakness in lower limbs, with a low potassium level and ECG changes of hypokalemia. The patients may have a history of similar weaknesses which may be several years old. An attack may be triggered by infections, stress, exercise and other stress-related factors.

The word ‘weakness’, can lead to physicians thinking about stroke, neurological deficits and other life-threatening illnesses such as spinal cord injuries associated with high morbidity and mortality which need to be ruled out in the ED.

In this case, history and examination are vital. Weakness in other parts of the body, a thorough neurological examination are important aspects.

Patients are monitored and treated with potassium supplements (oral/Intravenous) until the levels normalize. ECG monitoring is essential, as cardiac function may be affected. 

The patient should be examined to assess the strength and should be referred for further evaluation and to confirm the diagnosis.

The differential diagnosis for weakness in lower limb include :

  1. Spinal cord disease (https://iem-student.org/spine-injuries/)
  2. Guillain barre syndrome
  3. Toxic myositis
  4. Trauma
  5. Neuropathy
  6. Spinal cord tumour

References

Cite this article as: Sumaiya Hafiz, UAE, "Hypokalemic Periodic Paralysis in the ED," in International Emergency Medicine Education Project, September 7, 2020, https://iem-student.org/2020/09/07/hypokalemic-periodic-paralysis-in-the-ed/, date accessed: July 2, 2022

Troponin and nothing more

troponin and nothin more

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].
Cite this article as: Israa M Salih, UAE, "Troponin and nothing more," in International Emergency Medicine Education Project, August 19, 2020, https://iem-student.org/2020/08/19/troponin/, date accessed: July 2, 2022