Category Archives: Diseases

Hypertensive Emergencies

Say what?

Hypertensive emergency has no universally accepted definition. Actual numbers are often used to define hypertensive emergency, though strictly speaking a hypertensive emergency is any elevation in blood pressure in the presence of end-organ dysfunction.1,2,3

Aggressively treating severe asymptomatic hypertension (very high blood pressure without clear end organ damage) is not indicated, not supported by the literature and dangerous. First, do no harm.

No end-organ damage ≠ HTN emergency

Pathophys alert: the mechanism of HTN emergency is poorly understood but it generally results from an abrupt rise in systemic vascular resistance, direct endothelial injury, and a loss of the body’s ability to autoregulate flow in vital organs. This leads to a continued increase in BPs and end organ damage. 2,4,5 Furthermore extremes of pressure result in activation of the renin-angiotensin-aldosterone axis. This leads to further vasoconstrictor release and elevations in BP. Finally, many patients undergo a pressure-induced natriuresis. The resulting intravascular volume loss causes further mediator release that elevates BP.

Your patient may report (from most to least common) 6:

  • Dyspnea (up to 30%)
  • Chest pain
  • Headache
  • Altered Mental Status
  • Limb weakness or sensory changes
  • Seizures (eclampsia)

You should ask about:

  • History of hypertension
  • Compliance with medication
  • Illicit drug use
  • Pregnancy
  • Kidney disease

On physical examination you should look for: 

  • Changes in mental status
  • Focal neurological abnormalities
  • Papilledema
  • Rales
  • JVD/S3
  • Asymmetric blood pressures between limbs

Is this really it?

If you patient has an elevated blood pressure in the setting of end organ dysfunction, then yes, it is.

If there are no clear signs of end organ damage, then no, it isn’t.

What tests does my patient need?

When evaluating your hypertensive patient it is imperative to make the distinction between a patient with symptomatic and asymptomatic hypertension. The recommendations below are for symptomatic patients only. Testing is mostly based on your patient’s presentation.

Labs: obtain a creatinine to assess for renal failure. A troponin and BNP are indicated if your patient has signs and symptoms consistent with cardiac ischemia or pulmonary edema.

Urine: perform a urinalysis to assess for proteinuria, indicating renal failure. If a pheochromocytoma is suspected obtain urine metanephrines. Obtain a toxicology screen if illicit drug use is suspected.

ECG: obtain if your patient has chest pain, shortness of breath, or signs and symptoms of pulmonary edema. Assess for ischemic changes.

Chest X-ray: indicated if pulmonary edema is suspected.

CT/MRI-scan: a CT-scan of the chest is indicated if an aortic dissection is suspected. CT scan of the brain should be obtained in a patient who has a history and/or physical examination consistent with an ischemic or hemorrhagic stroke. An MRI is more sensitive than a CT-scan for detecting changes consistent with hypertensive encephalopathy.

Is there a cure, doc?

For HTN emergencies, first, do no harm. Traditionally, a reduction of your patient’s mean arterial pressure (MAP) of no more than 20-25% in the first hour of treatment has been recommended. Several studies have indicated that we often do not do this well, and that we drop our patient’s blood pressure too rapidly in the emergency department. 7 Rapid lowering of the blood pressure poses your patient at risk of ischemic events (occurring in up to 5% of patients with rapid blood pressure reduction), and should be avoided at all cost. Aim for a reduction of 15-20% in the first hour, and no more than 25% in first 2 hours. It is important to monitor your patient’s blood pressure very closely. For that reason, an arterial line is highly recommended in HTN emergency. 6,9,10

What is the best route of drug administration?

A continuous, short acting, titratable intravenous agent is indicated for initial treatment. A continuous infusion is likely to achieve more predictable blood pressure control compared to repeated doses of antihypertensives. Oral and transdermal antihypertensives are not indicated in hypertensive emergency. These agents have a high failure rate and cannot easily be reversed.

Which agent should I use?

There are few studies with head to head comparison of agents in HTN emergency. One 2011 study suggested nicardipine, when compared to labetalol, may be superior in time to BP reduction, less adverse events and less need for use of additional agents. 11 Of note: most of the studies comparing nicardipine to labetolol are manufacturer sponsored. None of these studies report patient centered outcome differences (i.e. mortality benefit).

Consider the agents below depending on the specific end organ damage: 7,10,11

Medication End Organ Damage Pearls
Nicardipine Aortic Dissection
Renal Failure
HTN encephalopathy
Hemorrhagic or ischemic stroke
If used in dissection, must give beta blocker first
Clevidipine Aortic Dissection
Renal Failure
HTN Encephalopathy
Hemorrhagic or ischemic stroke
Fast onset and shorter half life than nicardipine makes, hence, very titratable but not available in many institutions
Labetalol Aortic Dissection
Pre-eclampsia and eclampsia
Hemorrhagic or ischemic strokes
Safe in pregnancy
Can be used as signal agent in aortic dissection
Nitroglycerin Acute Pulmonary Edema
Acute Coronary Syndrome
May use sublingual or topical forms until IV access established
Esmolol Aortic Dissection Should be used before vasodilator in dissection
Bolus initially and then begin continuous infusion
Phentolamine Cocaine or amphetamine intoxication
Secondary treatment with cocaine or amphetamines after trial of benzodiazepines
Fenoldopam Acute Renal Failure
Furosemide Acute Pulmonary Edema Not a first line agent as patients are generally hypovolemic; furosemide is also slow to work so should be used as an adjunctive agent


Additional Treatment Pearls:

  • Aortic dissection: if your patient has aortic dissection, rapidly lower the heart rate to approximately 60 beats per minute to help prevent reflex tachycardia. Once the heart rate is controlled, rapidly lower the SBP to < 120 mm Hg. Aortic dissection is the one HTN emergency where the rule of a 15-20% reduction in MAP during the first hour does not apply.
  • There is no clear data to prove that aggressive blood pressure lowering reduces hematoma expansion if your patient has a intracerebral hemorrhage, however, early high blood pressures are associated with mortality. 12 Therefore, aggressive blood pressure management should be considered, and recent data indicated that this may be safe. 13,14,15
  • In stroke patients, blood pressure targets are guided by stroke subtype and presenting blood pressure. 12 Start with a MAP reduction of 15-20% in the first hour in the ED.

Miller table stroke SBP

  • Eclampsia: give intravenous magnesium sulfate combined with labetolol. Definitive treatment is delivery of fetus.
  • A headache does not equal hypertensive encephalopathy. Hypertensive encephalopathy is diagnosed after a CT scan of the brain ruled out a bleed or stroke. 9
  • Give IVF fluids – most patients with hypertensive emergency are intravascularly depleted. Providing IV fluids can help prevent dropped blood pressures after initiation of antihypertensives. 16,17

FOAM under pressure: blow of some steam with continued reading/listening





1. Chobanian AV, Bakris LG, et al. Seventh report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. Hypertension. 2003; 42:1206-52.

2. Kessler CS and Joudeh Y. Evaluation and treatment of severe asymptomatic hypertension. AFP. 2010; 81: 470-476.

3. Wolfe SJ, Lo B, et al. Clinical policy: critical issues in the evaluation and management of adult patients in the emergency department with asymptomatic elevated blood pressure. Ann Em Med. 2013; 62: 59-64.

4. Vaughan CJ and Delanty N. Hypertensive emergencies. The Lancet. 2000; 356: 411-7.

5. Papadopoulos DP, Mourouzis I, et al. Hypertension crisis. Blood Pressure. 2010; 19: 328-36.

6. Marik PE and Rivera R. Hypertensive emergencies: an update. Current Opinion in Critical Care. 2011; 17: 569-580.

7. Brooks TWA, Finch CK, Lobo BL, et al. Blood pressure management in acute hypertensive emergency. Am J Helath-Syst Pharm. 2007; 64: 2579-2582.

8. Emergency Medicine Updates – Hypertension and the Emergency Physician

9. Johnson W, Nguyen M, Patel R. Hypertension in the emergency department. Cardiol Clin. 2012; 30: 533-543.

10. Flanigan JS and Vitberg D. Hypertensive emergency and severe hypertension: what to treat, who to treat, and how to treat. Med Clin N AM. 2006;90:439-451.

11. Peacock WF, Varon J, et al. CLUE: a randomized comparative effectiveness trial of IV nicardipine versus labetalol use in the emergency department. Critical Care. 2011; 15: R157-64.

12. Miller J, Kinni H, Lewandowski C, Nowak R, Levy P. Management of hypertension in stroke. Ann Emerg Med. 2014 Sep;64(3):248-55.

13. Zazulia, A.R., Diringer, M.N., Videen, T.O. et al. Hypoperfusion without ischemia surrounding acute intracerebral hemorrhage. J Cereb Blood Flow Metab. 2001; 21: 804–810

14. Anderson CS, Heeley EH, Huang Y, et al. Rapid blood-pressure lowering in patients with acute intacerebral hemorrhage. NEJM. 2013; 368:2355-2365.

15. Anderson CS, Huang Y, Wang JG, et al. Intensive blood pressure reduction in acute cerebral haemorrhage trail (INTERACT): a randomized pilot trial. Lancet Neurol. 2008; 7: 391-9.

16. Marik PE, Rivera R. Hypertensive emergencies: an update. Curr Opin Crit Care 2011; 17:569-80.

17. UMEM Education Pearls- Hypertensive Emergencies


Written by: Phil Magidson, M.D., M.P.H. | Edited by: Maite Huis in ‘t Veld, M.D. | Peer reviewed by: Michael Winters | November 9th, 2014

Asthma in Adults

Say what?

Chronic inflammation of your patient’s bronchi. Their bronchi are hypersensitive to environmental or intrinsic stimuli, leading to reversible episodes of bronchial constriction and mucosal edema.

Your patient will report:

  • Wheezing
  • Cough
  • Dyspnea
  • Chest tightness
  • Chest pain

You will ask about:

  • Comorbid diseases – you do not want to overlook another etiology to your patient’s symptoms (COPD, CHF, pneumonia)
  • Inhaler use, especially recent increase in PRN inhalers
  • History of asthma related admissions (especially in the last month or twice or more last year)
  • History of symptoms worsening at night
  • History of asthma related ICU admissions
  • History of asthma related intubation

Remember: “a lack or risk factors does not necessarily confer a lack of risk”1

You will see and hear2

  • Tachypnea
  • Tachycardia
  • Wheezing
  • Prolonged expiratory phase
  • Diaphoresis
  • Limited or absent air movement on auscultation
  • Increased work of breathing: retractions, accessory respiratory muscle use
  • Hypoxemia
  • Altered mental status

Does my patient need any tests?

Peak expiratory flow/spirometry – obtain before and after treatment. Limited by selected patient’s inability to appropriately perform the test. Consider using this Youtube video to teach your patient how to properly perform the test. Data suggest that up to 83% of the total increase in peak flow occurs after the first treatment, so the utility of serial measurements might be limited.1,3 It should not be used in isolation as a disposition decision making tool.

Labs – only indicated if you have a concern for an alternative diagnosis. If your patient is on diuretics or has renal disease, check a BMP to assess for patient’s potassium, magnesium and phosphate levels, as beta agonists can decrease these.4

ABG – please do not violate your patient’s radial artery. Metabolic acidosis on a blood gas has been described as an indicator of impending arrest4, however, this can be assessed by getting a venous blood gas. Hypoxemia and hypercarbia on the ABG indicate a severe status asthmaticus, but again, a venous gas will suffice.5 The ABG can be normal in patients with impending respiratory arrest. Your clinical judgment is the best indicator of your patient’s need for therapy and intubation.

ECG – not routinely indicated, unless you are concerned about an alternative diagnosis. If obtained it might show signs of pulmonary disease, including signs of right atrial enlargement, right axis deviation, right bundle branch block, rhythm abnormalities or non-specific ST and T-wave abnormalities. The abnormalities are reversible.6

Chest radiograph – not routinely indicated, unless you have a concern for an alternative diagnosis or underlying pneumonia or pneumothorax.1 In a study of patients that were admitted with asthma 34% were found to have a abnormality on initial chest X-ray, of which 40% lead to a change in clinical management.7 The abnormalities included hyperinflation, focal infiltrates, increased interstitial markings and pneumothorax.

Is there a cure, doc?

Beta agonists – short acting beta agonists are the mainstay of treatment for your asthmatic patient in the emergency department. Use racemic albuterol, as multiple studies have not shown any benefit to the use of levalbuterol and it is more expensive.1 Long acting beta agonists have no role in the emergency department, and have even been linked to asthma related deaths.8

Albuterol dosing:9

  • Intermittent nebulizer: 2.5 – 5mg every 20 minutes up to 3 doses, followed by 2.5-10mg every 1-4 hours as needed
  • Continuous nebulizer: 10-15 mg/hour
  • MDI: 4-8 puffs every 20 minutes up to 4 hours, then space to every 1-4 hours

Cholinergics – efficacy as a solitary agent is inferior to use of albuterol, however, if used in combination with albuterol leads to improved peak expiratory flow and decreased hospitalization rates. Use 1-3 doses initially, no data to support use beyond the first 3 doses.10

Ipratropium bromide dosing:9

  • Nebulizer (0.5mg/2.5mL or 0.2mg/mL): 2.5 mL, give 3 doses, may repeat every 6 hours (limited data to support this)
  • MDI (18mcg/puff): 8 puffs every 20 minutes, repeat as needed (limited data to support this beyond the first 3 doses)

Intermittent vs. continuous – use continuous nebulizer treatments if your patient is suffering from a moderate or severe attack.11 Continuous nebulizers can reduces the hospitalization rate in some patients compared to intermittent treatments. There is no data on the use of continuous nebulizer in mild attacks.

MDI vs. nebulizers – there is no data suggesting nebulizers are superior to the use of MDI’s.12 MDIs are cheaper and require fewer personnel. It is also a great way to assess if you’re patient is capable of correctly administering MDI treatment doses, and educate them if necessary.

Corticosteroids – get steroids on board early. Administrating steroids in the first hour has shown to significantly reduce admission rates.13 There is no clear evidence that inhaled steroids alone or in combination with systemic steroids have any added benefit in the early treatment of your asthmatic patient.14 Steroids should be continued for 3-10 days after the first early dose, as it helps prevent bounce backs and late hospitalization rates.15 There is no clear data on exact duration and dosage of the short course of steroids. Five days of 40-60mg prednisone per day is most commonly prescribed. Intramuscular depo administration of steroids can be considered, Several studies have shown that one shot of intramuscular steroids has similar relapse rates compared to a 5 -7 days of oral steroids.16,17 You can use 12mg of bethamethasone or 40mg of triamcinolon i.m.

Magnesium – give magnesium early if your patient is suffering from a severe asthma attack, as it reduces admission rates in this patient population.18 Give 2 gm i.v. over 20 minutes. Data is limited, but magnesium has relatively few side effects. There is minimal evidence for administering magnesium if your patient is having a mild to moderate attack.

Antibiotics – only indicated if you have a high suspicion for bacterial illness.

Epinephrine – intramuscular or subcutaneous epinephrine may be considered as an adjunct if your patient has a severe asthma attack and you are concerned about the delivery of nebulized medication due to air-flow obstruction. However, keep in mind that if your patient has that much difficulty moving air intubation should be considered, and there is limited data that epinephrine helps prevent intubation. Mostly used in the peri-intubation setting.

Intubation and ventilation – the decision to intubate your asthmatic patient is not easy, as complications are prevalent and mortality is high. The decision is mostly made by your clinical judgment.1 Objective absolute indications include respiratory arrest or coma; relative indications include worsening hypercapnea, exhaustion and altered mental status. For an excellent discussion on ventilator management of your asthmatic patient please see the ‘EMCrit Lecture – Dominating the Vent: Part II’. If your patient is alert enough, a trial of NIPPV could be attempted. There are no large trials to support the use of NIPPV in asthmatic patients, but small trials suggest improvement in FEV1 measurements at 1 hour and decrease in hospitalization rate.19

Cutting edge:
At this time there is insufficient data to support the use of theophyline, aminiphylline, heliox or ketamine in the acute care setting.1

Treatment tips & tricks:

  • When hooking up your patient for nebs, set the gas flow rate at 6-8 L/min
  • Use a spacer when using MDI, even in adults
  • Albuterol can be mixed with ipratropium into same solution. When using premixed solution dose: 3mL nebulizer solution every 20 minutes for 3 doses, then as needed or when using an MDI 8 puffs every 20 minutes as needed up to 3 hours.

Can’t I just go home, doc?

Disposition is largely based on how your patient looks, how your patient responds to treatment, and if your patient has adequate, readily available outpatient follow up.1 Traditionally it has been proposed that the discharge goal for asthmatic patient was a return to 70% of predicted peak flow spirometry, but as stated above, peak expiratory flow measurements are limited by patient’s ability to perform the test. Therefore, disposition still largely depends on your clinical impression of your patient. Consider a walking pulse ox if your patient still don’t look right

Ready? Dive, my friend!





1. Schauer, SG, Cuenca PJ, Johnson JJ, et al. Management Of Acute Asthma In The Emergency Department. Emergency Medicine Practice 2013 Jun 15;(6):1-28

2. Dr. Carol Rivers’ Preparing for the Written Board Exam in Emergency Medicine Paperback, 6th edition (2011) Ohio Chapter, American College of Emergency Physicians.

3. Henderson SO, Ahern TL. The utility of serial peak flow measurements in the acute asthmatic being treated in the ED. Am J Emerg Med. 2010;28(2):221-223.

4. Papiris S, Kotanidou A, Malagari K, et al. Clinical review: severe asthma. Crit Care. 2002;6(1):30-44.

5. Kelly AM, Kyle E, McAlpine R. Venous pCO2 and pH can be used to screen for significant hypercarbia in emergency patients with acute respiratory disease. J Emerg Med. 2002;22(1):15-19.

6. Siegler D. Reversible electrocardiographic changes in severe acute asthma. Thorax. Jun 1977; 32(3): 328–332.

7. White CS, Cole RP, Lubetsky HW, et al. Acute asthma. Admission chest radiography in hospitalized adult patients. Chest. 1991;100(1):14-16.

8. Ducharme FM, Ni Chroinin M, Greenstone I, Lasserson TJ. Addition of long-acting beta2-agonists to inhaled steroids versus higher dose inhaled steroids in adults and children with persistent asthma. Cochrane Database Syst Rev. 2010 Apr 14;(4):CD005533.

9. National Heart Lung and Blood Institute. National Asthma Education Program. Expert Panel on the Management of Asthma, United States Department of Health and Human Services. National Institutes of Health (U.S.). Expert Panel report 3 guidelines for the diagnosis and management of asthma: full report. NIH publication No. 07-4051. Rev. June 2002, Aug. 2007. ed. Bethesda, MD.: U.S. Dept. of Health and Human Services, National Institutes of Health, National Heart, Lung, and Blood Institute; 2007.

10. Rodrigo GJ, Rodrigo C. First-line therapy for adult patients with acute asthma receiving a multiple-dose protocol of ipratropium bromide plus albuterol in the emergency department. Am J Respir Crit Care Med. 2000;161(6):1862-1868.

11. Camargo CA, Jr., Spooner CH, Rowe BH. Continuous versus intermittent beta-agonists in the treatment of acute asthma. Cochrane Database Syst Rev. 2003(4):CD001115.

12. Cates CJ, Welsh EJ, Rowe BH. Holding chambers (spacers) versus nebulisers for beta-agonist treatment of acute asthma. Cochrane Database Syst Rev. 2013 Sep 13;9:CD000052.

13. Rowe BH, Spooner C, Ducharme FM, Bretzlaff JA, Bota GW. Early emergency department treatment of acute asthma with systemic corticosteroids. Cochrane Database Syst Rev. 2001;(1):CD002178.

14. Edmonds ML, Milan SJ, Camargo CA Jr, Pollack CV, Rowe BH. Early use of inhaled corticosteroids in the emergency department treatment of acute asthma. Cochrane Database Syst Rev. 2012 Dec 12;12:CD002308. doi: 10.1002/14651858.CD002308.pub2.

15. NNT – Systemic steroids given during an asthma attack 

16. Schuckman H, DeJulius DP, Blanda M, Gerson LW, DeJulius AJ, Rajaratnam M. Comparison of intramuscular triamcinolone and oral prednisone in the outpatient treatment of acute asthma: a randomized controlled trial. Ann Emerg Med. 1998 Mar;31(3):333-8.

17. Chan JS, Cowie RL, Lazarenko GC, Little C, Scott S, Ford GT. Comparison of intramuscular betamethasone and oral prednisone in the prevention of relapse of acute asthma. Can Respir J. 2001 May-Jun;8(3):147-52.

18. Rowe BH, Bretzlaff JA, Bourdon C, Bota GW, Camargo CA Jr. Magnesium sulfate for treating exacerbations of acute asthma in the emergency department. Cochrane Database Syst Rev. 2000;(2):CD001490.

19. Soroksky A, Stav D, Shpirer I. A pilot prospective, randomized, placebo-controlled trial of bilevel positive airway pressure in acute asthmatic attack. Chest. 2003;123(4):1018-1025.


Written by: Maite Huis in ‘t Veld, M.D. | Peer reviewed by: Haney Mallemat, M.D. | August 27th, 2014

Pulmonary Embolism

Say what?

Virchow’s triad (stasis, endothelial injury, hypercoagulability) leads to thrombosis in your patient’s deep venous system. Part of the formed thrombus breaks loose, and gets stuck in your patient’s pulmonary vasculature.

Your patient will report (in decreasing order of frequency)1:

  • Dyspnea
  • Pleuritic chest pain
  • Cough
  • Hemoptysis
  • Diaphoresis
  • Nonpleuritic chest pain
  • Syncope (massive PE)
  • Nothing (asymptomatic)

You will see and hear (in decreasing order of frequency)1:

  • Tachypnea (RR>16/min)
  • Rales
  • Accentuated S2
  • Tachycardia (HR>100/min)
  • Hyperthermia (T>37.8)
  • Diaphoresis
  • S3 or S4 gallop
  • Clinically evident thrombophlebitis
  • Decreased breath sounds
  • Lower extremity edema
  • Cardiac murmur
  • Cyanosis
  • Hypotension (massive PE)
  • A normal exam – absence of physical findings does not rule out a PE

Is this really it?

Clinical scoring systems

One of the most important steps in the work up of your patient is to determine how likely it is that your patient has a PE. Low risk indicates you think that the patient has a 0-20% risk of having a PE, intermediate indicates a risk of 20-80% and high is a risk of 80-100% of PE.2 ED docs have been pretty good at the guessing game, but unfortunately not good enough with an accuracy of pretest probability of PE between 71-78%. As we do not want to send a patient home with a PE a bunch of clinical scoring systems have been proposed, two will be discussed here as they are most frequently used and have been prospectively validated.

First, the Wells score is used to risk stratify our patient.3 The patient will be given a score according to the criteria below.

  • Suspected DVT – 3.0 points
  • An alternative diagnosis is less likes than PE – 3.0 points
  • Heart rate >100/min – 1.5 points
  • Immobilization or surgery in the previous 4 weeks – 1.5 points
  • Previous DVT/PE – 1.5 points
  • Hemoptysis – 1.0 points
  • Malignancy (current treatment, treated in last 6 months or palliative) – 1.0 points

A score of 0-1 indicates a low risk, 2-6 is an intermediate risk and a score greater than 6 is a patient at high risk. If your patient is at low risk, the Pulmonary Embolism Rule out Criteria (PERC) can be used to assess if your low risk patient can be safely discharged home without ancillary testing.4  The following questions need to be answered with “no” in order to discharge without additional testing:

  • Is the patient >49 years of age?
  • Is the pulse rate > 99/min?
  • Is the pulse oximetry reading <95% while the patient breathes room air?
  • Is there a history of hemoptysis?
  • Is the patient receiving exogenous estrogen?
  • Does the patient have a prior diagnosis of venous thromboembolism?
  • Has the patient had recent surgery or trauma requiring endotracheal intubation or hospitalization in the previous 4 weeks?
  • Does the patient have unilateral leg swelling?


There is no evidence that ECG alone has sufficient sensitivity or specificity to rule out PE.5  It is mainly used to exclude alternative causes of your patient’s symptoms. It will be normal in 30% of cases.6,7

Most common ECG findings in patients with PE include:

  • Sinus tachycardia (36%)
  • Right axis deviation
  • (In)complete right bundle branch block (6-67%)
  • Non-specific T-wave inversions (68-80%)
  • S1Q3T3 – even though S1Q3T3 has been traditionally thought of as pathognomonic for PE, it only occurs in 20% of patients.


D-dimer – aids in excluding PE if your patient has a low pre-test probability. If your patient’s Wells score is 2 or less the D-dimer assay has a negative predictive value of 99%.8 A D-dimer assay is not indicated if your patient has an intermediate or high risk of having a PE.

  • “False” positive D-dimer in: your patient is elderly or has myocardial infarction, DIC, trauma, postoperative states, infection, malignancy, sickle cell crisis, pre-eclampsia, atrial fibrillation, aortic dissection, stroke or a superficial thrombophlebitis
  • False negative D-dimer in: small clot burden, older thrombus, fibrinolysis disorder

Troponin and pro-BNP – an elevated troponin is associated with adverse outcomes and hemodynamic instability in non-massive PE. A low pro-BNP indicates your patient will probably do well.

ABG – not helpful in making diagnosis, as multiple studies have shown that a normal ABG does not exclude PE. Do not routinely violate your patient’s radial artery when evaluating for PE.6


CXR – mainly used to exclude alternative causes of your patient’s symptoms. Commonly seen abnormalities in PE include cardiomegaly, elevated hemidiaphragm and pleural effusion.9  Westmark’s sign (peripheral oligemia) and Hampton’s hump (pleural wedge-based density) are classically described in PE, but occur in less than 20% of patients with PE and have low sensitivity and specificity.10

CTA – indicated if your patient has a high probabilty or is a low or indeterminate risk patient with a positive D-dimer. CTA has a false negative rate of 15-20%, even with multidetector scanners.11 Subsegmental PE’s are most likely to be missed, and it has been debated if these subsegmental PE’s are clinically relevant.12

V/Q scan – performed if your patient has a contra-indication to CTA. Results will be reported as low, intermediate or high probability of PE. If your patient has a high pretest probability and a high-probability V/Q scan a PE is reliably diagnosed. It is more complicated if your patient has a low or intermediate risk. The American College of Emergency Physicians has attempted to help you out here by leaving their recommendations.13 They state that if your patient has a low or intermediate risk of PE and has a non diagnostic V/Q, a negative D-dimer or a bilateral venous ultrasonographic scan will exclude a clinically significant PE. In low risk patients a single bilateral venous ultrasound will suffice, if your patient has an intermediate risk serial ultrasound scans are indicated.

Echocardiography – echo may reveal right ventricular dilatation, decreased ventricular wall contractility or ventricular filling if your patient has a (sub)massive PE. Worry about your patient if you find that their right ventricle is dilated, as that is a predictor of poor early outcome. A dilated right ventricle will also help you with decision making regarding thrombolytics (see below).14

Venous compression ultrasonography – use if your patient is pregnant and has an elevated D-dimer and you worry about the radiation risk.15 It can also be used in patients with a intermediate to high clinical risk of PE and a negative or inconclusive CTA or V/Q scan. In these intermediate to high risk patients it is necassary to repeat the US in 5 – 7 days to assess for clot progression.11

Is there a cure, doc?

Anticoagulation – indicated if your patient is hemodynamically stable. Start with low molecular weight heparin (LMWH) or unfractionated heparin. LMWH is just as effective as unfractionated heparin.11 Monitor partial thromboplastin. Recent studies support the initiation of oral warfarin on day one. Contra-indications to anticoagulation include active bleeding, vascular trauma, drug sensitivity, recent major surgery, lumbar puncture, history of GI bleed, severe hypertension or bleeding tendencies. has the data you need should you decide to go with that road.

Thrombolysis – only indicated in hemodynamically unstable patients, even though there is limited data that thrombolytics lead to improved mortality rates.11 There is no consensus on the use of thrombolytics in patient who are hemodynamically stable but have signs of right ventricular dilatation on echocardiography. Some data suggests that in hemodynamically stable patients with right ventricular dilatation on echocardiography might benefit from thrombolysis: your patient might have lower all cause mortality (if your patient is <75 years old), but at the cost of higher bleeding rates.16

Inferior vena cava filter – indicated if your patient has: a contraindication to anticoagulation, has had a complication from the use of anticoagulation or if they have failed to attain adequate anticoagulation while undergoing treatment.6

Surgical embolectomy – use is limited, ill defined indications, mostly used in critically ill with unsuccesful, prolonged resuscitation, high mortality rate.11

Congrats, you got your life vest, now dive into the FOAM:





1. Dr. Carol Rivers’ Preparing for the Written Board Exam in Emergency Medicine Paperback, 6th edition (2011) Ohio Chapter, American College of Emergency Physicians.

2. The PIOPED Investigators. Value of the ventilation/perfusion scan in acute pulmonary embolism diagnosis. Results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). JAMA. 1990;263:2753-2759.

3. Wells PS, Anderson DR, Rodger M, et al. Derivation of a simple clinical model to categorize patients probability of pulmonary embolism: Increasing the models utility with the SimpliRED d-dimer. Thromb Hamemost. 2000;83(3):416-420.

4. Kline JA, Courtney DM, Kabrhel C, et al. Propsective multicenter evaluation of the pulmonary embolism rule-out criteria. J Thromb Haemost. 2008;6(5):722-780.

5. BestBets “Diagnostic utility of ECG for diagnosing pulmonary embolism.”

6. Rogers RL, Winters M, Mayo D. Pulmonary Embolism: Remember That Patient You Saw Last Night? Emergency Medicine Practice 2004 Jun;6(6):1-20.

7. Stein PD, Terrin ML, Hales CA, et al. Clinical, laboratory, roentgenographic and electrocardiographic findings in patients with acute pulmonary embolism and no pre-existing cardiac or pulmonary disease. Chest 1991;100(3):537-543.

8. Wells PS, Anderson DR, Rodger M, et al. Excluding pulmonary embolism at the bedside without diagnostic imaging: management of patients with suspected pulmonary embolism presenting to the emergency department by using a simple clinical model and d-dimer. Ann Intern Med. 2001 Jul 17;135(2):98-107

9. Elliott CG, Goldhaber SZ, Visani L, et al. Chest radiographs in acute pulmonary embolism. Results from the International Cooperative Pulmonary Embolsim Registry. Chest 2000; 118 (1): 33-38.

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Written by: Maite Huis in ‘t Veld, M.D. | Peer reviewed by: Michael Bond, M.D. | August 4th, 2014

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