Introduction of Case 

47-year-old male presents for evaluation of right sided chest pain that started one week ago. He states that within the last five days, his pain has gotten progressively worse. He reports dyspnea, sharp pleuritic chest pain, worse with inspiration.

Vitals at triage note HR 96, O2 Sat 100% on RA, RR 14. He’s had no recent surgery or trauma, does not use hormones, and has no hemoptysis or hx of DVT/PE. 

What is a Pulmonary Embolism?

A pulmonary embolism is a blood clot that has settled into the pulmonary vasculature. PEs can be defined as acute, subacute, and chronic. Along with this, further classification is provided with massive, submassive and normal.

Acute PEs are defined as developing within minutes to hours whereas subacute can be days to weeks.

Massive is defined as causing cardiovascular instability. This is secondary to the right heart not being able to push blood forward due to the large amount of sudden pulmonary hypertension caused by the PE. This leads into the definition of submassive, in which there is evidence of right heart strain. Right heart strain can be found on EKG (right axis deviation, S1Q3T3), elevated troponin, and elevated BNP. 

Pulmonary emboli cause 100,000 deaths annually. The case rate has doubled over the past few years to 112 per 100,000 largely attributable to more sensitive testing. The 30 day and 1 year mortality after a PE is 4% and 13% respectively. 

What Causes Pulmonary Emboli? 

A pulmonary embolism(PE) is primarily a complication of deep vein thrombosis (DVT). Most DVTs originate in the calf but can originate in any deep vein of the body. The risk factors for development of PE and DVT all have their basis in Virchow’s Triad (Venostasis, hypercoagulability, vessel wall injury). 

The most common risk factors include: 

• Obesity
• Current DVT
• Prior DVT or PE
• Long time immobility
• Recent trauma or surgery
• Cancer 
• Estrogen use or Pregnancy 

PERC Criteria

Age > 50	Hemoptysis
HR > 100	Recent Surgery/Trauma (<4 weeks)
O2 sat <95%	History of DVT/PE
Unilateral Leg swelling	Hormone Use

Keep in mind if all of PERC criteria are negative and low suspicion by clinician based on gestalt, chance of PE is <2% and no further workup is warranted.

What Are the Clinical Signs of a PE?

The most common symptoms of PE include dyspnea (73%), pleuritic chest pain (66%), cough (37%), and leg swelling/pain (44%). Dyspnea, tachypnea or pleuritic chest pain are present in >95% of PEs, if the patient has low risk factors and these are not present, the likelihood of PE is low. 

The most common sign includes tachycardia (24%), tachypnea (54%), low O2 saturation (74%). PE is a common cause of sudden cardiac arrest or circulatory collapse (8 percent), especially among patients younger than 65 years old. Among such patients, either dyspnea or tachypnea is present in 91 percent.

How Do You Work up a PE?

EKG
Most common finding is sinus tachycardia but not at all specific. It can be totally normal in 9-26% of patients. Other big things to look for are evidence of right heart strain (peaked p-wave in lead II, right axis deviation, afib, S1Q3T3). 

Chest X-ray 

Most PEs will actually have some very non-specific signs on X-ray (effusion, atelectasis, etc.) but 12 to 22 percent will be completely normal. Some very uncommon findings that are fairly specific include Hampton’s hump (wedge shaped infarct on X-ray) and Westermark’s Sign (dilation of the proximal vessels with sharp demarcation and cut off of distal vessels at site of embolism). 

Labs

BNP- can be elevated in people with PE and right heart strain

D-dimer

VERY Sensitive but non-specific. Only order this if you are prepared to CTA this person if its positive. Don’t forget to age adjust. Although the complete criteria is dictated my facility, age adjusted literature suggests age x5 for people >50 years old. While others suggest age x10, if the sum is less than the D-Dimer, it is considered negative. Be sure to check which criteria your facility uses.

Troponin

Although not really correlated with PE too well, can show evidence of heart strain

ABG

Hypoxemia seen in 74% of PEs, and is considered very non-specific. A-a gradient is also very common and generally more specific if you don’t suspect ARDS. A-a gradient can be calculated by : 150- (PO2 + PCO2/0.8). The normal A-a gradient varies by age and can be calculated as: Age/4 +4 (ET Tube anyone?). 

V/Q Scan

Hotly debated on the usefulness of this scan. The consensus is that you should only do this when CTA is contraindicated. At Arnot we most of the time do a Perfusion scan primarily because the ventilation is assumed to be normal. It gives a few possible outcomes; normal scan, and low/middle/high probability for PE. It provides more radiation to the patient but does not rely on contrast, which would be contraindicated in patients who have baseline kidney damage or have already received a contrasted scan that day. 

CTA

Gold standard for PE imaging. Very sensitive and specific and has the added benefit of finding just about anything else that could be causing SOB. Main limitation is patient ability to comply with the 30 seconds of holding their breath that produces optimal results and the timing of the contrast to make sure it is in the pulmonary vasculature. The other thing we run into all the time is contrast induced nephropathy. The EM literature suggests that it is negligible and that the risk of missing our primary diagnosis outweighs the risk of CIN (SGEM Episode #234). It is always good to consider the risks before ordering this test but be prepared to defend your position if you think its necessary. 

Our Patient’s Workup

Our patient was ordered a standard “cardiac workup” which turned out to be mostly normal except for his X-ray. The radiology read was a pleural effusion in the right middle lobe, but we noticed that the effusion was not present on the lateral view. CURIOUS. 

We were thinking that effusion was actually a Hampton’s Hump. A d-dimer was ordered which came back elevated at 967 and a CTA was subsequently added on. This showed a segmental PE causing infarction of the tissue behind it, confirming our diagnosis of PE!  

Treatment of Pulmonary Embolisms

For the majority of PEs that we see (not massive or submassive) treatment will be directed by hemodynamic and oxygen support first and blood thinners second. If found incidentally with low overall risk factors, you can treat outpatient. An Example of risk scoring is below: 

If a patient is deemed low risk per this score, they could be potentially treated outpatient based on your clinical gestalt as well. 

Choice of agent has been shown to be equivocal between heparin, LMWH and DOACs (dabigitran, enoxaparin and apixaban). 

For inpatient therapy the standard of care is heparin infusion. For the average patient in our department we’d start them on a bolus followed by a drip depending on weight. Heparin has a number of advantages in the inpatient setting over LMWH, namely that the half life is much shorter. If there’s a chance that the patient will need a procedure then regular heparin is preferred.  

For massive and submassive PEs you should be giving TPA. The dosing is 100 mg over 2 hours. There have been many studies on the effectiveness of half dosing, but they have returned insignificant evidence. If you are already running heparin on these patients and then decided to thrombolyze, you can stop the heparin infusion and then immediately start the TPA. Choice of agent in the US is commonly altepase. 

Embolectomy is another choice of treatment, would need to be transferred from our facility for this option and would likely not be a good choice for a severely unstable patient. 

Take Home Points

• Clinical gestalt beats PERC
• D-dimer is sensitive and not specific, should not be used in a high pre-test probability patient
• The incidence of PE over the last ten years has doubled, mostly as a result of increasingly sensitive testing. Mortality has greatly decreased
• CTA is the best for definitive testing but not 100% sensitive or specific
• You can treat PEs outpatient if low risk
• You should be using TPA in massive and submassive PE

Written by: Max Brown, DO

Peer reviewed and edited by: Robert Wicelinski, DO

References:

• Milne, Ken. “SGEM#295: Teacher Teacher – Tell Me How to Do It (Diagnose a PE).” The Skeptics Guide to Emergency Medicine, 25 June 2020, http://www.thesgem.com/2020/06/sgem295-teacher-teacher-tell-me-how-to-do-it-diagnose-a-pe/.
• Rivers, Carol. Guide to EM: Pulmonary Embolisms.
• Thompson, Taylor, and Christopher Kabrhel. UpToDate, http://www.uptodate.com/contents/overview-of-acute-pulmonary-embolism-in-adults?search=pulmonary+embolism&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1.