POTD: Pulmonary Embolism Decision Rules - Beyond the Basics

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Special thanks to Dr. Errel Khordipour for giving this amazing review and Dr. Anna Bona for taking meticulous notes during this talk!

TL;DR

  • PE carries an 8% 30-day mortality after diagnosis (some studies higher)

  • CTA has a very high false positive rate

  • Step 1: based on the patient's history and presentation, do you think the patient has a PE? If yes, proceed. If no, STOP

    • Read more below for nuances re: features that makes a patient risky for PE

  • Step 2: Using your clinical decision rules (Well's, Geneva, or clinical gestalt), is the patient low, medium, or high risk?

    • Low risk: PERC

    • Medium: D-dimer --> then CTA if positive

      • Age adjust your d-dimer if possible

    • High Risk: CTA

  • Step 3: Treat! (or don't treat!)

    • Unstable --> tPA and MICU

    • Stable --> get labs, echo

      • Labs abnormal or echo w/ RV strain --> heparin +/- half-tPA

      • Labs/echo normal --> determine the pt's PESI score

        • High --> heparin

        • Low --> lovenox and discharge

  • Subsegmental PEs in patients < 50 with stable vitals have a very low risk of adverse outcome

    • May consider discharging without anticoagulation if no DVT is present and there are no risk factors for recurrence

  • If the study is inadequate, refer to the d-dimer

    • If d-dimer positive, get bilateral lower extremity dopplers

      • Discharge if negative

      • If positive, consider anticoagulation based on risk factors and labs and f/u with PMD for repeat doppler in 3-7 days. 

Interested? Let's get more specific!

Let’s consider a patient that rolls into your emergency department. They’re complaining of chest pain and shortness of breath. You’re working with a medical student and they list pulmonary embolism as a differential diagnosis. How do we risk stratify our patients using our decision making tools.

Background
First off, why do we care? First off, PE is a very much-feared missed diagnosis, which carries an 8% 30-day mortality** after diagnosis (this was much lower than I expected, to put this into context, hemorrhagic strokes carry a 25-40% mortality depending on your source and hip fractures carry a 4-10% mortality rate depending on your source).

**some studies show a 30% mortality, however those were autopsy studies, so it is unknown whether the patients died with a PE or as a result of a PE.

That being said, our testing methods are very much imperfect! The false positive rate on CTA for segmental PE is 25% and even scarier, the false positive rate for subsegmental PEs is 60%!! Not a great test! Plus, a CTA is not a benign test. Contrast can cause anaphylactoid reactions and lifetime risk of malignancy increases with each CT. Plus, once a patient is labeled as having a PE (even subsegmental), they’re much more likely to get scanned in the future.

So let’s talk about how we can determine who is high risk and who is low risk.

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Step 1: Consider the patient’s presentation and history

Vital signs:

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Risk Factors

Prior VTE (PE/DVT): Was the last PE/DVT unprovoked or provoked? More concerning if the last PE/DVT was unprovoked (e.g. the patient was not immobilized for a long period of time). This does not change if testing for hypercoagulability was negative. If provoked, this is less concerning.

Malignancy History: Higher risk with active cancer. This either means active treatment within the last 6 months or metastatic disease. Chemotherapy patients are also more at risk. Not all malignancies are created equal, though! Your risk is even higher with pancreatic cancer, multiple myeloma, colon cancer, glioblastoma, and melanoma.

Immobility: certain types of immobility are higher risk than others! Examples: patients in casts, hospitalized trauma patients (others not at higher risk). Surgical patients are higher risk if they were intubated, received general anesthesia, or received an epidural (e.g. knee surgery, abdominal surgery, neurological surgery). Being in a continuous seated position for > 6 hours might be a risk factor.

OCPs: estrogen of any form increases risk (e.g. OCPs, estrogen replacement, intra-vaginal estrogen). For transgendered patients, more study is needed to determine increased risk.

Pregnancy: Highest risk 2 weeks postpartum. If a patient is pregnant and symptomatic, they have a 70% risk of PE.

Increased risk at age 50: Risk of PE perpetually increases with age. 

Symptoms:

Chest painpleuritic chest pain suggest peripheral PE (65%)

Hemoptysis: more indicative of pulmonary hemorrhage, not infarct

Exertional Dyspnea: concerning! You do not need to have chest pain to have a PE!! There is a syndrome that consists of subacute dyspnea that gets worse over days that is predictive of central PE.

Calf pain/Calf swelling: unilateral calf pain (the symptom) and calf swelling (the physical exam finding) are both concerning.

Syncope: corresponds to a large clot burden, but syncope  (likely does not confer an increased likelihood of PE)

Anticoagulation: if they are compliant with anticoagulation, they are less likely to have PE. While this is definitely true with NOACs, with Coumadin, it’s less certain because levels will vary regardless of compliance with medication. Symptoms that are not significant: orthopnea, palpitations, anxiety, dizziness 

Physical Exam Findings:

Abnormal pulmonary exam - decreases likelihood of PE

Clinical signs of DVT - such as calf swelling, redness, etc. increases likelihood 

STEP 1 (cont): Do you, based on the information above, feel that a PE is possible? Meaning, it is ABOVE the 2% threshold for PE. 

Professional recommendation: if the patient has risk factors in 2 or more of the above categories (e.g. vital sign and risk factors, or risk factors and exam findings), and there is no alternative explanation for the patient's presentation, you can say adequately that you have suspicion for PE. 

If you have less than a 2% clinical suspicion for PE, STOP. You do NOT think there is a PE and you do not evaluate further. I repeat - STOP! Evaluate for other suspected pathologies). ACEP Guidelines: 2% is an acceptable cutoff recognizing limitations of testing and risk of false positives (in latest NSTEMI guidelines) Now that you truly think your differential should include PE...  


STEP 2: RISK STRATIFY

It doesn't matter if you use Well's Score vs. Geneva vs. Gestalt; all have been shown to be equal. Keep in mind these decision tools SHOULD NOT used to rule out. They are only to RISK STRATIFY. Meaning that you clinically have a suspicion of said disease before you use them. This means you should NEVER document "Well's score low, not likely PE". 

 High risk: get a CTA! May consider empiric heparin before or after CTA.  

Moderate: D-dimer. 

  • In general, you should use age adjusted cutoffs for patients > 50. The conversion depends on which unit you use. 

    • FEU (fibrinogen unit, cutoff usually ~ 500): add the age x 10

    • DDU (d-dimer unit, cutoff usually ~ 250): add the age x 5

Low: PERC


STEP 3: Further Management

Ever get a reading that said "evaluation for sub-segmental suboptimal due to motion artifact? What do you do? (Only if vital signs are stable)

  • Get a d-dimer (if not already obtained)

  • Positive --> LE dopplers

    • Yes DVT: anticoagulate!

    • No DVT: discharge with or without anticoagulation based on risk factors and lab values; follow-up with PMD for repeat surveillance ultrasound in 3-7 days. 

  • Negative -->  Discharge 

Now let's go over what you do if a PE is found...

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Disposition: depends on if the patient is stable or unstable

Unstable: hypotensive, signs of shock, etc

  • Give tPa and admit to MICU

Stable: labs (BNP, troponin), echo

  • If the patient as abnormal labs or right heart strain, give heparin +/- half-dose tPA and admit to ICU/tele

  • If normal, determine the patient's PESI Score

    • High PESI score --> give heparin and admit to floor

    • Low PESI score --> give lovenox** and discharge

** There inadequate evidence and no FDA approval for NOACs at this time
  Subsegmental PEs in patients < 50 with stable vitals have a very low risk of adverse outcome, so you may consider discharging without anticoagulation if no DVT is present and there are no risk factors for recurrence and have the patient f/u with PMD for surveillance of PE symptoms

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POTD: TB in the ED

Approach to TB in the ED.

TB might be more common than you think: In NY alone, in 2016, 3.9 cases per 100,000 people, 761 cases in NY in 2016.

Reactivation TB is about 90% of active TB in the United States. 

Who is at high risk?

Those with no “usual source of care”

  • ethnic minorities

  • foreign born

  • HIV patient

  • drug users

  • nursing home patients

  • homeless patients

  • prisoners

Why is it often missed?

Non-specific presentation of TB

  • Cough present: 64%

  • Cough was chief complaint: 20%

  • Only 36% had respiratory complaint at triage

What to do if for high suspicion of TB:

  • Negative pressure isolation room

  • N95 fitted masks

  • CXR and rapid HIV

    • Why HIV test?

      • HIV increases risk of having reactivation TB

      • Immunosuppression will give you atypical cxr findings

  • Looking primarily for active tuberculosis 

Confirmatory testing:

  • PPD: Sensitivity 60-100%

  • QuantiFERON Gold: Sensitivity 81-96%

  • Sputum Looking for AFB on smear (Ziehl-Neelson stain)

    • Variable Sensitivity: 20-60%

    • High specificity: 90-100%

  • Culture

    • Slower results: 7days- 8 weeks

    • Gold standard: 99% sensitivity

  • Rapid TB testing/ Cepheid Xpert MTB/RIF PCR assay

    • Respiratory for assistance in collection

    • 5 ml specimen

    • Rifampin resistance detection

    • Supposed to be a 2 hr turnaround

    • 2 negative sputum specimens at least 8 hrs apart: can remove from isolation

    • Sensitivity about 75-93%

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*This is a sample rule out TB protocol that I adapted from Annals of Emergency Medicine October 2016 : http://www.annemergmed.com/article/S0196-0644(16)30920-9/fulltext

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Crashing Asthmatic POD

We treat asthma on a daily basis, especially in the peds ED. But what if duonebs x3, steroids, and mag isn’t doing the trick?

THE CRASHING ASTHMATIC

  • Nebulized epinephrine may help.

  • If no improvement, start dosing IM epi as if it were anaphylaxis: 0.5 mg (0.01 mg/kg) q 10 min, or start a drip at 5 mcg/min and titrate to effect.

  • Keep going with continuous albuterol nebs.

  • If pharmacy isn’t around to make an epi drip, consider a “dirty” epi drip: 1 mg epi (an entire vial of code cart epi) added to 1 L NS or LR, start at 2 drops per second and titrate up.

  • Alternatively, terbutaline IV can be started: 10 mcg/kg bolus over 10 min and then drip starting at 0.4 mcg/kg/min and titrate up. Terbutaline is a systemic beta agonist. Perhaps they’re so tight that the albuterol you’re nebulizing is not getting where it needs to go due to profound bronchoconstriction. The main adverse effect is here is vasodilation-related hypotension.

By this point, your intubation stuff should be ready and the patient should be in resus.

They also will be having insensible losses so should get as 20 cc/kg IVF bolus.

Still getting worse.

Now this gets interesting.

We are really trying to avoid intubating any asthmatic because of historically poor outcomes with intubation, but sometimes it is unavoidable.

Next step is to try BiPAP. BiPAP could also be started simultaneously with epi. If they can’t tolerate BiPAP, consider ketamine to help them tolerate BiPAP. Ketamine can be dosed numerous ways. If sub-dissociative dosing is pursued, you risk them freaking out. If dissociative dosing, there’s a higher risk of laryngospasm. But consider this, they’re on the brink of getting intubated anyway. If your last-ditch-effort-ketamine gives them laryngospasm, that might be your cue to push a paralytic.

Ketamine and BiPAP has failed.

Time to intubate. Preoxygenate as much as possible. Use the largest ETT possible. First pass success is key. Induce with ketamine 2 mg/kg if they’re not already in the K-Hole. Roc or Sux.

Now they’re intubated

  • They have OBSTRUCTIVE LUNG PHYSIOLOGY. It will take them way longer than usual to exhale. Thus:

  • Low respiratory rate! 8 breaths/min

  • Lung protective tidal volume: 7 cc/kg ideal body weight

  • Minimal PEEP: 0 (ZEEP) - 2 cc H2O

  • High inspiratory flow rate: 90 LPM or I:E 1:5

  • FiO2 100%

  • The ventilator will alarm due to high PEAK pressures. This is OK. Have the respiratory therapist fix it to raise the alarm threshold. The high peak pressures are a consequence of their tight bronchioles.

  • If running into issues with ventilator dyssynchrony, consider paralyzing with cisatracuium

  • Relative hypoxia (sat mid 80s, goal >90%) and hypercarbia (goal >7.15) is OK

  • Aggressive airway suctioning

  • If they begin crashing, disconnect from vent and push on chest to ensure breath stacking is not the issue; rule out pneumothorax; rule out displaced/clogged/kinked ETT

Still doing poorly

  • Call the ECMO team for VV ECMO

  • Anesthesia to set up inhaled anesthetics! e.g. desflurane, sevoflurane. Not tons of evidence, but in case series' and anecdotally, this works really well.

  • Fun fact, CO2 can be dialyzed out of someone rather than ventilated out of someone. However, you need to be in a center where ECMO is also done, because it’s basically putting a piece of the ECMO circuit into a CVVHD circuit. Yes. Blew my mind too.

See Reuben’s algorithm on this at https://emupdates.com/when-the-patient-cant-breathe-and-you-cant-think-the-emergency-departement-life-threatening-asthma-flowsheet/

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