SonoCase: 46yo shortness of breath – guest post by Jacob Avila @UltrasoundMD #FOAMed

Our newest guest post is by one of the best emergency medicine resident educators I know – of course, you dont want to miss his educational pearls on twitter too – Dr. Jacob Avila. He discusses a case that illustrates how bedside ultrasound can help in your unexplained short of breath patient, and even cancel that triage bias that your attending can do to sway you away from the truth. Let’s give it to Dr. Avila for highlighting (with a great literature review) how ultrasound can help you too. Here it is – enjoy! (note: not all images were of this patient, but were taken from other resources)

“You arrive to the emergency department for your first night shift of the month, and as you place your bag on the desk, the attending walks towards you with a chart in his hand. “Do you mind seeing this patient? It’s a COPD’er with dyspnea.  It’s probably just a COPD exacerbation.”  You look at the chart and see that it’s a 46 year old female with shortness of breath.  As you walk into the room, you notice the patient appears slightly pale, is afebrile, has an O₂ saturation of 91% and is tachycardic in the 110’s with a blood pressure of 105/76, temperature of 98.5° and respiratory rate of 26.  While taking the history, you note that the patient is a smoker and recently returned from a 12 hour car ride to see relatives.  Suspecting that this may be something other than simple COPD exacerbation, you grab your ultrasound machine and start with the cardiac echo (as described in the RADiUS protocol) and are able to get the following image:

This apical 4-chamber view shows severe right heart dilation, defined as a RV:LV ratio >1.  However, you remember that the patient has a history of COPD, and chronic pulmonary hypertension can cause chronic right ventricular dilation1.  At that moment, the patient becomes hypotensive with a systolic blood pressure in the 70’s and develops severe respiratory distress. What should we do?

Early diagnosis of a pulmonary embolism (PE) is exceedingly important, as two thirds of patients with mortality associated with a PE die within the first hour of their presentation², and intuitively, those who are treated earlier generally have a better prognosis ³.  The definitive diagnosis of a PE requires the use of a CT scanner ⁴, but in a patient who is unstable, like this one, that isn’t an option. Looking at the right ventricular to left ventricular ratio is a maneuver that can rapidly change your differential diagnosis or confirm what you previously suspected. A recent study by Dresden et al found right ventricular dilatation identified by emergency physicians had a specificity of 98% for a PE.  That number is impressive, but when you look at the methodology section of the publication, only 10% of the patients they included had coexisting COPD, and all of the false positives in the study were in patients with COPD⁵.   One  technique that may help differentiate between chronic and acute dilation is looking at the RV free wall in the subxiphoid view while in end diastole. A free wall size >0.5 cm is more likely to be chronic RV dilation⁶ⁱ. However, this view is not always possible in all patients.  Another echo sign you could look for is the McConnell sign (apical winking of the right ventricle during systole), which previously was reported to have an impressive 94% specificity and 77% sensitivity for an acute PE^7l, but a subsequent and larger study found the McConnell sign to be only 70% sensitive and 33% specific for a PE⁸. Take a look at what the McConnell sign looks like”

 

Another, less commonly seen finding would be directly seeing the clot in the right atrium (RA) or in the pulmonary arteries.

Clot in RA:

Clot in pulmonary artery:

Of more practical use are two other sonographic findings: Deep venous thrombosis (DVT) and distal pulmonary infarction.

In a study that included 199 examinations, bedside 2-point compression evaluation of the greater saphenous/femoral vein junction and the popliteal veins of patients with suspected DVT was found to be 100% sensitive and 99% specific for DVT ⁹.   However, it is possible for a patient to present with an acute PE and have a negative DVT, and only about 40-50% of patients with DVT’s will end up having a PE^{10, 11}

DVT on one side diagnosed by noncompressible vein:

More recently, lung ultrasound has been explored for the assessment of a suspected PE. A recent systematic review and meta-analysis by Squizzato et al which included 10 studies and a total of 887 patients found lung ultrasound to have a mean sensitivity of 87% and a mean specificity of 82% for acute PE¹².  What they looked for in the lung was the presence of triangular, wedge or rounded hypoechoic, pleural based lesions.  These lesions are thought to be due to embolic occlusions that resulted in either focal atelectasis with extravasation of blood or focal infarction of the lung parenchyma . However, they state in their publication that “Several methodological drawbacks of the primary studies limit any definite conclusion”.

Lung infarction:

 

Instead of looking at just one specific sonographic finding for the diagnosis of acute PE, a better method may the use of multi-organ sonography.  Recently, Nazerian et al. published a study utilizing multi-organ sonography in the diagnosis of PE.  This study used echo, lung and DVT ultrasound to diagnose PE and found that when the three ultrasounds were combined, they yielded a sensitivity of 90%, which was significantly higher than each of the exams by themselves¹³.

Like any physical exam finding, lab reports or other radiographic assessments, the sonographic analysis of a patient with a suspected pulmonary embolism should be used as part of your diagnostic quiver, and not the silver bullet.  Any of the above mentioned ultrasound findings of acute PE can potentially be found in other,  non-PE causes of dyspnea.  DVT’s can just be DVT’s, RV enlargement can be chronic or from an RV infarction, and subpleural fluid collections can be seen in contusions, pneumonia  and cancer.  This doesn’t mean not to use it though.  Just think about all the other tests we use in the emergency department, such as EKG’s, chest x-rays, troponins, BNP, and the d-dimer.  All of these can be abnormal in PE and in non-PE entities.

Now back to our patient.  She is a 46 year-old female with COPD that had right heart enlargement, which we learned above can be  seen in COPD without the presence of a PE.  You were unable to get a good subcostal view of the heart to measure the lateral wall, mostly because the  patient did not tolerate being laid flat.  You move on to the lungs and in the lower right thorax and there you find two hypoechoic, pleural based lesions.  Heparin and a CT scan are ordered, and the CT scan shows a large clot located in the right main pulmonary artery.

Here is the CT scan showing the clot:

To see a recent podcast by Ultrasoundpodcast on multi-organ US for PE, go here.

References:

1. Otto, Catherine M.. Textbook of clinical echocardiography. 5th ed. Philadelphia, PA: Elsevier/Saunders, 2013. Print. p 247
2. Wood KE. Major pulmonary embolism: review of a pathophysiologic approach to the golden hour of hemodynamically significant pulmonary embolism. Chest. 2002;121:877-905
3. Jelinek GA, Ingarfield SL, Mountain D, et al. Emergency department diagnosis of pulmonary embolism is associated with significantly reduced mortality: a linked data population study. Emerg Med Australas. 2009;21:269-276
4. Goldhaber SZ, Bounamenaux H. Pulmonary embolism and deep vein thrombosis. Lancet 2012:379:1835-46
5. Dresden S1, Mitchell P2, Rahimi L2, Leo M2, Rubin-Smith J2, Bibi S2, White L3, Langlois B2, Sullivan A4, Carmody K5 Right ventricular dilatation on bedside echocardiography performed by emergency physicians aids in the diagnosis of pulmonary embolism. Ann Emerg Med. 2014 Jan;63(1):16-24. doi: 10.1016/j.annemergmed.2013.08.016. Epub 2013 Sep 27.
6. Rudski LG, Lai WW, Afilalo J, Hua L, Handschumacher MD, Chandrasekaran K et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American Society of Echocardiography endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography. J Am Soc Echocardiogr. 2010;23:685-713
7. McConnell MV, Solomon SD, Rayan ME, Come PC, Goldhaber SZ, Lee RT. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol 1996;78:469e73.
8. Casazza F, Bongarzoni A, Capozi A, Agostoni O. Regional right ventricular dysfunction in acute pulmonary embolism and right ventricular infarction. Eur J Echocardiogr. 2005;6:11-4
9. Crisp JG, Lovato LM, Jang T. Compression ultrasonography of the lower extremity with portable vascular ultrasonography can accurately detect deep venous thrombosis in the emergency department. Ann Emerg Med. 2010;56:601-610
10. Kearon C. Natural history of venous thromboembolism. Circulation. 2003;107:22-30
11. Moser KM, Fedullo PF, Littlejohn JK, Crawford R. Frequent asymptomatic pulmonary embolism in patients with deep venous thrombosis. JAMA 1994;271:223-225
12. Squizzato A1, Rancan E, Dentali F, Bonzini M, Guasti L, Steidl L, Mathis G, Ageno W. Diagnostic accuracy of lung ultrasound for pulmonary embolism: a systematic review and meta-analysis. J Thromb Haemost. 2013 Jul;11(7):1269-78. doi: 10.1111/jth.12232.

13. Nazerian P, et al. Accuracy of Point-of-Care Multiorgan Ultrasonography for the Diagnosis of Pulmonary Embolism.Chest. 2014 May 1;145(5):950-7. doi: 10.1378/chest.13-1083

SonoStudy: Thoracic ultrasound in identifying pneumothorax progression in the intubated – the lung point

In the Feb 2013 issue of Chest, Oveland et al studied porcine models, introducing air at incremental levels to identify if thoracic ultrasound is as accurate as CT scanning for the detection pneumothorax progression in the intubated patient. They found that “the accuracy of thoracic ultrasonography for identifying the lung point (and, thus, the PTX extent) was comparable to that of CT imaging. These clinically relevant results suggest that ultrasonography may be safe and accurate in monitoring PTX progression during positive pressure ventilation.”

“Background:  Although thoracic ultrasonography accurately determines the size and extent of occult pneumothoraces (PTXs) in spontaneously breathing patients, there is uncertainty about patients receiving positive pressure ventilation. We compared the lung point (ie, the area where the collapsed lung still adheres to the inside of the chest wall) using the two modalities ultrasonography and CT scanning to determine whether ultrasonography can be used reliably to assess PTX progression in a positive-pressure-ventilated porcine model.

Methods:  Air was introduced in incremental steps into five hemithoraces in three intubated porcine models. The lung point was identified on ultrasound imaging and referenced against the lateral limit of the intrapleural air space identified on the CT scans. The distance from the sternum to the lung point (S-LP) was measured on the CT scans and correlated to the insufflated air volume.

Results:  The mean total difference between the 131 ultrasound and CT scan lung points was 6.8 mm (SD, 7.1 mm; range, 0.0-29.3 mm). A mixed-model regression analysis showed a linear relationship between the S-LP distances and the PTX volume (P < .001).

Conclusions:  In an experimental porcine model, we found a linear relation between the PTX size and the lateral position of the lung point. The accuracy of thoracic ultrasonography for identifying the lung point (and, thus, the PTX extent) was comparable to that of CT imaging. These clinically relevant results suggest that ultrasonography may be safe and accurate in monitoring PTX progression during positive pressure ventilation.”

Full article found here.

To see the lung point, you visualize the pleural line using the linear probe (indicator toward the patient’s head) starting from anterior chest wall (2nd intercostal space, mid-clavicular line) to inferior-lateral chest wall, and look out for the area where the lack of lung sliding or comet tail artifacts reverts back to normal lung sliding with comet tail artifacts. Blaivas, et al, studied this, showing that bedside ultrasound can detect size of pneumothorax through identification of the lung point location. Below is a video fo the lung point:

SonoCase: 55 yr old healthy male, short of breath, appears ill – guest post by Dr. Viveta Lobo

I’d like to introduce everyone to our amazing Ultrasound Fellow, Dr. Viveta Lobo (otherwise known as “VLo” to our team – of course!). She came to us by way of Drexel, tolerates out antics, appreciates our quirks, and laughs at our jokes. We love her! Enjoy this post about a healthy guy who looked very sick, short of breath, and only bedside ultrasound, using the RADIUS protocol, could help diagnose it so quickly and get the patient what he needs and fast….

I’m about 4 months into my Ultrasound (US) Fellowship at Stanford, and while I am thrilled to have greatly improved my US skills, and image acquisition during a scanning shift, it is in no comparison to the thrill, and satisfaction I felt, after using my bedside US skills to navigate through the following case.

A 55-year-old healthy male, with no past medical history, presents with progressively worse shortness of breath over the past 2 weeks. Within 30 seconds of being in the room, he is getting more short of breath, dusky, diaphoretic, and requiring to now sit up and lean forward while speaking to me in 1 word sentences. He is on a 100% non re-breather, sating about 93%. The rest of his vitals – BP 124/84 RR 41 HR 124 Temp 97.8

Even as a new attending, I was pretty certain, that if I did not figure this out in the next few minutes, this once very healthy patient is going to decompensate, and likely end up with grave morbidity. However, given that he had no known history, I had nothing to go by, except…. I grabbed my US probe, and within 3 minutes, I gained a wealth of information. I first took a look at his chest by using the phased array low frequency probe on each side of his chest in 8 total areas (4 on each side). This is what I see throughout:

…. >2 large B lines bilaterally, rays from the pleural line on the top to the end of the screen.

When I switched to a RUQ and LUQ views, my suspicions were confirmed :
RUQ:
LUQ:

…Now, the US images are on cardiac presets so the resolution is a touch different than what we are used to, but the findings are obvious which heightened my concern for the patient even more: large pleural effusions noted bilaterally. Seen as a black (anechoic) area above the diaphragm. Black is fluid on ultrasound, and you can even see the lung trying to breathe on each of the images above.

Next, I quickly assessed his IVC, and saw a plump dilated IVC, consisted with fluid overload state, which prompted me to stop my nurse from hanging any IV fluids. I then performed a bedside echo:
Subxiphoid view: (placing the phased array low frequency probe in the subxiphoid area and pressing down while flattening the probe, using the liver as an acoustic window to see the heart):

Apical 4-chamber view: (placing the probe just underneath the nipple line, at the point of maximal impulse and angling toward the body center):

…. I was able to rule out a pericardial effusion and cardiac tamponade as well as any significant RV strain to suggest a hemodynamically unstable pulmonary embolism, but I appreciated significant left ventricle dysfunction, and hypokinesis.

I then took a look using the linear probe on the anterior chest wall at the 2nd intercostal space and saw:

So, there is great lung sliding but we see it almost too well! The reason is because fluid is the lover of ultrasound and will allow you to see tissue deep to it better due to enhancing of echoes. There is fluid between the parietal and pleural layers, more and more from superior to inferior chest – on both sides. That’s quite a bit of pleural effusion if it goes all the way up to the upper lung zones! While I was putting the pieces together and realizing the diagnosis, my nurse informs me that his istat troponin comes back elevated. His initial EKG:

…..showed sinus tachycardia with ischemic changes inferior and laterally, with t waves inversions. We also see multiple PVCs. No old one EKG for comparison. Ah, the evolution of an MI on EKG – love it!

So to recap, I have an otherwise healthy gentlemen, with progressive sob, no chest pain, but with positive family history of ACS, with confirmed LV dysfunction on US and bilateral pleural effusions and a positive troponin, and some possible ischemic changes on EKG. Sounds like a post ischemic cardiac event presenting with ventricular infarct! From door to diagnosis in 5 minutes! I placed him on BIPAP, gave him a big shot of Lasix IV, aspirin PO, and called my cardiologist! The patient started to improve after the medication, avoiding intubation. The Chest Xray was then done:

….showing bilateral diffuse opacities which could be typical for ARDS.

After a brief cardiology evaluation, my patient was admitted to the CCU and shortly after went to the Cath lab, and was found to have a complete LAD occlusion.

While I initially had a very broad differential including PE, new onset CHF, cardiac tamponade, myocarditis, pneumonia; my bedside ultrasound was quickly able to prioritize my differential, and consult the right service, with a specific question of – should this patient go to the cath lab? Without bedside US, this patient could have easily been a Medical ICU evaluation for respiratory distress, with an extensive work up, including CT Chest, intubation, and more time than the patient needed for a diagnosis to have bee made while we sorted through the differential.

This case is one of many that completely validates bedside ultrasound for me, and my decision to pursue this awesome fellowship!

As a follow up: Patient went on to get an LVAD, and is on the heart transplant list.

SonoCase: 60 yr old male, lethargic, respiratory distress, shock – “RUSH” to bedside

The great thing about bedside ultrasound is that you can get a really REALLY good idea of what is going on with a patient within 5-10 minutes of their arrival, particularly patients who can’t tell you whats going on (whether it’s because they are lethargic and tachypneic – like this case – or altered, unconscious, or speak another language) , but, because you are a great doc, you do know by just walking through the doorway and looking at the patient that he is S.I.C.K. This case discusses exactly that and highlights the RUSH protocol, (see my prior post on the evidence based approach to the RUSH) ,but also how interpreting those applications when correlating to your exam and clinical history is key and adds greatly to your evaluation of the patient.

60 yr old guy (with an amazingly nice wife and family) with a history of cutaneous T-cell lymphoma (chemo/radiation 3 months earlier), Sezary syndrome (with chemo) and Sjogren’s syndrome walks in (yes, thats right, walks in…) to the emergency department waiting room, leaning on his wife after just getting off a plane from Seattle (about a 3 hour flight) after a 1 week cruise.

SonoCase: Motorcycle victim: needs OR! But wait…

So, this case that I just had the other day is an example of an “oldy but goody” reason why bedside ultrasound rocks, especially in the blunt trauma victim with multiple injuries. 40 year-old motorcycle helmeted driver going moderate speed was T-boned by a car and fell onto his left side. He c/o severe left leg pain and mild left lower back pain, with STABLE (and yes, I mean, stable/normal/not worrisome vitals – HR 72, RR 16, BP 148/90, O2 sat 97%RA) with a clear primary trauma survey, and a secondary that revealed a small abrasion on his cheek, no left sided chest wall tenderness, nontender abdomen, no pelvis instability, an obvious deformed open fracture of his left tibia/fibula, and left lower posterior rib cage tenderness without crepitance or bruising. An E-FAST was done…