The case presentation...
Our patient is a middle aged male with a past medical history notable for asthma and laparotomy for multiple GSWs a few months prior. he presented to the emergency department complaining of shortness of breath. This had been progressively worsening over the past two months to the point that he could not walk more than a few steps without becoming severely winded. He had not been able to lie flat at night and instead has been sleeping upright in a reclining chair. He has no known cardiac or pulmonary history other than his asthma. He reports that he has tried his albuterol inhaler for his symptoms with no relief.
On initial vital signs in triage, he is hypoxic to the low 90s and mildly tachycardic. His oxygen saturation drops down into the 70s when walking to the exam room from the lobby. On exam, his lungs are clear to auscultation and he has 1+ pitting edema below the knee in the left leg only.
His workup is notable for an elevated troponin and BNP and his EKG showed T wave inversions in the inferior and lateral leads and an elevated creatinine. He had a portable chest x-ray which demonstrated clear lungs. The treating physicians had a high degree of diagnostic uncertainty about the etiology of his symptoms with cardiomyopathy, myocarditis, pulmonary hypertension and pulmonary embolism (PE) at the top of the list. To narrow down their differential, bedside ultrasound was performed.
And now for the ultrasound images...
Evaluation of dyspnea can be challenging due to the wide differential which is a minefield of of potential life threats. In the emergency department, we start by considering these potential life threats and work backwards to benign and self-limited causes. This patient's presentation was particularly challenging because he had progressive symptoms over a period of months, which would argue for a chronic cause, but also had hemodynamic instability and distress which could be secondary to any number of acute conditions.
On the images here we see a deep vein thrombosis and evidence of right heart strain. Taking a closer look at the right heart, the right ventricle appears thick-walled, which argues for a more chronic process such as pulmonary hypertension. Can ultrasound help differentiate between these two entities that share a high degree of clinical overlap? As emergency physicians become more facile with the use of bedside ultrasound, are there more comprehensive ways in which we can be using it for diagnosing PE?
As to the first question, there are two measurements that we can use to distinguish chronic pulmonary hypertension from acute RV failure caused by PE. They will require a bit of practice to obtain the necessary views, and also the aid of a calculator, but with the potential to alter a patient's trajectory in these cases in which CTPA is an unavailable test, they are worthwhile to have in your back pocket. These measurements are the right ventricular systolic pressure (RVSP) and pulmonary acceleration time (PAT), and together they comprise the "60/60 sign" (1).
The remodeling of the right ventricle that happens with chronic pulmonary hypertension can produce RVSP greater than 60mmHg (the first 60), so values less than 60 are probably from an acute process. In acute PE, there is no time for the right ventricle to remodel it cannot generate such force and pressure. The second 60 refers to PAT, which is the amount of time it takes for the blood flow across the pulmonic valve reach peak velocity. Chronic pulmonary hypertension allows a longer time to peak because the problem lies in smaller distal branches and spares some of the compliance of the proximal circulation, whereas in acute proximal PE compliance is more affected and peak flow velocity is reached more quickly. For details on how to obtain these measurements and a link to the online calculator, check out the great explanation and diagrams at Ultrasound of the Week.
Yet another measurement that has some promise to differentiate these two entities is right ventricular outflow tract systolic excursion (RVOT_SE). This refers to the distance traveled by the anterior wall endocardium of the RVOT during systole and is measured using M-mode in the parasternal short axis at the level of the aortic valve. A study published in the Journal of Echocardiography found that values less than 0.54cm were 98% sensitive and 96% specific for reduced RV function and were better than other measurements such as TAPSE and McConnell's sign because it measures an area that is less affected by ischemia from other causes such as coronary artery disease (2). Another very small study found that this reduced RVOT_SE was much more common in acute PE than chronic pulmonary hypertension (3).
As to the second question of broadening the ways in which ultrasound is used to diagnose PE, there have been some interesting papers focused on amalgamating ultrasound with more traditional tools and aids. Symptoms of PE run the gamut from none at all to sudden death and everything in between. Of course there is the “classic” presentation of the patient with non-exertional respirophasic chest pain, shortness of breath, and vital sign abnormalities of tachycardia, tachypnea, hypoxia, and potentially hypotension. However, as in many disease processes, the classic presentation is not actually the most common and diagnosis can be elusive without a high degree of suspicion. Some studies even suggest that we should not be falsely reassured by normalization of vital signs (something that subjectively many of us attempt to do), as this does not serve to sufficiently rule out PE (4).
There exist a myriad of cognitive aids and decision tools to aid in the process. The definitive test (CT angiography of the pulmonary arteries or CTPA) is not benign, carrying the potential harms of radiation exposure and risks of contrast media (although contrast-induced nephropathy is currently a debated topic) and sending everyone with suspicion of PE for CTPA is not feasible. Most commonly we employ something like the Wells’ score, or PERC if the patient is low enough risk. The Wells’ Criteria were originally described in 2001 (5) and then later validated in 2004 (6) and have since become a widely-employed tool to improve patient care and aid diagnosis of PE.
With the expansion of applications for ultrasound in the emergency department we now have the ability to look for secondary signs. These include RV dilation, septal flattening (the “D sign”), McConnell sign, elevated pulmonary arterial pressure, and plethoric IVC.
Several studies have looked at expanding the role of ultrasound in the diagnosis of PE. Nazerian and Vanni et al looked at the use of multiorgran ultrasound and found that by combining thoracic ultrasound with DVT scan they were able to increase the sensitivity and accuracy of clinical pretest probability and reduce the amount of CTPAs performed (7). A few years later Nazerian and Volpicelli revisited this concept by modifying the Wells’ Criteria to include ultrasound. In this second study they replaced the “clinical signs and symptoms of DVT” criterion with an actual 2-point compression DVT scan and the “PE is #1 diagnosis or equally likely” criterion with lung ultrasound (8). The authors concluded that this ultrasound-enhanced version of the Wells’ Score performed significantly better than the standalone Wells' Score, increasing both sensitivity and specificity, and effectively reducing the number of CTPAs performed (8).
Take Away Pearls
Differentiating acute RV strain due to PE from chronic RV failure due to pulmonary hypertension can be clinically difficult, but understanding RVOT systolic excursion and the 60/60 sign can help distinguish the two.
Perform multi-organ ultrasound including lung and DVT to increase sensitivity of your exam for PE.
Our providers attempted to optimize the patient’s respiratory status first with oxygen via nasal cannula. He continued to worsen and was moved to the SRU where he was placed on optiflow but still could not achieve sats higher than mid 80s on max settings. Discussion of intubation took place, a trial of inhaled nitric oxide was attempted first. With this, his oxygen saturation improved significantly. Although there was great concern for PE the patient could not tolerate lying flat for CTPA and so he was started empirically on heparin and admitted to the MICU.
During his MICU course he was stabilized and was able to undergo CTPA which showed a large bilateral burden of emboli. Consultative TTE showed severe RV dilation with flattening of the interventricular septum and severely increased PA pressure. Consultative venous duplex showed bilateral popliteal and posterior tibial venous thromboses. The patient had signs of both an acute PE and undiagnosed chronic pulmonary hypertension.
Case and Post by Jared Ham, MD
Peer Review by Lori Stolz, MD RDMS
Alsoos F, Almobarak M, Shebli H. Right ventricular outflow tract systolic excursion: a useful method for determining right ventricular systolic function. J Echocardiogr. 2014;12(4):151-8.
López-candales A, Edelman K. Right ventricular outflow tract systolic excursion: a distinguishing echocardiographic finding in acute pulmonary embolism. Echocardiography. 2013;30(6):649-57.
Kline JA, Corredor DM, Hogg MM, Hernandez J, Jones AE. Normalization of vital signs does not reduce the probability of acute pulmonary embolism in symptomatic emergency department patients. Acad Emerg Med. 2012;19(1):11-7.
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;135(2):98-107.
Wolf SJ, Mccubbin TR, Feldhaus KM, Faragher JP, Adcock DM. Prospective validation of Wells Criteria in the evaluation of patients with suspected pulmonary embolism. Ann Emerg Med. 2004;44(5):503-10.
Nazerian P, Vanni S, Volpicelli G, et al. Accuracy of point-of-care multiorgan ultrasonography for the diagnosis of pulmonary embolism. Chest. 2014;145(5):950-957.
Nazerian P, Volpicelli G, Gigli C, et al. Diagnostic Performance of Wells Score Combined With Point-of-care Lung and Venous Ultrasound in Suspected Pulmonary Embolism. Acad Emerg Med. 2017;24(3):270-280.