Role of Echocardiography in a Patient With Suspected Acute Pulmonary Embolism

A Case Report

Julio Miranda-Bacallado; María Manuela Izquierdo-Gómez; Javier García-Niebla; Juan José Jiménez; José Luis Iribarren; Ignacio Laynez-Cerdeña; Juan Lacalzada-Almeida

Disclosures

J Med Case Reports. 2019;13(37) 

In This Article

Discussion

This case report illustrates the fundamental role of echocardiography in the ICU for a patient admitted for community-acquired pneumonia with severe shock. The combined use of echocardiography, especially TEE in our patient, with an electrocardiogram, allowed for all possible causes of shock to be quickly ruled out at the patient's bedside, avoiding unnecessary intrahospital transfers of an unstable patient. In addition, the echocardiographic findings suggestive of PE with repercussion on the RV were recognized, allowing for a suspected diagnosis to be made and for the initiation of fibrinolytic and anticoagulant treatment without further delay, with excellent outcomes in our patient. Although this case is not unique in the literature, it highlights the value of TEE over TTE in patients in the ICU, who, due to the clinical situation (mechanical ventilation, supine position, and so forth), usually have a poor transthoracic window.

Approximately half of PE cases are diagnosed in an emergency setting.[1–3] Dyspnea, chest pain, and syncope are key symptoms that can lead to diagnosis, but these symptoms are absent in ICU patients who are under sedation and on mechanical ventilation.[4] In this scenario, after the development of sudden, severe hypotension, PE must be considered and included in a differential diagnosis according to the cause of admission.[5] TEE played a pivotal role in our patient due to the poor echocardiographic window, which is common in ICU patients. TEE was useful in the differential diagnosis of the cause of shock, ruling out pericardial tamponade, acute valvular dysfunction, severe global or regional LV dysfunction, aortic dissection, or hypovolemia, as recommended by the guidelines of the European Society of Cardiology,[6] and resulting in a diagnosis of PE as the most prevalent etiology. Direct visualization of the thrombus is infrequent, and it was not observed in our patient. The echocardiographic diagnosis is based on indirect signs of the physiopathological consequences of increased pressure on the right side of the heart. In addition to TEE findings similar to those of our patient, clinicians may also observe an enlarged pulmonary artery diameter, tricuspid regurgitation that allows for an estimation of the pulmonary artery systolic pressure, an enlarged right atrium, and a dilated inferior vena cava. In the absence of these findings, PE is unlikely.[7] TTE has been established as a valuable tool for evaluating the different causes of hemodynamic instability. Furthermore, TEE has been shown to be of additional value in many instances for critically ill patients because of its ability to provide excellent visualization of cardiac structures. In this context, TTE has a diagnostic success rate of 50% and can occasionally lead to inadequate images that are not able to establish a diagnosis, compared with a 90% success rate for TEE.[5] TEE has 70% sensitivity and 81% specificity for the confirmation of PE.[8] The gold standard for the diagnosis of PE is pulmonary angiography and spiral CT. The PIOPED II trial showed a sensitivity of 83% and a specificity of 96% for multidetector computed tomographic (MDCT) angiography. That trial also highlighted that in patients with a low or intermediate clinical probability of PE as assessed by the Wells rule, a negative CT result had a high negative predictive value for PE (96% and 89%, respectively), whereas this value was only 60% in those with a high pretest probability. Conversely, the positive predictive value of a positive CT result was high (92–96%) in patients with an intermediate or high clinical probability, but much lower (58%) in patients with a low pretest likelihood of PE. Therefore, the PIOPED II trial concluded by warning clinicians to be cautious in cases of discordance between clinical suspicion of PE and MDCT outcome.[9] These techniques require the transport of an unstable patient, which causes a certain risk when performing crucial tests for diagnostic confirmation.[5,10] In these cases, TEE is a very useful bedside technique for patients in an ICU environment. The recent guidelines of the European Society of Cardiology do not recommend diagnostic echocardiographic studies in patients with suspected (not high-risk) PE. However, signs of RV overload in patients with high-risk PE without another important alternative diagnosis warrant emergency treatment if CT or other confirmatory test results are not immediately available.[6] Thus, although it does not allow an initial PE diagnosis, TEE helps identify when PE is the cause of RV dilation (RV end-diastolic diameter/LV end-diastolic diameter ratio > 0.9) and exclude other causes, such as pericardial effusion or acute myocardial infarction.[11] Echocardiography, on the other hand, has the noninvasive ability to evaluate and monitor the RV and LV function. It also allows the serial determination of different measures of ventricular function, analyzing its response to medical interventions such as fluid and drug therapy. In the specific case of a patient with PE, it is useful for monitoring RV function and pulmonary artery systolic pressure when thrombolytics are administered.[12] In patients with massive PE, serial assessment of RV size and fractional area change, determination of RV systolic pressure, and inferior vena cava assessment can be performed using the American Society of Echocardiography RV guidelines for the normal ranges.[13]

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