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


J Med Case Reports. 2019;13(37) 

In This Article

Case Presentation

A 44-year-old Caucasian man, a construction worker in an urban area, married and with two children, with no past medical history, previous treatment, or toxic habits, presented 1 week before entering the hospital with general weakness and respiratory difficulty that gradually increased in intensity, accompanied by cough without expectoration. He had also experienced recent fever (38.9 °C, 102.0 °F) and some episodes of vomiting and diarrhea. He was admitted to the ICU with a diagnosis of community-acquired pneumonia and respiratory failure. At the time of admission to the ICU, the patient was conscious, oriented, and collaborative, without presenting any neurological alteration. The patient was febrile (38 °C, 100.4 °F) and tachycardic (heart rate 110 beats/min), his blood pressure was 120/80 mmHg, and he was tachypneic (28 breaths/min), without intercostal print, with an oxygen saturation of 88% with a Ventimask (Flexicare Medical, Mountain Ash, UK) at 50%. Lung auscultation showed conserved vesicular murmur and basal and midfields bilateral crackles. His heart sounds were regular, rhythmic, and without murmurs. No heart failure data were recorded. We observed a soft and depressible abdomen with peristalsis present, without visceromegalies. The patient's lower limbs were without edema and had symmetric palpable peripheral pulses. Empiric antibiotic treatment was started with ceftriaxone (2 g/24 h, 7 days), levofloxacin (500 mg/24 h, 7 days), and oseltamivir (150 mg/12 h, 5 days), and 24 h after the admission, the patient was diagnosed with influenza A(H1N1) pneumonia after the virus was isolated in the nasopharyngeal swab samples taken at admission by PCR (DNA isolation). In the patient's medical history, he did not highlight any history of toxic habits; information on medication taken regularly or any drug allergies was not recorded.

The patient required mechanical ventilation, and his initial evaluation was favorable with stable hemodynamics. On day 12 of the admission, he developed acute severe hypotension (systolic blood pressure < 80 mmHg) with tachycardia (heart rate > 140 beats/min) and a markedly worsening respiratory status. Arterial acid-base balance at that time showed fraction of inspired oxygen 60%, pH 7.39, partial pressure of carbon dioxide 26.7 mmHg, partial pressure of oxygen 55.9 mmHg, bicarbonate 15.9 mmol/L, base excess − 8.1, lactic acid 0.9 mmol/L, and oxygen saturation 91.2%. The patient's respiratory status failed to respond to high-dose vasopressors and ventilatory support. The laboratory findings at that time showed the following: red blood cells 3.4 × 106/mm3, hemoglobin 9.7 g/dl, mean corpuscular volume 96.5 fl (normal reference value 80–100), average corpuscular hemoglobin 28.5, leukocytes 14.8 × 103/mm3 (normal reference value 4.5–11.1 × 103), 74.9% neutrophils, 14.8% lymphocytes, international normalized ratio 1.29, basal glucose 155 mg/dl (normal reference value 65–110), blood urea nitrogen 33 mg/dl (normal reference value 5–20), creatinine 1.10 mg/dl, sodium 145 mEq/L, potassium 3.9 mEq/L, troponin I 0.022 ng/dl, (normal reference value < 0.034), D-dimer > 10,000 ng/ml (normal reference value < 500), and C-reactive protein > 90 mg/L (normal reference value 0–12).

The cultures of the bronchial secretion (sputum of the patient) and of urine and blood (direct puncture of a peripheral artery) were negative for both aerobic and anaerobic bacteria, as were urine antigens for Pneumococcus and Legionella. An anteroposterior chest radiograph showed right basal infiltrate (Figure 1a). To determine the cause of this acute hemodynamic instability and facilitate patient management, TTE was performed for a differential diagnosis of hypovolemia, acute LV or RV dysfunction, cardiac tamponade, aortic dissection, severe valvular regurgitation, dynamic LV outflow tract obstruction, or PE. Poor-quality images were obtained, necessitating the completion of the study with TEE.

Figure 1.

a Anteroposterior chest x-ray obtained in the intensive care unit showing basal pulmonary infiltrate. b Posteroanterior chest x-ray taken prior to discharge and showing disappearance of the pulmonary infiltrate

TEE demonstrated a small and hyperdynamic LV and a severely dilated and dysfunctional RV. In the midesophageal four chambers view with TEE, the RV end-diastolic area to LV end-diastolic area ratio was 1.7 (normal reference value < 0.6), and the RV end-diastolic diameter to LV end-diastolic diameter ratio was 1.4 (normal reference value < 0.9). TEE also showed McConnell's sign, normokinesia of the RV apical segment, and akinesia of the RV mid-free wall (Figure 2a, Additional file 1) and a systolic flattening of the interventricular septum (Figure 2b, Additional file 2), suggesting RV pressure overload. There was no evidence of a thrombus either on the right side of the heart or in the pulmonary arteries. These findings of acute RV failure due to pressure overload raised the possibility of a PE or RV myocardial infarction.[1] A 12-lead electrocardiogram showed T-wave inversion in leads V1 to V4 and an S1Q3T3 pattern without abnormalities in the ST segment (Figure 2c). The combined use of electrocardiography and TEE in this clinical setting suggested a high probability of PE. The unfavorable hemodynamic situation of the patient prevented transfer to carry out other complementary tests that could confirm the diagnosis of PE. Fibrinolytic and anticoagulant therapies were administered immediately, achieving a favorable clinical outcome.

Figure 2.

a A 45-degree TEE view showing a severely dilated right ventricle with normokinesia of the apical segment and akinesia of the remaining segments of the free wall. b Transgastric TEE view showing systolic flattening of the interventricular septum. c A 12-lead electrocardiogram shows T-wave inversion in leads V1 to V4 and an S1Q3T3 pattern without abnormalities in the ST segment. TEE Transesophageal echocardiography

Twenty-four hours later, with the patient stable from a hemodynamic and respiratory point of view, computed tomography (CT) pulmonary angiography showed multiple filling defects in both the pulmonary artery and bilateral lobar arteries; this outcome is consistent with PE and peripheral pulmonary consolidations that were more extensive on the right side with hypodense zones compatible with areas of hypoperfusion (Figure 3a). The diagnosis of PE was confirmed. The patient continued with anticoagulant and antibiotic treatment during admission, progressing favorably from both a hemodynamic and respiratory point of view. Mechanical ventilation was removed on the 27th day. After 11 days of admission, he showed acute renal failure secondary to the nephrotoxic effects of tobramycin, with subsequent normalization of renal function on the 31st day of admission. After completing approximately 2 weeks of rehabilitation, on the 45th day after admission, the patient was discharged without complications. He achieved normalization of the chest x-ray (Figure 1b) and normalization of RV morphology (Figure 3b, Additional file 3) and functionality (Figure 3c). Three years and five months after discharge, the patient remained free of symptoms and was living a normal life.

Figure 3.

a Axial CT slice showing multiple repletion defects in both the pulmonary artery and bilateral lobar arteries, along with peripheral pulmonary consolidations with hypodense zones compatible with areas of hypoperfusion. b Four-chamber apical view of TTE showing the right ventricle with normal diameter and contractility after PE treatment. c Normal (a) TAPSE and (b) TASV as an expression of functionality of the normal right ventricle after PE treatment. CT Computed tomography, TTE Transthoracic echocardiography, PE Pulmonary thromboembolism, TAPSE Tricuspid annular plane systolic excursion, TASV Tricuspid annular systolic velocity