Abstract
In the present report, the case of a 60-year-old man who presented with syncope secondary to chronic thromboemboli of the main pulmonary arteries and pulmonary arterioles is described.
BACKGROUND
Chronic pulmonary thromboembolism is a potentially lethal, highly prevalent entity in clinical practice.
As a consequence of the lack of specificity of the signs and symptoms, as well as the low diagnostic sensitivity of the physical examination and basic complementary tests, computed tomographic angiography (CTA) takes on a particularly meaningful role.
CASE PRESENTATION
A 60-year-old retired worker presented with twice-witnessed syncopal episodes of duration of a few minutes each over the past 3 days, accompanied by an oppressed feeling after paroxysmal palpitation; there were no symptoms suggestive of a seizure, and temporary loss of consciousness was with spontaneous recuperation without sequelae. The patient had experienced hypertension for over 10 years. He denied prior syncope or diabetes. The patient was a 20-pack per day smoker and had experienced alcohol-related seizures for 30 years.
INVESTIGATIONS
On arrival, the patient was afebrile and normotensive, with a normal heart rate, and his respiratory rate was 29 breaths/min. Cardiac auscultation revealed the aortic (A2) and the pulmonary (P2) components of the second heart sound to be A2 > P2, compatible with hypertension. There was no calf or thigh swelling or tenderness. The patient’s vital signs were remarkable for cyanosis because of a partial O2 value of 40% and a saturated O2 value of 82% (room air). The cell blood count, electrolytes, coagulation parameters, D-dimer and urinalysis were normal, and echocardiogram (ECG) demonstrated sinus rhythm at 83 beats/min with abnormal Q-wave in the inferior leads in V1–V3 and avF, the presence of incomplete right bundle-branch block. The chest radiograph showed no infiltrates. No x ray findings indicated pulmonary embolism. Ultrasound of the lower extremities revealed deep venous thrombosis in the left popliteal, posterior tibial and peroneal veins. Ultrasound of the carotid revealed no stenosis. The patient was admitted to the hospital; myocardial infarction was ruled out by serial cardiac enzyme levels, and an ambulatory ECG monitor was placed. As the possibility of a cardiac aetiology for syncope was entertained, the patient was admitted to the hospital for continuous telemetry and serial cardiac enzymes, the results of both of which were negative. The patient underwent two-dimensional echocardiography that confirmed slight tricuspid regurgitation (right ventricular (RV) dilatation and hypokinesia were not detected) with an estimated pulmonary systolic pressure of 45/17 mm Hg by cardiac catheterisation. The patient subsequently underwent an infused spiral CT of the chest, which demonstrated bilateral chronic pulmonary emboli in the main pulmonary arteries; the lung field showed no locational infiltrates. Contrast-enhanced multidetector CT pulmonary angiography revealed masses of chronic pulmonary embolus in the right pulmonary artery (figs 1–3).
Figure 1.
No infiltrated lung field and masses of embolus in the pulmonary artery could be visualised on transsexual CT section.
Figure 3.
Contrast-enhanced examination shows a mass of embolus in the pulmonary artery visualised on coronal and oblique sagittal multiplanar reformat.
Figure 2.
Contrast-enhanced examination shows masses of embolus in the pulmonary artery visualised on transaxial CT section.
DIFFERENTIAL DIAGNOSIS
Cardiac aetiology for syncope
Vasogenic syncope
Neurogenic syncope
TREATMENT
A regimen of low molecular weight heparin and warfarin was initiated to reduce prothrombin time and prevent deep vein thrombosis.
OUTCOME AND FOLLOW-UP
The patient was continued on anticoagulation therapy and was discharged. On subsequent clinic follow-ups CT was repeated to check the response to anticoagulation therapy and lifestyle modification advised for risk factor management; embolectomy and vena cava inferior filters were suggested to be performed later.
DISCUSSION
Chronic pulmonary thromboembolism is a potentially lethal, highly prevalent entity in clinical practice, which can often generate diagnostic difficulties.1-3 The mean (SD) attenuation in patients with chronic pulmonary embolism is 87 (30) Hounsfield units (HU). This value was significantly higher than the mean for patients with acute pulmonary embolism (p<0.001).4 When pulmonary thromboembolism occurs and is properly treated, the estimated mortality is 8%; that value can reach up to 40% if the diagnosis is delayed.3 This is due to the lack of specificity of the signs and symptoms, as well as to the low diagnostic sensitivity of the physical examination and basic complementary tests, such as chest radiography,5 arterial gas analysis, electrocardiography, prothrombin time and D-dimer. Physical examination for things such as chest pain and basic complementary tests, such as abnormality in prothrombin time and D-dimer are the differentiating factors between acute and chronic thrombi. Syncope is three times more common in older patients. Stein et al demonstrated syncope as a presenting syndrome in only 8% of a total of 150 patients with documented pulmonary embolism, but it is interesting to see that the mean age in their subgroup was 66 years old and they showed more severe disease.6 When present, syncope is, most of the time, the initial manifestation of the embolic accident and is usually reported as resulting from a sudden decrease in cardiac output due to massive pulmonary arterial obliteration.3,6 The presence of deep vein thrombosis was associated with greater risk of recurrence and/or death. Various studies have demonstrated that residual deep vein thrombosis is associated with an increased risk of recurrence.7,8 This case reminds us that one should entertain the diagnosis of pulmonary embolism presenting with syncope.
LEARNING POINTS
Chronic pulmonary thromboembolism is a potentially lethal, highly prevalent entity in clinical practice, which can often generate diagnostic difficulties.
When pulmonary thromboembolism diagnosis is delayed, this is often due to the lack of specificity of the signs and symptoms.
Syncope is three times more common in older patients (mean age in subgroup was 66 years old).
Due to the lack of specificity of the signs and symptoms, as well as to the low diagnostic sensitivity of the physical examination and basic complementary tests, computed tomographic angiography (CTA) takes on a particularly meaningful role.
Footnotes
Competing interests: none.
Patient consent: Patient/guardian consent was obtained for publication.
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