Systemic arterial to pulmonary arterial shunt masquerading as acute pulmonary embolism

Description

We present the case of a middle-aged man in his early 40s who came to the emergency department with sudden-onset chest pain and dyspnoea. The patient had a history of antitubercular drug intake 6 years ago. He also complained of two episodes of haemoptysis in the past 6 months. General examination was within normal limits except for tachycardia and tachypnoea, blood oxygen saturation level was 97% and TROP-T assay was negative. ECG showed sinus tachycardia and 2D-echocardiogram did not reveal any significant abnormality (figure 1B,C).

Figure 1.

(A) Chest X-ray in Postero-anterior (PA) projection showing radio-opacity with cavitation and focal bronchiectatic changes in the right lung upper zone (marked by red arrow). (B,C) Show unremarkable ECG and echocardiogram.

Routine blood investigations showed elevated leucocyte count, 18 000/mL (range 4–10 000/mL), raised CRP, 155 mg/L (range 0–5 mg/L) and D-dimer, 1.03 μg/mL (range <0.2 μg/mL).

Chest X-ray showed findings of volume loss, radio-opacity with cavitations and focal bronchiectasis changes in the right upper lung zone (figure 1A). These findings were thought to be consistent with the history of pulmonary tuberculosis.

Clinically acute pulmonary thromboembolism was suspected and CT pulmonary angiography (CTPA) was advised. As the patient had a history of intermittent haemoptysis, an aortic phase was also included to look for any hypertrophied bronchial or non-bronchial systemic collaterals.

CTPA depicted partially occluding hypodense filling defect in the right main pulmonary artery and its upper lobar branch (figure 2A,B). This finding was thought to be consistent with the clinical suspicion of pulmonary embolus. However, on the subsequent aortic phase, retrograde flow of the systemic arterial blood was noted into the right pulmonary artery (figure 2C,D), likely through an underlying acquired systemic arterial to pulmonary arterial (SAPA) shunt. In order to confirm the filling defect seen in the pulmonary phase, a delayed scan was also taken. Complete resolution of the filling defect was noted (figure 3A,B). The High Resolution Computed Tomography (HRCT) reconstruction images revealed lung destruction with volume loss and associated tractional bronchiectasis changes involving the right upper lobe (figure 3C). Neovascularisation (figure 3D) was also noted in this region with branches arising from the right upper intercostal arteries and hypertrophied right bronchial artery.

Figure 2.

(A,B) Show filling defect in the right main pulmonary artery and its upper lobar branch in the pulmonary angiography phase. Contrast jet noted in the region of filling defect on subsequent aortographic phase shown by arrows in (C,D).

Figure 3.

(A,B) Show resolution of the filling defect that was seen in the pulmonary angiography phase. (C) Shows fibrobronchiectatic changes in the right upper lobe with changes of neovascularisation depicted by arrow in (D).

CT values of hypodense filling defect were measured and it is of mean value 70 HU on pulmonary angiographic phase mimicking thrombus (figure 4B), however on aortographic phase it got resolved and contrast jet is seen at the site of hypodensity of mean HU 289 that is of contrast admixed blood (figure 4C). 3D-CT showed undulations over the surface of right pulmonary artery likely due to systemic shunt collaterals (figure 5A,B).

Figure 4.

(A) Plain axial CT cut at the level of pulmonary artery, appears unremarkable. (B) Hypodense filling defect in the right main pulmonary artery of mean HU 70 in angiographic phase, shown by red arrow. (C) Contrast jet at the site of hypodensity of mean HU 289 in aortographic phase, shown by green arrow.

Figure 5.

(A,B) Three-dimensional pulmonary arterial vasculature in grey and colour format, respectively. Slight undulations noted over the surface of right pulmonary artery, likely due to systemic shunt collaterals, shown by red arrows in (A,B).

There are few case reports where SAPA shunt was misinterpreted on imaging as pulmonary emboli, leading to delay in the definitive management of the patient. It also leads to inadvertent administration of anticoagulants in a patient with haemoptysis, thus further worsening the situation. Dissaux et al¹ reported SAPA shunt as a rare cause of filling defects in the pulmonary arteries on CTPA. Toupchiani et al² reported the case of a middle-aged woman whose CT pulmonary angiogram showed a pulmonary arterial filling defect, which was subsequently found to be false positive due to an underlying SAPA shunt. These shunts are acquired shunts as they develop in the vicinity of prior tubercular cavity and the patient was asymptomatic in childhood until the development of pulmonary TB.

Patient’s perspective.

I had two episodes of fresh blood in sputum in last 6 months. I developed chest pain and difficulty in breathing, for which I came to the emergency department of All India Institute Of Medical Sciences (AIIMS) Patna. I was very apprehensive. After imaging and other investigations, I was explained that my symptoms were due to previous tubercular infection and not because of some new sinister disease. This immensely helped in relieving my anxiety.

Learning points.

• Systemic arterial to pulmonary arterial (SAPA) shunts are a rare cause of filling defects in the pulmonary arteries on CTPA, which can be misinterpreted as a pulmonary embolus.

• In the presence of chronic lung parenchymal disease with haemoptysis, radiologists should consider SAPA shunt as a differential for filling defect on CTPA. In case of diagnostic dilemma, an additional contrast phase will help avoid false-positive diagnosis of pulmonary embolism.

• It will also help in preventing the unwarranted use of anticoagulation in patients with haemoptysis.

Ethics statements

Patient consent for publication

Consent obtained directly from patient(s).