Abstract
Acute pulmonary thromboembolism (PTE) can range from asymptomatic cases to severe presentations with cardiogenic shock. We report a 67-year-old male with diabetes and hypertension, presenting with progressive dyspnea and hemodynamic instability. Clinical examination revealed sinus tachycardia, right ventricular dysfunction on echocardiography, and elevated biomarkers indicative of PTE. Chest X-ray showed classic signs including Westermark's, Palla's, Fleischner's and Chang's signs, raising suspicion for PTE, which was confirmed via CT pulmonary angiogram showing extensive thrombi. The patient was treated with intravenous thrombolysis and anticoagulation, resulting in clinical improvement and normalization of imaging findings. This case underscores the diagnostic relevance of chest X-ray in emergency settings for suspected PTE.
Introduction
Pulmonary thromboembolism (PTE) is a critical medical condition with diverse clinical presentations, ranging from asymptomatic sub-segmental emboli to life-threatening events characterized by cardiogenic shock and multi-organ failure. The rapid and unpredictable onset of PTE poses significant diagnostic challenges, especially in emergency settings [1]. Although computed tomography pulmonary angiography (CTPA) is the gold standard for diagnosis, the role of chest X-ray (CXR) in suggesting PTE through specific radiographic signs should not be overlooked. Classical signs such as Westermark's sign, Palla's sign, Fleischner's sign and Chang's sign, although uncommon, may provide vital clues to prompt further diagnostic evaluation. This case highlights the diagnostic value of these CXR signs, emphasizing the importance of early imaging in suspected PTE.
Case report
A 67-year-old male with a history of diabetes and hypertension presented to the emergency department with progressive dyspnea over four days. On arrival, he exhibited signs of hemodynamic instability, including a respiratory rate of 26 breaths per minute, heart rate of 120 beats per minute, blood pressure of 90/60 mmHg, and oxygen saturation (SpO₂) of 88% on room air. Electrocardiography (ECG) revealed sinus tachycardia, inverted T waves in the precordial leads, and an S1Q3T3 pattern, which are suggestive of right ventricular strain. Given the clinical presentation, an urgent chest X-ray was performed to evaluate differential diagnoses such as pulmonary embolism (PE), pneumothorax, pneumonia, or pleural effusion.
The chest X-ray demonstrated several key findings:
Bilateral focal areas of translucency (oligemia) in the middle and lower lung zones (Westermark's sign, yellow circle in Fig. 1A) [2, 3].
Prominent right descending pulmonary artery (RDPA), also referred to as Palla's sign or Fleischner's sign (black arrow in Fig. 1A) [2–5].
Dilated RDPA with abrupt vascular cutoff, consistent with Chang's sign (white arrowhead in Fig. 1A) [6].
(A) Pre-thrombolysis chest radiograph showing: focal oligemia in the right and left lung zones (yellow circles), consistent with Westermark's sign; a prominent right descending pulmonary artery (RDPA) (black arrow), indicative of Palla's sign; and an abrupt cutoff of the dilated RDPA (white arrowhead), referred to as Chang's sign.
(B) Post-thrombolysis chest radiograph demonstrating improved visualization of the pulmonary vasculature in both lung fields and clearer delineation of the RDPA
Citation: Imaging 2025; 10.1556/1647.2024.00264
These radiographic findings (Fig. 1A) strongly raised the suspicion of an acute pulmonary thromboembolism (PTE), prompting further diagnostic evaluation with a computed tomography pulmonary angiogram (CTPA). The CTPA confirmed the diagnosis by revealing large thrombi in both the right and left pulmonary arteries, nearly occluding the lumens and extending into the segmental and sub-segmental branches (Fig. 2).
Contrast-enhanced CT pulmonary angiograms (axial view) showing thrombi within the bilateral pulmonary arteries (PA) and their segmental branches
Citation: Imaging 2025; 10.1556/1647.2024.00264
Echocardiography further supported the diagnosis, showing severe pulmonary hypertension and right ventricular (RV) dysfunction. Laboratory tests revealed elevated biomarkers, including NT-proBNP (14,437 pg mL−1), Troponin T (0.06 ng mL −1), D-dimer (8,000 ng mL −1 FEU), and a creatinine level of 1.6 mg dL−1, further corroborating the severity of the condition. These findings classified the patient as having a high-risk PE, necessitating immediate systemic thrombolysis.
The patient was promptly admitted to the intensive care unit due to hemodynamic instability, hypotension, hypoxia, and RV dysfunction. Treatment commenced with intravenous Tenecteplase 35 mg as a bolus, followed by anticoagulation with subcutaneous enoxaparin (1 mg kg−1) administered twice daily for five days. The patient responded favorably to the treatment, exhibiting improved oxygenation, stabilization of blood pressure, and recovery of renal function over the subsequent three days. On the fourth day, the patient was transferred to the ward, continuing subcutaneous enoxaparin for an additional two days. A follow-up chest X-ray showed marked improvement in the visualization of the right descending pulmonary artery and pulmonary vasculature (Fig. 1B), and repeat echocardiography demonstrated a reduction in pulmonary artery pressures and improvement in RV function. The patient was discharged after five days of hospitalization on oral rivaroxaban 20 mg once daily, with instructions for outpatient follow-up.
Discussion
Acute pulmonary thromboembolism (PTE) spans from asymptomatic, incidentally found sub-segmental thrombi to severe cases with cardiogenic shock and multi-organ dysfunction. While anatomical obstruction primarily compromises physiology, platelet-derived vasoactive agents like serotonin can disrupt ventilation-perfusion matching. Increased right ventricular afterload may result in its dilation, dysfunction, and ischemia, ultimately leading to right ventricular failure and death [1]. PTE remains a leading cause of cardiovascular morbidity and mortality. Its clinical presentation can be highly variable, which makes early diagnosis challenging. While CTPA is the preferred diagnostic modality due to its high sensitivity (83%) and specificity (96%), chest X-ray is often the first imaging modality obtained in an emergency setting [5, 7, 8]. Although the majority of CXRs in PTE are normal or nonspecific, certain radiographic signs, such as Westermark's sign (focal oligemia distal to a large vessel occluded by embolus), Palla's sign (prominent right descending pulmonary artery), Fleischner's sign (enlarged central pulmonary artery) and Chang's sign (abrupt cutoff in pulmonary vasculature), can strongly suggest the diagnosis of PTE [2–6, 8].
In this case, the presence of all these classical radiographic signs on CXR was highly suggestive of PTE, leading to prompt confirmation with CTPA. These signs are pathophysiological reflections of the mechanical obstruction and the hemodynamic alterations caused by the emboli in the pulmonary arteries. Westermark's sign indicates reduced blood flow to the lung parenchyma distal to the embolism, while Palla's, Fleischner's and Chang's signs reflect enlargement and obstruction of the pulmonary vasculature. Identifying these signs on CXR in an acute setting can expedite the diagnostic process and guide immediate management [2–6, 8].
The importance of chest X-ray in suspected PTE should not be underestimated, particularly in resource-limited settings where CTPA may not be readily available. Early recognition of these radiographic signs, along with clinical and laboratory findings, can lead to timely initiation of life-saving therapies such as thrombolysis and anticoagulation.
Conclusion
This case underscores the diagnostic value of chest X-ray in acute pulmonary thromboembolism, highlighting the significance of recognizing classical radiographic signs such as Westermark's, Palla's, Fleischner's and Chang's signs. While CTPA remains the definitive diagnostic tool, the role of CXR in the initial evaluation of suspected PTE, especially in emergency settings, should be acknowledged. Early detection through CXR can facilitate prompt management, improving patient outcomes.
Contributors
SD, CM, and KL reported the case and wrote the manuscript. KL, PP, and MJ reviewed and edited the manuscript. KL, MJ, and PR managed the case. All authors approved the final version of the manuscript.
Disclosure of interest
None of the authors has any conflicts of interest or financial interest to disclose. The authors report there are no competing interests to declare.
Funding
No financial support is received for the research, authorship, and/or publication of this article.
Patient consent
Obtained.
Acknowledgements
Nil.
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