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The Pulmonary and Bronchial Vessels, Pulmonary Vascular Abnormalities including Embolism, Pulmonary and Bronchial Angiography, and A/V Malformations.
Published in Fred W Wright, Radiology of the Chest and Related Conditions, 2022
Acute embolism causes a sudden reduction in the pulmonary circulation to the affected part(s) or the lung. This may be accentuated by vascular spasm, perhaps due to sudden hypoxia in the affected lobe or lung. Reduced perfusion may lead to reduced fluid within the lung producing increased translucency, narrowing of the arteries on the affected side and contralateral dilatation. If the condition is bilateral, then the changes may be reflected in the vessels of the affected lobes. With major blockages, it is untrue to state, as often appears in text-books that the chest radiograph is likely to be normal. Westermark (1938), Shapiro and Rigler (1948) and Chang (1967) described the 'characteristic appearance of ischaemic lung' as the 'Westermark sign' i.e. - a marked increased radio-lucency of the involved lung, with elevation of the hemidiaphragm (from decreased lung volume), the hilar shadow being small, the descending pulmonary artery (and its branches) small and spastic - often accompanied by compensatory dilatation of the pulmonary vessels in the contralateral lung.
Paper 2
Published in Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw, The Final FRCR, 2020
Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw
Large pulmonary embolus may cause the imaging features of reduced lung markings. The ‘Westermark’ sign is a radiographic sign of focal increased lucency of the lung, thought to be secondary to occlusion of the pulmonary artery or due to vasoconstriction distal to the embolus. This sign is not commonly seen and the patient in the main stem is asymptomatic.
Practice Paper 3: Answers
Published in Anthony B. Starr, Hiruni Jayasena, David Capewell, Saran Shantikumar, Get ahead! Medicine, 2016
Anthony B. Starr, Hiruni Jayasena, David Capewell
PE is a blood clot in the lung vasculature. Most PEs (75%) derive from a deep vein thrombosis. Features include acute-onset pleuritic chest pain and shortness of breath, often with fever and tachycardia. The chest X-ray may show a wedge-shaped opacity due to consolidation associated with pulmonary infarction (Hampton’s hump). The Westermark sign is a focus of oligaemia on X-ray distal to an occluded blood vessel. The ECG most commonly demonstrates a sinus tachycardia, although the S1Q3T3 pattern is characteristic (S-wave in lead I, Q-wave and inverted T-wave in lead III). An arterial blood gas reveals type I respiratory failure (normal pH, low Po2). D-dimers are a breakdown product of clots: a low D-dimer can be used to exclude a PE, but a high level does not confirm it. The next investigation in PE depends on the chest X-ray: if the chest X-ray is clear, a ventilation–perfusion scan is performed to look for areas that are getting air but not blood. If the chest X-ray is not clear, or if a scan is inconclusive, a spiral CT (CT pulmonary angiography) is the best investigation. Patients with a confirmed PE are started on heparin or LMWH and then warfarinized for 6 months (aiming for an INR between 2 and 3). Patients who have suffered a massive PE need urgent thrombolysis.
Pulmonary artery twisting during lung transplantation
Published in Baylor University Medical Center Proceedings, 2018
Andrew Lichliter, Joseph Oros, Louba Laurie
An anteroposterior chest radiograph was acquired when the patient arrived in the intensive care unit (Figure 1). The support apparatus was appropriately positioned. Asymmetric lucency was identified throughout the right lung. The nonspecific findings could be due to edema or hemorrhage in the left lung, a right anterior pneumothorax or left layering pleural effusion in a supine patient, or right-sided oligemia, such as a Westermark sign. An indwelling Swan-Ganz catheter revealed a PA pressure of 54/24 mm Hg. Arterial blood gas demonstrated respiratory acidosis with a pH of 7.25. Inhaled nitric oxide was added to the treatment regimen with a goal of keeping systolic PA pressure <40 mm Hg and oxygen saturation >92% on the ventilator. Over the next 14 hours, the systolic PA pressure was weaned to 33 mm Hg, but this required increasing requirements of nitric oxide, up to 27 ppm. Although hemodynamically stable, the patient remained acidotic in this period, with arterial blood gas pH ranging from 7.25 to 7.36 despite multiple ventilator changes. Quantitative perfusion scintigraphy performed 16 hours posttransplant revealed little to no visualization of and only 6% of total perfusion to the right lung (Figure 2), suggestive of a PA complication. For confirmation and treatment planning, a computed tomography (CT) angiogram with PA embolism protocol was performed. This demonstrated twisting of the right main PA (Figures 3and4), and the patient was immediately taken to the operating room.