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| CASE REPORT |
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| Year : 2020 | Volume
: 9
| Issue : 4 | Page : 273-275 |
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“Bubbly lung consolidation” - A highly specific imaging marker for pulmonary infarction
Srinivas Dandamudi1, Raghuram Palaparti2, P S S Chowdary2, Purnachandra Rao Kondru2, Sudarshan Palaparthi2, Gopala Krishna Koduru2, Somasekhar Ghanta2, Boochi Babu Mannuva2
1 Department of Radiology, Aayush Hospitals, Vijayawada, Andhra Pradesh, India
2 Department of Cardiology, Aayush Hospitals, Vijayawada, Andhra Pradesh, India
| Date of Submission | 25-Nov-2019 |
| Date of Decision | 05-Apr-2020 |
| Date of Acceptance | 13-Apr-2020 |
| Date of Web Publication | 6-Jan-2021 |
Correspondence Address:
Dr. Raghuram Palaparti
Consultant Cardiologist, Aayush Hospitals, Vijayawada, Ramachandra Nagar - 520 008, Andhra Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/JDRNTRUHS.JDRNTRUHS_111_19
A 23-year-old male with a history of smoking presented with dyspnea and pleuritic chest pain. His CXR showed pleural-based wedge-shaped opacity in the right lower zone. Non-contrast CT thorax showed central air lucencies without air bronchogram in the opacity (bubbly lung consolidation), suggestive of pulmonary infarction. CT pulmonary angiogram showed a large thrombus involving the right pulmonary artery. Pulmonary infarction affects only a minority of patients with pulmonary embolism. Recent literature suggests that younger individuals without major cardiovascular disease states present more commonly with pulmonary infarction contrary to the earlier studies. “Bubbly lung consolidation” is a highly specific imaging marker for pulmonary infarction and CT pulmonary angiogram has to be expedited to rule out pulmonary embolism. Our case report demonstrates this classical finding and highlights the importance of identifying various CT signs of pulmonary infarction.
Keywords: Bubbly lung consolidation, pulmonary infarction, specific imaging marker
How to cite this article:
Dandamudi S, Palaparti R, Chowdary P S, Kondru PR, Palaparthi S, Koduru GK, Ghanta S, Mannuva BB. “Bubbly lung consolidation” - A highly specific imaging marker for pulmonary infarction. J NTR Univ Health Sci 2020;9:273-5 |
How to cite this URL:
Dandamudi S, Palaparti R, Chowdary P S, Kondru PR, Palaparthi S, Koduru GK, Ghanta S, Mannuva BB. “Bubbly lung consolidation” - A highly specific imaging marker for pulmonary infarction. J NTR Univ Health Sci [serial online] 2020 [cited 2023 Feb 4];9:273-5. Available from: https://www.jdrntruhs.org/text.asp?2020/9/4/273/306118 |
| Case Report | |  |
A 23-year-old male with a history of smoking presented to the medical outpatient department for progressive dyspnea, pleuritic chest pain for 2 weeks and low-grade intermittent fever for 1 week. Clinical examination revealed sinus tachycardia (110 bpm), decreased room air saturation at 94% and right basal hypoventilation. Serum D-dimer levels were elevated to 3050 ng/mL with mild neutrophilic leucocytosis. Chest X-ray (CXR) showed a right lower zone wedged-shaped opacity. Electrocardiography showed sinus tachycardia. 2D Echo showed mild dilatation of right atrium (RA) and right ventricle (RV) without significant RV dysfunction. Non-contrast thoracic computed tomography (CT) demonstrated wedge-shaped opacity with bubbly consolidation in the right lower lobe. CT pulmonary angiogram showed a large thrombus involving the right pulmonary artery [Template 1]. He was started on anticoagulation and other supportive measures. He improved gradually and was discharged on oral vitamin K antagonists (VKA) therapy with optimal International Normalized Ratio (INR). Other than smoking, he did not have any predisposing factors such as prolonged immobilisation, recent major trauma or surgery, history of heart disease, etc., Evaluation of deep venous thrombosis was negative. He was evaluated later in the follow-up for any hypercoagulable states, the workup of which was also negative. Considering sub-massive unprovoked PE, it was decided to continue him on oral VKA therapy for an extended period and assess his risk vs. benefit of continuing the oral anticoagulant therapy at the end of 1 year. Presently he is doing well and is in the regular follow-up.
| Discussion | | |
The most common cause of pulmonary infarction (PI) is pulmonary embolism (PE). However, PI affects only a minority of the patients with PE, around 10–32%.[1] An earlier autopsy study by Kirchner et al. showed that the incidence of PI is around 31% in patients with PE and is more common in patients dying of cardiovascular or malignant diseases.[2] In another study by Hongying et al., evaluating the PI in PE by CT found that the PI occurs in nearly 32% of patients.[3] Other conditions that can lead to PI include infection, malignancy, sickle cell disease[4] and vasculitis. Smoking is also a known risk factor for PI. Young age is associated with an increased likelihood while interestingly, obesity is associated with a reduced likelihood of developing a PI in patients with PE.[5] Though earlier literature suggested that patients with underlying cardiac disease are at greatest risk for developing a PI, recent literature suggests that the younger patients without cardiopulmonary disease were found to be more likely to suffer a PI secondary to a PE.[6] Impedance of blood flow from the three major sources of blood flow to the lung parenchyma, namely, pulmonary arteries, bronchial circulation and direct diffusion from the alveoli can cause PI. Inflammatory mediators from ischaemic parenchyma limit gas exchange following vasoconstriction and bronchoconstriction.[1],[7]
A unilateral infarct occurs in 77% to 87% of PI, with the strongest predilection for the right lower lobe like in our patient. The predilection to lower lobe has been related to gravity's influence on the relationship between alveolar pressure, pulmonary arterial pressure and bronchial arterial pressure.[8] The treatment of PI is guided by the underlying condition. PE initially requires anticoagulation and supportive therapy. In patients requiring admission, heparin or low-molecular-weight heparin are started to transition to oral VKA or novel oral anticoagulants (NOACs) for continued outpatient therapy. In patients with haemodynamic instability due to a sub-massive or massive PE, systemic fibrinolytic or catheter-based lytic therapies are commonly employed. Surgical interventions like pulmonary embolectomy are less commonly considered. Various radiological signs have been described concerning PI.[9],[10] The ischaemic necrosis in PI can result in either complete or incomplete PI resulting in either fibrotic scar or resolving opacity in few days, respectively (Melting Ice Cube Sign). Sub-pleural wedge-shaped consolidation with convex borders in the area of low attenuation is a common finding. Consolidation can have truncated apex (Hampton hump sign) or central air lucencies (bubbly consolidation) or thickened vessels leading to the apex of the opacity (vascular sign). The consolidation may also be surrounded by focal ground-glass opacities (halo sign) secondary to adjacent alveolar haemorrhage or vice versa (reversed halo sign). Of all the signs, bubbly consolidation is a very specific radiological marker for PI on CT. According to Revel et al.[10] The presence of central lucencies on CT had 98% specificity and 46% sensitivity for PI. When the vessel sign and negative air bronchogram were combined with central lucencies, specificity increased to 99% but sensitivity decreased to 14%.
| Conclusion | | |
- Identification of air space opacities in a peripheral acinar opacity on non-contrast CT is considered a highly specific imaging marker for PI.
- It can be due to various causes including the embolism, infection, haemorrhage, bronchoalveolar cell carcinoma, etc., and by far the commonest cause is PE. CT pulmonary angiography is to be expedited in such cases.
- Our case report demonstrates this classical finding and highlights the importance of identifying various CT signs of PI.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorships
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Tsao MS, Schraufnagel D, Wang NS. Pathogenesis of pulmonary infarction. Am J Med 1982;72:599-606.  |
| 2. | Kirchner J, Obermann A, Stückradt S, Tüshaus C, Goltz J, Liermann D, et al. Lung infarction following pulmonary embolism: A comparative study on clinical conditions and CT findings to identify predisposing factors. ROFO 2015;187:440-4. |
| 3. | He H, Stein MW, Zalta B, Haramati LB. Pulmonary Infarction: Spectrum of findings on multidetector helical CT. J Thoracic Imaging 2006;21:1-7. |
| 4. | Knight J, Murphy TM, Browning I. The lung in sickle cell disease. Pediatr Pulmonol 1999;28:205-16. |
| 5. | Miniati M, Bottai M, Ciccotosto C, Roberto L, Monti S. Predictors of pulmonary infarction. Medicine (Baltimore) 2015;94:e1488. |
| 6. | Chengsupanimit T, Sundaram B, Lau WB, Keith SW, Kane GC. Clinical characteristics of patients with pulmonary infarction-A retrospective review. Respir Med 2018;139:13-8. |
| 7. | Islam M, Filopei J, Frank M, Ramesh N, Verzosa S, Ehrlich M, et al. Pulmonary infarction secondary to pulmonary embolism: An evolving paradigm. Respirology 2018. doi: 10.1111/resp. 13299. |
| 8. | Terry PB, Buescher PC. Pulmonary infarction: In the beginning: The natural history of pulmonary infarction. Chest 2017;152:1135-9. |
| 9. | Bray TJP, Mortensen KH, Gopalan D. Multimodality imaging of pulmonary infarction. Eur J Radiol 2014;83:2240-54. |
| 10. | Revel M-P, Triki R, Chatellier G, Couchon S, Haddad N, Hernigou A, et al. Is it possible to recognize pulmonary infarction on multisection CT images? Radiology 2007;244:875-82. |
| This article has been cited by | | 1 |
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