Pulmonary infarction characterized by bloody pleural effusion in a young male patient without underlying risk factors: a case report

Pulmonary infarction characterized by bloody pleural effusion in a young male patient without underlying risk factors: a case report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Pulmonary infarction characterized by bloody pleural effusion in a young male patient without underlying risk factors: a case report Akira Kawamura, Kazuki Tanaka, Naoki Kawaguchi, Ryo Suzuki, Takumi Nagasaki, and 7 more This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-6268109/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background Pulmonary infarction, caused by an obstruction of the pulmonary artery, sometimes occurs in young healthy individuals with pulmonary thromboembolism. Thoracentesis is rarely performed because of a small volume of pleural effusion in such cases. We report a case of pulmonary infarction initially diagnosed as bacterial pneumonia and pleurisy, exhibited bloody and exudative pleural effusion on thoracentesis later. Case presentation A 23-year-old male patient previously visited a medical institution after exhibiting left chest pain and bloody sputum for 1 week. The patient was initially diagnosed with bacterial pneumonia and started on oral antibiotics. Chest computed tomography scan revealed a small volume of pleural effusion in the left lung and an extensive consolidation in the left lower lung lobe. He was then diagnosed with left lobar bacterial pneumonia and pleurisy and was started on intravenous antibiotics. However, his condition worsened. After being referred to our hospital, the patient underwent thoracentesis, which revealed bloody and exudative pleural effusion. Deep vein thrombus and pulmonary artery thrombus were detected on contrast-enhanced computed tomography scan performed on the 5th day of admission. The patient was then diagnosed with pulmonary infarction caused by pulmonary thromboembolism, and treatment with anticoagulants was started. After the initiation of anticoagulation therapy, the symptoms and imaging findings gradually improved. Conclusions Pulmonary infarction caused by thromboembolism should be considered for bloody pleural effusion with chest pain and bloody sputum even in young people, particularly those without a predisposition to thrombosis. Pulmonary infarction Pulmonary thromboembolism Bloody pleural effusion Case report Figures Figure 1 Figure 2 Figure 3 Background Pulmonary infarction is caused by an obstruction of the pulmonary artery, resulting in ischemia, hemorrhage, and lung parenchyma necrosis. Pulmonary infarction is associated with bloody sputum, chest pain, and pleuritic friction noise. Further, it occurs in 16–39% of patients with pulmonary thromboembolism (PTE) [ 1 , 2 ]. Patients with pulmonary infarction are more likely to be young and healthy, and the factors associated with pulmonary infarction are increased height and smoking [ 3 ]. Young patients with an uncomplicated cardiopulmonary disease are at high risk of pulmonary infarction if they develop PTE because of their underdeveloped collateral blood vessels. Pulmonary infarction is characterized by semicircular to wedge-shaped infiltrate shadows located basal to the pleural side and thrombi in the pulmonary arteries upstream of the infiltrate shadows on contrast-enhanced computed tomography (CT) scan [ 2 ]. The presence of central lucencies within a peripheral consolidation strongly indicates pulmonary infarction [ 4 ]. According to previous reports on pleural effusions caused by pulmonary embolism, pulmonary infarction is an independent risk factor for developing pleural effusions. The degree of pleural effusion caused by pulmonary embolism is often minimal, which is managed with thoracentesis in a few cases. Nevertheless, it is classically considered an exudative pleural effusion. The bloody appearance is also one of the most characteristic features. In the absence of trauma or malignancy, testing should be initiated to validate or rule out the diagnosis of pulmonary embolism [ 5 ]. Herein, we report a case of pulmonary infarction initially diagnosed as bacterial pneumonia and pleurisy. This case might provide a valuable example of pulmonary infarction attributed to idiopathic PTE in a young male patient diagnosed with pulmonary infarction based on bloody pleural effusion. Case presentation A 23-year-old Japanese male patient visited a general medical practitioner after exhibiting left chest pain and bloody sputum for 1 week. He smoked five cigarettes per day. He was diagnosed with bacterial pneumonia and was started on amoxicillin/clavulanate 4 days back. Upon admission, his body temperature was 37.0°C; blood pressure, 106/55 mmHg; and oxygen saturation on room air, 98%. Auscultation of the left chest revealed coarse crackles. The patient’s chest pain worsened upon inspiration. Electrocardiogram showed a heart rate of 94 beats per minute, and ST-T change was not observed. Chest radiography revealed consolidation in the left lower lung field, and chest CT scan showed consolidation along with ground-glass opacity in the left lung field and pleural effusion (Fig. 1 a and 1 b). Based on the laboratory findings, there was a neutrophil-dominant increase in the white blood cell count of 12.1 × 10 9 /L (normal range [NR] 3.3–8.6 × 10 9 /L) and an increase in the C-reactive protein level of 2.0 mg/L (NR 0.1–1.4 mg/L). The other laboratory values were commonly within the normal range. The blood and sputum culture yielded negative results. Based on the clinical symptoms and radiological findings, the patient’s initial diagnosis was bacterial pneumonia with pleuritis. Treatment with imipenem/cilastatin and azithromycin was initiated. However, the patient’s symptoms gradually worsened. Thoracentesis was performed on the 4th day because of an increase in the pleural effusion volume (Fig. 2 ). The pleural effusion was bloody and exudative and had a high lactate dehydrogenase level. Nevertheless, the culture and cytology results were negative, and there were no other notable findings. Bronchoscopy was scheduled on the 5th day to identify the cause of the effusion. However, contrast-enhanced CT scan was performed on the 5th day to consider the possibility of vascular involvement, such as disruption of arteriovenous malformation, due to the presence of bloody effusion. Contrast-enhanced CT scan revealed consolidation with thromboembolism in the bilateral pulmonary arteries, worsening pleural effusion, and extensive deep vein thrombosis from the right common iliac vein to the popliteal vein (Fig. 3 ). Hence, pulmonary infarction was suspected due to PTE. The patient’s D-dimer level increased to 91.1 µg/dL. The laboratory findings did not show congenital (coagulation factor deficiency) or acquired (e.g., malignancy and opportunistic infection) predisposition to thrombosis. Echocardiography revealed a normal left ventricular contractility and right heart load. After the initiation of anticoagulation therapy (apixaban 20 mg/day), the patient’s symptoms and imaging findings gradually improved (Fig. 3 ). The patient was discharged from the hospital on the 22nd day of admission and was continuously receiving anticoagulation therapy. Discussion and conclusions This is a rare case of pulmonary infarction in a healthy young man diagnosed based on the presence of bloody pleural effusion. According to the physical symptoms and imaging findings upon admission, the patient was initially diagnosed with bacterial pneumonia and pleurisy. This was because he was a healthy young man and did not present with evident risk factors for thrombosis upon admission. Pulmonary infarction commonly occurs in patients with pulmonary embolism. The lungs receive oxygen supply from three sources: pulmonary circulation, bronchial circulation, and airways. Thus, pulmonary infarction is a relatively rare pulmonary complication. However, its actual prevalence is higher than previously believed. One-third of patients with pulmonary embolism develop pulmonary infarction. Younger patients without cardiopulmonary disease are more likely to develop the condition. There are two important lessons that can be learned from this case. First, 96% of patients with pulmonary infarction are at risk for thrombosis [ 6 ], and the risk factors of the condition are current smoking and height [ 3 ]. The patient was assessed for other risk factors for thrombosis. However, none were identified other than smoking. Smoking triggers an inflammatory response that eventually leads to the narrowing of the small airways and emphysema. Therefore, it is considered a major risk factor for chronic obstructive pulmonary disease [ 7 ]. Moreover, smoking increases the permeability of the alveolar capillary barrier in regular smokers [ 8 ]. Thus, it is associated with an increased risk of pulmonary infarction. There are no reports on the association between number of cigarettes smoked and the risk of pulmonary infarction. In this case, the patient had a smoking history of 1.25 pack years. However, the association between smoking and pulmonary infarction may be poor. Young patients with uncomplicated cardiopulmonary disease, as in the current one, are at high risk of pulmonary infarction if they develop PTE. This is because their collateral blood vessels have not yet developed [ 9 ]. A study on predisposition to thrombosis is important. Nevertheless, the patient also had prostatitis prior to being diagnosed with bacterial pneumonia. Considering the possibility of a host being at high risk for infection, such as human immunodeficiency syndrome (HIV) infection [ 10 ], the patient was assessed for HIV infection. However, his test was negative. Second, pulmonary infarction should be suspected in patients with hematologic sputum, chest pain, and pleural effusion, as in the current one. The three signs of suspected pulmonary infarction are bloody sputum, chest pain, and dyspnea, which occur in 16–39% of patients with PTE. In addition, previous reports have assessed PTE in patients with or without pleural effusions. Results showed that patients with pleural effusions are more likely to present with severe pulmonary embolism (with a higher incidence of central involvement and right heart failure) and increased inflammation (as evidenced by findings such as high C-reactive protein levels and pulmonary infarction), as in this case. The risk of pulmonary infarction attributed to pulmonary embolism should be noted at an early stage in this case. PTE causes pleural effusions in 26% of all cases. If causes other than PTE are ruled out, pleural effusions caused by PTE itself are observed in approximately 14% of cases. The pleural effusion volume itself is low in most cases, and pleural drainage is rarely performed [ 11 ]. Several studies have analyzed the characteristics of pleural effusions in patients with PTE who present with pleural effusions [ 12 – 14 ]. Numerous patients have bloody or blood-tinged pleural effusions, and pleural effusions caused by PTE are usually exudative, which is consistent with the current case. In this case, CT scan performed after thoracentesis showed infiltrating and wedge-shaped shadows, which are characteristic findings of pulmonary infarction. However, the first and second CT scan images were not clear due to the presence of extensive consolidation and pleural effusion, which contributed to the time required for the diagnosis. Notably, pulmonary infarction caused by pulmonary thromboembolism should be considered when bloody pleural effusion is identified in a healthy young male patient. Declarations Ethics approval and consent to participate Ethics approval is not needed for case reports according to our institutional (Fujieda Municipal General Hospital) review board. Written informed consent for publication of this case and accompanying images was obtained from the patient. Consent for publication Written informed consent was obtained from the patient for publication of this case report and any accompanying images. Availability of data and materials This study is a case report, and all analyzed data are presented within the manuscript. Images related to the case have been provided with the submission, and no additional datasets are available. Competing interests The authors declare no competing interests. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Authors' contributions AK performed the thoracentesis procedure and case report writing. AK and NK contributed to the patient follow-up. KT and SM wrote the revision of the manuscript. All authors have reviewed the manuscript and approved the final version for submission. Acknowledgements The authors would like to acknowledge the patient’s contribution to this report. The authors also thank Enago (www.enago.jp) for editing a draft of this manuscript. Abbreviations PTE Pulmonary thromboembolism CT Computed tomography NR Normal range HIV Human immunodeficiency syndrome References Miniati M. Pulmonary Infarction: An Often Unrecognized Clinical Entity. Semin Thromb Hemost. 2016;42(8):865–9. https://doi.org/10.1055/s-0036-1592310 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;23(9):866–72. https://doi.org/10.1111/resp.13299 Miniati M, Bottai M, Ciccotosto C, Roberto L, Monti S. Predictors of Pulmonary Infarction. Medicine (Baltimore). 2015;94(41):e1488. https://doi.org/10.1097/MD.0000000000001488 Revel MP, 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(3):875–82. https://doi.org/10.1148/radiol.2443060846 Cha SI, Shin KM, Lee J, Hwangbo Y, Yoo SS, Lee J, et al. Clinical relevance of pulmonary infarction in patients with pulmonary embolism. Thromb Res. 2012;130(3):e1–5. https://doi.org/10.1016/j.thromres.2012.03.012 He H, Stein MW, Zalta B, Haramati LB. Pulmonary infarction: spectrum of findings on multidetector helical CT. J Thorac Imaging. 2006;21(1):1–7. https://doi.org/10.1097/01.rti.0000187433.06762.fb Global Initiative for Chronic Obstructive Lung Disease. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease, 2025 Report (accessed 5 March 2025). Mason GR, Uszler JM, Effros RM, Reid E. Rapidly reversible alterations of pulmonary epithelial permeability induced by smoking. Chest. 1983;83(1):6–11. https://doi.org/10.1378/chest.83.1.6 Gwozdz AM, de Jong CMM, Fialho LS, Likitabhorn T, Sossi F, Jaber PB, et al. Development of an international standard set of outcome measures for patients with venous thromboembolism: an International Consortium for Health Outcomes Measurement consensus recommendation. Lancet Haematol. 2022;9(9):e698–706. https://doi.org/10.1016/S2352-3026(22)00215-0 Akaba T, Kondo M, Kobayashi F, Yagi O, Takeyama K, et al. A case of pulmonary infarction induced by undiagnosed HIV. Respir Med Case Rep. 2020;31:101293. https://doi.org/10.1016/j.rmcr.2020.101293 Findik S. Pleural effusion in pulmonary embolism. Curr Opin Pulm Med. 2012;18(4):347–54. https://doi.org/10.1097/MCP.0b013e32835395d5 Porcel JM, Madroñero AB, Pardina M, Esquerda MVA, Light RW. Analysis of pleural effusions in acute pulmonary embolism: radiological and pleural fluid data from 230 patients. Respirology. 2007;12(2):234–9. https://doi.org/10.1111/j.1440-1843.2006.01026.x Candeira SR, Blasco LH, Soler MJ, Aranda AMI. Biochemical and cytologic characteristics of pleural effusions secondary to pulmonary embolism. Chest. 2002;121(2):465–9. https://doi.org/10.1378/chest.121.2.465 Bynum LJ, Wilson JE 3 rd . Characteristics of pleural effusions associated with pulmonary embolism. Arch Intern Med. 1976;136(2):159–62. https://doi.org/10.1001/archinte.1976.03630020019005 Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-6268109","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":458196810,"identity":"bed3c213-4a27-44d7-8319-9ce716ef708b","order_by":0,"name":"Akira Kawamura","email":"","orcid":"","institution":"Fujieda Municipal General Hospital","correspondingAuthor":false,"prefix":"","firstName":"Akira","middleName":"","lastName":"Kawamura","suffix":""},{"id":458196812,"identity":"e5b1b0e6-b7a7-48d8-ba48-20ac9254b8af","order_by":1,"name":"Kazuki 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Hospital","correspondingAuthor":false,"prefix":"","firstName":"Naoki","middleName":"","lastName":"Koshimizu","suffix":""}],"badges":[],"createdAt":"2025-03-20 09:23:07","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-6268109/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-6268109/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":83199370,"identity":"ac9dbe03-a7eb-4c9d-bc33-d7f7ce4f34ac","added_by":"auto","created_at":"2025-05-21 06:07:48","extension":"jpg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":129988,"visible":true,"origin":"","legend":"\u003cp\u003eChest imaging findings on admission\u003c/p\u003e\n\u003cp\u003e(\u003cstrong\u003eA\u003c/strong\u003e) Chest radiography showed consolidation in the left lower lung field.\u003c/p\u003e\n\u003cp\u003e(\u003cstrong\u003eB\u003c/strong\u003e) Chest computed tomography scan showed mixture of consolidation and ground glass opacity in left lower lobs with small amount of left pleural effusion.\u003c/p\u003e","description":"","filename":"1.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6268109/v1/4b361d8992a07f46d29b53d9.jpg"},{"id":83200674,"identity":"699b25b4-ec1a-485f-b7fe-8972e34aae15","added_by":"auto","created_at":"2025-05-21 06:15:48","extension":"jpg","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":124197,"visible":true,"origin":"","legend":"\u003cp\u003eChest computed tomography (CT) imaging 4 days after admission\u003c/p\u003e\n\u003cp\u003eCT scan revealed a dense consolidation in left lower lobe, pleural effusion was increased and pressure-drainage atelectasis was seen, and consolidation was seen on the right lower lobe pleural side.\u003c/p\u003e","description":"","filename":"2.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6268109/v1/5fce7c70c697ce31764add07.jpg"},{"id":83200675,"identity":"f40db897-6fca-4808-8391-6f9558b59de7","added_by":"auto","created_at":"2025-05-21 06:15:48","extension":"jpg","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":131172,"visible":true,"origin":"","legend":"\u003cp\u003e(\u003cstrong\u003eA\u003c/strong\u003e) Chest contrast-enhanced computed tomography (CT) scan revealed deterioration of pleural-based consolidation and ground glass opacity in left lower lobes 5 days after admission. Multiple thromboses were detected in pulmonary arteries. The decrease of pleural effusion was seen in left lung after thoracentesis.\u003c/p\u003e\n\u003cp\u003e(\u003cstrong\u003eB\u003c/strong\u003e) Chest CT revealed improvement of consolidation and pleural effusion in both lungs one month after treatment. Thromboses in pulmonary arteries has shrunk.\u003c/p\u003e","description":"","filename":"3.jpg","url":"https://assets-eu.researchsquare.com/files/rs-6268109/v1/06366cfa7900ce21503ff834.jpg"},{"id":84535233,"identity":"8dd79351-079f-4e51-8f64-85fe24e6d6a1","added_by":"auto","created_at":"2025-06-13 07:01:45","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":819305,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-6268109/v1/765ff99c-37dc-4c79-9604-1eb7559d58f7.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Pulmonary infarction characterized by bloody pleural effusion in a young male patient without underlying risk factors: a case report","fulltext":[{"header":"Background","content":"\u003cp\u003ePulmonary infarction is caused by an obstruction of the pulmonary artery, resulting in ischemia, hemorrhage, and lung parenchyma necrosis. Pulmonary infarction is associated with bloody sputum, chest pain, and pleuritic friction noise. Further, it occurs in 16\u0026ndash;39% of patients with pulmonary thromboembolism (PTE) [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. Patients with pulmonary infarction are more likely to be young and healthy, and the factors associated with pulmonary infarction are increased height and smoking [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. Young patients with an uncomplicated cardiopulmonary disease are at high risk of pulmonary infarction if they develop PTE because of their underdeveloped collateral blood vessels. Pulmonary infarction is characterized by semicircular to wedge-shaped infiltrate shadows located basal to the pleural side and thrombi in the pulmonary arteries upstream of the infiltrate shadows on contrast-enhanced computed tomography (CT) scan [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. The presence of central lucencies within a peripheral consolidation strongly indicates pulmonary infarction [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. According to previous reports on pleural effusions caused by pulmonary embolism, pulmonary infarction is an independent risk factor for developing pleural effusions. The degree of pleural effusion caused by pulmonary embolism is often minimal, which is managed with thoracentesis in a few cases. Nevertheless, it is classically considered an exudative pleural effusion. The bloody appearance is also one of the most characteristic features. In the absence of trauma or malignancy, testing should be initiated to validate or rule out the diagnosis of pulmonary embolism [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. Herein, we report a case of pulmonary infarction initially diagnosed as bacterial pneumonia and pleurisy. This case might provide a valuable example of pulmonary infarction attributed to idiopathic PTE in a young male patient diagnosed with pulmonary infarction based on bloody pleural effusion.\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cp\u003eA 23-year-old Japanese male patient visited a general medical practitioner after exhibiting left chest pain and bloody sputum for 1 week. He smoked five cigarettes per day. He was diagnosed with bacterial pneumonia and was started on amoxicillin/clavulanate 4 days back. Upon admission, his body temperature was 37.0°C; blood pressure, 106/55 mmHg; and oxygen saturation on room air, 98%. Auscultation of the left chest revealed coarse crackles. The patient’s chest pain worsened upon inspiration. Electrocardiogram showed a heart rate of 94 beats per minute, and ST-T change was not observed. Chest radiography revealed consolidation in the left lower lung field, and chest CT scan showed consolidation along with ground-glass opacity in the left lung field and pleural effusion (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003ea and \u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eb). Based on the laboratory findings, there was a neutrophil-dominant increase in the white blood cell count of 12.1 × 10\u003csup\u003e9\u003c/sup\u003e/L (normal range [NR] 3.3–8.6 × 10\u003csup\u003e9\u003c/sup\u003e/L) and an increase in the C-reactive protein level of 2.0 mg/L (NR 0.1–1.4 mg/L). The other laboratory values were commonly within the normal range. The blood and sputum culture yielded negative results. Based on the clinical symptoms and radiological findings, the patient’s initial diagnosis was bacterial pneumonia with pleuritis.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eTreatment with imipenem/cilastatin and azithromycin was initiated. However, the patient’s symptoms gradually worsened. Thoracentesis was performed on the 4th day because of an increase in the pleural effusion volume (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). The pleural effusion was bloody and exudative and had a high lactate dehydrogenase level. Nevertheless, the culture and cytology results were negative, and there were no other notable findings. Bronchoscopy was scheduled on the 5th day to identify the cause of the effusion. However, contrast-enhanced CT scan was performed on the 5th day to consider the possibility of vascular involvement, such as disruption of arteriovenous malformation, due to the presence of bloody effusion. Contrast-enhanced CT scan revealed consolidation with thromboembolism in the bilateral pulmonary arteries, worsening pleural effusion, and extensive deep vein thrombosis from the right common iliac vein to the popliteal vein (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e). Hence, pulmonary infarction was suspected due to PTE. The patient’s D-dimer level increased to 91.1 µg/dL. The laboratory findings did not show congenital (coagulation factor deficiency) or acquired (e.g., malignancy and opportunistic infection) predisposition to thrombosis. Echocardiography revealed a normal left ventricular contractility and right heart load. After the initiation of anticoagulation therapy (apixaban 20 mg/day), the patient’s symptoms and imaging findings gradually improved (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003e). The patient was discharged from the hospital on the 22nd day of admission and was continuously receiving anticoagulation therapy.\u003c/p\u003e "},{"header":"Discussion and conclusions","content":"\u003cp\u003eThis is a rare case of pulmonary infarction in a healthy young man diagnosed based on the presence of bloody pleural effusion. According to the physical symptoms and imaging findings upon admission, the patient was initially diagnosed with bacterial pneumonia and pleurisy. This was because he was a healthy young man and did not present with evident risk factors for thrombosis upon admission. Pulmonary infarction commonly occurs in patients with pulmonary embolism. The lungs receive oxygen supply from three sources: pulmonary circulation, bronchial circulation, and airways. Thus, pulmonary infarction is a relatively rare pulmonary complication. However, its actual prevalence is higher than previously believed. One-third of patients with pulmonary embolism develop pulmonary infarction. Younger patients without cardiopulmonary disease are more likely to develop the condition. There are two important lessons that can be learned from this case. First, 96% of patients with pulmonary infarction are at risk for thrombosis [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e], and the risk factors of the condition are current smoking and height [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. The patient was assessed for other risk factors for thrombosis. However, none were identified other than smoking. Smoking triggers an inflammatory response that eventually leads to the narrowing of the small airways and emphysema. Therefore, it is considered a major risk factor for chronic obstructive pulmonary disease [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e]. Moreover, smoking increases the permeability of the alveolar capillary barrier in regular smokers [\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. Thus, it is associated with an increased risk of pulmonary infarction. There are no reports on the association between number of cigarettes smoked and the risk of pulmonary infarction. In this case, the patient had a smoking history of 1.25 pack years. However, the association between smoking and pulmonary infarction may be poor. Young patients with uncomplicated cardiopulmonary disease, as in the current one, are at high risk of pulmonary infarction if they develop PTE. This is because their collateral blood vessels have not yet developed [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. A study on predisposition to thrombosis is important. Nevertheless, the patient also had prostatitis prior to being diagnosed with bacterial pneumonia. Considering the possibility of a host being at high risk for infection, such as human immunodeficiency syndrome (HIV) infection [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e], the patient was assessed for HIV infection. However, his test was negative. Second, pulmonary infarction should be suspected in patients with hematologic sputum, chest pain, and pleural effusion, as in the current one. The three signs of suspected pulmonary infarction are bloody sputum, chest pain, and dyspnea, which occur in 16–39% of patients with PTE. In addition, previous reports have assessed PTE in patients with or without pleural effusions. Results showed that patients with pleural effusions are more likely to present with severe pulmonary embolism (with a higher incidence of central involvement and right heart failure) and increased inflammation (as evidenced by findings such as high C-reactive protein levels and pulmonary infarction), as in this case. The risk of pulmonary infarction attributed to pulmonary embolism should be noted at an early stage in this case. PTE causes pleural effusions in 26% of all cases. If causes other than PTE are ruled out, pleural effusions caused by PTE itself are observed in approximately 14% of cases. The pleural effusion volume itself is low in most cases, and pleural drainage is rarely performed [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e]. Several studies have analyzed the characteristics of pleural effusions in patients with PTE who present with pleural effusions [\u003cspan additionalcitationids=\"CR13\" citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e–\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e]. Numerous patients have bloody or blood-tinged pleural effusions, and pleural effusions caused by PTE are usually exudative, which is consistent with the current case. In this case, CT scan performed after thoracentesis showed infiltrating and wedge-shaped shadows, which are characteristic findings of pulmonary infarction. However, the first and second CT scan images were not clear due to the presence of extensive consolidation and pleural effusion, which contributed to the time required for the diagnosis. Notably, pulmonary infarction caused by pulmonary thromboembolism should be considered when bloody pleural effusion is identified in a healthy young male patient.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eEthics approval is not needed for case reports according to our institutional (Fujieda Municipal General Hospital) review board. Written informed consent for publication of this case and accompanying images was obtained from the patient.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWritten informed consent was obtained from the patient for publication of this case report and any accompanying images.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis study is a case report, and all analyzed data are presented within the manuscript. Images related to the case have been provided with the submission, and no additional datasets are available.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors' contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAK performed the thoracentesis procedure and case report writing. AK and NK contributed to the patient follow-up. KT and SM wrote the revision of the manuscript. All authors have reviewed the manuscript and approved the final version for submission.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors would like to acknowledge the patient’s contribution to this report. The authors also thank Enago (www.enago.jp) for editing a draft of this manuscript.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003ePTE\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Pulmonary thromboembolism\u003c/p\u003e\n\u003cp\u003eCT\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Computed tomography\u003c/p\u003e\n\u003cp\u003eNR\u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp; \u0026nbsp;Normal range\u003c/p\u003e\n\u003cp\u003eHIV \u0026nbsp; \u0026nbsp; \u0026nbsp; Human immunodeficiency syndrome\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eMiniati M. Pulmonary Infarction: An Often Unrecognized Clinical Entity. Semin Thromb Hemost. 2016;42(8):865\u0026ndash;9. https://doi.org/10.1055/s-0036-1592310\u003c/li\u003e\n\u003cli\u003eIslam M, Filopei J, Frank M, Ramesh N, Verzosa S, Ehrlich M, et al. Pulmonary infarction secondary to pulmonary embolism: An evolving paradigm. Respirology. 2018;23(9):866\u0026ndash;72. https://doi.org/10.1111/resp.13299\u003c/li\u003e\n\u003cli\u003eMiniati M, Bottai M, Ciccotosto C, Roberto L, Monti S. Predictors of Pulmonary Infarction. Medicine (Baltimore). 2015;94(41):e1488. https://doi.org/10.1097/MD.0000000000001488\u003c/li\u003e\n\u003cli\u003eRevel MP, 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(3):875\u0026ndash;82. https://doi.org/10.1148/radiol.2443060846\u003c/li\u003e\n\u003cli\u003eCha SI, Shin KM, Lee J, Hwangbo Y, Yoo SS, Lee J, et al. Clinical relevance of pulmonary infarction in patients with pulmonary embolism. Thromb Res. 2012;130(3):e1\u0026ndash;5. https://doi.org/10.1016/j.thromres.2012.03.012\u003c/li\u003e\n\u003cli\u003eHe H, Stein MW, Zalta B, Haramati LB. Pulmonary infarction: spectrum of findings on multidetector helical CT. J Thorac Imaging. 2006;21(1):1\u0026ndash;7. https://doi.org/10.1097/01.rti.0000187433.06762.fb\u003c/li\u003e\n\u003cli\u003eGlobal Initiative for Chronic Obstructive Lung Disease. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease, 2025 Report (accessed 5 March 2025).\u003c/li\u003e\n\u003cli\u003eMason GR, Uszler JM, Effros RM, Reid E. Rapidly reversible alterations of pulmonary epithelial permeability induced by smoking. Chest. 1983;83(1):6\u0026ndash;11. https://doi.org/10.1378/chest.83.1.6\u003c/li\u003e\n\u003cli\u003eGwozdz AM, de Jong CMM, Fialho LS, Likitabhorn T, Sossi F, Jaber PB, et al. Development of an international standard set of outcome measures for patients with venous thromboembolism: an International Consortium for Health Outcomes Measurement consensus recommendation. Lancet Haematol. 2022;9(9):e698\u0026ndash;706. https://doi.org/10.1016/S2352-3026(22)00215-0\u003c/li\u003e\n\u003cli\u003eAkaba T, Kondo M, Kobayashi F, Yagi O, Takeyama K, et al. A case of pulmonary infarction induced by undiagnosed HIV. Respir Med Case Rep. 2020;31:101293. https://doi.org/10.1016/j.rmcr.2020.101293\u003c/li\u003e\n\u003cli\u003eFindik S. Pleural effusion in pulmonary embolism. Curr Opin Pulm Med. 2012;18(4):347\u0026ndash;54. https://doi.org/10.1097/MCP.0b013e32835395d5\u003c/li\u003e\n\u003cli\u003ePorcel JM, Madro\u0026ntilde;ero AB, Pardina M, Esquerda MVA, Light RW. Analysis of pleural effusions in acute pulmonary embolism: radiological and pleural fluid data from 230 patients. Respirology. 2007;12(2):234\u0026ndash;9. https://doi.org/10.1111/j.1440-1843.2006.01026.x\u003c/li\u003e\n\u003cli\u003eCandeira SR, Blasco LH, Soler MJ, Aranda AMI. Biochemical and cytologic characteristics of pleural effusions secondary to pulmonary embolism. Chest. 2002;121(2):465\u0026ndash;9. https://doi.org/10.1378/chest.121.2.465\u003c/li\u003e\n\u003cli\u003eBynum LJ, Wilson JE 3\u003csup\u003erd\u003c/sup\u003e. Characteristics of pleural effusions associated with pulmonary embolism. Arch Intern Med. 1976;136(2):159\u0026ndash;62. https://doi.org/10.1001/archinte.1976.03630020019005\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Pulmonary infarction, Pulmonary thromboembolism, Bloody pleural effusion, Case report","lastPublishedDoi":"10.21203/rs.3.rs-6268109/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-6268109/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cb\u003eBackground\u003c/b\u003e\u003c/p\u003e \u003cp\u003ePulmonary infarction, caused by an obstruction of the pulmonary artery, sometimes occurs in young healthy individuals with pulmonary thromboembolism. Thoracentesis is rarely performed because of a small volume of pleural effusion in such cases. We report a case of pulmonary infarction initially diagnosed as bacterial pneumonia and pleurisy, exhibited bloody and exudative pleural effusion on thoracentesis later.\u003c/p\u003e\u003cp\u003e\u003cb\u003eCase presentation\u003c/b\u003e\u003c/p\u003e \u003cp\u003eA 23-year-old male patient previously visited a medical institution after exhibiting left chest pain and bloody sputum for 1 week. The patient was initially diagnosed with bacterial pneumonia and started on oral antibiotics. Chest computed tomography scan revealed a small volume of pleural effusion in the left lung and an extensive consolidation in the left lower lung lobe. He was then diagnosed with left lobar bacterial pneumonia and pleurisy and was started on intravenous antibiotics. However, his condition worsened. After being referred to our hospital, the patient underwent thoracentesis, which revealed bloody and exudative pleural effusion. Deep vein thrombus and pulmonary artery thrombus were detected on contrast-enhanced computed tomography scan performed on the 5th day of admission. The patient was then diagnosed with pulmonary infarction caused by pulmonary thromboembolism, and treatment with anticoagulants was started. After the initiation of anticoagulation therapy, the symptoms and imaging findings gradually improved.\u003c/p\u003e\u003cp\u003e\u003cb\u003eConclusions\u003c/b\u003e\u003c/p\u003e \u003cp\u003ePulmonary infarction caused by thromboembolism should be considered for bloody pleural effusion with chest pain and bloody sputum even in young people, particularly those without a predisposition to thrombosis.\u003c/p\u003e","manuscriptTitle":"Pulmonary infarction characterized by bloody pleural effusion in a young male patient without underlying risk factors: a case report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-05-21 06:07:43","doi":"10.21203/rs.3.rs-6268109/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"4fb252ec-5000-4ec7-bc51-294e721293bf","owner":[],"postedDate":"May 21st, 2025","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2025-06-13T06:53:40+00:00","versionOfRecord":[],"versionCreatedAt":"2025-05-21 06:07:43","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-6268109","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-6268109","identity":"rs-6268109","version":["v1"]},"buildId":"8U1c8b4HqxoKbykW_rLl7","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}