Intrapericardial Corticosteroid Therapy for Recurrent Malignant Pericardial Effusion: A Case Series | 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 Intrapericardial Corticosteroid Therapy for Recurrent Malignant Pericardial Effusion: A Case Series Nuri Lee, Yoojin Kim, Hyukjin Park This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8660978/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 28 Mar, 2026 Read the published version in Cardio-Oncology → Version 1 posted 9 You are reading this latest preprint version Abstract Background Malignant pericardial effusion (PE) and subsequent effusive-constrictive pericarditis (ECP) are significant clinical challenges in patients with advanced cancer. Case presentation: We report three cases of patients with metastatic breast or lung cancer who experienced recurrent, life-threatening cardiac tamponade despite multiple pericardiocenteses (PCC) and systemic anti-inflammatory treatment (AIT). In all cases, pericardial disease remained refractory to conventional management, and chronic systemic corticosteroid use led to debilitating side effects. Following complete drainage of the PE, a single high-dose bolus of 200 mg triamcinolone was administered via an intrapericardial catheter with a 12-hour clamping protocol. This intervention resulted in sustained pericardial stabilization for 8 to 47 months across all three patients. Remarkably, this cardiac stability was maintained independently of the underlying oncological status. Conclusion High-dose (200 mg) intrapericardial corticosteroid therapy is an effective and safe intervention for refractory malignant PE. pericardiocentesis cancer pericardial effusion Figures Figure 1 Figure 2 Figure 3 Figure 4 Background Pericardial effusion (PE) is increasingly observed in patients with cancer, likely reflecting advancements in cancer therapies and improved survival. While malignant infiltration remains the predominant cause, some cases arise from treatment-related or cancer-associated inflammation [ 1 , 2 ]. PE can progress to cardiac tamponade, requiring urgent pericardiocentesis (PCC). However, a subset of patients develop persistent symptoms due to pericardial adhesion and constrictive physiology (CP) after PCC, which may disrupt cancer treatment and worsen clinical outcomes [ 3 , 4 ]. Though anti-inflammatory therapy (AIT) can potentially reverse CP, the risks associated with systemic corticosteroid often limit their use in this population [ 5 , 6 ]. Here, we report three cases in which intrapericardial triamcinolone administration improved the clinical outcomes of cancer patients who required repeated PCC for malignant PE. Case presentation Case 1 A 40-year-old female patient with hormone receptor-negative and human epidermal growth factor receptor 2 (HER2)-positive metastatic breast cancer (MBC) presented to our emergency department (ED). She had been diagnosed with MBC six years prior, and had been managed with dual HER2-targeted therapy consisting of trastuzumab and pertuzumab for four years. Two years ago, the patient experienced her first episode of cardiac tamponade, necessitating urgent PCC, after which malignant cells were identified in the PE (Fig. 1 A, additional file 1). Though the PE was successfully drained, she subsequently developed effusive-constrictive pericarditis (ECP) (Figs. 1 B, 1 C, and additional file 2). Systemic AIT with prednisolone (started with 0.5 mg/kg/day, gradually tapered for 2 months) and colchicine (0.6 mg/day) was initiated to manage the inflammatory process and CP. Concurrent with this event, her breast cancer showed progression in follow-up imaging studies, leading to regimen change from dual HER2 blockade to trastuzumab emtansine (T-DM1). For the following two years, she required two additional PCC procedures and repeated cycles of systemic AIT for recurrent PE, but the patient’s overall oncological status remained stable under T-DM1 therapy. Over the past six months, the frequency of PE recurrence accelerated significantly, with two episodes of cardiac tamponade occurring at three-month intervals. Each episode was managed with PCC and systemic AIT. The current admission was prompted by a rapid and severe clinical decline. Only two weeks after her most recent PCC, the patient returned to the ED with overt cardiac tamponade. She presented with New York Heart Association (NYHA) class IV dyspnea and profound peripheral edema. Transthoracic echocardiography confirmed a massive PE with signs of cardiac tamponade, indicating her condition had become refractory to conventional systemic AIT and repeated drainage. Beyond the refractory nature of the PE, the patient suffered significantly from the adverse effects of chronic systemic AIT. She reported severe generalized weakness and muscle wasting attributed to prolonged corticosteroid use, alongside persistent diarrhea caused by colchicine. Consequently, we decided to shift our management strategy. Systemic AIT was maintained at a minimal dose (prednisolone 10 mg/day, colchicine 0.6 mg/day, and azathioprine 50 mg/day). A repeat PCC was performed. Following complete drainage, we initially attempted a fragmented dosing protocol: 40 mg (1 mL) of triamcinolone acetonide was injected via the catheter daily for three consecutive days (total 120 mg). After each injection, the catheter was clamped for 12 hours to maximize local drug exposure. However, a follow-up echocardiogram performed one week later revealed a rapid recurrence of large PE (Fig. 1 D, additional file 3), indicating that this low-dose fragmented dosing was ineffective in controlling the intense pericardial inflammation. So we chose a more aggressive dosing. After another complete drainage of the PE, a single high-dose bolus of 200 mg of triamcinolone was administered through the intrapericardial catheter (Fig. 2 ). Simultaneously, given the previous oncological stability but cardiac instability, her anticancer therapy was switched from T-DM1 to trastuzumab deruxtecan (T-DxD). One week after the 200 mg triamcinolone injection, follow-up echocardiography showed significant improvement. Though residual pericardial thickening, adhesions, CP persisted, the PE had been reduced to a scanty amount (Fig. 1 E, additional file 4). The patient’s heart failure (HF) symptoms became tolerable, and her N-terminal pro-B-type natriuretic peptide (NT-proBNP) level decreased from 1,480 pg/mL (when CP developed during the index hospitalization) to 508 pg/mL (at the time of discharge), so she was successfully discharged. Recognizing that systemic AIT had provided marginal benefit while causing substantial adverse effects, we completely withdrew all systemic AIT. Remarkably, during the 16 months of T-DxD therapy, the patient remained free of cardiac tamponade or any heart-related hospitalizations, with only a stable, small amount of PE observed on serial imaging. Importantly, the stabilization of the pericardial disease appeared independent of her oncological status. Despite the transition to T-DxD, the MBC eventually showed signs of disease progression. Consequently, several lines of salvage therapy were administered, including four cycles of doxorubicin/cyclophosphamide followed by capecitabine and lapatinib. Despite these therapies, the MBC continued to progress, ultimately leading to the patient’s death (47 months after intrapericardial triamcinolone therapy). But it’s noteworthy that the pericardial disease remained stable throughout this period – following the administration of 200 mg of intrapericardial triamcinolone, the patient experienced no significant increase in PE or clinical events such as cardiac tamponade. Remarkably, even on imaging obtained only one month before her death, the PE remained at a scanty amount (Fig. 1 F, additional file 5). Case 2 A 63-year-old female with lung adenocarcinoma and multi-organ metastases, who had been treated with dacomitinib for one year, presented to the ED with NYHA class IV dyspnea. Echocardiography revealed a massive PE with tamponade physiology, necessitating emergency PCC, which revealed malignant cells in the PE. Follow-up echocardiography the next day confirmed complete drainage but also showed significant pericardial thickening, adhesions, and CP (Fig. 3 A, additional file 6). Elevated NT-proBNP level of 1,070 pg/mL and serum C-reactive protein (CRP) level of 7.03 mg/dL supported the diagnosis of inflammatory constrictive pericarditis. Systemic AIT was initiated with prednisolone (0.25 mg/kg/day, tapered for 2.5 months) and colchicine (1.2 mg/day). Initially, the patient showed a favorable response: at two weeks, the NT-proBNP level decreased to 220 pg/mL, and HF symptoms nearly resolved. However, one month after complete discontinuation of prednisolone, she was readmitted with recurrent pleuritic chest pain, dyspnea, and moderate PE. For this ECP, we resumed systemic AIT with a higher dose of prednisolone (0.5 mg/kg/day) and added methotrexate (15 mg/week). Colchicine was omitted due to severe treatment-limiting diarrhea. Despite intensified AIT and stable oncological status under dacomitinib, cardiac tamponade recurred within one month, requiring a second PCC (five months after the first procedure) (Fig. 3 B, additional file 7). Post-procedure imaging showed persistent CP, though inflammatory markers were only mildly elevated (CRP 3.36 mg/dL). Systemic AIT was withdrawn due to lack of efficacy and progressive sarcopenia caused by prednisolone treatment. However, cardiac tamponade recurred again just one month later, even without significant progression of the lung cancer. Following a third PCC, the PE re-accumulated within another month. At this stage, slight progression of abdominal and pelvic metastases was observed, leading to a switch from dacomitinib to a pemetrexed and cisplatin regimen. Nevertheless, cardiac tamponade recurred for the fourth time, only four months after the third procedure. Because of the repetitive and refractory cardiac tamponade events, we performed a fourth PCC followed by intrapericardial injection of 200 mg of triamcinolone, as the same protocol as case 1 (complete drainage and triamcinolone injection, followed by a 12-hour catheter clamping). Post-procedure echocardiography revealed no significant PE, though pericardial thickening and CP remained (Fig. 3 C, additional file 8). Though the NT-proBNP level rose to 968 pg/mL, the patient’s HF symptoms improved significantly to NYHA class II. Consequently, no further systemic AIT was administered, and the pemetrexed-based chemotherapy was maintained (cisplatin was discontinued after four cycles). The patient remained on pemetrexed for a total of 15 months. Though the lung cancer began to show gradual progression after eight months, the pericardial disease has remained remarkably stable (Fig. 3 D, additional file 9). During the 17 months since the fourth PCC and intrapericardial triamcinolone injection, the PE has been maintained at a scanty to small amount. Most importantly, there have been no recurrences of cardiac tamponade or any hospitalizations related to cardiovascular diseases. Case 3 A 46-year-old female with MBC was admitted to our ED with NYHA class III dyspnea, Her oncological history was as follows: six years prior, she was diagnosed with estrogen receptor positive/progesterone receptor positive breast cancer and underwent six cycles of neoadjuvant chemotherapy (docetaxel and epirubicin), follow by a left breast-conserving surgery. After completing adjuvant radiation therapy, eight cycles of capecitabine and transitioning to tamoxifen maintenance, she remained stable for four years until lung metastases were detected. Her treatment was then switched to letrozole, ribociclib, and goserelin, however, the patient was lost to follow-up for ten months due to concerns over treatment-induced alopecia. Upon her return, multiple (hepatic, peritoneal, uterine, skeletal, pleural, and pericardial) metastases were detected, and she resumed capecitabine therapy. The current presentation to the ED with dyspnea occurred three months after resuming capecitabine. Though a chest computed tomography (CT) indicated stable disease of her MBC, it revealed a new, large PE causing cardiac tamponade. Urgent PCC was performed and presence of malignant cells in the PE was cytologically confirmed. While complete drainage was achieved, follow-up echocardiography showed diffuse pericardial thickening, adhesions, and CP (Fig. 4 A, additional file 10). Laboratory findings showed mildly elevated NT-proBNP level of 548 pg/mL and CRP level of 0.83 mg/dL. She was discharged on systemic AIT consisting of prednisolone (0.5 mg/kg/day with a 5 mg/day taper every two weeks) and colchicine (0.6 mg/day). Despite being on active systemic AIT and capecitabine therapy, cardiac tamponade recurred only 1.5 months after the first PCC (Fig. 4 B, additional file 11). At this point, the patient presented with significant sarcopenia due to her prolonged disease course, raising concerns about the morbidities of escalating or continuing systemic corticosteroids. Also, since the tamponade recurred while she was still receiving systemic AIT, the pericardial disease was deemed refractory to systemic AIT. Rather than escalating the systemic dose, we performed a second PCC followed by an intrapericardial injection of 200 mg of triamcinolone using the same protocol as the previous cases. Following this, echocardiography showed persistent pericardial thickening and adhesions, but only a small amount of residual PE. Levels of biomarkers remained stable (NT-proBNP 371 pg/mL, CRP 0.62 mg/dL). One month after the second PCC, the patient returned to the ED with NYHA class III dyspnea. However, CT imaging confirmed that this was due to bilateral pleural effusions, with only a small PE (Fig. 4 C). The relief of symptoms after thoracentesis confirmed that this event was not a recurrence of cardiac tamponade. At this point, her MBC was deemed to have progressed significantly. Accordingly, capecitabine, which had been withheld since the second episode of cardiac tamponade, was replaced with nanoparticle albumin-bound paclitaxel and administered for four months. Ongoing disease progression subsequently necessitated a switch to gemcitabine and carboplatin, which has been administered for three months to date. While her MBC has shown such progression, her pericardial disease has remained remarkably quiescent. During the eight months since the intrapericardial triamcinolone therapy, the PE has remained small in amount (Fig. 4 D, additional file 12), and her subjective dyspnea has been well-managed in the outpatient setting without any further cardiac events. Discussion The main finding of this case series is the remarkable stabilization of the pericardial disease after high-dose intrapericardial corticosteroid (IPC) therapy in patients with metastatic cancer and malignant PE. In all three cases, the patients suffered from recurrent, refractory PE and life-threatening cardiac tamponade despite initial management with PCC and systemic AIT. Crucially, these cardiac events occurred independently of the status of their extra-pericardial metastases. Cardiac tamponade recurred even when the primary malignancy remained stable, but after a single intrapericardial injection of 200 mg triamcinolone, the pericardial disease achieved sustained stabilization, remaining free of significant recurrence for 8 to 47 months. Remarkably, this cardiac stability persisted even as the underlying metastatic cancers eventually progressed in other organs. The management of pericardial disease in oncology patients presents a unique clinical challenge. CP and ECP remain well-documented sequelae of PCC and are significant predictors of poor prognosis [ 3 ]. While systemic AIT can be effective in resolving pericardial inflammation, its application in oncology patients is frequently restricted by the risk of opportunistic infections, glycemic burden, and potential interference with the efficacy of immunotherapies [ 5 , 6 ]. Furthermore, as shown in our cases, chronic systemic corticosteroid use often leads to debilitating side effects such as sarcopenia and generalized weakness, which can compromise the patient’s ability to continue essential oncological treatments. Localized corticosteroid instillation offers targeted anti-inflammatory effects by achieving high drug concentrations directly at the site of inflammation and minimizing systemic toxicity [ 7 , 8 ]. Our findings are supported by prior reports suggesting the feasibility of IPC therapy in non-cancer cohorts [ 9 , 10 ]. The pharmacological advantage of triamcinolone acetonide is its low solubility, which allows it to remain within the pericardial space for an extended period, providing sustained local anti-inflammatory action. A notable finding in our first case was the failure of fragmented, low-dose intrapericardial triamcinolone (40 mg/day for 3 days). Despite a cumulative dose of 120 mg, the PE recurred rapidly within one week. In contrast, the subsequent administration of a single high-dose bolus of 200 mg triamcinolone resulted in long-term stabilization. This suggests that in the setting of intense, refractory pericardial disease, especially in patients with advanced malignancy and PE, a certain concentration above the threshold may be required to effectively suppress the inflammatory cascade and prevent progression of pericardial diseases. Maintaining the continuity of cancer treatment is a critical determinant of prognosis in advanced malignancy. By ensuring the long-term stabilization of the pericardial disease, IPC therapy played a vital role in preventing both systemic physical deconditioning and recurrent heart-related hospitalizations. Crucially, this cardiac stability precluded the need to interrupt or delay life-saving cancer treatments due to cardiovascular emergencies. Furthermore, by minimizing the requirement for systemic AIT, IPC therapy helped mitigate debilitating side effects such as steroid-induced muscle wasting and colchicine-related diarrhea, thereby preserving the patient’s performance status and allowing them to tolerate multiple subsequent lines of chemotherapy. Lastly, though our sample size is limited, IPC therapy did not appear to increase procedural complications, even in heavily pre-treated patients. Conclusion In conclusion, our case series suggests that a single high-dose (200 mg) intrapericardial triamcinolone injection is a highly effective and safe intervention for patients with recurrent malignant PE and refractory ECP. This localized approach provided sustained pericardial stabilization for up to 47 months, remarkably independent of the underlying oncological progression. From a cardio-oncological perspective, the clinical utility of high-dose IPC therapy extends beyond symptomatic relief. By preventing recurrent cardiac emergencies and mitigating the side effects of chronic systemic corticosteroids, this intervention preserved the continuity of oncological therapies. While further prospective studies are warranted to validate these findings, high-dose IPC therapy may be considered for cancer patients with recurrent pericardial disease who are refractory to conventional management. Abbreviations AIT Anti-inflammatory therapy ED Emergency department CP Constrictive physiology CRP C-reactive protein CT Computed tomography ECP Effusive-constrictive pericarditis HER2 Human epidermal growth factor receptor 2 HF Heart failure IPC Intrapericardial corticosteroid MBC Metastatic breast cancer NT-proBNP N-terminal pro-B-type natriuretic peptide NYHA New York Heart Association PCC Pericardiocentesis PE Pericardial effusion T-DM1 Trastuzumab emtansine T-DxD Trastuzumab deruxtecan Declarations Ethics approval and consent to participate The study was approved by the Institutional Review Board of Chonnam National University Hwasun Hospital (IRB No. CNUHH-2025-114) and was performed in accordance with the latest version of the Declaration of Helsinki and its amendments (2013). Consent for publication Written consent was obtained from all patients or their families. Competing interests The authors declare that they have no competing interests. Author’s information The patients presented in this case report were enrolled in an ongoing prospective study at our institution comparing the efficacy of intrapericardial corticosteroid therapy and conventional therapy in patients with recurrent malignant pericardial effusion. Funding This study was supported by a grant from the Working Group on Cardio-Oncology of the Korean Society of Cardiology (Grant No. 2022-01-03). Chonnam National University Hwasun Hospital Biomedical Research Institute. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Author Contribution NL collected and organized the patient’s clinical and diagnostic data and drafted the initial version of the manuscript. YK contributed to drafting and revising the manuscript. HP conceived and designed the study and critically revised the manuscript. All authors participated in the analysis and interpretation of the cases and approved the final version of the manuscript. Acknowledgements Not applicable. Availability of data and materials Data sharing is not applicable to this article, as no datasets were generated or analysed during the current study. References Strobbe A, Adriaenssens T, Bennett J, et al. Etiology and long-term outcome of patients undergoing pericardiocentesis. J Am Heart Assoc. 2017;6:e007598. Gornik HL, Gerhard-Herman M, Beckman JA. Abnormal cytology predicts poor prognosis in cancer patients with pericardial effusion. J Clin Oncol. 2005;23:5211–6. Park H, Yoon HJ, Lee N, et al. Characteristics and Clinical Outcomes of Cancer Patients who Developed Constrictive Physiology After Pericardiocentesis. Korean Circ J. 2022;52:74–83. Cho IJ, Chang HJ, Chung H, et al. Differential impact of constrictive physiology after pericardiocentesis in malignancy patients with pericardial effusion. PLoS ONE. 2015;10:e0145461. Kim SR, Kim EK, Cho J, et al. Effect of anti-inflammatory drugs on clinical outcomes in patients with malignant pericardial effusion. J Am Coll Cardiol. 2020;76:1551–61. Lee N, Bang H, Park H, Shim HJ. Case report: Successful treatment of malignant pericardial effusion with pericardiocentesis, concurrent anti-inflammatory therapy and cancer therapy. Front Cardiovasc Med. 2023;10:1285233. Maisch B, Pankuweit S, Brilla C, et al. Intrapericardial treatment of inflammatory and neoplastic pericarditis guided by pericardioscopy and epicardial biopsy–results from a pilot study. Clin Cardiol. 1999;22(1 Suppl 1):I17–22. Maisch B, Ristić AD, Pankuweit S. Intrapericardial treatment of autoreactive pericardial effusion with triamcinolone; the way to avoid side effects of systemic corticosteroid therapy. Eur Heart J. 2002;23:1503–8. Mainzer G, Zaidman I, Hatib I, Lorber A. Intrapericardial steroid treatment for recurrent pericardial effusion in a patient with acute lymphoblastic leukaemia. Hematol Oncol. 2011;29:220–1. Romero JE, Matos CD, Garcia F, et al. Intrapericardial Corticosteroids and Colchicine Prevent Pericarditis and Atrial Fibrillation After Epicardial Ablation of Ventricular Arrhythmias. JACC Clin Electrophysiol. 2025;11:498–508. Additional Declarations No competing interests reported. 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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-8660978","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":583204780,"identity":"b2ee93f8-d7c1-456d-83a5-dbabec183677","order_by":0,"name":"Nuri Lee","email":"","orcid":"","institution":"Chonnam National University Hwasun Hospital","correspondingAuthor":false,"prefix":"","firstName":"Nuri","middleName":"","lastName":"Lee","suffix":""},{"id":583204781,"identity":"93a73e45-b214-42ba-b08e-e91aff6db60d","order_by":1,"name":"Yoojin Kim","email":"","orcid":"","institution":"Chonnam National University","correspondingAuthor":false,"prefix":"","firstName":"Yoojin","middleName":"","lastName":"Kim","suffix":""},{"id":583204782,"identity":"a14b0b6b-8d4c-4611-8f27-af635a225d2f","order_by":2,"name":"Hyukjin Park","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAxUlEQVRIiWNgGAWjYBACAwYGZgYJAwY5EOfAA1K0GIO1JBCtBQgSG0AkUVrMJXKMDSwK7qTPDzv8EGiLnZxuAwEtljNyjBMkDJ7lbrydZgDUkmxsdoCQw27kGB+QMDicu3F2AkjLgcRtxGpJN5yd/oF4LUCHHU6Ql84h1pYzz4oNgFoMN0jnFBxIMCDGL8eTN0tL/DksLz87ffOHDxV2cgS1MAgkMDBLgPSCVRoQUg4C/AcYGD8AafkGYlSPglEwCkbBiAQAu61GjqxhvlMAAAAASUVORK5CYII=","orcid":"","institution":"Chonnam National University Hwasun Hospital","correspondingAuthor":true,"prefix":"","firstName":"Hyukjin","middleName":"","lastName":"Park","suffix":""}],"badges":[],"createdAt":"2026-01-21 14:25:59","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8660978/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8660978/v1","draftVersion":[],"editorialEvents":[{"content":"https://doi.org/10.1186/s40959-026-00479-x","type":"published","date":"2026-03-28T16:11:27+00:00"}],"editorialNote":"","failedWorkflow":false,"files":[{"id":101787639,"identity":"e2077f99-a243-4050-9d7b-473bfc12af67","added_by":"auto","created_at":"2026-02-03 15:49:42","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":1428287,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eSequential transthoracic echocardiography findings of case 1.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eA: large pericardial effusion (PE) resulting in cardiac tamponade. B: pericardial thickening with adhesions following initial pericardiocentesis. C: prominent expiratory hepatic venous flow reversal suggesting constrictive physiology. D: rapidly reaccumulated large PE observed seven days after pericardiocentesis. E: scanty PE after intrapericardial corticosteroid therapy. F: minimal residual PE seen in the final follow-up echocardiogram.\u003c/p\u003e\n\u003cp\u003ePE; pericardial effusion.\u003c/p\u003e\n\u003cp\u003eAsterisks (*) indicate PE; arrows indicate visceral and parietal pericardium.\u003c/p\u003e","description":"","filename":"Figure120260114.png","url":"https://assets-eu.researchsquare.com/files/rs-8660978/v1/f3faf94c3d21db021a128b5b.png"},{"id":101880935,"identity":"d725bed9-4f66-45e7-ab56-fd8a97526c70","added_by":"auto","created_at":"2026-02-04 15:08:05","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":4447811,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eIntrapericardial instillation of 200 mg triamcinolone acetonide via a pigtail catheter.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eA syringe containing 200 mg of triamcinolone acetonide is prepared for administration into the pericardial space. The medication was delivered through the previously inserted 8.5-French pigtail catheter. Following the administration, the catheter was clamped for 12 hours to ensure optimal drug retention.\u003c/p\u003e","description":"","filename":"Figure220260114.png","url":"https://assets-eu.researchsquare.com/files/rs-8660978/v1/01e2b25f9580aa45b159bcf6.png"},{"id":101787642,"identity":"1a305620-d42d-467b-8655-a33d3a9fd004","added_by":"auto","created_at":"2026-02-03 15:49:42","extension":"png","order_by":3,"title":"Figure 3","display":"","copyAsset":false,"role":"figure","size":917284,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eSequential transthoracic echocardiography findings of case 2.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eA: pericardial thickening with adhesions following initial pericardiocentesis. B: reaccumulated pericardial effusion (PE) resulting in cardiac tamponade. C: scanty PE after intrapericardial corticosteroid therapy. D: minimal residual PE seen in the final follow-up echocardiogram.\u003c/p\u003e\n\u003cp\u003ePE; pericardial effusion.\u003c/p\u003e\n\u003cp\u003eAsterisk (*) indicates PE; arrows indicate visceral and parietal pericardium.\u003c/p\u003e","description":"","filename":"Figure320260114.png","url":"https://assets-eu.researchsquare.com/files/rs-8660978/v1/0d598a6e991a77dc6ff9b2a0.png"},{"id":101787644,"identity":"2779138a-ce06-497c-ae93-734306c58a01","added_by":"auto","created_at":"2026-02-03 15:49:42","extension":"png","order_by":4,"title":"Figure 4","display":"","copyAsset":false,"role":"figure","size":822044,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eTransthoracic echocardiography and chest computed tomography of case 3.\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eA: pericardial thickening with adhesions following initial pericardiocentesis. B: reaccumulated pericardial effusion (PE) resulting in cardiac tamponade. C: chest computed tomography showing scanty PE. D: minimal residual PE seen in the final follow-up echocardiogram.\u003c/p\u003e\n\u003cp\u003ePE; pericardial effusion.\u003c/p\u003e\n\u003cp\u003eWhite asterisks (*) indicate pleural effusion; Yellow asterisks (*) indicate PE; and arrows indicate visceral and parietal pericardium.\u003c/p\u003e","description":"","filename":"Figure420260114.png","url":"https://assets-eu.researchsquare.com/files/rs-8660978/v1/695cc9f8bb0236d25187c691.png"},{"id":105755622,"identity":"c9f1366c-b92e-4ed0-a1ee-23c0f4490ced","added_by":"auto","created_at":"2026-03-30 16:28:36","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":8884233,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8660978/v1/9f858941-4d9b-4168-abef-a0f3e32c28fd.pdf"},{"id":101787640,"identity":"9ac6e9cb-7357-4102-9f4e-2f80d739c7a3","added_by":"auto","created_at":"2026-02-03 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15:49:42","extension":"mp4","order_by":10,"title":"","display":"","copyAsset":false,"role":"supplement","size":2082580,"visible":true,"origin":"","legend":"","description":"","filename":"Additionalfile11.mp4","url":"https://assets-eu.researchsquare.com/files/rs-8660978/v1/4fab2375003e04eebfdcb10b.mp4"},{"id":101880545,"identity":"90c6f710-19a7-4488-9dd1-2d51e968e7d6","added_by":"auto","created_at":"2026-02-04 15:03:26","extension":"mp4","order_by":11,"title":"","display":"","copyAsset":false,"role":"supplement","size":2725275,"visible":true,"origin":"","legend":"","description":"","filename":"Additionalfile12.mp4","url":"https://assets-eu.researchsquare.com/files/rs-8660978/v1/98055a9a1248d5c99b1e7833.mp4"}],"financialInterests":"No competing interests reported.","formattedTitle":"Intrapericardial Corticosteroid Therapy for Recurrent Malignant Pericardial Effusion: A Case Series","fulltext":[{"header":"Background","content":"\u003cp\u003ePericardial effusion (PE) is increasingly observed in patients with cancer, likely reflecting advancements in cancer therapies and improved survival. While malignant infiltration remains the predominant cause, some cases arise from treatment-related or cancer-associated inflammation [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e, \u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. PE can progress to cardiac tamponade, requiring urgent pericardiocentesis (PCC). However, a subset of patients develop persistent symptoms due to pericardial adhesion and constrictive physiology (CP) after PCC, which may disrupt cancer treatment and worsen clinical outcomes [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]. Though anti-inflammatory therapy (AIT) can potentially reverse CP, the risks associated with systemic corticosteroid often limit their use in this population [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. Here, we report three cases in which intrapericardial triamcinolone administration improved the clinical outcomes of cancer patients who required repeated PCC for malignant PE.\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cp\u003e \u003cstrong\u003eCase 1\u003c/strong\u003e \u003cp\u003eA 40-year-old female patient with hormone receptor-negative and human epidermal growth factor receptor 2 (HER2)-positive metastatic breast cancer (MBC) presented to our emergency department (ED). She had been diagnosed with MBC six years prior, and had been managed with dual HER2-targeted therapy consisting of trastuzumab and pertuzumab for four years. Two years ago, the patient experienced her first episode of cardiac tamponade, necessitating urgent PCC, after which malignant cells were identified in the PE (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eA, additional file 1). Though the PE was successfully drained, she subsequently developed effusive-constrictive pericarditis (ECP) (Figs.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eB, \u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eC, and additional file 2). Systemic AIT with prednisolone (started with 0.5 mg/kg/day, gradually tapered for 2 months) and colchicine (0.6 mg/day) was initiated to manage the inflammatory process and CP. Concurrent with this event, her breast cancer showed progression in follow-up imaging studies, leading to regimen change from dual HER2 blockade to trastuzumab emtansine (T-DM1). For the following two years, she required two additional PCC procedures and repeated cycles of systemic AIT for recurrent PE, but the patient\u0026rsquo;s overall oncological status remained stable under T-DM1 therapy. Over the past six months, the frequency of PE recurrence accelerated significantly, with two episodes of cardiac tamponade occurring at three-month intervals. Each episode was managed with PCC and systemic AIT.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003c/p\u003e \u003cp\u003eThe current admission was prompted by a rapid and severe clinical decline. Only two weeks after her most recent PCC, the patient returned to the ED with overt cardiac tamponade. She presented with New York Heart Association (NYHA) class IV dyspnea and profound peripheral edema. Transthoracic echocardiography confirmed a massive PE with signs of cardiac tamponade, indicating her condition had become refractory to conventional systemic AIT and repeated drainage. Beyond the refractory nature of the PE, the patient suffered significantly from the adverse effects of chronic systemic AIT. She reported severe generalized weakness and muscle wasting attributed to prolonged corticosteroid use, alongside persistent diarrhea caused by colchicine. Consequently, we decided to shift our management strategy. Systemic AIT was maintained at a minimal dose (prednisolone 10 mg/day, colchicine 0.6 mg/day, and azathioprine 50 mg/day).\u003c/p\u003e \u003cp\u003eA repeat PCC was performed. Following complete drainage, we initially attempted a fragmented dosing protocol: 40 mg (1 mL) of triamcinolone acetonide was injected via the catheter daily for three consecutive days (total 120 mg). After each injection, the catheter was clamped for 12 hours to maximize local drug exposure. However, a follow-up echocardiogram performed one week later revealed a rapid recurrence of large PE (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eD, additional file 3), indicating that this low-dose fragmented dosing was ineffective in controlling the intense pericardial inflammation. So we chose a more aggressive dosing. After another complete drainage of the PE, a single high-dose bolus of 200 mg of triamcinolone was administered through the intrapericardial catheter (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e2\u003c/span\u003e). Simultaneously, given the previous oncological stability but cardiac instability, her anticancer therapy was switched from T-DM1 to trastuzumab deruxtecan (T-DxD).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eOne week after the 200 mg triamcinolone injection, follow-up echocardiography showed significant improvement. Though residual pericardial thickening, adhesions, CP persisted, the PE had been reduced to a scanty amount (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eE, additional file 4). The patient\u0026rsquo;s heart failure (HF) symptoms became tolerable, and her N-terminal pro-B-type natriuretic peptide (NT-proBNP) level decreased from 1,480 pg/mL (when CP developed during the index hospitalization) to 508 pg/mL (at the time of discharge), so she was successfully discharged.\u003c/p\u003e \u003cp\u003eRecognizing that systemic AIT had provided marginal benefit while causing substantial adverse effects, we completely withdrew all systemic AIT. Remarkably, during the 16 months of T-DxD therapy, the patient remained free of cardiac tamponade or any heart-related hospitalizations, with only a stable, small amount of PE observed on serial imaging. Importantly, the stabilization of the pericardial disease appeared independent of her oncological status. Despite the transition to T-DxD, the MBC eventually showed signs of disease progression. Consequently, several lines of salvage therapy were administered, including four cycles of doxorubicin/cyclophosphamide followed by capecitabine and lapatinib. Despite these therapies, the MBC continued to progress, ultimately leading to the patient\u0026rsquo;s death (47 months after intrapericardial triamcinolone therapy). But it\u0026rsquo;s noteworthy that the pericardial disease remained stable throughout this period \u0026ndash; following the administration of 200 mg of intrapericardial triamcinolone, the patient experienced no significant increase in PE or clinical events such as cardiac tamponade. Remarkably, even on imaging obtained only one month before her death, the PE remained at a scanty amount (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e1\u003c/span\u003eF, additional file 5).\u003c/p\u003e \u003cp\u003e \u003cstrong\u003eCase 2\u003c/strong\u003e \u003cp\u003eA 63-year-old female with lung adenocarcinoma and multi-organ metastases, who had been treated with dacomitinib for one year, presented to the ED with NYHA class IV dyspnea. Echocardiography revealed a massive PE with tamponade physiology, necessitating emergency PCC, which revealed malignant cells in the PE. Follow-up echocardiography the next day confirmed complete drainage but also showed significant pericardial thickening, adhesions, and CP (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eA, additional file 6). Elevated NT-proBNP level of 1,070 pg/mL and serum C-reactive protein (CRP) level of 7.03 mg/dL supported the diagnosis of inflammatory constrictive pericarditis. Systemic AIT was initiated with prednisolone (0.25 mg/kg/day, tapered for 2.5 months) and colchicine (1.2 mg/day). Initially, the patient showed a favorable response: at two weeks, the NT-proBNP level decreased to 220 pg/mL, and HF symptoms nearly resolved. However, one month after complete discontinuation of prednisolone, she was readmitted with recurrent pleuritic chest pain, dyspnea, and moderate PE. For this ECP, we resumed systemic AIT with a higher dose of prednisolone (0.5 mg/kg/day) and added methotrexate (15 mg/week). Colchicine was omitted due to severe treatment-limiting diarrhea.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003c/p\u003e \u003cp\u003eDespite intensified AIT and stable oncological status under dacomitinib, cardiac tamponade recurred within one month, requiring a second PCC (five months after the first procedure) (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eB, additional file 7). Post-procedure imaging showed persistent CP, though inflammatory markers were only mildly elevated (CRP 3.36 mg/dL). Systemic AIT was withdrawn due to lack of efficacy and progressive sarcopenia caused by prednisolone treatment. However, cardiac tamponade recurred again just one month later, even without significant progression of the lung cancer. Following a third PCC, the PE re-accumulated within another month. At this stage, slight progression of abdominal and pelvic metastases was observed, leading to a switch from dacomitinib to a pemetrexed and cisplatin regimen. Nevertheless, cardiac tamponade recurred for the fourth time, only four months after the third procedure.\u003c/p\u003e \u003cp\u003eBecause of the repetitive and refractory cardiac tamponade events, we performed a fourth PCC followed by intrapericardial injection of 200 mg of triamcinolone, as the same protocol as case \u003cspan refid=\"FPar1\" class=\"InternalRef\"\u003e1\u003c/span\u003e (complete drainage and triamcinolone injection, followed by a 12-hour catheter clamping). Post-procedure echocardiography revealed no significant PE, though pericardial thickening and CP remained (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eC, additional file 8). Though the NT-proBNP level rose to 968 pg/mL, the patient\u0026rsquo;s HF symptoms improved significantly to NYHA class II. Consequently, no further systemic AIT was administered, and the pemetrexed-based chemotherapy was maintained (cisplatin was discontinued after four cycles). The patient remained on pemetrexed for a total of 15 months. Though the lung cancer began to show gradual progression after eight months, the pericardial disease has remained remarkably stable (Fig.\u0026nbsp;\u003cspan refid=\"Fig3\" class=\"InternalRef\"\u003e3\u003c/span\u003eD, additional file 9). During the 17 months since the fourth PCC and intrapericardial triamcinolone injection, the PE has been maintained at a scanty to small amount. Most importantly, there have been no recurrences of cardiac tamponade or any hospitalizations related to cardiovascular diseases.\u003c/p\u003e \u003cp\u003e \u003cstrong\u003eCase 3\u003c/strong\u003e \u003cp\u003eA 46-year-old female with MBC was admitted to our ED with NYHA class III dyspnea, Her oncological history was as follows: six years prior, she was diagnosed with estrogen receptor positive/progesterone receptor positive breast cancer and underwent six cycles of neoadjuvant chemotherapy (docetaxel and epirubicin), follow by a left breast-conserving surgery. After completing adjuvant radiation therapy, eight cycles of capecitabine and transitioning to tamoxifen maintenance, she remained stable for four years until lung metastases were detected. Her treatment was then switched to letrozole, ribociclib, and goserelin, however, the patient was lost to follow-up for ten months due to concerns over treatment-induced alopecia. Upon her return, multiple (hepatic, peritoneal, uterine, skeletal, pleural, and pericardial) metastases were detected, and she resumed capecitabine therapy.\u003c/p\u003e \u003c/p\u003e \u003cp\u003eThe current presentation to the ED with dyspnea occurred three months after resuming capecitabine. Though a chest computed tomography (CT) indicated stable disease of her MBC, it revealed a new, large PE causing cardiac tamponade. Urgent PCC was performed and presence of malignant cells in the PE was cytologically confirmed. While complete drainage was achieved, follow-up echocardiography showed diffuse pericardial thickening, adhesions, and CP (Fig.\u0026nbsp;\u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eA, additional file 10). Laboratory findings showed mildly elevated NT-proBNP level of 548 pg/mL and CRP level of 0.83 mg/dL. She was discharged on systemic AIT consisting of prednisolone (0.5 mg/kg/day with a 5 mg/day taper every two weeks) and colchicine (0.6 mg/day).\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eDespite being on active systemic AIT and capecitabine therapy, cardiac tamponade recurred only 1.5 months after the first PCC (Fig.\u0026nbsp;\u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eB, additional file 11). At this point, the patient presented with significant sarcopenia due to her prolonged disease course, raising concerns about the morbidities of escalating or continuing systemic corticosteroids. Also, since the tamponade recurred while she was still receiving systemic AIT, the pericardial disease was deemed refractory to systemic AIT. Rather than escalating the systemic dose, we performed a second PCC followed by an intrapericardial injection of 200 mg of triamcinolone using the same protocol as the previous cases. Following this, echocardiography showed persistent pericardial thickening and adhesions, but only a small amount of residual PE. Levels of biomarkers remained stable (NT-proBNP 371 pg/mL, CRP 0.62 mg/dL).\u003c/p\u003e \u003cp\u003eOne month after the second PCC, the patient returned to the ED with NYHA class III dyspnea. However, CT imaging confirmed that this was due to bilateral pleural effusions, with only a small PE (Fig.\u0026nbsp;\u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eC). The relief of symptoms after thoracentesis confirmed that this event was not a recurrence of cardiac tamponade. At this point, her MBC was deemed to have progressed significantly. Accordingly, capecitabine, which had been withheld since the second episode of cardiac tamponade, was replaced with nanoparticle albumin-bound paclitaxel and administered for four months. Ongoing disease progression subsequently necessitated a switch to gemcitabine and carboplatin, which has been administered for three months to date. While her MBC has shown such progression, her pericardial disease has remained remarkably quiescent. During the eight months since the intrapericardial triamcinolone therapy, the PE has remained small in amount (Fig.\u0026nbsp;\u003cspan refid=\"Fig4\" class=\"InternalRef\"\u003e4\u003c/span\u003eD, additional file 12), and her subjective dyspnea has been well-managed in the outpatient setting without any further cardiac events.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eThe main finding of this case series is the remarkable stabilization of the pericardial disease after high-dose intrapericardial corticosteroid (IPC) therapy in patients with metastatic cancer and malignant PE. In all three cases, the patients suffered from recurrent, refractory PE and life-threatening cardiac tamponade despite initial management with PCC and systemic AIT. Crucially, these cardiac events occurred independently of the status of their extra-pericardial metastases. Cardiac tamponade recurred even when the primary malignancy remained stable, but after a single intrapericardial injection of 200 mg triamcinolone, the pericardial disease achieved sustained stabilization, remaining free of significant recurrence for 8 to 47 months. Remarkably, this cardiac stability persisted even as the underlying metastatic cancers eventually progressed in other organs.\u003c/p\u003e \u003cp\u003eThe management of pericardial disease in oncology patients presents a unique clinical challenge. CP and ECP remain well-documented sequelae of PCC and are significant predictors of poor prognosis [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. While systemic AIT can be effective in resolving pericardial inflammation, its application in oncology patients is frequently restricted by the risk of opportunistic infections, glycemic burden, and potential interference with the efficacy of immunotherapies [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e, \u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. Furthermore, as shown in our cases, chronic systemic corticosteroid use often leads to debilitating side effects such as sarcopenia and generalized weakness, which can compromise the patient\u0026rsquo;s ability to continue essential oncological treatments.\u003c/p\u003e \u003cp\u003eLocalized corticosteroid instillation offers targeted anti-inflammatory effects by achieving high drug concentrations directly at the site of inflammation and minimizing systemic toxicity [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. Our findings are supported by prior reports suggesting the feasibility of IPC therapy in non-cancer cohorts [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e]. The pharmacological advantage of triamcinolone acetonide is its low solubility, which allows it to remain within the pericardial space for an extended period, providing sustained local anti-inflammatory action. A notable finding in our first case was the failure of fragmented, low-dose intrapericardial triamcinolone (40 mg/day for 3 days). Despite a cumulative dose of 120 mg, the PE recurred rapidly within one week. In contrast, the subsequent administration of a single high-dose bolus of 200 mg triamcinolone resulted in long-term stabilization. This suggests that in the setting of intense, refractory pericardial disease, especially in patients with advanced malignancy and PE, a certain concentration above the threshold may be required to effectively suppress the inflammatory cascade and prevent progression of pericardial diseases.\u003c/p\u003e \u003cp\u003eMaintaining the continuity of cancer treatment is a critical determinant of prognosis in advanced malignancy. By ensuring the long-term stabilization of the pericardial disease, IPC therapy played a vital role in preventing both systemic physical deconditioning and recurrent heart-related hospitalizations. Crucially, this cardiac stability precluded the need to interrupt or delay life-saving cancer treatments due to cardiovascular emergencies. Furthermore, by minimizing the requirement for systemic AIT, IPC therapy helped mitigate debilitating side effects such as steroid-induced muscle wasting and colchicine-related diarrhea, thereby preserving the patient\u0026rsquo;s performance status and allowing them to tolerate multiple subsequent lines of chemotherapy. Lastly, though our sample size is limited, IPC therapy did not appear to increase procedural complications, even in heavily pre-treated patients.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003e \u003cdiv class=\"BlockQuote\"\u003e \u003cp\u003eIn conclusion, our case series suggests that a single high-dose (200 mg) intrapericardial triamcinolone injection is a highly effective and safe intervention for patients with recurrent malignant PE and refractory ECP. This localized approach provided sustained pericardial stabilization for up to 47 months, remarkably independent of the underlying oncological progression. From a cardio-oncological perspective, the clinical utility of high-dose IPC therapy extends beyond symptomatic relief. By preventing recurrent cardiac emergencies and mitigating the side effects of chronic systemic corticosteroids, this intervention preserved the continuity of oncological therapies. While further prospective studies are warranted to validate these findings, high-dose IPC therapy may be considered for cancer patients with recurrent pericardial disease who are refractory to conventional management.\u003c/p\u003e \u003c/div\u003e \u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003e\u003cstrong\u003eAIT\u003c/strong\u003e Anti-inflammatory therapy\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eED\u003c/strong\u003e Emergency department\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCP\u003c/strong\u003e Constrictive physiology\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCRP\u003c/strong\u003e C-reactive protein\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCT\u003c/strong\u003e Computed tomography\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eECP\u0026nbsp; \u0026nbsp;\u0026nbsp;\u003c/strong\u003e Effusive-constrictive pericarditis\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eHER2\u003c/strong\u003e Human epidermal growth factor receptor 2\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eHF\u003c/strong\u003e Heart failure\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eIPC\u003c/strong\u003e Intrapericardial corticosteroid\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eMBC\u0026nbsp; \u0026nbsp;\u003c/strong\u003e Metastatic breast cancer\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eNT-proBNP\u003c/strong\u003e N-terminal pro-B-type natriuretic peptide\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eNYHA\u003c/strong\u003e New York Heart Association\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003ePCC\u003c/strong\u003e Pericardiocentesis\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003ePE\u003c/strong\u003e Pericardial effusion\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eT-DM1\u003c/strong\u003e Trastuzumab emtansine\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eT-DxD\u003c/strong\u003e Trastuzumab deruxtecan\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e \u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e \u003cp\u003eThe study was approved by the Institutional Review Board of Chonnam National University Hwasun Hospital (IRB No. CNUHH-2025-114) and was performed in accordance with the latest version of the Declaration of Helsinki and its amendments (2013).\u003c/p\u003e \u003c/p\u003e \u003cp\u003e \u003cstrong\u003eConsent for publication\u003c/strong\u003e \u003cp\u003eWritten consent was obtained from all patients or their families.\u003c/p\u003e \u003c/p\u003e\u003cp\u003e \u003ch2\u003eCompeting interests\u003c/h2\u003e \u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e \u003c/p\u003e\u003cp\u003e \u003ch2\u003eAuthor\u0026rsquo;s information\u003c/h2\u003e \u003cp\u003eThe patients presented in this case report were enrolled in an ongoing prospective study at our institution comparing the efficacy of intrapericardial corticosteroid therapy and conventional therapy in patients with recurrent malignant pericardial effusion.\u003c/p\u003e \u003c/p\u003e\u003ch2\u003eFunding\u003c/h2\u003e \u003cp\u003eThis study was supported by a grant from the Working Group on Cardio-Oncology of the Korean Society of Cardiology (Grant No. 2022-01-03). Chonnam National University Hwasun Hospital Biomedical Research Institute. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.\u003c/p\u003e\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eNL collected and organized the patient\u0026rsquo;s clinical and diagnostic data and drafted the initial version of the manuscript. YK contributed to drafting and revising the manuscript. HP conceived and designed the study and critically revised the manuscript. All authors participated in the analysis and interpretation of the cases and approved the final version of the manuscript.\u003c/p\u003e\u003ch2\u003eAcknowledgements\u003c/h2\u003e \u003cp\u003eNot applicable.\u003c/p\u003e\u003ch2\u003eAvailability of data and materials\u003c/h2\u003e \u003cp\u003eData sharing is not applicable to this article, as no datasets were generated or analysed during the current study.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eStrobbe A, Adriaenssens T, Bennett J, et al. Etiology and long-term outcome of patients undergoing pericardiocentesis. J Am Heart Assoc. 2017;6:e007598.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eGornik HL, Gerhard-Herman M, Beckman JA. Abnormal cytology predicts poor prognosis in cancer patients with pericardial effusion. J Clin Oncol. 2005;23:5211\u0026ndash;6.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePark H, Yoon HJ, Lee N, et al. Characteristics and Clinical Outcomes of Cancer Patients who Developed Constrictive Physiology After Pericardiocentesis. Korean Circ J. 2022;52:74\u0026ndash;83.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eCho IJ, Chang HJ, Chung H, et al. Differential impact of constrictive physiology after pericardiocentesis in malignancy patients with pericardial effusion. PLoS ONE. 2015;10:e0145461.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKim SR, Kim EK, Cho J, et al. Effect of anti-inflammatory drugs on clinical outcomes in patients with malignant pericardial effusion. J Am Coll Cardiol. 2020;76:1551\u0026ndash;61.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLee N, Bang H, Park H, Shim HJ. Case report: Successful treatment of malignant pericardial effusion with pericardiocentesis, concurrent anti-inflammatory therapy and cancer therapy. Front Cardiovasc Med. 2023;10:1285233.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMaisch B, Pankuweit S, Brilla C, et al. Intrapericardial treatment of inflammatory and neoplastic pericarditis guided by pericardioscopy and epicardial biopsy\u0026ndash;results from a pilot study. Clin Cardiol. 1999;22(1 Suppl 1):I17\u0026ndash;22.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMaisch B, Ristić AD, Pankuweit S. Intrapericardial treatment of autoreactive pericardial effusion with triamcinolone; the way to avoid side effects of systemic corticosteroid therapy. Eur Heart J. 2002;23:1503\u0026ndash;8.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMainzer G, Zaidman I, Hatib I, Lorber A. Intrapericardial steroid treatment for recurrent pericardial effusion in a patient with acute lymphoblastic leukaemia. Hematol Oncol. 2011;29:220\u0026ndash;1.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eRomero JE, Matos CD, Garcia F, et al. Intrapericardial Corticosteroids and Colchicine Prevent Pericarditis and Atrial Fibrillation After Epicardial Ablation of Ventricular Arrhythmias. JACC Clin Electrophysiol. 2025;11:498\u0026ndash;508.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"
[email protected]","identity":"cardio-oncology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"caon","sideBox":"Learn more about [Cardio-Oncology](http://cardiooncologyjournal.biomedcentral.com)","snPcode":"40959","submissionUrl":"https://submission.nature.com/new-submission/40959/3","title":"Cardio-Oncology","twitterHandle":"@OncoBioMed","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"em","reportingPortfolio":"BMC/SO AJ","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"pericardiocentesis, cancer, pericardial effusion","lastPublishedDoi":"10.21203/rs.3.rs-8660978/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8660978/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eMalignant pericardial effusion (PE) and subsequent effusive-constrictive pericarditis (ECP) are significant clinical challenges in patients with advanced cancer.\u003c/p\u003e\u003ch2\u003eCase presentation:\u003c/h2\u003e \u003cp\u003eWe report three cases of patients with metastatic breast or lung cancer who experienced recurrent, life-threatening cardiac tamponade despite multiple pericardiocenteses (PCC) and systemic anti-inflammatory treatment (AIT). In all cases, pericardial disease remained refractory to conventional management, and chronic systemic corticosteroid use led to debilitating side effects. Following complete drainage of the PE, a single high-dose bolus of 200 mg triamcinolone was administered via an intrapericardial catheter with a 12-hour clamping protocol. This intervention resulted in sustained pericardial stabilization for 8 to 47 months across all three patients. Remarkably, this cardiac stability was maintained independently of the underlying oncological status.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eHigh-dose (200 mg) intrapericardial corticosteroid therapy is an effective and safe intervention for refractory malignant PE.\u003c/p\u003e","manuscriptTitle":"Intrapericardial Corticosteroid Therapy for Recurrent Malignant Pericardial Effusion: A Case Series","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-02-03 15:49:37","doi":"10.21203/rs.3.rs-8660978/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-03-02T13:41:01+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-02-26T16:35:31+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-02-16T10:13:10+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"230999308294361805580789679758906348975","date":"2026-01-30T17:01:03+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"306546671942000437660877787170770231185","date":"2026-01-29T22:06:48+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-01-29T15:36:25+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-01-28T17:32:56+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-01-22T06:22:00+00:00","index":"","fulltext":""},{"type":"submitted","content":"Cardio-Oncology","date":"2026-01-21T13:58:32+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"
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