ABSTRACT
Metastatic gastric adenocarcinoma rarely manifests initially with massive pleuropericardial effusions and life‐threatening cardiac tamponade. Identifying the primary tumour source in such acute and complex clinical presentations represents a significant diagnostic challenge. A 44‐year‐old man with a history of heavy tobacco smoking and chronic opium use presented with acute‐onset dyspnea and chest pain. Imaging revealed massive pleural and pericardial effusions causing cardiac tamponade, necessitating urgent pericardial drainage. Initial investigations, including pleural and pericardial fluid analyses, were non‐diagnostic and demonstrated lymphocyte‐predominant exudative effusions. Definitive diagnosis was achieved through video‐assisted thoracoscopic surgery (VATS) with pleural biopsy, revealing metastatic adenocarcinoma. Immunohistochemical profiling (CK7+/CK20+/TTF‐1−) supported a primary origin of gastric carcinoma. The patient's clinical course was complicated by ventilator‐associated pneumonia and septic shock, ultimately resulting in death before initiation of systemic therapy. This case highlights the diagnostic challenge of occult gastric adenocarcinoma presenting with pleuropericardial effusions and tamponade. In unexplained lymphocyte‐predominant effusions, malignancy should be considered, and early VATS‐guided pleural biopsy may be required when noninvasive tests are inconclusive. Prognosis remains poor in advanced disease.
Keywords: cardiac tamponade, gastric adenocarcinoma, gastric cancer, metastasis, pleuropericardial effusion, sepsis
This case highlights the diagnostic challenge of occult gastric adenocarcinoma presenting with pleuropericardial effusions and tamponade. In unexplained lymphocyte‐predominant effusions, malignancy should be considered, and early VATS‐guided pleural biopsy may be required when noninvasive tests are inconclusive. Prognosis remains poor in advanced disease.

1. Introduction
Metastatic gastric cancer rarely presents initially with pleuropericardial involvement, accounting for approximately 2% of malignant pleural effusions [1]. A large cohort study demonstrates that while lung and breast cancers are the most common sources, gastrointestinal (GI) malignancies account for approximately 6.1% of malignant pericardial effusions, highlighting their clinical diagnostic relevance [2]. According to the most recent global estimates from the Global Cancer Observatory (GLOBOCAN 2022), stomach cancer accounted for approximately 969,000 new cases and 660,000 deaths worldwide in 2022 [3, 4]. Approximately 90% of gastric malignancies are adenocarcinomas, representing a substantial global health burden. The most common metastatic sites of gastric cancer are the liver (48%) and peritoneum (32%), followed by the lung (15%) and bone (12%) [5]. Pleuropericardial effusions with lymphocytic predominance pose a significant diagnostic challenge. Current guidelines for the management of pericardial diseases provide a crucial framework for risk stratification and intervention in cases presenting with effusions and cardiac tamponade [6].
In this case report study, we present a rare case of metastatic GI adenocarcinoma initially manifesting as massive pleuropericardial effusions and cardiac tamponade, highlighting the complexity of early recognition and the necessity of a comprehensive diagnostic approach.
2. Case Report
A 44‐year‐old man from Tehran presented to the emergency department with acute‐onset severe dyspnea and chest pain. His medical history was notable for a previous episode of deep vein thrombosis following prolonged bed rest after a motor vehicle accident, for which he was receiving apixaban. He reported a 50‐pack‐year history of tobacco smoking and chronic opium use. Home medications included apixaban, aspirin and omeprazole. He denied any significant family history of malignancy or other chronic diseases.
On admission, the patient appeared acutely ill and was in respiratory distress. Vital signs revealed tachypnea (respiratory rate, 25 breaths/min), tachycardia (heart rate, 110 beats/min), hypoxemia (SpO2, 85% on room air), and a markedly narrowed pulse pressure (blood pressure, 101/98 mmHg). Physical examination revealed bilaterally diminished breath sounds, more pronounced over the left hemithorax, accompanied by bilateral crackles on auscultation. The jugular veins were not distended. Scleral pallor was noted. Abdominal examination revealed distension without tenderness, guarding, or rebound tenderness.
Chest computed tomography (CT) demonstrated a large left‐sided pleural effusion and a concomitant pericardial effusion (Figure 1). Pulmonary CT angiography excluded pulmonary embolism. Transthoracic echocardiography demonstrated a large pericardial effusion with right ventricular diastolic collapse, consistent with cardiac tamponade (Figure 2). Pleural fluid analysis revealed an exudative, lymphocyte‐predominant effusion, while pericardial fluid analysis showed elevated lactate dehydrogenase levels but was non‐diagnostic for malignancy (Table 1). Bronchoscopy with bronchoalveolar lavage did not reveal infectious or malignant pathology.
FIGURE 1.

Chest CT scan revealed left‐sided pleural effusion (marked by ‘*’) and pericardial effusion (shown by ‘#’).
FIGURE 2.

Cardiac echocardiography showing pericardial effusion (dotted line).
TABLE 1.
Pleural fluid and pericardial fluid analysis.
| Characteristics | Pleural fluid | Pericardial fluid |
|---|---|---|
| Appearance | Turbid | Turbid |
| Colour | Yellow | Reddish |
| WBC (cells/μL) | ||
| Total | 2816 | 2350 |
| Segment (cells/μL) | 1126 | 1528 |
| Lymphocyte (cells/μL) | 1690 | 822 |
| RBC (cells/μL) | 500 | 830,000 |
| Glucose (mg/dL) | 10 | 15 |
| Protein (g/dL) | 3.2 | 3.8 |
| Albumin (g/dL) | 2.0 | 2.6 |
| LDH (U/L) | 1440 | 4982 |
Abbreviations: LDH, lactate dehydrogenase; RBC, red blood cell; WBC, white blood cell.
During diagnostic video‐assisted thoracoscopic surgery (VATS), a lesion involving the left pleura was identified, and biopsy specimens were obtained. Histopathological examination showed adenocarcinoma on haematoxylin and eosin staining, and immunohistochemical analysis demonstrated CK7 positivity, CK20 positivity, and TTF‐1 negativity (CK7+/CK20+/TTF‐1−), consistent with metastatic adenocarcinoma of upper GI origin (Figure 3) [7, 8]. Subsequent contrast‐enhanced CT of the abdomen and pelvis revealed an irregular mass lesion in the upper GI tract, consistent with a primary gastric malignancy (Figure 4).
FIGURE 3.

Haematoxylin and eosin (H&E) staining showing lung parenchyma infiltrated by nests of tumour cells with a high nuclear‐to‐cytoplasmic ratio and eosinophilic cytoplasm floating in air spaces (A). H&E high‐power view demonstrating nests of tumour cells within air spaces (B). Immunohistochemical staining for CK7 showing positive reaction in tumour cells (C). Immunohistochemical staining for TTF1 showing negative reaction in tumour cells (D). Immunohistochemical staining for CK20 showing positive reaction in tumour cells (E). The combined immunophenotype profile (CK7+/CK20+/TTF‐1−) supports an upper gastrointestinal origin (gastric/upper GI) rather than a primary pulmonary adenocarcinoma, and together with subsequent CT imaging [see also Figure 4], confirmed the diagnosis of metastatic gastric adenocarcinoma.
FIGURE 4.

Axial CT scan demonstrating irregular thickening of the gastric wall with heterogeneous enhancement. The area marked with asterisk * indicates a focal abnormality, consistent with gastric adenocarcinoma.
Laboratory blood analysis demonstrated hypochromic–microcytic anaemia consistent with iron deficiency, with reduced haemoglobin and red blood cell indices, and an elevated red cell distribution width. Inflammatory markers were markedly increased, as evidenced by elevated erythrocyte sedimentation rate and C‐reactive protein levels. Coagulation studies showed a prolonged prothrombin time, a prolonged partial thromboplastin time, and an elevated international normalized ratio. Liver enzymes and lactate dehydrogenase were significantly elevated, while renal function parameters remained within normal limits. Electrolyte analysis revealed hyponatremia and mild hypocalcemia. Cardiac markers showed elevated levels of pro–B‐type natriuretic peptide and creatine kinase–MB. Iron studies were consistent with iron deficiency. Autoimmune markers were negative, and tumour marker evaluation was largely unremarkable, except for elevated CA19‐9 and beta‐human chorionic gonadotropin levels. A summary of the laboratory blood analysis is presented in Table 2.
TABLE 2.
Laboratory blood analysis of the patient.
| Measured variables | Unit | Result | Reference range |
|---|---|---|---|
| WBC | Cells/μL | 6900 | 4000–11,000 |
| RBC | Cells/μL | 4.09 × 106 | 4.7–6.1 × 106 |
| Haemoglobin | g/dL | 8.9 | 13.5–17.5 |
| MCV | fL | 73.8 | 80–100 |
| MCH | pg | 21.8 | 27–33 |
| MCHC | g/dL | 29.5 | 32–36 |
| Platelet | Cells/μL | 278 × 103 | 150–450 × 103 |
| RDW | % | 17.7 | 11.5–14.5 |
| ESR | mm/h | 36 | < 15 |
| CRP | mg/L | 80 | < 10 |
| BUN | mg/dL | 13 | 7–20 |
| Cr | mg/dL | 1.1 | 0.7–1.3 |
| Sodium (Na) | mmol/L | 128 | 135–145 |
| Potassium (K) | mmol/L | 4.7 | 3.5–5 |
| Calcium (Ca) | mg/dL | 8.2 | 8.5–10.5 |
| Phosphorus (P) | mg/dL | 3.8 | 2.5–4.5 |
| Magnesium (Mg) | mg/dL | 1.9 | 1.7–2.2 |
| Albumin | g/dL | 2.8 | 3.5–5 |
| CPK | U/L | 71 | 52–336 |
| CPK‐MB | U/L | 18 | 0–5 |
| AST | U/L | 390 | 10–40 |
| ALT | U/L | 111 | 7–56 |
| ALP | U/L | 239 | 40–130 |
| Total bilirubin | mg/dL | 0.9 | 0.1–1.2 |
| Direct bilirubin | mg/dL | 0.2 | 0–0.3 |
| LDH | U/L | 519 | 140–280 |
| Iron | μg/dL | 43 | 65–176 |
| TIBC | μg/dL | 238 | 240–450 |
| Ferritin | ng/mL | 70 | 24–336 |
| Blood sugar | mg/dL | 127 | 70–140 |
| Pro‐BNP | pg/mL | 277 | < 125 |
| Amylase | U/L | 38 | 30–110 |
| Lipase | U/L | 29 | 10–140 |
| Bicarbonate | mmol/L | 24.5 | 22–26 |
| PCO2 | mmHg | 41.3 | 35–45 |
| PH | — | 7.39 | 7.35–7.45 |
| Anti‐dsDNA | IU/mL | 21 | Negative |
| CA‐125 | U/mL | 7.2 | < 35 |
| CA19‐9 | U/mL | 141 | 0–36 |
| CEA | ng/mL | < 0.5 | Smoker: < 10 |
| Beta‐HCG | mIU/mL | 26.67 | UP to 10 |
| Alpha Phytoprotein | ng/mL | 1.6 | 0–10 |
| PSA | ng/mL | 0.62 | 0.4–6.1 |
| ANA | Index value | 0.05 | Negative |
| Cardiolipin IgG | GPL‐U/mL | 11 | < 12–15 |
| Cardiolipin IgM | MPL‐U/mL | < 3 | < 12–15 |
| Anti‐CCP | U/mL | < 3 | < 20 |
Abbreviations: ALP, lkaline phosphatase; ALT, alanine aminotransferase; Anti‐CCP, anti‐cyclic citrullinated peptide antibody; AST, aspartate aminotransferase; BUN, blood urea nitrogen; CEA, carcinoembryonic antigen; CPK, creatine phosphokinase; CPK‐MB, creatine phosphokinase‐myocardial band; Cr, Creatinine; CRP, C‐reactive protein; ESR, erythrocyte sedimentation rate; INR, international normalized ratio; LDH, lactate dehydrogenase; MCH, mean corpuscular haemoglobin; MCHC, mean corpuscular haemoglobin concentration; MCV, mean corpuscular volume; PCO2, partial pressure of CO2; PH, potential of hydrogen; Pro‐BNP, ProB‐type natriuretic peptide; PSA, prostate specific antigen; PT, prothrombin time; PTT, partial thromboplastin time; RBC, red blood cell; RDW, red cell distribution width; TIBC, total iron‐binding capacity; WBC white blood cell.
Due to hemodynamic instability and confirmed cardiac tamponade, emergent pericardial drainage was performed, resulting in transient clinical stabilization. The patient received supportive care, including oxygen therapy, broad‐spectrum antimicrobial treatment, and intensive monitoring. Definitive oncologic therapy was planned but deferred due to rapid clinical deterioration.
The patient's hospital course was complicated by ventilator‐associated pneumonia, followed by sepsis and septic shock. Owing to progressive organ dysfunction, systemic chemotherapy could not be initiated. Despite maximal supportive care, the patient died from septic shock during hospitalization.
3. Discussion
Metastatic gastric adenocarcinoma rarely presents with acute cardiothoracic manifestations, particularly as the initial clinical presentation. Malignant pleural and pericardial effusions are most commonly attributed to lung and breast malignancies, whereas GI cancers account for a minority of cases [1, 2]. The simultaneous occurrence of massive pleural and pericardial effusions complicated by cardiac tamponade, as observed in this patient, is exceptionally uncommon and underscores the diagnostic complexity of such presentations. Recognition of this rare pattern is clinically important, as early manifestations dominated by cardiopulmonary symptoms may delay identification of the underlying malignancy.
The pathogenesis of gastric adenocarcinoma is multifactorial. Helicobacter pylori infection remains the most established risk factor; however, tobacco smoking, alcohol use, dietary factors, obesity, and prior gastric surgery are also implicated [9, 10]. Emerging evidence has identified opium use as an independent risk factor for gastric cancer, with a recent meta‐analysis demonstrating a significant association between chronic opium consumption and GI malignancies [11]. The patient's extensive tobacco exposure and chronic opium use may have acted synergistically, contributing to carcinogenesis and aggressive disease progression. Metastatic involvement of the pleural and pericardial spaces likely reflects haematogenous or lymphatic dissemination, signifying advanced disease.
Lymphocyte‐predominant exudative pleuropericardial effusions present a broad differential diagnosis, including infectious, inflammatory, autoimmune, and malignant aetiologies. Initial minimally invasive diagnostic procedures, including thoracentesis, pericardiocentesis and bronchoalveolar lavage, frequently yield inconclusive results in malignant effusions. In this case, definitive diagnosis was achieved only after VATS with pleural biopsy. Current British Thoracic Society guidelines recommend thoracoscopic or image‐guided pleural biopsy when cytology is negative or inconclusive [12]. Thoracoscopic pleural biopsy has a high diagnostic yield in malignant pleural effusions, ranging from 85% to nearly 100%, reinforcing its value in complex cases [13].
Immunohistochemical profiling played a pivotal role in identifying the primary tumour origin. The tumour's CK7‐positive, CK20‐positive, and TTF‐1–negative immunophenotype strongly supported an upper GI primary, effectively excluding a pulmonary source [7, 8]. This highlights the importance of integrating histopathology, immunohistochemistry, and radiologic findings to establish the diagnosis in metastatic disease of unknown primary origin.
Pleural and pericardial involvement by metastatic disease typically indicates advanced‐stage cancer and is associated with poor prognosis. Management of this patient was further complicated by ventilator‐associated pneumonia and subsequent septic shock, which precluded initiation of systemic chemotherapy. Hospital‐acquired infections, particularly VAP, are well‐recognized contributors to mortality in critically ill patients with malignancy. This case illustrates how rapid clinical deterioration and infectious complications can limit therapeutic options, even when a definitive diagnosis is achieved.
Pleuropericardial effusion with cardiac tamponade as the initial manifestation of metastatic gastric adenocarcinoma is an exceptionally rare presentation. Although malignancy is a well‐recognized cause of lymphocyte‐predominant pleural effusions, this case highlights the diagnostic challenges posed by occult malignancies presenting primarily with cardiothoracic manifestations. In patients with unexplained recurrent pleural and pericardial effusions, particularly when initial investigations are inconclusive, comprehensive evaluation, including VATS‐guided pleural biopsy, should be considered to establish an early diagnosis. This case underscores the importance of maintaining a broad differential diagnosis and recognizing atypical metastatic presentations that may delay identification of the primary malignancy. Despite advances in diagnostic and therapeutic approaches, metastatic gastric cancer with pleuropericardial involvement remains associated with a poor prognosis.
Author Contributions
Reza Ghaderi provided the clinical case. Mahta Moradi and Samira Nakhaie drafted the manuscript and assisted in preparing the radiographic images. Pegah Babaheidarian prepared the pathological images and reports. Seyed Arash Javadmoosavi supervised the overall project. Mehdi Karimi reviewed, conceptualized, and revised the manuscript. All authors read and approved the final manuscript.
Consent
The authors declare that written informed consent was obtained for the publication of this manuscript and accompanying images, and attest that the consent form used to obtain patient consent complies with the Journal's requirements as outlined in the author guidelines.
Conflicts of Interest
The authors declare no conflicts of interest.
Moradi M., Karimi M., Babaheidarian P., Moosavi S. A. J., Nakhaie S., and Ghaderi R., “Metastatic Gastric Adenocarcinoma Presenting With Pleuropericardial Effusions and Cardiac Tamponade: A Diagnostic Challenging Case Report,” Respirology Case Reports 14, no. 7 (2026): e70676, 10.1002/rcr2.70676.
Associate Editor: Tracy Leong
Data Availability Statement
The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.
