Gallbladder cancer causing superior vena cava syndrome treated by palliative surgery: A case report

Abstract

Superior vena cava syndrome (SVCS) caused by gallbladder cancer is extremely rare, with tumor thrombus potentially leading to right atrial obstruction or fatal pulmonary embolism. This report presents a 56-year-old female with gallbladder cancer who developed SVCS due to tumor metastasis. The patient presented with cough, hoarseness, dyspnea, headache, and facial-cervical swelling. Contrast-enhanced chest computed tomography confirmed tumor thrombi in the left brachiocephalic vein, right brachiocephalic vein, and superior vena cava (SVC). Under cardiopulmonary bypass, SVC thrombectomy was performed, revealing two massive thrombi (20 × 80 mm, 10 × 80 mm). At the 11-month follow-up, the patient showed good recovery without thrombus-related complications. Surgical intervention directly relieved mechanical obstruction caused by tumor or thrombus, demonstrating its crucial role in palliating life-threatening obstruction and improving quality of life in advanced cancer with SVCS.

Introduction

Gallbladder cancer, an aggressive malignancy of the biliary system, shows increasing global incidence and mortality rates in recent years. ¹ This disease exhibits highly invasive biological behavior, typically manifesting as early local invasion and distant metastasis through direct infiltration, lymphatic spread, and hematogenous dissemination.^2,3 In hematogenous metastasis, while liver, lungs, and bones are common target organs, superior vena cava (SVC) metastasis with tumor thrombus formation is extremely rare. SVC tumor thrombus can cause mechanical vessel obstruction, leading to superior vena cava syndrome (SVCS). The etiology of SVCS can be broadly classified into extrinsic compression (e.g. tumor or fibrosis) and intraluminal obstruction (e.g. thrombus or tumor invasion). Treatment strategy selection is highly dependent on the underlying cause; endovascular stenting is typically the first-line approach for extrinsic stenosis, but its use remains controversial and is generally not preferred for intraluminal obstruction caused by malignant tumors. We report a rare case of gallbladder cancer secondary to SVCS in which the malignant obstruction was successfully relieved by open surgery as a palliative measure, resulting in significant symptomatic relief and restored eligibility for systemic therapy.

Case report

A 56-year-old female with a history of cholecystolithiasis was diagnosed with gallbladder cancer in January 2024. After receiving four cycles of chemotherapy with cisplatin, gemcitabine, and durvalumab, she underwent laparoscopic partial hepatectomy with extended cholecystectomy in May 2024. Histopathology revealed moderately to poorly differentiated adenocarcinoma. Postsurgery, the patient received consolidation therapy with cisplatin and gemcitabine. During the third month of consolidation therapy, she developed sudden onset of cough, hoarseness, dyspnea, headache, and facial-cervical swelling. Enhanced chest computed tomography (CT) revealed patchy filling defects in the left brachiocephalic vein, right brachiocephalic vein, and SVC, highly suggestive of extensive tumor thrombus (Figure 1). In contrast, Positron emission tomography-computed tomography (PET-CT) showed metabolically active soft tissue masses within the SVC and right brachiocephalic vein. Additionally, it revealed hypermetabolic right iliac lymph nodes, increased metabolism in the right fourth rib, left lung nodules, and bilateral pleural effusion. Notably, the lesion in the left brachiocephalic vein was not hypermetabolic (Figure 2). Echocardiography showed normal cardiac valve structure and function.

Figure 1.

Enhanced chest CT revealed patchy filling defects in the left brachiocephalic vein, right brachiocephalic vein, and superior vena cava.

CT: Computed tomography.

Figure 2.

PET-CT demonstrated hypermetabolic soft tissue masses within the lumen of the right brachiocephalic vein and superior vena cava.

PET-CT: Positron emission tomography-computed tomography.

Subsequently, a multidisciplinary team comprising cardiac surgery, vascular surgery, thoracic surgery, oncology, and radiology specialists was urgently convened. After weighing the patient’s distant metastatic tumor burden against the acute mortality risk of SVCS, we decided to perform SVC thrombectomy under systemic circulation. We explicitly discussed with the patient and their family the palliative purpose of this surgery, solely to relieve life-threatening SVCS, thereby improving quality of life and enabling subsequent systemic treatment, rather than curing the underlying metastatic cancer. They signed a written informed consent form. The procedure was performed through a median sternotomy. Following pericardiotomy, the SVC, azygos vein, brachiocephalic veins, and bilateral internal jugular veins were mobilized to achieve adequate exposure. After systemic heparinization, a venous drainage cannula was inserted through the right atrial appendage, and an arterial perfusion cannula was inserted via the ascending aorta to establish partial cardiopulmonary bypass. During the bypass, the flow rate was maintained at approximately 2.0–2.4 L/min/m², and the mean arterial pressure was kept between 50–70 mmHg. We then sequentially clamped the proximal SVC and distal right brachiocephalic vein. Upon longitudinal incision of the SVC, we discovered dark red thrombotic tissue (approximately 10 × 80 mm) in the left brachiocephalic vein (A in Figure 3), and yellow adipose-like tissue with dark red thrombotic material (approximately 20 × 80 mm) in the SVC and right brachiocephalic vein (B in Figure 3). Using a vascular dissector, the thrombus was separated and delivered to the distal right brachiocephalic vein, and the lumen was repeatedly flushed with copious saline. We then performed a parallel incision on the left brachiocephalic vein, completely removed the thrombotic tissue, and thoroughly irrigated with saline until no debris remained, followed by suturing the vascular incisions. After neutralizing heparin with protamine, we ensured stable blood pressure before removing the arterial perfusion cannula. One drainage tube each was placed in the pericardium and mediastinum. The sternum was secured with steel wires and plates, and the chest was closed in layers, completing the surgical procedure.

Figure 3.

Tumor thrombus removed from superior vena cava and brachiocephalic vein.

Pathological examination confirmed the resected tissue as moderately to poorly differentiated adenocarcinoma. Postoperatively, the patient was transferred to the intensive care unit for close monitoring. Six hours after surgery, the facial and cervical edema gradually subsided, and respiratory distress improved. With stable conditions, the patient was transferred to the general cardiac surgery ward on postoperative day two. Enhanced chest CT on postoperative day four showed no residual tumor thrombus in the SVC and brachiocephalic vein. The patient was discharged uneventfully on postoperative day five without any complications or adverse events.

The successful thrombectomy of the SVC immediately relieved the mechanical obstruction caused by the tumor thrombus. The patient showed significant improvement in symptoms, including reduced chest tightness and facial edema – typical manifestations of SVCS. This intervention not only effectively alleviated the patient’s clinical symptoms but also secured valuable time for subsequent antitumor therapy, significantly improving quality of life and extending survival. Following surgery, the patient received planned standardized chemotherapy in outpatient care. The patient subsequently underwent standardized adjuvant chemotherapy. Contrast-enhanced chest CT scans were performed at 1, 2, 3, and 5 months postoperatively, followed by PET-CT monitoring at 7 and 11 months. All imaging studies confirmed patency of the SVC and cephalic-brachial venous systems with no evidence of recurrent tumor thrombus. The patient’s other metastatic sites (including ribs, lungs, and lymph nodes) remained stable under continued systemic therapy, with no new symptomatic progression. Echocardiography at 1 month demonstrated normal cardiac structure and function. At the 11-month evaluation, the patient was in good general condition and had a satisfactory quality of life.

Discussion

SVCS is most commonly caused by lung cancer and lymphoma, with approximately 15,000 new cases annually in the United States. ⁴ Gallbladder cancer metastasis to the SVC with secondary SVCS is exceptionally rare, with limited literature reports. The severity of SVCS depends on the degree of obstruction, onset speed, and collateral circulation. ⁵ This patient presented with acute symptoms including cough, hoarseness, dyspnea, headache, and facial-cervical edema, indicating significant obstruction with inadequate collateral compensation. Without timely intervention, conditions may progress to respiratory failure, cerebral herniation, right atrial obstruction, or fatal pulmonary embolism, directly threatening patient survival.^5,6

Imaging plays a crucial role in evaluating SVCS. ⁷ In this case, contrast-enhanced CT anatomically delineated tumor thrombi in both brachiocephalic veins and the SVC, while PET-CT highlighted metabolically active components primarily in the right brachiocephalic vein and SVC. This discrepancy underscores the complementary roles of anatomical and functional imaging.

Currently, there are no standardized treatment guidelines for malignant SVCS. Traditional treatment approaches include chemotherapy, radiotherapy, supportive care, endovascular stenting, and surgical intervention. ⁸ In 2010, Batra et al. ⁹ the first reported case of gallbladder cancer with SVCS. Despite receiving antithrombotic therapy and radiotherapy, the patient died within 6 months of diagnosis, indicating that conservative treatment alone is insufficient to resolve mechanical obstruction. Sudden onset of dyspnea and headache indicates acute symptoms of airway compression and increased intracranial pressure, constituting an indication for surgical emergency. Stanford and Doty ¹⁰ confirmed this view in their study of SVCS patients with cerebral or airway symptoms, showing that the median survival was only 1.4 months in the nonsurgical group compared to 10.8 months in the surgical intervention group (p < 0.001).

While endovascular stenting is minimally invasive, it carries risks of restenosis and thrombus fragmentation with potential pulmonary embolism, particularly in brachiocephalic bifurcation lesions. In contrast, surgery provides prompt symptom relief by directly restoring venous flow, enabling subsequent antitumor therapy. In 2022, Kawaida et al. ¹¹ reported a case of radical surgery for invasive thymoma-induced SVCS, where the patient recovered well with symptom relief and showed no recurrence during 4 years of follow-up. This long-term disease-free survival contrasts sharply with Batra’s reported 6-month survival, highlighting the crucial role of active surgical intervention in improving malignant SVCS prognosis.

We acknowledge that percutaneous mechanical thrombectomy (such as AngioVac) is a minimally invasive and valuable option for managing SVC syndrome in selected patients. ¹² In this case, however, the decision for open surgery was based on a multidisciplinary assessment of several factors. First, the thrombus was extensive (8 cm) and involved both brachiocephalic veins and the SVC, which raised concerns about achieving complete clearance and immediate restoration of flow via a percutaneous approach, given the acute, life-threatening nature of the symptoms. While the risk of thrombus fragmentation is a consideration with any mechanical thrombectomy, the primary rationale was the need for immediate and definitive decompression. Open surgery under cardiopulmonary bypass provided direct visualization and control, allowing for thorough thrombus removal and immediate confirmation of venous patency.

The decision for radical thrombectomy was based on multidisciplinary risk–benefit analysis. The surgery aimed solely at relieving the life-threatening SVCS, not at treating the underlying metastatic burden. Although metastatic disease typically shifts the paradigm toward systemic therapy, acute local complications that threaten immediate survival warrant surgical intervention. Without urgent relief, the patient’s performance status would have rapidly deteriorated, precluding further antitumor treatment. This approach aligns with the oncologic principle of managing symptomatic dominant sites to provide rapid symptomatic relief and create a window for systemic therapy.

Despite the generally poor prognosis of gallbladder cancer, timely surgical management of SVCS as a local complication can meaningfully improve quality of life and extend survival. Our patient’s 11-month follow-up demonstrated durable symptomatic relief and maintained vascular patency, supporting the role of aggressive local palliation in selected patients with advanced cancer.

Conclusion

Acute SVCS may represent the most life-threatening emergency in advanced gallbladder cancer, posing a risk that even exceeds the direct threat of systemic metastasis. Emergency surgical thrombectomy can provide rapid, definitive palliative relief, restoring venous flow and enabling continued systemic treatment. The decision should be guided by a multidisciplinary evaluation that weighs the acute SVCS mortality risk against the overall disease course, reinforcing the principle that aggressive local intervention remains a critical component of palliative care for dominant symptomatic complications.