Malignancy-associated internal jugular venous thrombosis following chemoradiation for oropharyngeal carcinoma

Abstract

Abstract Background: Head and neck squamous cell carcinoma (HNSCC), particularly HPV-associated oropharyngeal cancer, frequently requires multimodal therapy (surgery, radiation, chemotherapy). These treatments induce significant morbidity, including tissue changes and vascular compromise, elevating thrombotic risk. Upper extremity deep vein thrombosis (UEDVT), especially involving the internal jugular vein (IJV), is uncommon in HNSCC and presents diagnostic and therapeutic challenges, compounded by comorbidities like chronic kidney disease (CKD) and contraindications to contrast imaging. Cancer-associated thrombosis (CAT) risk is heightened by tumor biology, therapy-induced endothelial injury, and extrinsic compression. Optimal management must balance thrombotic risk against bleeding susceptibility and renal limitations. This case illustrates these complexities. Case Presentation: A 74-year-old male with stage IV CKD (creatinine 2.6 mg/dL, GFR 25 mL/min/1.73m²), hypertension, dyslipidemia, and history of smoking presented with 4 days of painless right upper extremity and neck swelling. Six months prior, he was diagnosed with HPV-positive (p16+) oropharyngeal SCC with nodal involvement, treated with carboplatin/fluorouracil chemotherapy and 14 days of radiation. Initial symptoms were misdiagnosed as infection. Post-treatment, he experienced significant GI toxicity and anemia (Hb 8.4 g/dL), requiring transfusions and erythrocyte stimulating agent, and declined surveillance scans. Examination confirmed right neck/upper limb swelling; a portacath was present on the left chest. Ultrasound confirmed right IJV thrombosis. CT neck without contrast showed post-treatment changes and reduced right neck mass size but could not assess vessel patency due to CKD prohibiting contrast. Laboratory findings included persistent anemia and stable stage IV CKD. Management and Outcome: The patient was admitted and initiated on a heparin drip for acute UEDVT management. Given CKD stage IV and the need for ongoing anticoagulation, he was transitioned to apixaban on discharge. He was discharged the same day with instructions to continue apixaban and follow up for management of his thrombosis, HNSCC, CKD, and other comorbidities. Discussion: This case highlights a rare right IJV thrombosis in a high-risk HNSCC patient post-chemoradiation. The etiology is multifactorial: 1) Cancer Hypercoagulability: HPV+ oropharyngeal SCC with nodal involvement inherently increases CAT risk via procoagulant factors. 2) Treatment Effects: Chemotherapy (carboplatin/5-FU) and radiation cause endothelial injury, inflammation, and disrupt coagulation balance. Post-treatment edema/fibrosis likely caused venous stasis or compression in the right neck, supported by imaging. 3) Comorbidities: Stage IV CKD contributes to both thrombotic and bleeding diatheses. While a left-sided portacath was present, contralateral thrombosis is unlikely to be the primary cause. Unilateral swelling and lack of SVC involvement on imaging argued against SVC syndrome. Diagnostic challenges arose due to contraindication to contrast CT, necessitating reliance on ultrasound. Anticoagulation choice (apixaban) required careful consideration of renal function and bleeding risk (history of GI toxicity, anemia). This case underscores the heightened thrombotic risk in HNSCC patients due to the confluence of disease biology, aggressive local therapy, and patient-specific factors like CKD. Vigilance for atypical UEDVT presentations and individualized anticoagulation strategies are crucial in this complex population.