Esophageal squamous cell carcinoma in a Dachshund with congenital type 9 vascular ring anomaly: a case report

Article information

Korean J Vet Res. 2025;65.e2

Publication date (electronic) : 2025 March 31

doi : https://doi.org/10.14405/kjvr.20240050

Hongju Lee^1,2, Gukil Joung¹, Seong-Gyu Jeong¹, Tae-Sung Hwang³, Joong-Hyun Song^1,

¹Department of Veterinary Internal Medicine, College of Veterinary Medicine, Chungnam National University, Daejeon 34134, Korea

²Ulsan S Animal Medical Center, Ulsan 44726, Korea

³Institute of Animal Medicine, Department of Veterinary Medical Imaging, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Korea

^*Corresponding author: Joong-Hyun Song College of Veterinary Medicine, Chungnam National University, 99 Daehak-ro, Yuseong-gu, Daejeon 34134, Korea Tel: +82-42-821-6756 E-mail: jh.song@cnu.ac.kr

Received 2024 August 1; Revised 2025 January 10; Accepted 2025 January 14.

Esophageal neoplasia in dogs is rare and usually malignant, often locally invasive with metastasis [1]. Esophageal squamous cell carcinoma (ESCC) originates from the squamous epithelial cells lining the esophagus, and is relatively uncommon in dogs [1,2]. Treatment options for ESCC include surgery, chemotherapy and radiotherapy [2,3]; however, the response rate to treatment is often poor owing to the tumor's aggressive growth and location [2]. The etiology of ESCC in dogs is unclear. However, potential risk factors include chronic esophageal inflammation, carcinogen exposure, and genetic predisposition [4].

Vascular ring anomaly (VRA) is a congenital malformation of the aortic arch and its branches, forming a complete or partial ring around the trachea and esophagus, causing compression and chronic inflammation of the esophagus [5–7]. Nine types of VRA exist. Among them, type 9 VRA is characterized by an anatomically normal left aortic arch with aberrant intercostal arteries, leading to partial esophageal compression due to the first two intercostal arteries branching off the dorsal aorta [6,7].

A 9-year-old spayed female Dachshund has been experiencing chronic regurgitation and weight loss for the past three months. Over the past two weeks, the dog has developed additional symptoms, including anorexia, lethargy, and excessive salivation. Physical examination revealed a decreased body condition score (1 on a 9-point scale), severe muscle loss, elevated rectal temperature (39.8°C), and enlarged bilateral submandibular lymph nodes (right, 22 × 15 mm; left, 22 × 32 mm). Fine-needle aspiration of the lymph nodes showed no malignancy or metastasis, indicating reactive lymph nodes. No other remarkable findings were noted upon physical examination.

Blood analysis using ProCyte Dx (IDEXX, USA) revealed normocytic-normochromic non-regenerative mild anemia (hematocrit 32.2%; reference interval, 37.0%–61.0%), significant leukocytosis (40.08 × 10³/μL; reference interval, 5.05–16.76 × 10³/μL) with a left shift, and thrombocytosis (655.9 × 10³/μL; reference interval, 148.0–484.0 × 10³/μL), confirmed via manual pack cell volume and blood film examination. The serum biochemical profile using Catalyst One (IDEXX) showed elevated C-reactive protein (9.8 mg/L; reference interval, 0.1–1.0 mg/L) and decreased glucose (53 mg/dL; reference interval, 70–143 mg/dL), albumin (1.9 g/dL; reference interval, 2.2–3.9 g/dL), and creatinine (0.4 mg/dL; reference interval, 0.5–1.6 mg/dL).

Radiographs revealed a well-defined circular mass in the esophagus, approximately 5 cm in diameter, prompting the need for computed tomography (CT) scanning to accurately localize the tumor and evaluate for metastasis. The CT scan revealed dilation and a distal esophageal mass measuring 54 × 40 × 40 mm (Fig. 1A and B), and a VRA classified as type 9 (Fig. 1B and C). This anomaly consists of a right-sided aortic arch along with a left-sided brachiocephalic trunk, which gives rise to both the right and left common carotid arteries and the left subclavian artery. Additionally, the CT scan revealed focal consolidation and a ground-glass opacity pattern in the left cranial, right cranial, and right middle lung lobes. These findings suggested aspiration pneumonia, though differentiation from pulmonary metastasis remained challenging.

Fig. 1.

Computed tomography (CT) findings (soft tissue window); sagittal plane (A), transverse plane (B) and volume-rendered three-dimensional (3D) CT reconstruction (C). (A) An esophageal mass (red arrow) and dilation (yellow arrow) were identified. (B) A mass in the esophagus (red arrow), and a VRA characterized by a right-sided aortic arch (green arrow), was identified. (C) Volume-rendered 3D CT reconstruction showing the vascular ring anomaly type 9. The right-sided aortic arch (A) and the left-sided brachiocephalic trunk are highlighted, With the labeled components as follows: A, aorta; RSA, right subclavian artery; RC, right common carotid artery; LC, left common carotid artery; LSA, left subclavian artery; VRA, vascular ring anomaly.

Esophagoscopy (EVIS EXERA III CLV-190; Olympus, USA) revealed a mass in the distal esophagus with erosion and ulceration around it (Fig. 2A and B). The esophageal lumen was narrowed, and torsion due to the mass and the VRA was observed. An endoscopic biopsy was performed on the lesion of the esophageal mass, and histological examination confirmed ESCC and chronic inflammation of the esophagus (Fig. 2C and D).

Fig. 2.

Endoscopic images and histopathological findings of esophagus. (A) Endoscopic image of esophageal mass in the distal esophagus (arrow), with esophageal dilation and considerable saliva accumulation. (B) Endoscopic image of esophagus with erythematous lesion (arrowhead) around the mass. (C) Histological sections of esophageal wall with epithelial hyperplasia, indicating chronic inflammation (hematoxylin and eosin staining [H&E], scale bar = 200 µm), (D) Histological sections of esophageal luminal mass, diagnosed as esophageal squamous cell carcinoma (H&E, scale bar = 50 µm).

At the time of diagnosis, chemotherapy was selected over immediate surgical resection due to the tumor’s size, location, and invasiveness, which posed a high risk for severe complications with surgery. Chemotherapy was therefore pursued to reduce tumor size and potentially downstage the tumor for future surgical intervention. The patient received carboplatin chemotherapy, and supportive management with assistant feeding was started. However, after 4 weeks of chemotherapy, clinical symptoms did not improve. Consequently, cytoreductive surgery was scheduled; however, during thoracostomy, extensive adhesions to neighboring tissue were discovered, and a diffuse lung lesion was suspected. The dog was subsequently euthanized 35 days after diagnosis. At necropsy, esophageal mass, VRA, and esophageal dilation were identified (Fig. 3). Post-mortem histopathological examination of the esophageal mass revealed squamous cell carcinoma with extensive transmural neutrophilic and histiocytic inflammation, serositis, and multifocal mucosal thrombosis (Fig 3B and C). No evidence of metastasis to adjacent organs including the heart, bronchial lymph nodes, and liver, was identified in the post-mortem histopathological sections. However, a histopathological examination of the lungs could not be performed due to the compromised tissue integrity at the time of necropsy.

Fig. 3.

Histopathological findings of esophageal mass and bronchial lymph node and gross necropsy observations. (A) Gross examination at the time of necropsy revealed an esophageal mass (black arrow), a vascular ring anomaly (red arrow), a suspected metastatic lung lesion (blue arrow), and an esophageal dilation (yellow arrow). (B) Histological section of esophageal mass with extensive transmural neutrophilic and histiocytic inflammation (hematoxylin and eosin staining [H&E], scale bar = 50 µm), (C) Histological section of bronchial lymph nodes accompanied by chronic lymphoid hyperplasia (H&E, scale bar = 200 µm).

In veterinary medicine, the reports of canine ESCC are rare, with no documented cases of coexistence with VRA [2,4]. Chronic irritation and inflammation of the esophagus are considered risk factors for ESCC, and esophageal achalasia, commonly associated with VRA, is one such factor that causes chronic inflammation in the esophagus [8,9]. In our case, VRA may have influenced the development of ESCC. Additionally, the dog had a rare type 9 VRA, which likely results in more irritation and inflammation than other types of VRA [6,7]. Chronic inflammation can create a pro-carcinogenic environment through mechanisms such as the production of reactive oxygen species and repeated epithelial damage [9]. Although a direct causal relationship between VRA and ESCC has not been conclusively established, several human cases suggest that chronic irritation from VRA-associated compression may contribute to the development of ESCC [9,10]. In veterinary medicine, this potential link remains largely unexplored, but the chronic inflammation observed in this case suggests a similar risk [1,3,11]. Persistent inflammatory stimuli, such as those associated with VRA-induced esophageal compression, can lead to epithelial cell damage and increased cellular turnover, which in turn elevates the risk of malignant transformation [8,9]. Furthermore, oxidative stress generated by chronic inflammation promotes DNA damage, contributing to cancer development [9]. Thus, the role of chronic inflammation in the pathogenesis of ESCC in this case cannot be overlooked, and early surgical correction of VRA may reduce the risk of malignancy.

Accurate anatomical classification of VRA is essential for surgical planning [5–7]. In veterinary medicine, although the traditional classification system included four types [5], recent advancements in diagnostic technology have expanded this to system to nine types for better categorization [6,7]. Type 9 VRA, as identified in this case, is rare, with no reported in dogs since 1989 [6,7]. Given the rare nature of type 9 VRA and its potential to cause significant esophageal irritation, future studies should focus on investigating the role of early VRA correction in reducing the risk of esophageal neoplasia [6,7]. Additionally, long-term follow-up of similar cases may help establish a clearer link between chronic esophageal conditions and cancer development. Therefore, we recommend prompt surgical correction of VRA.

Reports of ESCC in veterinary medicine are rarely reported [1,3]. Based on the safe application of carboplatin in combination with paclitaxel as a neoadjuvant chemotherapy for the treatment of ESCC in humans [12], and the evidence of partial remission achieved with carboplatin monotherapy in canine tonsillar squamous cell carcinoma [13], we selected carboplatin as a palliative chemotherapeutic agent for this case. To date, no established treatment method for ESCC exists in either humans or dogs; although treatments for other esophageal tumors may be applied, the rapid and invasive nature of ESCC results in poor treatment response rates [1,3]. The 5-year overall survival rate of a human study ranges from 15% to 50%, depending on the stage at diagnosis and treatment method [14]. Accordingly, early detection and a multimodal approach—including surgery, chemotherapy, and radiation therapy—are known to be crucial for improving patient prognosis. In this case, surgical tumor resection was deemed likely to cause significant surgery-related complications (e.g., poor exposure, poor surgical margin, tension on the anastomosis, etc.) without substantially impacting the patient’s prognosis. Therefore, a chemotherapeutical trial with carboplatin was explored. However, the patient showed no response to chemotherapy. To address the limitations in treating ESCC, various attempts have been made in human medicine, including photodynamic therapy and chemoradiotherapy, though the outcomes remain limited [9,15]. This highlights the extremely poor prognosis and poor response to carboplatin chemotherapy of advanced ESCC and underscores the need for further research into effective treatment strategies.

Our case had a considerable limitation in that the causal relationship between the VRA and ESCC could not be definitively established. The advanced stage of diagnosis and multiple confounding factors further limited the assessment of therapeutic efficacy. Despite these limitations, this case highlights the potential link between chronic esophageal compression caused by VRA and the development of ESCC, underscoring the need for more aggressive diagnostic and therapeutic approaches in similar cases.

In conclusion, this is the first case report of concurrent VRA and ESCC and of type 9 VRA in veterinary medicine. Although the causal relationship between VRA and ESCC cannot be definitively established, VRA may be a risk factor for ESCC by inducing chronic inflammation and irritation in the esophagus. Furthermore, given the poor prognosis when VRA and ESCC coexist, prompt correction of VRA is recommended.