Recurrent canine cervical sialocele is most often caused by incomplete excision of the mandibular–sublingual gland complex, leading to anatomical distortion and concealment of residual tissue. This case describes the multimodal management of a repeatedly recurrent cervical sialocele in a young, small-breed dog following multiple previous revision surgeries. A stepwise bridging strategy was adopted before definitive salvage surgery. Oral phenobarbital was instituted, resulting in partial reduction in fluid accumulation and improved comfort. Ultrasound-guided intracavitary sclerotherapy with OK-432 was then performed, inducing a localized fibrotic response but without durable cure. Final resolution was achieved only after salvage ventral paramedian (VPM) sialoadenectomy, which provided wide exposure for complete excision of deeply concealed sublingual remnant tissue within a fibrotic pseudocapsule. Histology confirmed a cervical sialocele. Transient neuropraxia resolved within 3 weeks, and no recurrence was observed at 6 months postoperatively. To the authors’ knowledge, this is the first report describing intracavitary OK-432 sclerotherapy as part of a staged multimodal strategy for canine cervical sialocele. This case illustrates the feasibility of integrating medical salivary suppression and minimally invasive sclerotherapy as bridging measures before salvage VPM surgery for refractory cervical sialocele.

Carcinoma of unknown primary origin (CUP) involving the skeletal system is rare in dogs and may closely mimic primary bone neoplasia or multicentric lymphoma, creating substantial diagnostic challenges. A 15-year-old spayed female Jindo-mix dog was referred for rapidly progressive tetralimb lameness and inability to stand following a 2-week history of worsening forelimb lameness. Computed tomography revealed aggressive multifocal osteolytic and osteoproliferative lesions involving the pelvis, distal femur, and lumbar vertebra, accompanied by generalized lymphadenopathy, raising differential diagnoses including osteosarcoma, lymphoma, and metastatic neoplasia. Serial CT examinations demonstrated rapid progression of the dominant left ischial lesion, which was considered most consistent with a primary bone neoplasm and was surgically excised for definitive diagnosis. MRI failed to identify clinically significant neurologic disease. Histopathologic examination of a surgically excised ischial lesion favored poorly differentiated epithelial malignancy, although lymphoma could not initially be excluded. During hospitalization, serial thromboelastography (TEG) and coagulation testing demonstrated a predominantly hypercoagulable profile despite antithrombotic therapy. Following acute clinical deterioration, contrast-enhanced CT identified thrombosis involving the splenic vein and caudal vena cava, pulmonary thromboembolism (PTE), and concurrent multi-organ infarction. Cytology of an enlarged peripheral lymph node suggested metastatic carcinoma, and postmortem immunohistochemistry supported epithelial differentiation, and in the absence of an identifiable primary tumor despite comprehensive diagnostic evaluation, the case was clinically classified as carcinoma of unknown primary origin. This case highlights an unusual diagnostic presentation of skeletal CUP mimicking osteosarcoma or lymphoma and complicated by fatal cancer-associated thrombosis. Rapidly progressive multifocal bone lesions accompanied by hypercoagulability should prompt consideration of metastatic carcinoma, including carcinoma of unknown origin, even in the absence of an identifiable primary tumor.

Small bowel obstruction (SBO) in dogs is most commonly caused by foreign bodies or neoplasia; however, SBO secondary to transmural fibroplasia remains a rare clinical complication of canine chronic enteropathy. This report describes the complex case of mechanical SBO caused by transmural ileal fibroplasia and inflammation at the ileocolic junction in a 9-year-old mixed-breed dog with concomitant hyperadrenocorticism (HAC). The primary presentation involved chronic severe weight loss and intermittent anorexia, contrasting with the acute presentation typical of most SBO cases. Imaging studies revealed severe, circumferential thickening up to 10 mm of the small intestine wall at the ileocolic junction (ICJ), resulting in complete luminal stricture and marked proximal dilation. Surgical intestinal resection and anastomosis were performed for alleviation of the obstruction, and histopathology confirmed severe mural and serosal enteritis with extensive fibroplasia extending into the adjacent mesentery, thereby excluding neoplastic processes. Quantitative PCR analysis demonstrated a significant upregulation of mRNA expression for PDGFRB and FGFR compared to normal tissue. Postoperative recovery was rapid; although soft feces persisted for one month, normal stool consistency was subsequently restored, and the patient achieved significant weight gain. This case underscores the diagnostic and therapeutic challenges associated with non-neoplastic, inflammation-driven SBO and suggests that activation of the PDGFR-β/FGFR pathways may play a key role in fibroplasia-related intestinal strictures, offering a novel molecular perspective beyond conventional SBO etiologies.