In human medicine, hemostatic disorders such as thrombocytopenia, hyperfibrinolysis, and disseminated intravascular coagulopathy (DIC) have been associated with many cancers. Acute hemorrhage secondary to hyperfibrinolysis has been predominantly reported with prostatic adenocarcinoma in human patients. To the author’s knowledge, severe bleeding due to paraneoplastic hyperfibrinolysis has not yet been reported in veterinary medicine. The case involves an 8-year-old neutered male Border Collie who was evaluated for progressive and recurrent epistaxis, having a history of 1 year of treatment for metastatic nasal adenocarcinoma. A progressive and severe coagulopathy thought to be related to the known cancer was diagnosed. Advanced coagulation testing was consistent with a chronic DIC and secondary hyperfibrinolysis. Throughout 1 week of hospitalization, the dog was treated with multiple blood products, vitamin K₁, and anti-fibrinolytic medications. While the dog was initially discharged home, the dog re-presented the following day and was humanely euthanized due to a perceived poor quality of life. Post-mortem analysis revealed a histopathologic diagnosis of disseminated adenocarcinoma. In dogs with disseminated nasal adenocarcinoma that are experiencing severe bleeding, paraneoplastic secondary hyperfibrinolysis should be considered as a differential. Knowing this association could help guide treatment recommendations for optimal patient management.

Case summary: Dynamic intrapelvic urinary bladder displacement (DIUBD) is an uncommon condition where the urinary bladder intermittently displaces caudally into the pelvic canal, resulting in episodic lower urinary tract obstruction. Although this phenomenon is recognized more commonly in canine patients with perineal hernias, documented feline cases remain rare. Trauma or pelvic fractures can compromise the strength and conformation of local musculature and fascia, permitting the bladder to slip caudally under changing pressure gradients. In this case, an 8-year-old spayed female domestic shorthair cat, previously affected by multiple healed pelvic fractures, developed progressive urinary and defecatory straining. Initial imaging, including abdominal radiographs and ultrasonography, confirmed a caudally displaced bladder occasionally reverting to a more cranial position. Blood work and repeated urinalyses indicated post-renal azotemia on re-presentation. Surgical exploration revealed a mobile bladder without a distinct muscular defect, prompting cystopexy to anchor the bladder in a stable cranial position. Postoperative monitoring showed rapid improvement in clinical signs and renal values, and follow-up imaging confirmed that the bladder retained its corrected orientation. This case supports the importance of thorough imaging and an early corrective procedure for cats with recurrent lower urinary obstruction and a history of pelvic fractures. Relevance and novel information: Although DIUBD is more often recognized in dogs, this case indicates that it can similarly arise in cats with a history of pelvic trauma. Targeted imaging coupled with cystopexy can successfully address the intermittent obstruction.

An 8‐year‐old spayed female Spanish Mastiff dog presented with a five‐month history of polyuria, polydipsia, persistent isosthenuria to hyposthenuria, urinary incontinence, and bilateral otitis externa, progressing to acute vestibular dysfunction. Endocrine testing excluded hypo‐ and hyperadrenocorticism, and the clinical signs were inconsistent with primary psychogenic polydipsia. Magnetic resonance imaging revealed severe left‐sided otitis media and interna and mild pituitary enlargement with signal characteristics suggestive of depleted arginine vasopressin stores. Transient central diabetes insipidus (CDI) was diagnosed secondary to chronic otitis media/interna based on imaging findings and a rapid response to desmopressin acetate. Treatment consisted of targeted otitis therapy, desmopressin acetate (DDAVP), and anti‐inflammatory glucocorticoids. Although glucocorticoids transiently reduced DDAVP responsiveness, this resolved after the course of glucocorticoids was completed. Following resolution of the otitis, DDAVP was discontinued and the dog’s water balance normalized without recurrence, confirming a reversible CDI secondary to localized inflammatory disease.

Adverse drug events are classified into type A (dose‐dependent and common) or type B (idiosyncratic and uncommon) reactions. Benzimidazole toxicosis in veterinary medicine typically induces nonspecific signs such as gastrointestinal distress and infrequent myelosuppression. Pancytopenia from benzimidazoles is exceptionally rare, with only one reported case. We present a 12‐year‐old, female, spayed, mixed‐breed dog with acute lethargy, anorexia, pyrexia and severe leukopenia after high‐dose benzimidazole therapy for suspected liver fluke infection. Despite hospitalisation, the dog remained unresponsive to antimicrobial therapies, developed neutropenic sepsis and was euthanized. Bone marrow analysis indicated marked haematopoietic hypoplasia suggestive of a type A adverse drug event secondary to an incidental, high‐dose fenbendazole administration.

Background: Fibrosing mediastinitis (FM) is a rare but serious condition characterized by excessive fibrous tissue proliferation in the mediastinum, often leading to compression of vital structures. Although considered benign, in people, clinical manifestations of FM can range from asymptomatic incidental findings on imaging studies to severe respiratory compromise and hemodynamic instability. While documented in people, FM has not yet been reported in dogs. Case Presentation: A 5‐year‐old male neutered Labrador Retriever presented with progressive respiratory distress, leading to pleural effusion and facial swelling. Thoracic radiographs revealed mediastinal mass‐like structures and pleural effusion. Computed tomography demonstrated a mediastinal mass‐like structure, enlarged tracheobronchial lymph nodes, multifocal narrowing of lobar bronchi and pulmonary veins and compression of the oesophagus and trachea. The dog was humanely euthanized due to poor response to empiric therapy and the owner's perception of suffering. A post‐mortem examination confirmed severe chronic mediastinal inflammation with fibrosis and vasculitis consistent with fibrosing mediastinitis. Conclusions: This report presents a unique case of FM in a dog.

Tubulointerstitial nephropathy and uveitis, otherwise more broadly known as oculorenal syndrome in human medicine, is a condition that has, to the authors’ knowledge, not been described in veterinary medicine. This report describes an 8‐year‐old, male, neutered, mixed breed dog with a 6‐year history of idiopathic epilepsy, chronically receiving zonisamide, who was presented for sub‐acute and recurrent episodes of severe generalised weakness, altered mentation and inappropriate urination. Throughout the dog's hospital visits, recurrent anterior uveitis, progressive severe metabolic acidosis, proteinuria, persistent granular casts and severe renal tubular acidosis, which progressed to renal insufficiency, were evident. Due to a poor prognosis and perceived poor quality of life, the dog was humanely euthanased. Postmortem examination and histopathology revealed tubulointerstitial nephropathy. In conjunction with clinical uveitis, this presentation reflects similarities with the human oculorenal syndrome, here referred to as canine oculorenal syndrome suspected secondary to chronic zonisamide administration.