Case summary: A 7-year-old neutered male Maine Coon cat was referred for an 18-month history of chronic mixed small- and large-bowel diarrhoea with tenesmus, marked weight loss and severe debilitation. Abdominal ultrasonography revealed focal ileal and colonic mural thickening with regional lymphadenomegaly, and colonoscopy identified a severe colonic stenosis precluding biopsy collection. Subtotal colectomy with ileocolic anastomosis was performed. Histopathology demonstrated severe transmural chronic inflammation of the ileum and colon, with deep ulceration, fibroplastic remodelling and a mixed lymphoplasmacytic and neutrophilic infiltrate. Surgery, dietary optimisation and cobalamin supplementation resulted in clinical improvement and weight regain, but a new colonic stenosis developed seven months later and was treated by endoscopic balloon dilation. Repeated fluorescence in situ hybridisation analyses failed to identify adherent or invasive bacteria. Immunosuppressive therapy was subsequently introduced, but clinical deterioration eventually progressed despite treatment, and the cat was euthanised following presentation in decompensated hypovolaemic shock. Relevance and novel information: This report describes an unusual fibrostenotic phenotype of feline chronic inflammatory enteropathy, characterised by recurrent intestinal strictures and transmural mixed lymphoplasmacytic–neutrophilic inflammation. The repeated absence of adherent or invasive bacteria argues against a primary bacterial-driven process. The clinicopathological features closely resemble the fibrostenosing phenotype of human Crohn’s disease, including ileocolonic involvement, deep ulceration, transmural inflammation and postoperative recurrence. This case expands the recognised spectrum of feline chronic inflammatory enteropathy and suggests that proactive monitoring may help identify disease progression earlier and guide more timely control of inflammation, even during periods of apparent clinical stability.
Case Summary Case 1: A 5‑month‑old male Ragdoll cat demonstrated acute anorexia, mild tachypnoea, and dull mentation. Cardiac auscultation revealed a grade 4/6 systolic murmur at the right cardiac apex. Echocardiography revealed marked right atrial enlargement, apical displacement of the tricuspid valve leaflets, and partial atrialization of the right ventricle, which were consistent with Ebstein’s anomaly (EA). Medical treatment was discontinued at the owner's request after 1 month. The cat remained relatively stable for several months but died from heart failure 16 months after the initial diagnosis. Necropsy confirmed apical displacement of the tricuspid septal leaflet and partial displacement of the anterior leaflet. Case 2: A 4-year-6-month-old spayed female domestic cat presented with lethargy, hyporexia, and acute tachypnea. Echocardiography revealed marked right atrial enlargement, apical displacement of the tricuspid septal leaflet, severe tricuspid regurgitation (peak regurgitant velocity 2.8 m/s), and partial atrialization of the right ventricle, which confirmed the diagnosis of EA. Clinical signs improved following medical treatment; however, the cat died at home 1 month later. Necropsy was declined, and the cause of death remained undetermined. Relevance and Novel Information This report describes two cases of feline EA and documents a rare morphological variant involving partial displacement of the anterior tricuspid leaflet. These findings expand current knowledge of anatomical variation in feline EA and may have implications for diagnosis and interpretation of echocardiographic findings.
Case summary: An 8-year-old neutered male domestic shorthair cat was evaluated for stertor, sneezing and right-sided nasal discharge. Rhinoscopy identified a mass occupying the choanae and nasopharynx. Histopathological examination of samples from two endoscopic debulking procedures revealed well-differentiated thyroid tissue composed of colloid-containing follicles lined by uniform cuboidal cells. Computed tomography (CT) demonstrated a right nasal and nasopharyngeal mass; both cervical thyroid lobes appeared normal. Serum total thyroxine concentration was within the reference interval (2.21 µg/dl; reference interval 1.0–4.0) with no evidence of hyperthyroidism. Technetium-99m pertechnetate scintigraphy revealed faint, poorly delineated activity over the right nasal cavity. As radiotherapy was unavailable and invasive surgery was declined, 370 MBq (10 mCi) iodine-131 was administered following progression. Four weeks later, worsening respiratory signs and epistaxis prompted repeat CT, which documented destruction of the ethmoidal turbinates, medial orbital wall and cribriform plate, with retrobulbar and intracranial extension. Given the extensive disease and poor prognosis, the owner elected euthanasia. The progressive, destructive behaviour supported a diagnosis of well-differentiated, non-hypersecretory ectopic follicular thyroid carcinoma despite its bland histological appearance. Relevance and novel information: To the authors’ knowledge, this is the first reported ectopic follicular thyroid carcinoma arising in the nasal cavity and choanae of a cat. Well-differentiated thyroid tissue in a feline nasal mass should raise suspicion of ectopic thyroid neoplasia despite normal cervical thyroid glands and absent hyperthyroidism. Rapid recurrence and progressive local invasion demonstrate that bland histological features do not exclude malignant behaviour, supporting cross-sectional staging and early consideration of definitive local treatment.
Case summary: A 10-year-old, male neutered, 7.5kg Sphynx cat was referred for patient stabilization for presumed acute congestive heart failure (CHF). On presentation, the patient was tachypnoeic (44 breaths/min) and tachycardic with poor femoral pulses (HR 300bpm). Emergency cardiac assessment identified sustained monomorphic ventricular tachycardia (VT) associated with hypertrophic cardiomyopathy phenotype and concurrent B-lines. Four boluses of IV lidocaine (0.5mg/kg) and subsequently IV esmolol (0.1 mg/kg) were administered with no success. The VT acutely deteriorated into ventricular fibrillation, at which point the patient lost consciousness, with absent pulses. Emergency biphasic defibrillation was performed at 30 J and was successful in restoring sinus rhythm; return to spontaneous circulation did not require additional chest compressions. Oral sotalol and CHF treatment were started. A complete echocardiogram identified an area of hypokinesia in the left ventricular free wall. Speckle tracking echocardiography identified global reduction in longitudinal and circumferential systolic function. High-sensitivity troponin I was 7.75ng/ml at presentation and decreased over time (7 days later 0.43 ng/ml and 0.44 2 months later). The patient was free from clinical signs for 4 months, after which he developed refractory CHF. Relevance and novel information: Ventricular tachycardia is an uncommon clinical presentation in cats with hypertrophic cardiomyopathy and can acutely deteriorate leading to cardiac arrest. In the present case, cardiac defibrillation was effective in restoring sinus rhythm and preventing arrhythmic death. Although prognosis in the acute setting seemed poor, good quality of life was achieved for 4 months since emergency presentation.
Case summary: A 6-day-old female domestic shorthair kitten weighing 140 g was presented with poor nursing and severe cardiogenic pulmonary oedema. Initial echocardiography revealed bilateral atrial enlargement, a membranous ventricular septal defect (VSD), and aortic narrowing. Follow-up assessment demonstrated progression of cardiomegaly and identification of a patent ductus arteriosus (PDA). On day 48, multidetector CT confirmed a focal, severe narrowing of the aorta between the origin of the left subclavian artery and the insertion of the ductus arteriosus, consistent with aortic coarctation with concurrent VSD and PDA. Owing to the extremely low birth weight, surgical intervention was not feasible, and medical management was continued. The kitten developed transient atrial fibrillation on day 72, which resolved with diltiazem. Despite comprehensive medical therapy, refractory congestive heart failure recurred, and the kitten died on day 160. Postmortem examination confirmed focal aortic narrowing adjacent to a cylindrical PDA, marked biatrial dilatation, biventricular concentric hypertrophy, a membranous VSD and a right atrial mural thrombus. Histopathology of the pulmonary artery and PDA demonstrated elastic artery-like remodelling, consistent with chronic haemodynamic loading and secondary pulmonary hypertension. Relevance and novel information: aortic coarctation is an exceptionally rare congenital cardiovascular anomaly in cats. This report describes the clinical presentation and detailed postmortem characterisation of aortic coarctation with concurrent VSD and PDA in a kitten, highlights the diagnostic utility of advanced antemortem imaging, and illustrates the limitations of medical management in the presence of complex structural disease.
