Thoracoscopic Assisted PleuralPortTM Application in Seven Dogs Affected by Chronic Pleural Effusion.

Chronic non-septic pleural effusion is a condition that frequently may occur because of lung or pleural neoplasia, or chylothorax refractory to surgical treatment, in dogs. Effusion management can be performed with multiple pleurocenteses or the application of chest drains. New modified vascular devices have been used for patients with chronic diseases; they offer the advantage of allowing home management and do not require hospitalization. Eight PleuralPortTM devices were applied in seven dogs during thoracoscopic exploration and biopsy procedures; five were affected by mesothelioma; one by lung metastases from a mammary carcinoma; and one by chronic chylothorax. The median time of surgical procedure was 51 min; one developed pneumothorax post-operatively that resolved within 12 h after repeated drainage; one device was obstructed after 45 days and was successfully managed by flushing. All patients were discharged after 24 h. The median duration of port insertion in cancer patients was 5 months and those dogs were euthanized because of tumor progression; in the dog with chylothorax, the device was removed after 1 year when the effusion had resolved.

Etiopathogenesis of Canine Cruciate Ligament Disease: A Scoping Review.

The spontaneous rupture of the cranial cruciate ligament in dogs remains a pathoetiologic puzzle. Despite much progress in research over the past years, the systemic and local mechanisms leading to ligament degeneration and structural failure remain largely obscure. This scoping review focuses on pathogenesis and aims at summarizing and interpreting today's knowledge on causes of canine cruciate ligament rupture, i.e., the multifactorial mechanisms leading to degenerative stifle joint disease with collagen matrix degeneration and structural failures. Thus, the initial view of traumatic ligament rupture, fostered by "wear and tear", has clearly been replaced by a new concept of systemic processes linked to progressive degenerative joint disease and ligament failure; thus, the term "cranial cruciate ligament disease" has been coined and is generally accepted. In addition, cruciate ligament rupture in people shares some similarities with the lesion in dogs; therefore, the review also includes comparative studies. The methods used were based on the PRISMA-ScR model (Preferred Reporting Items for Systematic Reviews and Meta-Analyses Extension for Scoping Reviews).

Immunoexpression of Relaxin and Its Receptors in Stifle Joints of Dogs with Cranial Cruciate Ligament Disease.

The etiology of spontaneous cranial cruciate ligament rupture in dogs is unknown despite being one of the most impacting orthopedic diseases in dogs. Numerous studies have contributed to the understanding of a multifactorial pathogenesis, this, however, without identifying a pivotal link to explain progressive collagen degeneration and osteoarthritic changes. In human medicine, recent reports have identified relaxin as a triggering factor in ligament ruptures in knee and metacarpal joints. We thus hypothesized that relaxin might also play a role in canine cruciate ligament rupture. Relaxin's primarily known property is connective tissue remodeling through collagenolysis. We therefore investigated relaxin and its cognate receptors LGR7/LGR8 in 18 dogs with cranial cruciate ligament disease (CCLD) and compared them to a group of dogs with normal stifle joints. Applying immunohistochemistry (IHC), double immunofluorescence (dIF), and western blot analysis (WB), we found strong and significantly increased expression of both relaxin and its receptors in ruptured cruciate ligaments, and in synovial membranes. Pattern of immuno-staining on dIF strongly suggests relaxin binding to primed receptors and activation of signaling properties, which in turn may have affected collagen matrix metabolism. Thus, in canine cranial cruciate ligament disease, relaxin/receptor signaling may be a primary trigger for collagen fiber degradation and collagen lysis, eventually followed by ligament rupture.

On the nature of canine aural haematoma and its treatment with continuous vacuum drainage.

OBJECTIVES: To evaluate continuous vacuum drainage from the convex side of the pinna for surgical treatment of aural haematoma in dogs. To investigate aural haematoma fluid and cartilage samples harvested during surgery in an attempt to elucidate the etiopathogenesis of the lesion. MATERIALS AND METHODS: Ten client-owned dogs with aural haematoma were treated by convex-side vacuum drainage using different types of vacuum drains and containers and were followed-up for at least 6 months. Systemic blood samples and aural haematoma fluids were analysed for biochemical, haematologic and electrophoretic content. Cartilage samples were examined histologically. RESULTS: Nine of the 10 dogs were successfully treated without recurrence at 6 months postoperatively and with excellent cosmetic results. In one case, infection required early drain removal and delayed healing was associated with wrinkling of the pinna. Fluid sample analysis suggested that "aural haematoma" contains a transudate that accumulates within a cartilage-lined cavity. Histologic examination of the tissue samples revealed clefts of the pinna cartilage, with the luminal surface often lined with granulation tissue. Fluids and cartilage lacked evidence of inflammation. CLINICAL SIGNIFICANCE: This technique was characterised by patient comfort, tolerance of drains, absence of dressings and good cosmetic outcome. The results of fluid analysis suggest that the term "aural seroma" would be more appropriate for this condition.

Relaxin of prostatic origin might be linked to perineal hernia formation in dogs.

Perineal hernia occurs spontaneously in older male dogs after idiopathic weakening of the pelvic diaphragm. Hernias invariably contain cystic paraprostatic tissues. Castration reduces incidence and recurrence after surgical repair. Although cystic prostatic hypertrophy is a consistent feature in patients with perineal hernia, an endocrine link of the disease to steroid sex hormones has not been demonstrated. Employing immunohistochemistry, we found intense relaxin immunoreactivity in dogs with perineal hernia within the epithelia of hypertrophic prostates and in periprostatic tissues. The prostate of normal dogs exhibited similar but less intense relaxin staining. In neutered dogs with prostatic atrophy, relaxin immunostaining was weak or absent. Periprostatic cysts highly expressed relaxin precursors in the fluid phase as shown by SDS-gel electrophoresis. Relaxin of prostatic origin, therefore, is possibly a local factor in connective tissue weakening and subsequently in perineal hernia formation.