Surgical Site Infection Rate after Hemilaminectomy and Laminectomy in Dogs without Perioperative Antibiotic Therapy.

OBJECTIVE: The aim of this study was to retrospectively review the surgical site infection (SSI) rate in dogs undergoing laminectomies without perioperative antibiotics, and compare those data with the expected infection rate for clean surgical wounds in dogs undergoing similar procedures. METHODS: This was a retrospective single-centre study composed of dogs that underwent hemilaminectomies or laminectomies for thoracolumbar disc herniation or lumbosacral disease during a 2-year period (during 2015 and 2016). All incisional complications within 30 days were recorded and divided into superficial, deep or organ/space infections. Those dogs that received perioperative or postoperative antibiotics due to non-related comorbidities and those with incomplete medical records during the study period were excluded. RESULTS: Of 221 consecutive hemilaminectomy and laminectomy procedures, 154 were included in this research study. One superficial wound infection was recorded and treated with antimicrobials. Overall, the SSI rate was 0.6%, while the expected SSI rate in clean operative wounds in dogs and cats is 2.0 to 4.8%. The SSI rate in human spinal surgery is 0.7 to 4.3%. CLINICAL SIGNIFICANCE: Considering the low incidence of SSI in our study group, the routine use of perioperative antibiotic prophylaxis in dogs undergoing laminectomy procedures should be reconsidered to help address the global problem of bacterial resistance.

Cooperative and redundant roles of VEGFR-2 and VEGFR-3 signaling in adult lymphangiogenesis.

Activation of vascular endothelial growth factor (VEGF) receptor-3 (VEGFR-3) by VEGF-C initiates lymphangiogenesis by promoting lymphatic proliferation and migration. However, it is unclear whether VEGFR-3 signaling is required beyond these initial stages, namely during the organization of new lymphatic endothelial cells (LECs) into functional capillaries. Furthermore, the role of VEGFR-2, which is also expressed on LECs and binds VEGF-C, is unclear. We addressed these questions by selectively neutralizing VEGFR-3 and/or VEGFR-2 for various time periods in an adult model of lymphangiogenesis in regenerating skin. While blocking either VEGFR-2 or VEGFR-3 with specific antagonist mAbs (DC101 and mF4-31C1, respectively) prior to lymphatic migration prevented lymphangiogenesis, blocking VEGFR-3 subsequent to migration did not affect organization into functional capillaries, and VEGFR-2 blocking had only a small hindrance on organization. These findings were confirmed in vitro using human LECs and anti-human antagonist mAbs (IMC-1121a and hF4-3C5): both VEGFR-2 and -3 signaling were required for migration and proliferation, but tubulogenesis in 3D cultures was unaffected by VEGFR-3 blocking and partially hindered by VEGFR-2 blocking. Furthermore, both in vitro and in vivo, while VEGFR-3 blocking had no effect on LEC organization, coneutralization of VEGFR-2, and VEGFR-3 completely prevented lymphatic organization. Our findings demonstrate that cooperative signaling of VEGFR-2 and -3 is necessary for lymphatic migration and proliferation, but VEGFR-3 is redundant with VEGFR-2 for LEC organization into functional capillaries.

Low-field Mri and arthroscopy of meniscal lesions in ten dogs with experimentally induced cranial cruciate ligament insufficiency.

Little is known about the magnetic resonance imaging (MRI) appearance of canine meniscal lesions. The aim of this study is to describe the MR appearance of meniscal lesions in dogs with experimentally induced cranial cruciate ligament (CCL) deficiency. The pilot study revealed dogs weighing approximately 10 kg to be too small for meniscal evaluation on low-field MRI. In the main study, dogs weighing approximately 35 kg were used. The left CCL was transected and low-field MRI was performed regularly until 13 months post-surgery. Normal menisci were defined as grade 0. Intrameniscal lesions not reaching any surface corresponded to grade 1 if focal and to grade 2 if linear or diffuse. Grade 3 lesions consisted in linear tears penetrating a meniscal surface. Grade 4 lesions included complex signal changes or meniscal distortion. Between 2 and 13 months post-surgery, all dogs developed grade 4 lesions in the medial meniscus. Most of them corresponded to longitudinal or bucket handle tears on arthroscopy and necropsy. Two dogs showed grade 3 lesions reaching the tibial surface of the lateral meniscus on MRI but not in arthroscopy. Such tears are difficult to evaluate arthroscopically; MRI provides more accurate information about the tibial meniscal surface. Grades 1 and 2 lesions could not be differentiated from presumably normal menisci with our imaging technique. An MRI grading system better adapted to canine lesions has yet to be developed. MRI is a helpful tool for the diagnosis of complete tears in the canine meniscus, especially in larger dogs.

Treatment of nonunions with nonglycosylated recombinant human bone morphogenetic protein-2 delivered from a fibrin matrix.

OBJECTIVE: To report the results of the treatment of nonunions with nonglycosylated recombinant human bone morphogenetic protein-2 (nglBMP-2) delivered from a designed fibrin matrix. STUDY DESIGN: Experimental trial in rodents and prospective clinical study in dogs and cats with nonunion fractures. ANIMALS: Twenty adult female, albino, Sprague-Dawley rats; 8 client-owned cats and dogs. METHODS: After development of a fibrin matrix and evaluation of nglBMP-2 in a rodent femoral defect model, 8 consecutive long bone nonunion fractures (no progression in healing in > or = 3 months), were treated using 300 microg nglBMP-2 in a liquid fibrin precursor, injected into the defect gap after fracture revision and stabilization, or through a stab incision into the fracture site. The fibrin matrix was designed to clot in the wound after 60 seconds and to release the nglBMP-2 continuously over several days. RESULTS: Using only fibrin gel, 7% of the rat femoral defect was filled with new formed bone compared with 79% defect filling using 2 microg nglBMP-2 (P=.006). Five and 10 microg nglBMP in fibrin resulted in union of all femoral defects with complete filling of the gap with new bone. Bony bridging and clinical healing was achieved in 7 patients within 24 weeks of administration of nglBMP-2. CONCLUSIONS: Application of nglBMP-2 in a functional matrix can induce bone healing. Controlled release of nglBMP-2 from a fibrin matrix mimics the natural fracture hematoma. CLINICAL RELEVANCE: nglBMP-2/fibrin can successfully replace a cancellous bone autograft in fracture treatment with an associated reduction in graft donor site morbidity and surgical time.