A large-scale epidemiological study was conducted to determine breeds at risk for 12 developmental orthopedic diseases (DODs). Developmental orthopedic diseases investigated included canine hip dysplasia (CHD); craniomandibular osteopathy (CMO); fragmented coronoid process; hypertrophic osteodystrophy; Legg-Calvé-Perthes disease; osteochondrosis of the medial humeral condyle, caudal humeral head, femoral condyles, and talar trochlear ridges; panosteitis; patella luxation; and ununited anconeal process. Dogs that were diagnosed with any one of the diseases of interest at any of 10 veterinary teaching hospitals participating in the Veterinary Medical Database from 1986 to 1995 were included as cases. Odds ratios and corresponding 95% confidence intervals were calculated to determine risk. Frequency of diagnosis during the 10-year period ranged from 35 cases (CMO) to 10,637 cases (CHD). The number of breeds at increased risk for a disease ranged from one (CMO) to 35 (CHD). Breed susceptibility for a DOD may suggest a genetic component in the disease etiology. The results of this study serve to increase veterinarians' awareness of breeds susceptible to DODs and may facilitate the control of such diseases by identifying breeds that might benefit from breeding programs or environmental intervention such as dietary modification.

Prevalence of CHD in these 2 breeds may be much higher than previously reported in the United States. Results suggest substantial bias in the OFA database, which causes lower estimates of prevalence of CHD.

Objective: To determine the frequency of postoperative pulmonary complications (PPCs) in dogs following laparotomy, characterize the nature of PPCs, and identify disease-related risk factors for PPCs in dogs. Design: Retrospective clinical study. Setting: University-affiliated small animal teaching hospital. Animals: One hundred and sixty-two dogs without preoperative pulmonary pathology that underwent laparotomy surgery. Interventions: None. Measurements and main results: Cases were evaluated for factors including patient signalment, preexisting disease, primary and ancillary surgical procedure(s), development of postoperative pulmonary disease, characteristics of perioperative hospitalization and therapy, and survival. Twenty-two percent of dogs in the study developed PPCs. PPCs included respiratory arrest (n 5 4), acute respiratory distress syndrome (ARDS) (n 5 3), pneumonia (n 5 8), hypoventilation (n 5 13), and transient hypoxemia (n 5 8). Dogs that developed PPCs had a significantly longer duration of oxygen therapy, longer duration of stay in intensive care unit (ICU), and decreased survival. Dogs with perioperative vomiting or regurgitation were more likely to develop PPCs. Animals that underwent exploratory laparotomy for biliary or septic peritonitis were also more likely to develop PPCs. Conclusions: PPCs occur in dogs following laparotomy and contribute significantly to the morbidity and mortality of these surgical patients. In this patient population, animals with vomiting, regurgitation, or peritonitis may be at a higher risk of developing PPCs. Animals with the identified risk factors should be monitored carefully postoperatively for development of pulmonary complications.

A 6-year-old, spayed female Himalayan cat with idiopathic chylothorax, which failed to respond to medical management, was successfully treated by advancement of the omentum into the thorax. Exploratory thoracotomy revealed severe, constrictive pleuritis as a sequela to chylothorax. Because of the poor prognosis for recovery from chylothorax in cats with thoracic duct ligation alone, and the lack of success in performing thoracic duct ligation in this cat, the omentum was advanced into the thorax through a hole created in the diaphragm and sutured within the thoracic cavity. The cat recovered from surgery and is clinically normal 13 months postoperatively. Omental advancement may be an effective surgical management technique for this challenging disease in cats.

In vivo visualization of subclinical osteochondrosis(OC) lesions, characterized by necrosis of epiphyseal growth cartilage, is necessary to clarify the pathogenesis of this disease. Hence, our objectives were to demonstrate induced necrosis of the epiphyseal cartilage in vivo using MRI and to monitor progression or resolution of resulting lesions. We also aimed to improve the goat model of OC by introducing controlled exercise. Vascular supply to the epiphyseal cartilage was surgically interrupted in four 5-day-old goats to induce ischemic cartilage necrosis in a medial femoral condyle. Starting 3 weeks postoperatively, goats underwent daily controlled exercise until euthanasia at 6, 10, 11 (n=2) weeks postoperatively. T2 maps of operated and control femora were obtained in vivo at 3(n=4), 6(n=4), 9(n=3) and 11(n=2) weeks postoperatively using a 3T MR scanner. In vivo MRI findings were validated against MRI results obtained ex vivo at 9.4T in three goats and compared to histological results in all goats. Surgical interruption of the vascular supply caused ischemic cartilage necrosis in 3 out of 4 goats. T2 maps obtained in vivo at 3T identified regions of increased relaxation time consistent with discrete areas of cartilage necrosis 3 to 11 weeks postoperatively and demonstrated delayed progression of the ossification front at 9(n=1) and 11(n=2) weeks postoperatively. In vivo MRI findings were confirmed by ex vivo MRI at 9.4T and by histology. Identification of cartilage necrosis in clinical patients in the early stages of OC using T2 maps may provide valuable insight into the pathogenesis of this condition.