AN INFECTED HIP PROSTHESIS IN A DOG DIAGNOSED WITH A 99mTC-CIPROFLOXACIN (INFECTON) SCAN

This case report describes the use of the 99mTc-labeled radiopharmaceutical ciprofloxacin (Infecton) in a case of hip prosthesis loosening in a dog. Serial planar radiographs were not conclusive, and culture of the synovial fluid was negative. Antibiotic treatment did not result in improvement of the lameness. Scintigraphy was performed with 99-Tc-Infecton, a tracer claimed to be specific for infection. Antibiotic treatment was interrupted 6 weeks prior to the examination. Planar and tomographic images at 3 h and at 24 h postinjection showed increased activity along the acetabulum and the proximal femoral bone surrounding the femoral prosthesis, indicating focal infection. Bacteriology performed after removal of the implant revealed Pseudomonas aeruginosa.     

CANINE BRAIN ANATOMY ON MAGNETIC RESONANCE IMAGES

Magnetic resonance (MR) images of the canine brain were acquired during investigation of dogs with neurologic disease. A paramagnetic contrast medium was used for enhancement. MR provided images with excellent contrast between grey and white matter, as well as brain tissue and cerebrospinal fluid. Good resolution and anatomic detail of the canine brain were obtained. A series of images was compiled and labelled as a reference for MR anatomy of the canine brain.     

The Medial Saphenous Fasciocutaneous Free Flap in Dogs

The purpose of this study was to identify the angiosome of the medial saphenous artery and vein and to evaluate the use of this cutaneous angiosome as a free skin flap in the dog. In phase 1 of this study, selective angiography of the medial saphenous artery performed in six canine cadavers showed that the skin covering the entire medial femorotibial area, the distal half of the caudal head of the sartorius muscle, and the gracilis muscle were perfused by the medial saphenous artery. In phase 2, a medial saphenous fasciocutaneous island flap was raised and sutured back to the skin edges of the donor wound in three dogs. One hundred percent survival of all of the flaps occurred. In phase 3, a medial saphenous fasciocutaneous microvascular free flap was transferred to a wound that was created over the dorsal metacarpal (n = 3) or metatarsal region (n = 3). The mean length ± SD of the medial saphenous vascular pedicle was 80 ± 13 mm (n = 5); the mean diameter ± SD of the medial saphenous artery was 2.8 ± 0.2 mm (n = 5) and the mean diameter ± SD of the medial saphenous vein was 4.2 ± 0.2 mm (n = 5). One hundred percent of all flaps survived (n = 6). Selective angiography of the distal cranial tibial artery (metatarsal wounds, n = 3) and the median artery (metacarpal wound, n = 3) was performed 3 weeks after surgery. All of the vascular anastomoses were patent and neovascularization of the wound beds was present. This free flap was found to be acceptable for cosmetic reconstruction of wounds located on the distal extremity.     

Effects of Growth Factors and L-Arginine on Ischemic Skin Flaps in Rats

This study determined the effect of the polypeptide growth factors transforming growth factor-beta (TGF-β), insulin-like growth factor-I (IGF-I), and growth hormone (GH) alone and in combination with dietary L-Arginine HCL (ARG) on skin flap survival in rats. Caudally based dorsal skin flaps were created in 110 Sprague-Dawley rats. The rats were randomly assigned into three treatment groups, based on drinking water supplementation. Group 1 (n = 50) received ARG in their drinking water, group 2 (n = 50) received tap water alone, and group 3 (n = 10) received N-omega-nitro-L-arginine (L-NA) and hydralazine. Groups 1 and 2 were divided into subgroups of 10 rats each based on treatment with either: TGF-β, IGF-I, GH, or IGF-I + GH. All subgroups that received GH had significantly greater ( P <.0001) median body weight gains when compared with subgroups not receiving GH. L-arginine HCL when added to IGF-I negated the positive effects of IGF-I on both flap survival and weight gain. Although the rats in all subgroups from groups 1 and 2 had an increase in mean percent skin flap survival when compared with the water alone subgroup, only rats receiving IGF-I, or the combination of ARG with either TGF-β or GH, had statistically significant enhanced skin flap survival. Rats in group 3 did not show an increase in skin flap survival when compared with the control subgroup.     

Clinical and topographic magnetic resonance characteristics of suspected brain infarction in 40 dogs

Medical records of 40 dogs presented for evaluation of acute-onset, nonprogressive, intracranial dysfunction by means of magnetic resonance imaging (MRI) diagnosis of brain infarction were reviewed. Location of the brain infarcts was: 11 of 38, telencephalic; 8 of 38, thalamic/midbrain; 18 of 38, cerebellar; and 3 of 38, multifocal. Telencephalic infarcts developed within the territory of the middle cerebral (4/11), rostral cerebral (2/11), and striate (5/11) arteries. Thalamic/midbrain infarcts developed within the territory of perforating arteries of the caudal portion of the thalamus and rostral portion of the brainstem (8/8). All cerebellar infarcts (18/38) were within the territory of the rostral cerebellar artery or one of its branches. All infarcts appeared nonhemorrhagic, with marked contrast enhancement observed in only 3 of 38 dogs, all of which were imaged more than 7 days after the onset of signs of neurologic dysfunction. Diffusion-weighted imaging (DWI) sequences were available from 6 dogs, all imaged within 5 days of the onset of signs of neurologic dysfunction. Suspected infarcts were hyperintense on DWI sequences and were hypointense on the apparent diffusion coefficient map. Telencephalic infarcts caused abnormal mental status, contralateral postural reaction deficit, contralateral nasal hypalgesia, contralateral menace deficit, and ipsilateral circling. Thalamic/midbrain infarcts caused contralateral or ipsilateral postural reaction deficit, contralateral menace deficit, ipsilateral head tilt or turn, nystagmus, ventrolateral strabismus, and anisocoria. Cerebellar infarcts caused ipsilateral asymmetric cerebellar quality ataxia, head tilt, intermittent opisthotonus, nystagmus, and ipsilateral menace deficit with apparent normal vision.