Acta Scientiae Veterinariae, 2013. 41(Suppl 1): 25
Rafael Oliveira Chaves, Diego Vilibaldo Beckmann, Rosmarini Passos dos Santos, Amanda Oliveira Andrades, Matheus Macagnan, Graciane Aiello, André Vasconcelos Soares & Alexandre Mazzanti
Background: Fibrocartilaginous embolic myelopathy is a syndrome of spinal cord infarction caused by fi brocartilaginous emboli identical to the nucleus pulposus of intervertebral disk. The signals were acute and not progressive, asymmetric in 92% and neuroanatomic regions were affected C6-T2 (n = 2), L3-T3 (n = 5) and L4-S3 (n = 5). The diagnosis was based on history, fi ndings on physical and neurological examination and exclusion of differential diagnosis. The aim of this study was to report twelve dogs treated at Hospital Veterinário Universitário (HVU), Universidade Federal de Santa Maria (UFSM) with a presumptive diagnosis of fi brocartilaginous embolism. Cases: Seven males and fi ve females dogs were referred to the Veterinary Teaching Hospital of the Federal University of Santa Maria: three rottweiler dogs, two labradors retrievers, one fi la brasileiro, one chow-chow, one boxer, one schnauzer, one German shepherd, one mixed breed and one greyhound, aged between one year and three months and eleven. In all cases, the owners reported during the anamnesis partial or complete loss of movement of member(s) involved(s) acutely with no history of trauma. For anatomical localization of the lesion was performed neurological examination. As complementary exams were requested blood count, serum biochemistry, urinalysis, and radiography of the spine. Contrast radiography (myelography) and cerebrospinal fl uid analysis were performed only in eight dogs. Front of the historical, clinical fi ndings, neurological and complementary exams the presumptive diagnosis was fi brocartilaginous embolism. The dogs were subjected to passive physical therapy and showed satisfactory clinical improvement in the first month after onset of clinical signs. Discussion: The myelopathy fi brocartilaginous embolism is commonly reported in dogs of large and giant breed. In this study, 92% were of large breeds. The mean age of onset of clinical signs in this study was 4.5 years, and male dogs, the most affected, result similar to that found in other studies. Neurological signs vary depending on the location and severity of ischemic lesions of the spinal cord and asymmetric signals in 55% to 61% of the dogs. Of the twelve dogs of this study, signals were asymmetric and eleven of them were affected neuroanatomic regions C6-T2 (n = 2), L3-T3 (n = 5) L4-S3 (n = 5). In other studies, the most affected areas were T3-L3 and L4-S3. Intensive physical activity seems to be involved in about half the cases of embolism few hours. Except for two dogs of breed rottweiler and SRD in this study, all had a history of physical activity at the onset of clinical signs. There were no changes in blood count, serum biochemistry, urinalysis, and radiography of the spine in the twelve dogs. With the exception of four dogs, the other underwent contrast radiography (myelography) and cerebrospinal fl uid analysis and only in German Shepherd and Labrador was observed intramedullary compression standard to myelography and mild lymphocytic pleocytosis and increased protein in the CSF, respectively. Diagnosis of fi brocartilaginous embolism cases in this study was based on history, fi ndings on physical and neurological examination, exclusion of differential diagnosis by laboratory tests and clinical evolution. In ten dogs of this study, was performed only physical therapy and nine of them were observed clinical signs of recovery between one and fi ve weeks. The study brings to clinical relevance, the importance of fi brocartilaginous embolism in the differential diagnosis of dogs with a history of acute loss of limb movements, with or without asymmetry, non-progressive, no pain on palpation of the spine. This may be favorable prognosis in patients with signs of recovery during the first month.