RESUMO
Following spinal cord stimulator (SCS) implantation, postoperative pain is commonly incisional or neuropathic from neurological damage. Occasionally, this new pain may mimic symptoms caused by preexisting pathology. This article presents a case of immediate, severe, postoperative leg pain secondary to a lower extremity deep vein thrombosis (DVT) and subsequent pulmonary embolism after percutaneous SCS implantation for failed back syndrome. The risk factors of DVT after spine surgery and perioperative prophylaxis are further discussed with a brief literature review. LEVEL OF EVIDENCE: V.
Assuntos
Terapia por Estimulação Elétrica/efeitos adversos , Perna (Membro)/irrigação sanguínea , Dor Lombar/terapia , Dor Pós-Operatória/etiologia , Embolia Pulmonar/etiologia , Trombose Venosa/etiologia , Humanos , Medição da Dor , Dor Pós-Operatória/diagnóstico por imagem , Dor Pós-Operatória/terapia , Embolia Pulmonar/diagnóstico por imagem , Embolia Pulmonar/terapia , Trombose Venosa/diagnóstico por imagem , Trombose Venosa/terapiaRESUMO
BACKGROUND: Inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) exhibit marked differences in neointimal formation after arterial injury when deficient in apolipoprotein E (apoE(-/-)) and fed a Western diet. Quantitative trait locus (QTL) analysis was performed on an intercross between B6.apoE(-/-) and C3H.apoE(-/-) mice to determine genetic factors contributing to the phenotype. METHODS AND RESULTS: Female B6.apoE(-/-) mice were crossed with male C3H.apoE(-/-) mice to generate F(1)s, which were intercrossed to generate 204 male F(2) progeny. At 10 weeks of age, F(2)s underwent endothelium denudation injury to the left common carotid artery. Mice were fed a Western diet for 1 week before and 4 weeks after injury and analyzed for neointimal lesion size, plasma lipid and MCP-1 levels. One significant QTL, named Nih1 (61cM, LOD score: 5.02), on chromosome 12 and a suggestive locus on chromosome 13 (35cM, LOD: 2.67) were identified to influence lesion size. One significant QTL on distal chromosome 1 accounted for major variations in plasma non-HDL cholesterol and triglyceride levels. Four suggestive QTLs on chromosomes 1, 2, and 3 were detected for circulating MCP-1 levels. No correlations were observed between neointimal lesion size and plasma lipid levels or between lesion size and plasma MCP-1 levels. CONCLUSIONS: Neointimal formation is controlled by genetic factors independent of those affecting plasma lipid levels and circulating MCP-1 levels in the B6 and C3H mouse model.