RESUMEN
Introduction: Coats disease is a rare vasculature pathology that usually presents as retinal telangiectasia with possible progression to exudative retinal detachment (RD). Intravitreal anti-VEGF injections, cryotherapy, laser photocoagulation, and surgery are commonly used to control the disease and prevent its progression. Although iatrogenic tractional RDs secondary to anti-VEGF injections have been reported in patients with Coats disease, RDs in Coats disease are exudative, secondary to retinal exudation and vascular abnormalities. In this article, we present the first reported case of a severe exudative RD accompanied by retinal traction and two retinal holes in a patient with Coats disease. Case Presentation: A 32-year-old male initially presented with Coats disease stage 2A, which then progressed to 3A1 within a month of close follow-ups, finally leading to exudative RD. Following cryotherapy and bevacizumab injections, the exudative RD progressed, with the emergence of retinal traction and two retinal holes. This complex case was successfully treated with a scleral buckle vitrectomy accompanied by radial elements to support the RD, pars plana vitrectomy, silicon oil tamponade, and post-surgical bevacizumab injections. Six months following the surgical intervention, the patient's vision is restored at 20/30, and retinal imaging shows a totally flattened retina. Conclusion: We present the first reported case of a severe exudative RD accompanied by retinal traction and two retinal holes in a patient with Coats disease. The combination of surgical treatment and bevacizumab injections is thought to have collectively contributed to our patient's favorable outcome.
RESUMEN
Background and objectives: In recent years, spinal cord stimulation (SCS) has emerged as a promising management option for chronic pain of multiple etiologies. While its effectiveness has been strongly suggested in many patients, the exact mechanism of action of SCS is incompletely understood. This article reviews the leading mechanisms underlying the analgesic and cardiovascular effects of SCS and reports its novel benefits in a case of recurrent pericarditis. Literature review: Throughout history, the analgesic properties of SCS were thought to arise via stimulation of the spinothalamic tract. Although this mechanism has been thoroughly reported, new research and patient outcomes from SCS have revealed various additional properties that cannot be fully explained by this mechanism alone. Evidence suggests that SCS enhances calcitonin gene-related peptide release and modulates inflammatory cytokine secretion, sympathetic tone, and inhibitory neurotransmitter secretion. These distinct mechanisms likely collectively contribute to the therapeutic effects of SCS on the cardiovascular system and pain management. Case report: We report the case of a 48-year-old male patient with recurrent pericarditis, characterized by refractory angina-like pain and reduced left ventricular ejection fraction (LVEF). After 1 year of having a spinal cord stimulator implanted, the patient is free from pain and narcotics, with a reduction of 428â mg equivalent dose of morphine. The patient's LVEF increased from 40% to 45% without changes to his previous medical treatment. This is the first reported case of refractory pericarditis managed with spinal cord stimulation. Conclusion: Recognizing the improved pain management, reduced narcotic usage, and improved LVEF in our patient following SCS is critical to paving the way toward a complete understanding of the mechanism of action of SCS. This case reveals the therapeutic potential of SCS for cardiovascular pathologies other than refractory angina pectoris.