5 resultados para concentric muscle contraction


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An 80 years old man suffered a cardiac arrest shortly after arrival to his local health department. Basic Life Support was started promptly and nine minutes later, on evaluation by an Advanced Life Support team, the victim was defibrillated with a 200J shock. When orotracheal intubation was attempted, masseter muscle contraction was noticed: on reevaluation, the victim had pulse and spontaneous breathing.Thirty minutes later, the patient had been transferred to an emergency department. As he complained of chest pain, the ECG showed a ST segment depression in leads V4 to V6 and laboratory tests showed cardiac troponine I slightly elevated. A coronary angiography was performed urgently: significant left main plus three vessel coronary artery disease was disclosed.Eighteen hours after the cardiac arrest, a quadruple coronary artery bypass grafting operation was undertaken. During surgery, a fresh thrombus was removed from the middle left anterior descendent artery. Post-operative course was uneventful and the patient was discharged seven days after the procedure. Twenty four months later, he remains asymptomatic.In this case, the immediate call for the Advanced Life Support team, prompt basic life support and the successful defibrillation, altogether, contributed for the full recovery. Furthermore, the swiftness in the detection and treatment of the acute reversible cause (myocardial ischemia in this case) was crucial for long-term prognosis.

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In cases of extensive damage to the foot, with significant bone loss, it is generally accepted that reconstruction must include bone flaps or grafts either in the emergency setting or subsequently. In this report, we describe the case of an 18-year-old student with an avulsion injury of the dorsum of his right foot. Consequently, he lost most of the soft tissue over the dorsum of the foot and the cuboid, navicular, and cuneiform bones. A latissimus dorsi free flap was used to reconstruct the defect. A functional pseudoarthrosis developed between the remaining bones of the foot, and the patient experienced satisfactory foot function after rehabilitation. For this reason, no additional reconstructive procedure was undertaken. This case suggests that it might be adequate to use the latissimus dorsi muscle flap more liberally than previously reported in the reconstruction of extensive defects of the dorsum of the foot, including cases with significant bone loss. This option could avoid the morbidity and inconvenience of a second surgery and the need to harvest a bone flap or graft.

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Introduction and hypothesis Puborectalis avulsion is a likely etiological factor for female pelvic organ prolapse(FPOP). We performed a study to establish minimal sonographic criteria for the diagnosis of avulsion. Methods We analysed datasets of 764 women seen at a urogynecological service. Offline analysis of ultrasound datasets was performed blinded to patient data. Tomographic ultrasound imaging (TUI) was used to diagnose avulsion of the puborectalis muscle. Results Logistic regression modelling of TUI data showed that complete avulsion is best diagnosed by requiring the three central tomographic slices to be abnormal. This finding was obtained in 30% of patients and was associated with symptoms and signs of FPOP (P<0.001). Lesser degrees of trauma (‘partial avulsion’) were not associated with symptoms or signs of pelvic floor dysfunction. Conclusions Complete avulsion of the puborectalis muscle is best diagnosed on TUI by requiring all three central slices to be abnormal. Partial trauma seems of limited clinical relevance.

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Giant cell arteritis (GCA) is a systemic large vessel vasculitis, with extracranial arterial involvement described in 10-15% of cases, usually affecting the aorta and its branches. Patients with GCA are more likely to develop aortic aneurysms, but these are rarely present at the time of the diagnosis. We report the case of an 80-year-old Caucasian woman, who reported proximal muscle pain in the arms with morning stiffness of the shoulders for eight months. In the previous two months, she had developed worsening bilateral arm claudication, severe pain, cold extremities and digital necrosis. She had no palpable radial pulses and no measurable blood pressure. The patient had normochromic anemia, erythrocyte sedimentation rate of 120 mm/h, and a negative infectious and autoimmune workup. Computed tomography angiography revealed concentric wall thickening of the aorta extending to the aortic arch branches, particularly the subclavian and axillary arteries, which were severely stenotic, with areas of bilateral occlusion and an aneurysm of the ascending aorta (47 mm). Despite corticosteroid therapy there was progression to acute critical ischemia. She accordingly underwent surgical revascularization using a bilateral carotid-humeral bypass. After surgery, corticosteroid therapy was maintained and at six-month follow-up she was clinically stable with reduced inflammatory markers. GCA, usually a chronic benign vasculitis, presented exceptionally in this case as acute critical upper limb ischemia, resulting from a massive inflammatory process of the subclavian and axillary arteries, treated with salvage surgical revascularization.

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INTRODUCTION: Ryanodine receptor gene (RYR1) mutations have been associated with central core disease (CCD), multiminicore/minicore/multicore disease (MmD), and susceptibility to malignant hyperthermia (MH). METHODS: Patients with muscle symptoms in adulthood, who had features compatible with CCD/MmD, underwent clinical, histological, and genetic (RYR1 and SEPN1 genes) evaluations. Published cases of CCD and MmD with adult onset were also reviewed. RESULTS: Eight patients fulfilled the criteria for further analysis. Five RYR1 mutations, 4 of them unreported, were detected in 3 patients. Compound heterozygosity was proven in 1 case. CONCLUSIONS: To our knowledge, this is the only report of adult onset associated with recessive RYR1 mutations and central core/multiminicores on muscle biopsy. Although adult patients with CCD, MmD, and minimally symptomatic MH with abnormal muscle biopsy findings usually have a mild clinical course, differential diagnosis and carrier screening is crucial for prevention of potentially life-threatening reactions to general anesthesia.