Objectives: The purpose of this study was to determine the relative accuracies of mammography, sonography, MRI and clinical examination in predicting residual tumour size and pathological response after neoadjuvant chemotherapy for locally advanced or inflammatory breast cancer. Each prediction method was compared with the gold standard of surgical pathology. Methods: 43 patients (age range, 25-62 years; mean age, 42.7 years) with locally advanced or inflammatory breast cancer who had been treated by neoadjuvant chemotherapy were enrolled prospectively. We compared the predicted residual tumour size and the predicted response on imaging and clinical examination with residual tumour size and response on pathology. Statistical analysis was performed using weighted kappa statistics and intraclass correlation coefficients (ICC). Conclusion:Predictions of response and residual tumour size made on MRI were better correlated with the assessments of response and residual tumour size made upon pathology than were predictions made on the basis of clinical examination, mammography or sonography. Thus, the evaluation of predicted response using MRI could provide a relatively sensitive early assessment of chemotherapy efficacy.
Although protein C and/or S deficiency has frequently been associated with venous thromboembolic events, instances of arterial thromboses have been reported. However, the exact incidence of protein C and/or S deficiency in patients with peripheral arterial insufficiency has not been established. Furthermore, given the lack of adequate studies to define the natural history and angiographic findings of these patients, the treatment has not been well delineated. Therefore, we conducted a prospective study to investigate the prevalence, characteristic angiographic findings and optimal treatments in patients with peripheral arterial insufficiency associated with protein C and/or S deficiency. Between September 2000 and August 2004, 133 patients who presented with peripheral arterial insufficiency underwent hypercoagulability tests before the initiation of any treatments. Of these, 11 patients (8.3%) with protein C and/or S deficiency were included in this study. There were nine males and two females. The ages ranged from 38 years to 72 years (mean 57 years). All patients showed characteristic angiographic findings: long segment thrombotic occlusion of a main peripheral artery without evidence of atherosclerosis or with mild atherosclerotic changes in the aorta and other major arterial trees. Surgical or endovascular procedures were performed in nine patients: bypass graft in four, thrombectomy in four and catheter-directed thrombolysis in one. Conservative treatment with full anticoagulation was performed in two patients. All patients received pre- and post-operative anticoagulation. Except for one amputated case, clinical and vascular laboratory improvements were achieved in 10 patients. Mean follow-up period was 21 months (range 4-45 months). However, one patient, in whom re-vascularization surgery was performed successfully, discontinued warfarin therapy himself at 10 months after surgery, graft occlusion and limb loss occurred at 30 months after surgery. This initial experience suggests that protein C and/or S deficiency may be an independent risk factor for peripheral arterial insufficiency. Patients who present with peripheral arterial insufficiency and protein C and/or S deficiency demonstrate characteristic angiographic findings. Once the diagnosis of protein C and/or S deficiency is made, patients should be treated with life-long anticoagulation.
The syndrome of CSF hypovolaemia has been a recognized cause of orthostatic headache (a headache in the upright position relieved by recumbancy) (1-3). Among other clinical manifestations, a change in hearing has also been described in this syndrome (1,2,4,5). However, the pathogenesis of hearing changes in CSF hypovolaemia is unclear.We report a patient with CSF hypovolaemia who had orthostatic hypacusis (hearing impairment in the upright position relieved by recumbancy) that was clearly demonstrated by pure tone audiometry. The anatomical and physiological relationship between CSF space and inner ear structure may explain the pathogenesis of orthostatic hypacusis in CSF hypovolaemia. Case reportA 34-year-old previously healthy man presented with severe headache. The headache consistently occurred within 1 min of assuming the upright posture, and was relieved within 2 min of lying flat. The headache was pressing in nature, and was associated with posterior neck pain. Two days after the onset of his symptoms, he developed a change in hearing that was provoked by standing or sitting, and relieved by lying down. The patient's hearing change was described as 'muffled' or 'distant'. This orthostatic change in hearing had gradually worsened, and was severe enough to impede his daily life.Neurological examination 5 days after the onset of headache was unremarkable. He continued to develop the orthostatic change in hearing 5-10 min after he assumed an upright position. The orthostatic hypacusis of both ears was clearly demonstrated with pure tone audiometry. When he assumed an upright position for 10 min, the average hearing intensity thresholds at lower frequencies (250, 500 and 1000 Hz) were 26.7 dBHL in the right ear and 23.3 dBHL in the left (Fig. 1A). Upon lying flat, average hearing intensity thresholds normalized: 10.0 dBHL in the right ear and 11.7 dBHL in the left (Fig. 1B). The hearings at higher frequencies were stable. The summating potential to action potential ratio (SP/AP) of electrocochleography (ECoG), performed only in the supine position, was 0.36 in the left ear and 0.25 in the right ear.On CSF examination, the opening pressure was unmeasurably low and other CSF composition was normal. A brain T1-weighted gadolinium-enhanced MRI showed diffuse pachymeningeal enhancement but no evidence of brain sagging or subdural fluid collection. A spine MRI revealed extradural fluid collection at the level of thoracic spine, and engorgement of the epidural venous plexus at the level of cervical spine. MR myelography showed multiple hyperintense lesions along the bilateral paradural space at the level of upper thoracic spine ( Fig. 2A). Radioisotope cisternography demonstrated multiple paradural uptakes of tracer at the level of the thoracic spine. The orthostatic headache and orthostatic hypacusis were simultaneously resolved after treatment of four epidural blood patches. MR myelography, performed 1 month after treatment, showed the resolution of multiple hyperintense lesions along the bilateral paradural space a...
Introduction The aim of this study was to determine the effect of hand positioning on the quality of external chest compression (ECC) by novice rescuers. Methods This observational simulation study was conducted for 117 included participants. After completion of an adult cardiopulmonary resuscitation (CPR) training program for 3-h, the participants selected which of their hands would be in contact with the mannequin during ECC and performed 5 cycles of single rescuer CPR on a recording mannequin. The participants were assigned to 2 groups: the dominant hand group (DH; n=40) and the non-dominant hand group (NH; n=29). The depth and rate of ECC were analysed to compare the effectiveness of ECC between 2 groups. Results The rate of ECC was significantly faster in the DH group (mean, 117.3 ±11.4/min) than in the NH group (mean, 110.9±12.2/min) (p=0.028). However, the depth of ECC in the dominant hand group (mean, 52.4±5.9 mm) was not significantly different from that in the non-dominant hand group (mean, 50.8±6.0 mm) (p=0.287). Similarly, the portion of ECC with inadequate depth in the dominant hand group (mean, 1.8±4.3%) was not significantly different from that in the non-dominant hand group (mean, 5.3±15.6%) (p=0.252). Conclusions ECC can be performed with an acceptably higher rate of compressions when the dominant hand of the novice rescuer is placed in contact with the sternum. However, the position of the dominant hand does not affect the depth of ECC. (Hong Kong j.emerg.med. 2014;21:382-386)
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