Venous thromboembolic events are a major cause of morbidity and mortality in patients with acute stroke and their prevention presents a significant challenge. This article outlines the clinical trial evidence for prevention of venous thromboembolic events in acute stroke, and the current UK clinical practice recommendations.
A 50-year-old female developed problems using her right hand and a right sided facial droop; she described drooling of liquids and difficulty operating a computer mouse. She was assessed at 4 h post onset for inclusion in the IST-3 trial. She was found to have a mild dysarthria and right arm weakness but a more obvious ataxia affecting the right side, arm more than leg. A diagnosis of ataxic hemiparesis was made. CT imaging was normal but follow-up imaging revealed a small cortical infarct in the left frontal lobe and a severe left internal carotid stenosis. Ataxic hemiparesis is widely thought to be a lacunar or pontine vascular syndrome, but it can result from cortical infarcts. This case illustrates an important lesson for the neurologist faced with increasing involvement in hyperacute care. Impairment such as weakness, ataxia and sensory loss can be immature and changing in the hyperacute setting, making it difficult for the clinician to be confident about their origin and relevance. The same applies to the resulting disabilities the patient has not yet had a chance to understand or assimilate. Awareness of this is crucial when faced with the need for immediate decision making, particularly if plain CT, effectively an ‘excludogram’, is the imaging modality used. A new ‘rule book’ may be required for the neurologist basing important diagnostic and treatment decisions on the clinical signs in the first few hours after the onset of a significant neurological disability.
Abstract In the current medical lexicon, the lay term ‘faint’ generally refers to reflex (neurocardiogenic, usually vasovagal) syncope (Chapter 2), whereas ‘cardiac syncope’ refers to syncope caused by a heart disorder, either structural or functional. In this chapter, we highlight the importance of awareness of cardiac syncope to clinicians (particularly neurologists) diagnosing epilepsy. We describe the clinical features of cardiac syncope and their relation to its underlying cause, and outline the investigation and treatment of suspected cardiac syncope, emphasizing the relevance of the 12-lead electrocardiogram (EKG) in clinical assessment. Finally, we focus on complex situations, such as where seizures result from cardiac syncope, or where cardiac syncope (asystole) results from seizures.
BACKGROUND: Adenosarcoma in a patient with extraovarian endometriosis is a rare event and can be easily overlooked. CASE: A woman with a history of endometriosis underwent multiple resections of a vaginal mass and medical treatment for presumed recurrent endometriosis. Eventually, a vaginal adenosarcoma was diagnosed. CONCLUSION: The possibility of adenosarcoma should be considered if an enlarging mass occurs at the site of extraovarian endometriosis.
Summary A patient with recurrent convulsions in childhood and associated ketotic hypoglycaemia is described. Hypoglycaemic attacks started at the age of 3 years and 4 months and continued until 9. At present (aged 15) the patient is mentally retarded, has epilepsy, high tone deafness and a major behaviour disturbance. Prednisone therapy failed to prevent hypoglycaemic convulsions and eventually irreversible brain damage. Intramuscular glucagon and adrenaline were ineffective in raising the blood glucose during acute hypoglycaemic attacks. Investigations at 3 years and 7 months and at 14 years showed a persistent and markedly abnormal sensitivity to a small dose of exogenous insulin with severe hypoglycaemia with convulsions, absence of clinical hyperadrenalism during hypoglycaemia, and a metabolic block in gluconeogenesis. The demonstration of a persistent biochemical abnormality of glucose metabolism at the age of 14 strongly suggests that ketotic hypoglycaemia of childhood is not another aspect of nutritional deprivation, as recently suggested (Buist, 1974), but the result of a defect in glucose homeostasis.
Abstract Background Endocrine therapy is commonly recommended in the adjuvant setting for patients as treatment for ductal carcinoma in situ (DCIS). However, it is unknown whether a neoadjuvant (preoperative) anti-estrogen approach to DCIS results in any biological change. This study was undertaken to investigate the pathologic and biomarker changes in DCIS following neoadjuvant endocrine therapy compared to a group of patients who did not undergo preoperative anti-estrogenic treatment to determine whether such treatment results in detectable histologic alterations. Methods Patients (n = 23) diagnosed with ER-positive pure DCIS by stereotactic core biopsy were enrolled in a trial of neoadjuvant anti-estrogen therapy followed by definitive excision. Patients on hormone replacement therapy, with palpable masses, or with histologic or clinical suspicion of invasion were excluded. Premenopausal women were treated with tamoxifen and postmenopausal women were treated with letrozole. Pathologic markers of proliferation, inflammation, and apoptosis were evaluated at baseline and at three months. Biomarker changes were compared to a cohort of patients who had not received preoperative treatment. Results Median age of the cohort was 53 years (range 38–78); 14 were premenopausal. Following treatment, predominant morphologic changes included increased multinucleated histiocytes and degenerated cells, decreased duct extension, and prominent periductal fibrosis. Two postmenopausal patients had ADH only with no residual DCIS at excision. Postmenopausal women on letrozole had significant reduction of PR, and Ki67 as well as increase in CD68-positive cells. For premenopausal women on tamoxifen treatment, the only significant change was increase in CD68. No change in cleaved caspase 3 was found. Two patients had invasive cancer at surgery. Conclusion Preoperative therapy for DCIS is associated with significant pathologic alterations. These changes may be clinically significant. Further work is needed to identify which women may be the best candidates for such treatment for DCIS, and whether best responders may safely avoid surgical intervention. Trial Registration ClinicalTrials.gov NCT00290745
We have determined the sites of hypoxic vasoconstriction in ferret lungs. Lungs of five 3- to 5-wk-old and five adult ferrets were isolated and perfused with blood. Blood flow was adjusted initially to keep pulmonary arterial pressure at 20 cmH2O and left atrial and airway pressures at 6 and 8 cmH2O, respectively (zone 3). Once adjusted, flow was kept constant throughout the experiment. In each lung, pressures were measured in subpleural 20- to 50-microns-diam arterioles and venules with the micropipette servo-nulling method during normoxia (PO2 approximately 100 Torr) and hypoxia (PO2 less than 50 Torr). In normoxic adult ferret lungs, approximately 40% of total vascular resistance was in arteries, approximately 40% was in microvessels, and approximately 20% was in veins. With hypoxia, the total arteriovenous pressure drop increased by 68%. Arterial and venous pressure drops increased by 92 and 132%, respectively, with no change in microvascular pressure drop. In 3- to 5-wk-old ferret lungs, the vascular pressure profile during normoxia and the response to hypoxia were similar to those in adult lungs. We conclude that, in ferret lungs, arterial and venous resistances increase equally during hypoxia, resulting in increased microvascular pressures for fluid filtration.
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