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http://projects.csail.mit.edu/courseware/?term=friendship-essay-conclusion friendship essay conclusion A comprehensive meta-analysis. Stroke. A journal of cerebral circulation. 2008;39:3029-3035. 14. Badjatia n. Hyperthermia and ever control in brain injury. Crit care med. 2009;37:S250-s257. 15. Broessner g, beer r, lackner p, helbok r, fischer m, p ausler b, et al. Prophylactic, endovascularly based, longterm normothermia in icu patients with severe 16. 17.

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http://manila.lpu.edu.ph/about.php?test=summary-essay summary essay A. Make the ophthalmologic examination part o your routine. Look or blurred borders o the optic disc and presence o spontaneous venous pulsations to assess or raised intracranial pressure. B. Look or ptosis. You will miss a horner syndrome unless you look care ully, as the ptosis in this neurologic emergency is very subtle. Compare one side to another or symmetry. Compare with a picture on an old driver’s license i you are uncertain whether a ptosis is new or chronic. C. As with most signs in neurology, a pathologic ptosis does not typically appear in isolation. Assess the size o the pupils. Myosis (constricted pupil) on the same side as a subtle ptosis is a horner syndrome unless another cause can be determined. I you are uncertain, shut the lights o in the room. I the di erence in size between the pupils gets larger (constricted pupil dilates minimally, while other pupil gets larger), this would support 361 altered mental status a sympathetic de cit on the side o the contracted pupil, consistent with horner syndrome. I , a er turning o the light, the di erence in size between pupils gets smaller, this may suggest that the dilated pupil is abnormal, raising concern or a cn iii compression (the parasympathetic bers travel along cn iii).

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http://cs.gmu.edu/~xzhou10/semester/thesis-on-energy-industry.html thesis on energy industry 2001;86:3568–3573. 31. Sonino n, boscaro m. Medical therapy for cushing’s disease. Endocrinol metab clin. 1999;28:211–22.

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my native land essay Fever, almost universally present in patients presenting with hyperleukocytosis, can be an important clue to the presence o the syndrome. Prompt intravenous hydration and cytoreduction interventions, such as leukapheresis, are warranted to reduce the risk o complications.8 how does hyperviscosity syndrome from acute leukemia present?. Hemorrhagic complications occur in 20% o acute leukemia cases. Leukemic cell in ltration rom hyperleukocytosis is an important cause o intracranial hemorrhage in acute leukemia but typically occurs only in the setting o marked leukocytosis where white blood cell counts exceed 300,000 leukemic cells/µl. Other common causes o intracranial hemorrhage in acute leukemia include dic, disseminated aspergillosis or mucormycosis, and thrombocytopenia.19 what are other neurologic manifestations of leukemia?. Leukemic parenchymal tumors, known as chloromas, have been reported, although these solid tumors consisting o leukemic blasts more o en result in epidural spinal cord compression due to their predilection or bone or dural attachment. Encephalopathy and meningitis are additional complications that can arise rom direct leukemic in ltration, as a result o malignant immunosuppression, or even as an adverse e ect o treatment o acute leukemia.19 are any leukemic processes not associated with hyperviscosity syndrome?. Fortunately, not all leukemic cells behave aggressively.

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