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ORANGE EKSTRAKLASA



Dołączył: 21 Lut 2011
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PostWysłany: Pią 6:30, 25 Mar 2011  

Cerebral salt wasting syndrome of


Death, the death rate 11.76%. 3 Discussion CSWS or SIADH is due to hypothalamic-pituitary damage caused by various reasons (adrenocorticotropichormone, ACrH) and (antidiuretichormone, ADH) abnormal secretion, so that the increase in renal water reabsorption, urinary sodium excretion increased, on the basis appear on the lower plasma osmolality and serum sodium [1】. CSWS is the danger of reduced plasma osmolality and serum sodium to promote water transport to the cells, resulting in intracellular edema, cerebral edema, in which the most dangerous [2】. It has been reported in 2Ah sharp decline in serum sodium to 120mmol / L or less up to 50% mortality due to cerebral edema is irreversible 【3】. 5 patients in this group, 2 patients died in critically ill patients. CSWS clinical diagnosis, the current gold standard for diagnosis is n】: serum sodium 80mmol/24h; urinary osmolality / plasma osmolality> 1. The key is to have a vigilance, I believe that if the general stability of post-operative patients,[link widoczny dla zalogowanych], 72h after surgery or after a sudden decline in progressive state of consciousness, no other reasons could explain, consider SIADH. Analysis of clinical manifestations can be found, who showed mild gastrointestinal symptoms and progressive fall in consciousness, and consciousness is manifested in patients with severe conditions to deteriorate rapidly. CSWS is the significance of early detection: the result of other causes brain edema and cerebral edema in the treatment of the existence of different points. General cerebral edema preferred hypertonic dehydration,[link widoczny dla zalogowanych], but CSWS cerebral edema, is not only ineffective treatment for critically ill patients can increase the symptoms. Hypertonic dehydration due to further promote urinary sodium excretion of 25, leading to clinical symptoms. For mild cases of high dose furosemide have more significant effect, but no significant effect of critically ill patients, should adopt an integrated treatment. I also found that there are limitations restrict water intake: elderly patients with a longer time limit water intake (48 ~ 72h or more), while high doses dehydration or diuretics, can cause a significant amount of water exceeds intake of water, the blood concentration , blood viscosity increased, decreased effective circulating blood volume, induced heart, brain hypoperfusion, and adequate cerebral perfusion is a decisive factor influencing the prognosis. While limiting the intake of water can be too viscous airway secretions,[link widoczny dla zalogowanych], cough, or aspiration is not easy,[link widoczny dla zalogowanych], easy to induce lower respiratory tract infection,[link widoczny dla zalogowanych], tracheotomy patients, especially for the disadvantaged. The author's experience is for mild cases: fluid in the appropriate amount of control on the basis of (15 (~ ml/24h so), make appropriate use of furosemide and sodium increased with the drug in plasma osmotic pressure, can achieve the desired effect; for critically ill patients: First, large doses of albumin (20 ~ 30g/24h) and furosemide (O.5 ~ 1.0/24h) control the cerebral edema, and actively make sodium. hypertonic salt water should be used (3% ~ 5 %), the serum sodium in a short time rose to 130mmol / L. hypertonic sodium current found in water treatment has a positive role in brain edema. Further also added ACTH (50 ~ 100U/24h), by negative feedback inhibition of ACTH ADH role. At the same time the serum sodium, urine sodium and urine osmolarity is to assess the efficacy of active surveillance to determine the gold standard for further treatment. 【
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