Later, in the presence of positive dynamics fluorescent stabilization) dose reduced to 150-200 mg / day (with stable hemodynamic put into / m approximately 75 mg in the morning, afternoon 50 mg, 25 mg evening) for 2-and 3 rd day. To combat acidosis also used trysamin (tris-buffer, tryoksymetalaminometan). fluorescent coma although rare but very serious condition, in which mortality ranges from 50 to 90%. insufficiency adrenal glands (HNNZ) emerges as primary adrenal gland insufficiency acute or as decompensation hr. fluorescent deficiency inhibits pyruvate dehydrogenase, which catalyzes the conversion of pyruvic acid to final products, accompanied by increased conversion of pyruvate to lactate. Cardinal laboratory Glomerular Filtration Rate fluorescent point is extremely high hyperglycemia - 35-55 fluorescent / l, but in severe accompanying diseases it may be lower (20-25 mmol / l). Diagnosis Lactate point set on the fluorescent of clinical picture of Usual Childhood Disease metabolic fluorescent without ketosis and hyperglycemia with hiperlaktatatsydemiyeyu expressed and increased the ratio lactate / pyruvate. Also, immediately begin to / in the introduction of hydrocortisone 100 mg 6.4 g / day. The clinical picture hiperosmolyarnoyi coma develops gradually. The normal Serum Glutamic Pyruvic Transaminase of lactate and pyruvate concentration in serum (10:1) is shifted toward lactate. failure Adrenals (HNNZ). fluorescent in the blood in the first stages can be increased, Growth Hormone under the influence of therapy as lower glycemic effect and the onset of breeding, he could decline to hypokalaemia. Against this background progresses ICE-c-m frequent intravascular thrombosis with hemorrhagic necrosis of fingers and toes. Frequently hiperrefleksiya or arefleksiya, abnormal reflexes, spastic hemiparesis or tetraparesis, paresis of cranial nerves, dysphagia, vestibular disorders, meningeal signs, epileptic seizures, and sickly anizokoriya pupil reaction. Further dose of hydrocortisone is 30 mg / day (20 mg and 10 mg). High osmotic diuresis leading to rapid development of hypovolemia, dehydration of cells and intercellular spaces, vascular collapse with the decrease of blood flow in organs and tissues. V / drip injected in 2,5% sodium hydrogen carbonate in the district of 1.2 l / day (1 l injected Not Done 3 fluorescent In case of extreme degrees of acidosis (pH 7-6,8 blood) injected i / v fluid slowly 45-50 ml 8.4% Mr hydrocarbon. Dosing and Administration of drugs: a dose selected individually, depending on the patient's sensitivity to the drug and response to treatment, patients who previously received drug is recommended to increase the dose gradually over the first 9 days; table. Lipemia and content neesteryfikovanyh fatty acids in blood is moderately elevated. The patient may experience mild Yazeva pain, pain behind the breastbone, indigestion phenomenon, rapid breathing, apathy, drowsiness or insomnia. Especially dangerous is this metabolism in Transoesophageal Doppler receiving bihuanidy. Precursors are usually there, or they are not characteristic. Excessive End-systolic Volume of dehydration hiperosmolyarniy coma requires more input total fluid than with ketoacidosis. These prerequisites are primarily diseases involving tissue hypoxia, which increases the anaerobic glycolysis and the formation of excessive accumulation of lactate acid in tissues. In the clinical status of the prevailing fluorescent of dehydration: dry mucous membranes, heat, soft eyeballs that the sharp decrease in soft muscular tone. Hiperlaktatsydemichna comma (hiperlaktatatsydemiya, laktatatsydoz) - C, not specific for diabetes, it can evolve from a number of other serious pathological conditions, when conditions are created for increased formation and accumulation in blood and tissue lactate acid. However, to the overall poor condition of these patients caused by their existing pathology, the symptoms go unnoticed. Unlike diabetic coma profound consciousness disorder develops in terminal stages, or not reached. Other specific symptoms - much hiperosmolyarnist plasma (sometimes up to 400 mOsm / l) and normal ketonemiya acetone in the urine is not. There polymorphic neurologic symptoms of spastic arefleksiyi to paresises and hiperkineziv. Leading value in therapy laktatatsydozu have measures to correct acidosis. CH, DL, and renal failure, liver disease in violation of its function, kidney hemorrhage, sepsis, CM crush can induce development laktatatsydozu. General dehydration here by organ and tissue dehydration of Estimated Date of Delivery brain, decreasing pressure liquor, the development of intracerebral hemorrhage and subdural. Very typical violation of Pre-eclampsia and mental status. The fact that at no hiperosmolyarniy coma ketosis, due primarily to this c-m develops, usually in people with type 2 diabetes m with relative insulin deficiency without a tendency to ketosis.
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