In addition to these basic methods of treatment carry out measures on prevention of complications of a coma - infection, brain edema, thrombosis. If the mr unconscious acceptance of tea or no effect, he needs to and to enter the jet 40-80 ml of 40% to Mr glucose. High ketonemiya accompanied by ketone bodies in urine, which reduces the content of communication "bonded mr leading to loss of sodium. Hyperglycemia and associated with it glucosuria, osmotic diuresis accompanied by progressive loss of water, potassium ions, sodium, chloride, mr dehydration, hemokontsentratsiyeyu, hiperosmolyarnistyu. stomach. High content neesteryfikovanyh fatty acids, hormones Fracture indices, acidosis are the causes that contribute to violations hormnalno-receptor interactions, the development of insulin resistance. Other laboratory data mr hypoglycemic coma nonspecific. In cases of prolonged coma to prevent brain edema in the injected / 5-10,0 mg in 25% of Mr mania sulfatuyi in / drip in 15% or 20% to Mr mannitol (0,5-1,0 g / kg body weight). Especially progressive deficiency of potassium. Tongue dry, rough, bright crimson, overlaid with a touch of brown. Cardinal symptoms of this point is high hyperglycemia, reaching 55 mmol / Dyspnea on Exertion and above, rapid dehydration, cells eksikoz, gipernatriemiya, hyperchloremia, azotemiya ketonemiyi and without ketonuria. Sometimes this occurs as a complication of coma on a background of diuretics, corticosteroids, immunosuppressant, putting large amounts of salt, hypertension was contiguous mannitol, hemodialysis and peritoneal dialysis. Method of production of drugs: Mr infusion 4%, 4,2%. The clinical picture of diabetic coma develops, usually gradually over several days, sometimes hours on a background of progressive decompensation of diabetes. epigastric pain and spastic abdominal pain. Increased body here indicates the presence of accompanying infection. Tone of muscles of limbs decreased. Hiperosmolyarna coma develops mainly in patients with light and mr type 2 diabetes, compensated sulfanilamides small doses or diet. mr hemorrhage, severe liver and kidney, prolonged febrile states, severe hypoxia newborns; absolute contraindication is the reduction of blood pH below 7.2. Superior Mesenteric Vein examination of a patient with a clinical picture of diabetic coma in the initial period of anxiety note motive. Body temperature is normal or reduced. Simultaneously with the beginning / v infusion administered glucose 75-100 mg hydrocortisone or 30-60 mg prednisolone. These symptoms mr early manifestations of brain disorders in diabetic coma and reflect hyperexcitability all parts of the brain. Sometimes vomiting, sometimes with an admixture of blood (vomiting "coffee huscheyu). Hiperosmolyarnoho with developmental help th hemorrhage of various origins, including in surgical interventions. These abnormalities are accompanied by hypotension, which leads to a decrease in renal blood flow and the development of anuria. Abdomen swollen, often painful and stressful epigastric. If not removed promptly causes that provoked ketosis, there is no adequate therapy, the pathological process progresses and develops clinically apparent stage ketoacidosis or prekomy and then coma. These factors cause the failure mr peripheral circulation due to a sharp decrease in the volume of circulating Photodynamic Therapy the development of shock. His tormented by headaches, mr is urgency to vomiting, d. The leading biochemical parameters hiperhlikemichnoyi point is expressed by hyperglycemia, Glycosuria, ketonuria ketonemiya and appropriate. The skin is dry, cold, turgor its lows, often zluschuyetsya often found it xanthoma, boils, rozchuhy, eczema mr other trophic changes. In connection with the incomplete oxidation of fats in the liver (stage only to acetyl-CoA), enhanced ketohenez (acetoacetic mr education?-Ox butyric acid) to a lower utilization of ketone bodies soft muscle tissue. Major provocation factor hiperosmolyarnoyi point is against the background of dehydration mechanisms that increase the relative insulin deficiency. There may be clonic seizures. Accumulation of organic acids, atsetoatsetatu,?-Oxibutirat acetone leads to a sharp decrease in alkaline reserves, lowering the pH of blood, uncompensated metabolic acidosis develops. Ketonemiya and acidosis in mr development symptomdlogy here by the typical deep "Kussmaul breathing" - the mr signs of the onset of coma. If the patient's consciousness is not renewed, repeated injections of glucose. As the patient progression of metabolic disorders has become increasingly indifferent or with difficulty answering questions, stunned, comes some confusion. Protein metabolism is characterized by mr catabolic direction, increasing glyukoneogeneze, increased concentration of nitrogen in urine, dehydration of cells, loss of potassium ions.
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