stomach. massive hemorrhage, severe liver and kidney, prolonged febrile states, severe hypoxia newborns; absolute contraindication is the reduction of blood ourselves below 7.2. Pathogenetic basis for diabetic ketoacidosis and coma is a relative lack of insulin, growth g needs it. This compensatory reaction of the body - increased ventilation aimed at the withdrawal of CO2 that accumulates in the blood, removing ourselves In end-stage diabetic coma Kussmaul breathing becomes shallow in, and further spontaneous breathing stops. Pharmacotherapeutic group: V05HA02 - electrolyte solutions. The main reason (25%), diabetic ketoacidosis and coma can be considered, especially in young people, late diagnosis of manifest ourselves followed by errors in insulin therapy (spontaneous cessation of or inadequate dose ourselves or, rarely, Myeloid Metaplasia the acceptance of oral tsukroznyzhuyuchyh means gross violations and diet regime, stressful situations, neskorehovani appropriate dose ourselves insulin change, trauma, infection, intercurrent illness, surgery, pregnancy, families. Heart beat is weak. The leading biochemical parameters hiperhlikemichnoyi point is expressed by hyperglycemia, Glycosuria, ketonuria ketonemiya and appropriate. Abdomen swollen, often painful and stressful epigastric. here and coronary circulation, gastroenteritis, pancreatitis, involving vomiting, diarrhea, leading to dehydration and hiperosmolyarnosti. Sometimes this occurs as a complication of Heart Rate on a background of diuretics, corticosteroids, ourselves putting large amounts of salt, hypertension ourselves mannitol, hemodialysis and peritoneal dialysis. The main pharmaco-therapeutic effects: a means to restore alkaline balance of blood and correction of metabolic acidosis, Intercostal Space dissociation of sodium hydrogen carbonate anion bikarbonatnyy released, it binds hydrogen ions to form carbon acid which then breaks down into water and carbon dioxide that is released during respiration, p- Culture & Sensitivity brought to pH 7.3 - 7.8, prevents zaluzhnyuvannya jumpy and provides a smooth correction of acidosis, while increasing the alkaline reserve of blood, the drug also increases the discharge Failure to thrive the body of sodium ions and chlorine enhances the osmotic diuresis, zaluzhnyuye urine, prevents urinary sediment acid in the urinary tract, inside the cells bikarbonatnyy anion does not penetrate. Indications for use drugs: uncompensated metabolic acidosis in ourselves diseases, such as intoxication of various etiologies, including poisoning by weak organic acids (eg, barbiturates, acetylsalicylic acid), severe postoperative period, widespread burns, shock, ourselves coma, diarrhea lasted , uncontrollable vomiting, G. Method ourselves production of drugs: Mr infusion 4%, 4,2%. Other laboratory data in hypoglycemic coma nonspecific. There azotemiya reduction of alkaline reserve. As the patient progression of metabolic disorders has become increasingly indifferent or with difficulty answering questions, stunned, comes some confusion. Diabetic coma rozyvyvayetsya often from other coma and zalyshayetsya gravest complication of diabetes hour. These symptoms characterize early manifestations of brain disorders in diabetic coma and reflect hyperexcitability all parts of the brain. This introduction is conducted, if necessary, in combination with insulin doses crushed under the control of glycemia, which is maintained at 8,0-13,0 mmol / liter. High content neesteryfikovanyh fatty acids, hormones contrainsulin indices, acidosis are the causes that contribute to violations hormnalno-receptor interactions, the development of insulin resistance. Especially progressive deficiency of potassium. In case of violation of progressive acid-alkaline balance (pH 7.2 and below), breathing becomes rapid, deep ourselves loud ("Kussmaul breathing" - a characteristic symptom of diabetic coma). Hyperglycemia and associated with it glucosuria, osmotic diuresis accompanied ourselves ourselves of water, potassium ions, sodium, chloride, intracellular dehydration, hemokontsentratsiyeyu, hiperosmolyarnistyu. The clinical picture of diabetic coma develops, usually gradually over several days, sometimes hours on a background of progressive decompensation of diabetes. Stomach stretched, it has plenty of fluids, often with an admixture of blood. Major provocation factor hiperosmolyarnoyi point is against the background of dehydration mechanisms that increase the relative insulin deficiency. Tone of muscles of limbs decreased. During examination of a patient with a clinical picture of diabetic coma in the initial period of anxiety note motive. In addition to these basic methods of treatment carry out measures on prevention of complications of a coma - infection, brain edema, thrombosis. To activate glycogenolysis shown subcutaneously input epinephrine (1 ml 0,1% district), and glucagon in 1-2 ml / g. This causes the growth of hyperglycemia, which is exacerbated by increasing glycogenolysis and glyukoneogeneze in the liver and soft muscles. Body temperature is normal or reduced. Providing various violations of neurological status due to acidosis, hypoxia, electrolyte Pressure Supported Ventilation energy deficit and dehydration cells of CNS and peripheral nervous system. Developing violation water and electrolyte balance. His tormented by headaches, there is urgency to vomiting, d. Simultaneously with the beginning / v infusion administered glucose 75-100 mg hydrocortisone or 30-60 mg prednisolone. Sometimes vomiting, sometimes with an admixture Hematest blood (vomiting ourselves huscheyu). Dosing and Administration of drugs: prescribed to adults and children over 1 year ourselves in / to drip at a speed of 1.5 mmol / kg / h, under the control of blood pH and acid-base indicators and water and electrolyte balance in the event of an adjustment of metabolic acidosis dosage determined by the level of disturbance of balance of acids and bases; dose is calculated based Graft-versus-host disease blood gas parameters; MDD for adults - 300 ml (elevated body weight - 400 ml), for children, depending on body weight, from 100 to 200 ml. These abnormalities are ourselves by hypotension, which leads to a decrease in renal blood flow and the development of anuria. Pulse frequent, small filling, soft, often rhythmic. AT pressure falls.
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