Giperosmolyarny coma

Description:

The Giperosmolyarny coma is a complication of a diabetes mellitus of which the hyperglycemia (more than 38,9 mmol/l), the hyper osmolarity of blood (more than 350 ¼«ß¼/kg) expressed to dehydration, absence of ketoacidosis are characteristic.
Epidemiology of a giperosmolyarny coma
The Giperosmolyarny coma meets at 6-10 times less than ketoatsidotichesky. In most cases it arises at patients with a diabetes mellitus 2 types, is more often at elderly. It develops in 90% of cases against the background of a renal failure.

Reasons of a giperosmolyarny coma:

The Giperosmolyarny coma can develop owing to:
- sharp dehydration (at vomiting, diarrhea, burns, prolonged treatment by diuretics);
- insufficiency or lack of endogenous and/or exogenous insulin (for example, owing to an inadequate insulin therapy or in its absence);
- the increased need for insulin (at gross violation of a diet or introduction of strong solutions of glucose, and also at infectious diseases, especially pneumonia and infections of uric ways, other serious associated diseases, injuries and operations, dative therapy by the medicines having properties of antagonists of insulin - glucocorticosteroids, drugs of sex hormones, etc.).

Pathogeny:

The pathogeny of a giperosmolyarny coma is up to the end not clear. The expressed hyperglycemia arises owing to excess intake of glucose in an organism, the raised products of glucose to cookies, glyukozo-toxicity, suppression of secretion of insulin and utilization of glucose peripheral fabrics, and also owing to organism dehydration. Was considered that availability of endogenous insulin interferes with a lipolysis and a ketogenesis, but it is not enough to suppress formation of glucose liver. Thus,  the gluconeogenesis  and  a glycogenolysis leads to the expressed hyperglycemia. However concentration of insulin in blood at diabetic ketoacidosis and a giperosmolyarny coma is almost identical.
According to other theory, at a giperosmolyarny coma of concentration of somatotropic hormone and cortisol it is less, than at diabetic ketoacidosis; besides, at a giperosmolyarny coma a ratio the insulin/glucagon is higher, than at diabetic ketoacidosis. Гиперосмолярностъ leads plasmas to suppression release of SZhK from fatty tissue and the lipolysis and a ketogenesis oppresses.
The mechanism of hyper osmolarity of plasma includes the increased development of Aldosteronum and cortisol in response to a dehydrational hypovolemia; as a result the hypernatremia develops. The high hyperglycemia and a hypernatremia results in hyper osmolarity of plasma which in turn causes sharply expressed intracellular dehydration. At the same time the content of sodium increases also in liquor. Disturbance of water and electrolytic balance in cells of a brain leads to development of neurologic symptomatology, wet brain and a coma.

Symptoms of a giperosmolyarny coma:

The Giperosmolyarny coma develops within several days or weeks.
At the patient accrues symptoms of a dekompensirovanny diabetes mellitus, including:
- polyuria;
- thirst;
- xeroderma and mucous membranes;
- decrease in body weight;
- weakness, adynamia.
Besides, dehydration symptoms are noted:
- decrease in turgor of skin;
- decrease in a tone of eyeglobes;
- lowering of arterial pressure and body temperatures.
Neurologic symptoms are characteristic:
- hemiparesis;
- hyperreflexia or areflexia;
- consciousness disturbances;
- spasms (at 5% of patients).
At a serious, nekorrigirovanny giperosmolyarny condition the sopor and a coma develop. Carry to the most widespread complications of a giperosmolyarny coma:
- epileptic seizures;
- deep vein thrombosis;
- pancreatitis;
- renal failure.

Diagnosis:

The diagnosis of a giperosmolyarny coma is made on the basis of the anamnesis of a diabetes mellitus, usually the 2nd ooze (however it is necessary to remember that the giperosmolyarny coma can develop also at persons with earlier not diagnosed diabetes mellitus, in 30% of the cases the giperosmolyarny coma is the first manifestation of a diabetes mellitus) characteristic clinical manifestation of data of laboratory diagnosis (first of all a sharp hyperglycemia, a hypernatremia and hyper osmolarity of plasma in the absence of acidosis and ketonic bodies. To similarly diabetic ketoacidosis of an ECG allows to reveal signs of a hypopotassemia and disturbance of a heart rhythm.

Laboratory manifestations of a giperosmolyarny state include:
- a hyperglycemia and a glucosuria (the glycemia usually makes 30-110 mmol/l);
- sharply increased osmolarity of plasma (usually> 350 ¼«ß¼/kg at normal 280-296 ¼«ß¼/kg); osmolality can be calculated by a formula: 2 x ((Na) (K)) + glucose level in blood / the 18th level of an urea nitrogen in blood / 2,8.
- a hypernatremia (also lowered or normal concentration of sodium in blood at the expense of a water exit from intracellular space in extracellular is possible);
- absence of acidosis and ketonic bodies in blood and urine;
- other changes (the leukocytosis to 15 000-20 000/mkl, not necessarily connected with an infection, increase in level of hemoglobin and a hematocrit, moderate increase in concentration of an urea nitrogen in blood is possible).

Differential diagnosis of a giperosmolyarny coma.
The Giperosmolyarny coma is differentiated with other possible causes of infringement of consciousness.
Considering advanced age of patients, most often the differential diagnosis is carried out with disturbance of cerebral circulation and a subdural hematoma.
Extremely important task is differential diagnosis of a giperosmolyarny coma from diabetic ketoatsidotichesky and especially gipeglikemichesky komama.

Treatment of a giperosmolyarny coma:

Patients with a giperosmolyarny coma need to be hospitalized in department of resuscitation / an intensive care. After establishment of the diagnosis and the beginning of therapy patients need constant control the state including monitoring of the main indicators of a hemodynamics, body temperature and laboratory indicators. If necessary to patients carry out IVL, bladder catheterization, installation of the central venous catheter, parenteral food. In department of resuscitation / an intensive care carry out:
- the express analysis of glucose of blood of 1 times an hour at intravenous administration of glucose or 1 time 3 hours upon transition to hypodermic introduction;
- definition of ketonic bodies in serum in blood 2 times a day (at impossibility - definition of ketonic bodies in urine 2 р / days);
- determination of level K, Na in blood 3-4 times a day;
- a research of an acid-base state 2-3 times a day before permanent normalization рН;
- hourly control of a diuresis before elimination of dehydration;
- monitoring of an ECG,
- control of arterial pressure, ChSS, body temperature each 2 h;
- X-ray analysis of lungs,
- the general blood test, wet 1 time in 2-3 days.
As well as at diabetic ketoacidosis, the main directions of treatment of patients with a giperosmolyarny coma are the regidratation, an insulin therapy (for decrease in a glycemia and hyper osmolarity of plasma), correction electrolytic disturbance and disturbances of an acid-base state).

Regidratation.
Enter:
Sodium chloride, 0,45 or 0,9% solution, intravenously kapelno 1-1,5 l within 1 hour of infusion, 0,5-1 l during the 2nd and 3rd, 300-500 ml in the next hours. Concentration of solution of sodium of chloride is defined by sodium level in blood. At the Na level + 145-165 ¼Ý¬ó/l enter chloride sodium solution into concentration of 0,45%; at the Na level +< 145 мэкв/л - в концентрации 0,9%; при уровне Na+ > 165 ¼Ý¬ó/l introduction of saline solutions is contraindicated; at such patients for a regidratation use glucose solution.
Dextrose, 5% solution, intravenously kapelno 1-1,5 l within 1 hour of infusion, 0,5-1 l during the 2nd and 3rd, 300-500 ml - in the next hours. Osmolality of infusion solutions:
0,9% of sodium of chloride - 308 ¼«ß¼/kg;
0,45% of sodium of chloride - 154 ¼«ß¼/kg,
5% of a dextrose - 250 ¼«ß¼/kg.
The adequate regidratation promotes decrease in a hypoglycemia.

Insulin therapy.
Use medicines of short action:
Insulin soluble (human genetic engineering or semi-synthetic) intravenously kapelno in solution of sodium of a chloride/dextrose with a speed of 00,5-0,1 PIECE/kg/h (at the same time glucose level in blood has to decrease no more than on 10 мосм/кг/ч).
In case of a combination of ketoacidosis and a giperosmolyarny syndrome treatment is carried out according to the general principles of treatment of diabetic ketoacidosis.

Assessment of efficiency of treatment.
Consciousness recovery, elimination clinical manifestation of a hyperglycemia, achievement target glucose levels in blood and normal osmolality of plasma, disappearance of acidosis and electrolytic frustration are signs of effective therapy of a giperosmolyarny coma.

Mistakes and unreasonable appointments.
Bystry regidratation and sharp decrease in level of glucose in blood can lead to bystry decrease in osmolarity of plasma and edematization of a brain (especially at children).
Considering advanced age of patients and existence of associated diseases, even adequately carried out regidratation quite often can lead to a decompensation of heart failure and a fluid lungs.
Bystry decrease in level of glucose in blood can cause transition of extracellular liquid in cells and aggravate arterial hypotonia and an oliguria.
Potassium use even at a moderate hypopotassemia at persons with oligo-or an anury can lead to a life-threatening hyperpotassemia.
Purpose of phosphate at renal is contraindicated not to sufficiency.

Forecast.
The forecast of a giperosmolyarny coma depends on efficiency of treatment and development of complications. The lethality at a giperosmolyarny coma reaches 50-60% and is defined first of all by the heavy accompanying pathology.