Hyperosmolar coma

Hyperosmolar coma is a complication of diabetes mellitus, which is characterized by hyperglycemia (more than 38.9 mmol / l), hyperosmolarity of blood (more than 350 mosm / kg), marked dehydration, the absence of ketoacidosis.

[1], [2], [3], [4], [5], [6]

Epidemiology

Hyperosmolar coma occurs 6-10 times less frequently than ketoacidotic. In most cases, it occurs in patients with type 2 diabetes, more often in the elderly. In 90% of cases, it develops on the background of renal failure.

[7], [8], [9], [10], [11]

Causes of the hyperosmolar coma

Hyperosmolar coma may develop due to:

• severe dehydration (vomiting, diarrhea, burns, long-term diuretic treatment);
• insufficiency or absence of endogenous and / or exogenous insulin (for example, due to inadequate insulin therapy or in its absence);
• increased need for insulin (with a gross violation of the diet or the introduction of concentrated glucose solutions, as well as with infectious diseases, especially pneumonia and urinary tract infections, other severe concomitant diseases, injuries and surgeries, dative therapy with insulin antagonists, - glucocorticosteroids, drugs of sex hormones, etc.).

[12], [13]

Pathogenesis

The pathogenesis of hyperosmolar coma is not completely clear. Severe hyperglycemia occurs due to excessive glucose uptake in the body, increased glucose production by the liver, glucose toxicity, suppression of insulin secretion and utilization of glucose by peripheral tissues, as well as due to dehydration of the body. It was believed that the presence of endogenous insulin interferes with lipolysis and ketogenesis, but it is not enough to suppress the formation of glucose by the liver.

Thus, gluconeogenesis and glycogenolysis leads to severe hyperglycemia. However, the concentration of insulin in the blood in diabetic ketoacidosis and hyperosmolar coma is almost the same.

According to another theory, the concentration of somatotropic hormone and cortisol is less in hyperosmolar coma than in diabetic ketoacidosis; in addition, in hyperosmolar coma, the insulin / glucagon ratio is higher than in diabetic ketoacidosis. Hyperosmolar plasma leads to the suppression of the release of FFA from adipose tissue and inhibits lipolysis and ketogenesis.

The mechanism of hyperosmolarity of plasma includes an increased production of aldosterone and cortisol in response to dehydration hypovolemia; as a result, hypernatraemia develops. High hyperglycemia and hypernatremia leads to plasma hyperosmolarity, which in turn causes a pronounced intracellular dehydration. At the same time, the sodium content rises in the liquor. Disruption of water and electrolyte balance in brain cells leads to the development of neurological symptoms, brain edema and coma.

[14], [15], [16], [17], [18]

Symptoms of the hyperosmolar coma

Hyperosmolar coma develops over several days or weeks.

The patient is growing symptoms of decompensated diabetes, including:

• polyuria;
• thirst;
• dry skin and mucous membranes;
• weight loss;
• weakness, weakness.

In addition, symptoms of dehydration are noted;

• reduced skin turgor;
• reduced tone of the eyeballs;
• lowering blood pressure and body temperature.

Characterized by neurological symptoms:

• Gimparasse ;
• hyperreflexia or areflexia;
• disturbance of consciousness;
• convulsions (in 5% of patients).

In severe, uncorrected hyperosmolar state, stupor and coma develop. The most common complications of hyperosmolar coma include:

• epileptic seizures;
• deep vein thrombosis;
• Pancreatitis ;
• renal failure.

[19], [20]

Diagnostics of the hyperosmolar coma

The diagnosis of hyperosmolar coma is made on the basis of the history of diabetes mellitus, usually 2 nd of tina (however, it must be remembered that hyperosmolar coma can also develop in patients with previously not diagnosed diabetes mellitus, in 30% of cases hyperosmolar coma is the first manifestation of diabetes mellitus), characteristic clinical the manifestation of laboratory diagnostic data (especially sharp hyperglycemia, hypernatremia and plasma hyperosmolarity in the absence of acidosis and ketone bodies. Similarly to diabetic ketoacidosis, ECG allows you to detect Induce signs of hypokalemia and heart rhythm disturbances.

Laboratory manifestations of the hyperosmolar state include:

• hyperglycemia and glucosuria (glycemia is usually 30-110 mmol / l);
• sharply increased plasma osmolarity (usually> 350 mosm / kg with a normal 280-296 masm / kg); osmolality can be calculated by the formula: 2 x ((Na) (K)) + blood glucose level / 18 blood urea nitrogen level / 2.8.
• hypernatremia (it is also possible reduced or normal concentration of sodium in the blood due to the release of water from the intracellular space in the extracellular);
• the absence of acidosis and ketone bodies in the blood and urine;
• other changes (possible leukocytosis up to 15 000-20 000 / μl, not necessarily associated with infection, increased hemoglobin and hematocrit, a moderate increase in the concentration of urea nitrogen in the blood).

[21], [22], [23], [24]

Differential diagnosis

Hyperosmolar coma differentiate with other possible causes of impaired consciousness.

Given the elderly age of patients, most often the differential diagnosis is carried out with impaired cerebral circulation and subdural hematoma.

An extremely important task is the differential diagnosis of hyperosmolar coma with diabetic ketoacidotic and especially hyperglycemic coma.

[25], [26], [27], [28], [29], [30]

Treatment of the hyperosmolar coma

Patients with hyperosmolar coma should be hospitalized in the intensive care unit / intensive care unit. After diagnosis and initiation of therapy, patients need constant monitoring of the condition, including monitoring of the main hemodynamic parameters, body temperature and laboratory parameters.

If necessary, patients undergo mechanical ventilation, bladder catheterization, central venous catheter installation, parenteral nutrition. In the intensive care unit / intensive care unit, the following is performed:

• rapid analysis of blood glucose 1 time per hour with intravenous glucose or 1 time 3 hours when switching to subcutaneous administration;
• determination of ketone bodies in the serum in the blood 2 times a day (if not possible - determination of ketone bodies in the urine 2 p / day);
• determining the level of K, Na in the blood 3-4 times a day;
• the study of the acid-base state 2-3 times a day until stable pH normalization;
• hourly control of diuresis to eliminate dehydration;
• ECG monitoring
• control of blood pressure, heart rate, body temperature every 2 hours;
• radiography of the lungs
• complete blood count, urine 1 time in 2-3 days.

As with diabetic ketoacidosis, the main areas of treatment for patients with hyperosmolar coma are rehydration, insulin therapy (to reduce blood glucose and hyperosmolar plasma), correction of electrolyte disorders and disorders of the acid-base state).

Regidratatsiya

Enter:

Sodium chloride, 0.45 or 0.9% solution, intravenous drip 1-1.5 l for the 1st hour of infusion, 0.5-1 l for the 2nd and 3rd, 300-500 ml in subsequent hours. The concentration of sodium chloride solution is determined by the level of sodium in the blood. At the level of Na ⁺  145-165 meq / l, sodium chloride solution is introduced at a concentration of 0.45%; when the level of Na ⁺  <145 mEq / l - in a concentration of 0.9%; when the level of Na ⁺  > 165 mEq / l, the introduction of saline solutions is contraindicated; in such patients, glucose solution is used for rehydration.

Dextrose, 5% solution, intravenous drip 1-1.5 l for the 1st hour of infusion, 0.5-1 l for the 2nd and 3rd, 300-500 ml - in the next hours. Osmolality of infusion solutions:

• 0.9% sodium chloride - 308 mosm / kg;
• 0.45% sodium chloride - 154 mosm / kg,
• 5% dextrose - 250 mosm / kg.

Adequate rehydration helps to reduce hypoglycemia.

[31], [32], [33]

Insulin therapy

Apply short-acting drugs:

Insulin soluble (human genetically engineered or semi-synthetic) intravenously drip in sodium chloride / dextrose solution at a rate of 00.5-0.1 U / kg / h (and the level of glucose in the blood should be reduced by no more than 10 mos / kg / h)

In the case of a combination of ketoacidosis and hyperosmolar syndrome, treatment is carried out in accordance with the general principles of treatment of diabetic ketoacidosis.

[34], [35], [36], [37], [38], [39]

Evaluation of the effectiveness of treatment

Signs of effective treatment of hyperosmolar coma are recovery of consciousness, elimination of the clinical manifestations of hyperglycemia, achievement of target blood glucose levels and normal plasma osmolality, disappearance of acidosis and electrolyte disorders.

[40], [41], [42], [43], [44], [45], [46]

Errors and unreasonable assignments

Rapid rehydration and a sharp decrease in the level of glucose in the blood can lead to a rapid decrease in plasma osmolarity and the development of cerebral edema (especially in children).

Given the elderly age of patients and the presence of comorbidities, even adequately performed rehydration can often lead to decompensation of heart failure and pulmonary edema.

A rapid decrease in blood glucose levels can cause the extracellular fluid to pass into the cells and aggravate hypotension and oliguria.

The use of potassium, even in moderate hypokalemia in individuals with oligo- or anuria, can lead to life-threatening hyperkalemia.

Prescribing phosphate in renal failure is contraindicated.

[47], [48], [49], [50], [51]

Forecast

The prognosis of hyperosmolar coma depends on the effectiveness of treatment and the development of complications. Mortality in hyperosmolar coma reaches 50-60% and is determined primarily by severe concomitant pathology.

[52], [53], [54]