Ketoacidotic coma

Ketoacidotic coma is an acute complication of diabetes mellitus, resulting from insulin deficiency due to inadequately selected insulin therapy. This condition is dangerous for human life and can lead to death. According to statistics, this complication of occurs in 40 patients from 1000 patients.

In 85-95% of cases the coma ends favorably, and in 5-15% of cases it ends with death for the patient. The most vulnerable people are over 60 years old. For older people, it is especially important to clarify the correctness of insulin therapy and compliance with the dosage of the drug.

Etiology of the onset of

The reasons for which there is such a serious complication are somewhat. All of them are formed due to non-compliance with the regime of therapy, violation of the recommendations prescribed by the doctor, as well as the attachment of a secondary infection. If you analyze the reasons in more detail, then we can identify the following factors that provoke the development of such a disease, as ketoacidotic coma:

• consumption of alcohol in large quantities;
• abolition of the intake of sugar reducing drugs without the permission of the doctor;
• unauthorized transition to a tablet form of treatment for insulin-dependent diabetes mellitus;
• missed insulin injection;
• violation of technical regulations for the introduction of insulin;
• creation of unfavorable conditions for metabolic disorders;
• joining of infectious and inflammatory diseases;
• trauma, surgical intervention, pregnancy;
• stress;
• stroke, myocardial infarction;
• taking medications that do not combine with insulin therapy.

The occurrence of complications in all of the above cases is due to a decrease in the sensitivity of tissue cells to insulin or an increase in the secretory function of the contrinsular hormones( cortisol, adrenaline, norepinephrine, STH, glucagon). Approximately 25% of cases of the development of ketoacidotic coma fail to recognize the cause of its occurrence.

Pathogenesis of the ketoacidotic coma

After the onset of some of the triggers of the development of complications of diabetes mellitus, a chain of pathological processes begins in the body that lead to the development of complication symptoms, as well as possible consequences. How does the ketoacidotic coma develop and its symptoms?

Firstly, appears in the body as insulin deficiency of , as well as the production in excess of the amount of contrinsular hormones. Such a violation leads to insufficient provision of tissues and cells with glucose and a reduction in its utilization. In this case, the liver suppresses glycolysis and develops a hyperglycemic state.

Secondly, under the influence of hyperglycemia, there is hypovolemia ( decreased bcc), loss of electrolytes in the form of potassium, sodium, phosphates and other substances, as well as dehydration( dehydration).

Third, due to the decrease in the volume of circulating blood( BCC), begins to intensify the production of catecholamines , which causes an even greater deterioration in the functional action of insulin in the liver. And in this state, when excess catecholamines and insulin deficiency are observed in this organ, the mobilization of fatty acids from adipose tissue begins.

The final stage of the complication mechanism is the enhancement of ketone bodies ( acetone, acetoacetate, beta-hydroxybutyric acid).Because of this pathological condition, the body is unable to metabolize and remove ketone bodies that bind to accumulating hydrogen ions, resulting in a decrease in blood pH and bicarbonate content and the formation of metabolic acidosis. Compensatory response of the body occurs in the form of hyperventilation and lowering the partial pressure of carbon dioxide. The ketoacidotic coma starts to show symptoms under the influence of such pathogenesis.

Symptoms of complication

Symptoms of complications develop gradually and take from several hours to several days of time. At the very beginning of ketoacidotic coma, the patient notes dry mouth, thirst and polyuria. All these symptoms speak of decompensation of diabetes mellitus. Further clinical picture is supplemented with skin itch due to dry skin, anorexia, weakness, adynamia, pain in the limbs and headaches .

Because of a violation of appetite and loss of electrolytes, abdominal pain, nausea and vomiting of "coffee grounds" begin. Pain in the abdomen can sometimes be so acute that at first there is a suspicion of pancreatitis, ulcer or peritonitis. Increasing dehydration increases the intoxication of the body, which can lead to irreversible consequences. Scientists have not yet studied the toxic effect on the central nervous system, but the main assumptions of death are the dehydration of brain neurons, which occurs as a result of the hyperosmolarity of the plasma.

The main clinical picture of a ketoacidotic coma is the typical symptoms for this complication, expressed in rapid, but deep breathing( Kussmaul breath) with the odor of acetone on exhalation. In patients, the turgor( elasticity) of the skin is reduced, and the skin and mucous membranes are dry. Because of the decrease in BCC, the patient may experience orthostatic hypotension, accompanied by confusion, gradually turning into a coma. It is very important to notice the presence of the presented symptoms in time to provide timely assistance.

Emergency care for a ketoacidotic coma

Probably, it is not worth mentioning that the diabetic patient himself, as well as his relatives and relatives around him, should know everything about this disease, including the provision of emergency care. Nevertheless, it is possible to repeat the algorithm of actions in case of occurrence of ketoacedosis:

1. If the worsening of the patient's condition, and even more so the disturbance of consciousness, is noted up to the transition to a coma, first of all the brigade of "first aid" is called.
2. Further it is necessary to check up heart rate, ЧДД and the HELL and to repeat these actions down to arrival of physicians.
3. To assess the patient's condition, you can use questions that must be answered or resorted to rubbing the lobes of the ears and slight slaps on the face.

In addition, pre-hospital care can be identified, which is provided in an ambulance carriage and includes the following actions:

1. Introducing saline solutions in the form of an isotonic solution in a volume of 400-500 ml IV at a rate of 15 ml / min. This is done to alleviate the symptoms of dehydration of the body.
2. Introduction of subcutaneously small doses of insulin.

After arrival in the hospital, the patient is identified in the intensive care unit, where the patient continues to be treated in a ketoacidotic coma.

Treatment

Inpatient treatment of a patient implies the fight against hypovolemic shock and dehydration, normalization of electrolyte balance, elimination of intoxication, restoration of physiological functions of the body and treatment of concomitant diseases.

Principles of care and treatment for ketoacedotic coma:

1. Rehydration. An important link in the chain of elimination of complications. In ketoacidosis, dehydration of the body occurs and physiological liquids are introduced in the form of 5-10% glucose and 0.9% sodium chloride solution to replenish the lost fluid. Glucose is prescribed to restore and maintain blood osmolarity.
2. Insulin therapy. A similar method of treatment begins immediately after the diagnosis of a ketoacidonic coma. In this case, as, indeed, in other urgent states with diabetes mellitus, short-acting insulin is used( Insuman Rapid, Actrapid NM, Actrapid MS, Humulin R).Initially, it is injected intramuscularly into the rectus abdominis muscle or intravenously drip. After the glucose level reaches 14 mmol / l, the patient begins the administration of short-acting insulin subcutaneously. As soon as the level of glycemia is fixed at the rates of 12-13 mmol / L, the dose of insulin administered is reduced by half. You can not reduce the glycemic index below 10 mmol / l. Such actions can trigger the onset of hypoglycemia and hyposmolarity of the blood. As soon as all symptoms of ketoacedomic coma are eliminated, the patient is transferred to 5-6 single-dose insulin administration for a short period of time, and with stabilizing dynamics, combined insulin therapy is then carried out.
3. Recovery of electrolyte balance and hemostasis. Such activities are an important part of ongoing therapy. With the introduction of the necessary drugs, calcium deficiency and acid-base blood state are restored, thereby ensuring the normalization of kidney functions to reabsorb bicarbonates.
4. Improvement of the rheological properties of blood. And also to prevent intravascular coagulation, heparin can be administered intravenously, necessarily under the control of the coagulogram.
5. Treatment of secondary infections. If the patient is experiencing secondary infection, and to prevent their occurrence, broad-spectrum antibiotics may be prescribed.
6. Symptomatic therapy. To restore blood pressure and eliminate the effects of shock, therapeutic measures are carried out aimed at improving cardiac activity. In addition, after a coma patient is prescribed a gentle diet, rich in potassium, carbohydrates and proteins. Fats from the diet are excluded for at least 7 days.

Prevention of ketoacedotic coma

Nothing is better than just not getting sick. If a moment happens in life that a chronic disease requires increased attention, it is with special responsibility that this circumstance.

First, you need to take special care with all the recommendations prescribed by your doctor. Secondly, you need to monitor the shelf life of insulin, observe the technique of administration, dosage and time of injections. It is necessary to store the medicinal product according to all the rules. In case the patient feels an ailment and a worsening of his condition, which he can not cope on his own, one should immediately consult a doctor where he will be given emergency care.

Complications of coma

A ketoacedotic coma with a correctly diagnosed diagnosis and timely correction of biochemical disorders carries a favorable outcome and does not cause serious consequences. The most dangerous complication of this condition can be cerebral edema, which in 70% of cases ends in a fatal outcome.