Hyperosmolar coma is most often diagnosed in patients over 50 years of age who suffer from mild to moderate diabetes mellitus, easily compensated by diet and special drugs. It develops against the background of dehydration of the body as a result of taking diuretics, diseases of the vessels of the brain and kidneys. Mortality from hyperosmolar coma reaches 30%.
Reasons
Hyperosmolar coma, caused by glucose levels, is a complication of diabetes mellitus and occurs as a result of a sharp increase in blood sugar (more than 55.5 mmol / l) in combination with hyperosmolarity and the absence of acetone in the blood.
The reasons for this phenomenon may be:
- severe dehydration due to severe vomiting, diarrhea, burns, or prolonged treatment with diuretic medications;
- insufficiency or complete absence of insulin, both endogenous andexogenous (the cause of this phenomenon may be the lack of insulin therapy or the wrong treatment regimen);
- increased need for insulin, which can occur as a result of gross violations of the diet, the introduction of concentrated glucose preparations, the development of an infectious disease (especially pneumonia and urinary tract infections), after operations, injuries, taking medications that possess the properties of insulin antagonists (in particular, glucocorticoids and sex hormone preparations).
Pathogenesis
Unfortunately, the mechanism of development of this pathological condition is not fully understood. It is believed that the development of this complication is affected by the blockade of glucose excretion by the kidneys, as well as the increased intake of this substance into the body and its production by the liver. At the same time, the production of insulin is suppressed, as well as blocking the utilization of glucose by peripheral tissues. This is all combined with dehydration of the body.
In addition, it is believed that the presence of endogenous (formed inside the body) insulin in the human body interferes with processes such as lipolysis (fat breakdown) and ketogenesis (formation of germ cells). However, this insulin is not enough to suppress the amount of glucose produced by the liver. Therefore, the introduction of exogenous insulin is necessary.
With a sharp loss of fluid in large quantities, the BCC (volume of circulating blood) decreases, which leads to thickening of the blood and an increase inosmolarity. This happens precisely due to an increase in the concentration of glucose, potassium and sodium ions.
Symptoms
Hyperosmolar coma develops, the symptoms of which appear in advance, within a few days or weeks. At the same time, the patient develops signs that are characteristic of decompensated diabetes mellitus (sugar levels cannot be adjusted with drugs):
- polyuria (increased urine production);
- increased thirst;
- increased dryness of the skin, mucous membranes;
- drastic weight loss;
- constant weakness;
- the consequence of dehydration is a general deterioration in well-being: a decrease in the tone of the skin, eyeballs, blood pressure, temperature.
Neurological symptoms
In addition, symptoms can also be observed from the nervous system:
- hallucinations;
- hemiparesis (weakening of voluntary movements);
- violation of speech, it is slurred;
- constant cramps;
- areflexia (lack of reflexes, one or more) or hyperlefxia (increased reflexes);
- muscle tension;
- impaired consciousness.
Symptoms appear days before hyperosmolar coma develops in children or adults.
Possible Complications
With untimely assistance, complications may develop. Frequent are:
- epileptic seizures that canbe accompanied by twitching of the eyelids, face (these manifestations may be invisible to others);
- deep vein thrombosis;
- pancreatitis (inflammation of the pancreas);
- kidney failure.
Changes also occur in the gastrointestinal tract, which are manifested by vomiting, bloating, abdominal pain, intestinal motility disorders (intestinal obstruction is sometimes observed), but they can be almost invisible.
Vestibular disorders also observed.
Diagnosis
If a diagnosis of hyperosmolar coma is suspected, diagnosis is based on laboratory tests. In particular, when examining blood, a high level of glycemia and osmolarity is detected. In addition, elevated sodium levels, high total whey protein, and residual nitrogen are possible. Urea levels may also be elevated. When examining urine, ketone bodies (acetone, acetoacetic and betahydroxybutyric acid) are not detected.
In addition, there is no smell of acetone in the air exhaled by the patient and ketoacidosis (impaired carbohydrate metabolism), which are pronounced hyperglycemia and blood osmolarity. The patient has neurological symptoms, in particular, the pathological sign of Babinski (foot extensor reflex), increased muscle tone, bilateral nystagmus (involuntary oscillatory eye movements).
Among other surveysstand out:
- ultrasound and x-ray examination of the pancreas;
- electrocardiography;
- blood glucose test.
Differential diagnosis is of particular importance. This is due to the fact that hypermolar coma can be the result of not only diabetes mellitus, but also hepatic-renal failure when taking thiazide diuretics.
Treatment
If hyperosmolar coma is diagnosed, emergency care is to eliminate dehydration, hypovolemia and restore plasma osmolarity.
To combat the hydration of the body, a hypotonic sodium chloride solution is used. Introduced from 6 to 10 liters per day. If necessary, the amount of solution is increased. Within two hours after the onset of the pathological condition, it is required to inject 2 liters of sodium chloride solution intravenously, after which the administration takes place by drip at a rate of 1 l / h. These measures are taken up to the normalization of blood osmolarity and pressure in the venous vessels. A sign of the elimination of dehydration is the appearance of the patient's consciousness.
If hyperosmolar coma is diagnosed, treatment requires reduction of hyperglycemia. For this purpose, insulin is administered intramuscularly and intravenously. This requires strict control of blood sugar levels. The first dose is 50 IU, which is divided in half and introduced into the body in various ways. In the case of hypotension, the method of administration is only intravenous. More insulinadministered in the same amount by drip intravenously and intramuscularly. These measures are carried out until the level of glycemia reaches 14 mmol / l.
The insulin regimen may be different:
- one-time 20 IU intramuscularly;
- 5-8 units every 60 minutes.
In the event that the sugar level has dropped to a level of 13.88 mmol / l, the hypotonic sodium chloride solution must be replaced with a glucose solution.
During the treatment of hyperosmolar coma, constant monitoring of the amount of potassium in the blood is necessary, since the introduction of potassium chloride is required to remove it from the pathological state.
In order to prevent cerebral edema as a result of hypoxia, patients are intravenously injected with a solution of glutamic acid in an amount of 50 ml. Heparin is also required, as the risk of thrombosis increases dramatically. This requires monitoring of blood clotting.
As a rule, hyperosmolar coma develops in patients with mild or moderate diabetes mellitus, so we can safely say that the body takes insulin well. Therefore, it is recommended to administer precisely small doses of the drug.
Prevention of complications
The cardiovascular system also needs prevention, namely, the prevention of cardiovascular insufficiency. For this purpose, "Kordiamin", "Strophanthin", "Korglikon" are used. With reduced pressure, which is at a constant level, the introduction of a solution of DOXA is recommended, as well as intravenousadministration of plasma, gemodez, human albumin and whole blood.
Be alert…
If you are diagnosed with diabetes mellitus, you must constantly undergo examinations by an endocrinologist and follow all his instructions, in particular, control blood sugar levels. This will avoid complications of the disease.
