Hyperosmolar coma is an acute complication of type 2 diabetes mellitus characterized by impaired glucose metabolism and an increase in its blood level, a sharp increase in plasma osmolarity, pronounced intracellular dehydration, and the absence of ketoacidosis. The main symptoms are polyuria, dehydration, muscle hypertonia, convulsions, increasing drowsiness, hallucinations, incoherent speech. For diagnosis, anamnesis is collected, the patient is examined, a number of laboratory blood and urine tests are performed. Treatment involves rehydration, restoration of a normal amount of insulin, elimination and prevention of complications.
ICD 10
E11.0
Meaning
Hyperosmolar coma (HOC) was first described in 1957, its other names are non–ketogenic hyperosmolar coma, diabetic hyperosmolar condition, acute hyperosmolar non-acidotic diabetes. The name of this complication describes its main characteristics – the concentration of kinetically active serum particles is high, the amount of insulin is sufficient to stop ketonogenesis, but does not prevent hyperglycemia. Hyperosmolar coma is rarely diagnosed, in about 0.04-0.06% of patients with diabetes. In 90-95% of cases, it is found in patients with type 2 diabetes and on the background of renal insufficiency. Elderly and senile people are at high risk.
Causes
GONK develops on the basis of severe dehydration. Frequent previous conditions are polydipsia and polyuria – increased urinary excretion and thirst for several weeks or days before the manifestation of the syndrome. For this reason, the elderly are particularly at risk – they often have impaired perception of thirst, altered kidney function. Among other provoking factors , there are:
- Incorrect treatment of diabetes. The occurrence of complications is caused by an insufficient dose of insulin, skipping the next injection of the drug, skipping the intake of oral hypoglycemic drugs, spontaneous cancellation of therapy, errors in the insulin injection procedure. The danger of hyperosmolar coma is that the symptoms do not appear immediately, and patients do not pay attention to the permissible errors of treatment.
- Concomitant diseases. The addition of other severe pathologies increases the likelihood of hyperosmolar hyperglycemic coma. Symptoms develop in infectious patients, as well as in acute decompensated pancreatitis, trauma, shock, myocardial infarction, stroke. In women, pregnancy is a dangerous period.
- Changing the power supply. The cause of the complication may be an increase in the amount of carbohydrates in the diet. Often this happens gradually and is not regarded by patients as a violation of the therapeutic diet.
- Fluid loss. Dehydration occurs when taking diuretics, burns, hypothermia, vomiting and diarrhea. In addition, the RACE is provoked by the systematic situational impossibility of quenching thirst (the inability to distract from the workplace and make up for the loss of fluid, the shortage of drinking water in the area).
- Taking medications. The appearance of symptoms can be triggered by taking diuretics or laxatives that remove fluid from the body. “Dangerous” drugs also include corticosteroids, beta-blockers and some other drugs that violate glucose tolerance.
Pathogenesis
When insulin is insufficient, glucose circulating in the bloodstream does not enter the cells. A state of hyperglycemia develops – an elevated sugar level. Cellular starvation triggers the breakdown of glycogen from the liver and muscles, which further increases the flow of glucose into the plasma. Osmotic polyuria and glucosuria occur – a compensatory mechanism for the excretion of sugar in the urine, which, however, is disrupted by dehydration, rapid loss of fluid, and impaired renal function. Due to polyuria, hypohydration and hypovolemia are formed, electrolytes (K+, Na+, Cl–) are lost, the homeostasis of the internal environment and the work of the circulatory system change. A distinctive feature of hyperosmolar coma is that the insulin level remains sufficient to prevent the formation of ketones, but too low to prevent hyperglycemia. The production of lipolytic hormones – cortisol, growth hormone – remains relatively intact, which further explains the absence of ketoacidosis.
Symptoms
Maintaining the normal level of ketone bodies in plasma and long-term maintenance of the acid-base state explains the features of the clinical picture of hyperosmolar coma: there is no hyperventilation and shortness of breath, there are practically no symptoms at the initial stages, deterioration of well-being occurs with a pronounced reduction in blood volume, dysfunction of important internal organs. The first manifestation is often a violation of consciousness. It ranges from confusion and disorientation to deep coma. Local muscle cramps and/or generalized seizures are observed.
For days or weeks, patients experience intense thirst, suffer from arterial hypotension, tachycardia. Polyuria is manifested by frequent urges and copious urination. Disorders of the central nervous system include mental and neurological symptoms. Confusion occurs according to the type of delirium, acute hallucinatory delusional psychosis, catatonic seizures. Characterized by more or less pronounced focal symptoms of central nervous system damage – aphasia (disintegration of speech), hemiparesis (weakening of limb muscles on one side of the body), tetraparesis (decreased motor function of the arms and legs), polymorphic sensory disorders, pathological tendon reflexes.
Complications
In the absence of adequate therapy, fluid deficiency is constantly increasing and averages 10 liters. Violations of the water-salt balance contribute to the development of hypokalemia and hyponatremia. Respiratory and cardiovascular complications occur – aspiration pneumonia, acute respiratory distress syndrome, thrombosis and thromboembolism, bleeding due to disseminated intravascular coagulation. Pathology of fluid circulation leads to edema of the lungs and brain. The cause of death is dehydration and acute circulatory failure.
Diagnostics
Examination of patients with suspected hyperosmolar coma is based on the determination of hyperglycemia, plasma hyperosmolarity and confirmation of the absence of ketoacidosis. Diagnosis is carried out by an endocrinologist. It includes the clinical collection of information about the complication and a set of laboratory tests. To make a diagnosis, the following procedures must be performed:
- Collection of clinical and anamnestic data. The endocrinologist studies the medical history, collects an additional anamnesis during the patient’s survey. The presence of a diagnosis of “type II diabetes mellitus”, age over 50 years, impaired kidney function, non-compliance with doctor’s prescriptions regarding DM therapy, concomitant organ and infectious diseases testifies in favor of hyperosmolar coma.
- Inspection. During a physical examination by a neurologist and an endocrinologist, signs of dehydration are determined – tissue turgor, eyeball tone are reduced, muscle tone and tendon physiological reflexes are changed, blood pressure and body temperature are reduced. Typical manifestations of ketoacidosis – shortness of breath, tachycardia, acetone breath – are absent.
- Laboratory tests. The key signs are glucose levels above 1000 mg/ dl (blood), plasma osmolarity usually exceeds 350 mosm / l, ketone levels in urine and blood are normal or slightly elevated. According to the level of urine glucose, its ratio to the concentration of the compound in the bloodstream, the preservation of kidney function and compensatory capabilities of the body are evaluated.
In the process of differential diagnosis, it is necessary to distinguish between hyperosmolar non-ketone coma and diabetic ketoacidosis. The key differences of hyperosmolar coma are a relatively low ketone index, the absence of clinical signs of ketone accumulation, the appearance of symptoms in the late stages of hyperglycemia.
Treatment
First aid to patients is provided in intensive care units, and after stabilization of the condition – in general hospitals and outpatient. Treatment is aimed at eliminating dehydration, restoring normal insulin activity and water-electrolyte metabolism, preventing complications. The therapy scheme is individual, includes the following components:
- Rehydration. Injections of hypotonic sodium chloride solution, potassium chloride are prescribed. The level of electrolytes in the blood and ECG indicators are constantly monitored. Infusion therapy is aimed at improving the circulation and excretion of urine, increasing blood pressure. The rate of fluid administration is corrected according to changes in blood pressure, heart function, and water balance.
- Insulin therapy. Insulin is administered intravenously, the rate and dosage are determined individually. When the glucose indicator approaches normal, the amount of the drug is reduced to basal (previously administered). In order to avoid hypoglycemia, sometimes it is necessary to add dextrose infusion.
- Prevention and elimination of complications. To prevent brain edema, oxygen therapy is performed, glutamic acid is injected intravenously. The balance of electrolytes is restored with the help of glucose-potassium-insulin mixture. Symptomatic therapy of complications from the respiratory, cardiovascular and urinary systems is carried out.
Prognosis and prevention
Hyperosmolar hyperglycemic non-ketone coma is associated with a risk of death, with timely medical care, the mortality rate decreases to 40%. Prevention of any form of diabetic coma should be focused on the fullest possible compensation for diabetes. It is important for patients to follow a diet, limit the intake of carbohydrates, regularly give the body moderate physical activity, not to allow independent changes in the scheme of using insulin, taking sugar-lowering medications. Pregnant women and maternity women need correction of insulin therapy.
Literature.
1. Comatose states. Scientific and educational material. – 2010.
2. Medicine of critical conditions. Book 2/ Marini D., Wheeler A. – 2002.
3. Acute complications of diabetes mellitus in the practice of a doctor/ Torshkhoeva H.M., Vertkin A.L., Gorodetsky V.V.// The attending physician. – 2003.