Diabetic coma is one of the variants of diabetic coma, in which there is a sharp increase in glucose levels without ketoacidosis. The condition occurs with prolonged dehydration, excessive intake of carbohydrates, relative insufficiency of insulin. Pathology is manifested by loss of consciousness, convulsions, decreased skin turgor and other signs of dehydration. To diagnose an emergency condition, biochemical blood and urine tests, ECG and ultrasound of the heart, neuroimaging methods are carried out. Treatment includes infusion therapy, insulin therapy, prevention of thrombotic complications.
ICD 10
E10.0 E11.0
Meaning
Diabetic (hyperglycemic) coma accounts for 5-10% of all types of diabetic coma and is characterized by high mortality. It is more common in patients over 50 years of age. The condition requires intensive and urgent medical care, which is carried out in the intensive care unit. Since the prevalence of comatose conditions in diabetes remains consistently high, the task of endocrinologists is to improve the hypoglycemic therapy regimen and increase patient compliance.
Causes
The development of diabetic coma is associated with severe insulin deficiency and its tissue effects. In practical endocrinology, the condition is most often found in patients with type 2 diabetes mellitus who have a long history of the disease and severe metabolic disorders. The risk factor is old age, concomitant pathologies of the urinary system. The immediate causes of diabetic hyperglycemia:
- Dehydration. Pathological fluid loss is most often observed with diarrhea and vomiting that occur against the background of acute gastroenteritis, food toxicoinfection, acute pancreatitis. Dehydration develops with extensive burns, massive bleeding, irrational use of diuretics.
- Climatic factors. Dehydration occurs with increased sweating in a hot climate. At risk are people who work in the open sun or in hot workshops, do not monitor the balance of the liquid they drink.
- Excessive intake of glucose. Hyperglycemic conditions can occur with the simultaneous use of a large amount of simple carbohydrates. Coma is possible with intravenous administration of hypertensive glucose solutions.
- Relative insulin deficiency. A comatose state is formed when there is a discrepancy between the level of insulin and the need of tissues for this hormone. Such situations develop against the background of exacerbation of a chronic disease, injuries, surgical operations.
Pathogenesis
Diabetic coma occurs with absolute or relative insulin insufficiency. Hormone deficiency blocks the transport of glucose from the blood to the muscles, liver and adipose tissue. Against the background of hyperglycemia, the intracellular glucose content decreases, as a result of which the processes of glycogenolysis and gluconeogenesis are triggered. The amount of carbohydrates in the blood increases even more, but the cells experience an energy deficit – “hunger among abundance”.
With hyperglycemia, the osmolarity of the blood increases, so the fluid passes from the cells into the vascular bed. To remove excess glucose, the renal filter is activated and diuresis increases. Together with urine, the body rapidly loses water, potassium, sodium and other electrolytes. These processes aggravate cellular dehydration, cause general dehydration and disrupt biochemical processes in all tissues.
The absence of ketoacidosis in diabetic coma is explained by the presence of endogenous insulin, which is produced in the islets of Langerhans. The hormone enters directly into the liver, where it inhibits the reactions of lipolysis and diabetic ketogenesis. Hyperosmolarity of the blood suppresses the release of free fatty acids from subcutaneous tissue, which indirectly prevents the development of ketoacidotic coma.
Symptoms
Diabetic coma develops within 1-2 weeks and is characterized by a long period of precoma. Initial manifestations include increased thirst, dry mouth, weakness and drowsiness. The symptoms are similar to the usual signs of diabetes mellitus, so patients do not pay due attention to it and do not consult a doctor. Then there is copious and frequent urination. Due to dehydration, the skin loses elasticity, becomes dry and flabby.
Hyperglycemic precoma is characterized by pronounced neurological symptoms. Patients experience disorientation in time and space, severe coordination disorders, and true hallucinations. Brain damage is manifested by convulsive syndrome, nystagmus, impaired perception and reproduction of speech. Occasionally, local paresis and paralysis occur.
If the patient does not receive treatment in time, the precoma goes into the stage of diabetic coma. Neurological symptoms are represented by lack of consciousness, generalized convulsions, pathological reflexes. A third of patients have a high fever. On external examination, there is a sharpness of facial features, dry skin, lips and tongue. Shortness of breath, deafness of heart tones, and a decrease in blood pressure are determined.
Complications
Progressive dehydration and increased blood viscosity disrupt adequate tissue perfusion. The kidneys are among the first to suffer from ischemic processes, which is clinically manifested by anuria, hyperazotemia and acute renal failure. Possible thrombosis in the vessels of the lower extremities, pulmonary and coronary artery thrombosis. Untreated diabetic coma ends with multiple organ failure.
At an early stage of treatment of a comatose condition, there is a risk of brain edema. Pathology mainly occurs due to erroneous calculation of infusion therapy and unjustified use of bicarbonates, however, cases of the disease have been described against the background of properly administered treatment. Cerebral edema can be suspected by bradycardia, convulsions, lack of reaction of pupils to light.
Diagnostics
The examination is carried out by a doctor of the intensive care unit together with an endocrinologist. To make a diagnosis, it is necessary to conduct a physical examination, identify typical neurological signs, and clarify the presence of diabetes mellitus in the anamnesis. Diagnosis is carried out in parallel with the provision of first aid. To confirm diabetic coma , the following research methods are prescribed:
- Blood test. A pathognomonic sign of diabetic hyperosmolar coma is the level of glucose in blood plasma over 30 mmol/l. The osmolarity index, which is calculated taking into account the indicators of electrolyte metabolism, is over 330 mosmol/l.
- Urinanalysis. Biochemical examination shows a high level of glucosuria and the absence of ketone bodies in the urine – an important sign for differential diagnosis with ketoacidotic coma in diabetes mellitus.
- ECG. Cardiography demonstrates conduction disorders, signs of ischemia of the heart muscle and other consequences of pathologies of electrolyte metabolism. According to the indications, a comprehensive examination of the patient is complemented by ultrasound of the heart.
- CT scan of the brain. Multiple neurological symptoms require the exclusion of organic brain diseases. With a complicated course of diabetic coma, signs of cerebral edema are detected on CT scans.
Differential diagnosis
Differential diagnosis is performed with other types of diabetic com:
- ketoacidotic;
- lactatacidotic;
- hypoglycemic.
The key differences of hyperosmolar coma are the absence of ketoacidosis and Kussmaul respiration, a high level of glycemia, and a normal lactic acid index. Pathology is also differentiated with encephalopathy, neuroinfections, epilepsy.
Treatment
The condition requires urgent care, which is aimed at combating dehydration, eliminating insulin deficiency and restoring the water-electrolyte balance. Treatment is carried out according to the basic principles of emergency correction. When selecting medications, the current biochemical parameters of blood and their dynamics are taken into account. The main components of hyperosmolar coma therapy:
- Infusion therapy. In case of critical hypernatremia, treatment starts with a hypoosmolar glucose solution, in other cases, a hypotonic or isotonic sodium chloride solution is used. The infusion rate is calculated taking into account the central venous pressure and the volume of diuresis.
- Insulin therapy. Hormone replacement therapy is carried out with small doses of short-acting insulins. The blood glucose level is reduced by no more than 5.5 mmol / l per hour, so as not to provoke ricochet hypoglycemia.
- Anticoagulants. For preventive purposes, heparin drugs are prescribed, which stabilize blood clotting and prevent thromboembolic complications.
After reducing glycemia to 10-12 mmol / l and normalizing the acid-base balance of the blood, patients are transferred to subcutaneous insulin administration. According to the indications, prevention of thrombosis with oral antiplatelet agents is carried out. With full recovery of consciousness and the ability to swallow, you can switch to fractional enteral nutrition with a moderate amount of protein and limited carbohydrates.
Prognosis and prevention
Despite the progress in the treatment of diabetic coma, the mortality rate is 35-40%. The prognosis is more favorable for young and middle-aged patients who do not have concomitant diseases. For the prevention of hyperosmolar conditions, rational selection of hypoglycemic therapy, dispensary observation of patients with diabetes mellitus, self-control of eating habits and water balance is necessary.