Hypoglycemia most often complicates the course of diabetes mellitus in patients receiving insulin or tableted sugar-lowering drugs. Hypoglycemia is a clinical syndrome caused by an abnormally low plasma glucose level. Hypoglycemia can be mild when the patient self-suppresses it with a sufficient amount of carbohydrates. In the case of severe hypoglycemia, loss of consciousness is noted, which requires intravenous administration of glucose or glucagon. In most cases, the state of hypoplycaemia is noted in patients undergoing intensive insulin therapy. Especially often, the state of hypoglycemia develops in elderly patients suffering from type II diabetes and receiving glibenclamide group drugs with a hypoglycemic goal, which have a long half-life and a cumulative effect. Quite often, hypoglycemia in such patients is recurrent in nature. An extreme manifestation of the hypoglycemic state is a hypoglycemic coma. It is defined as an acute condition with a threat to the lives of patients, caused by a rapid and pronounced decrease in blood glucose level, which in turn causes the development of energy starvation of the body cells, swelling of the brain substance, and in far advanced cases – decorting and even decerebration. Hypoglycemia in diabetes mellitus usually occurs with a rapid decrease in the level of glucose to the lower limit of the norm — 3.3 mmol / l. Symptoms of hypoglycemia can develop already with glycemia 4-6 mmol / l.
In such cases, there is a pronounced drop in the level of blood glucose in a short period of time. In addition, in the case of permanent and prolonged hyperglycemia in diabetes mellitus, passive diffusion of glucose into the tissue is simulated. Since the cell membranes are adapted to hyperglycemia during sadiabetes, as the blood glucose level decreases, the passive diffusion of glucose in the tissue stops, which leads to energy starvation of brain cells.
The main reason for the development of hypoglycemia is an excess of insulin in the body in relation to the amount of carbohydrates supplied with food or from endogenous sources (glucose production by the liver), as well as accelerated utilization of carbohydrates during intensive muscular work. The development of hypoglycemia is provoked by the following factors: excessive physical exertion, alcohol intake, a violation of the diet in the form of an improper dietary regime or insufficient carbohydrate content in it, as well as an overdose of insulin or tableted sugar-lowering drugs. The development of hypoglycemia is promoted by the first trimester of pregnancy, childbirth, chronic hepatitis and hepatosis in diabetes mellitus, nephropathy with renal insufficiency, insufficiency of the adrenal cortex and gland, and the use of certain drugs, such as salicylates.
A decrease in the level of glucose in the blood primarily affects the state of the central nervous system, since it is the only substrate of brain metabolism. With a decrease in the level of glucose in the blood below the physiological level, its admission to brain cells decreases, which leads to their energy starvation. This condition is called neuroglycopenia. It manifests itself at different stages by various neurological disorders, which ultimately lead to loss of consciousness and the development of a hypoglycemic coma. The individual structures of the central nervous system have different sensitivity to energy starvation. Initially, hypoglycemia affects the cells of the gray matter, located in the cerebral cortex, as they have the greatest intensity of metabolic processes. This fact explains the appearance of symptoms of neuroglycopenia in all more or less pronounced hypoglycemic conditions. The least sensitivity to hypoglycemia is give the centers of the medulla oblongata, such as: respiratory and vasomotor. This explains the fact that respiration, vascular tone and cardiac activity persist for a long time even in cases where prolonged hypoglycemia leads to irreversible decortication. To maintain the level of glucose in the blood while its entry into the brain cells in the body decreases, the processes of glycogenolysis, gluconeogenesis, proteolysis, lipolysis are activated, and the process of glucose utilization by peripheral tissues is inhibited. These mechanisms are carried out under the control of continsulin hormones, which include glucagon, catecholamines, glucocorticoids, somatotropic hormone, adrenocorticotropic hormone. The concentration of these hormones on the background of hypoglycemia sharply increases, which leads to the stimulation of the autonomic nervous system and the emergence of a set of autonomic symptoms. In addition, the development of hypoglycemia is accompanied by a compensatory increase in cerebral blood 2-3 times, which provides a higher level of oxygen. All compensatory mechanisms that are activated during the development of the state of hypoglycemia can maintain brain viability for a relatively short period of time. If the duration of a hypoglycemic coma is less than 30 minutes, then with adequate treatment and a quick return, the state of complications and consequences, as a rule, is not observed. Protracted hypoglycemia is a danger to the life of the patient. As a result of prolonged energy starvation, edema of the brain substance develops, small-point hemorrhages in the brain tissue appear. In the end, these pathological changes are the cause of structural disturbances in the cells of the cerebral cortex, and subsequently – to their death.
Hypoglycemic coma is characterized by a sudden development against the background of a satisfactory condition. The development of coma is preceded by a state of mild hypoglycemia, which is bought by taking a sufficient amount of carbohydrates. The period of hypoglycemia is accompanied by the appearance of precursors of hypoglycemic coma. They appear next to vegetative symptoms such as increased sweating, hunger, anxiety, anxiety, palpitations, mydriasis, and increased blood pressure. In the case of the development of a state of hypoglycemia during sleep, patients are disturbed by nightmares. Quite often, the appearance of autonomic symptoms is ahead of the symptoms of neuroglycopenia. Such symptoms can be inadequate behavior, disorientation of orientation in space, aggressiveness, mood changes, amnesia, headache and headache, as well as visual disorders in the form of diplopia, the appearance of “fog” and the flickering of the “front sights”.
If untreated, neuroglycopia is aggravated, which is clinically manifested by the development of psychomotor arousal, muscle hypertonus, tonic or clonic, and seizures. This state continues for a short period of time and is replaced by a coma. Hypoglycemic coma is characterized by the following clinical signs: profuse sweating, increased muscle tone, and the appearance of a carotid syndrome.
The brightness of the clinical picture depends on the rate of decrease in the level of glucose in the blood: the faster this happens, the brighter the clinical manifestations. Precursors of hypoglycemic coma are not in all cases. If diabetes occurs for a sufficiently long time and is accompanied by the development of autonomic neuropathy, as well as frequent hypoglycemic comas, patients do not feel the precursors of the onset of this pathological condition. If the hypoglycemic coma takes a long time, then signs of brain edema appear.
Such signs are usually hemiplegia, stiff neck and other pathological neurological symptoms. The appearance of shallow breathing, a decrease in blood pressure is also noted, reflexes are reduced or completely drop out, and bradycardia is detected. Death occurs as a result of decortication and decerebration. The sign of the onset of these conditions is the lack of reaction of the pupils to light.
Laboratory and instrumental diagnostic methods
In the study of blood, there is a decrease in the level of glucose to 3 mmol / l and below. The reaction to acetone in the urine may be positive, which is associated with previous decompensation of diabetes. Differential diagnosis with acute cerebrovascular accident, inflammatory diseases of the brain, craniocerebral injury and other pathological conditions requires an echoencephaloscopy, computed tomography and spinal puncture.
Treatment must be prompt. Lack of treatment for 2 h from the onset of hypoglycemic coma significantly worsens the prognosis. Initially, it is necessary to conduct an intravenous jet injection of a 40% glucose solution in a volume of 20–60 ml. Typically, the amount of glucose is determined by the recovery of the patient’s consciousness. If the consciousness is not restored, then the volume of glucose injected can be increased to 100 ml, before the arrival of the medical team of the ambulance it is necessary to intramuscularly inject 1 ml of glucagon. This event is ineffective in the case of alcoholic hypoglycemia, as well as in the case of hypoglycemia as a result of overdosage of insulin. The absence of the effect of the introduction of glucagon in the first case is explained by the fact that the production of glucose in the liver is blocked by ethanol. In the second case, glycogen stores in the liver are depleted against the background of an insulin overdose. If, after the introduction of glucose solution, the patient’s mind quickly returned to normal, then hospitalization can be avoided. In other cases, it is necessary to urgently hospitalize the patient in the endocrinological or therapeutic department. Medical events start at the pre-hospital.