Hypoglycemia and hypoglycemic coma

Hypoglycemia is a clinical syndrome caused by a decrease in blood glucose and characterized by clinical signs of activation of the autonomic nervous system and neuroglycopenic symptoms.

[1], [2], [3], [4]

Epidemiology

The hypoglycemic state of various severity often develops both in patients with type 1 diabetes and type 2, and in individuals without diabetes. The exact prevalence of hypoglycemia is unknown, but hypoglycemic coma cause death of 3-4% of patients with diabetes mellitus. 

[5], [6], [7]

Causes of the hypoglycemia and hypoglycemic coma

At the heart of hypoglycemia is an excess of insulin with a relative deficiency of carbohydrates or their accelerated utilization.

The main factors provoking the development of hypoglycemia in diabetes mellitus:

• accidental or intentional overdose of insulin or BSSS;
• skipping the next meal or not enough of it,
• increased physical activity (against the background of taking a constant dose of PTSS);
• alcohol use (inhibition of gluconeogenesis under the influence of alcohol);
• change in the pharmacokinetics of insulin or BCC in case of improper administration (for example, accelerated absorption of insulin by intramuscular injection instead of subcutaneous), renal insufficiency (cumulation of BCC in the blood), drug interaction (eg, beta blockers, salicylates, MAO inhibitors and others potentiate the effect of PCB);
• autonomic neuropathy (inability to sense hypoglycemia).

To rare causes of hypoglycemia (not only for diabetes) include:

• insulinoma  (a benign insulin-producing tumor from beta-cells of the pancreas);
• non-beta-cell tumors (usually large mesenchymal tumors, possibly producing insulin-like factors), defects in carbohydrate metabolism enzymes (with glycogenoses, galactosemia, intolerance to fructose),
• hepatic insufficiency (due to a violation of gluconeogenesis in massive liver damage);
• adrenal insufficiency (due to hypersensitivity to insulin and inadequate release of counterinsulant hormones in response to hypoglycemia).

[8], [9],

Pathogenesis

Glucose is the main source of energy for the cells of the cerebral cortex, muscle cells and red blood cells. Most other tissues use starvation in fasting conditions.

Normally, glycogenolysis and gluconeogenesis support the concentration of glucose in the blood, even with prolonged starvation. At the same time, the insulin content is reduced and maintained at a lower level. With a glycemic level of 3.8 mmol / l, an increase in the secretion of the contrinsular hormones glucagon, epinephrine, growth hormone and cortisol is noted (the level of growth hormone and cortisol increases only with prolonged hypoglycemia). Following the vegetative symptoms appear neuroglycopenic (due to insufficient intake of glucose in the brain).

With an increase in the duration of diabetes in just 1 to 3 years, there is a decrease in glucagon secretion in response to hypoglycemia. In subsequent years, glucagon secretion continues to decrease until complete cessation. Later, reactive secretion of epinephrine decreases even in patients without autonomic neuropathy. Decreased secretion of glucagon and adrenaline hypoglycemia increases the risk of severe hypoglycemia.

[10], [11], [12], [13]

Symptoms of the hypoglycemia and hypoglycemic coma

Symptoms of hypoglycemia are diverse. The faster the blood glucose level decreases, the more vivid the clinical manifestations. The threshold of glycemia, in which clinical manifestations appear, is individual. In patients with prolonged decompensation of diabetes mellitus, symptoms of hypoglycemia are possible even at a blood sugar level of 6-8 mmol / l.

The early signs of hypoglycemia are vegetative symptoms. These include symptoms:

• activation of the parasympathetic nervous system:
  • hunger;
  • nausea, vomiting;
  • weakness;
• activation of the sympathetic nervous system:
  • anxiety, aggressiveness;
  • sweating;
  • tachycardia;
  • tremor;
  • mydriasis;
  •  hypertonic muscle.

Later, there are symptoms of CNS damage, or neuroglycopic symptoms. They include:

• irritability, decreased ability to concentrate, disorientation;
• headache, dizziness,
• violation of coordination of movements;
• primitive automatisms (grimaces, grasping reflex);
• convulsions, focal neurological symptoms (hemiplegia, aphasia, double vision);
• amnesia;
• drowsiness, impaired consciousness, to whom;
• respiratory and circulatory disorders of the central genesis.

Features of the clinical picture of alcoholic hypoglycemia are the delayed nature of the occurrence and the probability of recurrences of hypoglycemia (due to suppression of gluconeogenesis in the liver), as well as frequent prevalence of neuroglycemia symptoms over autonomic symptoms.

Night hypoglycemia can be asymptomatic. Their indirect signs are sweating, nightmarish dreams, anxious sleep, morning headaches, and sometimes post-hypoglycemic hyperglycemia in the early morning hours (the Somogy phenomenon). Such posthypoglycemic hyperglycaemia develops in response to hypoglycemia in patients with a conserved system of contention. However, most often morning hyperglycemia is due to an insufficient evening dose of prolonged insulin.

Clinical manifestations of hypoglycemia are not always determined by the level of sugar in the blood. Thus, patients with diabetes mellitus complicated by autonomic neuropathy may not feel a drop in blood glucose levels <2 mmol / l, and patients with long-term decompensated diabetes feel symptoms of hypoglycemia (symptoms of activation of the autonomic nervous system) at a glucose level of> 6.7 mmol / l.

[14]

Diagnostics of the hypoglycemia and hypoglycemic coma

The diagnosis of hypoglycemia is based on an anamnesis corresponding to the clinical picture and laboratory studies. Given the individual sensitivity of patients to hypoglycemia, a normal blood glucose level does not exclude this diagnosis in the presence of symptoms of hypoglycemia and the effect of glucose administration. Laboratory manifestations:

• decrease in blood glucose level <2.8 mmol / l, accompanied by clinical symptoms;
• a decrease in blood glucose <2.2 mmol / l, regardless of the presence of symptoms.

When hypoglycemia and especially hypoglycemic coma should be excluded other causes of impaired consciousness.

Patients with  diabetes  most often have to differentiate hypoglycemia and hypoglycemic coma with diabetic ketoacidosis, diabetic ketoacidotic coma, and hyperosmolar coma.

Identification of hypoglycemia in patients requires clarification of its causes (malnutrition, insulin regimen, load, concomitant diseases, etc.).

In the case of development of hypoglycemia in people without diabetes mellitus in history, it is first of all necessary to exclude newly diagnosed diabetes mellitus, alcoholic hypoglycemia, drug hypoglycemia in persons with mental disorders (the criterion for diagnosis of drug hypoglycemia is a low level of C-peptide that does not correspond to a high level of insulin, insulin preparations for injections do not contain C-peptide). Other possible causes of hypoglycemia are also identified.

[15]

Treatment of the hypoglycemia and hypoglycemic coma

The main goal is the prevention of hypoglycemia. Each patient receiving the MTSP should know the causes of hypoglycemia, its symptoms and the principles of treatment.

Before the planned physical activity it is necessary to reduce the dose of insulin. In case of an unplanned load, you should additionally take carbohydrate food.

Light hypoglycemia

For the treatment of mild hypoglycemia (consciousness is preserved), it is advisable to take inwardly digestible carbohydrates in an amount of 1.5-2 XE (for example, 200 ml of sweet fruit juice, 100 ml of pepsi-cola or phantoms, 4-5 slices of sugar-refined sugar).

On average, 1XE increases blood glucose by 2.22 mmol / l. Easily assimilated carbohydrates are taken until the symptoms of hypoglycemia disappear completely.

Do not recommend sandwiches with butter, cheese, sausage, since fats interfere with the absorption of glucose.

Severe hypoglycemia and hypoglycemic coma

In severe hypoglycemia with loss of consciousness, parenteral administration of a solution of glucose and glucagon is used. After restoration of consciousness continue treatment as in patients with mild hypoglycemia.

• Glucagon subcutaneously or intramuscularly 1 ml, once (if 10-15 minutes after the injection the patient does not regain consciousness, repeat the administration in the same dose) or
• Dextrose, 40% solution, intravenously struyno 20-60 ml, once (if after 20 minutes the patient does not regain consciousness, 5-10% dextrose solution is injected intravenously until the consciousness is restored and the blood glucose level reaches 11.1 mmol / L) .

With prolonged hypoglycemic coma, to control the edema of the brain,

• Dexamethasone. Intravenously spray 4-8 mg, once or
• Prednisolone intravenously struino 30-60 mg, once.

Evaluation of treatment effectiveness

Signs of effective therapy for hypoglycemia and hypoglycemic coma are the restoration of consciousness, the elimination of clinical manifestations of hypoglycemia, the achievement of normal for the patient's glucose level in the blood.

[16], [17]

Errors and unreasonable appointments

Glucagon stimulates the endogenous production of glucose by the liver to be ineffective in alcohol hypoglycemia, as well as with high insulinemia (ie, with the deliberate administration of a high dose of insulin or PSM)

If the patient receives acarbose, the intake of edible sugar will not lead to the reduction of hypoglycemia, since acarbose blocks the enzymes of a-glucosidase and the sugar does not split into fructose and glucose. Such patients need the introduction of pure dextrose (grape sugar).

[18], [19]

Forecast

The prognosis of hypoglycemia depends on the speed of recognition of the condition and the adequacy of therapy. Not recognized in time hypoglycemic coma can lead to the death of the patient.

[20]