Hypoglycemia and hypoglycemic coma

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

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Epidemiology

Hypoglycemic conditions of varying severity often develop in patients with type 1 and type 2 diabetes, as well as in individuals without diabetes. The exact prevalence of hypoglycemia is unknown, but hypoglycemic comas cause death in 3-4% of patients with diabetes.

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Causes hypoglycemia and hypoglycemic coma.

Hypoglycemia is based on an excess of insulin with a relative deficiency of carbohydrates or their accelerated utilization.

The main factors that provoke the development of hypoglycemia in diabetes mellitus:

• accidental or intentional overdose of insulin or PSSS;
• skipping meals or eating insufficient amounts of food,
• increased physical activity (while taking a constant dose of PSSS);
• alcohol consumption (inhibition of gluconeogenesis under the influence of alcohol);
• changes in the pharmacokinetics of insulin or PSSS due to incorrect administration (for example, accelerated absorption of insulin with intramuscular administration instead of subcutaneous), renal failure (accumulation of PSSS in the blood), drug interactions (for example, beta-blockers, salicylates, MAO inhibitors and others potentiate the action of PSSS);
• autonomic neuropathy (inability to sense hypoglycemia).

Rare causes of hypoglycemia (not just diabetes) include:

• insulinoma (a benign insulin-producing tumor of the beta cells of the pancreas);
• non-beta-cell tumors (usually large tumors of mesenchymal origin, possibly producing insulin-like factors), defects in carbohydrate metabolism enzymes (in glycogenoses, galactosemia, fructose intolerance),
• liver failure (due to impaired gluconeogenesis in case of massive liver damage);
• adrenal insufficiency (due to increased sensitivity to insulin and inadequate release of counter-insulin hormones in response to hypoglycemia).

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Pathogenesis

Glucose is the primary energy source for cerebral cortex cells, muscle cells, and red blood cells. Most other tissues use FFAs under starvation conditions.

Normally, glycogenolysis and gluconeogenesis maintain blood glucose levels even during prolonged starvation. In this case, insulin levels decrease and are maintained at a lower level. At a glycemia level of 3.8 mmol/l, an increase in the secretion of counter-insular hormones is observed - glucagon, adrenaline, somatotropic hormone and cortisol (with the level of somatotropic hormone and cortisol increasing only during prolonged hypoglycemia). Following vegetative symptoms, neuroglycopenic symptoms appear (caused by insufficient glucose supply to the brain).

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

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Symptoms hypoglycemia and hypoglycemic coma.

Symptoms of hypoglycemia are varied. The faster the blood glucose level decreases, the more pronounced the clinical manifestations. The glycemia threshold at which clinical manifestations appear is individual. In patients with long-term decompensation of diabetes mellitus, symptoms of hypoglycemia are possible already at a blood sugar level of 6-8 mmol/l.

Early signs of hypoglycemia are autonomic symptoms. These include symptoms of:

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

Later, symptoms of CNS damage, or neuroglycopenic symptoms, appear. These include:

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

The clinical picture of alcoholic hypoglycemia is characterized by the delayed nature of its onset and the likelihood of relapses of hypoglycemia (due to the suppression of gluconeogenesis in the liver), as well as the frequent predominance of neuroglycemia symptoms over vegetative symptoms.

Nocturnal hypoglycemia may be asymptomatic. Its indirect signs include sweating, nightmares, restless sleep, morning headaches, and sometimes posthypoglycemic hyperglycemia in the early morning hours (Somogyi phenomenon). Such posthypoglycemic hyperglycemia develops in response to hypoglycemia in patients with an intact counterinsular system. However, morning hyperglycemia is more often caused by an insufficient evening dose of prolonged insulin.

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

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Diagnostics hypoglycemia and hypoglycemic coma.

The diagnosis of hypoglycemia is made based on the anamnesis, the corresponding clinical picture and laboratory tests. Given the individual sensitivity of patients to hypoglycemia, normal blood glucose levels do not exclude this diagnosis in the presence of hypoglycemic symptoms and the effect of glucose administration. Laboratory manifestations:

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

In hypoglycemia and especially hypoglycemic coma, it is necessary to exclude other causes of impaired consciousness.

In patients with diabetes mellitus, it is most often necessary to differentiate hypoglycemia and hypoglycemic coma from diabetic ketoacidosis, diabetic ketoacidotic coma, and hyperosmolar coma.

Detection of hypoglycemia in patients requires clarification of its causes (nutrition disorders, insulin administration regimen, stress, concomitant diseases, etc.).

In case of hypoglycemia in individuals without diabetes mellitus in the anamnesis, it is necessary first of all to exclude newly diagnosed diabetes mellitus, alcohol hypoglycemia, drug-induced hypoglycemia in individuals with mental disorders (the criterion for diagnosing drug-induced hypoglycemia is a low level of C-peptide that does not correspond to a high level of insulin; insulin preparations for injection do not contain C-peptide). Other possible causes of hypoglycemia are also identified.

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Treatment hypoglycemia and hypoglycemic coma.

The main goal is to prevent hypoglycemia. Every patient receiving PSSS should know the causes of hypoglycemia, its symptoms and principles of treatment.

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

Mild hypoglycemia

For the treatment of mild hypoglycemia (consciousness is preserved), it is advisable to take easily digestible carbohydrates orally in the amount of 1.5-2 XE (for example, 200 ml of sweet fruit juice, 100 ml of Pepsi-Cola or Fanta, 4-5 pieces of refined sugar).

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

Sandwiches with butter, cheese, and sausage are not recommended, as fats interfere with the absorption of glucose.

Severe hypoglycemia and hypoglycemic coma

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

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

In case of prolonged hypoglycemic coma, the following is prescribed to combat cerebral edema:

• Dexamethasone. Intravenous jet stream 4-8 mg, single dose or
• Prednisolone intravenously by jet stream 30-60 mg, once.

Evaluation of treatment effectiveness

Signs of effective therapy for hypoglycemia and hypoglycemic coma include restoration of consciousness, elimination of clinical manifestations of hypoglycemia, and achievement of a normal blood glucose level for the patient.

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Errors and unjustified appointments

Glucagon stimulates endogenous glucose production by the liver and is ineffective in alcohol-induced hypoglycemia, as well as in high insulinemia (i.e., with the deliberate administration of a high dose of insulin or PSM)

If the patient is receiving acarbose, taking table sugar will not relieve hypoglycemia, since acarbose blocks the enzymes a-glucosidase and sugar is not broken down into fructose and glucose. Such patients need to be given pure dextrose (grape sugar).

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Forecast

The prognosis of hypoglycemia depends on the speed of recognition of the condition and the adequacy of therapy. Hypoglycemic coma that is not recognized in time can lead to the death of the patient.

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