Hypoglycemia is a decrease in the concentration of glucose in the blood plasma in full-term newborns to less than 2.7 mmol/l, in older children - less than 2.2 mmol/l. The causes of hypoglycemia in diabetes mellitus are insufficient food intake, heavy physical activity, and overdose of sugar-lowering drugs. The main non-diabetic causes of hypoglycemic conditions in children are: starvation, diseases accompanied by malabsorption syndrome, hormonal regulation disorders (adrenocortical insufficiency, hypothyroidism), chronic renal failure, poisoning (ethanol, salicylates, β-blockers).
Clinical manifestations of hypoglycemia
Precursors are weakness, anxiety, trembling of arms and legs, sweating, and the appearance of hunger. Advanced stage: psychomotor agitation, then stupor, stupor or coma develops. The face is mask-like, severe sweating, tissue turgor is normal, muscle tone is high; tachycardia, blood pressure is initially increased, then it decreases. Clonic-tonic convulsions often occur. Sometimes hypoglycemic coma develops suddenly and is characterized by a triad of symptoms: loss of consciousness, muscle hypertonicity, and convulsions. With prolonged hypoglycemia, a clinical picture of cerebral edema develops. In a patient with diabetes mellitus, hypoglycemic coma is differentiated from hyperglycemic ketoacidotic coma.
Emergency measures for manifestations of hypoglycemia:
- if consciousness is preserved, take carbohydrate-containing products (sweet tea, apple or orange juice); in the absence of positive dynamics after 10-15 minutes. – repeated intake of easily digestible carbohydrates;
- calling an ambulance;
- in case of impaired consciousness - slowly inject 40% glucose solution intravenously - 1-2 ml / kg until the patient comes out of coma and the convulsions stop;
- when regaining consciousness, administer easily digestible carbohydrates orally;
- if there is no effect after 10-15 minutes. – repeated intravenous administration of 40% glucose solution up to 5 ml/kg;
- in the absence of positive dynamics, administer intravenous hydrocortisone 0.5-10 mg/kg body weight (prednisolone, dexamethasone are not administered due to the high risk of developing cerebral edema);
If the child’s consciousness has not recovered, enter:
- intravenous, intramuscular glucagon in a dose of 0.5 ml for children weighing up to 20 kg and 1.0 ml;
- with a weight of more than 20 kg or 0.18% solution of epinephrine (adrenaline) 0.1 ml/kg s.c.
If the patient does not regain consciousness, suspect cerebral edema! For cerebral edema, administer:
- 1% solution of furosemide (Lasix) 0.1-0.2 ml/kg intravenously or intramuscularly;
- 10% mannitol solution 0.5–1.0 g/kg intravenous drip in 10% glucose solution,
- dexamethasone solution 0.5-1 mg/kg (1 ml - 4 mg) intravenously,
- oxygen therapy.
Attention! If acute intracranial hypertension is suspected, limit intravenous infusion, but do not stop - catheter thrombosis is possible
Hospitalization in the intensive care unit (in the absence of consciousness), if the patient is conscious - in the endocrinology department of the hospital.
Hyperglycemic comas
In children suffering from diabetes mellitus, ketoacidotic (ketonemic) coma is most common, and hyperosmolar and hyperlactic acidemic coma is less common.
Diabetic ketoacidotic coma
In the pathogenesis, the leading place belongs to hyperglycemia, hyperketonemia, ketonuria, the consequence of which is pronounced disturbances in water-electrolyte metabolism and a shift in the acid-base balance towards acidosis. The causes of ketoacedotic coma in children are late diagnosis of diabetes mellitus, insufficient insulin administration, the addition of intercurrent diseases, injuries and surgical interventions, and emotional stressful situations.
Clinical manifestations. Precomatose state: general weakness, lethargy, drowsiness, headache, tachypnea, smell of acetone in exhaled air, sinus tachycardia, blood pressure within normal limits, blood glucose level more than 15 mmol/l, polyuria, glycosuria and ketonuria, thirst, vomiting, possible "acute abdomen" syndrome
Stage of coma: the patient is unconscious (stupor turns into coma), the skin is dry, cold, with “marbling”, tissue turgor is reduced, facial features are sharpened, skin folds are poorly straightened, decreased tendon reflexes, breathing is noisy, deep, rare (Kussmaul) , the smell of acetone in the exhaled air, the pulse is frequent and weak, low blood pressure, high glycemia (20-30 mmol/l), glucosuria and ketonuria, decreased diuresis to anuria.
Diabetic hyperosmolar coma
A less common complication of diabetes mellitus, with a slower progression compared to ketoacidotic coma. Hyperosmolar coma is based on disturbances in water-electrolyte metabolism, which are the result of significant hyperglycemia and polyuria. The main causes are adequately treated or unrecognized diabetes mellitus, the development of severe dehydration of the body (vomiting, diarrhea, blood loss, burns and frostbite), treatment with diuretics and steroid drugs, surgical interventions and extensive trauma.
Clinical diagnosis: pronounced signs of dehydration, hyperthermia, nystagmus, muscle hypertonicity, weakly positive meningeal symptoms, convulsions, sinus tachycardia, arterial hypotension, hyperglycemia (more than 40 mmol/l), oliguria up to anuria, severe glycosuria without ketonuria, absence of Kussmaul respiration and odor acetone in exhaled air.
Hyperlactic acidemic coma
A rare variant of coma, characterized by the accumulation of lactic acid in the blood (normally 0.62-1.33 mmol/l) and, in the presence of tissue hypoxia, a change in the ratio between pyruvic and lactic acids (>10:1). Diabetic causes are distinguished: insufficient food intake, heavy physical activity (without insulin dose adjustment), insulin overdose, alcohol intake and non-diabetic causes: insulinomas, renal and liver failure, galactosemia, fructosemia, glycogenosis, etc.
Clinical manifestations: rapid development of coma (within several hours, preceded by pain in the muscles and behind the sternum); nausea, vomiting, diarrhea; impairment of consciousness to the point of stupor as acidosis worsens. The skin is pale, cold, with “marbling”, dehydration is not expressed, blood pressure is sharply reduced until the development of collapse, symptoms of heart failure, severe heart rhythm disturbances, symptoms of hyperventilation (Kussmaul breathing), hyperglycemia (12-20 mmol/l), ketosis no, oliguria followed by anuria.
Emergency conditions for diabetes mellitus at the prehospital stage
TO
omas are acute complications of diabetes mellitus (DM) and often lead to death. It is a direct result of changes in blood glucose in the form of hyperglycemia or hypoglycemia and associated metabolic disturbances. If left uncorrected, hyperglycemia can lead to diabetic ketoacidosis (DKA) or nonketonic hyperosmolar coma. They are characterized by varying degrees of insulin deficiency, excess production of counter-insulin hormones and dehydration. In some cases, signs of diabetic ketoacidosis and hyperosmolar coma may develop simultaneously.
Hypoglycemia is caused by an imbalance between the medication used to treat diabetes (insulin or blood glucose-lowering tablets) and food intake or exercise. A sharp drop in glucose concentration leads to loss of consciousness, since the normal functioning of the brain is almost entirely dependent on glucose. Patients with diabetes mellitus may develop the following comatose states, directly related and specifically caused by the underlying disease - ketoacidotic, hyperosmolar and hypoglycemic.
The speed and timeliness of providing care to comatose patients largely determine the prognosis. Therefore, from these positions, the correct management of patients at the prehospital stage seems to be the most important.
Hypoglycemic coma ranks third (5.4%) in the structure of comas at the prehospital stage, and diabetic coma (3%) ranks fifth (data from the National Emergency Medical Center).
Diabetic ketoacidotic coma
Diabetic ketoacidotic coma (DKA) is a serious complication of diabetes mellitus, characterized by metabolic acidosis (pH less than 7.35 or bicarbonate concentration less than 15 mmol/L), an increase in the anion gap, hyperglycemia above 14 mmol/L, and ketonemia. More often develops in type 1 diabetes. The frequency is from 5 to 20 cases per 1000 patients per year (2/100). Mortality rate is 5–15%, for patients over 60 years old – 20%. More than 16% of patients with type 1 diabetes die from ketoacidotic coma. The cause of DKA is an absolute or pronounced relative deficiency of insulin due to inadequate insulin therapy or an increased need for insulin.
Provoking factors:
- Insufficient dose of insulin or skipping an insulin injection (or taking tablets of hypoglycemic drugs).
- Unauthorized withdrawal of glucose-lowering therapy.
- Violation of insulin administration technique.
- The addition of other diseases (infections, trauma, operations, pregnancy, myocardial infarction, stroke, stress, etc.).
- Diet disorders (too many carbohydrates).
- Physical activity with high glycemia.
- Alcohol abuse.
- Insufficient self-monitoring of metabolism.
- Taking certain medications (corticosteroids, oral contraceptives, thyroid hormones, calcitonin, saluretics, ethacrynic acid, acetazolamide, b-blockers, diltiazem, adrenaline, dobutamine, diazoxide, nicotinic acid, isoniazid, asparaginase, cyclophosphamide, diphenine, morphine, lithium carbonate and etc.).
Often the etiology of DKA remains unknown. It should be remembered that up to 25% of cases of DKA occur in patients with newly diagnosed diabetes mellitus.
Clinical picture and classification
There are three stages of diabetic ketoacidosis (Table 1):
1.
Moderate ketoacidosis
.
2. Precoma, or decompensated ketoacidosis
.
3. Coma
.
Complications of ketoacidotic coma - deep vein thrombosis, pulmonary embolism, arterial thrombosis (myocardial infarction, cerebral infarction, necrosis), aspiration pneumonia, cerebral edema, pulmonary edema, infections, rarely - gastrointestinal tract and ischemic colitis, erosive gastritis, late hypoglycemia. Severe respiratory failure, oliguria and renal failure are noted. Complications of therapy are cerebral and pulmonary edema, hypoglycemia, hypokalemia, hyponatremia, hypophosphatemia.
Diagnostic criteria
1. The peculiarity of DKA is its gradual development, usually over several days.
2. The presence of symptoms of ketoacidosis (the smell of acetone in the exhaled air, Kussmaul breathing, nausea, vomiting, anorexia, abdominal pain).
3. The presence of symptoms of dehydration (decreased tissue turgor, tone of the eyeballs, muscle tone, tendon reflexes, body temperature and blood pressure).
It should be remembered that with type 2 diabetes, one should always look for an intercurrent disease as the cause of decompensation of diabetes.
List of questions required when diagnosing DKA at the prehospital stage:
– Does the patient suffer from diabetes?
– was there a history of DKA?
– is the patient receiving glucose-lowering therapy, what kind, and the last dose of the drug?
– when was the last meal or inadequate meal or skipping?
– was there too much physical activity or alcohol intake?
– what recent diseases preceded the coma (infectious diseases)?
– Was there polyuria, polydipsia and weakness?
Possible errors in therapy and diagnosis at the prehospital stage:
1. Insulin therapy at the prehospital stage without the ability to determine the level of glycemia and its control.
2. The emphasis in treatment is on intensive insulin therapy in the absence of effective rehydration.
3. Insufficient volume of fluids administered.
4. Administration of hypotonic solutions, especially at the beginning of treatment. This can lead to cerebral edema and intravascular hemolysis.
5. Use of forced diuresis instead of rehydration. The use of diuretics simultaneously with the administration of fluids will only slow down the restoration of water balance, and in hyperosmolar coma, the use of diuretics is strictly contraindicated.
6. Starting therapy with the administration of sodium bicarbonate can lead to the death of the patient. It has been proven that adequate insulin therapy in most cases helps eliminate acidosis. Correction of acidosis with sodium bicarbonate carries an exceptionally high risk of complications. The introduction of alkalis increases hypokalemia and disrupts the dissociation of oxyhemoglobin; carbon dioxide formed when bicarbonate is administered increases intracellular acidosis (although the blood pH may increase); paradoxical acidosis is also observed in the cerebrospinal fluid, which can contribute to cerebral edema; the development of “rebound” alkalosis cannot be ruled out. Rapid administration of sodium bicarbonate (boost) can cause death due to the rapid development of hypokalemia.
7. Administration of sodium bicarbonate solution without additional administration of potassium preparations, which causes pronounced hypokalemia, which becomes the cause of death of patients.
8. Withdrawal or non-prescription of insulin for DKA in a patient who is unable to eat.
9. Subcutaneous administration of insulin to patients in a diabetic coma in whom insulin absorption is impaired due to impaired microcirculation.
10. Intravenous injection of insulin. The half-life of insulin when administered intravenously is 3–5 minutes, and only the first 15–20 minutes its concentration in the blood is maintained at a sufficient level, and therefore this route of administration is ineffective.
11. 3-4 times the prescription of short-acting insulin (RAI) subcutaneously (in the initial stages of DKA, when the condition is moderate and there is no loss of consciousness, it is possible to prescribe insulin subcutaneously). The effective duration of action of ICDs is 4–5 hours, especially in the setting of ketoacidosis. Therefore, ICDs should be prescribed at least 5–6 times a day without a night break.
12. Use of sympathotonic drugs to combat collapse. Firstly, they are counter-insulin hormones and, secondly, in diabetic patients their stimulating effect on glucagon secretion is much more pronounced than in healthy individuals.
13. Incorrect diagnosis of DKA. With DKA, the so-called “diabetic pseudoperitonitis” often occurs, which simulates the symptoms of an “acute abdomen” - tension and pain in the abdominal wall, a decrease or disappearance of peristaltic sounds, and sometimes an increase in serum amylase. The simultaneous detection of leukocytosis can lead to an erroneous diagnosis and the patient ends up in the infectious (“intestinal infection”) or surgical (“acute abdomen”) department. In all cases of “acute abdomen” or dyspeptic symptoms in a patient with diabetes, it is necessary to determine glycemia and ketonuria.
14. Failure to measure glycemia in any unconscious patient often leads to erroneous diagnoses - “cerebrovascular accident”, “coma of unknown etiology”, while the patient has acute diabetic metabolic decompensation.
Prehospital therapy is presented in Table 2.
Hyperosmolar ketoacidotic coma
Hyperosmolar ketoacidotic coma is characterized by severe dehydration, significant hyperglycemia (often above 33 mmol/l), hyperosmolarity (more than 340 mOsm/l), hypernatremia above 150 mmol/l, characterized by the absence of ketoacidosis (maximum ketonuria (+)). It develops more often in elderly patients with type 2 diabetes. It is 10 times less common than DKA. Characterized by a higher mortality rate (15–60%). The reason for the development of hyperosmolar coma is a relative deficiency of insulin and factors accompanied by dehydration.
Hyperosmolar ketoacidotic coma is characterized by severe dehydration, significant hyperglycemia (often above 33 mmol/l), hyperosmolarity (more than 340 mOsm/l), hypernatremia above 150 mmol/l, characterized by the absence of ketoacidosis (maximum ketonuria (+)). It develops more often in elderly patients with type 2 diabetes. It is 10 times less common than DKA. Characterized by a higher mortality rate (15–60%). The reason for the development of hyperosmolar coma is a relative deficiency of insulin and factors accompanied by dehydration.
Provoking factors:
- insufficient dose of insulin or missing an insulin injection (or taking tableted hypoglycemic drugs);
- unauthorized withdrawal of glucose-lowering therapy;
- violation of insulin administration technique;
- addition of other diseases (infections, acute pancreatitis, trauma, surgery, pregnancy, myocardial infarction, stroke, stress, etc.);
- dietary irregularities (too many carbohydrates);
- taking certain medications (diuretics, corticosteroids, b-blockers, etc.);
- cooling;
- inability to quench thirst;
- burns;
- vomiting or diarrhea;
- hemodialysis or peritoneal dialysis.
It should be remembered that one third of patients with hyperosmolar coma do not have a previous diagnosis of diabetes mellitus.
Clinical picture
Severe thirst, polyuria, severe dehydration, arterial hypotension, tachycardia, focal or generalized convulsions increasing over several days or weeks. If, in DKA, disorders of the central nervous system and peripheral nervous system occur according to the type of gradual loss of consciousness and inhibition of tendon reflexes, then hyperosmolar coma is accompanied by a variety of mental and neurological disorders. In addition to the soporous state, also often noted in hyperosmolar coma, mental disorders often occur as delirium, acute hallucinatory psychosis, and catotonic syndrome. Neurological disorders are manifested by focal neurological symptoms (aphasia, hemiparesis, tetraparesis, polymorphic sensory disorders, pathological tendon reflexes, etc.).
Diagnostic criteria
1. Develops more slowly (over 5–14 days) than DKA.
More pronounced dehydration (decreased tissue turgor, tone of the eyeballs, muscle tone, tendon reflexes, body temperature and blood pressure).
2. Often polymorphic neurological symptoms that disappear when hyperosmolar coma is relieved.
3. Absence of ketoacidosis (smell of acetone in exhaled air, absence of Kussmaul respiration, nausea, vomiting, anorexia, abdominal pain).
4. Absence or mild ketonuria.
5. Anuria and azotemia occur earlier.
6. Elderly and senile age.
Possible errors in therapy and diagnosis include:
1. Administration of hypotonic solutions at the prehospital stage.
2. Long-term administration of hypotonic solutions.
3. Hyperosmolar syndrome is often mistakenly regarded as reactive psychosis, cerebrovascular paroxysm or other acute mental or neurological disease.
Therapy is discussed in Table 3.
Hypoglycemic coma
Hypoglycemic coma develops due to a sharp decrease in blood glucose levels (below 3–3.5 mmol/l) and severe energy deficiency in the brain.
Hypoglycemic coma develops due to a sharp decrease in blood glucose levels (below 3–3.5 mmol/l) and severe energy deficiency in the brain.
Provoking factors:
– insulin overdose
– skipping or inadequate meals
– increased physical activity
– excessive alcohol intake
– taking medications (b-blockers, salicylates, sulfonamides, phenylbutazone, anabolic steroids, calcium supplements, tetracycline, lithium carbonate, pyridoxine, MAO inhibitors, clofibrate).
Clinical picture
Symptoms of hypoglycemia are divided into early (cold sweat, especially on the forehead, pale skin, severe paroxysmal hunger, trembling hands, irritability, weakness, headache, dizziness, numbness of lips), intermediate (inappropriate behavior, aggressiveness, palpitations, poor coordination of movements, double vision, confusion) and late (loss of consciousness, convulsions).
Diagnostic criteria
1. Sudden development, usually over several minutes, less often hours.
2. The presence of characteristic symptoms of hypoglycemia.
3. Glycemia below 3–3.5 mmol/l.
It should be remembered that the absence of symptoms does not exclude hypoglycemia, and in patients with diabetes mellitus, symptoms of hypoglycemia may occur even with normal blood glucose concentrations.
Standard questions from a doctor at the prehospital stage:
– whether the patient suffers from diabetes, its duration;
– is he receiving glucose-lowering therapy (what kind, last dose of the drug);
– inadequate food intake or skipping, last meal;
– any episodes of hypoglycemia in the past;
– too heavy physical activity;
– drinking excessive amounts of alcohol.
It should be remembered that the most common cause of loss of consciousness in type 1 diabetes is severe hypoglycemia.
After removing the patient from a hypoglycemic coma, it is recommended to use drugs that improve microcirculation and metabolism in brain cells for 3–6 weeks. Repeated hypoglycemia can lead to brain damage.
Possible errors in diagnosis and therapy:
1. An attempt to introduce carbohydrate-containing products (sugar, etc.) into the oral cavity of an unconscious patient. This often leads to aspiration and asphyxia.
2. Use of unsuitable foods (bread, chocolate, etc.) to relieve hypoglycemia. These products do not have a sufficient sugar-raising effect or increase blood sugar too slowly.
3. Incorrect diagnosis of hypoglycemia. Some of the symptoms of hypoglycemia can imitate an epileptic seizure, stroke, “vegetative crisis”, etc. In a patient receiving glucose-lowering therapy, in almost any unclear paroxysmal state, it is advisable to urgently determine blood sugar. In the absence of the ability to determine the level of glycemia or the relatively slow performance of this analysis by express laboratories (30–40 minutes), if there is a reasonable suspicion of hypoglycemia, its relief should begin immediately, even before receiving a response from the laboratory.
4. The risk of relapse after recovery from severe hypoglycemia is often not taken into account. In case of an overdose of long-acting insulin preparations and sulfonylurea preparations, hypoglycemia may recur and therefore the patient requires intensive monitoring, monitoring of glycemic levels and, if necessary, its correction for several days.
Therapy for hypoglycemic coma is presented in Table 4. Differential diagnostic criteria for comatose states with diabetes are presented in Table 5.
Conclusion
In patients who are in a comatose state of unknown origin, it is always necessary to study glycemia. If it is reliably known that the patient has diabetes mellitus and at the same time it is difficult to differentiate the hypo- or hyperglycemic genesis of the coma, intravenous injection of glucose in a dose of 20–40–60 ml of 40% solution is recommended for the purpose of differential diagnosis and emergency assistance for hypoglycemic coma In the case of hypoglycemia, this will significantly improve symptoms and thus allow differentiation between the two conditions. In the case of hyperglycemic coma, such an amount of glucose will have virtually no effect on the patient’s condition.
In patients who are in a comatose state of unknown origin, it is always necessary to study glycemia. If it is reliably known that the patient has diabetes mellitus and at the same time it is difficult to differentiate the hypo- or hyperglycemic genesis of the coma, intravenous injection of glucose in a dose of 20–40–60 ml of 40% solution is recommended for the purpose of differential diagnosis and emergency assistance for hypoglycemic coma In the case of hypoglycemia, this will significantly improve symptoms and thus allow differentiation between the two conditions. In the case of hyperglycemic coma, such an amount of glucose will have virtually no effect on the patient’s condition.
In all cases where it is impossible to measure glycemia, highly concentrated glucose should be immediately administered empirically. Emergency untreated hypoglycemia can be fatal.
Basic drugs for patients in a coma in the absence of the possibility of clarifying the diagnosis and immediate hospitalization are considered to be thiamine 100 mg IV, glucose 40% 60 ml and naloxone 0.4–2 mg IV. This combination is effective and safe in many cases.
