Assessment of the severity of the condition of patients in the provision of emergency therapeutic and surgical medical care at the prehospital stage.

Diseases that are characterized by taste disturbances:

1.Iron deficiency anemia, B12-deficiency anemia.

2.Inflammatory diseases of the oral mucosa (stomatitis) and tongue (glossitis).

3.Neuralgia of the cranial nerves, herpetic lesions of the trigeminal nerve.

4.Acute respiratory infections.

5.New coronavirus infection COVID-19.

6.Damage to sensory nerves and receptors in diabetes mellitus, hypothyroidism (thyroid insufficiency).

7.Strokes and other focal damage to the brain.

8.Fungal infections in the mouth with taste and olfactory disorders.

9.Mental disorders.

Olfactory research. The sense of smell is a sense that enriches our emotions and is capable of firmly fixing a smell in memory. In everyday life, we do not remember it, taking its presence for granted. Moreover, its loss is the clearest symptom of a number of diseases.

Anosmia (ICD-10 — R43) is a complete loss of smell (a person ceases to feel and distinguish odors). Anosmia is often combined with another symptom — loss of taste (ageusia). This is due to the fact that taste and olfactory receptors are in close cooperation. Anosmia is more common in men. In both sexes it can be a transient condition or persist for a long time.

Impaired sense of smell can lead to serious psychological complexes. A person may think that there is a bad smell coming from him or his things, but he does not feel it. Another situation: loss of smell (anosmia) leads to the fact that danger cannot be recognized in time, for example, a gas leak, the appearance of a burning or smoke smell. For chefs, anosmia can actually cost them their careers.

Causes of anosmia.

There are two mechanisms for the development of anosmia:

1.Lesions inside the nasal cavity and pathological processes at the level of olfactory receptors — this can be seasonal allergies, polyps of the nose and paranasal sinuses, respiratory viral infections, prolonged inhalation of toxic substances and prolonged use of vasoconstrictor drops.

2.Involvement of the olfactory pathways in the brain in the pathological process — this mechanism is observed in traumatic brain injuries, Alzheimer's disease, multiple sclerosis, infectious brain damage, hypertensive encephalopathy, etc.

Very rarely, anosmia may indicate the presence of a tumor in the brain, nasal cavity, or paranasal sinuses.

Anosmia is unilateral and bilateral.

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Impaired sense of smell can be combined with the following symptoms:

–memory problems;

–double vision;

–difficulty swallowing;

–speech problems;

–runny nose;

–cough;

–general weakness.

A different combination of symptoms helps the doctor differentiate peripheral (impairments at the level of olfactory receptors and nerve fibers) anosmia from central (associated with brain damage at the level of the olfactory center).

In order to distinguish unilateral from bilateral loss of smell, the doctor conducts a special test — alternately applying substances with a strong odor (vanilla, coffee, etc.) to one or the other nostril.

Features of loss of smell due to coronavirus. Every third patient with COVID experiences anosmia. Usually this symptom appears at the beginning of the disease. The frequency of anosmia with coronavirus is so high that it is proposed to consider it an indicator of coronavirus at the level of PCR smear analysis. The sense of smell returns in the first month in over 90 % of patients. The whole point is that the coronavirus infects the receptors that support the olfactory cells; the virus does not attack the receptor itself and the olfactory nerve, but the cells from which new receptor cells are formed to replace the old ones.

Hearing test. Sensorineural, or sensorineural, hearing loss is a hearing loss associated with damage to the sensitive nerve cells of the organ of hearing or the auditory nerve. The pathological process develops in the deepest part of the ear — in the inner ear, which is located in the cavity inside the temporal bone, behind the eardrum.

Sensorineural hearing loss may be one of the symptoms of some other ear disease (for example, acute purulent otitis media — inflammation in the middle ear cavity, otosclerosis, Meniere's disease, ear injury), or it may be an independent disease.

Sensorineural hearing loss can be unilateral or bilateral, and can develop either suddenly (acute) or slowly, gradually over many years (chronic hearing loss).

Chronic sensorineural hearing loss:

1.Gradual and slow loss of hearing in both ears over several months.

2.Speech intelligibility deteriorates: it is difficult to distinguish words in noisy environments.

3.The perception of high frequencies deteriorates: the ringing of a mobile phone, the microwave timer, the squeak of a mosquito, the speech of a child are worse heard, while a low male voice is heard better.

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4. Often accompanied by a constant hissing, rustling noise in the ears (patients describe it “like a radio”, “like the sound of the sea”).

Acute sensorineural hearing loss:

–severe, sudden hearing loss;

–often occurs only on one side, accompanied by ringing in the ear, dizziness, imbalance, and nausea;

–this is always some kind of catastrophe in the ear: a sharp disruption of the blood supply to the cochlea, intoxication, acoustic trauma (after an explosion, a gunshot), an acute infectious disease, traumatic brain injury, blockage of the ear canal with wax, a consequence of a stroke.

Causes of hearing loss:

1. Heredity: this type of hearing loss develops due to a genetic predisposition and disruption of the normal development of the hearing organ even before birth.

2. Age: similar to the gradual decline in visual acuity, after 50 years of age there is a natural decline in hearing due to a slowdown in metabolism in the sensitive cells of the ear, which is called “presbycusis”.

3. Infectious diseases: many acute infectious diseases such as influenza, meningococcal infection, measles, etc. often lead to complications.

4. Long-term exposure to noise: at work.

2.7.EXAMINATION OF THE STATE OF THE ENDOCRINE SYSTEM

Diabetes mellitus, emergencies and complications.

Early signs of diabetes mellitus are weight loss, polyuria, polydipsia, inflammatory diseases of the skin and mucous membranes that are difficult to treat, and dry mouth.

Signs of poorly compensated diabetes mellitus: exacerbation of infectious lesions of the skin and mucous membranes, dry, hyperemic skin, dry mucous membranes, slight decrease in tissue turgor, smell of acetone from the mouth, rapid breathing. If there are symptoms of insufficient compensation of diabetes mellitus, poor healing and infectious complications are possible after various surgical or other medical interventions.

Emergency conditions in diabetes mellitus (DM) differ in etiology and pathogenesis.

The following clinical and metabolic options for acute complications in diabetology are distinguished:

–diabetic ketoacidosis and ketoacidotic coma;

–hyperosmolar coma and hyperosmolar hyperglycemic state;

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–lactic acidosis (lactic acidosis);

–hypoglycemia and hypoglycemic coma.

However, in the prehospital setting, it is more important to distinguish between hyperglycemic and hypoglycemic comas.

Hyperglycemic comas (ketoacidotic, hyperosmolar, lactic acidotic) develop relatively slowly, over a day or more.

Hypoglycemic coma develops quickly, within a few minutes, and is dangerous both for the functioning of the central nervous system and for life if assistance is provided slowly. Hypoglycemic coma ranks third (5.4 %) in the structure of comas at the prehospital stage, and diabetic (3 %) is fifth. 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.

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.

Ketoacidotic coma.

Diabetic ketoacidosis (DKA) is an emergency condition in diabetes mellitus, which develops as a result of absolute insulin deficiency or severe relative insulin deficiency, leading to the development of ketoacidotic coma with severe hormonal and metabolic disorders.

Etiology. DKA is caused by an absolute deficiency of insulin. In the development of DKA, psychological problems with eating disorders and insulin therapy are important. In ketoacidotic coma, profound metabolic disorders occur, decompensation of carbohydrate, lipid, protein, and electrolyte metabolism. The toxic effect of ketone bodies on the cells of the central nervous system, inhibition of enzyme systems, decreased utilization of glucose by brain cells, oxygen starvation leads to impaired consciousness and the development of ketoacidotic coma.

Clinical symptoms of DKA include polyuria, polydipsia, weight loss, diffuse abdominal pain, diabetic pseudoperitonitis, dehydration, severe weakness, breath odor of acetone or a fruity odor, and a gradual decrease in consciousness to stupor. When examining patients, signs of dehydration, skin turgor and eyeball density, tachycardia, and hypotension are revealed. With the development of coma in patients, severe respiratory disturbances occur and Kussmaul breathing develops. Many patients develop vomiting, which may resemble coffee grounds in color.

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Diagnostics. Based on clinical picture data, indications that the patient has type 1 diabetes, as well as laboratory test data. DKA is characterized by hyperglycemia (in some cases slight), ketonuria, metabolic acidosis, and hyperosmolarity.

Hyperosmolar coma.

Hyperosmolar hyperglycemic state — acute decompensation of diabetes mellitus with hyperglycemia above 35 mmol/L) with high plasma osmolarity and severe dehydration, in the absence of ketoacidosis, is rare, mortality is 12–15 %, with inadequate treatment it reaches 50–60 %.

Etiology. Hyperosmolar coma develops, as a rule, in elderly people, in 20–30 % of newly diagnosed diabetes mellitus. Provoking factors are diseases accompanied by severe dehydration and severe relative insulin deficiency — infectious diseases with fever, vomiting, diarrhea, acute cardiovascular diseases, myocardial infarction, stroke, pulmonary embolism, massive bleeding, acute pancreatitis, extensive burns, renal failure, peritoneal dialysis, operations, injuries, heat stroke, endocrinopathies (acromegaly, thyrotoxicosis, hypercortisolism).

The causes of coma are the use of β-blockers, diuretics, calcium channel blockers, glucocorticoids, somatostatin analogues, as well as limiting fluid intake.

Clinical manifestations. The clinical picture for hyperosmolar coma is complex of signs and complications of dehydration and hypoperfusion:

–thirst, dry mucous membranes, tachycardia, arterial hypotension, nausea, weakness, shock;

–focal and generalized seizures;

–fever, nausea and vomiting (40–65 % of cases).

Patients are often diagnosed with concomitant diseases — thrombosis of the veins of the lower extremities, pneumonia, cerebrovascular accidents, and intestinal motility disorders.

Lactic acidotic (lactic acid) coma.

Lactic acidotic (lactic acid) coma is a fairly rare complication of diabetes mellitus; it develops as a result of excessive accumulation of lactic acid in the blood and tissues and the acidosis caused by it. Often, lactic acidosis can be combined in 10–20 % of cases with ketoacidosis and in almost 50 % of cases with a hyperosmolar state, which significantly worsens the condition of patients. Lactate acidosis (LA) or lactic acidosis is a nonspecific syndrome, its causes are varied.

The main reason is mixed: increased formation and decreased utilization of lactate and hypoxia. Lactic acidosis is a metabolic acidosis with a large anion gap (≥ 10) and a blood lactate level > 4 mmol/L (according to some definitions > 2 mmol/L).

Most often, diabetes mellitus develops lactic acidosis of mixed etiology (type A, B), the pathogenesis of which involves several provoking factors. The concepts

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of biguanide-induced and biguanide-associated lactic acidosis should also be differentiated. The latter should be understood as lactic acidosis, in the pathogenesis of which the intake of biguanides plays not a major, but a secondary role.

Etiology. Lactic acid coma develops, as a rule, in elderly and senile patients suffering from type 2 diabetes mellitus, with severe concomitant diseases of the liver, kidneys, cardiovascular and respiratory systems, chronic alcoholism, accompanied by tissue hypoxia. Lactic acidosis is a pathological reaction to situations associated with any type of hypoxia.

Factors that provoke the development of lactic acidosis in diabetes mellitus:

–increased formation of lactate (taking biguanides, severe decompensation of diabetes mellitus, diabetic ketoacidosis, acidosis of another origin);

–decreased clearance of lactate and/or biguanides (impaired liver function, kidney function, alcohol intoxication, intravenous administration of radiocontrast agents);

–tissue hypoxia (chronic heart failure, obliterating diseases of peripheral arteries, severe respiratory diseases, anemia, severe infections);

–the combined effect of several factors leading to the accumulation of lactate (acute stress, severe late complications of diabetes, severe general condition, age over 65 years, advanced stages of malignant neoplasms);

–pregnancy.

Clinical picture. Lactic acid coma develops quite quickly, within a few hours. Patients develop thirst, nausea, vomiting, weakness, headaches, abdominal pain, diffuse muscle pain that is not relieved by analgesics, increased breathing, pain in the heart area that is not relieved by antianginal drugs. Loss of consciousness is sometimes preceded by excitement and delirium, Kussmaul breathing occurs, and symptoms of acute cardiovascular failure. The skin is pale, with a cyanotic tint, the pulse is frequent, arrhythmias often occur, blood pressure decreases, collapse occurs with oliguria and anuria, hypothermia occurs, shock occurs, and thrombosis develops in the veins of the lower extremities.

Diagnostics. The diagnosis is based on the clinical picture, the presence of severe metabolic acidosis with hyperlactic acidemia and an increase in the lactate/pyruvate ratio without ketosis and severe hyperglycemia. The content of lactic acid in the blood rises to more than 2 mmol/L (a specific sign is more than 4.0 mmol/L) when the norm is 0.4–1.4 mmol/L. Characterized by a decrease in reserve alkalinity of the blood, a shift in pH towards acidosis (< 7.3), a decrease in blood bicarbonates (HCO3– < 18 mEq/L) in combination with anion deficiency (Na+ – (Cl– + HCO3–) > 10–15 mEq/L). Along with lactic acidemia, pyruvatemia

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(from 0.3 to 0.5 mmol/L) is noted with moderate hyperglycemia, the absence of ketonemia and acetonuria.

Main components:

–reduction of lactate formation;

–removal of lactate and biguanides from the body (if used);

–combating shock, hypoxia, acidosis, electrolyte disturbances;

–elimination of provoking factors.

At the prehospital stage: intravenous infusion of 0.9 % NaCl.

Hypoglycemic coma.

Hypoglycemic coma is an emergency condition in diabetes mellitus, caused by an imbalance between the amount of insulin and glucose in the blood, with the subsequent development of neuroglycopenic and adrenergic syndromes.

Etiology. The main reasons for the development of hypoglycemic coma are the following:

1)overdose of insulin and its analogues, as well as sulfonylureas;

2)drinking alcoholic beverages;

3)insufficient food intake against the background of unchanged glucoselowering therapy;

4)physical activity against the background of constant glucose-lowering therapy and/or without additional intake of carbohydrates;

5)violation of insulin administration technique (intramuscular injection instead of subcutaneous);

6)artificial hypoglycemia (deliberate overdose of glucose-lowering drugs by the patient himself);

7)organic hyperinsulinism — insulinoma.

Clinical manifestations. There are two main groups of symptoms: adrenergic, associated with activation of the sympathetic nervous system and the release of adrenaline by the adrenal glands, and neuroglycopenic, associated with dysfunction of the central nervous system.

Adrenergic symptoms include:

–tachycardia, mydriasis;

–anxiety, aggressiveness;

–trembling, cold sweat, paresthesia;

–nausea, severe hunger, hypersalivation;

–diarrhea, excessive urination.

Neuroglycopenic symptoms include:

–asthenia;

–decreased concentration;

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–headache;

–feeling of fear;

–confusion;

–disorientation;

–hallucinations;

–speech, visual, behavioral disorders;

–amnesia, impaired consciousness;

–convulsions, transient paralysis;

–to whom.

In some cases, despite restoration of normoglycemia and ongoing therapy, patients may remain in a stuporous or even comatose state for several hours or even days. Prolonged hypoglycemia or its frequent episodes can lead to irreversible changes in the central nervous system (primarily in the cerebral cortex), the manifestations of which vary significantly from delirious and hallucinatory-paranoid episodes to typical epileptic seizures, the inevitable outcome of which is persistent dementia.

Emergency conditions for thyroid diseases.

Thyrotoxic crisis is a syndrome manifested by a sharp increase in the severity of symptoms of thyrotoxicosis in patients with diffuse or diffuse nodular toxic goiter. Most often, a crisis develops after a strumectomy, or after treatment with radioactive iodine preparations.

Provoking factors are:

–cessation of thyreostatic therapy;

–trauma, surgery;

–massive load of iodine;

–mental trauma, stress;

–TELA;

–ONMC.

Clinical picture. Subacute phase — the period from the appearance of the first signs to impaired consciousness and the development of coma.

Acute (comatose) phase develops after 24–48 hours with an unfavorable course of the subacute phase.

Clinical manifestations:

1)increased sweating in combination with hyperthermia (without signs of in-

fection);

2)cardiovascular disorders, tachycardia, arrhythmia;

3)nervousness, anxiety, fear, aggression, agitation and other manifestations of the central nervous system;

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4)gastrointestinal manifestations — nausea, vomiting, gastrointestinal motility disorders, the appearance of jaundice.

Lethal outcomes occur as a result of acute heart failure, acute adrenal insufficiency, acute liver failure.

Hypothyroid coma.

Hypothyroid coma is an emergency disease of the thyroid gland and is one of the outcomes of decompensated hypothyroidism.

Etiology. Develops with primary hypothyroidism, mortality ranges from 50% to 80 % depending on the timeliness of emergency care.

Provoking factors are:

– inadequate treatment of thyroid diseases with thyroid-stimulating hormones;

– infectious diseases;

– stress;

– hypothermia;

– injuries;

– alcohol;

– bleeding;

– surgical interventions;

– anesthesia.

Clinical picture:

1)bradycardia, arrhythmia, hypotension;

2)gastrointestinal bleeding;

3)acute urinary retention;

4)impaired intestinal motility;

5)depression of the central nervous system — lethargy, drowsiness, hyporeflexia, stupor;

6)development of hypoglycemia;

7)polyserosites;

8)hypothermia.

Lethal outcomes occur as a result of the development of cardiovascular and respiratory failure.

Acute adrenal insufficiency.

Acute adrenal insufficiency develops due to a sharp drop in the level of corticosteroids in the body, mortality reaches 40–50 %.

Etiology:

–tumor diseases leading to the development of chronic adrenal insufficiency;

–injuries of the kidneys and adrenal glands;

–congenital malformations of the adrenal glands;

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–hemorrhagic infarction of the adrenal glands on both sides;

–acute pituitary failure;

–acute somatic and infectious diseases leading to the development of adrenal insufficiency.

Clinical picture. Arises and develops over several days.

The following clinical manifestations are characteristic:

1) gastrointestinal disorders — nausea, vomiting, abdominal pain, flatulence, peritonism;

2) loss of appetite;

3) weight loss;

4) physical inactivity;

5) weakness;

6) depression;

7) skin pigmentation;

8) hemorrhagic gastritis, enteritis;

9) oliguria, anuria;

10) clonic convulsions;

11) meningeal symptoms.

Lethal outcomes occur from dehydration, pulmonary edema, coma, and cardiovascular disorders.

Catecholamine crisis.

Catecholamine crisis is a pathological condition associated with a massive release of hormones (adrenaline, norepinephrine, dopamine) into the blood of the adrenal glands by pheochromocytoma, leading to cardiovascular complications — pulmonary edema, arterial hypertension, myocardial infarction, acute cerebrovascular accident and death.

Etiology. Development of pheochromocytoma in the adrenal glands on one or both sides. The incidence is 3–11 cases per 10 000 population, i.e. per 1 000 patients with arterial hypertension there is 1 patient with pheochromocytoma.

Provoking factors in the presence of pheochromocytoma itself provoke its activity by the following factors:

–stressful situations;

–fasting;

–physical stress;

–hypothermia;

–use of insulin, cardiac glycosides;

–abuse of citrus fruits, cheeses, chocolate, red wine, mustard;

–operations;

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