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Файл:Emergency medical care at the prehospital stage. Assessment of the severity of the condition of patients. Study aid
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4) cerebrovascular accident, increased liquor (intracerebral fluid), stroke, trau-
matic brain injuries.
Intracranial pressure affects the state of the fundus, nerve cells of the retina are
affected, and peripheral vision suffers from this.
Examination of taste sensations. Taste sensation is one of the five main feelings of a person. On the one hand, the determination of the taste of food is necessary
to increase appetite and reflex the operation of the gastrointestinal glands, which contributes to normal digestion; on the other hand, the taste sensation helps to distinguish
inedible or spoiled food products, protecting against poisoning. Taste is perceived using taste buds. Most of them are located on the surface of the tongue in structures
called taste papillae. We feel salty, sweet, bitter, sour flavours. Impulses from taste
papillae are transmitted through nerve fibers to the cells of the subcortical centers and
cortex of the brain, where a particular taste feeling is formed. The system of taste
buds, nerves and areas of the brain in which information received from receptors is
processed is called a taste analyzer.
Varieties of taste disturbance.
The first type is an exacerbation of taste (hypergeusia), which is characterized
by the occurrence of a taste sensation of high intensity, disproportionate to the
usual level.
The second type is a decrease in the severity of taste (hypogeusia). This state is
characterized by the occurrence of a taste sensation of low intensity, up to a complete
lack of taste, the so-called ageusia.
The third type is the perversion of the taste sensation (dysgeusia). At the same
time, for example, irritation of receptors normally responsible for the development of
a sweet feeling leads to another feeling — acute, bitter, salty.
Often enough, the cause of taste disturbance lies in a change in the mucous
membrane of the oral cavity and tongue, which leads to direct damage to the taste papillae or the inability to deliver a chemical to them. Most often, infectious processes
and the consequences of deficiency in the body of certain nutrients lead to changes in
the mucous membrane.
For the normal operation of taste papillae, it is necessary to dissolve chemical
stimuli in saliva. Taste disorders are associated with this when impaired secretion by
the salivary glands. Taste sensation is closely related to smell sensation (smell). That
is why in acute and chronic rhinitis (inflammation of the mucous membrane of the
nasal cavity) there is a violation of taste perception. Taste sensations change or even
disappear completely when nerves and brain centers belonging to the taste analyzer
are damaged. It is worth saying that a change in taste perception can be observed in
mental disorders.
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Pregnant women complain about taste disorders, which is associated with
a specific restructuring of metabolism during this period. Dull taste also causes smoking. Changes in taste are recorded after some medicines, as well as when consuming
individual foods with an extremely intense taste (for example, lemon).
Diseases characterized by taste disorder:
iron deficiency anemia, B12-deficient anemia;
inflammatory diseases of the oral mucosa (stomatitis) and tongue (glossitis);
cranial neuralgia, herpetic trigeminal nerve involvement;
acute respiratory infections;
new coronavirus infection COVID-19;
lesions of sensitive nerves and receptors in diabetes mellitus, hypothyroidism
(thyroid insufficiency);
strokes and other focal lesions of a brain substance;
fungal lesions in the mouth with taste-olfactory disorders;
mental disorders.
Sense of smell research. The sense of smell is a feeling that enriches our emotions and can firmly capture the smell in memory. In everyday life, we do not remember him, taking his presence as a given. At the same time, its loss is the brightest
symptom of a number of diseases.
Anosmia (ICD-10 — R43) is a complete loss of smell (a person ceases to feel
and distinguish odors). Often anosmia is combined with another symptom — loss of
taste (ageusia). This is due to the fact that the taste and olfactory receptors are in
close association. Anosmia is more common in men, in both sexes it can be a transient condition or persist for a long time.
Violation of the sense of smell can lead to serious psychological complexes.
A person may feel that a bad smell comes from him or from his things, but he does
not feel it. Another situation: loss of smell (anosmia) leads to the fact that the danger
cannot be recognized in time, for example, gas leakage, the appearance of the smell
of burning or smoke. For chefs, anosmia can cost a career at all.
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 ol-
factory receptors, these can be seasonal allergies, nasal and paranasal polyps, respiratory viral infections, prolonged inhalation of toxic substances and prolonged intake of
vasoconstrictive droplets;
2) involvement in the pathological process of olfactory pathways in the brain.
Such a mechanism is observed in traumatic brain injuries, Alzheimer's disease, multiple sclerosis, infectious brain damage, hypertensive encephalopathy, etc.
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Extremely rarely, anosmia can indicate the presence of a tumor in the brain,
nasal cavity, or paranasal sinuses.
Anosmia is one-sided and two-sided.
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
(disorders at the level of olfactory receptors and nerve fibers) anosmia from central
(associated with damage to the brain at the level of the olfactory center).
In order to distinguish a unilateral loss of smell from a bilateral one, the doctor
conducts a special test: alternately brings a substance with a strong smell (vanilla,
coffee, etc.) to one or the other nostril.
The peculiarity of the loss of smell in coronavirus. Every third patient with
COVID faces anosmia. Usually this symptom appears at the beginning of the disease.
The frequency of anosmia in coronavirus is so high that it is proposed to consider it
an indicator of the disease at the level of PCR smear analysis. The sense of smell returns in the first month in more than 90 % of patients. It's all about the peculiarities of
the coronavirus lesions of receptors that support sense of smell cells: the virus does
not affect the receptor itself and the olfactory nerve, but the cells from which new receptor cells are formed to replace the old ones.
Hearing research. Sensorineural, or sensorineural, hearing loss is a decrease in
hearing associated with damage to the sensitive nerve cells of the hearing organ or
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), and may be an independent disease.
Sensorineural hearing loss is unilateral or bilateral, can develop either suddenly
(in an acute form), or slowly, gradually over many years (chronic hearing loss).
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Chronic sensorineural hearing loss:
a gradual and slow reduction in hearing on both ears over several months;
the intelligibility of speech deteriorates: it is difficult to distinguish words in
noisy environments;
perception of high frequencies worsens: a mobile phone call, a microwave
timer, a mosquito squeak, a child's speech are worse heard, while a low male voice is
heard better;
often accompanied by constant hissing, rustling noise in the ears (patients de-
scribe it “as a radio receiver”, “as a noise of the sea”).
Acute sensorineural hearing loss:
1) abrupt, sudden hearing loss;
2) often happens only on the one hand, accompanied by ringing in the ear, diz-
ziness, imbalance, nausea;
3) this is always some kind of catastrophe in the ear: a sharp violation of the
blood supply to the cochlea, intoxication, acoustic injury (after an explosion, shot),
acute infectious disease, traumatic brain injury, blockage of the ear canal with a sulfur plug, the consequence of a stroke.
Causes of hearing loss:
heredity: this type of hearing loss develops with a genetic predisposition and
violation of the normal development of the hearing organ even before birth;
age: like a gradual decrease in visual acuity after 50 years, there is a natural
decrease in hearing due to a slowdown in metabolism in sensitive ear cells, called
“presbyacusis”;
infectious diseases: many acute infectious diseases, such as influenza, me-
ningococcal disease, measles, etc., often lead to complications;
long-term noise exposure: at work, etc.
2.7. ENDOCRINE SYSTEM STUDY
Diabetes mellitus, medical emergencies and complications.
Early signs of diabetes mellitus are weight loss, polyuria, polydipsia, poorly
treatable inflammatory diseases of the skin and mucous membranes, dry mouth.
Signs of poorly compensated diabetes mellitus: exacerbations 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. In the presence of symptoms of insufficient compensation for diabetes
mellitus, poor healing and infectious complications after various surgical or other
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medical interventions are possible. Diabetes mellitus emergencies vary in etiology
and pathogenesis.
The following clinical and metabolic variants of acute complications in diabetology are distinguished:
diabetic ketoacidosis and ketoacidotic coma;
hyperosmolar coma and hyperosmolar hyperglycemic state;
lactic acid acidosis (lactate acidosis);
hypoglycemia and hypoglycemic coma.
However, at the prehospital stage, it is more important to distinguish between
hyperglycemic and hypoglycemic comas.
Hyperglycemic comas (ketoacidotic, hyperosmolar, lactacidotic) develop rela-
tively slowly, within a day or more.
Hypoglycemic coma develops rapidly, within a few minutes, and is dangerous
both for the functioning of the CNS and for life in the event of slow care. Hypoglycemic coma ranks third (5.4 %) in the structure of coma at the prehospital stage, and
diabetic (3 %) — fifth. Hypoglycemia is associated with an imbalance between
a drug used in the treatment of diabetes (insulin or tableted sugar-lowering agents)
and eating or exercising. A sharp drop in glucose concentration leads to loss of consciousness, since the normal functioning of the brain is almost completely dependent
on glucose.
The speed and timeliness of providing care to patients in a comatose state
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
that develops due to absolute insulin deficiency or pronounced relative insulin deficiency, leading to the development of ketoacidotic coma with severe hormonal metabolic disorders.
Etiology. The cause of DKA is absolute insulin deficiency. In the development
of DKA, psychological problems with nutritional disorders and insulin therapy are
important. In ketoacidotic coma, deep metabolic disorders occur, decompensation of
carbohydrate, lipid, protein, electrolyte metabolism. Toxic effect of ketone bodies on
CNS cells, inhibition of enzyme systems, reduced utilization of glucose by brain
cells, oxygen starvation lead to impaired consciousness, development of ketoacidotic
coma.
Clinical symptoms of DKA include polyuria, polydipsia, weight loss, spilled
abdominal pain, diabetic pseudoperitonitis, dehydration, pronounced weakness, ace-
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tone odor at mouth or fruit odor, gradual reduction of consciousness to soporotic. Examination of patients reveals signs of dehydration, skin turgor and density of eyeballs, tachycardia, hypotension. With the development of coma, patients have pronounced respiratory disorders, Kussmaul breathing develops. Many patients develop
vomiting, which in color can resemble coffee grounds.
Diagnosis. Based on clinical data, indications of the patient's SD-1, as well as
laboratory data. DKA is characterized by hyperglycemia (in some cases minor), ketonuria, metabolic acidosis, hyperosmolarity.
Hyperosmolar coma.
Hyperosmolar hyperglycemic state — acute decompensation of diabetes
mellitus with hyperglycemia above 35 mmol/L, high plasma osmolarity and pronounced dehydration in the absence of ketoacidosis, is rare, mortality is 12–15 %,
with inadequate treatment reaches 50–60 %.
Etiology. Hyperosmolar coma develops, as a rule, in elderly people, in
20–30 % with newly diagnosed diabetes mellitus. Provoking factors are diseases accompanied by sharp dehydration and pronounced relative insulin failure — infectious
diseases with fever, vomiting, diarrhea, acute cardiovascular diseases, myocardial infarction, stroke, pulmonary embolism, massive bleeding, acute pancreatitis, extensive
burns, renal failure, peritoneal dialysis, surgery, injuries, heat stroke, endocrinopathies (acromegaly, thyrotoxicosis, hypercorticism).
The causes of coma are taking β-blockers, diuretics, calcium channel blockers,
glucocorticoids, somatostatin analogues, as well as limiting fluid intake.
Clinical manifestations. Hyperosmolar coma is characterized by a complex of
signs and complications of dehydration and hypoperfusion:
thirst, dry mucous membranes, tachycardia, hypotension, nausea, weakness,
shock;
focal and generalized seizures;
fever, nausea and vomiting (40–65 % of cases).
Often, patients are diagnosed with concomitant diseases — thrombosis of the
veins of the lower extremities, pneumonia, cerebral circulation disorders, intestinal
motility disorders.
Lactacidotic (lactic acid) coma.
Lactacidotic (lactic acid) coma is a rather rare complication of diabetes melli-
tus, develops due to excessive accumulation of lactic acid in the blood and tissues and
the acidosis caused by it. Often lactate acidosis can be combined in 10–20 % of cases
with ketoacidosis and almost, in 50 % of cases with a hyperosmolar condition, which
significantly worsens the condition of patients. Lactate acidosis, or lactic acid acidosis, is a nonspecific syndrome, its causes are diverse.
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The main reason is mixed: increased formation and reduced utilization of lactate and hypoxia. Lactate acidosis is a metabolic acidosis with a large anion differ-
ence (≥ 10) and a blood lactate level of more than 4 mmol/L (according to some defi-
nitions, more than 2 mmol/L).
Most often, with diabetes mellitus, lactic acidosis of mixed etiology (type
A, B) develops, in the pathogenesis of which several provoking factors are involved.
The concepts of biguanide-induced and biguanide-associated lactate acidosis should
also be differentiated. The latter should be understood as such lactate acidosis, in the
pathogenesis of which the intake of biguanides plays not the main, but a seconddary role.
Etiology. Lactacidotic 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. Lactate acidosis is a pathological response to situations related to any
type of hypoxia.
Factors that provoke the development of lactate acidosis in diabetes mellitus:
1) increased lactate formation (ingestion of biguanides, severe decompensation
of diabetes mellitus, diabetic ketoacidosis, acidosis of another origin);
2) reduced clearance of lactate and/or biguanides (impaired liver, kidney func-
tion, alcohol intoxication, intravenous administration of radiopaque agents);
3) tissue hypoxia (chronic heart failure, peripheral artery obliterating diseases,
severe respiratory diseases, anemia, severe infections);
4) combined effect of several factors leading to lactate accumulation (acute
stress, severe late complications of diabetes mellitus, severe general condition, age
over 65 years, advanced stages of malignancies);
5) pregnancy.
Clinical presentation. Lactacidotic coma develops quickly enough, within
a few hours. Patients develop thirst, nausea, vomiting, weakness, headaches, abdominal pain, diffuse muscle pain that does not stop with analgesics, increased
breathing, heart pain that does not stop with anti-anginal drugs. Loss of consciousness is sometimes preceded by agitation and delirium, Kussmaul's breathing occurs,
symptoms of acute cardiovascular failure. The skin is pale, with a cyanotic tint, the
pulse is frequent, arrhythmias often occur, blood pressure decreases, collapse with
oliguria and anuria occurs, hypothermia, shock, thromboses develop in the veins of
the lower extremities.
Diagnosis. Diagnosis is based on clinical presentation, presence of severe
metabolic acidosis with hyperlactacidemia and increased lactate/pyruvate ratio with-
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out ketosis and severe hyperglycemia. The content of lactic acid in the blood rises
more than 2 mmol/L (specific sign — more than 4.0 mmol/L) at a rate of
0.4–1.4 mmol/L. Characteristic is a decrease in reserve blood alkalinity, pH shift towards acidosis (< 7.3), a decrease in blood bicarbonates (NSO3 < 18 mEq/L) in combination with anion deficiency (Na+ – (Cl– + HCO
3
–
) > 10–15 mEq/L). Along with
lactate acidemia, pyruvatemia (from 0.3 to 0.5 mmol/L) is noted in moderate hyperglycemia, the absence of ketonemia and acetonuria.
The main components are:
reducing lactate formation;
excretion of lactate and biguanides from the body (if used);
combating shock, hypoxia, acidosis, electrolyte disorders;
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 due to an
imbalance between the amount of insulin and glucose in the blood, followed by the
development of neuroglycopenic and adrenergic syndromes.
Etiology. The main causes of hypoglycemic coma are:
1) overdose of insulin and its analogues, as well as sulfonylureas;
2) taking alcoholic beverages;
3) insufficient food intake against the background of constant sugar-lowering
therapy;
4) physical activity against the background of constant sugar-lowering therapy
and/or without additional intake of carbohydrates;
5) impaired insulin administration technique (intramuscular injection instead of
subcutaneous injection);
6) artificial hypoglycemia (conscious overdose of sugar-lowering drugs by the
patient himself);
7) organic hyperinsulinism — insulinoma.
Clinical manifestations. Two main groups of symptoms are distinguished: ad-
renergic, associated with activation of the sympathetic nervous system and adrenaline
release by the adrenal glands, and neuroglycopenic, associated with impaired functioning of the CNS.
Adrenergic symptoms include:
tachycardia, mydriasis;
anxiety, aggressiveness;
trembling, cold sweat, paresthesia;
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nausea, severe hunger, hypersalivation;
diarrhea, abundant urination.
Neuroglycopenic symptoms include:
asthenia;
reduced concentration of attention;
headache;
a sense of fear;
confusion;
disorientation;
hallucinations;
speech, visual, behavioral disorders;
amnesia, impaired consciousness;
seizures, transient paralysis;
to whom.
In some cases, despite the restoration of normoglycemia and ongoing therapy,
patients can remain in a stupor or even comatose state for several hours or even days.
Prolonged hypoglycemia or its frequent episodes can lead to irreversible changes in
the CNS (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.
Medical emergencies in thyroid diseases. Thyrotoxic crisis.
Thyrotoxic crisis is a syndrome manifested by a sharp increase in the severity
of symptoms of thyrotoxicosis in patients with diffuse or diffuse nodal toxic goiter.
The most common crisis occurs after strumectomy or after treatment with radioactive
iodine drugs.
The provoking factors are:
discontinuation of thyroostatic therapy;
trauma, surgery;
massive iodine load;
mental trauma, stress;
TELA;
ONMK.
Clinical presentation. Subacute phase — the period from the appearance of the
first signs to impaired consciousness and the development of coma. The acute (coma-
tose) phase develops after 24–48 hours with an unfavorable course of the subacute
phase.
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Clinical manifestations:
1) increased sweating combined with hyperthermia (no signs of infection);
2) cardiovascular disorders, tachycardia, arrhythmia;
3) nerves, anxiety, fear, aggression, agitation and other CNS manifestations;
4) gastrointestinal manifestations — nausea, vomiting, impaired gastrointesti-
nal motility, the appearance of jaundice.
Deaths occur as a result of acute heart failure, acute adrenal insufficiency,
acute liver failure.
Hypothyroid coma.
Hypothyroid coma — an emergency disease of the thyroid gland, is one of the
outcomes of decompensated hypothyroidism.
Etiology. Develops in primary hypothyroidism, mortality ranges from 50 to
80 %, depending on the timeliness of emergency care.
The provoking factors are:
1) inadequate treatment of thyroid diseases with thyroid-stimulating hormones;
2) infectious diseases;
3) stresses;
4) hypothermia;
5) injuries;
6) alcohol;
7) bleeding;
8) surgical interventions;
9) anesthesia.
Clinical presentation:
bradycardia, arrhythmia, hypotension;
gastrointestinal bleeding;
acute urinary retention;
impaired intestinal motility;
CNS depression — inhibition, drowsiness, hyporeflexion, sopor;
development of hypoglycemia;
polyserosites;
hypothermia.
Deaths 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 %.
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