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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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Brudzinsky's symptom (upper, middle, lower);
zygomatic symptom of Bekhterev;
Mondonesi symptom;
photophobia, phonophobia;
headache;
hyperesthesia of the skin and mucous membranes.
Focal symptoms.
Cranial nerves.
I pair (n. olfactorius). The sense of smell is not disturbed; hyposmia, anosmia
(right, left); dysosmia, hyperosmia; olfactory hallucinations — yes, no.
II pair (n. opticus). Visual acuity — not impaired; amblyopia (decreased visu-
al acuity), amaurosis (blindness); visual fields — not disturbed; scotoma (loss of field
of view); hemianopsia: homonym (right, left), heteronym (bitemporal, binazal); visual hallucinations — yes, no.
III (n. oculomotorius), IV (n. trochlearis), VI (n. abducens). Arbitrary eye
movements — in full, strabismus (strabismus): converging, diverging, vertically.
Pupils OD > < = OS, deformed; width of pupils: corresponds to illumination,
miosis (narrow), mydriasis (wide).
Photoreactions direct, commonwealth: saved, reduced, absent (right, left).
Eye paresis, tonic eye diversion: right, left.
V (n. trigeminus). Facial sensitivity — preserved, reduced: neural type
(I, II, III branches); segmental type (inner, middle, outer brackets); conductor type
(right, left).
The strength of the chewing muscles is preserved; reduced (right, left).
Corneal reflexes — preserved, reduced, absent (right, left).
Mandibular reflex — unchanged, elevated.
VII (n. facialis). Mimic musculature. The face is symmetrical, facial muscle
paresis: central — the nasolabial fold is smoothed, peripheral — the inability to raise
the eyebrow, clamp the eye, the nasolabial fold is smoothed (right, left).
Taste disturbance on the front 2/3 of the tongue (right, left).
Lacrimation (lacrimation), dryness of sclera; hyperacusis (increased sound perception).
VIII (n. vestibulocohlearis). Hearing preserved, reduced, absent (right, left).
Vestibular syndrome — absent; systemic dizziness; nausea, vomiting; nystagmus (horizontal, vertical, rotator, coarse-fine-sweeping), ataxia, decreased muscle tone.
IX (n. glossopharingeus), X (n. vagus). Swallowing — preserved, a dys-
phagia. Phonation — saved, a dysphonia.
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Articulation — preserved, a-dysarthria.
Bulbar syndrome — paresis of the soft palate (right, left), decreased pharyngeal reflex (right, left). Pseudobulbar syndrome — paresis of the soft palate on both
sides (there is, no), increase in pharyngeal reflexes (there is, no), reflexes of oral automatism (distance-oral, palmar-chin, nasolabial, proboscis), violent laughter or crying. Taste disturbance on the back 1/3 of the tongue (right, left). Dry mouth (yes, no).
XI (n. accessorius). Trapezoidal muscle strength, strength of the forging muscle (unchanged, reduced, right, left).
XII (n. hypoglossus). Language along the midline, language deviation to the
right, left; hypotrophy of the tongue, fibrillation (yes, no).
Motor system.
The volume of active movements in the extremities is complete, limited (Barre
sample upper and lower; test with anti-retention, pronational phenomenon, symptom
of the rotated foot of Bogolepov).
Muscle tone — not changed, increased: spastic, plastic; decreased (in which
muscle groups).
Tendon reflexes — unchanged, reduced, elevated (from biceps tendon S5–6,
triceps S7–8, knee L2–4, achilles S1–2) on the right, left.
Clones of the chin, hand, gluteal muscles, kneecap, foot (right, left).
Periosteal reflexes — carporadial S5–8 (unchanged, decreased, elevated,
right, left).
Superficial reflexes — abdominal, cremaster, plantar (unchanged, reduced).
Pathological reflexes — extensory (Babinsky, Oppenheim, Gordon, Schaeffer,
etc.), flexural (Jacobson — Laska, Rossolimo, Bekhterev I and II, Zhukovsky, etc.).
Protective reflexes — shortening, elongating (the level from which the reflex is
called).
Pathological synkinesias are global, coordinating, imitative.
Fasciculations, fibrillaci (in which muscle groups).
Hypotrophy, hypertrophy (in which muscle groups).
Tremor (at rest, with movements, frequency).
Hyperkinesis — chorea, athetosis, tremor, myoclonia, tics (simple/complex;
motor, vocal), dystonias (blepharospasm, oromandibular, laryngeal, spastic crank,
scribal spasm, foot dystonia, torsion dystonia).
Coordination system.
Static ataxia — Romberg's pose, a test for Babinsky's synergy.
Dynamic ataxia — palsenos, heel-colic, index test, Stewart — Holmes symptom, Schilder test, diadochokinesis test, dysmetry tests (negative, positive).
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Chanted speech.
Nystagmus.
Micro- or megalography.
Gait — not changed, atactic, steppe, stamping, “sample of a star”.
Sensitivity system.
Types of sensitivity:
superficial sensitivity: pain, temperature, tactile;
deep sensitivity: articulomuscular feeling, vibrational, kinesthetic, feeling of
pressure and weight;
complex types of sensitivity: discriminatory sensitivity, sense of localization,
two-dimensional spatial feeling.
Nature of sensitivity disturbances:
1) anesthesia — complete loss of a particular type of sensitivity;
2) hepaesthesia — a decrease in a particular type of sensitivity;
3) hyperesthesia — an increase in a particular type of sensitivity;
4) hyperpathy — perversion of sensitivity with unpleasant pain;
5) dysesthesia — perversion of sensitivity (cold, it seems, hot; touch feels
like pain);
6) paresthesia — a feeling of cold, numbness, tingling, crawling “goosebumps”
that occurs without disturbing external irritations;
7) pains — aching, dull, stabbing, pulsating, cutting, etc.
Types of sensitivity disturbance distribution:
neural (indicate nerve);
polyneuritic — “socks” and/or “gloves”;
segmental (root) (indicate segment, presence of pain, tension symptoms);
segmental dissociated (specify segment);
conductor spinal — mono-, hemi-, para-, tetra-type (indicate the level of
damage by segments);
conductor cerebral — mono-, hemi-, tetra-type.
Aphasia's higher mental functions:
1) efferent motor (Broca) — complete absence of expressive speech/embolus/
perseveration;
2) afferent motor — a violation of the pronunciation of closely articulated
sounds (table — elephant — groan);
3) sensory (Wernicke) — violation of expressive and impressive speech (literal
and verbal paraphasies, “verbal salad”);
4) optical-mnestic — disorders of the connections between the visual image of
an object and its name;
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5) acoustic-mnestic — decrease in hearing-speech memory, inability to re-
member a series of 3–5–10 words, impoverishment of speech;
6) semantic — violation of understanding of complex logical-grammatical con-
structions, temporal and comparative relationships;
7) dynamic — absence of expanded speech, elementary phrases;
8) total; sensorimotor.
Apraxia:
kinetic — “fist-rib-palm” test;
kinesthetic — the test “carried postures”.
Agnosia: visual (subject, facial, letter), auditory, olfactory, taste.
Amnesia: Impaired short-term memory, impaired long-term memory.
Vegetative system.
Dermographism — red, white, spilled, sublime.
Bernard — Gorner symptom (sympathetic denervation of the eye) — narrowing of the eye gap, miosis, hypohidrosis of the 1/2 face (right, left).
Clinostatic test — heart rate, blood pressure standing heart rate, blood pressure
lying down.
Orthostatic test — HR, BP lying down HR, BP standing.
Plan for neurological examination of a patient in a comatose state. Primary
actions in the management of a patient with a coma: assessment of the state of vital
functions (functions of external respiration and cardiovascular system), elimination of
hypoxia (restoration of patency of the upper respiratory tract, installation of an air
duct or intubation of the trachea, inhalation of oxygen or mechanical ventilation),
normalization of hemodynamics. Then the naked patient is examined (sequentially
embracing the head, eyes, ears, nose and pharynx, as well as the lungs, heart, abdomen, limbs and skin, including thermometry).
To assess the condition of a patient with a coma, pathological disorders should
be determined:
1. Assess the degree of respiratory impairment (normal, tachypnea, bradypnea,
Grock, Cheyne — Stokes, Biot, Kussmaul respiration), BP + HR (Cushing phenomenon).
2. Meningeal symptoms with assessment of indirect signs of paresis (see
above): stiffness of the neck muscles is not investigated if the patient is suspected of
having a cervical spinal injury.
3. Pupil diameter and reactivity, ciliospinal reflex.
4. Position of the eyeballs (strabismus: convergent, divergent, including vertically, horizontally), adversion (or paresis) of the eye.
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5. Corneal reflex.
6. Eyeball movement: oculocephalic reflex, nystagmus (spontaneous).
7. Posture (decortization, decerebration), different position of limbs.
8. Limb movement: spontaneous, stimulated.
9. Babinsky's reflex (skin (abdominal, plantar) and tendon-periosteal reflexes).
10. Presence or absence of myoclonias.
Eye movements in a patient in a coma. In a comatose state, there is no eye fixation, so there are no tracking movements and in most cases nystagmus is observed.
The deviation of the eyeballs to the side indicates a pathological focus in the ipsilateral hemisphere or in the contralateral sections of the Varolian bridge. Only in epileptic seizures can transient nystagmus and tonic turning of the eyes to the opposite side
of the focus be observed. Slow floating eye movements in a shallow coma indicate
the safety of trunk functions. Other spontaneous eye movements, such as bobbing or
ping-pong, always serve as a sign of brain damage.
Ocular bobbing (from the English bobbing — a blow or squat) is a quick
downward diversion of the eyeballs, accompanied by a longer return to the original
position. Reflex eye movements in this state are not caused.
Bobbing points, as a rule, to a severe defeat of the Varolian bridge. Reverse
bobbing (or ocular dipping, from English dipping — immersion) is an alogical
movement in the opposite direction.
Ping-pong (periodic alternating deviation of the gaze in the horizontal plane):
eyeballs change direction of movement every few seconds, indicating diffuse bilateral
lesion of the cortex.
Examination of eye movements. The only way to assess oculomotor functions
in a patient in a coma is to study vestibuloocular and oculocephalic (oculocephalic)
reflexes. Based on the study of these two reflexes, one can conclude about the state of
the middle brain, the bridge, the oblong brain. Before examining the oculocephalic
reflex, you need to make sure that there is no injury with a fracture or subluxations of
the cervical vertebrae.
Oculocephalic reflex (CRR). The head of the patient in the coma lying on the
back is covered with two hands and rotated to the sides (in the horizontal plane),
while the eyelids are raised with the help of the thumbs to observe the movement of
the eyes.
The normal reaction is that the eyeballs first turn slightly passively with the
head, but then make a movement in the opposite direction (positive CRF is a phenomenon of the doll's eyes). The pathological reaction consists in the loss of the
CRO: the eyeballs remain motionless relative to the eye socket and passively follow
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the turn of the head (negative CRO). The patient's head is then tilted forward and returned to its original position (moving in the sagittal plane). With the preserved function of the brainstem, the eyeballs in this case also move towards the opposite direction of movement of the head (the phenomenon of the doll's eyes). When the middle
brain is affected, the study of the CRF causes normal movements of the eyes in the
horizontal plane, while in the vertical plane they cannot be caused, sometimes only
downward movements of the eyes are possible. When the Varolian bridge is affected,
the CRF is negative or pathological in both planes.
Violation of the commonality of eye movements in CRO indicates internuclear
ophthalmoplegia or damage to subnuclear structures, for example, the abducting
nerve. Impaired consciousness is a manifestation of dysfunction of the hemispheres,
upper parts of the brain stem or both at the same time.
Metabolic or infectious diseases can have an inhibitory effect on the function
of the hemispheres and brainstem through the pathological content of blood components or a direct toxic effect.
Impaired consciousness can also be observed in cerebrovascular accident or in
changes in the bioelectric activity of the brain, epilepsy. Inadequate brain blood flow
and chemical blood imbalances may also cause impaired electrical activity in the
brain. Concussion and psychological disorders cause impaired consciousness without
visible structural brain changes. Impaired consciousness can be short-term or profound. Short-term loss of consciousness is observed in syncopations. In convulsive
seizures, loss of consciousness can last longer, and in concussion, it can last up to
24 hours. Prolonged impairment of consciousness is observed in intracranial pathology or metabolic disorders.
Acute and subacute disorders of consciousness:
deafening: manifested by a decrease in wakefulness and usually accompa-
nied by sleepiness;
nullification (“nebula of consciousness”, English clouding of conscious-
ness) — a slight degree of stunning, slowing down reactions and a “clouded” percep-
tion of reality;
moderate deafening — partial disorientation, moderate drowsiness, execu-
tion of all commands;
deep deafening — disorientation, deep drowsiness, execution of only simple
commands;
sopor — severe depression of consciousness and pathological sleep, lack of
fulfillment of instructions by patients, it is possible to obtain an eye opening reaction
with strong stimulation (to pain or sound). In sopor, there is a deep oppression of
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consciousness, in which speech communication with the patient is impossible. Coordinated protective reactions have been preserved — opening the eyes to pain, sound
and other irritations. The patient is drowsy, lying with his eyes closed. It is possible
to remove it from the state of sleepiness with the help of various stimulations;
stupor is a concept in English literature similar to sopor. In addition, the
term is used in psychiatry to refer to a state of immobilization with mutism and
weakening reactions to irritations (including pain);
action editredlink — a slight violation of consciousness, in which the pa-
tient often falls asleep, slowed down, but adequate reactions can be caused by shortterm external stimuli.
Coma is characterized by a lack of reaction and the impossibility of awakening:
a) coma I: consciousness is lost, the patient does not open his eyes, in response
to pain irritations he responds with uncoordinated protective movements without localizing pain;
b) coma II, deep: consciousness is lost, there is no reaction to pain and sponta-
neous movements;
c) coma III, exorbitant: consciousness lost, bilateral mydriasis, areflexia, mus-
cular atonia, catastrophic state of vital functions.
Chronic disorders of consciousness:
1) akinetic mutism: sick in clear consciousness, lying motionless with his eyes
open, not talking or answering questions. All motor functions are suppressed (except
for movements that fix the eyeballs).
2) apallic syndrome (awake coma) — a state in which consciousness remains
preserved, the patient's eyes are open, he rotates them in the eye sockets, but does not
fix the gaze, there are no speech and emotional reactions, verbal commands are not
perceived by the patient and contact with him is impossible, but the patient does not
lie motionless;
3) “locked person” syndrome (isolation syndrome): reflects the patient's condi-
tion in which consciousness is preserved, but contact with it is impossible due to bilateral paralysis of all parts of the body, with the exception of movements with which
the patient encodes his response. Various diseases can lead to this condition, which is
the result of a bilateral lesion of the cortico-spinal tract between the midbrain and the
varolium bridge or massive damage to the lower motor neurons (anterior antlers of
the spinal cord). A given state is also sometimes called a pseudocome;
4) autonomic state — the absence of the possibility of spontaneous mental ac-
tivity due to extensive damage or dysfunction of the cerebral hemispheres with the
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preservation of the activity of the diencephalic region and the brainstem, preserving
motor reflexes and the sleep-wake cycle;
5) brain death — a state of complete loss of consciousness and all brain
functions.
Mind-darkening syndromes in psychiatry.
Darkening consciousness, disorders of reflection of environmental reality:
amenative syndrome;
the aura of consciousness;
delirious syndrome;
oneuroid syndrome;
twilight darkening of consciousness.
The most common causes of impaired consciousness.
The effect of lateral displacement of the median structures of the brain on
the level of loss of consciousness:
1) 0–3 mm — complete consciousness (alert);
2) 3–4 mm — drowsiness (drowsy);
3) 6–8.5 mm — stupor (stuporous);
4) 8–13 mm — coma (comatose).
Pathological conditions leading to displacement of the median structures of
the brain and impaired consciousness:
supratentorial volumetric processes;
epidural hematoma;
subdural hematoma;
cerebral infarction or intracerebral hemorrhage;
brain tumor;
brain abscess;
subtentorial lesions;
cerebral stem infarction;
a brain stem tumor;
cerebral stem hemorrhage;
cerebellar hemorrhage;
brain stem injury;
diffuse and metabolic brain disorders;
injury (concussion, brain injury or bruises);
anoxia or ischemia (syncopations, cardiac arrhythmia, pulmonary infarction,
shock, pulmonary insufficiency, carbon monoxide poisoning, vascular collagen diseases);
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epilepsy;
condition after epileptic seizure;
infections (meningitis, encephalitis);
subarachnoid bleeding;
exogenous toxins (alcohol, barbiturates, glutetimide, morphine, heroin, me-
thyl alcohol, hypothermia);
endogenous toxins and metabolic disorders (uremia, hepatic coma, diabetic
acidosis, hypoglycemia, hyponatremia);
psychomotor epileptic status.
Brain death. The possibility of conducting mechanical ventilation to maintain
the activity of the lungs and heart for a long time is largely based on the diagnosis of
human death by the complete absence of brain activity and brain stem structures. In
order to establish the diagnosis of “brain death, the doctor” should be based on
knowledge of the structural or metabolic causes of brain death, while excluding the
possibility of the influence of anesthetic or paralyzing drugs, especially those taken
by patients on their own. In this case, attention should be paid to reliable signs of
clinical and biological death.
Signs of clinical death include coma, apnea, lack of pulse on the main arteries.
This triad concerns the early period of death (when several minutes have passed since
asystole) and does not apply to those cases when there are already distinct signs of
biological death. The shorter the period between the statement of clinical death and
the start of resuscitation measures, the greater the chances of life in the patient, therefore, diagnosis and treatment are carried out in parallel.
Coma is diagnosed based on lack of consciousness and pupil reflex.
Apnea is recorded visually by the absence of respiratory movements of
the chest.
The absence of pulse on the main vessels can be observed with asystole, ventricular fibrillation or electromechanical dissociation.
Additional signs of clinical death are:
wide pupils;
areflexia (no corneal reflex and pupil reaction to light);
pallor, cyanosis of the skin.
Biological death (true death) represents an irreversible cessation of physiological processes in cells and tissues. Over time, the possibilities of medicine for resuscitating dead patients change. Therefore, signs of biological death at each stage of the
development of medicine are specified.
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Early signs of biological death include the appearance of a symptom of Beloglazov (cat's eye): with lateral compression of the eyeball, the pupil transforms into
a vertical fusiform gap, similar to a cat's pupil (10–15 minutes).
Late signs of biological death include:
drying of the skin and mucous membranes;
cooling (decreased body temperature after death);
cadaveric spots in sloping places;
cadaveric mortification;
autolysis (decomposition).
2.6. EXAMINATION OF THE STATE OF THE SENSES —
VISION, TASTE, HEARING
Vision research. There are two types of visual perception — central and pe-
ripheral. Central vision is provided by the central part of the retina, where nerve cells,
cones, are located, which are responsible for vision clarity and color perception. Pe-
ripheral vision is responsible for the nerve cells of the retina, rods, which allow a person to better navigate space and see in low light.
To separate peripheral vision from the central one, you should find an object in
the room, fix the look on it. However, in addition to this object, some other objects
that are nearby also come into view. These objects are not clearly seen, because the
look is fixed on another object. Peripheral vision is necessary for the perception of
objects located not in the field of central vision. Peripheral vision boundaries are
normally considered to be a field of 120°.
When the work of some areas of the retina weakens, the field of vision narrows, in some cases, peripheral vision may disappear altogether. This pathology is
called tunnel vision.
Causes of peripheral vision impairment may be:
1) glaucoma. This disease appears due to an increase in intraocular pressure,
leads to a deterioration in the visual field. At the initial stage, peripheral vision narrows, and when the disease develops, it is completely impaired, then central vision
deteriorates, as a result — complete blindness;
2) retinal damage, in which nerve cells of the eye suffer, as a result, the periph-
eral field of vision is narrowed. For example, detachment, dystrophy, dissection, retinal degeneration;
3) weak vascular circulation of the optic nerve, as well as various types of eye
tumors;
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