Examination of patients in a coma

Coma is the most profound oppression of consciousness, in which the patient is unable to enter into verbal contact, execute commands, open eyes and react in a co-ordinated manner to pain stimuli. The coma develops with a bilateral diffuse lesion (anatomical or metabolic) of the cortex and subcortex of the cerebral hemispheres, brainstem or with combined lesions at these levels.

General principles of the survey

When examining patients who are in a coma, it is advisable to follow the following steps.

• Evaluation of vital (vital) functions - breathing and circulation. Determine the patency of the respiratory tract, the nature of breathing, the presence of pathological types of breathing; frequency, filling and rhythm of pulse; arterial pressure.
• Assessment of the degree of oppression of consciousness (depth of coma).
• A brief elucidation of the circumstances of the development of the coma, the factors preceding it, and the rate of disturbance of consciousness.
• General examination of the patient, in which special attention should be paid to signs of trauma (abrasions, bruises, swelling, etc.); bleeding from the ears and nose; presence of periorbital hematoma; change in color, humidity, skin temperature; odor from the mouth ; body temperature; any other symptoms of acute pathology.
• A brief neurologic examination, in which special attention is fixed on stem reflexes ( pupillary responses, position and movements of the eyeballs); posture, muscle tone, deep reflexes, pathological signs, involuntary motor activity; symptoms of irritation of meninges.

Examination of a patient in a coma is necessary to combine with the implementation of urgent measures to eliminate life-threatening respiratory and circulatory disorders.

Evaluation of vital functions

The vital functions are primarily respiration and circulation. Assess the patency of the respiratory tract, the characteristics of breathing, heart rate and blood pressure. The results of such an assessment are extremely important for timely correction of the revealed violations.

Patients in a coma often identify pathological types of respiration. According to the variant of respiratory failure, it is possible to assume localization, and sometimes also the nature of the pathological process.

• Cheyne-Stokes breathing is a series of gradually increasing and then decreasing in frequency and depth of breaths alternating with periods of shallow breathing or short-term stops of breathing (the amplitude and frequency of respiratory movements increase and decrease in wave form until the respiratory movement appears paused). The periods of hyperpnoea are longer than the periods of apnea. The Cheyne-Stokes breathing testifies to the defeat of the hypothalamic (diencephalic) region or to the bilateral dysfunction of the cerebral hemispheres. Observed with metabolic disorders, rapid increase in intracranial pressure, somatic diseases (for example, with severe heart failure).
• Superficial slowed, but rhythmic breathing is characteristic for someone who developed against a background of metabolic disorders or toxic effects of drugs.
• Kussmaul's breathing is a deep and noisy breathing, characterized by rhythmic rare breathing cycles, a deep noisy inspiration and an exhaled breath. It is typical for ketoacidotic, hepatic, uremic coma and other conditions, accompanied by metabolic acidosis ( lactic acidosis, poisoning with organic acids). Hyperventilation can also occur with respiratory alkalosis ( hepatic encephalopathy, salicylate poisoning) or hypoxemia.
• True central neurogenic hyperventilation ("mechanical respiration") is a rapid (more than 30 per minute) rhythmic deep breathing, usually with a reduced amplitude of the chest excursion; occurs with dysfunction of the bridge of the brain or the midbrain and usually serves as an unfavorable prognostic sign, since it indicates a deepening of the coma. The neurogenic nature of hyperventilation is established only after the exclusion of its other possible causes, which were mentioned above.
• Apneal breathing is characterized by an extended inhalation followed by a delay in breathing at inspiratory height ("inspiratory spasm") and has a topical significance, indicating a focus in the brain bridge region (for example, occlusal occlusion of the basilar artery).
• Cluster Breathing: periods of rapid irregular breathing alternate with periods of apnea; can resemble the Cheyne-Stokes breathing, combined with various variants of difficulty breathing. It occurs when the upper sections of the medulla oblongata or the lower sections of the bridge are affected and serves as a threatening sign. One option is breathing of the Biota: frequent even breathing movements, separated by periods of apnea. It is characteristic for the defeat of the bridge of the brain.
• Atactic breathing, characterized by a non-rhythmical alternation of deep and shallow breathing with pauses, occurs when the medulla oblongata (respiratory center) is damaged. This increases the sensitivity of cerebral structures to sedative and other medicinal substances, increasing the dose of which easily causes respiratory arrest. Such breathing is usually preterminal.
• Agonal sighs are single rare, short and deep convulsive respiratory movements on the background of apnea; arise during the agony and usually precede the complete cessation of breathing.

[1], [2], [3]

Blood pressure and pulse

Reduction in blood pressure can occur not only because of the pathological conditions that led to coma (internal bleeding, myocardial infarction ), but also due to oppression of the medulla oblongata (alcohol and barbiturate poisoning). Arterial hypertension also can either reflect the process that led to coma, or be a consequence of dysfunction of stem structures. Thus, an increase in intracranial pressure leads to an increase in systolic and diastolic blood pressure, with the pulse usually slowed down. The combination of arterial hypertension with bradycardia (Cushing phenomenon) indicates an increase in intracranial pressure.

[4], [5],

Estimation of the depth of coma

The most famous rapid quantitative method for determining the depth of coma is the use of the Glasgow coma scale. In accordance with this approach, the definition of the severity of oppression of consciousness is based on an assessment of the patient's reactions: eye opening, speech reaction, motor reaction to pain. The total score for the Glasgow Coma Scale can range from 3 to 15 points. A score of 8 or lower indicates a coma. Using this scale allows only a preliminary estimate of the depth of the disorder of consciousness; a more accurate conclusion is made after a neurologic examination.

• The mild (1st degree) coma is characterized by the appearance of general motor anxiety or by the withdrawal of the limb in response to the pain stimulus, the reflex response in the form of sneezing when the nasal mucosa is irritated with cotton wool soaked with ammonia; mimic reactions on the same side while percussion of the zygomatic arch. The corneal reflexes and pupillary responses to light are preserved, swallowing is not disturbed, breathing and circulation are sufficient to maintain the vital activity of the organism. Urination is involuntary; possible retention of urine.
• Expressed (II degree) coma is characterized by a complete lack of motor reaction to sound and moderate pain stimuli and the emergence of protective reflexes to strong pain stimuli. Observe pathological types of breathing, arterial hypotension and heart rhythm disturbances. Pupils are often narrow, rarely broad, their reactions to light and corneal reflexes are weakened. Swallowing is disturbed, but when the liquid enters the respiratory tract, there are coughing movements, indicating partial safety of bulbar functions. Deep reflexes are depressed. They reveal grasping and proboscis reflexes, a symptom of Babinsky.
• Deep (III degree) coma is characterized by the extinction of all, including vitally important, reflex acts. Typical inadequate breathing (bradypnoea with a frequency of less than 10 per minute, etc.), weakness of cardiac activity (collapse, arrhythmia, cyanosis of the skin and mucous membranes), lack of motor reactions, muscle hypotension. Eyeballs are in neutral position, pupils are wide, their reaction to light and corneal reflexes are absent, swallowing is disturbed.

[6], [7], [8]

Clarification of the development of coma

Find out from relatives or people surrounding the patient information about the circumstances of the development of coma, the rate of impairment of consciousness and the diseases that the patient suffered. This information is important for determining the cause of coma.

• The presence of a history of stroke, arterial hypertension, vasculitis or heart disease (may indicate a vascular nature of coma).
• In a patient with diabetes mellitus coma may be a consequence of diabetic ketoacidosis (ketoacidotic coma), hyperosmolar non-ketogenic state (hyperosmolar coma), lactate-acidosis (hyperlactacidemic coma), insulin-induced hypoglycemia (hypoglycemic coma).
• A coma in a patient with epilepsy may be the result of an epileptic status or a craniocerebral injury that occurs during a seizure.
• Indication of a recently received head injury suggests such causes of coma, as a brain contusion, intracerebral hematoma, diffuse axonal damage.
• Indications for alcoholism in the anamnesis increase the likelihood of alcohol coma, hepatic coma, encephalopathy of Gaye-Wernicke, and also allow one to suspect head injury as one of the possible causes of coma.
• Coma can be a consequence of an overdose of insulin, sedatives and hypnotics, antidepressants, neuroleptics, drugs, barbiturates.
• When infections are possible as metabolic (with meningitis, encephalitis, sepsis, neurosarcoidosis), and structural (with herpetic encephalitis, brain abscess with the development of a dislocation syndrome) causes coma.

[9], [10], [11], [12]

General examination of the patient

Examination of the skin and mucous membranes, as well as the examination of the chest, abdomen and extremities, conducted according to general rules, are aimed at identifying specific for certain manifestations.

• It is necessary to carefully examine the patient for signs of trauma (bleeding, bruising, bruising, swelling of the tissues). Thus, the signs of fracture of the base of the skull may be a symptom of Battle (hematoma in the mastoid region), local soreness, hemorrhage in the conjunctiva and in the peri-ocular cellulose ("glasses"), bleeding and liquorrhea from the ear and nose.
• When evaluating the skin condition, the "spiders", abrasions, venous pattern, injections injected are found to be of differential diagnostic significance; the condition of the skin turgor, its dryness or humidity. Pink or scarlet skin is characteristic for carbon monoxide poisoning and cyanide compounds, icteric skin for liver diseases, a yellowish-ashy shade of the skin with a whitish shade on the lips for uremia, a sharp pallor for anemia and internal bleeding, bluish skin with an aspidum gray or black-blue shade - for poisoning with methhemoglobin-releasing poisons, brown skin - for bromide poisoning.
• Important information about the condition of sclera, the tone of eyeballs, body temperature, color of vomit.
• The density of the eyeballs is determined by pressing the pulp of the nail phalanx of the index finger on the eyelids. Decrease in skin turgor and density of eyeballs are detected with uremia, chlorination, food poisoning, alimentary dystrophy, hyperglycemia, dehydration of the organism of any genesis. On the contrary, in those with severe craniocerebral trauma, even with a sharp decrease in hemodynamic parameters, the density of eyeballs is increased, and the possibility of their displacement into the depth of the orbit is limited. Injected sclera is most often observed with subarachnoid hemorrhage, epilepsy, fat embolism of cerebral vessels, alcohol intoxication.
• Multiple whitish scars on the lateral surfaces of the tongue with fresh bites are formed due to repeated convulsive seizures.
• Hyperthermia is observed in meningitis, encephalitis, septic thrombosis of cerebral sinuses, thyrotoxicosis, food poisoning, pneumonia, dehydration, poisoning with atropine-like drugs and tricyclic antidepressants, intracranial hematomas with symptoms of brainstem and hypothalamus. Hypothermia is typical for chlorphenia, uremia, alimentary depletion, adrenal insufficiency, as well as for poisoning with barbiturates, tranquilizers.

Evaluation of neurological status

The neurological examination is aimed at assessing the general motor reactions, stem reflexes and the detection of symptoms of irritation of the meninges.

[13], [14],

Motor sphere

We assess the patient's posture, muscle tone and deep reflexes, spontaneous and provoked motor activity.

Pathological poses:

• If the patient lies in a natural position, as in a normal dream, one can think of a shallow coma, which is confirmed by the preservation of yawning and sneezing. Other reflex acts in the form of coughing, swallowing, or hiccups are preserved even with deeper depression of consciousness.
• The patient in a coma is sometimes observed pathological poses, mostly flexor or extensor. Sometimes they use such terms, borrowed from pathophysiology, as "decortication" and "decerebration rigidity". With decortication rigidity, the hands are brought to the trunk, bent at the elbow and wrist joints, the brushes are supine; legs unbent in the hip and knee joints, rotated inward, the feet are in the position of plantar flexion. This posture develops as a result of the loss of inhibitory cortico-spinal influences and points to the lesion above the midbrain. In case of decerebral rigidity, the head is thrown back (opisthotonus), the teeth are clamped, the arms are bent and rotated to the inside, the fingers are bent, the legs are straightened and rotated to the inside, the feet are in the position of plantar flexion. When pinching the skin on the trunk and limbs, protective spinal reflexes appear, which in the legs often have the form of triple flexion (in the hip, knee and ankle joints). Decerebral rigidity indicates a lesion of the upper part of the brainstem at the level between the red and vestibular nuclei with the loss of central inhibitory influences on peripheral motoneurons with disinhibition of descending vestibular tonic pulses. The decortication pose, as compared with the decerebral pose, indicates a more rostral localization of the lesion and a more favorable prognosis, nevertheless it is impossible to reliably judge the localization of the lesion focus only by the patient's posture.
• Diagnostic value can have asymmetry of the position of the limbs, unusual posture of individual parts of the body. Thus, in a patient with hemiplegia, which developed as a result of damage to the inner capsule and nodes of the base of the brain, the tone of the muscle in the affected limbs in the acute period of the disease is reduced. If such a patient is in a coma, then his foot on the side of paralysis is rotated outwards (a symptom of Bogolepov). Fixed deviation of the head posteriorly and to the side is often noted in patients with tumors of the posterior cranial fossa. A pose with an upturned head and a curved back is often a sign of irritation of the meninges (with subarachnoid hemorrhage, meningitis). Bringing the legs to the abdomen is observed in many patients with uremic coma.

Muscle tone and spontaneous movement

• Repeated twitching of the muscles of the face, fingers and / or feet can be the only manifestation of an epileptic fit. The unfolded epileptic seizures do not have topico-diagnostic significance, however they indicate the preservation of the cortico-muscular path.
• Multifocal myoclonic seizures are often a sign of metabolic brain damage (azotemia, drug poisoning) or late stage of Creutzfeldt-Jakob disease. Asterixis also indicates metabolic encephalopathy (with uremia, liver failure).
• The preservation of complex reflex acts, such as defensive movements and other purposeful actions (such as scratching the nose in response to the tickling of the nostrils), indicates the safety of the pyramidal system on the appropriate side. The absence of automated movements in one limb in a comatose patient indicates paralysis of this side.
• Hormonal convulsions (attacks of increasing muscle tone, usually in the paralyzed limbs and following one another with short pauses) are observed with hemorrhage in the ventricles of the brain. The duration of such tonic spasms ranges from a few seconds to several minutes. Typically, a paroxysmal increase in the tone in the arm encompasses the adductor muscles of the shoulder and the pronotals of the forearm, and in the legs-the driving muscles of the thigh and the extensors of the shin.

Initiated motor activity - movements that arise reflexively in response to external stimulation (injections, tweaks, strokes).

• When the pain stimulus causes a purposeful withdrawal of the limb without its pronounced flexion, one can think of the preservation of the cortico-muscular path to this limb. If a similar targeted diversion occurs in all limbs with their pain stimulation, then the motor disorders in the patient are minimal. Thus, the retraction of the limb is a sign of the relative preservation of the motor system. On the contrary, if, in response to irritation of the limbs, a patient in a coma takes stereotyped poses, this indicates a severe bilateral defeat of pyramidal systems.
• The detection of the grasping reflex upon irritation of the palmar surface of the hand indicates the defeat of the opposite frontal lobe.
• The phenomenon of confrontation with the emergence of resistance to passive limb movements is characteristic of diffuse lesions of the anterior parts of the brain due to metabolic, vascular or atrophic pathological process.
• Normal muscle tone and safety of deep reflexes testify to the intactness of the cortex and cortico-spinal tract. The asymmetry of the muscle tone and reflexes is observed in the supratentorial localization of the lesion; it is not characteristic of a metabolic coma. Symmetrical reduction of muscle tone and depression of deep reflexes are typical for metabolic coma. The changing muscle tone and reflexes are usually observed with epileptic seizures and with psychiatric pathology.

Stem reflexes play an important role in the evaluation of the cerebral coma and reflect the degree of preservation of the cranial nerve nuclei (while deep reflexes in the limbs are spinal reflexes, so their diagnostic significance in patients in coma is limited). Violation of stem reflexes with a high probability indicates that depression is associated with dysfunction of the ascending activating system of the reticular formation of the brain stem. On the contrary, the safety of stem reflexes indicates intact stem structures (coma, most likely, is associated with extensive bilateral lesions of the cerebral hemispheres). To evaluate the function of the brain stem, the pupil responses, the corneal reflex and the movements of the eyeballs are examined first.

• Assess the pupil size and shape of the pupils, their direct and friendly reaction to light.
• One-sided dilatation of the pupil with no response to light in a patient in a coma (Hutchinson's pupil) most often indicates the compression of the oculomotor nerve as a result of temporo-tentorial wedging, especially if the pupil dilates with the deviation of the eyeball down and out. Less commonly, the enlarged and non-responsive pupil is observed in the defeat or compression of the midbrain itself.
• Bilateral point pupils with a weak reaction to light (for the evaluation of pupillary reactions using a magnifying glass in this case) testify to the defeat of the brain bridge cover with the descending sympathetic paths passing in this region (the sympathetic innervation of the pupils is lost and the parasympathetic nucleus begins to predominate, since the Edinger-Westphal nuclei remain intact).
• Bilateral fixed mydriasis (wide areactive pupils 4-6 mm in diameter) is observed with a gross defeat of the midbrain with destruction of parasympathetic nuclei of the oculomotor nerve, as well as in botulism and poisoning with atropine, cocaine, and fungi.
• The reaction of pupils to light can serve as a clue in determining the cause of coma. At metabolic disturbances of pupils' reaction to light in a coma in a coma most often remains, even in the absence of all other neurological reactions (with the exception of hypoxic encephalopathy and poisoning with anticholinergic drugs), while in focal lesions of the brain they disappear early. For example, in patients with traumatic brain injury, the weakened response of pupils to light is almost always observed and does not indicate a poor prognosis.
• Preservation of pupillary reactions is a sign of the integrity of the midbrain. Equal-sized and light-responsive pupils indicate the toxic / metabolic nature of coma, with some exceptions. Metabolic causes of fixed mydriasis are hypoxic encephalopathy and poisoning with anticholinergics (atropine) or botulinum toxin. Drug poisoning, as well as the use of narcotic analgesics or pilocarpine, causes a narrowing of the pupils (miosis) with a weak reaction to light, which sometimes can be detected only by using a magnifying glass.
• Pay attention to the closure of the eyelids (that is, the safety of the connections between the V and VII pairs of sculls) and the symmetry of the corneal reflexes. For corneal reflexes, a different pattern is characteristic than for pupillary reactions to light: when poisoning with drugs depressing the central nervous system, the corneal reflex decreases or disappears quite early, while in coma due to traumatic brain injury, on the contrary, the disappearance of the corneal reflex indicates severity of injury and is an unfavorable prognostic sign. Thus, the preservation of pupillary reactions in a patient in a deep coma, in the absence of corneal reflexes and eye movements, allows one to suspect a metabolic disorder (for example, hypoglycemia ) or poisoning with medicinal agents (in particular barbiturates).
• Assessment of the position and movements of eyeballs. When lifting the eyelids of a patient in a coma, they slowly descend. With incomplete closure of the eyelids on one side, one can assume defeat of the facial nerve (nuclear defeat on this side or supranuclear on the opposite side). If the patient is not in a coma, but in a hysterical fit, then with a passive opening of the eyes, they are resisted. The preservation of blinking in a patient in a coma is evidence of the functioning of the reticular formation of the brain bridge. After the opening of the eyelids, the position of the eyeballs and the spontaneous movements of the eyes are evaluated. In healthy people in the waking state, the axes of the eyeballs are parallel, and in the drowsy state, the eyeballs deviate. In patients in a coma, eyeballs can occupy the position along the middle line, be diverged along the horizontal or vertical axis, or be withdrawn up / down or to the side.
• A persistent friendly outward spacing of the eyeballs may indicate a lesion of the ipsilateral hemisphere or the contralateral area of the brain bridge. When the frontal lobe of the cerebral hemisphere is destroyed (the frontal center of the horizontal gaze), the eyeballs "look" towards the lesion, "turning away" from the paralyzed limbs. The reflex movements of the eyeballs are preserved (that is, the deviation of the eyeballs in the defeat of the frontal lobe can be overcome with the help of a sharp turn of the head - the phenomenon of "pupal eyes" is preserved). When the center of the horizontal eye is defeated in the brain bridge cover, the eyes, on the contrary, "turn away" from the hearth and "look" at the paralyzed limbs. Overcoming the deviation of eyeballs by turning the head fails due to the depression of the vestibulo-ocular reflex (the phenomenon of "pupal eyes" is absent). There is only one exception to the rule, which states that with supratentorial lesions, the eye deviates towards the source of destruction: with a hemorrhage into the medial parts of the thalamus, an "incorrect" deviation of the eye may appear - the eyes "turn away" from the affected thalamus and "look" at the paralyzed limbs.
• The deviation of the eyeballs downwards in conjunction with the violation of their convergence is observed when the thalamus or the prefectural area of the midbrain is affected. Can be combined with the reactivity of the pupils (Parino syndrome). Usually occurs with metabolic coma (especially when poisoning with barbiturates).
• The divergence of the eyeballs along the vertical or horizontal axis, or the retraction of both eyeballs up / down or to the side, usually indicates a focal brain lesion.
• The deviation of one eyeball to the inside occurs when the lateral rectus muscle of the eye paralyzes and indicates the defeat of the abducent nerve (most likely in the region of its nucleus in the bridge of the brain). The deviation of both eyeballs to the inside develops as a result of bilateral defeat of the excretory nerves as a symptom throughout with intracranial hypertension. The deviation of one eyeball from the outside indicates a lesion of the medial rectus muscle of the eye in the failure of the function of the nucleus of the oculomotor nerve.
• The divergence of the eyeballs along the vertical with the deviation of the eyeball on the side of the lesion down and inside, and on the opposite side - upward and outward (the symptom of Hertwig-Magendie) is characteristic for the disturbance of the vestibular connections with the medial longitudinal fascicle. This symptom is observed in tumors of the posterior cranial fossa or in circulatory disorders in the brainstem and cerebellum, as well as in the localization of the tumor in the cerebellar hemispheres with pressure on the roof of the midbrain.
• The constant tonic deviation of the eyeballs down (the phenomenon of the setting sun) most often occurs with hydrocephalus with expansion of the third ventricle.
• Spontaneous movements of eyeballs. "Floating" movements of the eyeballs in the horizontal direction are sometimes observed with a slight coma; they do not have much significance for topical diagnostics. Their appearance indicates the preservation of stem structures (the nuclei of the third pair of cranial nerves and the medial longitudinal fascicle). The usual nystagmus for patients in coma is not typical, because the coma disturbs the interaction necessary for its development between the cochleovestibular apparatus of the trunk (formation of the slow phase of the nystagmus) and the cerebral hemispheres (formation of the rapid phase of the nystagmus) and there is no arbitrary fixation of the view.
• Reflex movements of eyeballs (oculocephalic or vestibulo-reflex reflex) are mediated by pathways going through the brainstem, so oppression of these reactions indicates damage to stem structures. Reflex movements of eyeballs cause breakdown of "pupal eyes" and less often - cold breakdown (introduction to the external auditory canal of cold water).

Meningeal symptoms (in particular, stiff neck) can be a sign of meningitis, brain trauma or subarachnoid hemorrhage. They should not be checked if there is a suspicion of a fracture of the cervical spine.