Coma in children: causes, symptoms, diagnosis, treatment

Coma (Greek kota - deep sleep) is a syndrome characterized by impaired consciousness, absence of mental activity, impaired motor, sensory and somatovegetative functions of the body. Unlike adults, coma in children occurs more often due to anatomical and physiological features. It accompanies severe forms of various somatic, infectious, surgical, neurological and mental diseases.

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Causes of coma in children

In the development of comatose states, the main factors are hypovolemia, hypoxia, hypoglycemia, disturbance of the VEO and AOS, toxic and traumatic brain damage. In total, these effects lead to edema-swelling of the brain, closing the vicious circle of the pathogenesis of comatose states.

Hypovolemia

Plays a leading role in many types of coma in children and is the cause of irreversible changes in the brain. CNS metabolism is determined by blood flow. The critical level of cerebral perfusion is 40 mm Hg (at a lower level, blood circulation inside the brain is sharply disrupted until it stops completely).

Hypoxia

Brain tissue is very sensitive to oxygen deficiency, since it consumes 20 times more than skeletal muscles and 5 times more than the myocardium. Cardiovascular and respiratory failure usually lead to oxygen starvation of the brain. A decrease in blood sugar levels also significantly affects its functional state. When its level in the blood is below 2.2 mmol/l (in newborns below 1.7 mmol/l), loss of consciousness and seizures are possible. Water and electrolyte imbalance also impairs brain function. Impaired consciousness and the development of coma are possible both with a rapid decrease in blood plasma osmolarity (from 290 to 250 mosm/l and below) and with its increase (> 340 mosm/l). Hyponatremia (< 100 mmol/l), hypokalemia (< 2 mmol), hypokalemia (> 1.3 mmol/l), as well as an increase in the concentration of potassium (> 8-10 mmol) and magnesium (> 7-8 mmol/l) in the blood plasma are accompanied by loss of consciousness due to impaired cardiac function, hypocalcemic seizures or the development of so-called magnesium narcosis.

Brain injuries

Brain trauma associated with its direct mechanical damage due to a blow (concussion or contusion of the brain) or compression (for example, fluid or hematoma) leads to both morphological and functional disorders of the central nervous system. Trauma is always accompanied by diffuse or local cerebral edema, which worsens cerebrospinal fluid and blood circulation, contributing to brain hypoxia and aggravation of its damage.

Toxic encephalopathy has been a subject of research for many years in a variety of diseases. Most likely, the pathogenetic significance is not of one toxic substance, but of a complex of causes. At the same time, in the case of poisoning with neurotropic poisons or drugs, their triggering role is beyond doubt.

The most probable cause of coma in infants is primary or secondary CNS lesions due to an infectious process (meningitis, encephalitis, generalized infectious toxicosis). In preschool age, as a rule, poisoning, and in children over 6 years old - head trauma. Regardless of age, depression of consciousness is possible due to metabolic disorders (including hypoxia).

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Coma in children with infectious diseases

Impaired consciousness, convulsions, and hemodynamic disorders are typical manifestations of infectious toxicosis.

The resulting toxic-hypoxic brain damage is caused by the combined effects of circulatory disorders, imbalance of the VEO and AOS, DIC syndrome, organ failure, PON and other manifestations of the disease. Toxic syndrome in acute infections in children can be in the form of neurotoxicosis (encephalic reaction), shock (infectious-toxic or hypovolemic), toxicosis with exicosis (dehydration).

The choice and sequence of drug administration depend on the specific form of the pathological syndrome. The basic treatment regimen for coma developed during infectious toxicosis consists of a number of stages: anticonvulsant therapy (in the presence of convulsions); support of vital functions (apnea, circulatory arrest); antishock therapy (in the presence of shock); detoxification; correction of VEO and AOS; stabilization of hemostasis; control of cerebral edema and hypoxia; etiotropic and symptomatic therapy; rehydration (in exicosis).

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By origin, there are:

• somatogenic coma caused by pathology of internal organs or intoxication (metabolic or infectious-toxic encephalopathy);
• cerebral (brain) or neurological coma resulting from primary damage to the central nervous system.

Primary comas (with direct damage to the brain tissue and its membranes) and secondary comas (associated with dysfunction of internal organs, endocrine diseases, general somatic diseases, poisoning, etc.) are also distinguished. In addition, the following clinically significant designations are used: supratentorial, subtentorial and metabolic comas. Since coma may be accompanied by increased intracranial pressure, edema and dislocation of brain structures, a distinction is made between "stable" (with metabolic disorders, such as liver failure) and "unstable" comas (with traumatic brain injury, meningitis and encephalitis).

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Symptoms of Coma in Children

The defining clinical symptom of coma in a child is loss of consciousness.

The younger the child, the easier it is for him to develop comatose states with relatively equal impacts. At the same time, the compensatory capabilities and plastic reserve of brain tissue in young children are significantly higher than in older children and adults, so the prognosis for coma is more favorable, and the degree of restoration of lost CNS functions is more complete.

V. A. Mikhelson et al. (1988) propose to distinguish between somnolence, delirium, stupor, coma proper and terminal coma.

Somnolence, stupor - the patient sleeps, can be easily awakened, can answer questions correctly, but then immediately falls asleep. This condition is typical in cases of poisoning with barbiturates, neuroleptics. Young children quickly lose the skills achieved in accordance with their age.

Delirium - the patient is excited, can move, but consciousness is lost with loss of orientation in space and time, there is an abundance of visual and auditory hallucinations. Inadequate. Delirium usually accompanies the height of severe forms of acute infections, observed in poisoning with atropine, some plants (fly agaric).

Stupor - consciousness is absent, the patient is disoriented, immobilized, catatonia is possible - freezing in bizarre poses (waxy tone). Often observed with severe hydration.

Sopor - consciousness is absent, but inadequate, monosyllabic speech is possible in the form of mumbling in response to a loud shout. Retrograde amnesia, motor reaction to strong, including painful, stimuli, without proper coordination, more often in the form of protective movements of the limbs, grimaces are characteristic. Pupillary reflexes are preserved. Tendon reflexes are increased. Pyramidal signs and tremor are noted. Urination and defecation are not controlled.

In essence, all the above-mentioned variants of impaired consciousness are varieties of precoma.

Coma is accompanied by a lack of speech contact, complete loss of consciousness - amnesia (forgetfulness), as well as muscle atony and areflexia in terminal coma.

Classification of coma is based on the level of brain damage (rostral-caudal progression):

1. diencephalic coma (decortication position);
2. midbrain coma (decerebrate position). The "doll's eyes" test is positive;
3. Upper trunk (lower area of the bridge). The "doll's eyes" test is negative, flaccid tetraplegia or dissociation of tendon reflexes and muscle tone along the body axis, pauses in inspiration (Biot type). Hyperthermia;
4. lower-stem coma. Bulbar disorders: absence of spontaneous breathing, drop in blood pressure, transition from tachycardia to bradycardia and cardiac arrest. Hypothermia. Pupils are wide, no photoreaction. Muscle atony.

Coming out of a coma

The period of recovery from a coma may vary in time: from almost instantaneous and complete restoration of consciousness and nervous functions to a multi-month or multi-year process, which may also end with complete restoration of the central nervous system functions or stop at any time with the preservation of a persistent neurological defect. Let us note the amazing ability of children to compensate for brain damage, so it is necessary to make a prognosis at the height of the comatose state with extreme caution.

Recovery from a deep and long-lasting comatose state often occurs gradually; the rate of recovery depends on the degree of brain damage. Complete recovery from a coma is not always observed, and months and years of active rehabilitation therapy are often required to restore CNS function. The following stages of recovery from a coma are distinguished:

• vegetative state (spontaneous breathing, blood circulation, and digestion are provided independently at a minimum level sufficient for life);
• apallic syndrome (Latin: pallium - cloak). There is a disordered change of sleep and wakefulness. The patient opens his eyes, the pupillary photoreaction is lively, but the gaze is not fixed. Muscle tone is increased. There are some manifestations of tetraparesis or plegia. Pathological reflexes are determined - pyramidal signs. There are no independent movements. Dementia (feeblemindedness). The function of the sphincters is not controlled;
• akinetic mutism - motor activity increases somewhat, the patient fixes his gaze, follows objects, understands simple speech and commands. Emotional dullness and a mask-like face are noted, but the patient can cry (in the sense of "shedding tears"). There is no independent speech. The patient is unkempt;
• restoration of verbal contact. Speech is poor, monosyllabic. The patient is disoriented, demented, emotionally disinhibited (tearfulness or aggression, anger are most often observed, less often - euphoria). He quickly becomes exhausted, tired. Bulimia, polydipsia are often observed due to the loss of the feeling of satiety. Partial restoration of neatness skills is possible;
• restoration of verbal functions, memory, speech, and intelligence. The prognostic significance is attributed to the postures that become distinct 2-3 weeks after the development of coma: decortication - bent upper and extended lower limbs (boxer's posture). When pressing on the sternum, the shoulders are adducted, the forearms and hands are flexed, the fingers are flexed, and the limbs are extended;
• decerebration - straightened arms and legs, hypertonicity of muscles, in the classic version - up to opisthotonus. These poses demonstrate the level of brain damage, overcoming which in the future will be given with great difficulty.

Only deep stages of coma with depression of the respiratory and vasomotor centers have independent pathological significance. In addition to complete loss of consciousness and development of areflexia, characteristic changes in breathing appear as the severity of the coma worsens. In decortication (coma I), the pathological Cheyne-Stokes type of breathing is observed, in decerebration (coma II), the Kussmaul type of breathing and rare, shallow breaths occur in the final stage. In parallel, hemodynamic parameters change: arterial pressure and heart rate progressively fall.

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Diagnosis of coma in children

To verify a comatose state in children, three main reference points are used: the depth of impaired consciousness, the state of reflexes, and the presence of a meningeal symptom complex. When objectively assessing the patient's consciousness, the following are important: the reaction to the doctor's voice, understanding of speech (its semantic meaning and emotional coloring), the ability to answer (correctly or incorrectly) the questions asked, to navigate in space and time, as well as the reaction to the examination (adequate and inadequate). If the patient does not react to the above techniques, pain stimuli are used (compression of the superficial tissues with fingers at pain points - in the projection of the sternocleidomastoid or trapezius muscle, injections or light pricks of the skin with a special clean needle).

Signs	Characteristic	Rating, points
Opening the eyes	Arbitrary	4
	At the shout	3
	For pain	2
	Absent	1
Motor reactions	Commands are being executed	6
	Repulsion	5
	Withdrawal	4
	Bending	3
	Extension	2
	Absent	1
Speech function	Correct	5
	Confused	4
	Shouts	2
	Absent	1
Photoreaction of pupils	Normal	5
	Slow motion	4
	Uneven	3
	Anisocoria	2
	Absent	1
Cranial nerve response	Saved	5
	No reflexes:	4
	Ciliary	3
	Corneal	2
	"doll eyes" from the trachea	1
Cramps	No	5
	Local	4
	General transients	3
	General continuous	2
	Complete relaxation	1
Spontaneous breathing	Normal	5
	Periodic	4
	Hyperventilation	3
	Hypoventilation	2
	Apnea	1

G. Teasdale, B. Jennet in 1974 proposed a scale for determining the depth of coma. It was called the Glasgow scale and is widely used in the practical work of resuscitation physicians. This scale evaluates the functions of the central nervous system on 7 positions.

To assess the severity of coma, the Glasgow scale and its modified version for hospitals, the Glasgow-Pittsburgh scale, are used.

The Glasgow scale is used to assess the nature of the response to voice and pain - by such signs as opening of the eyes, verbal and motor response. The maximum score is 15 points. If the score is below 9 points, the condition is considered extremely severe. The minimum possible score is 3 points. The Glasgow-Pittsburgh scale additionally assesses the reactions of the cranial nerves, the presence of seizures and the nature of breathing. The maximum score on this scale is 35 points. In case of brain death - 7 points. If the patient is on mechanical ventilation (i.e. it is impossible to assess such parameters as "spontaneous breathing" and "speech reactions"), the score on the scale is reduced to 25 points and 5 points, respectively.

As the severity of coma worsens, the conjunctival and corneal reflexes are the first to be suppressed. The fading of corneal reflexes is considered an unfavorable prognostic sign. Diagnostically significant information in assessing the severity of coma is provided by checking the oculocephalic reflex. If an unconscious patient does not show a concomitant movement of both eyes when turning his head to the right and left and the gaze seems to be fixed on the midline (doll's eye effect), this indicates a pathology of the cerebral hemispheres (coma I) and the absence of damage to the brainstem.

To assess the condition of children in a coma, it is necessary to check Brudzinski's and Babinski's symptoms. The appearance of a unilateral Babinski's reflex in a child in a coma indicates a focal lesion of the brain on the side opposite to the limb being tested. A bilateral reflex with subsequent fading indicates a deepening of the coma, regardless of the local lesion of the brain tissue. In case of spinal lesions, the reflex is not determined. Positive Brudzinski's symptoms detected in a child in a coma indicate irritation of the membranes (meningitis, meningoencephalitis, subarachnoid hemorrhage). In addition, it is necessary to assess changes in the diameter of the pupils, movements of the eyeballs and the fundus, especially paying attention to possible asymmetry (the result of focal lesions of the brain tissue!). In metabolic comas, the reaction of the pupils to light is preserved.

The necessary diagnostic procedures (including those at the pre-hospital stage) include ECG assessment, determination of hemoglobin concentration, glycemia level, detection of ketonuria, testing for the presence of psychotropic drugs in urine and ethanol in saliva (using a visual test strip), as well as CT and MRI.

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Emergency care for coma in children

In case of stage II-III coma complicated by circulatory failure, after 100% O ₂ hyperoxygenation, tracheal intubation with preliminary premedication with atropine is performed. One should not forget about possible injury to the cervical spine, therefore its immobilization is necessary. A tube is inserted into the stomach to aspirate the contents and decompress it. Then, rheopolyglucin or crystalloids are infused at a rate that ensures maintenance of systolic blood pressure of more than 80 mm Hg in older children, and in case of traumatic brain injury, to maintain cerebral perfusion by 10 mm Hg above the lower limit of the age norm. If the airway is not protected, the patient is placed on his side (half-turned) during transportation. Monitoring of body temperature and diuresis is mandatory (possibility of bladder rupture!).

If hypoglycemia is suspected, a 20-40% glucose solution is administered. To prevent Wernicke's encephalopathy, thiamine should be administered before infusion of glucose solutions. To protect neurons in the brain of adolescents in a coma, modern antioxidants can be used: Semax, Mexidol, or Methylethylpyridinol (Emoxipin).

Such patients are also prescribed antihypoxants, such as actovegin. Antioxidants (ascorbic acid) and, in addition, preenergy protectors (reamberin and cytoflavin) are continued to be administered. In hospital, to activate reception, it is advisable to supplement the treatment with central cholinomimetics. For example, choline alfoscerate (gliatilin). It is not recommended to use respiratory analeptics and psychostimulants.

Patients in coma are subject to emergency hospitalization in the intensive care unit. It is extremely important to determine the need for consultation and surgical treatment in a neurosurgical hospital (supratentorial coma in traumatic brain injury, intracerebral and subdural hematomas, subarachnoid hemorrhage).

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