Coma in children: causes, symptoms, diagnosis, treatment

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

[1], [2], [3], [4]

The causes of coma in children

In the emergence of coma, hypovolemia, hypoxia, hypoglycemia, disturbance of VEOs and CBS, toxic and traumatic brain damage are of primary importance. In sum, these effects lead to edema-swelling of the brain, which closes the vicious circle of the pathogenesis of coma.

Hypovolemia

It plays a leading role in many variants of coma in children and is the cause of irreversible brain changes. Metabolism of the central nervous system is determined by the blood flow. The critical level of cerebral perfusion is 40 mm Hg. Art. (at a lower level, blood circulation inside the brain is severely disrupted until complete cessation).

Hypoxia

Brain tissue is very sensitive to lack of oxygen, because it consumes 20 times more than skeletal muscle, and 5 times more than myocardium. To oxygen starvation of the brain usually leads to cardiovascular and respiratory failure. Reducing the level of sugar in the blood also significantly affects its functional state. At a blood level below 2.2 mmol / l (in newborns below 1.7 mmol / L), loss of consciousness, convulsions, is possible. Water-electrolyte imbalance also worsens the work of the brain. Disturbance of consciousness and development of coma are possible both with a rapid decrease in osmolarity of blood plasma (from 290 to 250 mosm / L and below), and at its increase (> 340 mOsm / l). Hyponatremia (<100 mmol / L), hypokalemia (<2 mmol), hypokaladyema (> 1.3 mmol / L), as well as an increase in the potassium concentration (> 8-10 mmol) and magnesium (> 7-8 mmol / l ) in the blood plasma are accompanied by a loss of consciousness due to disruption of the heart, hypocalcemic convulsions or the development of so-called magnesia anesthesia.

Brain Injury

Trauma of the brain, associated with its immediate mechanical damage due to a stroke (concussion or bruise of the brain) or compression (for example, by liquid or hematoma), leads to both morphological and functional abnormalities of the CNS. Trauma is always accompanied by diffuse or local edema of the brain, worsening the liquor and blood circulation, which contributes to hypoxia of the brain and aggravation of its damage.

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

The most likely cause of coma in infants is the primary or secondary lesions of the central nervous system due to the infectious process (meningitis, encephalitis, generalized infectious toxicosis). At the preschool age, as a rule, poisoning, and in children older than 6 years - head trauma. Regardless of age, depression of consciousness is possible due to metabolic disorders (including hypoxia).

[5], [6], [7],

Coma in children with infectious diseases

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

The resulting toxic-hypoxic brain damage is due to the combined effects of circulatory disturbances, imbalance of VEO and CBS, 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 exsicosis (dehydration).

The choice and sequence of the use of drugs depend on the specific form of the pathological syndrome. The basic scheme of therapy for coma developed with infectious toxicosis consists of several stages: anticonvulsant therapy (in the presence of convulsions); support of vital functions (apnea, circulatory arrest); anti-shock therapy (in the presence of shock); detoxification; correction of VEO and CBS; stabilization of hemostasis; struggle with edema and hypoxia of the brain; etiotropic and symptomatic therapy; rehydration (with exsicosis).

[8], [9], [10], [11], [12],

By origin they distinguish:

• somatogenous coma due to pathology of internal organs or intoxication (metabolic or infectious-toxic encephalopathy);
• cerebral (cerebral) or neurological coma arising as a result of primary CNS damage.

Primary coma are also isolated (with direct damage to the brain substance and its membranes) and secondary (associated with insufficiency of the functions of internal organs, diseases of the endocrine system, obscheomatic diseases, poisoning, etc.). In addition, such clinically relevant designations are used: supratentorial, subtentorial and metabolic coma. Since coma may increase intracranial pressure, edema and dislocation of brain structures, distinguish between "stable" (in metabolic disorders, for example, in liver failure) and "unstable" coma (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 a loss of consciousness.

The smaller the age of the child, the easier it will develop comatose states with relatively equal strengths. At the same time, compensatory possibilities and plastic reserve of brain tissue in children of early age are significantly higher than in older children and adults, therefore, coma is more favorable in coma, and the degree of recovery of lost CNS functions is more complete.

VA Mikhelson et al. (1988) offer to distinguish between the doubt, delirium, sopor, actually to whom and the terminal coma.

Copulation, stunning - the patient sleeps, it can be easily awakened, he can correctly answer questions, but then immediately falls asleep. This condition is typical for poisoning with barbiturates, neuroleptics. Young children quickly lose their old-age skills.

Delirium - the patient is agitated, can move, but the consciousness is lost with the 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, is observed with atropine poisoning, some plants (fly agaric).

Stupor - there is no consciousness, the patient is disoriented, immobilized, catatonia phenomena are possible - congealing in freakish postures (waxy tone). Often observed with pronounced hydration.

Sopor - consciousness is absent, but possible inadequate, monosyllabic speech in the form of mutterings in response to a loud cry. Characteristic retrograde amnesia, motor reaction to strong, including pain, stimuli, without proper coordination, often in the form of defensive movements of the limbs, grimaces. Pupillary reflexes are preserved. Tendon reflexes are increased. There are pyramidal signs, tremor. Urination and defecation are not controlled.

In fact, all the above variants of the disturbance of consciousness are types of precoma.

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

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

1. diencephalic coma (decortication posture);
2. mid-cerebral coma (decerebrate posture). The puppet eyes test is positive;
3. upper-stem (lower area of the bridge). The puppet eye test is negative, flaccid tetraplegia or dissociation of tendon reflexes and muscle tone along the body axis, respiratory pause (Biota type). Hyperthermia;
4. lower-stem coma. Bulbar disorders: the absence of spontaneous breathing, the fall of blood pressure, the transition from tachycardia to bradycardia and cardiac arrest. Hypothermia. The pupils are wide, no photoreaction. Muscular atony.

Coming out of a coma

The period of coma release can vary in time: from almost instantaneous and complete restoration of consciousness and nervous functions to a multi-month or multi-year process, which can also end as a complete restoration of the CNS functions, and stop at any period while maintaining a persistent neurological defect. We note the amazing ability of children to compensate for brain damage, therefore, to build a prognosis at the height of the comatose state should be extremely cautious.

The way out of a deep and long-lasting comatose state often occurs gradually; The rate of exit depends on the degree of brain damage. Complete recovery from coma is not always observed, and it often takes months and years of active rehabilitation therapy to restore the function of the central nervous system. There are following stages of an exit from a coma:

• vegetative state (spontaneous breathing, blood circulation, digestion on a minimum level sufficient for life are provided on their own);
• Apallic syndrome (lat .: pallium - cloak). There is a disorderly change of sleep and wakefulness. The patient opens his eyes, the photoreaction of the pupils is alive, but the sight does not fix. Muscular tone is increased. There are some manifestations of tetraparesis or plethysm. Defined pathological reflexes - pyramidal signs. There are no independent movements. Dementia (dementia). The function of sphincters is not controlled;
• akinetic mutism - motor activity increases somewhat, the patient fixes his eyes, follows the objects, understands simple speech, commands. Emotional stupidity, a masklike face, is noted, but the patient can cry (in the sense: "pouring tears"). There is no independent speech. The patient is untidy;
• restoration of verbal contact. Speech scanty, monosyllabic. The patient is disoriented, demented, emotionally disinhibited (more often tearfulness or aggression, maliciousness, less often - euphoria). He is quickly exhausted, tired. Often observed bulimia, polydipsia due to loss of feeling of satiety. Perhaps a partial restoration of neatness;
• restoration of verbal functions, memory, speech, intelligence. Prognostic value has postures that become distinct 2-3 weeks after the development of coma: decortication - bent upper and bent lower limbs (boxer's pose). When pressing on the sternum, the shoulder should be reduced, the forearms bent, the wrists and bending of the fingers, the extension of the limbs;
• decerebration - unbent arms and legs, hypertonic muscles, in the classical version - to opisthotonus. These postures demonstrate the level of brain damage, the overcoming of which will later be given with great difficulty.

Only deep degrees of coma with oppression of the respiratory and vasomotor center have an independent pathological significance. In addition to complete loss of consciousness and the development of areflexia, as the coma severity worsens, characteristic changes in respiration appear. When dekortikatsii (coma I) observed pathological type of respiration Cheyne-Stokes, with decerebration (coma II), the type of respiration Kussmaul and rare, superficial breaths in the final stage. In parallel, the parameters of hemodynamics change: the blood pressure and the heart rate fall progrediently.

[14], [15], [16]

Diagnosis of coma in children

To verify the comatose state, children have three main reference points: the depth of the disturbance of consciousness, the state of reflexes, and the presence of a meningeal symptom complex. With an objective assessment of consciousness, the reaction to the doctor's voice, understanding of speech (its semantic meaning and emotional color), ability to respond (correctly or incorrectly) to the questions asked, to orientate in space and time, as well as reaction to examination (adequate and inadequate ). In the absence of reactions in the patient, pain stimuli are used in the above methods (fingerprints of the superficial tissues in the painful points - in the projection of the nipple or trapezius muscle, injections or light stabbing of the skin with a special clean needle).

Symptoms	Characteristic	Score, points
Opening the eyes	Arbitrary	4
	To shout	3
	To the pain	2
	Absent	1
Motor reactions	Commands are executed	6th
	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
	Slowed down	4
	Uneven	3
	Anisocoria	2
	Absent	1
Response of cranial nerves	Saved	5
	There are no reflexes:	4
	Ciliary	3
	Corneal	2
	"Puppet eyes" from the trachea	1
Convulsions	No	5
	Local	4
	General transient	3
	General continuous	2
	Full relaxation	1
Spontaneous breathing	Normal	5
	Periodic	4
	Hyperventilation	3
	Hypoventilation	2
	Apnea	1

G. Teasdale, V. Jennet in 1974 proposed a scale for determining the depth of coma. It is called the Glasgow scale and is widely used in the practical work of resuscitation physicians. On this scale, the functions of the central nervous system are evaluated in 7 positions.

To assess the severity of coma, use the Glasgow scale and its modified version for the hospital - the Glasgow-Pittsburgh scale.

The scale of Glasgow assesses the nature of the response to voice and pain - by such signs as opening the eyes, verbal and motor response. The maximum score is 15 points. At an estimation below 9 points a condition recognize the extremely heavy. The minimum possible score is 3 points. On the scale of Glasgow-Pittsburgh, the reactions of cranial nerves, the presence of convulsions and the character of respiration are additionally evaluated. The maximum score for this scale is -35 points. At death of a brain - 7 points. If the patient is on ventilator (ie, parameters such as "spontaneous breathing" and "speech reactions" can not be estimated "), the scale score is reduced to 25 points and 5 points, respectively.

With aggravation of coma severity, conjunctival and corneal reflexes are the first to be inhibited. The extinction of the corneal reflexes is attributed to unfavorable prognostic signs. Diagnostically significant information in assessing the severity of coma is provided by the examination of the oculocephalic reflex. If the patient is unconscious when turning his head to the right and left, do not note the friendly movement of both eyes and the gaze is fixed in the middle line (the effect of puppet eyes), this indicates the pathology of the cerebral hemispheres (coma I) and the absence of damage to the trunk.

To assess the condition of children in a coma, necessarily check the symptoms of Brudzinsky and Babinsky. The appearance of a one-sided reflex of Babinsky in a child in a coma indicates a focal lesion of the brain on the side opposite to the test extremity. A bilateral reflex followed by extinction indicates a deepening of the severity of the coma, regardless of the local damage to the brain substance. With spinal lesions, the reflex is not determined. Positive symptoms of Brudzinsky, revealed in a child in a coma, indicate irritation of the membranes (meningitis, meningoencephalitis, subarachnoid hemorrhage). In addition, it is necessary to evaluate changes in the diameter of pupils, movements of the eyeballs and the fundus, especially paying attention to possible asymmetry (the result of focal lesions of the brain substance!). With metabolic coma, the pupils' reaction to light is preserved.

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

[17], [18], [19], [20]

Emergency care for coma in children

With a coma of grade II-III, complicated by circulatory failure, after 100% _{of the} O2 hyperoxygenation intubation of the trachea is carried out with preliminary premedication with atropine. Do not forget about the possible injury of the cervical spine, in connection with which it is necessary to immobilize it. A probe is injected into the stomach to extract the contents and decompress the contents. Then, infusion of rheopolyglucin or crystalloids is carried out at a rate that maintains a systolic blood pressure level of more than 80 mm Hg. In older children, and with craniocerebral trauma to maintain cerebral perfusion by 10 mm Hg. Above the lower limit of the age norm. In the event that the respiratory system is not protected, the patient is placed on his side during transportation (half-turn). It is necessary to control the level of body temperature and diuresis (the possibility of rupture of the bladder!).

If suspected of hypoglycemia, 20-40% glucose solution is administered. For the prevention of Wernicke's encephalopathy before infusion of glucose solutions, it is necessary to administer thiamine. To protect neurons of the brain of adolescents in coma, you can use modern antioxidants: Semax, mexidol or methylethylpyridinol (emoxipine).

Such patients are also prescribed antihypoxants, such as Actovegin. Continue to introduce antioxidants (ascorbic acid) and, in addition. Pre-energy protectors (reamberin and cytoflavin). In the hospital for the activation of the reception it is advisable to supplement the treatment with central cholinomimetics. For example, choline alphoscerate (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 case of craniocerebral trauma, intracerebral and subdural hematomas, subarachnoid hemorrhage).

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