Syncope among children | MEDICH
Syncope among children

Syncope among children

Syncope among children

Syncope is a cerebral attack of anoxic ischemic origin, manifested by short-term loss of consciousness and transient hemodynamic disturbances due to insufficient homeostatic mechanisms.

 Pathogenesis

 Syncope occurs mainly in young people, often in children and adolescents. The main pathogenetic mechanism is the inferiority of the devices that regulate homeostasis and ensure adequate adaptation of the latter to changing environmental conditions and the needs of the organism. Usually, this insufficiency of regulation is manifested permanently – in the form of symptoms of vegetative dystonia. The latter may have a primary (constitutional) character, but much more often it is a result of a traumatic brain injury or associated with a psychogenic disease (neurosis), a disease of internal organs, endocrinopathy, infections, intoxication, etc. Often, vascular dystonia occurs during puberty and then passes. In individuals with vegetative-vascular dystonia, under normal conditions, hemodynamics, and in particular, cerebral blood flow, are in a compensated state, however, under the influence of certain factors that place increased demands on homeostasis, decompensation occurs, manifested by hemodynamic disorders and accompanied by transient symptoms of brain stem anoxia.

The direct pathogenetic mechanisms of syncope are: vascular factor – a drop in vascular tone with a significant decrease in blood pressure; cardiac factor – acute functional myocardial insufficiency or neurogenic cardiac arrhythmias. Syncope can also occur on the basis of the primary organic lesion of the heart – valvular disease and rhythm disturbances. However, this factor itself is often of relative importance and, with a good functional state of regulatory mechanisms, acts as a cause of syncopal states quite rarely. Nevertheless, along with the reflex syncope arising from the vasomotor and (or) cardiac mechanism, symptomatic syncope occurs, developing most often in primary heart diseases, with increased intrathoracic pressure, hyperventilation. With a predominantly vascular mechanism of syncope (vasomotor syncope), the main pathogenetic factor is usually acute vascular insufficiency, sometimes reaching the degree of collapse, with a predominantly cardiac mechanism, the heart rate is slowed down to asystole (vagal syncope).

Synocarotid syncope is also distinguished, in which the drop in blood pressure and slow pulse occur due to increased excitability of the carotid sinus. However, among young people, this mechanism in isolation is the cause of fainting extremely rarely, as a rule, in the presence of local pathological processes in the neck (lymphadenitis, etc.). Usually it is possible to identify vegetative dystonia. More often, the hypersyncity of the carotid sinus occurs in atherosclerosis of the carotid arteries and manifests itself in dysregulation of blood pressure, which may be accompanied by the occurrence of syncope. Also, the so-called vertebral syncope is the transient loss of consciousness and a fall during sharp turns of the head. The mechanism of these conditions is associated with short-term impaired blood circulation in the vertebrobasilar basin that occurs when the head turns in patients with osteochondrosis of the cervical spine and atherosclerosis of the vertebral arteries.

In a number of patients, insufficiency of regulatory homeostatic mechanisms occurs during a rapid transition from a horizontal to a vertical position, and in others, with prolonged standing. The mechanism is associated with the occurrence in the vertical position of the so-called postural hypotension – the fall of vascular tone with a decrease in blood pressure. Often, such syncope occurs during the recovery period after a serious illness with a long stay in bed or during the postoperative period, especially after operations on the sympathetic nervous system. Nikturic syncope, which usually occurs in men at night after rising and urinating, is close to a similar mechanism.

Reflex syncope always develops under the influence of a certain external influence and is usually the same for each patient. In some cases, these are psycho-emotional factors: type of blood, excitement, fear, etc., in others – physical: stay in the heat, a stuffy room, etc. Often there is a combination of psycho-emotional and physical factors, as is the case with various pain syndromes . The reflex syncope is vestibular one that occurs when traveling on transport, less often with sharp movements of the head.

Syncope clinic

 When fainting, loss of consciousness, as a rule, is preceded by feelings of nausea, blurring of vision or flickering before the eyes, tinnitus, etc. There is a weakness, sometimes yawning, the legs become deadened, a feeling of approaching loss of consciousness. Patients turn pale, the skin is covered with sweat. The seizure may end up with this (pre-unconsciousness, lipotemia), but more often the loss of consciousness occurs, the patient falls. Examination at this time reveals pronounced vegetative and hemodynamic disturbances: extreme pallor, coldness of the skin, weak pulse, sometimes its absence on the radial artery, a drop in blood pressure, muscular hypotension, a decrease in deep reflexes, mydriasis often with a weakening of the pupils’ reactions to light. With a predominantly vasomotor mechanism of fainting, the pulse is frequent, with a predominantly vagal one, the pulse is slowed down, in some cases absent, sometimes the heartbeat is not heard.

With a longer anoxia of the brain (usually due to asystole) at the height of fainting, convulsions may occur (convulsive form of fainting). It can lead to involuntary urination, foam from the mouth. The duration of fainting is 1-2 minutes. In most cases, reflex syncope does not develop in the horizontal position of the patient, and loss of consciousness does not occur if the patient has the opportunity to lie down with the onset of symptoms of the beginning attack.

With symptomatic fainting, along with a fainting clinic, symptoms of the underlying disease are identified. The most common cause of this syncope is a violation of the cardiac activity, accompanied by a significant decrease in the minute volume of the heart. The minute volume of the heart can fall in some cases with the intact stroke volume due to bradystolia, in others – due to a sharp decrease in the stroke volume, namely tachycardia and atrial fibrillation. The mechanism of the first type most often implements syncope in Adams – Stokes – Morgagni syndrome — disorders of atrioventricular conduction with the appearance of asynchronous ventricular and atrial rhythm due to ventricular bradysystolia. In the most severe cases, flutter or atrial fibrillation and even ventricles may occur.

Violation of the conductivity of the heart depends on its organic lesion, most often due to rheumatism (myogenic form) or from a disorder of the effects on the system by the vagus nerve (neurogenic form). The latter form with a known base could be referred to as reflex syncope, as usually heart rhythm disturbances and fainting can usually occur reflexively in response to stimulation of the afferent parts of the reflex arcs associated with the nuclei of the vagus nerve, for example, the gastrointestinal tract, nosopharyngeal areas and others. A characteristic feature of this syncope is that it can occur in the horizontal position of the patient.

Another type of symptomatic syncope develops with coughing fits, and some researchers consider it a variant of reflex epilepsy (betalepsy). In fact, bouts of loss of consciousness in these cases are usually fainting. Such conditions usually develop in patients with chronic lung diseases with signs of cardiopulmonary insufficiency. The provoking factors can be an overcrowded stomach, straining of the bowel movement, weight lifting, laughter, etc. At the height of the cough, as a result of increased intrathoracic pressure, signs of venous congestion appear, usually in the form of purple-cyanotic complexion, swelling of the veins of the neck. Then there is a loss of consciousness, during which patients can fall and get bruises. The mechanism of fainting when coughing is associated with twofold factors: firstly, with increased intrathoracic pressure, decreased filling of the left ventricle with blood, increased pressure in the system of the superior vena cava and venous pressure in the brain, impaired venous outflow and arterial blood flow to the brain tissue and, secondly, with a reflex effect from the pulmonary receptors of the vagus nerve.

Diagnosis

 Examination of patients suffering from fainting in the interictal stage, as a rule, reveals the symptoms of vegetative-vascular dystonia. Often there is a history of traumatic brain injury, severe infections, and somatic diseases. Often, you can identify diseases of the gastrointestinal tract, gallbladder, stomach, and with symptomatic fainting – rheumatic heart disease with conduction disorders, arrhythmia. Patients are often asthenic physique, emotionally labile. Often there is clinical symptoms of asthenic neurosis. A trip in transport is a factor that provokes fainting, usually there is an increased sensitivity of the vestibular apparatus: oculostatic and ocular vestibular phenomena, nystagmoid with extreme abductions of the eyeballs, increased optokinetic nystagmus, etc.

Differential diagnosis

 Diagnosis and differential diagnosis of fainting in some cases is not difficult, and in others – only a thorough examination of the patient and monitoring it allows to correctly diagnose the disease. It is the most complex differential diagnosis of syncope and vegetative-visceral epileptic seizures. In both cases, there are vegetative manifestations, dilated pupils, the relative short duration of paroxysms. It is not always easy to distinguish a convulsive syncope from an epileptic seizure.

A hypoglycemic condition can give a picture similar to fainting – weakness, pallor, arterial hypotension, sweating. However, hypoglycemic crises develop, as a rule, on an empty stomach, often at night or in the morning, sometimes after intense physical work and are accompanied by a decrease in blood sugar levels.

Treatment

 At the time of the attack:

  1. Try to catch a falling person in order to protect his/her head and other parts of the body from additional injuries;
  2. Put the patient so that his/her head is below the body, lift his/her legs (so that blood flows to the head);
  3. Provide fresh air (open the window, free the patient’s neck);
  4. Spray the patient’s face with cold water, let him/her breathe over a cotton wool moistened with liquid ammonia (a sharp irritating smell allows you to bring the person to consciousness);
  5. Give the patient an intravenous glucose solution (to improve brain nutrition) or give something sweet to eat (a piece of sugar, candy).
  6. During the interictal period, a general strengthening treatment is carried out.

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