Neurological diseases in children: causes, symptoms, treatment

27.10.2021

Fetal hypoxia is a syndrome caused by a lack of oxygen or impaired tissue oxygen absorption. This is not an independent disease, but a symptom that indicates a congenital or acquired pathology or a complicated course of pregnancy or childbirth. Oxygen starvation in the early stages of pregnancy can slow down the development of the child and lead to abnormalities, and in the later stages it can lead to damage to the nervous system, cerebral edema, kidney failure and other serious pathologies.

Intrauterine fetal hypoxia is detected, according to various sources, in 4-10.5% of cases of pregnancy and childbirth in our country.

Classification of fetal hypoxia

There are acute and chronic fetal hypoxia. The chronic form is observed for a long time and leads to pathologies in fetal development. The most common causes are diseases of the nervous, cardiovascular, endocrine systems of a pregnant woman, post-term pregnancy, multiple pregnancies, intoxication, and infectious diseases.

Acute hypoxia most often occurs during delivery. It can be caused by short or prolonged labor, premature loss of water, placental abruption, uterine rupture and other factors. Acute hypoxia requires immediate action. If she is observed at a late stage and labor has not yet begun, then doctors induce labor or perform a cesarean section.

Treatment

Clinical recommendations for asphyxia include the provision of first aid to the newborn as a priority. This is the most important step, which, if carried out competently, reduces the severity of the consequences of the pathological condition and the risk of complications. The key goal of resuscitation measures for asphyxia is to achieve the highest possible Apgar score by 5-20 minutes of the newborn’s life.

The stages and principles of ABC resuscitation allow for consistent and effective resuscitation of a newborn born with asphyxia. Source: Carrying out therapeutic hypothermia in newborns born with asphyxia. K. B. Zhubanysheva, Z. D. Beisembaeva, R. A. Maykupova, T. Sh. Mustafazade. Science of Life and Health, 2021. p. 60-67:

• Principle A (“airway”) is to ensure a clear airway during the first stage of resuscitation. To do this, you need to create the correct position: tilt your head back, lower it 15 degrees. After this, suck out mucus and amniotic fluid from the nose, mouth, trachea, and lower respiratory tract.
• Principle B (“breath”) – create ventilation, provide breathing. To do this, a jet oxygen flow is created - artificial ventilation of the lungs is performed using a resuscitation bag. If the child does not cry, tactile stimulation is added: stroking along the back, patting the feet.
• Principle C (“cordial”) – restore heart function. Indirect cardiac massage helps with this. If necessary, adrenaline, glucose, hydrocortisone and other drugs are administered. In this case, the auxiliary ventilation from the previous stage cannot be stopped.

Care for a newborn child who has suffered asphyxia is carried out in a maternity hospital. Babies with a mild form are placed in a special tent with a high oxygen content. In cases of moderate or severe asphyxia, infants are placed in an incubator - a special box where oxygen is supplied. If necessary, the airways are re-cleaned and freed from mucus.

The scheme of further treatment, recovery and care is determined by the attending physician. General care recommendations include:

• maintaining normal body temperature, blood pressure, heart rate;
• creating maximum comfort: optimal ambient temperature, comfortable position;
• carrying out respiratory therapy;
• conducting infusion therapy - administering fluid to meet needs Source: Protocol for therapeutic hypothermia for children born with asphyxia. Ionov O.V., Balashova E.N., Kirtbaya A.R., Antonov A.G., Miroshnik E.V., Degtyarev D.N. Neonatology: News. Opinions. Training, 2014. p. 81-83.

During rehabilitation, regular monitoring :

• baby's weight (twice a day);
• neurological and somatic status;
• volume of fluid consumed;
• nutrition composition;
• basic vital signs: pulse, blood pressure, saturation, respiratory rate;
• laboratory characteristics of blood, urine;
• X-rays of the chest, abdominal cavity;
• ultrasound examination of the abdominal cavity;
• neurosonography;
• electrocardiograms, echocardiograms.

After discharge, the baby should be regularly monitored by a pediatrician or neurologist.

Signs of fetal hypoxia during pregnancy

The gynecologist will be able to understand that the fetus has signs of hypoxia during the examination. The main manifestation at the initial stage will be a rapid heartbeat and increased respiratory activity. Meconium appears in the amniotic fluid.

If a child has severe hypoxia, then the heartbeat, on the contrary, will be slow. Significant oxygen deprivation leads to intracellular and tissue edema as a result of the blood condensing and plasma leaving the vascular bed. Tissue respiration is disrupted, embryo development slows down, and acidosis develops. Circulatory disorders cause tachycardia followed by bradycardia. Due to the increased fragility of the vascular walls, hemorrhages are possible.

A pregnant woman herself can identify signs of fetal hypoxia in the second and third trimester by changes in motor activity: the child behaves restlessly, moves too often and too much, and with progressive oxygen deficiency, on the contrary, practically stops moving. If such symptoms appear, you should immediately consult a doctor for diagnosis.

If chronic fetal hypoxia is suspected, doctors conduct the following examinations:

1. listening to the fetal heartbeat
2. Ultrasound, Dopplerography;
3. cardiotocography, phonocardiography of the fetus;
4. amnioscopy and amniocentesis through the cervical canal;
5. laboratory tests of blood and urine in a pregnant woman.

Early symptoms that should be addressed to a pediatric neurologist

- sluggish breastfeeding, choking during feeding, leakage of milk through the baby's nose - weak cry of the child, nasal or hoarse voice - frequent regurgitation and insufficient weight gain - decreased motor activity of the child, drowsiness, lethargy or severe anxiety - trembling of the chin, upper and/or or lower extremities, frequent startlings - difficulty falling asleep, frequent awakenings during sleep - throwing back the head - slowing or rapid increase in head circumference - low (flabby muscles) or high tone of the muscles of the limbs and torso - decreased activity of movements of the arm or leg on any side , limited hip separation or the presence of a “frog” position with pronounced hip separation, unusual position of the child - strabismus, torticollis - birth of a child by caesarean section, in breech presentation, with an anomaly of labor or with the use of obstetric forceps, extrusion, with the umbilical cord entwined around the neck - prematurity of the child - presence of convulsions during childbirth or in the postpartum period

Fetal hypoxia during childbirth

Hypoxia of the newborn during childbirth can be caused both by congenital pathologies and unfavorable course of pregnancy, and by problems directly during the birth process. The main danger is oxygen starvation of the brain, which leads to its dysfunction and can even cause the death of the baby.

The baby's condition is assessed in the first minute after birth using the Apgar scale. The following indicators are assessed:

• color of the skin
• breathing rate;
• reflex activity;
• heart rate;
• muscle tone.

For each point, 0 to 2 points are given, resulting in a maximum score of 10. If 6-7 points are scored, then mild hypoxia is observed, if 4-5 points - moderate, 0-3 - severe.

The examination is repeated after 5 minutes. In newborns with mild hypoxia, which is not caused by serious pathologies, by this time the indicators return to normal.

Hypoxic lesions of the central nervous system

Section I

Hypoxic lesions of the central nervous system

I. A) P 91.0 Cerebral ischemia (hypoxic-ischemic encephalopathy, perinatal hypoxic brain damage)

Cerebral ischemia grade I (mild)

a) Intrapartum hypoxia, mild asphyxia at birth;

b) Excitation of the central nervous system is more common in full-term infants, depression - in premature infants, lasting no more than 5-7 days;

c) Moderate hypoxemia, hypercarbia, acidosis;

NSG, CT, MRI - without pathological abnormalities;

DEG - compensatory increase in speed along the main arteries of the brain;

Diagnosis example:

P 91.0 “Cerebral ischemia stage I” or “Hypoxic-ischemic damage to the central nervous system stage I”

Cerebral ischemia degree II (moderate)

a) Factors indicating intrauterine fetal hypoxia; moderate asphyxia at birth; extracerebral causes of cerebral hypoxia that arise postnatally;

b) CNS depression, excitation or change of phases of cerebral activity (lasting more than 7 days);

Convulsions in premature infants are often tonic or atypical (convulsive apnea, stereotypical spontaneous oral automatisms, fluttering of the eyelids, myoclonus of the eyeballs, “rowing” movements of the arms, “pedaling” of the legs); in full-term infants - multifocal clonic; Attacks are usually short-term, single, less often repeated;

Intracranial hypertension (transient, more often in full-term infants);

Autonomic-visceral disorders;

c) Metabolic disorders (hypoxemia, hypercarbia, acidosis are more pronounced and persistent)

NSG - local hyperechoic foci in the brain tissue (in premature infants, more often in the periventricular region; in full-term infants, subcortically.

MRI - focal lesions in the brain parenchyma are determined in the form of changes in the nature of the magnetic resonance signal on T1 and T2-weighted images.

CT scan of the brain shows local foci of low density in the brain tissue (in premature infants, more often in the periventricular region; in full-term infants, subcortically and/or cortically.

DEG are signs of hypoperfusion in the middle cerebral artery in full-term infants and the anterior cerebral artery in premature infants. An increase in the diastolic component of blood flow velocity, a decrease in the resistance index.

Diagnosis example:

P 91.0 “Cerebral ischemia degree II” or “Hypoxic-ischemic damage to the central nervous system II degree.”

In cases of diagnosis of specific structural changes in the brain, an additional code is set (for example, P 91.2 cerebral leukomalacia of a newborn).

Cerebral ischemia grade III (severe)

a) Factors leading to intrauterine fetal hypoxia and/or severe perinatal asphyxia; extracerebral causes of persistent cerebral hypoxia (CHD, severe forms of SDR, hypovolemic shock, etc.);

b) Progressive loss of cerebral activity - over 10 days

(in the first 12 hours of life there is deep depression or coma, in the period from 12-24 there is a short-term increase in the level of wakefulness, from 24-72 hours there is an increase in depression or coma

• Repeated convulsions, epistatus is possible.
• Dysfunction of the brain stem (disturbances in breathing rhythm, pupillary reactions, oculomotor disorders).
• The position of decortication or decerebration (depending on the extent of the lesion).
• Severe autonomic and visceral disorders.
• Progressive intracranial hypertension.

c) Persistent metabolic disorders.

NSG - a diffuse increase in the echogenicity of the brain parenchyma - is characteristic of full-term infants. Increased echogenicity of periventricular structures is typical for premature infants. Narrowing of the lateral ventricles. Subsequently, cystic periventricular cavities (PVC) are formed in premature infants, and signs of atrophy of the cerebral hemispheres with passive expansion of the cerebrospinal fluid spaces appear.

CT scan - decreased density of brain parenchyma, narrowing of the cerebrospinal fluid spaces, multifocal cortical and subcortical foci of reduced density, changes in the density of the basal ganglia and thalamus - mainly in full-term infants, periventricular cystic cavities - in premature infants (Check with a radiologist)

MRI - lesions in the brain parenchyma are detected as changes in the magnetic resonance signal on T1 and T2-weighted images.

DEG - paralysis of the main arteries of the brain, with transition to persistent cerebral hypoperfusion. Decrease in diastolic blood flow velocity, change in the nature of the curve (its leasing or pendulum-like nature). Increase in resistance index.

Diagnosis example:

P 91.0 “Cerebral ischemia of the third degree” or “Hypoxic-ischemic damage to the central nervous system of the third degree.”

In cases of diagnosis of specific structural changes in the brain, an additional code is set (see Appendix).

I. B) R 52 INTRACRANIAL HEMORRHAGES

(hypoxic, non-traumatic)

P 52.0 Intraventricular hemorrhage of the 1st degree (subependymal)

a) Ante- and - intrapartum hypoxia, mild asphyxia at birth, repeated attacks of apnea, jet administration of hyperosmolar solutions.

b) Develops predominantly in premature or immature newborns Course: asymptomatic, absence of specific neurological disorders

c) Transient metabolic disorders

NSG - hyperechoic areas, unilateral or bilateral localization in the thalamo-caudal notch or in the region of the head of the caudate nucleus. The time frame for transformation of a subependymal hematoma into a cyst is 10-14 days or more.

CT, MRI - do not have diagnostic advantages over NSG.

DEG - without pathological changes.

P 52.1 Intraventricular hemorrhage of the second degree

(subependymal + intraventricular)

Develops predominantly in premature infants (35-65%).

a) Factors indicating intrauterine fetal hypoxia and/or moderate asphyxia at birth. Defects in the provision of primary resuscitation care, arterial hypertension or fluctuation of systemic blood pressure due to SDR, iatrogenic factors (inadequate mechanical ventilation regimens, rapid administration of large volumes or hyperosmolar solutions, functioning fetal communications, pneumothorax, etc.). Coagulopathies.

b) There are 2 main variants of the flow: gradual (wavy) and catastrophic.

• Catastrophic course: short-term motor excitation is suddenly replaced by progressive depression of cerebral activity with transition to coma. Deep apnea, increasing cyanosis and marbling of the skin. Tonic convulsions, oculomotor disorders, bradyarrhythmia, and thermoregulation disorders indicate increasing intraventricular hypertension.
• Gradual course (wavy): periodic changes in phases of cerebral activity, attacks of repeated apnea, muscle hypotension, atypical convulsive attacks.

c) Fluctuation and then a rapid decrease in systemic blood pressure (cf. blood pressure < 30 mm Hg)

Fall in hematocrit and decrease in hemoglobin level

Metabolic disorders: hypoxemia, hypercabia, acidosis, hypocalcemia, fluctuations in serum glucose levels

CSF - with an admixture of blood (the time of occurrence of bleeding and its intensity is judged by the microscopic characteristics and the number of red blood cells), reactive pleocytosis, increased protein levels, decreased glucose. During lumbar puncture, blood pressure is often elevated.

NSG changes depend on the time of the study; at the initial stages, hyperechoic zones are determined in the area of ​​the germinal matrix, then ventriculomegaly develops, and subsequently echo-positive formations (thrombi) are visualized in the lumens of the ventricles. In some cases, blockage of the cerebrospinal fluid pathways with the development of acute hydrocephalus is possible.

CT, MRI, PET - do not have diagnostic advantages in the neonatal period over NSG

DEG - fluctuation of blood flow in the main arteries of the brain before the development of intravetricular bleeding, stabilization - after hemorrhage, with the progression of ventriculomegaly (usually after 10-12 days) - increasing hypoperfusion.

P 52.2 Intraventricular hemorrhage of the third degree

(subependymal + intraventricular + periventricular)

Among all variants of IVH, their share accounts for 12 to 17%.

b) Most often observed in premature infants with extremely low body weight.

• Typically catastrophic. Rapid depression of cerebral activity with the development of coma, progressive disorder of vital functions (bradycardia, arrhythmia, apnea, respiratory rhythm pathology).
• Tonic convulsions and oculomotor disorders occur due to dislocation of the brain stem. High incidence of deaths in the first days of life.

c) Severe, difficult to correct, metabolic disorders (hypoxemia, hypercarbia, acidosis, electrolyte disturbances), disseminated intravascular coagulation syndrome.

A progressive fall in systemic blood pressure and cardiac arrhythmias. Critical drop in hematocrit and hemoglobin levels

CSF - with a significant admixture of blood (the time of occurrence of bleeding and its intensity is judged by the microscopic characteristics and the number of red blood cells), reactive pleocytosis, increased protein levels are often observed, and cerebrospinal fluid pressure is often increased.

Diagnostic lumbar puncture is performed according to strict indications and with extreme caution, due to the high risk of herniation of the brain stem into the foramen magnum.

NSG is an extensive hyperechoic area of ​​periventricular localization (hemorrhagic infarction - often unilateral in the fronto-parietal region), the lateral ventricle on the side of the hemorrhage is practically not visualized, later ventriculomegaly and deformation of the lateral ventricle are revealed due to the formation of a porencephalic post-hemorrhagic cystic cavity. Thrombi are often visualized in the lumen of the ventricles, in combination with pronounced dilatation of the ventricular system. Subsequently, an increase in the echogenicity of the ventricular walls is caused by the development of aseptic ventriculitis and hemosiderosis of the periventricular parenchyma. In a significant percentage of cases, occlusive hydrocephalus is formed.

CT, MRI, PET - do not have diagnostic advantages in the neonatal period over NSG

DEG - in the initial stages, a decrease in systolic and diastolic blood flow rates, an increase in the resistance index

Reduced diastolic blood flow velocity, decreased resistance index.

P 52.5 Primary subarachnoid hemorrhage (non-traumatic)

The frequency is about 20%, of which 75% are in premature and immature

a) Intranatal hypoxia, asphyxia at birth. Short gestation period, immaturity. Coagulopathies.

b) Clinical course options:

• Asymptomatic,
• Excitement syndrome with hyperesthesia and acute intracranial hypertension (tension and bulging of the large fontanel, divergence of the sagittal and coronal sutures, profuse regurgitation, intermittent Graefe's symptom);
• Convulsions that suddenly occur on the 2-3rd day of life (focal clonic - more often in full-term infants), atypical convulsions (in premature infants).

c) Metabolic disorders are not typical

NSG is not very informative for diagnosing PSC. In some cases, the expansion of the Sylvian fissure and/or interhemispheric fissure is visualized.

CT and MRI - accumulation of blood is detected in various parts of the subarachnoid space, but more often in the temporal regions.

DEG is not very informative (primary and secondary vasospasm).

CSF - increased pressure, increased erythrocyte content (including changed ones), increased protein concentration, neutrophilic pleocytosis.

R 52.4 Hemorrhage into the substance of the brain (non-traumatic)

parenchymal

P 52.6 hemorrhage in the cerebellum and posterior cranial fossa

(rare)

a) Intrauterine fetal hypoxia, severe or moderate asphyxia at birth. Coagulopathies. Prematurity. Vascular malformations.

b) The clinical picture depends on the location and volume of the hemorrhagic infarction.

• With scattered petechial hemorrhages of subcortical localization, an asymptomatic course is possible.
• With extensive parenchymal hematomas of hemispheric localization, the clinical course is similar to stage III IVH. Progressive loss of cerebral activity with transition to stupor or coma, focal neurological symptoms contralateral to the lesion (distinct asymmetry of muscle tone, focal or tonic convulsions, oculomotor disturbances, etc.); increasing intracranial hypertension.
• Hemorrhages in the posterior cranial fossa and cerebellum are characterized by increasing signs of intracranial hypertension (tension of the fontanelles, dehiscence of the nuchal suture, agitation, frequent tonic convulsions) and brainstem disorders (respiratory, cardiovascular disorders, oculomotor disorders, bulbar syndrome).

c) Severe metabolic disorders that are difficult to correct (hypoxemia, hypercarbia, acidosis, disseminated intravascular coagulation) are usually accompanied by massive hematomas. A progressive increase in systemic blood pressure is subsequently replaced by a fall. Heart rhythm disturbances. Decreases in hematocrit and hemoglobin levels correlate with the amount of bleeding.

CSF - increased pressure, increased erythrocyte content (including changed ones), increased protein concentration, neutrophilic pleocytosis in the cerebrospinal fluid. With the exception of cases of small focal parenchymal hemorrhages.

NSG is not very informative for small-point hemorrhages; massive hemorrhagic infarctions are visualized as asymmetric hyperechoic foci in the brain parenchyma. After 2-3 weeks, echo-negative cavities (pseudocysts, leukomalacia) form in their place. Possible contralateral displacement of the interhemispheric fissure and homolateral compression of the lateral ventricle.

CT scan shows areas of increased density in the brain parenchyma, varying in size and location, with concomitant deformation of the cerebrospinal fluid spaces.

MRI - change in the MR signal from foci of hemorrhage not in the acute stage.

DEG is asymmetric hypoperfusion in the cerebral arteries on the affected side.

I. B) Combined ischemic and hemorrhagic

CNS lesions (non-traumatic)

Occurs much more often

than all isolated forms of CNS damage discussed above

(occurs predominantly in premature infants)

a) Intrauterine hypoxia and asphyxia at birth. Premature infants with low body weight (1000-1500 g). Defects in the provision of primary resuscitation care, arterial hypotension, hypertension or fluctuations in systemic blood pressure. Coagulopathies, DIC syndrome.

B) The clinical picture depends on the leading type of damage to the central nervous system (ischemia or hemorrhage), its severity and location. There is significant variability in neurological symptoms and their dynamics. These types of damage are the most severe.

c) Metabolic disorders that are difficult to correct.

CSF - pressure is usually increased; morphological characteristics depend on the degree of hemorrhage into the cerebrospinal fluid spaces.

NSG, CT, MRI - various variants of deformation of the liquor-conducting system, foci of altered density, differing in intensity, predominantly periventricular localization.

DEG—fluctuation of cerebral blood flow; paralysis of the main arteries of the brain, decreased blood flow.

Diagnosis example:

“Combined (non-traumatic) ischemic-hemorrhagic damage to the central nervous system.”

In cases of diagnosing specific structural changes in the brain, combinations of codes corresponding to ischemic and hemorrhagic intracranial injuries are set (see Appendix).

Section II

Traumatic damage to the nervous system.

II. A) P 10 Intracranial birth injury

(Rupture of intracranial tissues and hemorrhage due to birth trauma)

R 10.8 Epidural hemorrhage

(occurs mainly in full-term,

with a frequency of about 2% among all intracranial hemorrhages).

a) Anomalies of childbirth: discrepancy between the birth canal and the size of the fetal head, anomalies of presentation, instrumental delivery.

b) Rapidly increasing intracranial hypertension in the first hours of life;

• Hyperexcitability;
• Convulsions;
• On the side of the hematoma, the pupil is sometimes dilated. Often combined with cephalhematoma.

c) Metabolic disorders in isolated epidural hematoma are not typical.

CSF is not informative.

NSG is not very informative (depends on the location and volume of the hematoma).

CT scan shows a ribbon-shaped, high-density formation between the dura mater and the covering bones of the skull. In some cases, the hematoma area has the shape of a “biconvex lens” adjacent to the integumentary bones of the skull.

DEG is not informative.

P 10.0 Subdural supratentorial hemorrhage

(True prevalence unknown, more common in full-term

over 4000 and post-term, in 40% of cases bilateral,)

a) See section “Epidural hemorrhage”

b) The following variants of clinical manifestations are found:

• Asymptomatic;
• Focal neurological disorders developing in the first 72 hours of life: hemiparesis (on the side opposite to the hematoma); deviation of the eyes in the direction opposite to hemiparesis (“eyes look” at the hematoma); dilation of the pupil on the side of the injury;
• Focal (focal) seizures
• Hypertension syndrome of varying severity or hyperexcitability.

c) Metabolic disorders in isolated subdural hematoma of convexital localization are not typical.

Transillumination of the skull is an accessible and informative diagnostic method. A limited focus of low luminescence above the hematoma is determined.

NSG - for small and flat subdural hematomas of convexital localization, is not very informative; for hemorrhages of significant size, there are signs of compression of the homolateral hemisphere and displacement of the median structures towards the side opposite to the focus.

CT and MRI are the most informative methods for diagnosing SDC of suprahemispheric localization. Hemorrhage is visualized as a “sickle-shaped” area of ​​​​increased density adjacent to the calvarium.

DEG is a decrease in blood flow velocity in the middle cerebral artery on the side of the hematoma.

CSF changes are not very specific; lumbar puncture should be performed with great caution due to the high risk of herniation of the cerebellar tonsils into the foramen magnum, or the temporal lobe into the notch of the tentorium of the cerebellum.

P 10.4 Subdural subtentorial (infratentorial) hemorrhage

(They are rare, more often in full-term babies weighing

over 4000 and post-term)

a) Anomalies of childbirth: (discrepancy between the birth canal and the size of the fetal head, rigid birth canal, etc.), pathological variants of fetal presentation (usually breech), instrumental delivery.

b) Flow options:

• Catastrophic - from the first minutes and hours of life, signs of compression of the brain stem develop: progressive loss of cerebral activity - coma, opisthotonus posture, divergent strabismus, impaired pupillary reactions, floating movements of the eyeballs, fixed gaze. Progression of respiratory and cardiovascular disorders.
• Delayed or subacute-progressive - after a period of relative well-being (lasting from several hours or days, less often weeks), signs of intracranial hypertension (tension of the fontanelles, dehiscence of the nuchal suture, agitation, frequent tonic convulsions) and compression of the brain stem (respiratory and cardiovascular) increase. disorders, oculomotor, bulbar syndrome).

The most common outcome is death.

c) Metabolic disorders that are difficult to correct. Progressive decrease in blood pressure, bradyarrhythmia, anemia.

NSG is a deformation of the fourth ventricle; in some cases, zones of increased echogenicity are identified in the area of ​​the structures of the posterior cranial fossa. Blood clots are detected in the cistern magna of the brain.

CT - allows you to detect extensive hematomas of the posterior cranial fossa, which are visualized as areas of increased density

MRI is the most informative for detecting hematomas of small volume in subacute cases.

CSF - lumbar puncture is not indicated due to the high risk of herniation of the cerebellar tonsils into the foramen magnum.

DEG is not informative.

R 10.2 Intraventricular hemorrhage, traumatic

(rarely encountered, mainly in full-term infants)

a) Prolonged labor, especially in combination with perinatal hypoxia, rapid rotation of the head, forced extraction of the fetus. Coagulopathies.

b) Manifestation - 1-2 days of life (in newborns with trauma and/or asphyxia) in newborns with unclear etiology (in 25%) - sometimes at 2-4 weeks of life.

• Hyperexcitability alternating with depression, convulsions (focal or multifocal), respiratory rhythm disturbances (secondary apnea).
• Progressive intracranial hypertension (vomiting, bulging fontanelle, dehiscence of cranial sutures).
• Hydrocephalus

c) There are no specific metabolic disorders.

NSG - ventriculomegaly, an uneven increase in the echogenicity of the choroid plexuses, deformation of their contours and an increase in size. Determination of echo-positive thrombi in the lumens of the ventricles.

CT, MRI - do not have obvious diagnostic advantages.

DEG is not informative

CSF - pressure is increased, blood admixture is determined in cases of blood penetration into the subarachnoid spaces, protein levels are increased, mixed pleocytosis (see above).

P 10.1 Parenchymal hemorrhage (hemorrhagic infarction)

(They are rare, more often in full-term babies weighing

over 4000 and post-term)

a) Anomalies of childbirth: (discrepancy between the birth canal and the size of the fetal head, rigid birth canal, etc.), pathological variants of fetal presentation, instrumental delivery. (Predisposing factors - hypoxia, foci of ischemia, coagulopathy, vascular malformations, tumors)

b) The clinical picture depends on the location and volume of hemorrhage.

Hemorrhages in the cerebral hemispheres - course:

• Asymptomatic;
• Increasing depression with a gradual loss of cerebral activity, transition to coma, often with focal symptoms (hemisyndromes, focal clonic convulsions),
• Intracranial hypertension (due to perifocal cerebral edema).

Intracerebellar hemorrhages - course

• Asymptomatic (with hemorrhage in the marginal parts of the cerebellar hemisphere);
• Increasing intracranial hypertension (tension of the fontanelles, dehiscence of the nuchal suture, agitation, frequent tonic convulsions).
• Compression of the brainstem (respiratory and cardiovascular disorders, oculomotor, bulbar syndrome) - with massive hemorrhages in the cerebellar hemispheres.

c) Metabolic disorders are not specific.

NSG - asymmetric hyperechoic areas of different size and location in the cerebral hemispheres; with a massive hematoma - signs of compression of the homolateral ventricle and displacement of the interhemispheric fissure. In the cerebellar hemispheres, hyperechoic foci are visualized (with significant intracerebellar hemorrhages).

CT and MRI are more informative for identifying parenchymal hematomas of various locations and sizes (especially subcortical and small ones).

DEG is not very informative in the acute period; later there are signs of cerebral hypoperfusion.

R 10.3 Traumatic subarachnoid hemorrhage

(rarely found, predominantly in full-term infants)

a) Anomalies of childbirth: (discrepancy between the birth canal and the size of the fetal head, rapid labor, rigid birth canal, etc.), pathological variants of fetal presentation, instrumental delivery, combined in 25% of cases with linear and depressed skull fractures. (Predisposing factors - hypoxia, coagulopathies, vascular malformations, tumors)

b) During the first 12 hours of life, depression of cerebral activity increases, up to coma. In some cases, a “waking” coma is observed: the eyes are wide open, a piercing cerebral scream, a decortication posture (flexion of the arms, extension of the legs).

• Hyperesthesia;
• Hyperexcitability;
• Rapidly growing external hydrocephalus (dehiscence of cranial sutures, bulging fontanelles);
• Generalized convulsions (occurring in the first hours of life).

c) Metabolic disorders are not specific. Posthemorrhagic anemia, blood pressure is reduced (vascular shock) in the first hours, subsequently uncontrolled systemic arterial hypertension.

NSG - possible increase in the echo density of the subcortical white matter on the side of the hemorrhage, expansion of the interhemispheric fissure and/or Sylvian fissure of the basal subarachnoid spaces. Subsequently, a progressive expansion of the convexital subarachnoid spaces is noted.

CT scan shows an increase in the density of the subarachnoid spaces, with their subsequent expansion.

MRI is not very informative in the acute period.

DEG is not very informative in the acute period; later there are signs of cerebral hypoperfusion.

CSF - high pressure, hemorrhagic cerebrospinal fluid, often reactive pleocytosis, elevated protein levels, by 3-6 days the macrophage reaction is pronounced.

II. B) Birth injury of the spinal cord

R 11.5 Hemorrhage into the spinal cord

(sprain, rupture, tear with or without spinal injury)

(rare, about 1% and mainly in full-term babies)

a) Anomalies of fetal presentation (gluteal and leg), incorrect implementation of obstetric aids (for example, excessive lateral traction or rotation of the body with a fixed head). Predisposing factors are hypoxia, coagulopathies, vascular malformations.

b) Three options for the clinical course:

• Catastrophic - stillbirth or death in the first hours after birth due to progressive respiratory and cardiovascular disorders. Observed at the craniospinal level of damage.
• Severe - accompanied by a picture of spinal shock lasting from several days to several weeks (adynamia, areflexia, atony), the abdomen is swollen, intestinal paresis, “paradoxical” diaphragmatic breathing, atony of the anal sphincter and bladder muscles, lack of pain sensitivity below the level of the lesion. Sometimes - Claude Bernard-Horner syndrome. Reflex reactions and sensitivity in the face and head are preserved.

The progression of respiratory failure often leads to death in the neonatal period. It is observed with damage to the middle and lower cervical, upper thoracic parts of the spinal cord.

• Moderately severe - the clinical picture of spinal shock is more short-lived, motor and reflex disorders are less pronounced.

c) Metabolic disorders characteristic of severe respiratory failure. Decreased systemic blood pressure, bradycardia, hypothermia.

NSG is not very informative.

CT, MRI - allow you to visualize the area and nature of the damage (MRI is more preferable).

ENMG - signs of denervation of skeletal muscles at the level of the lesion.

CSF - with hemorrhage, tears, ruptures - the cerebrospinal fluid is hemorrhagic, with ischemia - there may be an increase in protein levels.

II. B) P 14 Birth injury of the peripheral nervous system

Frequency of occurrence 0.1%, mainly in full-term infants

a) Incorrect implementation of obstetric care provided when it is difficult to remove the shoulders and head, or when the fetus’s arms are thrown back.

Traumatic injuries of the brachial plexus

b) P 14.0 Proximal (upper) Erb-Duchenne type

Flaccid paresis of the proximal arm: the arm is brought to the body, extended in all joints, the forearm is pronated, the hand is in palmar flexion, the head is tilted towards the sore shoulder, movements in the shoulder and elbow joints are limited, there is no reflex from the biceps brachii muscle, pain and tactile sensitivity reduced.

In approximately 5% of cases it is combined with paresis of the phrenic nerve.

P 14.1 Distal (lower) Dejerine-Klumpke type

Flaccid paresis of the distal arm: the arm is extended in all joints, lies along the body, pronated, the hand hangs passively. There are no spontaneous movements in the elbow and wrist joints, and movements in the fingers are limited. The grasping and palmo-oral reflexes on the affected side are not evoked. Often trophic disorders (edema, cyanosis, etc.). Sometimes this damage is accompanied by Claude Bernard-Horner syndrome on the affected side.

R 14.3 Total type (paresis of the brachial plexus).

Spontaneous movements in all parts of the arm are completely absent, diffuse muscle hypotonia, areflexia, impaired all types of sensitivity, trophic disorders. Often combined with Claude Bernard-Horner syndrome on the affected side.

c) There are no characteristic metabolic disorders.

NSG, CT, MRI, DEG are not informative.

CSF is not informative

ENMG - spontaneous bioelectrical activity in rest mode is absent; with active muscle effort, an interference type of curve is recorded with a reduced amplitude of oscillations in paretic muscles.

R 14.2 Traumatic injuries of the phrenic nerves

In 80-90% of cases it is combined with traumatic injuries of the brachial plexus

(total and proximal type), isolated paresis is extremely rare.

b) Unilateral paresis is clinically practically asymptomatic or with minimal manifestations of respiratory failure.

Bilateral paresis of the diaphragm leads to severe respiratory disorders from the first hours of life, which requires respiratory support in some cases.

c) Metabolic disorders characteristic of respiratory failure.

Ultrasound, chest X-ray - high standing and low mobility (relaxation) of the dome of the diaphragm on the affected side/sides.

R 11.3 Traumatic injury to the facial nerve

a) Abnormal presentation of the fetus, operative delivery - incorrect application of abdominal and exit obstetric forceps.

b) On the losing side:

• Lagophthalmos;
• Smoothness of the nasolabial fold;
• When screaming, the mouth is pulled to the healthy side, the search reflex is weakened.

c) NSG, CT, MRI are not informative.

ENMG - reveals a decrease in conductivity along the facial nerve.

R 14.8 Traumatic injuries to other peripheral nerves

(rare)

a) Anomalies of fetal presentation (breech and leg presentation), improper implementation of obstetric care. In the postnatal period - as a rule, of iatrogenic origin or of a secondary nature (inflammatory and traumatic changes in the bones and joints of the extremities).

b) Damage to the nerves of the extremities is clinically manifested by impaired movements and muscle tone in the corresponding areas of innervation: ulnar, radial, sciatic, obturator and tibial nerves.

c) If symptoms characteristic of damage to a particular peripheral nerve are identified, it is necessary to conduct a comprehensive examination to exclude traumatic and purulent-inflammatory processes in the bones, joints and soft tissues.

Continued >>

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Consequences of hypoxia in a newborn

A mild degree usually does not have serious consequences. Severe hypoxia can lead to damage to the central nervous system, cerebral edema, convulsions, and areflexia. Damage to the respiratory system leads to pneumopathy and pulmonary hypertension. Problems with the cardiovascular system can be heart and vascular defects.

You can tell that a newborn is suffering from hypoxia by frequent regurgitation, vomiting, and enterocolitis. The consequences of severe perinatal hypoxia are DIC syndrome and secondary immunodeficiency.

Prevention of newborn asphyxia

The expectant mother should be involved in the prevention of the pathological condition during pregnancy. To do this you should:

• attend routine gynecological consultations;
• adhere to the recommendations of the obstetrician-gynecologist;
• be sure to take vitamin complexes if prescribed by a doctor;
• monitor the condition of the fetus and placenta during routine ultrasound examinations;
• treat any diseases only under the supervision of a doctor, do not self-medicate;
• follow a daily routine, do not overload the body;
• get rid of bad habits;
• to walk outside.

In obstetrics, considerable attention is paid to the development of effective preventive methods that can reduce the risk of asphyxia during childbirth and during the first days of a baby’s life.

Sources:

1. Modern methods of treating newborn asphyxia. Cherednikova E.N., Sherstnev D.G. Bulletin of Medical Internet Conferences, 2016. p.824
2. Protocol for therapeutic hypothermia for children born with asphyxia. Ionov O.V., Balashova E.N., Kirtbaya A.R., Antonov A.G., Miroshnik E.V., Degtyarev D.N. Neonatology: News. Opinions. Training, 2014. p. 81-83
3. Carrying out therapeutic hypothermia in newborns born with asphyxia. K. B. Zhubanysheva, Z. D. Beisembaeva, R. A. Maykupova, T. Sh. Mustafazade. Science of Life and Health, 2021. p. 60-67
4. Asphyxia of newborns. Zhetpisova L.B. West Kazakhstan Medical Journal, 2011
5. Fetal hypoxia and asphyxia of the newborn. Kuznetsov P.A., Kozlov P.V. General Medicine, 2021. p. 9-15

The information in this article is provided for reference purposes and does not replace advice from a qualified professional. Don't self-medicate! At the first signs of illness, you should consult a doctor.

Treatment and prevention of intrauterine hypoxia

The most common causes of intrauterine hypoxia are placental insufficiency, fetal malformations, umbilical cord compression and maternal hypoxia. It is very difficult to help a fetus with hypoxia in utero - before birth you can only monitor the condition and carry out delivery in a timely manner.

One of the main recommendations for the prevention of intrauterine hypoxia for expectant mothers is to spend as much time as possible in the fresh air. Doctors recommend evening walks, preferably not in the city, where the air is polluted and the oxygen content in it is reduced, but in nature. An alternative or additional way to cope with hypoxia is to use an oxygen tank. Just a few breaths are enough to increase the oxygen level in the blood of mother and child. The cans are compact and lightweight, you can carry them with you to work or store them in your car. An additional advantage is that oxygen therapy procedures strengthen the immune system and help cope with toxicosis, relieving nausea, dizziness, and weakness.

The PRANA company offers wholesale purchase of oxygen cylinders of various sizes with delivery throughout Russia. As a manufacturer, we have set minimum prices for oxygen-containing products and guarantee the quality of cylinders.

General information about the disease

Asphyxia is diagnosed in 4-6% of children. Moreover, the percentage varies depending on the degree of prematurity of the fetus. In babies born before 36 weeks, the incidence of pathology reaches 9%, and in children born after 37 weeks it decreases to 1-2%.

Scientific definitions of newborn asphyxia boil down to the fact that the child cannot breathe independently or makes superficial convulsive breathing movements that do not allow the body to receive sufficient oxygen. The authors consider infant asphyxia as suffocation, in which other signs that the fetus is alive remain: there is a heartbeat, the umbilical cord is pulsating, the muscles are weak but contracting.

The reasons for the development of newborn asphyxia include a complex of risk factors that disrupt the blood circulation and respiratory functions of the fetus in the womb and during birth. The most common reasons include:

• conflict of Rh blood between mother and child;
• abnormal fetal development;
• pathologies of the nervous system in a baby;
• circulatory disorders, heart disease in the baby;
• intracranial injury that the baby received during the birth process;
• infections affecting the fetus in the womb (chlamydia, herpes, rubella, etc.);
• extragenital pathologies of the mother (thyrotoxicosis, anemia, diabetes mellitus);
• infectious diseases in the second and third trimesters;
• complicated childbirth;
• premature or post-term pregnancy;
• bad habits of the mother (effects of alcohol, nicotine, drugs on the body);
• malnutrition during pregnancySource: Asphyxia of newborns. Zhetpisova L.B. West Kazakhstan Medical Journal, 2011.

The most common cause of asphyxia is intrauterine hypoxia, that is, the baby lacks oxygen in the womb.

Whatever the causes of the pathological condition, it causes the same processes in the child:

• disrupts metabolism and blood circulation;
• thickens and increases blood viscosity;
• damage is caused to the brain, liver, heart, adrenal glands;
• organs swell, bleeding occurs;
• disruptions in the functioning of the central nervous system occur.

The longer the body feels a lack of oxygen, the more serious the degree of damage to tissues, organs and systems becomes.

Symptoms of neurological diseases in children

The first signs of neurological disorders can be noticed in a child at a very early age. You should consult a doctor for help if you experience the following symptoms:

• twitching of the chin and arms at rest;
• throwing your head back while crying;
• lack of reaction to bright light and the sound of a rattle;
• inability to hold a rattle 30 days after birth;
• inability to hold the head 30 days after birth;
• excessive salivation after feeding;
• hyperexcitability (frequent crying) or passive behavior (does not cry at all);
• increased anxiety, sleep disturbances (difficulty falling asleep, sleeping more than 20 hours a day);
• frequent regurgitation in a fountain;
• the occurrence of seizures with a slight increase in temperature;
• hypertonicity (constant tension) of the leg muscles, arching of the body or tilting of the head to the side, which makes it difficult to change the child’s clothes;
• difficulty swallowing food;
• temporary loss of consciousness;
• A 3-month-old baby does not imitate the speech of adults;
• sunken fontanelle;
• the child does not want to sleep on his stomach;
• When leaning on his legs, the child bends his fingers.

As for an older child, the symptoms of neurological diseases in children will be somewhat different:

• forgetfulness, absent-mindedness;
• fainting;
• urinary incontinence;
• delayed speech development;
• excessive nervousness;
• panic attacks;
• the child has difficulty making contact with other children;
• insomnia;
• poor appetite;
• constant despondency and melancholy attitude towards life;
• constant headache.

If parents detect even some of these signs, it is necessary to urgently consult a specialist.

Causes

The factors that provoke the development of hypoxia in the newborn are very numerous. Conventionally, they can be divided into 4 large groups:

Antenatal causes (acting during pregnancy)

These include:

• severe somatic diseases of the mother (cardiovascular, respiratory, endocrine pathology),
• chronic intoxication of a pregnant woman (smoking, drinking alcohol, using drugs, occupational hazards, disturbed ecology).

This list also includes:

• premature and post-term pregnancy,
• gestosis,
• severe pronounced anemia,
• bleeding during pregnancy (previa, placental abruption),
• intrauterine infection of the fetus with chronic maternal infections and acute infection suffered during pregnancy,
• polyhydramnios and oligohydramnios,
• multiple pregnancy.

In addition, hypoxia may be to blame for:

• Rhesus conflict pregnancy and antiphospholipid syndrome,
• permanent threat of miscarriage and development of fetoplacental insufficiency,
• constant stress, unfavorable living conditions, poor nutrition.

Intrapartum causes (complicated labor)

This group includes:

• protracted or, conversely, rapid labor,
• birth injury to the fetus (damage to the brain or spinal cord),
• labor stimulation with oxytocin,
• surgical delivery (application of obstetric forceps, caesarean section).

This group also includes:

• drop in blood pressure during childbirth,
• preeclampsia and eclampsia during childbirth,
• placental abruption during childbirth,
• hypoxia of a woman during general anesthesia,
• uterine ruptures,
• anomalies of labor (discoordination of labor forces).

Pathology from the umbilical cord

• true nodes and their tightening of the umbilical cord,
• rupture of the umbilical vessels,
• umbilical cord entanglement,
• umbilical cord compression.

Fetal causes (from the fetus).

These reasons include:

• hemolytic disease of the fetus and newborn (anemia due to hemolysis of red blood cells),
• fetal malformations (anomalies of the cardiovascular and pulmonary systems),
• infectious intrauterine diseases,
• hemorrhages in the brain, adrenal glands.

Asphyxia of the newborn

Asphyxia, which subsequently turns into hypoxia of the newborn, develops as a result of blockage of the respiratory tract (ingestion of amniotic fluid and meconium by the child, blockage of mucus, tight entanglement of the umbilical cord, prolonged and problematic birth of the head, and others).

List of neurological diseases in children

The list of neurological diseases in children is quite impressive, so we will limit ourselves to listing the most common ones.

• Epilepsy. The disease manifests itself by sudden, recurring convulsive attacks.
• Cerebral palsy . The disease is characterized by limited motor capabilities of the child, difficulties in maintaining an upright posture and walking. Often accompanied by reduced intelligence, delayed speech development and epilepsy.
• Neurosis (psychoneurosis, neurotic disorder) . This name unites a group of reversible disorders, which are characterized by obsessive, asthenic or hysterical manifestations, weakening of both mental and physical performance.
• Hyperactivity . The disease manifests itself in the child’s excessive energy and mobility, impaired attention and sleep, lack of appetite, anxiety and some bad habits, for example, the habit of biting nails.
• Asthenic syndrome . Often occurs as a consequence of traumatic brain injury. It manifests itself as rapid fatigue, irritability, isolation and self-doubt, or a complete loss of the ability to perform physical activity for a long time.

Treatment of neurological diseases in children

Treatment of neurological disorders in children includes taking medications that restore the functioning of the nervous system, physical and psychological correction. The child may be prescribed courses of therapeutic massage, special physical education, and exercises in water. Physiotherapeutic methods are often used - stimulation with a high-intensity magnetic field or electric current, laser therapy, ultraphonophoresis of enzyme preparations, electrophoresis and others.

What treatment the doctor will prescribe depends on the child’s age, concomitant diseases, the totality of all the features of the development of neurological pathology from beginning to end, as well as on the effectiveness of correction at the previous stage.

In the city of Penza, you can be examined by a pediatric neurologist and receive qualified assistance at the medical ]"Stoletnik"[/anchor], located at the address: st. Chaadaeva, 95 on the first floor of a five-story residential building. On Wednesdays from 9.00 to 12.00 and on Fridays from 13.00 to 15.00, consultations are conducted by a doctor of the highest qualification category.

MAKE AN APPOINTMENT

Therapeutic tactics of hypoxia

If fetal hypoxia occurs during the period of pushing or during contractions (decrease in heartbeat), a decision is made to complete the labor as soon as possible: a cesarean section or the application of obstetric forceps (in the case of labor stimulation with oxytocin, the administration of the drug is stopped). After the birth of the child, immediate medical care begins:

• clearing the respiratory tract from mucus, meconium and water (suction with a special aspirator);
• supplying a mixture of oxygen with air or pure humidified oxygen through a mask, nasal catheter or mechanical ventilation device (in case of severe hypoxia, the newborn is placed in an incubator, intubated and mechanical ventilation is started);
• heating the baby with radiant heat (on a special changing table), and in case of severe hypoxia, placing the baby in an incubator;
• administration of drugs that stimulate blood circulation and increase blood pressure (camphor, dopamine) and drugs that stimulate the respiratory center (etimizole);
• intravenous infusions solution, sodium bicarbonate (neutralization of carbon dioxide in the blood), glucose to restore the reduced volume of the vascular bed;
• transfusion of blood products if necessary (hemolytic disease of the newborn);
• prescribing antibiotics to prevent pulmonary infections in case of severe hypoxia or intrauterine infection of the fetus, as well as in respiratory distress syndrome during premature birth;
• prescription of anticonvulsants (phenobarbital, phenazepam);
• To reduce intracranial pressure, administration of diacarb and veroshpiron (diuretics with the effect of reducing cerebrospinal fluid production) is indicated.