Hypoxia of the fetus and newborn

Fetal hypoxia, or oxygen starvation, is a condition that occurs in the fetus and the newborn due to oxygen deficiency.

Intrauterine (antenatal) fetal hypoxia is an oxygen deficiency that occurs during pregnancy.

Intranatal hypoxia of the fetus is hypoxia, which develops in childbirth.

Perinatal hypoxia of the fetus is oxygen deficiency that occurs during pregnancy and / or childbirth and develops until the end of the early neonatal period.

Hypoxia of a newborn can have perinatal (associated with pregnancy and childbirth) and postnatal (after birth) origin.

In the practice of obstetrics, it is customary to call the oxygen deficiency that developed during pregnancy and / or childbirth, hypoxia, and oxygen deficiency in the child born asphyxia.

Asphyxia is a pathological condition caused by hypoxia and hypercapnia, characterized by the presence of cardiac activity and certain irregular respiratory movements or lack of breathing. Depending on the duration of the course, hypoxia can be chronic - from several days to several months (typical for intrauterine hypoxia of the fetus) and acute - from several minutes to several hours, which occurs with rapid disturbances of oxygen in the body (more often with intrapartum hypoxia).

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11]

Epidemiology of fetal hypoxia

Hypoxia and its consequences during pregnancy and childbirth rank first among causes of perinatal morbidity and mortality.

Against the background of a general decline in perinatal mortality rates, the frequency of cerebral pathology has increased as a consequence of fetal hypoxia, often resulting in severe neurologic child disability.

In premature and newborn children with morphological and functional immaturity, hypoxia develops 10-15 times more often and has less favorable course and outcome.

[12], [13], [14], [15], [16], [17], [18], [19]

What causes fetal hypoxia?

To the oxygen deficiency of the fetus and the newborn causes an extremely large number of complications during pregnancy and childbirth, as well as causes not related to pregnancy.

All the causes that cause antenatal, intranatal and perinatal fetal hypoxia can be divided into five groups.

1. The first group of causes is associated with abnormal placenta: anomaly of development and attachment, presentation and detachment of the placenta, trauma, hemorrhage, tumors, infection of the placenta.
2. The second group of causes is related to the pathology of the umbilical cord: anomaly of development, torso of the umbilical cord, the true node of the umbilical cord.
3. The third group of causes is due to fetal pathology: rhesus sensitization, intrauterine growth retardation, intrauterine infections, malformations, genetic diseases.
4. The fourth group of causes is associated with a complicated course of pregnancy and childbirth; The largest proportion in this group is gestosis and a prolonged threat of abortion. Other, no less important reasons include anemia of pregnant women, nephropathy, antiphospholipid syndrome, intrauterine infection, perenashivanie, polyhydramnios and hypochlorism, multiple pregnancies, premature birth, weakness of labor, discoordination of labor, prolonged labor.
5. The fifth group of causes is due to chronic pathology in the pregnant woman: cardiovascular (rheumatic disease, heart defects, neurocirculatory dystonia), endocrine (diabetes mellitus, thyroid pathology, obesity), chronic kidney disease, lung, liver, blood, cancer, drug addiction, alcoholism .

All of the above causes lead to utero-fruit-placental insufficiency - the main factor in the development of chronic hypoxia.

Chronic fetal hypoxia in some cases can be caused by the influence of the so-called exogenous factors arising under conditions of reduced partial oxygen pressure in the inspired air (high altitude, Far North, etc.).

The causes of acute fetal hypoxia are situations that cause a rapid cessation of oxygen supply to the body: prolapse of the umbilical cord, tight cord around the neck, tight cord umbilical cord, acute uterine bleeding, previa and premature detachment of the placenta in childbirth, abnormal fetal presentation, premature birth and t .

Chronic intrauterine fetal hypoxia

In response to the effects of certain causes that cause oxygen deficiency, compensation mechanisms are launched to maintain adequate oxygenation. These mechanisms include increased rates of placental circulation, hyperplasia of the fetal part of the placenta, an increase in the capillary bed capacity and increased fetal blood flow, which leads to an increase in heart rate. The increase in palpitation of the fetus is the most important sign of the onset of hypoxia. If the cause of hypoxia is not eliminated, there is fetoplacental insufficiency - the basis for the development of chronic fetal hypoxia. Further, in the pathogenesis of chronic (intrauterine) hypoxia, three links can be distinguished.

1. Oxygen deficiency triggers activation of the fetal adrenal cortex, accompanied by increased production of catecholamines and their entry into the bloodstream, which causes redistribution of blood, aimed at enhancing blood circulation in vital organs (heart, brain). As a result, blood pressure rises and a threat of hemorrhage develops.
2. Deficiency of oxygen stimulates the process of hemopoiesis as a compensatory reaction of the fetal organism. This leads to the development of erythrocytosis, thrombocytosis in the vascular bed, the viscosity of the blood increases, intravascular aggregation of cells occurs, including platelets in the microcirculatory bed, which in turn leads to the formation of microthrombi. There is a violation of microcirculation, the result of which may be the development of ischemia of any organ. Along with the process of microthrombogenesis, activation of the coagulating system of blood can occur, an increase in the consumption of coagulation factors and blood cells (erythrocytes, platelets) around the blood clots where the hypocoagulation zone is formed. This can provoke the development of DIC syndrome (hemorrhage and bleeding).
3. In response to oxygen starvation, metabolic changes occur, to which the fetal brain is particularly sensitive. First of all, tissue respiration is enhanced, glycogenolysis and anaerobic glycolysis are activated, as a result of which acidic metabolic products are formed. In conditions of pathological acidosis, the permeability of the vascular wall and cell membranes increases. Through the pores of the cells of the central nervous system, there is a loss of "exciting" amino acids (glutamine, glycine, succinic, etc.), which can cause depression (depression) of the central nervous system.

Under the conditions of anaerobic glycolysis, calcium accumulation occurs in the axons of CNS cells, which can lead to seizures.

Finally, potassium-sodium metabolism is disrupted in the cells of the brain. Loss of potassium by the cell causes the entry of sodium and water into the cells, as a result of which edema (swelling) of the brain develops. The blood increases the content of potassium, and the concentration of sodium decreases.

Thus, the consequences of chronic (intrauterine) fetal hypoxia can be:

• perinatal CNS damage;
• hemorrhages, bleeding, ischemia of internal organs (myocardium, lungs, kidneys, adrenals, intestines);
• retardation of fetal development;
• prematurity;
• death of the fetus.

[20], [21], [22], [23], [24], [25], [26], [27], [28], [29], [30]

Acute intrauterine fetal hypoxia

The pathogenesis of acute fetal hypoxia is characterized by the rapid inclusion of reflex-adaptive reactions of the fetal and neonatal cardiovascular system with minimal changes in metabolism.

Acute oxygen deficiency causes a rapid drop in its partial pressure in the fetus's blood, in response there is an activation of the adrenal system of the adrenal cortex, ejection of catecholamines into the vascular bed, an increase in cardiac output, and the appearance of a tachycardia that provides blood and, along with it, oxygen to vital organs. At the same time, compensatory spasm of peripheral vessels develops, where acidic metabolic products are deposited without penetrating into the central bloodstream.

If the oxygen balance is not restored, the compensatory mechanisms fail: the function of the adrenal cortex is depleted, bradycardia develops, and blood pressure in the central vessels falls. Blood flows from the central bloodstream into the peripheral channel, a sharp drop in oxygen perfusion occurs in vital organs, which leads to their hypoxia, anoxia, and ischemia. In this case, the child can be born in a state of hypoxic shock or coma. Cases of fetal or neonatal death are possible.

[31], [32], [33], [34], [35], [36], [37], [38]

Classification of fetal hypoxia

The severity of the fetal hypoxia is:

• moderate;
• heavy.

Assessment of the severity of hypoxia is carried out on the Virginia Apgar scale. The scale of assessing the state of the newborn at the first minutes of life was first presented at the 27th Congress of Anesthesiologists in 1952. The scale represents a system of criteria (5 indicators) for assessing the state of the newborn, including observation:

• for the nature of breathing (no breathing, slow or irregular, good or screaming);
• for reflexes - reaction to a catheter in the nose (no reaction, grimace of crying, coughing, sneezing or crying);
• for tonus of muscles (weak, bending of arms and legs, active movements);
• for the color of the skin (cyanotic, pale, pink body, cyanotic limbs, pink);
• (heart rate is less than 100 per minute, more than 100 per minute).

Each indicator is evaluated on a three-point system (0-1-2 points). The Apgar score is scored twice: in the first minute of life and five minutes after birth. A healthy newborn has an assessment of 8-10 points.

Most newborns in the first minute of life receive an estimate of 7-8 points due to cyanosis and decreased muscle tone. After five minutes, the score rises to 8-10 points, which indicates a good adaptation of the child.

The Apgar scores of 4-7 points indicate moderate hypoxia, an score of 0-3 indicates severe hypoxia (asphyxia).

Classification of fetal hypoxia by severity is important for assessing the child's condition in the first minutes after birth and addressing the need for resuscitation and intensive care tactics.

[39], [40], [41], [42], [43], [44]

Classification of hypoxic CNS lesions in neonates

The successes achieved in perinatology over the past decades, the active introduction of new medical diagnostic technologies into clinical practice of obstetrics and perinatology allow timely diagnosis of fetal hypoxia and its consequences, the most dangerous of which is the CNS lesion. For a long time hypoxic CNS damage was denoted by the terms "perinatal encephalopathy", "cerebral blood circulation disorder", etc. The lack of clear terminology adversely affected the timely diagnosis of the effects of perinatal damage to the nervous system, in particular the effects of hypoxic CNS lesions, on timely and adequate therapy, which led to an increase in neglected cases and the growth of a child's psycho-neurological disability.

The use of advanced technologies in perinatal practice made it possible to clarify the etiology, pathogenetic mechanisms, clinical and morphological structures, the localization of cerebral disorders typical for different gestational ages, to develop uniform approaches to terminology and to develop a new classification of perinatal neural lesions in newborns.

The classification was developed by the Russian Association of Specialists of Perinatal Medicine and approved at the VI Congress of Pediatricians of Russia in February 2000.

According to this classification, neurological disorders, depending on the leading mechanism of damage, are divided into four groups:

• I - hypoxic;
• II - traumatic;
• III - toxic-metabolic;
• IV - infectious.

In each of these groups, the nosological form, severity and basic neurological symptoms and syndromes are distinguished.

Fundamentally new in the classification is the separation of hypoxic brain damage into cerebral ischemia and intracranial hemorrhages.

Cerebral ischemia (hypoxic-ischemic encephalopathy, perinatal hypoxic brain damage)

In terms of severity, three nosological forms are distinguished.

1. Cerebral ischemia I degree (light) is characterized by excitation and / or depression of the central nervous system (no more than 5-7 days).
2. Cerebral ischaemia of II degree (moderate severity) is characterized by oppression and / or excitation of the central nervous system (more than 7 days), development of convulsions, intracranial hypertension, vegetative-visceral disorders.
3. Cerebral ischemia of the third degree (severe) is characterized by a progressive loss of cerebral activity (over 10 days), oppression, passing into a coma, or oppression, which turns into excitement and convulsions, or oppression, turning into convulsions and coma. Characteristic development of seizures, possibly the emergence of status epilepticus. There are dysfunction of the brain stem departments, decortication, decerebration, vegetovisceral disorders, progressive intracranial hypertension.

[45], [46], [47], [48], [49], [50]

Intracranial hemorrhages of hypoxic origin

There are five nosological forms.

1. Intraventricular hemorrhage of the 1st degree (subependymal) is characteristic of prematurity. Specific neurological symptoms are absent.
2. Intraventricular hemorrhage of the second degree (subependymal + intraventricular) is characteristic of prematurity. Clinical symptoms: shock, apnea, oppression, passing into coma; convulsions, intracranial hypertension (fast or slow progressing).
3. Intraventricular hemorrhage of the third degree (subependymal + intraventricular + periventricular) is characteristic of prematurity. Clinical symptoms: shock, apnea, deep depression, coma, seizures (more often tonic), intracranial hypertension (rapidly or slowly progressing with dysfunction of the caudal sections of the trunk).
4. Primary subarachnoid hemorrhage is more common in premature babies. Typical clinical syndromes: hyperexcitability of the central nervous system, hyperesthesia, partial (focal) clonic convulsions, intracranial hypertension (acute hydrocephalus).
5. Hemorrhage into the brain substance (parenchymal) is more common in premature babies. The clinical picture depends on the localization and volume of hemorrhage: hyperexcitability, turning into convulsions, deep oppression, passing into a coma, partial (focal) convulsions, intracranial hypertension. Perhaps an asymptomatic course.

Combined ischemic and hemorrhagic lesions of the central nervous system (non-traumatic)

The clinical picture and severity of the condition depend on the leading type of lesion and localization.

In the first days of life, the nosological diagnosis of CNS lesions is often difficult, since clinical neurologic manifestations are similar in different pathological states, and no additional information is available. For this reason, the setting of a syndromological diagnosis (for example, hyperexcitability syndrome, oppression syndrome, etc.) is permissible, which should be further clarified in the course of obtaining anamnestic, clinical and laboratory data.

[51], [52], [53], [54]

Criteria for the diagnosis of hypoxic lesions of the central nervous system

The principles of the diagnosis of perinatal CNS lesions in newborns should be based on data:

• anamnesis;
• clinical symptoms and syndromes;
• results of additional surveys.

[55], [56], [57], [58], [59]

Cerebral ischemia

Cerebral ischaemia of the 1st degree (light), or hypoxic-ischemic lesion of the central nervous system of the 1st degree.

• In the anamnesis: intranatal fetal hypoxia, mild asphyxia at birth.
• Clinical syndromes: excitation of the central nervous system (usually in term), CNS depression (in premature infants) with a duration of no more than 5-7 days.
• Survey results.
  • Metabolic disorders (moderate hypoxemia, hypercapnia, acidosis).
  • NSG, CT, MRI - without pathological abnormalities.
  • DEG - compensatory increase in the rate of blood flow along the main arteries of the brain.

Cerebral ischemia of the 2nd degree (moderate severity), or hypoxic-ischemic lesion of the central nervous system of the 2nd degree.

• In the anamnesis: intrauterine hypoxia of the fetus, asphyxia of moderate severity at birth.
• Clinical symptoms:
  • oppression of the central nervous system, excitation or change of phases of cerebral activity (duration more than 7 days); convulsions: in premature babies - tonic, or atypical (apnea, oral automatism, fluttering of eyelids, myoclonias of eyeballs, "rowing" movements of hands, "pedaling" of the legs); in full - clonic (short-term, single, rarely repeated);
  • intracranial hypertension (transient, often in term);
  • vegetative-visceral disorders.
• Survey results.
  • Metabolic disorders (hypoxemia, hypercapnia, acidosis) are more pronounced and persistent.
  • NSH: local hyperechoic foci in the brain tissue (in premature infants more often in the periventricular region, in full-term - subcortical). MPT: focal lesions in the parenchyma of the brain.
  • CT of the brain: local foci of reduced density in the brain tissue (in premature infants more often in the periventricular region, in full-term - subcortically and / or cortically).
  • FDEG: signs of hypoperfusion in the middle cerebral artery in the terminus and anterior cerebral artery in prematurity. An increase in the diastolic component of blood flow velocity, a decrease in the resistance index.

Cerebral ischaemia of the third degree (severe), or hypoxic-ischemic lesion of the central nervous system of the third degree.

• In the history: intrauterine hypoxia of the fetus and / or severe perinatal asphyxia, persistent hypoxia of the brain.
• Clinical symptoms:
  • progressive loss of cerebral activity (over 10 days);
  • repeated seizures (possible epileptic status);
  • dysfunction of the brain stem (abnormalities in the rhythm of breathing, pupillary reactions, oculomotor disorders);
  • posture of decortication and decerebration (depends on the extent of the lesion);
  • expressed vegetative-visceral disorders;
  • progressive intracranial hypertension.
• Survey results.
  • Persistent metabolic disorders.
  • NSH: a diffuse increase in echogenicity of the cerebral parenchyma (in term donors), periventricular structures (in prematurity). Narrowing of the lateral ventricles. Formation of cystic periventricular cavities (in premature infants). The appearance of signs of atrophy of the cerebral hemispheres with a passive expansion of the spaces of circulation of cerebrospinal fluid.
  • CT: reduction in the density of the cerebral parenchyma, narrowing of the spaces of circulation of the cerebrospinal fluid, multifocal cortical and subcortical foci of reduced density, changes in basal ganglia and thalamus density (in term donors), periventricular cystic cavities in premature infants (to be clarified by the radiologist).
  • MRI: damage to the parenchyma of the brain.
  • DEG: paralysis of the main arteries with the transition to persistent cerebral hypoperfusion. Decrease in diastolic blood flow velocity, change in character of the curve. Increase in the resistance index.

[60], [61], [62], [63], [64], [65], [66], [67]

Intracranial hemorrhage (hypoxic, non-traumatic)

Intraventricular hemorrhage I degree (subependimal).

• In the anamnesis: ante- and intranatal fetal hypoxia, mild asphyxia at birth, repeated apnea attacks, jet injection of hyperosmolar solutions.
• Clinical symptoms: it develops mainly in premature or immature neonates. The course is asymptomatic, there are no specific neurological disorders.
• Survey results.
  • Transient metabolic disorders.
  • NSH: hyperechoic regions of one- or two-sided localization in thalamo-caudal notch or in the region of the head of the caudate nucleus. The timing of the transformation of subependimal hematoma in the cyst is 10-14 days or more.
  • CT, MRI do not have diagnostic advantages over NSH.
  • DEG - without pathology.

Intraventricular hemorrhage of the second degree (subependymal, intraventricular) develops mainly in prematurity.

In the anamnesis: intrauterine fetal hypoxia, moderate birth asphyxia, defects in primary resuscitation, arterial hypertension or systemic BP fluctuation due to SDR, iatrogenic factors (inadequate ventilation, rapid administration of large volumes or hyperosmolar solutions, functioning fetal communications, pneumothorax, etc.) ), coagulopathy.

Clinical symptoms: two main variants of the flow are distinguished: gradual (wavy) and catastrophic.

Catastrophic course: short-term motor excitement is suddenly replaced by progressive suppression of cerebral activity with the transition to coma, deep apnea, increasing cyanosis and "marbling" of the skin, tonic convulsions, oculomotor disorders, bradyarrhythmia, thermoregulatory disturbances, indicative of increasing intraventricular hypertension.

• Gradual course: periodic phase change of cerebral activity, seizures of repeated apnea, muscle hypotension, atypical convulsive attacks.
• Survey results.
  • Decreased systemic blood pressure.
  • The fall of the hematocrit and the concentration of hemoglobin.
  • Metabolic disorders: hypoxemia, hypercapnia, acidosis, hypocalcemia, fluctuations in glucose in the blood plasma.
  • CSF with an admixture of blood, reactive pleocytosis, increase in protein concentration, decrease in glucose content.
  • NSH: in the initial stages - hyperechoic zones, then - ventriculomegaly, echopositive formations (thrombi) in the ventricles. Possible blockage of the outflow of cerebrospinal fluid with the development of acute hydrocephalus.
  • CT, MRI, PET have no diagnostic advantages over NSH in newborns.
  • DEG: fluctuation of blood flow in the main arteries of the brain until the development of intraventricular bleeding, stabilization after hemorrhage. With the progression of ventriculomegaly (after 10-12 days) - increasing hypoperfusion.

Intraventricular hemorrhage of the third degree (subependymal + intraventricular + periventricular).

In the anamnesis: the same, that at a grade 2 IVH.

Clinical symptoms:

• most often occurs in premature infants with extremely low body weight;
• typically a catastrophic course: the rapid suppression of cerebral activity with the development of coma, a progressive disorder of vital functions (bradycardia, arrhythmias, apnea, rhythm pathology, respiration), tonic convulsions, oculomotor disorders, high incidence of death in the first days of life.

Survey results.

• Severe, difficult to correct metabolic disturbances (hypoxemia, hypercapnia, acidosis, electrolyte disorders), DIC syndrome.
• A critical drop in hematocrit and hemoglobin concentration.
• Progressive fall of systemic blood pressure and cardiac arrhythmias.
• CSF: the admixture of blood is significant, reactive pleocytosis, an increase in protein concentration, and the pressure of cerebrospinal fluid is increased. Spinal puncture is performed according to strict indications and very carefully because of the high risk of wedging the brainstem into the large occipital foramen.
• NSH: an extensive hyperechoic region of periventricular localization (hemorrhagic infarction more often in the frontal-parietal region). Later - ventriculomegaly and deformation of the lateral ventricle as a result of the formation of the cystic cavity. Often in the lumen of the ventricles - clots. In most cases occlusal hydrocephalus is formed.
• CT, MRI, PET do not have diagnostic advantages in the period of the newborn before NSH.
• DEG: in the initial stages - a decrease in systolodiastolic blood flow velocity, an increase in the resistance index. Then - a decrease in the diastolic blood flow velocity, a decrease in the resistance index.

Primary subarachnoid hemorrhage (non-traumatic) - mainly in preterm and immature.

In the anamnesis: intranatal fetal hypoxia, asphyxia at birth, short gestation period, immaturity, coagulopathy.

Variants of clinical course:

• asymptomatic;
• excitation syndrome with hyperesthesia and acute intracranial hypertension (tension and swelling of the large fontanel, seam divisions, profuse regurgitation, unstable Gref symptom);
• seizures that suddenly appear on the 2-3th day of life (clonic - in term, atypical - in premature).

Survey results.

• Metabolic disorders are atypical.
• The NSG is not very informative. There may be an expansion of the interhemispheric fissure.
• CT and MRI: the accumulation of blood in various parts of the subarachnoid space, but more often in the temporal areas.
• DEG is poorly informative (primary and secondary vasospasm).
• CSF: pressure increased, increased red blood cell count, increased protein concentration, neutrophilic pleocytosis.

Hemorrhage into the brain substance (non-traumatic) parenchymal (rarely - cerebral hemorrhage and posterior cranial fossa).

In the history: intrauterine hypoxia of the fetus, severe or moderate asphyxia at birth, coagulopathy, prematurity, vascular malformations.

The clinical picture depends on the localization and volume of hemorrhagic infarction:

• with disseminated petechial hemorrhages of subcortical localization, there may be an asymptomatic course;
• with extensive petechial hematomas of hemispheric localization, clinical course is similar to grade III IVH. Progressive loss of cerebral activity with transition to stupor or coma, focal neurological symptoms contralateral to the lesion focus (asymmetry of muscle tone, convulsions, oculomotor disorders, etc.), increasing intracranial hypertension;
• hemorrhages in the posterior cranial fossa and cerebellum are characterized by increasing signs of intracranial hypertension and stem disorders (respiratory, cardiovascular disorders, oculomotor disorders, bulbar syndrome).

Survey results.

• Severe, hard-to-correct metabolic disorders, DIC-syndrome (accompanied by massive hematomas).
• Reduction of hematocrit and hemoglobin concentration.
• Progressive increase in systemic BP is followed by its fall.
• Violation of the heart rate.
• CSF: pressure increased, increased red blood cell content, increased protein concentration, neutrophilic pleocytosis (except for small focal parenchymal hemorrhages).
• NSH in small-point hemorrhages is poorly informative. Massive hemorrhagic infarcts are projected as asymmetric hyperechogenic foci in the brain parenchyma. After 2-3 weeks in their place pseudocysts, leukomalacies are formed.
• CT: foci of increased density in the parenchyma of the brain, deformation of the spaces of circulation of the cerebrospinal fluid.
• MRI: a change in the MR signal from foci of hemorrhage in the acute stage.
• DEG: asymmetric hypoperfusion in the cerebral arteries on the affected side.

Combined ischemic and hemorrhagic lesions of the central nervous system

Combined ischemic and hemorrhagic lesions of the central nervous system (non-traumatic) occur much more often than all isolated forms of CNS damage (occur primarily in prematurity).

In the anamnesis: intrauterine hypoxia and asphyxia at birth, premature infants with a small body weight (1000-1500 g), defects in primary resuscitation, arterial hypotension, hypertension or fluctuations in systemic blood pressure, coagulopathy, DIC syndrome.

The clinical picture depends on the leading type of CNS lesion (ischemia or hemorrhage), its severity and localization. These types of damage are most severe.

Survey results.

• Difficultly amenable to correction of metabolic disorders.
• CSF: pressure is increased, the morphological characteristics depend on the degree of hemorrhage in the space of circulation of the cerebrospinal fluid.
• NSG, CT, MRI: various variants of deformation of the system of cerebrospinal fluid outflow, foci of changed density of different intensity, mainly periventricular localization.
• DEG: oscillation of cerebral blood flow, paralysis of the main arteries of the brain, decreased blood flow.
• The diagnosis is formulated as follows: combined (non-traumatic) ischemic-hemorrhagic CNS lesion. In cases of diagnosis of specific structural changes in the brain, this is reflected in the diagnosis.

[68], [69], [70], [71], [72], [73], [74], [75]

Consequences of hypoxic lesions of the central nervous system

Perinatal lesions of the central nervous system, in particular hypoxic genesis, are not limited only to the period of the newborn. Their consequences are of particular importance in the first year of life. Timely and adequate therapy during this period can lead to more favorable outcomes and reduce the risk of developing persistent neurological disorders.

In connection with this, the Russian Association of Perinatal Medicine Specialists proposed the project "Classification of the effects of perinatal lesions of the nervous system in children of the first year of life".

The classification is based on the following principles.

• Etiology and pathogenetic basis of lesions of the nervous system of the perinatal period.
• Variants of clinical course: transient (transient) and persistent (organic) neurological disorders.
• Main clinical syndromes.
• Outcomes (full compensation, functional disorders or persistent neurological deficit by the 1st year of life). Hypoxic lesions of the CNS have the following consequences.
• The consequences of cerebral ischemia-hypoxia I-II degree - perinatal transient post-hypoxic-ischemic encephalopathy.
• Consequences of hypoxic intracranial hemorrhages I-II degree - perinatal transient posthemorrhagic encephalopathy.
• The consequences of cerebral ischemia-hypoxia and / or intracranial hemorrhage of grade II-III are perinatal persistent (organic) post-hypoxic and posthemorrhagic CNS lesions.

Clinical syndromes of the above first two variants of encephalopathies:

• hydrocephalus (unspecified);
• disorder of the autonomic nervous system (unspecified);
• hyperactive behavior, hyperexcitability;
• impairment (delay) of motor development;
• combined forms of developmental delay;
• symptomatic cramps and situationally conditioned paroxysmal disorders (curable epileptic syndromes).

Outcomes:

• full compensation of neurological abnormalities in the first year of life;
• may not be intractable functional disorders.

Clinical syndromes of the third variant of encephalopathies:

• various forms of hydrocephalus;
• severe organic forms of mental development disorder;
• severe forms of motor development disorder (cerebral palsy);
• symptomatic epilepsy and epileptic syndromes of early childhood;
• defeat of cranial nerves.

Outcomes:

• Neurological abnormalities are not compensated by the end of the first year of life;
• there is a total or partial neurological deficit.

[76], [77], [78], [79], [80], [81], [82], [83], [84]

Criteria for the diagnosis of fetal hypoxia

The criteria for diagnosing hypoxia include the following.

• Malodode.
• Meconium in the amniotic fluid.
• Change in the indices of feto- and placentometry (low water, structural changes in the placenta, condition of the membranes and umbilical cord).
• Change in the parameters of dopplerometry (pathological values of blood flow in the uterine artery, umbilical cord, middle cerebral artery of the fetus, pathological blood flow in the venous duct of the fetus in the second half of pregnancy).
• Change in cardiomonitoring indicators (fetal bradycardia less than 120 per minute, monotony of the rhythm of cardiac activity, periodic decelerations, anactive non-stress test).
• Change in the characteristics of amniotic fluid (the presence of meconium) during amnioscopy (if the maturity of the cervix reaches 6-8 points on the Bishop scale, when the cervical canal passes for one finger) or amniocentesis (if there are no conditions for amniascopy).

[85], [86], [87], [88], [89], [90], [91], [92], [93], [94]

Differential diagnosis of hypoxic lesions of the central nervous system

• The most important is differential diagnosis between intracranial hemorrhages of hypoxic genesis and intracranial birth trauma.
• Epidural, subdural, supratentorial, subtentorial hemorrhages are characteristic only for birth trauma and do not occur during hypoxia.
• Intraventricular, parenchymal and subarachnoid hemorrhages develop both with fetal hypoxia and with birth trauma. The main criteria for a differential diagnosis are:
  • history data;
  • features of the clinical picture;
  • results of surveys.

[95]

With intraventricular traumatic hemorrhage

• In the anamnesis: the fact of presence of a birth trauma (fast rotation of a head, forced extraction of a fruit).
• Clinically: often, but not always, the manifestation of a clinical picture on the 1-2 day of life or later, and not at birth.

Survey results.

• There are no specific metabolic disorders.
• NSH: deformation of the contours of vascular plexuses.
• CSF: an admixture of blood is detected only in cases of penetration of blood into the subarachnoid space.

With traumatic parenchymal hemorrhages (hemorrhagic infarction)

In the anamnesis: complicated birth (incompatibility of the birth canal with the size of the fetal head, pathological variants of the presentation of the fetus, etc.).

It is more common in full-term donors with a large mass (more than 4000 g) and those born.

Survey results.

• Metabolic changes are not typical.
• CT, MRI, DEG are poorly informative.

With subarachnoid traumatic hemorrhage

In the anamnesis: anomalies of childbirth (mismatch of birthmarks to the size of the fetal head, pathological variants of presentation, instrumental delivery). In 1/4 cases it is combined with fractures of the skull.

Clinical symptoms:

• occurs rarely, mostly in the term infants.
• oppression of the central nervous system or hyperexcitability and convulsions develop within 12 hours, vascular shock (in the first hours), followed by alternating hypertension; development of posthemorrhagic anemia.

Survey results.

• Metabolic changes are not typical.
• NSG: increased subcortical white substance echodensity on the side of hemorrhage, progressive expansion of subarachnoid space.
• CT: an increase in the density of the subarachnoid space and its subsequent expansion.

Intracranial birth trauma is characterized by a rupture of intracranial tissue and hemorrhage due to birth trauma.

Hypoxic lesions of the central nervous system can also in some cases differentiate from neuroinfections, brain tumors. In these cases it is necessary to use the information obtained during CT, MRI and CSF research.

Treatment of fetal hypoxia and its consequences

Treatment in an acute period depends on the severity of fetal hypoxia (asphyxia).

The tactics of conducting newborns with hypoxia in the delivery room is as follows.

• Release of the upper respiratory tract (suction of contents from the upper respiratory tract).
• Restoration of external respiration.
• Warming.
• Monitoring of vital functions and symptomatic therapy according to indications.

If a newborn who under the vital indications performed primary resuscitation measures in the delivery room, an Apgar score 5 minutes after birth did not reach 7 points, it must be urgently transferred to the intensive care ward.

After completion of resuscitation in the delivery room of a newborn with severe hypoxia, they are transferred to the intensive care unit.

The purpose of intensive care is the prevention or minimization of functional and organic disorders caused by the action of adverse perinatal factors.

The main task of intensive care is a rapid primary (or early) stabilization of the condition of sick newborns.

The complex of medical and diagnostic measures for primary stabilization of the state includes the following measures:

• Monitoring (dynamic assessment) of vital functions.
• Maintenance of adequate oxygenation (oxygen masks, oxygen tents). In the absence of independent breathing or its inefficiency, respiratory support is provided (forced or ancillary forced ventilation of the lungs). The partial pressure of oxygen in the respirable mixture in full-term children should be in the range of 60-80 mm Hg, in preterm infants - 50-60 mm Hg. Hyperoxygenation can lead to the formation of free radicals and the development of fibrotic changes in the lung tissue.
• Maintaining an adequate body temperature.
• Correction of the function of the cardiovascular system.

Drugs used to correct the function of the cardiovascular system

A drug	Doses	Method of administration	Act
Albumen	5% solution of 10-20 ml / kg xut)	Intravenously drip	Replenishment of BCC
Glucose	5-10% solution, 10 ml / kg xut)	Intravenously drip
Infukol	6% solution of 10 ml / kg xut)	Intravenously drip
Dopamine	2-10 μg / kg hmin)	Intravenously drip	Vazopro detectors

• Replenishment of the volume of circulating blood (BCC): 5-10% glucose solution 10 ml / kg, 5% albumin solution 10-20 ml / kg, 6% solution of hydroxyethyl starch (infusional HES) 10 ml / kg drip intravenously. When carrying out infusion therapy, it is necessary to strictly monitor the volume and rate of fluid administration. Increasing the volume or rate of administration can lead to hypertension.
• Introduction of vascular drugs: dopamine 2-10 μg / kghmin) intravenously drip.
• Posindromnoe treatment.

Preparations for congenital therapy

A drug	Doses	Method of administration	Indications
Furosemide	1 mg / kg xut)	Intravenously	Edema of the brain
		Intramuscularly
Dopamine	2-10 μg / kg hmin)	Intravenously
Dexamethasone	0.5-1 mg / kg xut)	Intravenously
		Intramuscularly
Magnesium sulfate	25% solution 0.1-0.2 ml / kg xut)	Intravenously	Intracranial hypertension
Phenobarbital	10-20 mg / kg xut)	Intravenously	Convulsions
	5 mg / kg xut) -supporting dose	Inside
Diazepam	0.1 mg / kg - single dose	Intravenously
Sodium oxybate	20% solution of 100-150 mg / kg	Intravenously
Anti-vascular therapy:		Diuretics	(furosemide

Dehydration therapy. With the development of intracranial hypertension recommend the appointment of 25% solution of magnesium sulfate 0.1-0.2 ml / kght) intravenously.

Anticonvulsant therapy is prescribed only with the development of seizures: phenobarbital 10-20 mg / kg intravenously [maintenance dose - 5 mg / kghsut]], 20% sodium oxybate solution 100-150 mg / kg intravenously, diazepam (Relanium) 0.1 mg / kg .

Hemostatic therapy: 1% solution of vicasol 1.0-1.5 mg / kg xut), 12.5% solution of etamzilate (dicinone) 10-15 mg / kg xut) (for 2-3 injections).

From the 2nd day of life additionally take into account the dynamics of body weight, electrolyte blood composition, the concentration of ionized calcium in the blood plasma, the concentration of protein, bilirubin, urea, creatinine, glucose in the blood.

Hemostatic preparations

A drug	Doses	Method of administration
Vikasol	1% solution of 1.0-1.5 mg / kg xut) 2-3 times a day	Intravenous, intramuscular
Dicycin	12.5% solution of 10-15 mg / kg xut)	Intramuscularly, intravenously

Treatment in the recovery period

Course treatment with drugs that improve cerebral circulation and metabolic processes of the brain:

• restoration of hemodynamics of the brain: 0.5% solution of vinpocetine (Cavinton) 1 mg / kg xut), vincamine 1 mg / kg xut);

Drugs that improve cerebral circulation (selective cerebrovascular action)

A drug	Doses	Method of administration
Vinpocetine	0.5% solution of 1 mg / kg xut)	Intravenously drip
	1 mg / kg 3 times a day	Inside
Winkamine	0.5% solution of 1 mg / kg xut)	Intramuscularly
	1 mg / kg 3 times a day	Inside

• Correction of metabolic disorders of the brain: gopanthenic acid (pantogam) 0.25-0.5 g / day, pyracetam (nootropil) 30-50 mg / kg xut), cerebrolysin 1 ml per 10 kg / day.

The treatment includes therapy with psychotropic (neurotropic) drugs: acetylaminosuccinic acid (cogitum) 0.5-1 ml inwards, gamma-aminobutyric acid (aminalon) 0.1-0.25 g 2-3 times a day, pyriginol (encephabol) 0.05 g 1-2 times a day, glutamic acid 0.1 g 2-3 times a day, glycine 0.3 g (1/2 tablet), 0.6 g (1 tablet) 2 times a day day.

• According to the indications, antiaggregant (anticoagulant) therapy: pentoxifylline (trental) 2-3 mg / kg xut), piracetam 20% solution 30-50 mg / kg 1-2 times a day.
• If necessary, postindromus therapy (sedative, anticonvulsant, dehydration, etc.) is performed.

Preparations of "metabolic" therapy (nootropic drugs)

A drug	Doses	Method of administration
Pantogam	0,25-0,5 g / day	Inside
Pyracetam	30-50 mg / kg xut)	Intravenously
	50-150 mg / kg three times a day	Inside
Cerebrolysin	1 ml / 10 (kgsut) once a day or every other day	Intramuscularly
Cogitum	0.5-1.0 ml	Inside
Aminalon	0.1-0.25 g 2-3 times a day	Inside
Pyrithinol	0.05 g (1/2 teaspoon) 1-3 times a day	Inside
Glutamic acid	0.1 g 2-3 times a day	Inside
Glycine	0.3 g ('/ 2 tablets) 2 times a day	Inside

Antiaggregant preparations

A drug	Doses	Method of administration
Pentoxifylline	2-3 mgDkgsut)	Intravenously drip
Pyracetam	20% solution 30-50 mg / kg 1-2 times a day	Intravenous, intramuscular

• Correct the focal disorders (massage, gymnastics, special piling).
• Carry out possible correction of impaired functions (visual, hearing impairment), speech therapy disorders, orthopedic disorders, psychological problems.
• They solve the problem of the possibility of performing surgical treatment with progressive hydrocephalus.
• Clinical follow-up at the polyclinic

A child who has suffered hypoxia should be observed by a pediatrician, a neurologist, an orthopedist, an oculist, an otorhinolaryngologist, a speech therapist, a psychologist and, in some cases, a sociologist.

Prevention of fetal hypoxia

• Prenatal diagnosis of uterine-fetoplacental insufficiency (MPPN) in pregnant women.
• Prevention of MPPN in pregnant women at risk.
• Timely and adequate treatment of MPPN in pregnant women.
• Treatment of complications of pregnancy leading to the development of hypoxia.
• Optimization of methods of delivery in pathology, which is the main cause of the development of MPPN.
• Diagnosis of PAP during pregnancy is carried out using the following methods:
  • US-fetometry and placentometry;
  • dopplerometry of blood flow in the vessels of the utero-placental complex;
  • monitoring cardiac activity of the fetus;
  • amniascopy;
  • amniocentesis.
• Prevention of MPPN in pregnant women at risk is performed with the help of preparations of vitamin E, glutamic acid and essential.
• Therapy of MPPN includes:
  • normalization of uteroplacental blood flow by restoring the vascular tone, rheological and coagulation properties of blood;
  • improving the metabolism of the placenta;
  • increase immunological reactivity of the pregnant woman;
  • normalization of structural and functional properties of cell membranes;
  • oxygen therapy.
• Treatment of complications of pregnancy leading to the development of hypoxia: correction of anemia, OPG gestosis, threatened termination of pregnancy, antiphospholipid syndrome, diabetes mellitus, etc.
• The decision of a question on timely delivery and a choice of a method of a delivery (operative sorts or through natural patrimonial ways).
• With increasing signs of hypoxia during pregnancy, preterm operative delivery is recommended (caesarean section).
• If acute fetal hypoxia is found in childbirth, the question of emergency operative delivery is decided.
• In case of delaying (at gestation terms of 41 weeks or more), one should adhere to the active management tactics of pregnancy (birth, amniotomy).