Cerebral ischemia in newborns

Signs and symptoms of cerebral ischemia in newborns

The disease manifests itself with obvious symptoms that attract attention.

• The child is easily excitable, cries for no reason, sleeps poorly, shudders, and has tremors.
• Muscle tone is reduced, the baby moves little, has difficulty sucking and swallowing.
• The fontanel is enlarged, intracranial pressure is increased due to the fact that fluid accumulates in the brain.
• Convulsions, twitching of the limbs and head, as well as comatose states with loss of coordination of movements and consciousness occur.
• The newborn's skin takes on a marbled hue.
• The functioning of the gastrointestinal tract is disrupted - bloating, constipation, and diarrhea are observed.

Treatment with folk remedies

It is impossible to cure cerebral edema in newborns using traditional methods, but they can alleviate the baby’s condition and have a calming effect. For example, you can try brewing medicinal herbs: mint, oregano and calendula. They are taken equally, poured with boiling water and left to cool completely. For 150 grams of herbs, three liters of water are needed. This product is filtered and poured into the bath. The duration of the procedure is about 10 minutes; All you need to do is three times a week.

A diagnosis such as cerebral edema in a newborn is given to many children at birth or in infancy. This does not mean that everything is very bad. But in order to cure the baby and avoid serious consequences, you need to contact a pediatrician as soon as possible. Timely treatment, as well as competent actions during the rehabilitation period, will help to cope with this disaster and keep the child healthy.

How does cerebral ischemia occur?

In 70% of cases, ischemia occurs in the fetus in the womb and is associated with the formation of a blood clot in one of the vessels supplying the brain, or with insufficient development of the vessel. Most often, the disease is diagnosed in premature babies whose vascular system is not yet fully formed.

As a result, an insufficient amount of blood enters the vital organ, and with it, oxygen. Delay in providing medical care leads to damage to larger areas of the brain, cerebral hemorrhage and other serious consequences.

Cerebral hemorrhage due to birth trauma

The most typical manifestations of any intracranial hemorrhage in newborns are: 1. sudden deterioration in the general condition of the child with the development of various variants of the depression syndrome with periodically occurring signs of hyperexcitability; 2. change in the nature of the cry; 3. bulging of the large fontanel or its tension, 4. abnormal movements of the eyeballs; 5. violations of thermoregulation (hypo- or hyper.1 army); 6. vegetovisceral disorders (regurgitation, pathological loss of body weight, flatulence, unstable stools, tachypnea, tachycardia, peripheral circulatory disorders); 7. pseudobulbar and motor disorders, convulsions; 8. progressive posthemorrhagic anemia; 9. acidosis, hyporbilirubgnemia and other metabolic disorders; 10. addition of somatic diseases (meningitis, sepsis, pneumonia, cardiovascular and adrenal insufficiency, etc.). Subdural hemorrhages . Depending on the location, there are: tentorial hemorrhages with damage to the direct and transverse sinuses of the vein of Galen or small infratentorial veins; occipital osteodiastasis - rupture of the occipital sinus; rupture of the falciform process of the dura mater with damage to the inferior sagittal sinus; rupture of the connecting superficial cerebral veins. Subdural hematomas can be unilateral or bilateral; they may be combined with parenchymal hemorrhages resulting from hypoxia.

Tentorial rupture with massive hemorrhage, occipital osteodiastasis, damage to the inferior sagittal sinus is characterized by an acute course with the rapid development of symptoms of compression of the upper parts of the brain stem such as stupor, eye deviation to the side, anisocoria with a sluggish reaction to light, the “doll’s eyes” symptom, muscle rigidity back of the head, opisthotonus pose; unconditioned reflexes are suppressed, the child does not suck or swallow, attacks of asphyxia and convulsions are observed. If the hematoma grows, symptoms of compression of the lower parts of the brain stem appear: coma, dilated pupils, pendulum-like eye movements, arrhythmic breathing. In the subacute course of the pathological process (hematoma and smaller rupture), neurological disorders (stupor, excitability, arrhythmic breathing, bulging of the large fontanelle, oculomotor disorders, tremor, convulsions) occur at the end of the first day of life or after several days and persist for several minutes or hours. Death, as a rule, occurs in the first days of a child’s life from compression of the vital centers of the brain stem.

Convexital subdural hematomas caused by rupture of the superficial cerebral veins are characterized by minimal clinical symptoms (restlessness, regurgitation, vomiting, tension of the large fontanelle, Graefe's symptom, periodic increase in body temperature, signs of local brain disorders) or their absence and are detected only during an instrumental examination of the child.

Primary subarachnoid hemorrhages are the most common. They occur when vessels of various sizes are damaged within the subarachnoid space, small veins of the leptomeningeal plexuses or connecting veins of the subarachnoid space. They are called primary in contrast to secondary subarachnoid hemorrhages, in which blood enters the subarachnoid space as a result of intra- and periventricular hemorrhages and aneurysm rupture. Subarachnoid hemorrhages are also possible with thrombocytopenia, hemorrhagic diathesis, and congenital angiomatosis. With primary subarachnoid hemorrhages, blood accumulates between separate areas of the brain, mainly in the posterior cranial fossa and temporal regions. As a result of extensive hemorrhages, the entire surface of the brain is covered with a red cap, the brain is swollen, and the vessels are filled with blood. Subarachnoid hemorrhages can be combined with small parenchymal hemorrhages.

The clinical picture of neurological disorders depends on the severity of the hemorrhage and its combination with other disorders (hypoxia, hemorrhages of other locations). More common are mild hemorrhages with clinical manifestations such as regurgitation, hand tremors, anxiety, and increased tendon reflexes. Sometimes neurological symptoms may appear only on the 2-3rd day of life after the baby is put to the breast. With massive hemorrhages, children are born with asphyxia, they experience anxiety, sleep disturbances, general hyperesthesia, stiffness of the neck muscles, regurgitation, vomiting, nystagmus, strabismus, Graefe's symptom, tremor, convulsions. Muscle tone is increased, tendon reflexes are high with an expanded zone, all unconditioned reflexes are clearly expressed. On the 3-4th day of life, Harlequin syndrome is sometimes noted, manifested by a change in the color of half the newborn’s body from pink to light red; the other half is paler than normal. This syndrome is clearly detected when the child is positioned on his side. A change in body color can be observed within 30 seconds to 20 minutes; during this period the child’s well-being is not disturbed. Harlequin syndrome is considered a pathognomonic sign of traumatic brain injury and asphyxia of the newborn.

Intraventricular and periventricular hemorrhages are most typical for premature babies born with a body weight of less than 1500 g. The morphological basis of these hemorrhages is the immature choroid plexus located under the ependyma lining the ventricles (germinal matrix). Until the 35th week of pregnancy, this area is richly vascularized, the connective tissue framework of the vessels is insufficiently developed, and the supporting stroma has a gelatinous structure. This makes the vessel very sensitive to mechanical stress, changes in intravascular and intracranial pressure. High risk factors for the development of hemorrhages are prolonged labor, accompanied by deformation of the fetal head and compression of the venous sinuses, respiratory disorders, hyaline membrane disease, various manipulations performed by the midwife (suction of mucus, replacement blood transfusion, etc.). In approximately 80% of children with this pathology, periventricular hemorrhages break through the ependyma into the ventricular system of the brain and blood spreads from the lateral ventricles through the foramina of Magendie and Luschka into the cisterns of the posterior cranial fossa. The most typical localization of the forming thrombus is in the region of the occipital cistern magna (with limited spread to the surface of the cerebellum). In these cases, abliterative arachnoiditis of the posterior cranial fossa may develop, causing obstruction through cerebrospinal fluid circulation. Intraventricular hemorrhage can also involve the periventricular white matter of the brain and be combined with cerebral venous infarctions, which are caused by compression of the venous outflow pathways by the dilated ventricles of the brain.

Hemorrhage usually develops in the first 12-72 hours of life, but may subsequently progress. Depending on the extent and speed of spread, three variants of its clinical course are conventionally distinguished: fulminant, intermittent and asymptomatic (low-symptomatic). With lightning-fast hemorrhage, the clinical picture develops over several minutes or hours and is characterized by deep coma, arrhythmic breathing, tachycardia, and tonic convulsions. The child’s eyes are open, the gaze is fixed, the reaction of the pupils to light is sluggish, nystagmus, muscle hypotonia or hypertension, bulging of the large fontanel are observed; metabolic acidosis, decreased hematocrit, hypoxemia, hypo- and hyperglycemia are detected.

The intermittent course is characterized by similar, but less pronounced clinical syndromes and an “undulating course, when a sudden deterioration is followed by an improvement in the child’s condition. These alternating periods are repeated several times over 2 days until the condition stabilizes or death occurs. With this variant of the pathological process, pronounced metabolic disorders are also observed.

Asymptomatic or low-symptomatic course is observed in approximately half of children with intraventricular hemorrhage. Neurological disorders are transient and mildly expressed, metabolic changes are minimal.

Cerebellar hemorrhages occur as a result of massive supratentorial intraventricular hemorrhages in full-term infants and hemorrhages in the germinal matrix in preterm infants. Pathogenetic mechanisms include a combination of birth trauma and asphyxia. Clinically, they are characterized by a rapid progressive course, as with subdural hemorrhages in the posterior cranial fossa: respiratory distress increases, hematocrit decreases, and death quickly occurs. A less acute course of the pathology, manifested by atony, areflexia, drowsiness, apnea, pendulum-like eye movements, and strabismus, is also possible.

Epidural hemorrhages - occur between the inner surface of the skull and the dura mater and do not spread beyond the cranial sutures. These hematomas are formed when there are cracks and fractures of the cranial vault with rupture of the vessels of the epidural space. Epidural hemorrhages are often combined with external cephalohematomas. In the clinic, the sequence of development of symptoms is characteristic: after a short “bright” interval (from 3 to 6 hours), brain compression syndrome develops, which manifests itself as severe anxiety 6-12 hours after the injury, progressive deterioration of the child’s condition, up to the development of coma after 2 hours-36 hours. Typical symptoms are pupil dilation (in 3-4 grooves) on the affected side, clonic-tonic convulsions, hemorrhoids on the opposite side of the hematoma, asphyxia, bradycardia, arterial hypotension, congestive optic nerve nipples.

Parenchymal (intracerebral) hemorrhages occur more often when the terminal branches of the cerebral arteries are damaged. With small-point hemorrhages, the symptoms are atypical and mild: lethargy, regurgitation, decreased muscle tone and reflexes, nystagmus, Graefe's symptom, etc. With large hematomas, the clinic is clear and manifests itself with symptoms characteristic of PIVC.

Atypical intracranial hemorrhages in newborns can be caused by vascular abnormalities, tumors, coagulopathies, and hemorrhagic infarction. The most common types of hemorrhagic diathesis are vitamin K-deficiency hemorrhagic syndrome, hemophilia A, and isoimmune thrombocytopenic purpura of newborns. Hemorrhagic disorders in newborns can also be caused by congenital thrombocytopathy due to the mother's prescription of acetylsalicylic acid and sulfonamide drugs before birth, while the hemorrhages are mainly subarachnoid and mild. Neonatal intracranial hemorrhages can cause congenital arterial aneurysms, arteriovenous anomalies, coarctation of the aorta, brain tumors (teratoma, glioma, medulloblastoma).

Flow. The following periods of the course of birth brain injury are distinguished: acute - 7-10 days, sometimes up to 1 month; subacute (early recovery up to 3-4-6 months and late - from 4 months to 2 years). During the acute period in full-term infants, phases of excitation and depression of the central nervous system are distinguished. Manifestations of intracranial hemorrhage are gradually eliminated. The prognosis depends on the severity of the process, the gestational age of the child and concomitant diseases. The survival rate is 50-70%, the rest retain various neurological disorders (hemisyndrome, hydrocephalus, cysts, etc.).

In premature infants, ICH may be asymptomatic or have a poor atypical clinical picture; with dominance of signs of respiratory disorders, apnea attacks; with the prevalence of general depression syndrome or hyperexcitability syndrome, etc.

Causes

In the vast majority of cases, the causes of cerebral ischemia in newborns are various disorders of gestation in recent weeks, as well as non-standard situations during childbirth.

• Detachment of the placenta or disruption of blood flow in it.
• Compression of the umbilical cord, suffocation of the fetus.
• Congenital heart defects.
• Circulatory problems.
• Intrauterine hypoxia.
• Infection during childbirth.
• Openness of the ductus arteriosus.
• Acute placental insufficiency.

Diagnosis of placental insufficiency

It is almost impossible to treat already developed placental insufficiency, so doctors are actively seeking to identify pregnant women at risk of developing placental dysfunction. If placental insufficiency is detected in the 3rd trimester of pregnancy, unfortunately, there is no effective treatment. Therefore, all methods of identifying in the early stages of pregnancy those women whose placenta formation has undergone disturbances are being very actively used.

First of all, when registering for pregnancy, the most significant risk factors are identified - smoking, previous abortions, family history (low birth weight, tendency to thrombosis), the presence of chronic heart disease, vascular disease, diabetes mellitus.

Preventive measures against the development of placental insufficiency are especially relevant and necessary until 16-17 weeks of pregnancy, when the formation of placental structures occurs.

Prenatal screening, which is carried out at 11-14 weeks of pregnancy, provides significant assistance in assessing the risk of developing placental insufficiency. It is carried out to identify Down syndrome, Edwards syndrome and other chromosomal diseases in the fetus. Currently, the most urgent thing is to conduct comprehensive early screening of pregnant women to predict the risk of developing placental insufficiency, preeclampsia and intrauterine growth retardation. Since this type of diagnostics is one of the most modern and advanced, unfortunately, it is not yet included in the list of services provided in the antenatal clinic as part of compulsory medical insurance, but is available to everyone at prenatal diagnostic centers.

Determination of proteins produced by the placenta

First of all, the PAPP-A protein is determined; it is also a marker of fetal chromosomal abnormalities. A decrease in the concentration of PAPP-A in the blood at 11-14 weeks of pregnancy occurs in pregnant women who have a high risk of placental insufficiency and fetal growth retardation.

The second placental hormone that helps in assessing the risk of placental insufficiency is PIGF (placental growth factor). Its concentration in the blood decreases long before the first manifestations of placental insufficiency. Its definition is not used as widely as PAPP-A, but nevertheless, many laboratories have already included this protein in prenatal screening of the 1st trimester. Measuring blood flow in the vessels of the uterus is extremely important when conducting 1st trimester screening. It has been unequivocally proven that the narrowing of the vessels of the uterus, determined during the study, indicates the inferiority of the formation of the placenta, which will worsen with increasing gestational age and will lead to a decrease in the baby’s nutrition and oxygen supply, that is, to the development of placental insufficiency and delayed fetal development. With normal sizes of the uterine vessels at 11-14 weeks of pregnancy, the risk of severe placental insufficiency is negligible.

The next mandatory screening ultrasound examination is carried out at 20-21 weeks of pregnancy. In this case, it is necessary to take measurements of the fetus to assess whether there is growth retardation. Indeed, with oxygen starvation, the growth rate of the fetus slows down and its size begins to lag behind the norm for each stage of pregnancy. In addition, the doctor must evaluate the condition and maturity of the placenta. During ultrasound, Doppler measurements of the uterine vessels are also performed to identify early changes that precede the clinical manifestations of placental insufficiency.

In patients belonging to the high-risk group, in addition to ultrasound and Doppler measurements, daily monitoring of blood pressure fluctuations is also carried out, determination of the amount of protein in a urine test collected per day, and evaluation of blood coagulation system parameters.

The third ultrasound is performed for all expectant mothers at 30–34 weeks of pregnancy. The doctor measures the circumference of the baby's head and abdomen, the length of the bones of his arms and legs, and calculates the estimated weight of the fetus. These measurements allow the doctor to make sure that the baby is developing normally. Also important is the structure of the placenta, the presence of signs of aging in it, as a result of which it usually ceases to fully supply the baby with blood, which means that he ceases to have enough oxygen and nutrients and the child’s development is disrupted. During an ultrasound, the amount and type of amniotic fluid is assessed, which can also change with intrauterine fetal suffering.

Doppler

Doppler testing of the vessels of the placenta and umbilical cord (a method for studying the speed of blood flow in these vessels) also allows you to assess the baby’s well-being. The doctor examines the blood flow in the arteries of the uterus, umbilical cord, heart and brain of the child. This study allows you to determine whether the placenta is working well, whether there are signs of a lack of oxygen in the baby, or the development of gestosis in the mother. When the speed of blood flow in any vessel decreases, we can talk about fetal nutritional disorders of varying degrees of severity.

A timely examination allows us to identify the initial stages of blood supply deficiency. In such cases, treatment can prevent serious complications, such as hypoxia and intrauterine growth retardation. Dopperometry is carried out at 20–21 weeks and at 30–32 weeks of pregnancy; if there are changes, monitoring is carried out at least every two weeks.

Cardiotocography

This is an important method for assessing the condition of the fetus. CTG is performed during pregnancy of 33 weeks or more, since only at this stage of the baby’s intrauterine development is full regulation of the activity of the fetal cardiovascular system established by the centers of the spinal cord and brain. The fetal heartbeat is recorded for 20–40 minutes, and if necessary, the study can be extended to 1.5 hours.

The device detects and records the baby's heart rate. The obstetrician-gynecologist evaluates the heartbeat recording curve, episodes of decrease and sharp increase in the fetal heart rate and, based on these data, makes a conclusion about how comfortable the baby feels in the mother’s stomach. For example, when the concentration of oxygen in the blood of the fetus decreases, its supply to the cells of the nervous system also decreases, which in turn affects the heart rate. In the normal course of pregnancy, CTG is performed after 33 weeks once every 10–14 days, sometimes more often. Some clinics currently offer the service of continuous CTG monitoring, which becomes relevant if there are signs of placental insufficiency. A pregnant woman is given a monitor that records changes in the baby’s cardiac activity and this data is transmitted via the Internet to the attending physician.

Risk factors

Various vascular and neurological pathologies, problems with blood pressure (especially hereditary) in the mother should alert the doctor who is managing the pregnancy. Also, risk factors for cerebral ischemia in a child are:

• mother's age is more than 35 years;
• endocrine diseases;
• premature, prolonged labor;
• multiple pregnancy;
• late toxicosis;
• failure of the mother to follow a healthy lifestyle;
• exacerbation of chronic or acute diseases in the mother during pregnancy.

Reasons for the development of hydrocephalus in children

Factors that can lead to the internal form of the disease are:

• anomalies and malformations of the fetus during the period of intrauterine formation, associated with infections, injuries, and the influence of bad habits of the mother;
• various birth injuries;
• prematurity and premature birth with low body weight.

The causes of acquired hydrocephalus in a child can be infectious diseases of the brain and its structures: meningitis, malignant and benign neoplasms, encephalitis. In some cases, the starting mechanism is traumatic brain injuries and bruises resulting from falls, blows, accidents and other injuries.

Diagnostics

The disease is usually diagnosed within the first few hours.

The presence of pathology is indicated by deviations in checking reflexes and a general blood test . Typically, the analysis shows an increased level of carbon dioxide in the body.

If obvious symptoms of a serious illness are detected magnetic resonance imaging , as well as electroencephalography , which reveals hidden convulsions and other abnormalities in the functioning of the brain.

Consequences and complications

The pathology is quite dangerous and is one of the most common causes of child mortality. How favorable the prognosis will be depends on the severity of the baby’s condition and the Apgar indicator. If the score increases, the prognosis is considered favorableSource: Modern methods of treating neonatal asphyxia. Cherednikova E.N., Sherstnev D.G. Bulletin of Medical Internet Conferences, 2021. p.824.

However, with severe pathology, serious complications develop during the first year of life. Early consequences that may appear in the first few days after resuscitation include :

• respiratory arrest (the most common and dangerous complication);
• pulse failure;
• convulsions;
• cerebral edema;
• disruption of the urinary and digestive systems.

Later disorders include the following diagnoses:

• syndrome of increased excitability (hyperexcitability);
• increased intracerebral pressure (hypertension syndrome);
• lesions of the central nervous system (perinatal encephalopathy);
• disruptions in the functioning of the endocrine and vegetative-vascular systems (hypothalamic disorders).

With timely and competent medical intervention, as well as a high-quality recovery period, asphyxia of newborns may not have dangerous consequences in the future. Mild forms of asphyxia have almost no effect on the child; after the illness, his further development will proceed in the same way as in other babies.

Cerebral ischemia grade 2

A dangerous form of the disease. It is characterized by:

• severe apnea (stopping breathing during sleep);
• decreased grasping and sucking reflexes;
• weak muscle tone;
• increase in head shape due to fluid accumulation;
• lack of coordination;
• loss of consciousness;
• changes in skin color.

Most often, grade 2 ischemia manifests itself in the first day of a newborn’s life, and symptoms can be observed for 2-4 weeks. At this time, the child is carefully monitored by doctors, and he undergoes a course of therapy. If necessary, surgery is performed to remove the blood clot.

Classification of asphyxia according to the Apgar scale

To assess the severity of asphyxia in a newborn, the Apgar scale is used. With its help, the doctor evaluates heart rate, breathing, muscle tone, skin color and reflexes, and then determines the severity of the pathological condition.

To give a rating, the doctor evaluates each of the five signs as 0, 1 or 2 points. Accordingly, the maximum and best score is 10 points. The assessment is determined taking into account the following criteria:

The condition is assessed in the first and fifth minutes of life. Accordingly, the child receives two ratings: for example, 8/10. If the score is 7 or lower, the baby’s condition is assessed additionally at the 10th, 15th and 20th minutes.

Depending on the Apgar score, the degree of asphyxia is determined:

• 1-3 points – heavy;
• 4-5 points – average;
• 6-7 points – mild or moderate.

The Apgar score is not highly sensitive. Therefore, if a child has abnormalities, additional diagnostics are necessary to assess asphyxia.

Cerebral ischemia grade 3

The most severe form, in which:

• the baby has no reflexes;
• the child falls into a coma;
• heart rhythm is disrupted;
• blood pressure rises sharply;
• there are problems with independent breathing;
• strabismus is observed.

An experienced doctor can already determine the presence of signs and symptoms of grade 3 cerebral ischemia in the first 5 minutes of a newborn’s life. In this case, the child is sent to intensive care and, if necessary, connected to a ventilator.

Diagnosis and drug treatment

The disease is diagnosed in two ways. Firstly, this is an examination of the baby by a neurologist. The doctor checks the baby’s reaction to various stimuli, looks at his reflexes and evaluates the external manifestations of the disease. The second way is to conduct research: neuroophthalmoscopy, MRI, spinal cord puncture. Usually, to make a diagnosis it is necessary to use these methods in combination. This way you can most accurately assess the severity of the disease and the baby’s health condition. In addition, a blood test of the newborn is carried out to identify the presence of pathogens of infectious diseases.

Cerebral edema in a newborn is treated strictly in a hospital setting. It is impossible to remove it without hospitalization, since the destruction occurs too quickly. Drug therapy is aimed at restoring full oxygen metabolism in brain cells. As a rule, the child is on artificial ventilation. Treatment uses medications such as muscle relaxants, which help relieve cramps.

In addition, the baby is prescribed diuretics, which remove fluid and prevent the development of swelling, and agents that normalize blood circulation. From time to time, the method of hypothermia is used, when body temperature is artificially lowered. If drainage of fluid from the child's brain is ineffective, a ventriculostomy may be prescribed - removing excess fluid with a catheter.

Treatment of cerebral ischemia in newborns

The goal of treatment is to restore normal blood circulation in the brain tissue, prevent pathological changes and eliminate the consequences of ischemia. For stage 1 disease, treatment usually involves prescribing massage to improve blood circulation.

For diseases of the 2nd and 3rd degrees, drug therapy and surgery are used to remove a blood clot in the vessel and restore the structure of the vascular bed. In difficult cases, the baby undergoes a rehabilitation course of intensive therapy.

Possible consequences

If the disease is detected on time, it is most often treatable. True, the child will then have to register with a pediatrician and neurologist. In cases where there is a delay in speech and development, the baby will also be observed by a psychiatrist. Treatment is quite long and takes from several months to several years. If the situation develops favorably, sometimes there may be no trace of the disease at all.

However, the illness often causes certain negative consequences. First of all, they consist in reducing the child’s mental abilities. This happens because some of the cells die. The cause is an unregulated cerebral circulatory system. Much depends on at what stage the disease is overcome. Sometimes a baby already at one year of age catches up with his peers in development, in other cases this continues for several more years.

Brain edema in children also affects their physiological functions. It may be difficult for a child to hold his head up, and his limbs may also work worse. In the future, children who have suffered from such a disease may become hyperactive and easily excitable. In addition, such children may have an increased head circumference, and recovery over time, as a rule, does not occur.

In the most severe cases, children with this diagnosis may develop diseases such as epilepsy or cerebral palsy. There are also episodes of death if the disease is detected too late or the brain damage is extensive. To prevent such consequences, it is necessary to constantly monitor the baby’s health.

Prognosis and consequences of cerebral ischemia

It is much more effective to eliminate ischemia itself after the birth of a baby than to treat its complications. Among the consequences of cerebral ischemia of the 2nd degree:

• sleep disorders;
• headache;
• irritability;
• isolation;
• physical inactivity.
• Stage 3 disease has severe consequences:
• cerebral palsy;
• attention deficit disorder;
• mental retardation;
• Graefe's symptom, etc.

If all actions to eliminate ischemia were carried out by doctors in a timely manner, then the symptoms disappear during the rehabilitation period, which usually lasts 6-12 months.

Treatment of placental insufficiency

There are currently no specific treatments for placental insufficiency, since there are no drugs that selectively improve uteroplacental blood flow. That is why all measures to combat placental insufficiency are aimed at prevention. If the patient is at high risk for the development of placental insufficiency, from early pregnancy she is prescribed medications whose effectiveness is well proven and which prevent the early development of severe placental dysfunction.

If, during additional methods of assessing the condition of the fetus, initial disturbances in the supply of oxygen to the baby are detected, drug treatment is carried out aimed at increasing the flow of blood and oxygen through the placenta and mandatory control examinations during the therapy. If the changes are serious and the baby experiences a severe deficiency of oxygen and nutrients, his condition suffers, then in such cases an emergency delivery is performed.