Ischemic encephalopathy. Perinatal encephalopathy in newborns

Perinatal hypoxic-ischemic encephalopathy (HIE) - this is a consequence of insufficient blood supply to the brain of a child during pregnancy, childbirth or during the first month of his life. Hypoxia-ischemia of the brain is the main cause of neurological damage in newborns. One of the main parameters characterizing the severity of hypoxic-ischemic brain damage during childbirth and during pregnancy is the Apgar score and the presence of meconium in the amniotic fluid.

The consequences of HIE can be different: from a slight decrease in attention and restlessness of the child to severe forms of cerebral palsy.

Children with moderate brain damage may appear healthy during the first days and even months of life. Pathology in them is detected during an ultrasound of the brain in the first month of life, when examined by a neurologist and other specialists.

Babies with severe HIE and birth asphyxia usually require intensive care and are treated step by step in the maternity hospital and neonatal pathology department.

Perinatal hypoxic-ischemic encephalopathy of moderate and severe degree is one of the main risk factors for the development of cerebral palsy.

The course of HIE is very individual, but, as a rule, it is accompanied by the death of some brain cells and requires timely and correct treatment. Compliance with this principle allows you to achieve significant improvement even with severe brain damage.

What is the treatment for HIE?

The best treatment for HIE is prevention and early treatment of intrauterine hypoxia and neonatal asphyxia. But, despite significant progress in the prevention of complications of childbirth, moderate and severe hypoxic-ischemic encephalopathy still occurs with a frequency of 1-2 per 1000 children born. Until recently, medicine could offer such children only supportive therapy for organ dysfunction.

Since 2010, induced hypothermia has become the standard of care for HIE. This method consists in the fact that starting from 6 hours after birth, the child's body temperature is maintained at 33.5 ° C for 72 hours. Unfortunately, even after the use of induced hypothermia, a significant number of infants with HIE retain neurological disorders of varying severity.

Today, for the treatment of newborns with HIE, scientists offer a new method - regenerative therapy with cord blood stem cells.

New treatment for HIE

In HIE, cord blood mononuclear fraction containing stem cells is used. When it is administered intravenously to a child, brain cells are restored and regenerated, and the immune system is regulated. If the therapy was started at an early stage of the disease, then encephalopathy can be cured due to the powerful regenerative potential of the umbilical cord blood and the restoration of the population of nerve cells. The uniqueness of cell therapy in encephalopathy lies in the achievement of high treatment results in each case. To date, more than 330 children suffering from cerebral palsy have already been saved in Russia with the help of harvested cord blood.

Treatment of hypoxic-ischemic encephalopathy with cord blood mononuclear fraction in the early stages is the most important factor in a favorable prognosis, reducing the risk of developing cerebral palsy, as well as the proper development of the child and improving his quality of life in subsequent years.

Thus, having decided to preserve cord blood, parents give their baby a wonderful "biological insurance" against cerebral palsy: if necessary, treatment can be started from the first day of a newborn's life, using his own cord blood cells, right in the maternity hospital.

Parents - be vigilant: prepare your child's umbilical cord blood and thus you will save him from many diseases.

Hypoxic-ischemic encephalopathy (HIE) is brain damage caused by hypoxia. They lead to movement disorders, seizures, mental development disorders and other types of cerebral insufficiency.

The conventionality of the term hypoxic-ischemic encephalopathy is obvious, but the modern development of medicine does not allow for a more accurate differentiation of etiology (what is the contribution of hypoxia and arterial hypotension, reduced cerebral blood flow, i.e. ischemia, to brain damage) and topics of lesions of the cerebral cortex in newborns.

The frequency of HIE has not been established. In the US and other industrialized countries, the incidence of cerebral palsy is 1-2 cases per 1000 full-term, but today there is an opinion that HIE is the cause of only 10% of them. According to M. Levin et al. (1985), in the UK, the frequency of HIE is 6:1000 full-term babies, with 1:1000 having severe neurological disorders or dying from the effects of perinatal hypoxia. In France (Wayenberg J.L. et al., 1998), mild posthypoxic encephalopathy is 2.8 per 1000, moderate - 2.7 per 1000 and severe - 0.2 per 1000. These values are slightly lower in England (Pharoah P.O. et al., 1998), where moderate and severe cerebral insufficiency due to perinatal it was diagnosed in 1 6 4 9 out of 7 8 9 411 children born in 1984-1989 (frequency of PHEP - 2.1 per 1000).

According to A.B. Palchik et al. (1998), the frequency of HIE among newborns of one of the observational maternity hospitals in St. Petersburg, using the classification of H.B. Sarnat and M.S. Sarnat (1976), was 15.6 among full-term and 88 per 1000 among premature infants.

Etiology. According to modern concepts, any unfavorable course of pregnancy in the mother for the fetus is transformed primarily into hypoxia. The causes leading to intrauterine hypoxia and asphyxia of the newborn are set out in Chapter VII. There is no doubt that some of the etiological factors of hypoxia (alcohol, drugs, certain drugs taken by the mother, as well as occupational and environmental hazards) directly affect the fetal brain. And this means that in some children, antenatal brain damage leads to hypoxia, rather than hypoxia - to brain damage.

Postnatal episodes of hypoxia leading to HIE are usually associated with sleep apnea, cardiac arrest, shock, and persistent seizures.

Pathogenesis, despite numerous studies, cannot be considered fully elucidated. The role of the following factors in the pathogenesis of HIE is currently being discussed.

Decreased cerebral blood flow. Analyzing the available clinical and experimental data on disorders of cerebral blood flow during perinatal hypoxia, J.J. Volpe (1995) notes that initially perinatal hypoxia causes a redistribution of blood flow between organs, as well as hypoxemia and hypercapnia, which, in turn, lead to impaired vascular autoregulation. Further persistence of hypercapnia and hypoxemia leads to a decrease in blood pressure and cerebral blood flow, which causes ischemic brain damage. On the other hand, an increase in blood pressure as a reaction to hypoxia naturally leads to an increase in the rate of cerebral blood flow, which can contribute to hemorrhages.

Cerebral hypoperfusion is diagnosed at a cerebral blood flow rate of less than 10 ml per 100 g of tissue/min and is more common in preterm infants. This indicator depends on the severity of hypoxia, as well as the presence of hypo- or hypercapnia; Normally, in a full-term baby, it ranges from 20 to 60 ml per 100 g of tissue / min (Zhetishev R.A., 1990; Lou N.S., 1988). R.A. Zhetishev (1990) established the relationship between indicators of cerebral blood flow, vascular resistance, systolic pressure and intracranial cerebrospinal fluid pressure in healthy newborns and in children with acute asphyxia of varying severity with and without antenatal hypoxia. The influence of a decrease in systolic pressure and a change in the resistance of cerebral vessels on the severity of hypoxic disorders, the age of the child - on a decrease in cerebral perfusion and an increase in intracranial pressure was noted. Hypoxic damage to endothelial cells leads to a sharp narrowing of the lumen of the brain capillaries, as a result of which resistance to blood flow increases, a phenomenon called no-reflow (blood flow deficiency, non-restoration of blood flow to normal after reoxygenation after a period of hypoxia) occurs.

Of particular importance in conditions of changing systemic arterial pressure is the preservation or violation of cerebrovascular autoregulation - a mechanism in which vasoconstriction and vasodilation of arterioles provide relatively constant perfusion with wide fluctuations in systemic pressure. It has been shown that the plateau of autoregulation of cerebral blood flow, which is characteristic of healthy full-term infants, sharply decreases in premature infants.

G.M. Fenichel (1983) emphasizes that the loss of autoregulation leads to a violation of the linear relationship between these indicators and makes the brain defenseless against wide fluctuations in blood pressure. This contributes to either ischemic damage (stroke) or hemorrhage. In the work of L.T. Lomako (1990) it is noted that with perinatal brain lesions in newborns in the first days of life, the hypokinetic type of hemocirculation predominates, which subsequently turns into hyperkinetic. In the first days of life, there is a decrease in stroke and minute volumes of blood flow, a decrease in cardiac output with an increase in the tone of arterial vessels. A pronounced pressor reaction of the precapillaries is the cause of an increase in diastolic pressure and a decrease in pulse pressure. D.E.Ballot et al. (1993) revealed an inverse relationship between the development of hypoxic brain lesions and the presence of persistent pulmonary hypertension. The authors suggest that persistent pulmonary hypertension may reduce the production of free radicals, and hence the occurrence of brain damage.

The delivery of oxygen to tissues also depends significantly on the rheological properties of the blood. Preservation of the liquid state of circulating and deposited blood is one of the tasks of the hemostasis system, which, in addition, provides stopping and preventing bleeding in case of violation of the integrity of the vascular wall. The central component of hemostasis as an autoregulatory process is the platelet, which carries out the relationship between the endothelium of the vascular wall with plasma proteins, blood cells and performs a number of non-hemostatic functions - regulation of tissue growth, angiogenesis, proliferation of neuroglia, etc.

The provoking role of hyperviscosity and polycythemia in the pathogenesis of thrombosis is well known. Structural blood viscosity increases significantly with severe asphyxia, polycythemia - risk factors for the development of hypoxic-ischemic brain lesions. For healthy newborns in the first hours of life, a thrombogenic orientation of hemostasis with disseminated intravascular coagulation (RVC) of the blood is characteristic, changing to 3-4 days of life with a tendency to hypocoagulation and hypoaggregation. In children with severe and acute asphyxia at birth, the thrombogenic orientation of hemostasis is more pronounced than in healthy newborns (Weber I.N., 1988; Ivanov D.O., 1996; Chumakova G.N., 1987, 1998; Shabalov N.P. et al., 1982-1997). The functional state of the hemostasis system significantly depends on the course of pregnancy: in premature babies born to mothers who suffered from prolonged preeclampsia (more than 4 weeks), who have chronic diseases of the gastrointestinal tract, hypo-coagulation and hypoaggregation orientation of hemostasis can be detected already at birth, and in connection with this, various hemorrhages, including intracranial, may occur.

It should be emphasized that the features of autoregulation of cerebral vessels in hypoxic-ischemic brain lesions depend on the electrolyte balance and a number of biochemical factors. It has been shown that during brain hypoxia there is an increase in the concentration of K+ and H+ in the extracellular fluid, which leads to an increase in the activity of cortical neurons, dilatation capacity of blood vessels and a decrease in their constrictive capacity. A similar effect has an increase in the concentration of adenosine and osmolarity. At the same time, hypoxia causes a decrease in the concentration of extracellular calcium with a decrease in the activity of cortical neurons, an increase in the contractility of cerebral vessels and a decrease in their dilatation ability (Sjosjo VK, 1984). In the studies of O.Pryds et al. (1988) using mXe showed a significant increase in cerebral blood flow in response to hypoglycemia (less than 1.7 mmol/l).

Despite the relative resistance to intracranial hypertension in newborns compared to older children and adults, with severe hypoxic-ischemic brain damage in full-term children, severe peri- or intraventricular hemorrhage in preterm infants, an increase in intracranial pressure is possible, which often leads to extensive necrosis of the brain tissue (Hill A. et al., 1992). The maximum intracranial hypertension falls on the period between the second and third days of life, which is confirmed by measurements of intracranial pressure in the subarachnoid spaces (V o l p e J.J., 1995). In premature infants, changes in intracranial pressure due to cerebral ischemia have a certain specificity: its increase occurs mainly at the end of the first day of life.

Intracranial hypertension is a poor prognostic sign: out of 32 children who underwent severe hypoxia, 7 had intracranial hypertension on the first day of life, three of them died and four developed severe neurological disorders. At the same time, extensive necrosis of the medulla was found in deceased children at autopsy (Lupton B.A. et al., 1988).

R.A. Zhetishev (1990) convincingly showed that with moderate asphyxia in newborns on the 3rd - 5th day of life, an increase in intracranial pressure develops, a decrease in the intensity of cerebral blood flow (after normalization by the end of the second day of life, blood flow reduced at birth and on the 1st day of life) and an increase in resistance to blood flow in the brain. At the same time, on the first day of life in children with acute moderate asphyxia, the resistance of cerebral vessels was reduced compared to healthy children (adaptive mechanism of autoregulation of cerebral blood flow). In children with severe asphyxia or moderate asphyxia, but developed against the background of chronic hypoxia, the resistance to blood flow of cerebral vessels was higher than in the control group of children during all periods of observation.

The role of prostaglandin metabolism features (excessive synthesis of vasoconstrictor - thromboxane, etc., deficiency of vasodilator - prostacyclin, etc.), excessive synthesis of leukotrienes by the vascular endothelium, as well as hormones in cerebral blood flow deficiency, cerebral edema during perinatal hypoxia has not been fully studied.

Localization of brain lesions. An essential moment in the development of hypoxic-ischemic lesions of the brain is the relationship between cerebral hypoperfusion and vascular architectonics of the brain. In term infants, cerebral hypoperfusion predominantly involves the cerebral cortex and parasagittal zones at the site of division of the basins of the anterior, middle, and posterior cerebral arteries; in premature babies, these areas are less vulnerable due to the presence of anastomoses with the meningeal arteries, and the periventricular white matter is more vulnerable in the areas between the subependymal vessels and the penetrating branches of the anterior, middle and posterior cerebral arteries (De Reuck J.L., 1984; Hill A. et al., 1992; Volpe J.J., 1995).

Premature infants with HIE are characterized by periventricular softening of the white matter of the brain - periventricular leukomalacia (PVL), mainly in the region of the outer corners of the lateral ventricles near the foramen of Monro. The term periventricular leukomalacia is due to the whitish tint of lesions detected on the section. PVL may be limited to one or more areas or be diffuse. Microscopically, at the beginning of the process, coagulative necrosis is determined with further centrilobular sclerosis and the absence of myelination, the reaction of neuroglia and the possible formation of microcavities after 2 weeks. According to serial ultrasound studies, the walls of the microcavities further collapse, the white matter surrounding the ventricles shrinks, and the ventricles expand. The affected area includes descending motor pathways, in particular, providing innervation of the lower extremities, which leads to spastic paresis of the legs. If more external parts are affected, then the nerve fibers that innervate the muscles of the hands also suffer, and then spastic diplegia and tetraplegia occur. Approximately 25% of children with PVL develop PVK and IVH at the site of the lesion. In conclusion, it is worth noting that Rudolf Virchow, the originator of PVL, considered infections to be the cause of the lesion.

Alfred Brann and James Schwartz (1987) in an experiment on newborn monkeys showed that the same damage to the cerebral cortex as in full-term newborns with asphyxia causes partial prolonged intrauterine hypoxia. In experimental monkeys, after birth, convulsions, retinal hemorrhages, and cytotoxic cerebral edema with subsequent foci of necrosis were noted in the section. Monkeys who were induced with total acute asphyxia at birth (according to the CBS indications, more severe than in the first group of monkeys) did not have convulsions, retinal hemorrhages, or cerebral edema. On the section in such monkeys, morphological lesions of the cortex were not observed either, but they were found in the region of the brainstem, thalamus, basal ganglia, and in the spinal cord. A. Brann and J. Schwartz believe that in acute short-term asphyxia, centralization of blood flow with increased blood flow in the brain, heart, adrenal glands and reduced blood flow in the kidneys, lungs, and intestines protects the cerebral cortex from damage.

In cases of acute asphyxia that developed against the background of chronic intrauterine hypoxia, the adaptive possibilities of hemodynamics are exhausted and cerebral blood flow decreases sharply. In chronic intrauterine hypoxia, changes in the basal ganglia and thalamus are typical, which, apparently, determine the narrowing of the adaptive possibilities of hemodynamics in response to increasing intranatal hypoxia. It is these basal parts of the brain that consume glucose most actively, which means that they are affected in placental insufficiency, reduced blood and energy delivery to the brain.

Focal ischemic lesions of the cortex in acute asphyxia are mainly the result of thrombosis, hemorheological disorders, while in prolonged acute asphyxia (or developed in a child who has undergone chronic intrauterine hypoxia) - cytotoxic edema, damage to the blood-brain barrier (BBB) and attraction of macrophages and neutrophils to the lesion.

In premature babies, due to the presence of a large number of meningeal anastomoses of the arterioles of the basins of the anterior, posterior and middle cerebral arteries, ischemic parasagittal strokes do not occur, paraventricular lesions (PVL) are typical for them. In the mature cerebral cortex of a full-term baby, there is a process of progressive deepening of the cortical furrows, and it is the deep sections of the bottom of the furrows that are sensitive to hypoxia. Under the bottom of the furrows in the parasagittal areas, infarctions occur (loss of both neurons and glial cells), foci of coagulation necrosis - subcortical leukomalacia (SCL), leading to subsequent subcortical atrophy, ulegiriya, gyrus atrophy.

Of the other posthypoxic brain lesions typical for a full-term child, selective necrosis of neurons of the cortex and hippocampus (even in the absence of convulsions, cerebral edema), as well as a peculiar pathological process in the basal ganglia, called Status marmoratus (marbling) in the English literature, are noted - neuron death, gliosis and an increase in the number of myelinated fibers, which gives the basal ganglia a marble appearance. These disorders can lead to bilateral choreoathetosis. An isolated deficiency of hippocampal neurons may be the cause of further minimal brain dysfunction and learning difficulties.

Cytotoxic edema. Hypoxia and ischemia naturally lead to anaerobic glucose metabolism, which results in a decrease in the synthesis of high-energy phosphates, energy suppliers for the neuron - ATP, creatine phosphate, impaired electron transport in mitochondria and the formation of excess free radicals. A decrease in the content of ATP naturally causes a deficiency of Na + - and K + - dependent ATP-ase and depolarization of presynaptic neurons. As a result, there is a release of excitatory amino acids - aspartate and glutamate (excitotoxicity), which act on kainate, AMPA (oc-amino-3-hydroxy-5-methyl-4-isoxoselepropionate) and NMOA (N-methyl-0-aspartate) receptors of the postsynaptic neuron. Activation of these receptors leads to the opening of Na+, K+ and Ca2+ channels, the flow of these electrolytes and water into the neuron, swelling and death of the neuron. The flow of Ca2+ in addition causes the activation of phospholipase and an increase in the synthesis of NO, which promote lipid peroxidation and death of the neuron membrane. The activation of proteases due to an increase in intracellular Ca2+ leads to the same effect. Free radicals, together with eicosanoids, activate platelets, which leads to release reactions from platelets, blockage of previously functioning vessels and the spread of ischemia. The development of ischemia is also facilitated by damage to the capillary endothelium by an excess of free radicals, activation of their production of leukotrienes, which stimulates the adhesion of leukocytes, the release of chemoattractants, and vascular thrombosis. It is important to emphasize that the glutamate-calcium cascade, due to the excitation of NMDA receptors of neighboring neurons, contributes to the spread of the lesion to non-ischemic areas of the brain.

In addition, the flow of Ca2+ into the endothelium of cerebral vessels provokes vasospasm and aggravation of cerebral ischemia, thus creating a vicious circle. According to the specified mechanism of death of the nervous tissue, necrosis develops. 6-48 hours after an episode of hypoxia or cerebral ischemia, the mechanism of genetically programmed cell death, apoptosis, is activated. The process of apoptosis in the nervous system is carried out mainly by the activation of microglia, which acquires the functions of phagocytosis. Normally, about 50% of the laid cells of the nervous system die in the fetus by the mechanism of apoptosis, and poorly differentiated and defective cells die. The regulation of this process is carried out by the interaction of apoptotic, or suicidal, genes ced-3 and ced-4 and antisuicidal bcl-2. All mechanisms of apoptosis induction involve the transcription factor p53, whose synthesis is activated at the first signs of DNA destruction. The polymorphism of the p53 gene and the relationship between the volume of brain damage in ischemic strokes and the p53 genotype have been established (Skvortsov V.A., 2003).

It should be emphasized that the process of necrosis prevails in neurons during acute and severe hypoxia, with an excess of Ca2+; the process of apoptosis dominates in neuroglia under milder and longer hypoxia, with an insignificant flow of Ca2+, and is more dependent on the content of Zn2+.

Animal experiments (including fetuses and newborns) showed a preventive effect in hypoxic brain damage (reducing it and improving the neurological outcome) of the administration of drugs that block NMDA-glutamate receptors (magnesium ions), calcium antagonists (verapamil, etc.), platelet inhibitors (indomethacin, etc.), inhibiting the formation of peroxide compounds (xanthine oxidase inhibitor - allopurinol), binding peroxides (su peroxide dismutase, vitamin E, dimethylthiourea), endogenous components of cell membranes (GMj-gangliosides), glutamate antagonists (derivatives of the inhibitory mediator in the brain of gamma-aminobutyric acid - piracetam, phenibut), craniocerebral hypothermia.

Background conditions can also affect the severity of glutamate cascade activation. So, with hypoglycemia after 2 hours, the level of glutamate in the brain increases 15 times. Yu.A. Yakunin et al. (1993) showed both in the experiment on animals and on sections of the brain of newborns who died from asphyxia, a sharp inhibition of pyridoxalkinase activity. There is a deficiency of pyridoxal phosphate, which leads to a decrease in the activity of the pyridoxal-dependent enzyme catalyzing the decarboxylation of glutamic acid, and hence to a violation of the formation of gamma-aminobutyric acid (GABA).

Early (immediately after birth) cytotoxic cerebral edema, the mechanism of which is described above, against the background of normalization of blood gas composition and hemodynamics in children with acute asphyxia during childbirth, resolves on its own (without drug treatment) in the first hours of life. In children with birth asphyxia, which developed against the background of chronic intrauterine hypoxia or with an Apgar score of 3 points or less remaining at the 5th minute after birth, the intensity of cerebral blood flow remains significantly reduced, both due to its non-recovery due to increased vascular resistance of the brain, and as a result of lower systemic pressure. This, in combination with severe metabolic acidosis (pH less than 7.0, BE more than -12 mmol / l), the metabolic disorders described above, leads to the development of the second stage of cerebral edema - vasogenic edema, swelling of the brain.

Attention should be paid to the role of antidiuretic hormone (ADH) in the genesis of brain lesions after hypoxia. With asphyxia, the syndrome of excessive production of ADH (SIPADH) is typical, and with IVH, hypoxic lesions of the hypothalamic pituitary tract - the syndrome of insufficient secretion of ADH (SIADH). Both conditions can contribute to the development of interstitial cerebral edema. CIPADH is characterized by hyponatremia, reduced plasma osmolarity, relatively high urinary osmolarity, urinary sodium excretion equivalent to its intake, improvement after fluid restriction, administration of spirolactone (veroshpiron) or indomethacin. SIADH is manifested by polyuria with low osmolarity and density of urine and hypernatremia, which is often observed in children with asphyxia and cerebral edema. There are descriptions in the literature of newborns in whom cerebral edema due to asphyxia was eliminated with a single injection of vasopressin (ADH).

The experiment shows that when newborn animals are injected with Escherichia coli endotoxin, changes can occur in their brain similar to those observed during chronic intrauterine hypoxia - PVL and SCL. In this regard, we note that N.N. Shabalova and N.A. Akhmina are developing a hypothesis about the trigger (stimulating, intermediate, supporting) role of endotoxins of the intestinal flora of a pregnant woman in the pathogenesis of preeclampsia, and it is in children from such mothers that HIE develops.

Depending on the characteristics of the course of the prenatal period, childbirth, drug therapy of the mother, affecting the metabolism of the child, in some children after hypoxia in childbirth, the effect of accumulation of excitatory mediators (mainly glutamate) dominates in the clinic - anxiety, hyperexcitability, etc., while in others - the effect of accumulation of inhibitory mediators (gamma-aminobutyric acid), adenosine, endogenous opiates, and then lethargy is noted, years argy, decreased activity of reflexes, muscle tone, regurgitation, etc.

Thus, the pathogenetic mechanisms of HIE are: disorders of hemostasis (maximum deficiency of vitamin K-dependent blood coagulation factors, platelet dysfunction can cause or increase intracranial hemorrhage); general metabolic disorders (hypoglycemia, hypocalcemia, hypomagnesemia, etc. can cause seizures that sharply increase brain hypoxia), which are sharply aggravated by starvation of the child, irrational parenteral nutrition; deficiency of inhibitory (GABA) and the predominance of the synthesis of excitatory mediators (glutamate); activated macrophages and neutrophils that enter the brain due to damage to the blood-brain barrier (activated macrophages can synthesize glutamate, peroxides, proteolytic enzymes, induce sclerotic processes, etc.).

The pathogenesis of the posthypoxic process in the brain is not completely clear. Perhaps the infection comes into its own. In this regard, it is worth recalling again R. Virchow, who in 1867 introduced the concept of early acquired leukoencephalopathy to describe infectious lesions of the brain of the fetus and newborn. The role of perinatal infections (mycoplasma, viral), as well as intestinal dysbacteriosis in the pathogenesis of perinatal hypoxic brain lesions is not yet clear.

The most recognized biochemical indicator of brain damage is the content in the blood serum of the brain fraction (BB-isoenzyme) of creatine phosphokinase, which is released into the blood with defects in the outer membrane of neurons or their death. The maximum level of this isoenzyme in the plasma of children born in asphyxia is observed at the end of the first day of life. Its plasma concentration is highest if the child has suffered chronic intrauterine hypoxia.

However, it has been established that intravenous administration of piracetam (5 g in 10% glucose solution in drops, and if the child has not yet been born, then 2 g every 2 hours) leads to an improvement in uteroplacental blood flow and, therefore, the state of the fetus, reduces the frequency of birth of children in severe asphyxia and reduces the severity of the rise in the concentration of BB-creatine phosphokinase in the blood.

Experimental data on the study of intrauterine hypoxia in animals showed wave-like changes in the brain, when, after a short period of neurodystrophic processes, under the direct influence of hypoxia, synthetic, reparative processes begin to dominate in the brain, which are again replaced by neurodystrophic, etc. (Zhukova T.P., Purin R.V. et al., 1984).

Thus, brain damage occurs not only during hypoxia, but also in the period following it. In some cases, this may be due to postresuscitation disease, according to V.A. Negovsky (Negovsky V.A. et al., 1987), namely:

the effect of reoxygenation (oxygen paradox - a damaging effect on the neuron and glia of high oxygen concentrations);

prolonged hypoperfusion and arterial hypotension;

activity of proteolytic enzymes;

the formation of free radicals and lipid peroxidation;

intracellular accumulation of Ca2.

At the same time, it should be remembered that the brain of young children has great plastic and reparative capabilities, including compensation for defects in its antenatal formation. In an adult, the number of nerve cells and synapses in 1 mm3 of brain tissue is only 40% of that in children aged 1 to 7 years, and the number of synapses per nerve cell by this time is 20% less.

The clinical picture of HIE is characterized by wavelike, staging flow. There are several clinical classifications of HIE. The first staged classification of HIE that has become a classic was proposed by H.B. Sarnat and M.S. Sarnat in 1976 (see Table 11.3).

A static assessment of the neurological status in the first hours and day of life does not allow one to judge with sufficient reliability the severity and prognosis of DIE. The dynamics of the child's condition is of primary importance for such judgments.

I.I.Volpe (1995) emphasizes that hyperexcitability, non-inhibition of reflexes, sympathicotonia (tachycardia, tachypnea, dilated pupils, etc.) with mild (I degree) HIE usually last no more than 1-2 days. The prognosis for the vast majority of these children is favorable.

In case of HIE of moderate severity, along with the symptoms listed in the table, already in the first hours of life there may be periodic sighs of the gasp type or periodic breathing of the Cheyne-Stokes type, attacks of bradypnea or bradycardia, and a decrease in spontaneous motor activity. In the second half of the first day of life, these children develop convulsions, but they are usually satisfactorily controlled by anticonvulsant therapy. On the second day of life, muscle tone in children improves, but a piercing, high-pitched cry, regurgitation, myoclonic seizures, tremor, and scattered movements may appear. By the end of the second - the beginning of the third day of life

sleep apnea, signs of intracranial hypertension or cerebral edema are possible. A certain improvement in the condition of a child with HIE II degree develops by the end of the first week of life. If neurological symptoms (lethargy, hypotension, poor movements, soporous condition, severe weakness of sucking) persist for more than a week, then, according to I.I. Volpe (1995), neurological consequences develop in 20 - 40% of children.

In severe HIE (grade III), consciousness is absent for the first 12 hours of life, then a false improvement may follow, but then consciousness is again lost in the middle of the second or third day of life. The most likely reason for this is the development of destructive, necrotic processes in the brain without or with cytotoxic edema. Attacks of respiratory arrest in such children appear already in the second half of the first day of life, and convulsions - even in the first half. The earlier posthypoxic seizures appeared, the more severe the encephalopathy and the worse the prognosis. The most unfavorable occurrence of hypoxic convulsions in the first 2-6 hours of life. Seizures are often refractory to anticonvulsant therapy. It should not be forgotten that in children with severe perinatal hypoxia, a frequent cause of seizures, even in the first hours of life, may be metabolic disorders - hypoglycemia, hypocalcemia, hypomagnesemia and hyperammonemia, and therefore monitoring of these indicators is necessary.

Motor disorders, muscle hypotension in different children with HIE may have some features. In full-term children with acute severe asphyxia of newborns due to ischemia of the parasagittal regions, shoulder weakness may develop by the end of the first day of life - in a child supported in the armpits, the head goes into the shoulders. This can also be indicated by the weakness of the proximal sections - a symptom of the seal's foot. In premature babies, leg weakness, lethargy, apnea attacks with bradycardia, immobility, lack of sucking, regurgitation, etc. are more typical.

Of course, the features of the course of HIE in the early neonatal period significantly depend on the background - comorbidity and complications of asphyxia present in the child (see Chapter VII). Early diagnosis of pulmonary, cardiovascular and metabolic disorders is especially important. A number of studies have shown that persistent oliguria (urine output less than 15 ml/kg/day) in the early neonatal period correlates with poor neurological outcome, i.e. with a high frequency of neurological complications both in the neonatal period and in follow-up.

Periventricular leukomalacia (PVL) is one of the most typical complications of hypoxic conditions in premature infants. Moreover, as a rule, we are talking about long-term persistent hypoxia in children born in asphyxia, followed by the development of pneumopathy, pneumonia. At the same time, the decisive role of free radicals in the pathogenesis of PVL, and therefore inadequate oxygen therapy, is emphasized. There are no specific clinical symptoms of PVL. In preterm infants with PVL, diagnosed by computed tomography or on section, hypotension, hyporeflexia, incomplete Moro reflex (its phase I), lethargy, weak cry, adynamia, convulsions (as their equivalent can be rotator nystagmus and other opercular paroxysms), spastic paralysis and paresis (spastic diplegia of the lower extremities, which can be combined with spastic paresis of the upper extremities), absence of sucking and swallowing reflexes, attacks of hypoxia (cyanosis).

With neurosonography, PVL is detected in 10-15% of children with very and extremely low body weight. Ultrasonographically, the following degrees of severity of PVL are distinguished (de Vries L.S., 1994):

the first degree - a transient increase in the echo density of the periventricular zones for more than 7 days;

the second degree - an increase in periventricular echo density in combination with small local frontoparietal cysts;

third degree - increased periventricular echo density in combination with extensive periventricular cystic lesions;

fourth degree - increased periventricular echo density with spread to the white matter of the brain and white matter cysts.

The surviving children can develop both the syndrome of minimal cerebral dysfunction, visual defects, and the spastic form of cerebral palsy after the cystic form of PVL, a pronounced mental deficit. According to V.I. Guzeva and A.E. Ponyatishin (1998), in 88.9% of cases, the cystic form of PVL leads to the development of spastic forms of cerebral palsy and in 44.4% - severe intellectual disorders; in the non-cystic form, 37.5% of children had persistent motor disorders in the residual period of the disease.

The diagnosis of HIE is possible only when taking into account a complex of anamnestic data (the course of pregnancy, the state of the fetus, the course of childbirth, childbirth benefits, drug therapy for the mother during pregnancy and childbirth, assessment of the child's condition at birth according to the Algar scale) and analysis of the dynamics of the clinical picture in the child. Clinical diagnosis of HIE is based on the use of clinical classifications and standard neurological scales, which make it possible to distinguish between normal and deviant neurological status. Within the framework of the deviant neurological status, it is necessary to differentiate adaptive, transient deviations in the neurological status of the infant (transient neurological dysfunction of the newborn) and clinical manifestations of HIE.

Modern imaging methods (neurosonography, axial computed tomography, magnetic resonance imaging, γ-scintigraphy) make it possible to assess the macrostructure of the medulla, the presence or absence of malformations, the size and shape of CSF spaces. Magnetic resonance imaging is the most informative imaging modality; with its help, it was possible to establish the phases of the course of DIE: acute (up to 5 days), subacute (up to 20 days) and chronic (up to 56 days).

Among the methods of neurophysiological diagnosis of DIE, electroencephalography (EEG) should be noted. To diagnose NGIE, a routine EEG is used, which allows to recognize various stages of DIE, a total EEG, an EEG with mapping. The use of EEG mapping made it possible to identify the patterns of the main neurological syndromes of HIE. The complexity of EEG diagnostics in newborns lies in the recognition of patterns of cerebral immaturity and pathological patterns.

Evoked potentials (EPs) are the most informative diagnostic method, which with 100% accuracy allows predicting an unfavorable outcome of DIE and deafness (auditory brainstem EPs), blindness (visual EPs), and the development of cerebral palsy (somatosensory EPs).

Forecast. As mentioned above, the prognosis for HIE depends on the severity of the transferred hypoxia, confirmed by the CBS parameters, the severity of encephalopathy (at stage I of HIE, according to H.B. Sarnat and M.S. Sarnat, the prognosis is favorable, at stage II - doubtful, at stage III - unfavorable for complete recovery).

In children born with asphyxia, the most threatening symptoms in terms of poor prognosis and long-term neurological consequences are: retention of an Apgar score of 3 points or lower at the 5th minute of life (such an assessment at the 15th and 20th minutes is the most unfavorable prognosis both in terms of survival and in case of survival, because most survivors will have severe brain damage), the appearance of seizures in the first 8 hours of life, recurrent convulsions, persistent muscle hypotension and transitions of the phase of lethargy and hypotension into a state of pronounced hyperexcitability and hypertension of the extensor muscles. Unfortunately, after a clinically clear period (i.e., in the absence of gross deviations from the norm), the child may develop motor or sensory disorders and other adverse outcomes of HIE, which include cerebral palsy, mental retardation, epileptic seizures, hydrocephalus, attention deficit hyperactivity disorder, damage to the visual and auditory analyzer,.

Both the course of the antenatal period and the features of the neonatal period have a significant impact on the prognosis in HIE. Thus, L.A. Fedorova (2003) showed that the presence of multiple organ failure in the acute period in children with a birth weight of less than 1500 g sharply worsens the neurological outcome. If in the acute period the insufficiency of two functional systems is registered, then cerebral palsy, severe psychomotor retardation and / or blindness, hearing loss at the age of 1 year are recorded in 47%, with insufficiency of three systems - in 77.7% and four or more functional systems - in 90% of children. The neurological prognosis of HIE worsens the development of BPD, sepsis, and necrotizing enterocolitis in a premature baby.

Possible long-term consequences of perinatal HIE depending on the nature of brain damage are shown in Table 11.4.

Treatment. The best treatment is the prevention and early treatment of intrauterine hypoxia and asphyxia of the newborn. It is impossible to treat the brain in isolation. Measures aimed at the main pathogenetic mechanisms of brain damage include: 1) the speedy restoration of normal airway patency and adequate ventilation of the lungs - VV L or mechanical ventilation in the mode of creating hypocapnia, but without hyperoxemia; 2) elimination of possible hypovolemia; 3) maintaining adequate brain perfusion both by preventing even short-term systemic (arterial) hypotension and hypertension, polycythemia and blood hyperviscosity, hypervolemia, in particular, due to the rapid intravenous injection of liquid; 4) protective mode - prevention of cooling,

overheating, infection, limiting unnecessary traumatic and irritating environmental influences; 5) systematic delivery of energy to the brain in the form of glucose (initially with the help of infusion therapy - 10% glucose solution, the volume of which in the first day of life is up to 50 ml / kg / day); 6) correction of pathological acidosis, prevention and treatment of hypoglycemia, hypocalcemia, hypomagnesemia, etc. It is very important to monitor the main parameters of vital activity and biochemical blood parameters (volume - see Chapter VII).

Individual maintenance and corrective therapy, taking into account the peculiarities of central and cerebral hemodynamics, the state of the main metabolic indicators both before and during treatment, along with the listed measures, is the golden rule for treating children with severe asphyxia, including cerebral edema.

Edema of the brain. The basis of treatment is compliance with the principles of maintenance therapy listed above, including mechanical ventilation in hyperventilation mode, limited both in volume (no more than 50 ml / kg / day) and infusion therapy. The following directions of pharmacotherapy of patients with cerebral edema are discussed: 1) osmotically active substances; 2) hormone therapy - dexamethasone; 3) nootropic drugs (instenon, piracetam, pantogam, glycine, gliatilin, semax); 4) high doses of barbiturates; 5) anticalcium drugs; 6) saluretics. Depending on the anamnesis and clinical picture of cerebral edema in a particular child, each of the listed directions of therapy can be either effective or not give any positive effect. Basically, pharmacological preparations are indicated for vasogenic, interstitial cerebral edema. If the edema is cytotoxic, then the effectiveness of these drugs is small or non-existent.

Of the osmotically active substances, sorbitol is preferred at a dose of 0.25-0.5 g/kg intravenously; the drug is administered once slowly drip in the form of a 10% solution.

Dexamethasone is also administered once at a dose of 0.5 mg/kg.

Numerous studies have shown that parenteral administration of phenobarbital at a dose of 10 mg/kg twice (in the first hours after birth and again after 12–24 hours) significantly improves the resistance of neurons to hypoxia and long-term neurological consequences. However, in most neonatal centers, such therapy is used only for convulsions that developed in the first hours of life. Maintenance dose of phenobarbital (after loading on the first day 20 mg/kg) - 3-4 mg/kg of body weight per day.

In the first day of life, especially with unrecovered diuresis (i.e. against the background of oliguria), saluretics and other diuretics are usually ineffective. Furosemide at a dose of 1-2 mg / kg 2 times a day is prescribed only for children older than 2 days of life with large increases in body weight (of course, against the background of limited infusion therapy).

Therapy with anticalcium drugs in the acute period of neonatal asphyxia is in a research situation, and the regimens for the use of these drugs have not been worked out.

Nootropic drugs (from the Greek noos - thinking) are actively introduced into neonatology. Studies by N.V. Bogatyreva and I.V. Sirotina showed that the pharmacokinetics of piracetam (nootropil) in children older than 5-7 days of life is basically similar to that in adults. R.A. Zhetishchev showed that intravenous injection of piracetam at a dose of 50 mg/kg to children born in asphyxia contributes to the normalization of cerebral blood flow. According to our data, the use of piracetam at the above doses twice during the first hours of life (at birth and after 4-6 hours) followed by repeated administration from the 6th day of life orally at a daily dose of 200-300 mg/kg improves the condition of children born with asphyxia and contributes to their faster neurological rehabilitation. Of the side effects, we noted some stimulation of convulsive activity, but only in children with a history of convulsions. In addition, according to the data of G.N. Chumakov, piracetam reduces platelet aggregation, but this effect is minimal at a single dose of the drug 35 mg/kg. And yet, if a child is already receiving several platelet inhibitors for various indications, then it is better not to prescribe piracetam. Piracetam promotes faster removal of a child from a coma, including cerebral edema.

I.V. Sirotina used piracetam in childbirth in women with severe placental insufficiency (diagnosed by ultrasound examination of the placenta) according to the following scheme: the first injection - with the onset of labor - 25 ml of 20% solution of piracetam in 100 ml of 5% glucose solution or isotonic sodium chloride solution intravenously for 20 - 30 minutes, subsequent injections (from 1 up to 4 times with an interval of 2 hours) - 10 ml of a 20% solution is also intravenous drip. It has been established that such therapy improves the course of labor and does not increase blood loss; increases the resistance of the fetus to hypoxia, which is manifested both in an improvement in the Apgar score of children at birth, and in a decrease in the frequency of neurological complications both in the early neonatal period and in follow-up studies during the first year of life. In randomized groups of children born in asphyxia, the level of BB isoenzyme of creatine phosphokinase (brain fraction of creatine phosphokinase) in blood plasma was significantly lower on the 3rd day of life in newborns whose mothers received piracetam during childbirth.

As nootropic drugs that improve trophic processes in the brain, newborns with HIE also use instenon (10-15 mg/kg/day, according to etofilin), pantogam (40 mg/kg/day), pyriditol (5 drops of suspension per 1 kg of body weight per day), phenibut (40 mg/kg/day), cortexin (10 mg/kg/day), etc. Of these drugs, pantogam does not stimulate convulsions new activity. Cerebrolysin, courses of vitamins Bj, B^, B12 are prescribed for children with GID, usually older than 2 weeks. Cerebrolysin is contraindicated in children with a history of seizures.

It should be emphasized that the above drugs in neonatology are widely used only in Russia and the CIS countries, and randomized trials in which their benefits have been proven have not been conducted. Abroad, these drugs are not used in newborns and infants. According to neurologists specializing in the treatment of adults, randomized studies have shown that gliatilin (Odinak M.M., Voznyuk I.A., 1999), instenon (Skoromets A.A., 1999), glycine and semax (Skvortsova V., 2003) are effective in cerebral ischemia in the first 3-6 hours. You can read more about the use of nootropics in children in our review (Shabalov N.P. et al., 2001).

Shoshina Vera Nikolaevna

Therapist, education: Northern Medical University. Work experience 10 years.

Articles written

The lack of oxygen in the human body sometimes causes irreparable harm in a matter of seconds. Hypoxic-ischemic encephalopathy (HIE) sometimes sounds like a terrible sentence for both a child and an adult. Let's see what kind of disease it is, its symptoms and how dangerous hypoxic-ischemic brain damage is at any age.

Oxygen deficiency inevitably affects the functioning of the body. Hypoxic-ischemic encephalopathy in newborns occurs frequently: both in full-term babies and premature babies. In 10% of infants who have had it, they are later diagnosed with cerebral palsy. That is why the expectant mother should be in the fresh air more often and strictly follow the recommendations of the doctor in order to reduce to a minimum.

In adults, injuries or existing serious diseases are a common cause of pathology. If help is not provided on time during an asthma attack, then there is a serious risk of death or disability. An important role is played by the severity of the pathology, the higher it is, the less chance a person has of returning to a full life.

When oxygen starvation occurs in the most important part of the central nervous system, this leads to a deficiency of this substance in the brain cells, which slows down blood flow and all metabolic processes. With such a lack of nutrition, brain neurons in some parts of the body begin to die, leading to neurological disorders.

Accelerates the process, which also occurs due to a failure in blood circulation. The pressure builds up and the cells begin to die faster. The faster the process goes, the greater the chance that the damage will be irreversible.

Causes

Hypoxic encephalopathy in adults and children occurs for different reasons. It is important to know them in order to take all measures to prevent it.

In adults

Hypoxic ischemic encephalopathy occurs against the background of a lack of oxygen, which is caused by the following reasons:

state of suffocation;
suffocation;
failure of the respiratory system of any kind;
drug addiction, overdose;
pathologies of the circulatory system, leading to its obstruction or rupture;
cyanide, carbon monoxide - poisoning;
prolonged stay in a smoky place;
tracheal injury;
heart failure;
diseases leading to paralysis of the muscular tissue of the respiratory system.

Acute hypoxic encephalopathy occurs if oxygen has not been supplied to the body for several minutes. This is a severe course of pathology, which most often ends in death. Isolated cases have been recorded when people survived, but for them it ended in a severe form of serious mental illness.

In newborns

The cause of this condition in a newly born child may be:

suffocation during childbirth due to weak labor activity;
premature birth process or with pathological factors, such as prolapse of the umbilical cord;
diseases of infectious genesis in the mother;
a number of physical factors from dirty air to radiation.

It is asphyxia in infants that is the most common factor leading to HIE. Doctors identify the following risk factors for its occurrence:

hypotension of an acute form in a woman in labor;
underdevelopment of the lungs, which leads to a lack of oxygen in the blood;
difficulties in the work of the heart;
injury to the fetus by the narrow pelvis of the mother or due to problems with the umbilical cord;
difficulties in labor, trauma, stress;
hypoxia;
birth bleeding;
negligence of medical personnel;
placental abruption;
change in the shape of the fetal skull due to pressure;
birth trauma, uterine rupture;
low placenta previa.

Severity and characteristic symptoms

Hypoxic-ischemic encephalopathy has 3 degrees of severity, which are characterized by their manifestations. According to them, doctors often give a preliminary description of damage to brain activity and an approximate prognosis.

Light degree

With this degree, the patient will:

the pupil is dilated and the eyelids are wide open;
lack of concentration;
impaired coordination of movements, wandering behavior;
revealed either drowsiness or hyperexcitability;
high degree of irritability;
lack of appetite;
impaired cerebral circulation.

Average degree

Neurology with it will be more pronounced, because the violation of oxygen saturation of the brain is longer:

the baby has spontaneous cries for no reason;
the protective and supporting reflex is either weakened or absent altogether;
signs of muscle weakness;
drooping of the upper eyelid;
increase in cerebrospinal fluid pressure;
metabolic acidosis of the blood;
neuralgic attacks;
failure in the swallowing process.

Severe degree

The defeat in such cases is more severe, which manifests itself in:

convulsions;
cyanosis of the skin;
loss of consciousness;
hypertension;
lack of motor abilities;
strabismus;
coma or precoma;
lack of pupillary reaction to light;
failure of the respiratory process with severe arrhythmia;
tachycardia.

PEP is a type of hypoxic-ischemic encephalopathy in young children. It is diagnosed both immediately after birth and in the first year of life. PEP develops both in utero, during labor, and in the first 10 days from birth.

It can be of three degrees of severity with characteristic symptoms and proceed in an acute form - up to a month, in early recovery of functions - up to 4 months, with late recovery - up to 2 years.

Diagnostics

Perinatal ischemia syndrome against the background of cerebral hypoxia begins to be diagnosed by making a visual examination of the child. It's the same with adults. Despite all the advances in medicine, a unique test that accurately detects HIE has not yet been invented. All laboratory techniques are aimed at identifying how badly the brain is damaged and the current state of the whole organism.

What the research will be depends on the symptoms, and how they developed. To decipher the analyzes, there are special biomarkers that give a complete picture of the degree of HIE. For the study, the patient's blood is needed.

Neuroimaging is carried out using:

neurosonograph and / or, a tomograph showing internal brain damage and changes in it;
, fixing the work of cerebral blood flow;
electroneuromyograph to determine the sensitivity of the fibers of the periphery of the nervous system.

Additional can be used:

an electroencephalograph to detect developmental delay at an early stage and whether there is epilepsy;
video monitoring to study the motor activity of babies.

If necessary, the victim is examined by an ophthalmologist to determine the condition of the optic nerves and the fundus, as well as for the presence of genetic diseases in this area.

Treatment and care

There should be special care for the victims, and for children who have undergone HIE, it is based on control over:

room temperature - no more than 25 degrees;
his comfortable posture, so tight swaddling is prohibited;
so that the light is soft and muffled;
silence;
feeding, which should be with skin-to-skin contact and according to the needs of the baby;
breathing, in case of failure in which a special apparatus is connected.

Therapy is carried out:

Surgically, to restore and improve blood circulation in the brain. Most often, for these purposes, an endovascular technique is used that does not violate the integrity of tissues.
Medication, choosing drugs depending on how severe the degree of damage and its clinical picture.
On anticonvulsants that stop seizures. Usually it is Phenobarbital, the dosage of which is selected individually. The intravenous method is the fastest. But the drug itself is contraindicated in hypersensitivity, severe hypoxic and hypercaptic respiratory failure, kidney and liver problems, and pregnancy. Lorazepam can be used, it has a similar effect and a list of contraindications.
On cardiovascular agents, to increase systemic vascular resistance and myocardial contractility, resulting in increased cardiac output. All drugs in this group affect the kidneys, and in case of an overdose, side effects are difficult to predict. The most commonly used are Dopamine, Dobutamine.

Further observation

They are discharged from the hospital only after completing a full course of physical therapy and a comprehensive assessment of neuropsychic development. Most often, after discharge, patients do not require specific care, but regular examinations in the clinic are mandatory, especially for children.

If the disease was severe, then the child will be observed in a special center, where he will be assisted by a doctor for neuropsychic development.

Treatment for seizures depends on central nervous system symptoms and test results. Discharged only with a slight deviation from the norm or even within it. Phenobarbital is removed gradually, but it is usually drunk after discharge for at least 3 months.

Forecast and consequences

In adults, the prognosis depends on the degree of brain damage by pathology. The most common consequences of perinatal HIE are:

delay in the development of the child;
brain dysfunction in terms of attention, focus on learning;
unstable work of the internal systems of the body;
epileptic seizures;
hydrocephalus;
vegetative dystonia.

There is no need to think that this is a sentence, even the disorder in the central nervous system is corrected, ensuring a normal life for patients. A third of people with this disorder are completely cured.

Prevention

If we are talking about adults, then all preventive measures should be aimed at the complete rejection of bad habits. At the same time, you need to regularly play sports, avoiding excessive stress, eat right, undergo regular medical examinations in order to identify dangerous pathologies at an early stage for their successful relief.

No one is immune from injuries, but if you behave more carefully, then they can be minimized.

To reduce the risk of HIE in a newborn, only his mother can still during pregnancy. For this you need:

strictly monitor the daily routine and personal hygiene;
give up nicotine and alcohol even at the minimum dosage;
undergo timely examinations by doctors and diagnostics, especially by a neurologist;
entrust childbirth only to qualified personnel.

Hypoxic-ischemic encephalopathy is a dangerous disease, but it can be prevented and even cured, but only if help is provided on time and medical recommendations are not violated in the future.

Hypoxic ischemic encephalopathy is a brain lesion characterized by hypoxia (low oxygen content in the body) caused by impaired motor functions, convulsions, and other mental developmental disorders.

In newborns, hypoxic ischemic encephalopathy can occur immediately after birth or during the first two days of the baby's life.

If a child or an adult is without oxygen for a long period of time, brain cells (neurons) are gradually destroyed and their irreversible death occurs.

I distinguish the following 3 degrees of severity of the disease:

For mild severity:

pupil dilation;
the patient cannot concentrate;
body coordination is disturbed;
sleepy state;
hyperemotionality;
increased irritability;
eyelids open wide;
lack of appetite;
the phenomenon of wandering is observed;
cerebrovascular accident.

Medium severity:

periodic causeless screams of the child;
reflexes are partially weakened or completely absent (protective, supporting);
muscle weakness (muscle tone decreases and then involuntarily increases);
drooping of the upper eyelid;
increased pressure of cerebrospinal fluid;
metabolic acidosis of the blood;
neurological disorders;
violation of the swallowing process.

In more severe cases:

convulsive state;
cyanosis of the skin;
loss of consciousness;
hypertension;
strabismus;
lack of response to pain and motor activity;
pre-coma or coma;
pupillary reaction to light is practically absent;
violation of the respiratory process, accompanied by arrhythmia;
rapid heartbeat (tachycardia).

Determination of the severity of the disease is carried out directly in the maternity hospital by specialist doctors. If necessary, appropriate treatment is prescribed.

Hypoxic ischemic encephalopathy occurs due to circulatory disorders, as a result of which the nerve cells do not receive the required amount of oxygen.

Causes

In newborns

The causes of hypoxic ischemic encephalopathy in newborns may be as follows:

asphyxia during childbirth (weak contractions);
premature and pathological childbirth (prolapse of the umbilical cord);
infectious diseases of the mother;
physical factors (polluted air, radiation).

In adults

In adults, the disease occurs as a result of:

carbon monoxide poisoning;
when suffocated;
sharply low blood pressure;
drug or alcohol overdose;
consequences after general anesthesia;
complications after head trauma.

All of the above causes are due to a decrease in the supply of oxygen to the brain.

Asphyxia during childbirth is the main cause of brain damage and can lead to disability or death, so obstetric care should be carried out professionally, taking into account the anatomy of the birth canal and body parts of the fetus.

Symptoms

increased excitability;
convulsive seizures;
inhibition of reflexes;
hypotension.

Treatment

Treatment of hypoxic ischemic encephalopathy must be carried out in a hospital.

Correct and timely drug treatment will prevent further consequences and complications, and in most cases the prognosis of the disease will be favorable.

Treatment should be aimed at eliminating the underlying problem of lack of oxygen in the body.

Treatment of the disease includes:

Taking medications.
Physiotherapy procedures.

Treatment of this disease requires an integrated approach and immediate prescription of drugs.

Adult patients should give up all kinds of bad habits (alcohol, smoking). It is necessary to review your diet and, if necessary, correct it by including vegetables and fruits. For a full recovery, it is necessary to undergo several courses of treatment during the year.

With a mild degree, homeopathic remedies are used.

To prevent convulsive reactions, anticonvulsants are prescribed:

diazepam;
Phenobarbital.

To improve metabolic processes in the brain, apply:

Piracetam;
Cinnarizine;
Actovegin.

To reduce intracranial pressure appoint:

Mannitol.

All of the above drugs are prescribed by the attending physician. Self-medication is strictly prohibited!

In some cases, if the central nervous system is damaged, anticonvulsant drugs are continued for three months or six months. Cancellation of drug treatment is determined by the attending physician, guided by the clinical picture and electroencephalogram studies.

There are several risk factors for the disease :

early or late pregnancy;
infectious diseases during pregnancy;
hereditary diseases;
violation of the diet;
unfavorable environmental conditions;
pathological pregnancy.

Hepatic encephalopathy is a disorder in the functioning of the brain as a result of severe liver damage. Here you will learn how this complication develops and how to cure the patient.

Recovery period

After completion of the course of treatment and discharge from the medical institution, it is necessary to assess the neuropsychic development of the child.

Most of the patients after discharge do not need community care, only periodic supervision of a pediatrician is necessary.

For a quick recovery you need:

communicate with the child;
keep silence;
monitor nutrition;
create all conditions to maintain health at the proper level and minimize adverse outcomes.

Consequences

The consequences after a mild or moderate form can be favorable and full recovery can be achieved.

If the clinical picture persists for 10 days in newborns who have undergone this disease, then the probability of a complete recovery is very small.

In severe form, death is possible in 30% of cases, treatment must be carried out strictly in the intensive care unit

In the recovery period, the effectiveness of physiotherapeutic procedures and pharmacological agents is high.

Prevention of hypoxic ischemic encephalopathy is very important, because disease is easier to prevent than to cure.

In young children, the disease is much easier than in adults. With the right approach to this disease, the brain is fully restored and the child achieves a full recovery. The earlier the diagnosis is made and the course of treatment is prescribed, the more likely it is to recover without pathological consequences. The consequences depend entirely on active treatment and rehabilitation.

What is encephalopathy?

Encephalopathy is an organic non-inflammatory lesion of the neurons of the brain, in which, under the influence of pathogenic factors, dystrophic changes occur, leading to disruption of the brain. The impetus for the development of this disease is a chronic oxygen deficiency caused by traumatic, toxic, infectious causes. Oxygen starvation of brain tissues disrupts the natural metabolic processes in them. As a result, the complete death of neurons triggers the shutdown of damaged areas of the brain.

As a rule, encephalopathy is a sluggish disease, but in some cases, for example, in severe renal and hepatic insufficiency, it develops rapidly and unexpectedly.

Currently, doctors divide all types of encephalopathies into 2 large groups, each of which is divided into subspecies:

Congenital. It usually occurs with an unfavorable course of pregnancy, anomalies in the development of the brain in the fetus, genetic disorders of metabolic processes.
Acquired. It occurs at any age, but is more common in adults. It is characterized by the influence of pathogenic factors on the brain during human life.

Varieties

Encephalopathy in children is a multietiological disease, but in all cases it has the same morphological changes in the brain. This is the destruction and reduction in the number of fully functioning neurons, foci of necrosis, damage to the nerve fibers of the central or peripheral nervous system, swelling of the meninges, the presence of areas of hemorrhage in the substance of the brain.

The table below shows the main types of this pathology.

Types of encephalopathy	Etiology of occurrence	Clinical manifestations
Hypoxic-ischemic (perinatal encephalopathy in newborns)	The impact of damaging factors on the fetus in the perinatal (from the 28th week of pregnancy) and postnatal (up to the 10th day of life) periods.	Hyperexcitability, poor sleep, frequent regurgitation, impaired thermoregulation, head tilt, pathological tone.
Bilirubin	Pathological jaundice, hemolytic disease, subcutaneous hemorrhages.	Lethargy, poor sucking reflex, rare delayed breathing, increasing tension in the extensor muscles.
epileptic	Pathologies of brain development.	Epileptic seizures, mental disorders, speech, mental retardation.
Residual (unspecified)	Infections of a bacterial and viral nature, intranatal injuries, cephalohematomas.	Neurological and cognitive dysfunctions, headache, hydrocephalus, psychomotor retardation.
Vascular	Vascular pathologies (atherosclerosis of cerebral vessels, arterial hypertension).	Depression, mood changes, headaches, sleep disturbance, poor memory, fatigue, pain of unknown origin in various organs.
toxic	Systematic impact on the body of neurotropic and toxic substances.	Mental, vegetovascular, motor, thermoregulatory disorders; parkinsonism; epileptic syndrome.
Post-traumatic	Traumatic brain injuries and fractures.	Headache, dizziness, sleep disturbances, decreased attention and concentration, paresis, vestibular disorders.

Bilirubin encephalopathy

The severity of the disease

The severity of symptoms of encephalopathy in each patient depends on the stage of the disease. Doctors distinguish 3 degrees of severity of the disease:

Easy (first). It is characterized by an almost complete absence of symptoms, aggravated after excessive exertion or stress. Minor changes in the brain tissues are fixed only with the help of instrumental diagnostic methods. It responds well to treatment in the first year of a child's life when medical recommendations are followed.
Medium (second). Symptoms are mild and may be temporary. There is a violation of some reflexes and coordination of movements. In the study of the brain revealed foci of hemorrhage.
Heavy (third). Severe disorders of motor and respiratory functions are observed. Severe neurological disorders seriously impair the patient's quality of life, often leading to disability. At this stage, dementia develops, a person cannot serve himself in everyday life.

Associated syndromes

Each type of encephalopathy in a child is characterized by the presence of syndromes indicating neurological dysfunction.

The most common of them are:

Hypertension-hydrocephalic syndrome. Caused by increased intracranial pressure and excessive accumulation of cerebrospinal fluid in the ventricular system of the brain. Among the signs of the syndrome in infants, there is a rapid increase in head circumference (by 1 cm monthly), opening of the sagittal suture, tension and bulging of the fontanel, mild congenital reflexes, strabismus and Graefe's symptom (a white strip between the pupil and the upper eyelid in a child) (more in the article:).
Syndrome of movement disorders. It manifests itself as pathological muscle tone - hypertonicity, hypotonicity or muscular dystonia. At the same time, it is difficult for a newborn to take physiological postures, and as the child grows older, there is a lag in physical and mental development. Parents should pay attention to too monotonous crying or crying of the baby, its delayed reactions to light, visual and sound stimuli, and at the first appearance of a pathological reaction, show the child to the doctor.

Syndrome of hyperexcitability. It implies an increased nervous reaction to any stimuli: touch, sounds, change in body position. Often there is hypertonicity and tremor of the limbs, chin. The crying of the baby resembles a squeal and is accompanied by tilting the head. He burps frequently and profusely (fountain), while weight gain is slow. Sleep and wakefulness is disturbed.
Convulsive syndrome. It is a pathological reaction of the body to external and internal stimuli and is manifested by involuntary muscle contractions of a local (local) and generalized (covering the whole body) character. Attacks may be accompanied by vomiting, foaming at the mouth, regurgitation, respiratory failure and cyanosis.
coma syndrome. In newborns, it is a consequence of birth trauma, infectious lesions, metabolic disorders and functional respiratory disorders. It is expressed in the oppression of three vital functions - consciousness, sensitivity and motor activity. With it, there is a lack of a sucking and swallowing reflex in children.
Syndrome of vegetative-visceral disorders. Manifested by pathological changes in the cardiovascular, respiratory systems, disorders of the gastrointestinal tract, abnormal color or pallor of the skin, impaired thermoregulation.
Attention deficit hyperactivity disorder. It is a neurological-behavioral developmental disorder in which children have difficulty concentrating and perceiving information. The child is too impulsive and does not cope well with his emotions.

Diagnostic methods

The diagnosis should be made only by a qualified doctor, guided by the results of clinical and diagnostic studies - the collection of anamnesis of the patient, external examination, laboratory and instrumental diagnostics.

For older children, special tests are also offered to help assess memory, attention and mental state. To date, the following modern research methods are used:

Neurosonography. It is prescribed for children from birth until the overgrowth of a large fontanel (see also:). With the help of a special ultrasonic sensor, brain structures are examined and their pathologies are revealed: hypertension and hydrocephalic syndromes, hypoxic-ischemic lesions, cysts and hematomas, inflammation of the meninges.
Doppler ultrasound. Allows you to assess the state of the vessels of the brain and detects a violation of the speed of blood flow, pathologies and aneurysms of the vessels supplying the brain, blockage or narrowing of the arteries.
Electroencephalography. Registers the electrical activity of the brain, allowing to draw conclusions about inflammatory processes, tumors, vascular pathologies in the brain, epileptic foci.
Rheoencephalography. It is the simplest method for studying and evaluating the vascular walls and cerebral vessels. Detects blood flow disorders and vascular hypertonicity.
Blood analysis. Allows you to determine the presence of leukocytosis, indicating inflammatory processes in the body, and the level of bilirubin, which is important in the development of bilirubin encephalopathy.

Neurosonography procedure

Treatment of encephalopathy in children

Encephalopathy is a serious diagnosis that requires immediate medical attention. Self-medication in this case is not only inappropriate, but can also lead to irreversible consequences. Only a specialist will select such an individual - home or inpatient - treatment, depending on the age, anthropometric data of the child, the severity of the pathology and the severity of its signs, which will not inhibit a number of important brain functions.

Medicines

Drug therapy is based on the following main groups of drugs:

Nootropics, or neurometabolic stimulants. Activate the work of nerve cells and improve blood flow. These include: Piracetam, Vinpocetine, Pantogam, Phenotropil, Actovegin, Cerebrolysin (we recommend reading:).
Vasodilators, or vasodilators. Expand the lumen of blood vessels, normalizing blood flow. Among them are Papaverine and Vinpocetine.
Psycholeptics, or sedatives. Aimed at the removal of increased excitability. These include Citral, Valerianahel, Elenium.
Analgesics, or painkillers. The purpose of their use is the relief of severe pain. It's Aspirin, Ibuprofen.
Anticonvulsants, or antiepileptic drugs. They are aimed at reducing epileptic activity and stopping convulsions of any origin. Among them are Valparin, Phenobarbital.

In addition to these drugs, the doctor may prescribe antispasmodics and centrally acting muscle relaxants. As part of inpatient treatment, physiotherapy procedures have proven themselves well - electrophoresis, amplipulse therapy. For bilirubin encephalopathy, treatment with phototherapy is appropriate.

To effectively combat the consequences of perinatal or acquired encephalopathy, medications alone are not enough. Parents should be patient and give strength to the physical and mental recovery of their child. To do this, you should establish a regime of wakefulness and rest for the baby, provide his diet with food rich in vitamin B, regularly conduct physiotherapy exercises and massage sessions.

As the child grows up, if necessary, it is recommended to involve correctional teachers - speech therapists, defectologists. They assist in social adaptation, the formation of positive motivation and draw up a development plan using the necessary methods, tools and techniques that take into account the age, individual and psychological characteristics of the baby.

Consequences for the child

The consequences of encephalopathy are serious. This is a delay in speech, mental and physical development, brain dysfunction, expressed by a lack of attention and memorization, epilepsy, hydrocephalus, cerebral palsy (we recommend reading:). The prognosis, depending on the severity of the disease, varies from complete recovery to disability and death.

Ischemic encephalopathy. Perinatal encephalopathy in newborns

What is the treatment for HIE?

New treatment for HIE

Causes

In adults

In newborns

Severity and characteristic symptoms

Light degree

Average degree

Severe degree

Diagnostics

Treatment and care

Further observation

Forecast and consequences

Prevention

Causes

In newborns

In adults

Symptoms

Treatment

Recovery period

Consequences

Related video

What is encephalopathy?

Varieties

The severity of the disease

Associated syndromes

Diagnostic methods

Treatment of encephalopathy in children

Medicines

Consequences for the child