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Hypoxia and Asphyxia

According to P.S. Gurevich (1989), intrauterine asphyxia is acute fetal hypoxia (anoxia) resulting from a sudden violation of the uteroplacental or placental-fetal circulation in a previously healthy fetus. However, the term “asphyxia” is recognized as very conditional, because does not quite accurately reflect the essence of pathology. In this regard, the WHO scientific team has proposed replacing the term “asphyxia” with the term “newborn depression”. However, many authors believe that the new term is largely conditional, because, when determining the clinical significance of the manifestation of oxygen deficiency, it does not reflect its pathogenetic basis.

The human fetus makes up to 70 respiratory movements per minute (N.L. Garmasheva, 1977), which is necessary for the instantaneous implementation of the act of breathing after birth (T.A. Adzhimolaev, 1989). Preparation for the possibility of extrauterine breathing is carried out through the system of the hypothalamus> pituitary gland> adrenal glands> lungs of the fetus.

Hypoxia of the fetus and asphyxia of the newborn are the most severe violations of external gas exchange, which cause acute oxygen deficiency, accompanied by hypercapnia and the development of a whole complex of interconnected disorders of the basic vital functions of the newborn's body.

Being a typical and non-specific pathological process, hypoxia to one degree or another accompanies many forms of brain pathology. With ischemia and concomitant hypoxia, a complex set of pathological changes occurs, including the lack of glucose supply and the action of locally formed substances that are not “removed” by the bloodstream. In the population of neurons, interconnected extra- and intracellular processes arise, which are the trigger mechanism for triggering events, resulting in the degeneration and death of neurons (G.N. Kryzhanovsky, 1997).

Many brain injuries are attributed to hypoxia and asphyxia. L.S. Persianinov (1963) described 17 possible causes of fetal and newborn asphyxiation and considered it a consequence of many types of obstetric pathology. T.P. Zhukova et al. (1984) indicate that a long list (about 40 items) of hypoxic damage to the nervous system can be compiled, ranging from hydroencephalus to diffuse neuronal prolapse in various parts of the brain, not to mention the numerous hemorrhages of varying prevalence.

Chronic intrauterine hypoxia is often combined with acute intra- and postnatal hypoxia (L.O. Badalyan, 1984; G. Eggers et al., 1984). Hypoxia of the fetus and asphyxia of the newborn are, in fact, a single pathophysiological process caused by the cessation or reduction of oxygen supply to the body under various conditions of its existence (S.N. Kopshev, 1985). B.N. Klosovsky, E.N.Kosmarskaya (1956 - cited by K.A.Semenova et al., 1972) and others considered asphyxiation in childbirth to be the end result of damage and impaired fetal development and attached even greater importance to it, than a brain hemorrhage. According to I.N.Ivanitskaya (1993), in determining the role of asphyxia in the development of cerebral palsy, it is necessary to determine whether it involves antenatal hypoxia (ischemia) or chronic antenatal asphyxia - chronic symptomatic fetal hypoxia.

Circulatory hypoxia causes a complex complex of disorders in the fetus. This allows us to talk about multi-organ oxygen deficiency, and not only about isolated central nervous system hypoxia (T.P. Zhukova et al., 1984). In relation to the prognosis, the most unfavorable combination of asphyxiation with infection of the child (G.V. Yatsyk et al., 1984).

G.M.Dementieva (1984) emphasizes that chronic symptomatic fetal hypoxia differs from acute intrauterine asphyxia in that it is accompanied by manifestations of a prolonged violation of the intrauterine development of the fetus - hypoxic fetopathy. The latter is expressed by various types of immaturity, found in 6.74% of all full-term, 17.95% of those born prematurely and 41.9% of those who died in the perinatal period. According to N.L. Garmasheva (1967), some violations of placental blood flow, which are classified as chronic, because they cause a lag in the development of the fetus, are often repeated acute disorders of the placental blood flow, the effect of which on the fetus is summarized.

The volume of amniotic fluid, although it does not reflect the functional state of the central nervous system of the fetus, is directly related to the outcome of pregnancy. G. M. Saveliev et al. (1991) explains the relationship between the decrease in the amount of amniotic fluid and the pathological outcome of pregnancy for the fetus as follows. Firstly, a decrease in the amount of amniotic fluid may be due to chronic hypoxia and the associated decrease in the “contribution” of the fetus to the production of amniotic fluid as a result of decreased excretion of fetal urine. Secondly, with a decrease in the amount of amniotic fluid, the risk of compression of the umbilical cord increases. The relationship between the amount of amniotic fluid and the frequency of fetal growth retardation was also revealed by PFChamberlain et al. (1984 - cited by G.M. Saveliev et al., 1991).

B.N.Klosovsky, E.M.Kosmarskaya (1968) showed that asphyxia drastically slows down the processes of germ cell propagation and adventitia cell division, which underlies the construction of the cerebro-vascular capillary network. These processes are especially active in the hemispheres of the brain and in the cerebellum in the second half of fetal life. Therefore, the hemisphere and cerebellum with hypoxia or temporary asphyxia suffer more than others and are clearly reduced in size. Asphyxia, which developed in the fetus of sick mothers, entails diffuse atrophy of the brain substance, single or multiple destruction of areas of the brain tissue, the formation of porencephaly.

According to JJVolpe (1979 - cited by: Ann. By pediatrician. 1981), the pathogenetic role of hypoxia can be associated, firstly, with venous congestion, which appears, apparently, secondarily as a result of circulatory failure, and secondly, possibly with the degree of endothelial damage. Due to the anatomical features of the venous network in the ventricular tissue, most pronounced in the subependymal germ matrix at the level of the monroe opening and the head of the caudate nucleus (where most of the ventricular hemorrhages occur), venous congestion can precede hemorrhage. Reynolds et al. (1977 - cited from: Annual. By pediatrician., 1981) believe that this contributes to excessive arterial blood flow, especially in combination with increased venous pressure. Since hypercapnia and the increase in perivascular concentration of H + in the brain associated with it are very strong stimulants of vasodilation and increased blood flow in the central nervous system, apnea, hypoventilation and / or the introduction of bicarbonate in respiratory failure, according to these authors, are especially dangerous. Moreover, the unreasonable use of agents that increase the volume of circulating blood can also play a pathogenetic role in these conditions. This is partially due to reperfusion oxygenation after ischemia, when instead of attenuation, there is an increase in degeneration and an increase in the number of dead neurons, which is explained by an increase in lipid peroxidation (lipid peroxidation) under the influence of oxygen entering the damaged neurons (G.N. Kryzhanovsky, 1997).

Secondary, postischemic hyperoxic damage to the central nervous system exacerbates a violation of the reactivity of cerebral vessels. In addition, hypoxia itself changes the vascular reactivity through the production of oxidants that cause obliterating damage to the vascular wall, especially vessels with a diameter of less than 40 microns (L.M. Reid, P. Davis, 1995). Studies of lipid peroxidation and antioxidant activity of blood serum, conducted by IB Kushch (1985), confirmed the possibility of using these parameters to diagnose placental dysfunction, accompanied by intrauterine growth retardation.


Some stimuli, including hypoxia, can lead to the simultaneous release of the precursors of lipid vasoactive mediators - eicosanoids, which, when metabolized, can produce various vasoconstrictive substances: prostaglandins containing sulfidopeptides, leukotrienes, thromboxanes and platelet activating factors (FHChilton 1986, FHChilton. The cell source of a vasoconstrictor from metabolites of the cyclooxygenase or lipoxygenase cycle of arachidonic acid metabolites is not precisely known. Possible sources include polymorphonuclear leukocytes (RALevis, KFAusten, 1984), platelets (EJGoetzl, 1980), and vascular wall cells (PGPiper, SAGalton, 1984).

A prolonged increase in vascular tone through hypertrophy of the muscle layer and proliferation of connective tissue in it, as shown by the example of pulmonary arteries DSShort (1957) and DWChapman et al. (1957), it itself initiates vascular damage, leading to “arterial contracture”. Hypoxic vasoconstriction is also accompanied by vascular compression by perivascular edema. This combined obstruction of large and small vessels is accompanied by their thrombosis, platelet sequestration, leukocyte aggregation and vacuolization or swelling of endothelial cells.

At the same time, it is known that with mild and even moderate degree of hypoxia, the compensatory mechanisms of the fetus, primarily from the enzymatic systems of the redox and energy series, can prevent the occurrence of oxygen deficiency. This is confirmed by modern data that a defect in the biochemical function of an organ can be compensated for by 1-10% of the cells of this organ (V. S. Repin, G. T. Sukhikh, 1998). Neurons are incomparably more resistant to pathogenic factors than is commonly believed, and continue to function quite intensively even with significant damage to their structure (D.S. Sarkisov, 1993). Embryonic cells and tissues survive after the cessation of blood supply in the embryo from 60 minutes to 12 hours (for different tissues) (V.S. Repin, G.T. Sukhikh, 1998). Moderate, dosed hypoxia can play the role of an adaptogenic factor that increases the resistance of neurons and the brain (G.N. Kryzhanovsky, 1997), and oxygen deficiency regulates the growth of capillary networks in the cortical plate (I.A. Zambrzhitsky, 1989).

According to T.P. Zhukova et al. (1984), there are no satisfactory hypotheses about the pathogenesis of posthypoxic changes. The consequences of hypoxia are not predetermined immediately, but regardless of at what stage of intrauterine development the conditions of oxygen deficiency act, they entail a long-running process.

Asphyxia in childbirth is a continuation of fetal hypoxia. If intrauterine hypoxia of the fetus does not go beyond the compensatory capabilities of the fetus, then the baby can be born in a satisfactory condition. However, already during the early neonatal period, they reveal signs indicating tension in the processes of adaptation to extrauterine life (L.O. Badalyan, 1984; G.L. Golubeva, 1986 - cited by: R.V. Tonkova-Yampolskaya et al. ., 1989).

G.M.Savelieva et al. (1991) showed that for every third child undergoing hypoxia, tissue Po2 (partial oxygen tension) was below normal limits and combined with instability of the hemostasis system. When conducting an oxygen test, the authors revealed differences in the response of tissues to inhalation of a 60% oxygen-air mixture in healthy children and newborns who underwent chronic hypoxia. The percentage of tissue oxygen saturation during fetal hypoxia is significantly higher (230%) than in healthy children, which indicates tissue oxygen debt and the newborn's high oxygen demand. Even more informative, according to the same authors, is an ischemic test that reveals a violation of the processes of oxygen utilization by the body tissues of newborns in a post-hypoxic state. If in healthy newborns after the termination of ischemia, the initial level of Po2 is restored relatively quickly and at a constant rate, then after chronic hypoxia, the time of restoration of Po2 to the initial level is 1.6 times higher than the control level, and in most children a stepwise rise in the curve is observed, which may Indirectly indicate a violation and microcirculation.

S.M. Grombach (1981) in the study of children who had perinatal hypoxia during the first year of life revealed neurological changes in 45% of children during the first 4 months, and in 10% during the entire first year. The author concludes that even hypoxia, which does not go beyond the compensatory and adaptive capabilities of the fetus and newborn, adversely affects the development of newborns and young children. This is consistent with evidence that the brain as a whole is more sensitive to anoxia than individual neurons (G.N. Kryzhanovsky, 1997).

Intranatal hypoxic brain damage in newborns may be due to birth trauma during the passage of the fetus through the birth canal. JM Freeman et al. (1988) consider intrauterine hypoxia and birth asphyxia as one of the causes of cerebral palsy. KBNelson, JHEllenberg (1986), on the contrary, do not associate most cases of cerebral palsy with these pathological conditions.

There is a connection between birth asphyxia and cerebral palsy in babies born prematurely (LVKuban, DEClark, 1991). It is believed (A. Jonson, RAKing, 1989; R. Naege, E. Peters, 1989) that such children are more sensitive to hemorrhage and ischemia of the brain tissue, which can subsequently lead to permanent damage to the nervous system and the appearance of cerebral palsy.

According to Gurevich P.S. (1989), intrauterine asphyxia most often occurs precisely intranatally with premature complete or partial detachment of a normally located placenta, when it is presented with detachment, massive placental infarction. This occurs during discoordination of the uterine muscles, stiffness of the birth canal, mismatch in the size of the fetal head and the birth canal. The action of the mechanical factor can be aggravated by a violation of the uteroplacental circulation with premature detachment of the placenta or tight cord entanglement, which leads to the occurrence of hypoxic and circulatory hypoxia of the fetus. Hypoxia of various origin during childbirth, accompanied by venous congestion, swelling and loosening of tissues, reduces the mechanical strength of the veins and leads to their rupture.

H. Madsen et al. (1991) suggest that low pH in the umbilical artery is a more likely cause of cerebral palsy than asphyxiation in labor. K.A. Semenova et al. (1972) do not consider asphyxia in childbirth and acidosis developing at the same time as the main link in the pathogenesis of cerebral pathology.

Postnatal hypoxia is caused by damage to one or more parts of the oxygen transport system. The pathology of its first component - respiratory - is associated with pulmonary and non-pulmonary factors. In case of trauma to the phrenic nerve, C3-C5 segments of the spinal cord or the corresponding roots, large fetuses with difficult removal of the head or shoulders develop birth paresis of the diaphragm, which can be one of the causes of postnatal hypoxia, including due to the addition of pneumonia or other respiratory complications. Circulatory hypoxia in the postnatal period may be associated with primary damage to the heart and blood vessels and numerous extracardial factors. Hemic variants of postnatal hypoxia occur with anemia, especially in children with hemolytic disease or with various hemoglobinopathies. Histotoxic oxygen deficiency in newborns is caused by depression of enzymes involved in aerobic cell metabolism (T.P. Zhukova et al., 1984).
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Hypoxia and Asphyxia

  1. Intrauterine Hypoxia. ASPHIXIA AND RESUSCITATION OF BABIES
    Asphyxia of a newborn is the lack of effective gas exchange in the lungs immediately after birth in a child with at least one sign of live birth. Signs of life: spontaneous breathing, palpitations, umbilical cord pulsation, voluntary muscular movement. Asphyxia of newborns is the cause of death of about a million children in the world every year and about the same number of children
  2. TEST CONTROL ON THE TOPIC: INNERIOTIC HYPOXIA. ASPHIXIA AND RESUSCITATION OF BABIES
    Signs of live birth are considered: 1) Spontaneous breathing 2) Cardiac activity 3) Umbilical cord pulsation 4) Arbitrary muscle movements 5) At least one of the listed signs 2. A rating on which scale indicates the presence or absence of asphyxia in a child at birth: 1) Silverman 2 ) Dementieva 3) Apgar 4) Downs 3. Risk factors for birth
  3. Fetal Hypoxia and Asphyxia of the Newborn
    FETAL HYPOXIA AND ASPHIX
  4. Neumann Elena Georgievna. Intrauterine hypoxia. Asphyxia and resuscitation of the newborn, 2003
    The manual reflects modern approaches to the diagnosis of asphyxia of newborn children and its early and late complications, etiology, pathogenesis, classification, clinic of asphyxiation in newborns are highlighted, modern approaches to providing emergency
  5. CLINICAL TASKS ON THE SUBJECT OF INNERABETAL HYPOXIA. ASPHIXIA AND RESUSCITATION OF BABIES
    TASK 1. Newborn S. from the 2nd pregnancy, 1st birth at 36 weeks. Первая беременность 3 года назад закончилась мед. абортом без осложнений. Матери 29 лет, страдает артериальной гипертонией. Данная беременность протекала с угрозой прерывания в 10 недель, фарингитом в 26-27 недель, повышением АД в 32 недели беременности, анализы мочи нормальные, отеков не было. Первый период родов 10
  6. ПЛАЦЕНТАРНАЯ НЕДОСТАТОЧНОСТЬ ГИПОКСИЯ ПЛОДА И АСФИКСИЯ НОВОРОЖДЕННОГО
    ХРОНИЧЕСКАЯ ФЕТОПЛАЦЕНТАРНАЯ НЕДОСТАТОЧНОСТЬ Фетоплацентарная недостаточность (ФПН) составляет в структуре причин перинатальной смертности более 20 %. Многолетние наблюдения многих авторов за развитием детей, рожденных матерями с диагностированной ФПН, позволили прийти к выводу, что указанная патология обусловливает не только резкое увеличение перинатальной смертности, но и многочисленные
  7. ПЛАЦЕНТАРНАЯ НЕДОСТАТОЧНОСТЬ ГИПОКСИЯ ПЛОДА И АСФИКСИЯ НОВОРОЖДЕННОГО
    ХРОНИЧЕСКАЯ ФЕТОПЛАЦЕНТАРНАЯ НЕДОСТАТОЧНОСТЬ Фетоплацентарная недостаточность (ФПН) составляет в структуре причин перинатальной смертности более 20 %. Многолетние наблюдения многих авторов за развитием детей, рожденных матерями с диагностированной ФПН, позволили прийти к выводу, что указанная патология обусловливает не только резкое увеличение перинатальной смертности, но и многочисленные
  8. Перегрузочная гипоксия («гипоксия нагрузки»)
    Возникает при напряженной деятельности органа или ткани, когда функциональные резервы систем транспорта и утилизации кислорода при отсутствии в них патологических изменений оказываются недостаточными для обеспечения резко увеличенной потребности в кислороде (чрезмерная мышечная работа, перегрузка сердца). Для перегрузочной гипоксии характерно образование «кислородного долга» при увеличении
  9. Асфиксия
    ОПРЕДЕЛЕНИЕ В клинической практике термином «асфиксия новорождённых» обозначают клинический синдром, проявляющийся в первые минуты жизни затруднением или полным отсутствием дыхания у ребёнка. Помимо нарушения дыхания у большинства детей, родившихся в состоянии асфиксии, отмечают угнетение безусловной нервно-рефлекторной деятельности и острую сердечно-сосудистую недостаточность. КОД ПО МКБ-Р21.0
  10. Механическая асфиксия
    Гипоксия - кислородное голодание органов и тканей, вплоть до полного прекращения поступления кислорода в организм. Асфиксия - состояние организма, когда в нем, наряду с недостатком кислорода, накапливается углекислый газ. Механическая асфиксия возникает от действия внешнего механического фактора. По темпу развития гипоксию подразделяют на: острую, развивающуюся и приводящую к
  11. Первичная и реанимационная помощь при асфиксии новорожденных
    Гипоксия плода и асфиксия новорожденного (перинатальная асфиксия) — патологические состояния, развивающиеся вследствие острой или хронической кислородной недостаточности и метаболического ацидоза, проявляющиеся расстройствами деятельности жизненно важных систем (ЦНС, кровообращения, дыхания). Перинатальная асфиксия является одной из основных причин перинатальной смертности, составляя в ее
  12. Асфиксия новорожденных
    Тяжесть асфиксии оценивается в баллах по шкале Апгар к концу 1 и 5 минут: умеренная асфиксия — 6-4 баллов, тяжелая — 3-1. Шкала Апгар Признаки 0 1 2 Частота сердечных Отсутствует Меньше 100 в Свыше 100 в сокращений 1 минуту 1 минуту Дыхание Отсутствует Слабый крик, Сильный крик, гиповентиляция достаточное дыхание Мышечный тонус
  13. Асфиксия
    Асфиксия новорожденных представляет собой синдром, характеризующийся отсутствием дыхания, нерегулярными или неэффективными дыхательными движениями при рождении, у ребенка с наличием сердечной деятельности. Различают асфиксию плода, которая подразделяется на антенатальную и интранатальную, и асфиксию новорожденного. Асфиксию новорожденного делят на первичную, когда новорожденный после перевязки
  14. Асфиксия новорождённых. Etiology
    Асфиксия новорожденных – патологическое состояние ребенка, обусловленное длительным или острым воздействием кислородной недостаточности. Этиология Внутриутробная острая или хроническая гипоксия плода могут быть обусловлены заболеваниями матери, вызывающими гипоксию у нее и, соответственно, у плода (анемия, хронические заболевания бронхо-легочной и сердечно-сосудистой системы),
  15. АСФИКСИЯ НОВОРОЖДЕННОГО
    Определение Асфиксия новорожденного есть снижение артериального рО, и повышение артериального рСО^ в результате неадекватного плацентарного или легочного газообмена. Этиология Дь1хательная недостаточность новорожденного. Сердечная недостаточность новорожденного. Типичные случаи Асфиксия новорожденного часто сопутствует внутриутробной асфиксии или дистрессу плода, которые могут быть
  16. Асфиксия
    Физическая блокировка Асфиксия - это крайнее затруднение дыхания, или удушье, в результате которого человек может умереть. При асфиксии в организме возникает недостаток кислорода и избыток углекислого газа. Эмоциональная блокировка Асфиксия может возникать в тех случаях, когда человек слишком долго скрывает в себе парализующий его страх. Возможно, ему какое-то время удается этот страх
  17. Асфиксия новорожденных
    Объем обследования 1. Асфиксия новорожденных на догоспитальном этапе возможна при приеме родов на дому или в салоне санитарного автомобиля. 2. Тяжесть асфиксии оценивается в баллах по шкале Апгар к концу 1 и 5 минут: легкой асфиксии соответствуют 6-5 баллов, средней тяжести — 4-3, тяжелой — 2. Медицинская помощь 1. При легкой асфиксии необходимо восстановить свободную проходимость
  18. Асфиксия плода и новорожденного. Внутричерепная родовая травма
    style="background-color:#ffffff;">Асфиксия (asphyxia, греч.— без пульса) — остро или подостро возникающее патологическое состояние, характеризующееся нарушением газообмена (гипоксия и гиперкапния) и функции органов и систем плода или новорожденного. Проблема этого состояния не решена, несмотря на появление новых способов диагностики и лечения. По данным отечественных и зарубежных авторов,
  19. Анестезиологическое пособие при асфиксии новорожденных
    В родовспомогательных учреждениях, в которых отсутствует круглосуточная служба педиатров-неонатологов, экстренную помощь новорожденным, родившимся в состоянии асфиксии, оказывают акушеры и анестезиолог. Под асфиксией новорожденных следует понимать состояния, характеризующиеся нарушениями спонтанной вентиляции (вплоть до апноэ), что ведет к развитию кислородной недостаточности с последующим
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