Perinatal hypoxemic encephalopathy

Description:

Perinatal hypoxemic  encephalopathy is a frequent complication of pathology of pregnancy and childbirth and is diagnosed for newborns to 5% of cases. Perinatal injuries of a brain make more than 60% of all pathology of a nervous system of children's age, directly participate in development of such diseases as cerebral palsy, epilepsy, the minimum brain dysfunction.

Symptoms of Perinatal hypoxemic encephalopathy:

In a clinical picture of hypoxemic encephalopathy allocate three periods - acute (the 1st month of life of the child), recovery (from 1st month to 1 year, and at premature unripe children up to 2 years) and an outcome.
  In the acute period on severity are allocated the easy form of defeats of a nervous system reflecting passing disturbances of a gemolikvorodinamika; a moderately severe form with edematous and hemorrhagic changes, a gliosis, single leykomalyation; severe form characteristic of generalized wet brain, multiple leykomalyation and hemorrhages. The scale Apgar is applied to definition of severity and expressiveness of disturbances of cerebral circulation.
  In the acute period allocate 5 clinical syndromes: increase in neuroreflex irritability, convulsive, gipertenzionno-gidrotsefalny, oppression syndrome, coma. The combination of several syndromes is usually observed. Feature of the acute period is domination of all-brain disturbances without the expressed local symptoms. At an easy form of damage of a brain (assessment on a scale Apgar of 6 - 7 points) the syndrome of the increased neuroreflex irritability is characteristic. The main manifestations of a syndrome are strengthening of a spontaneous physical activity, an uneasy superficial dream, lengthening of the period of active wakefulness, difficulty of backfilling, frequent unmotivated crying, revival of instinctive congenital reflexes, muscular dystonia, increase in knee jerks, a tremor of extremities and a chin. At premature the neuroreflex irritability syndrome in 94% of cases is a clinical sign of reduction of the threshold of convulsive readiness that is confirmed by data of an electroencephalography (EEG). Patients who, according to EEG, have a reduction of the threshold of convulsive readiness have to be considered in risk group on a convulsive syndrome.
  The medium-weight form of hypoxemic encephalopathy (Apgar of 4 - 6 points is estimated on a scale) is shown by a gipertenzionno-gidrotsefalny syndrome and a syndrome of oppression.
  For a gipertenzionno-gidrotsefalny syndrome increase in the sizes of the head by 1 - 2 cm in comparison with norm (or a thorax circle), disclosure of a sagittal seam more than 0,5 cm, increase and protrusion of a big fontanel is characteristic. The brakhiotsefalichesky shape of the head with the increased frontal hillocks or dolichocephalic - with the nape hanging kzad is typical. The symptom Gref, a symptom "setting the sun", a non-constant horizontal nystagmus, the descending squint is noted. Muscular dystonia comes to light, it is more in distal departments of extremities in the form of a symptom of "seal pads" and "calcaneal piles". At most of children, especially in the first days of life, these phenomena are combined with paroxysms of starts, a spontaneous reflex of Moro, a sleep disorder, Arlekino's symptom, the general and local cyanosis. Development of a gipertenzionno-gidrotsefalny syndrome on 3 - the 5th day of life can be a symptom of periventrikulyarny hemorrhage. The Gipertenzionno-gidrotsefalny syndrome can be isolated, but is more often combined with a syndrome of oppression or a coma syndrome. The syndrome of oppression is shown by slackness, a hypodynamia, decrease in spontaneous activity, the general hypomyotonia, a hyporeflexia, oppression of reflexes of newborns, decrease in reflexes of suction and swallowing. Local symptoms in the form of the dispersing and meeting squint, a nystagmus, asymmetry and an otvisaniye of a mandible, asymmetry of mimic muscles, bulbar and pseudobulbar symptoms are observed. The syndrome characterizes a current of the acute period of hypoxemic encephalopathy and at the end of the first month of life usually disappears. In the acute period the syndrome of oppression can be a harbinger of wet brain and development of a coma syndrome.
  The coma syndrome is manifestation of serious condition of the newborn, on a scale Apgar is estimated 1 - 4 point. In a clinical picture come to light the expressed slackness, the adynamia, a hypomyotonia to an atony, congenital reflexes do not come to light, pupils are narrowed, the photoharmose insignificant or is absent. There is no reaction to painful irritants, the "floating" movements of eyeglobes, a horizontal and vertical nystagmus, tendon jerks are oppressed. Breath is arrhythmic, with a frequent apnoea, bradycardia, cardiac sounds deaf, pulse arrhythmic, arterial pressure low. Attacks of spasms with dominance of a tonic component can be noted. Serious condition remains 10 - 15 days, there are no reflexes of suction and swallowing. Emergence in the acute period of hydrocephaly with protrusion and tension of a big fontanel, discrepancy of cranial seams, a protrusion of eyeglobes, rapid growth of the head demonstrates intracraneal hemorrhage.
  The convulsive syndrome in the acute period is, as a rule, combined with a syndrome of oppression or coma. Results from hypoxemic wet brain, a hypoglycemia, a gipomagnemiya or intracraneal hemorrhages. It is shown in the first days of life by toniko-clonic or tonic spasms. Along with it local clonic spasms or gemikonvulsiya are observed. Convulsive attacks at newborns differ in short duration, the sudden beginning, lack of pattern of repetition and dependence on a condition of a dream or wakefulness, the mode of feeding and other factors. Spasms are observed in the form of a melkoamplitudny tremor, a short-term apnoea, a tonic spasm of eyeglobes as look paresis up, imitations of a symptom "setting the sun", a nystagmus, automatic chewing movements, paroxysms of a clonus of feet, vasomotor reactions. These spasms in character sometimes remind the spontaneous movements of the child that complicates diagnosis.
  The recovery period of a hypoxemic entsefaloratiya includes the following syndromes: increase in neuroreflex irritability, gipertenzionno-gidrotsefalny, vegetovistseralny dysfunctions, motive disturbances, delay of psychomotor development, epileptic.
  The syndrome of the increased neuroreflex irritability in the recovery period has two options of a current. At favorable option of a current disappearance or reduction of expressiveness of symptoms of the increased neuroreflex irritability in terms from 4 - 6 months till 1 year is noted. At adverse option, especially at premature, the epileptic syndrome can develop.
  The Gipertenzionno-gidrotsefalny syndrome has two options of a current:
  1) a gipertenzionno-gidrotsefalny syndrome with a favorable current at which disappearance of gipertenzionny symptoms at a delay of gidrotsefalny is observed;
  2) the adverse option of a gipertenzionno-gidrotsefalny syndrome entering a symptom complex of an organic cerebral syndrome.
  Outcomes of a gipertenzionno-gidrotsefalny syndrome:
  1. Normalization of growth of a circle of the head by 6 months.
  2. The compensated gidrotsefalny syndrome in 8 - 12 months.
  3. Development of hydrocephaly.
  The syndrome of vegeto-visceral dysfunctions begins to be shown after 1 - 1,5 month of life against the background of increase in neuroreflex irritability and a gipertenzionno-gidrotsefalny syndrome. In a clinical picture persistent vomiting, a persistent hypotrophy, disturbance of a respiratory rhythm and an apnoea, change of coloring of integuments, a Crocq's disease, paroxysms takhi-and bradipny, disorders of thermal control, digestive tract dysfunction, temporal baldness are noted.
  The epileptic syndrome can be shown at any age (as continuation of spasms after the birth or against the background of a somatic infection). At newborns and babies it has the so-called age person, i.e. convulsive paroxysms imitate that athletic potential which the child by the time of their emergence has.
  At newborns and babies (especially at premature) the convulsive syndrome is characterized by variety of clinical forms of attacks. Generalized convulsive attacks (toniko-clonic, clonic, tonic), abortal, focal, gemikonvulsivny, polymorphic attacks, simple and difficult absentias epileptica are observed. On frequency polymorphic forms of attacks prevail. With perinatal encephalopathy propulsive and impulsive paroxysms in the isolated look do not occur at premature children, and are observed only as a part of polymorphic attacks. The greatest difficulty in diagnosis is presented by abortal and convulsiveless forms of paroxysms.
  Imitation of instinctive motive reflexes in the form of paroksizmalno the arising manifestations of a cervical and tonic symmetric reflex with a ducking and tonic tension of hands and legs is observed; a cervical and tonic asymmetric reflex with turn of the head aside and extension of the hand of the same name and legs; the first phase of a reflex of Moro with disclosure of handles. There are paroxysms in the form of an oculogyric crisis and a nystagmus, imitation of "the symptom setting the sun". Attacks of reddening and blanching of integuments with the strengthened sweating, sometimes vomiting are quite often observed. After 3 - 4 months of life, in process of emergence of ability to hold the head, there are "nods", "klivka", and from 6 - 7 months - "bows" (bending of a trunk back and forth).
  Such features of a convulsive syndrome at premature children as instability of clinical manifestations with dominance of polymorphic spasms, existence of abortal forms of attacks, and also difficult absentias epileptica with imitation of instinctive reflexes of newborns (the first phase of a reflex of Moro, an asymmetric cervical and tonic reflex) are probably a consequence of immaturity of structures of a brain. However increase in frequency of attacks, increase of polymorphism of their manifestations, resistance to anticonvulsant therapy have to guard concerning formation of rough organic forms of damage of a brain.
  Polymorphism of attacks, their resistance to therapy is predictively an adverse sign.
  The syndrome of motive disturbances comes to light from first weeks of life, can proceed with a hypomyotonia or a hypertension. At emergence of a syndrome of motive disturbances with a hypomyotonia decrease in a spontaneous physical activity, oppression of tendon jerks and congenital instinctive reflexes of newborns is noted. The syndrome of motive disturbances a hypomyotonia meets separately, and also in combination with a gipertenzionno-gidrotsefalny syndrome, a syndrome of the increased neuroreflex irritability reduction of the threshold of convulsive readiness. The combination of a syndrome of motive disturbances and a convulsive syndrome is adverse.
  Increase of a muscular hypertension at the full-term children, emergence of a storonnost of focal symptoms have to guard in the development plan for cerebral palsy.
  The syndrome of a delay of psychomotor development begins to be shown from 1 - 2 months. In structure of a syndrome disturbance of a reduction of instinctive congenital reflexes is noted. Gets a big diagnostic role cervical and tonic symmetric and asymmetric reflexes, a delay of formation of vypryamitelny labyrinth chain tonic reflexes. In the presence in structure of this syndrome of a delay of mental development in children to monthly age insufficiently steady fixing of a look, short-term tracing with bystry exhaustion is observed. There is no reaction to a voice of mother, acoustical concentration. To 2 - to 3-month age insufficient revival at communication is observed, shout is expressionless, the festivities are absent, children find a sound source eyes without turn of the head, there is a rare, difficult raised smile. To half a year - are in toys and surrounding objects insufficiently actively interested, react to presence of mother, festivities low-active and short insufficiently, manipulations with objects are detained, there is no active attention. If the arrest of development is "tempo", it at the correct nursing begins to disappear. This group of children in 4 - 5 months as if "jump" becomes more active, and mental development advances motor. Appear emotional reaction on people around, interest in toys.
  Age motive functions begin to be compensated actively after 6 - 7 months and are, as a rule, recovered by 1 - 1,5 years. Predictively the long delay of mental development is adverse.

Reasons of Perinatal hypoxemic encephalopathy:

For recognition of clinical signs of a perinatal hypoxia it is necessary to consider the risk factors contributing to its development:
  • Boundary age of mother (is younger 20 and 35 years are more senior)
  • Premature placental detachment
  • Placental presentation
  • Preeclampsia
  • Premature or late births
  • Coloring of amniotic waters meconium
  • Bradycardia, fruit tachycardia, muting of cardiac sounds of a fruit
  • Multiple pregnancy
  • Long anhydrous interval
  • Diabetes of mother
  • Any diseases of mother during pregnancy
  • Reception by mother of drugs, potentially dangerous to fruit
  Among the reasons of disturbances is ventilation of the lungs and allocate to oxygenation of blood a peripheral and central hypoxia. Pathology of respiratory tracts or an alveolar blood-groove takes part in a peripheral hypoxia, in the central hypoxia a basis is dysfunction of a respiratory center.
Etiology of hypoxemic encephalopathy.
Peripheral:
1. Respiratory distress syndrome
2. Aspiration of amniotic waters
3. Pheumothorax
4. Bronchopulmonary dysplasia
5. Congenital anomalies (Pierre-Robena's syndrome)

Central:
1. The lowered pressure at mother
2. Anemia of mother
3. Arterial hypertension
4. Placental insufficiency
5. Brain malformations

Treatment of Perinatal hypoxemic encephalopathy:

Treatment of the acute period.

  In the acute period timely correction of a respiratory respiratory disstress-syndrome and adequate ventilation of the lungs is necessary. At premature endotracheal introduction of a kolfostseril of palmitate of 5 ml/kg is carried out. Use of analogs of surfactant leads to considerable regress of neurologic syndromes of hypoxemic encephalopathy.
  1. Correction of a homeostasis and hypovolemia: freshly frozen plasma of 5 - 10 ml/kg, 10% albumine of 5 - 10 ml/kg, реополиглюкин 7 - 10 ml/kg, Haemodesum of 10 ml/kg.
  2. Decrease in permeability of vessels: 12,5% etamsylate solution intramusculary or intravenously, 1% Vikasolum of 0,1 ml/kg.
  3. Metabolic and antioxidant therapy: piracetam of 50 mg/kg, 10% glucose of 10 ml/kg, Actovegin intravenously, 5% vitamin E of 0,1 ml a day. As antioxidant soy oil of 2 - 3 ml of 4 - 6 days on stomach skin is used.
  4. Vascular therapy: Vinpocetine 1mg/kg intravenously.
  5. Dehydrational therapy: hydrocortisone of 3 - 10 mg/kg, Prednisolonum of 1 - 2 mg/kg, 25% of magnesium sulfate of 0,2 ml/kg.
  6. Improvement of fabric metabolism of a cardiac muscle: cocarboxylase of 8 mg/kg, ATP of 10 mg/kg.
  7. Antikonvulsantny therapy: diazepam 1mgkg intramusculary or intravenously, GOMK of 50 mg/kg, barbiturates when benzodiazepines are not effective, 5 mg/kg.

Treatment of the recovery period.

  Treatment of the recovery period is carried out by the syndromologic principle.
  1. At a syndrome of the increased neuroreflex irritability with displays of vegetovistseralny dysfunctions sedative drugs are shown: diazepam of 0,001 g 2 times a day, Tazepamum of 0,001 g 2 times a day, mixture with цитралью - solution of citral 2,0, magnesium % sulfate 3,0, 10 glucose 200,0 solution - on a teaspoon 3 times a day; from 2-month age soothing cocktail from herbs (a valerian root, a motherwort, a sage) on 1 teaspoon 3 times a day are appointed.
  2. At a gipertenzionno-gidrotsefalny syndrome it is reasonable to appoint g/kg furosemide 0, 002 a day with Pananginum, глицерол on 1 teaspoon 3 times a day. At the expressed manifestations of a gipertenzionno-gidrotsefalny syndrome use acetazoleamide on 0,02 g/kg a day once according to the scheme: 3 days - reception, 1 put a break, a course of 3 weeks up to 1 - 1,5 month with Pananginum.
  3. At a syndrome of motive disturbances: mg B6 5 vitamin, B1 2 vitamin of mg, ATP of 0,5 ml of 10 - 12 injections, Pyritinolum of 10 - 20 drops on 1 kg of body weight 2 times a day in the first half of day of 1 - 3 month. Massage. Remedial gymnastics, training of mother in skills of rehabilitation is provided.
  4. At a syndrome of a delay of psychomotor development: piracetam of 30 - 50 mg/kg in 3 receptions, Pyritinolum. Since 6 months Cerebrolysinum of 0,5 ml No. 20 (it is contraindicated at a convulsive syndrome), B6, B1 vitamins. Gamma аминобутировая acid on 0,06 g 2 - 3 times a day.
  5. At a convulsive syndrome: Valproatum of sodium of 20 - 50 mg/kg, clonazepam to 1 - 2 mg a day, phenobarbital of 1 - 2 mg/kg. At resistant spasms ламотригин 1 - 2 mg/kg.
  6. Surgical treatment is applied at the combined periventrikulyarny hemorrhages and development of posthemorrhagic hydrocephaly, ventrikulyarny shunting is carried out.
  Therapeutic actions are individualized further depending on the result of process. To one-year-old age at most of mature children with the advent of verticalization and speech functions it is possible to reveal outcomes of perinatal hypoxemic encephalopathy. Recovery occurs at 15 - 20% of children. Frequent effects of the postponed encephalopathy are the minimum brain dysfunction, a gidrotsefalny syndrome. The heaviest outcomes are cerebral palsy and epilepsy.
  Certainly, achievements of perinatal medicine, adequate conducting childbirth and the acute period of hypoxemic encephalopathy will allow to lower psychoneurological outcomes of a disease.