Perinatal edema

The term "Birth trauma, perinatallesions of the central nervous system "- understand the violation of the integrity of the tissues and organs of the child that arise during childbirth Perinatal hypoxia and asphyxia often accompany the birth trauma.

Frequency birth injuries by R.E. Bermanu (1991) is from 2 to 7 per 1,000 live births, according to other authors - up to 6-8%

1. Perinatal brain damage

Intracranial hemorrhage (VCK). Distinguish subdural, epidural, sub-rachnoidal, peri- and intraventricular, parenchymal, intracerebral and other VChK.

The frequency of VChK varies greatly. Among the term, it is 1: 1000, in premature babies weighing less than 1500 g, it reaches 50%.

Perinatal hypoxia and severehemodynamic (especially pronounced arterial hypotension) and metabolic disorders (pathological acidosis, excessive activation of lipid peroxidation);</ li>
  • perinatal features of coagulation and platelet hemostasis (in particular, deficiency of vit. K-dependent factors of coagulation hemostasis):
  • small gestational age of the child;
  • intrauterine virus and mycoplasmic infections, causing both damage to the walls of blood vessels, and the liver, the brain. a;
  • irrational care and atatrogenic interventions (rapid intravenous infusions, uncontrolled excessive dyslipidemia, etc .;

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    Predisposing factors: mismatch between fetal head and ancestralpathways, rapid or rapid delivery, improper application of obstetric forceps, vacuum extraction of fetus, delivery by cesarean section, chronic intrauterine hypoxia

    Birth injury of the brain and hypoxia pathogeneticallysvyachachy with each other and, as a rule, combined, and in some cases damage to the brain tissue and ZCHK is a consequence of severe hypoxia, in others - its cause. The ratio of traumatic and non-rhythmic hemorrhages to the brain and its soft membranes is 1:10.

    Pathogenesis. Subdural (SDC), epidural (EDC) andhemorrhages in the cerebellum are the result of traumatic injury in childbirth (there is excessive compression of the "skull in the vertical and frontal-occipital planes with rupture of superficial veins of the cerebral hemispheres or venous sinuses of the posterior cranial fossa), intraventricular (IVC), subarachnoid (KDK) and periortraventricular hemorrhages (PESC) are more common in premature infants and are mainly caused by hypoxic-ischemic damage to the endothelium of the capillaries and zenul with the development of venous stasis and the subsequent appearance Niemi punctate hemorrhages of the brain substance.

    To the main causal factors of the impairedhemostasis in all children with VChK can also carry a deficiency of procoagulants and a wide spectrum'1, other factors of coagulating, ayatriptoring and fibrinolytic systems predisposing to ischemic-lobotic lesions of the brain.

    Clinic. The most typical manifestations of any intracranial hemorrhage in newborns are:
    sudden deterioration of the general condition of the child with the development of "various variants of the syndrome of oppression with recurring symptoms of hyperexcitability;</ li>
  • change in the nature of the scream;
  • bulging of a large fontanel or its tension,
  • abnormal movements of the eyeballs;
  • violations of thermoregulation (gypsum or hyper. army);
  • vegetovisceral disorders (regurgitation, abnormal rate of thalassemia, flatulence, unstable stool, tchypnea, tachycardia, peripheral circulatory disorders);
  • pseudobulbar and motor disorders; ', convulsions;
  • progressing posthemorrhagic anemia;
  • acidosis, gigkulikbmiya, giporbilirubgnemia and other metabolic disorders;
  • attachment of somatic diseases (meningitis, sepsis, pneumonia, cardiovascular and adrenal gland failure, etc.).

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    Subdural hemorrhages (SDC) - occur when the skull is deformed with an offsethis .asgin. The source of hemorrhages is the veins of the sinuses: the vessels of the cerebellar gland. KFOR are observed in gas supply and are often combined with subaraknoy-distant hemorrhages. Sympumes hematomas appear after 4-14 days after injury and later

    Epidural hemorrhage (EDC) - arise between the inner surface of the handsthe skull and the dura mater and do not extend beyond the cranial sutures. These hematomas are formed in the cracks and fractures of the brachium of the cranial vault with the rupture of the vessels of the epidural space. EKD is often combined with external cephalo-tomas. In the clinic, the sequence of development of symptoms, after a short "fresh" interval (from 3 to 6 hours), develops a syndrome of compression of the brain, which manifests itself in acute anxiety 6-12 hours after injury, progressive deterioration of the child's condition, 2 hours to 36 hours. Typical symptoms are the dilatation of the pupil (in 3-4 grooves) on the affected side, clonic-tonic convulsions, hemipnies on the opposite side of the hematoma, asphyxia, bradycardia, arterial rot, stagnant nipples of the optic nerve.

    Subarachnoid hemorrhage (SAH) arise in the re-delta-tion of disorders of the whole bodymeningeal vessels. Their most frequent localization is the parietal-in combination with the cerebral hemispheres and the cerebellum. Blood, settling on the membranes of the brain, causes their aseptic chospalenia and subsequently leads to a scar of EO-atrophic changes in the brain and its membranes, a breakdown of the liquorice. Clinical manifestations of SAK: either immediately after birth or in a few days there are signs of general excitement-anxiety, brain cry, sleep inversion, children lie with wide-eyed, face alert or anxious, increased motor activity due to hyperesthesia, muscle tone and congenital reflexes. The hypertensive-hydro-cephalic syndrome is manifested by tilting the head, convulsive readiness or convulsions, strabismus, Gref's symptom, smoothening of nasolabial folds, bulging fontanels, diverging cranial sutures, stiff neck muscles, etc. There is jaundice in somatic status, more often hyperthermia, anemia. Characteristic for SAK are: erythrocytes in CSF, elevated protein level, xanthochromia, lymphocytic cytosis.

    Periortraventricular hemorrhage (PIVK) - are one- and two-sided. In 60-70% of patients, they are "clinically mute" and diagnosed with computed tomography and ultrasound. With massive hemorrhages, hematocrit rita, anemia, swelling of the large fontanel, changes in motor activity, a drop in muscle tone, the disappearance of sucking and swallowing reflexes, attacks of apnea, eye symptoms (nystagmus, lack of response to light, etc.), a decrease in blood pressure, are noted; less often, convulsions, bradycardia and hyperthermia.

    Parenchymal (intracerebral) hemorrhages occur more often when the end(terminal) branches of the cerebral arteries. When punctate hemorrhages and atypical symptoms are mild: lethargy, vomiting, decreased muscle tone and reflexes, nystagmus, Graefe symptom, etc. When large hematomas and manifests distinct clinical symptoms characteristic of beer (see above.)..

    Flow. Allocate such periods of flow birth injury brain: acute -7-10 days, sometimes up to 1 month; subacute (early recovery to 3-4-6 months and later - from 4 months to 2 years). In the course of the acute period, the phases of excitation and CNS depression are distinguished in terminus. The manifestations of the Cheka are being gradually eliminated. The prognosis depends on the severity of the process, the gestational age of the child and the concomitant diseases. Survival rate is 50-70%, the rest of them retain various neurological disorders (hemisinpid, hydrocephalus, cysts, etc.).

    Preterm infants have a high incidence of infectionasymptomatic or poor atypical clinic; with the predominance of signs of respiratory disorders, attacks of apnea; with the prevalence of the syndrome of general oppression or the syndrome of increased excitability, etc.

    II. Hypoxic-ischemic encephalopathy (HIE)

    Hypoxic-ischemic encephalopathy -brain damage due to perinatal hypoxia, which lead to motor disorders, seizures, mental development disorders and other signs of cerebral insufficiency.

    Etiology and predisposing factors of intrauterine fetal hypoxia and intra-natal asphyxia of the newborn are described in the section of asphyxia.

    Pathogenesis. In the pathogenesis of GIE attach importance to such discussed factors:
    reduction of cerebral blood flow, the main causeswhich is the loss of ability to autoregulate it, arterial system hypotension, reduced cardiac output due to hypoxic damage to the myocardium, impaired venous outflow from the brain, and increased vascular resistance in the brain itself;</ li>
  • the role of prostaglandins, excessive synthesis of leukotriene and hormone vessels (to be specified), and also the role of antidiuretic hormone (ADH) in the genesis of brain lesions after hypoxia;
  • localization of brain damage - amazedmainly the parts of the cerebral cortex of the frontal and parietal regions, where the arterioles and the capillaries are thinner. In chronic intrauterine hypoxia, changes in the basal ganglia, the thalamus are typical, because of which the adaptive capabilities of hemodynamics become disturbed. There are areas of ischemia due to thrombosis, hemorheological disorders, edema and damage to the blood-brain barrier, mark selective necrosis of neurons of the cortex and gi-pachampa;
  • cytotoxic edema of the brain. It is believed that it can be caused by a cascade of amino acids - primarily glutamate (neurotransmitter) in combination with severe metabolic acidosis (pH less than 7.0 and BE over 12 mmol / l);
  • disorders of hemostasis (low levelK-dependent factors of blood coagulation, platelet dysfunctions can enhance intracranial hemorrhage), metabolic disorders - cause seizures, etc. - 34 -

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    Clinic. On the first day of life of pregrown newborns, three clinical stages of HIE are distinguished

    At easy (I stage) GIE signs stickusually no more than 1-2 days. At the average severity of GIEH stage), along with the symptoms listed in the table, in the first hours of life there may be abnormalities in the rhythm of breathing, bouts of bradypnoea or bradycardia, decreased motor activity, later there are convulsions, high-pitched screaming, regurgitation, tremors, . By the end of the second - the beginning of the third day of life, there may appear attacks of apnea, signs of intracranial hypertension or cerebral edema. Heavy GIE (stage III) - consciousness is absent for the first 12 hours of life, then a "false improvement" can follow, but then the consciousness is lost again for 2-3 days; all the symptoms of the stage are sharply expressed, as well as the syndromes of the "weakness of the shoulders", "the head that goes into the shoulders", "the seal's paw", etc. The most probable causes are destructive necrotic lesions of the brain or cytotoxic edema.

    Current and forecast. The most formidable symptoms in terms ofan unfavorable prognosis and distant neurological consequences are the preservation of the score for Apgar 3 points and lower at the 5th minute of life, the appearance of seizures in the first 8 hours of life, persistent muscular hypotension. The child can develop cerebral palsy, delay psychomotor and mental development, epilepsy.

    Diagnostics of the Cheka and GIE. Diagnosis is possible with the complexanamnestic (during pregnancy and childbirth, benefits in childbirth, drug therapy of the mother during pregnancy and childbirth, etc.), analysis of the dynamics of the clinical picture in the child and evaluation of the results of such diagnostic methods:
    Neurosonography - ultrasound scanningthe brain through a large fontanel. This method is highly informative, non-invasive, not burdened by radiation and gives an image of various structures of the brain;</ li>
  • computed tomography of the brain - allows you to analyze both the state of the bones of the skull and the brain parenchyma;
  • nuclear magnetic resonance and emissiontomography is a very delicate method of investigation, it allows to reveal pathological changes in the brain, to determine the difference between white and gray substances of the brain and to clarify the degree of myelination (maturity) of different parts of the brain;
  • Treatment of VChK and HIE
    Organization of a protective regime. It is necessary to reduce the intensity of sound and light stimuli; gentle inspections, swaddling and performing various procedures; Minimizing painful appointments; "temperature protection", preventing cooling and overheating, mother's participation in childcare.
  • Power depending on the condition - eitherparenteral, either through a permanent or a single probe or from a bottle. The child should not starve. It is important to comply with parenteral nutrition rhythm, do not overload the volume, prevent the development of hypovolemia, hypotension, dehydration, hyperviscosity; do not administer heparin, because even its small doses (1-2 U / kg body weight per hour) increase the risk of the VCCH.
  • Monitoring of the basic parameters of vital activity: blood pressure and pulse, the number of respiration, body temperature, etc.
  • Early recovery of normal airway patency and adequate ventilation.
  • With GIE - maintenance of adequate perfusion of the brain;correction of pathological acidosis and other biochemical indicators (hypoglycemia, hypocalcemia, etc.); systematic delivery to the brain of energy in the form of glucose - 10% solution in the first day of life to 50 ml / kg / day.
  • Prevention and early treatment of intrauterine hypoxia and asphyxia of the newborn.
  • Newborns in a state of coma and edema-swelling of the brain are prescribed:
    IVL in the mode of hyperventilation (ratio of inspiration to expiration 1: 2, pCO ^ within 28-30 mm Hg);
  • Barbiturates (phenobarbital) of 3-5 mg / kg every6-8 hours or seduxen at 0.5 mg / kg every 8-12 hours intravenously. Barbiturates also reduce increased intracranial pressure in swelling-swelling of the brain;
  • With the exclusion of intracranial hemorrhageconduct intravenous dehydration with concentrated dry plasma (5-10 ml / kg drip once a day), mannitol (0.25 g / kg drip for 10-15 minutes), and at the end of its administration - 2-4 mg / kg Lasix is ​​also intravenously sprayed. The introduction of mannitol in the absence of the effect can be repeated at a dose of 0.5 g / kg in combination with lasics at intervals of 6 hours;
  • With the progression of symptoms of brain edemanewborns with HIE used osmodiuretics in combination with corticosteroids (dexamethasone at an initial dose of 0.2 mg / kg, followed by 0.1 mg / kg of body weight with an interval of 6 hours); Neotropical preparations (panto-gam 40 mg / kg / day, pyriditol 5 drops of suspension per 1 kg of body weight per day, Phenibut 40 mg / kg / day, etc.) in order to improve trophic processes in the brain;
  • Conduct a sanation of the tracheobronchial tree with preliminary oxygenation of 80% 0 ^ for 2-4 minutes.

  • </ ol> </ li> </ ol> Therapy of neonatal seizures:
    With hypoglycemic convulsions:
    1-2 g / kg 10-20% glucose solution intravenously struino, maintaining a dose of 5-8 mg / kg / min 10% solution intravenously drip;</ li>
  • when persistent hypoglycemia - hydrocortisone hemisuccinate 1-2 mg / kg / day intravenously or -muscle.
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  • With hypocalcemic convulsions - 1 ml / kg 10% calcium gluconate solution intravenously slowly.
  • With magnesium cramps - 0.2 ml / kg 25% solution of magnesium sulfate is single-intramuscularly.
  • With pyridoxine-dependent seizures, 2 ml of a 5% solution of pyridoxine is intravenous or intramuscular; maintenance dose of pyridoxine - 25 mg / kg / day.
  • Standard anticonvulsant therapy for emergency cramping of seizures:
    100-150 mg / kg 20% ​​solution of sodium oxybutyrate intravenously slowly, in the absence of effect - 0.5 mg / kg of 0.5% solution of seduxene intravenously;
  • 15-20 mg / kg of phenobarbital once intravenously for 15 minutes, maintaining a dose of 3-4 mg / kg / day intravenously orally;
  • when the standard therapy is ineffective -barbiturates - thiopental sodium - 15 mg / kg intravenously struino slowly under the control of blood pressure and pulse. The maintenance dose is not more than 80 mg / day continuously drip; Ventilation in the mode of moderate hyperventilation.

  • </ ol> </ li> </ ul> Plasma fresh-frozen or 1-2-day fresh blood 10-15 ml / kg intravenously once a day.</ li>
  • Vicasol 0.2-0.5 ml (2-5 mg) of a 1% solution intravenously or intramuscularly daily for the first 3 days of life.
  • Etamsylate (dicinone) - 1 ml of a 12.5% ​​solution at one time intravenously to obtain a rapid effect. Further enter 0.3-0.5 ml 3-5 days.

  • </ ol> Therapy to improve the metabolism of brain cells:
    Drugs that improve microcirculation:
    0.05-0.1 ml of a 0.5% solution of curantyl (dipyridamole) is intravenously sprayed or drip;</ li>
  • 0.5 ml / kg of 2% trental solution intravenously;
  • 0.1 ml / kg 0.5% Cavinton solution intravenously;
  • 0.1 ml / kg of a 15% solution of xanthinal nicotinate intravenously.
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  • 0.4-0.5 ml / kg 20% ​​solution (80-100 mg / kg) of sodium oxybutyrate intravenously in combination with potassium chloride at a dose of 1/10 dose of sodium oxybutyrate (to prevent hypokalemia);
  • 200-400 mg / kg piracetam (inside more, intravenously or intramuscularly - less) 4 times a day in 5-10% glucose solution;
  • 8-10 mg / kg of cocarboxylase in 10% glucose solution intravenously;
  • 1-3 ml of 5% solution of ascorbic acid intravenously drip;
  • 2-4 ml of a 0.05% solution (1-2 mg) of riboflavin mononucleotide intravenously by striae or intramuscularly once a day;
  • 3 mg / kg / day 0.25% solution of cytochrome C intravenously striated.

  • </ ol> 3. Antioxidants - stabilizers of cell membranes:
    alpha-tocopherol acetate for premature infants 15-20mg / kg for the first 24 hours. Then during intensive oxygenation - 15 mg / kg every 6 hours, then every 12 hours in the same dose until 7-10 days of life;</ li>
  • 0.2 ml / kg 5% solution of unithiol intravenously or intramuscularly 4 times a day,

  • </ ol> </ li> </ ul> Neurosurgical intervention to evacuate blood;</ li>
  • lumbar puncture for draining blood from subarachnoid spaces to prevent adhesion and secondary hydrocephalus.

  • </ ul> With slowly progressive ventriculodilation:
    reduce the production of cerebrospinal fluid (CSF) using furosemide 1 mg / kg / day and diacarp 80-100 mg / kg / day in 2-3 doses;</ li>
  • improve the outflow of CSF with osmotic preparations - 2mg / kg 50% isosorbide solution inside; glycerol 1 g / kg 4 times a day inside; serial punctures (10-15 ml / kg CSF are taken out); external ventriculostomy.

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    Perinatal damage to the spinal cord and brachial plexus

    Etiology: The forced increase in the distance betweenshoulders and the base of the skull, which happens when pulling the head with fixed shoulders and pulling the shoulders with the fixed head (with breech presentation) and excessive rotation (with facial presentation). At the time of the birth of such children, the use of forceps and manual aids were often used.

    Hemorrhages in the spinal cord and its membranes</ li>
  • Ischemia in the area of ​​vertebral arteries due to stenosis, spasm or occlusion of their
  • Intervertebral disc damage
  • Damage to the cervical roots and brachial plexus

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    When the trauma of the cervical spine is notedpainful syndrome with a change in the position of the child, a sharp crying; possible - a fixed torticollis, a shortened or elongated neck, bruising, a lack of sweat, dry skin over the place of injury.

    If the upper segments of the neck are damaged, C, -CdAthere is lethargy, adynamia, diffuse muscle hypotension, hypothermia, arterial hypotension, hypo- or areflexia, paralysis of movements, SDR; with the change in the position of the child - increased respiratory disorders up to apnea.

    Characteristic are delayed urination orurinary incontinence, "frog pose", spasmodic torticollis, symptoms of defeat III, VI, VII, IX, X pairs of cranial nerves. The cause of death is SDR, asphyxia attacks, shock.

    Paresis of the diaphragm is the result of a shoulder injuryplexus, spinal cord at the level of St-Sd. Leading symptoms: SDR, asymmetry of the chest, lag in the act of breathing the affected half, paradoxical breathing, weakened breathing, crepitus in the lungs, severe pneumonia. On the side of defeat is the high standing of the dome of the diaphragm. There is a shift in the mediastinal organs in the opposite direction, heart failure, etc.

    Light forms of the paresis can be restored withouttreatment, with severe - possible complete or partial recovery within 6-8 weeks. The prognosis is worse, if simultaneously there is total paralysis of the upper limb.

    Paresis and Duchenne-Erba paralysis develop atdefeat of the spinal cord at the level of C-C or brachial plexus. Clinic: The affected limb is brought to the trunk, unbent at the elbow joint, turned inward, rotated in the shoulder joint, penetrated into the forearm, the hand flexed in the palm and turned back and out. The head is more often inclined. The neck appears short with a lot of transverse folds. The turn of the head is caused by the presence of a spastic or traumatic torticollis. Passive movements in the paretic limb are painless; reflexes Moro, Babkin, grasping reduced, tendon reflex absent; can appear a symptom of a "click" and the contracture of the shoulder and forearm is formed. With severe Su-S damage, pyramidal pathways are involved in the process - the muscle tone of the hip increases. Paralysis of Duchenne-Erba often appears on the right, maybe double-sided.

    In addition to the above birth injuries are also:
    the lower distal paralysis Dejerine-Clumpke, occurs when a spinal cord injury is at the level of SD-T. It manifests as a violation of the function of the hand - a decrease in the function of flexor flexors and fingers, etc .;</ li>
  • total paralysis of the upper limb (paralysisKerer) is observed when the C "-T | segments of the spinal cord or brachial plexus, more often unilateral; symptoms - lack of active movements and reflexes, muscle hypotension, trophic disorders;
  • damage to the thoracic spinal cord T, -Ted, manifested by respiratory disorders, sometimes spastic lower paraparesis;
  • trauma of the lower thoracic segments of the spinal cord - manifested by the symptom of the "flattened abdomen", anxiety;
  • trauma of the spinal cord in the lumbosacral region - manifested by lower flaccid paraparesis, reduced tone of the lower limbs and restriction of active movements (legs in the "frog pose");
  • partial or complete rupture of the spinal cord. Symptoms: flaccid paresis (paralysis), involuntary urination and defecation or constipation with the attachment of a urinary tract infection, etc.

  • </ ul> Intracranial birth trauma, the period of early manifestations; the phase of oppression, the violation of hemolytic dystrophy of traumatic genesis, the medium-severe form, the cephalo-tom.</ li>
  • Innate muscular torticum
  • Birth injury of the spinal cord. Duchenne-Erba paralysis.

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    Diagnosis and differential diagnosis

    Diagnosis of spinal cord injuryis established on the basis of a history and accounting of clinical symptoms, radiography of the spine and thorax, the results of electromyography, craniography, and examination of the ophthalmologist.

    Differential diagnosis of paralysis of the upper limb is performed with:
    osteomyelitis of the shoulder (there is swelling and hyperemia of the joint, crepitus, soreness, etc.);</ li>
  • congenital hemihypoplasia - there is craniofacial asymmetry with underdevelopment of half of the trunk;
  • malformations of the spinal cord - there is a lack of positive dynamics in the background of treatment.

  • </ ol> immobilization of the head and neck is one of the firstactivities in case of suspected genital trauma of the spine and spinal cord. It is produced by a cotton-gauze collar of the Shantz type (donut method), and when subluxations and dislocations are detected - by stretching with weights of 150-300 g until the pain syndrome disappears or by using a ring-shaped cotton gauze bandage according to Yukhnova (1988): measure the circumference of the child's head using a centimeter tape, make the bandage so that its internal diameter is 2-3 cm less than the circumference of the head and put it in this bandage. The period of immobilization is 10-14 days;</ li>
  • relieve the pain syndrome Seduxenom, Relanium0.1 mg / kg 2-3 times a day, and for severe pains - fentanyl 2-10 μg / kg every 2-3 hours or promedol at the same dose as Seduxen (0.1 mg / kg to 0, 2 mg / kg). Apply analgin 0.05 ml of 50% solution 2-3 times a day;
  • intramuscularly administered vitamin K, if not injected at birth;
  • gentle care, careful swaddling with the support of the neck, feeding from a bottle or through a probe to the removal of pain and stabilization of the child's condition;
  • in the subacute period appoint treatment,aimed at normalizing the function of the central nervous system (nootropil, paktogam), to improve the trophic processes (ATP, vitamins B. Wu B,;, in the dose of up to 15-20 injections). Restoration of neuromuscular conduction (dibazol, galantamine, proserin, oxazil, etc.); preparations of resolving action (lidase, collagenase) and improving myelination (cerebrolysin + ATP + vitamin B "- 15-20 injections);
  • from 8-10 days is shown simultaneously a physiotherapy(electrophoresis with a solution of euphyllin, nicotinic acid on the cervical spine), thermal procedures (paraffin, ozocerite), diadynamic currents, electrostimulation, and later acupuncture. The course of procedures is 10-12; *
  • when the acute phenomena abate - massage,hydrokinetic therapy from the 3-4th week of life (water temperature 36-37 ° C, bath time 10 min, sea salt is added to the water, coniferous extract - 10-15 procedures), adaptogens (ginseng, eleutherococcus).

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    Forecast. With an easy degree of spinal cord injurycome spontaneous recovery; with moderate and severe - restoration of impaired functions is slow, long-term restorative treatment is required, orthopedic therapy is sometimes necessary.

    Compliance with the principles of antenatal fetal protection, improving obstetric tactics.</ li>
  • The woman should give birth whenever possible independently, and the midwife does not extract the fruit, but only supports it from sagging during birth.

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    Clinic of purely obstetric injuries

    1. Injuries of soft tissues are manifested in the form of petechiae, ecchymoses, abrasions in various parts of the body: in the place of the fetal part in the birth, the application of forceps, the collection of blood from the fetal head, and so on.

    Small abrasions and cuts require only local treatment with alcohol solutions of aniline dyes and dressing. Petechia and ecchymoses dissolve on their own.

    2. Adiponecrosis - focal necrosis of subcutaneous adipose tissue. These are delimited dense nodes, infiltrates of 1-5 cm in diameter in the region of buttocks, back, shoulders, limbs. Sometimes they are painful on palpation. In the center of the infiltrates, softening and opening them develop with the release of a white, crumbly mass. The general condition is not disturbed, the temperature is normal. Differentiate with a sclera and a sclera. The forecast is favorable. Infiltrates disappear independently without treatment or are limited to the appointment of thermal procedures (solux, microwave, dry bandages with cotton wool) and vitamin E.

    3. Damage and hemorrhage in the sternocleidomastoid muscle - are when applying forceps, manual benefits. Muscle rupture usually occurs in the lower third (the sternal part). In the area of ​​injury and hematoma, a moderately dense or testicular tumor is probed. By the end of the first week of life, torticollis develops - the child's head is tilted toward the injured muscle, and the chin is turned in the opposite direction. Differentiate with congenital muscular torticollis, the pathogenesis of which is not clear. The diagnosis is based on the detection of the altered position of the head, the asymmetry of the face, etc. In the bilateral process, the head is tilted forward, the cervical lordosis is strengthened, and the mobility of the spine in the cervical region is limited.

    Treatment - correction of the head position (roller), dry heat, physiotherapy (electrophoresis with potassium iodide), massage. With inefficiency - surgical correction in the first half of life.

    4. Generic swelling is a cyanotic swelling of the soft tissues of the head with a headache with a lot of petechiae or ecchymoses. Treatment does not require, it passes independently after 1-3 days. Differentiate with a cephalothorem (see below), a hemorrhage for aponeurosis.

    5. Hemorrhage under aponeurosis is manifested by dough swelling, edema of the parietal and occipital part of the head. The swelling is not limited to the limits of one bone, it can increase in intensity after birth. It is often infected and causes the development of anemia and hyperbilirubinemia. Hemorrhage resorbed after 2-3 weeks.

    6. Kefalogematoma external - hemorrhage under the periosteum of any bone of the cranial vault several hours after birth (more often in the area of ​​one or both parietal, less often - the occipital bone). The tumor is elastic, never passes to the neighboring bone, pulsates, is painless, fluctuates and has a roller along the periphery. The surface of the skin over the cephalohematoma is not changed, sometimes there are petechia. Often, jaundice is observed due to increased extra-suicidal formation of bilirubin. Dimensions of the cephalohematoma gradually decrease and by 6-8 weeks there is complete resorption (rarely calcification and suppuration).

    Causes: an abruption of the periosteum with movements of the head at the time of its eruption, less often - a crack in the skull, very rarely - hereditary coagulopathy.

    Differentiate with the cephalohematoma with. generic tumor (passes through the seams, disappearsin 2-3 days); hemorrhage under the aponeurosis (flat, testate consistency, passes over the sutures, fluctuates); cerebral hernia (protrusion of the meninges and brain substance through the fontanelle and bone defects). They pulsate, reflecting respiratory movements, are located more often in the forehead, on the roentgenogram of the skull, a bone defect is visible.

    Feed the expressed breast milk from the bottle for the first 3-4 days of life, and then, in a stable condition, the baby is applied to the chest.</ li>
  • Vitamin K (if not administered at birth) is once intramuscular.
  • Symptomatic therapy. It is not excluded the need for surgical intervention in connection with the thinning of the underlying bone plate or the formation of bone outgrowths in place of the cephalohematoma.

  • </ ul>

    Causes: damage by superimposed output obstetric forceps on the facial nerve and its branches.

    Symptoms: omission and immobility of the mouth, its swelling, absence of nasolabial fold, superciliary reflex, loose closure of eyelids on the side of the lesion, asymmetry of the mouth when crying, lacrimation.

    Treatment together with neuropathologists.