Lesson 2. Perinatal CNS lesions of hypoxic-ischemic and traumatic origin in newborns. Etiology, pathogenesis, clinical forms, diagnosis, treatment, prevention. Asphyxia at birth is a syndrome characterized by a lack of effective gas exchange in the lungs immediately after birth, inability to breathe independently in the presence of a heartbeat and /or other signs of live birth (spontaneous muscle movement, pulsation of the umbilical cord). Severe asphyxia at birth is a condition characterized by low blood pressure. Apgar score and complex of clinical and laboratory signs of violation the child's condition. Hypoxic ischemic encephalopathy (HIE) – brain damage that develops in the first hours of life and is characterized by a complex neurological disorder of varying severity that occurred as a result of asphyxia at birth. Cerebral ischemia – brain ischemia is a condition that occurs as a result of a wide range of causes leading to brain ischemia, such as sepsis, shock, HIE, respiratory distress syndrome, and so on. Risk factors for neonatal asphyxia: - preterm birth; - diabetes mellitus in the mother; - obesity in the mother; - preeclampsia; eclampsia; - chronic hypertension (maternal hypertension); - rh-immunization of the mother - ultrasound signs of anemia or dropsy of the fetus; - stillbirths or the birth of previous children in a state of severe asphyxia; - clinical signs immediately before or during labor (chorioamnionitis, fever before or immediately during labor); - suspicion of a congenital infection of the fetus; - polyhydramnios. - lack of water. - multiple pregnancies. - discrepancy between the estimated fetal body weight and gestational age; - drug or alcohol dependence of the mother; - the use of medications by the mother, respiration and cardiac activity of the newborn; - the presence of malformations of the child; - inhibition of fetal motor activity before childbirth; - lack of data on prenatal follow-up; - long waterless period (more than 18 hours). Intra-natal risk factors: - preterm birth (less than 37 weeks); - delayed delivery (more than 42 weeks); - acute fetal hypoxia at birth; - uterine rupture; - amniotic fluid embolism; - collapse/shock in a woman in labor (of any etiology) during delivery - placental abruption; -placenta previa; - placental ingrowth; - loss of umbilical cord loops; - abnormal position of the fetus; - the use of general anesthesia during delivery; - anomalies of labor activity; - the presence of meconium in the amniotic fluid; - violation of the fetal heart rhythm; - instrumental delivery (obstetric forceps, vacuum extraction). There are four main causes of neonatal asphyxia: 1. Maternal blood oxygenation disorders (anemia, shock, cardiovascular and / or respiratory failure). 2. Inadequate hemoperfusion of the maternal placenta (hypotension or hypertension in the mother, uterine dysfunction). 3. Disorders of placental gas exchange (heart attacks, calcifications, edema and inflammatory changes of the placenta, premature placental abruption and its presentation). 4. Violations of the umbilical cord blood flow (true nodes of the umbilical cord, its compression, tight wrapping of the umbilical cord around the neck or other parts of the child's body, loss of umbilical cord loops). In the pathogenesis of HIE, there are phases of primary and secondary damage to the nervous system tissues. Primary damage develops at the time of exposure to asphyxia and is characterized by irreversible death of brain cells, the volume of which depends on the type of injury depth and duration of hypoxia. Secondary damage is activated in the phase of reoxygenation – reperfusion 2-12 hours after the initial injury. Secondary damage is caused by activation of a number of pathogenetic mechanisms: glutamate and calcium stress, free radical damage, aseptic inflammatory process, activation of apoptosis, leading to an increase in the volume of neuronal damage and a deterioration in the prognosis for life and health Clinical picture The clinical picture depends on the severity of asphyxia. With moderate asphyxia at birth, the child's condition after birth is moderate to severe. At the age of the first minutes of life, the child is sluggish, motor activity and reaction to examination is reduced or absent. The cry, if present, is low-emotional. Neonatal period reflexes are reduced, depressed or missing. During auscultation of the heart – normal rhythm or tachycardia, the tones are increased or muted. Breathing is irregular or intermittent, often involving auxiliary musculature, the presence of wired wheezing of different calibres is possible. Spilled cyanosis is detected, however, against the background of restoration of oxygenation, the skin quickly turns pink. At the same time, acrocyanosis often persists. During the first two or three days of life, these newborns are characterized by a change from depression syndrome to hyperexcitability syndrome, which is manifested by fine-grained tremor of the limbs, hyperesthesia, regurgitation, sleep disturbance, spontaneous Moreau reflex (phase I), decreased or inhibited reflexes of support, step, crawling, muscle hypotension, adynamia. However, changes in the physiological reflexes of newborns and muscle tone are individual and may depend on other concomitant diseases and conditions. In case of severe asphyxia at birth, the child's condition at birth is severe or extremely difficult. The reaction to the examination is often absent or very sluggish. The reflexes of newborns are depressed or sharply reduced. Muscle tone is absent or sharp reduced, no spontaneous movements. In the neurological status, there are signs of coma or sopor (lack of reaction to examination and pain stimuli, adynamia, areflexia, atonia, pupil reaction to light is sluggish or absent, local ocular symptoms are possible). The skin is cyanotic, pale with a "marble pattern" (microcirculation disorder). Independent breathing is arrhythmic, shallow, or absent. Auscultation shows weakening of breathing. Palpation of the abdomen shows a moderate increase in the liver. There may be pronounced signs of peripheral blood disorders (a "white spot" symptom for more than 3 seconds) and central hemodynamics (arterial hypotension). There are signs of multiple organ failure. APGAR SCALE Attributes Scores 0 1 2 1. Heartbeat No Heartbeat Less than 100 beats / min 100-148 beats / min 2. Breath No breathing Sharp single breaths Good, cry 3. Skin color White or sharply cyanotic Pink, limbs blue Pink 4. Muscle tone is absent Reduced Physiological hypertonus is reduced 5. Reflex excitability There is no reaction to irritation There is a grimace or movement of the soles Movement, loud cry The high risk of perinatal pathology includes children with an Apgar score of 0-4 points, an average score of 5-7 points, and a low score of 8-10 points. Semiotics of perinatal lesions of the nervous system: 1) Depression syndrome (hypo-excitability syndrome; cerebral apathy): - Reduced physical and mental activity.  - Muscle hypotension (decreased muscle tone). - Hyporeflexia (reduced expression of reflexes).  - Weakening of the sucking and swallowing reflexes. - Lethargy, apathy, a faint monotonous cry. - Extreme manifestation-coma with areflexia, atony and severe respiratory and cardiac disorders. 2) The syndrome of increased neuro-reflex excitability (hyperexcitability syndrome): - Motor restlessness, emotional lability. - Sleep disturbance (shallow, intermittent).  - Strengthening of innate reflexes (for example, the Moreau reflex).  - Tremor (trembling) of the chin, tongue, and limbs.  - Horizontal nystagmus (involuntary oscillatory eye movements).  - Tendency to regurgitate.  - Increased reflex excitability. 3) Intracranial hypertension syndrome (hydrocephalus syndrome): - Excessive increase in head circumference, divergence of cranial sutures. - Bulging and straining of the large fontanel. - Loud, high-pitched, monotonous crying ("brain cry"). - A symptom of the "setting sun "(lagging of the upper eyelid when looking down). - Convergent strabismus. - Hypersensitivity to external stimuli (hyperesthesia). - Throwing the head back until the torso is arched (opisthotonus). 4) Convulsive syndrome: - Clonic convulsions (muscle contractions that quickly follow each other at short, uneven intervals); - Tonic cramps (prolonged muscle contractions) - Generalized convulsions-cover a large number of muscles in different parts of the body at the same time; - Partial seizures-limited to muscle contraction in only one area, manifested by clonic twitching of the facial muscles, head turns and deviation of the eyeballs to the side. 5) Syndrome of vegetative-visceral disorders - Violations of thermoregulation. - Transient cyanosis (cyanosis). - Tachycardia, tachypnea (rapid breathing and palpitations). - Arrhythmias. - Marbling of the skin (uneven coloration due to imperfection of vascular tone). - Hypothermia of the extremities. - Regurgitation, vomiting, unstable stools. Classification by severity: Mild: Symptoms of hyperexcitability predominate: small-scale tremor, sleep disturbances, regurgitation, spontaneous Moreau reflex (phase I). Reflexes are elevated, and muscle tone may be normal or slightly reduced. Medium: Change of syndromes: first CNS depression (lethargy, decreased motor activity), then hyperexcitability syndrome. Possible violations of muscle tone, convulsions. Severe: Severe depression of all levels of the nervous system (coma or deep deafness). Seizures are frequent, severe, and may be multifocal. Disorders of vital functions (respiration, heart activity). Laboratory and instrumental diagnostics When conducting laboratory and instrumental research methods for HIE, the following changes are determined: 1. Acid-base state and blood gases-hypoxemia, hypercapnia, mixed or metabolic acidosis, lactate acidosis. 2. Clinical blood test –normoblastosis (an increase in the number of nucleated red blood cells), thrombocytopenia. 3. Biochemical blood analysis – changes in the level of electrolytes, glucose; increased levels of AST, ALT, LDH, creatinine, total bilirubin, due to the indirect fraction. 4. Instrumental research methods: a) electroencephalography – the presence of excitability, the appearance of epi-waves; b) neurosonography (NSG, brain edema can be detected with a diffuse increase in echogenicity of brain tissues, narrowing of internal and external CSF spaces and a decrease in differentiation of brain structures, has advantages over CT due to the lack of radiation exposure); c) computed tomography (for hemorrhagic infarction, basal ganglia of increased density); d) magnetic resonance imaging (focal changes); e) echocardiography (ECHO-KG, assess the degree of myocardial contractility, signs of persistent pulmonary hypertension). 5. Examination by an ophthalmologist (there may be retinal hemorrhages, signs of brain edema). Treatment Treatment of perinatal CNS lesions of hypoxic-ischemic origin is a complex and multi-stage process that begins in the neonatal period and continues in the recovery period. Its goal is to stabilize vital functions, minimize brain damage and create conditions for its recovery.  Acute period (first days of life) At this time, the main task is to support the body's work and create conditions for neuroprotection.  - Therapeutic hypothermia. This is the main method of neuroprotection for severe asphyxia at birth. The procedure is performed at a gestational age of at least 36 weeks. Cooling to 33.5 °C (whole body) or 34.5-36.5 °C (head area selectively) for 48-72 hours helps reduce the metabolic needs of the brain, reduce glutamate release, oxidative stress, and inflammation.  - Infusion therapy and nutrition. Control the balance of fluid and electrolytes (sodium, potassium, calcium). In the absence of contraindications, parenteral nutrition is prescribed with a gradual increase in protein, fat and carbohydrate subsidies. Early initiation of enteral nutrition (optimal — mother's milk) is important even against the background of hypothermia.  - Anticonvulsant therapy. It is prescribed for the appearance of convulsive syndrome-diazepam, relanium, sibazone.  - Correction of metabolic disorders. Recovery period After the condition stabilizes, the focus shifts to restoring CNS functions. Drug therapy. It is prescribed strictly according to the indications. The following may apply: - Neuroprotectors and nootropics (for example, "Cortexin", "Cerebrolysin", "Pantogam") — to stimulate the restoration of nerve cells and improve higher brain functions. - Vascular drugs ("Vinpocetine", "Nicergoline") — to improve cerebral circulation and metabolism.  - Anti-spastic agents (Tolperizon, Tizanidin, Baclofen) - with increased muscle tone. - Diuretics ("Diacarb") - only with a confirmed increase in intracranial pressure. Rehabilitation services Non-drug methods of rehabilitation. They play a key role in recovery. - Kinesotherapy: therapeutic massage, gymnastics, hydrokinesiotherapy (classes in water), Voit method (stimulation of reflex motor reactions).  - Physical therapy: electrophoresis, magnetic therapy, laser therapy, sinusoidal modulated currents.  - Treatment by position (laying, splints, "collars") to correct muscle tone. - Dry immersion (weightless simulation).  - Psychological, pedagogical and speech therapy correction. It includes classes with a speech pathologist, psychologist, sensory education, and work with the family. Perinatal lesions of the central nervous system of traumatic origin are a group of pathological conditions of the brain, spinal cord and peripheral nerves in newborns caused by mechanical damage in the period from the 22nd week of intrauterine development to the 7th day of life.  Reasons Traumatic injuries occur due to the action of mechanical forces during childbirth. The main risk factors include: Discrepancy between the size of the fetal head and the mother's pelvis. Rapid or prolonged labor. Use of obstetric forceps or a vacuum extractor. Extensor insertion of the head, asynclitic insertion of the head. Pelvic presentation. Obstetric aids and manipulations (traction for the head, pressure on the bottom of the uterus). Mechanical force can lead to compression, crushing or rupture of brain structures, blood vessels, membranes, nerve roots and nerve plexuses. Types of traumatic injuries Depending on the location of the damage, there are: 1) Intracranial birth trauma. These include epidural, subdural, intraventricular, parenchymal, and subarachnoid hemorrhages. 2) Spinal cord injury. This can be a spinal cord hemorrhage, damage to the craniospinal (upper neck) or lower cervical/upper thoracic region. 3) Damage to the peripheral nervous system. Most often, the facial nerve suffers (VII pair), less often — the glossopharyngeal (IX pair). Brachial plexus injuries are also possible Clinical manifestations Symptoms depend on the location and severity of the injury. Intracranial hemorrhages may include: - Syndrome of increased neuro-reflex excitability (tremor, restless sleep, reviving reflexes).  - CNS depression syndrome (decreased motor activity, weakened reflexes, impaired sucking and swallowing).  - Focal disorders: paresis and paralysis (spastic hemiplegia, paraparesis, monoparesis).  - Dysfunction of the autonomic nervous system (lability of pulse and pressure, marbling of the skin, hyperhidrosis, thermoregulation disorders).  In spinal cord injury, the symptoms depend on the level of damage: - Damage to the craniospinal region often leads to rapid death in the neonatal period. - Damage to the lower cervical or upper thoracic region can cause lower spastic paraparesis, spastic tetraparesis, or a combination of lower spastic paraparesis with flaccid upper paresis. -Severe vegetative-trophic disorders, muscle atrophy, bone growth retardation, and urination disorders are also possible. When peripheral nerves (for example, facial) are affected, characteristic clinical signs occur – paresis, paralysis of the innervated area. Diagnostics Clinical data are used for diagnosis, as well as instrumental methods: neurosonography, CT, and MRI.  Stages of providing assistance 1. Acute period (resuscitation and intensive care). At this stage, the main task is to stabilize vital functions: normalize the acid-base state, glucose levels, blood pressure, and cardiac output. According to the indications, the following are used: - Dehydration therapy (osmotic and loop diuretics) to reduce intracranial pressure. - Antihemorrhagic agents (vitamin K, ethamzylate, etc.) to stop bleeding. - Anticonvulsant therapy in the presence of seizures. - Creating a gentle regime with temperature comfort and limiting external stimuli. 2. Early recovery period (Department of Neonatal Pathology). Correction of neurological disorders, treatment of concomitant diseases and preparation for rehabilitation continue here. 3. Rehabilitation stage (specialized departments and outpatient treatment). At this stage, non-drug methods are actively used, which often play a leading role in recovery. 4. Dispensary observation (polyclinic). Regular checkups with a neurologist and other specialists to monitor the dynamics and correct the rehabilitation program. Drug therapy Medications are prescribed strictly according to the indications and under the supervision of a doctor. Symptomatic remedies: - Anticonvulsants (phenobarbital, valproates, etc.) for convulsions. - Sedatives (magnesium sulfate). - Antispasmodics and prokinetics for vegetative disorders. Pathogenetic therapy: - Neuroprotectors and nootropics (cortexin, cerebrolysin, pantogam, glycine) to stimulate the recovery of nerve cells. - Vasoactive drugs (vinpocetine, cinnarizine) to improve cerebral circulation. - Antioxidants and antihypoxants (mexidol, actovegin) to protect neurons from damage.

I don't understand?

Make a quick-reference PDF for neonatal CNS lesions

Summarize neonatal HIE diagnosis and treatment guidelines