Obstetrics and Gynecology - A. M. Hromova 2000

Fetoplacental Insufficiency
Fetal Hypoxia and Neonatal Asphyxia
Neonatal Asphyxia

Neonatal asphyxia is a terminal condition caused by impaired gas exchange, characterized by the absence of breathing or its severe depression (irregular or shallow breathing) while Cardiac Activity is either preserved or suppressed.

In a healthy newborn, regular breathing should be established no later than 60 seconds after birth, and by 5 minutes, the respiratory rate should be 40–60 breaths per minute.

The tidal volume averages about 30 mL, and the minute ventilation ranges from 500 to 1200 mL. The oxygen tension in capillary Blood is 8.0–10.67 kPa, and p_СО2 is 4.0–6.0 kPa.

The absence of Respiration during the transition from intrauterine to extrauterine life leads to acute oxygen deprivation—an impairment in tissue oxygen supply and carbon dioxide elimination from the body. This necessitates prompt resuscitation measures, followed by intensive care to manage post-hypoxic complications and Metabolic Disorders during the early neonatal period.

Neonatal asphyxia is directly caused by the following:

- intrapartum Hypoxia in healthy women, most commonly resulting from fetal gas exchange impairments caused by acute uteroplacental Circulatory Disorders (nuchal cord, premature placental abruption, Uterine rupture, uterine inertia, etc.);

- certain medications administered to the mother during the Second Stage of labor, which may lead to respiratory depression in the newborn (promedol, fluorothane, ether, relanium, seduxen);

- birth trauma (intracranial Hemorrhage);

- airway obstruction resulting from the aspiration of Amniotic Fluid, meconium, or blood;

- congenital intrauterine pulmonary aplasia, tracheoesophageal fistula, diaphragmatic hernia, choanal atresia, and Pulmonary Hemorrhage.

In most cases, neonatal asphyxia in high-risk pregnant women results from chronic Fetal hypoxia and shares a common Pathogenesis with it. During uterine contractions or pushing, There is a further progressive decline in uteroplacental blood flow, which, against the Background of pre-existing chronic hypoxia, exacerbates fetal oxygen deprivation, depletes energy reserves, and serves as the direct cause of neonatal asphyxia.

In this scenario, acute intrapartum hypoxia superimposed on chronic fetal hypoxia transitions into neonatal asphyxia and is accompanied by pronounced metabolic disorders in the post-resuscitation period. This dictates The Need for intensive care aimed at normalizing pulmonary ventilation, the cardiovascular and nervous systems, and metabolic processes.

Resuscitation and intensive care for high-risk newborns must be administered strictly on a differentiated basis, taking into account the course of Pregnancy and labor, the severity of the experienced hypoxia, and the compensatory-adaptive mechanisms and reserve capacities of the fetus.

Neonatal asphyxia is generally a continuation of fetal hypoxia. The scoring system for assessing a newborn's condition was developed and proposed by Virginia Apgar in 1953, and in 1965, this system was recommended by a WHO group for universal use.

Class="center">Apgar score for assessing the condition of the newborn

The Scope of resuscitation measures in newborns depends on the severity of asphyxia. An Apgar score of 7 or less indicates that the newborn is in a state of asphyxia. Mild asphyxia corresponds to a score of 6–7, moderate to 4–5, and severe asphyxia to 1–3. At the same time, in most cases, an Apgar score of 4 or lower points to a critical condition of the infant.

The Apgar score is evaluated twice—at 1 and 5 minutes after birth, regardless of the infant's gestational age and birth weight. In preterm infants, In addition to the general condition assessed by the Apgar score, the severity of respiratory distress is evaluated using the Silverman-Andersen score. During neonatal resuscitation, it is crucial to monitor the dynamics of the resolution of primary asphyxia signs. If, after 5 minutes, the condition of a newborn delivered in asphyxia improves and the Apgar score rises to 8 or higher, the child has a favorable chance of being healthy.

Promptly initiated resuscitation for newborns delivered in asphyxia includes measures aimed at:

- restoring airway patency;

- body oxygenation;

- stimulating vital Functions—pulmonary respiration and cardiac activity.

Resuscitation measures for an infant born in a state of asphyxia are performed in accordance with Order No. 4 of the Ministry of Health of Ukraine dated January 5, 1996.

The extent of care provided to the newborn depends on their clinical condition, vital signs, and the presence or absence of meconium in the amniotic fluid.

In cases where the amniotic fluid is free of meconium, the infant is placed under a radiant warmer and dried with warm, sterile towels. Suctioning the Contents of the Mouth and nasal passages ensures maximal airway patency. If spontaneous breathing fails to initiate, tactile stimulation is applied by stroking the skin along the spine or soles, or by gently flicking the soles of the feet.

If delivery occurs with meconium-stained amniotic fluid, suctioning of the Upper Respiratory Tract is performed immediately after the baby's HEAD is born. Under a radiant warmer, the Trachea is intubated, and the contents of the tracheobronchial tree are suctioned directly through the endotracheal tube. These Procedures must be completed within the first 20 seconds after birth. Afterward, the infant's condition is evaluated for the first time based on respiratory effort, heart rate, and skin color.

The Apgar score is not used to determine the need for resuscitation because it is obtained too late—the first assessment is at the end of the first minute of life. The 1- and 5-minute Apgar scores are instead used to evaluate the effectiveness of ongoing resuscitation efforts.

If spontaneous breathing is present, the newborn's heart activity is assessed. If breathing is absent, positive pressure ventilation (PPV) is initiated using 90–100% oxygen via a bag and mask. The effectiveness of ventilation is determined by observing chest wall movement and by Auscultation.

After 15–30 seconds of positive pressure ventilation, the infant's condition is reassessed and The Heart rate (HR) is determined.

If the heart rate exceeds 100 bpm and spontaneous breathing is present, mechanical ventilation is discontinued, and skin color is assessed. If spontaneous ventilation is absent, mechanical ventilation is continued until breathing begins. If the heart rate is below 100 bpm, ventilation is maintained regardless of spontaneous breathing. When the heart rate ranges between 60 and 100 bpm and continues to rise, ventilation is continued. If the heart rate remains around 80 bpm despite ventilation, chest compressions are initiated by pressing on the lower third of the Sternum (located below the imaginary line connecting the nipples). It is critical to avoid pressing on the xiphoid process to prevent Liver rupture.

Heart rate is monitored every 10–15 seconds until it exceeds 100 bpm and spontaneous breathing is established. At this point, the final evaluation of the infant's condition is performed by assessing skin color. A pink skin tone in the newborn is considered the primary indicator of effective ventilation and Circulation.

Acrocyanosis, common in the first hours after birth, is a normal vascular response to environmental Temperature changes and does not indicate hypoxia. General cyanosis, however, is a sign of hypoxia in an infant. In such cases, the newborn requires an increased oxygen concentration in the inspired gas mixture, which is delivered as a free-flowing stream from an oxygen tubing. By positioning the end of the tubing 1.0–1.5 cm away from the nostrils, the inspired oxygen concentration will be approximately 80%.

The disappearance of cyanosis indicates the resolution of hypoxia. The tubing is then gradually moved away from the nostrils. If the skin remains pink when the tubing is moved 5 cm away, it indicates that an elevated oxygen concentration is no longer needed.

During resuscitation in the delivery room, epinephrine, volume expanders, sodium bicarbonate, and antagonists of anesthetic agents are used.

Epinephrine is indicated in cases of asystole and when the heart rate remains at around 80 bpm after 15–30 seconds of 100% oxygen ventilation. Epinephrine is administered intravenously or endotracheally as a 1:10000 solution in normal saline at a dose of 0.1–0.3 mL/kg of body weight. For endotracheal administration, the 1:10000 solution is further diluted 1:1 with isotonic saline. If there is no response, the dose is repeated every 5 minutes (for a maximum duration of 30 minutes).

Among volume expanders, 5% albumin solution and normal saline are used. It is generally assumed that all infants requiring resuscitation have some degree of hypovolemia. Clinical manifestations of hypovolemic Shock include skin pallor, a weak pulse despite an adequate heart rate, and hypotension. In cases of metabolic acidosis, 4.2% sodium bicarbonate is administered slowly intravenously at a dose of 4 mL/kg.

If severe depression due to anesthetics is evident, administration of anesthetic antagonists—naloxone (0.1 mg/kg) or bemegride (0.1 mg/kg)—is indicated.

Following resuscitation procedures, the newborn is transferred to the neonatal intensive care unit (NICU) for ongoing management and Treatment.

In the intensive care unit, infants born with asphyxia continue to receive interventions to restore vital functions (heart rate and respiration) and correct the primary pathophysiological disturbances caused by asphyxia, including metabolic and electrolyte imbalances, microcirculatory failure, and cerebral disorders. Differentiated, targeted intensive care is guided by the newborn's clinical status.

Patient monitoring during intensive care is carried out through rigorous clinical observation, bedside monitors, and laboratory testing. Special attention is paid to respiratory rate and rhythm, lung auscultation findings, heart rate, blood pressure, skin color, and neurological status.

Electroencephalography (EEG), rheoencephalography, ECG, and cerebral Ultrasonography are utilized for continuous monitoring.

In Addition to a complete blood count, laboratory monitoring includes the evaluation of Water-electrolyte balance, acid-base status, hematocrit, and blood glucose levels. The results of clinical and Laboratory tests, administered medications, body weight trends, and urine output are meticulously recorded in the neonatal intensive care chart.

During the first days of life, an incubator environment is maintained with humidified oxygen and minimal sensory disturbance for the newborn. All procedures should ideally be performed inside the incubator.

Vibration massage, which helps regulate muscular tone and body temperature, provides significant assistance in managing respiratory distress syndrome.

When indicated by predominant respiratory distress and moderately impaired cerebral hemodynamics, hyperbaric Oxygen therapy is administered in a KB-02 hyperbaric chamber at an oxygen pressure of 0.3 atm for 1–2 hours, under the guidance of echoencephalography.

Cardiac Glycosides are administered to normalize myocardial contractility, reduce venous return and pulmonary Hypertension, and correct volume overload and hyperhydration. Indications for their use include signs of pulmonary congestion combined with paroxysmal tachycardia (pulmonary congestion, cyanosis, dyspnea, edema syndrome). Most commonly, 0.05% strophanthin solution or 0.06% corglycon solution (0.02 mL) is administered intravenously along with 10% glucose solution (10 mL).

If there is no response to cardiac glycosides, Glucagon is administered by continuous intravenous infusion at a rate of 5–7 mL/h.

Glycosides are best used in combination with metabolic myocardial support agents: cocarboxylase (10 mg/kg intramuscularly), cytochrome c (0.25% solution, 1 mL), ATP (0.5 mL intramuscularly), and ascorbic acid (5% solution, 1 mL).

To restore vascular tone, prednisolone (1 mg/kg) or hydrocortisone (5 mg/kg) is used. In cases of arterial hypotension, dopamine (10 mcg/kg/min) in 10% glucose solution is infused intravenously.

For bradycardia, 0.05–0.1 mL of 0.1% atropine sulfate solution is administered intravenously. If bradycardia persists, the dose may be repeated in combination with epinephrine.

In right ventricular failure, a 2.4% solution of aminophylline (0.1 ml/kg) is administered.

One of the most critical tasks in intensive care units is the early rehabilitation of children with hypoxic CNS injuries. Interventions aimed at this goal focus on combating cerebral edema and hemorrhagic syndrome, as well as correcting metabolic and hemodynamic disorders.

To manage hypertensive syndrome, a 25% magnesium sulfate solution (0.5 ml/kg) is administered intramuscularly.

Children who have suffered moderate to severe birth asphyxia are prescribed osmodiuretics and sedatives. Dehydration therapy includes the intravenous administration of 10% sorbitol (10 ml/kg), 5% albumin (10 ml/kg), or 0.5–1.0 g of dry mannitol per kg of body weight in 10 ml of a 5% glucose solution, along with rheopolyglucin or hemodesis (10 ml/kg). When necessary, these drugs should be combined with sedatives and anticonvulsants (sodium oxybutyrate at 75–100 mg/kg).

Administration is continued with a 20% glucose solution (10 ml/kg), 2.4% aminophylline solution (0.1 ml/kg), cocarboxylase (10 mg/kg), 5% ascorbic acid solution (0.5 ml/kg), and Essentiale (1 ml/kg). The Use of hemostatic agents is indicated (1% dicynone solution at 0.5 ml, 1% vikasol solution at 0.2–0.3 ml, and 10% calcium gluconate solution at 0.5 ml/kg).

Infusion therapy is carried out at a slow rate (8 drops/min) while monitoring diuresis, acid-base balance, hematocrit, and body weight dynamics. Upon completion of infusion therapy, saluretics (Lasix 1 mg/kg) are administered. The total volume of administered fluid must not exceed 50 ml/kg. Medications that improve cerebral METABOLISM (ATP, B-group Vitamins, glutamic acid) are prescribed.

As a result of asphyxia, the majority of newborns develop hypoxic encephalopathy. The Clinical presentation of hypoxic encephalopathy includes:

- hyperexcitability syndrome;

- CNS depression syndrome;

- convulsive syndrome;

- hypertensive syndrome;

- motor disorder syndrome.

Hypoxic encephalopathy is dominated by symptoms of increased neuro-reflex excitability. For hyperexcitability syndrome, sodium oxybutyrate (100 mg/kg) is administered intravenously, or seduxen or relanium (0.1 ml/kg) intramuscularly, or droperidol (0.5 mg/kg), and luminal (0.003) per os twice daily.

Moderate encephalopathy is characterized by prevailing symptoms of Central Nervous system depression, followed by The Development of hypertension-Hydrocephalus and convulsive syndromes.

Focal neurological symptoms in hypoxic encephalopathy are mild, which significantly distinguishes it from birth trauma and can be utilized in the Differential Diagnosis between these two forms of nervous system injury in newborns.

Considering manifestations of central hemodynamics and CSF circulation disorders as early as the first days of life in newborns who have suffered birth asphyxia, the therapeutic regimen includes dehydration therapy and agents that improve cerebral metabolism (cerebrolysin, B vitamins, cocarboxylase, ATP, glucose, essential Phospholipids, gamma-aminobutyric acid preparations, and glutamic acid).

In cases of marked intracranial pressure elevation, determined via echolocating, a lumbar puncture is indicated, during which 3–5 ml of CEREBROSPINAL FLUID is evacuated. The administration of vasoactive drugs, such as cavinton, is advisable. The latter selectively enhances Blood Circulation, improves microcirculation and cerebral metabolism. In addition to its cerebrovascular effects, cavinton also exerts a nootropic action. It is administered intravenously at a dosage of 1 mg/kg of body weight.

All children who have suffered birth asphyxia are subject to phased treatment and follow-up care by a pediatrician and a neurologist. To properly organize the rehabilitation of these children, the newborn's medical record should indicate the time of onset of asphyxia (intra- or antenatal), its severity and duration, the severity of hypoxic encephalopathy, dominant neurological syndromes, and the therapeutic measures performed. At the rehabilitation stage, treatment with cavinton is continued, followed by its replacement with nootropic agents:

- piracetam 20% solution 200 mg/kg three times a day, treatment course ranging from 2-3 weeks to 2-6 months;

- aminalon - 0.125 (1/4 dragee) twice a day orally or 1% solution 1 teaspoon three times a day, treatment course - 6-8 weeks;

- pyriditol (encephabol) - 1 ml of syrup two to three times a day 15-30 minutes after feeding. Treatment course - one month;

- glutamic acid 0.05-0.1 twice to three times a day 15-30 minutes before meals;

- cerebrolysin - 0.5-1 ml intramuscularly up to 20-30 injections per treatment course.

Newborns must be under the dispensary supervision of pediatric psychoneurologists.

Control questions

1. Define the term "placental insufficiency".

2. What is the difference between Primary and secondary placental insufficiency?

3. List the causes of placental insufficiency.

4. How is placental insufficiency diagnosed?

5. Name the functional tests used to diagnose placental insufficiency.

6. Outline a treatment plan for a patient with placental insufficiency.

7. Name the types of oxygen deprivation.

8. Describe the Classification of hypoxia according to intensity, duration, and clinical course.

9. What causes acute fetal hypoxia during labor?

10. What are the causes of chronic fetal hypoxia?

11. State the main symptoms of fetal hypoxia.

12. Describe the comprehensive management approach for fetal hypoxia.

13. Which medications are prescribed to improve fetoplacental complex function?

14. Define birth asphyxia (neonatal asphyxia).

15. What causes birth asphyxia?

16. What criteria are used to evaluate the newborn's condition using the Apgar score?

17. Describe the resuscitation protocols for newborns in the presence of meconium-stained amniotic fluid.

18. Describe the resuscitation protocols for newborns in the absence of meconium-stained amniotic fluid.

19. What resuscitation measures are performed in cases of impaired spontaneous breathing in newborns?

20. What resuscitation measures are performed when a newborn presents with impaired cardiac activity?