PRIMARY NEONATAL RESUSCITATION
Prepared by D.M.S., professor S.N.Heryak
Ternopol medical state univercity
by I.Ya. Gorbachevsky
FETAL HYPOXIA AND ASPHYXIA OF NEWBORN. FETAL DISTRESS AND FETAL DAMAGE. DEFINITION OF FETAL DISTRESS
The words fetal distress are too broad and vague to be applied with any precision to clinical situations. For example, some element of fetal distress (danger) is almost universal at some time during normal human parturition. Uncertainty about the diagnosis of fetal distress based upon interpretation of fetal heart rate patterns has given rise to use of descriptions such as reassuring or nonreassuring. “Reassuring” suggests a restoration of confidence by a particular pattern, whereas “nonreassuring” suggests inability to remove doubt. These patterns during labor are dynamic, such that they can rapidly change from reassuring to nonreassuring and vice versa. In this situation, obstetricians essentially experience surges of both confidence and doubt. Put another way, most diagnoses of fetal distress using heart rate patterns occur when obstetricians lose confidence or cannot assuage doubts about fetal condition. These fetal assessments are entirely subjective clinical judgments inevitably subject to imperfection and must be recognized as such.
Why is diagnosis of fetal distress based on heart rate patterns so tenuous? One explanation is that these patterns are more a reflection of fetal physiology than pathology. Physiological control of heart rate includes a variety of interconnected mechanisms that depend on blood flow as well as oxygenation. Moreover, the activity of these control mechanisms is influenced by the preexisting state of fetal oxygenation, as seen, for example, with chronic placental insufficiency. Importantly, the fetus is tethered by an umbilical cord, where blood flow is constantly in jeopardy, which demands that the fetus have a strategy for survival. Moreover, normal labor is a process of increasing acidemia (Dildy and associates, 1994). Thus, normal parturition is a process of repeated fetal hypoxic events resulting in acidemia. Put another way, and assuming that “asphyxia” can be defined as hypoxia leading to acidemia, then normal parturition is an asphyxiating event for the fetus.
DIAGNOSIS OF FETAL DISTRESS
Diagnosis of fetal distress based upon fetal heart rate patterns is too often oversimplified. Fetal heart rate decelerations provide clues about in utero events; but do not define fetal damage. A critical dimension—duration of the in utero event—is essentially ignored in deliberations on fetal distress. There have been several research efforts aimed at quantifying the duration of abnormal heart rate patterns necessary to portend significant fetal effects. The most common, due to umbilical cord occlusion, requires considerable time to significantly affect the fetus in experimental animals. Watanabe and associates (1992) showed that sequential complete occlusion of the umbilical cord for 40 seconds followed by 80 seconds of release for 30 minutes in sheep resulted in only moderate fetal acidemia. Similarly, Clapp and colleagues (1988) partially occluded the umbilical cord for 1 minute every 3 minutes in fetal sheep and observed brain damage after 2 hours.
Myers and co-workers (1972) observed that more than 20 late decelerations were necessary in humans for a depressed Apgar score. Low and co-workers (1977), using profound fetal metabolic acidemia as an endpoint, reported that heart rate patterns could only be correlated with outcome during the last 2 hours of labor, and moreover, only in those 2-hour segments showing decelerations with more than 35 percent of uterine contractions. Fleischer and co-workers (1982) observed that abnormal heart rate patterns had to persist for 120 to 140 minutes before fetal acidemia increased significantly.
Significant fetal impact cannot be attributed to severely abnormal fetal heart rate deceleration patterns when these patterns are intermittent and of short duration. The prognostic significance of fetal heart rate changes is further increased by combining several patterns. For example, Gaziano (1979) observed that variable decelerations in conjunction with abnormal baseline rate (either tachycardia or bradycardia) and loss of variability more often predicted poor fetal condition compared with variable decelerations without baseline changes. Nelson and associates (1996) found that although multiple late decelerations and/or decreased beat-to-beat variability were associated with a 4- to 6-fold increased risk for cerebral palsy, these cases accounted for only 0.2 percent of all fetuses with such tracings during labor.
Inevitably, the timing and route of delivery are scrutinized in deliberations about fetal distress. It is generally assumed that cesarean delivery would have improved the infant outcome. Keegan and associates (1985) emphasized that prompt intervention—within 30 minutes of diagnosis of fetal distress—did not prevent newborn seizures. Moreover, Krebs and colleagues (1982b) observed that fetuses with abnormal heart rate patterns in the last portion of labor were in worse metabolic condition when delivered by cesarean delivery compared with those delivered vaginally. The most frequent cause of worrisome patterns is umbilical cord compression. Management of variable fetal heart decelerations, in the absence of baseline changes, is difficult because of the unpredictability of cord occlusion.
Interestingly, cesarean delivery itself, as well as the choice of anesthetic, can affect the fetal heart rate. Prolonged decelerations have been reported during abdominal wall scrubbing in 10 percent of cesarean deliveries (Petrikovsky and co-workers, 1988). Another 10 percent of fetuses exhibited decelerations as a result of the uterine incision provoking excessive contractility.
MECONIUM IN THE AMNIONIC FLUID
Obstetrical teaching throughout this century has included the concept that meconium passage is a potential warning of fetal asphyxia. J. Whitridge Williams, writing in 1903, observed that “a characteristic sign of impending asphyxia is the escape of meconium.” He attributed meconium passage to “relaxation of the sphincter ani muscle induced by faulty aeration of the (fetal) blood.” Obstetricians, however, have also long realized that the detection of meconium during labor is problematic in the prediction of fetal distress or asphyxia. In their review, Katz and Bowes (1992) emphasized the prognostic uncertainty of meconium by referring to the topic as a “murky subject.” Indeed, although 12 to 22 percent of human labors are complicated by meconium, few such labors are linked to infant mortality. In a recent investigation from Parkland Hospital, meconium was found to be a “low-risk” obstetrical hazard because the perinatal mortality attributable to meconium was 1 death per 1000 live births (Nathan and co-workers, 1994).
Three theories have been suggested to explain fetal passage of meconium and may, in part, explain the tenuous connection between the detection of meconium and infant mortality. The pathological explanation proposes that fetuses pass meconium in response to hypoxia, and that meconium therefore signals fetal compromise (Walker, 1953). Alternatively, in utero passage of meconium may represent normal gastrointestinal tract maturation under neural control (Mathews and Warshaw, 1979). Third, meconium passage could also follow vagal stimulation from common but transient umbilical cord entrapment and resultant increased peristalsis (Hon and colleagues, 1961). Thus, fetal release of meconium could also represent physiological processes. Naeye (1995) has postulated that meconium, and perhaps bile acids, can cause constriction of umbilical and placental surface veins.
In a study by Ramin and co-authors (1996) that included almost 8000 pregnancies delivered at Parkland Hospital with meconium in the amnionic fluid, meconium aspiration syndrome was significantly associated with fetal acidemia at birth .
Other significant correlates of aspiration included indices of fetal jeopardy such as cesarean delivery, forceps to expedite delivery, and intrapartum heart rate abnormalities. Similarly, indices of condition at birth, to include depressed Apgar scores and need for assisted ventilation in the delivery room, also implicated fetal compromise during labor and/or delivery. Analysis of the type of fetal acidemia based on umbilical blood gases suggested that the fetal compromise associated with meconium aspiration syndrome was an acute event, because most acidemic fetuses had abnormally increased PCO2 rather than the pure metabolic acidemia.
Interestingly, hypercarbia in fetal lambs has been shown to induce fetal gasping and resultant increased amnionic fluid inhalation (Boddy and colleagues, 1974; Dawes and co-workers, 1972). Jovanovic and Nguyen (1989) later observed that meconium gasped into the fetal lungs caused aspiration syndrome only in asphyxiated animals. Ramin and co-authors (1996) hypothesized that the pathophysiology of meconium aspiration syndrome includes, but is not limited to, fetal hypercarbia, which stimulates fetal respiration leading to aspiration of meconium into the alveoli, and lung parenchymal damage secondary to acidemia-induced alveolar cell damage in the presence of meconium. The results of this study could thus be interpreted to implicate meconium as a fetal hazard when acidemia supervenes rather than a result of fetal compromise. In this pathophysiological scenario, meconium in amnionic fluid is a fetal environmental hazard rather than a marker of preexistent compromise.
This proposed pathophysiological sequence is not exclusive, because it does not account for approximately half of cases of meconium aspiration syndrome in which the fetus was not acidemic at birth. It was concluded that the high incidence of meconium observed in the amnionic fluid of women during labor often represents fetal passage of gastrointestinal contents in conjunction with normal physiological processes. Such meconium, however, can become an environmental hazard when fetal acidemia supervenes. Importantly, fetal acidemia occurs acutely, and therefore meconium aspiration is unpredictable and likely unpreventable.
l Preparation of delivery room to resuscitation
Two sets of equipment and materials on delivery - for primary and complete resuscitation.
l Set for initial resuscitation always should be in every delivery room. In anticipation of the birth of the child at high risk, resuscitation equipment for full resuscitation (both sets) should be ready for immediate use.
l Resuscitation bag and mask,
laryngoscope blade and suction
meconium should be sterile, and
the rubber pear, catheters, probes,
endotracheal tubes - disposable.
l For initial resuscitation of newborns
l Optional set for resuscitation
l Responsible personnel of delivery room before every birth should:
l prepare well-lighted place for possible neonatal resuscitation with a clean, dry and warm surface
l check the temperature of indoor air (not below 25° С) and ensure there is no draft
l switch on a radiant heat source in advance to heat the surface of the table and diaper before the baby's birth;
l check two sets of equipment, materials and medicines; cushion under the shoulders;
l connect oxygen tubing to the oxygen source and check its availability in the tank;
l Further assistance during newborn resuscitation based on the simultaneous evaluation of three clinical signs:
l availability and adequacy of of independent breathing
l heart rate
l color of skin and mucous membranes
l After every 30 seconds of intensive care of newborn necessarily :
l evaluate three signs
l using a common algorithm resuscitation decide what to do next
l perform the appropriate action
l re-evaluate the three features; decide what intervention is necessary at this point, and act
l continue the cycle "evaluation-decision-action" until the end of resuscitation.
Availability and adequacy of independent breathing - the main feature that determines the need of providing of neonatal resuscitation
l Assessment of the availability and adequacy of independent breathing is conducted:
l immediately after birth to decide to start resuscitation actions;
l end of 1 and 5 minutes (and later, if necessary) to assess Apgar;
l during resuscitation actions;
l during the stay of the newborn in the delivery room
l Signs of adequate breathing baby - scream and / or satisfactory excursions chest:
l frequency and depth of respiratory movements should grow a few seconds after birth
l normal newborn respiratory rate is 30-60 for 1 min.
l If a child undergoes artificial ventilation then the process should be stopped for 6 seconds to assess the availability and adequacy of independent breathing
l convulsive respiratory movements (“gasping"), or bradypnea breathing <30 breaths in 1 minute are ineffective and their presence is an indication for the immediate start of mechanical ventilation of newborn;
l appearance of expiratory groan or other respiratory disorders during resuscitation indicates that the baby needs further post-reanimation care.
l HR Assessment - heart rate is counted within 6 seconds to get the figure for 1 minute, the result is multiplied by 10
l Methods for heart rate determining :
l listening of heartbeat by stethoscope over the left side of the chest
l Palpation of pulse at umbilical cord directly into the area of its accession to the anterior abdominal wall
l Normal heart rate of just born child ≥ 100 for 1 minute.
l Bradycardia heart rate <100 for 1 minute of a newborn is always an indication for starting of mechanical ventilation.
l Evaluation of mucous membranes and skin colour
l Persistent central cyanosis (hypoxemia) requires intervention: first - oxygen therapy, and in case of its failure - ALV
l Acrocyanosis (blue hands and feet) without central cyanosis, usually does not indicate a low level of oxygen in the blood of the child, but may indicate the cold stress (hypothermia) of newborn.
l Pale skin or marble pattern may be nonspecific signs of reduced cardiac output, severe anemia, hypovolemia, hypothermia or acidosis.
l Initial help steps
l Providing of proper positioning of the child on the surface under radiant heat source and releasing of airways, especially in the case of meconium aspiration threat.
l Final drying of the newborn and repeated providing of proper head position.
l Reevaluation of the newborn.
l A – airways
l Firstly, you should suck from the mouth, then from the nose with a disposable rubber pear or sterile disposable catheter;
l input-depth should be no deeper than 3 cm from the lips of term infants and 2 cm in premature babies
l suck briefly, carefully, slowly removing the catheter or rubber pear out;
l length of suction should not exceed 5 seconds.
l During aggressive suctioning stimulation of the posterior pharyngeal wall is possible, which can cause a vagal reaction (severe bradycardia or apnea) and delay independent breathing.
l If during the suction bradycardia of newborn appeared, necessary to stop manipulation and re-evaluate HR.
l In the case of a significant accumulation of secretions, blood, mucus advisable during suctioning turn the child's head to the side and repeat the procedure.
l While using suction negative pressure should not exceed 100 mm Hg. (13.3 kPa or 136 cm aq.).
l Special initial help steps are necessary for a child who was born after the outpouring of amniotic fluid contaminated with meconium
At the absence of independent breathing or breathing type “gasping" or bradypnea (RR <30 for 1 minute), or clearly decreased muscle tone (no active movements, hanging limbs), or heart rate <100 for 1 minute:
l avoiding tactile stimulation as soon as possible under the control of direct laryngoscopy suck the contents of the lower pharynx, then intubate trachea and carry on sucking it.
l Ensure airway
Provide child supine or side position with moderate straighten back head with the caution beneath shoulders
l Check whether skin and hair of newborn are completely dried; conduct additional drying if needed.
l Remove wet diaper and then provide the correct position of the baby.
l Re-evaluate the child's condition
l B - breathing
l If there is central cyanosis it’s necessary to set oxygen therapy despite appropriate independent breathing and heart rate> 100 for 1 minute
l B - breathing
The aim of oxygen therapy - to ensure proper oxygen levels in the blood of newborn
Saturation of blood - less than 95% (according to pulsoxymetrie).
l Equipment for oxygen therapy:
l oxygen tube and palm composed in the form of a funnel
l resuscitation bag, that is filled by stream (anesthetical) and resuscitation mask: mask loosely placed upon the face of the child
l free flow of oxygen can’t be served by mask attached to a bag that is filled independently
l oxygen mask and oxygen tube
l B - breathing
If there is still central cyanosis despite oxygen therapy for at least 5 minutes it’s necessary to begin ventilation by resuscitation bag and mask
l Indications for mechanical ventilation by resuscitation bag and mask
l Absence / inadequate independent breathing, heart rate <100 for 1 minute
l Absence or inadequate independent breathing after the initial steps of care conducted within 30 seconds after birth
l HR <100 per 1 minute regardless of the availability and adequacy of independent breathing after the initial steps of care conducted within 30 seconds after birth.
l Persistent central cyanosis, despite the presence of adequate independent breathing, heart rate> 100 for 1 minute and feed the free flow of 100% oxygen for at least 5 minutes.
l Technique of the primary ventilation during neonatal resuscitation
l The correct position of the child
l To stay in front of the head
l Apply mask of appropriate size, attached to resuscitation bag hermetically
l To fix the head position.
l APPLICATION OF MASKS
l Monitoring the ventilation effectiveness
l rapid increasing of heart rate, what must be checked immediately after the ventilation
l movements of the chest during compression of the sack should be subtle and symmetrical.
l additional signs of effective ventilation:
l symmetric breathing is auscultated over the lungs;
l appearance of independent breathing;
l Improving of skin colour (reduction or disappearance of central cyanosis);
l Improving of newborn muscle tone.
l In the case of absence of effective ventilation evidence by bag and mask it’s necessary to:
l check the fit of the mask to the face (re-apply mask);
l check the airway (change head position, suctioning of the upper airway, ventilate by opening child’s mouth);
l increase ventilation pressure : compress the resuscitation bag stronger by more fingers or the whole hand, but avoid too sharp and vigorous compression;
l predict the necessity of trachea intubation.
l INDICATIONS FOR TRACHEA INTUBATION
l Absolute indications:
l the necessity of meconium suction from the trachea;
l presence of child diaphragmatic hernia.
l Not Absolute indications:
l bag and mask ventilation is ineffective or long-term;
l necessity of endotracheal entering of medicine;
l birth of a child with extremely low birth weight (<1000 g);
l INDIRECT CARDIAC MASSAGE C - CIRCULATION
l Heart rate < 60 for 1 minute after 30 seconds of effective ventilation.
l 2 techniques of indirect cardiac massage are used
l thumbs method - press the breast by pads of two thumbs, while the rest of the fingers of both hands support the child back (this method is preferred)
l two fingers method - press the breasts by tips of two fingers of one hand: the second and third or third and fourth, during this second hand supports the child back. This method is used if access to the vessel umbilical cord is needed.
l C - CIRCULATION
l The frequency of pressing on the chest is 90 per 1 minute.
l after every three presses on the chest a pause is made for ventilation, then pressing should be repeated.
l You should press on the chest 3 times for 2 seconds (90 for 1 minute) and do 1 ventilation (30 in 1 minute) - together - 120 action for 1 minute.
l heart rate increasing
l indirect heart massage should be stopped, if the heart rate is ≥ 60 beats per minute.
l After every 30 seconds of indirect massage you should re-evaluate heart rate and breathing to decide what to do next
l THE USE OF MEDICINE
l Despite adequate ventilation by 100% oxygen and indirect cardiac massage for 30 seconds, the heart rate remains < 60 for 1 minute.
l Means that normalize vascular volume - saline.
l Sodium bicarbonate.
l Heart rate < 60 for 1 minute after at least 30 seconds of indirect cardiac massage and artificial ventilation by 100% oxygen
l No cardiac activity of newborn at any moment of resuscitation (necessary ventilation, indirect cardiac massage and injection of epinephrine).
l Prepare a 0.01% solution of epinephrine[1:10000]:
l To 1 ml of 0.1% solution of epinephrine hydrochloride or 0.18% solution of epinephrine gidrotartrata must be added 9 ml of 0.9% sodium chloride.
l Gaining in a 1-5 ml syringe prepared solution [1:10000].
l intravenous dose– 0,1-0,3 ml/kg (0,01-0,03 mg/kg);
l endotracheal dose– 0,3-1,0 ml/kg (0,03-0,1 mg/kg).
l Do not use larger doses of intravenous epinephrine during neonatal resuscitation, as their input can cause brain and heart damage of a child. Smaller endotracheal doses are ineffective
l If no effect, and there are indications injection of epinephrine are repeated every 3-5 minutes. Repeated injection of epinephrine is performed only intravenously.
During mechanical ventilation check the heart rate and the presence of independent breathing every 30 seconds until the heart rate does not exceed 100 for 1 minute and is established adequate independent breathing.
Neonatal resuscitation can be terminated if, in spite of timely, proper and full implementation of all its activities, the cardiac activity of child is absent for at least 10 minutes