45-fetal & Neonatal Asphyxia

FETAL & NEONATAL ASPHYXIA

DEFINITION  Fetal

asphyxia is a state of inadequate oxygenation and inadequate elimination of CO2, which if allowed to be continued, will result in metabolic acidemia (umbilical arterial blood pH < 7.2).

PATHOPHYSIOLOGY The fetal respiratory centers in the medulla are inhibited by higher centers in the diencephalon.  The mild temporary anoxia at birth (due to stoppage of the placental circulation) depresses the higher cortical centers, thus releasing the medullary centers from inhibition. 

PATHOPHISIOLOGY The medullary centers become stimulated by:  a. Sensory stimuli from the skin, muscles & joints;  b. Relative increase in carbon dioxide concentration (chemoreceptors)  c. Rise in blood pressure at birth (pressor receptors).

PATHOPHYSIOLOGY 

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However, if the anoxia is marked or prolonged, the lower respiratory centers in the medulla together which the vasomotor centers become paralyzed leading to asphyxia & shock. Thus, if prompt resuscitation is not done at an early stage, the irreversible damage to the respiratory center will result in failure of all attempts at recovery.

ONSET of RESPIRATION(causes) 

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Mild temporary anoxia at birth (due to stoppage of placental circulation), which depresses higher cortical centers thus releasing medullary centers from inhibition. Physical stimulation: afferent sensory stimuli from the skin, muscles & joints. The compression of the fetal thorax incident to vaginal delivery & the expansion that follows delivery may be an auxiliary factor in the initiation of respiration.

Aetiology of Intrauterine fetal distress (asphyxia) I - MATERNAL CAUSES: (conditions leading to imperfect oxygenation of maternal blood)  Severe anemia, Hemorrhage & shock, Respiratory failure, and heart failure.  Eclamptic convulsions, advanced pulmonary T.B., pneumonia, and pulmonary edema.

Aetiology of intrauterine asphyxia ( cont….) II- PLACENTAL CAUSES:  Placental compression: interfering with its circulation as in tonically contracted uterus, prolonged labour after rupture of the membranes or as a method of control of bleeding in placenta previa.  Placental separation as in accidental hemorrhage.  Placental insufficiency e.g. extensive degeneration, multiple infarcts & abnormally small placenta.

Aetiology (cont…) III- CAUSES IN THE UMBILICAL CORD: Obstruction of the circulation, which may be due to:  Tight coils around the neck.  True knots of the cord.  Prolapsed cord.  Compression of the vessels by haematoma of the cord or by blades of the forceps.  Rupture of vasa praevia.

Aetiology ( cont…) IV-PROLONGED COMPRESSION OF THE FETAL HEAD: This will cause edema and ischemia, which interfere with the blood supply of the medulla leading to depression of the respiratory center. Prolonged compression may be due to:  Contracted pelvis (C/P disproportion).  Rigid perineum.  Intracranial hemorrhage.  Forceps application for a long time.  Depressed fracture

CLINICAL FEATURES 1-F.H.R. >160 (tachycardia), or <100 (bradycardia, which is more dangerous) or irregular. 2-Delay of return of the FHR to their normal rate after uterine contraction. (FHR normally slows down during the uterine contraction, and returns rapidly to normal after it ends).

Clinical features 3-If continuous electronic monitoring of the fetal heart rate and uterine contractions is available, the following criteria would suggest fetal distress: a-Late deceleration (see assessment of fetal well being). b-Variable deceleration. C-Loss of beat-to-beat variation in fetal heart rate. d-A sinusoidal fetal heart rate pattern.

Clinical features 3-Passage of meconium in cephalic presentations, due to relaxation of the anal sphincter due to anoxia & ­­ intestinal peristalsis. 4-Fetal acidosis: Detected by taking blood samples from the scalp of the fetus during labour; pH below 7.2 indicates fetal asphyxia (N. 7.257.35).

MANAGEMENT OF INTRAUTERINE ASPHYXIA Try to eliminate the cause if possible:  The patient should be turned onto her side: this may relieve either umbilical cord compression, or alleviate poor return of blood to maternal heart caused by occlusion of the maternal aorta or IVC by the gravid uterus.  Oxytocin infusion, if started, should be discontinued to _ uterine activity & improve placental perfusion.  Any hypotension should be corrected by position change, intravenous hydration or vasopressor treatment if severe hypotension due to induction anesthesia develops

Management 2-Oxygen (100%) should be administered to the mother by facemask. 3-Atropine given to the mother may be beneficial in some cases of fetal bradycardia.( of no proven value ) 4-If the situation improves, careful follow up; preferably by the aid of electronic fetal monitoring is essential.

Management 5-If fetal distress is not relieved within several minutes, immediate delivery is indicated. Vaginal examination is done to detect degree of cervical dilatation, presentation, position & to rule out cord prolapse & the fetus is delivered by:  Breech extraction or forceps if the cervix is fully dilated.  C.S., if cervix is not fully dilated.

CAUSES OF POSTNATAL ASPHYXIA (ASPHYXIA NEONATORUM 1-Persistence of a state of severe intrauterine asphyxia after birth. 2-Obstruction of respiratory passages by mucus, amniotic fluid, blood or meconium. 3-Paralysis of cardiorespiratory centers, due to cerebral hemorrhage.

Cont… 4-Depression of the respiratory centers by drugs (morphine or pethidine) or narcotics & anesthetics given during labour. 5-Congenital malformations: e.g. congenital atelectasis of the lungs or congenital abnormality in respiratory or circulatory system. 6-Prematurity (R.D.S.). 7-Congenital debility.

CLINICAL FEATURES OF ASPHYXIA NEONATORUM: # With initial oxygen deprivation the new born develops rapid breathing pattern followed by a period of APNEA. .: # Clinically, primary and secondary apnea, are indistinguishable. The older classification of asphyxia neonataorum into asphyxia Livida and asphyxia Pallida has been abandoned and is nowadays

Postnatal asphyxia  Primary

apnea: It represents the initial phase of apnea  Secondary apnea: If oxygen deprivation persists

CLINICAL ASSESSMENT (APGAR SCORE) Virginia Apgar (1953)In this system the child’s condition is assessed one minute and five minutes after birth utilizing five features

APGAR score  1.

Appearance (color)  2. Pulse (heart rate)  3. Grimace (reflex irritability)  4. Activity (muscle tone)  5. Respiration (respiratory effort) Either 0, 1 or 2 is given for each clinical feature and a total degree out of ten is given for the 5 clinical features.

Apgar score should be done at one and 5 minutes after birth  1.

One minute Apgar score: determines the need for immediate resuscitation  2. Five minutes Apgar score is useful index of the effectiveness of resuscitation methods, when low is indicative of infant at higher risk of morbidity and mortality (prognostic)

IMPORTANCE  1.

One minute Apgar score: determines the need for immediate resuscitation  2. Five minutes Apgar score is useful index of the effectiveness of resuscitation methods, when low is indicative of infant at higher risk of morbidity and mortality (prognostic)

MANAGEMENT OF ASPHYXIA NEONATORUM PROPHYLAXIS:  1.

Proper antenatal care for detection and proper management of probable cause of intrauterine asphyxia.

Management ( prophylaxis) 2. Proper intranatal care:  Careful observation of FHR.  Avoid operative trauma (forceps)  Avoid morphia within 3 hours before labor  Proper oxygenation during anesthesia

Cont..  Episiotomy

is strongly recommended especially for breech and premature infants.  Proper delivery of the after coming head  Vitamin K for all premature and breech deliveries  Aspiration of the mucus and meconium from fetal larynx before it starts breathing.

ACTIVE MANAGEMENT (ACTIVE RESUSCITATION 

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Resuscitation of the new born is an excellent example of a team work that needs cooperation and harmony between each member, namely the obstetrician, the neonatologyst, the anaesthesiologyst and the nursing team. The first few minutes in the new born's life may be crucial in determining both its potential for survival and its future health performance which may not be revealed except after several months or even

Active management 1-Clearing the air passages: Holding the infant from the feet and aspirating mucus from the mouth and upper pharynx by a rubber catheter.

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N.B.: The infant's head should not be lowered if intracranial hemorrhage is suspected. 1-Warming the infant:Warming is necessary to decrease oxygen requirements and to avoid attacks of apnea.

Active Management 3-Oxygen therapy : When necessary, may be supplied by:

Small mask or stream in front of the mouth and nose (O2 saturation …).  Endotracheal tube is indicated if: 

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1 minute Apgar score < 3 Persistent Apnea. Persistent Bradycardia < 100.

4-Artificial respiration: by:  Endotracheal tube with intermittent positive pressure insufflation  Mouth to mouth breathing until endotracheal tube is available.

Active Management 5-Cardiopulmonary resuscitation: Cardiac resuscitation together with Endotracheal entubation (or mouth to mouth breathing) – – –

No audible heart beats or Heart rate < 100. Thumbs are put at the junction of lower and middle 1/3 of sternum to compress the chest gently 100 times per minute.

Active Management 6-Use of Drugs:     

Nalorphine: ½ mg into umbilical vein if asphyxia is due to morphia. Sodium bicarbonate 8.4%: If the infant develops acidosis with severe asphyxia. Epinephrine: May be used for cardiac resuscitation (if absent heart beats). Up to 0.5 cc are injected either into umbilical vein or intracardiac Antibiotics: To prevent pneumonia especially if resuscitation has been difficult.