Perinatal Asphyxia: Cause, Management, Complications

Perinatal asphyxia is an insult to the fetus or newborn infant due to lack of oxygen (hypoxia) and /or a lack of perfusion (ischemia) to various organs, which will manifest as difficulty in establishing spontaneous respiration evident by delayed cry after birth, at least after 1 minute.

Essential Criteria:

  • Profound metabolic or mixed acidemia (pH<7) on umbilical cord arterial blood sample, if obtained.
  • Persistance of an Apgar Score of <3 for more than 5 minutes.
  • Neurologic manifestations in the immediate neonatal period- seizure, hypotonia, coma, or hypoxic ischemic encephalopathy.
  • Multi-organ system dysfunction in the immediate neonatal period.

Etiology:

1. Fetal Hypoxia

  • Inadequate oxygenation of maternal blood as a result of hypoventilation during anesthesia, cyanotic heart disease, pneumonia, respiratory failure.
  • Low maternal blood pressure as a result of hypotension, e.g., in anesthesia, compression of the vena caval and aorta by the gravid uterus.
  • Inadequate relaxation of uterus in uterine tetany cause by excessive oxytocin.
  • Premature separation of placenta
  • Impedance to the circulation of blood through the umbilical cord as a result of knotting of the cord.
  • Placental insufficiency (in toxemia, postmaturity)

2. After Birth

  • Severe anemia (in hemorrhage or hemolytic disease)
  • Shock (in severe infection, massive blood loss, intracranial or adrenal hemorrhage or adrenal hemorrhage)
  • Failure to breathe adequately (trauma, narcosis, cerebral defect)
  • Failure of oxygenation (in pulmonary or heart disease)
  • Unscientific delivery

Physiology:

When babies become asphyxiated (in utero or after delivery), they undergo a well-defined sequence of events.

  • Primary Apnea: An initial brief period of rapid breathing followed by a cessation of respiratory movements; heart rate begins to fall, muscle tone gradually diminishes, baby enters a period of apnea, known as primary apnea.
  • Secondary Apnea: If asphyxia continues following primary apnea, the infant develops deep gasping respiration (3-6 breaths/min), heart rate continues to decrease, the blood pressure begins to fall, and the baby becomes nearly flaccid. This is secondary apnea.

Clinically, primary apnea and secondary apnea are virtually indistinguishable. An infant may go through primary and secondary apnea while in utero. So when an infant is apneic at birth, it is very difficult to say whether it is primary of secondary apnea.

A newborn in primary apnea may re-establish breathing without extensive intervention, but an infant in secondary apnea will not recover without help.

Oxygen is required to establish respiration. This means that when anybody faces an apneic infant at delivery, assuming it as secondary apnea he should begin resuscitation immediately. Delay in initiating resuscitation will delay in establishing spontaneous and regular respiration.. Note that that the longer an infant is in secondary apnea, the greater the chance of brain damage.

During hypoxia, anaerobic metabolism produces lactic acid; there is fall in pH and a decrease in ATP. As hypoxia progresses, so the acidosis, there is decreased heart rate, decreased cardiac regulation; all these causes combined hypoxic-ischemic insult.

 

Effects of asphyxia on different organ systems:

  • On Central nervous system: Hypoxic-ischemic encephalopathy, Infarction, intracranial hemorrhage, seizures, cerebral edema, hypotonia
  • On Cardiovascular system: Myocardial ischemia, poor contractility, hypotension.
  • On Pulmonary System: Pulmonary hypertension, pulmonary hemorrhage, respiratory distress syndrome
  • On Renal System: Acute tubular or cortical necrosis.
  • Adrenal glands: Adrenal hemorrhage
  • Gastrointestinal: Perforation, ulceration with hemorrhage, necrosis
  • Metabolic: Inappropriate secretion of antidiuretic hormone, hyponatremia, hypoglycemia, hypocalcemia
  • Integument: Subcutaneous fat necrosis
  • Hematology: Disseminated intravascular coagulation.

 

Clinical Features:

Prenatal

The signs of hypoxia in a fetus are usually apparent a few minutes to a few days before delivery. Fetal heart rate slows- periodic deceleration of fetal heart rate in response to uterine contraction associated with fetal hypoxemia. At delivery, the sign of fetal distress may be evidenced by meconium staining of amniotic fluid.

Postnatal:

1. Babies may present with primary or secondary apnea. The degree of depression can be asessed by Apgar score (Not considered  now-a-days for resuscitation). One-minute Apgar score usually predicts immediate neonatal outcome of the baby, while 5-minute or later Apgar score is fairly predictive of future mental prognosis of such infant. Degree of depression is minimum when Apgar Score is more than or equal to 8; increased frequency of mortality occurs when score is 0-3.

Apgar Scoring System:

(After Professor Virginia Apgar, Anesthetist, New York)

Signs Score 0 Score 1 Score 2
Appearance (Color) Blue or Pale Body Pink, limbs blue Pink all over
Pulse (Heart Rate) Nil <100/min >100/min
Grimace (response to catheter put into nostril) Nil Grimace, feeble cry Cough or sneezing
Activity and tone Limp Some flexion of limbs Active movements
Respiration Nil Slow, irregular Good, crying

 

2. Some babies may present with CNS complications, like hypoxic ischemic encephalopathy (HIE), manifested by drowsiness, seizure, altered muscle tone, etc. HIE may be mild, moderate or severe. HIE is an important cause of premature damage to central nervous system cells. HIE may result in neonatal death (15.2%). and may be manifested later as cerebral palsy, mental deficiency. HE in term infants result in neuronal injury of cortex (later cortical atrophy) and parasagittal ischemic injury. Preterm infants with HIE demonstrate periventricular leukomalacia (later spastic diplegia), IVH, changes in basal ganglia,. There may be focal or multifocal infarcts (later focal seizures, hemiplegia) in both preterm and term babies.

 

3. Other Organ dysfunction symptoms, e.g., congestive cardiac failure and shock, persistent pulmonary hypertension (persistent fetal circulation) may by present. Respiratory distress syndrome, GI perforation, hematuria acute tubular necrosis or DIC may also be associated with perinatal asphyxia.

 

Management of Perinatal Asphyxia:

If the baby’s history is suggestive of asphyxia but its color is normal, reflex and activities are good, vital signs are nromal, and can maitain SpO2 without oxygen (87-92%), the parents of the baby can be advised come for follow up later on.

Perinatal Treatment:

Monitoring of heart rate, ultrasound, fetal scalp pH, etc are valuable information about fetal condition, asphyxia and progress of labor. These will guide the obstetrician to take decision about to perform cesarean section, augment vaginal delivery or to allow progression to labor.

Delivery Room Treatment:

The steps of neonatal resuscitation include:

  • A. establish a patent airway by suctioning, if necessary by endotracheal intubation;
  • B. initiate breathing by tactile stimulation or PPV with a bag and mask or through endotracheal tube;
  • C. maintain circulation with chest compression and medications if needed.

 

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