Birth Asphyxia

MABUKU SANKOMBO
201301623
 Outline
 Definition
 Epidemiology
 Etiology
 Clinical presentation
 Investigations
 Management
 Prognosis
 Definition
 Birth Asphyxia-defined as the inability to initiate respirations and requiring
resuscitation.

 Asphyxia is a biochemical term that is characterized by progressive

hypoxia, hypercarbia and acidosis and is a consequence of compromise
in placental blood flow – the definition that is commonly agreed upon is a
cord arterial pH < 7.00 (severe or pathologic fetal acidemia )
 Epidemiology

 Asphyxia/HIE in 2-9/1000 live births.

 Cerebral palsy in 1-2/1000 live births, but only 8-17% of CP explained by
probable perinatal asphyxia.
 Death rate ~11% in term infants, severe sequela in 0.3%o
 In premature infants incidence of HIE, deaths and handicap much higher
Causes of Asphyxia in the neonate
 Interrupted umbilical circulation (cord compression)
 Inadequate maternal-placental perfusion (hypotension,
hypertension, abnormal uterine contractions)
 Impaired maternal oxygenation (cardiopulmonary disease,
anemia)
 Altered placental gas exchange (abruption, p. previa,
insufficiency)
 Failure of the neonate to accomplish lung inflation and
successful transition from fetal to neonatal cardiopulmonary
circulation (heart, lung, chest, brain, nerves, muscles,
metabolic)
 Pathophysiology
 Adaptive responses: redistribution of blood to brain, heart and
adrenals; term infant more resistant than adults and premature
infants.
 Impairment of cerebrovascular autoregulation due to cellular
injury and acidosis/hypercarbia.
 Circulatory changes during asphyxia (brain injury occurs only
when asphyxia severe enough to impair cerebral blood flow
(CBF))
 Loss of cerebrovascular autoregulation due to hypercapnia,
hypoxemia and acidosis;
 Initially secondary increase in CBF
 After prolonged asphyxia decrease in CBF
 Clinical Presentation
The majorities do not exhibit overt neurological
features or subsequent neurological evidence ofbrain
injury.
 Occurrence of neonatal neurologic syndrome shortly
after birth is a sign for recent (i.e., intrapartum)
severe insult.
 Occurrence of seizures within the first12-24 hrs after
insult
 Posturing- opisthotonus, extension
 HIE
 Hypoxic Ischemic Encephalopathy
 Stages 1- 24-48 hrs
hyperalert, awakefulness state,
sympathetic stimulation, Increased muscle tone, brisk reflexes
 Stage 2- 4-5 days
lethargic, suppressed primitive reflexes,
hypotonic, seizures,
 Stage 3- 7-14 days or more
stuporous, comatose, flaccid, posturing
abnormally, seizures, ±↑ICP
 Depressed reflexes and cranial nerve palsies are common findings.
 F. Hypoxic ischemic injury
 + or – coexistence of skull fracture
 + or -subdural hematoma
 + or – subarachnoid haemorrhage
 Asphyxia in the Neonate
9
- Multiple Organ involvement -
 CVS: shock, hypotension, TI, myocardial necrosis, congestive
heart failure, ventricular dysfunction
 Renal: oligo-anuria, tubular/cortical necrosis, renal failure
 Liver: cell injury, hyperbilirubinemia, decreased clotting factors -
bleeding
 GIT: paralytic ileus, NEC after 5-7 days
 Lungs: RDS, pulmonary hemorrhage, PPHN
 Hematologic: thrombocytopenia, DIC, increased nucleated red
blood cells
 Metabolic: acidosis, hypoglycemia, hypocalcemia, hyponatremia,
SIADH
 Asphyxia in the Neonate
10
- Diagnosis -
 FHR patterns, obstetric and delivery history
 careful history, physical exam, lab studies
 Ultrasonography with Doppler (method of choice for IVH, necrotic
changes in the brain)
 EEG (best in first few hours after birth)
 CT scan (later valuable)
 MRI (best! delayed myelinization, even in mild cases)
 Management
Optimal management is prevention
 Immediate resuscitation
 –adequate ventilation
 -adequate oxygenation
 adequate perfusion (Monitor BP, fluid rescusc, dopaminejkg
 correct metabolic acidosis
 -A normal serum glucose level
 -control of seizures
 -prevention of cerebral oedema
 Asphyxia in the Neonate
12
- Treatment -

 Immediate resuscitation of apneic infant (may be

primary (spontaneous resuscitation possible) or
secondary apnea (spontaneous resuscitation not
possible))
 Adequate ventilation (pCO2 35-45 mmHg): Resolve
hypercarbia
 adequate oxygenation (pO2 > 40 mmHg in preterm,
pO2 > 50 mmHg in term): hyperoxia may lead to
further secondary damage
 Asphyxia in the Neonate
13
- Treatment -
 seizures: phenobarbital first choice, use high dose (40
mg/kg), better outcome, prophylactic use
controversial, stop when EEG normal and no seizures
during last 2 months; alternatives - phenytoin
 prevent cerebral edema: fluid restriction (60
ml/kg/day), look out for SIADH, steroids and osmotic
agents controversial
 support all vital systems: may require ventilation,
pressure support, TPN, diuretics etc.
 Asphyxia in the Neonate 14
-Prognosis -

 Most survivors do not have any sequelae!

 death 12.5%, neurologic handicap 14.3%
 low predictive value of depressed FHR, Apgar score, meconium-stained
amniotic fluid, low pH, neurologic depression after birth
 Asphyxia in the Neonate
15
-Poor prognosis -
 Apgar score 0-3 at 20 min
 presence of multiorgan failure (oliguria > 24 hrs)
 HIE stage 3: 80% deaths, survivors severely affected
 HIE stage 2 beyond 5 days
 duration of neurological signs > 1-2 weeks (but ability to nipple feed carries
excellent prognosis)
 neonatal seizures in first 12 hrs
 abnormal MRI in first 72 hrs
 poor EEG patterns (burst-suppression on any day; normal initial EEG good
prognosis)
 Prevention

 Easy access to good ANC.

 Optimal Mnx of Labour and Delivery.

 Resuscitation equipment and personnel trained in its use to be

available for each delivery!
References

 Behrman, R. E. (et el) Nelson Essentials of Pediatrics (6th ed). Saunders

Elsevier.,Philadelphia, 2011.
 Clayden, G. , Lissauer, T. Illustrated Textbook of Paediatrics (4th ed).
Mosby Elsevier, China, 2012.
 Wittenberg D. F. , Coovadia’s paediatrics & Child health (6th ed). Oxford
University press, South Africa, 2009.
 Medscape: Hypoxic ischaemic encephalopathy