Perinatal Asphyxia

Prepared by
Johannes Negesse
Terminology
• Hypoxemia , a decreased arterial concentration of oxygen
• Hypoxia , decreased oxygenation to cells or organs
• Ischemia ,refers to blood flow to cells or organs that is inadequate to
maintain physiologic function.
• Anoxia , is complete lack of oxygen as a result of a number of primary
causes.
• Asphyxia
• World Health Organization (WHO) defines birth asphyxia as failure to initiate
and sustain breathing at birth
• It can also be defined as placental or pulmonary gas exchange impairment
leading to hypoxemia and hypercarbia.
Cont...
Multiorgan Systemic Effects of Asphyxia

Central nervous Hypoxic-ischemic encephalopathy, infarction, intracranial hemorrhage, seizures,

cerebral edema,hypotonia, hypertonia

Cardiovascular Myocardial ischemia, poor contractility,hypotension, tricuspid insufficiency

Pulmonary Pulmonary hypertension, pulmonary hemorrhage, respiratory distress syndrome
Renal Acute tubular or cortical necrosis
Adrenal Adrenal hemorrhage
Gastrointestinal Perforation, ulceration with hemorrhage, necrosis
Metabolic SIADHS, hyponatremia, hypoglycemia, hypocalcemia,

Integumentary Subcutaneous fat necrosis

Hematologic Disseminated intravascular coagulation
HIE
• Hypoxic-ischemic encephalopathy (HIE) is a leading cause of neonatal
brain injury, morbidity, and mortality globally
• developed world, incidence is 1-8 per 1,000 live birth
• and in the developing world, as high as 26 per 1,000.
• Hypoxic ischaemic encephalopathy can result from lack of oxygen to vital organs
before, during or immediately after birth
Etiology
• Most neonatal encephalopathy and seizure are caused by
• congenital malformations
• metabolic
• genetic syndromes
• perinatal events
Clinical manifestation
• The encephalopathic neonate may have
• low Apgar scores at delivery
• metabolic acidosis documented in the cord blood
• Within 24 hours ,infant may develop apnea and seizures with EEG
abnormality
• Abnormal EEG results may be helpful in the prediction of clinical outcome,
like death and neurologic sequelae, such as spastic quadriplegia or diplegia
Clinical features cont.…
 Encephalopathy manifest as:
Mildly affected infants
 Jittery, irritable, some degree of feeding problem
Moderate degree
 Irritable, vomiting, increased muscle tone, high pitched cry
Severely degree
 Deeply stuporous or comatose
 Seizure in 50% (usually within 24 hr)
 Hypotonia hyperotonia
Stages of HIE
SIGNS STAGE 1 STAGE 2 STAGE 3
Level of CON Hyperalert Lethargic Stuporous, coma

Muscle tone Normal Hypotonic Flaccid

Posture Normal Flexion Decerebrate

Tendon reflexes Hyperactive Hyperactive Absent

Myoclonus Present Present Absent

Moro reflex Strong Weak Absent

Pupils Mydriasis Miosis Unequal, poor light reflex

Seizures None Common Decerebration

EEG Normal Low voltage changing to seizure Burst suppression to isoelectric

activity
Duration <24 hr 24 hr to 14 days Days to weeks

Outcome Good Variable Death, severe deficits

Diagnosis
• MRI is the most sensitive imaging modality for detecting hypoxic brain
injury in neonate
• Diffusion-weighted sequences obtained in the 1st 3-5days following a
presumed sentinel event are optimal for identifying acute injury
• CT is least sensitive for evaluation of HIE because of high water in
neonatal brain and high protein of the CSF result in poor parenchymal
contrast resolution.
• CT scans may be helpful in ruling out focal hemorrhagic lesions or
large arterial ischemic strokes
• Sonography is sensitive for the detection of hemorrhage,
periventricular leukomalacia (PVL), and hydrocephalus
• US has limited utility in evaluation of hypoxic injury in term infant, but
it can be useful for excluding hemorrhagic lesions
• US is the initial preferred (and sometimes only feasible) modality in
evaluation of the preterm infant
Cont...
MAJOR CONVENTIONAL MR FINDINGS IN 1ST WEEK

• Cerebral cortical gray-white differentiation lost (on T1W or T2W)

• Cerebral cortical high signal (T1W and FLAIR), especially in parasagittal perirolandic cortex
• Basal ganglia/thalamus, high signal (T1W and FLAIR), usually associated with the cerebral cortical
changes but possibly alone with increased signal in brainstem tegmentum in cases of acute severe
insult
• Parasagittal cerebral cortex, subcortical white matter, high signal (T1W and FLAIR)
• Periventricular white matter, decreased signal (T1W) or increased signal (T2W)
• Posterior limb of internal capsule, decreased signal (T1W or FLAIR)
• Cerebrum in a vascular distribution, decreased signal (T1W), but much better visualized as
decreased diffusion (increased signal) on diffusion-weighted MRI
• Diffusion-weighted MRI more sensitive than conventional MRI, especially in 1st days after birth,
when former shows decreased diffusion (increased signal) in injury
Management

Generalized treatment:
Ventilation: CPAP, Mechanical ventilation
Circulation: Dopamine/Dobutamine
Energy: normal glucose
Fluid: restriction < 60-80ml/kg/d
Treatment
• Therapeutic hypothermia
• head cooling or systemic cooling
• High-dose erythropoietin
• Seizures associated with HIE
• Tx by phenobarbital
• for referactory levetiracetam
Prognosis
Depend on the severity of brain damage & medical treatment,
usually:
Mild or moderate cases could be cured completely, but severe cases
represent poor prognosis with high mortality or cerebral
complications such as mental retardation & cerebral palsy.
Mild HIE: complete recovery
Moderate HIE: 6% died,30% neurologic disability
Severe HIE: 70 -80% died, 100% neurologic disability
Shock In The Neonates
Significant reduction of systemic perfusion resulting in low tissue
oxygen and nutrient delivery.
Hypovolemic shock
Distributive shock
Cardiogenic shock
Obstructive shock
Septic shock
Hypovolemic shock
Commonest cause of shock in neonates
 Hemorrhage (Intracranial/extracranial)
Abruption of placenta
Fetomaternal hemorrhage, DIC
infections (Increased capillary leak/Gastroenteritis)
Excessive volume depletions (Diuresis)
Distributive shock
Sepsis related to increased inflammatory responses
Rapid heating
Abnormal vaso response
Cardiogenic shock
Asphyxia
Myocarditis
Arrhythmia
Obstructive shock
It is due to decreased cardiac output
Cont….
Tachycardia, BP is maintained (early)
Cold, pale skin, oliguria and ileus
Wide pulse pressure hypotension
Decreased systolic BP
Altered mentation
Irreversible organ damage.
Management
Supportive treatment
ABC of life
Intranasal oxygenation
Correction of hypoglycemia, hypocalcemia, acidosis
If large amount of fluid is given 2ml/kg/dose of Calcium gluconate 10% can be
administered
Cont…
Fluid treatment in hypovolemic shock
Crystalloids (NS 20ml/kg with in 30min to hour)
Can be given three times (60ml/kg
End goal directed treatment until V/S, urine output, capillary refill and
mentation become stable.
Cont…
Acute blood loss
Whole blood 20ml/kg less than 7 days over one hour.
 If blood is not available volume expanders like 0.9% N/S can be used .
Cont…
Resistant to fluid treatment consider septic shock or cardiogenic
shock.
As much as 60-80ml/kg of NS
Broad spectrum antibiotics
Blood transfusion of 20ml/kg of whole blood
Hydrocortisone administration in suspected septic shock
Inotropes
Dopamine
Dobutamine
 Epinephrine
 Milrinone