PERINATAL ASPHYXIA

Professor Bogale Worku

Oct 2009

PERINATAL ASPHYXIA

Insult to the fetus / Newborn

Lack of oxygen (Hypoxia)

Lack of perfusion (Ischemia)

Effect of hypoxia & Ischemia are inseparable

Both contribute to tissue injury

PERINATAL ASPHYXIA

• There may be associated lactic acidosis

• If there is hypoventilation there may be hypercarbia

Definition • Profound umbilical arterial metabolic or

mixed acidemia with PH <7.2

• APGAR score of <3 for > 5 minutes• Neonatal neurologic sequelae:

– seizures, hypotonia, coma

• Multi-organ dysfunction

PERINATAL ASPHYXIA

Western Scenario

India (NNF data Base)

Incidence

Cause of Perinatal death

Still Birth + P. Mort.

1 – 1.5 / 1000

20%

50%

10%

26%

59%

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4 million newborn deaths – Why?almost all are due to preventable conditions

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Estimated causes of neonatal deaths (2000)

34%

22%15%

15%

4%4% 6%

Infection

Asphyxia

Preterm

Tetanus

Diarrhea

Congenital

Others

35% 35%

20% 10%

During deliveryDuring labor

After deliveryBefore labor

ETIOLOGY

• Intrapartum or Antepartum (90%)–Placental Insufficiency

–Cord accident

–Maternal CP arrest

–MAS

ETIOLOGY• Post partum (10%)–Pulmonary–Cardiovascular–neurological

I - MATERNAL CAUSES: (conditions leading to imperfect oxygenation of maternal blood)

• Severe anemia, Hemorrhage & shock, Respiratory failure, and heart failure.

• Eclamptic seizure, pneumonia, and pulmonary edema.

ETIOLOGY

II- PLACENTAL CAUSES:• Placental compression: interfering with its

circulation as in tonically contracted uterus, prolonged labor 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.

ETIOLOGY

III- CAUSES IN THE UMBILICAL CORD: Obstruction of the circulation, which may be due to:

• Tight nuchal cord• True knots • Prolapsed cord• Compression of the vessels by hematoma of the

cord • Rupture of vasa praevia.

ETIOLOGY ( 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

FACTORS Mat. Oxygenation

Blood flow mother to placenta

Blood flow placenta to fetus

Gas Exchange across placenta or fetal tissue

Fetal O2 Req.

Circulatory depressionRespiratory depression

Hypoxemia

Hypercarbia

Respiratory acidosis

Low cardiac output

Decreased tissue perfusion

Ischemia

Metabolic acidosis

Capillary leak, edema

Multi-organ dysfunction

NONE BRAIN ORGAN DAMAGE

PATHOPHYSIOLOGYAcute asphyxia

Diving reflex

Shunting of blood to brain adrenals & heart

Away from lungs, kidney gut & skin

CEREBRAL CORTICAL LESIONS

PATHOPHYSIOLOGYAsphyxia continues

Shunting within the brain

Anterior Circulation

Suffers

Posterior Circulation Maintained

THALAMUS & BRAIN STEM INJURY, CORTEX SPARED

PATHOPHYSIOLOGY

• Hypoxia – ABRUPT & SEVERE– Complete abruption– Cord accident – Maternal CP arrest

PATHOLOGY• Target organs of perinatal asphyxia

– Kidneys 50%

– Brain 28%

– Heart 25%

– Lung 23%

– Liver, Bowel, Bone marrow < 5%

NEUROPATHOLOCIAL CHANGES

Pattern seen in term infants

Selective neuronal necrosis (Spastic CP)

Status Marmoratus (Chorea, Athetoid, Dystonia)

Parasagittal cerebral injury (Prox Spastic Quadriparesis)

Focal and multifocal ischemic brain injury (sp. Hemiparesis, cognitive defects, seizure)

Pattern predominant in preterm

PERIVENTRICULAR LEUKOMALACIA

PATHOLOGY

Cerebral O2

Substrate supply

Synaptic inactivation (Reversible)

Energy failure

Memb. pump failure

Further in perfusion

At cellular level

CHANGES IN SUBSTRATE METABOLISM AND NEURTRANSMITTERS

• Hypoxic effect–Changes that are increased

• An initial increase Cerebral blood flow• Increase of glucose influx to brain• Increase in glycogenolysis (increase cAMP)• Increase in glycolysis (increase cAMP)• Increase lactate and hydrogen ions

CHANGES IN SUBSTRATE METABOLISM AND NEURTRANSMITTERS

–Changes that are decreased• Decreased oxidative phosphorylation• Eventual decrease brain glucose• Decreased phosphocreatinine (PCr) and ATP

– These changes are more pronouned in the white matter compared to the gray matter

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GASTROINTESTINAL EFFECTS

• The asphyxiate infants is at risk for bowel ischemia and

• NECROTIZING ENTEROCOLITIS

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HEMATOLOGICS EFFECTS

• DIC

• THE LIVER MAY FAIL TO MAKE CLOTTING FACTORS

• THE BONE MARROW MAY NOT PRODUCE PLATELETS

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PULMONARY EFFECTS• Increased pulmonary resistance• pulmonary hemorrhage• Pulmonary edema secondary to cardiac failure• Failure of surfactant production with secondary

HMD• Meconium aspiration may be present.

Management of HIE

1.1. Maintain Maintain O2O2 and and CO2CO2 in normal ranges. in normal ranges.

2.2. HyperventilationHyperventilation not recommended and may be not recommended and may be detrimentaldetrimental..

3.3. Monitor Monitor arterial blood pressure arterial blood pressure because cerebra because cerebra perfusion pressure is dependent on MAPperfusion pressure is dependent on MAP

4.4. Administer Administer volume volume slowlyslowly: overall fluid restriction: overall fluid restriction5.5. Monitor Monitor electrolyteselectrolytes and glucose and glucose6.6. Control Control seizuresseizures

7.7. HYPOTHERMIAHYPOTHERMIA THERAPY THERAPY

HYPOTHERMIA THERAPY

• Entry criteria– PH < 7.0– Base deficit 16mmole/l in 1st hour– APGAR score < 5 at 10 minutes.– Less than 6 hrs old.

• Technique– Keep core temp at 33 *C for 72 hrs– Continuous EEG monitoring– Continue medical management

MULTISYSTEMIC EFFECTS

• Seizures – Often resistant to anticonvulsant therapy in severe HIE(possibly

because of a lack of cortical inhibition Vs. excessive cortical activity– 50% are subtle, focal ,multifocal or myoclonic– Typically first noted at age 12 to 24 hrs and often resolve by 5 to 7

days– Must also assess for other metabolic derangements (eg;

hypoglycemia, hypocalcemia, hypomagnesemia)– Phenobarbital is the first line agent followed by dilantin (may also

consider lorazepam)

MULTISYSTEMIC EFFECTS

• ACUTE ASPHYXIA– elicits diving reflex with preferred blood flow to the brain, heart, and

adrenal gland

• CARDIAC MANIFESTATIONS– Transient myocardial ischemia, congestive heart failure, left or right

ventricular dysfunction, tricuspid regurgitation murmur within the first 24 hrs

• RENAL– Oliguria and possible acute tubular necrosis

• PULMONARY– Pulmonary hypertension especially after MAS

PREDICTORS OF POOR NEURO DEVELOPMENTAL OUTCOME

• Failure to establish respiration by 5 minutes• Apgar 3 or less in 5 mts• Onset of Seizure in 12 hrs• Refractory convulsion• Inability to establish oral feed by 1 wk• Abnormal EEG & failure to normalize by 7

days of life• Abnormal CT, MRI in neonatal period

PREVETION IS THE BEST MEDICINE!!!!

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PREVETION IS THE BEST MEDICINE!!!!

Thank you