1. neonatal asphyxia
DESCRIPTION
NATRANSCRIPT
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%
04/10/23 6
4 million newborn deaths – Why?almost all are due to preventable conditions
04/10/23 7
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
04/10/23 27
GASTROINTESTINAL EFFECTS
• The asphyxiate infants is at risk for bowel ischemia and
• NECROTIZING ENTEROCOLITIS
04/10/23 28
HEMATOLOGICS EFFECTS
• DIC
• THE LIVER MAY FAIL TO MAKE CLOTTING FACTORS
• THE BONE MARROW MAY NOT PRODUCE PLATELETS
04/10/23 29
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!!!!
04/10/23 36
PREVETION IS THE BEST MEDICINE!!!!
Thank you