BIRTH ASPHYXIA an updated approach .pptx

Birth Asphyxia (Perinatal Asphyxia)

Definition:
Birth asphyxia refers to impaired gas exchange leading to hypoxemia, hypercapnia, and metabolic acidosis during the perinatal period (immediately before, during, or after birth). It results in failure to initiate and sustain breathing at birth.
(AAP, 2023; WHO, 2022)


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Pathophysiology

Primary insult: Interruption of placental blood flow or umbilical circulation → ↓O₂ delivery → hypoxemia.

Secondary effects:

Anaerobic metabolism → lactic acidosis.

Cellular energy failure → sodium–potassium pump dysfunction → cell swelling and death.

Organ dysfunction, especially in the brain, heart, kidneys, and lungs.

Reperfusion injury after resuscitation can worsen damage via free radicals and inflammation.




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Causes

Antenatal:

Maternal hypoxia (e.g., anemia, cardiac/respiratory disease)

Placental insufficiency or abruption

Severe preeclampsia or eclampsia

Intrauterine growth restriction (IUGR)


Intrapartum:

Prolonged or obstructed labor

Cord prolapse, compression, or true knot

Uterine rupture

Meconium aspiration

Abnormal presentation


Postnatal (less common):

Respiratory distress syndrome

Pneumonia

Congenital heart disease



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Clinical Features

Immediately after birth:

Low or absent cry

Poor respiratory effort or apnea

Bradycardia

Hypotonia

Cyanosis or pallor


Later signs:

Poor feeding

Seizures (often within 24–48 hours)

Altered level of consciousness




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Diagnosis

1. Clinical Criteria (AAP & WHO):

Birth asphyxia is suspected when ≥1 of the following:

Apgar score ≤5 at 5 minutes

Need for positive pressure ventilation >1 minute

Umbilical arterial pH <7.0 or base deficit ≥12 mmol/L

Evidence of multisystem involvement, particularly hypoxic-ischemic encephalopathy (HIE)


2. Investigations:

Arterial blood gas (cord or early sample)

Neuroimaging: MRI brain (best for HIE pattern)

EEG/aEEG: Detects subclinical seizures

Renal/liver function tests

Cardiac enzymes (troponin, CK-MB)



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Complications

Neurological: Hypoxic-ischemic encephalopathy, seizures, cerebral palsy, developmental delay

Renal: Acute tubular necrosis

Cardiac: Myocardial dysfunction

Pulmonary: Persistent pulmonary hypertension

Metabolic: Hypoglycemia, hyponatremia



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Management

1. Immediate (Delivery Room)

Follow Neonatal Resuscitation Program (NRP) guidelines:

Ensure warmth, clear airway, and adequate ventilation.

If not breathing → positive pressure ventilation (PPV).

If HR <60 bpm → chest compressions + epinephrine as indicated.


2. Post-resuscitation Care

Therapeutic hypothermia (33–34°C for 72 h) within 6 hours if moderate/severe HIE.
(AAP, 2020; TOBY and NICHD trials)

Maintain oxygenation (SpO₂ 90–95%), normocapnia, and normal glucose.

Anticonvulsants (phenobarbital) if seizures occur.

Monitor urine output, electrolytes, and perfusion.



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Prognosis

Depends on severity and duration of hypoxia.

Mild HIE: Usually full recovery.

Moderate HIE: Risk of neurodev

1. BIRTH ASPHYXIA Hypoxic-Ischemic Encephalopathy(HIE) Dr. Mohsen AL- Solaimani

2. DEFINITION: It is an insult occur in fetus or newborn that result in anoxia, hypoxia or ischemia which may injure any organ of the body especially the brain (which is more susceptible to irreversible damage).

3. ETIOLOGY: Prenatal events are those which cause fetal hypoxia/ischemia e.g. maternal hypoxia/hypotension, uterine tetany , premature separation of placenta, impedance of blood through umbilical cord, or placental insufficiency due to toxemia or postmaturity . Perinatal events of newborn are the most common (80%), it include:- ✓ Hypoxia e.g. severe cardiac or pulmonary disease. ✓ Anemia e.g. severe hemorrhage or hemolytic disease. ✓ Shock e.g. overwhelming sepsis, massive blood loss, and intracranial or adrenal hemorrhages .

4. PATHOPHYSIOLOGY The initial response of hypoxic-ischemic insult is ↑ pulmonary vascular resistance & preferential perfusion of circulation to the brain, heart & adrenals. The response to HIE is different between full-term versus premature infant in that: in term infant it usually → focal or multifocal cortical infarcts & necrosis, whereas in premature infant → periventriculer leucomalasia (PVL), intraventricular hemorrhage (IVH ), or status marmoratus of basal ganglia.

5. CLINICAL MANIFESTATIONS The severity of neonatal encephalopathy depends on the duration and timing of injury. The need to define severity is rooted in the need to determine eligibility for therapeutic hypothermia , a treatment that decreases death and disability in moderate to severe HIE. Infants with moderate to severe HIE are characterized by disturbed neurologic function, altered level of consciousness, depressed tone, abnormal reflexes, and difficulty maintaining spontaneous respirations, and seizures. An empirically validated definition of mild HIE within 6 hours uses two steps: the first step is screening for fetal acidosis and acute perinatal events, and the second step has an examiner use a modified Sarnat scoring, which is expanded to include mild in addition to moderate and severe abnormalities

6. modified Sarnat scoring

7. MANAGMENT It should be started before, during, & immediately after delivery. Before delivery; Fetal hypoxia can be detected by IUGR & ↑ vascular resistance which should alert the obstetrician about the treatable causes of fetal distress. During delivery; Fetal distress is indicated by: bradycardia , ↓ beat-to beat variability, late (type II) deceleration, & acidosis (pH <7.20) detected by fetal scalp blood analysis. These signs necessitate administration of high concentrations of oxygen to the mother and immediate delivery (probably by C/S)

8. MANAGMENT After delivery; Asphyxiated infant is indicated by ↓ Apgar scores e.g. pallor, cyanosis, apnea, bradycardia , unresponsive to stimuli and may has meconium-stained amniotic fluid. Thus he need vigorous resuscitation with the following measures :- Systemic (or selective) cerebral hypothermia should be done within the 1st 6 hr after birth to core temp of 33.50C. It cans ↓ mortality & neurodevelopmental impairment in term or near-term infants with HIE because it may ↓ the rate of apoptosis and suppresses production of neurotoxic mediators . SE of cerebral hypothermia includes: thrombocytopenia ( usually without bleeding), reduced heart rate, subcutaneous fat necrosis, and the potential for overcooling and the cold injury syndrome.

9. MANAGMENT Seizures due to HIE is usually severe & refractory to the usual doses of anticonvulsants, thus Phenobarbital loading dose may be given initially as 20 mg/kg, but can be given up to 40-50 mg/kg to control the seizure. Phenytoin 20 mg/kg, Lorazepam 0.1 mg/kg, or levetiracetam can also be used . Note: Remember & treat other causes of convulsion in asphyxiated infant e.g. hypoglycemia, metabolic disturbances, infection...etc.

10. MANAGMENT Supportive Care directed at management of other organ system dysfunction. Hyperthermia has been found to be associated with impaired neurodevelopment, so it is important to prevent hyperthermia before initiation of hypothermia. Careful attention to ventilatory status and adequate oxygenation, BP, hemodynamic status, acid–base balance, and possible infection is important. • All survivors of moderate to severe encephalopathy require comprehensive medical and developmental follow-up .

11. PROGNOSIS It ranges from complete recovery to death depending on the timing and severity of insult. The area of injury can also determine short & long term sequelae as follows :-