Post -resuscitation management of an asphyxiated neonate
Dr Mohd Maghayreh
PRTH
Perinatal asphyxia Common neonatal problem Contributes significantly to neonatal morbidity & mortality Second most important cause of neonatal death Accounts for 25 % of neonatal deaths
Perinatal asphyxia
Insult to the fetus / newborn
Lack of oxygen - hypoxia &/or Lack of perfusion – ischemia
Effect of ischemia & hypoxia – inseparable Both contribute to tissue injury
ESSENTIAL CRITERIA FOR PERINATAL ASPHYXIA Prolonged metabolic or mixed acidemia (pH < 7.00) on an
umbilical cord arterial blood sample
Persistence of an Apgar score of 0-3 for > 5 minutes
Clinical neurological manifestations e.g. seizure, hypotonia, coma or hypoxic-ischaemic encephalopathy in the immediate neonatal period
Evidence of multiorgan system dysfunction in the immediate neonatal periods
Incidence
1. Perinatal asphyxia is about 1%-1.5% of life births.
2. It is inversely related to gestational age and birth weight .
3. It occur in (o.5%(of live born infants with gestational age >36wk
4. It account for 20% of perinatal deaths
Risk factors
Ante partum events (20%) Maternal: cardiac arrest, hemorrhage, diabetes ,pre
eclamptic toxemia, fetal: IUGR, congenital anomalies
Intrapartum events (35%) birth trauma, abruption, uterine rupture, uteroplacental
insufficiency Ante partum and Intrapartum (35%) Postpartum events (10%)
apnea, bradycardia, septic shock, pulmonary disease, some CHD (LVOT obstr), PDA (premie
FACTORS
Mat. Oxygenation
Blood flow mother to placenta
Gas Exchange across placenta or fetal tissue
Fetal O2 Req.
PATHOPHYSIOLOGY
Hypoxia
Diving seal reflex
Away from lungs, kidney gut & skin
Shunting of blood to brain adrenals & heart
CEREBRAL CORTICAL LESIONS
PATHOPHYSIOLOGYAsphyxia continues
Shunting within the brain
Anterior Circulation
Suffers
Posterior Circulation Maintained
PNA is produced by the interaction of one of the following
factors: 1- Impaired maternal oxygenation. 2- Decreased blood flow from mother to placenta
or placenta to fetus 3- impaired gas exchange across the placenta or
at the fetal tissue.
4- 4- Increase fetal O2 requirementsIncrease fetal O2 requirements..
Circulatory depressionRespiratory depression
Hypoxemia
Hypercarbia
Respiratory acidosis
Low cardiac output
Decreased tissue perfusion
Ischemia
Metabolic acidosis
Capillary leak, edema
Multi-organ dysfunction
PATHOLOGY Target organs of perinatal asphyxia
Kidneys 50%
Brain 28 %
Heart 25%
Lung 23%
Liver, Bowel, Bone marrow < 5%
Clinical consequences of perinatal asphyxia Brain ( Hypoxic Ischemic Encephalopathy,
HIE ) Altered sensorium Irritability, lethargy, deeply comatose Tone disturbances - Hypotonia of proximal girdle muscles (lack of head control & weakness of
shoulder muscle in term infants )
Clinical consequences of perinatal asphyxia (contd.) Brain ( Hypoxic Ischemic
Encephalopathy,HIE ) Autonomic disturbances eg. hypotension,
increase salivation, abnormal pupillary reflex Altered neonatal reflexes -Moro’s, sucking , swallowing Seizures
PATHOLOGY
At cellular level
Cerebral O2
Substrate supply
Synaptic inactivation (Reversible)
Energy failure
Memb. pump failure
ROS Release
ISCHEMIA AND REPERFUSION INJURY
Ischemia ATP depletio
n
Calcium influx
Phospholipase activation
Arachidonic acid release
Prostaglandins Proteases, lipases
VasodilationMicrovascular permeabilityReperfusion
MECHANISM
RESUSCITATION ATP ASPHYXIA
HYPOXANTHINE
XANTHINE
URIC ACID
Oxygen
Oxygen free radicals
Oxygen
Oxygen free radicals
BLOCKED
BLOCKED
EFFECT OF ROS
ROS
DNA strand
breakage
Lipid peroxidation
Neutrophil accumulation
Release of proteases,
myeloperoxidase, prostaglandins
Tissue damage
Phagocytosis
PMN plugging of capillaries
Ischemia
Membrane damage
Cell death
Fetal and neonatal assessment
1. A- Fetal Heart rate monitoring
2. B- Passage of Meconium
3. C- Failure to establish spontaneous respiration
4. D- low Apgar Scores
5. E- Hypoxic - Ischemic Encephalopathy
6. F- Multi organ Involvement
CLINICAL MANIFESTATIONS OF HIE Altered consciousness Tone problems Seizure activity Autonomic disturbances Abnormalities of peripheral and stem reflexes
Principles of management
Prevent further organ damage Maintain oxygenation, ventilation & perfusion Correct & maintain normal metabolic & acid
base milieu Prompt management of complications
CLASSIFICATION OF HIE (LEVENE)
Mild Moderate
Consciousness
Tone
Seizure
Sucking / Resp.
Irritable
Hypotonia
No
Poor Suck
Lethargy
Marked
Yes
Unable to suck
Feature Severe
Comatose
Severe
Prolonged
Unable to sustain
spont. Resp.
Grade 1 (mild)Grade2 (moderate)Grade 3 (severe)
Level of consciousnessIrritable/hyperalertLethargyComa
Muscle toneNormal or hypertoniaHypotoniaFlaccid
Tendon reflexesIncreasedIncreasedDepressed or absent
SeizuresAbsentFrequentFrequent
Complex reflexesNormalweakAbsent
PrognosisGoodVariableHigh mortality and neurologicl disability
Sarnat staging of hypoxic-ischemic encephalopathy.
According to Sarnat classification of severity
stage 1 100 % normal
stage 2 80 % normal
stage 3 50 % death 50 % major sequalae
Initial management
Admit in nursery,if -Apgar score <3 at 1 minute -Babies requiring intubation, chest compressions
or medications Nurse in thermo-neutral temperature to maintain skin
temperature at 36.5oC Secure IV line , fluids 2/3 rd of maintenance Fluid bolus if CRT > 3 secs or blood pressure low Inj vit k Stomach wash
Clinical monitoring
HR, RR, colour, CRT, O2 saturation, BP & temperature Assessment of neurologic status
Tone, seizures, consciousness, pupillary size & reaction, sucking, swallowing
Abdominal circumference Urine output
Biochemical monitoring
Blood gases & pH Bedside blood sugar by Dextrostix Hematocrit S. electrolytes ( Na, K) S. calcium BUN, creatinine
Other investigations
Sepsis screen & blood culture to exclude in- utero or acquired infection during resuscitation
X-ray chest to look for pneumothorax, malformations, cardiac enlargement
Other investigations contd..
Neuroimaging CT scan -brain edema as suggested by small
compressed ventricles -hemorrhage Ultrasound -small compressed ventricles -intraventricular hemorrhage EEG
Aims of specific management
Maintain temperature, perfusion, oxygenation, ventilation & normal metabolic state Temperature 36.5 C – 37.5 C Perfusion:
BP Mean 40-60 mm Hg ( Term) CRT maintain < 3 sec
Oxygen PaO2 60-80mmHg saturation 90-93 %
CO2 35-45 mm of Hg Glucose 70-110 mg/dl Calcium 9-11 mg/dl
Specific management
Maintain perfusion Normal blood pressure CRT < 3 secs Normal urine output ( >1ml/kg/hr) Absence of metabolic acidosis
Specific management
Maintain perfusion Maintain mean arterial pressure and CRT by giving
slow bolus of crystalloid 10 ml/kg over 20 minutes. Repeat one more time , if still does not improve
Use vasopressors Dopamine and /or Dobutamine to increase BP
Sodium bicarbonate 1-2 ml/kg diluted in 5 % dextrose can be used for babies with documented acidosis after establishing respiration
SUBSEQUENT MANAGEMENT
Oxygenation & ventilation Adequate perfusion Normal glucose & calcium Normal hematocrit Treat seizure
Oxygenation & ventilation Adequate perfusion Normal glucose & calcium Normal hematocrit Treat seizure
TREATMENT OF SEIZURESTREATMENT OF SEIZURES
Correction of hypoglycemia, hypocalcemia & electrolyte
Prophylactic Phenobarbitone ?
Therapeutic Phenobarbitone 20 mg / kg (loading), 5 mg / kg / d (maintenance)
Lorazepam – 0.05 – 0.1 mg / kg
Diazepam to be avoided
Correction of hypoglycemia, hypocalcemia & electrolyte
Prophylactic Phenobarbitone ?
Therapeutic Phenobarbitone 20 mg / kg (loading), 5 mg / kg / d (maintenance)
Lorazepam – 0.05 – 0.1 mg / kg
Diazepam to be avoided
Predictors of poor neuro-developmental outcome Failure to establish resp. by 5 minutes Apgar score of 3 or less at 5 minutes Onset of seizures with in 12 hours Refractory seizures Inability to establish oral feeds by 1 wk Abnormal EEG, neuro-imaging
Preventing asphyxia
Perinatal assessment Regular antenatal check ups High risk approach Anticipation of complications during labour Timely intervention ( eg. LSCS)
Perinatal management Timely referral Management of maternal complications
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