Curs Asfixia

8/13/2019 Curs Asfixia

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ASPHYXIA OF THE NEWBORN


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IntroductioN

Definition:

An event or condition during the perinatalperiod that is likely to severely reduce

oxygendelivery (Apgar Score


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Incidence:The incidence of neonatal encephalopathyprobably lies between 0.3 and 1.8%

Risk factors:

Hypertensive disease of pregnancy or pre-

eclampsia, Intrauterine growth restriction,

Placental abruption,

Fetal anaemia (eg rhesus incompatibility), Postmaturity,

Unphysiological labour (eg induction), and

Malpresentation including vasa praevia.


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Detection of infants at risk of perinatal asphyxia:

Only about half of the infants needing resuscitation

are predicted by antenatal history or signs duringlabour. The following predictors have been assessedfor their ability to predict low Apgar scores:

Fetal movement counting Non-stress testing

Fetal biophysical profile

Abnormal fetal heart rate (FHR) Fetal scalp pH

Reduction of liquor volume, and

Meconium staining of the liquor.


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ConsequencesPerinatal asphyxia may result in fetal demise, neonatal death, or a period ofrecovery during which there is organ dysfunction with possible long-termeffects, particularly in neurological function1. Clinical manifestations ofperinatal asphyxia include6:

Depression of the neonate at birth with a low Apgar score andacidosis, Hypoxic ischaemic encephalopathy(HIE), Multiorgan system dysfunction(% of infants with HIE):

Renal compromise with oliguria and elevated creatinine (40%), Hypoxic cardiomyopathy (ECHO or ECG abnormality) (25%),

Pulmonary complications including respiratory distress and persistent pulmonaryhypertension of the neonate (25%), Disseminated intravascular coagulation, Hepatic failure Necrotising enterocolitis.

Fluid, electrolyte and metabolic abnormalitiesincluding:

Fluid overload, hyperkalaemia, hypoglycaemia, and acidosis.One third or more of infants with HIE will have 2 or more organ systemsinvolved, which may include lung, heart, liver, brain, kidneys andhematological.


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Prediction of outcome:

No single clinical factor predicts outcome (death orneurodevelopmental abnormality) of perinatal

asphyxia or HIE with absolute certainty. DuringResuscitation:

Apgar scores

Cord blood gas Time to spontaneous respiration: the

overall risk of death or handicap was 72%in the pooled series of infants with > 30

minutes to sustained spontaneousrespiration


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Clinical assessment of encephalopathy:Degree of encephalopathy:the overall risk ofdeath or severe handicap in a pooled series ofinfants was:

Grade 1 HIE: 1.6%

Grade 2 HIE: 24%

Grade 3 HIE: 78%

More prolonged encephalopathy (eg. > 6 days stage 2) isalso highly predictive of severe neurological abnormality.

EEG abnormality:the rates of death or severehandicap for grade of EEG abnormality from pooledstudies were:

Severe abnormality (burst suppression, low voltage orisoelectric) = 95%,

Moderate abnormality (slow wave activity) = 64%, and

Mild or no abnormality = 3.3%


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Imaging and evoked potentials:

Ultrasound abnormality: May detect haemorrhage. Infantswith small or poorly visualised ventricles, andhypoechogenicities are at increased risk of abnormal

neurodevelopment. The ultrasound tends to underestimatecortical damage. Lesions may take 2-3 days to develop.

Computerised tomography:Hypodensities may take 10-14days to develop. Abnormalities include haemorrhages andhypodensities. The risk of death or severe neurologicaldisability is 82% in infants with severe hypodensities orhaemorrhage.

Nuclear magnetic resonance:NMRI (proton NMR) andNMRS (31 P NMRS) provide information on brain structure and

function that is highly predictive of outcome. Somatosensory evoked potentials:There is a close

correlation between outcome and SEP. Infants with normaloutcome have a normal SEP by 4 days of age, whereas thosewith abnormal or absent responses beyond 4 days have

abnormalities at follow up.

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Diagnosis On basic principles the assessment should include a history of maternal and

intrapartum risk factors, problems of pregnancy, abnormalities identifiedantenatally in the fetus, the presence of meconium stained liquor, CTGabnormalities, scalp pH, maternal indicators of infection, presentation andmethod of delivery.Document:

Apgar score:(see resuscitation - Apgar score) at 1 and 5 minutes andevery 5 minutes until Apgar > 7.

Umbilical arterial and venous blood gases (from placenta if no cord blood -veins cross arteries on placental surface),

Time to sustained spontaneous respiration, Neurological status (grading of HIE), Multiorgan system function including:

Respiratory status, Cardiac status (hypotension, cardiac ECHO), Renal impairment - urine output, creatinine and electrolytes (watch for fluid

overload and hyperkalaemia), Liver dysfunction - LFT's, DIC - coagulation profile (APTT, PI - if abnormal: fibrinogen degradation

products and fibrinogen level), Gastrointestinal - feed intolerance and NEC.


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Neurological examination:

Perinatal asphyxia may result in hypoxic ischaemicencephalopathy(Sarnat)

Grade 1: mild encephalopathy with infant hyperalert, irritable,and over-sensitive to stimulation. There is evidence ofsympatheticover-stimulation with tachycardia, dilated pupilsand jitteriness. The EEG is normal.

Grade 2: moderate encephalopathy with the infant displayinglethargy, hypotonia and proximal weakness. There isparasympatheticoverstimulation with low resting heart rate,small pupils, and copious secretions. The EEG is abnormal and

70% of infants will have seizures.

Grade 3: severe encephalopathy with a stuporous, flaccidinfant, and absent reflexes. The infant may have seizures and

has an abnormal EEG with decreased background activityand/or voltage suppression.


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Interventions

1. appropriate obstetric monitoring of pregnancy and

labour2. appropriate and adequate resuscitation of the

newborn is logical (see resuscitation).

Principles: clinical management is directed atappropriate and rapid resuscitation, and preventinghypoxia, hypercarbia and acidosis. Early arterialblood gasand blood sugarlevel should be

performed and acidosis and hypoglycaemia treated.The infant's cardiorespiratory status should bemonitored and signs of multiorgan systemdysfunctionsought and treated where appropriate.


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Correction of hypoglycaemia:

Correction of acidosis:

Treatment of seizures:

Temperature:

Respiratory status

Cardiac status

Fluid therapy and renal impairment

DIC

Gastrointestinal -feeding:


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Interventions to decrease severity of hypoxicischaemic encephalopathy:

Proven to be effective:

Need further evaluation:

Hypothermia: Allopurinol:

Steroids:

Mannitol: Magnesium sulphate:


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Proven to be ineffective:

Barbiturates:there is no data to support

the use of prophylactic barbiturates forHIE

Naloxone:there is no data to support

the use of prophylactic Naloxone for HIE

K P i t


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Key Points

Key Points Level of Evidence'Perinatal asphyxia'is "acondition in the neonate where there is the followingcombination:

an event or condition during the perinatal period that is likely toseverely reduce oxygen delivery and lead to acidosis; and

A failure of function of at least two organs consistent with the

effects of acute asphyxia." Grade of HIE (Sarnat) provides the best prediction of outcome

For hypoxic-ischaemic encephalopathy:

Naloxone and barbiturates are ineffective

For hypoxic-ischaemic encephalopathy:Hypothermia, allopurinol, MgSO4, Mannitol and steroids

require further study

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