asphyxia neonatorum
TRANSCRIPT
Dr Varsha Atul ShahSenior Consultant
Department of Neonatal and Developmental MedicineSingapore General Hospital
ASPHYXIA NEONATORUMASPHYXIA NEONATORUM
Defined as impaired respiratory gas exchange
accompanied by the development of acidosis
ASPHYXIA NEONATORUMASPHYXIA NEONATORUM
Definition of perinatal asphyxiaWHO :
A failure to initiate and sustain breathing at birth.
NNF :Moderate asphyxia
Slow gasping breathing or an apgar score of 4-6 at 1 minute of age
Severe asphyxiaNo breathing or an apgar score of 0-3 at 1 minute of age
HOW DOES ASPHYXIA OCCUR? Interruption of umbilical cord blood flow, eg: cord
compression during labour
Failure of exchange across the placenta, eg: abruption
Inadequate perfusion of maternal side of placenta, eg: maternal hypotension
Compromised fetus who cannot tolerate transient intermittent hypoxia of normal labour
Failure to inflate lungs
CHARACTERSITICS OF PERINATAL ASPHYXIA
Profound metabolic acidosis (pH<7.00)Persistence of an Apgar score of 0 to 3 beyond 5 minutesClinical neurologic sequelae in the immediate neonatal
periodEvidence of of multiorgan system dysfunction in the
immediate neonatal period
- derived from the 1992 joint statement of the AAOP and ACOG and the 1999 International Cerebral Palsy Task Force
TO ASSESS THE SEVERITY OF ASPHYXIA - Apgar Scores
Signs 0 1 2
Colour Blue/pale Blue peripheries Pink
Heart rate 0 <100 >100
Respiration 0 Weak, gasping Regular
Suction response 0 Slight Cries
Tone 0 Fair Active
A -Appearance P- Pulse G- Grimace A-Activity R-Respiration
Quiz:At birth, a newborn infant is noted to have the following findings: heart rate – 70/min, respiratory effort – poor and irregular, limp, no reflex irritability, blue all over the body.
The Apgar score of the baby at this point is?
HR 1, RR 1, Tone 1, reflex 0, color 0
APGAR=3
PREDISPOSING FACTORS
Maternal Causes
Medical conditions eg Pulmonary hypertension Chronic HPT
Antenatal conditions eg Abnormal uterine contraction Antepartum haemorrhage Prolapsed cord Malpositions etc
PREDISPOSING FACTORS
Fetal Causes
Multiple pregnancies
Big baby with CPD
Fetal anomalies - Congenital abnormalities
of the lung
PATHOPHYSIOLOGY
Fetal adaptation to oxygen lack
1. Preferential flow to heart, brain and adrenals
aerobic anaerobic metabolism
glucose pyruvic acid lactic acid Acidosis
Acidosis failure of autoregulation impaired perfusion
increasing acidosis Death unless resuscitated
PATHOPHYSIOLOGY
2. Primary and Secondary apnoea
Occur as an attempt to minimize metabolic work
3.Fetal response to asphyxia
Respiratory metabolic acidosis
4. EEG changes
Loss of faster rhythm iso-electric rhythms Prolonged voltage suppression with burst of spike waves indicating risk of significant brain damage
CLINICAL FEATURES Apnoea, bradycardia
Altered respiratory pattern - grunting, gasping
Cyanosis
Pallor-shock
Hypotonia
Unresponsiveness
ORGANS INVOLVED IN ASPHYXIA (1)
Asphyxia results in alteration in blood flow to various organs, hence multiple organ injury
Kidney abnormalities occur in 50% of asphyxiated infants CNS abnormalities in 30% & CVS & pulmonary abnormalities in 25%
• Renal abnormalities - Oliguria, elevated β2 , microglobulin, • azotaemina, elevated serum creatinine, acute tubular necrosis
ORGANS INVOLVED IN ASPHYXIA (2)
CNS abnormalities - HIE, PV-IVH
CVS abnormalities - Ventricular failure (R > L) Tricuspid regurgitation
Hypotension
Pulmonary abnormalities - PFC, pulmonary haemorrhage
GIT abnormalities - bleeding GIT, NEC
Bone marrow abnormalities - Thrombocytopenia etc
PATHOLOGY OF BRAIN DAMAGEAcidosis alteration in cell membrane permeability fluid shift cerebral edema
Anoxia chromatolytic changes in neuron
neuron necrosis and neuroglia reactions
Neuron necrosis may be focal, multifocal or
diffusely over the cerebral cortex, brainstem,
thalamus, basal ganglia etc
PATHOLOGY OF BRAIN DAMAGEExtent of damage depends on:
duration of asphyxia
severity of asphyxia
gestational age
alteration in cerebral blood flow
changes in glucose/glycogen metabolism in vulnerable areas of brain.
Pathology
•Severity and distribution is dependent on several factors
•Certain vulnerable areas
- cerebral cortex , hippocampus , basal ganglia, thalamus, brain stem, subcortical and periventricular white matter
•In full term infants gray matter structures affected and in premature infants white matter
•Four basic and clinically important lesions
- Neuronal necrosis, status marmoratus, para-sagittal cerebral injury, periventricular leucomalacia
In hypoxic-ischaemic encephalopathy, as the
cerebral edema develops, the brain function is
affected in descending order.
PATHOCLINICAL CORRELATIONFull term infant
Pathology Clinical Signs
• Parasagittal cortical and Spastic quadriplegia subcortical neurosis especially arms
Intellectual deficits
• Cerebellum Ataxia
• Brainstem Pseudobulbar palsy
PATHOCLINICAL CORRELATION Preterm infant
Pathology Clinical Signs
• Periventricular leukomalacia Spastic diplegia
• Status marmoratus of Dystonia,
• Basal ganglia choreoathetosis
• Thalamus Mental retardation
• Cerebral Cortex Mental retardation
SEVERITY OF HIE - SARNAT & SARNAT STAGE Stage I Stage II Stage III
Consciousness Hyperalert Lethargic Stuporose
Muscle Tone NAD Mild Hypotonia Flaccid Reflexes active Reflexes active intermittent
decerebration
Primitive Reflexes Present Incomplete Absent sucking weak suck weak or -ve suck -ve
Autonomic Function Sympathetic Parasympathetic Both depresseddepressed depressed
Seizures None Common None
EEG Normal Seizure, Isopotential background burst mildly abnormal suppression
Mild HIE
• Muscle tone may be increased slightly • Deep tendon reflexes may be brisk during the first
few days. • Transient behavioral abnormalities, such as poor
feeding, irritability, or excessive crying or sleepiness, may be observed.
• By 3-4 days of life, the CNS examination findings become normal.
Moderate HIE
• Lethargic, significant hypotonia • Diminished deep tendon reflexes. • Grasp, Moro, and sucking reflexes may be sluggish
or absent. • Occasional periods of apnea. • Seizures may occur within the 1st 24 hours of life. • Full recovery within 1-2 weeks is possible and is
associated with a better long-term outcome.
Severe HIE
• Stupor or coma is typical. • may not respond to any physical stimulus. • Breathing may be irregular, and the infant often requires ventilatory
support. • Generalized hypotonia and depressed deep tendon reflexes are
common. • Neonatal reflexes (e.g., sucking, swallowing, grasping, Moro) are
absent.• Disturbances of ocular motion, such as a skewed deviation of the
eyes, nystagmus, bobbing, and loss of "doll's eye" (i.e., conjugate) movements may be revealed by cranial nerve examination.
• Pupils may be dilated, fixed, or poorly reactive to light.
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 Prevention,
PREVENTION
Recognition of at risk pregnancies
Antenatal monitoring fetal movements, fetal growth CTG for change in baseline, loss of variability, decelerations fetal scalp pH < 7.2 --------------------- immediate delivery 7.2 - 7.25 ------------- repeat in 1 hour 7.25 ------------------- normalCo-ordinated care at delivery by paediatrician
MANAGEMENT-InvestigationsHx - of pregnancy and resuscitation
O/E to exclude other abnormality
Metabolic tests - sugar, Ca/P04/Mg, cord BG, ABG, metabolic screen
CSF - to exclude infection; assay brain specific creatine kinase
EEG - to help with seizure Dx and prognosis
Tech. scan - for abnormal uptake in damaged area
MANAGEMENT U/S - to exclude PV-IVH
CT scan - to exclude IVH/trauma, demonstrate severity of edema and for prognosis
MRI scan
• Supportive care Monitor B/p, To, blood sugar, correct acidosis and electrolyte
inbalance Care of renal failure - low fluid, dialysis Care of cardiac failure - Dopamine, restrict fluid Management of inappropriate ADH secretion - prevent overhydration
MANAGEMENT-1
BASIC CARE :Should be a daily routine in the management of all these babies -
1. Strict asepsis.2. Ensure neutral thermal environment.3. Monitor vital parameters – HR,RR,BP,and Pulse Oximetry.4. Urine output.5. Daily weight.6. Nutrition.
1. Management of shock
1.Hypovolumic shock needs replacement with fluids, plasma, or blood.
2.Cardiogenic shock warrants use of pressors like dopamine and / or dobutamine. In case of refractory shock inspite of use of pressors of 20 microgram/kg/mt steroids may be tried.
3.Septic shock should be suspected based on intrapartum risk factors for sepsis, core axillary mismatch and results of sepsis screen.
2-MANAGEMENT of Cerebral Oedema
• Minimise cerebral edemaVentilation - to prevent apnoea and maintain PC02 of 25 - 30
mmHgEnsure adequate oxygenationRestrict fluid intakeMannitol/frusemide - if urine output is established
• Not all seizures require treatment. Only lif seizures are more than 3 in a hour or lasting for 3 mts or more they warrant anticonvulant.
• Phenobarbitone,Phenytoin,initially by loading dose followed by maintenance dose are the first line drugs.
• In refractory seizures use of drip of midazolam,lorazepam or diazepam may be required.
• Role of sodium valproate is occasional. Use of newer anticonvulants like lamotrigene,clobazam,gabapentin etc is not well known in neonates.
3-Manangement of seizures
4-MANAGEMENT OF KIDNEY FAILUREUrine output is by itself not a reliable marker renal
parameters need to be monitored.
2.Fluid restriction is required once renal failure sets in. A careful evaluation of electrolytes would direct the fluid management.
3.Daily monitoring of urine output, urine specific gravity, and body weight are adjuvant to basic care.
4.Rarely peritoneal dialysis is required in case of persistent oliguria
5-Management of metabolic derangement
1.Hypoglycemia needs to be corrected by 10 % D.Only if it is symptomatic it warrants a bolus otherwise in asymptomatic cases maintenance infusion is all that is required.
2.Only symptomatic hypocalcemia needs correction.Evaluate for hypomagnesemia in case of persistent hypocalcemia.
3.Hyponatremia should be anticipated and prevented by restricted fluid administration.
Newer modalities
• Antagonists of excitotoxic neurotransmitter receptors - NMDA receptor blockers
• Free radical inhibitors / scavengers- vitamin E, superoxide dismutase
• Ca channel blockers• Nitric oxide synthetase inhibitors
•Hypothermia
Hypothermia as a Treatment for HIE
• Studies have shown that hypoxic ischemic injury can be reduced by brain cooling.
• Favorable effect on many of the pathways contributing to brain injury– Excitatory amino acids– Cerebral energy state– Cerebral blood flow and metabolism– Nitric oxide production – Apoptosis
Whole Body Hypothermia Selective Head Cooling
OUTCOMEDeath CNS sequelae
Stage I 0% 0%
Stage II 5% 21%
Stage III 75% 100%
Outcome generally good in those who do not reach stage III and spend < 5/7 in stage II
DIFFERENTIAL DIAGNOSISDrug depression - maternal drugs, GA
Prematurity
Trauma - tentorial tear
Anaemia
Neuromuscular disorder
Infection
Inborn error of metabolism - Pyridoxine Dependency
Respiratory tract malformation
Prognosis based on Apgars•Score at 1, 5 minutes does not give prognosis indicator •The longer the score remains lower, the greater its significance•0-3 @ 1min has mortality of 5-10%•may be increased to 53% if at 20min apgars score 0-3 •0-3 @ 5min , CP risk app. 1%•may be increased to 9%if for 15min•dramatic rise to 57% CP risk if for 20min
Predictors of poor neuro-developmental outcome
1. Failure to establish resp. by 5 minutes2. Apgar score of 3 or less at 5 minutes3. Onset of seizures with in 12 hours4. Refractory seizures5. Inability to establish oral feeds by 1 wk6. Abnormal EEG, neuro-imaging
That’s a wrap
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