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Asphyxia neonatorum


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Asphyxia neonatorum

  1. 1. ASPHYXIA NEONATORUM Dr Varsha Atul Shah Senior ConsultantDepartment of Neonatal and Developmental Medicine Singapore General Hospital
  2. 2. ASPHYXIA NEONATORUMDefined as impaired respiratory gas exchangeaccompanied by the development of acidosis
  3. 3. Definition of perinatal asphyxia WHO : 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 asphyxia No breathing or an apgar score of 0-3 at 1 minute of age
  4. 4. 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
  5. 5. CHARACTERSITICS OF PERINATAL ASPHYXIA Profound metabolic acidosis (pH<7.00) Persistence of an Apgar score of 0 to 3 beyond 5 minutes Clinical neurologic sequelae in the immediate neonatal period Evidence 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
  6. 6. 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 ActiveA -Appearance P- Pulse G- Grimace A-Activity R-Respiration
  7. 7. Quiz:At birth, a newborn infant is noted to have the following findings: heartrate – 70/min, respiratory effort – poor and irregular, limp, no reflexirritability, 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
  8. 8. PREDISPOSING FACTORSMaternal Causes Medical conditions eg Pulmonary hypertension Chronic HPT Antenatal conditions eg Abnormal uterine contraction Antepartum haemorrhage Prolapsed cord Malpositions etc
  9. 9. PREDISPOSING FACTORSFetal Causes Multiple pregnancies Big baby with CPD Fetal anomalies - Congenital abnormalities of the lung
  10. 10. PATHOPHYSIOLOGYFetal adaptation to oxygen lack1. 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
  11. 11. PATHOPHYSIOLOGY2. 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
  12. 12. CLINICAL FEATURES Apnoea, bradycardia Altered respiratory pattern - grunting, gasping Cyanosis Pallor-shock Hypotonia Unresponsiveness
  13. 13. 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
  14. 14. 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
  15. 15. PATHOLOGY OF BRAIN DAMAGE Acidosis 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,
  16. 16. 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.
  17. 17. 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 inpremature infants white matter•Four basic and clinically important lesions - Neuronal necrosis, status marmoratus, para-sagittal cerebral injury,periventricular leucomalacia
  18. 18. In hypoxic-ischaemic encephalopathy, as thecerebral edema develops, the brain function isaffected in descending order.
  19. 19. PATHOCLINICAL CORRELATION Full term infant Pathology Clinical Signs• Parasagittal cortical and Spastic quadriplegia subcortical neurosis especially arms Intellectual deficits• Cerebellum Ataxia• Brainstem Pseudobulbar palsy
  20. 20. 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
  21. 21. SEVERITY OF HIE - SARNAT & SARNAT STAGE Stage I Stage II Stage IIIConsciousness Hyperalert Lethargic StuporoseMuscle Tone NAD Mild Hypotonia Flaccid Reflexes active Reflexes active intermittent decerebrationPrimitive Reflexes Present Incomplete Absent sucking weak suck weak or -ve suck -veAutonomic Function Sympathetic Parasympathetic Both depresseddepressed depressedSeizures None Common NoneEEG Normal Seizure, Isopotential background burst mildly abnormal suppression
  22. 22. 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.
  23. 23. 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.
  24. 24. 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 "dolls eye" (i.e., conjugate) movements may be revealed by cranial nerve examination.• Pupils may be dilated, fixed, or poorly reactive to light.
  25. 25. 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,
  26. 26. PREVENTIONRecognition of at risk pregnanciesAntenatal 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 ------------------- normalCo-ordinated care at delivery by paediatrician
  27. 27. MANAGEMENT-Investigations Hx - 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
  28. 28. 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
  29. 29. MANAGEMENT-1BASIC 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.
  30. 30. 1. Management of shock1.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.
  31. 31. 2-MANAGEMENT of Cerebral Oedema• Minimise cerebral edema Ventilation - to prevent apnoea and maintain PC02 of 25 - 30 mmHg Ensure adequate oxygenation Restrict fluid intake Mannitol/frusemide - if urine output is established
  32. 32. 3-Manangement of seizures• 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.
  33. 33. 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
  34. 34. 5-Management of metabolic derangement1.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.
  35. 35. 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
  36. 36. 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
  37. 37. Whole Body Hypothermia Selective Head Cooling
  38. 38. OUTCOME Death CNS sequelaeStage I 0% 0%Stage II 5% 21%Stage III 75% 100%Outcome generally good in those who do not reach stageIII and spend < 5/7 in stage II
  39. 39. DIFFERENTIAL DIAGNOSIS Drug depression - maternal drugs, GA Prematurity Trauma - tentorial tear Anaemia Neuromuscular disorder Infection Inborn error of metabolism - Pyridoxine Dependency Respiratory tract malformation
  40. 40. 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
  41. 41. Predictors of poor neuro-developmental outcome1. 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
  42. 42. That’s a wrap Got questions?