Birth asphyxia 2

Birth asphyxia 2

1. Birth Asphyxia Dr.Anup John Thomas Assistant Professor Department of Pediatrics MGMC&RI

2. 2010 Guidelines for Neonatal Resuscitation

3. Techniques for Achieving Effective Ventilation (MR. SOPA)

4. NRP Video

5. Neonatal Evaluation and Resuscitation APGAR Scoring A Appearance P Pulse G Grimace A Activity R Respirations Take the APGAR score at one minute and five minutes.

6. APGAR Score

7. APGAR Score 7-10 points - The newborn should be active and vigorous. Provide routine care. 4-6 points - The newborn is moderately depressed. Provide stimulation and oxygen. 0-3 points - The newborn is severely depressed and requires extensive resuscitation.

8. Apgar Score Total Score = 10 score 7-10 normal score 5-6 mild birth asphyxia score 3-4 moderate birth asphyxia score 0-2 severe birth asphyxia

9. Causes of Neonatal Mortality

10. Asphyxia neonatorum is respiratory failure in the new-born, a condition caused by the inadequate intake of oxygen before, during, or just after birth.

11. Definition Birth asphyxia is defined as a reduction of oxygen delivery and an accumulation of carbon dioxide owing to cessation of blood supply to the fetus around the time of birth.

12. ESSENTIAL CRITERIA FOR PERINATAL ASPHYXIA AAP and ACOG Profound metabolic or mixed acidemia (pH< 7.00) in umbilical cord blood Persistence of low Apgar scores less than 3 for more than 5 minutes Signs of neonatal neurologic dysfunction (e.g., seizures, encephalopathy, tone abnormalities) Evidence of multiple organ involvement (such as that of kidneys, lungs, liver, heart and intestine).

13. Etiology Pathologically , any factors which interfere with the circulation between maternal and fetal blood exchange could result in the happens of perinatal asphyxia. These factors can be maternal factor, delivery factor and fetal factor.

14. Etiology—High Risk Factors Maternal factor: hypoxia Anemia Diabetes Hypertension Smoking Nephritis heart disease too old or too young Delivery condition: Abruption of placenta placenta Previa prolapsed cord premature rupture of membranes Fetal factor: Multiple birth congenital or malformed fetus

15. Pathophysiology When fetal asphyxia happens, the body will show a self-defended mechanism which redistribute blood flow to different organs called “inter-organs shunt” in order to prevent some important organs including brain, heart and adrenal from hypoxic damage.

16. PATHOPHYSIOLOGY Hypoxia Diving sea reflex Shunting of blood to brain adrenals & heart Away from lungs, kidney gut & skin NON BRAIN ORGAN INJURY

17. PATHOPHYSIOLOGY Asphyxia continues Shunting within the brain Anterior Circulation Suffers Posterior Circulation Maintained CEREBRAL CORTICAL LESIONS

18. PATHOPHYSIOLOGY Hypoxia – ABRUPT & SEVERE No time for compensation THALAMUS & BRAIN STEM INJURY, CORTEX SPARED

19. Pathophysiology(I) Hypoxic cellular damages: Reversible damage(early stage): Hypoxia may decrease the production of ATP, and result in the cellular functions . But these change can be reversible if hypoxia is reversed in short time.

20. b. Irreversible damage: If hypoxia exist in long time enough, the cellular damage will become irreversible that means even if hypoxia disappear but the cellular damages are not recovers. In other words, the complications will happen.

21. Pathophysiology(II) Asphyxia development: Primary apnea breathing stops but normal muscular tone or hypertonia, tachycardia (quick heart rate), and hypertension Happens early and shortly, self-defended mechanism No damage to organ functions if corrected quickly

22. b. Secondary apnea Features of severe asphyxia or unsuccessful resuscitation, usually result in damage of organs function.

23. PATHOLOGY Target organs of perinatal asphyxia Kidney 50 % Brain 28 % Heart 25 % Lung 23 % Liver, Bowel, Bone marrow < 5%

24. Clinic manifestations Fetal asphyxia fetal heart rate: tachycardia bradycardia fetal movement: increase decrease amniotic fluid: meconium-stained

25. Assessment Fetal heart rate slows Electronic fetal monitoring • persistent late deceleration of any magnitude • persistent severe variable deceleration • prolonged bradycardia • decreased or absent beat-to-beat variability Thick meconium-stained amniotic fluid Fetal scalp blood analysis show pH less than 7.2

26. Effects of Asphyxia Central nervous system intracranial hemorrhage hypoxic-ischemic encephalopathy Cardiovascular Bradycardia Arrhythmia Hypotension myocardial ischemia

27. Effects of Asphyxia Respiratory system Apnea KUB acute tubular necrosis Gastrointestinal tract necrotizing enter colitis

28. Effects of Asphyxia Hematology Disseminated intravascular coagulation Metabolic Hypoglycemia Hyperglycemia Hypocalcemia hyponatremia

29. 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.

30. SPECIFIC MANAGEMENT PREVENT FURTHER BRAIN DAMAGE Maintain temperature, perfusion, oxygenation & ventilation Correct & maintain normal metabolic & acid base milieu Prompt management of complications

31. Management of a neonate with perinatal asphyxia Delivery room care Obtain arterial cord blood for analysis Transfer the infant to NICU if Apgar score 0-3 at 1 minute Prolonged bag and mask ventilation (60 seconds or more ) Chest compression

32. Management of a neonate with perinatal asphyxia NICU care 1 . Maintain normal temperature Avoid Hyperthermia 2. Maintain normal oxygenation and ventilation Maintain saturations between 90% and 95% and avoid any hypoxia or hyperoxia Avoid hypocarbia, as this would reduce the cerebral perfusion Avoid hypercarbia , which can increase intracranial pressure and predispose the baby to intracranial bleed.

33. Management of a neonate with perinatal asphyxia NICU care 3. Maintain normal tissue perfusion Start intravenous fluid Administer dobutamine (preferred) or dopamine to maintain adequate cardiac output, as required. Do not restrict fluid as this practice may predispose the babies to hypo perfusion. Restrict fluid only if there is hyponatremia (Sodium<120 mg%) secondary to syndrome of inappropriate secretion of ADH (SIADH) or if there is renal failure. 4 . Maintain normal hematocrit and metabolic milieu maintain blood glucose levels between 75 mg/dL and 100 mg/dl. Correct Anaemia and maintain haematocrit between 45% and 55%. Check blood gases to detect metabolic acidosis as needed and maintain pH above 7.30. In case of severe asphyxia, provide calcium in a maintenance dose of 4 mL/kg/day (of 10% calcium gluconate )

34. Management of a neonate with perinatal asphyxia NICU care 5. Treat seizures 6 . Nutrition: Start oral feeding once baby is hemodynamically stable 7. Miscellaneous Administer Vitamin K (1 mg IM) to all infants with perinatal asphyxia

35. Role of special investigations Electroencephalography (EEG): The prognosis is likely to be poor if the EEG shows: Long periods of inactivity (more than 10 seconds) Brief period of bursts (less than 6 seconds) with small amplitude bursts Interhemispheric asymmetry and asynchrony Isoelectric and low voltage (less than 5 microvolts) 25 Amplitude-integrated electroencephalography (aEEG ) simplified form and can be performed on continuous basis in NICU. Following abnormalities would indicate poor prognosis: Wide fluctuations in the amplitude with the baseline voltages dropping to near zero Peak amplitudes under 5 mV Seizure spikes

36. Role of special investigations Cranial ultrasound (US) : Cranial US is not good for detecting changes of HIE in the term babies . hypoechoic areas can be seen in very severe cases In preterm babies, periventricular leukomalacia and intraventricular-periventricular haemorrhage. Computed tomography (CT) : CT is more useful after a traumatic delivery and suspected of having an extra-axial haemorrhage Magnetic resonance imaging (MRI) : Abnormalities of thalami and basal ganglia in term infants Abnormalities of white and grey matter in preterm infants Second most common pattern of injury is injury to the watershed regions. MRI is preferred over CT as it has no radiation exposure.

37. Newer modes of therapy 1 . Therapeutic hypothermia 33 C to 34 C in infants of at least 36 wk. moderate to severe encephalopathy initiated within 4- 6 hr continued for 72 hr of age reduce mortality and neuro-morbidity by 18 months of age. selectively cooling the head or the whole body.

38. Newer modes of therapy 2 . Prophylactic phenobarbitone A dose of 40 mg/kg administered prophylactically was associated with a better neuro-developmental outcome at 3 years of age 3. Drugs under investigation A large number of drugs are under investigation for neuro-protection in HIE which need to be used in the early period. blockade of free radical generation (allopurinol, oxypurinol) scavenging of oxidants (superoxide dismutase, glutathione, N-acetyl cysteine and alpha tocopherol) calcium channel blockade (flunarizine, nimodipine) blockage of NMDA receptors (magnesium, MK801, dextromethorphan) blockage of inflammatory mediators (phospholipase A2, indomethacin).

39. PREDICTORS OF POOR NEURO DEVELOPMENTAL OUTCOME Failure to establish respiration by 5 minutes Apgar 3 or less in 5 mts Onset of Seizure in 12 hrs. Refractory convulsion Stage III HIE Inability to establish oral feed by 1 wk. Abnormal EEG & failure to normalize by 7 days of life Abnormal CT, MRI, MR spectroscopy in neonatal period

40. HIE OUTCOME (METAANALYSIS) Severe Moderate Risk of Death Risk of Severe disability 61% 72% 5.6% 20% Mild < 1% < 1%

41. Prognosis Apgar score < 5 at 10 minutes : nearly 50 % death or disability (Leicester ) No spontaneous respiration after 20 min :60 % disability in survivors (USA). No spontaneous respiration after 30 minutes : nearly 100 % disability in survivors (Newcastle).