5 Perinatal Asphyxia.pptx9999999999999999999999999999999

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1. Perinatal Asphyxia By Dr. Abu Bakarr Kanu

2. Outline Review of foetal circulation Definition of terms Pathophysiology Risk factors/Causes Assessment Investigations Complications Management Questions & feedback

3. Review of foetal circulation DISCUSSION………………

4. Ductus Venosus Patent Foramen Ductus Arteriosus

5. Definition A condition in the newborn where there is reduced oxygen saturation ( hypoxaemia ) and increased acid in blood ( acidaemia ) from CO 2 retention and lactic acid accumulation . The newborn fails to initiate and sustain breathing after birth . Hypoxic- ischaemic encephalopathy (HIE) – abnormal neurobehavioural state in which the predominant pathogenic mechanism is impaired cerebral blood flow.

6. Risk factors Impairment of maternal oxygenation Decreased blood flow from mother to the placenta Impaired gas exchange across the placenta Decreased blood flow from placenta to the fetus Impaired gas exchange at the fetal tissue level Increased foetal oxygen requirement

7. Aetiology/Predisposing factors 1. Maternal (Prenatal) Factors Infection – chorioamnionitis Lungs – Pneumonia, Asthmatic attack etc. Cardiac – Arrhythmias, heart failure etc. Vascular – Anaemia due to haemoglobinopathy , poor nutrition & leukaemia Diabetes mellitus – due to arteriosclerosis Hypertension - due to arteriosclerosis Hypoperfusion

8. Aetiology/Predisposing factors contd. Uterus Uterine hypertonia Malformations Uterine rupture Others Narcotics – via respiratory depression in mother of direct effect on the baby Anaesthetic agent Alcohol

9. Aetiology/Predisposing factors contd. 2. Placental problems Abruptio placenta Placenta praevia Placental insufficiency   3. Foetal factors Prematurity – affect respiratory centre Postmaturity – due to placental insufficiency Developmental anomalies - Diaphragmatic hernia, Hypolplasia , Choanal atresia Cord problems : Knotting, compression or Prolapse Infection : Congenital

10. Aetiology/Predisposing factors contd. 4. Delivery factors Delayed second stage e.g. prolonged obstructed labour . Placental insufficiency

11. Assessment Done using the APGAR score. APGAR score is assessed at 1 & 5 minutes though it may be extended to assess the extent of resuscitation required. 1 minute: To determine the amount of resuscitation. 5minutes: To prognosticate (especially on brain) If it is low after 5 minutes, the child is likely to have long term sequelae.

12. APGAR SCORE Score 1 2 Appearance/ colour Pale or central cyanosis Peripheral cyanosis Completely pink Pulse rate /Heart rate Absent < 100 b/min > 100b/min Grimace / Irritability None Grimace Cry /sneezing Activity /Muscle tone Flaccid Some flexion Well flexed Respiration Absent Weak irregular Regular Maximal score = 10

13. Practice As the intern oncall in labour ward you were informed that a teenage girl with severe eclampsia just delivered a baby who is limp, gasping, has blue hands and lips and makes no response to stimulation had a HR of 120 beats/min by the 1 st minute of life. You got there by the 5 th minute and noted that the baby was now breathing normally, lips were pink but the nurses said all other findings were as before . What is this baby’s Apgar score at 1&5mins ?

14. GRADING Score Grade Management ≥ 7 Resguires no active resuscitation 6 Mild birth asphyxia Suctioning 4 – 5 Moderate birth asphyxia More suctioning, but avoid vigorous suctioning to avoid vagal reflex Oxygen by face mask, occasionally bag & mask 1 – 3 Severe Birth Asphyxia Clearing of airways Endotracheal intubation & ventilation by bag and mask

15. Investigations Fetal heart rate monitoring Fetal scalp blood pH Cardiotocography –to assess FHR variability Arterial blood gases E/U/Cr ECG Other ancillary investigations as required

16. Complications 1.Central Nervous system Hypoxic IschaemicEncephalopathy (HIE) Seizures Hypotonia Mental retardation Learning disability Speech disorders Cerebral palsy (spastic diplegia, spastic quadriparesis) Syndrome of InappropiateADH secretion (SIADH) Intracranial haemorrhage

17. Spastic Diplegia- Usually seen in preterm infants as a result of the high incidence of IVH & periventricular leukomalacia.

18. Complications (2) Respiratory System Respiratory distress syndrome Persistent pulmonary hypertension Cardiovascular System Left ventricular dysfunction -due to myocardial ischaemia Patent ductus arteriosus Cardiogenic shock

19. Complications(3 ) Renal Acute tubular necrosis –causing haematuria Acute cortical necrosis Haematuria Gastrointestinal Necrotising enterocolitis –due to ischaemia which causes bacterial proliferation Liver dysfunction

20. Complications(4) Haemopoeitic DIC –due to generalized hypoxia Increased risk of infection Metabolic Hypo or hyperglycaemia Hyponatraemia –from renal failure Hypocalcaemia Acidosis

21. Hypoxic Ischaemic Encephalopathy Most feared complication of perinatal asphyxia Impacts on long term neurodevelopmental outcomes It is clinically staged by doing a sequential, systematic evaluation of brain injury Sarnat staging commonly used

22. Level of consciousness Muscle tone Tendon reflexes Seizures Irritable / hyperalert Normal or hypertonia Increased present Absent Suck Moro Grasp Oculocephalic (Doll’s eye) Active Exaggerated Normal to exaggerated Normal Pupils Respirations Heart rate EEG Dilated, reactive Regular Normal or tachycardia Normal Prognosis Good Sarnat staging of hypoxic – ischemic encephalopathy Grade 1 (mild)

23. Level of consciousness Lethargy Muscle tone Hypotonia Tendon reflexes Increased Seizures Present Suck Weak Moro Incomplete Grasp Exaggerated Oculocephalic (Doll’s eye) Overactive Pupils Constricted, reactive Respirations Periodic Heart rate Bradycardia EEG Low – voltage periodic or paroxysmal Prognosis Variable Coma Flaccid Depressed or absent Absent Absent Absent Absent Reduced or absent Variable or fixed Ataxic, apnoeic Bradycardia Periodic or isoelectric High mortality and neurologic disability Grade 2 (moderate) Grade 3 (severe) Sarnat staging of hypoxic – ischemic encephalopathy

24. Management Treatment is supportive Anticipate need for neonatal resuscitation from maternal obstetric and labour history (including CTG tracing) Maintain breathing and circulation Avoid : Hypo-or hyperventilation (keep PaC02 in the normal range) Hypoxemia Hypotension

25. Management contd. Give inotropes for hypotension or myocardial dysfunction Maintain normal blood glucose, calcium and magnesium Correct metabolic acidosis Restrict fluid intake and monitor urine output Control seizures Avoid overheating, re-warm slowly if hypothermic Nutritional support Family support

26. Outcome In general: A normal neurologic exam and feeding well by 2 weeks of age suggest good prognosis. Mild HIE usually normal outcome. Moderate HIE increased risk for motor and cognitive abnormalities, including cerebral palsy. Severe HIE mortality rate 75%. 80 % of survivors will have neurologic sequelae.

27. Poor prognostic features Persistence of clinical seizures Persistently abnormal neurologic exam Not feeding orally by 2 weeks of age EEG with burst suppression or isoelectric pattern on any day Abnormal basal ganglia or marked brain atrophy on MRI Poor postnatal head growth

28. By now we should have………….. Reviewed the foetal circulation Learnt some related terms Listed some risk factors/causes of perinatal asphyxia Learnt the parameters of the APGAR score and its application in perinatal asphyxia

29. THANKS FOR YOUR ATTENTION

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