Birth Asphexia by Dr Iqra Osman Abdulle.pptx

Birth asphexia................................

1. Birth Asphyxia Dr.Iqra Osman

2. Contents Introduction Definition Etiology Pathophysiology HIE Diagnosis Management

3. Perinatal Asphyxia:  There is no universal definition of perinatal asphyxia.  Depending on the setting, different criteria are taken into consideration  Perinatal asphyxia is an insult to the fetus or newborn due to lack of oxygen(hypoxia) or lack of perfusion ( ishchemia ) to various organs.  It is often associated with tissue lactic acidosis and hypercarbia . 2

4. Definition: It refers to a condition during pregnancy and labor in which impaired gas exchange leads to; Hypoxemia, and Hypercarbia . Fetal acidosis, It is evidenced by fetal acidosis as measured in umbilical arterial blood pH <7.0 [ Cloherty and Stark’s Manual of Neonatal Care ; pg .820]

5. National Neonatology Forum (NNF) of India defined perinatal asphyxia as gasping or no breathing at 1 minute or Apgar Score of 4 or less at 1 minute. WHO : Failure to initiate and sustain breathing at birth.

6. Diagnosing Criteria • Prolonged metabolic or mixed academia (pH <7) on an umbilical arterial blood sample • Persistent APGAR score of 0-3 for >5 mins • Neurological manifestations: e.g.- seizure, coma, hypotonia or HIE in the immediate neonatal period • Evidence of multi organ dysfunction in the immediate neonatal period 3 These are the Essential Criteria recommended by the American Academy of Pediatrics

7. Apgar Scoring :

8. Severe  perinatal asphyxia APGAR score at 1 min is 0–3. Mild and moderate  perinatal asphyxia Apgar score at 1 min is 4-7 . International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10 WHO Version 2016), P20 Intrauterine hypoxia, P21 Birth asphyxia .

9. Complications of Perinatal Asphyxia : Immediate Complications: Multi-organ damage May end up with long term sequelae May lead to immediate death Long term sequelae

10. Immediate Complications

11. Long Term Sequelae : Cognitive delay Cerebral palsy Dystonia Seizure disorders Hemiparesis or Quadriparesis/ plegia Visual and auditory processing difficulty

12. HIE :Hypoxic Ischemic Encephalopathy Abnormal neurologic behavior in the neonatal period arising as a result of a hypoxic-ischemic event. It is an important cause of permanent damage to CNS tissues that may result in neonatal death or manifest later as cerebral palsy or developmental delay. It is the term used to designate the clinical and neuropathological findings of an encephalopathy that occurs in a full term infant who has experienced a significant episode of intrapartum asphyxia.

13. HIE: About 20-30% of infants with HIE die in the neonatal period, and ≈ 33-50% of survivors are left with permanent neurodevelopmental abnormalities (cerebral palsy, mental retardation). The greatest risk of adverse outcome is seen in infants with severe fetal acidosis (pH <6.7) (90% death/impairment) and a base deficit >25 mmol/L (72% mortality). Multiorgan failure can occur 10

14. Neurological pattern of HIE: Premature newborns : Selective subcortical neuronal necrosis Periventricular leukomalacia Focal and multifocal ischemic necrosis Periventricular hemorrhage or infarction Term newborns Selective cortical neuronal necrosis (spastic CP) Status marmoratus of basal ganglia and thalamus( choreo-athetoid CP) Parasagittal cerebral injury (spastic quadreperesis ) Focal and multifocal ischemic cerebral necrosis ( hemiparesis, cognitive defect, seizure)

15. Risk Factors: Inadequate oxygena ti o n of maternal blood Low BP Oxytocin- contraction of uterus Maternal Uteroplacental Prem a ture separation Knotting of cord - impedance to the circulation Placental in s uff i ciency Failure of oxygena ti o n Severe an e m i a - b lo o d loss or hemolysis Shock Fetal

16. E t i o l o g y Cardiac arrest Asphyxiation Severe an a p h ylaxis Status epilepticus Hypovole mic shock Placental a b rup t ion Cord prolapse Uterine rupture Hyperstimulation with oxytocic agents F e tom a te r nal hemorrhage Twin to twin transfusion Severe isoimmune hemolytic disease Cardiac arrhythmia Maternal Uteroplacental Fetal

17. Pathophysiology Other organs ( pericardium, pleura, heart, adrenal, meninges etc .) Increased capillary p e r m e ab ili ty Fluid leak and c o n g est i o n C oa g ul at i o n necrosis

18. Pathophysiology: Brain Damage Hypoxia and ischemia Increased lactate and inorganic phosphate Accumulation of cytotoxic product Cerebr a l edema Increased shunting (diving seal reflex)

19. Clinical Manifestations: Asphyxia Intrauterine growth restriction Fetal bradycardia Meconium stained liquor Depressed infant Hypotonic Pallor Cyanosis Apnea Unresponsive to stimulation Seizure due to brain edema in 24hr after birth

20. DIAGNOSIS Perinatal assessment of risk includes awareness of preexisting maternal or fetal problems placental and fetal conditions ascertained by - Ultrasonographic examination, - Biophysical profile and - Non stress tests Umbilical cord or first blood gas determination Serum CK-BB may be increased in asphyxiated newborns within 12 hours of the insult. Others-Protein S-100,NSE and urine markers.

21. D i a g n o s i s MRI is the preferred imaging modality in neonates with HIE CT scans are helpful in identifying focal hemorrhagic lesions, diffuse cortical injury, and damage to the basal ganglia; CT has limited ability to identify cortical injury during the 1st few days of life. Ultrasonography has limited utility in evaluation of hypoxic injury in the term infant; it is the preferred modality in evaluation of the preterm infant. 18

22. A- MRI showing focal neuronal injury; B- Diffuse weighted MRI showing HIE

23. Staging of HIE in term infants: Sarnat & Sarnat Signs Stage 1 Stage 2 Stage 3 Level of consciousness Hyperalert Lethargic Stuprous/coma Muscle tone Normal Hypotonic Flaccid posture Normal Flexion Decerebrate Tendon Reflex Hyperactive Hyperactive Absent Myoclonus Present Present Absent Moro reflex strong weak Absent Pupils Mydriasis Miosis Unequal Seizure None Common Decerebration EEG findings Normal Low voltage Burst suppression Duration <24hr 24hr-14days Days to weeks Outcome Good Variable D e ath/ se v ere deficit

24. Management of HIE Selective cerebral or whole body (systemic ) therapeutic hypothermia reduces mortality or major neurodevelopmental impairment in term and near-term infants with HIE. core temperature of 33.5 o C within the 1st 6 hr after birth Note: Prevent hyperthermia first Phenobarbital, the drug of choice for seizures, is given with an intravenous loading dose (20 mg/kg); additional doses of 5-10 mg/kg (up to 40-50 mg/kg total) may be needed. Phenytoin (20 mg/kg loading dose) or lorazepam (0.1 mg/kg) may be needed for refractory seizures. Additional therapy for infants with HIE includes supportive care directed at management of organ system dysfunction

25. Summary of potential neuroprotective strategies

26. P r o g n o s i s Depends upon the timing and severity of the insult Initial cord or initial blood pH <6.7 have a 90% risk for death or severe neurodevelopmental impairment at 18 month of age Apgar scores of 0-3 at 5 min High base deficit (>20-25 mmol /L) Decerebrate posture Lack of spontaneous activity Increas e d risk for death or imp a irme nt