Birth Asphyxia in Pediatrics in 2024.pptx

Birth Asphyxiation in pediatrics

1. Birth ashyxia kibaru

2. defination Asphyxia is considered in infants with fetal acidosis (pH <7.0) a 5-min Apgar score of 0-3 hypoxic-ischemic encephalopathy (altered tone, depressed level of consciousness, seizures), and other multiorgan system signs

3. It results from 1)Hypoxia refers to an arterial concentration of oxygen that is less than normal, 2) ischemia refers to blood flow to cells or organs that is insufficient to maintain their normal function

4. Hypoxic-ischemic encephalopathy is an important cause of permanent damage to CNS cells that may result in neonatal death or be manifested later as cerebral palsy or mental deficiency.

5. aetiology Hypoxic ischaemic encephalopathy can result from lack of oxygen to vital organs before, during or immediately after birth .

6. A)Fetal hypoxia may be caused by (1) inadequate oxygenation of maternal blood as a result of hypoventilation during anesthesia cyanotic heart disease respiratory failure carbon monoxide poisoning

7. (2) low maternal blood pressure as a result of the hypotension that may complicate spinal anesthesia result from compression of the vena cava and aorta by the gravid uterus

8. (3) inadequate relaxation of the uterus to permit placental filling as a result of uterine tetany caused by the administration of excessive oxytocin (4) premature separation of the placenta (5) impedance to the circulation of blood through the umbilical cord as a result of compression or knotting of the cord .

9. (6) uterine vessel vasoconstriction by cocaine; (7) placental insufficiency from numerous causes, including toxemia and postmaturity

10. After birth, hypoxia may be caused by: (1) anemia severe enough to lower the oxygen content of the blood to a critical level, as after severe hemorrhage or hemolytic disease

11. (2) shock severe enough to interfere with the transport of oxygen to vital organs as a result of overwhelming infection, massive blood loss, and intracranial or adrenal hemorrhage

12. (3) a deficit in arterial oxygen saturation from failure to breathe adequately postnatally because of a cerebral defect, narcosis, or injury

13. 4) failure of oxygenation of an adequate amount of blood as a result of severe forms of cyanotic congenital heart disease or pulmonary disease.

14. Pathophysiology and Pathology Within minutes of the onset of total fetal hypoxia, bradycardia , hypotension, decreased cardiac output, and severe metabolic as well as respiratory acidosis occur. The initial circulatory response of the fetus is increased shunting through the ductus venosus , ductus arteriosus, and foramen ovale

15. transient maintenance of perfusion of the brain, heart, and adrenals in preference to the lungs (because of pulmonary vasoconstriction), liver, kidneys, and intestine.

16. Effects of Asphyxia Central nervous system Hypoxic-ischemic encephalopathy infarction intracranial hemorrhage seizures cerebral edema hypotonia hypertonia

17. Cardiovascular Myocardial ischemia poor contractility tricuspid insufficiency hypotension

18. Pulmonary Pulmonary hypertension pulmonary hemorrhage, respiratory distress syndrome Renal Acute tubular or cortical necrosis Adrenal Adrenal hemorrhage

19. Gastrointestinal Perforation ulceration with hemorrhage necrosis Metabolic Inappropriate secretion of antidiuretic hormone hyponatremia hypoglycemia hypocalcemia integument Subcutaneous fat necrosis

20. Hypoxic-Ischemic Encephalopathy in Term Infants SIGNS STAGE 1 STAGE 2 STAGE 3 Level of consciousness Hyperalert Lethargic Stuporous , coma Muscle tone Normal Hypotonic Flaccid Posture Normal Flexion Decerebrate Tendon reflexes/ clonus Hyperactive Hyperactive Absent Myoclonus Present Present Absent Moro reflex Strong Weak Absent Pupils Mydriasis Miosis Unequal, poor light reflex Seizures None Common Decerebration EEG Normal Low may remain normal 24 hr to 14 dys Days to weeks Outcome Good Variable Death severe deficits

21. DIAGNOSIS. Ultrasound has limited utility in evaluation of hypoxic injury in the term infant it is the preferred modality in evaluation of the preterm infant. CT scans are helpful in identification of focal hemorrhagic lesions, diffuse cortical injury, and damage to the basal ganglia; CT has limited ability to identify cortical injury within the 1st few days of life.

22. MRI is the preferred imaging modality because of its increased sensitivity and specificity early in the process and its ability to outline the topography of the lesion.

23. The initial treatment is effective resuscitation supportive care directed at management of organ system dysfunction. Careful attention to ventilatory status and adequate oxygenation, blood pressure, hemodynamic status, acid-base balance, and possible infection is important.

24. Secondary hypoxia or hypotension due to complications of HIE must be prevented. Aggressive treatment of seizures is critical and may necessitate continuous EEG monitoring

25. Problems during the days after birth Convulsions: Treat with phenobarbital ensure hypoglycaemia is not present (check blood glucose). Apnoea: common after severe birth asphyxia; sometimes associated with convulsions.

26. Inability to suck: Feed with expressed breast milk via a nasogastric tube. Avoid delayed emptying of the stomach, which may lead to regurgitation of feeds. Poor motor tone: fl oppy or with limb stiffening (spasticity

27. prognosis Fifteen to 20% of infants with hypoxic-ischemic encephalopathy die in the neonatal period 25-30% of survivors are left with permanent neurodevelopmental abnormalities (cerebral palsy, mental retardation).

28. The prognosis varies depending on whether the metabolic and cardiopulmonary complications (hypoxia, hypoglycemia, shock) are treated the infant's gestational age (outcome is poorest if the infant is preterm the severity of the encephalopathy

29. Factors asssociated with poor prognosis Severe encephalopathy stage 2 and 3 A low Apgar score at 20 min absence of spontaneous respirations at 20 min of age persistence of abnormal neurologic signs at 2 wk of age MRI and EEG abnormalities

30. Follow-up All survivors of moderate to severe encephalopathy require comprehensive high-risk medical and developmental follow-up.

31. Early identification of neurodevelopmental problems allows prompt referral for developmental, rehabilitative, neurologic care, and early intervention services so that the best possible outcome can be achieved

32. prevention Prevention is critical because no specific therapy can reverse the CNS injury. Death and disability may sometimes be prevented through symptomatic treatment with oxygen or artificial respiration and correction of the associated multiorgan system dysfunction

33. Focused antenatal follow up Better management of labour