Birth asphyxia (asphyxia neonatarum)

1. Birth asphyxia (asphyxia neonatarum)

2. Asphyxiais considered in the presence of fetal acidosis (PH less than 7), a 5-min Apgar score of 0-3, hypoxic-ischemic encephalopathy (altered tone, depressed level of consciousness, seizures), and other multiple organ systems signs. Physiologyof asphyxia: The initial response to hypoxia is an increase in respiratory and heart rates and rise in blood pressure.

3. Then the heart rate and blood pressure begin to fall and respiration cease (primary apnea) which lasting for 30-60 seconds. With out resuscitation, gasping breathing (3-6 cycles/min) then begin, while heart rate and blood pressure gradually decline. Secondary or terminal apnea then occurs with further decline in heart rate and blood pressure. The longer the duration of secondary apnea, the greater the risk for hypoxic organ injury.

4. The major body defense mechanism against hypoxia is by decrease of blood flow to the skin, muscles, kidneys, and GIT and shifting the major blood flow to core organs (heart, brain and adrenal glands). During the period of primary apnea, any physical stimuli (like tactile stimulation to the chest wall) causes the baby to initiate respiration, while infants in secondary apnea required positive pressure ventilation.

5. The first sign of recovery is an increase in the heart rate, followed by an increase in blood pressure with improved perfusion. The time required for rhythmic, spontaneous respiration to occur is related to the duration of secondary apnea.

6. Risk factors for birth asphyxia: 1. Maternal diseases e.g. diabetes, pregnancy- induced hypertension, heart and renal diseases ,and collagen vascular diseases. 2. Fetal conditions: e.g. prematurity, multiple pregnancy, IUGR, and congenital anomalies. 3. Labor and delivery conditions: e.g. fetal distress with or without meconium in the amniotic fluid, and administration of anesthetics and narcotic analgesics.

7. Etiology of asphyxia: A. fetal hypoxia:its result from: 1. Inadequate oxygenation of maternal blood due to hypoventilation during anesthesia, cyanotic heart diseases, respiratory failure or Co poisoning. 2. Maternal hypotension due to spinal anesthesia during labor or as a result from compression of vena cava and aorta by gravid uterus.

8. 3. Inadequate relaxation of the uterus to permit placental filling due to excessive use of oxytocin during labor 4. Premature separation of placenta. 5. Prevention of blood circulation through the umbilical cord due to compression or knotting of the cord. 6. Uterine vessels vasoconstriction by cocaine used by the mother. 7. Placental insufficiency due to pre-eclampsia and postmaturity.

9. B. after birth asphyxia: its result from: 1. Severe anemia due to severe Hge or hemolytic disease. 2. Severe shock due to infections, massive blood loss, intracranial Hge, and adrenal Hge. 3. Inadequate breathing after birth due to cerebral defects, narcosis or injury. 4. Severe hypoxia due to severe cyanotic heart diseases or pulmonary diseases.

10. Clinical manifestations: 1. Yellow, meconium-stained amniotic fluid, umbilical cord and newborn skin. 2. Depressed infant and failed to breath spontaneously after birth. 3. During few hours after birth, infant may remain hypotonic or change from hypotonia to extreme hypertonia or the tone may appear normal. 4. Pallor, cyanosis, apnea, bradycardia, and unresponsiveness to stimulations.

11. 5. Cerebral edema may develop during the next 24hr, causing profound brain stem depression. 6. Seizure which might be severe and refractory to the usual doses of anticonvulsant drugs. **causes of seizure in asphyxiated infants: a. HEI (most common cause). b. Hypocalcaemia. c. Hypoglycemia.

12. **Treatment of hypoxic seizure: a. Phenobarbital, is the drug of choice, given as I.V. loading dose (20mg/kg) additional doses of 10mg/kg(up to 40-50mg/kg total) may be needed, then maintenance dose of 5mg/kg/24hr started after 24hr of loading dose. b. Phenytoin (20mg/kg loading dose), or lorazepam (0.1mg/kg) may be needed for refractory seizures. 7. Multiple organ systems signs of asphyxia.

13. Complications of asphyxia (or multiple organ systems signs of asphyxia): System Effects 1. CNS HIE, intracranial hemorrhage, seizure, cerebral edema, Hypotonia and hypertonia. 2. CVS myocardial infarction, cardiac failure, tricuspid Insufficiency, hypotension 3. Pulmonary pulmonary HT, pulm.Hge, system respiratory distress synd. 4. Renal acute tubular or cortical necrosis, system hematuria

14. 5. Adrenal glands adrenal Hge. 6. GIT perforation, ulceration with Hge. 7. Metabolic IADH secretion, Hyponatremia, hypoglycemia, hypocalcaemia 8. Skin subcutaneous fat necrosis. 9. Hematology DIC

15. Treatment of asphyxia: Treatments are supportive and directed to the organ affected, including: 1. Cardiopulmonary resuscitation. 2. Maintenance of fluid and electrolyte balance (Na, Ca). 3. Maintenance normal blood glucose levels. 4. Treatment of seizures. 5. Symptomatic treatment according to the organ affected

16. Prognosis of asphyxia: Its depend on: 1. If the metabolic and cardiopulmonary complications (hypoxia, hypoglycemia, shock) can be treated or not. 2. Gestational age at birth (out come is poorest in preterm infants) 3. Severity of HIE (The most important). 4. Low Apgar score at 20 min. 5. Absence of spontaneous respirations at 20min age. 6. Persistence of abnormal neurological signs at age of 2 wks.

17. Long term complications of asphyxia: 1. Cerebral palsy. 2. Mental retardation. 3. Epilepsy.

18. Meconium aspiration syndrome Its result from the aspiration of thick meconium particles which pass from the fetus to the amniotic fluid during fetal distress in to the lungs in utero or more often with the 1st breath after delivery.

19. Clinical features: Aspiration of meconium particles causing obstruction of small airways producing respiratory distress within the first hours after birth with tachypnea, retractions, grunting breathing and cyanosis in severely affected infants. Pneumothorax or pneumomediastinum or both may results from partial obstruction of some airways Chest XR shows patchy infiltrates, coarse streaking of both lung fields, increase anteroposterior diameter and flattening of the diaphragm.

23. Prevention: 1. Early detection of fetal distress and rapid delivery in the presence of fetal acidosis, late decelerations or poor beat-to-beat variability. 2. Delee suctioning of the oropharynx after the head is delivered.

24. Treatment: A. mild cases (thin meconium-stained amniotic fluid, no respiratory distress, Apgar score 8 or more) required no treatment. B. Sever cases (thick or pea-soap meconium- stained amniotic fluid, hypotonia, bradycardia, fetal acidosis, or apnea) especially those without Delee suctioning treated with: 1. Endotracheal intubation and suctioning directly through the tube to remove meconium from the airway. 2. Supportive measures and respiratory resuscitation.

25. Congenital diaphragmatic hernia Its herniation of abdominal contents in to the thoracic cavity as a result of congenital defects in the diaphragm.

26. Types: 1. Hiatal D.H.: if the defect at the esophageal hiatus. 2. Paraesophageal D.H: if the defect adjacent to the hiatus. 3. Morgagni D.H: if the defect is retrosternal. 4. Bochdalek D.H (most common type): if the defect is posterolateral at foramen of Bochdalek.

27. Clinical features: 1. Majority of cases presents with sever respiratory distress within first hours of life. 2. Some cases presented beyond neonatal period with repeated vomiting due to intestinal obstruction or with mild respiratory distress 3. Some times, incarcenation of the intestine will proceed to ischemia with sepsis and cardiorespiratory collapse. 4. Unrecognized cases cause sudden death in the infants. 5. Absence of breath sounds and shift of heart sounds to the right side with scaphoid abdomen.

29. Diagnosis: 1. Prenatal diagnosis by fetal ultrasonography. 2. Lateral chest X-R: shows intestinal loope passing through the diaphragm into the thoracic cavity with lung hypoplasia on the same side.

30. 3. Postnatal ultrasonography or injection of contrast media in to stomach or umbilical artery catherization to identify intestine above diaphragm.

31. Treatment: 1. Initial resuscitation with oxygen, ventilation, I.V. fluids, bicarbonate and dopamine to establish adequate cardiopulmonary functions and stabilization of general conditions of infants. 2. Extracorporeal membrane oxygenation (ECMO). 3. Surgical repair of the hernia which should be done as surgical emergency.

32. Thank you for your attention