Birth Asphyxia.pptx

Approach to Perinatal and birth asphyxia

1. Birth Asphyxia (PERINATAL ASPHYXIA) Dr. Jwan Ali Ahmed AlSofi

2. Contents Pathophysiology Causes Clinical presentation Treatment Prognosis

3. PERINATAL ASPHYXIA Is a mixture of  hypoxia ,  hypercapnia , and a combination of both respiratory and metabolic  acidosis.

4. Pathophysiology : Asphyxia results in a series of changes in the fetus and newborn , corresponding to changes in the pH of the blood . Interruption in blood flow and oxygen supply will result in the fetus or newborn transitioning to anaerobic respiration , with a resultant buildup of lactic acid , leading to a decrease in the pH of the blood and an acidotic state .

5. Causes of Perinatal Asphyxia

6. CLINICAL MANIFESTATIONS :

7. Signs before delivery:- The signs of hypoxia in the fetus are usually noted a few minutes to a few days before delivery.  IUGR with increased vascular resistance may be the first indication of fetal hypoxia.  The fetal heart rate slows , and the beat-to-beat variability declines. Fetal scalp blood analysis may show a pH less than 7.20. The acidosis is made up of varying degrees of metabolic or respiratory components. 

8. Action These signs should lead to Administration of high concentrations of oxygen to the mother And immediate delivery to avoid fetal death CNS damage .

9. Signs at delivery:- Presence of yellow, meconium-stained amniotic fluid is evidence that there has been fetal distress. Infants are frequently depressed and fail to breath spontaneously . 

10. Signs Few hours after delivery:- The tone change from hypotonia to extreme hypertonia, or may appear normal. Pallor. Cyanosis and apnea . Slow heart rate. Unresponsiveness to stimulation.

11. Clinical Presentation Apnea Vascular redistribution Hypoxic-ischemic brain injury

12. Apnea :- Primary apnea : Primary apnea can result from acidosis secondary to decreased fetal circulation. It is often recoverable with stimulation . It may progress into a period of gasping and, without intervention, may develop into secondary apnea . Secondary apnea : Results after a more prolonged period of decreased oxygenation and will lead to a decreased heart rate, as well as additional cardiovascular compromise if not corrected. Secondary apnea can only be corrected with improved ventilation , usually via positive-pressure ventilation (PPV) through a mask or endotracheal tube. Because after delivery of an infant it is impossible to differentiate between primary apnea and secondary apnea , assume the infant is in secondary apnea and begin resuscitation immediately .

13. The asphyxiated infant passes through a series of events: rapid breathing and fall in heart rate primary apnea irregular gasping, further fall in heart rate and drop in blood pressure secondary apnea Most infants in primary apnea will resume breathing when stimulated . Once in secondary apnea , infants are unresponsive to stimulation .

14. Vascular redistribution:

15. Prolonged intrauterine hypoxia may result in periventricular leukomalacia (PVL ) . Pulmonary arterioles smooth muscle hyperplasia may develop, predisposes the infant to pulmonary hypertension. If fetal distress produces gasping, the amniotic fluid contents (meconium, squamous, lanugo) are aspirated into the trachea or lungs .

16. Hypoxic-ischemic encephalopathy This occurs after a hypoxic or ischemic event resulting in asphyxia, shortly before or at the time of delivery . Is an important cause of permanent damage to central nervous system cells, which may result in: 1 . Neonatal death Or may be manifest later as: 2 . Cerebral palsy 3 . Mental deficiency

17. Hypoxic-ischemic brain injury- Mechanism Primary energy failure Occurs Immediately after the insult , there is a depletion of (ATP),. Results in immediate necrotic cell death , from which the brain metabolism may be able to recover . Necrosis occurs after cellular membrane breakdown (from lack of ATP) results in the leakage of cellular contents, resulting in inflammation and necrotic cell death . Secondary energy failure Occurs if the injury is sufficiently severe, after a brief period of attempted recovery. may occur hours to days after the initial insult (usually, 6–48 hours ). Glutamate, an excitatory amino acid, accumulates in the extracellular space due to increased production, as well as decreased reuptake by damaged cells. This results in an increased Ca2+ influx and activation of degradative enzymes, as well as reactive oxygen species, which lead to delayed, apoptotic cell death .

18. This will lead to Neonatal neurologic abnormalities : hypotonia to extreme hypertonia , or may appear normal . Multiple organ involvement : congestive heart failure, pulmonary hypertension, respiratory distress syndrome, gastrointestinal perforation , acute tubular necrosis hematuria .

19. Definition of hypoxic-ischemic encephalopathy (HIE) due to perinatal asphyxia, as given by the American Academy of Pediatrics (AAP) and American College of Obstetrics and Gynecology (ACOG): Significant metabolic or mixed acidosis in an umbilical arterial sample. pH <7.00 or BE > −12— high-risk fetal compromise Apgar score of <4 for longer than 5 minutes Neonatal neurologic abnormalities Multiple organ involvement Umbilical venous blood—reflects supply from placenta (blood from placenta to fetus ): average pH, 7.20–7.40; Po2, 30 mm Hg; Pco2, 40 mm Hg; base excess (BE) = −3 Umbilical artery blood – reflects condition of fetus (blood returning from fetus to placenta): average pH, 7.15–7.35; Po2, 16 mm Hg; Pco2, 55 mm Hg; BE = −3 Normal values

20. Severe encephalopathy characterized by: Flaccidity Coma Refractory seizures Apnea a marked decrease of cortical attenuation on CT, Is associated with a poor prognosis.

21. Apgar scores This developed to provide a more consistent and objective way to describe the condition of an infant in the delivery room . Can be used to describe the infant’s condition response to delivery room interventions. Scores assigned at 1 and 5 minutes after birth. If the score remains less than 7 at 5 minutes, score should continue to be assigned every 5 minutes until 20 minutes of life . Poor scores have been shown to be associated with increased mortality , but scores are not predictive of long term neurologic outcome .

22. Treatment:

23. Immediate resuscitation of the neonate AIRWAY AND VENTILATION Establishing a patent and secure airway that allows for adequate ventilation is crucial in the successful resuscitation of the neonate because most episodes of bradycardia will respond to improved ventilation . Most infants can be effectively ventilated with a bag and mask device and do not require the placement of an advanced airway, such as a laryngeal mask airway or endotracheal intubation .  Intubation for direct suctioning of meconium below the cords is no longer recommended. Chest compressions should be coordinated with ventilation breaths in a 3:1 (compression-to-breath) ratio. The goal is for 120 events in a 60-second period—that is, 90 compressions and 30 breaths. Indicated when HR remains less than 60 bpm after at least 30 seconds of PPV that inflates the lungs (effective ventilation) Drug used in resuscitation: is epinephrine in 0.1mg/ml concentration ( 1:10000 ), this is the only concentration that should be used in neonatal resuscitation The volume given during resuscitation is 0.1-0.3ml/kg/dose IV or 0.5-1ml/kg /dose via endotracheal tube (0.01–0.03 mg/kg/dose IV or 0.05–0.1 mg/kg/ dose via ETT).

24. Therapeutic cooling Therapeutic head and whole-body cooling have shown improved neurodevelopmental outcomes in infants with moderate to severe encephalopathy at birth . The goal of therapies, such as whole-body cooling, is to prevent the onset or lessen the impact of secondary energy failure by Decreasing cellular metabolism in the brain,So Suppress cell death by decreasing proapoptotic proteins and increasing antiapoptotic proteins and neurotropic factors. Suppress inflammation by decreasing activated microglia and neutrophils, decreasing reactive oxygen species and proinflammatory cytokines Criteria for diagnosis of HIE that qualify neonates for therapeutic cooling include clinical and biochemical components : History of perinatal asphyxia event Evidence of acute acidosis on umbilical artery gas Apgar < 5 at 10 minutes or continued need for mechanical ventilation at 10 minutes after birth. Neurologic criteria Seizure Or evidence of moderate to severe encephalopathy on examination (must have at least three to six components in the moderate to severe category )

25. Prognosis: Depends on whether: It’s metabolic and cardiopulmonary complications (hypoxia, hypoglycemia , shock) can be corrected or not . On the infant's gestational age (outcome is poorest if infant is preterm). And on the severity of the hypoxic-ischemic encephalopathy.     The outcome ranges between normal to severe in the form of cerebral palsy, seizure, deafness.

26. Cases - MCQS

27. At delivery room, the obstetrician informed you about a pregnant woman on delivery, that there is fetal distress . The delivery was by normal vaginal delivery, the neonate was depressed , gasping respiration and APGAR score at first minute was 2 after resuscitation at 5 th minute the APGAR was 5. Describe the clinical diagnosis of the neonate. What are active measures you are going to do for this neonates.

28. Asphyxia Immediate resuscitation

29. A 2 months old infant presented to your office with history of birth asphyxia , family had concern about the future of this infant, he delivered prematurely by 4 weeks, the fetal monitoring result was bad, and decision for cesarean section was late. What other important Question you will ask in regard to explain the prognosis for family? Would you ask for any imaging tools for diagnosis confirmation.   MRI What are important evidences for severe encephalopathy ?

30. Clinical manifestations of fetal hypoxia includes: Normal birth weight Normal beat to beat variation Metabolic acidosis only Increased vascular resistance Answer : d There will be IUGR, acidosis could be metabolic or respiratory or both components and beat to beat variation declines.

31. CASE-1 You are called to the delivery of a 39-week infant, with no known maternal complications of pregnancy. Meco - nium was noted at the time of delivery. You arrive in the delivery room ∼1 minute after birth and find the infant is on a warmer, apneic , and being vigorously stimulated by nursing staff. The HR is noted to be less than 100 bpm. Of the following, which is the most appropriate next step to improve the patient’s heart rate? a. Continue vigorous stimulation of the patient b. Deep-suction the posterior pharynx c. Provide positive-pressure ventilation via bag-mask ventilation d. Intubate the patient e. Obtain umbilical access and administer intravenous epinephrine

32. CASE1 c. This patient is likely in secondary apnea . The appro - priate next step is to provide effective positive-pressure ventilation. Continuous stimulation is unlikely to induce spontaneous respirations and improvement in heart rate in this infant. Deep suctioning may fur- ther exacerbate bradycardia by inducing a vagal nerve stimulatory response. If the patient does not respond to effective bag-mask ventilation, obtaining a more secure airway and administration of epinephrine may become necessary, but not before a period of effective positive-pressure ventilation and chest compressions has been attempted.

33. CASE-2. Based on current evidence and practice guidelines, which of the following describes an infant who would most benefit from therapeutic whole-body cooling? a. 33-week infant born due to maternal preeclampsia, required intubation at birth, Apgar scores—1 at 1 minute, 3 at 5 minutes, 8 at 10 minutes b. 37-week infant born after prolonged shoulder dysto - cia , Apgar scores—1 at 1 minute, 3 at 5 minutes, 8 at 10 minutes—and an arterial cord gas of pH 6.98/ CO2 88 mmHG /PaO2 24 mmHg/ Bicarbonate 20 mmol /L/base excess–17 who at 1 hour of age appears hyperalert , with mildly increased tone, a weak suck, HR of 190 beats/min, and respiratory rate (RR) of 75 breaths/min. c. 39-week infant born after uterine rupture, Apgar scores—1 at 1 minute, 3 at 5 minutes, 8 at 10 minutes—and an arterial cord gas of pH 6.98/CO2 88 mmHG /PaO2 24 mmHg/ Bicarbonate 20 mmol /L/ base excess–17 who at 1 hour of age appears coma- tose , remains intubated, is lethargic, with decreased activity, hypotonia , incomplete Moro reflex and suck, and intermittent spontaneous respirations on the ventilator. d. 37-week infant, now 12 hours old, found in mother’s room to be unresponsive and received CPR with two doses of epinephrine before spontaneous return of cir - culation .

34. case2 c. The infant in choice c presents with signs of moder - ate encephalopathy after a known perinatal hypoxic event and is most likely to have a neurologic benefit from whole-body cooling. The infant in (b) has also experienced a significant hypoxic event at birth but shows signs of only mild encephalopathy on examina - tion and therefore does not meet the criteria for whole- body cooling. The infant in (a) is preterm; cooling in this population has not yet been established to be beneficial. The infant in (d) had an unwitnessed hypoxic event 12 hours after birth; whole-body cooling for neonates who experience this type of arrest is not the standard of care.

35. CASE-3 Which of the following is the preferred dose of epineph - rine to be given during a neonatal resuscitation? a. 0.01-mL/kg/dose of a 1:10,000 solution IV b. 0.5-mL/kg/dose of a 1:1000 solution via ETT c. 0.0-mL/kg/dose of a 0.1-mg/mL solution (1:10,000) IV d. 1-mL/kg/dose of a 1:10,000 solution via ETT

36. Case 3 c. This is the preferred dosage and route of administra - tion for epinephrine during a neonatal resuscitation.

37. 4 Which of the following is an advantage of a self-inflating bag over a T-piece resuscitator? a. It can administer PPV without a source of compressed air or oxygen b. It can provide PEEP when applied continuously to the face c. It provides consistent PIP and PEEP with each breath, with minimal variation between breaths d. It can be used to deliver oxygen concentrations > Fio2 21%

38. 4 4. a. Of the most commonly used devices used in neona - tal resuscitation, the self-inflating bag is the only device that can deliver positive-pressure breaths without being attached to a source of compressed air or flow. A self- inflat - ing bag cannot deliver PEEP unless additional valves or mechanisms are attached to the device, whereas a T-piece resuscitator can. Additionally, the benefit of a T-piece resuscitator is that it will deliver consistent PIP and PEEP to the patient, provided that a good seal is made between the mask and the patient’s face and/or the ETT remains in place. Both devices can deliver PPV with an increased Fio2 concentration if attached to an oxygen source.

39. 5 The hypercapnia, hypoxemia, and acidosis that result from asphyxia will initially cause a redistribution of blood flow to which organs? a. Heart, kidneys, and adrenal glands b. Heart, intestines, and brain c. Heart, brain, and adrenal glands d. Brain, intestines, and kidneys e. Brain, kidneys, and heart

40. 5 c. The hypercapnia, hypoxemia and acidosis that result from asphyxia will initially cause a redistribution of blood flow to the most vital organs, the heart, brain and adrenal glands.

41. 6 Which of the following is a feature of primary energy failure from hypoxic brain injury? a. Occurs 6−48 hours after hypoxic injury b. Necrotic cell death c. Apoptosis d. Decreased glutamate reuptake by damaged cells e. Increases in cerebral ATP stores

42. 6 b. Necrotic cell death occurs after primary energy failure due to depletion of cerebral ATP stores and inactivation of the Na/K membrane pumps. Secondary energy failure occurs 6−48 hours after the initial hypoxic injury and results in decreased glutamate reuptake, which leads to the induction of apoptosis.

43. The END