Lecture 5 - Neonatology - Birth Asphyxia PDF

Summary

This document discusses birth asphyxia, a medical condition of a newborn infant caused by oxygen deprivation. It details definitions, causes, and risk factors related to this medical issue. It is a detailed medical summary, probably from a lecture or presentation.

Full Transcript

Neonatology Dr. Karrar Alibek Lecture:5 (( Birth Asphyxia )) Birth Asphyxia, Neonatal Asphyxia, Asphyxia Neonatorum or Perinatal Asphyxia is the medical condition resulting from deprivation of oxygen to a newborn infant that caus...

Neonatology Dr. Karrar Alibek Lecture:5 (( Birth Asphyxia )) Birth Asphyxia, Neonatal Asphyxia, Asphyxia Neonatorum or Perinatal Asphyxia is the medical condition resulting from deprivation of oxygen to a newborn infant that causes physical harm, mainly to the brain. Definition : Birth Asphyxia may be defined as hypoxic insult to the fetus severe enough to cause metabolic acidosis, neonatal encephalopathy, and multi-organ system dysfunction. It is a pathologic condition referred to a neonate who have no spontaneous breathing or represented irregular breathing movement after birth. Perinatal asphyxia describes a clinical entity whereby the fetus or the newborn infant sustains in impairment of respiratory gas exchange reflecting acute respiratory failure. Anoxia : Complete lack of oxygen in the cells or organ. Hypoxia : Decreased availability of oxygen in the cells or organ. Hypoxemia : Decreased arterial concentration of oxygen. Ischemia : Insufficient blood flow to the cells or organ resulting in interrupted metabolism and death of the cells or organ affected. Incidence : In developing countries: 2/1000 live birth. In developing countries: 10 times greater. Mortality rate:15-20% in the neonatal period , 25% of survivors will have permanent neurologic deficits. In the USA, intrauterine hypoxia & B. asphyxia was listed as the 10th leading cause of neonatal death. Perinatal asphyxia is one of the 3 common causes of U5 MR (11%) following preterm birth (17%) and pneumonia (15%). 1 Prenatal Risk Factors for Asphyxia : 1. Extreme maternal age (35 year) 2. Placental abruption 3. Placenta previa 4. Pre-eclampsia 5. Preterm gestation 6. Post term gestation 7. Meconium stained amniotic fluid 8. Fetal bradycardia 9. Malpresentation and abnormal lie 10. Multiple pregnancy 11. PROM 12. Maternal Diabetes Mellitus 13. Maternal use of drugs Etiology : Pathologically, any factor which interferes with the circulation between maternal and fetal blood exchange could result in the happening of perinatal asphyxia. So these factors could be : A. Antenatal Factors. B. Intranatal Factors. C. Postnatal Factors. A. Antenatal factors : “ Placental insufficiency ” 1. Impaired maternal oxygenation due to anemia, pulmonary or cardiac or neurologic disease in mother. 2. Decreased blood flow from the mother to the placenta due to maternal Infection, shock, dehydration or hypotension. 3. Decreased blood flow from placenta to fetus due to placental abruption, cord prolapse, cord entanglement, true knot, cord compression, or abnormality of the umbilical vessels. 4. Impaired gas exchange across placenta or fetal tissues due to maternal hypertension, vascular disease, Diabetes Mellitus, drug abuse, postmaturity, placental calcification, infarct or fibrosis. 5. Increased fetal oxygen requirement due to fetal anemia, fetal infection, or intra uterine growth retardation. 2 B. Intranatal factors : 1. Inadequate oxygenation of maternal blood due to hypoventilation during anesthesia, cyanotic heart disease, respiratory failure or CO poisoning. 2. Low maternal BP due to acute blood loss, spinal anesthesia, great vessels compression by gravid uterus. 3. Uterine tetany (oxytocin induced). 4. Premature separation of placenta. 5. Compression or knotting of umbilical cord. 6. Placental insufficiency due to toxemia or postmaturity. C. Postnatal factors : 1. Failure of oxygenation due to severe respiratory distress or fetal cyanotic congenital heart disease. 2. Severe anemia due to severe hemorrhage or hemolytic disease. 3. Shock due to sepsis, massive blood loss like intracranial hemorrhage or adrenal Hemorrhage. 4. A deficit in arterial oxygen saturation due to failure of breathing adequately after birth because of a cerebral defect, narcosis or injury. Physiology of Asphyxia : When babies become asphyxiated (either in utero or after delivery), they undergo a well-defined sequence of events, i.e., primary apnea followed by secondary apnea. 3 Primary Apnea : When an infant is deprived of oxygen, an initial brief period of rapid breathing occurs. If the asphyxia continues, the respiratory movements cease, the HR begins to fall, muscle tone gradually diminishes, and the infant enters a period of apnea known as primary apnea. The initial steps will induce breathing. Secondary Apnea : If the asphyxia continues, the infant develops deep gasping respiration, the HR continues to decrease, the BP begins to fall, and the infant becomes nearly flaccid. The respirations become weak and weaker until the infant takes a last gasp and enters a period of apnea called secondary apnea. During secondary apnea the infant does not respond to initial steps. Resuscitation of Newborn Baby : Routine Care :  Provide warmth.  Clear airway, if needed.  Dry.  Initiate Breastfeeding.  Monitor : breathing, heart rate & color. NNR (Neonatal Resuscitation) :  Initial steps.  Assisted ventilation : bag & mask and/or endotracheal intubation.  Chest Compression.  Medication. 4 Apgar Score :  It is an objective method to quickly summarize the health of newborn children.  It is performed on a baby at 1 and 5 minutes after birth.  The 1-minute score determines how well the baby tolerated the birthing process.  The 5-minute score tells how well the baby is doing outside the mother's uterus.  In rare cases, the test will be done 10, 15 and even 20 minutes after birth.  It is developed in 1952 by an American anesthesiologist Virginia Apgar. ((Apgar)) : Appearance, Pulse, Grimace, Activity, and Respiration. Each of these objective signs can receive 0, 1, or 2 points. 5 SIGN SCORE 0 1 2 Color Blue or Pale Pink body with Acrocyanosis Completely Pink Heart Rate Absent < 100 BPM > 100 BPM Reflex Irritability No Response Grimace Cough or Sneeze Muscle Tone Limp Some Flexion Active Movement Respiration Absent Weak, irregular Gasping Strong, regular Active cry Apgar Score Assessment :  7-10 : No depression, Good Health  4 - 6 : Moderate Asphyxia  0 - 3 : Severe Asphyxia Effects of Birth Asphyxia :  Hypoxic damage to most of the infant's organs (heart, lungs, liver, gut, kidneys), but brain damage is of most concern and perhaps the least likely to heal.  In more pronounced cases, an infant will survive, but with damage to the brain manifested as either mental or physical disability, such as developmental delay or intellectual disability, or physical, such as spasticity. CNS : Hypoxic-ischemic encephalopathy, infarction, intracranial hemorrhage, seizures, cerebral edema, hypotonia or hypertonia. CVS : Myocardial ischemia, poor contractility, tricuspid insufficiency or hypotension. Pulmonary : Pulmonary hypertension, pulmonary hemorrhage, RDS. Renal : Acute tubular or cortical necrosis. Adrenal : Adrenal hemorrhage. GIT : Perforation, ulceration with hemorrhage and necrosis. Metabolic : SIADH, hyponatremia, hypoglycemia, hypocalcemia or myoglobinuria. 6 Integument : Subcutaneous fat necrosis. Hematology : DIC.  The most vulnerable organ is the brain because it has a very high requirements for oxygen and basal blood flow. Hypoxic insult to the fetus initiates Mammalian Diving Reflex : Shunting of blood to brain, heart and adrenals and away from lungs, gut, kidneys, liver, spleen and skin, in an attempt to maintain perfusion to more vital organs. Biochemical Changes : A. Hypoxia impairs cerebral oxidative metabolism resulting in : - Increase in lactate. - Fall in pH (acidosis). - Decrease in ATP level. B. Acidosis : - Myocardial Depression - Reduced Cardiac Output. C. Respiratory acidosis may also occur because of the rapid elevation of PaC02. D. Increased production of free radicals and nitric oxide in damaged tissues. 7 Circulatory Response of Fetus : 1. ↑ shunting through Ductus Venosus, Ductus Arteriosus and Foramen Ovale. 2. Transient maintenance of perfusion of the brain, heart, and adrenals in preference to the lungs, liver, kidneys, and intestine 3. Inadequate perfusion of periventricular white matter leading to PVL (periventricular leukomalacia). 4. Hypotension : due to myocardial dysfunction, capillary leak syndrome and hypovolemia. 8 Clinical Manifestation of B. Asphyxia : Before delivery :  Intrauterine growth restriction.  Abnormal heart rate or rhythm.  Increased movements of fetus. At delivery :  Presence of meconium stained amniotic fluid is an evidence of fetal distress.  No spontaneous breathing or breathing with difficulty. After delivery :  The neonate may remain hypotonic or change to hypertonic state.  Pallor, cyanosis, apnea, bradycardia and no response to stimulation.  Cerebral “cytotoxic” edema may develop during the next 24hr and result in profound brainstem depression.  Seizures may occur, it may be refractory to the usual doses of anticonvulsants. American Academy of Pediatrics (AAP) and American College of Obstetricians and Gynecologists (ACOC) criteria for Birth Asphyxia : 1. Profound metabolic or mixed acidemia (pH 20 -25 mmol/l) 4. Decerebrate posture 5. Lack of spontaneous activity  Moderate Encephalopathy : – Mortality : 10 - 30%  Severe Encephalopathy : – Mortality : 60% ; – Disability : 100% Long Term Handicaps :  Developmental Delay  Microcephaly  Cerebral Palsy  Deafness  Seizures  Blindness  Problems with cognition, memory, fine motor skills and behavior 12

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