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High-Risk Neonate & neurodevlopmental outcome


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Lecture given during Port said fifth neonatology conference, 23-24 October 2014 by Dr.Osama Arafa Abd EL Hameed M. B.,B.CH - M.Sc Pediatrics - Ph. D. Consultant Pediatrician & Neonatologist Head of Pediatrics Department - Port-Fouad Hospital

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High-Risk Neonate & neurodevlopmental outcome

  1. 1. High-Risk Neonate & neurodevlopmental outcome By Dr.Osama Arafa Abd EL Hameed M. B.,B.CH - M.Sc Pediatrics - Ph. D. Consultant Pediatrician & Neonatologist Head of Pediatrics Department - Port- Fouad Hospital
  2. 2. GOALS • Perinatal prevention • Resuscitation and stabilization • Evaluate and manage • Monitoring and therapeutic modalities • Family centered care
  3. 3. Predisposing factors • Pregnancy between the age of 15-19yrs • Elderly women • Wrong dates • Multiple pregnancy • Fetal anomalies • Hereditary
  4. 4. Introduction: Definition of High-risk Neonate: Any baby exposed to any condition that make the survival rate of the neonate at danger. Factors that contribute to have a High-risk Neonate: A) High-risk pregnancies: e.g.: Toxemias B) Medical illness of the mother: e.g.: Diabetes Mellitus
  5. 5. C) Complications of labor: e.g.: Premature Rupture Of Membrane (PROM), Obstructed labor, or Caesarian Section (C.S). D) Neonatal factors: e.g.: Neonatal asphyxia
  6. 6. Classification of High Risk Newborns • Gestational Age – Preterm – (Late Preterm) – Term – Postterm • Gestational Age & Birth Weight – SGA – AGA – LGA
  7. 7. Some Definitions: - Low Birth Weight Infant: Is any live born baby weighing 2500 gram or less at birth. (VLBW: <1500 gm, ELBW:<1000 gm). - Preterm: When the infant is born before term. i.e.: before 38 weeks of gestation. - Premature: When the infant is born before 37weeks of gestation.
  8. 8. - Full term: When the infant is born between 38 – 42 weeks of gestation. - Post term: When the infant is born after 42 weeks of gestation.
  9. 9. Identification of some High-risk Neonates: The previous conditions often will result in: Premature birth, Low birth weight infants, or infants suffering from: Hypothermia, Hyperthermia, Hypoglycemia, Infant of Diabetic Mother (IDM), Neonatal Sepsis, Hyperbilirubinemia, and Respiratory Distress Syndrome (RDS).
  10. 10. Physiologic Challenges of the premature infant
  11. 11. Physiologic Challenges of the premature infant • Respiratory and Cardiac • Thermoregulation • Digestive • Renal
  12. 12. Physiologic Challenges of the premature infant • Respiratory and Cardiac – Lack of surfactant – Pulmonary blood vessels – Ductus arteriosus
  14. 14. Definition: It is a condition characterized by lowering of body temperature than 36°C. Types of Hypothermia: It could be classified according to: Causes and according to Severity.
  15. 15. I) According to Causes: 1- Primary Hypothermia: (immediately associated with delivery) In which the normal term infant delivered into a warm environment may drop its rectal temperature by 1 – 2°C shortly after birth and may not achieve a normal stable body temperature until the age of 4 – 8 hours. In low birth weight infants, the decrease of body temperature may be much greater and more rapid unless special precautions are taken immediately after birth. (loss at least 0.25 °C/ min.) (careful dryness).
  16. 16. Situations which contribute to develop Primary Hypothermia: e.g.: Low birth weight infants. 2- Secondary Hypothermia: This occurs due to factors other than those immediately associated with delivery. Important contributory factors are: e.g.: Acute infection especially Septicemia.
  17. 17. II) According to Severity: (1) Mild Hypothermia: When the infant’s body temperature is less than 36°C. (2) Moderate Hypothermia: When the infant’s body temperature is less than 35.5°C. (3) Severe Hypothermia: When the infant’s body temperature is less than 35°C.
  18. 18. *) Clinical Picture: 1- Decrease in body temperature measurement. 2- Cold skin on trunk and extremities. 3- Poor feeding in the form of poor suckling. 4- Shallow respiration. 5- Cyanosis. 6- Decrease activity, e.g.: Weak crying.
  19. 19. The Four modalities by which the infant lost his/ her body temperature: 1- Evaporation: Heat loss that resulted from expenditure of internal thermal energy to convert liquid on an exposed surface to gases, e.g.: amniotic fluid, sweat. Prevention: Carefully dry the infant after delivery or after bathing.
  20. 20. 2- Conduction: Heat loss occurred from direct contact between body surface and cooler solid object. Prevention: Warm all objects before the infant comes into contact with them.
  21. 21. 3- Convection: Heat loss is resulted from exposure of an infant to direct source of air draft. Prevention: · Keep infant out of drafts. · Close one end of heat shield in incubator to reduce velocity of air.
  22. 22. 4- Radiation: It occurred from body surface to relatively distant objects that are cooler than skin temperature.
  24. 24. *) General management: 1- Infant should be warmed quickly by wrapping in a warm towel. 2- Uses extra clothes or blankets to keep the baby warm. 3- If the infant is in incubator, increase the incubator’s temperature. 4- Use hot water bottle (its temperature 50 °C). 5- Food given or even intravenous solution should be warm. 6- Avoid exposure to direct source of air drafts. 7- Check body temperature frequently. 8- Give antibiotic if infection is present.
  26. 26. Definition: It is a condition characterized by an elevation in body temperature more than 38°C. Causes: 1- Disturbance in Heat Regulating Center caused by intracranial hemorrhage, or intracranial edema. 2- Incubator temperature is set too high. 3- Dehydrating fever
  27. 27. *) Management : 1) Undress the infant. If at home; keep light cloths, cover that containing light sheet, Or only a diaper if the infant is inside an incubator. 2) Reduction of incubator temperature. 3) Provide Tepid sponge bath. 4) If available; fill the water mattress with tape water, and keep it in contact with the infant’s skin. 5) Increase fluid intake in the form of 5cc of Glucose 5% between feeds to prevent dehydration.
  28. 28. HYPOGLYCEMIA Untreated hypoglycemia can result in permanent neurological damage or death.
  29. 29. Ideally, neonatal hypoglycemia would be defined as the blood glucose concentration at which intervention should be initiated to avoid significant morbidity, especially neurologic sequelae. However, this definition remains elusive because the blood glucose level and duration of hypoglycemia associated with poor neurodevelopmental outcome has not been established. Neonatal hypoglycemia, defined as a plasma glucose level of less than 30 mg/dL (1.65 mmol/L) in the first 24 hours of life and less than 45 mg/dL (2.5 mmol/L) thereafter
  30. 30. Definition: Neonatal hypoglycemia is usually defined as a serum glucose value of < 40-45 mg/dl. For the preterm infant a value of < 30 mg/dl is considered abnormal (hypoglycemia).
  31. 31. N.B.: The normal plasma glucose concentration in the neonate is approximately 60 to 80 percent of the maternal venous glucose level, or nearly between 70 – 80 mg/dl in neonates of normoglycemic mothers. A steady-state level occurs by approximately three hours after birth.
  32. 32. *) Neonates at risk for developing hypoglycemia: 1- The main cause may become maternal malnutrition during pregnancy which leads to fetal malnutrition and of course a low birth weight. 2- Those infants whom are Small for gestational age infants (SGA), that manifested by decrease in their birth weight and subcutaneous fat and hepatic glycogen. 3- Those infants’ of diabetic mothers (IDM) or those named as large for gestational age (LGA).
  33. 33. 4- Those whom placentas were abnormal, e. g.: placenta previa . 5- Those whom their mothers had toxemia during pregnancy, e. g.: eclampsia or pre-eclampsia induction of labor preterm infant. 6- Those very ill or stressed neonates whom their metabolic needs were increased due to hypothermia, infection, respiratory distress syndrome, or cardiac failure.
  34. 34. Pathophysiology: The fetus receives glucose from the mother continuously across the placenta. As soon as the cord is cut, within 2 hours the normal neonate’s blood glucose level falls from 70 – 80 mg/dl to 50 mg/dl. At this time, hepatic glucose is released into the blood and the serum glucose level returns to its normal level at birth (70 – 80 mg/dl). So, after birth the neonate must kept well nourished because of the newly acquired stressors as; abrupt transition from warm intrauterine environment to a relatively cold extra-uterine one, beginning the respiratory cycles by the neonate own self, muscular activity, and suckling effort to prevent carbohydrates storage consumption and the neonate become at risk for developing hypoglycemia.
  35. 35. Clinical manifestations: 1- Hypotonia. 2- Feeding poorly after feeding well. 3- Tremors. 4- Cyanotic spells. 5- Lethargy. 6- Seizures.
  36. 36. 7- Hypothermia. 8- Irregular respiratory pattern (Apnea). 9- Irritability. 10- High pitched cry followed by weak cry. 11- poor reflexes, especially sucking reflex.
  37. 37. Management of the Neonate at Risk: Prevention: first of all, providing a warm environment. Early enteral feeding is the single most important preventive measure. If enteral feeding is to be started, breast or artificial milk should be used if the infant is able to tolerate nipple or naso-gastric tube feeding.
  38. 38. These infants should have glucose values monitored until they are taking full feedings and have three normal pre-feeding readings above 40-45 mg/dl. Care must be taken to ensure that breast-feeding mothers are providing an adequate intake. If the infant at risk for hypoglycemia is unable to tolerate nipple or tube feeding, maintenance IV therapy with 10% glucose should be initiated and glucose levels monitored.
  39. 39. Management of the Neonate with Hypoglycemia: Infants who develop hypoglycemia should immediately be given 2cc/kg of 10% dextrose over 5 minutes, repeated as needed.
  40. 40. A continuous infusion of 10% glucose at a rate of 8-10 mg/kg/min should be started to keep glucose values normal (NOTE: 10 mg/kg/min of 10%dextrose = 144cc/kg/day). Frequent bedside glucose monitoring is necessary. When feedings are tolerated and frequent bedside glucose monitoring values are normal, the infusion can be tapered gradually.
  41. 41. Infant of Diabetic Mother
  42. 42. Infant of Diabetic Mother
  43. 43. Introduction: Good control of maternal diabetes is the key factor in determining fetal outcome. Recent data indicates that perinatal morbidity and mortality rates in the offspring of women with diabetes mellitus have improved with dietary management and insulin therapy. Infants of diabetic mothers are large plump with plethora faces resembling patients receiving cortisone.
  44. 44. Infant of Diabetic Mother
  45. 45. Pathophysiology: Maternal hyperglycemia fetal hyperglycemia (because the placental barrier passes from 70 – 75% of maternal glucose level to the fetus) fetal hyperinsulinemia which in turn increased glycogen synthesis and storage in the liver and increased fat synthesis weight and size of all infants organs except the brain (Macrocosmic infant). Sudden placental separation and cord clamping interrupts the transplacental glucose supply to the newly born infant without a similar effect on the hyperinsuilinemia (Pancreatic Hyperplasia), this leads to hypoglycemia during the first 2 hours after birth.
  46. 46. Specific Disorders frequently encountered in Infants of Diabetic Mothers (IDM): *) Hypoglycemia. *) Hypocalcemia. *) Hypomagnesemia. *) Cardio-respiratory disorders. *) Hyperbilirubinemia (Unconjugated) *) Birth injuries *) Congenital malformations
  47. 47. Management: I) For the mother: Through good antenatal care for proper control of maternal diabetes.
  48. 48. II) For an infant: All IDMs should receive continuous observation and intensive care. Serum glucose levels should be checked at birth and at half an hour, 1, 2, 4, 8, 12, 24, 36 and 48 hours of age: - If clinically well and normoglycemic; oral or gavage feeding should be started and continued within 2 hours intervals. - If hypoglycemic; give 2 – 4 ml/kg of 10% dextrose over 5 minutes, repeated as needed. A continuous infusion of 10% glucose at a rate of 8-10 mg/kg/min. Start enteral feeding as soon as possible. Give Corticosteroids in persistent hypoglycemia.
  49. 49. Treatment of other complications should also start; oxygen therapy for RDS, calcium gluconate 10% for hypocalcemia, phototherapy for hyperbilirubinemia…………….. etc.
  50. 50. Neonatal Sepsis
  51. 51. Introduction: The newborn infant is uniquely susceptible to acquire infection, whether bacterial, viral or fungal. Bacterial sepsis and meningitis continue to be major causes of morbidity and mortality in the newborn. The mortality rate due to sepsis ranges from 20% to as high as 80% among neonates. Surviving infants can have significant neurologic squeal because of CNS involvement.
  52. 52. Definition: Neonatal sepsis is a disease of neonates (who are younger than one month) in which they are clinically ill and have a positive blood culture.
  53. 53. Risk Factors: I) Maternal risk factors: - e.g.: Premature rupture of membrane. II) Neonatal risk factors: - e.g.: Prematurity (less immunologic ability to resist infection + more liable to penetrate their defensive barriers).
  54. 54. Bacteria can reach the fetus or newborn and cause infection in one of the following ways: • Bacteria can pass through the maternal blood through placenta as rubella, toxoplasma, and syphilis. • Bacteria from the vagina or cervix can enter the uterus, as groups B streptococci. • The newborn may be come contract with bacteria as it passes through the birth canal as gram negative organisms. • The newborn may come in contact with bacteria in its environment after birth (Coagulate positive or negative staphylococci.) • When a susceptible host acquires the pathogenic organism, and the organism proliferates and overcomes the host defense, infection results.
  55. 55. Classification of neonatal sepsis: Neonatal sepsis may be categorized as early or late onset . Newborns with early-onset infection present within 24 hours till 72 hours. Early-onset sepsis is associated with acquisition of microorganisms from the mother during pregnancy (transplacental infection), or during labor (an ascending infection from the cervix).
  56. 56. Late-onset sepsis; occurs beyond the first 72 hours of life (most common after the 3rd day till the 7th day after birth) and is acquired from the care giving environment (Nosocomial infection).
  57. 57. Clinical presentation of neonatal sepsis: Physical findings may be nonspecific and are often subtle. e.g.: apnea , Jaundice , Hypothermia , Bulging or full fontanel , Seizures , hypotonia
  58. 58. Laboratory indicators of sepsis include: - Total leukocytic count (WBC count) - C – reactive Protein (CRP) - Erythrocyte Sedimentation Rate (ESR) - Cultures:
  59. 59. Management of Sepsis: - Prevention: through proper application to infection control practices. - Early onset sepsis; give intrapartum antimicrobial prophylaxis (IAP) to the mother.
  60. 60. - Neonates with clinically suspected sepsis: *) Culture should be obtained first. *) The recommended antibiotics are ampicilin and gentamicin. *) Third generation cephalosporins (Cefotaxime) may replace gentamicin if meningitis is clinically suspected or if gram-negative rods are dominant in the unit. - Late onset neonatal sepsis: Vancomycin in combination with either gentamicin or cephalosporins should be considered in penicillin resistant cases. Note: Administer all medications IV.
  61. 61. Nursing consideration • Prevention • Curative
  62. 62. Prevention 1- Demonstrate the effect of hand washing upon the prevention of the noscomical infections. 2 -Standard precautions should be applied in the nursery for infection prevention. 3- Instillation of antibiotics into newborn’s eye 1-2 hours after birth is done to prevent the infection. 4- Skin car should be done using worm water and may use mild soup for removal of blood or meconium and avoid the removal of vernix caseosa. 5- Cord care should be cared out regularly using alcohol or an antimicrobial agent.
  63. 63. Curative • Encourage breast feeding from the mother. • Adequate fluid and caloric intake should be administered by gavage feeding or intravenous fluid as ordered. • Extra-measure for hypothermia or hyperthermia that may take place to the newborn. • Administering medications as doctor order. • Follow the isolation precautions. • Monitoring intravenous infusion rate and antibiotics are the nurse responsibility.
  64. 64. • Administer the medication in the prescribed dose, route, and time within hour after it is prepared to avoid the loss of drug stability. • Care must be taken in suctioning secretions from the newborn as it may be infected. • . Isolation procedures are implemented according to the isolation protocols of the hospital. • Observe for the complication e.g. meningitis and septic shock. • Encourage in-service programs and continuing education of nurses regarding the infection control precautions.
  65. 65. Hypoxic Ischemic Encephalopathy (HIE)
  66. 66. Grade I HIE: - Alternating periods of lethargy and irritability, hyper-alertness and jitteriness. - Poor feeding. - Exaggerated and/or a spontaneous Moro reflex. - Increased heart rate and dilated pupil. - No seizure activity. - Symptoms resolved in 24 hours.
  67. 67. Grade II HIE: - Lethargy. - Poor feeding, depressed gag reflex. - Hypotonia. - Low heart rate and papillary constriction. - 50-70% of infants display seizures, usually in the first 24 hours after birth. - Oliguria.
  68. 68. ( HIE )
  69. 69. Grade III HIE: - Coma. - Flaccidity. - Absent reflexes. - Pupils fixed, slightly reactive. - Apnea, bradycardia, hypotension. - Oliguria. - Seizures are uncommon.
  70. 70. Management of Hypoxic Ischemic Encephalopathy: - Prevention is the best management. - Primary supportive measures. - Treat seizures: e.g: Phenobarbital
  71. 71. Hyperbilirubinemia
  72. 72. Definition: Hyperbilirubinemia is an elevation in the neonatal serum bilirubin characterized by JAUNDICE, which is defined as “yellowish discoloration of skin and mucous membranes”. In the neonate clinical jaundice is diagnosed if the total serum bilirubin is ≥ 7 mg/dl.
  73. 73. N.B.: The normal adult range of Total Serum Bilirubin is 0.2 – 1 mg/dl (Direct: 0 – 0.2 mg/dl and Indirect: 0.2 – 0.8 mg/dl).
  74. 74. Pathophysiology: = Neonatal Bile Pigment Metabolism. Destruction of RBCs Hemoglobin Salts Water Heme globin (protein portion reused by the body). + O2 Biliverdin
  75. 75. + more O2 Unconjugated Bilirubin + Plasma protein Liver Which released from plasma protein inside the liver and connected with Glucuronic acid and Glucuronyl Transferese Enzyme (in the presence of normal Ph, O2, and normal body temperature) to become Conjugated Bilirubin , that has 3 pathways: Bile duct Kidney Gastrointestinal tract To digest fat. (Urobilin Urobilinogen) (Stercobilin Stercobilinogen) to obtain normal color of urine. to obtain normal color of stool.
  76. 76. The following are possible causes of hyperbilirubinemia in the newly born infants: 1. Over production of bilirubin. 2. Under excretion of bilirubin. 3. Combined over production and under excretion. 4. Physiological jaundice. 5. Breast milk associated jaundice.
  77. 77. Complication: The most common complication of hyperbilirubinemia is Kernicterus (Bilirubin Encephalopathy), which usually occurs when the unconjugated serum bilirubin level exceeds than 20 mg/dl. In small, sick preterm infants, even a bilirubin level in a low range may cause Kernicterus.
  78. 78. Clinical Presentation: Kernicterus progresses through 4 stages: Stage I: Poor Moro reflex, poor feeding, vomiting, high-pitched cry, decreased tone and lethargy. Stage II: Spasticity, seizures, fever. Neonatal mortality is high at this stage (80%). Stage III: A symptomatic (Spasticity decreases and all remaining clinical signs and symptoms may disappear). Stage IV: Appears after the neonatal period. Long-term sequelae can include: spasticity quadriplegia, deafness and mental retardation (for the 20%).
  79. 79. •Management of unconjugated hyperbilirubinemia: ·
  80. 80. •Phototherapy: Nursing care for those infants receiving Phototherapy: 1. Cover the infant’s eyes and genital organs. 2. The infant must be turned frequently to expose all body surface areas to the light. 3. Serum bilirubin level /4 – 12 hours. 4. Each shift, eyes are checked for evidence of discharge or excessive pressure on the lids and eye care should be done using warm water, then apply eye drops or ointment.
  81. 81. 5. Eye cover should be removed during feeding, and this opportunity is taken to provide visual and sensory stimuli. 6. Avoid oily lubricants or lotion on the infant’s exposed skin, because this can act as a barrier that prevent penetration of light through the skin. 7. Increase feeds in volume and calories. Add 20% additional fluid volume to compensate for insensible and intestinal water loss. 8. Intake and output chart.
  82. 82. • Blood exchange transfusion Carry out this technique Beside the Crash Cart.
  83. 83. Neonatal Respiratory Disorders
  84. 84. Common Neonatal Respiratory disorders: · Respiratory distress syndrome (RDS) = Hyaline membrane disease (HMD). · Transient tachypnea of the newborn (TTN). · Meconium aspiration syndrome (MAS). · Apnea.
  85. 85. A) Respiratory distress syndrome (RDS) = Hyaline membrane disease (HMD). Definition: Respiratory distress syndrome is A low level or absence of surfactant system.
  86. 86. Risk factors (High risk group): e.g: Prematurity and low birth weight.
  87. 87. Clinical Presentation: Grade I: (Mild distress): Rapid respiratory rate (tachypnea >60 breaths per minute) + nasal flaring (alae nasai). Grade II: (Moderate distress): GI + intercostals and substernal retractions. Grade III: (Severe distress): GI + GII + expiratory grunting. Grade IV: (Advanced distress): GI + GII + GIII + central cyanosis and disturbed consciousness.
  88. 88. Management of RDS: A) General: * Basic support including thermal regulation and parentral nutrition and medications (antibiotics). * Oxygen administration, preferably heated and humidified B) Specific: Surfactant replacement therapy through ET tube.
  89. 89. B) Transient Tachypnea of the Newborn (TTN). Definition: TTN is a benign disease of near-term or term infants who display respiratory distress shortly after delivery. It occurs when the infant fails to clear the airway of lung fluid or mucus or has excess fluid in the lungs, this limit the amount of alveolar surface available for gas exchange, leading to respiratory rate and depth to better use of the surface available.
  90. 90. Risk factors: · Secondary to hypothermia. · Infant born by Cesarean section, in which the thoracic cavity is not squeezed by the force of vaginal pressure, so that less lung fluid is expelled than normally happen.
  91. 91. Clinical presentation: * The infant is usually near-term or term. * Exhibits tachypnea (> 80 breaths/min) shortly after delivery. * The infant may also display mild grunting, nasal flaring, intercostals retraction, and cyanosis. * Spontaneous improvement of the neonate, which considered as the most important marker of TTN.
  92. 92. Management of TTN: - Oxygenation. - Fluid restriction. - Start feeding as tachypnea improves. Outcome and prognosis: ·Peaks intensity reached at 36 hours of infant’s life. ·The disease is self-limited (respiratory symptoms improve as intrapulmonary fluid is naturally absorbed or artificially mobilized using diuresis). ·No risk of recurrence or further pulmonary dysfunction.
  93. 93. C) Meconium Aspiration Syndrome (MAS). Definition: This respiratory disorder is caused by meconium aspiration by the fetus in utero or by the newborn during labor and delivery. MAS is often a sign that the neonate has suffered asphyxia before or during birth. The mortality rate can be as high as 50% and survivors may suffer long-term sequelae related to neurological damage.
  94. 94. Causes and Pathophysiology: 1. Fetalis hypoxia; e.g. cord prolapse that comes around the neck of the fetus many days before delivery. 2. Babies born breech presentation. In both cases; intrauterine hypoxia Or breech presentation vagal nerve stimulation relaxation of the sphincter muscle releasing of the first stool (meconium) in the intrauterine life and becomes mixed with the amniotic fluid, with the first breath the baby can inhale meconium.
  95. 95. Dangerous of MAS: The aspirated meconium can cause airway obstruction clinical manifestations of RDS, and an intense inflammatory reaction.
  96. 96. Management of MAS: *) Suctioning of the oropharynx by obstetricians before delivery of the shoulders. *) Immediate insertion of an ET tube and tracheal suctioning before ambu bagging (Maintain a neutral thermal environment). *) Gastric lavage, and emptying of the stomach contents to avoid further aspiration.
  97. 97. *) Postural drainage and chest vibration followed by frequent suctioning. *) Pulmonary toilet to remove residual meconuim if intubated. *) Antibiotic coverage (Ampicillin & Gentamicin). *) Oxygenation ( maintain a high saturation > 95%) *) Mechanical ventilation to avoid hypercapnia & respiratory acidosis.
  98. 98. D) Apnea. Definition: Apnea is the cessation of respiration accompanied by bradycardia and/or cyanosis for more than 20 second. Types: 1- Pathological apnea: Apnea within 24 hours of delivery is usually pathological in origin. 2- Physiological apnea: Apnea developing after the first three days of life and not associated with other pathologies, may be classified as apnea of prematurity.
  99. 99. Management of apnea: · Monitor at-risk neonates of less than 32 weeks of gestation. Begin with tactile stimulation ; gentle shaking or prick the sole of the foot often stimulate the infant to breath again.
  100. 100. · If no response to tactile stimulation, bag and mask ventilation should be used during the spell. · Provide CPAP or ventilatory support in recurrent and prolonged apnea. · Pharmacological therapy: - Theophylline. Treat the cause, if identified, e.g., Sepsis, Hypoglycemia, Anemia ………….. etc.
  101. 101. Neonatal Brain Monitoring
  102. 102. Monitoring the neonatal brain Can we do more? More direct monitoring parameters are needed: • Stable and recognizable parameters • Bedside monitoring possible for extended periods of time
  103. 103. Monitoring the brain • Near Infrared Spectroscopy (NIRS) • 1 or 2 channel EEG: aEEG
  104. 104. Near Infrared Spectroscopy (NIRS) • Monitoring technique for cerebral oxygenation and haemodynamics • Based on absorption of near-infrared light by oxygenated [O2Hb] and deoxygenated Hb [HHb] • Absorption-changes in NIR-light (D ODs) can be converted in changes of [DO2Hb] and [DHHb] • Regional (mixed) cerebral O2-saturation: rScO2
  105. 105. Reproducibility is good when used for trend monitoring Menke et al, Biol Neon 2003 Fronto-parietal position (r= 0.88, p <0.01) rScO2-Right (%) rScO2-Left (%) Lemmers et al, Pediatr Res, 2009
  106. 106. 100 90 80 70 60 50 40 30 20 10 0 Interpretation of rScO2 values High values (> +2SD) Avoid if possible!1,2,3 2:02 2:05 2:08 2:11 2:14 2:17 2:20 2:23 2:26 2:29 2:32 2:35 2:38 2:41 2:44 2:47 2:50 2:53 2:56 2:59 3:02 3:05 3:08 3:11 3:14 3:17 3:20 3:23 3:26 3:29 3:32 rScO2 % Expected “normal” values (±2SD) Low values (< -2SD) 1) Hou, Physiol Meas 2007; 2) Kurth, J Cereb Blood Flow Metab 2005; 3) Dent, J Thorac Cardiovasc Surg 2002
  107. 107. aEEG • Filtered (2-15 Hz) • Amplification • Compressed (6 cm/hr) • Semilogarithmic scale • 1 channel (2 parietal leads) • 1 channel for impedance
  108. 108. Continuous Background patterns Burst Suppression Discontinuous Cont. Low Voltage Flat Trace = 10 min Thanks to LdeVries/MToet
  109. 109. Has cerebral monitoring add any additional value in clinical care for the neonate in N.I.C.U
  110. 110. Brain monitoring in clinical practice non invasive monitoring Preterm infants <32 wks Term infants after hypoxic ischemic events Preterm infants <32 wks for 72 h Neonates after perinatal asphyxia
  111. 111. Brain monitoring in clinical practice • Arterial saturation (pulse oxymetry) • Arterial blood pressure • Heart rate • Cerebral oxygenation by NIRS (rScO2) • aEEG
  112. 112. Monitoring the neonatal brain • aEEG and NIRS in clinical practice • Relation with other clinical conditions • Blood pressure • Patent ductus arteriosus • Autoregulatory ability • (Mechanical) ventilation • Surgery
  113. 113. Relation brain monitoring • Blood pressure • Patent ductus arteriosus • Autoregulatory ability • (Mechanical) ventilation • Surgery
  114. 114. Limits of normal blood pressure in neonates • Not well defined • Mostly used definition MABP (mmHg)<GA (wks) • Hypotension is related with brain damage • Hypotension is not directly related to outcome (Dammann 2002; Limperopoulos 2007) • Recent papers show good outcome when accepting lower limits for MABP (Dempsey 2013)
  115. 115. Dopamine 5μg/kg/min $ * $ p<0.05 vs controls; * p<0.05 vs before dopa N=38 Bonestroo et al, Pediatrics 2011 $ N=39
  116. 116. Surgical closure of PDA
  117. 117. Thanks to Toet/ de Vries
  118. 118. Conclusion aEEG should be continued for at least 48 hrs to be able to detect late onset seizure after HI
  119. 119. Suggestion • Brain monitoring by NIRS and aEEG could be a useful approach to judge the need of blood pressure support in infants with low blood pressures
  120. 120. Relation brain monitoring • Blood pressure • Patent ductus arteriosus • Autoregulatory ability • (Mechanical) ventilation • Surgery
  121. 121. Hemodynamically important PDA • Ductal steal phenomenon in cerebral arteries is a risk factor for cerebral damage in the preterm infant (Perlman 1981)
  122. 122. PDA surgery after failure medication * GA 26.7 ±1.8 wks PNA 7 days [4-39] surger y p<0.05 vs pre-clip
  123. 123. Suggestions • Monitoring of rScO2 during surgical ductal closure can prevent surgery-related brain damage • Cerebral oxygenation should play a role in the ultimate decision to close of a hemodynamically important ductus arteriosus
  124. 124. Relation brain monitoring • Blood pressure • Patent ductus arteriosus • Autoregulatory ability • (Mechanical) ventilation • Surgery
  125. 125. Autoregulatory ability rScO2 CCeerreebbrraall bblloooodd ffllooww (corr) (no corr) (corr) MABPBrady, Stroke 2007/2010 CCeerreebbrraall ppeerrffuussiioonn pprreessssuurree Wong, Pediatrics 2008 De Smet Adv Exp Med Biol. 2010 Aciado Ped Res 2011
  126. 126. 200 180 160 140 120 100 80 60 40 20 0 Absence of cerebral autoregulation 0:00:07 0:18:07 HR (b/min) 21:00 21:18 21:36 21:54 22:12 22:30 22:48 23:06 23:24 23:42 0:54:07 1:12:07 1:30:07 1:48:07 2:06:07 2:24:07 2:42:07 3:00:07 3:18:07 3:36:07 3:54:07 4:12:07 0:36:07 4:48:07 4:30:07 5:06:07 5:24:07 5:42:07 Erythrocyt es Thrombo+FF P Dopamine 15 Dobutamine and steroids Dopamine 10 ♂, sepsis, † SaO2 (%) rScO2 (%) MABP (mmHg)
  127. 127. Presence cerebral autoregulation 40 50 60 70 80 90 100 18:01 18:03 18:05 18:07 18:09 18:11 18:13 18:15 18:17 18:19 18:21 18:23 18:25 18:27 18:29 18:31 18:34 18:36 18:38 18:40 18:42 18:44 18:46 18:48 18:50 18:52 18:54 18:56 18:58 19:00 19:02 19:04 19:06 19:08 19:10 19:12 19:14 19:16 19:18 19:20 10 MABP (mmHg) 20 30 40 SaO 50 2 (%) rScO2 (%) ♂, 30 wk 945 g, day 1
  128. 128. Suggestions • Monitoring MABP and rScO2 can, within certain limits, identify infants with absence of autoregulatory ability • Identification of absence of autoregulatory ability may help to prevent brain damage
  129. 129. Relation brain monitoring • Blood pressure • Patent ductus arteriosus • Autoregulatory ability • (Mechanical) ventilation • Surgery
  130. 130. Suggestion • Brain monitoring during (artificial) ventilation can help to prevent hypo/hyper perfusion and hyper/hypoxemia and so brain damage
  131. 131. Relat ion br ain monit or ing Hypotension Patent ductus arteriosus Autoregulatory ability (Mechanical) ventilation Surgery
  132. 132. Neonatal cardiac surgery Low cerebral saturations (<35%-45% ) related with adverse outcome Toet et al Exp Brain Res 2009 Phelps et al 2009 Sood et al J Thorac Cardiovasc surg 2013
  133. 133. Conclusions • The current results of these studies in neonates strongly suggest that SaO2 does not always reflect oxygenation of the neonatal brain. • Thus monitoring of cerebral oxygenation by NIRS and brain function by aEEg in addition to SaO2 and blood pressure, can help to prevent brain damage but also prevent unnecessary treatment.
  134. 134. • The number of infants with (minor) neurodevelopmental problems is high in infants undergoing surgical procedures in neonatal period So • Neurodevelopmental delay needs to be investigated in relation to brain injury : • brain monitoring • (pre-existing) riskfactors • brain injury by neuro-imaging • longterm follow-up • larger cohorts • collaboration between disciplines in hospitals and multi-center
  135. 135. Study design
  136. 136. Neonatal brain damage • Leading to neuro developmental problems • Cerebral palsy • Behaviour/sch ool problems
  137. 137. Thank you