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  2. 3. Neonatal respiratory distress syndrome ( NRDS ) <ul><li>Infant respiratory distress syndrome ( IRDS ) </li></ul><ul><li>Respiratory distress syndrome of newborn </li></ul><ul><li>Hyaline membrane disease </li></ul>
  3. 4. Introduction <ul><li>A syndrome caused in premature infants by </li></ul><ul><li>developmental insufficiency of surfactant production </li></ul><ul><li>and structural immaturity in the lungs . It can also </li></ul><ul><li>result from a genetic problem with the production of </li></ul><ul><li>surfactant associated proteins. affects RDS about </li></ul><ul><li>1% of newborn infants and is the leading cause of </li></ul><ul><li>death in preterm infants.The incidence decreases </li></ul><ul><li>with advancing gestational age .The syndrome is </li></ul><ul><li>more frequent in infants of diabetic mothers and in </li></ul><ul><li>premature twins. </li></ul>
  4. 5. DEFINITION <ul><li>NRDS is a condition caused by insufficient pulmonary development or alveolar stability.It is a major cause of death in the neonatal period, with characteristic radiographic ,clinical, and physiologic signs that show difficult initiating normal respiration,progressive dyspnea, cyanosis,and respiratory failure developed within hours of life. </li></ul>
  6. 7. About incidence <ul><li>An estimated 30% of all neonatal deaths result from RDS or/and its complications. </li></ul><ul><li>RDS occurs primarily in premature infants; incidence is inversely proportional to the gestational age and birthweight.It occurs in 60-80% of infants less than 28wk of gestational age, in 15-30% of those between 32-36wk , in about 5% beyond 37wk ,and rarely at term. </li></ul>
  7. 8. Table 1 <ul><li>A <28wk(60-80%) </li></ul><ul><li>B 32-36wk(15-30%) </li></ul><ul><li>C >37wk(5%) </li></ul>
  8. 9. Associated factors <ul><li>An increased frequency is associated with infant of </li></ul><ul><li>diabetic mothers </li></ul><ul><li>Prematurity </li></ul><ul><li>Multifetal </li></ul><ul><li>cesarean section </li></ul><ul><li>Asphyxia </li></ul><ul><li>cold stress </li></ul><ul><li>prior affected and etc. </li></ul>
  9. 10. ETIOLOGY AND PATHOPHYSIOLOGY <ul><li>The absence of surfactant </li></ul><ul><li>The failure to develop a </li></ul><ul><li>functional residual capacity </li></ul><ul><li>The tendency of affected </li></ul><ul><li>lungs to become atelectatic correlate </li></ul><ul><li>with high surface tensions </li></ul>
  10. 11. about Surfactant <ul><li>The lungs of infants with respiratory distress syndrome are developmentally deficient in a material called surfactant , which helps prevent collapse of the terminal air- spaces throughout the normal cycle of inhalation and exhalati- on. </li></ul>
  11. 12. about Surfactant <ul><li>Surfactant is a complex system of lipids , proteins and glycoproteins which are produced in specialized lung cells called Type II cells or Type II pneumocytes. The surfactant is packaged by the cell in structures called lamellar bodies , and extruded into the air-spaces. The lamellar bodies then unfold into a complex lining of the air-space. This layer reduces the surface tension . </li></ul>
  12. 13. about Surfactant <ul><li>With progressive gestational age ,increasing amounts of Surfactant are synthesized and stored in type Ⅱ alveolar cells . These active agents are released into the alveoli,reducing the surface tension and maintain alveolar stability by preventing the collapse of small air spaces at end-expiration. </li></ul>
  13. 14. about Surfactant <ul><li>By reducing surface tension, surfactant prevents the air-spaces from completely collapsing on exhalation. In addition, the decreased surface tension allows re-opening of the air-space with a lower amount of force. Therefore, without adequate amounts of surfactant, the air-spaces collapse and are very difficult to expand. </li></ul>
  14. 15. Table 2 (composition)
  15. 16. about Surfactant <ul><li>Surfactant is present in high concentrations in fetal lung homogenates by 20 wk of gestation but does not reach the surface of the lung until later. It appears in the amniotic fluid between 28 and 32 wk. Mature levels of pulmonary surfactant are usually present after 35 wk. </li></ul><ul><li>So the amounts produced or released may be insufficient to meet postnatal demands because of immaturity. </li></ul>
  16. 17. about Surfactant <ul><li>Surfactant synthesis depends in part on normal PH, temperature, and pulmonary perfusion. </li></ul><ul><li>Asphyxia, hypoxemia, and pulmonary ischemia, particularly in association with hypovolemia, hypotention, and cold stress,may supress surfactant synthesis. </li></ul><ul><li>The epithelial lining of the lung may also be injured by high oxygen concentrations , resulting in further reduction in surfactant . </li></ul>
  17. 18. lungs less compliant <ul><li>Alveolar atelectasis </li></ul><ul><li>Hyaline membrane formation </li></ul><ul><li>Interstitial edema </li></ul><ul><li>make the lungs less compliant, requiring greater pressure to expend the small alveoli and airways. </li></ul>
  18. 19. about hyaline membranes <ul><li>Microscopically, a surfactant deficient lung is characterized by collapsed air-spaces alternating with hyper-expanded areas, vascular congestion and, in time, hyaline membranes. Hyaline membranes are composed of fibrin , cellular debris, red blood cells , rare neutrophils and macrophages . They appear as an eosinophilic, amorphous material, lining or filling the air spaces and blocking gas exchange . </li></ul>
  19. 20. about hyaline membranes <ul><li>As a result, blood passing through the lungs is unable to pick up oxygen and unload carbon dioxide. Blood oxygen levels fall and carbon dioxide rises, resulting in rising blood acid levels and hypoxia .. </li></ul>
  20. 21. Structural immaturity <ul><li>Structural immaturity, as manifest by decreased number of gas-exchange units and thicker walls, also contributes to the disease process. </li></ul>
  21. 22. highly compliant chest wall <ul><li>In these infants, the lower chest wall is pulled in as the diaphragm descends and the intrathoracic pressure becomes negative, thus limiting the amount of intrathoracic pressure that can be produced; the result is a tendency for atelectasis to develop. </li></ul><ul><li>The highly compliant chest wall of the premature infant , offers less resistance than that of the mature infant against the natural tendency of the lungs to collapse. </li></ul>
  22. 23. Table 3
  23. 24. Atelectasis <ul><li>Atelectasis resulting in perfused but not ventilated alveoli, which causes hypoxia, decreased lung compliance, small tidal volumes, increased physiologic dead space ,increased work of breathing, and insufficient alveolar ventilation eventually resulting in hypercarbia. </li></ul>
  24. 25. Table 4
  25. 26. Pathology <ul><li>The characteristic pathology seen in babies who die from RDS was the source of the name &quot;hyaline membrane disease&quot;. These waxy-appearing layers line the collapsed tiny air sacs (&quot; alveoli &quot;) of the lung. In addition, the lungs show bleeding, over-distention of airways and damage to the lining cells. </li></ul>
  26. 27. Clinical manifestations <ul><li>This condition usually occurs in premature infants ,with normal crying at birth ,in 6-12 hours, progressive dyspnea can be found . </li></ul>
  27. 28. Clinical manifestations <ul><li>This condition is self-limited ,if the baby can live for three days ,improvement will set in .But many baby with complications such as phneumonia ,the condition will depravation,until infection is restrained. </li></ul>
  28. 29. Clinical manifestations <ul><li>Signs of HMD usually appear within minutes of birth, although they may not be recognized for several hours until rapid, shallow respirations have increased to ≧60/min . Some patients require resuscitation at birth because of intrapartum asphyxia or initial severe respiratory distress . </li></ul>
  29. 30. Clinical manifestations <ul><li>Characteristically, tachypnea , prominent(often audible) grunting, intercostal and subcostal retractions, nasal flaring , and duskiness are seen. There is increasing cyanosis, which is often relatively unresponsive to oxygen administration. Breath sounds may be normal or diminished with a harsh tubular quality, and on deep inspiration, fine rales may be heard, especially over the posteriorly lung bases. </li></ul>
  30. 31. Clinical manifestations <ul><li>The natural course is characterized by progressive worsening of cyanosis and dyspnea. If inadequately treated, blood pressure and body temperature may fall; fatigue, cyanosis , and pallor increase, and grunting decreases or disappears as the condition worsens. Apnea and irregular respirations occur as infants tire. These </li></ul><ul><li>are ominous signs requiring immediate intervention. There may also be a mixed respiratory-metabolic acidosis, edema, ileus, and oliguria. </li></ul>
  31. 32. Clinical manifestations <ul><li>As the disease progresses, the baby may develop ventilatory failure (rising carbon dioxide concentrations in the blood), and prolonged cessations of breathing (&quot; apnea &quot;). </li></ul>
  32. 33. The clinical course <ul><li>Whether treated or not, the clinical course for the acute disease lasts about 2 to 3 days. </li></ul><ul><li>the first , the patient worsens and requires more support. </li></ul><ul><li>the second the baby may be remarkably stable on adequate support and resolution is noted </li></ul><ul><li>the third day, heralded by a prompt diuresis </li></ul>
  33. 34. Clinical manifestations <ul><li>Signs of asphyxia secondary to apnea or partial respiratory failure occur when there is rapid progression of the disease.In many cases the symptoms and signs may reach a peak within 3 days, after which gradual improvement sets in . </li></ul>
  34. 35. Clinical manifestations <ul><li>Improvement is often heralded by a spontaneous diuresis and the ablilty to oxygenate the infant with lower inspired oxygen levels . Death is rare on the 1 st day of illness,but usually occurs between days 2 and 7. </li></ul>
  35. 36. Diagnosis <ul><li>clinical course </li></ul><ul><li>roentgenogram </li></ul><ul><li>blood gas and acid-base </li></ul>
  36. 37. roentgenogramⅠ <ul><li>There may be considerable variation among films, depending on the phase of respiration and the use of CPAP, often resulting in poor correlation between the roentgenograms and clinical course. </li></ul>
  37. 38. roentgenogramⅡ <ul><li>Ⅰ fine reticular granularity of the parenchyma ,the degree of pervious </li></ul><ul><li>to light decrease. </li></ul><ul><li>Ⅱ empty bronchograms beyond </li></ul><ul><li>the cardiac shadow. </li></ul><ul><li>Ⅲ the edge of the cardiac and costal are indeterminate. </li></ul><ul><li>Ⅳ white shadow called “white lung”. </li></ul>
  38. 39. blood gas and acid-base <ul><li>The laboratory findings are characterized initially by hypoxemia and later by progressive hypoxemia, hypercarbia, and variable metabolic acidosis.we can see PH , BE ,CO2CP decline,and sometime Na,K,Cl increase. </li></ul>
  39. 40. DiagnosisⅡ- Foam test <ul><li>Extract amnoitic fluid or bronchial secretion ,mixed with equivalent 95% alcohol,shake for 15 second </li></ul><ul><li>and stay for 15 minutes.Then observe the surface of the liquid. </li></ul><ul><li>If we can see foam </li></ul><ul><li>we can exclude this condition. </li></ul>
  40. 41. Prevention <ul><li>Most cases of hyaline membrane disease can be ameliorated or prevented if mothers who are about to deliver prematurely can be given one of a group of hormones glucocorticoids . This speeds the production of surfactant. </li></ul>
  41. 42. Prevention <ul><li>For very premature deliveries, a glucocorticoid is given without testing the fetal lung maturity. In pregnancies of greater than 30 weeks, the fetal lung maturity may be tested by sampling the amount of surfactant in the amniotic fluid, obtained by inserting a needle through the mother's abdomen and uterus . </li></ul>
  42. 43. Several tests are available <ul><li>lecithin-sphingomyelin ratio </li></ul><ul><li>For assessing fetal lung maturity </li></ul><ul><li>The presence of </li></ul><ul><li>Phosphatidol glycerol ( PG ) </li></ul><ul><li>usually indicates fetal lung maturity </li></ul><ul><li>The S/A ratio </li></ul><ul><li>the result is given as mg of surfactant per gm of protein. An S/A ratio <35 indicates immature lungs, between 35-55 is indeterminate, and >55 indicates mature surfactant production (correlates with an L/S ratio of 2.2 or greater). </li></ul>
  43. 44. lecithin-sphingomyelin ratio <ul><li>Lungs require surfactant , a soapy sort of substance, to lower the surface pressure of the alveoli in the lungs. This is especially important for trying to expand their lungs for that first critical breath after birth. </li></ul><ul><li>Surfactant is a mixture of lipids, proteins, and gly n coproteins . Lecithin and sphingomyeli being two of them. </li></ul>
  44. 45. lecithin-sphingomyelin ratio <ul><li>Lecithin makes the surfactant mixture more effective. An L/S ratio of 2 indicates a relatively low risk of infant respiratory distress syndrome , and less than 1.5 is associated with a high risk of infant respiratory distress syndrome. </li></ul><ul><li>If preterm delivery is necessary and the L/S ratio is low, the mother may need to receive steroids to hasten the fetus's surfactant production . </li></ul>
  45. 46. Prevention <ul><li>prevention of prematurity </li></ul><ul><li>glucocorticoid therapy </li></ul><ul><li>Surfactant therapy </li></ul>
  46. 47. Prevention <ul><li>Most important is the prevention of prematurity , including avoidance of unnecessary poorly-timed cesarean section, appropriate management of the high-risk pregnancy and labor. In timing cesarean sections or inducing labor, estimation of the fetal head circumference by ultrasound and determination of the lecithin concentration in the amniotic fluid should be considered. </li></ul>
  47. 48. prevention of prematurity <ul><li>Preventing prematurity is the most important way to prevent neonatal RDS. Ideally, this effort begins with the first prenatal visit, which should be scheduled as soon as a mother discovers that she is pregnant. </li></ul><ul><li>Good prenatal care results in larger, healthier babies and fewer premature births. </li></ul>
  48. 49. management of the high-risk pregnancy and labor <ul><li>If a mother does go into labor early, a lab test will be done to determine the maturity of the infant's lungs. When possible, labor is usually halted until the test shows that the baby's lungs have matured. This decreases the chances of developing RDS. </li></ul>
  49. 50. treatment of pulmonary immaturity <ul><li>In some cases, medicines called corticosteroids may be given to help . </li></ul><ul><li>It is not clear if additional doses of corticosteroids are safe or effective. </li></ul>
  50. 51. Prevention <ul><li>The administration of dexamethasone or betamethasone to women 48-72 hr before delivery of fetuses at 24 and 34 weeks of gestation significantly reduces the incidence and the mortality and morbidity from HMD. </li></ul><ul><li>It is appropriate to administer these corticosteroids intramuscularly to pregnant women whose lecithin in amniotic fluid indicates fetal lung immaturity and who are likely to deliver in 1 wk or whose labor may be delayed 48 hr or more. </li></ul>
  51. 52. Prevention <ul><li>Prenatal glucocorticoid therapy </li></ul><ul><li>Decreases the severity of RDS </li></ul><ul><li>Reduces the incidence of other complications of prematurity (intraventricular,hemorrhage,patent ductus arteriosus, and pneumothorax). </li></ul>
  52. 53. Prevention <ul><li>Administration of one dose of surfactant into the trachea of premature infants immediately after birth during the first 24 hr of life reduces the mortality from HMD . </li></ul>
  53. 54. Treatment <ul><li>The basic defect requiring treatment is inadequate pulmonary exchange of oxygen and carbon dioxide; </li></ul><ul><li>metabolic acidosis and circulatory insufficiency are secondary manifestations. </li></ul>
  54. 55. Treatment <ul><li>Basic inadequate pulmonary exchange of oxygen and carbon dioxide </li></ul><ul><li>second metabolic acidosis and circulatory insufficiency </li></ul>
  55. 56. Treatment <ul><li>Despite greatly improved RDS treatment in recent years, many controversies still exist. </li></ul>
  56. 57. Treatment <ul><li>Early supportive care of the LBW infant,especially in the treatment of acidosis ,hypoxia, hypotension, and hypothermia, appears to lessen the severity of HMD.Therapy requires careful and frequent monitoring of heart and respiratory rates, arterial PO 2 , PCO 2 , PH, bicarbonate, electrolytes,blood glucose,hematocrit, blood pressure,and temperature. </li></ul>
  57. 58. Treatment <ul><li>Since most cases of HMD are self-limited, the goal of treatment is to minimize abnormal physiologic variations and superimposed iatrogenic problems. The management of these infants is best carried out in a specially in stalled and equipped hospital unit,the neonatal intensive care nursery . </li></ul>
  58. 59. Treatment <ul><li>(1)Supportive care </li></ul><ul><li>(2)Oxygenation and artificial ventilation (3)Surfactant replacement </li></ul><ul><li>(4) Correction of metabolic acidosis </li></ul><ul><li>(5) Symptomatic treatment </li></ul><ul><li>(6) Antibacterial therapy for preventing infections. </li></ul>
  59. 60. Treatment <ul><li>(1)Supportive care </li></ul><ul><li>The general principles for supportive care of any LBW infant shoud be adhered to ,including gentle handling and minimal disturbance consistent with management.To avoid chilling and to educe the metabolic rate, infants should be placed in an Isolette and core temperature maintained between 36.5 to 37℃ . Calories and fluids should be provided intravenously. </li></ul>
  60. 61. Treatment <ul><li>(2)Oxygenation and artificial ventilation Warm humidified oxygen should be provided at a concentration sufficient initially to keep atrerial levels between 55 and 70mm Hg with stable vital signs to maintain normal tissue oxygenation while minimizing the risk of oxygen toxicity. If the atrerial oxygen tension cannot be maintained above 50mm Hg at inspired oxygen concentrations of 70% ,applying CPAP . </li></ul>
  61. 62. oxygen toxicity <ul><li>Infants will be given warm, moist oxygen. This is critically important, but needs to be given carefully to reduce the side effects associated with too much oxygen . </li></ul><ul><li>Injury retina,lead to blindness. </li></ul><ul><li>Lead to bronchopulmonary dysplasia . </li></ul>
  62. 63. CPAP <ul><li>A treatment called continuous positive airway pressure (CPAP) that delivers slightly pressurized air through the nose can help keep the airways open and may prevent the need for a breathing machine for many babies. Even with CPAP, oxygen and pressure will be reduced as soon as possible to prevent side effects associated with excessive oxygen or pressure. </li></ul>
  63. 64. assisted mechanical ventilation <ul><li>Infants with severe HMD or </li></ul><ul><li>those who develop complications </li></ul><ul><li>resulting in persistent apnea </li></ul><ul><li>require assisted mechanical ventilation. </li></ul>
  64. 65. assisted mechanical ventilation <ul><li>A breathing machine can be lifesaving, especially for babies with the following: </li></ul><ul><li>High levels of carbon dioxide in the arteries </li></ul><ul><li>Low blood oxygen in the arteries </li></ul><ul><li>Low blood pH (acidity) </li></ul>
  65. 66. assisted mechanical ventilation <ul><li>There are a number of different types of breathing machines available. However, the devices can damage fragile lung tissues, and breathing machines should be avoided or limited when possible. </li></ul>
  66. 67. assisted mechanical ventilation <ul><li>(1)arterial blood pH of less than 7.20; </li></ul><ul><li>(2)arterial blood Pco2 of 60mm Hg or more; </li></ul><ul><li>(3)arterial blood Po2 of 50mm Hg or less at oxygen concentrations of 70-100%; </li></ul><ul><li>(4)persistent apnea. </li></ul><ul><li>These are reasonable indications </li></ul>
  67. 68. assisted mechanical ventilation <ul><li>. Assisted ventilation by pressure or flow limited conventional respirators through an endotracheal tube including positive end-expiratory pressure(PEEP). </li></ul>
  68. 69. Treatment <ul><li>(3)Surfactant replacement </li></ul><ul><li>Partially synthesized or subtraction from calf lung or amniotic fluids . Surfactant therapy can improve the oxygenation dramatically. </li></ul>
  69. 70. Surfactant replacement <ul><li>Delivering artificial surfactant directly to the infant's lungs can be enormously important, but how much should be given and who should receive it and when is still under investigation </li></ul>
  70. 71. Treatment <ul><li>(4)Correction of metabolic acidosis </li></ul><ul><li>The dosage of sodium bicarbonate should be calculated as follows: </li></ul><ul><li>5% NaHCO3(ml)= CO2CP X BW(kg)X 1.2 </li></ul>
  71. 72. Treatment <ul><li>(5)Symptomatic treatment </li></ul><ul><li>20% manitol in a dosage of 5-10ml/Kg/dose IV to relieve cerebra edema. Furosemide in a dosage of 1-2 mg/Kg/dose to increase urine output. </li></ul><ul><li>Sod. Luminal in a dosage of 5-10mg/Kg/dose to sedate the patient. </li></ul><ul><li>Digoxin ,0.025mg/Kg/dose to correct heart failure. </li></ul><ul><li>Corticotoid to promote the production of the surfactant. </li></ul>Ⅻ
  72. 73. Treatment <ul><li>(6)Antibacterial therapy for preventing infections. </li></ul>
  73. 74. Treatment <ul><li>A variety of other treatments may be used, including: </li></ul><ul><li>Extracorporeal membrane oxygenation (ECMO) to directly put oxygen in the blood if a breathing machine can't be used </li></ul><ul><li>Inhaled nitric oxide to improve oxygen levels </li></ul>
  74. 75. Reduce the infant's oxygen needs <ul><li>It is important that all babies with RDS receive excellent supportive care, including </li></ul><ul><li>Few disturbances </li></ul><ul><li>Gentle handling </li></ul><ul><li>Maintaining ideal body temperature </li></ul>
  75. 76. Nonphysilogic jaundice Pathological jaundice
  76. 77. Incidence and definition <ul><li>Jaundice is observed during the 1 st wk of life in approximately 60% of term infants and 80% of preterm infants.The color usually results from the accumulation in the skin of unconjugated, nonpolar, lipid-soluble bilirubin pigment (indirect-reacting) </li></ul><ul><li>Jaundice with peak serum bilirubin of more than 12 mg/dl for full-term infant or 15 mg/dl for premature is named as nonphysiologic jaundice. </li></ul>
  77. 78. Metabolic features of neonatal bilirubin <ul><li>The newborn infant ’ s metabolism of bilirubin is in transition from the fetal stage, during which the placenta is the principal route of elimination of the lipid-soluble bilirubin,to the adult stage , during which the water-soluble conjugated form is excreted from the hepatic cell into the biliary system and then into the gastrointestinal tract . </li></ul>
  78. 79. Metabolic features of neonatal bilirubin <ul><li>(1) Increased production of bilirubin </li></ul><ul><li>( A )Increased blood cell destructions </li></ul><ul><li>( B )Shortened blood cell life </li></ul><ul><li>(2) Inadequate Y and z protein function </li></ul><ul><li>(3) Glucuronyl transferase deficiency </li></ul><ul><li>(4) Increased enter hepatic circulation of bilirubin </li></ul>
  79. 80. Some explaining <ul><li>The haemoglobin concentration falls rapidly in the first days after birth from heamolysis (1g of heamoglobin yields 35mg of bilirubin) </li></ul><ul><li>The red cell life span of newborn infant(70 days),is markedly shorter than that of adults(120 days). </li></ul><ul><li>Hepatic bilirubin metabolism is less efficient in the first days of life. </li></ul>
  80. 81. Etiology <ul><li>Unconjugated hyperbilirubinemia may be caused or increased by any factor that (1) increases the load of bilirubin to be metabolized by the liver (hemolytic anemias, shortened red cell life due to immaturity or to transfused cells, increased enterohepatic circulation, infection); (2) may damage or reduce the activity of the transferase enzyme(hypoxia, infection, possibly hypothermia and thyroid deficiency); (3) may compete for or block the transferase enzyme (drugs and other substances requiring glucuronic acid conjugation for excretion);or (4) leads to an absence of or decreased amounts of the enzyme or to reduction of bilirubin uptake by the liver cell (genetic defect,prematurity) </li></ul>
  81. 82. EtiologyⅡ <ul><li>The risk of toxic effects from elevated levels of unconjugated bilirubin in the serum is increased by factors that reduce the retention of bilirubin in the circulation , or by factors that increase the permeability of the blood-brain barrier or nerve cell membanes to bilirubin or the susceptibility of brain cells to its toxicity such as asphyxia, prematurity, and infection. </li></ul>
  82. 83. Clinical ManifestationⅠ <ul><li>Jaundice may be present at birth or may appear at any time during the neonatal period , depending on the condition responsible for it. Jaundice usually begins on the face and, as the serum level increases, progresses to the abdomen and then the feet. </li></ul>
  83. 84. Clinical ManifestationⅡ <ul><li>.A serum bilirubin level is determined for those patients with progressing jaundice, symptoms, or a risk for hemolysis or sepsis. </li></ul>
  84. 85. Color <ul><li>Jaundice resulting from deposition of indirect bilirubin in the skin tends to appear bright yellow or orange </li></ul><ul><li>jaundice of the obstructive type(direct bilirubin), a greenish or muddy yellow </li></ul><ul><li>This difference is usually apparent only in severe jaundice. The infant may be lethargic and may feed poorly. </li></ul>
  85. 86. Differential Diagnosis Ⅰ <ul><li>1. PHYSIOLOGIC JAUNDICE </li></ul><ul><li>2. JAUNDICE ASSOCIATED WITH BREAST-FEEDING </li></ul><ul><li>3 OBSTRUCTIVE JAUNDICE </li></ul><ul><li>4. KERNICTERUS </li></ul>
  86. 87. PHYSIOLOGIC JAUNDICEⅰ <ul><li>Definition : Under normal circumstances, the level of indirect-reacting bilirubin in umbilical cord serum is 1-3 mg/dL and rises at a rate of less than 5 mg/dL/24 hr ; thus,jaundice becomes visible on the 2 nd -3 rd day, usually peaking between the 2 nd -4 th days at 5-6 mg/dL and decreasing to below the 2 mg/dL between the 5 th and 7 th days of life . </li></ul>
  87. 88. PHYSIOLOGIC JAUNDICEⅱ <ul><li>Jaundice associated with these changes is designated “ physiologic” and is believed to be the result of increased bilirubin production following breakdown of fetal red blood cells combined with transient limitation in the conjugation of bilirubin by the liver. </li></ul>
  88. 89. PHYSIOLOGIC JAUNDICEⅲ <ul><li>The diagnosis of physiologic jaundice in term or preterm infants can be established only by excluding known causes of jaundice on the basis of the history and clinical and laboratory findings . </li></ul>
  89. 90. PHYSIOLOGIC JAUNDICEⅳ <ul><li>In general,a search to determine the cause of jaundce should be made if </li></ul><ul><li>(1) it appears in the first 24 hr of life; </li></ul><ul><li>(2) serum bilirubin is rising at a rate greater than 5 mg/dL ; </li></ul><ul><li>(3) serum bilirubin is greater than 12 mg/dl in full-term or 10-15 mg/dL in preterm infants; </li></ul><ul><li>(4) jaundice persists after the 2 nd wk of life; </li></ul><ul><li>(5) direct-reacting bilirubin is greater than 1 mg/dL ; at any time. </li></ul><ul><li>(6) appears again after disappeared. </li></ul>
  90. 91. JAUNDICE ASSOCIATED WITH BREAST-FEEDINGⅰ <ul><li>An estamated 1 of 200 breast-fed term infants develops significant elevations in unconjugated bilirubin between 4 th and 7 th days of life ,reaching maximum concentrations as high as 10-30 mg/dl during the 2 nd -3 rd wk.if breast-feeding is continued,the serum bilirubin gradually decreases and then may persist for 3-10wkat lower levels. </li></ul>
  91. 92. JAUNDICE ASSOCIATED WITH BREAST-FEEDINGⅱ <ul><li>If breast-feeding is discontinued,the serum bilirubin level falls rapidly,usually reaching the normal levels within a few days. </li></ul><ul><li>Cessation of breast-feeding for 1-2 days and substitutions of formula for breast milk results in a rapid decline in serum bilirubin,after which nursing can be resumed without a return of the hyperbilirubinimia to its previously high levels. </li></ul>
  92. 93. OBSTRUCTIVE JAUNDICE <ul><li>COLOUR </li></ul><ul><li>SKIN: greenish or muddy yellow </li></ul><ul><li>URINE: deep yellow </li></ul><ul><li>STOOL: pale </li></ul><ul><li>for an example: congenital biliary atresia </li></ul>
  93. 94. Kernicterus ⅰ <ul><li>Definition </li></ul><ul><li>Kernicterus is a neurologic syndrome resulting from the deposition of uncojugated bilirubin in brain cells. </li></ul>
  94. 95. Kernicterusⅱ <ul><li>Lipid-soluble indirect bilirubin may cross the blood-brain barrier and enter the brain by diffusion if the bilirubin-binding capacity of albumin and other plasma proteins is exceeded and plasma free bilirubin levels increase. Alternatively, bilirubin may enter the brain following damage to the blood-brain barrier by asphyxia or hyperosmolatity. </li></ul>
  95. 96. Kernicterus ⅲ <ul><li>The precise blood level above which indirect-reacting bilirubin or free bilirubin will be toxic for an individual infant is unpredictable, but kernicterus is rare in healthy term infants and in the absence of hemolysis if the serum level is under 25mg/dL. There is little evidence to suggest that the level of indirect bilirubin affects the IQ of healthy term infants without hemolytic disease. </li></ul>
  96. 97. Kernicterusⅳ <ul><li>Nonetheless the less mature the infant, the greater the susceptibility to kernicterus . Factors that potentiate the movement of bilirubin into brain cells and its adverse effects on them are discussed in the last class n. In exceptional circumstances, kernicterus in VLBW infants with serum bilirubin concentrations as low as 8-12 mg/dL has been associated with an apparentlly cumulative effect of a number of these factors. </li></ul>
  97. 98. Kernicterus ⅴ <ul><li>CLINICAL MANIFESTATIONS . Signs and symptoms of kernicterus usually appear 2-5 days after birth in term infants and as late as the 7 th day in premature ones, but hyperbilirubinemia may lead to the syndrome at any time during the neonatal period . </li></ul>
  98. 99. Kernicterus ⅵ <ul><li>The early signs may be subtle and indistinguishable from those of sepsis, asphyxia, hypoglycemia, intracranial hemorrhage, and other acute systemic illnesses in the neonatal infant. Lethargy, poor feeding, and loss of the Moro reflex are common initial signs. </li></ul>
  99. 100. Kernicterusⅶ <ul><li>Subsequently, the infant may appear gravely ill and prostrated with diminished tendon reflexes and respiratory distress. Opisthotonos, with bulging fontanel, twitching of face or limbs, and a shrill high-pitched cry may follow. In advanced cases convulsions and spasm occur, with the infant stiffly extending his or her arms in inward rotation with fists clenched. Rigidity is rare at this late stage. </li></ul>
  100. 101. Kernicterusⅷ <ul><li>Many infants who progress to these severe neurologic signs die; the survivors are usually seriously damaged but may appear to recover and for 2-3 mo manifest few abnormalities. Later in the 1 st yr of life opisthotonos, muscular rigidity, irregular movements, and convulsions tend to recur. In the 2 nd yr opisthotonos and seizures abate but irregular, involuntary movements, muscular rigidty, or, in some infants, hypotonia increase steadily. </li></ul>ⅷ
  101. 102. Kernicterus ⅸ <ul><li>By 2 yr of age the complete neurologic syndrome is often apparent, consisting of bilateral choreoathetosis with involuntary muscle spasm, extrapyramidal signs, seizures, mental deficiency, dysarthric speech, high-frequency hearing loss, squints, and defective upward movement of the eyes. Pyramidal signs, hypotonia, and ataxia occur in a few infants. </li></ul>
  102. 103. Kernicteruⅹ <ul><li>In mildly affected infants the syndrome may be characterized only by mild to moderate neuromuscular incoordination, partial deafness, or “minimal brain dysfunction,” occurring singly or in combination; these problems may be inapparent until the child enters school. </li></ul>
  103. 104. Kernicterⅹⅰ <ul><li>PATHOLOGY. The surface of the brain is usually pale yellow. On cutting, certain regions are characteristically stained yellow by unconjugated bilirubin, particularly the corpus subthalamicum, hippocampus and adjacent olfactory areas, striate bodies, thalamus, globus pallidus, putamen, inferior clivus, cerebellar nuclei, and cranial nerve nuclei. </li></ul>
  104. 105. Kernicterⅹⅱ <ul><li>INCIDENCE AND PROGNOSES . Using pathologic criteria, one third of infants (all gestational ages) with untreated hemolytic disease and bilirubin levels in excess of 20 mg/dL will develop kernicterus. The incidence at autopsy in hyperbilirubinemic premature infants is 2-16% . </li></ul><ul><li>Reliable estimates of the freqency of the clinical syndrome are not available because of the wide spectrum of manifestations. </li></ul>
  105. 106. Kernicterⅹⅲ <ul><li>Overt neurologic signs have a grave prognosis; 75% or more of such infants die,and 80% of affected survivors have bilateral choreoathetosis with involuntary muscle spasm. Mental retardation, deafness, and spastic quadriplegia are common. </li></ul>
  106. 107. Treatment TreatmentⅧ <ul><li>Feeding </li></ul><ul><li>Correct acidosis and replenish glucose </li></ul><ul><li>Phototherapy </li></ul><ul><li>Chinese herbal medicine </li></ul><ul><li>Enzyme inducer </li></ul><ul><li>Blood plasma or albumin </li></ul>
  107. 108. Correct acidosis and replenish glucose <ul><li>They can help bilirubin transporting and combining in the liver. </li></ul>
  108. 109. Phototherapy <ul><li>Indication:TB>12 to 15 mg/dl </li></ul><ul><li>Colour: blue </li></ul><ul><li>Wave length:420to 470 nm </li></ul><ul><li>Distance: 50cm </li></ul>
  109. 110. Feeding <ul><li>It can reduce the amount of unconjugated bilirubin produced by enterohepatic circulation . </li></ul>
  110. 111. Chinese herbal medicine <ul><li>Yinchen 1.5g </li></ul><ul><li>Gancao 1.5g </li></ul><ul><li>Zhidahuang 3g </li></ul><ul><li>Huangqin 9g </li></ul><ul><li>One dose daily,continue to 3-5 days . </li></ul>
  111. 112. Blood plasma or albumin <ul><li>Offering the albumin to combine bilirubin to reduce the free unconjugated bilirubin. </li></ul>
  112. 113. Enzyme inducer <ul><li>Both phenobarbital and nikethamide can induce the activity of glucuronly </li></ul><ul><li>transferase in the smooth endoplasmic reticulum of hepatocyte,speeding its combining with unconjugated bilirubin. </li></ul>
  113. 114. Adrenl cortica hormone <ul><li>It can restrain the antigenantibody reaction ,reduce hemolisis, and promote the cell enzyme system. </li></ul>
  114. 115. Scleredema neonatorum <ul><li>Scleredema is a syndrom ,caused primarily by cold injury,usually occurs in cold season, so we sometime call it cold injury syndrom.on the other hand ,it is associated with agents such as prematurity,axphysia,infection and so on.For an example, it can occur in the durition of severe septicaemia. </li></ul>
  115. 116. Defition <ul><li>Scleredema neonatorum is a disorder of adipose tissue that occurs primarily in preterm.Infections,asphysia and cold injury may also be the etiologic is one of the major cause of death in neonatal period in china . </li></ul><ul><li>It’s clinical character:adipose tissue sclerosis and edema. </li></ul>
  116. 117. Etiology <ul><li>External agent </li></ul><ul><li>Internal agent </li></ul>
  117. 118. External agents <ul><li>Cold injury </li></ul><ul><li>Intake absence </li></ul><ul><li>disease </li></ul>
  118. 119. Cold injury
  119. 120. Intake absence
  120. 121. Disease <ul><li>Pneumonia </li></ul><ul><li>Septicaemia </li></ul><ul><li>Asphysia and so on </li></ul>
  121. 122. Internal agents <ul><li>When body temperature is lower than 35℃ ,we call hypothermia .After born ,the environmental temperature is much lower than in utroe for the infant .so hypothermia may occur. </li></ul>
  122. 123.    Etiology <ul><li>Deficiency of enzyme </li></ul><ul><li>decreased response to cold stress </li></ul><ul><li>more susceptible to heat loss </li></ul><ul><li>immature thermotaxic center </li></ul>
  123. 124. Deficiency of enzyme <ul><li>  Deficiency of enzyme which converts saturated to unsatured fatty acid in neonatal period. The thawing point of the former is higher and is easy to be coagulated when it is exposed to cold. </li></ul>Ⅰ
  124. 125. decreased response to cold stress <ul><li>  All newborns have decreased response to cold stress. Newborns do not have a capacity to shiver (increase muscle activity to generate heat).they rely on non-shivering thermogenisis (brown fat), brown fat is important origin of heat when exposed to cold stress. Prematures have relatively small amount of brown fat, and asphyxiated or Infectious infants is likely to be involved, that is because of hypoxic acidosis, shock which leads to chemical heat production inhibited. </li></ul>
  125. 126. more susceptible to heat loss <ul><li>  they have smaller subcutaneous store of isolating fat, a smaller mass-to-body surface ratio, enhancing heat loss, a more open and exposed resting posture allowing more surface convective and radiate losses and an immature temperature mechanism. </li></ul>
  126. 127. immature thermotaxic center <ul><li>  The immature thermotaxic center of premature is the another etiological factor of scleredema. </li></ul>
  127. 128. Clinical manifestions <ul><li>History </li></ul><ul><li>Symptom </li></ul>
  128. 129. History <ul><li>Cold season </li></ul><ul><li>Prematurity </li></ul><ul><li>Asphysia </li></ul><ul><li>Infection </li></ul><ul><li>Intake absence and so on </li></ul>
  129. 130. Symptom <ul><li>Typical symptoms:apathy, refusal of feeding, no crying, hypothermia, not doing well, immobility, sclerosis edema of the adipose tissue and redness of the skin. </li></ul>
  130. 131. <ul><li>  Dyspnea, oliguria , acidosis and cardiovascular injury are common in some patient. Pulmonary hemorrhage is the fatal complication of scleredema. Shock and DIC can be found in severe case. </li></ul>
  131. 132. symptom <ul><li>Turns: legs breech face upper limbs trunk </li></ul><ul><li>Temperature: 29℃ 35 ℃ </li></ul><ul><li>Color :redness achromachia </li></ul><ul><li>and cyanosis </li></ul>
  132. 133. Hardness degree <ul><li>A.      Patient with mild scleredema showed subcutaneous tissues with a little decreased elasticity and a negative pitting edema. </li></ul><ul><li>B.       Moderate scleredema showed subcutaneous tissues with pitting edema but elasticity. </li></ul><ul><li>C.      Severe scleredema showed rubber-like subcutaneous tissues in association with compromised joint mobility. </li></ul>
  133. 134. Degree
  134. 135. Tretment <ul><li>Preventive measures </li></ul><ul><li>Rewarming </li></ul><ul><li>Nursing </li></ul><ul><li>Fluid therapy </li></ul><ul><li>drugs </li></ul>
  135. 136. Preventive measures <ul><li>Keeping the body out off draft, keeping the body warm and improving perinatal care of mother to premature delivery. </li></ul>
  136. 137. Nursing care <ul><li>Meeting the caloric needs is the most important, initial needs being 50 cal/Kg/day , gradually increase the caloric supply after normal temperature reached (100-120 </li></ul><ul><li>kcal/kg/day). </li></ul>
  137. 138. Fluid therapy <ul><li>10% Glucose with 1/4 or 1/5 of normal saline, 60-80ml/Kg/day . </li></ul>
  138. 139. Drugs <ul><li>Anti-infection with Ampicillin 200-400mg/Kg/day IV, </li></ul><ul><li>Anti- shock with Dopamine 5ug/Kg/min IV </li></ul><ul><li>Anti-DIC with Heparin 0.5-1.0mg-Kg-dose IV drip. </li></ul><ul><li>correction acidosis with 5% Nat. Bicarbonate 3-5ml/ Kg/dose IV . </li></ul><ul><li>Supportive therapy include Plasma (5-10ml/Kg/dose), Prednison (1-2ml/Kg/dose) and Vit.E (5-15mg/day). </li></ul><ul><li>  </li></ul><ul><li>  </li></ul>
  139. 140. Rewarming <ul><li>The patient rapidly or gradually according to the severity of the disease, making the body temperature at 36.5 0 C . The rewarming methods including incubator , electric capet, radiant warmer and thermostatic bathing. </li></ul>