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JAUNDICE Just Call Me Yellow Mary Johnson RNC/MSN Gwinnett Hospital System.

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Presentation on theme: "JAUNDICE Just Call Me Yellow Mary Johnson RNC/MSN Gwinnett Hospital System."— Presentation transcript:

1 JAUNDICE Just Call Me Yellow Mary Johnson RNC/MSN Gwinnett Hospital System

2 Objectives At the end of the presentation; the participant will be able to: List 2 factors that place a neonate at risk for jaundice Describe the common treatment modalities for jaundice Discuss the difference between physiologic jaundice and pathologic jaundice

3 Jaundice Jaundice: An elevated bilirubin level Bilirubin: Results from the breakdown of hemoglobin

4 Bilirubin Metabolism The breakdown of “heme” is usually a normal physiologic process… Heme is initially converted to biliverdin via the enzyme heme oxygenase Biliverdin is then further reduced to bilirubin by biliverdin reductase

5 Bilirubin Metabolism Bilirubin is insoluble in water and must be placed into the plasma circulation by being bound to albumin In the liver, bilirubin is changed to a water soluble compound by being conjugated by the enzyme UDPGT (uridine diphosphylgluronosyn transferase)

6 Bilirubin Metabolism This changed (or conjugated) bilirubin is released, after several enzymatic reactions, from the liver into the bile duct and then to the GI tract for elimination. Some bilirubin is also excreted through the urine via similar processes. This all depends on adequate amounts of oxygen and glucose.

7 Bilirubin Binding Bilirubin/albumin binding explains how bilirubin can be toxic to the brain. Small amounts of unconjugated (unchanged) bilirubin are not bound to albumin, but circulate as free bilirubin. This unbound, insoluble bilirubin crosses the lipid containing cell membranes-including the blood brain barrier and causes kernicterus

8 Before Birth Metabolism and clearance of fetal bilirubin is accomplished through the maternal liver There is limited conjugation in the fetus because there is limited fetal blood flow in the fetal liver Unconjugated bilirubin in the fetus is cleared by the placenta

9 Before Birth Conjugated bilirubin in the fetus is not cleared by the placenta and may accumulate in fetal tissues

10 Factors influencing bilirubin levels Racial and ethnic groups Perinatal events Maternal Diabetes Higher bilirubin production in neonates Limited conjugation of bilirubin in neonates Delayed excretion due to increased enterohepatic circulation

11 Enterohepatic Circulation Excretion is delayed because the small intestine of the neonate contains an enzyme (B-glucoronidase) which converts conjugated bilirubin back to its unconjugated form. Bilirubin is then re-absorbed into the circulation Neonatal intestines are slow to become colonized with bacteria that degrade bilirubin into non-re- absorbable urobilogen

12 Measurement of Jaundice May be serum blood level- most accurate Trancutaneous bilirubin monitoring acceptable.

13 Physiologic Jaundice Almost universally observed in all neonates due to: Larger RBC mass Shorter RBC lifespan Greater amount of bilirubin produced from sources other than RBCs Increased enterohepatic circulation Defective conjugation Decreased excretion

14 Physiologic Jaundice Bilirubin levels generally peak on day 3 to 5 of life in term babies and day 5 to 6 in preterm babies Hyperbilirubinemia in premies is an exaggerated form of physiologic jaundice because of decreased glucuronyl transferase activity in the liver.

15 Treatment of Physiologic Jaundice Phototherapy Works by “photoisomerization”: a process that converts bilirubin to a water soluble component excreted by the liver

16 Optimal Phototherapy Expose as much skin as possible Eye patches except for feeding Turn frequently Monitor temperature Monitor intake and output: increased insensible water loss is common Monitor for diarrhea

17 Phototherapy Information Place lights at the distance from the infant recommended by the manufacturer (generally 8 to fourteen inches from the baby) Place lights so that they are centered over the baby

18 Phototherapy Information Use radiometer: Place parallel to the light unit and directly under the light at the level of the baby’s skin. An irradiance level of 20 microwatts or greater is acceptable An irradiance level of 30 microwatts or greater is considered to “intensive” or double phototherapy

19 Phototherapy Information Higher levels of irradiance are not known to be detrimental to the infant

20 Bili Blankets Acceptable to use bili blankets in conjunction with regular phototherapy If only bili blanket used: eye patches are not needed

21 Phototherapy Side effects Loose stools/diarrhea/dehydration Hyper/hypothermia Skin rashes lethargy

22 Pathologic Jaundice Differs from physiologic jaundice: Begins earlier (sometimes before 24 hours) Rises more quickly (>5 mg/dl/day) Lasts longer (> 1 week in term babies and greater than 2 weeks in preterms)

23 Pathologic Jaundice Causes Hemolytic disease Rh incompatibility ABO incompatibility G6PD deficiency Breastfeeding Jaundice Breastmilk Jaundice

24 Rh Incompatibility Fetal blood cells containing Rh antigen (Rh + cells) enter the maternal circulation. The maternal cells have no Rh antigen (Rh-) and the maternal immune system then produces antibodies against the fetal antigens. Finally, the maternal antibodies enter the fetal circulation and hemolyze (destroy) the fetal red cells.

25 Rhogam Given to protect hemolysis in the neonate Given at 28 weeks and within 72 hours after delivery

26 ABO Incompatibility Less severe; more frequent than Rh Most often seen in mothers with Blood type O with blood type A or B babies Fetal cells enter the maternal circulation as with Rh disease Infant presentation includes: Hemolysis; anemia Jaundice

27 G6PD Deficiency A deficiency of the enzyme glucose 6 phosphate dehydroginase Autosomal dominant Caused by: Impaired conjugation Hemolysis: G6PD protects the RBC membranes from oxidation. In G6PD deficiency; the red cell is very likely to hemolyze

28 G6PD Deficiency More common in African Americans Greeks Italians Sephardic Jews Asians Males

29 G6PD Deficiency Once diagnosed: usually a good outcome Diagnosis with G6PD testing Treatment includes dietary restrictions No fava beans

30 Breastfeeding Jaundice Breastfeeding is associated with more significant and prolonged jaundice than formula feeding Early onset (2 to 4 days of age) Inadequate nursing (inadequate feeding and calories) Encourage nursing/pumping times a day No water supplement needed

31 Breastmilk Jaundice Late onset (4-7 days of life) Prolonged physiologic jaundice Related to the ingredients in breast milk Decreased conjugation from Interference of UDGT enzyme Increased concentration of free fatty acids because of the lipoprotein in human milk Increased enterohepatic circulation because of lipoprotein in breast milk

32 Breastmilk Jaundice: Treatment Discontinue breastfeeding for 24 hours Have mom pump and then resume breastfeeding

33 Kernicterus Bilirubin induced neurological dysfunction with yellow staining and neuronal injury in the ganglia Classic signs Cerebral palsy Gaze abnormalities Hearing impairment Dental dysplasia

34 Kernicterus Usually associated with bilirubin levels Greater than 30 in term babies Greater than 20 in preterm babies Severity of symptoms varies from baby to baby

35 Other Treatments Early feedings Phenobarbital IVIG Exchange transfusion Decision based on bili level; age in hours of baby; gestational age; rate of rise of bilirubin Blood removed from UAC and replaced with whole blood as ordered by the physician

36 Exchange Transfusion Major complication is hypocalcemia READ THE POLICY


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