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‫الرحيم‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬
Neonatal jaundice
‫عماد‬ ‫علياء‬
‫احمد‬ ‫فاطمة‬
‫حسين‬ ‫فاطمة‬
‫حسن‬ ‫فاطمة‬
Definition:is a yellowing of the skin and sclera
of a newborn infant caused by accumulation of
Bilirubin( Hyperbilirubinem...
Hyperbilirubinemia is a common and in most
cases benign problem in neonates. Jaundice is
observed during the 1st wks. of l...
Metabolism and secretion of bilirubin
Bilirubin -breakdown of hemoglobin
Unconjugated bilirubin (insoluble in water)
trans...
Clinical Manifestations
• Yellow skin and sclera
• Poor feeding
• Brown urine
• Fever
• High pitch cry
• Vomiting
• withou...
Physiologic jaundice : (Icterus Neonatorum)
Physiologic jaundice is a common cause of
hyperbilirubinemia among newborns. I...
Physiological jaundice is jaundice that is
present between day 2 and day 10
Characteristics:-
1-The clinical pattern of physiologic jaundice in
term infants includes a peak indirect-reacting
bilirub...
Pathologic jaundice
• Appears within 24 hours of age
• Increase of bilirubin > 5 mg / dl / day
• Total Serum bilirubin > 1...
Risk factors for jaundice
1-low birth wt & prematurity
2-polycythemia
3-A sibling affected
4-male sex
5-hemolytic conditio...
Types of neonatal jaundice
In Hemolytic disease of the
newborn (ABO / Rh)
Rh incompitability:
• is the most common cause
• < 1 mL of Rh-positive feta...
Not all mother produce hemolysis in their
baby ??
1. The baby may be Rh negative
2. Not all mother produce enough Abs
3. T...
ABO incompatibility
• if Mother is type O and the baby is either type A
or B. O +ve Mothers makes antibodies which are
IgM...
Physiologic jaundice is a common cause of hyperbilirubinemia
among newborns. It is a diagnosis of exclusion, made
after ca...
Crigler-Najjar syndrome is a serious, rare, autosomal
recessive, permanent deficiency of glucuronosyltransferase
that resu...
Breast milk jaundice
may be associated with unconjugated hyperbilirubinemia without
evidence of hemolysis during thefirst ...
Direct-reacting hyperbilirubinemia (defined as a direct bilirubin
level >2 mg/dL or >20% of the total bilirubin) is never
...
Best classified by age of onset and duration:
Early: within 24 hrs of life
Intermediate: 2 days to 2 weeks
Late: persists ...
Causes of neonatal jaundice
Early Intermediate Late/prolonged
• Haemolytic causes:
– Rh isoimmunisation
– ABO incompatibil...
Kernicterus ( bilirubin encephalopathy):
is a neurologic syndrome results when indirect bilirubin is
deposited in brain ce...
Kernicterus usually is noted when the bilirubin level is
excessively high for gestational age. It usually does not
develop...
Pathalogy
Yellow staining of the brain with neuronal injury, there are necrosis, neuronal
loss and gliosis
Its commonly se...
Risk factor for Kernicterus
1. Sever hyperbilirubinemia
2. Prematurity
3. Asphyxia
4. Acidosis ,hemolysis, hypoxia, hypoth...
Clinical feature
The earliest clinical manifestations of kernicterus are
lethargy
Hypotonia
irritability
poor Moro respons...
Complication of Kernicterus
Infants with severe cases of kernicterus die in the neonatal
period.
Spasticity resolves in su...
Diagnosis of hyperbilirubiniemia
:
• History
 ask about Antenatal history
 Drugs
 Trauma
 Family H/O of jaundice
 Liver disease
 H/O delayed feeding
...
Examination :
• Look for yellowish discoloration of the skin,
sclera and mucous membrane
• Gently pressing by finger on th...
Kramer index:
1.Face-5 mg/dl
2.Abdomen 15 mg/dl
5.Palms & sloes 20 mg/dl
LABORATORY TESTS
Physical evidence of jaundice is observed in infants when
bilirubin levels reach 5 to 10 mg/dL (versus 2 ...
These tests must be
performed before treatment of hyperbilirubinemia with
phototherapy
or exchange transfusion. In the abs...
Treatment
phototherapy
•is an effective and safe method for reducing indirect bilirubin
levels, particularly when initiated before s...
The therapeutic effect of phototherapy depends on
1. the light energy emitted in the effective range of wavelengths
2. the...
Serum bilirubin levels and hematocrit should be monitored every
4-8 hr in infants with hemolytic disease and those with
bi...
Late complication:
• Risk of skin malignancies
• Damage to intracellular DNA
• Retinal damage
• Testicular damage
Intensive phototherapy
using light source above and beneath the infant using
in sever cases with risk of kernicterus
Home ...
Intravenous Immunoglobulin
The administration of intravenous immunoglobulin
use in treatment for hyperbilirubinemia due to...
Exchange blood transfusion
usually is used for infants with dangerously high
indirect bilirubin levels who are at risk for...
Indication:
• The appearance of clinical signs suggesting
kernicterus
• Rh and ABO incompatibility
• Unconjugated billirub...
Complications
1. Problems related to the blood (transfusion reaction,
metabolic instability,or infection)
2. Problems rela...
Prevention of neonatal jaundice :
1. Promote and support breast feeding
2. Establish nursery protocols for identifying and...
‫علي‬&‫فاطمة‬
•‫لكما‬ ‫هللا‬ ‫بارك‬
‫عليكما‬ ‫وبارك‬
‫بينكما‬ ‫وجمع‬
‫خيـــر‬ ‫في‬
‫الخطوبة‬ ‫مبروك‬
Neonatal jaundice
Neonatal jaundice
Neonatal jaundice
Neonatal jaundice
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Neonatal jaundice

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Neonatal jaundice

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Neonatal jaundice

  1. 1. ‫الرحيم‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬
  2. 2. Neonatal jaundice ‫عماد‬ ‫علياء‬ ‫احمد‬ ‫فاطمة‬ ‫حسين‬ ‫فاطمة‬ ‫حسن‬ ‫فاطمة‬
  3. 3. Definition:is a yellowing of the skin and sclera of a newborn infant caused by accumulation of Bilirubin( Hyperbilirubinemia) in the skin & mucous mambrene
  4. 4. Hyperbilirubinemia is a common and in most cases benign problem in neonates. Jaundice is observed during the 1st wks. of life in approximately 50- 60% of term newborns and 80% of premature infants. Its clinically visible when exceeds 5 mgm/dl.
  5. 5. Metabolism and secretion of bilirubin Bilirubin -breakdown of hemoglobin Unconjugated bilirubin (insoluble in water) transported to liver- Bound to albumin Transported into hepatocyte (Ligandin / y- protein ) & conjugated - With glucuronic acid → now water soluble Secreted into bile In ileum & colon, converted to stercobilin 10-20% (Deconjugated by β glucuronidase) reabsorbed into portal circulation (Enterohepatic circulation )and re-excreted into bile or into urine by kidneys - urobilinogen
  6. 6. Clinical Manifestations • Yellow skin and sclera • Poor feeding • Brown urine • Fever • High pitch cry • Vomiting • without treatment can progress to acute bilirubin Encephalopathy (kernicterus)
  7. 7. Physiologic jaundice : (Icterus Neonatorum) Physiologic jaundice is a common cause of hyperbilirubinemia among newborns. It is adiagnosis of exclusion, made after careful evaluation has ruled out more serious causes of jaundice, such as hemolysis, infection, and metabolic diseases.
  8. 8. Physiological jaundice is jaundice that is present between day 2 and day 10
  9. 9. Characteristics:- 1-The clinical pattern of physiologic jaundice in term infants includes a peak indirect-reacting bilirubin level of no more than 12 mg/dL on day 3 of life. In premature infants, the peak is higher (15 mg/dL) and occurs later (fifth day). 2-its disappears by one weak in full term infants & two weeks in preterm infants. 3-serum bilirubin is rarly rising at a rate faster than 5 mg/dL/24 hr 4- Healthy baby.
  10. 10. Pathologic jaundice • Appears within 24 hours of age • Increase of bilirubin > 5 mg / dl / day • Total Serum bilirubin > 13 mg / dl in term infant or 10 mg/dl in preterm .The direct bilirubin fraction is greater than 1.5 mg/dL May associated with acute hemolysis • Signs of an underlying illness
  11. 11. Risk factors for jaundice 1-low birth wt & prematurity 2-polycythemia 3-A sibling affected 4-male sex 5-hemolytic conditions 6-sepsis 7-ABO incompatibility
  12. 12. Types of neonatal jaundice
  13. 13. In Hemolytic disease of the newborn (ABO / Rh) Rh incompitability: • is the most common cause • < 1 mL of Rh-positive fetal blood is sufficient to sensitize the Rh negative mother • 90% sensitization during delivery/abortion So , most first born infants are not affected due to the short period of exposure which is insufficient to produce a significant maternal IgG antibody response. Sensitized mother produces Ab –IgG types—crosses placenta sensitized –small doses of Ag stimulate high Ab titer . So, risk and severity of sensitization response increases with each subsequent pregnancy with Rh-positive blood fetus
  14. 14. Not all mother produce hemolysis in their baby ?? 1. The baby may be Rh negative 2. Not all mother produce enough Abs 3. The mother might have been immunized by anti D immunoglobin 4. Fetomaternal trasfusion occurs only in 50% of preg 5. When mother and baby ABO incompatibale
  15. 15. ABO incompatibility • if Mother is type O and the baby is either type A or B. O +ve Mothers makes antibodies which are IgM & IgG types , IgG types crosses the placenta • No effects if the mother & baby have same blood group or baby is grp O, as there is nothing to make antibodies against. • If mother - type A or B Makes antibodies (IgM) type so does not cross the placenta So, even if baby has a different blood type no effect
  16. 16. Physiologic jaundice is a common cause of hyperbilirubinemia among newborns. It is a diagnosis of exclusion, made after careful evaluation has ruled out more serious causes of jaundice, such as hemolysis, infection, and metabolic diseases. Physiologic jaundice is the result of many factors that are normal physiologic characteristics of newborns: 1- increased bilirubin production resulting from an increased RBC mass, 2- shortened RBC life span, 3- hepatic immaturity of ligandin and glucuronosyltransferase. Physiologic jaundice
  17. 17. Crigler-Najjar syndrome is a serious, rare, autosomal recessive, permanent deficiency of glucuronosyltransferase that results in severe indirect hyperbilirubinemia. Type II responds to enzyme induction by phenobarbital, producing an increase in enzyme activity and a reduction of bilirubin levels. Type I does not respond to phenobarbital and manifests as persistent indirect hyperbilirubinemia, often leading to kernicterus Gilbert disease is caused by a mutation of the promoter region of glucuronosyltransferase and results in a mild indirect hyperbilirubinemia. In the presence of another icterogenic factor (hemolysis), more severe jaundice may develop
  18. 18. Breast milk jaundice may be associated with unconjugated hyperbilirubinemia without evidence of hemolysis during thefirst to second week of life. Bilirubin levels rarely increase to more than 20 mg/dL. Interruption of breastfeeding for 1 to 2 days results in a rapid decline of bilirubin levels, which do not increase significantly after breastfeeding resumes. Breast milk may contain an inhibitor of bilirubin conjugation or may increase enterohepatic recirculation of bilirubin because of breast milk glucuronidase
  19. 19. Direct-reacting hyperbilirubinemia (defined as a direct bilirubin level >2 mg/dL or >20% of the total bilirubin) is never physiologic and should always be evaluated thoroughly according to the diagnostic categories Etiology of Direct Conjugated Hyperbilirubinemia Direct-reacting bilirubin (composed mostly ofconjugated bilirubin) is not neurotoxic to the infant but signifies a serious underlying disorder involving cholestasis or hepatocellular injury.
  20. 20. Best classified by age of onset and duration: Early: within 24 hrs of life Intermediate: 2 days to 2 weeks Late: persists for >2 weeks Causes of neonatal jaundice
  21. 21. Causes of neonatal jaundice Early Intermediate Late/prolonged • Haemolytic causes: – Rh isoimmunisation – ABO incompatibility – G6PD deficiency • Congenital infection • Physiological jaundice • Breast milk jaundice (inadequate intake) • Sepsis • Haemolysis • Crigler-Najjar syndrome (glucuronyl transferase absent/reduced) • Polycythaemia, bruising • Conjugated (dark urine, pale stools): – Bile duct obstruction – Biliary atresia – Neonatal hepatitis • Unconjugated: – Physiological – Breast milk jaundice – Infection – Hypothyroidism
  22. 22. Kernicterus ( bilirubin encephalopathy): is a neurologic syndrome results when indirect bilirubin is deposited in brain cells and disrupts neuronal metabolism and function, especially in the basal ganglia. Indirect bilirubin may cross the blood-brain barrier because of its lipid solubility. Other theories propose that a disruption of the blood-brain barrier permits entry of a bilirubin-albumin or free bilirubin–fatty acid complex Its characterized by severe athetoid cerebral palsy, paralysis of upward gaze, hearing loss & intellctual impairment & its preventable Kernicterus
  23. 23. Kernicterus usually is noted when the bilirubin level is excessively high for gestational age. It usually does not develop in term infants when bilirubin levels are less than 20 to25 mg/dL, but the incidence increases as serum bilirubin levels exceed 25 mg/dL
  24. 24. Pathalogy Yellow staining of the brain with neuronal injury, there are necrosis, neuronal loss and gliosis Its commonly seen in the basal ganglia, hypocampus,cerebellum,brainstem & spinal cord
  25. 25. Risk factor for Kernicterus 1. Sever hyperbilirubinemia 2. Prematurity 3. Asphyxia 4. Acidosis ,hemolysis, hypoxia, hypothermia 5. Hypoglycemia, sepsis, meningitis, Other risks for kernicterus in term infants are hemolysis, jaundicenoted within 24 hours of birth, and delayed diagnosis of hyperbilirubinemia
  26. 26. Clinical feature The earliest clinical manifestations of kernicterus are lethargy Hypotonia irritability poor Moro response poor feeding. A high-pitched cry and emesis also may be present. Early signs are noted after day 4 of life. Later signs include bulging fontanelle opisthotonic posturing pulmonary hemorrhage Fever Hypertonicity paralysis of upward gaze and seizures
  27. 27. Complication of Kernicterus Infants with severe cases of kernicterus die in the neonatal period. Spasticity resolves in surviving infants, who may manifest later nerve deafness choreoathetoid cerebral palsy mental retardation enamel dysplasia and discoloration of teeth as permanent sequelae Prevention Kernicterus may be prevented by -avoiding excessively high indirect bilirubin levels -avoidingconditions or drugs that may displace bilirubin from albumin.
  28. 28. Diagnosis of hyperbilirubiniemia
  29. 29. : • History  ask about Antenatal history  Drugs  Trauma  Family H/O of jaundice  Liver disease  H/O delayed feeding  Sepsis  Sibling jaundice  Splenectomy in family
  30. 30. Examination : • Look for yellowish discoloration of the skin, sclera and mucous membrane • Gently pressing by finger on the tip of the nose • Examination of liver and spleen for hepatosplenomegaly • Look for the color of urine and • stool
  31. 31. Kramer index: 1.Face-5 mg/dl 2.Abdomen 15 mg/dl 5.Palms & sloes 20 mg/dl
  32. 32. LABORATORY TESTS Physical evidence of jaundice is observed in infants when bilirubin levels reach 5 to 10 mg/dL (versus 2 to 3 mg/dL in adults). When jaundice is observed, the laboratory evaluation for hyperbilirubinemia should include a total bilirubin measurement to determine the magnitude of hyperbilirubinemia. Bilirubin levels greater than 5 mg/dL on the first day of life or greater than 13 mg/dL thereafter in term infants should be evaluated further with measurement of indirect and direct bilirubin levels blood typing Coombs test complete blood count, blood smear and reticulocyte count.
  33. 33. These tests must be performed before treatment of hyperbilirubinemia with phototherapy or exchange transfusion. In the absence of hemolysis or evidence for either the common or the rare causes of nonhemolytic indirect hyperbilirubinemia, the diagnosis is either physiologic or breast milk jaundice. Jaundice present after 2 weeks of age is pathologic and suggests a direct-reacting Direct-reacting hyperbilirubinemia (defined as a direct bilirubin level >2 mg/dL or >20% of the total bilirubin) is never physiologic and should always be evaluated thoroughly according to the diagnostic categories Direct-reacting bilirubin (composed mostly of conjugated bilirubin) is not neurotoxic to the infant but signifies a serious underlying disorder involving cholestasis or hepatocellular injury.
  34. 34. Treatment
  35. 35. phototherapy •is an effective and safe method for reducing indirect bilirubin levels, particularly when initiated before serum bilirubin increases to levels associated with kernicterus. •In term infants, phototherapy is begun when indirect bilirubinlevels are between 16 and 18 mg/dL. • Under the effects of phototherapy light with maximal irradiancein the 425- to 475-nm wavelength band, bilirubin is transformed into isomers that are water soluble and easily excreted. • Blue lights and white lights are effective in reducing bilirubin
  36. 36. The therapeutic effect of phototherapy depends on 1. the light energy emitted in the effective range of wavelengths 2. the distance between the lights and the infant 3. the surface area of exposed skin, 4. the rate of hemolysis During phototherapy : 1. Cover the eyes and Genitals 2. Supplemental hydration 3. monitoring for side effects 4. Monitering of bilirubin level
  37. 37. Serum bilirubin levels and hematocrit should be monitored every 4-8 hr in infants with hemolytic disease and those with bilirubin levels near toxic range . Complications of phototherapy Early complication: 1. loose stools 2. erythematous macular rash 3. dehydration (increased insensible water loss, diarrhea) 4. bronze baby syndrome (which occurs in the presence of direct hyperbilirubinemia) 5. lethargy, masking of cyanosis, nasal obstruction by eye pads
  38. 38. Late complication: • Risk of skin malignancies • Damage to intracellular DNA • Retinal damage • Testicular damage
  39. 39. Intensive phototherapy using light source above and beneath the infant using in sever cases with risk of kernicterus Home phototherapy This is an option way of treatment where facilities are available and fiber optic blankets are commonly used .the family should be well instructed and a well trained nurse should be present it is usually used for simple jaundice
  40. 40. Intravenous Immunoglobulin The administration of intravenous immunoglobulin use in treatment for hyperbilirubinemia due to isoimmune hemolytic disease. (0.5-1.0 g/kg/dose; repeat in 12 hr) has been shown to reduce the need for exchange transfusion in both ABO and Rh hemolytic disease, by reducing hemolysis
  41. 41. Exchange blood transfusion usually is used for infants with dangerously high indirect bilirubin levels who are at risk for kernicterus . The exchange transfusion usually is performed through an umbilical venous catheter placed in the inferior vena cava or,if free flow is obtained, at the confluence of the umbilical veinand the portal system.
  42. 42. Indication: • The appearance of clinical signs suggesting kernicterus • Rh and ABO incompatibility • Unconjugated billirubin > 20 -25mg/dl in term, >15 -18mg/dl preterm babies. • Other disease :Septicemia ,DIC,Severe anemia,…
  43. 43. Complications 1. Problems related to the blood (transfusion reaction, metabolic instability,or infection) 2. Problems related to the catheter (vessel perforation or hemorrhage) 3. problems related to the procedure (hypotension or necrotizing enterocolitis ) 4. Unusual complications include thrombocytopenia and graft-versus-host disease.
  44. 44. Prevention of neonatal jaundice : 1. Promote and support breast feeding 2. Establish nursery protocols for identifying and evaluating hyperbilirubinemia 3. Measure bilirubin levels in all neonate with jaundice in the first 24 hrs 4. Recognize that visual estimation of bilirubin level inaccurate 5. Interpret all bilirubin levels according to baby age in hrs 6. Identify preterm ,breast fed infant and provide close monitoring 7. Risk assessment for all newborn baby . 8. Give written and verbal information to familly 9. Treat newborns when indicated and appropriate follow up
  45. 45. ‫علي‬&‫فاطمة‬ •‫لكما‬ ‫هللا‬ ‫بارك‬ ‫عليكما‬ ‫وبارك‬ ‫بينكما‬ ‫وجمع‬ ‫خيـــر‬ ‫في‬ ‫الخطوبة‬ ‫مبروك‬

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