NEONATAL JAUNDICE (??????? ???????)

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NEONATAL JAUNDICE(??????? ???????)

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Definition

• JAUNDICE yellowish discoloration of skin, sclera
  and mucus membrane
• Results from accumulation of un conjugated
  bilirubin pigment in the skin occur in 60 of
  term infant and 80 of preterm infant.

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Bilirubin production

• Bilirubin is a product of heme catabolism.
  Approximately 80 to 90 of bilirubin is produced
  during the breakdown of hemoglobin from red blood
  cells (RBCs).
• Hemoglobin globin heme co
  biliverdine
• Bilirubin albumin hepatocyte (glucuronic
  acid)
• bilirubin diglucuronides bilirubin
  monoglucuronides. Conjugated bilirubin
• Conjugated bilirubin is secreted into the bile,
  and then excreted into the digestive tract.
  conjugated bilirubin is reduced to urobilin.
• Un conjugated bilirubin lipid soluble can cross
  blood brain barrier and its neurotoxic.
• Conjugated bilirubin water soluble not
  neurotoxic it indicates serious liver disorder .

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CAUSES OF HYPERBILIRUBINEMIA

• Increased production Isoimmune-mediated
  hemolysis (eg, ABO or Rh(D) incompatibility),
  Inherited red cell membrane defects (eg,
  hereditary spherocytosis and elliptocytosis),
  Erythrocyte enzymatic defects (eg,
  glucose-6-phosphate dehydrogenase (G6PD)
  deficiency, pyruvate kinase deficiency),Sepsis
  Other causes due to increased red blood cell
  breakdown include polycythemia( infants of
  diabetic mothers )or cephalohematoma.
• Decreased clearance defects in UGT decrease
  bilirubin conjugation, reducing hepatic bilirubin
  clearance and increasing TSB levels. These
  disorders include Crigler-Najjar syndrome types I
  and II and Gilbert's syndrome
• Increased enterohepatic circulation The major
  causes are breastfeeding failure jaundice, breast
  milk jaundice, or impaired intestinal motility
  caused by functional or anatomic obstruction.
• Risk factors
• Hypoprotenemia, displacement of bilirubin
  from its binding sit on albumin by competitive
  binding of drug such as sulfisoxasole ,and
  moxalactam ,acidosis and increase free fatty acid
  concentration secondary to hypoglycemia ,
  starvation or hypothermia . Drugs such as
  oxytocin used in the nursery may produce
  hyperbilirubinimia . other risk factors include
  polycythemia, infection, prematurity , and being
  infant of diabetic mother.a

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Diagnostic feature of the various types of
neonatal jaundice
Notes Rate of accumulation Peak conce. J. disappear j. appears Diagnosis
Us.relate to degree of maturity. lt5mg/dl lt5mg/dl 10-12mg/dl 15mg/dl 4-5days 7-9days 2-3days 3-4days Physiological Fullterm premature
Hypoxia,RDS,lack of carbohydrate lt5 lt5 gt12 gt15 Variable variable 2-3days 3-4days Metabolic Fullterm premature
Rh,ABO,spherocytosis, drugs.vit. k Us.gt5 unlimited Variable 1st 24 hr Hemolysis hematoma
Biliary atresia,Cholestasis ,hepatitis,Galactosemia Infection,(directindirect) Usuallygt5 unlimited Variable Us.2-3d. may app. By2nd wk. Hepayocellular damage
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CLINICAL MANIFESTATIONS

• presence of jaundice its not a reliable method to
  assess TSB concentration or identify infants at
  risk for rapidly rising bilirubin, especially in
  those with dark skin. The examination for
  jaundice should be performed with adequate
  ambient light or under daylight fluorescent
  light. Pressing on the skin with a finger reduces
  local skin perfusion and facilitates detection of
  jaundice.
• Jaundice progresses in a cephalocaudal direction,
  appearing first in the face and sclerae at
  bilirubin levels of 5 mg/dL. The abdomen
  15mg/dl, soles20mg/dl. TSB levels should
  always be measured in an infant with jaundice
  below the umbilicus.
• Other findings on physical examination may
  suggest an increased risk for hyperbilirubinemia.
  They include pallor, enclosed hemorrhage (eg,
  cephalohematoma), bruising, and
  hepatosplenomegaly

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Acute bilirubin encephalopathy

• Term and nearterm infants are at risk for
  bilirubin neurotoxicity when TSB concentrations
  exceed 20mg/dl . unconjugated bilirubin, which is
  not bound to albumin, can enter the brain and
  cause cell death
• Acute bilirubin encephalopathy (ABE) typically
  progresses through three phases
• In the early phase which occurs in the first few
  days of life(1-2days), the infant may exhibit
  lethargy, hypotonia, poor sucking, and
  high-pitched cry.
• the intermediate phase evolves later in the
  first week of life If there is no intervention,.
  The infant can be moderately stuporous ,irritable
  with a high-pitched cry, and usually develops
  hypertonia, often with backward arching of the
  neck (retrocollis) and trunk (opisthotonus), and
  fever. An emergent exchange transfusion at this
  stage might prevent permanent BIND.
• The advanced phase(after 1 st wk) is
  characterized by hypertonia with marked
  retrocollis and opisthotonus, stupor or coma, a
  shrill cry, and sometimes seizures and
  death.called Kernicterus (the chronic and
  permanent sequelae of BIND) develops during the
  first year after birth. Cognitive function
  usually is relatively spared. The major features
  of kernicterus include
• Choreo-athetoid cerebral palsy (chorea,
  ballismus, tremor). Sensorineural hearing loss,
  Gaze abnormalities, especially limitation of
  upward gaze. Dental-enamel dysplasia.

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SCREENING LABORATORY STUDIES

• measurement of total serum bilirubin (TSB) is
  dependent on clinical findings of jaundice and
  risk factors for hyperbilirubinemia, including
  whether the infant is breast or formula fed.
• All term and nearterm infants should be routinely
  assessed for the presence of jaundice every 8 to
  12 hours while in the hospital. Infants who are
  jaundiced before 24 hours of life are at
  increased risk for severe hyperbilirubinemia,
  often due to hemolytic disease. In these infants,
  TSB measurement should be performed.
• TSB also should be measured in infants gt24 hours
  of age when jaundice appears excessive for age
  (eg, jaundice below the level of the umbilicus)
• Term infants are at risk for bilirubin-induced
  neurologic dysfunction (BIND) when TSB
  concentrations exceeds 20 mg/d. free bilirubin is
  more likely to cross the blood-brain barrier and
  cause brain injury. Most bilirubin is normally
  bound to albumin, resulting in low levels of
  unbound bilirubin.Preterm and sick infants often
  have decreased serum albumin concentrations and a
  reduced binding capacity resulting in a higher
  proportion of unbound bilirubin for a given TSB
  compared to healthy term infants?

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ADDITIONAL EVALUATION

• Initial tests that should be obtained are
• Blood type and direct Coombs test Complete blood
  count and smear Reticulocyte count
  Glucose-6-phosphate dehydrogenase (G6PD)
  measurement, if clinically appropriate Direct or
  conjugated bilirubin
• TSB should be repeated in 4 to 24 hours depending
  upon the infant's age and TSB value. The mother's
  blood type usually should be known from prenatal
  testing.

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Treatment of severe hyperbilirubinemia

• PHOTOTHERAPY is the most commonly used
  intervention to treat and prevent severe
  hyperbilirubinemia. In term and large preterm
  infants, phototherapy is safe based upon its
  extensive use
• Phototherapy exposes the infant's skin to light
  of a specific wavelength, which reduces TSB by
  the following mechanism
• Structural isomerization to lumirubin
  Phototherapy converts bilirubin into lumirubin
  via structural isomerization that is not
  reversible. Lumirubin, a more soluble substance
  than bilirubin, is excreted without conjugation
  into bile and urine
• photoisomerization does reduce the amount of
  potentially toxic bilirubin by rapidly converting
  15 percent of it to a non-toxic form
• phototherapy should be administered continuously,
  until the TSB falls below save level. Once this
  occurs, phototherapy can be interrupted for
  feeding and parental visits. During phototherapy,
  the area covered by the diaper should be
  minimized. The eyes should be shielded with an
  opaque blindfold and care should be taken to
  prevent the blindfold from covering the nose.

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Phototherapy indications

• For infants at low risk (38 weeks gestation and
  without risk factors)
• -  24 hours of age gt12 mg/dL
•   48 hours of age gt15 mg/dL
•   72 hours of age gt18 mg/dL
• For infants at medium risk (38 weeks gestation
  with risk factors or 35 to 37 weeks gestation
  without risk factors).
• -  24 hours of age gt10 mg/dL
•   48 hours of age gt13 mg/dL
•   72 hours of age gt15 mg/dL
• For infants at high risk (35 to 37 weeks
  gestation with risk factors).
• -  24 hours of age gt8 mg/dL
•   48 hours of age gt11 mg/dL
•   72 hours of age gt13.5 mg/dL
• Adverse effects include transient erythematous
  rashes, loose stools, and hyperthermia,Increased
  insensible water loss may lead to dehydration.
  bronze baby syndrome, retinal degeneration may
  occur after 24 hours of continuous exposure. As a
  result, it is essential that the eyes of all
  neonates treated with phototherapy are
  sufficiently covered to eliminate any potential
  eye exposure.

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EXCHANGE TRANSFUSION

• is the most effective method for removing
  bilirubin rapidly, and is indicated when
  intensive phototherapy cannot prevent a continued
  rise in the TSB or in infants who already display
  signs indicative of BIND.
• Indications
• Infants with signs of acute bilirubin
  encephalopathy (ABE), such as significant
  lethargy, hypotonia, poor sucking, or
  high-pitched cry, irrespective of the TSB level.
• In infants who have not yet been discharged from
  the birth hospital, exchange transfusion is
  recommended if the TSB reaches the threshold
  level despite intensive phototherapy
• For infants at low risk (38 weeks gestation and
  without risk factors).
•       -  24 hours of age gt19 mg/dL
•        48 hours of age gt22 mg/dL
•      72 hours of age gt24 mg/dL
•       Any age 25 mg/dL (428 micromol/L)
• For infants at medium risk (38 weeks gestation
  with risk factors or 35 to 37 weeks gestation
  without risk factors).
•       -  24 hours of age gt16.5 mg/dL
• 48 hours of age gt19 mg/dL
•    72 hours of age gt21 mg/dL
• For infants at high risk (35 to 37 weeks
  gestation with risk factors).
•       -  24 hours of age gt15 mg/dL
• 48 hours of age gt17 mg/dL
•    72 hours of age gt18.5 mg/dL

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Risks

• result from the use of blood products and from
  the procedure itself. Complications include
• Blood-borne infection ,Thrombocytopenia and
  coagulopathy Graft-versus-host disease,
  Necrotizing enterocolitis, Portal vein thrombosis
  Electrolyte abnormalities (eg, hypocalcemia and
  hyperkalemia), Cardiac arrhythmias

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