Neonatal Jaundice Flashcards
Bile metabolism الصوره ب صفحه ٢٧
اوكيه ولا مش اوكيه
Direct vs indirect bilirubin
DIRECT BILIRUBIN (CONJUGATED)
- Water Soluble
- Excreted in bile and urine
- Can not cross BBB
INDIRECT BILIRUBIN (UNCONJUGATED)
- Lipid soluble; bind to albumin
- Can not Excreted in the urine
- Can Cross BBB
What is neonatal jaundice?
a) A skin rash in newborns
b) A condition characterized by blue discoloration of the skin
c) The yellow discoloration of mucous membranes and skin due to increased bilirubin levels
d) A common digestive disorder in newborns
At what age does neonatal jaundice usually occur?
a) Within the first month of life
b) Within the first day of life
c) During the second month of life
d) During the first week of life
What type of hyperbilirubinemia is most frequently the cause of neonatal jaundice?
a) Direct (conjugated) hyperbilirubinemia
b) Total (mixed) hyperbilirubinemia
c) Indirect (unconjugated) hyperbilirubinemia
d) Hemolytic hyperbilirubinemia
At what serum bilirubin level does visible jaundice occur in a neonate?
a) 1 mg/dL
b) 5 mg/dL
c) 10 mg/dL
d) 15 mg/dL
In what type of neonates is jaundice more likely to occur, those with polycythemia or anemia?
a) Polycythemia
b) Anemia
c) Both are equally at risk
d) Neither are at risk
Describe the typical pattern of jaundice progression in neonates
———of term babies develop jaundice during the —- —of life
———of preterm babies develop jaundice during the ——-of life
c) The yellow discoloration of mucous membranes and skin due to increased bilirubin levels.
d) Within the first week of life.
c) Indirect (unconjugated) hyperbilirubinemia.(physiological in nature)
b) 5 mg/dL.
a) Polycythemia.
Cephalocaudal → start from head & goes down to the trunk & limbs.
60% first week
80-100% first 2 weeks
Physiologic Jaundice Quiz
What characterizes physiologic jaundice in newborns?
a) Severe and long-lasting hyperbilirubinemia
b) Benign and self-limited indirect hyperbilirubinemia
c) Conjugated hyperbilirubinemia
d) A life-threatening condition that requires immediate treatment
How long does it typically take for physiologic jaundice to resolve in newborns?
a) Within a few hours after birth
b) By the end of the first week of life require no treatment
c) Within the first month of life
d) It requires lifelong treatment
What are the causes of physiologic jaundice in newborns?
a) A genetic mutation
b) Increased bilirubin load on hepatocytes due to the breakdown of red blood cells after birth and Delayed activity of the hepatic enzyme glucuronyl transferase
c) Exposure to environmental toxins
d) Viral infection
B
B
B
Clinical features of physiological jaundice
well-appearing infants with elevated indirect bilirubin levels.
In normal full-term:
Peak serum concentrations infants reach 5–16 mg/dL by 3–4 days of life
Begin decreasing before the end of the first week of life.
In preterm infants:
Bilirubin levels continue to rise later than in term infants
Reaching peak levels after 5–7 days
Requiring 10–20 days before decreasing without treatment
Breastfeeding vs breastmilk jaundice
الجدول صفحه ٢٨
Non-physiologic jaundice:
Is a
Jaundice on ——- is always pathological
Classifications
❖ Jaundice that is secondary to pathophysiologic causes
❖ Jaundice on the first day of life is always pathologic
Direct and indirect hyperbilirubinemia
Direct and INDIRECT HYPERBILIRUBINEMIA definition
Direct : Is an elevated bilirubin in which the conjugated or direct component is >20% of the total bilirubin level
Indirect:Is an elevated bilirubin in which the conjugated or direct component is <20% of the total bilirubin level
Crigler-Najjar syndrome
Inheritance
Types
Autosomal recessive
Permanent deficiency of glucuronosyltransferase
Type I:
Does not respond to phenobarbital o Manifests as persistent indirect hyperbilirubinemia often leading to kernicterus
Type II:
Responds to enzyme induction by phenobarbital, producing an increase in enzyme activity and a reduction of bilirubin levels.
Gilbert disease:
Is caused by a mutation of the promoter region of glucuronosyltransferase (Extra TA insertion in the UGT1A1 promoter Contains the sequence (TA)6 TAA)
Results in a mild indirect hyperbilirubinemia.
In presence of another icterogenic factor (hemolysis), more severe jaundice may develop
Autosomal recessive
Kernicterus Spectrum Disorder (Bilirubin Encephalopathy): definition
Indirect bilirubin cross the blood-brain barrier because of its lipid solubility
Results when indirect bilirubin is deposited in brain cells and irreversibly disrupts neuronal metabolism and function, especially in the basal ganglia.
Kernicterus Spectrum Disorder (Bilirubin Encephalopathy): risk factors
Risk factors
Rapid rising in bilirubin (more important than the level itself)
Incidence increases as serum bilirubin levels exceed 25 mg/dL
Premature babies (their BBB is more immature)
Hypoalbuminemia
Kernicterus Spectrum Disorder (Bilirubin Encephalopathy) earliest signs
The earliest (noted after day 4 of life) clinical manifestations of kernicterus are:
Lethargy
Hypotonia
Irritability
Poor Moro response
Poor feeding
A high-pitched cry
Emesis
Kernicterus Spectrum Disorder (Bilirubin Encephalopathy) late signs
Later signs include:
Bulging fontanel
Hypertonicity
Opisthotonic posturing
Pulmonary hemorrhage
Fever
Paralysis of upward gaze
Seizures
Hearing loss
Oculomotor paralysis.
Choreoathetoid cerebral palsy:
Chorea: Continuous, irregular movements of the extremities and trunk
Athetosis : Involuntary writhing movements of the fingers, hands, feet, and, less commonly, arms, legs, and neck
Cause of hemolysis in neonate
Hemolysis lead to ——-hyperbilirubinemia
- ABO Incompatibility:
Happens when the mother is O and her baby is from A or B blood group The mother will have Ig G against A and B antigens of RBCs, that can cross the placenta and attack the fetus A or B antigens on fetus RBCs. - Rh antigen:
When the mother is Rh negative and the fetus is Rh positive.
But this type of hemolysis usually do not occur in the first time of Rh + pregnancy:
Because the mother don’t normally have antibodies against the Rh+ blood group.
She needs to have a previous exposure to Rh antigen in order to synthesis these Antibodies
The type of Immunoglobulins produced first will be IgM → can’t cross the placenta.
Then the type of Immunoglobulin produced by the mother will be changed to IgG that can cross the placenta freely
Management:
Anti-Rh+ immune globulin (RhoGAM):
✓ Given prophylactically at weeks 26 to 28 & again within 72 hours of delivery of an Rhpositive infant
✓ Attach to the Rh antigen & prevent the immune system of the mother to recognize it
Indirect
DIRECT HYPERBILIRUBINEMIA important info
This is always pathologic in neonates
Not toxic to CNS
INVESTIGATIONS of neonatal jaundice
➢ Bilirubin level: is the first test and the most important to be done
➢ CBC & blood film: is the 2 nd test usually done after bilirubin level to see if there is anemia or not
➢ Direct Combs test: to determine whether we are dealing with immune mediated hemolytic anemia or not immune
Management of neonatal jaundice
➢ Phototherapy:
Wave-length → 420-470 nanometer
Is an effective & safe method for reducing indirect bilirubin levels, make it more water soluble Complications:
Increased insensible water loss → Dehydration
Diarrhea
Retinal damage
Testicular & ovarian damage
➢ Exchange transfusion:
Usually is reserved for infants with dangerously high indirect bilirubin levels who are at risk for kernicterus :
1 Infants with hemolysis with weight more than 2000g: Done exchange at level of 20mg/dL
2 Asymptomatic infants with physiologic or breast milk jaundice:
Not require exchange transfusion, unless the indirect bilirubin level exceeds 25 mg/dL.
Performed through an umbilical venous catheter placed in the inferior vena cava
➢Liver transplantation: for conjugated hyperbilirubinemia
Jaundice according to time:
Early Onset ( First 24 hours)
Always pathological
Intermediate Onset (First 2 weeks)
Physiological Jaundice
Breast feeding Jaundice
Late onset
Breast milk Jaundice
Infection
Cystic fibrosis
Hypothyroidism
Trisomy 21
