approach to the diagnosis of neonatal jaundice
TRANSCRIPT
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Approach to the diagnosis of Neonatal jaundice
By
Gelaye Mandefro
Ambo Universit
y
Department of
Medicine
August 2015
outline Definitions
Clinical classification
Clinical Assessment
Principles of management
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Definition and Basic concept
Jaundice is the visible manifestation of increased level of
bilirubin in the body
It is not a disease rather a symptom of diseases
In adults sclera appears jaundiced when serum bilirubin
exceeds 2 mg/dl
However it is difficult to see sclera in newborn due to difficulty
in opening eye
But in new born it is very easy to see jaundice in skin.
Definition and Basic concept…
Burden:
Important problem in the 1st week of life
Almost all neonates (60% Term and 80% Preterm) will have bilirubin >
5 mg/dl in the 1st week of life and become visibly jaundiced, vast
majority being benign
Some of the term babies (8 to 9%) have levels exceeding 15 mg/dl in
1st 7 days of life
High bilirubin level is toxic to the developing CNS(KERNICTERUS;
Bilirubin≥25mg/dl)
Definition and Basic concept…
Bilirubin:
End product of hemoglobin metabolism that is excreted in bile
In neonates
-75% : from catabolism of circulating RBCs
-25% :*from ineffective erythropoiesis (bone marrow)
*from turnover of heme proteins & free heme(liver).
Normal Bilirubin Metabolism
Hemoglobin----Bilivervdin-----Bilirubin---Uptake in the liver---
Conjugation----Excretion
Unconjugated bilirubin bind albumin
Unconjugated and un bound bilirubin cross blood brain barrier
Conjugated bilirubin (direct bilirubin) is non toxic to the brain and
not cross blood brain barrier
Conjugated bilirubin is excreted via bile ducts to the gut and pass
through feces
Conjugated bilirubin damages liver if not excreted
Neonatal jaundice
Clinical classification
1. Physiologic Jaundice
Jaundice becomes evident as physiologic in neonates B/c :
Short life span of RBCs(70-90days)
RBC mass is increased
Immature ligandine
Less UDPGT
High activity β-glucuronidase (gut)
Decreased flora in the gutcommon neonatal problems
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Preterm Term
Peak time 4th -7th days 2nd – 4th day
Peak level 8 – 12 mg/dl 5 -6 mg/dl
Resolution time
Before 10th day
5th – 7th day
common neonatal problems
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Clinical classification…Physiologic jaundice ( Icterus neonatorum)
05/03/23
Clinical classification…
2. Pathologic jaundiceJaundice detected on the first day of life
Jaundice persisting more than two weeks
Jaundice rising at a rate more than 0.5mg/dl/hr
Direct bilirubin more than 2mg/dl
Underlying systemic illness
Clinical classification…Physiologic Vs pathologic
Signs PhysiologicJx Pathologic JxClinical Jx Visible in 2-3day With in 24hrs
TSB rise <5mg/dl/day >5mg/dl/day
TSB Term<12mg/dl Preterm<15mg/dl
Term>12g/dl Preterm>15mg/dl
Conj BBn <1.5mg/dl >1.5(2)mg/dl
Jaundicepersisting
Term <1 week Preterm <2weeks
Term >1week Preterm >2weeks
common neonatal problems
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Causes of pathologic jaundice
Increased production Hemolytic diseases (ABO and RH)
Enclosed hemorrhage
Polycythemia
Decreased clearance Sepsis
Prinatal asphyxia
Prematurity
Hypothyroidism
Crigler-Najjar syndrome
Causes of pathologic jaundice
Increased enterohepatic circulation
Breast milk jaundice
Gastro intestinal obstruction
Breast feeding jaundice
Obstructive lesions (Direct Bilirubin)
Choledochal cyst
Biliary atresia
Sepsis and congenital infections
Causes of pathologic jaundice…
Blood Group Incompatibilities
Rh negative mother & Rh positive infant
ABO incompatibilities
Strongly considered if there is jaundice in the first 24 hours of lifeNon-Immune Hemolytic Anemias:
G6PD Deficiency:
Deficiency-decreased NADPH- decreased reduced Glutathione –
decreased protection of RBCs from oxidants-hemolysis
Causes of pathologic jaundice…
Structurally Abnormal RBCs: Spherocytosis
Pyknocytes ( irregular borders)
Thyroxine Deficiency: Thyroxine increases the activity of Glucoronyl transferase which promotes
conjugation of bilirubin.
Inhibition of Conjugation: Sulfonamides and Vitamin K results in competitive conjugation inhibition of bilirubin. GALACTOSEMIA:
Absent or deficient Galactose 1-phosphoate uridyl transferase which is needed in
glucoronidaton of indirect bilirubin.
RH hemolytic disease
RH negative woman conceiving RH positive fetus
IgG crosses the placenta and results in fetal red blood cell hemolysis
Anemia, jaundice, heart failure and generalized edema (hydrops fetalis) develop in utero
Affected new borns are delivered prematurely and may be still birth
Moderately affected new borns may show anemia, hepatosplenomegaly and signs of congestive heart failure
Early exchange transfusion is life saving
Unsensitized woman should take anti –D every delivery of RH positive neonate
Jaundice Risk Factors for Neonatal Hyperbilirubinemia
Jaundice visible on the 1st day of life
A sibling with neonatal jaundice or anemia
Unrecognized hemolysis (ABO, Rh, other blood group, incompatibility); UDP-
glucuronyl transferase deficiency (Crigler-Najjar, Gilbert disease)
Non-optimal feeding (formula or breast-feeding)
Deficiency of glucose-6-phosphate dehydrogenase
Infection (viral, bacterial). Infant of diabetic mother. Immaturity (prematurity)
Cephalohematoma or bruising. Central hematocrit >65% (polycythemia)
East Asian, Mediterranean, Native American heritage
Clinical assessment of jaundice
Jaundice in the newborn progresses in cephalocaudal direction Face =5-7mg/dlChest =10mg/dllower abdomen /thigh= 12mg/dlSole/palms≥15mg/dl
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Work up neonates with JxHistory
Age of onset
Family history of Jaundice,pallor,splenectomy
Previous sibling with Jaundice
Maternal illness during pregnancy
Maternal drug intake
Delivery history e.g. PROM ,sepsis, prolonged labor
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Cont’d
P/EProper classification of the newborn according to GA, & wgt.
Pallor, petechea
Bruises and cephalhematoma
Dark urine and clay colored stool
Examination geared to specific cause
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Schematic approach to the diagnosis of neonatal jaundice
Investigations
TSB with conjugated fraction
Hct with RBC morphology and reticulocyte count
Bg of the baby with direct coomb’s test
Bg of the mother with indirect coomb’s test.
Specific investigations for suspected specific problems
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Management
Aim lower serum billirubin decrease neurtoxicity
Principles of treatment Avoid drugs w/c interfere with BBn metabolism Treat factors w/c↑ neurotoxicity Give adequate feeding Specific therapy Decrease serum billirubin
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Management…
Physiological jaundice Explain about benign nature of the disease
Encourage to breastfeed frequently & exclusively
Ask Mother to bring baby back if baby looks deep yellow or palms &
soles have yellow staining.
Pathological jaundice
Mainly 2 modalities of treatment:
Phototherapy
Exchange transfusion
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Management…
Lower serum Billirubin Phototherapy Exchange transfusion
1. Phototherapy Mainstay of treatment
Under blue-green light(460-490nm), insoluble bilirubin is converted into
soluble isomers that can be excreted in urine & feces. Indicated when TSB rises more than normal but not exchange
transfusion level May be therapeutic or prophylactic
To be effective, bilirubin must be present in skin; hence nor role for
prophylactic phototherapy
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Prophylactic phototherapyINDICATIONS
RH isoimmunization with sever hemolysisBirth weight<1000gm(EVLBW)Sever multiple bruises
SIDE EFFECTSErythematous skin rashRetinal damageIncreased insensible water lossBronze baby syndromeLoose stoolLow calcium
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Exchange transfusion( ET)Most effective way of treating Jaundice and anemiaCould be partial or double exchange transfusion
INDICATIONSRh isoimmunization with hydrops fetalisCord blood Billirubin >5mg/dlRise in Billirubin >0.5mg/dl/hr despite phototherapyHemoglobin <11gm/dlTSB >20mg/dlVLBW, preterm, sepsis
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Choice of blood for exchange BT
ABO incompatibility Use O blood of same Rh type
Rh isoimmunization Emergency 0 -ve blood Ideal 0 -ve suspended in AB plasma or baby's blood group but Rh –ve
Other situations Baby's blood group
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Exchange transfusionCOMPLICATIONS
Portal vein thrombosis Umbilical vein perforation/bleeding Necrotizing enterocolitis Cardiac arrest/arrhythmia Hypoglycemia, hypocalcemia,
hypomagnisemia, hyperkalemia Increased risk of infection Respiratory and metabolic acidosis
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KERNICTERS (Billirubin encephalopathy)
Definition: neurologic syndrome resulting from deposition of unconjugated billirubin in brain cells .
Sites of billirubin staining and necrosis include -Basal ganglia , Hippocampal cortex, Sub
thalamic nucleus & cerebellum Cerebral cortex is spared
Half of the neonates with kernicters at autopsy have extra neuronal lesions
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Pathophysiologic mechanism
Unconjugated BBn is nonpolar ,lipid soluble and can traverse BBB.
Factors that ↑ billirubin toxicity Hypoxia (asphyxia) Hypothermia & hypoglycemia sepsis Prematurity Acidosis Hypoalbuminemia
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Clinical progression of encephalopathy34
Thank you!35