2. Neonatal Jaundice
• Def:- Jaundice is yellow discoloring of the skin
and mucous membrane.
• it is not in itself a disease but a sign of the
presence of excessive amounts of bilirubin
circulating in the blood stream.
3. Neonatal Jaundice
– Is observed during the first week of life in 60% of
term and 80% of preterm infants.
– Color results from accumulation in the skin of
unconjugated bilirubin. It may also be due in part
to the deposition of conjugated bilirubin.
– Unconjugated bilirubin is neurotoxic to
infants.[kernicterus]
4. Physiological jaundice
• Immaturity in bilirubin metabolism at multiple
steps results in the occurrence of
hyperbilirubinemia in the first few days of life.
These are:
– Increased bilirubin load on the hepatic cell
– Defective uptake from plasma into liver cell
– Defective conjugation
– Decreased excretion
– Increased entero-hepatic circulation
5. Characteristics of physiological jaundice
• First appears between 24-72 hours of age
• Maximum intensity seen on 4-5th day in
term and 7th day in preterm neonates
• Does not exceed 15 mg/ dl
• Clinically undetectable after 14 days.
• No treatment is required but baby should
be observed closely for signs of
worsening jaundice.
6. Pathological jaundice
• Presence of any of the following signs denotes that the
jaundice is pathological.
• Treatment is required in the form of phototherapy or
exchange blood transfusion.
• One should investigate to find the cause of pathological
jaundice.
– Clinical jaundice detected before 24 hours of age
– Rise in serum bilirubin by more than 5 mg/ dl/ day
– Serum bilirubin more than 15 mg/ dl
– Clinical jaundice persisting beyond 14 days of life
– Clay/white colored stool and/or dark urine staining the clothes
yellow
– Direct bilirubin >2 mg/ dl at any time
7. Causes of jaundice
• Hyperbilirubinemia in the first week of life is
usually of the indirect variety.
• Causes are usually classified based on the
time of onset of jaundice.
– Appearing within 24 hours of age
• Hemolytic disease of newborn: Rh, ABO and minor
group incompatibility
• Infections: intrauterine viral, bacterial; malaria
8. Causes of jaundice
• Appearing between 24-72 hours of life
– Physiological
– Sepsis neonatrum
– Polycythemia
– Concealed hemorrhages: cephalhematoma,
subarachnoid bleed, IVH.
– Increased enterohepatic circulation
–
9. Causes of jaundice
• Appearing after 72 hours
– Sepsis neonatrum
– Neonatal hepatitis
– Extra hepatic biliary atresia
– Metabolic disorders
12. Assessment
• The examination should be done in natural
daylight, since jaundice can then be most easily
seen.
• The color of the nails, sclera, mucous
membranes, and skin, including the palms and
soles, is observed.
• Blanching of the skin by applying direct pressure
over bony areas, such as sternum or the nose,
allows the nurse to more readily see the yellow
coloring.
13. Assessment
• In deeply jaundiced newborn one must also
evaluate for presence or absence of bilirubin
toxicity (kernicterus). Kernicterus is identified
by lethargy and poor feeding, poor or absent
Moro's reflex, opisthotonus or convulsions.
15. Management of jaundice
• is directed towards reducing the level of
bilirubin and preventing CNS toxicity.
– Prevention of hyperbilirubinemia
• Early and frequent feeding
– Reduction of bilirubin:
• This is achieved by phototherapy or/and exchange
transfusion.
16. Management of jaundice
1. Give glucose 4 hourly, this will help the liver to
improve its production of glucuronyl
transferees.
2. Increase fluid intake which will help excretion
3. Keep the baby in a light place light sunlight or
fluorescent light is best as it destroys bilirubin.
This is called photo therapy. The baby's eyes
must be protected and he must be turned
frequently
4. Phenobarbitone is help full to facilitate the
conversion&excreation of bilirubin
Metalloporphyrins — Synthetic metalloporphyrins, such as tin mesoporphyrin (SnMP), reduce bilirubin production by competitive inhibition of heme oxygenase [ 59-66 ]. There are limited data upon the safety of SnMP [ 66 ], and SnMP is not available for general use.
Brush border beta-glucoronidase – deconjugates it.
Bowel bacteria – convert it to urobilinogen and stercobilinogen.