NEONATAL JAUNDICE

YEE WEI HOONG121303147

31B (L1)1

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DEFINITION

• Jaundice is a yellowish discolouration of skin, sclerae, mucous membranes & nails from accumulation of bilirubin.

• Hyperbilirubinemia refers to an excessive level of bilirubin in blood.

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Neonatal Jaundice• One of the most common medical

conditions in newborn babies• All babies have transient rise in

serum bilirubin, but only 75% are visibly jaundiced.

• Jaundice is clinically detectable when serum bilirubin levels are >5mg/dL (85 umol/L)

• Jaundice is more common in Asian babies

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Day 1 Day 7 Day 14/21

PATHOLOGICAL jaundice

PHYSIOLOGICAL jaundice

PROLONGED jaundice

Time Frame for Jaundice

CLASSIFICATIONS• Physiological

1. Appears after 24hrs2. Maximum intensity by 3rd -5th day in term, 7th day in preterm3. TSB <15mg/dL (<255umol/L)4. Not detectable clinically after 14days5. No underlying cause6. Disappears spontaneously

• Pathological 1. Appears within 24hrs of age2. Serum bilirubin level increase >6mg/dl/day3. TSB >20mg/dL(340umol/dL)4. Conjugated/Direct bilirubin >2mg/dL(34umoLdL) 5

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Pathophysiology of Physiological Jaundice

1. Decreased erythrocyte life span (80 to 90 days) in a full term infant

2. Increased erythrocyte volume3. Increased bilirubin load on the hepatic cell4. Defective uptake from plasma into liver cell –

decreased ligandin5. Defective conjugation - relatively low activity of the

enzyme glucuronosyltransferase which normally converts unconjugated bilirubin to conjugated bilirubin

6. Low conversion of bilirubin to urobilinogen by the intestinal flora resulting in higher entero-hepatic circulation

7. Decreased excretion

RBC vol & RBC survival

Bil monoglucoronide Bil Diglucoronide

UCB

Prod

uctio

nTr

ansp

ort

Uptake

Excretion

Conjugation

ineffective erythropoiesis & haem turnover

Non availability of albumin binding sites

Defective conjugation

Ligandin

Decreased excretion

gut motility Poor evacuation beta glucoronidase, intestinal

bacteria

BILIRUBIN load

Defective uptake from plasma

Entero-hepatic circulation

Bilirubin Load Causing Jaundice in Newborn

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CAUSES OF PATHOLOGICAL JAUNDICE

1. Haemolytic disease of newborn: Rh, ABO & minor group (anti-Kell, Duffy) incompatibility

2. Infections: Intrauterine infection (Bacterial, viral)

3. Membrane defects: Spherocytosis, elliptocytosis

4. RBC enzyme defects: G6PD deficiency, pyruvate kinase deficiency

5. Polycythemia

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NNJ & Mother’s Knowledge

• A Malaysian study found that less than 50% of the mothers had good knowledge & awareness about the risks & complications of NNJ.1

1. Boo NY, et al. Med J Malaysia. 2011 Aug;66(3):239-243

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MONITORING• Extract (1) from Malaysia CPG :

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MONITORING• Extract (2) from Malaysia CPG :

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MONITORING• Extract (3) from Malaysia CPG :

82. Division of Family Health Development, Ministry of Health. Integrated Plan for Detection and Management of Neonatal Jaundice. Putrajaya: MoH; 2009

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MONITORING• Extract (4) from Malaysia CPG :

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P.P.A.P Physiological, Pathological and Prolonged

Physiological Jaundice

Pathological Jaundice

Prolonged jaundice

Starts within 24 hours

Starts after 24 hours; usually disappear by 14th day

Jaundice lasting >14 days

MIX & MATCH!!!

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Maybe Previous Q was too easy…Try This Pulak.

In the development of physiological NNJ, there is:a.decreased bilirubin load F b.defective uptake of bilirubin from plasma  Tc.defective conjugation  Td.increased excretion  Fe.decreased entero-hepatic circulation  F

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Three Components of Assessment

• History• Physical Examination• Lab Investigations

*Phototherapy must always be started while awaiting further assessment & investigation

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Objectives of Proper Assessment (History, Physical Examination, Lab

Investigations)

End Point

Prevention of bilirubin neurotoxicity(acute/ chronic)

To identify

Risk Factors (for severe NNJ and neurotoxicity)

Severity of NNJ(level of SB or extent of hemolysis)

Complications (signs of ABE)

To decide on

Management (phototherapy, exchange transfusion)

Follow-up (ABR, MRI, development)

But not at the cost of overinvestigating or overtreating low risk babies

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1. Risk Factor Identification

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2. ASSESSMENT OF SEVERITY

• Visual assessment

• Transcutaneous measurement

• Analysis of blood serum

VISUAL ASESSMENT-KRAMER’s RULE

Kramer’s rule describes the relationship between serum bilirubin levels & the progression of skin discolouration 20

Transcutaneous bilirubinometer (TcB)

• The transcutaneous bilirubinometer is a hand-held device that measures the amount of bilirubin in the skin.

Bilicheck (Philips)Does not require any disposable material & less time consuming

JM 103 (Draeger)

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Serum Bilirubin (SB) Measurement

• Gold standard for detecting & determining the level of hyperbilirubinaemia.

• May be estimated on either a capillary or a venous blood sample.

• Blood sample should be analysed as soon as possible & should be shielded from light during transport (exposure to light rapidly & significantly decreases bilirubin).

• Remove phototherapy prior to sample collection.

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CPG says…

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3. Assessing Complications

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Dangers of Hyperbilirubinemia• If untreated, it will lead to acute & chronic bilirubin

encephalopathy, eventually kernicterus.• C/F:

Refusal of feeds, shrill cry, setting sun sign, convulsions, retrocollis & opisthotonus

Sluggish Moro’s response, lethargy, poor feeding Preterm – Non specific. Die due to apnoeic attacks Infancy – Athetoid cerebral palsy, choreo-athetosis, brownish

staining of teeth, dental dysplasia, deafness, paralysis of upward gaze, intellectual retardation & learning disabilities

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Images taken from: Vinod K, et al. Bilirubin Neurotoxicity in Preterm Infants: Risk and Prevention. J Clin Neonatol. 2013 Apr-Jun; 2(2): 61–69.

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Acute Bilirubin Encephalopathy (ABE)

• ABE: Changes of mental (behavioural) status & muscle tone during the neonatal period when the baby is having hyperbilirubinaemia.

• Identifying & Monitoring of ABE:• Term Babies: Use BIND Score • Preterm Babies: Difficult, as signs are

subtle. Auditory Brainstem Response (ABR) could be used.

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BIND Score

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Indications for Referral to Hospital

• Jaundice within 24hours of life• All babies that require phototherapy• Jaundice below umbilicus• Jaundice extending to soles and feet• Rapid increase of bilirubin level (>0.5mg/h)• Diagnosed with G6PD deficiency• Haemolytic disorder• Symptoms and signs of sepsis

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Investigations • *Total serum bilirubin• *G6PD status• Others as indicated:-infant’s blood group-Maternal blood group-Direct coombs’ test (indicated in day 1 jaundice and severe jaundice)-FBC, reticulocyte count, peripheral blood smear-Blood culture, urine microscopy, and culture (infection

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TREATMENT1. Phototherapy

• Light with wavelenght of 450nm convert unconjugated bilirubin into harmless water soluble pigment excreted predominantly in the urine

2. Exchange Transfusion• Twice the infant’s blood volume 2x80ml/kg is exchange

3. IVIG (Intravenous immunoglobulin)• high dose IVIG (0.5-1 gm/kg over 2hours) reduce the need for ET in Rh and

ABO hemolytic disease• Give as early as possible in hemolytic disease with positive Coomb’s test or

when the serum bilirubin increasing despite intensive phototherapy.

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Hmm…Final Q• Following vessels can be utilised

for exchange transfusion, except:A. Femoral VeinB. Umbilical ArteryC. Umbilical VeinD. Subclavian VeinE. Peripheral Artery

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Measures to Prevent Severe Neonatal Jaundice

• Promote & support breastfeeding.• Advise a frequency of 8 to 10 feedings per day • Formula milk for term infants should be 1 to 2 ounce every 2 to 3

hrs in the 1st week.• If phototherapy in infants with hemolytic jaundice is initiated early

and discontinue before infant 3-4 days old, must monitor for rebound jaundice and adequacy of breast feeding within the next 24-48 hours.

• Routine supplements with water or dextrose water will not help prevent hyperbilirubinemia

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Follow up

• All infant discharge < 48hrs after birth should be monitor in ambulatory setting or at home

• Infants with risk factors for severe neonatal jaundice, early follow up is a must to detect rebound jaundice

• Infant with hemolytic diseases not requiring ET should be closely followed up for anemia until risk of ongoing hemolysis is minimal.

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REFERENCES

1. Malaysia Clinical Practice Guidelines: Management of Neonatal Jaundice, 2nd edition, 2014.

2. Paediatric Protocol. 3rd ed: KKM,20153. Tom Lissauer, Illustrated TextBook of

Paediatrics, 4th ed.20124. Nelson essential of pediatrics.5. http://emedicine.medscape.com/

article/974786