Jaundice results from deposition of bilirubin in the skin premature infants are also more likely to develop jaundice

 

INTRODUCTION

 

          Bilirubin is a yellow pigment that arises from the break down of red blood cells haemoglobin.  Jaundice’s the yellow discolouration of the skin and mucous membrane, due to accumulation of bilirubin in the serum.  Neonatal jaundice become apparent at serum bilirubin concentration of 5-7 mg/d.

1. DEFINITION:

          Jaundice is yellow discolouration of skin and mucosa is caused by accumulation of excess bilirubin in the tissues and the plasma conjugated.  Neonatal jaundice becomes apparent at serum bilirubin concentrations of 5-7 mg/dl. (Bilirubin level should be in excess 2mg/dl).

 

2.  INCIDENCE

          Neonatal jaundice is observed during first week of life.  More than 50% of full term infants and 80% preterm neonates.

 

3. TYPES

          Neonatal jaundice is divided into two groups.

a.    Physiological jaundice

b.    Pathological jaundice

 

a) Physiological Jaundice

          The jaundice usually appears on 2^nd and 3^rd day and disappears by 7^th -10^th day a little later in premature neonates.  In a term infant the level may be 6-8 mg/dl on 3^rd day.  A rise of uncongugated serum bilirubin to 12mg/dl is in the physiological range in a fulterm well baby, physiological jaundice never appears before 24 hrs of age.

 

Causes

1.  Increased red cell break down

          The newborns red blood cells have a shorter life span (100 days in term infants and 60-80 days in preterm infants as opposed to 120 days in adults).  The average concentration of serum conjugated bilirubin in neonates is three to seven times higher than that of adults.  Whereas the concentration of unconjugated bilirubin is four to 24 times higher.

 

2. Demand albumin binding capacity

          The ability of neonates to actively transport bilirubin to the lives for conjugation is reduced because of lower albumin concentration, decreased albumin capacity.

 

3. Enzyme deficiency

          New born infants have low levels of uride diphospho Glucuronyl transferance (UDP-GT) enzyme activity during the first 24 hours of life.

 

 

4.  Increased entro hepatic reabsorption

          Increased enterhepatic circulation due to decreased gut motility.

 

MANAGEMENT

          No specific treatment is generally required

a.   Adequate feeding

Early frequent feeding helps newborns deal with their increased bilirubin load.  Demand feeding ensures adequate volume of colostrums and milk in the intestine.

b.   Careful observation of newborn

It will help to distinguish between healthy babies with normal, physiological response and those for whom serum bilirubin is required.

c.    In premature babies:

Rising bilirubin level to critical level require use of phototherapy or phenobarbitone administration.

 

b) PATHOLOGICAL JAUNDICE

          Pathological jaundice usually appears within 24 hours of birth, and is characterized by a rapid rise in serum bilirubin and prolonged jaundice.

FEATURES OF PATHOLOGICAL JAUNDICE

a)    Clinical jaundice appears within the first 24 hours of life.

b)   Increase in bilirubin > 5mg/dl pr day.

c)    Total bilirubin > 13 mg/dl

d)   Persistence of clinical jaundice for 7-10 days in full term infants and two weeks in premature infants

 

CAUSES OF PATHOLOGICAL JAUNDICE

1)   Excessive red cell haemolysis

a.   Haemolytic disease of the newborn Feto – maternal blood group incompatibilities Rh incompatibility, ABO incompatibility immunization against kell antigen

                                         i.    Increased red cell fragility – congenital sphirocytosis.

                                       ii.    Deficient red cell enzyme (Glucose 6-phosphate) dehydrogenase)

b.   Neonatal sepsis specially with E.coli

c.    Polycythemia, delayed cord clamping and infants of diabetic mothers.

d.   Extravasated blood, such as incephal haematoma and bruising

2)   Defective conjugation

a.   Congenital deficiency of gluconyl transferase

                                         i.    Immature liver cells as in premature babies.

                                       ii.    Dehydration, starvation, hypoxia and sepsis because oxygen and glucose are required for conjuation.

3)   Breast Milk jaundice: The enzyme – cluclaronyl transferase activity of the liver is inhibited by a specific steroid 3a, 20b pregnaediol and increased fatty acids of breast milk.

4)   Metabolic disorders: Galactosemia, hypothyrodism may be associated with unconjugated hyper bilirubinemia

5)   Transport and excretion failure

a.   Hepatic obstruction caused by congenital anomalies such as biliary atresia, bile plugs or absence of common bile duct

b.   Excess conjugated bilieubin caused by infection or idiopathic neonatal jaundice.

c.    Umbilicas cord sepsis leading to ascending thrombophlebitis, obstruction of biliary cancaliculi and destruction of liver cells.

 

 

 

CLINICAL MANIFESTATIONS

 

a.   Urine become yellow

b.   Stool are often pace or clay coloured peuritis

c.    Fatigue

d.   Lethargy

e.    Scleral appearance yellow

f.     Refusal of feed

g.    Presence of dehydration, starvation hypothermia, acidosis, hypoxia.

h.   Presence of irritability, a high pitched cry, dark urine or light stools

 

DIAGNOSTIC EVALUATION

a)   History collection

i. Maternal history of infection or administration of       drugs during pregnancy.

ii. Previous sibling affected by jaundice and anemia.

iii. Ethnic groups of the parents and ancestors.

iv. Time of onset of jaundice

v. General condition of the infant, whether healthy        having no feeding difficulty, no fever no rash.

 

 

b)   Laboratory Investigation

i. Haemoglobin

ii. Serum bilirubin

iii. Direct coomb’s test

iv.Indirect coomb’s test.

v. Reticulocyte count.

vi. ABO blood group and Rhesus type for possible   incompatibility.

vii. Peripheral blood smear

viii.White cell count

ix. Glucose 6-phosphate dehydrogen are assay

 

MANAGEMENT

        Three methods of treatment are used to reduce the level of unconjugated bilirubin.

1.    Phototherapy

2.    Pharmacologic therapy

3.    Exchange transfusion

 

1) Phototherapy

          During phototherapy the neonates skin surface is exposed to high intensity light, which photochemically converts fat soluble, unconjugated bilirubin into water soluble bilirubin, which can be exerted in bile and urine.

 

Indications

a)   Who are smaller or preterm

b)   Who are sick particularly with hemolysis

c)    In whom jaundice appears within 12-24 hrs.

d)   17-22 mg / dl for teem infants who become jaundiced after 48 hrs.

e)    8-10 mg/dl for preterm infants > 1,500 gm.

f)     5-8 mg / dl for preterm babies < 1500 gm

 

Length Of Phototherapy

          Just 24-28 hours exposure is generally long enough to bring down serum bilirubin levle to safe limit.

 

Special Precuation

Male baby: Protect the eyes and genetalia from exposure to phototherapy.

Female baby – Protect the eyes using mask

 

Types Of Phototherapy

1. Conventional systems

Flurescent lamps are used deliver high intensity light.

2. Fiberoptic light systems

Side effects

a.   Lethargy

b.   Hyperthermia

c.    Dehydration

d.   Fluid losses

e.    Skin rashes

f.     Retinal haemorrhage

g.    Skin Malignancy

h.   Delayed puberty

 

Care of the baby undergoing phototherapy

a.   Observing any visible side effects.

b.   Check the baby’s temperature

c.    Apply eye pads.  The infant is also observed for any eye discharge or weeping.

d.   Estimation of bilirubin level.

e.    Undress the baby

f.     Apply genital pads

g.    Put on the photo therapy machine

h.   Fluid intake and urine output are to be monitored

i.     Neurobehavioural status

j.     Sensory deprivation

          To reduce the effects of isolation when feeding  the eye patches are to be taken off and the infant is removed from lights.

a.   Place on each side small pillow or a rolled sheet for safely.

b.   Turn the baby frequently to exposure all the body parts.

c.    Check the serum bilirubin level as per order.

d.   Maintain intake and output chart.

e.    Remove the eye pads when mother is feeding.

f.     Check in weight twice daily

g.    Hypocalcemia.

 

          Serum calcium level decreases in some babies and a level < 7 mg / dl is considered hypocalcaemia in neonates.

 

After Care

Ø  Switch of the phototheraphy machine.

Ø  Remove the eye pad from the baby.

Ø  Inspect the baby for any sign of complication.

Ø  Give the baby to the mother for feeding.

 

Complications

Ø  Watery diarrhoae

Ø  Skin rashes

Ø  Dehydration

Ø  Bronze baby syndrome

Ø  Retinal damage

 

2. Pharmacological Therapy

Ø  Phenobarbital therapy induces hepatic microsomal enzymes and increase bilirubin conjugation and excretion.  A dore of 5-8 mg / kg every 24 hrs is used it takes 3-7 days to be effective.

Ø  Metalloporphyrins decrease bilirubin production by inhibiting heme oxygenace.

 

Salt free albumin

          It may be prescribed about one gram per kg of the body weight.  The salt free albumin increases bilirubin binding capacity.

 

3. Exchange blood transfusion

          It is necessary to remove the excess serum bilirubin mechanically by exchange blood transfusion.

Indications

a.   Progressive rise of bilirubin > 1mg / dl / hr inspite of phototherapy.

b.   Cord blood bilirubin level > 5mg / dl and haemoglobin level < 12 gm / dl

c.    Total bilirubin 20 mg / dl or more

 

Objectives

a.   To remove circulatory antibodies.

b.   To correct the anaemia by replacing the Rh positive sensitized red cells.

c.    To eliminate the circulating bilirubin

 

Complications

a.   Air embolism

b.   Cardiac failure

c.    Sepsis

d.   Hyperkalaemia

e.    Coagulopathesis due to thrombocytopenia

 

NURSING MANAGEMENT

 

a.   Constant observation is necessary to detect early changes.

b.   Skin color is observe for increase or decrease yellowness.

c.    Urination is checked for frequency amount of colour.

d.   Vital Signs should bechecked.

e.    Maintain the body temperature specially when the baby is under phototherapy.

f.     Any behavioural changes, convulsion or sluggishness should be noted and reported.

g.    Enough fluid intake is necessary to help in the excretion of bile to prevent dehydration.

h.   Eye of the baby should be covered with eye pads to protect from high intensity light in the care of the baby under phototherapy.

i.     Check the weight twice daily.

j.     Check the serum bilirubin level

k.   Maintain intake and output chart.

l.     Advice mother to give lactore free milk feeding for the baby suffering from Glactosemia.

 

 

CONCLUSION

 

          Jaundice results from deposition of bilirubin in the skin premature infants are also more likely to develop jaundice.  Asian and native American babies tend to have higher bilirubin levels than white babies who in turn have higher level than black infants.

 

 

BIBLIOGRAPHY

 

1.   D.C. Dutta “Text Book of Obstetric Including Perinatology and contraception”.

Sixth edition 2004, New Central Book Agency (P) Ltd., Page.No.447-481.

2.   Annamma Jacob “A comprehensive Text Book of Midwifery”, Second Edition Jaypee brothers Medical Publishers Page.No.588-594.

3.   V.Ruth Benet and Linda K. Brown Myles Text Book for Midwives Thirteenth Edition, Page.No.816-822, 827-830.