JAUNDICE THE NEWBORN INFANT

Made by: Resident Clim Georgiana

Resident Dumitru Liliana
 JAUNDICE THE NEW-born infant

ABSTRACT

Jaundice is one of the most important events that require medical attention in newborns. The
yellow coloration of teguments and mucous membranes in newborns with jaundice is due to
accumulation of unconjugated bilirubin. Intensity or persistence of jaundice in the neonatal
period can be a first sign of subsequent pathology, that is why it should be very well assessed and
followed.

Definition : jaundice represents the yellow coloration of teguments and mucous membranes,
which occurs due to the increase of the concentration of the sero bilirubin. In new-born infant
jaundice becomes apparent to the values of the serum bilirubinei 5- 7 mg%.
There are 3 types of jaundice: physiological, pathological, nuclear material.

Metabolism bilirubinei:
Steps:
1. The training system bilirubin reticulo-histiocitar (SRH) in the liver, spleen, bone marrow
2. The carriage bilirubin in blood
3. The metabolism of hepatic bilirubin
4. Excretion bilirubin in the intestin
The mechanisms involved in the accumulation bilirubin to new born: hepatic ligandina deficit,
the summary and low activity of UDP-GT, delayed, excretion hepatic circulation enterohepatic
circulation increased (6 x value to adult), increased activity of beta glucuronidazei (10 times
higher that the adult).

The intensity and severity of jaundice can be appreciated the clinical trial, always at the natural
light, using the strip Kramer (Table No. I). The absence of jaundice does not automatically mean
absence of hyperbilirubinaemia, but can be used for the prediction with accuracy of the new-born
infants who will not develop sever hyperbilirubinaemia. Clinical assessment of jaundice has no
value at babies that make phototherapy and the ones with constitutional hyperpigmentation.

Icterica area Indirect bilirubin (mg%)

The head, neck strap 4-8
Chest 5-12
The abdomen, thigh 8-16
Arms, calf 11-18
The palms, plants 15 -20
Table No. I- clinical judgment of the intensity of the bilirubine areas (Kramer)

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I.Physiologic jaundice: Unconjugated hyperbilirubinaemia the value of the total bilirubin is
below 12 mg/100 ml serum and direct bilirubinemia value below 15%.
Jaundice appears after 48 hours from his birth, to a new-born with the general status of the good,
without hepatosplenomegaly, indirect bilirubin values below 12 mg/dl. It occurs at 50- 80% in
term newborn; the 90% at premature.

Cause:
The physiological jaundice causes are: blood volume increased, short life of fetal erythrocytes,
ineffective erythropoiesis, poor hepatic conjugation, increased enterohepatic circulation.

Jaundice of prematurity
Shall be carried out by simple exaggerating neonatal simple jaundice.
 The production of bilirubin increased (the deficit of vitamin E stressed the prematurely
→ hiperhemoliza more accentuated)
 The capacity of the mounting plasma bilirubin is low by the shortage of albumin
(increase the risk of Jaundice nuclear material for the same values of unconjugated
bilirubin)
 Capturing glucuronoconjugarea hepatic, and excretion in the bile ducts bilirubinei ways
more deficiencies from the new born in the period
 Special conditions circulatory problems (this thing liver part of circulating unconjugated
bilirubin).

Prophylactic treatment: early: food at the breast, colostrum having purgative effect
curative: Phototherapy

II.Pathological Jaundice: Hyperbilirubinaemia published in the first 24 hours after birth, with
the total bilirubinemia over 12 mg/100 ml serum to the new-born infant and more than 15
mg/100 ml of serum from prematurely; or direct bilirubinemia over 1.5+2 mg%.
Jaundice extended with a duration of 10 days to the new-born infant and over 2 weeks at
prematurely.

Cause: disturbance of production, metabolism disorders, disorders of excretion of indirect

bilirubinemia.

Types of Jaundice pathological to new-born after the mechanism of production:

1. (Prehepatic Haemolytic jaundice) - with increased indirect bilirubin

 The incompatibility Rh;

 Incompatibility AB0;
 Hemoglobinopathies: congenital spherocytosis, eliptocitoza, alpha-thalasemia, the
shortage of G6PDH;
 polyglobulus after late umbilical cord oclusion, fetal transfusion feto-load in the twin
pregnancy;
 resorbtion jaundice: cephalhematoma, ecchymosis;

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  diabetic fetophaty;
 hypothyroidism
 metabolic jaundice of Crigler-Najjar and Lucey-Driscol syndrome.

2. Jaundice with mixed bilirubin:

 Infections: syndrome, TORCH, viral hepatite;

 Galactosemia;
 Shortage of alpha 1-antitripsina;
 fibrosis cystic

3. Jaundice with increased direct bilirubin - cholestatic jaundice:

 The thick ball syndrome;

 Atrezia-biliary intra- and extrahepatic;
 Food for parenteral use extended.

Neonatal congenital hemolytic disease represents a Rh native incompatibility Rh or ABO

incompatibility. Appears in the following situations: Rh negative mother and child Rh positive,
the mother A(I) and the child(II) or (B)(III).
When the fetus produce antibodies in maternal blood, passing in the fetal movement and produce
the haemolysis.

Clinic: anemia, jaundice, hepatosplenomegaly, bleeding and neurological manifestation.

Clinical forms :
 foeto placental anasarca, the most serious form of Rh isoimmunization, which frequently
unfavorable outcome. New baby has generalized edema, ascites, hepatosplenomegaly,
pale, heart failure, anemia, birth asphyxia.
 haemolytic jaundice: the new-born infant is apparent normally at birth, has anemia, but
Hgb is above 12 mg%, increased jaundice, hepatosplenomegaly, edema localized,
bilirubin has more than 3-4 mg%.
 Congenital hemolytic anemia: the new-born infant shows small Apgar score, Hgb below
12 mg%, Bilirubin 3-4 mg% hepatosplenomegaly.

The laboratory diagnosis:

 Blood group and Rh to parents and child
 The titre of antibodies to pregnant
 Positive Coombs test reveals antibodies in the serum mother
 The CBC newborn: thrombocytopenia, anemia
 Smear peripheral: more than 25% erythroblasts, reticulocytes more than 6%
 Indirect bilirubin cord blood more than 4 mg%
Prophylactic treatment: imunoprophylaxis with anti-D(specific Ig) at the woman with Rh
negative (300mg in 72 hours after the abortion/ birth new born Rh positive); the new-born Rh
negative sex female of the mothers Rh positive.
Curative treatment:

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  phototherapy and phenobarbital 5-8 mg / day, 3-4 days
 exchange transfusion double-volume (160 ml/kg)
 Whole blood (Htc 40-45%, OI group, Rh-negative or izogup the newborn, but negative
Rh
 Monitoring of indirect bilirubin/ 6h, exchange transfusion is repeated if bilirubin
increases by 1 mg/h
 Blood is extracted through the umbilical artery, umbilical vein transfused

III. Kernicterus - serious complication of hemolytic disease is installed, usually on the third day
of life. Kernicterus occurs due to indirect bilirubin passage across the blood-brain or blood-brain
barrier is broken.
A number of factors increase the risk of kernicterus: prematurity, because hypoalbuminemia;
acidosis, hypoxia hipercarbie and factors that increase the permeability of the blood-brain barrier.
The unbound free bilirubin to albumin, fat soluble substance is impregnated in the brain,
especially in the nucleus basalis, hippocampus and nucleus of the anterior horn of the spinal
cord. Microscopic highlighted phenomena of neuronal loss and gliosis with necrosis. Important
in the treatment of hemolytic jaundice, indirect bilirubin is maintaining below 20 mg / dL, above
this level considering the level of bilirubin toxicity.

Clinical signs of kernicterus: acute bilirubin encephalopathy occurs in term newborns with Rh
incompatibility, with bilirubin exceeding 20 mg / dl. From Clinically, there are three clinical
stages:
Stage 1: Hypotonia, lethargy, crying sharp and weak sucking reflex. Term newborns who are
treated at this stage have very good prognosis, with normalization of clinical signs after lowering
bilirubin.
Stage 2: Extensor muscle hypertonia with opistotonus, stiffness, seizures oculogyric, fever and
convulsions, many of newborns dying at this stage or developing chronic encephalopathy.
Stage 3: Hipotonia replaced hipertonia after one week. Death is the most frequently at this stage.
Infants with significant hyperbilirubinemia (> 25 mg / dL) should be carried craniocerebral MRI
to highlight abnormal signals in the nuclei of basal and evoked installation auditors to detect
hearing loss. Chronic bilirubin encephalopathy is marked by classical clinical signs up tetrad
Perlstein: abnormal extrapyramidal partial or complete sensorineural deafness, limiting upward
gaze, deciduous teeth dental dysplasia.

Treatment:

 Phototherapy increase in the risk of exceeding the capacity of bilirubineimiei indirect

albumin-binding.
 Exchange transfusion is carried out in the first hours after birth if the baby jaundice,
pallor, swelling, hepatomegaly, malaise; newborn with a good general status, but a
positive direct Coombs test, Hgb less than 10 g% neonate mature and less than 14 wt%
prematurely.

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