Hyperbilirubinemia – Definition, Classification, Etiology, Signs and Symptoms

Hyperbilirubinemia - definition, classification, etiology, signs and symptoms 1

Definition of Hyperbilirubinemia

Hyperbilirubinemia is a condition where the rate of bilirubin in the blood reaches a value that has the potential to create nuclear icterus if not handled well, or have a relationship with a pathological condition. Brown set hyperbilirubinemia when the rate of bilirubin reached 12 mg% in full-term and 15 mg% in infants less than month. Utelly prescribe 10 mg% and 15 mg%.

Increased bilirubin can occur in some circumstances. Genesis is often found when there is an increased bilirubin load on liver cells in excess. This can be found when it was increasing destruction of erythrocytes, polycythemia. Plasma bilirubin breakdown disorder can also cause an increase of bilirubin body. This can happen when Y and Z protein in infants less or hypoxia, acidosis. Other conditions that saw an increase in the rate of bilirubin conjugation is when found from liver disorders or neonate with a disorder such as excretion of bile duct obstruction.

In a certain degree, bilirubin is toxic and damaging body tissues. Toxicity is mainly found in indirect bilirubin which is poorly soluble in water but soluble in fat. This trait allows the pathological effects on brain cells when bilirubin was able to penetrate the blood-brain barrier. Abnormalities that occur in the brain called the nucleus jaundice. It is generally considered that abnormalities in the central nervous might arise if indirect bilirubin levels over 20 mg / dl.

Easily least bilirubin passes through the blood brain barrier is not only dependent on the state of the neonate. Indirect bilirubin will easily through the blood brain barrier where there is a state of low birth weight infants, hypoxia, and hypoglycemia.

Classification and Etiology of Hyperbilirubinemia

1. Physiological Hyperbilirubinemia
Criteria :
Not occur on the first day of life (appearing after 24 hours). Increased total bilirubin normally no more than 5 mg% per day. In just months reaching a peak at 72 hours. Serum bilirubin 6-8 mg%. On the fifth day will go down to 3 mg%. for 3 days bilirubin 2-3 mg%. Down slowly to normal at the age of 11-12 days. At low birth weight / preterm, bilirubin peak at 120 hours of serum bilirubin of 10 mg% (10-15%) and decreased after 2 weeks.

Etiology :
Erythrocyte lifespan is shorter (80-90 days), whereas in adults 120 days. The amount of blood in newborn infants more (± 80 ml ??/ kg), in adults 60 ml / kg. Another source of more bilirubin than adults. Amount of albumin for bilirubin transport relatively less, especially on premature. Intestinal flora has not been much, an increase in the activity of the Intestinal flora has not been much, an increase in the activity of the enzyme ? glukoronidase deconjugation.

2. Pathologic Hyperbilirubinemia
Criteria :
Jaundice arising within the first 24 hours of life , the serum total bilirubin increased by more than 5 mg % per day. In term infants serum total bilirubin more than 12 mg %, in premature infants > 15 mg %. conjugated bilirubin > 1.5 to 2 mg %. jaundice lasting> 1 week in term infants and 2 weeks in premature infants.

Etiology :
1) The formation of bilirubin due to excessive hemolysis
Caused by hemolytic disease or increased destruction of erythrocytes as :

  • Abnormal hemoglobin and erythrocytes (Hb S in sickle cell anemia)
  • Inkompabilitas ABO
  • G6PD deficiency
  • sepsis
  • Drugs such as oxytocin
  • 2) Impaired transport of bilirubin, is influenced by :
  • Hypoalbuminemia
  • Prematurity
  • Drugs such as sulfonamides, salicylates, diuretics, and FFA ( free fatty acid ) which competes with albumin
  • Hypoxia, acidosis, hypothermia
  • Cutting the umbilical cord is slow
  • Polycythemia
  • Hemorrhage extravasation in the body such as cephalhematoma, bruises.

3) Impaired uptake of bilirubin, because :

  • Reduced ligandin
  • Increased acceptor Y and Z by other anions (novobiocin)

4) Impaired conjugation of bilirubin

  • Deficiency of the enzyme glucuronyl transferasi, hepatic immaturity
  • Persistent jaundice in breast-fed babies
  • Hypoxia and hypoglycemia

5) The decrease in bilirubin excretion due to a blockage in the bile duct.
6) Impaired elimination of bilirubin

  • Breastfeeding slow
  • Meconium slow spending
  • Mechanical obstruction.

Signs and Symptoms of Hyperbilirubinemia

According Surasmi (2003), hyperbilirubinemia symptoms are grouped into:
Acute symptoms: symptoms that are considered as the first phase kern jaundice in neonates are lethargic, do not want to drink, and hypotonia.
Chronic symptoms: the shrill cries (high pitch cry) include hypertonus and opisthotonos (infant survivors usually suffer sequelae such as cerebral paralis with Athetosis, hearing loss, partial paralysis of eye muscles and dental dispasia).
Meanwhile, according Handoko (2003), the symptoms are yellow (jaundice) of the skin, mucous membranes and the white part (sclera) eye, visible as blood bilirubin levels reached about 40 mol / l.

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