Transitory Hyperbilirubinemia

Temporal and laboratory criteria

Physiological jaundice has strict timeframes and biochemical thresholds. Yellowish discoloration of the skin and visible mucous membranes does not occur immediately after birth, but strictly on the 2nd–3rd day of life.

The manifestation of the clinical picture directly depends on the concentration of unconjugated bilirubin in blood serum. At the same time, the threshold of tissue sensitivity to staining varies depending on the maturity of the infant:

• In full-term infants, jaundice becomes visually noticeable when the concentration of unconjugated bilirubin reaches 80–90 µmol/L.
• In preterm infants, this threshold is significantly higher and amounts to over 120 µmol/L.

The total duration of the condition is 1–2 weeks after birth. During this time, the symptoms gradually subside, and the condition normalizes independently. The prognosis for this form of hyperbilirubinemia is exceptionally favorable, as the process is strictly transient in nature.

Clinical presentation and patient assessment

The most important criterion for the physiological nature of the process is the absence of severe systemic disorders. As a rule, the general condition of the newborn is not compromised.

However, with high intensity of the yellowish discoloration and a significant increase in bilirubin levels, signs of mild central nervous system depression may be observed. These include:

• General lethargy and increased drowsiness in the infant.
• Decreased sucking reflex (the infant poorly takes the breast or bottle).
• Occurrence of rare regurgitation or episodes of vomiting.

Such symptoms require careful monitoring, but within the framework of transient hyperbilirubinemia, they are expected and resolve as bilirubin levels decrease.

Differential diagnosis

To ensure that the jaundice is physiological in nature and not a symptom of a severe disease (e.g., infection, biliary atresia, or hemolytic disease), it is necessary to rely on strict physiological criteria:

1. Stool color: The infant's stool retains its normal color. Complete stool discoloration (acholia) is absolutely uncharacteristic of transient hyperbilirubinemia.
2. Urine characteristics: Urine remains light, and the laboratory test for bile pigments in the urine yields a negative result.
3. Complete blood count: All red and white blood cell parameters remain within age-appropriate normal limits. There are no signs of active hemolysis or a systemic infectious process.

Pathogenesis: causes of hyperbilirubinemia

The logic of the development of transient jaundice is entirely due to the functional immaturity of bilirubin metabolism systems in the infant. Failures occur at virtually all stages of pigment metabolism:

• Hyperproduction of bilirubin. Accelerated formation of free (unconjugated) bilirubin occurs. This is associated with the presence of physiological polycythemia (elevated red blood cell volume) in newborns and a shortened lifespan of these erythrocytes.
• Impaired transport. The infant's serum albumin has a reduced capacity to bind and transport bilirubin. Additionally, there is a deficiency of a specific carrier protein responsible for transporting the pigment across the hepatocyte membrane.
• Impaired conjugation. The newborn's liver demonstrates transient immaturity of enzyme systems. First and foremost, this is expressed in the extremely low activity of the enzyme UDP-glucuronosyltransferase, which is necessary for converting unconjugated bilirubin into the conjugated (water-soluble) form.
• Impaired excretion. The excretory function of the liver in the first weeks of life is also significantly reduced, which slows down bile outflow.
• Intestinal phase. In the intestine, there is an increased reabsorption of free bilirubin back into the systemic circulation, which leads to a sharp increase in the enterohepatic circulation of the pigment.

Class and exam questions

What else to study on this topic

• Mechanisms of development of physiological polycythemia in newborns
• The role and function of the enzyme UDP-glucuronosyltransferase in the liver
• Features of the enterohepatic circulation of bilirubin in the neonatal period
• Clinical differences between transient jaundice and hemolytic disease of the newborn
• Differential diagnosis with pathologies accompanied by acholic stools

Other topics in «Chapter 2. Neonatology»

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