When is neonatal jaundice dangerous? What is and why does jaundice occur in newborns?

Jaundice (jaundice) is essentially a clinical manifestation that involves yellowing of the skin, mucous membranes, and sclera.

It is caused by an increase in the concentration of extracellular (extracellular) bilirubin in serum and intracellular (intracellular) bilirubin in tissues above the physiological value.

Neonatal jaundice (jaundice neonatorum) is the most common pathological condition in newborns.
It affects on average every second newborn, with about 55% of mature newborns and up to 90% of immature newborns.

• Normal bilirubin production in mature neonates is approximately 3 to 4 mg/kg/day.
• The normal value for bilirubin is 17-25 µmol / l at each age.

When bilirubin rises above 35 µmol / l, a yellow discoloration of the sclera appears.
When bilirubin rises above 60 µmol / l, yellowing of the skin and mucous membranes is associated.

What exactly is bilirubin?

Bilirubin is a tetrapyrrole bile dye that is formed in the liver as a final waste product of the metabolism of the red blood pigment hemoglobin from extinct red blood cells.

Its role in the body is to scavenge free radicals and slow down lipid damage by oxidative processes.

It is synthesized mainly in the liver, spleen, bone marrow, but also in the skin from where it enters the blood.

1. In the blood, unconjugated bilirubin binds to albumins (proteins without a carbohydrate component) and is transported by the bloodstream to the liver.
2. In the liver, it is converted to conjugated bilirubin, which is excreted in the bile, from where it travels to the intestine and finally out of the body through the stool.

At high concentrations of bilirubin in the blood, a certain amount is excreted in the urine, the rest is stored in the skin, mucous membranes and tissues.
In its absence, the stool lacks its characteristic brown coloration, the stool is white cholic.

When the intestinal microflora changes, biliverdin can be produced and the stool turns green.

Also read the article in the magazine:
Stool - what does its consistency, color or odor signal?

Table with values ​​of total bilirubin in newborns

Thus, the cause of neonatal jaundice is a high level of bilirubin, which is caused by the breakdown of erythrocytes with the subsequent release of hemoglobin and its metabolism.

Defined as elevated serum or plasma bilirubin - hyperbilirubinemia above 95% of Bhutani nomogram.

Bilirubin is a product of the catabolism of hemoglobin, which is stored in tissues, skin, and sclera.
On the outside, it shows yellow color.

Disorders of bilirubin metabolism in the neonate are due to:

• high levels of erythrocytes in the blood of the newborn
• hepatic insufficiency, which normally degrades bilirubin

Pathophysiology of neonatal jaundice

The fetus in the womb is not able to breathe independently.
Oxygen transmission, therefore, provides an increased number of red blood cells (erythrocytes).

After giving birth, the baby inhales spontaneously for the first time, and from that moment on, breathing becomes part of the life of every living creature.

Excess blood cells are no longer needed to carry oxygen and thus become unnecessary.
The body deals with unnecessary red blood cells so that they break down - hemolysis.

Upon disintegration, they release a red blood pigment, hemoglobin, into the bloodstream, which is further metabolized until it becomes a yellow blood pigment, bilirubin.

In the fetal period, bilirubin is transported to the fetus via the placenta (transplacentally), the liver is only slightly active.

Bilirubin, like the original erythrocytes, is a large amount (hyperbilirubinemia), which means that the child's body and underdeveloped liver do not manage to break it down, it accumulates in the skin, mucous membranes, sclera, and tissues, which is manifested by yellowing of the skin and sclera.

Why is hyperbilirubinemia dangerous?

Neonatal hyperbilirubinemia is a condition in which the value of concentrated serum or plasma bilirubin is greater than 95% (> 25 mg/dl, 428 μmol / l).

Up to 85% of hyperbilirubinemia is caused by the breakdown of erythrocytes, only 15% are caused by a liver problem or the breakdown of other hemoproteins.
It is caused by increased production and at the same time reduced excretion of bilirubin.

After complete elimination of excess bilirubin, the condition resolves spontaneously, the skin of the newborn is pink again and the sclera is white.

But ...

If bilirubin levels do not return to normal, free unconjugated bilirubin in the blood can cross the blood-brain barrier, where it is neurotoxic, and causes further health complications.

Neonatal jaundice is unmissable.

On the one hand, its origin is expected in this period, on the other hand, the manifestations are typical and visible to the naked eye of the layman.

The symptoms of neonatal jaundice are better observed in daylight.
Artificial light can distort or they may not be so clear.

It is typically manifested by a change in the color of the skin, with it being most pronounced in the areas of greatest congestion.

The dominant is the face, head, chest, abdomen, and finally the limbs.

In some newborns, the skin has a pronounced yellow color, in others only a slight hint of yellow color, or it has a mild shape, where the yellow color is missing and the baby has a gray color only in certain places of the skin.

Instead of healthy white sclera, their yellowing of the whites can also be observed.

The yellow discoloration of the mucous membranes is less pronounced, and the yellowing of other tissues is invisible to the naked eye.

This excessive yellow coloration is caused by two to three times the production of bilirubin compared to a healthy adult. 2-3 times higher than in adults.

Table with degrees of neonatal jaundice

If bilirubin levels cannot be controlled, other health problems may arise due to its neurotoxicity.

The most common is acute hepatic encephalopathy - damage to the brain caused by high levels of this bile pigment.

Then other symptoms are associated with yellowing.

The most common manifestations of jaundice complications:

• disorders of consciousness - the child is usually asleep - somnolence, lethargic, apathetic. The condition can progress to recommendation, which is a deeper disorder of consciousness, or to a deep coma when convulsions and fevers also occur. Ultimately, respiratory arrest and death can occur.
• Disorder of muscle tone - muscle tone newborn can be flaccid, so it is a hypotonia varying degrees, and there is the increase - hypertension muscle tone.
• cry - the child is often dissatisfied, poorly tuned and annoyed times during jaundice. It manifests itself in a sharp and inconsolable crying, which at the same time exhausts the baby. As the condition progresses, the crying becomes less and less intense, and eventually very weak. In the end, she cries only during external stimulation.

Diagnosis of neonatal jaundice is not complicated at all.

However, the principle of diagnosis is not its determination, which is trivial, but the distinction of physiological jaundice from pathological.

1.) Neonatal jaundice is, so to speak, expected in this period, and the clinical picture is typical of most neonates.

The neonatal type of jaundice is manifested by external yellowing of the skin, mucous membranes, and whites of the eyes.

2.) In addition, laboratory diagnostics are performed to determine the exact level of bilirubin in the blood, usually immediately after the birth of the baby as part of comprehensive examinations of the newborn.

Serum bilirubin levels can be repeatedly detected in infants in poor condition when it is necessary to know the most accurate parameters. 

One possibility is the examination of bilirubin from capillary blood, which is based on spectrophonometry. 

If the concentration of bilirubin is too high, it is necessary to do additional blood tests such as blood counts, conjugated bilirubin, blood group and  Rh factor newborn and the mother, direct Coombs test and examination albumin.

In some cases, blood, urine, and cerebrospinal fluid cultures are also performed to detect the presence of infection and to test for erythrocyte enzyme deficiency.

Can we find out who will develop pathological jaundice?

Yes, we know.

Pathological jaundice can be predicted on the basis of:

• visual monitoring of the newborn
• transcutaneous bilirubin (TCB) screening
• serum bilirubin (TSB) screening 
• risk factors

Screening and the use of risk factors to detect pathological jaundice are the most effective identifiers.
With the help of them, it is possible to identify the most risky children with up to 95% success.

TB and TSC measurements should be taken by all neonates with a positive clinical picture, due to the early detection of severe hyperbilirubinemia.

Interesting:
Based on some studies, TCB is not recommended in neonates born before 30 weeks of gestation and in immature neonates.
The reason is the fluctuation of the relationship between TCB and TSB measurements.

By default, the disease begins to manifest itself on the second to third day of the newborn's life.

Sometimes it may appear earlier, or a few days later.

Normal course of physiological jaundice of the newborn

In the vast majority of newborns, resp. in almost all of them, physiological jaundice occurs, i.e. the increase in the level of unconjugated bilirubin and its reduced elimination is still at acceptable values.

This means that this condition is normal and transient.

The child may turn yellow temporarily, but the condition improves spontaneously within a few days to weeks and does not cause him any more serious problems.

The manifestation of the clinical picture occurs in mature newborns on the second to third day, not earlier than 36 hours after birth.
It resolves in about 5-7 days.

In immature newborns , the symptoms occur a little later, ie for 5 to 7 days.
The yellow discoloration of the skin, mucous membranes and sclera lasts longer, about 2-3 weeks, then subsides.

The course of pathological jaundice

Every newborn's jaundice should be controlled.

The most important aspect is the early distinction between physiological jaundice and pathological jaundice, which is manifested by the same yellowing of the skin.

Division of pathological jaundice based on the mechanism of origin:

• jaundice caused by increased bilirubin production,
• jaundice caused by reduced conjugation
• jaundice caused by insufficient excretion of bilirubin from the body

What are the most common types of pathological jaundice we know?

Pathological jaundice as the so-called prolonged neonatal jaundice, ie prolonged jaundice.
The baby is visibly yellow, the symptoms do not subside in normal time (5-7 days), but last for more than two weeks in a mature newborn, in an immature it can be almost a month.

In fully breastfed infants, the time of jaundice may be extended up to 4 months.

Similar is persistent jaundice, i.e. persistent, lasting more than 1 to 2 weeks in a full-term newborn, and more than 2 to 3 weeks in a full-term newborn. Sometimes it lasts up to 2-3 months.

Another example of pathological jaundice is the so-called unconjugated hyperbilirubinemia, which is jaundice caused by an increase in serum levels of unconjugated bilirubin.

Manifestations of unconjugated hyperbilirubinemia appear very early, usually within 24 hours after birth and last up to 2 weeks in mature neonates, in immature children it is more than 2 weeks.

If it lasts longer, we speak of prolonged unconjugated hyperbiliruninemia, which is caused by the immaturity of the newborn, severe hemolysis, or genetic diseases.

The most common causes of unconjugated hyperbilirubinemia are hemolysis, polycythemia, bleeding conditions, increased blood circulation through the enterohepatic circulation, or other metabolic and endocrine diseases.

In case of decreased hepatic excretion of conjugated bilirubin, conjugated hyperbilirubinemia develops.

With this type of neonatal jaundice, it is necessary to examine the newborn due to the early diagnosis of other diseases such as liver, gallbladder, infections or congenital diseases.

The most common causes of conjugated hyperbilirubinemia may be long-term parenteral nutrition of the child, neonatal cholestasis, biliary obstruction, asphyxia, erythroblastosis or various infections.

Interesting:
Have you ever heard of jaundice of a breastfed newborn, or so-called jaundice from breast milk?
Is that not possible?
There are cases of jaundice in breastfed babies that are healthy, thriving and have good liver tests.
In these children, some substances in the mother are thought to affect the metabolism of bilirubin.
Jaundice resolves spontaneously within one to four months.

What complications of jaundice can we encounter?

In most newborns, jaundice is considered a physiological condition that occurs due to a change in the intrauterine oxygen supply to spontaneous breathing. It is the physiological jaundice of a newborn.

However, in the first days of life, it can be a symptom of a serious illness of the newborn, so we are talking about pathological jaundice.

A more complicated course of jaundice in a newborn requires a longer hospital stay in the neonatal unit, and in some cases a medical intervention. Prolonged (persistent) jaundice can be such a problem.

However, jaundice can be complicated, which is usually the case in immature newborns, or if hyperbilirubinemia is detected late and treated late.

Complications of neonatal jaundice

Acute bilirubin encephalopathy is a rare complication affecting 1 in 10,000 newborns.

Acute kernicterus is even rarer and occurs in 1 in 100,000 newborns. 
It is manifested by changes in muscle strength, sometimes weakness, sometimes stiffness, convulsions, and even epileptic seizures.
Some cases are fatal.

Chronic kernikterus means lifelong brain damage manifested by varying degrees of mental retardation and associated seizures.
Patients may also suffer from deafness or blindness.