Prolonged jaundice in newborns!

Complexes with this research

Hospital complex Infectious screening for prevention and hospitalization 1,270 RUR Composition
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Preparation for partner childbirth for a man Tests necessary to accompany a woman in labor RUB 2,470 Composition

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• Expanded hospital complex 4,520 RUR
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Jaundice due to breastfeeding disorders

A decrease in intestinal activity in a newborn leads to increased enterohepatic circulation. Jaundice in the absence or insufficient breastfeeding and intestinal obstruction are common conditions associated with increased enterohepatic circulation, which leads to unconjugated hyperbilirubinemia. Non-breastfeeding jaundice occurs in the first week of life and is caused by insufficient breast milk intake, which leads to dehydration and sometimes high sodium levels in the baby. Lack of breastfeeding leads to decreased intestinal motility and decreased excretion of bilirubin in feces or meconium. This jaundice occurs at the end of the first week, peaks in the second, and usually resolves by 12 weeks of age.

When do you need to get tested for Hepatitis B, HBs Ag (quality)?

1. Suspicion of infection with viral hepatitis B;
2. Changes in liver biochemistry, indicating liver damage;
3. Development of jaundice;
4. Screening during pregnancy;
5. Comprehensive examination before hospitalization;
6. Pre-employment screening for specialists in certain professions (medical workers and others);
7. Examination of people from groups at high risk of infection (receiving intravenous injections, undergoing hemodialysis, blood donors and others).

What is the nature of jaundice in newborns?

Jaundice or, scientifically speaking, unconjugated hyperbilirubinemia in newborns occurs due to physiological or pathological reasons. More than 75% of cases of neonatal jaundice are due to physiological reasons. Physiological jaundice is also called non-pathological jaundice because it is mild and disappears spontaneously. This occurs due to the peculiarities in the metabolism of bilirubin in the neonatal period. Increased bilirubin load in newborns occurs due to its increased production, which is caused by a higher mass of red blood cells (RBCs) with a decrease in the duration of their existence in newborns. At the same time, a newborn’s liver is still very inactive, and it processes water-soluble bilirubin into conjugated bilirubin, which is water-insoluble, 100 times slower than in an adult.

Physiological jaundice usually occurs between days 2 and 4 of life, peaks between days 4 and 5, and resolves within 2 to 3 weeks. Physiological jaundice never occurs in the first 24 hours of a newborn's life.

Detailed description of the study

Hepatitis B virus is a potentially life-threatening infection that affects the liver. The pathogen is found in body fluids such as blood, semen and vaginal secretions.

The main mechanisms of transmission of hepatitis B infection are as follows:

1. Horizontal transmission - through unprotected sexual intercourse or contact with the mucous membranes of saliva, vaginal secretions, semen and blood of an infected person$
2. Vertical transmission - from mother to newborn.

The incubation period of the disease lasts on average from 30 to 180 days. The virus penetrates the liver, where it attaches to the surface of the hepatocyte (liver cell) using the HBs antigen (HBsAg). Next, the virus penetrates the cell itself and begins replication, that is, reproduction. The human immune system identifies infected hepatocytes and secretes appropriate antibodies to proteins on the membrane, which ultimately causes cell destruction.

People infected with hepatitis B virus may have acute symptomatic illness or asymptomatic infection. Initial symptoms are nonspecific and may include:

1. Flu-like condition (weakness, fever, aches in joints and muscles);
2. Nausea or vomiting;
3. Discomfort and pain in the right hypochondrium;
4. Lack of appetite.

Jaundice may then occur. An infected person notices darkening of urine, discoloration of stool, and yellowing of the whites of the eyes and skin. Recovery is the usual outcome for people with normal immunity (about 95% of cases), but in a small number of people (5% on average) the disease can develop into chronic hepatitis B, which is defined as the presence of HBsAg for more than six months.

With chronic infection, people can experience both asymptomatic carriage and chronic hepatitis with possible progression to liver cirrhosis, when hepatocytes die and are replaced by tissue that is unable to perform the necessary functions. As a result, liver failure develops. Its signs are:

1. Increase in abdominal volume due to fluid accumulation (ascites);
2. Constant bloating, indigestion;
3. Nausea, vomiting;
4. Swelling of the legs;
5. Dysfunction of the central nervous system (CNS);
6. Jaundice;
7. Increased body temperature;
8. Decreased or lack of appetite;
9. Sarcopenia is a decrease in the muscles of the arms and legs;
10. Tendency to bruise;
11. Bleeding gums;
12. A rash on the body that looks like spider veins;
13. Redness of the palms.

In case of severe liver failure, jaundice, impaired consciousness (encephalopathy), and gastrointestinal bleeding may develop. People who have been infected with hepatitis B for a long time have an increased risk of hepatocellular carcinoma - liver cancer.

Diagnosis is based on blood tests in people with symptoms and associated risk factors for the disease. Detection of HBsAg serves as the basis for the primary diagnosis of viral hepatitis B. Its appearance in the blood is observed at the end of the incubation period of the disease and persists in the chronic form of the infection.

Pediatrician, physiotherapist, head of the pediatric medical department

Neonatal jaundice is a change in the color of the skin, conjunctiva and sclera (whites of the eyes) in newborns to a yellowish tint due to increased levels of bilirubin (a pigment that is formed when hemoglobin breaks down) in the blood plasma during the newborn period. Neonatal jaundice is usually mild and transient. However, it is important to monitor newborns with severe jaundice or whose jaundice does not resolve naturally, as this may lead to long-term negative consequences. Severe neonatal hyperbilirubinemia is associated with a neurological dysfunction known as bilirubin-induced neurological dysfunction (BIND). In severe hyperbilirubinemia, unconjugated bilirubin crosses the blood-brain barrier, binds to the basal ganglia and brainstem nuclei, leading to acute bilirubin encephalopathy, or progresses to permanent neurological dysfunction that manifests as cerebral palsy, seizures, buckling, and sensorineural hearing loss.

References

1. Ivashkin, V.T., Mayevskaya, M.V., Pavlov, Ch.S. and others. Clinical recommendations of the Russian Society for the Study of the Liver and the Russian Gastroenterological Association for the treatment of complications of liver cirrhosis. - Russian Journal of Gastroenterology, Hepatology, Coloproctology, 2021. - V. 26(4). — P. 71-102.
2. Schwarz, W., Heidi, M., Nancy, E. False positive hepatitis B surface antigen test caused by hepatitis B vaccine, The Pediatric Infectious Disease Journal, 2001. - Vol. 8(2). — P. 189-193.
3. Tripathi, N., Mousa, O. Hepatitis B. - In: StatPearls, 2020.
4. Anjum, Q. False positive Hepatitis B Surface Antigen due to recent vaccination. - IntJHealthSci (Qassim), 2014. - Vol. 8(2). — P. 189-193.

What is pathological jaundice of newborns?

The causes of pathological unconjugated hyperbilirubinemia are also associated with an increase in bilirubin production, a decrease in its excretion from the body and increased blood circulation in the liver and intestines. Pathological jaundice can occur in a newborn in the first 24 hours of life and is characterized by a rapid increase in bilirubin levels of more than 5 mg/dL per day.

The causes of increased bilirubin production in pathological jaundice are immune-mediated hemolysis (destruction of red blood cells) arising due to Rh conflict with the mother, blood group incompatibility or non-immune-mediated causes such as cephalhematoma, defects in red blood cell membranes (hereditary spherocytosis and elliptocytosis), defects enzyme system (glucose-6-phosphate dehydrogenase and pyruvate kinase), which most often affects boys.

Incompatibility of blood groups according to the ABO system occurs in mothers with blood group O, who have IgG antibodies to factors A and B, which penetrate the placenta into the child’s body and cause hemolysis in newborns with blood group A or B. In case of Rh incompatibility, Rh- a negative mother exposed to Rh positive blood from a previous pregnancy becomes sensitized to such blood. This leads to hemolysis in a fetus with Rh-positive blood. To prevent Rh conflicts, anti-D gamma globulin is currently used, which reduces the incidence of hemolysis.

Decreased bilirubin clearance is also observed with hereditary diseases such as Crigler-Najjar and Gilbert syndrome, as well as with diabetes in the mother or congenital hypothyroidism in the baby. For Crigler-Najjar syndrome, newborns may require liver transplantation or long-term use of phototherapy. In Gilbert syndrome, a mutation of the UGT1A1 gene is observed, causing unconjugated hyperbilirubinemia. Gilbert syndrome is usually diagnosed during adolescence, although the first manifestations may occur as early as the neonatal period. It can be diagnosed using genetic testing.

How is jaundice treated?

To prevent acute bilirubin encephalopathy and kernicterus, severe hyperbilirubinemia is treated with phototherapy, intravenous immunoglobulin, or exchange transfusion. There are nomograms for determining bilirubin levels at which phototherapy and replacement blood transfusion are indicated.

Phototherapy is initiated taking into account risk factors and serum bilirubin levels on a nomogram. Bilirubin optimally absorbs light in the blue-green range (460 to 490 nm) and is either photoisomerized and excreted in bile or converted to lumirubin and excreted in urine. During phototherapy, the newborn's eyes should be protected and as much of the body's surface area should be illuminated as possible. It is important to maintain hydration and urine output because most bilirubin is excreted in the urine as lumirubin. The use of phototherapy is not indicated for conjugated hyperbilirubinemia and may result in “bronze baby syndrome” with grayish-brown skin discoloration.

After cessation of phototherapy, there is an increase in total serum bilirubin levels, known as “reverse bilirubin.” The level of "reverse bilirubin" is usually lower than the level at the beginning of phototherapy and does not require restarting phototherapy.

Intravenous immunoglobulin is recommended if bilirubin levels increase as a result of isoimmune hemolysis despite phototherapy. Intravenous immunoglobin is started when bilirubin levels are between 2 and 3 mg/dL.

Replacement blood transfusion is indicated if there is a risk of neurological dysfunction, either with or without phototherapy. It is used to remove bilirubin from the bloodstream and, in isoimmune hemolysis, also removes circulating antibodies and sensitized red blood cells. Blood transfusions are performed in neonatal or pediatric intensive care units. A double exchange blood transfusion (from 160 to 180 ml/kg) is performed to replace the newborn’s blood. Phototherapy should be restarted and continued after blood transfusion until bilirubin reaches a safe level.

How common is jaundice in newborns?

Almost all newborns will have a total bilirubin level above the upper limit of normal for adults and older children of bilirubin of 1.5 mg/dL with less than 5% total conjugated bilirubin. Up to 60% of full-term infants and 80% of newborns at 35 weeks' gestation or more will have jaundice, which occurs when plasma bilirubin levels exceed 5 mg/dL. Neonatal jaundice is more common in people living at high altitudes and in people living around the Mediterranean Sea, especially in Greece.

Jaundice resulting from impaired bile transport

Conjugated hyperbilirubinemia is always a pathology and occurs due to defects in the formation or transport of bile caused by mechanical obstructions to its outflow or systemic diseases that can affect the liver. Such conditions include biliary atresia, common bile duct cysts, idiopathic neonatal hepatitis, and Alagille syndrome. Congenital metabolic disorders such as galactosemia, tyrosinemia, antitrypsin-1 deficiency also manifest themselves in the form of conjugated hyperbilirubinemia. Biliary atresia is the most common cause of conjugated neonatal hyperbilirubinemia. It affects both intrahepatic and extrahepatic bile ducts and usually appears during the first 2–4 weeks of life along with pale stools. Initial diagnosis is by ultrasound, which may show the absence of the gallbladder. Ultrasonography can also detect cysts with normal or dilated intrahepatic bile ducts, or sclerotic ducts in biliary atresia.