Infectious Mononucleosis | Johns Hopkins Medicine

What is infectious mononucleosis?

Infectious mononucleosis is characterized by swollen lymph glands, fever, sore throat, and extreme fatigue. It’s often spread through contact with infected saliva from the mouth. Symptoms can take between 4 to 6 weeks to appear and usually do not last beyond 4 months. Transmission is impossible to prevent because even symptom-free people can carry the virus in their saliva.

What causes infectious mononucleosis?

Infectious mononucleosis is caused by the Epstein-Barr virus (EBV). A variant of mononucleosis that is milder than EBV infectious mononucleosis is caused by the cytomegalovirus (CMV). Both EBV and CMV are members of the herpes virus family:

• In the U.S., most adults between 35 and 40 years old have been infected with the Epstein-Barr virus. This is a very common virus. When children are infected with the virus, they usually do not experience any noticeable symptoms. However, uninfected adolescents and young adults who come in contact with the virus may develop an illness very similar to infectious mononucleosis.

• The Epstein-Barr virus (EBV) may cause infectious mononucleosis in adolescents and young adults. However, even after the symptoms of infectious mononucleosis have disappeared, the EBV will remain dormant in the throat and blood cells during that person’s lifetime. The virus can reactivate periodically, however, usually without symptoms.

What are the symptoms of infectious mononucleosis?

Mononucleosis usually lasts for 1 to 2 months. The following are the most common symptoms of mononucleosis. However, each person may experience symptoms differently. Symptoms may include:

• Fever

• Swollen lymph glands in the neck, armpits, and groin

• Extreme fatigue

• Sore throat

• Enlarged spleen

• Head and body aches

• Liver involvement, such as mild liver damage that can cause temporary jaundice, a yellow discoloration of the skin and whites of the eyes due to abnormally high levels of bilirubin (bile pigmentation) in the bloodstream

Once a person has had mononucleosis, the virus remains dormant in the throat and blood cells for the rest of that person’s life. Once a person has been exposed to the Epstein-Barr virus, a person is usually not at risk for developing mononucleosis again.

The symptoms of mononucleosis may resemble other medical conditions. Always talk with your healthcare provider for a diagnosis.

How is infectious mononucleosis diagnosed?

A diagnosis of mononucleosis is usually based on reported symptoms. However, diagnosis can be confirmed with specific blood tests and other lab tests, including:

• White blood cell count, which is not diagnostic, but the presence of certain types of white blood cells (lymphocytes) may support the diagnosis

• Heterophile antibody test or monospot test, which, if positive, indicates infectious mononucleosis

How is infectious mononucleosis treated?

Your healthcare provider will figure out the best treatment for you based on:

• How old you are

• Your overall health and past health

• How sick you are

• How well you can handle specific medicines, procedures, or therapies

• How long the condition is expected to last

• Your opinion and preference

Treatment for mononucleosis may include:

• Rest (to give the body’s immune system time to destroy the virus)

• Drink plenty of liquids

• Take over-the-counter medicine as directed for discomfort and fever

• Corticosteroids only when necessary to reduce swelling of the throat and tonsils

What are the complications of infectious mononucleosis?

Complications of infectious mononucleosis don’t happen often. Complications may include:

• Ruptured spleen

• Kidney inflammation

• Hemolytic anemia

• Nervous system problems, such as encephalitis, meningitis, and other conditions

• Inflammation of the heart muscle

• Heart rhythm problems

• Obstruction of the upper airways

Can infectious mononucleosis be prevented?

Avoid kissing or sharing dishes, food utensils, or personal items with anyone who has the infection.

When should I call my healthcare provider?

If your symptoms get worse or you have new symptoms, let your healthcare provider know.

Key points about infectious mononucleosis

• Infectious mononucleosis is characterized by swollen lymph glands, fever, sore throat, and extreme fatigue

• Mononucleosis usually lasts for 1 to 2 months.

• Symptoms may include fever, swollen lymph glands in the neck, armpits, and groin, constant fatigue, sore throat, enlarged spleen, and jaundice, a yellow discoloration of the skin.

• Treatment includes rest and plenty of liquids.

46 Infectious Mononucleosis with clinical jaundice in 14 year old

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General Pediatrics

46 Infectious Mononucleosis with clinical jaundice in 14 year old

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1. R Bhamkar,
2. S Davison,
3. M Selter,
4. H Sammons,
5. A Arend,
6. D Dalton

1. Department of Paediatrics, North Devon District Hospital, Barnstaple, UK

Abstract

Glandular fever or Infectious Mononucleosis (IMN) is caused by Ebstein-Bar Virus (EBV). It is characterised by fever, sore throat and lymphadenopathy. Mild elevation of liver enzymes or transaminitis is common in the illness, but is rarely associated with clinical jaundice.

There are very few case reports of EBV with symptomatic hepatitis. We report a case of EBV infection with very high liver enzymes and clinical jaundice.

A 14 year old girl presented with history of fever, sore throat and cervical lymphadenopathy. Her blood investigations showed white cell counts of

14000/mm3 with lymphocytic predominance and numerous atypical lymphocytes in the smear. Her IMN monospot test was positive. Her alanine aminotransferase

(ALT) was 370 IU/L. She was discharged home with diagnosis of glandular fever on symptomatic treatment. A week later, she represented with jaundice, pruritus, nausea and anorexia. Her liver functions showed ALT: 1956 IU/L, aspartate aminotransferase (AST): 1007 IU/L, alkaline phosphatase (ALP): 162 IU/L, total bilirubin: 70 µmol/L, direct bilirubin: 47 µmol/L and albumin:

45 g/L. Her renal functions and clotting was normal.

Her viral markers (hepatitis B virus surface antigen, anti-hepatitis C virus, hepatitis A virus immunoglobulin IgM) were negative. Hepatitis E IgG antibody was positive whereas IgM was negative. Antinuclear, anti-mitochondrial and anti-smooth antibody profile was negative. Ultrasound abdomen showed mild splenomegaly (14cm). Her copper level was 35.8 µmol/L

(N: 11-22 µmol/L) and ceruloplasmin level was 0.52 g/L (0.16-0.45 g/L). EBV viral capsid antigen IgM and IgG were positive and EBV nuclear antigen IgG was negative. Cytomegalovirus IgM was negative and IgG were positive. Her IgA and IgM antibody levels were mildly elevated 3.36 g/L (N: 0.8-2.8 g/L) and 2.8 g/L (N: 0.5-1.9 g/L) respectively. She was treated with ursodeoxycholic acid and fat soluble vitamins. Her liver functions improved but were still deranged 4 weeks later.

Symptomatic hepatitis in IMN is rare, more so in paediatric population compared to elderly. The elevation in aminotransferases levels are usually less than fivefold and hyperbilirubinaemia is seen in up to 5% of patients.

In our patient ALT increased more than 30 times and she became clinically jaundiced and symptomatic. Fulminant hepatitis is very rare. Possible mechanisms are lymphocytic infiltration of hepatocytes, cholestasis and auto-immune hepatitis. Treatment is mainly symptomatic and supportive.

Conclusion Patients with IMN should be observed for jaundice and subsequently monitored for liver function in case of hepatitis. EBV should be considered in patients presenting with clinical jaundice.

http://dx.doi.org/10.1136/archdischild-2021-europaediatrics.46

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full description, symptoms and causes

Bilirubin is formed when hemoglobin is destroyed. As a result, the skin of the child turns yellow.

Neonatal jaundice of the newborn is one of the most common conditions in babies during the first 2 weeks of life and is a common cause of hospitalization in this age group. This condition manifests itself clinically in the first week after birth in about 60% of term babies and 80% of premature babies. Fortunately, severe and prolonged neonatal jaundice is less common and is often a mild, self-limiting condition. But if the content of bilirubin is very high, then this can lead to persistent neurological disorders and even death.

Causes of development

Erythrocytes in human blood live only 120 days. Then they collapse, and new ones come to replace them. Normally, this process of self-renewal occurs constantly. The hemoglobin of the destroyed red blood cells is converted to bilirubin, which is then neutralized in the liver and enters the intestine with bile. When these processes are disturbed, bilirubin accumulates in the blood.

Speaking about the causes of jaundice in newborns, for starters it is important to understand that it happens conjugated and non-conjugated – it depends on which fractions of bilirubin predominate. With conjugative jaundice, direct (conjugated) bilirubin predominates – it is neutralized and ready to be excreted from the body. In non-conjugated, indirect (non-conjugated) bilirubin predominates – it is insoluble, has not yet been neutralized, and therefore is more toxic.

Causes of non-conjugated jaundice

Non-conjugative jaundice is the most common type of neonatal hyperbilirubinemia. It accounts for 75% of cases of physiological jaundice. In the blood of a newborn, there are a lot of red blood cells with the so-called fetal hemoglobin, which, after the baby is born, becomes unnecessary and must be replaced by “normal” hemoglobin. These erythrocytes are characterized by a short life, they are rapidly and massively destroyed. The situation is aggravated by the fact that the activity of the enzyme uridine diphosphate glucuronosyltransferase (UGT), which is necessary for the conjugation of bilirubin, in a newborn is only 1% compared to an adult. In other words, the resources of the liver are simply not enough to neutralize and remove all bilirubin from the body. Most often, such jaundice is a physiological phenomenon and is not dangerous: it develops 24 hours after birth, reaches a maximum after 36-48 hours and disappears within 2-3 weeks.

Also, the following pathologies can become the cause of this condition:

• Rhesus conflict between a pregnant woman and a fetus . At the same time, maternal antibodies pass through the placenta and destroy the erythrocytes of the fetus
• Blood type conflict AB0
• Defects in erythrocyte membranes in pathologies such as hereditary spherocytosis and elliptocytosis
• Disorders in the work of erythrocyte enzymes
• Intracranial hemorrhages
• Polycythemia – when red blood cells are excessively increased in the blood

• Sepsis is a generalized inflammatory process that leads to the destruction of blood cells.

Causes of conjugative jaundice

Conjugational jaundice in neonates is characterized by an increase in direct bilirubin greater than 1.0 mg/dL. Such hyperbilirubinemia is extremely rarely physiological. It is usually associated with pathologies of the liver and bile ducts that require treatment:

• Obstruction of the bile ducts – their narrowing. It is usually caused by pathologies such as cysts of the choledochus (common bile duct), biliary atresia, neonatal cholelithiasis (cholelithiasis), neonatal sclerosing cholangitis.
• Many infections can lead to conjugative jaundice in infants . They are caused by rubella, herpes, HIV, cytomegaloviruses, pathogens of toxoplasmosis, syphilis, etc. Hyperbilirubinemia develops with septicemia.
• Certain genetic diseases
• Idiopathic neonatal hepatitis
• Gestational alloimmune liver disease
• Neonatal hemochromatosis
• Bile stasis caused by parenteral nutrition – when nutrient solutions are given intravenously (in diseases where nutrition is not possible naturally)

Risk factors

Several factors increase the risk of developing neonatal hyperbilirubinemia. These include:

• Prematurity . The liver of a premature baby copes worse with the metabolism and excretion of bilirubin. In addition, premature newborns often eat less, have fewer bowel movements, and thus less bilirubin is excreted in the feces.
• Birth injuries . The more petechiae / hematomas appear on the baby’s body during childbirth, the more red blood cells are subsequently destroyed in his body.
• The risk of jaundice is increased in infants who are not breastfeeding if the woman is not milking enough.
• Studies show that the risk of neonatal jaundice is higher in East Asian children .

Pathogenesis

So, jaundice in newborns develops due to the accumulation of bilirubin in the blood serum. Each of the above causes can be attributed to one of three groups, they correspond to the types of jaundice:

• Prehepatic (hemolytic neonatal jaundice). The destruction of hemoglobin occurs very quickly, as a result, a large amount of bilirubin is formed, and the liver ceases to cope with its neutralization and excretion. In this case, the level of indirect bilirubin in the blood first of all rises.
• Hepatic – when a normal amount of bilirubin is formed, but it is not properly utilized due to liver pathologies.
• Subhepatic, or mechanical – when the liver tissue normally copes with the neutralization of bilirubin, but it is not excreted due to a violation of the outflow of bile. The main reason is the pathology of the biliary tract, and the level of direct bilirubin in the blood increases.

In parallel, bilirubin is deposited in the tissues – because of this, the skin becomes yellow.

But this is not the only manifestation of hyperbilirubinemia. Bilirubin is a toxic compound that affects the entire body. If its level is significantly increased, then the brain suffers, encephalopathy develops, and persistent neurological disorders may occur. Bilirubin is able to penetrate the blood-brain barrier – the structure that separates the central nervous system (CNS) from the bloodstream – and accumulate in various structures of the brain: stem, hippocampus, cerebellum, nerve centers. Here it disrupts the work of mitochondrial enzymes, inhibits the synthesis of DNA and proteins, and causes breaks in DNA chains. There is such a term as kernicterus – a yellow staining of the nuclei in the brain.

Classification

We discussed some classifications of neonatal hyperbilirubinemia above. Jaundice in newborns is conjugated and non-conjugated; suprahepatic (hemolytic), hepatic and subhepatic (mechanical).

It is also important to know about another classification:

Physiological jaundice is not considered a disease, but a natural reaction of the child’s body to new conditions. Most often, this condition does not require treatment. Typical manifestations of physiological jaundice:
• occurs 24–36 hours after birth
• builds up over three to four days
• symptoms begin to disappear after the first week
• symptoms disappear completely at 2–3 weeks of age
Pathological jaundice in newborns is a consequence of certain pathologies. Examination is necessary to establish the cause, appropriate treatment. Suspicion of pathology in full-term newborns falls in the following cases:
• jaundice develops in the first 24 hours or after the first week of life
• jaundice persists for more than 2 weeks
• blood bilirubin level rises more than 18 mg/dl (more than 308 µmol/l in other units)
• bilirubin level rises by more than 5 mg/dl/day (or 86 µmol/l/day)
• a child with hyperbilirubinemia has symptoms indicating a serious illness


There are also two more types of jaundice in newborns:

• Breastfeeding jaundice occurs in about one in six breastfed babies in the first week of life. The reason is that the child is not getting enough food, calories and fluids. The situation is exacerbated by the fact that a small child does not have enough intestinal bacteria that convert bilirubin into compounds that cannot be absorbed back into the bloodstream.
• Breast milk jaundice develops on days 5–7 of life and reaches a maximum in the second week. It occurs when the concentration of the enzyme beta-glucuronidase is high in breast milk. Because of it, conjugated bilirubin in the intestine is converted to unconjugated and absorbed back into the bloodstream.

Symptoms

The main symptom of jaundice in newborns is yellowness of the skin, mucous membranes and whites of the eyes. Usually the face turns yellow first. As the level of bilirubin in the blood increases, the chest, abdomen, arms and legs acquire the same color. The easiest way to detect this is by examining the baby’s skin in good natural light. If you press on the skin with your finger, then in this place it will take on a natural color, and then quickly turn yellow again. In swarthy children, jaundice is more difficult to notice, but it is clearly visible on the whites of the eyes and the mucous membrane of the mouth.

For different types of neonatal hyperbilirubinemia, certain nuances in the clinical picture are characteristic:

Type of jaundice	Features of the course of the disease	Characteristic features in the clinical picture
Hemolytic	Symptoms appear on the first day of life, often within the first 12 hours. Jaundice of the skin increases within 3-5 days. Symptoms begin to decrease at the beginning of the second week of life and disappear completely by the third week.	In Rhesus incompatibility, the skin often has a lemon tint, as jaundice occurs against a background of pallor. In AB0 conflict, the skin is bright yellow. The child’s condition strongly depends on how quickly and massively erythrocytes are destroyed. Some children feel satisfactory, while others may be in serious condition. Feces and urine are usually of normal color. In the first days of life, the child may have an enlarged liver and spleen.
Conjugative jaundice	Symptoms usually begin at least 24 hours after birth. Jaundice continues to increase after 4 days of life and resolves by the end of 3 weeks.	The baby’s skin has an orange tint. Most often the child’s condition is satisfactory, but may worsen if the level of bilirubin rises very much. The color of urine and feces does not change. The liver and spleen are usually not enlarged.
Obstructive jaundice		The baby’s skin turns green. The liver usually enlarges and becomes more dense. The spleen is enlarged in more rare cases. Urine becomes darker and stools become discolored because bile is not supplied to the intestines.
Hepatic jaundice	Jaundice appears early and proceeds in waves.	The liver and spleen increase in size. There are signs of increased bleeding, such as bruising of the skin. Stool becomes discolored intermittently. Urine becomes dark yellow.

Which doctor should I contact?

Usually, jaundice in a newborn occurs even in the maternity hospital, so doctors notice it when they conduct periodic examinations (in the first 48 hours of a baby’s life, it is recommended to examine it every 8-12 hours). If symptoms appear at home, then you should contact your pediatrician. It is necessary to show the child to the doctor on the same day in the following cases:

• bright yellow or orange skin color
• the child constantly sleeps, wakes up with difficulty or, on the contrary, is restless and falls asleep badly
• baby does not suckle well at breast or bottle formula
• the child behaves very restlessly, is constantly acting up
• decrease in the number of urination and bowel movements: normally during the day there should be at least 4-6 urine-filled diapers and 3-4 bowel movements


If jaundice is accompanied by some symptoms, you should immediately call an ambulance:

• the child constantly cries, screams loudly, and it takes a long time to calm him down
• the child lies in an arched position with the head thrown back
• all the child’s muscles are very tense or, on the contrary, sluggish, with reduced tone
• the child makes unusual movements with the eyeballs, rolls his eyes

Diagnostic methods

As we noted above, usually the only manifestation of neonatal hyperbilirubinemia is icteric staining of the skin. This symptom is enough for the doctor to suspect this condition and prescribe the correct examination to clarify the diagnosis. Most modern clinics have special devices (bilirubinometers) that allow you to detect an elevated level of bilirubin in the blood by simply applying a special sensor to the skin – on the forehead or chest. This is the so-called percutaneous determination of the level of bilirubin. The study lasts only a couple of seconds, the doctor immediately sees the result on the display of the device.

A more accurate diagnostic method is to determine the level of bilirubin in the blood serum. To do this, you need to take blood from a child – usually it is taken from a newborn from the heel. Such an analysis helps to determine the level of not only total bilirubin, but also its fractions – conjugated, unconjugated.

With an increase in the level of total bilirubin more than 18 mg / dl (308 μmol / l) in full-term children and more than 10 mg / dl (171 μmol / l) in preterm infants, additional tests are prescribed:

• determination of the level of conjugated and unconjugated bilirubin
• evaluation hematocrit – percentage of blood cells in relation to its liquid part
• examination of blood smears – allows you to count the number of cells and evaluate their appearance
• count reticulocytes – young forms of erythrocytes
• Coombs test is a test that is used to detect erythrocyte-binding antibodies on the surface of erythrocytes
• determination of blood type AB0 and Rh factor in mother and child

According to the indications, doctors prescribe other studies. For example, if sepsis is suspected, cultures of blood, urine, and cerebrospinal fluid are performed . If it is not possible to identify the cause of the destruction of red blood cells, then is prescribed to measure the levels of erythrocyte enzymes .

Also, the doctor may prescribe a biochemical blood test , which helps to assess the condition and function of the liver. Investigate such indicators as the levels of AST and ALT, albumin, fibrinogen, cholesterol, etc. According to indications, ultrasound of the liver and other abdominal organs is performed.

Methods of treatment

Physiological jaundice in newborns most often does not lead to health problems, does not cause long-term consequences and does not require treatment, as it resolves on its own. The doctor may recommend breastfeeding more often and, if necessary, mixtures (10-12 times a day): this helps to improve intestinal motility and speed up the excretion of bilirubin from the body.

With breastfeeding jaundice, the recommendation is the same – increase the frequency of feedings. If the level of bilirubin in the blood rises more than 18 mg / dl, then it is recommended to transfer the child to formulas for artificial feeding for 1-2 days. At this time, a woman needs to express milk regularly in order to maintain lactation and subsequently return to breastfeeding her baby.

In other cases, special methods of treatment are used, pursuing two goals:

• fight against the underlying disease that caused pathological jaundice;
• therapy aimed at reducing the level of bilirubin .

Phototherapy and exchange transfusion are used to combat unconjugated hyperbilirubinemia.

Phototherapy

If translated from “medical” language to “ordinary”, then phototherapy is a treatment with light. The child is undressed and placed under a special lamp – only a diaper and an eye mask remain on him. In this case, not ultraviolet, but ordinary light is used. The most effective rays are blue with a wavelength of 425 to 475 nm.

The essence of the procedure is that under the action of light, unconjugated trans-bilirubin is converted into a soluble form – cis-bilirubin. It does not need to be conjugated, it is already easily excreted by the liver and kidneys, quickly leaving the body with feces and urine. Usually treatment lasts 1-2 days. Indications for phototherapy are determined by the degree of jaundice in newborns and the gestational age at which the birth occurred:

Due dates (weeks of pregnancy)	Blood bilirubin level for which phototherapy is indicated
up to 28	5–6 mg/dl
28–30	6–8 mg/dl
30–32	8–10 mg/dl
32–34	10–12 mg/dl
after 34	12–14 mg/dl

Exchange transfusion

Exchange transfusion is a second line treatment. It is used when the level of bilirubin is very high, or when it is not possible to get the effect of phototherapy. This procedure helps to quickly remove bilirubin from the bloodstream in immune hemolysis. With the help of a catheter inserted into the umbilical vein or other blood vessel, some blood is removed from the child and replaced with a donor. As a result, antibodies that destroy red blood cells are removed from the blood, as well as red blood cells, which are already partially destroyed and covered with antibodies. If hyperbilirubinemia is caused by Rh-conflict, then the donor must be Rh-negative, and if there is a conflict in AB0, the donor blood must be of the first group.

Bilirubin levels at which exchange transfusion is indicated are shown in the table:

Due dates (weeks of pregnancy)	Blood bilirubin level at which exchange transfusion is indicated
up to 28	11–14 mg/dl
28–30	12–14 mg/dl
30–32	13–16 mg/dl
32–34	15–18 mg/dl
after 34	17–19 mg/dl

Treatment of conjugative jaundice

The treatment regimen for conjugative jaundice in newborns depends on the cause of hyperbilirubinemia:

• In case of atresia of the biliary tract , surgical intervention is indicated aimed at restoring the outflow of bile. It is advisable to perform it in the first two months of life – this helps to achieve the best result. The Kasai operation (portoenterostomy according to Kasai) is performed: the surgeon removes the atrezated ducts and connects the remaining ones with the intestines.
• In case of infectious diseases that cause a violation of the outflow of bile, antimicrobial preparations are used, in accordance with the nature of the pathogen.
• Cholic and chenodeoxycholic acid preparations help in most cases in case of violation of the synthesis of bile acids as a result of a deficiency of the corresponding enzymes.
• metabolic disorders are treated with fight the underlying disease and improve liver function .
• In gestational alloimmune liver disease (when maternal antibodies cross the placenta and damage the fetal liver), intravenous immunoglobulin and exchange transfusion are effective.

Possible complications

A rare but formidable complication of neonatal hyperbilirubinemia – kernicterus . When the level of bilirubin in the blood is very high, it crosses the blood-brain barrier and damages the brain and spinal cord. Brain damage in this case is called hepatic (bilirubin) encephalopathy. The risk of developing kernicterus occurs with a very high level of bilirubin in the blood, its rapid increase, and the absence of treatment for jaundice in a newborn.

In the early stages, kernicterus is manifested by symptoms such as:

• poor appetite
• restlessness irritability
• frequent loud crying
• lethargy, drowsiness
• short episodes of apnea – respiratory arrest
• reduced muscle tone – the child becomes like a “rag doll”

As this condition progresses, seizures, muscle spasms may occur, due to which the child arches his back and neck, throws his head back.

With further progression, damage to the central nervous system leads to persistent neurological consequences of jaundice in newborns:

• cerebral palsy
• Hearing loss ranging from mild to severe, almost total deafness
• retardation in psychomotor development, decreased ability to learn
• impaired gaze: people with this consequence of kernicterus usually do not look straight ahead, but look up or side to side

Treatment of kernicterus is carried out by exchange transfusion of blood .

Forecast

In most cases, the prognosis is favorable if the diagnosis is made on time and treatment is started. The situation worsens if kernicterus develops. This condition is accompanied by the risk of developing persistent neurological disorders and death of the child.

Prevention

An effective method for preventing jaundice in newborns is proper feeding. If the child is breastfed, then in the first days of life there should be 8-12 feedings per day. With artificial feeding during the first week of life, the baby should receive 30-60 ml of the mixture every 2-3 hours.

At the risk of Rh conflict during pregnancy, the following preventive measures are taken:

• Rh-negative pregnant women, even if no antibodies are detected in their blood, undergo three courses of desensitization – their immune system is “trained” not to react to the Rh-positive blood of the fetus. Courses of therapy are carried out at 10-22, 22-24 and 32-34 weeks of pregnancy, they will last for 10-12 days.
• If a pregnant woman has a high level of Rh antibodies, and she has a history of miscarriage or the birth of a child with severe hemolytic disease, plasmapheresis is prescribed. This procedure helps to remove Rh antibodies from the blood. Plasmapheresis begins at 23–24 weeks of gestation and is performed once a week until delivery.
• Pregnant women with a high risk of Rh conflict are referred for hospitalization from 34-36 weeks of pregnancy – from this period they are in the hospital under the supervision of doctors. In some cases, hospitalization may be indicated at an earlier date.

Main

• Newborn jaundice is a condition in which the level of bilirubin in the blood rises – a substance formed when the hemoglobin of red blood cells is destroyed.
• Often this is a physiological state, a manifestation of the adaptation of the body of a newborn to new conditions.
• The main and often the only manifestation of jaundice in newborns is yellow staining of the skin, mucous membranes and whites of the eyes.
• This condition is usually detected by doctors in the maternity hospital. If symptoms occur after discharge from the hospital, you should immediately show the child to the doctor.
• The diagnosis is established by the results of the examination of the child and laboratory tests.
• Treatment depends on the cause of jaundice. Most often, phototherapy is used, in more severe cases, exchange transfusion.
• The prognosis is most often favorable if treatment is started in a timely manner.
• In some cases, kernicterus develops, a condition in which the central nervous system is affected. It can lead to persistent neurological disorders and sometimes death of the child.

Volodin N.N., Antonov A.G., Aronskind E.V., Baibarina E.N., Degtyarev D.N., Degtyareva A.V., Kovtun O. P., Mukhametshin F.G., Parshikova O.V. Protocol for the diagnosis and treatment of hyperbilirubinemia in newborns // Russian Association of Perinatal Medicine Specialists, 2006

• Zakharova I. N., Goryainova A.N., Kholodova I.N., Maikova I.D., Belenovich E.V., Tambieva E.V., Bolbikova E.V., Melenkina A.N., Khudyakova A.A. Differential diagnosis of jaundice in young children // Medical Council, 2016
• Pervishko O.V., Shashel V.A., Muravieva V.N. Stages of treatment and outcomes of conjugative jaundice in young children // Medical Bulletin of the North Caucasus, 2015
• Shabalov N.P. Neonatology: textbook. allowance: in 2 volumes // MEDpress-inform, 2006
• Volodina N.N., Mukhina Yu.G., Subarova A.I. Children’s diseases: textbook. // Dynasty, 2011

Laboratory diagnosis of jaundice

Jaundice is an icteric coloration of the skin and mucous membranes that accompanies an increase in the level of total bilirubin (hyperbilirubinemia). Bilirubin is a bile pigment, formed mainly as a result of the breakdown of hemoglobin in the blood. In the blood, bilirubin binds to proteins and is transported to the liver, where it combines with glucuronic acid (bound / direct bilirubin) and is part of the bile. Then it enters the intestines, where it participates in the breakdown of fats. Partially, bilirubin is transformed into urobilinogen and excreted by the kidneys, giving a yellow color to the urine. The other part turns into stercobilin and is excreted in the feces, giving it a dark color.

Also sources of bilirubin, in addition to erythrocytes, are myoglobin, cytochromes and heme-containing enzymes. Normally, the concentration of bilirubin in the blood is from 3.4 to 17.1 µmol/l. At a bilirubin concentration of more than 27-34 µmol / l, jaundice appears.

Jaundices are hemolytic, parenchymal and obstructive.

Hemolytic jaundices

Hemolytic, or suprahepatic, jaundice is associated with massive hemolysis of red blood cells – a violation of their integrity. In this case, a large amount of bilirubin enters the blood, and the body does not have time to utilize it.

Reasons:

• Acute and chronic hemolytic anemia.
• B ₁₂ – deficiency anemia.
• Thalassemia.
• Extensive hematomas.
• Jaundice caused by the action of drugs that increase the breakdown of red blood cells (for example, acetylsalicylic acid, tetracycline, etc.).
• “Physiological jaundice” in newborns, etc.

Parenchymal jaundice

The cause of parenchymal (hepatic) jaundice is liver disease. Damaged or destroyed liver cells are not able to fully bind bilirubin with glucuronic acid, thereby neutralizing its toxic properties, and it enters the blood in large quantities. In the blood, the level of bilirubin increases, both bound and unbound (direct and indirect)

• Acute and chronic diffuse liver diseases
• Primary and metastatic liver cancer
• Secondary dystrophic lesions of the liver in various diseases of internal organs and right ventricular heart failure
• Cholestatic hepatitis
• Primary biliary cirrhosis
• Toxic liver damage: hydrogen tetrachloride, chloroform, trichlorethylene, halothane, alcohol
• Drug poisoning: paracetamol, isoniazid, rifampicin
• Toxic damage to the liver due to fly agaric poisoning (alpha-amanitin)

Obstructive jaundices

Obstructive (subhepatic, mechanical, congestive, cholestatic) jaundices. The increase in total bilirubin in the blood occurs due to both of its fractions. These jaundices, as the name implies, are associated with a violation of the outflow of bile along the excretory pathways from the liver. Most often this is due to a barrier in the biliary tract, such as a stone, or compression of the ducts from the outside, such as tumors or helminths.

• Extrahepatic bile duct compression
• Gallstone disease
• Neoplasms of the liver
• Neoplasms of the pancreas
• Biliary cirrhosis of the liver
• Helminthiases

Along with these forms of jaundice, congenital and acquired functional (constitutional) hyperbilirubinemias are distinguished:

• Gilbert’s syndrome (idiopathic unconjugated hyperbilirubinemia – increased indirect bilirubin in the blood)
• Post-hepatitis hyperbilirubinemia Kalka
• “Physiological” neonatal jaundice
• Crigler-Najjar Syndrome
• Jaundice due to myxedema (hypothyroidism)
• Jaundice in children born to mothers with diabetes mellitus
• Dubin-Johnson Syndrome
• Rotor Syndrome

“Physiological jaundice” of newborns

Physiological jaundice occurs in about 60% of newborns.

The reason for the increase in bilirubin in the blood of newborns is accelerated hemolysis (decay) of red blood cells due to the functional “immaturity” of the liver in the first days of life. Physiological jaundice is a transient condition, usually appears on the third day, gradually increases by the fifth, and slowly disappears by 2-3 weeks of a child’s life.

Elevated bilirubin in newborns and “physiological” jaundice in most cases are safe, do not require treatment and do not leave consequences for the child.

Laboratory diagnosis of jaundice

For jaundice, changes in the parameters of a biochemical blood test are characteristic.

Normally, the concentration of bilirubin in the blood is from 3.4 to 17.1 µmol/l. At a bilirubin concentration of more than 27-34 µmol / l, jaundice appears.

There are three forms of jaundice:

• Light. The concentration of bilirubin in the blood up to 86 µmol/l
• Medium. The concentration of bilirubin in the blood 87-159µmol/l
• Heavy. The concentration of bilirubin in the blood over 160 µmol/l

In the CMD laboratory, when total bilirubin and direct bilirubin are performed at the same time, indirect bilirubin is calculated, the calculation is free of charge.

The concentration of cholesterol in the blood with parenchymal jaundice can both decrease and increase, with obturation it increases. Alanine aminotransferase, aspartate aminotransferase, gamma-glutamine transferase and alkaline phosphatase increase in parenchymal and obstructive jaundice.

• Bilirubin total (Bilirubin total)
• Bilirubin direct (Bilirubin direct)
• Gamma-glutamyl transferase (Gamma-glutamyl transferase)
• Alanine aminotransferase (Alanine aminotransferase)
• Aspartate aminotransferase (Aspartate aminotransferase)
• Alkaline phosphatase

With hemolytic jaundice, changes can be detected in the general blood test.