Neonatal jaundice

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Neonatal jaundice is a yellowish discoloration of the whites of the eyes and skin of newborns due to high bilirubin levels. Other symptoms may include excessive sleepiness or poor food. Complications may include seizures, cerebral palsy, or kernicterus.

In many cases there is no specific underlying (physiological) disorder. In other cases it results from damage to red blood cells, liver disease, infections, hypothyroidism, or metabolic (pathological) disorders. The bilirubin level is more than 34? Mol/l (2 mg/dL) can be seen. Concerns, in healthy babies, occur when the levels are over 308? Mol/L (18 mg/dL), jaundice seen on the first day of life, there is a rapid increase in the level, jaundice lasts more than two weeks, or the baby appears unhealthy. On those with related findings, further investigation to determine the underlying cause is recommended.

The need for treatment depends on the level of bilirubin, the age of the child, and the underlying cause. Treatment may include frequent feeding, phototherapy, or exchange transfusion. In those born early, aggressive care is likely to be necessary. Physiological jaundice generally lasts less than seven days. This condition affects more than half of infants in the first week of life. Babies born early are about 80% affected.

Video Neonatal jaundice

Signs and symptoms

The main symptom is a yellowish discoloration of the whites of the eyes and skin of newborns. Other symptoms may include excessive sleepiness or poor food.

The bilirubin level is more than 34? Mol/l (2 mg/dL) can be seen. For the foot to be exposed the level should generally be more than 255Ã? Mol/l (15 mg/dL).

Complications

Prolonged hyperlilirubinemia (severe jaundice) may lead to chronic bilirubin encephalopathy (kernicterus). Rapid and accurate treatment of jaundice neonatal helps to reduce the risk of neonates developing kernicterus.

Babies with kernicterus may experience fever or seizures. High pitched cry is the effect of kernicterus. Scientists used computers to record and measure cranial nerves 8, 9 and 12 in 50 infants divided into two groups equally dependent on bilirubin concentrations. Of the 50 babies, 43 have a high-pitched crying trail.

The exchange of transfusions performed to lower high bilirubin levels is an aggressive treatment.

Maps Neonatal jaundice

Cause

In newborns, jaundice tends to develop due to two factors - the breakdown of fetal hemoglobin because it is replaced by adult hemoglobin and a relatively immature metabolic pathway of the liver, which can not conjugate and secrete bilirubin as early as adults. This causes the accumulation of bilirubin in the blood (hyperbilirubinemia), leading to symptoms of jaundice.

If neonatal jaundice is unclear with simple phototherapy, other causes such as biliary atresia, progressive familial intrahepatic cholestasis, bile duct deficiency, Alagille syndrome, alpha 1-antitrypsin deficiency, and other pediatric liver disease should be considered. Evaluations for this include blood work and various diagnostic tests. Prolonged neonatal jaundice and should be acted upon immediately.

Severe neonatal jaundice may indicate the presence of other conditions that contribute to elevated bilirubin levels, where there is a wide range of possibilities (see below). These should be detected or excluded as part of the differential diagnosis to prevent the development of complications. They can be grouped into the following categories:

Unconjugated

Hemolytic

Causes of intrinsic hemolysis

• Membrane condition
  • Spherocytosis
  • hereditary eliptocytosis
• Enzyme Conditions
  • Deficiency of glucose-6-phosphate dehydrogenase (also called G6PD deficiency)
  • Pyruvate kinase deficiency
• Globin synthesis defects
  • sickle cell disease
  • Alpha-thalassemia, eg. HbH Disease

Causes of extrinsic haemolysis

• Systemic conditions
  • Sepsis
  • Open arterial malformations
• Alloimunitas (Blood of neonatal or umbilical cord gives direct positive test and mother blood give positive indirect Coombs test)
  • Hemolytic disease in newborns (ABO)
  • Rh disease
  • Hemolytic disease in newborns (anti-Kell)
  • Hemolytic disease in newborns (anti-Rhc)
  • Incompatibility of other blood types causes hemolytic disease in newborns

Non-hemolytic causes

• Breastfeeding jaundice
• Breast milk jaundice
• Cephalohematoma
• Polycythemia
• Urinary tract infection
• Sepsis
• Hypothyroidism
• Gilbert's syndrome
• Crigler-Najjar Syndrome
• High GI obstruction (Pyloric Stenosis, bowel obstruction)

Konjugated (Direct)

Heart causes

• Infection
  • Sepsis
  • Hepatitis A
  • Hepatitis B
  • TORCH infections
• Metabolic
  • Galactosemia
  • Alpha-1-antitrypsin deficiency, which is usually missed, and should be considered in DDx
  • Cystic fibrosis
  • Dubin-Johnson Syndrome
  • Rotor Syndrome
• Drugs
• Total parenteral nutrition
• Idiopathic

Post-heart

• biliary atresia or bile duct obstruction
  • Alagille Syndrome
  • Choledochal cyst

Non-organic causes

Breastfeeding jaundice

"Breastfeeding jaundice" or "lack of breastfeeding jaundice," caused by inadequate breast milk intake, results in an inadequate amount of bowel movements to remove bilirubin from the body. This leads to increased enterohepatic circulation, resulting in increased bilirubin reabsorption of the intestine. Usually in the first week of life, most cases can be corrected with frequent breastfeeding sessions with sufficient duration to stimulate adequate milk production.

Breast milk jaundice

While breastfeeding jaundice is a mechanical problem, breast milk jaundice is a biochemical occurrence and higher bilirubin may act as an antioxidant. Breast milk jaundice occurs later in the newborn period, with bilirubin levels usually peaking on the sixth day until the 14th of life. This slow onset jaundice can develop up to one-third of healthy breast-fed infants.

• First, at birth, infertile intestines, and normal bowel flora take time to develop. The bacteria in the adult intestine convert the conjugated bilirubin into stercobilinogen which is then oxidized to stercobilin and excreted in the stool. In the absence of sufficient bacteria, bilirubin is not conjugated by the brush border? -glucuronidase and reabsorbed. This process of reabsorption is called enterohepatic circulation. It has been suggested that intake of bilirubin (enterohepatic circulation) is increased in breast-fed infants, possibly as a result of increased levels of epidermal growth factor (EGF) in breast milk. Breast milk also contains glucoronidase which will increase the deconjugation and recirculation of enterohepatic bilirubin.
• Secondly, breast milk in some women contains a progesterone metabolite called 3-alpha-20-beta pregnanediol. This substance inhibits the action of uridine diphosphoglucuronic acid (UDPGA) glucuronyl transferase which is responsible for subsequent conjugation and excretion of bilirubin. In the newborn, glucuronyl transferase activity is only 0.1-1% of the adult level, so bilirubin conjugation is reduced. Further inhibition of bilirubin conjugation causes an increase in blood levels of bilirubin. However, these results have not been supported by subsequent research.
• Thirdly, an enzyme in breast milk called lipoprotein lipase results in an increase in the concentration of free fatty acids that do not detetify inhibiting liver glucathonic transferase, again causing decreased conjugation and subsequent excretion of bilirubin.

Physiological jaundice

Most babies experience jaundice seen as an increase in concentration of unconjugated bilirubin during the first week. This is called physiological jaundice. This pattern of hyperbilirubinemia has been classified into two distinct periods functionally.

• First phase

1. The term infant - jaundice lasts for about 10 days with a rapid increase in serum bilirubin up to 204Ã? mol/l (12 mg/dL).
2. Premature babies - jaundice lasts for about two weeks, with a rapid increase of serum bilirubin up to 255Ã,? mol/l (15 mg/dL).

• Stage two - the level of bilirubin decreases to about 34Ã ¢ â,¬? mol/l (2 mg/dL) for two weeks, eventually mimicking the adult value.

1. Premature babies - the second phase can last more than a month.
2. Exclusively breastfed babies - phase two can last more than a month.

The mechanisms involved in physiological jaundice are mainly:

• The relatively low activity of the glucoronosyltransferase enzyme that normally converts unconjugated bilirubin into conjugated bilirubin that can be excreted into the gastrointestinal tract. Before birth, this enzyme is actively re-regulated, since bilirubin must remain unconjugated to cross the placenta in order not to accumulate in the fetus. After birth, it takes some time for this enzyme to function.
• A shorter lifetime of fetal red blood cells, to about 80 to 90 days in term infants, compared with 100 to 120 days in adults.
• Relatively low conversion of bilirubin to urobilinogen by intestinal flora, resulting in a relatively high absorption of bilirubin into the circulation.

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Diagnosis

Diagnosis is often done by measuring serum bilirubin levels in the blood. In those who are born after 35 weeks and more than one day only transmissal bilirubinometer can also be used. The use of a icterometer, a transparent piece of plastic painted in five graduated yellow line horizontally, is not recommended.

Transmissible Bilirubinometer

It is handy, portable and rechargeable but expensive. When pressure is applied to the photoprobe, the xenon tube produces a strobe light, and this light passes through the subcutaneous tissue. Light is reflected back through the second optical fiber bundle to the spectrophotometric module. The intensity of the yellow color in this light, after correcting the hemoglobin, is measured and directly displayed in the arbitrary unit.

pathological jaundice

One of the following features shows pathologic jaundice:

1. clinical jaundice appears in the first 24 hours or more than 14 days of life.
2. Increased total bilirubin levels more than 8.5? mol/l (0.5 Âμg/dL) per hour or (85 μmol/l) 5 mg/dL per 24 hours.
3. Total bilirubin more than 331,5Ã,? mol/l (19.5 mg/dL) (hyperbilirubinemia).
4. Direct bilirubin is more than 34 Ã,Âμ mol/l (2.0Ã, mg/dL).

Signs that help detect pathologic jaundice are intrauterine growth restriction, intrauterine infection stigma (eg cataract, small head, and enlarged liver and spleen), cephalohematoma, bruising, signs of bleeding in the ventricle of the brain. The history of the disease is worth noting. Family history of jaundice and anemia, family history of neonatal or neonatal death due to liver disease, maternal disease suggestive of viral infection (fever, rash or lymphadenopathy), maternal medicine (eg sulfonamides, anti-malarial causes red blood cell destruction in G6PD deficiency) suggestive pathological jaundice in the neonate.

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Treatment

The rate of bilirubin for phototherapy initiatives varies depending on the age and health status of the newborn. However, every newborn with a total bilirubin serum is more than 359? Mol/l (21 mg/dL) should receive phototherapy.

Phototherapy

Babies with neonatal jaundice can be treated with a colored light called phototherapy, which works by converting trans-bilirubin into a water-soluble cis-bilirubin isomer.

Phototherapy involved is not an ultraviolet light therapy but a certain frequency of blue light. Light can be applied with lights above the head, which means that the baby's eyes need to be covered, or by a device called biliblanket, which is under baby clothes close to the skin.

The use of phototherapy was first discovered, accidentally, at Rochford Hospital in Essex, England, when nurses there noticed that sun-exposed infants had less jaundice, and pathologists realized that a bottle of blood left in the sun had little bilirubin. A detailed randomized clinical trial published at Pediatrics in 1968; it took another ten years for the practice to become established.

Exchanging transfusions

Similar to phototherapy the rate at which exchange transfusions must occur depends on the health status and age of the newborn. But it should be used for every newborn with total bilirubin serum greater than 428? Mol/l (25 mg/dL).

Alternative therapy

Homeopathy, acupuncture, and traditional Chinese medicine should not be used.

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References

src: pediatrics.aappublications.org

External links

• Neonatal Hiperbilirubinemia Management and Learning Tool for Healthcare Providers
• Jaundice in the first two weeks of life
• BiliTool - Risk Assessment of Hiperbilirubinemia for Newborns
• Neonatal jaundice - Southern Illinois University Medical School
• The American Academy of Pediatrics has issued guidelines for managing the disease, which can be obtained for free.
• The National Institute for Health Care and Care (NICE) has issued guidelines for the recognition and treatment of neonatal jaundice in the UK.

Source of the article : Wikipedia