What Is Phototherapy for Jaundice?

Medically, the jaundice of newborns under the full moon (within 28 days of birth) is called neonatal jaundice. Neonatal jaundice refers to the neonatal period. Due to the abnormal metabolism of bilirubin, the blood bilirubin level rises High, and the appearance of symptoms characterized by yellow staining of the skin, mucous membranes and sclera is the most common clinical problem in newborns. The disease is divided into physiological and pathological. Physiological jaundice refers to temporary jaundice caused solely by bilirubin metabolism. It occurs in 2 to 3 days after birth, peaks in 4 to 6 days, and subsides in 7 to 10 days. The duration of preterm infants is longer, except for minor Apart from loss of appetite, there were no other clinical symptoms. If jaundice occurs 24 hours after birth, the daily serum bilirubin rises more than 5 mg / dl or> 0.5 mg / dl per hour; the duration is long, full-term infants> 2 weeks, and premature infants> 4 weeks will not return, or even Continue to deepen and aggravate or recur after recurrence or jaundice began to appear within a week to several weeks after birth, are pathological jaundice.

Basic Information

English name: neonatal jaundice
Visiting department: Pediatrics, neonatal
Multiple groups: Pathological jaundice occurs mostly in children with ABO hemolysis

Common locations: Skin, mucosa, sclera
Common causes: Excessive bilirubin production, liver bilirubin metabolism disorders, etc.
Common symptoms: Pathological jaundice is characterized by early onset, severe severity, and rapid progress
Contagious: no

Causes of neonatal jaundice

(A) physiological jaundice

Associated with neonatal bilirubin metabolism, including relatively high bilirubin production; insufficient uptake of bilirubin by hepatocytes; poor ability of plasma albumin to bind bilirubin; deficiency in bilirubin excretion capacity; intestinal liver Cycles increase. Therefore, 60% of term infants and 80% of premature infants can develop visible jaundice in the first week after birth.

(Two) pathological jaundice

1. Excessive bilirubin production

Due to the destruction of excessive red blood cells and increased intestinal liver circulation, serum unbound bilirubin increased. Common causes are: erythrocytosis, extravascular hemolysis, homologous immune hemolysis, infection, increased intestinal and liver circulation, red blood cell enzyme deficiency, abnormal red blood cell morphology, hemoglobinopathy, vitamin E deficiency, and hypozincemia.

2. Hepatic bilirubin metabolism disorders

Due to the poor uptake of hepatocytes and the function of binding bilirubin, the serum unbound bilirubin is increased. Common causes are: hypoxia and infection, Crigler-Najjar syndrome (congenital uridine diphosphate glucuronyltransferase deficiency), Gilbert syndrome (congenital non-hemolytic unconjugated bilirubin elevation), Lucey -Driscoll syndrome (familial transient neonatal jaundice), drugs (such as sulfa, salicylate, indomethacin, lanolin, etc.), congenital hypothyroidism, hypopituitarism, trisomy 21- Syndrome and so on.

3. Bile excretion disorder

Hepatocyte excretion combined with bilirubin disorder or bile duct obstruction can cause hyper-bound bilirubinemia, but if accompanied by impaired liver cell function, there may also be an increase in unbound bilirubin. Common causes are: neonatal hepatitis, congenital metabolic defects, bile duct obstruction, Dubin-Johnson syndrome (congenital non-hemolytic combined bilirubin elevation) and so on.

Clinical manifestations of neonatal jaundice

Physical jaundice

The lighter ones are pale yellow and confined to the face and neck, or spread to the trunk. The sclera can also be yellow-stained after 2 to 3 days, and the skin color returns to normal on the 5th to 6th days. In severe cases, jaundice can also spread throughout the whole body. Cerebrospinal fluid and cerebrospinal fluid can also be yellow stained for more than 1 week, especially in individual premature babies can continue to 4 weeks, the feces are still yellow, urine without bilirubin.

(1) Jaundice The light color is light color, the heavy color is darker, but the skin is ruddy and yellowish.

(2) Jaundice sites are more common in the trunk, sclera, and proximal limbs, but generally elbows and knees.

(3) Newborns are generally in good condition, without anemia, liver and spleen are not enlarged, liver function is normal, and nuclear jaundice does not occur.

(4) Premature babies are more common than full-term babies, and may appear slightly delayed for 1 to 2 days. The severity of jaundice subsides and is delayed, which can be delayed to 2 to 4 weeks.

2. Pathological jaundice

It often has the following characteristics: appear early, appear within 24 hours after birth; severe, full-term infants greater than 12.9mg / dl, premature infants greater than 15mg / dl; rapid progress, serum bilirubin rises more than 5mg / dl every day ; long duration, or recurring.

(1) Degree of jaundice In addition to the face and torso, it can also affect the extremities, hands, and feet with yellow stains.

(2) Color of jaundice: Unconjugated bilirubin is mainly elevated, showing orange or golden yellow; Combining bilirubin is mainly elevated, showing dark green or shade yellow.

(3) Accompanying manifestations Hemolytic jaundice is often accompanied by anemia, hepatosplenomegaly, bleeding points, edema, and heart failure. Infectious jaundice is often accompanied by fever, infection symptoms and signs. Obstructive jaundice is often associated with hepatomegaly, pale stools, and yellow urine.

(4) Systemic symptoms can occur in severe jaundice, with poor response, debilitating symptoms , and anorexia. Low muscle tone, followed by irritability, loud screams, dyspnea, convulsions or angulation, and increased muscle tone.

Neonatal jaundice examination

Bilirubin test

It is an important indicator for the diagnosis of neonatal jaundice. The venous blood or trace blood method can be used to determine the serum bilirubin concentration (TSB). Transdermal bilirubin tester is a non-invasive detection method with convenient operation. The correlation between transcutaneous bilirubin value (TcB) and the trace blood bilirubin value is good. Because this method is affected by the skin thickness and skin color in the measurement site, It can mislead jaundice and can be used for screening. Once a certain threshold is reached, the serum bilirubin needs to be detected.

2. Other auxiliary inspections

(1) Red blood cells, hemoglobin, reticulocytes, and nucleated red blood cells . Routine examination of neonatal jaundice is necessary to help the screening of neonatal hemolytic disease. When there is hemolytic disease, the red blood cell count and hemoglobin decrease, and reticulocytes increase.

(2) Blood type Including the blood type of the father, mother and newborn (ABO and Rh system), especially when suspicious neonatal hemolytic disease is very important. If necessary, further serum specific antibody tests are performed to help confirm the diagnosis.

(3) Red blood cell fragility test It is suspected that jaundice is caused by hemolysis, but blood group incompatibility hemolysis is ruled out. This test can be performed. If fragility is increased, consider hereditary spherocytosis, autoimmune hemolysis, and the like. If the fragility is reduced, it can be seen in hemoglobin diseases such as thalassemia.

(4) Methaemoglobin reduction rate is normal> 75%, and the value of G-6PD (glucose 6-phosphate dehydrogenase) deficiency is reduced. Further investigation of G-6PD activity measurement is needed to confirm the diagnosis.

(5) Blood, urine, and cerebrospinal fluid culture, serum-specific antibodies, C-reactive protein, and erythrocyte sedimentation tests. If jaundice due to infection is suspected, blood, urine, cerebrospinal fluid culture, serum-specific antibodies, C-reactive protein, and erythrocyte sedimentation tests should be performed. Blood routine white blood cell counts increased or decreased, and poisoned particles and nuclei shifted to the left.

(6) Examination of liver function Total blood bilirubin and combined bilirubin are tested. Alanine aminotransferase is a more sensitive method to reflect the damage of liver cells. Alkaline phosphatase can be increased in intrahepatic biliary obstruction or inflammation.

(7) Ultrasound Abdominal ultrasound is a non-invasive diagnostic technique, especially suitable for newborns. Diseases of the biliary tract, such as bile duct cysts, bile duct dilatation, gallstones, biliary atresia, and gallbladder absentness, can all show lesions.

(8) Electrophysiological examinations of auditory and visual functions, including brainstem auditory evoked potentials (BAEP), can be used to evaluate the functional status of auditory conduction nerve channels, to early predict brain damage caused by bilirubin toxicity, and to help temporary or subclinical biliary red Diagnosis of neurotoxicity.

Diagnosis of neonatal jaundice

Diagnosis can be made based on clinical manifestations and bilirubin and related laboratory tests. The focus is on identifying neonatal pathological jaundice, finding the cause, and early identifying the risk of bilirubin encephalopathy.

Differential diagnosis of neonatal jaundice

It should be distinguished from neonatal hemolysis, neonatal sepsis, breast milk jaundice, physiological jaundice, G-6-PD deficiency, neonatal hepatitis, complete intrahepatic obstruction, and biliary atresia.

Neonatal jaundice complications

A serious complication of neonatal jaundice is bilirubin encephalopathy. When serum bilirubin is severely increased or high-risk factors are present, unbound bilirubin can enter the brain through the blood-brain barrier, resulting in bilirubin encephalopathy. More common within 1 week after birth, neurological symptoms can occur as early as 1 to 2 days after birth. Hemolytic jaundice occurs earlier, mostly occurring 3 to 5 days after birth. Premature babies or other causes are mostly seen 6 to 10 days after birth. When there are high risk factors such as premature birth, asphyxia, dyspnea or hypoxia, severe infection, hypoalbuminemia, hypoglycemia, hypothermia, acidosis or weight less than 1.5kg, serum bilirubin can also be lower than the threshold value. Bilirubin encephalopathy occurred. Symptoms usually occur 12 to 48 hours after the peak of severe jaundice.

Neonatal jaundice treatment

Light therapy

It is a simple and effective method to reduce serum unbound bilirubin. Unconjugated bilirubin can produce conformational isomers, structural isomers, and photooxidation products after exposure to light. Among them, the formation of structural isomers is the most important. It can be quickly excreted from bile and urine without the need. Metabolism through the liver is the main reason for reducing serum total bilirubin by phototherapy.

At present, the most commonly used in China is blue light irradiation. The newborn was lying in a phototherapy box, and both eyes were protected with black goggles to prevent damage to the retina. The perineum and anus were covered with diapers, and the rest were bare. Irradiate with single or double light for 2 to 48 hours (usually no more than 4 days). Continuous or intermittent irradiation can be used until the bilirubin drops below 7 mg / dL to stop the treatment.

2. Blood exchange therapy

Blood exchange can effectively reduce bilirubin, replace sensitized red blood cells and reduce anemia. However, certain conditions are required for blood transfusion, and some adverse reactions can also occur. Therefore, the indications should be strictly grasped, and it is generally used when phototherapy fails.

3. Drug treatment

Application of drugs to reduce bilirubin production, accelerate bilirubin clearance or inhibit enterohepatic circulation of bilirubin, including supply of albumin, correction of metabolic acidosis, liver enzyme inducers (such as phenobarbital), intravenous use Immunoglobulin.

4. Supportive treatment

It is mainly to actively prevent and treat hypoxia, hypercapnia, cold injury, hunger, infection, and hypertonic drug infusion to prevent the temporary opening of the blood-brain barrier and prevent the occurrence of bilirubin encephalopathy.