neonatal bilirubin encephalopathy

Introduction

Introduction to neonatal bilirubin encephalopathy Bilirubinencephalopathy refers to the pathological damage of brain tissue caused by bilirubin. In addition to the basal ganglia of the brain, the nucleus of the hypothalamic nucleus and the globus pallidus are yellow-stained, the cerebral cortex, meninges and endothelium. There has also been a spread in the past. In the past, it was said that Huang Wei was not comprehensive enough. For neonatal hyperbilirubinemia, it must be treated early to avoid the development of bilirubin encephalopathy. Failure to prevent early can lead to sequelae or death. basic knowledge The proportion of illness: the probability of neonatal disease is 2.1% Susceptible population: newborn Mode of infection: non-infectious Complications: eye movement disorders deafness

Cause

Causes of neonatal bilirubin encephalopathy

1. Excessive production of bilirubin in early life, immature liver of newborns, limited ability to treat bilirubin. The serum does not bind too much bilirubin and penetrates the blood-brain barrier to form bilirubin encephalopathy.

2. The blood-brain barrier is immature in the early neonatal period. In some pathological conditions, the permeability of the blood-brain barrier is increased, and free bilirubin is more likely to pass the blood-brain barrier and form bilirubin encephalopathy.

3. When the plasma albumin level is low, the free bilirubin is increased, and bilirubin is more likely to pass through the blood-brain barrier. Form bilirubin encephalopathy.

Prevention

Neonatal bilirubin encephalopathy prevention

For neonatal hyperbilirubinemia, it must be treated early to avoid the development of bilirubin encephalopathy.

1. Do prenatal care and health education before birth, try to prevent premature birth, dystocia and infection, and prepare for labor for those who have hemolytic disease.

2, postpartum for newborns, especially premature infants can not routinely use vitamin K3, sulfonamides, sodium benzoate caffeine and salicylic acid drugs, jaundice detection must pay attention to, the visual error of experienced people generally does not exceed 85.5mol / L (5mg / Dl), Shanghai neonatal medical engineering professional committee is studying the yellow enamel color palette, there are five different shades of yellow spline fixed on a piece of plexiglass plate, just press the newborn tip of the nose to see what yellow To the extent that the primary doctors and nurses can detect the neonatal jaundice and the estimated serum bilirubin content early, and can be used as the content of bilirubin in hyperbilirubinemia, and can be used as high bilirubin. Screening diagnosis and monitoring of blood loss, before the absence of special tools can also be roughly estimated according to the surface of the jaundice throughout the body surface, the general facial yellow is extremely light about 85.5mol / L (5mg / dl), the trunk is also yellow about 171mol /L (10mg / dl), the limbs see yellow about 256.5mol / L (15mg / dl), hands, feet see yellow is higher than 256.5mol, such as from apricot yellow to golden often exceeds 342mol / L (20mg / dl ), percutaneous bilirubin analyzer is good for newborns Dynamic observation and screening hyperbilirubinemia jaundice, but expensive, less experienced medical staff for value, because the decision to shake or trace amounts of serum bilirubin measurement is based.

Complication

Neonatal bilirubin encephalopathy complications Complications, eye movement disorders, deafness

The sequelae: often occurs 2 months or later after birth, manifested as hand and foot movement, eye movement disorders, deafness, mental retardation or enamel dysplasia.

Symptom

Symptoms of neonatal bilirubin encephalopathy Common symptoms Neonatal hand and foot Xu moving dyspnea angle bow anti-green teeth or tan teeth convulsions Bradycardia acne palsy tremors weak force hug reflection weakened or disappeared

The severity of symptoms is related to serum unconjugated bilirubin concentration, age and other factors, generally divided into four phases:

Warning period: younger age, serum bilirubin is less sensitive at 256.5mol (15mg/dl), mainly manifested as lethargy, refusal to eat, decreased muscle tone, impaired reflex or disappearance, and other symptoms of apnea. , the bradycardia, about half a day into the flood season.

Menstrual period: manifested as convulsions, fever, increased muscle tension, screaming, kindness, nystagmus, difficulty breathing, convulsions or angulation, and other symptoms of premature infants, such as convulsions, can not be obvious, survivors enter after 1 to 2 days Recovery period.

Recovery period: First, the sucking and reaction gradually recover, and then the breathing is improved, and the phlegm is reduced or disappeared. This period lasts about 2 weeks.

The sequelae period: generally occurs 2 months to 3 years after birth, hand and foot movements, eyeball difficulty or strabismus, hearing impairment, enamel hypoplasia with green teeth or brown teeth, mainly due to damage to the vertebral system The so-called quadruple syndrome, 48 cases of bilirubin encephalopathy seen in Shanghai 835 hemolytic disease follow-up, there are mental retardation, convulsions or clonic, head lift and runny symptoms.

In the presence of symptoms, serum bilirubin sometimes decreases, which may be due to the uptake of tissues such as the bilirubin central nervous system, so it is not possible to relax the vigilance. In recent years, partial brain bilirubin 171 was detected by brainstem auditory evoked potential detection. Children with ~342mol/L (1020mg/dl) had no neurological symptoms, but the IV and V waveforms of the potential curve disappeared, and the brainstem nerve transit time prolonged, indicating that the auditory nerve has dysfunction. Such changes are in bilirubin. After falling, it disappeared. Perlman (1988) called transient subclinical lilirubin neurotoxicity. It is believed that this bilirubin poisoning effect can be reversed and gradually restored.

Examine

Examination of neonatal bilirubin encephalopathy

Severe jaundice on the basis of drowsiness, decreased sucking reflex and decreased muscle tone, or two eyes gaze, paroxysmal muscle tension increased; heavy two hands clenched, forearm internal rotation, horn arch reversal, and sometimes screaming.

Neonatal bilirubin encephalopathy examination: meningeal irritation, brain CT examination, cerebrospinal fluid bilirubin, brain ultrasound, liver function examination.

1. Serum bilirubin levels were significantly increased, with unconjugated bilirubin as the main component.

2. Abnormal brainstem hearing evoked potential.

3. Head MIR can show imaging abnormalities of the basal ganglia, thalamus and internal capsule.

Diagnosis

Diagnosis and diagnosis of neonatal bilirubin encephalopathy

diagnosis

Can be diagnosed based on clinical symptoms and laboratory tests.

Differential diagnosis

1, JE: the main symptoms and signs of acute onset, high fever, headache, vomiting, lethargy, etc., severe patients have coma, convulsions, difficulty swallowing, cough and respiratory failure and other symptoms, signs of meningeal irritation, shallow reflection Disappeared, deep reflexes, tonic sputum and positive disease reflexes.

2, tetanus: tetanus generally begins to appear symptoms 1-2 weeks after bacterial invasion (very few people have as short as 24 hours or up to several months to appear symptoms). It usually occurs 6 to 10 days after injury, and it occurs after 24 hours or weeks after injury.

The onset time is short, the more severe the symptoms, the greater the risk of the patient. At first, there are fatigue, dizziness, headache, irritability, yawning and other prodromal symptoms, followed by strong muscle contraction, first of all, facial muscles begin. It is difficult to open the mouth, the teeth are tightly closed; the expression is tense, the patient has a "chat smile" face; the back muscles are paralyzed, and the so-called "corner arch reversal" appears in the back of the head; if respiratory muscles or sneezing occur, the breathing can be stopped, and the patient suffocates. death. This systemic muscle spasm lasts for a few minutes, and it recurs at intervals. Any slight irritation such as light, sound, speech, and hair can be induced.

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