green or tan teeth
Introduction
Introduction That is, the color of the teeth is abnormally green or brown, often caused by neonatal bilirubin encephalopathy. The sequelae of neonatal bilirubin encephalopathy usually occurs from 2 months to 3 years after birth. The hand and foot are moving, the eyeball is difficult to turn or strabismus, hearing disorder, and enamel hypoplasia has green teeth or brown teeth. The so-called quadruple syndrome dominated by system damage. In the 835 cases of hemolytic disease in Shanghai, 48 cases of bilirubin encephalopathy were found to be mentally retarded, with convulsions or convulsions, fatigue, and salivation.
Cause
Cause
The onset is related to the chemical properties of bilirubin.
Unbound bilirubin, which is not associated with albumin, is in a free state and has a small molecular weight. It can pass through the blood brain barrier (BBB) and enter the brain cells to dissociate the mitochondrial oxidative phosphorylation in brain cells. , that is, uncoupling. Therefore, the energy production of brain cells is inhibited, and brain cells are damaged. The permeability of Mirra et al. BBB increases with the increase of serum bilirubin, which may reduce cell surface tension and toxic effects on brain capillary endothelial cell wall, and increase BBB permeability.
Unbound bilirubin linked to albumin, a lipolysin albumin complex with large molecular weight, unable to pass BBB and cell membrane, but in recent years, it is considered to be in hypoxia, infection, dehydration, hypoglycemia, acidosis and hypertonic infusion Under the influence of BBB, BBB can be temporarily opened, so that unconjugated bilirubin, which links macromolecules with albumin, can also enter brain tissue and involve a wide range of sites. When there is an increase in the anion in the blood or a drop in pH, it can also become free bilirubin and pass through the cell membrane, and enter the nerve cells rich in phospholipids to form bilirubin encephalopathy.
Combined with glucuronic acid in hepatocytes, the bound bilirubin is water-soluble, excreted through the liver and kidney, and does not cause bilirubin encephalopathy. Bilirubin encephalopathy occurs almost exclusively in the neonatal period, mainly due to the following factors:
1. The enzyme system is immature: hepatocytes cannot effectively bind unbound bilirubin to bind bilirubin.
2, severe hyperbilirubinemia: more common, such as neonatal hemolytic disease, congenital non-hemolytic jaundice (K-Nan syndrome), and drug poisoning (vitamin K3), etc., can make unbound Increased bilirubin.
3, blood-brain barrier function is poor: unconjugated bilirubin is easy to pass and combined with brain tissue, premature infants are worse, various infections, asphyxia and hypoxia factors can affect the integrity of BBB barrier function.
4. Low plasma albumin content: limited ability to attach unconjugated bilirubin.
5, acidosis: neonatal disease is prone to acidosis, can promote the opening of BBB, so that the intake of cells increased.
6, seize the albumin linkage to make bilirubin free: external farming cattle have sulfamethoxazole, salicylate, sodium benzoate, novobiocin, cephalosporin, new penicillin II, indomethacin, etc., endogenous Heparin, cholic acid and hunger, hypoglycemia or increased free fatty acids in the body during cold stimulation.
Examine
an examination
Related inspection
Oral endoscopic oral X-ray examination of pulp temperature test (cold and hot diagnosis)
The severity of symptoms is related to factors such as serum unconjugated bilirubin concentration and age. Generally divided into four phases:
Warning period: The age is small, serum bilirubin is mild at 256.5mol (15mg/dl), mainly manifested as lethargy, antifeeding, hypotonia, diminished or disappeared, and other symptoms of apnea. Slow heartbeat, about half to one day into the flood season.
Stage: manifested as sputum, fever, increased muscle tension, screaming, kindness, nystagmus, difficulty breathing, convulsions or angulation, and other symptoms such as convulsions in premature infants. The survivors will enter after 1 or 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 are moving, eyeball is difficult to turn or strabismus, hearing disorder, enamel hypoplasia has green teeth or brown teeth, mainly due to damage of the extracorporeal system The so-called quadruple syndrome. In the 835 cases of hemolytic disease in Shanghai, 48 cases of bilirubin encephalopathy were found to be mentally retarded, with convulsions or convulsions, fatigue, and salivation.
Serum bilirubin sometimes decreases when symptoms appear. This may be due to the uptake of tissues such as the bilirubin central nervous system, so you can't relax your vigilance. In recent years, the brainstem auditory evoked potential test has found that some patients with serum bilirubin 171 ~ 342mol / L (10 ~ 20mg / dl) have no neurological symptoms, but the IV and V waveforms of the potential curve disappear, and the brain stem nerve transit time is prolonged. , indicating that the auditory nerve has dysfunction, such changes disappear after the decline of bilirubin. Perlman (1988) calls it transient subclinical lilirubin neurotoxicity, and believes that the effect of this bilirubin poisoning can be reversed and gradually restored.
Diagnosis
Differential diagnosis
1. JE:
The main symptoms and signs are acute, high fever, headache, vomiting, and lethargy. Severe patients have symptoms such as coma, convulsions, difficulty swallowing, coughing and respiratory failure. Signs of meningeal irritation, disappearance of shallow reflexes, deep reflex hyperthyroidism, tonic paralysis and positive disease reflexes.
2, tetanus:
Tetanus usually begins to develop symptoms 1 to 2 weeks after bacterial invasion (very few people have symptoms as short as 24 hours or as long as several months).
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 pre-existing symptoms such as fatigue, dizziness, headache, irritability, and yawning. Strong muscle contractions can then occur. The first is the beginning of facial muscles, difficulty in opening the mouth, tightness of the jaws; expression of tendons, the patient has a "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 stops and the patient suffocates and dies.
This systemic muscle spasm lasts for a few minutes and recurs at intervals. Any slight stimuli such as light, sound, speech, and hair can be induced.
The severity of symptoms is related to factors such as serum unconjugated bilirubin concentration and age. Generally divided into four phases:
Warning period: The age is small, serum bilirubin is mild at 256.5mol (15mg/dl), mainly manifested as lethargy, antifeeding, hypotonia, diminished or disappeared, and other symptoms of apnea. Slow heartbeat, about half to one day into the flood season.
Stage: manifested as sputum, fever, increased muscle tension, screaming, kindness, nystagmus, difficulty breathing, convulsions or angulation, and other symptoms such as convulsions in premature infants. The survivors will enter after 1 or 2 days. Recovery period. During the recovery period, the sucking and the reaction gradually recovered, and then the breathing improved, and the sputum was alleviated or disappeared. This period lasted about 2 weeks.
The sequelae period: generally occurs 2 months to 3 years after birth, hand and foot are moving, eyeball is difficult to turn or strabismus, hearing disorder, enamel hypoplasia has green teeth or brown teeth, mainly due to damage of the extracorporeal system The so-called quadruple syndrome. In the 835 cases of hemolytic disease in Shanghai, 48 cases of bilirubin encephalopathy were found to be mentally retarded, with convulsions or convulsions, fatigue, and salivation.
Serum bilirubin sometimes decreases when symptoms appear. This may be due to the uptake of tissues such as the bilirubin central nervous system, so you can't relax your vigilance. In recent years, the brainstem auditory evoked potential test has found that some patients with serum bilirubin 171 ~ 342mol / L (10 ~ 20mg / dl) have no neurological symptoms, but the IV and V waveforms of the potential curve disappear, and the brain stem nerve transit time is prolonged. , indicating that the auditory nerve has dysfunction, such changes disappear after the decline of bilirubin. Perlman (1988) calls it transient subclinical lilirubin neurotoxicity, and believes that the effect of this bilirubin poisoning can be reversed and gradually restored.
