neonatal respiratory distress syndrome
Introduction
Introduction to neonatal respiratory distress syndrome Neonatal respiratory distress syndrome (NRDS) indicates progressive dyspnea shortly after birth, cyanosis, expiratory sputum, inspiratory tri-concavity and respiratory failure, mainly found in premature infants, especially gestational age is less than 32 to 33 weeks. The basic characteristics are progressive alveolar atelectasis caused by immature lungs and pulmonary surfactant deficiency, pulmonary fluid transport disorders, and pulmonary capillary-alveolar high permeability exudative lesions. Its pathological features are the eosinophilic transparent membrane attached to the wall of the alveolar wall to the terminal bronchioles, also known as hyalinemiembranedisease (HMD). basic knowledge Sickness ratio: 0.05% Susceptible population: newborn Mode of infection: non-infectious Complications: pulmonary hypertension, respiratory failure, heart failure, emphysema
Cause
Causes of neonatal respiratory distress syndrome
Premature delivery (35%):
When the fetus is 22 to 24 weeks old, the lung type II cells can produce PS, but the amount is small, and rarely metastasize to the alveolar surface. As the gestational age increases, the synthesis of PS gradually increases, so the baby is born in the lungs. The lower the amount of PS, the higher the incidence of RDS. At the gestational age of 24 to 30 weeks, various hormones have the greatest effect on promoting lung maturation. This is the best stage for prenatal prevention. After 32 to 34 weeks, the hormone pair The effect of lung maturation is not very important. After 35 weeks of gestational age, the stage of PS rapidly entering the alveolar surface. The lungs of premature infants continue to develop after birth. The PS produced within 72 to 96 hours after birth can generally maintain normal breathing, so as long as The PS deficiency phase is supplemented so that premature babies can survive the storm and the survival rate can be increased.
Pregnant women with diabetes (25%):
The blood sugar of pregnant women with diabetes is high, and the blood sugar of the fetus is also increased. At this time, the secretion of fetal insulin must be increased to adapt to the needs of glucose metabolism, and the glucose is converted into glycogen. In this case, the fetus grows fat and huge, but The lungs are not necessarily mature, and insulin antagonizes the action of adrenocortical hormones and affects lung development.
Intrauterine distress (20%):
The distress in the palace occurs mostly in the fetus with insufficiency of the placenta. Due to long-term hypoxia, the development of fetal lungs is low, and the secretion of PS is low. The suffocation at birth is caused by dystocia, which is one of the causes of RDS in newborns.
The appearance of the lung is normal. Due to the high degree of stagnation, it is dark red, with a tough texture such as the liver. It sinks into the water. The cut surface is dark red. The lung tissue shows a wide resorption of atelectasis under the microscope. The alveolar walls are close to each other. There is only a small amount of dilated alveoli in the lung, and the wall is covered with a layer of eosinophilic homogeneous and unstructured substance, that is, a transparent membrane. Sometimes the transparent membrane is partially freed from the alveoli, the alveolar duct and bronchioles are dilated, and the wall is also With a transparent membrane, the lung tissue has edema, sometimes the process of edema fluid is concentrated into a transparent membrane, and large mononuclear and multinucleated cells are seen to exude. Those who survive for more than 32 hours often have pneumonia, and the transparent membrane has been absorbed. Or loose granular particles.
Pathogenesis
PS can reduce the surface tension at the junction of the alveolar wall and the alveolar gas, and make the alveolar open. Its half-life is short and needs to be supplemented continuously. When PS is lacking, the alveolar surface tension is increased, the alveolar collapses, the functional residual volume is decreased, and the lung compliance is improved. The curve moves down, the compliance decreases, the ineffective cavity ventilation, the respiratory work increases significantly, the energy is depleted, leading to systemic organ failure, according to the formula:
P (alveolar retraction rate) = 2T (surface tension) / r (alveolar radius).
The alveoli with the smallest radius during exhalation collapsed first, so progressive atelectasis occurred. The number of alveoli and ventilation area of immature lungs was too small, the alveolar space was wide, gas diffusion and exchange were severely insufficient, and end-expiratory alveolar collapse Difficulty in ventilation, hypoxemia, decreased ability of alveolar epithelial cells to synthesize surfactants, leading to clinical exacerbations of dyspnea and cyanosis, persistent hypoxia leading to pulmonary vasospasm, pulmonary hypertension, and reduced pulmonary blood flow Right outside the lung, shunt right and left, pulmonary arteriovenous shunt, imbalance of ventilation-perfusion, affecting blood and blood exchange, continuous hypoxia and acidosis can cause myocardial damage, decreased cardiac output, systemic hypotension, low perfusion, Finally, multiple organ failure mainly caused by respiratory failure is as follows: insufficient alveolar surfactant increased alveolar wall surface tension (increased alveolar retraction force) minimum radius of alveoli first collapse progressive atelectasis Hypoxia, acidosis pulmonary arteriolar spasm increased pulmonary artery pressure foramen ovale and arterial catheter opening right to left shunt (continuous fetal circulation) Decreased pulmonary perfusion lung tissue hypoxia heavier capillary permeability fibrin calm hyaline membrane formation hypoxia, acidosis is more severe, resulting in a vicious cycle.
Due to the decreased secretion synthesis of lung PS, the blockage of PS recirculation pathway, or due to excessive fluid in the alveolar space (transportation disorder, hyperosmotic), PS can be insufficient, and pathological exudate contains a large amount of plasma protein. Interference and inhibition of PS function in the alveolar cavity, inhalation at birth, pneumonia, lung dysplasia, pulmonary hemorrhage, and early hypoxic lesions such as asphyxia may be related to the above pathophysiology, etc., pulmonary intrapulmonary surface activity in preterm infants The total amount of phospholipids in the substance, only 10% to 30% of full-term children, or lower, and lack of major pulmonary surfactant proteins such as SP-A, B, C, etc., are inferior to full-term children in quantity and quality. It is the main reason for the occurrence of RDSN. The application of exogenous pulmonary surfactant preparation can rapidly increase the content of pulmonary surfactant in the lungs. After pulmonary surfactant is instilled into the lungs of children with RDSN, the surface activity of the lungs is activated. The substance phospholipids are immediately taken up by alveolar epithelial cells and gradually enhance the functional activity of endogenous pulmonary surfactants, especially the synthesis and secretion of SP-A, B, C. This process is related to the clinical response after administration. Owned by closely related.
Prevention
Neonatal respiratory distress syndrome prevention
First, prenatal prevention
Pregnant women with preterm birth may be given adrenal-cortical hormone (ACH) in the late pregnancy to prevent RDS or reduce RDS symptoms in premature infants. In 1969, Liggins first discovered intravenous infusion of dexamethasone. Promote the maturity of premature sheep lungs, and the same results can be obtained for other heterogeneous lungs. Later, gradually applied to pregnant women to promote the maturation of lungs in premature infants. The most commonly used hormones are betame-thasone and dexamethasone (betame-thasone) and dexamethasone (betame-thasone). Dexamethasone) Because they are easier to enter the fetus through the placenta than other ACHs, the effect of ACH is to stimulate the production of phospholipids and small proteins in fetal lung type II cells, reduce the permeability of capillaries in the lungs, reduce pulmonary edema, and thus reduce the incidence of RDS. Rate, even if the disease, the symptoms are lighter, can reduce the mortality rate, the oxygen concentration during treatment does not have to be too high, can prevent complications such as bronchopulmonary dysplasia (BPD) and post-fibrous fibrosis (ROP), due to reduced Oxygen should also reduce the incidence of neonatal necrotizing enterocolitis and hypoxic ischemic intracranial hemorrhage.
The preventive dose of ACH for pregnant women; 24 mg of betamethasone or dexamethasone, divided into 2 intramuscular injections, 24 hours apart, the commonly used dose in China is 5-10 mg, intramuscular or intravenous, once a day for 3 days. Prevention should be given 7 to 24 hours before the delivery of the pregnant woman, so that the drug has enough time to play its due role. ACH prevention does not increase the possibility of infection for pregnant women and fetuses, even if the amniotic membrane is broken, it will not be based on the original. Increasing the infection rate, intrauterine growth retardation is not a contraindication, the effect of preventing RDS is very inconsistent for the very low birth weight infants delivered. It is generally considered that the incidence of RDS cannot be reduced, but in the infants who have survived the ventricle The incidence of lower cerebral hemorrhage seems to be reduced, and ACH is less effective in infants with diabetes, Rh hemolytic disease, and multiple pediatric children.
Although ACH prevention has a positive effect, there are still 10% of premature infants with RDS. Therefore, considering the addition of other hormones to improve the efficacy, thyroxine has the effect of promoting lung maturation, but it is not clinically applicable because it is not easy to pass the placental barrier. Later, it was found that the structure of thyrotropin releasing hormone (TRH) in animal brain tissue is similar to that of thyroxine, and can pass through the placenta. It can be used as a preventive preparation. The dose is 0.4mg every time, every 8 hours, a total of 4 times. Some pregnant women may have side effects, showing nausea, vomiting and high blood pressure, which can be reduced to half. After the addition of TRH, the incidence and mortality of RDS are lower.
Second, postpartum prevention
It is pointed out that the lung surface activity and substances are given to the baby within half an hour after birth to prevent the occurrence of RDS or to alleviate the symptoms. Most of the infants who are not used for prenatal pregnancy are prevented. The better the prevention, the better, before the baby begins to breathe or Instillation from the tracheal intubation before the ventilator positive pressure breathing begins, the PS can be evenly distributed in the lungs, the preventive effect is shown in the incidence of RDS and the mortality rate is reduced, the incidence of the disease is lighter, because PS can be early Improve oxygenation in the body. Some babies can use ventilator, the oxygen concentration and average airway pressure can be lower, so the incidence of air leak and oxygen poisoning is significantly reduced, and the oxygen ischemic skull can also be reduced. Chronic lung diseases (CLD) are rare in the occurrence of internal hemorrhage. CLD refers to diseases requiring oxygen supply within 28 days after birth. Although the advantages of prevention are many, premature infants and asphyxia do not necessarily have RDS. Prevention of babies who are not ill will increase costs and unnecessary endotracheal intubation, and suffocation and premature babies often require more urgent resuscitation, and PS prevention will temporarily interrupt the continuous process of resuscitation. In preterm infants with a fetus <28 weeks or a birth weight <1000g in this delivery room, if antenatal pregnancies do not receive ACH prevention, PS can be prevented under the treatment of experienced and skilled resuscitation personnel, and other infants are in RDS. Immediately after use, the ventilator and the tracheal intubation were used to drip the PS and treated according to the treatment.
PS prevention and PS treatment are not easily separated. Many newborns who have just recovered have irregular breathing or distress, and need PS to continue treatment. The amount of prevention is similar to the amount of treatment, such as using natural PS (regardless of pig lung or bovine lung PS). 100 ~ 150mg / kg, such as the use of synthetic Exosurf infusion dose of 5ml / kg (containing DPPC 67mg / kg). See the treatment of respiratory distress syndrome and the third chapter of the third section of pulmonary surfactant and its clinical application Overview.
Third, joint prevention
Refers to the pre-natal use of ACH for pregnant women, postpartum for the joint prevention of neonatal PS, for 1 prenatal prevention started late, pregnant women have not delivered to 24 hours, 2 neonates with severe distress, RDS after birth It is also often serious, and this combination prevention is appropriate. Animal experiments prove that joint prevention is better than prevention alone.
Complication
Neonatal respiratory distress syndrome complications Complications pulmonary hypertension respiratory failure heart failure emphysema
Complications of hyaline membrane disease occur mostly during oxygen therapy or during the recovery period after treatment. Severe cases often have pulmonary hypertension, respiratory and heart failure.
1. Air leakage due to damage of the alveolar wall, gas spills into the pulmonary interstitial, or interstitial emphysema caused by excessive inspiratory peak pressure or mean airway pressure (MAP) during mechanical ventilation, gas along the blood vessel to the mediastinum, Causes mediastinal emphysema, interstitial emphysema can also cause pneumothorax, breathing is more difficult when air leaks.
2. Oxygen poisoning When the inhaled oxygen concentration (FiO2) is too high, or the oxygen supply time is too long, oxygen poisoning may occur, and bronchopulmonary dysplasia (BPD) and posterior lens fibrosis are most common. The former is the lung itself. The lesions make the ventilator difficult to remove, and the latter manifests as retinal hyperplasia or retinal detachment after the lens, which causes vision loss and even blindness.
3, the recovery of the arterial catheter open this disease after mechanical respiration and oxygen treatment, in the recovery period about 30% of cases of patent ductus arteriosus, premature infantile arterial catheter tissue is immature, can not spontaneously close, but in the transparent membrane of the lung The early pulmonary vascular resistance increases, not only does the left-to-right shunt occur, but sometimes the right-to-left shunt occurs. When the pulmonary vascular resistance decreases during the recovery period, the left-to-right shunt can occur, which is caused by the increase of pulmonary blood flow. Pulmonary edema, intermittent apnea and congestive heart failure, and even life-threatening, systolic murmur can be heard in the left sternal border of the anterior region of the anterior region, with the most complication between the 2nd and 3rd ribs, such as a large decrease in pulmonary vascular resistance, even Continuous murmurs can occur, chest X-ray films show enlarged heart shadows, lung field congestion, and B-mode echocardiography can directly detect patent ductus arteriosus.
Symptom
Symptoms of neonatal respiratory distress syndrome Common symptoms Difficulty breathing complexion Violet newborn hair sputum around the nose and mouth snoring breath sounds weakened Acute dyspnea newborn cyanotic lip hair sputum breathing irregular nose flapping
Mainly manifested as sudden, progressive respiratory distress, shortness of breath, cyanosis, often accompanied by irritability, anxious expression, sweating, etc., the characteristics of respiratory distress can not be improved by the usual therapy, nor can other primary cardiopulmonary Disease (such as pneumothorax, emphysema, atelectasis, pneumonia, heart failure) explained.
Examine
Examination of neonatal respiratory distress syndrome
[Laboratory Inspection]
Biochemical method
Generally, thin layer chromatography (TLC) is used. At the end of pregnancy (3rd trimaster), the amount of PC and S is about equal. When the gestational age is 34 weeks, the PC increases rapidly, while S is relatively stable or slightly reduced, so L/ The S ratio increased, and soon after that (about 35 weeks of gestational age) PG began to appear, and once it appeared, it rose rapidly, so the gestational age of 34 to 36 weeks was the best stage of the experimental examination.
(1) L/S ratio: L/S means lung maturation, 1.5 to 2 means transition value or suspicious, <1.5 means lung immature, amniotic fluid such as meconium is not seriously polluted or flows out from the vagina, The detection value has little effect. The L/S value of pregnant women with diabetes is often high. Sometimes, although it is >2, the infant can still develop RDS. Therefore, pregnant women can not rely on one kind of examination alone, and need to check with other examination results (such as PG). Control, more reliable.
(2) PG: PG can be expressed by thin layer chromatography when it reaches 3% in PS. As long as PG is present, it means the lung is mature, its sensitivity is high, but its specificity is poor (about 75%). .
(3) DPPC value: When the measured value is >500 mg/dl, the lung is mature, but about 10% of the subjects have NPDS even though the DPPC has reached 500-1000 mg/dl.
2. Foam test
It belongs to biophysical measurement method. The principle is that PS helps foam formation and stability, while pure alcohol prevents foam formation. Method: Take amniotic fluid or bronchial secretion 0.5~1.0ml, add equal amount of 95% alcohol, shake vigorously 15 In the second, stand for 15 minutes and observe the formation of foam around the liquid level of the test tube. No foam is (-), 1/3 of the tube has a small foam (+), > 1/3 tube circumference to a small tube circumference. Foam (++), the foam layer on the upper part of the test tube is (+++), (-) means less PS, can be diagnosed as lack of sign, (+) or (++) is suspicious, (+++) means PS more This method is a tube method in the foam method. It can also be used as a foam method with 4 test tubes. Refer to the physiology and function of amniotic fluid in Chapter 3, Section 3.
3. Gastric juice oscillation test 1ml of gastric juice plus 95% alcohol 1ml, shake for 15s and then let stand for 15min, if there is still a circle of foam along the tube wall is positive, HMD can be excluded first, negative indicates the disease, false positive only 1%, but false Negative up to 10%, the later the gastric juice, the more false negatives, because the amniotic fluid has entered the intestine.
4. Blood examination blood pH value, PaO2, HCO3- decreased and PCO2, BE increased, showing metabolic acidosis, blood potassium increased frequently in early stage, and decreased after diuresis in recovery period.
[Auxiliary inspection]
X-ray examination of the lungs should be performed before positive pressure breathing, otherwise the alveoli that collapsed soon can be reopened so that the chest radiograph has no positive performance, showing the early RDSN network of fine granules and the late vitreous (white lung) The signs, as well as the relatively enhanced bronchial aeration sign, with the characteristics of the chest and lung volume of premature infants, can be divided into four levels according to the severity of the disease:
1. The first stage is characterized by fine-grained frosted glass-like shadows, and the brightness of both lungs is reduced.
2. The second level of performance can be seen in addition to the shadow of the miliary bronchus beyond the heart shadow.
3. The third level performance is in addition to the above image, the heart and the edge are blurred.
4. The fourth level is characterized by a wide white shadow called "white lung", in which black bald leaf dendritic bronchial tree shadows extend from the hilum to the peripheral airway, forming a "bronchial inflation sign", using high pressure Oxygen is introduced into the lungs and X-ray changes can be improved.
Diagnosis
Diagnosis and diagnosis of neonatal respiratory distress syndrome
diagnosis
Diagnosis can be based on medical history, clinical symptoms, and laboratory tests.
Differential diagnosis
I. B group -hemolytic streptococcus infection
Group B hemolytic streptococcus pneumonia or sepsis infected during intrauterine or delivery, very similar to hyaline membrane disease, difficult to distinguish, such as pregnant women with a history of premature rupture of amnion or late pregnancy infection needs to consider the occurrence of B group hemolysis in infants The possibility of streptococcal infection, timely blood collection for culture to identify, before the diagnosis is not clear, should be treated as an infectious disease, given penicillin.
Second, wet lung
Wet lungs are more common in term infants. The symptoms are mild and the course of disease is short. It is not easy to distinguish from light lung hyaline membrane disease, but the X-ray manifestations of wet lung are different and can be identified.
Third, intracranial hemorrhage
Intracranial hemorrhage caused by hypoxia is more common in premature infants, showing respiratory depression and irregularity, accompanied by apnea. On the other hand, intracranial hemorrhage can also be caused by hypoxia after NRDS. Intracranial B-ultrasound can diagnose intracranial hemorrhage.
Fourth, the injury of the transverse nerve
Difficulties in dyspnea can occur in the injury of the diaphragmatic nerve (or the dysfunction of the diaphragmatic movement) and sputum, but the cardiopulmonary signs and X-ray findings can be identified.
