儿科学-培训课件PPT
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Lecture Notes for Nanshan class of Grade 2012Neonatal Respiratory Distress SyndromeSUN YIDepartment of Neonatology The 2nd Affiliated Hospital of Guangzhou Medical UniversityStudents Nanshan Class, Grade 2012 TextbookPediatricsby Chen Shubao, Science Press, 2012Teaching time 2015-09-16Classroom Yuexiu campus, class room 12-5C Class hour 1 class hoursTeaching objectivesAfter this class, students should:1. Understand the etiology and pathophysiology of respiratory distress syndrome (RDS) in newborns. Understand the relationship between prematurity and RDS. 2. Master the clinical presentations of neonatal respiratory distress syndrome.3. Know the management for neonatal respiratory distress syndrome.Key points1. The etiology of RDS is related to pulmonary surfactant deficiency2. Clinical characteristics and chest X-ray appearance of RDS. Master the diagnosis and differential diagnosis.3. The effects of assisted ventilation and surfactant replacement therapy in management.Difficult points1. The roles of pulmonary surfactant.2. Pathophysiology of RDS.Teaching methods Problem-based learningTeaching arrangement(1 class hour, 40 minutes)1. Overview of RDS(3min)2. Etiology(5min)3. Pathophysiology(4min)4. Risk factors(2min)5. Clinical presentations(8min)6. Diagnosis and differential diagnosis(5min)7. Management(7min)8. Prophylaxis(4min)9. Summary and questions(2min)Teaching contents1. OverviewToday our topic is neonatal respiratory distress syndrome. Usually we call its initialsRDS.RDS is also called hyaline membrane disease-HMD. A glassy translucent membrane formed in the alveoli. I think you can imagine how bad the gas diffusion is because of the membranes. Please look at these pictures. Well, how tiny this baby is, right? He is even smaller than your hand. This is an extremely preterm infant. This one is bigger, but still preterm. Preterm means the baby was borned too earlier than he should be, less than 37 weeks gestation. Both babies developed respiratory distress right after birth, deteriorated very fast and need respiratory support. This is the connection to a ventilator. RDS is very common in preterm infants. The survival rate is more than 90%, but there are still some severe cases died. Some babies although survived but left disease like chronic lung disease which is very sad and unfortunate for the babies and the families. So timely and correct diagnosis and appropriate treatment is very important. That means, as a doctor, you are very important. The incidence and severity increase with decreasing gestational age, the lower the gestation is ,the higher the incidence is. Less than 2% term babies develop RDS. In preterm infants less than 32 weeks gestation, the incidence is about 25%. But for babies borned more earlier, 26weeks gestation, most of them get RDS and some cases are very severe. Next we will discuss all these 6 parts of RDS. Like etiology, pathophysiology, clinical presentations, management and so on.2.EtiologyWhy do preterm infants develop RDS? Firstly, due to the immature lung structure. A mature lung has rich alveoli and large surface area for gas exchange like this. But an immature lung has much less and much smaller alveoli which is not enough for normal gas exchange. Also the chest wall muscles in preterm infants are very weak. They cant help breathing as much as term babies. But the most important cause for RDS is pulmonary surfactant deficiency.What is pulmonary surfactant? It is a complex mixture of phospholipids, neutral lipids and proteins which is synthesized and secreted by alveolar type 2 cells. There are two types of epithelial cells in alveoli: type 1 and type 2. Type 2 cells begin to produce surfactant from 24 weeks gestation and increases rapidly till 35 weeks. That may explain why the incidence and severity increase with decreasing gestational age. What is the roles of PS? We say it can decrease the surface tension at air-liquid interface of alveoli. You may ask me what the surface tension is. In the alveolar lumen, there is a thin layer of liquid which is constantly secreted to protect the alveolar epithelium. Like a water bubble. As we know there is air inside, an air-liquid interface is formed here. The water molecules in this liquid layer attract to each other and generate an attractive forces, we call it surface tension. This forces is not only to oppose the alveoli expanding, but contribute to its inward contraction. During expiration the alveolus contracts, contracts and contracts, then what will happen? Collapse, right? Surfactant is a monolayer of surface active material. During exhalation surfactant molecules compress together and disrupt the intermolecular forces in the liquid layer, then decreases surface tension, thereby prevents alveolar collapse. Not only to keep lung open but also stablize the functional residual capacity(FRC), then maintain normal oxygenation and ventilation. 3.PathophysiologyHow does pulmonary surfactant deficiency cause progressive respiratory distress? Surfactant is deficient in preterm babies. With diminished surfactant, the alveoli tend to collapse. So the patients develop generalized atelactasis. That means very little air enter into the alveoli, but the blood flow is still the same, that is what we called ventilation-perfusion mismatching. Normally ventilation perfusion ratio-V/Q ratio should be 1, anytime more than or less than 1 is called mismatching. Then you will see increased PCO2 which reflects decreased ventilation, subsequent low PO2hypoxemia and low PH-acidosis. Hypoxemia and acidosis injures lung capillary, increases capillary permeability, leads to leakage of proteinaceous debrisvery small pieces into the alveoli, results in hyaline membranes formation. This membrane may suppress gas effusion and cause more deteriorated blood gas. If this situation is not interrupted, it will impair the cellular metabolism then suppress the production and activity of surfactant when just little surfactant presents, lead to a vicious circle, get worse and worse. So respiratory distress is progressive, deteriorate very fast, may end in respiratory failure and death.4.Risk factorsOther than prematurity, are there any other risk factors for RDS? Yes, there are. Some term infants with maternal diabetes or are borned by cesarean sectiona surgery without labor, may develop RDS. Perinatal asphyxia as well as multiple birth are all risk factors. Male babies get more chance for RDS than females.5.Clinical presentations Are there any special clinical signs in RDS infants? Lets just go through it. Tachypnea is the first sign. Baby breathes very fast because the lung cant be opened enough, so the tidal volume is decreased, He has to increase the respiratory rate to maintain the minute ventilation. Like the video shows here. See, very fast, right? The respiratory rate is usually more than 60 times every minute. Grunting is a special sign in RDS. You may hear sounds like ee. during expiration. The baby is trying to help himself to close the vocal cord then keep more gas retained in the lung. Increase the FRC, avoid lung collapse. Nasal flaring means the wings of nose keep opening and closing like this. It is another way to help himself to inspire more air. At this time the accessory respiratory muscles try to help with retraction. Baby is working very hard in breathing with substernal、subcostal and intercostal retracting. If all these efforts fail, you will see cyonosis-a blue color around the lips. Because of decreased air entry, on auscultation you will hear decreased breath sounds bilaterally. These signs usually develops very early after birth, before 6 hours, and deteriorate very fast, we call it progressively. What can you see from the chest X-ray?Both lungs look hazy, right? There is a diffuse reticular-granular pattern in lung fields. Granular means small particles by alveolar collapse. Reticular signs is because of the hazy background, you can see a net of small bronchus. For a severe case, lung fields look like a ground glass, very coarse and unclear glass. You can see bronchial tree with air in it very clearly. It is called air bronchogram. Lung volume is small because of atelectasis. Case goes more severe, the cardiac border is very unclear and the whole lung looks white outwhite lung. All these signs could appear in RDS. The complications include patent ductus arteriosus,PDA, pulmonary air leak, pneumothorax, bronchopulmonary dysplasia, chronic lung disease, retinopathy of prematurity, ROP, and ventilator associated pneumonia. Patient with PDA has left to right shunt, so baby will show signs of increased FiO2,apnea,metabolic acidosis,feeding difficulty, increased pulse pressure, bounding pulse, heart murmur, increased heart rate and cardiomegaly6.Diagnosis and differential diagnosis Now lets discuss a case. Baby C is a boy, G2P2, the second pregnancy and second delivery. Born at 32 weeks gestation. It is a C-section delivery due to antenatal bleeding. Birth weight is only 1.8 kilograms, amniotic fluid is bloody, Apgar scores are 8 and 8 at 1 and 5 minutes after birth respectively which are normal. Grunting and retracting developed at 10 minutes after birth. Who can tell me what wrong is with baby C? The disease deteriorated very fast, Cyanosis was noticed, oxygen was given, then baby was transfered to NICU. This is the blood gas at 30 minutes after birth. PH 7.20 PCO2 65, PO2 48, Base excess minus 6, bicarbonate minus 18. What does the blood gas tell you? Yes, this is a mixed respiratory and metabolic acidosis, but mostly respiratory. Chest X-ray. Well, this is ground glass pattern. What is your impression? RDS? You maybe right. Yes, most likely this is a RDS. But you maybe wrong, because some special pneumonia looks very similarly. So dont forget to rule out infection, especially Group B streptococcal pneumonia infection. The differential diagnosis should also include wet lung and diaphragmatic hernia. 7.ManagementNow that you know the diagnosis, how should you treat the baby? General treatment include keep the baby warm, maintain balanced fluid and nutrition. Sometimes baby need cardiac support. Before ruling out infection, give antibiotics for a couple of days.But the most important management is respiratory support. Some mild cases only need oxygen by nasal canula. But most cases at least need the help of nasal CPAP which gives baby a continuous positive airway pressure all through the breath. This is the machine of CPAP. The pressure is given here from the nose into the lung. The pressure is usually between 4 to 6 centimeters of water. Why can nasal CPAP help? This is a RDS lung, inflates and deflates. If there is no positive airway pressure, the lung will close like this at the end of expiration. But if keep a pressure of 4 to 6, the lung will keep a bit open, so less efforts are needed to open the lung for next inspiration, Nasal CPAP may be not enough for severe cases. Then mechanical ventilation works. These are the ventilators. If blood gas shows a PaO250mmHg in high oxygen or a prominent respiratory acidosis, that is the time for mechanical ventilation. But a very specific therapy for RDS is surfactant replacement therapy. Surfactant is deficient in the babies lung. If we give surfactant into the lung, does it work? Absolutely it works very well. Surfactant is from either natural or synthetical. There are two products in Chinese markets which are extracted from animals lung such as pig or bovine. Surfactant is given through the endotracheal tube into the lung. Usually 100 to 200 miligrams every kilogram. The earlier you give it, The faster baby recovers. About the treatment with PDA, if the duct is hemodynamically symptomatic, we can close the duct with indomethacin or ibuprofen. Fluid limitation and diuretics are important. If medical closing failed, consider surgery ligation of the duct.8.ProphylaxisFor a hurtful disease like RDS, can we prevent it or at least alleviate it? Yes, we can. If you expect a woman very likely deliver a premature baby, give steroids like betamethasone or dexmethasone before delivery, that really helps, because steroids stimulates the production of surfactant. Of course, a regular prenatal care and prevention for preterm labor are both important. For very low birth weight infants, give surfactant before clinical signs appearance may alleviate subsequent signs. But the cutoff is still controversial. In western countries, doctors tend to give it to babies born before 28 weeks, but in our country, maybe 30 or 32 weeks is more acceptable. 9.Summary and questionsLets summarize the contents for today. RDS is a common disease in preterm infants due to surfactant deficiency and lung immaturity. Respiratory distress develops progressively before 6 hours after birth. The chest X-ray signs are characteristic. Surfactant replacement therapy has specific effects. These are questions to you and references. What is the roles for surfactant? What are the clinical characteristics for neonatal RDS? How do you treat? You should know the answers. Welcome to email me if you have any questions.OK, thanks for your attention. We really like to see this beautiful smile after your timely diagnosis and appropriate treatment. Thank you.- 5 -
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