Respiratory distress syndrome: Pathology Review

two people are admitted to the emergency department Mike a 55 year old man presents with shortness of breath high fever and cough a chest x-ray was ordered and it showed a right lower lobe infiltrate which is suggestive of pneumonia he was then started on IV antibiotics but the following day Mike became hypoxic and hypotensive because his hypotension didn't improve despite intubation IV fluids and vasopressors he is diagnosed with septic shock next a repeat x-ray detected newly developed bilateral alveolar opacities heart echography ruled out heart failure and arterial blood gas analysis revealed a PF ratio of 109 milligrams of Mercury then there was Donna an infant delivered by cesarean section at 36 weeks gestational age with an apgar score of 9 at Birth a few hours after delivery she develops tachypnea chest wall retractions with nasal flaring and tachycardia aside from increased work of breathing her physical examination findings are normal a chest x-ray was ordered and it showed diffuse reticulogranular ground glass appearance with air bronchograms now both people are in respiratory distress but first a bit of physiology normally when you breathe in the air reaches the alveoli which are made up of two types of pneumocytes first type 1 pneumocytes are thin and have a large surface area that can facilitate gas exchange more important for the exams are the type 2 pneumocytes which are smaller thicker and have the ability to proliferate in response to lung injury they are in charge of making a fluid called surfactant which contains various phospholipids this lets it act like droplets of oil that coat the inside of the alveoli decreasing surface tension so if it's missing the alveoli will collapse these cells also act like stem cells meaning they can give rise to type 1 cells and type 2 pneumocytes okay so acute respiratory distress syndrome or ards is characterized by rapid onset of widespread inflammation in the lungs which can lead to respiratory failure Arts is not a primary disease as it is usually triggered by conditions like sepsis aspiration trauma and pancreatitis now art starts when these conditions cause alveolar damage and a high yield fact is that the injury triggers the pneumocytes to secrete inflammatory cytokines like tnf Alpha and interleukin-1 this subsequently leads to neutrophil Recruitment and they will release toxic mediators like reactive oxygen species and proteases which will damage the lungs even more you'll need to know that the main site of injury is the alveolar capillary membrane which becomes more permeable causing fluid to move into the alveoli resulting in pulmonary edema this fluid can impair gas exchange leading to hypoxemia furthermore the edema can also wash away the surfactant coating of the alveoli to the point where it can't reduce surface tension anymore and as a result the alveoli collapse and finally dead cells and protein-rich fluids start to pile up in the alveolar space and over time it forms this waxy hyaline membrane which look like a layer of glassy material individuals with Arts present with serious symptoms and signs that require urgent investigation the inflammation process and impaired gas exchange lead to Fever shortness of breath tachypnea chest pain hypotension hypoxia and cyanosis more often than not ards will lead to shock due to hypotension the excess fluid in the lungs can cause a crackling sound called rails during auscultation which is the sound of collapsed alveoli popping open with inspiration keep in mind that additional symptoms might provide clues to the underlying cause for example epigastric abdominal pain radiating to the back along with the history of gallstones indicate acute pancreatitis diagnosis of ards is typically made when the individual presents all of the next four criteria which you should definitely remember for your exams first the symptoms have to be acute meaning an onset of one week or less second and particularly high yield a chest x-ray or CT scan shows opacities or white out in both lungs which is due to pulmonary edema the third is What's called the PF ratio it's the partial pressure of oxygen in the arterial blood divided by the percent of oxygen in the inspired air also called the fraction of inspired oxygen in ards gas exchange is defective so the PF ratio is below 300 millimeters of mercury and the lower this ratio gets the more severe the condition fourth the respiratory distress must not be due to cardiac causes like heart failure often this is assessed by using an echocardiogram to look for evidence of heart failure like an ejection fraction below 55 percent in systolic heart failure and abnormal relaxation of The myocardium and diastolic heart failure another clue is the pulmonary capillary wedge pressure which is measured by inserting a catheter into a small pulmonary arterial branch in heart failure this is elevated because more blood remains in the left side of the heart and it prevents pulmonary venous return the blood backs up into the pulmonary vessels and the increase in pressure pushes fluid into the interstitium of the lungs resulting in edema in ards the pressure is normal since the edema is caused by leaky capillaries instead of increased pressure treatment of ards ultimately comes down to treating the condition that triggered it however the most important initial step is supportive care like supplemental oxygen or mechanical ventilation a high yield fact to remember is that it's vital to maintain positive end expiratory pressure which is where the pressure in the lungs is kept slightly above atmospheric pressure even after exhalation because this prevents the alveoli from collapsing it's also good to have low tidal volumes to prevent over inflation of the damaged alveoli another important thing to watch out for is positive pressure ventilation which can cause compression of pulmonary vessels which leads to pulmonary hypertension decreased pulmonary venous return this will reduce cardiac output and hypotension might worsen now even with supportive care the macrophages clean up old cell debris that attract and activate fibroblasts which are cells that secrete collagen and form scar tissue in the alveolar walls if the there's enough Scar Tissue it can still lead to a decrease in lung compliance or the ability of lungs to expand and come back to their original size remember that this means the individual will have residual symptoms all of their lives next neonatal respiratory distress syndrome is a disease of the newborn caused by a deficiency of surfactant this results in alveoli that can't stay open and the newborn has to work hard to breathe resulting in the development of progressive and diffuse atelectasis now there are some risk factors associated with the disease that are commonly tested first there's prematurity usually because the lungs are not mature enough to produce surfactant next maternal diabetes can cause increased insulin levels in the infant which interferes with surfactant production C-section delivery is another cause normal birth is a very stressful process for the infant and this increases glucocorticoid levels which causes the pneumocytes to release more surfactant during a C-section there's no boost of glucocorticoids which can cause a deficiency of surfactant for symptoms at Birth the newborn might be asymptomatic because they receive oxygen via the umbilical cord before birth a few hours later initial clinical signs like dyspnea tachypnea tachycardia and hypoxemia will develop eventually respiratory failure will manifest and the baby will present with chest wall retractions expiratory grunting nasal flaring or nasal widening while breathing eventually they might become cyanotic another fact you need to remember is that since the O2 pressure in the blood will be lower than normal the ductus arteriosus might not close a small patent ductus arteriosus or PDA might not cause additional symptoms but a large one might lead to heart failure now you'll be able to diagnose neonatal respiratory distress syndrome by chest radiography or CT where typical findings include low lung volume and the classic diffuse reticulogranular ground glass appearance this shows up as a contrast between the black aerated alveoli and the white or gray ones where there's alveolar atelectasis another feature is air bronchogram where the air filled bronchi appears dark in contrast to the surrounding white or gray atelectatic tissue arterial blood gases usually show hypoxemia and hypercapnia now we can also assess lung maturity before the baby is born with amniocentesis where a sample of amniotic fluid is drawn to measure the lecithin single myelin ratio in amniotic fluid both of which are surfactant components a ratio under 1.5 is predictive of neonatal respiratory distress syndrome other tests include the foam stability index and surfactant albumin ratio which are similar to The lecithin sphingomyelin ratio test regarding treatment something essential to remember is that antenatal corticosteroid therapy should be administered to all pregnant individuals at 23 to 34 weeks gestation who are at an increased risk of preterm delivery this is done to prevent or decrease the severity of the syndrome in newborns without respiratory failure nasal continuous positive airway pressure is the preferred initial intervention however keep in mind that some complications of supplemental oxygen can include retinopathy of prematurity intraventricular hemorrhage and bronchopulmonary dysplasia if this fails endotracheal intubation and intratracheal surfactant therapy is needed all right as a quick recap acute respiratory distress syndrome happens when inflammation causes diffuse alveolar injury and pulmonary edema the four criteria of ards are it develops within a week affects both lungs causes the PF ratio to dip below 300 millimeters of mercury and is not due to heart failure or other cardiac causes treatment includes supplemental oxygen and mechanical ventilation neonatal respiratory distress syndrome is caused by a deficiency of surfactant often this is due to prematurity maternal diabetes or delivery through C-section diagnosis is based on a clinical picture of the infant with the onset of progressive respiratory failure and chest radiography showing low lung volume diffuse reticulogranular ground glass appearance and Air bronchogram treatment begins with nasal continuous positive airway pressure if this fails endotracheal intubation and intratracheal surfactant therapy are needed now back to our cases so Mike presents with a cute onset of shortness of breath high fever and cough which together with the chest x-ray showing a right lower lobe infiltrate led to a diagnosis of pneumonia he was then started on intravenous antibiotics but his respiratory symptoms only got worse the next day Mike developed hypoxemia and septic shock despite appropriate treatment the x-rays detected newly developed bilateral alveolar opacities heart echography ruled out heart failure and arterial blood gas analysis revealed a severely decreased PF ratio these four factors mean Mike met all the criteria needed for an Arts diagnosis Donna was delivered prematurely by C-section but she initially had a good apgar score however soon after delivery she developed signs of respiratory distress tachypnea and subcostal retractions with nasal flaring and tachycardia given her history and risk factors a diagnosis of neonatal respiratory distress syndrome should be high on the differential list this was actually confirmed by a chest x-ray showing the classic reticulogranular ground glass appearance with air bronchograms helping current and future clinicians Focus learn retain and Thrive learn more

Channel: Osmosis from Elsevier

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Keywords: Health (Industry), Medicine (Field of Study), Disease (Cause of Death), Osmosis, Pathology (Medical Specialty), what is, nursing (field of study), Nursing school (organization)

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Length: 13min 26sec (806 seconds)

Published: Tue Oct 18 2022