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Am J Gastroenterol 1995;90:1212-1220 222 Karjoo M, Kane R Omeprazole treatment of children with peptic esophagitis refractory to ranitidine therapy Arch Pediatr Adolesc Med 1995;149:267-271 223 Kuipers EJ, Lundell L, Klinkenberg-Knol EC, et al Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication N Engl J Med 1996;334:1018-1022 224 Wilde MI, McTavish D Omeprazole: an update of its pharmacology and therapeutic use in acid-related disorders Drugs 1994;48:91-132 225 Curry JI, Lander TD, Stringer MD Review article: erythromycin as a prokinetic agent in infants and children Aliment Pharmacol Ther 2001;15:595-603 e6 226 O’Kane G Inhalation of ammonia vapour Anaesthesia 1983;38: 1208-1213 227 Rorison DG, McPherson SJ Acute toxic inhalations Emerg Med Clin North Am 1992;10:409-435 228 Ruddy RM Smoke inhalation injury Pediatr Clin North Am 1994;41:317-326 229 Scannell G, Waxman K, Tominaga GT Respiratory distress in traumatized and burned children J Pediatr Surg 1995;30:612-614 230 Ainslie G Inhalational injuries produced by smoke and nitrogen dioxide Respir Med 1993;87:169-174 231 Fitzpatrick JC, Cioffi Jr WG, Cheu HW, Pruitt Jr BA Predicting ventilation failure in children with inhalation injury J Pediatr Surg 1994;29:1122-1126 232 Kulling P Hospital treatment of victims exposed to combustion products Toxicol Lett 1992;283:64-65 233 Perez-Benavides F, Riff E, Franks C Adult respiratory distress syndrome and artificial surfactant replacement in the pediatric patient Pediatr Emerg Care 1995;11:153-155 234 Rosenow EC, Myers JL, Swensen SJ, Pisani RJ Drug-induced pulmonary disease: an update Chest 1992;102:239-250 235 Fan LL, Deterding RR, Langston C Pediatric interstitial lung disease revisited Pediatr Pulmonol 2004;38:369-378 236 Barbato A, Panizzolo C Chronic interstitial lung disease in children Paediatr Respir Rev 2000;1:172-178 237 Canakis AM, Cutz E, Manson D, O’Brodovich H Pulmonary interstitial glycogenosis: a new variant of neonatal interstitial lung disease Am J Respir Crit Care Med 2002;165:1557-1565 238 Deterding R, Fan LL Surfactant dysfunction mutations in children’s interstitial lung disease and beyond Am J Respir Crit Care Med 2005;172:940-941 239 Deterding R Persistent tachypnea of infancy is associated with neuroendocrine cell hyperplasia Pediatr Pulmonol 2005;40:157-165 240 Dinwiddie R Treatment of interstitial lung disease in children Paediatr Respir Rev 2004;5:108-115 241 Langston C, Fan LL Diffuse interstitial lung disease in infants Pediatr Pulmonol 2001;(suppl 23):73-76 242 Edwards JR, Matthay KK Hematologic disorders affecting the lungs Clin Chest Med 1989;10:723-746 243 Kumar S, et al Pulmonary hemorrhage in a young infant Ann Allergy 1989;62:209 244 Noseworthy TW, Anderson BJ Massive hemoptysis CMAJ 1986; 135:1097-1099 245 Esterly S, Oppenheimer E Massive pulmonary hemorrhage in the newborn J Pediatr 1996;69:3-11 246 Cahill BC, Ingbar DH Massive hemoptysis: assessment and management (review) Clin Chest Med 1994;15:147-167 247 Donald KJ, Edwards RL, McEvoy JD Alveolar capillary basement membrane lesions in Goodpasture’s syndrome and idiopathic pulmonary hemosiderosis Am J Med 1975;59:642-649 248 Ingbar DH, White DA Acute respiratory failure Crit Care Clin 1988; 4:11-40 249 Coffin CM, Schechtman K, Cole FS, Dehner LP Neonatal and infantile pulmonary hemorrhage: an autopsy study with clinical correlation Pediatr Pathol 1993;13:583-589 250 Yeung CY Massive pulmonary hemorrhage in neonatal infection Can Med Assoc J 1976;114:135-138 251 Vice TJ, et al Diffuse alveolar hemorrhage in children In: Wilmott RW, Boat TF, Bush A, et al., eds Kendig and Chernick’s Disorders of the Respiratory Tract in Children Philadelphia: Elsevier; 2012: 676-685 252 Swischuk LE, L’Heureux P Unilateral pulmonary vein atresia AJR Am J Roentgenol 1980;135:667-672 253 Colombo JL, Stolz SM Treatment of life-threatening primary pulmonary hemosiderosis with cyclophosphamide Chest 1992;102: 959-960 254 Susarla SC, Fan LL Diffuse alveolar hemorrhage syndromes in children Curr Opin Pediatr 2007;19:314-320 255 States LJ, Fields JM Pulmonary hemorrhage in children Semin Roentgenol 1998;22:174-186 256 Gizzi C, Papoff P, Barbàra CS, Cangiano G, Midulla F, Moretti C Old and new uses of surfactant J Matern Fetal Neonatal Med 2010;23(suppl 3):41-44 257 Raju TN, Langenberg P Pulmonary hemorrhage and exogenous surfactant therapy: a meta-analysis J Pediatr 1993;123:603-610 258 Centers for Disease Control and Prevention Acute pulmonary hemorrhage among infants—Chicago, April 1992-November 1994 MMWR Morb Mortal Wkly Rep 1995;44:67, 73-74 259 Centers for Disease Control and Prevention Acute pulmonary hemorrhage/hemosiderosis among infants—Cleveland, January 1993-November 1994 MMWR Morb Mortal Wkly Rep 1995;43: 881-883 260 Dammacco F, Battaglia S, Gesualdo L, Racanelli V Goodpasture’s disease: a report of ten cases and a review of the literature Autoimmun Rev 2013;12:1101-1108 261 Fauci AS, Haynes BF, Katz P, Wolff SM Wegener’s granulomatosis: prospective clinical and therapeutic experience with 85 patients for 21 years Ann Intern Med 1983;98:76-85 262 Miller RW, Salcedo JR, Fink RJ, Murphy TM, Magilavy DB Pulmonary hemorrhage in pediatric patients with systemic lupus erythematosus J Pediatr 1986;108:576-579 263 Lhote F, Cohen P, Généreau T, Gayraud M, Guillevin L Microscopic polyangiitis: clinical aspects and treatment Ann Med Interne (Paris) 1996;147:165-177 264 Matsumoto T, Homma S, Okada M, et al The lung in polyarteritis nodosa: a pathologic study of 10 cases Hum Pathol 1993;24: 717-724 265 Erkan F Pulmonary involvement in Behỗet disease Curr Opin Pulm Med 1999;5:314-318 266 Erkan F, Kiyan E, Tunaci A Pulmonary complications of Behỗets disease Clin Chest Med 2002;23:493-503 267 Ference BA, Shannon TM, White Jr RI, Zawin M, Burdge CM Life-threatening pulmonary hemorrhage with pulmonary arteriovenous malformations and hereditary hemorrhagic telangiectasia Chest 1994;106:1387-1390 268 Pouwels HM, Janevski BK, Penn OC, Sie HT, ten Velde GP Systemic to pulmonary vascular malformation (review) Eur Respir J 1992;5:1288-1291 269 Kato R, Sawafuji M, Kawamura M, Kikuchi K, Kobayashi K Massive hemoptysis successfully treated by modified bronchoscopic balloon tamponade technique Chest 1996;109:842-843 270 Patel U, Pattison CW, Raphael M Management of massive haemoptysis Br J Hosp Med 1994;52:74, 76-78 271 Knott-Craig C, Oostuizen JG, Rossouw G, Joubert JR, Barnard PM Management and prognosis of massive hemoptysis: recent experience with 120 patients J Thorac Cardiovasc Surg 1993; 105:394-397 272 Merkel F, Netzer KO, Gross O, Marx M, Weber M Therapeutic options for critically ill patients suffering from progressive lupus nephritis or Goodpasture’s syndrome Kidney Int Suppl 1998; 64:S31-S38 273 Falk RJ, Nachman PH, Hogan SL, Jennette JC ANCA glomerulonephritis and vasculitis: a Chapel Hill perspective Semin Nephrol 2000;20:233-243 274 Ball JA, Young Jr KR Pulmonary manifestations of Goodpasture’s syndrome: antiglomerular basement membrane disease and related disorders Clin Chest Med 1998;19:777-791 275 Fox HL, Swann D Goodpasture syndrome: pathophysiology, diagnosis, and management Nephrol Nurs J 2001;28:305-310 276 Cipolli M, Perini S, Valletta EA, Mastella G Bronchial artery embolization in the management of hemoptysis in cystic fibrosis Pediatr Pulmonol 1995;19:334-347 277 Zhang JS, Cui ZP, Wang MQ, Yang L Bronchial arteriography and transcatheter embolization in the management of hemoptysis Cardiovasc Intervent Radiol 1994;17:276-279 e7 Abstract: Pneumonitis is one of the most common causes of lifethreatening lower respiratory tract disease in pediatric patients Pneumonitis can result from noninfectious etiologies but is more often secondary to an infection Early in the process, the lung injury is associated with increased cellularity but minimal fibrosis More advanced disease is associated with extensive fibrosis, with destruction of gas-exchange units Changes in physiology that have been observed are lower lung volumes, diminished compliance, impaired gas exchange, and airflow limitation This chapter addresses potential causes of parenchymal disease, which includes alveolar and interstitial disorders Key Words: Pneumonitis, interstitial, diffusion, infectious, hemorrhage 53 Diseases of the Pulmonary Circulation HUI ZHANG, CHRISTINE VOHWINKEL, ALINE MADDUX, AND KURT R STENMARK PEARLS • Updated definitions and classification of pulmonary hypertension have helped to advance the understanding of pulmonary hypertensive diseases and facilitate drug trials • Four classes of drugs have been extensively studied for the treatment of pulmonary hypertension: prostanoids, endothelin receptor antagonists, phosphodiesterase inhibitors, and calcium channel blockers The use of approved vasodilator drugs, either alone or in combination, has led to an improvement in the quality of life and clinical outcomes in pediatric patients with pulmonary hypertension Unfortunately, there has been no significant effect on mortality • Pulmonary vascular remodeling, as a characteristic of chronic pulmonary hypertension, is both the result of, and a contributor to, increased pulmonary vascular pressures • Emerging evidence suggests an important role of novel mechanisms contributing to pulmonary vascular and right ventricle remodeling, which are not adequately addressed by current therapies, perhaps explaining continuing disease morbidity and mortality • The observation of differences in genes associated with pulmonary hypertension in children compared with adults support the idea that it is at least in part a developmental lung disease when it presents early in life; technologic advances in genetic sequencing will provide important information to the patient, families, and caregivers • Therapy for pulmonary hypertension remains challenging, and gaps in the current clinical and lab-based research need to be addressed to more specifically define the pathology of the disease and accurately measure the symptoms correlated with disease progression with the future goal of identifying curative therapies Definition and Classification management approaches Since an increase in pulmonary pressure can be due to purely precapillary causes (as is described in groups 1, 3, 4, and in Box 53.1), it was determined that it is essential to include pulmonary vascular resistance (PVR) in the definition of precapillary PH.1 This allows a separation of the elevation in pulmonary artery pressure due to pulmonary vascular disease from those due to elevation of pulmonary artery wedge pressure or due to high cardiac output Measuring PVR and using a cutoff of PVR of units or more is important to separate precapillary PH (group 1) from combined or isolated pre- and postcapillary PH due to left heart disease (group 2; see Box 53.1) It is clear that the etiologic origins of PH are complex and can be associated with diverse pathologic conditions The classification system for PH in adults was first established in 1998 and has since gone through several revisions, the last one at the 6th World Symposium on PH in 2018.1 The general purpose of the clinical classification of PH was and continues to be to categorize clinical conditions associated with PH based on similar pathophysiologic mechanisms, clinical presentation, hemodynamic characteristics, and therapeutic management The most recent updated classification system is shown in Box 53.1.1,2 This classification system has Pulmonary hypertension (PH), defined as an increase in pressure in lung blood vessels, is a heterogeneous, complex, and often misunderstood condition PH is associated with diverse cardiac, pulmonary, and systemic diseases in both adults and children and is associated with significant morbidity and mortality Since the first World Symposium on PH in 1973, PH has been defined as mean pulmonary artery pressure (mPAP) of 25 mm Hg or greater measured by right heart catheterization in the supine position at rest However, at the 6th World Symposium on PH in 2018, discussions took place to determine whether the definition should be changed to an mPAP at rest of 20 mm Hg or greater.1 This was due to studies showing that, in normal subjects, comprising nearly 1200 patients from 47 studies, mPAP at rest was 14.0 3.3 mm Hg.2 Thus, two standard deviations suggest mPAP of 20 mm Hg or greater as above the upper limit of normal The committee determined that it was essential to emphasize that this value, used in isolation, cannot characterize a clinical condition and does not define the pathologic process, per se Indeed, increases in mPAP have several different causes with different outcomes as well as various 608 ... RL, McEvoy JD Alveolar capillary basement membrane lesions in Goodpasture’s syndrome and idiopathic pulmonary hemosiderosis Am J Med 1975;59:642-649 248 Ingbar DH, White DA Acute respiratory... observed are lower lung volumes, diminished compliance, impaired gas exchange, and airflow limitation This chapter addresses potential causes of parenchymal disease, which includes alveolar and interstitial... essential to include pulmonary vascular resistance (PVR) in the definition of precapillary PH.1 This allows a separation of the elevation in pulmonary artery pressure due to pulmonary vascular