Children’s Diffuse and Interstitial Lung Disease
Timothy J. Vece, MD
Introduction/Epidemiology/Pathophysiology
The Basics
•Children’s diffuse and interstitial lung disease (hereafter referred to as “children’s ILD”) is a heterogeneous group of individually rare disorders of the lung that can manifest at any age during childhood.
•Interstitial lung disease and diffuse lung disease are often used interchangeably to describe these disorders.
Epidemiology
•Disease prevalence ranges from 0.13 to 16.2 cases per 100,000 children. The range is large because there is no agreed-upon list of children’s ILD disorders. The classification schemes proposed by Deutsch et al in 2007 and Fan et al in 2015 are the most widely accepted (Box 85-1).
•There is no known racial or ethnic predisposition for any of the common children’s ILD disorders.
•The prevalence of specific disorders varies by age group.
Pathophysiology
•Alveoli and supporting cells of the lungs (interstitium) are most often affected. Exceptions are neuroendocrine cell hyperplasia of infancy (NEHI) and bronchiolitis obliterans, which affect the small airways.
•Gas exchange of the lung is compromised—most commonly oxygen transfer, which can lead to hypoxemia.
•Most disorders are inflammatory and lead to fibrosis of the interstitium and chronic lung disease.
•Lung involvement is usually diffuse at imaging (including chest computed tomography [CT]). Some disorders have specific patterns at imaging.
General Clinical Features
•Chronic and progressive tachypnea and increased work of breathing are typical.
•In infants, failure to thrive may be seen because of the increased caloric demand from the increased work of breathing.
Box 85-1. Children’s Diffuse and Interstitial Lung Disease
Classification Scheme
Age 0–2 classification
Disorders more prevalent in infancy
Diffuse developmental disorders
Alveolar capillary dysplasia with misalignment of the
pulmonary veins
Growth abnormalities
Alveolar simplification
Conditions of undefined etiologic origin
Neuroendocrine cell hyperplasia of infancy
Pulmonary interstitial glycogenosis
Disorders of surfactant metabolism
Disorders prevalent throughout childhood
Disorders of systemic disease
Diffuse alveolar hemorrhage
Rheumatologic disease–related lung disease
Disorders of the normal host
Postinfectious lung disease
Disorders of the immunocompromised host
Opportunistic infections
Damage related to chemotherapy or radiation therapy
Age 2–18 classification
Disorders in clinically immunocompetent patients
Disorders of infancy
Disorders of surfactant metabolism
Neuroendocrine cell hyperplasia of infancy
Disorders of the immunocompetent host
Postinfectious lung disease
Disorders of systemic diseases
Diffuse alveolar hemorrhage
Rheumatologic disease–related lung disease
Disorders in clinically immunocompromised patients
Opportunistic infections
Related to treatment
Chemotherapy
Radiation therapy
Related to transplant rejection
Diffuse alveolar damage
Lymphoid infiltrates
Lymphocytic interstitial lung disease
Lymphoprolific interstitial lung disease
Adapted from (a) Deutsch GH, Young LR, Deterding RR, et al. Diffuse lung disease in young children: application of a novel classification scheme. Am J Respir Crit Care Med. 2007;176(11):1120–1128 and (b) Fan LL, Dishop MK, Galambos C, et al. Diffuse lung disease in biopsied children 2 to 18 years of age. Application of the chILD classification scheme. Ann Am Thorac Soc. 2015;12(10):1498–1505.
• Older children often experience shortness of breath that is worse with exercise and progressive in nature.
•Hypoxemia is common.
•Physical examination often reveals crackles or rales on inspiration. Wheezing is an uncommon finding in most children’s ILD disorders.
•Digital clubbing can be present and denotes chronic hypoxemia.
•Routine laboratory testing is generally nonspecific in children’s ILD.
•Pulmonary hypertension is seen in advanced, severe cases and is a poor prognostic indicator, with up to a fourfold increase in mortality shown in some studies.
General Diagnostic Considerations
•A family history of interstitial lung disease or early death is important because a number of children’s ILDs are genetic.
•Timing of studies is based on severity of illnesses and age at presentation, with a more aggressive approach advocated for more severe forms
of children’s ILD, where a quick diagnosis is needed for medical decision-making.
Imaging
•Chest imaging is the first step in evaluation and usually leads to the suspicion of an interstitial lung process. However, chest CT is preferable to chest radiography because CT (usually thin-section CT) is more sensitive and shows specific patterns that may be helpful in classification.
•Patterns at CT may indicate specific diseases (NEHI, bronchiolitis obliterans) or can be suggestive but nonspecific, such as in disorders of surfactant metabolism.
Additional Diagnostic Testing
•Lung biopsy is often required for diagnosis.
—Certain disorders can be diagnosed without lung biopsy, including NEHI, bronchiolitis obliterans, disorders of surfactant metabolism if genetic changes are present, and alveolar hemorrhage syndromes if there are positive auto-antibodies and a compatible clinical picture.
•Genetic testing is becoming increasingly important for diagnosis, particularly in disorders of surfactant metabolism and immune dysregulation.
•A screening echocardiogram is recommended because some children’s ILD disorders can manifest with pulmonary hypertension at presentation. In addition, there are cardiac disorders, such as total anomalous pulmonary venous return and pulmonary veno-occlusive disease, that can mimic children’s ILD and need to be ruled out.
•Patients with children’s ILD who require supplemental oxygen should undergo yearly echocardiography for evaluation of potential pulmonary hypertension.
Neuroendocrine Cell Hyperplasia of Infancy
History and Symptoms
•Specific to young children, with all known cases manifesting symptoms <2 years of age.
•Patients generally present <1 year of age, with a typical onset of first symptoms at 2–4 months of age.
•Symptoms are often first recognized during a viral respiratory infection; however, the tachypnea and hypoxemia do not resolve after the infection.
Physical Examination
•Findings are nonspecific and demonstrate retractions, crackles, and increased diameter of the chest. Digital clubbing is not found, and wheezing is rare and intermittent.
•Failure to thrive is often seen because of increased work of breathing.
Imaging
•Chest CT shows ground-glass opacities in the right middle lobe, lingula, and medial portion of the upper and lower lobes (see Figure 85-1). This pattern on CT images can be diagnostic in the correct clinical setting and can obviate the need for lung biopsy.
Lung Biopsy
•Lung biopsy, when required for diagnosis in atypical cases, shows increased neuroendocrine cells surrounding the small airways.
Treatment
•Treatment is supportive because there are no known effective therapies for NEHI.
Prognosis
•Long-term prognosis is excellent—there are no reported deaths caused by NEHI.
•Significant morbidity is associated with chronic hypoxemia and exercise intolerance in children with NEHI that generally improves over time.
Disorders of Surfactant Metabolism
For a full discussion, see Chapter 66, Surfactant Metabolism Disorders, Including Surfactant Protein Deficiencies.
General Surfactant Biology
•Surfactant lines the alveoli and reduces surface tension, allowing for easier maintenance of patency of the alveoli and decreased work of breathing.
•Surfactant is composed primarily of phospholipids and specific proteins that either aid in surfactant structure or are part of the innate immunity of the lung.
•Surfactant proteins B and C, along with a trafficking protein called member A3 of the adenosine triphosphate–binding cassette family (ABCA3), as well as a transcription factor called thyroid transcription factor 1 (TTF-1), are implicated in children’s ILD disorders.
•ABCA3 likely plays a role in packaging and delivering surfactant into the apical membrane of the alveolar cells.
Specific Disorders of Surfactant Metabolism
•Surfactant protein B (SPB) is encoded by the SFTPB gene. Surfactant protein deficiency is inherited in an autosomal recessive pattern.
• Deficiency results in severe disease, with onset of symptoms in the neonatal period. Most patients die or require lung transplantation by 1 month after birth.
•Surfactant protein C (SPC) is encoded by the SFTPC gene and is inherited in an autosomal dominant fashion.
—SPC deficiency has a variable presentation, with patients presenting from infancy to adulthood. There is also a variable outcome, with some patients progressing to severe chronic lung disease in early childhood.
•ABCA3 disease is inherited in an autosomal recessive pattern.
—ABCA3 disease has a variable prognosis, with some patients having a severe SPB deficiency–like presentation, while others have a more chronic course, such as in SPC deficiency.
Diagnostic Considerations: Imaging
•Imaging patterns are nonspecific but can be suggestive of a disorder of surfactant metabolism. Chest CT is preferred to chest radiography.
•Young children often have diffuse ground-glass opacities with septal thickening (see Figure 85-2).
•Older children have fewer areas of ground-glass opacities and have increased areas of fibrosis on chest CT images.
Figure 85-2. Axial chest computed tomographic image from full-term infant with ABCA3 deficiency. Note the diffuse ground-glass opacities. Septal thickening is present but less obvious. From Guillerman RP. Imaging of childhood interstitial lung disease. Pediatr Allergy Immunol Pulmonol. 2010;23(1):43–68. The publisher for this copyrighted material is Mary Ann Liebert, Inc. publishers.
ABCA3, member A3 of the adenosine triphosphate–binding cassette family.
Diagnostic Considerations: Genetics
•Genetic testing is available for SPB, SPC, ABCA3, and NKX2.1, a newer gene that encodes TTF-1 (Table 85-1).
•Results are generally available in 2–4 weeks and can provide prognostic information in some cases.
•Genetic testing is preferred if there is a family history of a disorder of surfactant metabolism.
•Results are only positive in 70%–80% of surfactant cases. A lung biopsy may still be necessary.
Diagnostic Considerations: Lung Biopsy
•Lung biopsy findings have specific patterns that are associated with disorders of surfactant metabolism.
•Electron microscopy should be performed on all lung biopsy samples for which a disorder of surfactant metabolism is suspected, because it can have specific defects in SPB and ABCA3.
•All lung biopsy findings should be reviewed by a pediatric pathologist with experience in children’s ILD disorders.
Treatment
•No treatment has been well studied for any of the disorders of surfactant metabolism.
•Systemic steroids (typically administered as monthly pulse steroids), chronic azithromycin, hydroxychloroquine, or some combination have been tried with varying degrees of success.
When to Refer
•All patients with a suspected children’s ILD disorder should be referred to a pediatric pulmonologist who has experience in treating these disorders.
•Patients should be admitted for worsening respiratory symptoms or increased supplemental oxygen requirement.
•In general, these patients have chronic, severe lung disease and require frequent hospitalizations.
•Often, patients require hospitalization to establish the diagnosis.
Resources for Families
•Children’s Interstitial and Diffuse Lung Disease Foundation. www.child-foundation.com
•What Is Childhood Interstitial Lung Disease? (National Heart, Lung, and Blood Institute). www.nhlbi.nih.gov/health/health-topics/topics/chld
•What Is Interstitial Lung Disease in Children? (American Thoracic Society). www.thoracic.org/patients/patient-resources/resources/interstitial-lung-disease-in-children.pdf
Clinical Pearls
•Children with NEHI often appear much more ill than their image findings suggest.
•Oxygen saturation levels are often on the low side of normal (92%–95%), which should raise suspicion for NEHI.
•Most children with disorders of surfactant metabolism present in the first 12 months of life.
CHAPTER 71: BRONCHOPULMONARY DYSPLASIA
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•Groothuis JR, Makari D. Definition and outpatient management of the very low-birth-weight infant with bronchopulmonary dysplasia. Adv Ther. 2012;29(4):297–311
•Islam JY, Keller RL, Aschner JL, Hartert TV, Moore PE. Understanding the short- and long-term respiratory outcomes of prematurity and bronchopulmonary dysplasia. Am J Respir Crit Care Med. 2015;192(2):134–156
•Jobe AH, Bancalari E. Bronchopulmonary dysplasia. Am J Respir Crit Care Med. 2001; 163(7):1723–1729
CHAPTER 72: PNEUMOTHORAX
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•Robinson PD, Cooper P, Ranganathan SC. Evidence-based management of paediatric primary spontaneous pneumothorax. Paediatr Respir Rev. 2009; 10(3):110–117, quiz 117
•Seguier-Lipszyc E, Elizur A, Klin B, Vaiman M, Lotan G. Management of primary spontaneous pneumothorax in children. Clin Pediatr (Phila). 2011;50(9):797–802
•Dotson K, Johnson LH. Pediatric spontaneous pneumothorax. Pediatr Emerg Care. 2012;28(7):715–720
•O’Connor AR, Morgan WE. Radiological review of pneumothorax. BMJ. 2005; 330(7506):1493–1497
CHAPTER 73: PULMONARY ASPIRATION: FOREIGN BODIES AND MASSIVE ASPIRATION
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CHAPTER 74: GASTROESOPHAGEAL REFLUX AND RECURRENT SMALL-VOLUME ASPIRATION
•Owayed AF, Campbell DM, Wang EE. Underlying causes of recurrent pneumonia in children. Arch Pediatr Adolesc Med . 2000;154(2):190–194
•Tutor JD, Gosa MM. Dysphagia and aspiration in children. Pediatr Pulmonol. 2012; 47(4):321–337
•Trinick R, Johnston N, Dalzell AM, McNamara PS. Reflux aspiration in children with neurodisability—a significant problem, but can we measure it? J Pediatr Surg. 2012;47(2):291–298
CHAPTER 75: HYPERSENSITIVITY PNEUMONITIS
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•Lacasse Y, Girard M, Cormier Y. Recent advances in hypersensitivity pneumonitis. Chest. 2012;142(1):208–217
•Sisman Y, et al. Pulmonary function and fitness years after treatment for hypersensitivity pneumonitis during childhood. Pediatr Pulmonol. 2015
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CHAPTER 76: PULMONARY HEMORRHAGE
•Godfrey S. Pulmonary hemorrhage/hemoptysis in children. Pediatr Pulmonol. 2004;37(6):476–484
•Susarla SC, Fan LL. Diffuse alveolar hemorrhage syndromes in children. Curr Opin Pediatr. 2007;19(3):314–320
•Flume PA, Mogayzel PJ Jr, Robinson KA, Rosenblatt RL, Quittell L, Marshall BC; Clinical Practice Guidelines for Pulmonary Therapies Committee; Cystic Fibrosis Foundation Pulmonary Therapies Committee. Cystic fibrosis pulmonary guidelines: pulmonary complications: hemoptysis and pneumothorax. Am J Respir Crit Care Med. 2010;182(3):298–306
•Colson DJ, Mortelliti AJ. Management of pediatric hemoptysis: review and a case of isolated unilateral pulmonary artery agenesis. Int J Pediatr Otorhinolaryngol. 2005;69(9):1161–1167
CHAPTER 77: PULMONARY HYPERTENSION
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•Berger RM, Beghetti M, Humpl T, et al. Clinical features of paediatric pulmonary hypertension: a registry study. Lancet. 2012;379(9815):537–546
•Dadlani GH, Sosa P, Cobb H, Akshatha A. Pediatric pulmonary hypertension: diagnosis and management. Curr Opin Cardiol. 2016;31(1):78–87
•Del Pizzo J, Hanna B. Emergency management of pediatric pulmonary hypertension. Pediatr Emerg Care. 2016;32(1):49–55
•Ivy DD, Abman SH, Barst RJ, et al. Pediatric pulmonary hypertension. J Am Coll Cardiol. 2013;62(25 Suppl):D117–D126
•Krishnan U, Rosenzweig EB. Pulmonary hypertension in chronic lung disease of infancy. Curr Opin Pediatr. 2015;27(2):177–183
•Park M. Pulmonary Hypertension. In: Park’s Pediatric Cardiology for Practitioners. 6th ed. Philadelphia, PA: Elsevier Saunders; 2014:483–494
CHAPTER 78: VOCAL CORD DYSFUNCTION
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•Landwehr LP, Wood RP II, Blager FB, Milgrom H. Vocal cord dysfunction mimicking exercise-induced bronchospasm in adolescents. Pediatrics. 1996;98(5):971–974
•Sandage MJ, Zelazny SK. Paradoxical vocal fold motion in children and adolescents. Lang Speech Hear Serv Sch. 2004;35(4):353–362
CHAPTER 79: TIC COUGH (HABIT COUGH)
•Vertigan AE, Murad MH, Pringsheim T, et al; CHEST Expert Cough Panel. Somatic Cough Syndrome (Previously Referred to as Psychogenic Cough) and Tic Cough (Previously Referred to as Habit Cough) in Adults and Children: CHEST Guideline and Expert Panel Report. Chest. 2015;148(1):24–31
•Ramanuja S, Kelkar P. Habit cough. Ann Allergy Asthma Immunol. 2009;102(2):91–95; quiz 95–97, 115
•Irwin RS, Glomb WB, Chang AB. Habit cough, tic cough, and psychogenic cough in adult and pediatric populations: ACCP evidence-based clinical practice guidelines. Chest. 2006;129(1 Suppl):174S–179S
•Goldsobel AB, Chipps BE. Cough in the pediatric population. J Pediatr. 2010; 156(3):352–358
•Weinberger M, Hoegger M. The cough without a cause: habit cough syndrome. J Allergy Clin Immunol. 2016;137(3):930–931
CHAPTER 80: SMOKE INHALATION
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•Parish RA. Smoke inhalation and carbon monoxide poisoning in children. Pediatr Emerg Care. 1986;2(1):36–39
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CHAPTER 81: HYDROCARBON ASPIRATION
•Anas N, Namasonthi V, Ginsburg CM. Criteria for hospitalizing children who have ingested products containing hydrocarbons. JAMA. 1981;246(8):840–843
•Makrygianni EA, Palamidou F, Kaditis AG. Respiratory complications following hydrocarbon aspiration in children. Pediatr Pulmonol. 2016;51(6):560–569 y Sen V, Kelekci S, Selimoglu Sen H, et al. An evaluation of cases of pneumonia that occurred secondary to hydrocarbon exposure in children. Eur Rev Med Pharmacol Sci. 2013;17(Suppl 1):9–12
•Taussig LM, Castro O, Landau LI, Beaudry PH. Pulmonary function 8 to 10 years after hydrocarbon pneumonitis. Normal findings in three children carefully studied. Clin Pediatr (Phila). 1977;16(1):57–59
•Thalhammer G. Pneumonitis and Pneumatoceles Following Accidental Hydrocarbon Ingestion in Children. Graz, Austria: Wiener Klinische Wochenschrift; 2005
•Tormoehlen LM, Tekulve KJ, Nañagas KA. Hydrocarbon toxicity: a review. Clin Toxicol (Phila). 2014;52(5):479–489
CHAPTER 82: DROWNING
•Szpilman D, Bierens JJ, Handley AJ, Orlowski JP. Drowning. N Engl J Med. 2012; 366(22):2102–2110
•Caglar D, Quan L. Drowning and submersion injury. In: Kliegman R, ed. Nelson Textbook of Pediatrics. 20th ed. Philadelphia, PA: Elsevier; 2015:561–568
•Mtaweh H, Kochanek PM, Carcillo JA, Bell MJ, Fink EL. Patterns of multiorgan dysfunction after pediatric drowning. Resuscitation. 2015;90:91–96
•Kieboom JK, Verkade HJ, Burgerhof JG, et al. Outcome after resuscitation beyond 30 minutes in drowned children with cardiac arrest and hypothermia: Dutch nationwide retrospective cohort study. BMJ. 2015;350:h418
•American Academy of Pediatrics Committee on Injury, Violence, and Poison Prevention. Prevention of drowning. Pediatrics. 2010;126(1):178–185
CHAPTER 83: THORACIC TUMORS
•Kishore M, Gupta P, Preeti, Deepak D. Pulmonary hamartoma mimicking malignancy: a cytopathological diagnosis. J Clin Diagn Res. 2016;10(11):ED06–ED07
•Lal DR, Clark I, Shalkow J, et al. Primary epithelial lung malignancies in the pediatric population. Pediatr Blood Cancer. 2005;45(5):683–686
•Wassef M, Blei F, Adams D, et al; ISSVA Board and Scientific Committee. Vascular anomalies classification: recommendations from the International Society for the Study of Vascular Anomalies. Pediatrics. 2015;136(1):e203–e214
CHAPTER 84: PULMONARY COMPLICATIONS OF CANCER THERAPY
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•Ardura MI, Koh AY. Infectious complications in pediatric cancer patients. In: Principles and Practice of Pediatric Oncology. 7th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins Health; 2015:1010–1057
•Henry MM, Noah TL. Lung injury caused by pharmacologic agents. In: Kendig and Chernick’s Disorders of the Respiratory Tract in Children. 8th ed. Philadelphia, PA: Elsevier; 2012:1026–1035
•Ermoian RP, Fogh SE, Braunstein S, Mishra K, Kun LE, Haas-Kogan DA. General principles of radiation oncology. In: Principles and Practice of Pediatric Oncology. 7th ed. Philadelphia, PA: Wolters Kluwer/Lippincott Williams & Wilkins Health; 2015: 362–382
•Spahr J, Weiner DJ, Stokes DC, Kurland G. Pulmonary disease in the pediatric patient with acquired immunodeficiency states. In: Kendig and Chernick’s Disorders of the Respiratory Tract in Children. 8th ed. Philadelphia, PA: Elsevier; 2012:899–919 y Abugideiri M, Nanda RH, Butker C, et al. Factors influencing pulmonary toxicity in children undergoing allogeneic hematopoietic stem cell transplantation in the setting of total body irradiation-based myeloablative conditioning. Int J Radiat Oncol Biol Phys. 2016;94(2):349–359
CHAPTER 85: CHILDREN’S DIFFUSE AND INTERSTITIAL LUNG DISEASE
•Deutsch GH, Young LR, Deterding RR, et al; Pathology Cooperative Group; ChILD Research Co-operative. Diffuse lung disease in young children: application of a novel classification scheme. Am J Respir Crit Care Med. 2007;176(11):1120–1128
•Nogee LM. Genetic basis of children’s interstitial lung disease. Pediatr Allergy Immunol Pulmonol. 2010;23(1):15–24
•Vece TJ, Young LR. Update on diffuse lung disease in children. Chest. 2016;149(3): 836–845
•Kurland G, Deterding RR, Hagood JS, et al; American Thoracic Society Committee on Childhood Interstitial Lung Disease (chILD) and the chILD Research Network. An official American Thoracic Society clinical practice guideline: classification, evaluation, and management of childhood interstitial lung disease in infancy. Am J Respir Crit Care Med. 2013;188(3):376–394
•Fan LL, Dishop MK, Galambos C, et al; Children’s Interstitial and Diffuse Lung Disease Research Network (chILDRN). Diffuse lung disease in biopsied children 2 to 18 years of age. application of the chILD classification scheme. Ann Am Thorac Soc. 2015;12(10):1498–1505
•Bush A, Cunningham S, de Blic J, et al; chILD-EU Collaboration. European protocols for the diagnosis and initial treatment of interstitial lung disease in children. Thorax. 2015;70(11):1078–1084
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