Chronic obstructive pulmonary diseases in children

Ribeiro, Jose Dirceu; Fischer, Gilberto Bueno

doi:10.1016/j.jped.2015.06.003

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• J. Pediatr. (Rio J.) 91 (6 Suppl 1) • Nov-Dec 2015 • https://doi.org/10.1016/j.jped.2015.06.003 copy

Chronic obstructive pulmonary diseases in children^☆ ☆ Please cite this article as: Ribeiro JD, Fischer GB. Chronic obstructive pulmonary diseases in children. J Pediatr (Rio J). 2015;91:S11–25.

Authorship SCIMAGO INSTITUTIONS RANKINGS

Abstract

Objectives:

To verify and describe the main events related to the diagnosis and management of chronic obstructive pulmonary diseases in children (COPDC) and adolescents, considering the interrelated physiopathology, genetic, and environmental characteristics.

Sources:

Relevant literature from PubMed was selected and reviewed.

Summary of the findings:

COPDC have an environmental and/or genetic origin and its manifestation has manifold genotypes, phenotypes, and endotypes. Although COPDC has no cure, it can be clinically controlled. Chronic cough is the main symptom and bronchiectasis can be present in several COPDC patients. The management of COPDC is more effective if based on guidelines and when treatment regimen adherence is promoted. Oral and inhaled corticosteroids, bronchodilators, inhaled antibiotics, and treatment of pulmonary exacerbation (PE) are the bases of COPDC management, and should be individualized for each patient.

Conclusions:

Correct diagnosis and knowledge of risk factors and comorbidities are essential in COPDC management. Procedures and drugs used should be based on specific guidelines for each COPDC case. Treatment adherence is critical to obtain the benefits of management. COPDC clinical control must be evaluated by the decrease in PEs, improved quality of life, reduction of pulmonary function loss, and lung structural damage. For most cases of COPDC, monitoring by interdisciplinary teams in specialized reference centers with surveillance strategies and continuous care leads to better outcomes, which must be evaluated by decreasing pulmonary function damage and deterioration, better prognosis, better quality life, and increased life expectancy.

KEYWORDS
Child; Chronic obstructive pulmonary disease; Chronic cough

COPDC characteristics	ASTHMA	RWIs	BPD	BO and PIBO	CF	BP	PCD	NCFB	Classic adult COPD
Symptom onset	Before 5 years of life	<2 years	Newborn	<3 years	<2 years in classical forms	CHD: <5 years Asthma: >5 years	First year of life	After the second year of life	Adults >40 years
Age of higher prevalence	Childhood	1–2 years	First year of life	Childhood and adolescence	Up to 30 years	CHD: <5 years Asthma: >5 years	Childhood and adolescence	Childhood and adolescence	After 40 years
Main clinical marker	Family history of asthma, personal atopy and positive response to BD	Infection by respiratory viruses (RSV and RV)	Prematurity Oxygen use	Virus	Chronic colonization of the airways by Pseudomonas aeruginosa and pancreatic failure	Elimination of bronchial casts with sputum	Suppurative infections of the upper and lower airways	Recurrent infections and chronic cough	Smoking, emphysema, and biomass smoke
Prevalence	High (5–30%)	High (15–60%)	High; 26% in VLBW infants	Low ?	Low. Classified as rare disease. 1:2500–1:10,000 live births	Low ?	Low ?	Low ?	6–15.8% of the population older >40 years
Bases for diagnosis	Spirometry, positive response to BD, IgE, and skin prick test	>3 episodes of wheezing in infancy and positive API	Prematurity and oxygen therapy for more than 28 days in early life	Lung biopsy, HRCT and lung perfusion scintigraphy	NBS with a positive IRT, chloride >60 mEq/L in sweat, two mutations in the CFTR gene	Airway cast expectoration and bronchoscopy	Dextrocardia, chronic sinusitis, pneumonia and recurrent URTIs	HRCT	Smoking, emphysema and alpha1 antitrypsin deficiency
Genotype	Many chromosomes and polymorphisms	Many chromosomes and polymorphisms	Little known	Little known	Autosomal recessive with alterations in CFTR gene located on chromosome 7. 6 classes of mutations. Many polymorphisms	Unknown	Autosomal recessive	Depends on the etiology	–
Phenotype	Several	Several	M, Mo, S	Constrictive proliferative	Many. With and without pancreatic failure	Depending on the etiology, the bronchial mold has a different composition	With and without dextrocardia	Depends on the etiology	With and without asthma
BAL	Eosinophils	Neutrophils and/or eosinophils	Neutrophils	Neutrophils	Neutrophils	Mucin and fibrin	Neutrophils	Neutrophils	Neutrophils and macrophages
Markers in lymphocytes	High CD4/CD8	Varies whether the BAL is eosinophilic or neutrophilic	?	?	?	?	?	Depends on the etiology	High CD8/CD4
Inflammatory mediators	IL4, IL5, IL9, IL13, TNF-α, GM-CSF	Varies whether the BAL is eosinophilic or neutrophilic	TNF-α, IL-1, IL-6, IL-10	IL1β, IL6, IL8, TNF-α, and NFkβ	IL8	?	?	Depends on the etiology	IL8, LTB4, proteases, MMP9, TNF-α, TGF-β1
Main causes of PE	Viruses and aero-allergens	Viruses	Viruses	Viruses	Gram-negative bacteria	Influenza H1N1 ?	Viruses and bacteria	Bacteria and viruses	Viruses and bacteria
Response to BD	Yes	Little known	Unknown	Rare	Rare	?	?	No	Low
Obstruction	Intermittent in the mild cases and fixed in severe cases	Intermittent	Fixed	Fixed	Fixed	Intermittent	Fixed	Fixed	Fixed
Survival/ Mortality	Long/low	Long/low	Depends on the severity and gestational age	Depends on severity	<40 years – class I–III mutations. >40 years – class IV–VI mutations	Low/high	<40 years	Depends on the age of onset and etiology	Depends on the severity. High mortality in the elderly
Evolution to restrictive lung diseases	Rare	Rare	Rare	Frequent	Frequent	Rare	Frequent	Frequent	Frequent
Evolution to lung transplantation	No	No	No	Rare	Yes	No	Yes	Yes	No
Comorbidities	Allergic rhinitis, atopic dermatitis and GERD	GERD	GERD and prematurity	Severe adenovirus infection	Pancreatic failure, depression, diabetes, and osteoporosis	CHD, asthma, lymphatic disease, ABPA	Azoospermia and chronic rhinosinusitis	?	Asthma and GERD
Treatment	IC; SABA; LABA; Montelukast; omalizumab	IC; SABA; Montelukast	IC; SABA; Sildenafil and PH Diuretics	IC; SABA; LABA; corticoids; oxygen; tiotropium bromide	Mucolytics; IA; digestive enzymes, IC; SABA; LABA; corticosteroids; tiotropium; Oxygen	bronchoscopy; mucolytics and antifibrinolytics	Mucolytics, IA; IC; SABA; LABA; corticosteroids and oxygen	Mucolytics; IA IC; SABA; LABA; corticosteroids; oxygen; macrolides	IC; SABA; LABA; corticosteroids; Tiotropium and oxygen
Perspectives	Early intervention in utero and early in life at risk populations. Prophylaxis against RSV and RV. Immunomodulation with prebiotics, probiotics and bacterial lysates. Prevention of allergic sensitization.	Permissive hypercapnia and improved care to VLBW infants	Palivizumab; genes and polymorphisms; respiratory virus vaccines	Corrections by potentiators and carriers of CFTR protein and new tests for the diagnosis of atypical forms	Multicenter studies, national registries	Genetic studies and early diagnosis	Prophylaxis against viruses	Avoid smoking Asthma control

API criteria	Original API¹1 Duijts L, Reiss IK, Brusselle G, Jongste JC. Early origins of chronic obstructive lung diseases across the life course. Eur J Epidemiol. 2014;29:871-885.	Modified API³⁸38 Guilbert TW, Morgan WJ, Zeiger RS, Bacharier LB, Boehmer SJ, Krawiec M, et al. Atopic characteristics of children with recurrent wheezing at high risk for the development of childhood asthma. J Allergy Clin Immunol. 2004;114:6.
General	Convincing API: more than three episodes of wheezing/year during the first 3 years of life with a major criterion or two minor.	The child must have a history of four or more episodes of wheezing. At least one episode verified and confirmed by a physician.
General	Less convincing API: less than three episodes of wheezing/year during the first 3 years of life with a major criterion or two minor.
Major	History of parental asthma Atopic dermatitis	History of parental asthma Atopic dermatitis diagnosed by physician Allergic sensitization to one or more aeroallergens
Minor	Allergic rhinitis diagnosed by physician Wheezing unrelated to colds Eosinophilia ≥ 4%	Sensitization to cow's milk, egg, or peanut Wheezing unrelated to colds Eosinophilia ≥ 4%

Inhaled corticosteroids	Daily doses in children younger than 5 years			Daily doses (6–11 years)
	Low	Medium	High	Low	Medium	High
Beclomethasone Dipropionate HFA	100			50–100	>100–200	>200
Budesonide spray	200			100–200	>200–400	>400
Nebulized budesonide	250–500	>500–1000	>1000	250–500	>500–1000	>1000
Fluticasone propionate HFA spray	100			100–200	>250–500	>500
Fluticasone propionate dry powder				100–200	>250–400	>400
Ciclesonide	160			80	>80–160	>160
Mometasone	There are no studies			110	220 ≤ 440	440 or more
Triamcinolone	There are no studies			400–800	>800–1200	>1200

Sociedade Brasileira de Pediatria Av. Carlos Gomes, 328 cj. 304, 90480-000 Porto Alegre RS Brazil, Tel.: +55 51 3328-9520 - Porto Alegre - RS - Brazil
E-mail: jped@jped.com.br

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[1] * Corresponding author. E-mails:jdirceuribeiro@gmail.com, dirceu.unicamp@gmail.com (J.D. Ribeiro).

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Chronic obstructive pulmonary diseases in children☆ ☆ Please cite this article as: Ribeiro JD, Fischer GB. Chronic obstructive pulmonary diseases in children. J Pediatr (Rio J). 2015;91:S11–25.

Abstract

Objectives:

Sources:

Summary of the findings:

Conclusions:

Chronic obstructive pulmonary diseases in children^☆ ☆ Please cite this article as: Ribeiro JD, Fischer GB. Chronic obstructive pulmonary diseases in children. J Pediatr (Rio J). 2015;91:S11–25.