2014

1. ‫الرحيم‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬

2. CHRONIC BRONCHITIS IN
CHILDREN
Ahmad Abu-Naglah
Prof of chest diseases
Al Azhar university

3. Definition
• Defining chronic bronchitis and its prevalence
in childhood has been complicated by the
significant clinical overlap with asthma and
reactive airway disease states.

4. Definition
• Chronic bronchitis is recurring inflammation
and degeneration of the bronchial wall that
may be associated with active infection

6. • In adults, chronic bronchitis is defined as daily
production of sputum for at least 3 months in
2 consecutive years.
• Some have applied this definition to
childhood chronic bronchitis.

7. • Chronic bronchitis has also been defined as a
complex of symptoms that includes cough
that lasts more than 1 month or recurrent
productive cough that may be associated with
wheezing or crackles on auscultation.

8. Etiology
Chronic bronchitis may be caused by
1-Repeated attacks of acute bronchitis, which
can weaken and irritate bronchial airways over
time, eventually resulting in chronic
bronchitis.

9. 2- Industrial pollution is also a common cause;
however, the chief culprit is heavy long-term
cigarette smoke exposure
Tsai et al demonstrated that in utero and
postnatal household cigarette smoke exposure
is strongly linked to asthma and recurrent
bronchitis in children.

10. 3- Chronic aspiration or gastroesophageal reflux
4- Fungal infection

11. • Chronic bronchitis is often part of an
underlying disease process, such as asthma,
cystic fibrosis, dyskinetic cilia syndrome,
foreign body aspiration, or exposure to an
airway irritant.

12. • Recurrent tracheobronchitis may also be seen
in patients with tracheostomy or with certain
forms of immunodeficiency.

13. • In all of these patient groups, chronic
bronchitis should not be the primary
diagnosis, because it does not describe the
pathology of the underlying disorder.

14. Factors affecting persistent or
recurrent chest infection

15. Factors affecting persistent or
recurrent chest infection
1- Infants born prematurely, and particularly
those who develop bronchopulmonary
dysplasia after ventilation, frequently require
hospital admission for respiratory infections in
early childhood.
• The mortality from infection in these infants is
higher than in term infants.

16. 2- The immunoprotective effect of breast
feeding against respiratory infections.

17. 3- Parental smoking increases the risk of all
respiratory illnesses and symptoms, and
particularly lower respiratory tract infection,
in children.
• The effect is greater in infants than in older
children
• Related more to maternal than paternal
smoking
• Dose-related

18. • Both maternal smoking during pregnancy and
postnatal passive exposure predispose the
children of smokers to recurrent respiratory
infections .

19. 4- Exposure to other children influences the
number of infections children develop.
• Infants with older siblings or from over-
crowded homes, have more frequent
respiratory infections.
• When children first attend school or nursery,
the number of infections they contract rises.

20. 5- Children with congenital defects of the
respiratory tract, such as tracheo-oesophageal
fistula or sequestration, and children with
congenital heart disease, are at increased risk
of recurrent respiratory infection.
6- Neurologically handicapped children are
particularly vulnerable

21. 7- Defect in the complex system of defence
mechanisms

22. Lung defense
mechanisms

23. Physical and physiological defenses
• Airway filtration of particles
• Cough
• Sneezing
• Bronchoconstriction
• Mucociliary clearance
• Airway mucus
• Respiratory cilia
• Alveolar fluid movement

24. Cellular defences
• Lymphocytes (T- and B-cells)
• Pulmonary macrophages
• Neutrophils

25. Secretory defences
• Immunoglobulins G, A, M and E
• Collectins α1–Antitrypsin and α2-
macroglobulin
• Lysozyme
• Lactoferrin
• Complement α and β Defensins
• Interferon

26. Pathophysiology

27. Pathophysiology
• In children, chronic bronchitis follows either
an endogenous response (eg, excessive
inflammation) to acute airway injury or
continuous exposure to certain noxious
environmental agents (eg, allergens or
irritants).

28. • An airway that undergoes such an insult
responds quickly with bronchospasm and
cough, followed by inflammation, edema, and
mucus production.
• This helps explain the fact that chronic
bronchitis in children is often actually asthma

31. Mucociliary clearance
• It is an important primary innate defense
mechanism that protects the lungs from the
harmful effects of inhaled pollutants,
allergens, and pathogens.
• Mucociliary dysfunction is a common feature
of chronic airway disease states in humans.

32. The mucociliary apparatus
• consists of 3 functional compartments:
1- cilia
2- a protective mucus layer
3- airway surface liquid (ASL) layer
They work together to remove inhaled particles
from the lung

33. • ASL depletion resulted in reduced mucus
clearance and histologic signs of chronic
airway disease, including mucus obstruction,
goblet cell hyperplasia, and chronic
inflammatory cell infiltration.

34. Normal airway color and architecture

35. Airway of a child with chronic bronchitis

36. Bronchitis and Asthma
• Recurrent episodes of acute or chronic
bronchitis in children should alert the
clinician to the likelihood of asthma.
• Bronchitis is often repeatedly diagnosed in
children in whom asthma has remained
undiagnosed for many years.

37. • Similarly, a family history of asthma in parents
or siblings may be masked within a history of
“recurrent bronchitis.”
• The diagnosis of "asthmatic bronchitis" or
"wheezy bronchitis" is simply asthma.

38. Bronchitis and Immunodeficiency
• Recurrent episodes of acute or chronic
bronchitis may be associated with
immunodeficiency.

39. Stiehm identifies the 4 most common
immunodeficiencies in pediatric patients:
1-transient hypogammaglobulinemia of infancy (THI)
2-immunoglobulin G (IgG) subclass deficiency
3-impaired polysaccharide responsiveness (partial
antibody deficiency)
4- selective IgA deficiency (IgAD).
Stiehm ER. The four most common pediatric immunodeficiencies. J
Immunotoxicol. Apr 2008;5(2):227-34.

40. • A summary of immunodeficiency registries in
4 countries listed IgAD in 27.5% of the
patients, IgG subclass deficiency in 4.8%, and
THI in 2.3%.
• Patients typically have normal cellular
immune systems, phagocyte function, and
complement levels.

41. • All 4 immunodeficiency states are
characterized by recurrent bacterial
respiratory infections, such as purulent
rhinitis, sinusitis, otitis, and bronchitis.
• Only a few cases require the use of
intravenous IgG (IVIG) and the long-term
prognosis is generally excellent

42. • Ozkan studied immunoglobulin A (IgA) and IgG
deficiency in children who presented with
recurrent sinopulmonary infection.
• The overall frequency of antibody defects was
found to be 19.1%.
• IgA deficiency was observed in 9.3%, IgG
subclass deficiency was observed in 8.4%, and
both IgA and IgG subclass deficiencies were
observed in 1.4%.
• Ozkan H, Atlihan F, Genel F, Targan S, Gunvar T. IgA and/or IgG subclass deficiency in
children with recurrent respiratory infections and its relationship with chronic
pulmonary damage. J Investig Allergol Clin Immunol. 2005;15(1):69-74.

43. • The prevalence of IgA and/or IgG subclass
deficiency was 25% in patients with recurrent
upper respiratory tract infections, 22% in
patients with recurrent pulmonary infections,
and 12.3% in patients with recurrent
bronchiolitis.

44. Common variable immunodeficiency
• It is the most frequent of the primary
hypogammaglobulinemias.
• Kainulainen et al conducted a nationwide survey
of all patients with common variable
immunodeficiency who were receiving
immunoglobulin replacement therapy in Finland
Kainulainen L, Nikoskelainen J, Ruuskanen O. Diagnostic findings in 95 Finnish patients with
common variable immunodeficiency. J Clin Immunol. Mar 2001;21(2):145-9

45. • Sinopulmonary infections were the most
common clinical presentation; 66% had
recurrent pneumonia, 60% had recurrent
maxillary sinusitis, and 45% had recurrent
bronchitis.
• The mean interval from the time of onset of
symptoms to diagnosis was 8 years.

46. • Evidence of chronic lung damage was noted
in 17% of patients at the time of diagnosis,
highlighting the importance of early
recognition in the prevention of chronic
pulmonary sequelae.

47. • To improve the recognition of common
variable immunodeficiency, the authors
suggest consideration of this condition in
patients with recurrent sinopulmonary
infection.
• In addition to a low serum IgG concentration,
measurement of specific antibody production
is recommended to establish the diagnosis

48. Treatment
• General measures include rest, use of
antipyretics, adequate hydration, and
avoidance of smoke.
• Proper care of the underlying disorder is of
paramount importance.
• Consideration of asthma and adequate
therapy are critical to an early response.

49. • Bronchodilator therapy should be considered
and instituted; either a beta-adrenergic
agonist or theophylline.
• Beta-adrenergic agents are less toxic, have a
more rapid onset of action than theophylline,
and do not require monitoring of levels.
• Inhaled corticosteroids may be effective.

50. • In the child who continues to cough despite a
trial of bronchodilators and in whom the
history and physical examination findings
suggest a wheezy form of bronchitis, oral
corticosteroids should be added.

51. • If the response is suboptimal or if fever
persists, antibiotic therapy with an agent such
as a macrolide or beta–lactamase-resistant
antimicrobial may be considered.
• Too often, antibiotics are the primary therapy.
They usually do not result in a cure and may
delay the start of more appropriate asthma
therapies

52. Conclusions
• Chronic bronchitis is manageable with proper
treatment and avoidance of known triggers
(eg, tobacco smoke).
• Proper management of any underlying
disease process, such as asthma, cystic
fibrosis, immunodeficiency, heart failure,
bronchiectasis, or tuberculosis, is also key.

53. • These patients need careful periodic
monitoring to minimize further lung damage
and progression to chronic irreversible lung
disease.

54. THANK YOU