1. ((Wheezy chest in pediatric age group))
Prepared by:
Daniel Rawand Pols
Sajad Abdulridha Ali
Ghazwan Ardalab Slewa
Supervised by:
Dr. Siamand Yahya

3. What is wheezing?
High pitched, continuous, musical
(whistling) sound, occurs when air flows
through a narrowed airway.
-Can originate from airway of any size
-Heard mostly on expiration
-Manifestation of lower respiratory tract

4. Causes of Wheezing in Childhood
ACUTE
CHRONIC OR RECURRENT
Reactive airway disease…..
Reactive airway disease : Asthma
Bronchial edema :
•Infection
•Inhalation
•Increased PVP
Bronchial hypersecretion :
• Infection
• Inhalation
• Cholinergic drugs
Aspiration : Foreign body
Aspiration of gastric contents
Airway compression by mass or blood vessel:
• Vascular ring/sling
• Bronchial or pulmonary cysts
•Lymph node
Dynamic airway collapse:
Bronchomalacia/tracheomalacia
Aspiration : Foreign body
GORD
Bronchial hypersecretion : Bronchitis,
Bonchiectasis, Cystic fibrosis, Primary ciliary
dyskinesia
Intrinsic airway lesions: Endobronchial tumors
(carcinoid)

5. Approach to a wheezing child
Clinical History:
oPatient age at onset of wheeze
oCourse: acute vs gradual
oPattern of wheezing?
Episodic: asthma
Persistent: congenital
o Response
to bronchodilators?
oIs Wheezing associated with multiple systemic
illnesses?
Cystic fibrosis and Immunodeficiency diseases

6. oWheeze associated with feeding?
oWheeze associated with cough?
oChange in position? Worsening or improvement
oFamily hx of asthma?

7. Physical Examination
•General
•Vital signs including SpO2 %
•Chest examination
Inspection:
–Respiratory distress
–Chest wall deformity (increased AP diameter)
– allergic shiners/nasal polyps
–Skin: eczema
•Palpation: chest wall asymmetry with expansion, tracheal
deviation
•Percussion: difference in vocal resonance
•Auscultation:
•Location of wheeze
•Character of wheeze
•Other breath sounds associated with wheeze
•Cardiac: presence of murmur

9. Investigations
•CXR: AP and lateral views
–Children with new onset wheezing of undetermined etiology
–Chronic persistent wheezing not responding to treatment
–Suspected FB aspiration
•CXR findings:
Hyperinflation:
Generalized: suggests diffuse air trapping
Asthma/ Cystic fibrosis/ Primary ciliary dyskinesia
Localized hyperinflation:
Structural abnormalities/ FB aspiration
Other findings: atelectasis, bronchiectasis, mediastinal masses, enlarged
LN’s, cardiomegaly, enlarged pulmonary vessels or pulmonary edema.

10. •Chest CT scan:
–Mediastinal masses or LN’s
–Vascular anomalies
–Bronchiectasis
•Barium Swallow:
–GERD
–TEF
–Vascular rings
–Swallowing dysfunction
Pulmonary Function Tests (PFT’s)
Airway obstruction assessment
•Response to bronchodilator

11. Other investigations:
•Sweat Chloride Test: Cystic fibrosis screening in children with
chronic lung problems, failure to thrive and diarrhea
•Immunoglobulin levels: Screen for immunodeficiency.
•Rapid antigen testing, viral cultures, sputum gram stain and
culture.

12. Bronchiolitis

13. Bronchiolitis
It is inflammatory obstruction of small airways.
Age: first 2 years.
2- 12 months peak 6 months.
more sever at 1-3 months.
Seasonal disease, peak during winter & early spring.

14. Etiology & Epidemiology
Predominantly viral: RSV
Human metapeumovirus
Influenza
Adeno
Para influenza
Mumps, Entero, Rhino
Mycoplasma pneumonia
Chlamydia pneumonia, Chlamydia Trachomatis.

15. Etiology & Epidemiology
Bronchiolitis common in
•Male.
•Not being breast fed.
•Crowded condition.

16. Clinical manifestation
- Mild URTI, diminished appetite, fever(38.5-39)
- Respiratory distress with paroxysmal wheezy cough,
dyspnea& irritability.
- Infant is tachypnic which interfere with feeding
- No other systemic complain.
- Apnea(in 20% of hospitalized infants)
Infant at risk for apnea:
*premature infant
*very young infant(1-4 months)
* Chronic lung disease.

17. On examination
Sign of respiratory distress (nasal flaring, retraction)+
wheezing.
Auscultation :
Fine crackle or overt ronchi+ prolongation of expiratory
phase.
Barely audible breath sound suggest a very sever disease
with nearly complete bronchiolar obstruction.
Hyperinflation of the lung may permit palpation of liver
&spleen.

18. Investigation
CXR:
•Hyperinflated lung.
•Bilateral interstitial abnormalities with peribronchial
thickening.
•Up to 20% having lobar, segmental, or sub segmental
consolidation.

19. Investigation
WBC & differential count are usually normal.
Viral testing:
•Rapid immunofluorescene.
•Polymerase chain reaction
•Viral culture
Blood gas analysis: hypoxemia, hypercarbia

20. Treatment
Supportive : mainstay of treatment.
- Respiratory distress( hospitalization, positioning, cool&humidified
oxygen).
-Feeding :risk of aspiration( NG feeding) and parenteral fluids.
Bronchodilater.
Nebulized epinephrine.
Corticosteroid : (oral, inhaler, parentral).
Ribavirin .
Antibiotic.
RSV immunoglobulin.
Intubation &mechanical ventilation.

21. Complication
1-increasingly labored breathing
2-cyanosis
3-dehydration
4-fatigue
5-severe respiratory failure

22. Childhood
Asthma

25. Genetic
predisposition
Atopy
Bronchial inflammation
- Oedema
- Excessive mucus production
- Infiltration with cells
(eosinophils, mast cells,
neutrophils,
lymphocytes)
Bronchial
hyperresponsiveness
Environmental triggers
- Upper respiratory tract
infections
- Allergens (e.g. house dust mite,
grass pollens, pets)
- environmental tobacco smoke
- Cold air
- Exercise
-Emotional upset or anxiety
-Chemical irritants (e.g. paint,
aerosols)
Airway narrowing
Symptoms:
Wheeze
Cough
Breathlessness
Chest tightness

27. Onset of presentation
Transient wheezer
Onset ≤3 years of age then resolving
Initial risk factor is primarily diminished lung size
Normal lung function by 6 Years of age
Not associated with increased risk of developing clinical asthma
Persistent wheezer
Onset ≤3 years then persisting
Initial risk factors include passive smoke exposure, maternal asthma
history and elevated IgE level in the first year of life
Irreversible reduction in lung function at 6 years of age
An increase risk of developing clinical asthma
Late onset wheezer
Onset of wheeze between 3 to 6 years

28. EARLY CHILDHOOD RISK FACTORS FOR PERSISTENT ASTHMA
1) Parental asthma
2) Allergy
3) Severe lower respiratory tract infection:
4) wheezing apart from cold
5) Male gender
6) Low birth weight
7) Environmental tobacco smoke exposure

29. Clinical features
-Intermittent dry coughing
-expiratory wheezing
-Older children report associated
shortness of breath and
chest tightness
-Asthma should be suspected in any child
with wheezing on more than one occasion.

30. -Other key features:
•worse at night and in the early morning
•triggers
•Personal or family history of an atopic disease
•Positive response to asthma therapy.
Once suspected, the pattern or phenotype should be
further explored by asking:
•frequency
•triggers
•general activities
•sleep disturbance
•How much school has been missed due to
asthma?

31. Examination
-Examination of the chest is usually normal
between
attacks.
-In long-standing asthma
hyperinflation
Harrison sulci
generalized expiratory wheeze
and prolonged expiratory phase.
- Evidence of eczema
- the nasal mucosa for allergic
rhinitis.
-Growth

33. Investigations
CBC :Eosinophilia in a range of 15-20%
Eosinophilia in bronchial mucosa strongly suggest Asthma
Allergy testing
Pulse oximetry
Arterial blood gas analysis
Pulmonary function test : Applicable for children > 6
 CXR
years

35. Classification of chronic Asthma
Days with
symptoms
Night with
symptoms
Mild intermittent
<= 2/week
< 2/month
Mild persistent
> 2/week
< 1/day
>2/month
Moderate
persistent
Daily
> 1 week
Sever persistent
Continual
Frequent

36. Asthma pharmacotherapy
•B2 agonist
•corticosteroids
•Anticholinergic agent
•Leukotreine modifier
•NSAID
•theophylline

37. A stepwise approach to the treatment of
chronic asthma
Step 1 ( mild intermittent asthma)
-No daily medication needed
-Sever exacerbation may need systemic steroids
-Step 2 (mild persistent)
-Low dose inhaled corticosteroids daily

38. Step 3 (moderate persistent)
-low to medium dose inhaled corticosteroids + long acting
inhaled B2 agonist
Step 4 ( sever persistent)
- High dose inhaled corticosteroids + long acting inhaled B2
agonist + oral corticosteroids (if needed)

39. Classification of severity of acute asthma exacerbations
Mild
Moderate
Sever
Respiratory arrest
walking
Talking, feeding
difficulty
Rest, stop feeding
Can lie down
Prefers setting
Sits upright
Talk in
Sentences
Phrases
words
Alterness
May be agitated
Usually agitated
Usually agitated
RR
Increased
Increased
>30
Use of accessory
Muscles
No
Commonly
Usually
Paradoxical
respiration
Wheeze
Moderate on
expiration
Loud, through out
exhalation
Loud, inspiration &
expiration
Absence of wheeze
Pulse/Min
<100
100-120
>120
bradycardia
Pulsus paradoxus
Absent <100mmhg
10-25 mmhg
>25mmhg
absent
symptoms
breathlessness
Drowsy, confusion
signs

40. Management:
Acute asthma:
oSemi sitting position
oO2 to keep saturation > 92%.
oFluid if dehydrated.
oBeta-2 agonist: Salbutamol each 20 min by mask
until improved later on mask hourly if required.
oIpratropium bromide.
oSteroids: Prednisolone.
If sever give steroids directly since
the onset of action is slow (4 hrs)

41. Criteria for admission to hospital
1)Persisting breathlessness, tachypnoea
2)Exhausted
3)Still have a marked reduction in their predicted (or
usual) peak flow rate
4) Oxygen saturation (<92% in air).
5) Family in able to cope with the condition

42. (pMDI)
Nebuliser
Dry
powder
inhaler

43. Gastro-oesophageal
reflux

45. -It is extremely common in infancy.
- caused by
1) inappropriate relaxation of the lower oesophageal
sphincter as a result of functional immaturity.
2)A predominantly fluid diet,
3)A mainly horizontal posture
4)A short intra-abdominal length of oesophagus.
-resolves spontaneously by 12 months of age.

46. Severe reflux is more common in:
1)children with cerebral palsy or other
neurodevelopmental disorders.
2) preterm infants
3) following surgery for oesophageal atresia
or
diaphragmatic hernia.

47. Complications of gastro-oesophageal reflux
• Failure to thrive from severe vomiting
• Oesophagitis – haematemesis, discomfort on
feeding or heartburn, iron deficiency anaemia
• Recurrent pulmonary aspiration – recurrent
pneumonia, cough or wheeze, apnoea in preterm infants
• Dystonic neck posturing (Sandifer syndrome)
• Apparent life-threatening events (ALTE)

48. Investigation
May be indicated if
1)the history is atypical
2)complications are present
3)failure to respond to treatment.
Investigations include:
• 24-hour oesophageal pH monitoring
• 24-hour impedance monitoring.
• Endoscopy with oesophageal biopsies
• Contrast studies of the upper
gastrointestinal tract

49. Management
Uncomplicated gastro-oesophageal reflux can be managed by
1)Parental reassurance
2)adding inert thickening agents to feeds
(e.g. Nestargel, Carobel)
3) positioning in a 30° head-up prone position after feeds.
4) acid suppression with either : H2 receptor antagonists
(e.g. ranitidine)
or: proton pump inhibitors
(e.g. omeprazole)
5) If the child fails to respond to these
measures, other diagnoses such as cow’s milk protein
allergy should be considered
6) Surgical management: A Nissen fundoplication,

50. Cystic fibrosis

51. Cystic fibrosis
Cystic fibrosis (CF) is an inherited (AR) multisystem disorder
of children and adult, characterized chiefly by obstruction
and infection of airways and by mal digestion and its
consequence
CF is the major cause of severe chronic lung disease in
children and is responsible for most exocrine pancreatic
insufficiency in early life.

52. • Cystic Fibrosis is an inherited
disease.
• For a child to inherit CF, both
parents must be carriers of a
defective gene on chromosome 7.
- They then have a 50% chance of
becoming a carrier.
- A 25% chance of getting CF
- A 25% chance of not being a carrier
and not having CF

53. • A chromosome carries genetic information
• Chromosome 7 carries the cystic fibrosis transmembrane
conductance regulator (CFTR)
• CFTR controls salt and water movements in and out of
cells
• When CFTR is defective, cystic fibrosis occurs because the
CFTR doesn’t work or is completely missing.
• When salt and water don’t move in and out of cells
properly, sweat becomes 5 times saltier and a thick, sticky
mucus is produced outside the cell.

54. It affects the…
Lungs
Pancreas
• Mucus builds up and obstructs
airways
• Pancreas produces enzymes that help
with digestion
• Build up also makes a suitable
environment for bacterial growth
• Build up of mucus blocks ducts in
pancreas, stopping enzymes form reaching
intestines
Bacterial growth increases risk of
infections
Repeated infections cause lung
damage
Without enzymes, intestines can’t digest
food properly
Leads to loss of vitamins and nutrients

55. Respiratory:
- A persistent cough that produces thick mucus
- Wheezing or lack of breath
- A lowered ability to do exercise
- Repetitive lung infections
-A persistent stuffy nose and inflamed nasal passages
Digestive:
- Foul smelling and greasy stools
- Unusually small amount of weight gain or growth
- Intestinal blocking, especially in newborns
-Severe constipation
Other:
- Infertility is common in both males and females, though more frequently in males
- Salty tasting skin and sweat.

57. Diagnosis
- Screening: most newborn with CF can be identified by
determination of immunoreactive trypsinogene and limited
DNA testing on blood spots, coupled with confirmatory
sweat analysis. This screening test is about 95% sensitive.
-History: child having :
Cough and wheeze, SOB, sputum production, hemoptysis, stool
type( e.g fatty, oily, pale) and frequency , weight loss or poor
weight gain

58. Diagnosis
-Most children with CF present with:
malabsorption,
Failure to thrive,
Recurrent chest infection.
-Examination:
Full assessment of:
*Respiratory system.
*Liver and GIT system.
*Growth and development.

59. Diagnosis
Investigation:
Sweat test: most definite test. By chloridometer is
recommended for analysis of chloride in these samples
+ve when CL is equal or more than 60 meq/L which is dx for
CF in conjunction with one of the followings:
•Typical chronic obstructive pulmonary dis.
•Exocrine pancreatic insuffisiency
•Positive family hx.

60. Diagnosis
DNA testing
Pancreatic function test:
Microbiological studies:
Sputum culture:
Radiology:
Pulmonary function test:

61. Treatments for CF
• Medications
– Medications are used to treat lung disease
– Many are inhaled using a nebulizer
– Medications used are:
• Mucolytics, which loosen lung mucus
• Bronchodilators, which expand the airways
• Steroids, which decrease inflammation
• Antibiotics, fight infections
• Chest physical therapy
– Considered standard therapy
– Used to clear mucus from the lungs
– Person is clapped on the back

62. Treatments for CF (continued)
• Nutrition
– Good nutrition
– High-calorie diet
– Vitamins
• Pancreatic enzymes
– Pancreatic enzyme supplements, taken with everything consumed, help
absorb nutrients
• Transplantation
– Transplants are used for end-stage disease.
– The transplants used are:
• Double-lung transplant
• Heart-lung
• Liver

63. Gene Therapy
• Gene therapy is an experimental technique that uses genes to treat
diseases.
• Gene therapy can replace a mutated gene or inactivating a mutated
gene.
• It is promising but risky. It needs more research to see if it is safe.
• Gene therapy has been used for cystic fibrosis, in which the healthy
CFTR gene is inserted into the lung cells

64. Foreign bodies of the airways

65. Foreign bodies of the airways
Epidemiology and etiolagy:
•Most patient are younger than 4 years.
•73% are older infants and toddlers
•1/3 of aspirated objects are nuts
•Raw carrot, apple, dried beans, pop corn& sun flower or
water melon seeds
•Mainly in right side.

66. Clinical manifestation
- Sudden onset of cough, chocking & wheezing.
Stages of symptoms:
•Initial events; there is violent paroxysms of coughing,
chocking, gagging& possibly airway obstruction.
•Asymptomatic interval; foreign body become lodged.

67. Complication
•Obstruction, erosion or infection develops.
•Atelectasis, recurrent or persistent pneumania.
•Persistent wheezing unresponsive to bronchodilator&
diminished local breath sounds
•Persistent cough.

68. Diagnosis
Postero anterior & lateral chest radiogragh(expiratory
film)
obstructive emphysema (air trapping) with
shifting of mediastinum toward the opposite site.
Lateral decubitus chest film or fluoroscopy.
Flexible bronchoscoy.

69. FB aspiration
 FB occludes middle lobe
bronchus
 Atelectasis of Rt middle
lobe
 Hyperinflation of upper and
lower lobes

70. Treatment
ABC
Conscious : Heimlich maneuver
FB removal Back blow or chest thrusts (PALS)
Unconscious: 100% oxygen through the mask, rigid
bronchoscopy and object removal

72. Reference:
-Nelson Essentials of Pediatrics, 6th Edition
-nelson textbook of pediatrics 19th edition
-illustrated textbook of paediatrics 4th
http://www.medicinenet.com/anatomy_of_an_a
sthma_attack_pictures_slideshow/article.htm