This document provides an overview of common pediatric respiratory illnesses discussed over 9 sections. Section 1 covers acute respiratory infections, distinguishing between upper and lower respiratory infections. Pneumonia is then discussed in section 2, covering etiology, clinical features, diagnosis, and treatment approaches. Section 3 focuses on bronchiolitis, describing the viral etiology, pathophysiology, clinical presentation, and differential diagnosis. Key points covered include that bronchiolitis most commonly affects infants under 2 years old and is predominantly caused by respiratory syncytial virus.

1. Lecture notes on Pediatric Pulmonology1
S. No. Contents
9.1 Acute Respiratory Infections.
9.2 Pneumonias
9.2.1 Mycoplasma Pneumonia
9.3 Bronchiolitis
9.4 Wheezing in Infants.
9.5 Bronchial Asthma
9.5.1 Status Asthmaticus
9.6 Croup (Acute Laryngotracheobronchiolitis)
9.7 Laryngomalacia
9.8 Foreign bodies in the Airways
9.9 Empyema (Purulent Pleurisy)
9.10 Pneumothorax

2. 9.1. Acute Respiratory Infections (A.R.I.).
1. Definition: infection of any part of respiratory tract of less than 30days
duration except otitis media, which is of less than 14 days.
2. Classification:
1) Acute URI: Upper respiratory infection. It includes.
a) Commen cold.
b) Pharyngitis.
c) Laryngitis.
d) Tracheitis.
e) Epiglottitis.
f) Otitis media.
2) Acute LRI: Lower respiratory infection. It includes
a) Bronchitis.
b) Bronchiolitis.
c) Pneumonia.
3. Mode of presentation:
Pneumonia is present with symptoms of cough and difficulty in breathing.
Signs:
1) Fast breathing.
When respiratory rate in
• < 2months – 1year = ≥60/minute.
• 2months to 1 year = ≥50/minute.
• 1 year to 5year = ≥40/minute
2) Chest indrawing. (Intercostals) and subcostal retraction.
History Taking:
a) Age.
b) History of measles prior to disease.
c) Fever.
d) Inability to drink.
e) Drowsiness.
f) Convulsions.
g) Fast breathing.
h) Chest indrawing.
i) Abnormal sound – stridor, grunting.
4. Clinical Manifestation: Three Grades.
a) No Pneumonia: History of cough, no fast breathing, no chest
indrawing.
b) Pneumonia: history of cough and fast breathing no chest indrawing.
c) Severe Pneumonia with severe illness:
i. History of cough, with fast breathing, with chest indrawing.
ii. Inability to drink.
iii. Lethargic/ Excessive drowsiness.
iv. Stridor in calm child.
v. Cyanosis.
vi. Convulsions.
vii. Hypothermia.

3. 5. Management:
i. Drug therapy:
A. No pneumonia: Home treatment.
• Continue feeding.
• Give sufficient fluids.
• Paracetamol for fever.
• Clean nose with normal saline gives honey, ginger, tulsi.
B. Pneumonia. Drug of choice.
Amoxicillin – 15 mg/kg/8hrly orally for 5 – 7days.
Precautions:
a) Should not be given to premature babies.
b) In a child of<2months with rapid breathing should not be
given.
c) If no improvement in 2days patient should report
back to doctor
C. Severe Pneumonia.
S. No Antibiotics Dosage Interval Route
1 Benzyl Penicillin or 50,000/U/kg 6 hourly IM/IV
2 Ampicillin or 50mg/kg/dose 6 hourly IM/IV
3 Chloramphenicol 25mg/kg//dose 6 hourly IM/IV
If improvement continue for next 3 days.
If no improvement – change antibiotic.
• Cloxacillin - 25mg/kg/dose/6hourly IM/IV.
• Gentamycin – 2.5mg/kg/dose/ 8hourly/ IM or IV
Precaution: Avoid Chloramphenicol below 2months of
age.
ii. Symptomatic treatment for:
Fever: Paracetamol 10 – 15 mg/kg/dose/SOS or 6hrly.
Wheezing: O2 Nebulize with salbutamol or Terbutaline /oral
salbutamol.
iii. Regulate fluid and food intake.
iv. Prevention of recurrent LRI:
a) Excessive Breast feeding for 6months.
b) Avoid exposure to dusty and smoky environment.
c) Vaccination at right age.
d) Vitamin A prophylaxis.
e) Maintain adequate nutrition.

4. 9.2. Pneumonias.
1. Definition: Infection of lung parenchyma.
2. Classification:
a) Etiological:
1) Bacterial (Mainly cause lobar pneumonia)
I. Pneumococcus >3 years (90% cases)
II. Staphylococcus more in infants.
III. Klebsiella.
IV. H influenza – 3months to 2 years.
V. M. Tuberculosis.
VI. Group B Streptococcus.
2) Viral:
I. Influenza.
II. Measles.
III. RSV.
IV. Chicken pox.
3) Mycoplasma: Mycoplasma pneumonia.
4) Fungal: Coccidomycosis, Histoplasmosis.
5) Protozoal:
I. Pneumocystic jiroveci.
II. Toxoplasma gondi.
6) Rickettsial:
I. Typhus.
II. Rocky mountain spotted fever.
7) Miscellaneous:
I. Aspiration pneumonia.
II. Chemical pneumonias.
III. Loeffler pneumonia.
IV. Hypostatic pneumonia.
3. Clinical features:
1. Fever, Chills, Cough.
2. Respiratory distress.
3. Rapid respiration.
4. Chest indrawing.
5. Cyanosis, chest pain.
6. Chest signs of consolidation:
I. Increased V.F.
II. Dullness on percussion.
III. Auscultation.
• Decreased air entry.
• Bronchial breathing.
• Crepitation during resolution.
7. Laboratory Diagnosis:
1) Blood counts.
2) X – Ray chest.
o Staphylococcal pneumonia.
1) Pleural effusion, sepsis.
2) Pneumothorax or pneumatoceles are highly suggestive.
o Pneumococcal.

5. • Lobar consolidation.
8. Treatment:
1) Antibiotics:
a) For pneumococcal pneumonia:
I. Penicillin.
II. 3rd
Generation injectable Cephalosporin.
III. For drug resistant cases, beta lactam antibiotics can be used.
b) For staphylococcal:
I. Ampicillin + Cloxacillin
OR
II. Vancomycin.
OR
III. Linezolid.
c) For H. Influenza – intravenous 3rd
generation Cephalosporin.
d) For Klebsiella – intravenous 3rd
generation Cephalosporin.
e) For pseudomonas – Ceftazidime.
f) For pneumocystis jiroveci – Cotrimoxazole 20mg/kg/day.
g) For fungal – Amphotericin B.
h) For viral pneumonia – oseltamivir/Ribavirin.
i) For mycoplasma pneumoniae – Azithromycin for 10 – 14days.
2) General measures:
a) O2. Inhalation.
b) Bed rest.
c) Symptomatic treatment for fever, cough, bronchospasm.
d) Adequate fluids.
9. Complications:
1) Pleural effusion.
2) Empyema.
3) Collapse.
4) Pneumothorax.
5) Lung Abscess.
6) Bronchiectasis.
9.2.1. Mycoplasma Pneumonia:
1. Definition: It is major cause of respiratory infections in school aged children
and young adults.
2. Etiology:
Mycoplasma is the smallest self-replicating biological agent, which is
dependent on host cells. They contain double stranded DNA.
Epidemiology
Age: Peak incidence in school aged children (3to15yrs.)
Incubation period: 1 to 3 weeks.
Mode of infection: infection occurs through respiratory route by droplet
spread.
3. Pathogenesis:
1) Mycoplasma targets ciliated respiratory epithelium.
2) Virulent organism attaches to ciliated respiratory epithelial cell surface
and burrows down between cells, resulting in ciliostasis and sloughing
od cells.

6. 3) Immunological response of host ins also responsible for manifestations
of disease.
4. Clinical features:
1) Commonly it causes Bronchopneumonia.
2) Onset is abrupt characterized by gradual onset of headache, malaise,
fever and sore throat followed by hoarseness and cough.
3) Coryza is usually absent.
4) Cough is prominent symptom.
5) Severity of symptoms is usually greater than physical signs
6) Cough usually worsens in untreated patients during first 2 weeks and
resolves in 3 – 4 weeks.
9.2.2. Additional Respiratory illness.
1. Definition: Pharyngitis, sinusitis, croup, bronchiolitis, wheezing, otitis
media, bullous myringitis, are occasionally seen.
2. Diagnosis:
I. Diagnostic features: (Clinical)
1) Pneumonia in school aged children.
2) Cough is prominent symptom.
3) Coryza is absent.
II. Laboratory test:
1) Four-fold increase in IgG antibody titer by complement
fixation between 10 days to 3 weeks after onset of
illness is diagnostic.
2) PCR: Rapid and sensitive test.
3. Treatment:
1) Resistant to penicillin and cephalosporin.
2) Sensitive to macrolides:
a) Erythromycin 40 – 50mg /kg/day/orally for 10days.
b) Clarithromycin 15mg/kg/day in two divided doses P.O. for
10days.
c) Azithromycin:
i. Day1 – 10mg/kg/PO.
ii. Day2 5mg/kg/PO.
4. Complication:
1) Bacterial super infections.
2) Extra respiratory complications caused by autoimmune mechanism
are as follows:
a) Skin:
i. Erythema multiforme.
ii. Stevens – Johnson syndrome 3to21 days after initial
infection.
iii. Maculopapular rash.
b) Neurological complications (3 – 28 days after initial
infections)
i. Meningoencephalitis.
ii. Transverse myelitis.
iii. Aseptic meningitis.
iv. Cerebellar ataxia.
v. Bell’s palsy.

7. vi. Deafness.
vii. Brainstem syndrome
viii. Demyelinating encephalitis.
ix. Guillain – Barre syndrome.
c) Hematological: Hemolysis.
d) Hepatitis.
e) Pancreatitis.
f) Arrythmias.
Treatment of neurological complication is by
corticosteroids.

8. 9.3. Bronchiolitis.
1. Definition: Disease of lower Respiratory tract, resulting in inflammatory
obstruction of smaller airways.
2. Etiology:
a) Age: Commen age 1to3 months. Can be seen up to 2yrs of age.
b) Sex: More in males.
c) Season: Peak during winter and early springs.
d) Causes:
• Predominantly caused by virus >50% cases by respiratory syncytial
virus (RSV).
• Other: Parainfluenza, Adenovirus.
• Mycoplasma.
e) Predisposing factors:
• Non-breast-fed infants.
• Crowded living conditions.
3. Pathophysiology:
Airway inflammation is caused by:
A. Immunological factor: RS virus initiate complex immune response,
eosinophil degranulate and release eosinophil cationic protein which is
cytotoxic to airway epithelium.
B. Airway inflammation is also caused by interleukin 8, MIP (Macrophage
inflammatory protein 1 α) and RANTES (Regulation on activation, normal
T cell expressed and secreted)
C. Altered regulation of surfactant Protein A & B.
D. Pathological changes:
• Bronchiolar obstruction due to edema, mucus, cellular debris.
• Bronchiolar wall thickening.
E. Mucus plugs resulting in ball valve obstruction leads to early air
trapping and over inflation. It may also lead to atelectasis.
F. Ultimately resulting into impairment of pulmonary gas exchange and
Hypoxemia and hypercapnia.
4. Clinical features:
1) Infant first develops URI with sneezing and clear rhinorrhea, fever
and loss of appetite.
2) Gradually Respiratory distress increases with paroxysmal wheezy
cough, dyspnea, irritability and refusal to feed.
3) Apnea may be more prominent in preterm babies than wheezing.
4) Examination:
a) Tachypnea.
b) Wheezing.
c) Nasal flaring, intercostal & subcostal retractions.
d) Auscultation fine crackles or overt wheezes with prolongation of
expiratory phase of respiration, breath sound hardly audible.
e) Liver and spleen often palpable due to over inflation.
5) Respiratory distress is more than chest sign.
5. Lab Diagnosis:
1) X – Ray chest: Hyper inflated lungs with patchy atelectasis.
2) TLC, DLC: Normal

9. 6. Differential diagnosis:
1) Bronchial asthma:
2) Foreign body in trachea.
3) Tracheobronchomalacia.
4) Vascular rings.
5) CHF.
6) Pertussis TLC↑↑ with lymphocytosis.
7) Cystic fibrosis.
7. Treatment:
1) Hospitalize the patient.
2) Humidified oxygen.
3) Avoid sedatives.
4) Position: More comfortable if sitting with head and chest elevated at
30⁰ angle and neck extended.
5) Nasogastric tube feeding.
6) Parenteral fluids.
7) Inhaled bronchodilators may be helpful if associated atopic features
present.

10. 9.4. Wheezing in Infants.
1. Definition: Impairment in airflow due to reduction in airway diameter
results in wheezing.
2. Causes:
1) Infections:
a. Viral:
a) Respiratory syncytial virus.
b) Parainfluenza.
c) Adenovirus.
d) Influenza.
e) Rhinovirus.
b. Others:
a) Chlamydia trachomatis.
b) Tuberculosis.
c) Histoplasmosis.
2) Asthma: Three phenotype in children ≤ 5yrs.
I. Transient wheeze (≤ 3 yrs resolving).
II. Persistent wheeze (≤ 3 yrs then persisting).
III. Late onset wheeze onset 3 – 5 years of age.
3) Anatomic abnormalities:
i. Central airway abnormalities.
a) Malacia of larynx, trachea and bronchi.
b) TO fistula H. type.
c) Laryngeal cleft.
ii. Extrinsic airway abnormalities resulting in airway
compression.
a) Mediastinal lymph adenopathy.
b) Vascular ring.
c) Mediastinal tumor.
iii. Intrinsic airway anomalies.
a) Airway hemangioma.
b) Bronchial cyst.
c) Congenital, lobar emphysema.
d) Pulmonary edema due to CHD.
iv. Inherited:
a) Cystic fibrosis.
b) Immunodeficiencies.
c) AIDS.
d) Bronchiectasis.
v. Bronchopulmonary dysplasia.
vi. Aspiration syndrome.
vii. Bronchiolitis.
viii. Intestinal lung disease.
ix. Foreign body.
3. Pathophysiology: following two types of factors produce wheezing:
A. Virus specific factors:
Specific virus affect lower airways lower airways and Ig E Antibodies
are produced. These antibodies activate cytokines, which cause
wheezing.

11. B. Host specific factors:
1) Lung size.
2) Family history of asthma.
3) Elevated S. Ig E levels.
4) History of atopic dermatitis.
4. Clinical features:
1) Complaints: wheezing, stridor, cold, fever, respiratory difficulty.
2) History of rhinorrhea, conjunctivitis suggests viral infection.
3) Presence of stridor, wheeze and hoarseness suggest croup,
tracheomalacia, bronchomalacia.
4) Pulmonary edema suggests CHD.
5) Unilateral findings suggest foreign body.
6) Respiratory rate is increased along with subcostal retraction and
intercostal reactions.
7) Poor growth suggests cystic fibrosis, immunodeficiency,
gastroesophageal reflux.
8) Cutaneous hemangioma can point towards intrathoracic lesion.
5. Laboratory Diagnosis:
1) Blood counts.
2) X – ray chest.
3) CT or MRI.
4) Direct visualization under flexible bronchoscopy.
5) Pulmonary function test.
6) RAST radioimmune allergosorbant tests for atopy.
6. Treatment:
1) Treatment according to cause.
2) For viral infection:
a) Humidified oxygen.
b) I.V. fluid therapy.
c) Nebulized adrenaline.
d) Bronchodilators.
3) Inhaled corticosteroids.
4) Leukotriene modifying agent long-term medication for atopic
wheeze.

12. 9.5. Bronchial Asthma.
1. Definition: Chronic inflammation of airways of lung resulting in episodic
airflow obstruction.
2. Etiology:
I. Genetic factors:
More than 20 loci on 15 autosomal chromosomes have been linked to
asthma.
II. Environmental factors:
1. Viral infections of the airway.
2. Allergen exposure.
3. Tobacco smoke.
4. Air pollutants – Ozone, Sulfur dioxide.
5. Endotoxins.
6. Cold, dry, air.
7. Strong odors.
Above factors aggravate airways inflammation.
8. Dust.
9. Mycotoxins.
10. Exercise.
11. Crying.
12. Laughter.
13. GE reflux.
3. Types of childhood asthma:
1) Under 5 wheeze – Recurrent wheezing in early childhood. Triggered
commonly by respiratory viral infection.
2) Chronic asthma.
i. Associated with allergy.
ii. Persists during childhood or often adulthood.
3) Asthma association
i. Hyperplastic sinusitis.
ii. Nasal polyposis.
iii. Hypersensitivity to medication like aspirin, NSAIDs.
4. Pathogenesis:
1) Airway obstruction produced by:
a) Bronchoconstriction.
b) Epithelial damage.
c) Inflammatory cell fill airways.
d) Increase production of mucus.
e) Edema of surrounding tissue.
2) Airway inflammation, hyperresponsiveness and remodeling:
a) Cytokine and chemokines mediate inflammatory process.
b) Airway hyperresponsiveness is there to irritant exposure such
as cold air, dry air, and strong odors and smoke.
c) Airway remodeling is due to aberrant tissue repair in response
to persistent tissue injury.
d) It is in form of mucus gland hypertrophy and hyperplasia,
smooth muscle hypertrophy, sub-epithelial collagen
deposition, basement membrane thickening.

13. 3) Phase of asthma: Allergen causes two phases of airflow
obstruction:
A. Early phase: (15to30 min. causing Bronchoconstriction).
B. Late phase: 4to8 hours after allergen exposure leads to:
• Tissue inflammation.
• Immune cellular infiltration in airways.
• Airway edema.
• Increase mucous production.
4) Progression of severe asthma:
5. Clinical features:
 Chronic symptoms.
 Intermittent dry cough.
 Expiratory wheeze.
 Shortness of breath.
 Tightness of chest.
 Chest pain.
 Respiratory symptoms are worst at night.
 Fatigue.
 Symptoms provoked by triggering environmental factors, exercise.
 Chest examination:
1) Decrease breath sounds.
2) Expiratory wheeze.
3) Crackles, rales, rhonchi can be heard.
In severe exacerbations:
1) Chest retractions.
2) Nasal flaring.
3) Accessory respiratory muscle use.
4) Absent air entry.
5) Severe respiratory distress.
6) Cyanosis.
6. Investigation:
1) Lung function test:
• Spirometry: FEV1 low.
• Bronchodilator response to inhaled ꞵ2 agonist FEV1
increases >12%.
2) Broncho-provocation challenges: Exercise challenge – symptom
worsening by >15%
3) Peak expiratory flow monitoring (PEF) morning to evening variation
>20%.
4) Radiology: Chest X – Ray.
a) Hyperinflation.
b) Parabronchial thickening.
5) Allergy testing.
7. Treatment: Four components
a) Regular assessments and monitoring:
i. Asthma checkup 2-4 weekly.
ii. Lung function monitoring.
b) Control of triggering factors.
c) Asthma pharmacotherapy.

14. d) Patient education.
8. Pharmacotherapy:
• Classify Asthma severity first by four parameters:
1) Frequency of day time symptoms.
2) Frequency of night time symptoms.
3) Degree of airflow obstruction by spirometry.
4) PEF variability.
• There are four disease severity groups:
1) Intermittent.
2) Mid persistent.
3) Moderate persistent.
4) Severe persistent.
• Therapy can be divided in two groups:
1) Quick relief medication (Reliver)
A. Short acting inhaled ꞵagonist.
1) Salbutamol.
2) Terbutaline.
3) Levosalbutamol.
B. Inhaled anticholinergics.
1) Ipratropium.
C. Short course systemic glucocorticoids.
1) Prednisolone.
2) Methyl prednisolone sodium succinate. (Solu-medrol)
3) Hydrocortisone.
4) Dexamethasone.
2) Long term control medications (Controller).
a) Inhaled corticosteroids.
 Beclomethasone.
 Fluticasone.
 Budesonide.
 Ciclesonide.
 Mometasone.
b) Sustained release theophylline.
c) Long acting inhaled ꞵ2 agonist.
 Salmeterol.
 Formoterol.
d) Leukotriene modifiers.
 Montelukast
• 10mg >15yrs.
• 5mg. 6 to 12 yrs.
• 4mg 2 - 5yrs.
e) Oral glucocorticoids.
i. Prednisolone.
ii. Methyl Prednisolone.
iii. Deflazacort.
9. Approach:
1) “Three strike” rule helps in deciding type of therapy required:
a) Asthma patient requires quick relief medication more than three
times/week.

15. b) Awaken in night more than three times /month.
c) Require refill more than three times /year. Patient requires daily
controller therapy.
2) Step up, step down approach: start with higher level controller
therapy for prompt control. Once good control is achieved, step down
the therapy.
10. Inhalation technique:
1) Metered dose inhaler.
2) Space devices.
• Precaution: Mouth rinsing should be advised after inhaled
glucocorticoids.
• Advantage: Minimizes the risk of systemic absorption of
inhaled glucocorticoids.
3) Nebulizers.
S. No. Particular
Low Medium High
1 Beclomethasone dipropionate 200 – 500 >500 – 1000 >1000
2 Beclomethasone 100 – 200 >200 – 400 >400
3 Budesonide 200 – 400 >400 – 800 >800
4 Ciclesonide 80 – 160 >160 – 320 >320
5 Flunisolide 320 >320 – 640 >640
6 Fluticasone propionate DPI 100 – 200 >200 – 400 >400
7 Fluticasone propionate HFA 100 – 200 >200 – 500 >500
8 Mometasone furoate 110 – 220 >220 – 440 >440
9 Triamcinolone acetonide 400 – 1000 >1000 – 2000 >2000
Note: From the Global strategy for Asthma management and prevention 2015,
Global initiative for Asthma (GINA) All rights reserved. Available from
http://www.ginasthma.org.
Abbreviations: ICS, inhaled corticoids; HFA, hydrofluoroalkane inhaler, DPI,
dry powder inhaler.
9.5.1. Status Asthmaticus.
1. Definition:
Status asthmaticus refers to an acute asthma exacerbation in which
Bronchial obstruction is severe and continues to worsen or not improve
despite the institution of adequate standard therapy, leading to
respiratory failure. Severe attack of Bronchial asthma with Bronchial
obstruction from beginning or during the course of episode, in spite
administration of sympathetic agents as well as theophylline or
aminophylline.
2. Management:
1) Humidified O2.
2) Hydration by I/V fluids.
3) Nebulization with:
Salbutamol / terbutaline (every 20 min. × 3times)
Dose: 0.15 mg/kg diluted in 3ml of normal saline (Salbutamol neb
solution 5mg/ml) followed by every hourly.
4) Intravenous corticosteroids:
a. Glucocorticoids 2mg/kg/day or
b. Methyl prednisolone 1 – 2 mg/kg/I.V. /6hourly or

16. c. Hydrocortisone 10mg/kg stat max 100mg followed by 5mg/kg
six hourly.
5) I.V. magnesium sulphate 25 – 75 mg/kg (max 2gm)
Terbutaline as infusion.
6) Mechanical ventilation if respiratory failure.
7) Regular Assessment.

17. 9.6. Croup (Acute Laryngotracheobronchiolitis)
1. Definition: It is a viral infection of glottic and subglottic region.
2. Etiology:
• Primarily it is viral disease.
• Bacterial superinfection can occur.
3. Clinical features:
• Starts as upper respiratory infection in form of rhinorrhea, pharyngitis, mild
cough, mild fever.
• Within one to three days develops characteristic Barking cough,
hoarseness, inspiratory stridor.
• Symptoms are aggravated by crying may become worst at night.
• Examination shows nasal flaring, tachypnea, chest retraction, respiratory
distress and continuous stridor.
4. Investigations:
• X – Ray neck shows subglottic narrowing Steeple sign.
5. Differential Diagnosis:
1) Bacterial Tracheitis.
2) Diphtheritic croup.
3) Foreign body aspiration.
4) Retropharyngeal abscess.
5) Peritonsillar abscess.
6) Extrinsic compression of airways.
6. Treatment:
1) Humidified O2.
2) I.V. fluids.
3) Nebulized epinephrine.
4) Corticosteroids.
i. Dexamethasone – I.V. I. M. or Oral.
ii. Nebulized Busonide.
iii. Oral Prednisolone.
5) Antibiotics for superadded bacterial infections.

18. 9.7. Laryngomalacia.
1. Definition: Laryngomalacia is congenital abnormality of the laryngeal
cartilage. It is a dynamic lesion resulting in collapse of the supraglottic
structures during inspiration, leading to airway obstruction. It is thought to
represent a delay of maturation of the supporting structures of the larynx.
2. Cause of stridor: Collapse of supraglottic structures inwards during inspiration.
3. Clinical features:
A.Stridor is most commen presenting feature, which appears within first
2weeksof life and increase the severity up to 6months. Stridor is inspiratory
and low pitched and increase with exertion. I.E. while crying, feeding.
B. Rarely Dysphagia cyanosis, failure to thrive, cor. pulmonale can be occur in
severe cases.
C. Laryngopharyngeal Reflux is commonly associated.
4. Treatment:
1) Symptoms resolve spontaneously in most of cases by 9months to 1year.
2) Surgical intervention in severe obstruction.
3) Endoscopic Supraglottoplasty.

19. 9.8. Foreign bodies in the Airways.
Foreign bodies aspiration is often seen during childhood.
Age: Younger than 3years account for 73% cases.
Types of foreign bodies: Nuts, pieces of raw carrots, dried beans seeds, fruit pieces,
coins.
1. Clinical History:
a) History of foreign body aspiration is very important both positive history
as well as negative history.
b) Choking or coughing episodes accompanied by wheezing are highly
suggestive.
c) There are three stages of symptoms:
1. Initial stage: Severe paroxysm of coughing, choking, gaging and
possibly airway obstruction occur while foreign body is ingested.
2. Asymptomatic phase: Foreign body becomes logged; expulsion
reflexes fatigued and immediate irritating symptoms subside.
3. Complication phase: There are complication like:
 Obstruction of airway.
 Erosion of airway.
 Infections of Respiratory system.
d) Features: Fever, Persistent cough, Hemoptysis, pneumonia and atelectasis,
depending upon site of obstruction features are as follows:
1) Laryngeal FB: Manifest as croup, hoarseness, cough, stridor,
dyspnea.
2) Tracheal FB: Choking and aspiration in 90% cases followed by
stridor and wheezing X – Ray neck reveals soft tissue abnormality.
3) Bronchial FB: Features suggestive of obstructive emphysema and
shift of mediastinum to opposite side. X – Ray chest shows air
trapping. i.e. obstructive emphysema.
2. Treatment:
1) Rigid Bronchoscopic removal of foreign body at the earliest.
2) Adequate hydration.
3) Antibiotics to treat the infection.
9.9. Empyema (Purulent Pleurisy).
1. Definition: An accumulation of pus in the pleural space.
2. Causes:
1) Pneumonia due to:
 Streptococcus Pneumonae.
 Staphylococcus aureus.
 Hemophilus influenza.
 Streptococcus.
2) Due to rupture of lung abscess.
3) Trauma.
4) Due to mediastinitis
5) Extension of intraabdominal abscess.
3. Clinical features:
1) Features of bacterial pneumonia initially.
2) Fever, Respiratory distress, chest pain.
3) On Examination:
a) Bulging chest.

20. b) Decreased movements.
c) VF Decreased.
d) Stony dull on percussion.
e) Auscultation:
• Air entry decreased.
• V. R. decreased.
f) Mediastinal shift to opposite side.
4. Investigation:
1) X – Ray chest – obliteration of C. P. angle.
2) USG.
3) CT Scan.
5. Complications:
1) Bronchopleural fistula especially in staphylococcal pneumonia.
2) Pyopneumothorax.
3) Local:
• Purulent pericarditis.
• Pulmonary abscess.
• Peritonitis.
• Osteomyelitis of ribs.
4) Systemic complication:
• Septicemia.
6. Treatment:
1) Thoracentesis:
2) Systemic antibiotic therapy for 10 days to 4weeks depending upon type of
organism. For staphylococcus 3 – 4 weeks.
3) Decortication if no improvement.

21. 9.10. Pneumothorax.
1. Definition: Accumulation of extrapulmonary air within the chest.
2. Causes:
I. Primary spontaneous pneumothorax:
• Without trauma.
• Without underlying lung disease.
II. Secondary spontaneous pneumothorax:
1. Complication of underlying lung disease:
• Pneumonia with empyema.
• Lung abscess.
• Gangrene.
• Infarct.
2. Rupture of cyst or emphysematous bullae in asthma.
3. Foreign body in lung.
4. Staphylococcal pneumonia in infants.
5. Complication of cystic fibrosis.
6. With lymphoma or malignancies.
III. Traumatic:
IV. Iatrogenic as a complication of:
1. Tracheostomy.
2. Thoracentesis.
3. Transbronchial biopsy.
4. Subclavian line placement.
5. After acupuncture.
V. Catamenial pneumothorax:
Pneumothorax associated with menses resulting from passage of intra-
abdominal air through diaphragmatic defects.
VI. Associated with:
1. Hydropneumothorax.
2. Pyopneumothorax.
VII. Bilateral pneumothorax:
1. Rare beyond neonatal period.
2. Associated with lung transplantation.
3. With mycoplasma pneumonia infection.
3. Clinical features:
1. Acute onset.
2. Pain, dyspnea, cyanosis.
3. Examination:
a) Respiration difficulty.
b) Retractions.
c) Percussion note – hyper resonant.
d) Mediastinal shift to opposite side.
e) Air entry decreased.
4. Laboratory:
X – Ray chest.
5. Differential diagnosis:
1. Emphysema.
2. Large pulmonary cavity.
3. Gaseous distention of abdomen.

22. 6. Treatment:
1) Treatment of underlying lung disease.
2) Small to moderate may resolve spontaneously within 7days.
3) 100% O2 can fasten recovery.
4) Closed tracheostomy.
I. Insert chest tube.
II. Drain trapped air through catheter which is kept under water in a
dependent position.
5) Chemical pleurodesis for recurrent pneumothorax.
Induce adhesions by putting sclerosing agent like tetracycline or talc in plural
space.
6) Open thoracotomy for recurring pneumothorax.
References:
1. Parthasarathy, K Nedunchalian, Gowri Shankar HC, Textbook of Balram chowdhary’s Pediatrics
Lecture notes, PEE PEE Publication, 2nd edition, Pg no. 222 – 236.