RESPIRATORY SYSTEM

COMMON COLD
1. Introduction:
1. The common cold is a viral illness
2. The symptoms of rhinorrhea and nasal obstruction are prominent;
3. Systemic symptoms and signs such as myalgia and fever are absent or
mild.
4. It is often termed rhinitis but includes self-limited involvement of the
sinus mucosa and is more correctly termed rhinosinusitis
2. Etiology :
1. Mor Common:
1. Rhinoviruses
2. Less common:
1. Coronaviruses
2. Respiratory syncytial viruses
3. Human metapneumovirus
3. Occasional:
1. Influenza viruses
2. Parainfluenza viruses
3. Adenoviruses
4. Enteroviruses
3. EPIDEMIOLOGY
1. Rhinovirus infection : August October & AprilMay
4. Age
a. Young children have an average of 68 colds per year but 1015% of
children have at least 12 infections per year.
b. Minimum 3/year as per ARI (WHO) program
5. Attack rate is 100%
6. PATHOGENESIS
1. Infection of the nasal epithelium is associated with an acute
inflammatory response characterized by release of a variety of
inflammatory cytokines and infiltration of the mucosa by inflammatory
cells.
2. Inflammation can obstruct the sinus ostium or eustachian tube and
predispose to bacterial sinusitis or otitis media
7. CLINICAL MANIFESTATIONS
1. The onset of common cold symptoms typically occurs 13 days after
viral infection.
2. The 1st symptom noted is frequently:
a. Sore or scratchy throat,
b. Nasal obstruction
c. Rhinorrhea.
3. The sore throat usually resolves quickly and, by the 2nd and 3rd day of
illness, nasal symptoms predominate.
4. The usual cold persists for about 1 wk, although 10% last for 2 wk
8. The physical findings
1. Increased nasal secretion is frequently obvious to the examiner.

9.

2. A change in the color or consistency of the secretions is common

3. Examination of the nasal cavity may reveal swollen, erythematous
nasal turbinates,
Diagnosis and DD
CONDITION
Allergic rhinitis

DIFFERENTIATING FEATURES
Prominent itching and sneezing; Nasal eosinophils
Unilateral, foul-smelling secretions; Bloody nasal
Foreign body
secretions
Presence of fever, headache or facial pain, or
Sinusitis
periorbital edema or persistence of rhinorrhea or
cough for >14 days
Streptococcosis Nasal discharge that excoriates the nares
Pertussis
persistent or severe cough with woop
8. LABORATORY FINDINGS
1) Routine laboratory studies are not necessary for the diagnosis
2) A nasal smear for eosinophils for allergic rhinitis
3) Polymorphonuclear leukocytes in the nasal do not indicate bacterial
superinfection.
4) The viral pathogens associated with the common cold can be detected
by culture, antigen detection, polymerase chain reaction (PCR), or
serologic methods.
5) Bacterial cultures or antigen detection are useful only when:
a. group A streptococcus,
b. Bordetella pertussis
c. Nasal diphtheria is suspected.
6) The isolation of other bacterial pathogens is not an indication of
bacterial nasal infection and is not a specific predictor of the etiologic
agent in sinusitis
9. TREATMENT
1. The management of the common cold consists primarily of
symptomatic treatment.
2. Antiviral Treatment.
a. Specific antiviral therapy is not available for rhinovirus
b. Ribavirin is approved for treatment of RSV infections
c. The neuraminidase inhibitors oseltamivir and zanamivir have a
modest effect on influenza viral infections
d. pleconaril for treatment of rhinovirus infections is under
evaluation
3. Antibacterial therapy is of no benefit in the treatment of the common
cold.
10. Symptomatic Treatment
1. Fever is infrequently associated with an uncomplicated common cold and
antipyretic treatment is generally not indicated.
2. NASAL OBSTRUCTION.
1. xylometazoline, oxymetazoline, or phenylephrine are
available as either intranasal drops or nasal sprays

2. They are not approved for use in children <2 yr old.

3. RHINORRHEA.
1. The first-generation antihistamines reduce rhinorrhea by 25
30%.
2. Rhinorrhea can also be treated with ipratropium bromide,
4. SORE THROAT.
1. The sore throat is treated with mild analgesics
2. Aspirin should not be given to children with respiratory infections
because of the risk of Reye syndrome
5. COUGH
1. Cough suppression is generally not necessary
2. For cough due to postnasal drip, treatment with a first-generation
antihistamine may be helpful.
6. Ineffective Treatments
Vitamin C, guaifenesin, and inhalation of warm, humidified air
Zinc
Echinacea a popular herbal treatment
11. COMPLICATIONS
1. Otitis media: in 530% of children and treatment with oseltamivir may
reduce the incidence of otitis media in patients with influenza.
2. Sinusitis: fever, facial pain, or facial swelling develop
3. Exacerbation of asthma
4. Inappropriate use of antibiotics leads to increasing antibiotic resistance
of pathogenic respiratory bacteria.
12. Prevention
1. Chemoprophylaxis or immunoprophylaxis is generally not available for
the common cold.
2. Immunization or chemoprophylaxis against influenza may be useful
3. Vitamin c and echinacea do not prevent the common cold.
4. Isolation: interrupting the chain involved in the spread of virus by direct
contact may prevent colds.
5. Personnel wearing protective face shields to prevent hand-to-eye or
hand-to-nose contact.
6. Good handwashing by the infected individual and/or the susceptible
contact.
WHO CLASSIFICATION OF ARI

Definitions:
Acute respiratory tract infection: infection of R.S for less than 14 days and
that of middle ear less tha 4 weeks

Classification:
I.

No pneumonia:

II.

III.

IV.

a. Normal breathing
Pneumonia:
a. Increased respiratory rate:
i. > 60 infants
ii. > 50 2-12 months
iii. > 40 1-5 years
Severe Pneumonia:
a. Chest retraction
b. Grunting
c. Stridor
Severe disease:
a. Cyanosis
b. Unconsciousness
c. convulsions

Treatment of no pneumonia: Home care: by Mother

a. Treats fever with paracetamol
b. Gives more fluid
c. Gives more food than usual
d. Continues breastfeeding
e. Whicks the nostrils for nasal obstruction
f.

Gives home remedies for cough: Honey, Tulsi, ginger extracts

g. Watches for fast breathing and report to health facility

Treatment mild pneumonia: by health worker
a. Continue mother care as above
b. Give co trimoxazloe for 2 days and review
c. If child improves continue co tri for next 3 days
d. If the child remains in the same state give co trimoxazloe for 2 days
and review
e. If the child has developed severe pneumonia refer to hospital

(Severe)PENEUMONIA IN CHILDREN

Definition:
Pneumonia:
Inflammation of parenchyma of lungs; often focal involving some
lobes
Bronchopneumonia:
Acute inflammation of the walls of the bronchioles with
peribronchial inflammation of lung parenchyma; bilateral and
symmetrical involvement
Epidemiology: 19% of under 5 deaths are due to pneumonia
Etiology of Pneumonias:
1. Infection: viral, bacterial, fungal, parasitic
2. Aspiration: food; gastric juice
3. Foreign body bronchus
4. Hydrocarbons: kerosene ingestion
5. Lipoid substance: oil baths and nasal instillation of oil
6. Hypersensitivity : airy and grain products, animal dander and protein
7. Drugs: anticancer drugs like methotrexate
8. Radiation: x ray treatment for cancers
Leading Etiologic Agents of Pneumonia Infants and Children: Common
pathogens:

Age

Neonate

Bacterial pathogens

Viral Pathogens

Group B Streptocaccus

RSV

Gram-negative bacilli

Herpes simplex virus

( E.coli, K.pneumoniae,
Proteus sp, others)

CMV

Other

S.aureus

Adenovirus

S.pneumoniae
1-3 mo.

RSV

C.trachomatis

H.Infuenzae type b

Parainflenza virus1 and 3,

4 mo.-5
yrs

S.pneumoniae
Adenovirus
H.Influenzae type b
Influenza viruses A and B

5 yrs and
older

M.pneumoniae
S.pneumoniae
C.pneumoniae

1. Pathogensis:
Viral invasion Surface defense knocked down altered secretions
bacterial invasion Inflammation consolidation
2. Pathology
Specific to pathogens
Streptococcus peumoniae:

Focal often lobar pneumonia

G.A. Streptococcus:

Diffuse often involves pleura

Staphylococcus:
necrosis; cavitation;

Unilateral; extensive; hemorrhagic

Pneumatoceles; empyema
Mycoplasma:
shadow

Patchy; edema; airway obstruction; coin

3. Clinical features:
1. Starts as upper respiratory catarrh

2. Fever
3. Chills
4. Tachypnoea
5. Grunt
6. Cyanosis
7. Chest retraction
8. Working of accessory muscles of respiration
9. Crackles and wheeze
10.Restlessness
11.Delirium
12.Pleuritic pain
4. Additional symptos in Infants :
1. Diarrhea
2. Vomiting
3. Abdominal distension
4. Incessant cry
5. Diagnosis:
Lab:
TC normal in viral increased in bacterial
Lymphocytosis in viral
CRP increased
ESR increased
CXR:
1. Sun ray appearance

2. Airbronchogram
3. Lobar consolidation
4. Perbronchial cuffing
5. Silhouette sign
6. Treatment
Amoxicillin: high doses of amoxicillin (8090 mg/kg/24 hr)
Cloxacillin: 50 to 100 mg/kg/day orally divided every 6 hours.
Cefuroxim axitil: Parenteral cefuroxime (150 mg/kg/24 hr),
Azithrocyn
Levofloxacin
Gatrifloxacin
Aminoglycosides
7. Causes of Poor response:

Antibiotic resistance

Viral

Aspiration

Immunodeficiency

Cystic fibrosis
8. Complications

Septicemia

Meningitis

Osteomyelitis

Metastasis

Empyema

Death due to sepsis; resp.failure and other complications

STAPHYLOCOCCAL PNEUMONIA:

Viurlance of S.aureus:
1. Staphylococcus aureus is coagulase positive and has many virulence
factors that mediate various serious diseases. Eg:
a.

Coagulase causes plasma to clot by interacting with fibrinogen;

produce abscess formation

b.

Panton-Valentine leukocidin (PVL) is an exotoxin causes leukocyte

destruction and tissue necrosis

c. Protein A, preventing opsonins and thus inhibiting phagocytosis.

d. loose polysaccharide capsule interferes with opsonophagocytosis.
e. Catalase: inactivates hydrogen peroxide, promoting intracellular
survival of pathogens.
f.

toxin and -hemolysin that cause local tissue destruction.

g. B-lactamase which inactivates most penicillins

h. Methycillin resistant staphylococcus aureus (MRSA) are becoming
more prevalent
2. S. aureus is an important pathogen of pneumonia in patients with cystic
fibrosis
Features of Staph Pneumonia:
1. Staph pneumonia can occur both as community acquired and hospital
acquired infections and also ventilator associated pneumonia
2. Clinical features:
1. Infants:
a. Abdominal distention, high fever, respiratory distress, and
toxemia.
b. produce Pneumatoceles, pyopneumothorax, and empyema
c. Rapid progression of disease and death
2. Older children:
a. More common are high fever, abdominal pain, tachypnea,
dyspnea, and localized or diffuse bronchopneumonia or lobar
disease.
b. S. aureus often causes a necrotizing pneumonitis;

c. Empyema, pneumatoceles, pyopneumothorax, and

bronchopleural fistulas develop frequently.
3. Symptoms:
1. Starts as upper respiratory catarrh
2. Fever
3. Chills
4. Restlessness
5. Delirium
6. Pleuritic pain
4. Signs:
1. Tachypnoea
2. Grunt
3. Cyanosis
4. Chest retraction
5. Working of accessory muscles of respiration
6. Crackles and wheeze;
7. bronchial breathing
Complications:
1. Pneumatocoel formation
2. Pyopneumothorax
3. Bronchopulmonary fistulas
4. Lung abscess
5. Septicemia
6. Meningitis
7. Osteomyelitis

8. Metastasis
9. Empyema
10.pyopericardium
11.Death due to sepsis; &
12.Resp.failure
Diagnosis:
Staphylococcal pneumonia can be suspected on the basis of chest
roentgenograms that may reveal pneumatoceles, pyopneumothorax, or
lung abscess.
Treatment:
1. Antibiotic choice is decided by culture -sensitivity patterns
2. Drugs: Empiric therapy
i. Community acquired staph pneumonia:
1. Co Trimoxazole: 8-12 (TMP) mg/kg/day
2. Clindamycin: 20-30 mg/kg/day
ii. Methicillin sensitive Staph aureus:
1. Penicillinase resistant antibiotics such as:
a. Oxacillin
doses

} 100-150 mg /kg/day/IV in 4 divided

b. Nafcillin

c. Methicillin: 200-300 mg /kg/day/IV in 4 divided

doses
2. Cephalosporins:
a. Cefazolin:
doses

100-150 mg /kg/day/IV in 4 divided

b. Cephalexin: 50-100 mg /kg/day/orally in 4 divided

doses

iii. For methicillin resistant staph. aureus:

a. Vancomycin: 40 mg mg /kg/day/IV in 4 divided
doses
b. Linozolid is a recent drug
c. Rifampin may be added to vancomycin tharpy
3. Othyer measures:
i. Inter costal drainage of empyema
ii. Fresh blood transfusion

CROUP (ACUTE LARYNGOTRACHEOBRONCHITIS).

1. Croup syndrome is another name for acute laryngotracheo bronchitis,
inflammation mainly glottis and subglottic region and it produces brassy
cough and hoarse voice; laryngitis may cause life threatening airway
obstruction.
2. Etiology:
a. Viruses:
i. The parainfluenza viruses (types 1, 2, and 3) account for
approximately 75% of cases;
ii. Other viruses associated with this disease include influenza A
and B, adenovirus, respiratory syncytial virus (RSV), and
measles.
b. Spasmodic croup occurs most often in children 1-3 yr of age and is
clinically similar to acute laryngotracheobronchitis, except that the
history of a viral prodrome and fever in the patient and family are
frequently absent. The cause is viral in some cases, but allergic and
psychological factors may be important in others
c. Epidemiology:
i. Most patients with croup are between the ages of 3 mo and 5 yr,
with the peak in the second year of life.
ii. Higher in males,
iii. Most common during winter
iv. Approximately 15% of patients have a strong family history of
croup
c. Clinical features:
i. An upper respiratory tract infection with some combination of
rhinorrhea, pharyngitis, mild cough, and low-grade fever for 1 to
3 days before the signs and symptoms of upper airway
obstruction become apparent.
ii. The child then develops the characteristic "barking" cough,
hoarseness, and inspiratory stridor.

d.

e.

f.

g.

h.

iii. The low-grade fever may persist, although temperatures may

reach 39-40C (102.2-104F); some children are afebrile.
iv. Symptoms are characteristically worse at night and often recur
with decreasing intensity for several days and resolve
completely within a week.
v. Agitation and crying greatly aggravate the symptoms and signs.
vi. The child may prefer to sit up in bed or be held upright.
vii. Older children usually are not seriously ill.
Physical examination:
i. hoarse voice, coryza, slightly increased respiratory rate.
ii. On progression: increasing respiratory rate; nasal flaring;
suprasternal, infrasternal, and intercostal retractions; and
continuous stridor.
iii. The child may hypoxic, cyanotic, pale, or obtunded
Investigations:
i. Croup is a clinical diagnosis and does not require a radiograph of
the neck.
ii. Radiographs of the neck may show the typical subglottic
narrowing or "steeple sign" of croup on the posteroanterior view
Differential Diagnosis:
i. Diphtheritic croup
ii. Aspiration of a foreign body
iii. Retropharyngeal or peritonsillar abscess
iv. Angioedema of the subglottic areas
v. Hypocalcemic tetany,
Complications:
i. Pneumonia, cervical lymphadenitis, otitis media, or, rarely,
meningitis or septic arthritis may occur during the course of
epiglottitis.
Treatment:
i. The mainstay of treatment is airway management.
ii. provide cool mist through a tube held in front of the patient by
the parent: It moistens airway secretions to facilitate clearance,
iii. nebulized epinephrine:
A dose of 0.25 to 0.75 mL of 2.25% racemic epinephrine in 3 mL
of normal saline can be nebulized as often as every 20 min.
iv. Corticosteroids:
1. Decrease the edema in the laryngeal mucosa through
their anti-inflammatory action.
2. Dexamethasone used a single dose of 0.6 mg/kgIM
v. Antibiotics: are not indicated in croup.
vi. helium-oxygen mixture (Heliox) have shown clinical
vii. should be hospitalized progressive stridor

ACUTE EPIGLOTITIS
1. Epiglottitis is an infection of the epiglottis and supraglottic structures
2. Etilogy:
a. In the past, Haemophilus influenzae type b was the most commonly
identified etiology of acute epiglottitis.
b. After HiB vaccine invasive disease due to H. influenzae type b in
pediatric patients has been reduced

3.
4.

5.

3.

4.

5.

6.

c. Therefore, other agents, such as Streptococcus pyogenes, S.

pneumoniae, and Staphylococcus aureus, now represent a larger
proportion of pediatric cases of epiglottitis.
Age:
a. 2-4 yr of age,
Clinical features:
a. This is a dramatic, potentially lethal condition
b. High fever, sore throat, dyspnea, and rapidly progressing respiratory
obstruction.
c. Drooling is present and the neck is hyperextended in an attempt to
maintain the airway.
d. The child may assume the tripod position
e. Restlessness may be followed by rapidly increasing cyanosis and coma.
f. Stridor is a late finding and suggests near-complete airway obstruction.
g. The barking cough typical of croup is rare.
The diagnosis:
1. Visualization of a large, "cherry-red" swollen epiglottis by laryngoscopy.
2. Classic radiographs of a child who has epiglottitis show the "thumb
sign"
Management:
a. Establishing an airway by nasotracheal intubation or, less often, by
tracheostomy is indicated urgently.
b. The duration of intubation depends on the clinical course probably 2-3
days
c. Pneumonia, cervical adenopathy, or otitis media, Meningitis, arthritis
are rarely found in conjunction with epiglottitis.
Drugs:
a. Racemic epinephrine and corticosteroids are ineffective.
b. Cultures of blood, epiglottic surface, and, in selected cases,
cerebrospinal fluid, should be collected at the time of airway
stabilization.
c. Ceftriaxone, cefotaxime, or a combination of ampicillin and sulbactam
should be given parenterally pending culture
d. Epiglottitis resolves after a few days of antibiotics, and the patient may
be extubated; antibiotics should be continued for 7-10 days.
e. Rifampin prophylaxis (20 mg/kg orally once a day for 4 days;) should
be given to all household members
Prevention:
a. HiB vaccine is routinely given with DPT at 6,12,16 weeks and a booster
at 18 months
Prognosis:
a. Untreated epiglottitis has a mortality rate of 6% in some series,

Common causes of acute respiratoly distress in a 2 years old child:

1. Respiratory system:
a. epiglottitis,
b. retropharyngeal abscess,
c. peritonsillar abscess,
d. croup,
e. tracheitis,
f. bronchiolitis,

2.

3.

4.

5.
6.
7.
8.

g. pneumonia
h. Asthma
i. Anaphylaxis
j. Foreign Body
CVS:
a. Heart failure,
b. Pericarditis,
c. Myocarditis,
d. Cardiac tamponade
Nervous system
a. Depressed ventilation (ingestion, injury, infection),
b. Hypotonia,
c. Loss of protective reflexes
GIT:
a. GER,
b. Aspiration,
c. Abdominal distention
Metabolic/Endocrine:
a. Diabetic Keto Acidosis,
b. Sepsis
Hematology:
a. Severe anemia,
b. Methemoglobinemia
Trauma to chest wall
Inhalation injury: toxic gases
PLEURISY

Pleura
1. The pleura is a two layered sac that holds the lungs and separates them
from the chest wall, diaphragm, and heart.
2. The pleura that lines the inside of the chest is called the parietal pleura.
3. The pleura that covers the lungs is called the visceral pleura.
4. The pleura is separated by a thin layer of fluid. This lets the lungs expand
and contract easily during breathing.
5. Pleural cavity has negative pressure that helps in inspiration
Pleurisy
1. Inflammation of pleura
2. Inflammatory process is divided into 3 types:
1. Dry or plastic
2. Serofibrinous or serosanguinous
3. Purulent
Dry or Plastic pleurisy
Etiology
1. Bacterial
2. Viral
3. Tuberculous
4. Connective tissue: Rheumatic fever
Pathology
1. Pathology is usually limited to visceral pleura

2. Small amounts of yellow serous fluid collection

3. Adhesions between pleural surfacces
4. Deposition of fibrin in the space
5. Fibrothorax
Clinical manifestations
1. Stabbing Pain exaggerated by deep breathing, coughing and straining
2. It is a dull aching pain in some
3. Localized over the chest and also referred to shoulder or back
4. Grunting and guarding of respiration
5. Child lies on affected side to reduce respiratory movement
6. Audible friction rub may be present
7. Dull percussion note
8. There may be no symptoms in some cases; seen only CXR as haziness
DD
1. Epidemic pleurodynia: Bornholm disease; Coxsackie B
2. Trauma to the rib cage
3. Lesions of dorsal root ganglia
4. Tumors of spinal cord
5. Herpes zoster
6. Gall bladder disease
7. Trichinosis : Infection with the roundworm Trichinella spiralis. Fever;
Muscle pain with breathing, chewing, or using large muscles
8. Tuberculosis
Treatment
1. Treat primary cause
2. Immobilize the chest with adhesive plaster
3. Suppress cough
4. Analgesia with NSAID
SEROFIBRINOUS PLEURISY (EFFUSION)
Etiology:
1. Lung infections
2. Inflammatory bowel disease
3. SLE
4. Periarteritis
5. Rheumatic fever
6. Neoplasm
Clinical manifestations
1. As fluid accumulate pain may disappear
2. Large fluid collection leads to cough, dyspnea, retraction, tachypnea,
orthopnea and cyanosis
3. Signs:
1. Dull percussion note
2. Decrease of breath sounds
3. Diminished tactile fremitus
4. Mdiastinal push to opposite side

5.
6.
7.
8.
9.

Intercostal fullness
Rales and ronchi due to lung infection
Bronchial breathing
Friction rubs
Shifting dulness

Work up
1. CXR:
1. Homogeneous density
2. Absent lung markings
3. Absent air bronchogram
4. Obliteration of costo and cardio phrenic angles
5. Widening of interlobar septa
2. Ultrasonography
3. Diagnostic pleural tap:
1. Increase in protein; minimal leukocytosis; increase in LDH
2. AFB and gram stain
DD
1. Hydrothorax
2. Chylothorax
3. Hemorrahge
4. Pyothorax
5. Pleural thickening
Complications
1. Fluid may resolve with treatment of pneumonia
2. May turn purulent if untreated
3. Adhesions may develop between pleural layers
4. Pleural thickening may develop
5. Usual to resolve completely over time
Treatment
1. Treat underlying disease
2. Drain large collection; rapid draining may produce re expansion pulmonary
edema
3. Chest tube for re accumulation
4. Indication for thoracostomy: pleural fluid has:
1. pH < 7.2
2. Glucose < 50 mg/dL
3. Purulent fluid
PURULENT PLEURISY OR EMPYEMA
Definition: accumulation of pus in pleural space
Etiology:
1. Pneumonia: Strepto, staphylo, Pneumo
2. Rupture of lung abscess
3. Thoracic surgery
4. Extension of mediastinitis
5. Extension of intra abdominal abscess

Epidemiology:
5-10% bacterial pneumonia may develop empyema
Pathology
3 stages:
1. Exudative: fibrinous exudate forms on the pleural surface
2. Fibrinopurulent: fibrinous septae forms loculations of fluid and
thickening of parietal pleura
3. Organizational stage: fibroblast proliferation and thickening of
pleura; lung collapse
4. Clinical manifestations
1. Presents as bacterial pneumonia
2. High fever and chills
3. Respiratory distress
4. Toxemia
5. Frontal sweating
Work up
1. CXR
2. CT scan
3. Ultrasound
4. Thoracentesis :
1. gram stain and culture
2. pH < 7.2
3. >10 000 wbcs
5. High ESR
6. Leukocytosis
Complications
1. Bronchopleural fistula pyopneumothorax
2. Pyopericardium
3. Lung abscess
4. Peritonitis
5. Rib osteomyelitis
6. Rupture into subcutis
7. Meningitis
8. Orthritis
9. Osteomyelitis
10.Septicemia
11.Pleural thickening persistent fever
Treatment
1. Thoracenetsis
2. Chest tube drainage- fibrinolytics (strptokinase)
3. Antibiotics- 3-4 weeks
4. Decortication through video assisted thoracoscopy
PNEUMOTHORAX
1. Definition: accumulation of extrapulmonary air within the chest
2. Most often it is due to leakage of air from lung

3. Not so common in childhood

4. Types :
1. Primary spontaneous
2. Secondary spontaneous
3. Traumatic
4. Iatrogenic
5. Catamenial
Primary
Eetiology
1. Pneumonia : high in staph pneumonia
2. Bronchiolitis
3. Tuberculosis
4. Cystic fibrosis
5. Lung abscess
6. Pulmonary infarct
7. Rupture of cyst
8. Rupture of emphysematous bleb (asthma)
9. Foreign body in lung
10.Lymphoma
Secondary
Etiology
1. Traumatic:
1. Penetrating injury
2. Blunt trauma
3. Loud music
2. Iatrogenic:
1. Thoracotomy
2. Tracheostomy
3. Needle punctutre
4. Mechanical ventilation
5. Resuscitation
3. Catamenial: during menstruation
Pathophysiology
1. Air in pleural space abolishes negative pressure
2. Lung collapses upto 30%
3. In tension pneumothorax:
1. mediastinal shift
2. Decreased venous return
3. Decreased cardiac output
4. Hypoxemia
Clinical manifestations
1. Abrupt onset of symptoms
2. Dyspnea, chest pain, cyanosis
3. Chest retraction
4. Signs:
1. Decreased breath sounds
2. Tympanitic percussion note

3. Tracheal shift
DD
1. Diaphragmatic hernia
2. Emphysema
3. Large cyst or cavity
4. Compensatory expansion
5. Distended stomach
Treatment
1. Tension pneumothorax: emergency needle thoracostomy
2. Small and medium pneumothorax may resolve spontaneously
3. 100% O2 helps resolution
4. For collapse lung: chest tube drainage
5. Chemical pleurodesis (doxycyclin in pleural space)
6. Thoracoscopic blebectomy
Intercostal drainage with under water seal:
1. 4th or 5th intercostal space; between the mid- to anterior axillary line
2. 2nd intercostal space at mid-clavicular line
FOREIGN BODY ASPIRATION
1. Children younger than 3 yr of age account for 73% of cases.
2. One third of aspirated objects are nuts, particularly peanuts.
3. CLINICAL MANIFESTATIONS:
1. Initial event: Stage I
1. Violent paroxysms of coughing, choking, gagging, and airway
obstruction occur immediately when the foreign body is aspirated.
2. Asymptomatic interval: stage II
1. The foreign body becomes lodged and the immediate irritating
symptoms subside.
2. This stage accounts for a delayed diagnoses and overlooked foreign
bodies.
3. Complications: Satge III
1. Obstruction or infection develops
2. Complications include fever, cough, hemoptysis, pneumonia, and
atelectasis.
4. Symptoms:
a. Acute:
1. Respiratory distress-with stridor; leaning chin forward and
drooling.
2. Inability to speak or cough.
3. Partial obstruction: Violent paroxysms of coughing, and
wheezing.
5. Laryngial FB:
b. Complete obstruction asphyxiates the child unless promptly
relieved with the Heimlich maneuver.
6. Tracheal foreign bodies:
1.
Produce stridor and wheezing.
7. Bronchial foreign body:

1.

8. Acute
1.

2.

3.

4.

5.

6.

During expiration the bronchial foreign body

obstructs the exit of air from the obstructed lung, producing
obstructive emphysema
Management:
The current guidelines for pediatric basic life support recommend
that when airway obstruction from a foreign body is mild, no
intervention is required. The patient should be allowed to clear his
or her airway by coughing while the clinician watches for signs of
impending severe airway obstruction.
Blind finger sweeps should not be performed in infants or children
because the finger may actually push the foreign body further into
the airway
Step I: Jaw Thrust
1. The airway may be opened by jaw thrust, and if the foreign
body can be directly visualized, it should be removed;
2. If the patient resumes adequate spontaneous ventilation, the
patient's body is turned on its side to the recovery position
with the head to the side (if in the field).
Step II: Back flow and chest thrust
1. In the infant younger than 1 yr, a combination of five back
blows and five chest thrusts are administered. The foreign
body is removed if it is seen.
Step III:
1. A conscious child older than 1 yr is administered a series of
five abdominal thrusts (the Heimlich maneuver) with the child
standing or sitting.
2. If unconscious, this is done with the child lying down.
3. After the abdominal thrusts, the airway is examined for a
foreign body, which should be removed if visualized.
Step IV:
1. When the airway is obstructed and foreign body could not be
removed needle cricothyrotomy is indicated
2. For foreign body bronchus, child should be treated by
bronchoscopic removal of foreign body under anaesthesia.
WHEEZE IN CHILDREN

1.
Definition:
a. Wheezing is a high-pitched whistling sound made while breathing,
usually during expiration;
b. Factors producing wheeze: Bronchospam, mucosal edema and
secretions
2. Causes of wheeze
a. Wheeze from birth:
i. Congenital Tracheo bronchomalacia
ii. Congenital Bronchial stenosis
iii. Vascular rings
iv. CHD with Lt to Rt shunt
b. Isolated episode: Bronchiolitis
c. Persistent wheeze from 1 year:

3.

4.

5.

6.

7.

i. Cystic fibrosis
d. Recurrent wheeze:
i. Asthma
e. Sudden onset of severe wheeze in a healthy child:
i. Foreign body
Congenital Bronchial stenosis:
a. Rare
b. Focal bronchomalacia
c. Persistant wheeze from early chilhood
d. persistent dyspnoea and cyanosis after birth
e. Stenting or surgery
Tracheo broncheomalacia:
1. Male : female = 2 : 1
2. Insufficient cartilage
3. Dynamic collapse; >50 reduction of tracheal diameter during
expiration
4. Low pitched monophonic wheeze
5. Good prognosis
6. Associated anomalies: TEF
7. Improves over 3 yrs of age
Vascular rings
1. Double aortic arc
2. Right aortic arch with liganetum arteriosum
3. Aberrant innominate artery
4. Anomalous left pulmonary artery
5. Compression of trachea and esophagus
6. Wheeze from childhood;
7. Aggravated by crying, feeding and neck flexion
8. Diagnosis by barium swallow
9. Surgical correction
CVS causes compressing or narrowing bronchus:
1. Cardiomegaly
2. Left atrial enlargement,
3. Dilated pulmonary artery
4. Pulmonary edema
Foreign body LRT
1. Sudden onset
2. h/o chocking
3. Chronic cough
4. Persistent wheezing localized to one side
5. Recurrent pneumonia
6. CXR: pendulum sign in fluroscopy
7. Treatment: Bronchoscopy
8. BRONCHIOLITIS

Introduction:

1. Bronchiolitis is the most common serious acute respiratory illness in

infants and young children.
2. The diagnosis of bronchiolitis is based upon clinical findings including
an upper respiratory infection that has progressed to cough,
tachypnea, respiratory distress.
Etiology:
i. Respiratory syncytial virus (RSV) is responsible for >50% of cases.
ii. Other agents include parainfluenza, adenovirus, Mycoplasma; Human
metapneumovirus can occur as a co-infection with RSV.
iii. There is no evidence of a bacterial cause for bronchiolitis.
Epidemiology:
1.

Common among children <1 yr old

2. Bronchiolitis is more common in males, in those who have not been

breast-fed, and in those who live in crowded conditions.
Pathology:
1.

Eosinophils degranulate and release eosinophil cationic protein, which is

cytotoxic to airway epithelium.

2. Immunoglobulin E (IgE) antibody release may also be related to wheezing.

3. Other mediators such as interleukin 8 (IL-8) are also involved.
Clinical features:
1. The infant 1st develops a mild upper respiratory tract infection with
sneezing and clear rhinorrhea.
2. Fever of 38.539C
3. Incessant cry and poor feeding
4. Air trapping and overinflation.
5. Child may develop atelectasis.
6. Hypoxemia
7. The infant is often tachypneic, which may interfere with feeding.

8. No secondary bacterial infection.

The physical examination:
1. It is characterized most prominently by wheezing.
2. Nasal flaring and retractions.
3. Auscultation: fine crackles or overt wheezes, with prolongation of the
expiratory phase of breathing.
4. Barely audible breath sounds suggest very severe disease
5. Hyperinflation of the lungs may permit palpation of the liver and spleen.
X Ray:
In acute bronchiolitis, chest radiography reveals hyperinflated lungs
with patchy atelectasis.
Bow sign
Lab:
1. The white blood cell and differential counts are usually normal.
2.

The diagnosis is clinical

Management:
1. If hypoxemic, the child should receive cool humidified oxygen.
2. Sedatives are to be avoided because they may depress respiratory drive.
3. Frequent suctioning of nasal and oral secretions often provides relief of
distress or cyanosis.
4. Oxygen is indicated in all infants with hypoxia.
5. Nebulized epinephrine may be more effective than -agonists. A trial dose
of inhaled bronchodilator may be reasonable, with further therapy
predicated on response in the individual patient.
6. Nebulization with 3% NaCl has been found to be effective.
7. Corticosteroids are not recommended in previously healthy infants with
RSV.
8. Ribavirin, an antiviral agent administered by aerosol, has been used for
infants with congenital heart disease or chronic lung disease.
9. Antibiotics have no value unless there is secondary bacterial pneumonia.
10.Likewise, there is no support for RSV immunoglobulin administration

PROGNOSIS:
1. The case fatality rate is <1%, with death attributable to apnea,
uncompensated respiratory acidosis, or severe dehydration.
2. Infants with conditions such as congenital heart disease,
bronchopulmonary dysplasia, and immunodeficiency often have more
severe disease, with higher morbidity and mortality.
3. There is a higher incidence of asthma in children with a history of
bronchiolitis
PREVENTION:
1. Reduction in the severity and incidence of acute bronchiolitis due to
RSV is possible through the administration of pooled hyperimmune RSV
intravenous immunoglobulin before and during RSV season.
2. Meticulous handwashing is the best measure to prevent nosocomial
transmission.

1.
2.
3.
4.
5.
6.
7.
8.
9.

9. ACUTE BRONCHITIS SYNDROME

Viral origin;
Bacterial infection may supervene
More in winter
Fever malaise
Purulent sputum
Minimal wheeze
Severe wheeze is termed asthmatic bronchitis
Severe cough
Recovery over 1-2 weeks

10. CYSTIC FIBROSIS:

1. Inherited multisystem disorder; autosomal recessive
2. CF, an autosomal recessive disease, results in a syndrome of chronic
sinopulmonary infections, malabsorption, and nutritional abnormalities
3. Gene defect causes problems in salt and water movement across cell
membranes, resulting in abnormally thick secretions in various organ
systems and critically altering host defense in the lung.Chloride is not
secreted and hence water not transported; mucous secretions are thick
and tenacious ; obstructs air ways; mucus defect leads to respiratory
infection.
4. Chloride is not reabsorbed from sweat; seat chloride level is increased.
5. Pulmonary: cough,chronic bronchitis and recurrent pneumonias; Persistent
wheeze from 1 year
6. Gastrointestinal manifestations: meconium ileus in neonate; malabsorption
in older children
7. Liver: Dysfunction of epithelial surface; Biliary cirrhosis;
8. pancreas: hyperglycemia and glycosuria
9. More common in white population
10.Seat chloride greater than 60 mmol/L
11.Aerosol antibiotics and bronchodilators

11. BRONCHIAL ASTHMA

1. Chronic inflammatory airway disease
2. Airway hyper responsiveness to provocative exposures
3. Incidence: Boys 14%; Girls 10%; poor 16%
4. 80% get asthma before 6 years
Etiology: Br asthma results fro interplaynof 3 factors: genetic,biologic and
environmental
Genetic:
Multifacorial inheritance
Proallergic and proinflammatory gene clusters on chromosome 5
Biologic factors:
Younger age

Developing lung
airway responsiveness altered by infection in infancy
Environmental factors:
Exposure to tobacco smoke: mother or father
Viral infections in early childhood
Dust mites, animal dander, cockroaches and some molds
Food rarely provoke allergy
Exercise induced asthma
Aspirin induced asthma less common
Psychological exacerbation possible
High levels of cat allergens found to prevent asthma by inducing
Ig.G
Indoor and home allergens Cold air, ozone and strong odor produce
bronchospasm without inflammation
Types of childhood asthma
Acute asthma: triggered by viral infection only
Chronic asthma: due to allergy; persists to adulthood
Obese girl with early onset puberty developing asthma- produce
inflammatory mediators from adipose tissue plus reduced
pulmonary compliance
Pathology:
Shedding of epithelium
Mucosal edema and hypertrophy
Mucus plugs
Cellular infiltration
Hypertrophy of bronchial musculature
Increased goblet cells
Clinical manifestation:
Expiratory wheeze
Intermittent cough
Shortness of breath
Chest tightness
Chest pain
Nocturnal aggravation
Inaudible breath sounds or wheeze in severe cases

DD:
Sinusitis
Gastroesophegeal reflex
Tracheobronchomalacia
Foreign body aspiration
Tuberculosis
Cystic fibrosis
Ciliary dyskinesia
Meditational mass
Cardiomegaly
CCF
Diagnosis:
Peek flow meter: FEV1 recorded by 3 attempts ; highest taken; 220
L/mt normal for child

Bronchodilator response: imrovemnt by >12% or 200L/mt of FEV1

after therapy
CXR:
Hyperinflation of lung
Tubular heart
Flattening of diaphram
Peribronchial thickening
Birds wing sign
Treatment: step up step down approach:
Stepwise management of bronchial asthma.

1. Asthma is a chronic disease that varies over time, depending upon

each individuals circumstances. This means that the dosage of
medication used to control asthma must be monitored and sometimes
"stepped up" or "stepped down" to achieve asthma control and then
manage the symptoms.

2. Classification:
Step 1
Mild Intermittent

Step 2
Mild Persistent

Exacerbations are
brief
No activity
limitation
Symptoms < 2
times a
Week;

Activity may cause

exacerbations

Nocturnal
Symptoms < 2
times/month

> 2 times/month

Symptoms more than

2 times/week but less
than 1 time/day

1. Treatment: step up step down approach:

Step 3
Moderate
Persistent
May last days
Activity causes
exacerbations
Daily Symptoms
Exacerbations 2
or
more times a
week;
> 1 time/week

Step 4
Severe Persistent
Frequent
exacerbations
Limited physical
Activity
Continual
Symptoms

Frequent

Step 4: severe persistent:

1. Acute severe Asthma:
O 2 to maintain 90-95% saturation
Nebulization of salbutamol 3 doses at 20 mt interval
Nebulization of Ipratropium 0.5 to 1 ml every 20 mts 3
doses
IV methylprednisolone 1-2 mg/kg or hydrocotisone 1-2
mg/kg
IVF: 20 ml/kg Na Cl to treat shock
PMS 2/3 of requirement
2. Refractory asthma:
Aminophilline 5 mg/kg as infusion
Adrenalin .01 mg/kg/dose SC x 3 doses
IV Magnesium sulfate 25 mvereg/kg x 2 dose
Heliox ( Helium+ Oxygen)
Mechanical ventilation
3. Severe persistent asthma
a. High dose inhaled corticosteroid, 1000g/day
b. B2 agonist inhalation
c. + or - Oral prednisolone 2mg/kg
Step 3: moderate persistent
d. Medium dose inhaled corticosteroid, 500g/day
e. B2 agonist inhalation
Step 2: mild persistent:
f. Low dose inhaled corticosteroid, 300 g/day
g. Bronchodilators - sos
Step 1: mild intermittent:
B2 agonist inhalation or oral preparations
Refractory case:
Aminophilline 5 mg/kg as infusion
Adrenalin .01 mg/kg/dose SC x 3 doses
IV Magnesium sulfate 25 mg/kg x 2 dose
Heliox ( Helium+ Oxygen)
Mechanical ventilation
Prevention:
Family education
Avoid exposure to allergens
Avoid smoke
Exposure to microbes
Prolonged breast feeding
Nutrition

BRONCHIECTASIS:
Introduction:

Ren Laennec, inventor of the stethoscope, first described

bronchiectasis in 1819 while observing patients with tuberculosis and
the sequelae of pneumonia in the pre antibiotic era
Definition:
Irreversible abnormal dilatation of the bronchial tree; It represents the
end result of non specific and unrelated events
Types:
Bronchiectasis can be focal or diffuse.
Lung defense
Lower respiratory tract is sterile one
Immune defense is by:
leukocytes and Ig.A
Mucous coat
Ciliary clearance
Cough
Alterations in any above defences can lead to chronic suppurative lung
disease
Epidemiology

Decreasing incidence due to antibiotics and immunization Vit. A

prophylaxis
Male female ratio is 2:1
In developing countries, bronchiectasis is frequently encountered as
one of the sequelae of acute infection.
Causes:
A. Congenital causes:
1. Cystic fibrosis
2. Ciliary dyskinesia including Kartagener's syndrome
3. Immune deficiency syndromes
Immunoglobulin deficiency syndromes
White blood cell dysfunction
Complement deficiencies
6. Williams - Campbell syndrome: Absence of annular bronchial
cartilage
7. Marnier - Kuhn syndrome: Congenital tracheo bronchomegaly due to
connective tissue disorder; autosomal
8. Alpha 1 - antitrypsin deficiency:
9. Disorders of cilia- Ciliopathy Eg.
a) Primary ciliary dyskinesia:
b) Kartagener syndrome:
B. Acquired causes:
1. Infections: Pertusis; Measles; Tuberculosis; Pneumonia ; HIV
2. Foreignbody bronchus
3. Right middle lobe syndrome: Brock syndrome: Rt middle lobe
compression by hilar lymph nodes
4. Yellow nail syndrome: Pleural effusion, lymphedema and nail
discoloration
5. Rheumatoid arthritis
6. Inflammatory bowel disease
7. Youngs syndrome (secondary ciliary dyskinesia)
Pathogenesis:

Typically, bronchiectasis causes widening of medium-sized airways by 3

mechanisms
1. Obstruction:
}
2. Infection
}
vicious cycle
3. Inflammation
}
The above mechanisms lead to:
1. Alteration in the pulmonary defense mechanisms,
2. Bacterial colonization
3. Endogenous nitric oxide production: reacts with superoxide
anion, to form a highly cytotoxic compound thjat affects the
bronchial epithelium
Pathology:
Stages of Bronchiectasis:
Prebronchiectasis: Endobronchial infection and inflammation
Reversible bronchiectasis: seen only in HRCT: reversible stage
Established bronchiectasis: No resolution
Three important pathological types are:
1. Cylindrical bronchiectasis: is characterized by uniform dilatation of
bronchi
2. Varicose bronchiectasis: is characterized by irregular and beaded
outline of bronchi, with alternating areas of constriction and
dilatation.
3. Cystic or saccular bronchiectasis: is the most severe form of the
disease. The bronchi dilate, forming large cysts, which are usually
filled with air and fluid.
Microbiology of Bronchiectasis: The most commonly found
microorganisms are:
a) Hemophilus influenza (55%), followed by
b) Pseudomonas sp (26%) and
c) Streptococcus pneumonia (12%).
d) 30% of isolates are resistant to antibiotics
e) Patients infected with P. aeruginosa have greater extent of
bronchiectasis and worse lung function.
Clinical features:
1. Persistent or intermittent, sputum production; sputum could be mucoid,
mucopurulent or viscous
2. Cough more in the morning
3. Foul smelling breath
4. Hemoptysis may range from minor, to life threatening conditions
5. Fever, loss of appetite and shortness of breath
6. Some patients have pleuritic chest pain
7. Poor weight gain
8. Late stage: Cor pulmonale
9. Signs:
a) variable degrees of crackles or coarse rhonchi
b) Leathery rales
c) Clubbing of digits: Clubbing develops in five steps:
1. Fluctuation and softening of the nail bed (increased
ballotability)

2. Loss of the normal <165 angle (Lovibond angle) between

the nailbed and the fold (cuticula)
3. Increased convexity of the nail fold
4. Thickening of the whole distal finger (resembling a drumstick)
5. Shiny aspect and striation of the nail and skin
Diagnostic Testing:
a) CXR:
Hyperinflation, tram tracks, increased linear markings, focal
pneumonitis, ring shadows and atelectasis.
Honey comb pattern
b) High-resolution CT scan:
tram-track lines
ring shadows signet ring; tree in bud
Cysts (grapelike clusters)
Bronchiectasis sica or 'dry' bronchiectasis:
a) Recurrent dry cough associated with intermittent episodes of
haemoptysis.
b) The haemoptysis can be life threatening
c) There is usually a past history of granulomatous infection, particularly
tuberculosis.
d) The upper lobes are often primarily affected, allowing good drainage.
Lab. work up:
a) Sweat chloride test >60 mm/L are abnormal
b) Ciliary beat frequency, using high-speed digital video photography. This
requires a biopsy taken from nasal epithelium
c) Measurement of nasal nitric oxide which is low primary ciliary
dyskinesia
d) Bronchoscopy to exclude foreign body and any endobronchial lesion
Treatment:
a) Bronchopulmonary hygiene:
Physical therapy:
1. Postural drainage,
2. Chest percussion,
3. Forced exhalation with pursed lips;
4. Blowing a whistle
Drugs:
1. Mucolytics,
2. Inhaled broncho-dilators
3. Corticosteroids.
4. Antibiotics- 14 days (oral and nebulized)
5. Pneumococcal and influenza vaccines
b) Surgery
a) Indications:
Failure of medical treatment
Obstructing tumor or foreign body
Uncontrolled hemorrhage
Multi-drug resistant tuberculosis
b) Lobar resection
c) Lung transplantation
Prevention:
a) Childhood immunization
b) Vit.A prophylaxis

c) Foreign body removal

d) Management of pneumonia
e) Neonatal screening for Cystic Fibrosis.
Alpha 1 - antitrypsin deficiency:
i.
Emphysema bronchiectasis
ii.
Autosomal dominant
iii.
Defective release hepatocytes.
iv.
Serum levels of alpha1-antitrypsin are decreased,
v.
Low alveolar concentrations, where the alpha1-antitrypsin
molecule normally would serve as protection against
antiproteases.
vi.
Protease excess in alveoli destroys alveolar walls and
causes emphysema.
vii.
Emphysema brochiectasis
viii.
Cirrhosis liver
9. Disorders of cilia- Ciliopathy Eg.
a) Primary ciliary dyskinesia:
1. Autosomal recessive; defect in dynein
2. Disorder beatings of cilia and flagella of sperms
3. Abnormal ciliary motion and impaired mucociliary
clearance
4. Cilia also are involved in nitric oxide production. Nasal
nitric oxide (NO) concentration is dramatically reduced
PCD
5. The term immotile cilia syndrome (ICS) is no longer
used
6. It is an important cause for male infertility
7. Female subfertility and tendency to ectopic pregnancy
has also been suggested.
8. Infections of the middle ear are common
b) Kartagener syndrome:
1. Heterotaxia with ciliary dyskinesia (50% 0f PCD)
2. Triad of situs inversus, chronic sinusitis,
and bronchiectasis;
3. Mechanisn of heterotaxia:
1. Clockwise movement of cilia in vertebrate
embryos generates robust leftward movement of
the extraembryonic fluid
2. It triggers normal D-looping of the primitive
heart tube and normal asymmetrical cardiac
morphogenesis.
3. Motile cilia are required for normal development
of left-right asymmetry
c) Youngs syndrome (secondary ciliary dyskinesia)
a. Recurrent sinopulmonary infection ; lungs is usually
normal but the mucus is abnormally viscous
b. Obstructive azoospermia; epididymides were frequently
enlarged or cystic
c. Considerable symptomatic improvement after
adolescence.
d. Sweat chloride is normal
e. No ciliary defect

f. Not inherited
g. Several studies suggest that contact with mercury might
cause the syndrome
STRIDOR IN A CHILD
1. Stridor is an abnormal, high-pitched sound produced by turbulent airflow
through a partially obstructed airway at the level of the supraglottis, glottis,
subglottis, and/or trachea
2. Causes:
Acute stridor
a) Laryngotracheobronchitis:
b) Aspiration of foreign body :
c) Bacterial tracheitis:
d) Retropharyngeal abscess:
e) Peritonsillar abscess:
f) Spasmodic croup:
g) Allergic reaction (ie, anaphylaxis):
h) Epiglottitis:
Chronic stridor
i. Laryngomalacia:
1. It is the most common cause of inspiratory stridor in the
neonatal period and early infancy and accounts for up to
75% of all cases of stridor.
2. Stridor may be exacerbated by crying or feeding.
3. Placing the patient in a prone position with the head up
improves the stridor; supine position worsens the stridor.
4. Laryngomalacia is usually benign and self-limiting and
improves as the child reaches age 1 year.
5. If significant obstruction or lack of weight gain is present,
surgical correction or supraglottoplasty may be considered
if tight mucosal bands are present holding the epiglottis
close to the true vocal cords or redundant mucosa is
observed overlying the arytenoids.
ii. Subglottic stenosis:
iii. Vocal cord paralysis:
iv. Laryngeal webs
v. Laryngeal cysts
vi. Laryngeal hemangiomas
vii. Laryngeal papillomas
viii. Tracheomalacia
ix. Tracheal stenosis
x. Choanal atresia
Evaluation:
1. Physical examination for recurrent or persistent stridor is usually normal.
2. Anteroposterior and lateral roentgenograms, contrast esophagography,
fluoroscopy, CT, and MRI are potentially useful diagnostic tools.
3. In most cases, direct observation by laryngoscopy is necessary for
diagnosis.