Lower respiratory

tract diseases
Group 2-
Yugma pandya
Feba wilson
Akshay gosh
Siya wilson
 Overview
• There are many causes of lower airway diseases.
• Lower airway diseases often result in airway
obstruction.
• most common lower airway disease in children is
asthma.
• Virus-induced wheezing episodes are common,
especially in children under 3 years of age
• Wheezing that begins in the first weeks or months of
life or that persists despite aggressive asthma therapy
is likely not due to asthma, and further diagnostic
evaluation may be warranted.
CLINICAL MANIFESTATIONS
• In contrast to upper airway obstruction, obstruction below thoracic inlet
causes more wheezing on expiration than on inspiration.
• Intrathoracic P is increased relative to atmospheric P during exhalation,
which tends to collapse the intrathoracic airways and accentuates airway
narrowing on expiration.

DIAGNOSTIC STUDIES
• When asthma is suspected, empiric trials of therapy.
• In children >6 years, spirometry can assess airflow obstruction and
response to bronchodilators.
• Radiographic exam is not needed with each episode of wheezing, but
those with significant respiratory distress, fever, history consistent with
foreign body aspiration, or focal auscultatory findings should have
posteroanterior and lateral chest X-ray obtained.
• Generalized hyperinflation (flattening
of the diaphragms and ↑ AP chest
diameter) suggests diffuse obstruction Risk factors for severe acute lower
of small airways. respiratory infections (ALRI)
• Hyperinflation with patchy densities ● Birth weight <2.5 kg irrespective of
due to atelectasis is often seen in gestational age
asthma and mistaken for pneumonia. ● Lack of exclusive breastfeeding
● Crowding
• Localized hyperinflation suggests ● Indoor air pollution
localized bronchial obstruction. ● Undernutrition
● Incomplete immunization
• Dysphagia leading to aspiration and ● HIV in a child
airway inflammation can present with ● Passive smoking
● Being male
persistent wheezing. ● Preterm birth
● Vitamin D deficiency
● Vitamin A deficiency
● Anemia
 Asthma
• most common chronic lung disease in children.
• most common cause of cough in school-age children.
• Respiratory hypersensitivity, inflammation, and reversible airway obstruction.
• There is cellular infiltration of mucosa by eosinophils, activated helper T cells, and
mast cells.

Etiology
Hyper-responsiveness to stimuli:
• Respiratory infection.
• Air pollutants. URI is the most
important
• Allergens: Seasonal, dust, mold, animalfactor
triggering dander.
for
• Foods. patients of all
ages.
• Exercise. Emotions.
Pathophysiology
• Bronchospasm (acute).
• Mucus production (acute).
• Inflammation and edema of airway mucosa (chronic).
• Two types: (1) Extrinsic: Immunological response to allergies.
Develop in childhood.
(2) Intrinsic:
No identifiable cause, most likely stress, anxiety,
exercise, quality of air, irritants.
Late onset.
Worsen with age.
• Underlying abnormalities include ↑ pulmonary vascular pressure, diffuse
narrowing of airways, ↑ RV and FRC, and ↑ total ventilation maintaining
normal or reduced PCO2 despite ↑ dead space.
 Signs and Symptoms

• Cough, wheezing, dyspnea, and tachypnea.

• ↑ work of breathing (retractions, use of accessory muscles,
nasal flaring, abdominal breathing).
• ↓ breath sounds.
• Prolongation of expiratory phase.
• Acidosis and hypoxia may result from airway obstruction.

Diagnosis
• Mostly a clinical diagnosis.
• Peak expiratory flow rate (PEFR): to assess severity of an
acute exacerbation
• Maximal rate of airflow during forced exhalation after a
maximal inhalation.
• Normal values depend on age and height:
1. Mild (80% of predicted).
2. Moderate (50–80% of predicted).
3. Severe (<50% of predicted).
• Spirometry—preferred method to diagnose airflow
obstruction.
1. Recommended >5 years old
2. Measure FVC and FEV1
3. Airway obstruction present if FEV1< 80%; FEV1/FVC < 85%.
• Chest x-ray shows hyperinflation and used to look for pneumonia
• Pulse oximetry demonstrate hypoxia.
• ABG—hypoxia in severe exacerbations; hypercapnia suggestive of
impending respiratory failure
• Bloodwork should not be routinely ordered in the evaluation of
asthma.
Classifying severity of asthma
exacerbations in the urgent or
emergency care setting
Mild Dyspnea only with activity PEFR >70% predicted personal
best

Moderate Dyspnea interferes with or limits usual activity PEFR 40–69%

predicted personal best

Severe Dyspnea at rest, interferes with conversation PEFR <40%

predicted personal best

Life Too dyspneic to speak PEFR <25% predicted personal best

threatening
Treatment

Goals: Improve bronchodilation, avoid allergens,

↓ inflammation, educate patient.

First-Line Agents for Acute Exacerbations

1. Oxygen if O2 saturation <92% on room air.

O2 is indicated for all asthmatics to keep O2 saturation >95%

2. Inhaled β2 agonist:
■ Albuterol (2.5 mg) (nebulized).
■Short-acting/rescue medication—treats only symptoms, not
underlying process.
■ Bronchial smooth-muscle relaxant in increase airflow.
■ Side effects: Tachycardia, tremors, hypokalemia.
3. Corticosteroids:
• For treatment of chronic inflammation.
• Oral prednisone or IV methylprednisolone.
• Contraindication: Active varicella or herpes infection.

4. Anticholinergic agents:
• Ipratropium bromide (nebulized).
• Act synergistically with albuterol.
• Bind to cholinergic R in medium and large airways.

Second-Line Agents
• Magnesium sulfate—bronchodilation via direct effect on smooth
muscle.
• Epinephrine or terbutaline.
• No role in acute asthma for theophylline; not recommended.
Status Asthmaticus
• Life-threatening form of asthma.
• Condition in which a progressively worsening
attack is unresponsive to usual therapy.

Signs and Symptoms

• Pulsus paradoxus >20 mm Hg.
• Hypotension, tachycardia.
• Cyanosis.
• One- to two-word dyspnea.
• Lethargy.
• Agitation.
• Retractions.
• Silent chest (no wheezes—poor air exchange).
BRONCHIOLITIS
Viral infection of the lower respiratory tract (medium and small
airways) which occurs after upper respiratory symptoms.

Bronchiolitis is the most common serious respiratory infection in

children <2 years.
ETIOLOGY

■ RSV—most common cause.

■ Rhinovirus.

■ Adenovirus.

■ Parainfluenza 3.

■ Influenza.

■ Human metapneumovirus (hMPV): First recognized in 2001 and now

increasingly implicated.

■ Two or more viruses are found in one-third of children hospitalized with

bronchiolitis.
Pathophysiology
■ Inflammatory obstruction (edema and mucus) of the bronchioles secondary to
viral infection.

■ Alterations in gas exchange are most frequently the result of mismatching of

pulmonary ventilation and perfusion.

■ Can lead to atelectasis

Epidemiology:

■ Occurs in first 2 years of life.

■ Reinfection is common.
■ Occurs in winter and early spring.

■ Risks: Crowded conditions, not breastfed, mothers who smoke, male gender.

■ High-risk infants:

■ Cardiac disease.

■ Pulmonary disease and bronchopulmonary dysplasia.

■ Neuromuscular disease.

■ Premature infants.

■ Immunocompromised.
 SIGNS AND SYMPTOMS
■ Starts with mild upper respiratory symptoms: often profuse nasal discharge and
congestion with or without fever.

■ Respiratory distress gradually develops.

■ Paroxysmal wheezing—common but may be absent, cough, dyspnea.

■ Apneic spells—young infants should be monitored.

■ Frequent complications include bacteremia, pericarditis, cellulitis, empyema,

meningitis, and suppurative arthritis.

■ Most common complication is hypoxia.

■ Dehydration is the most common secondary complication.

DIAGNOSIS
■ Mostly clinical but if other DDx are suspected, then consider additional testing.

■ Viral detection in nasopharyngeal secretions via culture, polymerase chain

reaction (PCR), or antigen detection.

■ Chest x-ray (rule out pneumonia or foreign body)—hyperinflation of lungs, ↑

anteroposterior (AP) diameter of rib cage.

■ Oxygen saturation is the single best objective predictor.

TREATMENT
■ Low threshold for hospitalization for high-risk infants.
■ Humidified oxygen,Nasal suctioning

■ Trial of nebulized albuterol although no long-term benefit shown (only 20–50% are responders,
discontinue if no objective benefit).

■ Hypertonic saline neb tx—potential to reduce airway edema and mucous plugging.

■ Steroids not indicated in first episode of bronchiolitis.

■ Respiratory isolation.

■ Ribavirin (aerosol form) if high-risk patients such as immunocompromised, need for mechanical
ventilation, or <6 weeks old.

■ RSV intravenous immunoglobulin (RSV-IVIG) or palivizumab given prior to and during RSV season in
high-risk infants <2 years old.
TUBERCULOSIS
• Contagious infection caused by bacteria that mainly affects the lungs but
also can affect any other organ.
• Etiology: Mycobacterium tuberculosis—acid fast bacilli.
• Pathophysiology: Primary portal of entry into children is lung.

• EPIDEMIOLOGY:■ Children are never the primary source (look for adult
contacts).
• ■ Risk factors:
• Urban living. ■ Low income. ■ Recent immigrants. ■ HIV.
 SIGNS AND
SYMPTOMS
■ Chronic cough (nonproductive) for more than 3 weeks.
■ Hemoptysis.

■ Fever.

■ Night sweats.

■ Weight loss or failure to thrive.

■ Anorexia.

■ Lymphadenopathy.

■ Present to ED with: ■ Primary pneumonia. ■ Miliary TB (may mimic sepsis).

 DIAGNOSIS
■ Hilar adenopathy.

■ Pulmonary calcification or caseating granulomas.

■ Pneumonia with infiltrate and adenopathy.

■ Pneumonia with pleural effusion.

■ Painless unilateral cervical adenopathy (scrofula).

■ Meningitis of insidious onset.

■ Bone or joint disease.

■ When any of the above are unresponsive to antibiotics.

■ PPD test (Mantoux test).

■ QuantiFERON®-TB Gold test.

■ Culture (gastric aspirates, sputum, pleural fluid, cerebrospinal fluid, urine, or

other body fluids).

■ Look for the adult source.

■ Acid-fast stain or PCR.

 TREATMENT
■ Prompt treatment necessary as in very
young, can disseminate quickly.

■ Two to four or more drugs (isoniazid,

rifampin, pyrazinamide, ethambutol,
streptomycin) for a minimum of 6
months for active disease.

■ Isoniazid for 9 months for latent

disease.
PNEUMONIA
Lower respiratory tract infection resulting in inflammation of lung parenchyma.

ETIOLOGY

■ Viruses: RSV, influenza, parainfluenza, adenovirus.

■ Bacteria: Less common, but more severe—S. pneumoniae, S. pyogenes,

S. aureus, H. influenzae type B, M. pneumoniae.

Signs and Symptoms

■ Respiratory distress including tachypnea, hypoxemia,

increased work of breathing.

■ Fever, productive cough, difficult feeding in infants.

■ Afebrile pneumonia seen with Chlamydia trachomatis (pneumonitis syndrome) in

infants.
DIAGNOSIS
1. Lung exam
Can hear crackles, decreased breath sounds, and dullness to percussion, egophany
2.Chest xray
● Viral (hyperinflation, perihilar infiltrate, hilar adenopathy, and atelectasis).
● Bacterial (alveolar consolidation).
● Mycoplasma (interstitial infiltrates).
● Tuberculosis (hilar adenopathy).
● Pneumocystis (reticulonodular infiltrates).
3.CBC and blood culture (positive in 10–30% of bacterial cases)
 TREATMENT
INPATIENT:-
• IV ampicillin is first line, second- or third-generation cephalosporin with or without
vancomycin depending on degree of illness.
• Consider macrolide (pneumonitis syndrome) in 1- to 3–month-olds if suspected.

OUTPATIENT:-
• Patients should have normal O2 saturation and be able to take oral fluids in order to
be outpatients.
• First line: High-dose amoxicillin. Alternative, second- or third-generation
cephalosporin or azithromycin
RESPIRATORY DISTRESS
SYNDROME (RDS)
Also known as neonatal respiratory
• distress syndrome [NRDS]).
• Formerly known as hyaline membrane disease
• Most common cause of respiratory failure in preterm infants (affects > 70% of
infants born at 28–30 weeks’ gestation).

ETIOLOGY:-

Surfactant deficiency leads to poor lung compliance, alveolar collapse, and

atelectasis.

RISK FACTORS:-

Maternal DM, male gender, C section delivery, the second born of twins.
 SIGNS AND SYMPTOMS
• Presents in the first 48–72 hours of life with a respiratory rate > 60/min.
• Progressive hypoxemia, cyanosis, nasal flaring.
• Intercostal retractions, expiratory grunting.

DIAGNOSIS
1.Check ABGs, CBC, and blood cultures to rule out

infection.

2. Diagnosis is clinical and confirmed with

characteristic findings on CXR.

Disease Process Key Findings

1. NRDS Ground-glass appearance, air bronchograms, and lack of

focal opacities

2. Transient tachypnea of the newborn (retained Perihilar streaking in interlobular fissures

aminotic fluid in respiratory tract)

3. Meconium aspiration Coarse, irregular infiltrates, lung hyperexpansion, and

pneumothorax

4. Congenital pneumonia Nonspecific patchy infiltrates

TREATMENT:-
• Continuous positive airway pressure (CPAP) or intubation and mechanical
ventilation.
• Artificial surfactant administration ↓ mortality.
• Pretreat mothers at risk for preterm delivery (24 weeks to 33 6/7 weeks) in the
next 7 days with corticosteroids.

COMPLICATIONS:-
1. Persistent PDA

2. NEC

3. Barotrauma from positive pressure ventilation

4. ROP,IVH,BPD(due to therapeutic supply of O2)

Foreign Body Aspiration
Pathophysiology

Cough reflex usually protects against aspiration.

Epidemiology
• Twice as likely to occur in males, particularly 6-month-olds to 3-
year-olds.
• Most common age: 1–2 years.

■ Most are located in the bronchi.

■ Toddlers: R = L mainstem

■ Adults: R mainstem predominates

 Signs and Symptoms

• Narrowest portion of the pediatric airway is at the cricoid ring.

• Determined by nature of object, location, and degree of obstruction.
• If in the upper airway: Respiratory distress with severe retractions and stridor.
• If in the lower airway [80%]: Symptoms may be subtle.
• Initial respiratory symptoms may disappear for hours to weeks after incident
• Vegetal/arachidic bronchitis due to vegetable (usually peanut) aspiration causes
cough, high fever, and dyspnea.
• Most common aspirated foreign body: Peanut.
• Most common foreign body aspirations resulting in death: Balloons.
• Complications if object is not removed include pneumonitis/pneumonia,
abscess, bronchiectasis, pulmonary hemorrhage, erosion, and perforation.
Diagnosis/Treatment

Larynx
• Croupy cough; may have stridor, aphonia,
hemoptysis, cyanosis.
• Lateral x-ray.
• Direct laryngoscopy—confirm diagnosis
and remove object.

Trachea
• Stridor, audible slap, and palpable thud
due to expiratory impaction.
• Chest x-ray , bronchoscopy.
Bronchi
• Initial choking, gagging, wheezing, coughing.
• Latent period with some coughing, wheezing, possible hemoptysis,
recurrent lobar pneumonia, or intractable asthma.
• Tracheal shift, ↓ breath sounds.
• Midline obstruction can cause severe dyspnea or asphyxia.
• → chronic bronchopulmonary disease if not treated
• Direct bronchoscopic visualization
• Antibiotics for secondary infection if prolonged exposure.
• Emergency treatment of local upper airway obstruction if necessary.
• If the child can cough and verbalize
1. Provide supplemental oxygen.
2. Maintain position of comfort
3. Immediate consultation with ENT and anesthesia.
• If the child cannot cough or verbalize, initiate basic life support
Congenital lobar
Developmental anomaly of the lower respiratory tract that is characterized by
emphysema(infantile
hyperinflation of one or more of the pulmonary lobes. lobar

emphysema)
EPIDEMIOLOGY
Most common congenital lung lesion.
More common in males (3:1)

PATHOPHYSIOLOGY
No significant parenchymal destruction.
SIGNS AND SYMPTOMS
Normal at birth.
Cough, wheezing, dyspnea, and cyanosis within a few days.
Decreased breath sounds and hyper-resonant to percussion over involved
lobe.
DIAGNOSIS
Chest x-ray:
Distention of the affected lobe.
Can see compressive atelectasis of contralateral lung.
Radiolucency.
Mediastinal shift to opposite side.
Flattened diaphragm
TREATMENT
Lobectomy.
Case report
Chief complaint-2-year-old white girl with chronic crackles admitted to clinic.

HPI-after birth the child was healthy until the seventh month of life, when she developed RSV infection.

PMI-from then on she had a LRTI every month treated with antibiotics, mainly macrolides for presumed
bacterial pneumonia; symptoms persisted daily. She had been under the care of pulmonologists ,who
suspected childhood interstitial lung disease and prescribed systemic and inhaled steroids, short-acting β2-
mimetics, and antileukotriene. This treatment, however, did not lead to any clinical improvement; symptoms
of crackles were present at all times.
hospitalization-She was hospitalized eight times .At the age of 11 months she had computed tomography
which revealed lung areas of uneven aeration in the middle lobe of her right lung and small areas of densities
which indicated postinflammatory changes. Due to suspected Pneumocystis jirovecii infection, she was
unsuccessfully treated with sulfamethoxazole and trimethoprim.

Next, she was referred for bronchoscopy with bronchoalveolar lavage.The result showed: copious
purulent secretions in her lower throat; mucosal edema of the larynx ,trachea, and bronchial tree, and
retention of the purulent mucus in bronchi with normal movement of bronchial cilia.Microbiological
testing-isolated high colony count of Moraxella catarrhalis in the BAL fluid.
She was administered amoxicillin-clavulanate for 14 days with good clinical improvement in respiratory
rate, labored breathing, and cough and she was discharged.

Follow up-She was observed for 2 months after discharge from the hospital and showed no signs of
recurrence. Then, she had a few more respiratory tract infections (usually every other month) treated with
antibiotics (crackles were present at each time during infection); between infections she remained healthy,
without any crackles or wheezing.
This case indicates
the importance of
RSV infection in an
immunocompetent
child.