Respiratory Flashcards
(295 cards)
1
Q
What is acute bronchiolitis?
A
Acute bronchiolitis is a viral lower respiratory tract infection causing inflammation, edema, and obstruction of small airways (bronchioles) primarily in infants.
2
Q
What is the most common causative agent of bronchiolitis?
A
Respiratory syncytial virus (RSV) is the most common causative agent.
3
Q
Which age group is most commonly affected by bronchiolitis?
A
Primarily affects children under 2 years of age, especially infants <6 months.
4
Q
What are the risk factors for severe bronchiolitis?
A
Risk factors: prematurity, congenital heart disease, chronic lung disease, immunodeficiency, and age <3 months.
5
Q
What is the pathophysiology of bronchiolitis?
A
Viral infection leads to inflammation, mucosal edema, increased mucus production, and airway obstruction, resulting in impaired ventilation and hypoxia.
6
Q
What are the early clinical features of bronchiolitis?
A
Early features: rhinorrhea, cough, low-grade fever, poor feeding, and irritability.
7
Q
What are the signs of respiratory distress in bronchiolitis?
A
Respiratory distress signs: tachypnea, nasal flaring, retractions, grunting, cyanosis.
8
Q
What physical examination findings are typical in bronchiolitis?
A
Findings include wheezing, crackles (rales), prolonged expiratory phase, tachypnea, and hypoxia.
9
Q
How is the diagnosis of bronchiolitis made?
A
Diagnosis is clinical based on history and examination; routine virologic testing is not required for typical cases.
10
Q
What investigations are indicated in typical bronchiolitis?
A
Investigations are usually not needed; testing for RSV may be considered in hospitalized infants for infection control.
11
Q
When are chest X-rays indicated in bronchiolitis?
A
Chest X-rays are reserved for severe cases, atypical presentations, or suspicion of complications (e.g., pneumonia, pneumothorax).
12
Q
What are the differential diagnoses for bronchiolitis?
A
Differentials: pneumonia, asthma (first episode), foreign body aspiration, congenital airway anomalies, heart failure.
13
Q
What is the mainstay of management in bronchiolitis?
A
Mainstay is supportive care with monitoring, hydration, and oxygenation as needed.
14
Q
What supportive therapies are important in bronchiolitis?
A
Supportive therapies include supplemental oxygen for hypoxia, suctioning of nasal secretions, and ensuring adequate hydration (oral/IV fluids).
15
Q
When is hospitalization indicated for bronchiolitis?
A
Hospitalization criteria: hypoxia requiring oxygen, inability to maintain hydration, severe respiratory distress, apnea, or underlying high-risk conditions.
16
Q
Is bronchodilator therapy routinely recommended in bronchiolitis?
A
Routine bronchodilator therapy (e.g., salbutamol) is not recommended but may be trialed in select cases and discontinued if no benefit.
17
Q
What is the role of corticosteroids in bronchiolitis?
A
Corticosteroids are not routinely recommended for bronchiolitis as they have not shown consistent benefit.
18
Q
When should antiviral therapy (e.g., ribavirin) be considered in bronchiolitis?
A
Ribavirin may be considered in severe cases in high-risk infants (e.g., severely immunocompromised), but its routine use is controversial.
19
Q
What preventive measures are recommended for bronchiolitis?
A
Prevention includes hand hygiene, avoiding exposure to sick contacts, palivizumab prophylaxis for high-risk infants during RSV season.
20
Q
What is the prognosis for infants with bronchiolitis?
A
Most infants recover fully within 1–2 weeks, but some may have recurrent wheezing episodes later in childhood.
21
Q
What is pneumonia?
A
Pneumonia is an infection of the lung parenchyma leading to inflammation and consolidation of the alveoli.
22
Q
What are the common causative organisms of community-acquired pneumonia (CAP) in infants and children?
A
Common organisms: Streptococcus pneumoniae (most common), Haemophilus influenzae type B, Staphylococcus aureus, Mycoplasma pneumoniae (in older children).
23
Q
What are the common pathogens in neonatal pneumonia?
A
Neonatal pathogens: Group B Streptococcus, E. coli, Klebsiella species, Listeria monocytogenes.
24
Q
What are the typical bacterial causes of CAP in children over 5 years?
A
Older children: Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydophila pneumoniae.
25
What are the typical viral causes of CAP in children?
Viral causes: RSV, influenza, parainfluenza, adenovirus, human metapneumovirus.
26
What are risk factors for severe pneumonia in children?
Risk factors: prematurity, malnutrition, immunodeficiency, chronic lung disease, congenital heart disease, and lack of vaccination.
27
What are the classic clinical features of bacterial pneumonia?
Symptoms: high fever, productive cough, pleuritic chest pain, tachypnea, and localized findings on exam (e.g., decreased breath sounds, crackles).
28
What are the clinical features of viral pneumonia?
Symptoms: low-grade fever, dry cough, wheezing, and diffuse findings on chest exam without focal consolidation.
29
What are signs of respiratory distress in pediatric pneumonia?
Signs include tachypnea, nasal flaring, subcostal/intercostal retractions, grunting, cyanosis in severe cases.
30
What physical examination findings suggest pneumonia?
Findings: crackles (rales), bronchial breath sounds, decreased air entry, dullness to percussion, egophony over consolidated areas.
31
What laboratory tests may be helpful in pneumonia diagnosis?
Helpful labs: CBC (leukocytosis with left shift), blood cultures (if severe), viral PCR panels if viral etiology suspected.
32
When is a chest X-ray indicated in pediatric pneumonia?
Chest X-ray is indicated in hospitalized patients, severe disease, complications, or when diagnosis is uncertain.
33
What chest X-ray findings are typical of bacterial pneumonia?
Typical bacterial pneumonia: lobar consolidation, air bronchograms, pleural effusion; viral pneumonia: interstitial infiltrates or peribronchial cuffing.
34
What are complications of pneumonia in children?
Complications: pleural effusion, empyema, lung abscess, necrotizing pneumonia, bacteremia, sepsis.
35
How is the severity of pneumonia assessed in pediatrics?
Severity is assessed based on oxygen requirement, respiratory distress, feeding difficulties, hydration status, and underlying conditions.
36
What are the general principles of outpatient treatment for mild CAP?
Outpatient treatment: oral antibiotics, supportive care (hydration, fever control), close follow-up for worsening symptoms.
37
What is the recommended first-line antibiotic for bacterial CAP in previously healthy children?
First-line antibiotic: high-dose amoxicillin for typical bacterial CAP; macrolides (e.g., azithromycin) if atypical bacteria suspected.
38
When is hospitalization indicated for pediatric pneumonia?
Hospitalization if hypoxia (O2 sat <90%), severe respiratory distress, inability to maintain hydration, toxic appearance, or underlying comorbidities.
39
What is the management of parapneumonic effusion or empyema?
Management: antibiotics, chest drainage for large effusions, intrapleural fibrinolytics for loculated effusions, or surgical intervention if needed.
40
What preventive strategies are important to reduce pneumonia incidence in children?
Prevention: pneumococcal conjugate vaccine (PCV13), Hib vaccine, influenza vaccination, breastfeeding, good nutrition, and hand hygiene.
41
What is asthma?
Asthma is a chronic inflammatory disease of the airways characterized by reversible airflow obstruction, airway hyperresponsiveness, and airway remodeling.
42
What is the pathophysiology of asthma?
Inflammation leads to airway edema, mucus hypersecretion, bronchial smooth muscle contraction, and airflow limitation.
43
What are the major triggers for asthma in children?
Triggers include respiratory infections, allergens (dust mites, pollen, animal dander), exercise, cold air, air pollutants, and emotional stress.
44
What are the risk factors for developing childhood asthma?
Risk factors: family history of atopy (asthma, eczema, allergic rhinitis), personal history of atopy, viral respiratory infections (e.g., RSV), exposure to tobacco smoke.
45
What are the typical clinical features of asthma?
Symptoms: recurrent wheezing, cough (especially at night), shortness of breath, chest tightness, often triggered by specific exposures or infections.
46
What is the classic triad of asthma?
Classic triad: wheezing, cough, and shortness of breath.
47
How is the diagnosis of asthma made in children?
Diagnosis is based on clinical history, physical exam, and demonstration of reversible airflow obstruction (spirometry preferred if age >5 years).
48
What is the role of spirometry in asthma diagnosis?
Spirometry measures airflow obstruction and reversibility after bronchodilator use; it confirms diagnosis and assesses severity.
49
What are the typical spirometry findings in asthma?
Findings: decreased FEV1, decreased FEV1/FVC ratio, and ≥12% improvement in FEV1 after bronchodilator use.
50
What is the classification of asthma severity in children?
Severity is classified into four categories: intermittent, mild persistent, moderate persistent, and severe persistent.
51
What are the features of mild intermittent asthma?
Mild intermittent: symptoms <2 days/week, nighttime symptoms <2 times/month, normal PEF between exacerbations.
52
What are the features of mild persistent asthma?
Mild persistent: symptoms >2 days/week but not daily, nighttime symptoms 3–4 times/month, minor limitation of activity.
53
What are the features of moderate persistent asthma?
Moderate persistent: daily symptoms, nighttime symptoms >1 night/week, some activity limitation.
54
What are the features of severe persistent asthma?
Severe persistent: symptoms throughout the day, frequent nighttime symptoms, extreme activity limitation.
55
What are the goals of asthma management?
Goals: control symptoms, prevent exacerbations, maintain normal activity levels, minimize medication side effects, and preserve lung function.
56
What is the first-line controller therapy for persistent asthma?
First-line: low-dose inhaled corticosteroids (ICS) for persistent asthma.
57
What is the role of inhaled corticosteroids (ICS) in asthma?
ICS reduce airway inflammation, decrease symptoms, improve lung function, and reduce risk of exacerbations.
58
What are the quick-relief medications used during asthma exacerbations?
Quick-relief medications: short-acting beta-2 agonists (SABA) such as albuterol for relief of acute bronchospasm.
59
When should systemic corticosteroids be used in asthma management?
Systemic corticosteroids (e.g., oral prednisolone) are used in moderate-to-severe exacerbations or when SABA response is inadequate.
60
What are preventive strategies for asthma control in children?
Prevention includes adherence to controller therapy, allergen avoidance, vaccination (influenza, pneumococcal), asthma action plan education, and smoking cessation exposure.
61
What is cystic fibrosis (CF)?
CF is a genetic disorder characterized by dysfunction of exocrine glands leading to thick, viscous secretions affecting multiple organs, especially the lungs and pancreas.
62
What is the genetic basis of CF?
CF is caused by mutations in the CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) gene, inherited in an autosomal recessive pattern.
63
What is the pathophysiology of CF?
Defective CFTR protein impairs chloride and water transport across epithelial cells, leading to dehydrated mucus and obstruction of ducts and airways.
64
Which organs are primarily affected in CF?
Organs affected: lungs, pancreas, gastrointestinal tract, hepatobiliary system, reproductive tract, and sinuses.
65
What are the common respiratory manifestations of CF?
Respiratory manifestations: chronic cough, recurrent lung infections, bronchiectasis, nasal polyps, sinusitis, and progressive respiratory failure.
66
What are the gastrointestinal manifestations of CF?
GI manifestations: meconium ileus in neonates, pancreatic insufficiency (malabsorption, steatorrhea), distal intestinal obstruction syndrome, hepatobiliary disease.
67
What are other systemic manifestations of CF?
Other manifestations: male infertility (absent vas deferens), electrolyte abnormalities (hypochloremic metabolic alkalosis), osteoporosis, diabetes mellitus (CFRD).
68
What is the most common presenting symptom of CF in neonates?
Meconium ileus (intestinal obstruction due to thick meconium) is a common presenting symptom in CF neonates.
69
What infections are common in CF patients' lungs?
Common infections: Staphylococcus aureus, Haemophilus influenzae early; Pseudomonas aeruginosa and Burkholderia cepacia complex later.
70
What is the role of Pseudomonas aeruginosa in CF?
Pseudomonas colonization leads to chronic lung infection, progressive airway damage, and worse prognosis.
71
How is CF diagnosed?
Diagnosis is based on clinical features, positive sweat chloride test, and/or identification of two CFTR mutations.
72
What is the role of the sweat chloride test in CF diagnosis?
Sweat chloride test: elevated chloride concentration ≥60 mmol/L confirms diagnosis; intermediate results require further evaluation.
73
What genetic testing is used for CF?
Genetic testing identifies CFTR mutations and helps confirm diagnosis, especially in atypical or borderline cases.
74
What are the goals of respiratory management in CF?
Goals: maintain airway patency, prevent and treat infections, optimize nutrition, and manage complications.
75
What are airway clearance therapies in CF?
Airway clearance: chest physiotherapy, positive expiratory pressure devices, hypertonic saline, and dornase alfa (DNAse enzyme).
76
What are the roles of antibiotics in CF management?
Antibiotics are used for acute pulmonary exacerbations and chronic suppression (e.g., inhaled tobramycin for Pseudomonas).
77
What is the role of pancreatic enzyme replacement therapy?
Pancreatic enzyme replacement therapy improves fat absorption, weight gain, and reduces steatorrhea.
78
What is the role of CFTR modulators in CF?
CFTR modulators (e.g., ivacaftor, lumacaftor/ivacaftor) correct underlying protein defect and improve lung function and quality of life in specific mutations.
79
What is the prognosis of CF today with modern therapies?
Prognosis has improved significantly with modern therapies; median survival now exceeds 40 years in developed countries.
80
What are preventive strategies for complications in CF?
Preventive strategies: vaccination (influenza, pneumococcal), aggressive infection control, regular monitoring of lung function, early detection and treatment of complications.
81
What is foreign body aspiration (FBA)?
FBA is the inhalation of a solid or liquid object into the respiratory tract, causing partial or complete airway obstruction.
82
Which age group is most at risk for FBA?
Children aged 1–3 years are at highest risk due to immature swallowing coordination and tendency to explore objects orally.
83
What are common objects aspirated by children?
Common objects: peanuts, seeds, small toys, coins, buttons, food particles.
84
What is the pathophysiology of FBA?
The foreign body can cause mechanical obstruction, local inflammation, infection, or air trapping distal to the obstruction.
85
What are the classic clinical features of acute FBA?
Acute presentation: sudden onset of coughing, choking, gagging, wheezing, or respiratory distress.
86
What is the typical presentation of chronic FBA?
Chronic presentation: persistent cough, recurrent pneumonia, localized wheezing, or failure to respond to standard therapies.
87
What are the red flags suggesting FBA in a child with respiratory symptoms?
Red flags: sudden onset of symptoms in a previously well child, asymmetric breath sounds, localized wheezing or decreased air entry.
88
What physical exam findings may be seen in FBA?
Findings: unilateral decreased air entry, wheezing, stridor (if upper airway involved), crackles, or cyanosis if severe.
89
What are typical chest X-ray findings in FBA?
CXR may show hyperinflation (air trapping) on the affected side, atelectasis, mediastinal shift, or visible foreign body if radiopaque.
90
What is the role of inspiratory and expiratory films in FBA?
Inspiratory-expiratory films help detect air trapping, seen as asymmetric hyperinflation during expiration.
91
Can a normal chest X-ray rule out FBA?
No; a normal chest X-ray does not rule out FBA, especially if the foreign body is radiolucent (organic material).
92
When is CT scan indicated in suspected FBA?
CT scan may be used if chest X-ray is inconclusive but clinical suspicion remains high.
93
What is the gold standard for diagnosis and treatment of FBA?
Rigid bronchoscopy is the gold standard for both diagnosis and removal of aspirated foreign bodies.
94
What is the role of rigid bronchoscopy in FBA?
Rigid bronchoscopy under general anesthesia provides optimal airway control and allows removal of the foreign body.
95
When is flexible bronchoscopy used in FBA?
Flexible bronchoscopy may be used for diagnostic purposes or retrieval of small, distally located foreign bodies in selected cases.
96
What is the initial management of complete airway obstruction due to FBA?
If there is complete obstruction and inability to breathe, back blows and chest thrusts (infants) or Heimlich maneuver (older children) should be initiated immediately.
97
What is the Heimlich maneuver and its role in FBA?
The Heimlich maneuver involves abdominal thrusts to create an artificial cough and dislodge the foreign body.
98
What complications can arise from FBA?
Complications: airway trauma, pneumothorax, pneumomediastinum, infection, granulation tissue formation, and chronic lung disease if diagnosis is delayed.
99
What are preventive strategies for FBA?
Prevention: supervision during eating, avoiding high-risk foods (e.g., nuts, hard candies) in young children, keeping small objects out of reach.
100
What is the prognosis after removal of the foreign body?
Prognosis is excellent if the foreign body is promptly removed; delayed diagnosis increases risk of complications.
101
What is croup (laryngotracheobronchitis)?
Croup is an acute viral infection causing inflammation and narrowing of the larynx, trachea, and bronchi, leading to inspiratory stridor and barking cough.
102
What is the most common causative organism of croup?
Parainfluenza virus (especially type 1) is the most common causative agent.
103
Which age group is most affected by croup?
Croup typically affects children aged 6 months to 3 years, with peak incidence at 1–2 years.
104
What is the pathophysiology of croup?
Viral infection causes mucosal edema and narrowing of the subglottic airway, leading to airflow obstruction during inspiration.
105
What are the classic clinical features of croup?
Classic features: barking cough, inspiratory stridor, hoarseness, and varying degrees of respiratory distress, often worse at night.
106
What is the hallmark symptom of croup?
A harsh, barking (seal-like) cough is the hallmark symptom of croup.
107
What are signs of severe croup?
Signs of severe croup: marked stridor at rest, significant chest wall retractions, agitation or lethargy, and hypoxia.
108
How is the diagnosis of croup made?
Diagnosis is clinical, based on history and physical examination; imaging is not routinely necessary.
109
What are typical findings on neck radiographs in croup?
Neck radiographs may show subglottic narrowing, termed the 'steeple sign'.
110
What is the 'steeple sign' in croup?
The 'steeple sign' refers to tapering of the subglottic airway resembling a church steeple on anteroposterior neck X-ray.
111
What are the differential diagnoses for stridor in children?
Differential diagnoses: epiglottitis, bacterial tracheitis, foreign body aspiration, retropharyngeal abscess, anaphylaxis.
112
What factors increase the risk of severe airway obstruction in croup?
Younger age (<1 year), severe stridor at rest, and underlying airway anomalies increase risk of severe obstruction.
113
What is the initial management of mild croup?
Mild croup is managed with a single dose of oral dexamethasone and supportive care at home.
114
What is the role of corticosteroids in croup treatment?
Corticosteroids (e.g., dexamethasone 0.15–0.6 mg/kg) reduce airway inflammation and improve symptoms within hours.
115
What is the role of nebulized epinephrine in croup?
Nebulized racemic epinephrine provides rapid, temporary reduction in airway edema; used in moderate-to-severe croup.
116
When is hospitalization indicated in croup?
Hospitalization is needed if there is persistent respiratory distress after treatment, need for repeated nebulized epinephrine, hypoxia, or poor oral intake.
117
What are supportive therapies in croup?
Supportive therapies: maintaining calm environment, cool mist (optional), hydration, oxygen if needed.
118
What precautions should be taken when using nebulized epinephrine?
Children treated with nebulized epinephrine must be observed for at least 2–3 hours due to risk of symptom rebound after effects wear off.
119
What are complications of croup?
Complications: airway obstruction, respiratory failure, secondary bacterial infection (e.g., bacterial tracheitis).
120
What is the prognosis for children with croup?
Prognosis is excellent; most cases are self-limited and resolve within 3–7 days with supportive care.
121
What is epiglottitis?
Epiglottitis is an acute, life-threatening bacterial infection causing inflammation and swelling of the supraglottic structures, especially the epiglottis.
122
What is the most common causative organism of epiglottitis in children?
Historically, Haemophilus influenzae type B (Hib) was the most common cause; now Streptococcus species and Staphylococcus aureus are more common.
123
How has the incidence of epiglottitis changed since the Hib vaccine introduction?
The incidence has dramatically decreased due to widespread Hib vaccination.
124
Which age group is typically affected by epiglottitis?
Typically affects children aged 2–7 years, but can occur at any age, especially in unvaccinated individuals.
125
What is the pathophysiology of epiglottitis?
Infection leads to rapid swelling of the epiglottis and surrounding tissues, risking complete airway obstruction.
126
What are the classic clinical features of epiglottitis?
Rapid onset of fever, severe sore throat, muffled 'hot potato' voice, drooling, dysphagia, respiratory distress, and stridor.
127
What are the signs of impending airway obstruction in epiglottitis?
Signs: severe respiratory distress, anxiety, retractions, cyanosis, and tripod positioning to maximize airway patency.
128
What is the classic posture seen in children with epiglottitis?
Tripod posture: child leans forward, chin thrust forward, mouth open, drooling, and tongue protruding to maintain airway.
129
Why should the oropharynx not be examined in suspected epiglottitis?
Examining the oropharynx may provoke airway spasm and complete obstruction; it should only be done with airway personnel ready.
130
How is the diagnosis of epiglottitis confirmed?
Diagnosis is clinical but can be confirmed by visualization during controlled airway management or lateral neck X-ray showing 'thumbprint sign'.
131
What is the 'thumbprint sign' in epiglottitis?
The 'thumbprint sign' is a swollen epiglottis appearing as a thumb-like projection on lateral neck radiograph.
132
What is the most important initial step in the management of suspected epiglottitis?
Immediate securing of the airway is the priority before any other intervention; airway assessment must occur in a controlled setting (OR if possible).
133
How should the airway be secured in epiglottitis?
Endotracheal intubation under general anesthesia with skilled personnel (ENT, anesthesiologist) is preferred; surgical airway backup should be available.
134
What role does endotracheal intubation play in epiglottitis management?
Intubation stabilizes the airway, allowing safe treatment of infection and reducing mortality risk.
135
What antibiotics are used in the treatment of epiglottitis?
Empiric IV antibiotics: third-generation cephalosporin (e.g., ceftriaxone) plus coverage for MRSA if needed (e.g., vancomycin).
136
What is the role of corticosteroids in epiglottitis?
Corticosteroids may be used to reduce airway edema, although their benefit is less well established.
137
What are complications of epiglottitis if not treated promptly?
Complications: sudden airway obstruction, respiratory arrest, septicemia, and death if untreated.
138
What are the differential diagnoses for stridor and respiratory distress in children?
Differentials: croup, retropharyngeal abscess, peritonsillar abscess, bacterial tracheitis, foreign body aspiration.
139
What preventive strategies are effective against epiglottitis?
Hib vaccination is highly effective in preventing classic epiglottitis; proper immunization reduces incidence.
140
What is the prognosis for epiglottitis with appropriate management?
With timely airway management and antibiotics, prognosis is excellent; mortality is very low (<1%).
141
What is bronchopulmonary dysplasia (BPD)?
BPD is a chronic lung disease of preterm infants characterized by impaired alveolar and vascular development, leading to long-term respiratory problems.
142
Which population is most commonly affected by BPD?
BPD primarily affects premature infants (<32 weeks gestation) who require prolonged mechanical ventilation and oxygen therapy.
143
What are the main risk factors for developing BPD?
Risk factors: extreme prematurity, prolonged mechanical ventilation, oxygen toxicity, antenatal and postnatal infections, and poor nutrition.
144
What is the pathophysiology of BPD?
Injury to immature lungs from oxygen and ventilator-induced damage leads to inflammation, fibrosis, and arrested alveolarization.
145
What is the definition of BPD according to the NICHD 2018 criteria?
Definition: Need for supplemental oxygen at 36 weeks' postmenstrual age, with severity classified based on oxygen/respiratory support requirements.
146
What are the clinical features of BPD in infants?
Features: persistent oxygen requirement, tachypnea, increased work of breathing, poor feeding, and frequent respiratory infections.
147
How is the diagnosis of BPD made?
Diagnosis is clinical, based on history of prematurity, respiratory support, and persistent oxygen need beyond 28 days of life or 36 weeks PMA.
148
What are the radiographic findings in BPD?
Chest X-ray may show areas of hyperinflation, atelectasis, fibrosis, and a bubbly or spongy lung appearance.
149
What are the common complications associated with BPD?
Complications: pulmonary hypertension, recurrent respiratory infections, reactive airway disease, growth failure, and neurodevelopmental delay.
150
What is the role of oxygen therapy in BPD?
Oxygen therapy is used to maintain adequate oxygenation (>90% SpO2) and prevent pulmonary hypertension; careful titration avoids oxygen toxicity.
151
How is the severity of BPD classified?
Severity:
- Mild: Need for oxygen <28 days but not at 36 weeks PMA
- Moderate: Oxygen at 36 weeks PMA but FiO2 <30%
- Severe: Oxygen at 36 weeks PMA and FiO2 ≥30% or positive pressure support.
152
What supportive measures are important in BPD management?
Supportive measures: minimize oxygen and ventilator exposure, optimize nutrition, manage fluids, and prevent infections.
153
What is the role of diuretics in BPD management?
Diuretics (e.g., furosemide) reduce pulmonary edema but are used short-term due to risks of electrolyte imbalance and nephrocalcinosis.
154
What are the nutritional needs of infants with BPD?
Infants with BPD have higher caloric needs (120–150 kcal/kg/day) to support growth and lung development.
155
What is the role of corticosteroids in BPD prevention or management?
Systemic corticosteroids (e.g., dexamethasone) may reduce inflammation and facilitate extubation but are used cautiously due to neurodevelopmental risks.
156
What immunoprophylaxis is recommended for infants with BPD?
Palivizumab is recommended during RSV season to prevent severe lower respiratory tract infections.
157
What is the role of bronchodilators in BPD?
Bronchodilators may help reduce airway resistance in some infants but are not routinely recommended without documented benefit.
158
How can BPD be prevented in preterm infants?
Prevention strategies: gentle ventilation (lung-protective strategies), early use of non-invasive ventilation, minimizing oxygen exposure, and antenatal steroids.
159
What is the long-term prognosis for infants with BPD?
Prognosis varies; many infants improve over time, but some have persistent lung function abnormalities into adulthood.
160
What follow-up care is needed for infants with BPD?
Follow-up includes monitoring for respiratory symptoms, growth, neurodevelopment, and screening for pulmonary hypertension.
161
What is tuberculosis (TB)?
Tuberculosis is a chronic infectious disease caused by Mycobacterium tuberculosis, affecting primarily the lungs but can involve multiple organs.
162
How is TB transmitted?
TB is transmitted via inhalation of airborne droplets from a person with active pulmonary TB.
163
Which children are at highest risk for developing TB?
Highest risk: infants, young children (<5 years), immunocompromised children (e.g., HIV), and malnourished children.
164
What are the common forms of TB in children?
Forms: primary pulmonary TB, miliary TB, TB meningitis, pleural TB, lymphadenitis, osteoarticular TB.
165
What are the typical symptoms of pulmonary TB in children?
Symptoms: persistent cough, weight loss or failure to thrive, fever, night sweats, and fatigue.
166
What is primary TB in children?
Primary TB is the initial infection following exposure, often involving a Ghon focus and regional lymphadenopathy.
167
What is miliary TB?
Miliary TB refers to hematogenous dissemination of TB causing diffuse millet seed-like lesions throughout the lungs and other organs.
168
What are the extrapulmonary manifestations of TB in children?
Extrapulmonary TB: lymphadenitis (cervical nodes most common), meningitis, bone and joint TB, pericardial TB, renal TB.
169
What are risk factors for progression from latent to active TB?
Risk factors: age <5 years, HIV infection, malnutrition, recent infection, absence of BCG vaccination.
170
How is TB diagnosed in children?
Diagnosis is based on a combination of clinical, radiological, microbiological, and immunological findings.
171
What is the role of the tuberculin skin test (TST) in pediatric TB diagnosis?
TST detects delayed hypersensitivity to tuberculin; a positive result suggests TB infection but not necessarily active disease.
172
What is the role of interferon-gamma release assays (IGRAs) in TB diagnosis?
IGRAs measure T-cell release of interferon-gamma in response to TB antigens; useful especially in BCG-vaccinated children.
173
What is the role of chest X-ray in diagnosing pediatric TB?
Chest X-ray supports diagnosis by detecting parenchymal disease, lymphadenopathy, or miliary patterns.
174
What are common chest X-ray findings in pediatric TB?
Findings: hilar/mediastinal lymphadenopathy, parenchymal consolidation, cavitations (less common in young children), or miliary pattern.
175
What microbiological tests confirm TB infection?
Confirmation: sputum or gastric aspirate AFB smear and culture, nucleic acid amplification tests (e.g., GeneXpert MTB/RIF).
176
How is latent TB infection (LTBI) managed in children?
LTBI management: isoniazid monotherapy for 6–9 months or rifampin for 4 months (depending on local guidelines).
177
What is the standard treatment regimen for active TB in children?
Standard regimen: intensive phase (2 months) of isoniazid, rifampin, pyrazinamide ± ethambutol, followed by continuation phase (4 months) of isoniazid and rifampin.
178
What are common side effects of anti-TB medications in children?
Side effects: hepatotoxicity (isoniazid, rifampin, pyrazinamide), optic neuritis (ethambutol), rash, gastrointestinal upset.
179
What preventive measures can reduce TB transmission?
Prevention: BCG vaccination, early diagnosis and treatment of infectious cases, contact screening, and prophylactic therapy for contacts.
180
What is the prognosis for pediatric TB with appropriate treatment?
Prognosis is excellent with timely diagnosis and appropriate therapy; however, delayed treatment can lead to severe morbidity or mortality, especially in disseminated TB.
181
What is Neonatal Respiratory Distress Syndrome (RDS)?
Neonatal RDS is a respiratory disorder primarily of preterm infants caused by surfactant deficiency leading to alveolar collapse and impaired gas exchange.
182
What is the primary cause of RDS in neonates?
Primary cause: deficiency of pulmonary surfactant, which reduces surface tension and prevents alveolar collapse.
183
Which neonates are at highest risk for RDS?
Highest risk: premature infants (<34 weeks gestation), particularly those <28 weeks, infants of diabetic mothers, and cesarean deliveries without labor.
184
What is the pathophysiology of RDS?
Surfactant deficiency leads to atelectasis, decreased lung compliance, ventilation-perfusion mismatch, hypoxemia, and respiratory acidosis.
185
What are the clinical features of RDS in newborns?
Features: tachypnea, nasal flaring, grunting, retractions, cyanosis, and increasing oxygen requirement shortly after birth.
186
What is the typical timing of symptom onset in RDS?
Symptoms usually develop within minutes to a few hours after birth and progressively worsen without intervention.
187
What are the classic physical examination findings in RDS?
Exam: tachypnea (>60 breaths/min), subcostal and intercostal retractions, nasal flaring, expiratory grunting, and cyanosis.
188
How is RDS diagnosed clinically?
Diagnosis is based on clinical presentation in a premature infant, supported by characteristic chest X-ray findings.
189
What are the typical chest X-ray findings in RDS?
CXR: bilateral diffuse reticulogranular (ground-glass) opacities and air bronchograms with low lung volumes.
190
What is the 'ground-glass appearance' in RDS?
The 'ground-glass appearance' refers to diffuse, fine granular densities representing alveolar collapse and surfactant deficiency.
191
What are the differential diagnoses for neonatal respiratory distress?
Differentials: transient tachypnea of the newborn (TTN), pneumonia, meconium aspiration syndrome, congenital diaphragmatic hernia.
192
What antenatal therapies help prevent RDS?
Antenatal corticosteroids (betamethasone or dexamethasone) administered to mothers at risk of preterm delivery stimulate fetal surfactant production.
193
What is the role of surfactant replacement therapy in RDS?
Surfactant replacement therapy improves lung compliance, oxygenation, reduces need for mechanical ventilation, and lowers mortality.
194
When should surfactant therapy be administered?
Surfactant should be administered early (within first 2 hours) in infants with significant respiratory distress and confirmed/suspected RDS.
195
What is the role of respiratory support in RDS management?
Respiratory support maintains adequate oxygenation and ventilation while minimizing lung injury (lung-protective strategies).
196
What types of respiratory support are commonly used in RDS?
Support includes CPAP (Continuous Positive Airway Pressure), mechanical ventilation, or high-frequency oscillatory ventilation as needed.
197
What are complications of RDS?
Complications: pneumothorax, bronchopulmonary dysplasia (BPD), pulmonary hemorrhage, intraventricular hemorrhage.
198
What preventive strategies reduce the risk of RDS?
Prevention: antenatal corticosteroids, delayed elective delivery (<39 weeks), minimizing mechanical ventilation and oxygen exposure.
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What is the prognosis of RDS with modern management?
Prognosis is excellent with modern surfactant and respiratory support; survival rates have greatly improved even in extremely preterm infants.
200
What long-term sequelae may occur in survivors of severe RDS?
Long-term sequelae: chronic lung disease (BPD), neurodevelopmental impairment, recurrent respiratory infections.
201
What is pediatric obstructive sleep apnea (OSA)?
Pediatric OSA is a disorder characterized by repeated episodes of partial or complete upper airway obstruction during sleep, leading to disrupted ventilation and sleep fragmentation.
202
What is the pathophysiology of OSA in children?
Anatomic narrowing and dynamic collapse of the upper airway during sleep cause intermittent hypoxia, hypercapnia, and sleep disruption.
203
What are the most common causes of OSA in children?
Most common causes: adenotonsillar hypertrophy, obesity, craniofacial anomalies, neuromuscular disorders.
204
What risk factors predispose children to OSA?
Risk factors: adenotonsillar hypertrophy, obesity, Down syndrome, craniofacial syndromes, neuromuscular weakness, allergic rhinitis.
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What are the common symptoms of OSA in children?
Symptoms: snoring, gasping or choking during sleep, restless sleep, witnessed apneas, nocturnal enuresis, daytime sleepiness.
206
What behavioral symptoms may suggest OSA in school-aged children?
School-aged children may exhibit hyperactivity, inattention, learning difficulties, and behavioral problems resembling ADHD.
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What are complications of untreated OSA in children?
Complications: failure to thrive, systemic hypertension, pulmonary hypertension, right heart failure, neurocognitive deficits, behavioral problems.
208
How is OSA diagnosed in children?
Diagnosis is based on clinical suspicion and confirmed by objective sleep study testing.
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What is the gold standard for diagnosing OSA?
Polysomnography (overnight sleep study) is the gold standard for diagnosing pediatric OSA.
210
What is the role of overnight polysomnography in OSA?
Polysomnography measures apneas, hypopneas, oxygen desaturation, arousals, and sleep architecture to confirm OSA severity.
211
What are the physical exam findings suggestive of OSA?
Findings: enlarged tonsils/adenoids, mouth breathing, nasal obstruction, craniofacial anomalies, obesity-related changes.
212
What is the first-line treatment for most children with OSA?
First-line treatment: adenotonsillectomy for children with adenotonsillar hypertrophy and moderate-to-severe OSA.
213
What are indications for tonsillectomy and adenoidectomy in OSA?
Indications: moderate-to-severe OSA confirmed by polysomnography, significant symptoms, or OSA complications.
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What is the role of continuous positive airway pressure (CPAP) in pediatric OSA?
CPAP maintains airway patency by providing continuous positive airway pressure, preventing collapse during sleep.
215
When is CPAP therapy indicated in children?
CPAP is indicated if adenotonsillectomy is contraindicated, incomplete resolution of OSA post-surgery, or in cases with craniofacial or neuromuscular abnormalities.
216
What medical treatments may be helpful for mild OSA?
Medical therapies: intranasal corticosteroids or leukotriene receptor antagonists (e.g., montelukast) for mild OSA, especially if associated with allergic rhinitis.
217
How does obesity affect pediatric OSA?
Obesity exacerbates OSA severity by increasing pharyngeal adiposity; weight loss improves OSA control.
218
What preventive strategies are important in OSA management?
Strategies: weight control, treating allergic rhinitis, nasal airway management, and early recognition of sleep-disordered breathing.
219
What is the long-term prognosis after treatment of pediatric OSA?
Prognosis is good with early diagnosis and treatment; many children experience complete or significant resolution of symptoms after intervention.
220
What are the indications for follow-up sleep study after OSA treatment?
Follow-up polysomnography is recommended if symptoms persist after treatment, for high-risk groups, or if OSA severity was high before intervention.
221
What is a pleural effusion?
Pleural effusion is the abnormal accumulation of fluid in the pleural space between the lung and chest wall.
222
What are the main types of pleural effusion based on pathophysiology?
Types: transudative (due to systemic factors like hydrostatic/oncotic pressure imbalance) and exudative (due to inflammation or infection).
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What are common causes of transudative pleural effusions in children?
Transudates: congestive heart failure, nephrotic syndrome, liver cirrhosis, hypoalbuminemia.
224
What are common causes of exudative pleural effusions in children?
Exudates: parapneumonic effusion (bacterial pneumonia), tuberculosis, malignancy, connective tissue diseases.
225
What are the clinical features of pleural effusion?
Features: cough, dyspnea, chest pain, fever (if infectious cause), and reduced breath sounds.
226
How does the size of the effusion affect symptoms?
Small effusions may be asymptomatic; larger effusions cause respiratory distress and decreased exercise tolerance.
227
What physical exam findings suggest a pleural effusion?
Exam: decreased breath sounds, dullness to percussion, decreased tactile fremitus, asymmetrical chest expansion.
228
What imaging modality is most sensitive for detecting pleural effusions?
Ultrasound is more sensitive than chest X-ray for detecting and characterizing pleural effusions, especially small or loculated ones.
229
What are the typical chest X-ray findings in pleural effusion?
CXR findings: blunting of costophrenic angle, homogeneous opacity, mediastinal shift (if large).
230
What is the role of ultrasound in pleural effusion?
Ultrasound detects small effusions, guides thoracentesis, and distinguishes simple vs complex (loculated) effusions.
231
When is CT scan indicated for pleural effusion evaluation?
CT is used when empyema, abscess, loculation, or underlying lung pathology (e.g., mass) is suspected.
232
What is thoracentesis and why is it important?
Thoracentesis is the aspiration of pleural fluid for diagnostic and sometimes therapeutic purposes.
233
How is pleural fluid analyzed after thoracentesis?
Pleural fluid is analyzed for protein, LDH, glucose, pH, Gram stain, culture, cytology, and cell counts.
234
What are Light’s criteria for distinguishing exudate vs transudate?
Exudate meets at least one of Light’s criteria:
- Pleural fluid protein/serum protein >0.5
- Pleural fluid LDH/serum LDH >0.6
- Pleural fluid LDH >2/3 upper limit of normal serum LDH.
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What pleural fluid findings suggest empyema?
Features suggesting empyema: purulent fluid, low pH (<7.2), low glucose (<40 mg/dL), high LDH, and positive Gram stain/culture.
236
What is the initial management of a moderate-to-large pleural effusion?
Initial management: oxygen, antibiotics (if infectious), thoracentesis for diagnosis, and supportive care.
237
When is chest tube drainage indicated?
Chest tube drainage is indicated for large effusions causing respiratory compromise or complicated (loculated, purulent) effusions.
238
What is the role of intrapleural fibrinolytic therapy?
Intrapleural fibrinolytics (e.g., tPA) can break down septations and facilitate drainage in complicated empyema.
239
What are potential complications of pleural effusions in children?
Complications: empyema, fibrothorax, respiratory failure, sepsis, and in rare cases, chronic restrictive lung disease.
240
What is the prognosis after effective treatment of pleural effusion?
Prognosis is excellent with timely diagnosis and treatment; most children recover fully without long-term sequelae.
241
What is pneumothorax?
Pneumothorax is the accumulation of air in the pleural space causing lung collapse.
242
What are the types of pneumothorax based on etiology?
Types: spontaneous (primary or secondary), traumatic, and iatrogenic pneumothorax.
243
What are common causes of spontaneous pneumothorax in children?
Spontaneous causes: rupture of subpleural blebs, asthma exacerbation, cystic fibrosis, Marfan syndrome.
244
What is secondary pneumothorax?
Secondary pneumothorax occurs in children with underlying lung disease (e.g., asthma, cystic fibrosis, pneumonia, mechanical ventilation).
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What is a tension pneumothorax?
Tension pneumothorax occurs when air enters the pleural space and cannot escape, leading to increased intrathoracic pressure, mediastinal shift, and cardiovascular compromise.
246
What are the clinical features of pneumothorax in children?
Features: sudden onset of chest pain, dyspnea, tachypnea, cyanosis if large, respiratory distress.
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What are signs of tension pneumothorax?
Signs: severe respiratory distress, hypotension, distended neck veins, tracheal deviation away from affected side (late sign), cyanosis.
248
What physical exam findings suggest pneumothorax?
Exam: hyperresonance to percussion, decreased or absent breath sounds on the affected side, decreased chest wall movement.
249
What is the initial investigation for suspected pneumothorax?
Initial test: chest X-ray (anteroposterior view); bedside ultrasound if unstable patient.
250
What are chest X-ray findings in pneumothorax?
Findings: visible pleural line with absent lung markings peripheral to it, lung collapse, mediastinal shift if tension pneumothorax.
251
What is the role of ultrasound in diagnosing pneumothorax?
Ultrasound: absence of lung sliding and barcode (stratosphere) sign on M-mode confirms pneumothorax rapidly.
252
What is the emergency management of tension pneumothorax?
Emergency decompression with a needle (needle thoracostomy) followed by chest tube placement.
253
How is a needle decompression performed in tension pneumothorax?
Needle decompression is performed in the 2nd intercostal space at the midclavicular line or 4th–5th intercostal space anterior axillary line using a large-bore needle.
254
What is the definitive management of pneumothorax?
Definitive management: chest tube (thoracostomy) insertion to evacuate air and allow lung re-expansion.
255
When is chest tube insertion indicated in pneumothorax?
Chest tube is indicated for large, symptomatic, or tension pneumothoraces.
256
What is the management of a small, asymptomatic pneumothorax?
Observation with oxygen therapy may suffice for small, stable pneumothoraces without respiratory distress.
257
What are risk factors for recurrence of pneumothorax?
Risk factors: underlying lung disease, mechanical ventilation, tall thin adolescent males (primary spontaneous pneumothorax).
258
What are complications of untreated pneumothorax?
Complications: respiratory failure, cardiac arrest (in tension pneumothorax), persistent air leak, infection.
259
What preventive strategies are recommended for recurrent pneumothorax?
Preventive options: avoid smoking, surgical pleurodesis or pleurectomy for recurrent pneumothorax.
260
What is the prognosis of pediatric pneumothorax with appropriate treatment?
Prognosis is excellent with appropriate management; recurrence risk exists especially in spontaneous pneumothorax.
261
What is empyema?
Empyema is the collection of pus within the pleural space, usually as a complication of pneumonia.
262
How does empyema develop in children?
Empyema develops from a complicated parapneumonic effusion as infection progresses and pus accumulates in the pleural cavity.
263
What are the stages of parapneumonic effusion leading to empyema?
Stages:
- Exudative phase (sterile fluid)
- Fibrinopurulent phase (infection, loculations)
- Organizing phase (fibrosis, trapped lung).
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What are the common causative organisms of empyema in children?
Common organisms: Streptococcus pneumoniae, Staphylococcus aureus (including MRSA), Streptococcus pyogenes, anaerobes.
265
What are the clinical features of empyema?
Symptoms: fever, cough, pleuritic chest pain, dyspnea, failure to improve after initial pneumonia therapy, weight loss.
266
How does empyema differ clinically from simple parapneumonic effusion?
Empyema usually presents with more severe systemic illness, persistent fever despite antibiotics, and chest pain compared to simple effusion.
267
What physical exam findings suggest empyema?
Findings: decreased breath sounds, dullness to percussion, decreased chest wall movement, egophony above fluid level.
268
What imaging studies are used to diagnose empyema?
Chest X-ray, ultrasound, and sometimes CT scan are used to detect, characterize, and guide management of empyema.
269
What are typical chest X-ray findings in empyema?
Chest X-ray: homogeneous opacity, possible mediastinal shift, and air-fluid levels if associated with bronchopleural fistula.
270
What is the role of chest ultrasound in empyema?
Ultrasound: identifies fluid loculations, fibrinous septations, guides thoracentesis, and assesses complexity of effusion.
271
What are pleural fluid characteristics of empyema?
Pleural fluid is typically purulent with low pH (<7.2), low glucose (<40 mg/dL), high LDH, and positive Gram stain or culture.
272
What laboratory tests should be performed on pleural fluid?
Tests: Gram stain, culture, cell count, glucose, pH, LDH, differential cell count.
273
What is the initial antibiotic management of empyema?
Initial antibiotics: broad-spectrum IV antibiotics targeting S. pneumoniae, S. aureus (including MRSA if suspected), and anaerobes if aspiration suspected.
274
When is chest tube drainage indicated in empyema?
Chest tube drainage is indicated for moderate-to-large, loculated, or complicated effusions with respiratory compromise.
275
What is the role of intrapleural fibrinolytic therapy in empyema?
Intrapleural fibrinolytics (e.g., alteplase, DNase) help break down septations and improve drainage of thick or loculated effusions.
276
When is surgical intervention (VATS or thoracotomy) indicated in empyema?
Surgical intervention (video-assisted thoracoscopic surgery - VATS, or thoracotomy) is indicated if medical management fails or there is organized empyema.
277
What supportive measures are important in empyema management?
Supportive care: oxygen supplementation, hydration, nutrition support, analgesia, and respiratory physiotherapy.
278
What complications can arise from untreated or severe empyema?
Complications: sepsis, lung abscess, bronchopleural fistula, restrictive lung disease, scoliosis from chronic empyema.
279
What preventive measures reduce the incidence of empyema?
Prevention: timely vaccination (PCV, Hib), early recognition and treatment of pneumonia, prompt antibiotic therapy.
280
What is the prognosis for pediatric empyema with appropriate treatment?
Prognosis is excellent with appropriate treatment; most children recover full lung function over time.
281
Q: What is the primary goal of asthma management in pediatric patients?
A: To achieve and maintain optimal control of symptoms, reduce the risk of exacerbations, improve lung function, enhance quality of life, and minimize medication side effects, while promoting normal growth and development.
282
Q: What are the key components of asthma control in pediatric patients?
A: Symptom control, risk reduction, patient and family education, regular monitoring, and individualized asthma action plans.
283
Q: What is the preferred first-line controller medication for mild persistent asthma in children?
A: Low-dose inhaled corticosteroids (ICS), such as budesonide or fluticasone, which reduce airway inflammation and improve long-term outcomes.
284
Q: When should a long-acting beta-agonist (LABA) be added to asthma therapy in children?
A: In children with moderate to severe persistent asthma not adequately controlled on medium doses of ICS, often in combination inhalers (e.g., budesonide-formoterol, fluticasone-salmeterol).
285
Q: What is the preferred rescue medication for acute asthma symptoms in children?
A: Short-acting beta-agonists (SABA), such as albuterol or salbutamol, for rapid bronchodilation and symptom relief.
286
Q: How often should asthma control be assessed in pediatric patients?
A: Every 1 to 3 months for initial follow-up, then every 3 to 6 months once well controlled, with more frequent assessments during high-risk periods (e.g., viral seasons, allergy seasons).
287
Q: What are the criteria for stepping down asthma therapy in children?
A: Well-controlled symptoms for at least 3 to 6 months with minimal side effects, stable lung function, and no recent exacerbations.
288
Q: What role do leukotriene receptor antagonists (LTRAs) play in pediatric asthma management?
A: They are an alternative or add-on therapy for mild to moderate persistent asthma, especially in children with coexisting allergic rhinitis or exercise-induced bronchoconstriction.
289
Q: What is the recommended approach for exercise-induced bronchoconstriction in children?
A: Use of a SABA 15 to 30 minutes before exercise or daily ICS for better long-term control, with consideration of LTRA if symptoms persist.
290
Q: What non-pharmacological strategies are recommended for pediatric asthma management?
A: Allergen avoidance, trigger control, smoking cessation in the household, regular follow-up, patient and family education, and personalized asthma action plans.
291
Q: What is the role of biologic therapies in severe pediatric asthma?
A: Considered for children with severe asthma not controlled with high-dose ICS and additional controller medications, often with evidence of allergic or eosinophilic asthma (e.g., omalizumab, mepolizumab).
292
Q: What are the key components of an asthma action plan for children?
A: Instructions for daily management, early recognition of worsening symptoms, steps for emergency care, and clear guidance on medication adjustments based on symptom severity.
293
Q: How should asthma exacerbations be managed in the emergency setting?
A: Oxygen support, SABA administration (every 20 minutes as needed), systemic corticosteroids (oral or IV), and consideration of adjunct therapies like magnesium sulfate, ipratropium bromide, or noninvasive ventilation in severe cases.
294
Q: What is the preferred method for monitoring asthma control in children?
A:
Symptom diaries, peak flow monitoring, regular spirometry for older children, and fractional exhaled nitric oxide (FeNO) testing where available.
295
Q: When should pediatric asthma patients be referred to a specialist?
A: Frequent exacerbations, severe persistent asthma, difficulty confirming diagnosis, poor response to conventional therapy, or need for biologic therapy.
