Pediatrics
Final Professional MBBS — Pediatrics. Complete question bank: Long Questions (10 marks) and Short Notes (5 marks) across all 15 systems, with clinical pearls, drug doses, staging tables, mnemonics and key-point recaps.
15chapters180questions108High-Yield
DEFINITION
Bronchial asthma is a chronic inflammatory disorder of the airways characterised by reversible airflow obstruction, bronchial hyper-responsiveness and recurrent episodes of wheeze, cough, breathlessness and chest tightness. It is the commonest chronic respiratory disease of childhood.
ETIOLOGY & TRIGGERS
- Host factors — genetic predisposition and atopy (personal/family history of eczema, allergic rhinitis).
- Viral respiratory infections — the commonest trigger of exacerbations in children (rhinovirus, RSV).
- Allergens — house-dust mite, pollen, moulds, pet danders, cockroach.
- Irritants & others — tobacco/biomass smoke, air pollution, cold air, exercise, strong emotions and certain drugs (aspirin, NSAIDs).
PATHOPHYSIOLOGY
Trigger + atopic (Th2) inflammation → Mast cells, eosinophils, IgE activated → Bronchoconstriction + mucosal oedema + mucus plugging → Airflow obstruction (reversible) → Chronic inflammation → airway remodelling (fixed component)
The early phase (bronchoconstriction) is mediated by histamine and leukotrienes; the late phase (inflammation, oedema) occurs hours later. Persistent inflammation causes airway hyper-responsiveness and, over time, remodelling.
CLINICAL FEATURES
- Recurrent, episodic wheeze, cough (often nocturnal/early-morning), breathlessness and chest tightness.
- Symptoms show diurnal variation (worse at night) and are triggered by the above factors.
- History of atopy (eczema, allergic rhinitis) in the child or family.
- Examination in an attack — tachypnoea, prolonged expiration, polyphonic wheeze, use of accessory muscles, hyperinflated chest.
DIAGNOSIS & INVESTIGATIONS
- Largely a clinical diagnosis based on the recurrent, reversible pattern of symptoms.
- Spirometry (age > 5 yr) — an obstructive pattern (↓ FEV1/FVC) with reversibility (FEV1 improves ≥ 12% after a bronchodilator).
- Peak Expiratory Flow Rate (PEFR) — diurnal variability > 13% supports asthma and helps monitoring.
- Supportive — chest X-ray (to exclude other causes; may show hyperinflation), allergy testing, and a therapeutic trial of inhaled steroids.
ASSESSMENT OF ACUTE SEVERITY
Feature Mild–Moderate Severe Life-threatening Speech Sentences Words only Unable to speak SpO2 (air) > 92% < 92% < 92%, cyanosis Wheeze/chest Wheeze present Loud wheeze, accessory muscles Silent chest Sensorium Normal Agitated Drowsy / confused MANAGEMENT OF ACUTE EXACERBATION
- Oxygen to maintain SpO2 ≥ 94%.
- Inhaled SABA — salbutamol via MDI + spacer (2–6 puffs) or nebuliser, repeated every 20 min in the first hour.
- Add ipratropium bromide nebulisation in moderate–severe attacks.
- Systemic corticosteroids — oral prednisolone 1–2 mg/kg (or IV hydrocortisone) early in all but the mildest attacks.
- IV magnesium sulfate in severe/life-threatening attacks; consider IV salbutamol/aminophylline and ICU care/ventilation if not responding.
LONG-TERM (CONTROLLER) MANAGEMENT — Stepwise (GINA)
- Reliever — inhaled SABA (or low-dose ICS-formoterol) as needed.
- Controller — inhaled corticosteroid (ICS) is the cornerstone; step up to ICS + LABA, then higher-dose ICS.
- Add-on — leukotriene receptor antagonist (montelukast); biologics for severe allergic asthma.
- Step up if poorly controlled, step down once controlled for ~3 months; use the lowest effective dose.
PATIENT & FAMILY EDUCATION
- Correct inhaler technique (MDI + spacer) — check at every visit.
- Trigger avoidance; a written asthma action plan; recognise danger signs.
- Adherence to controller therapy; treat allergic rhinitis; annual influenza vaccine.
COMPLICATIONS
- Acute — status asthmaticus, pneumothorax, respiratory failure.
- Chronic — airway remodelling with fixed obstruction, growth & school impact, and steroid side-effects.
DIFFERENTIAL DIAGNOSIS OF RECURRENT WHEEZE
- Bronchiolitis (first episode in an infant, viral), foreign body (sudden onset, unilateral).
- Gastro-oesophageal reflux; recurrent aspiration; tuberculosis; suppurative lung disease.
- Cystic fibrosis (with failure to thrive/steatorrhoea); congenital heart disease; structural airway anomaly (vascular ring).
ASSESSMENT OF CONTROL (GINA)
- In the past 4 weeks — daytime symptoms > twice/week, any night waking, reliever use > twice/week, or any activity limitation.
- None → well-controlled; 1–2 → partly controlled; 3–4 → uncontrolled.
- Control guides stepping up or down of therapy at each review.
SPECIAL PATTERNS
- Exercise-induced asthma — wheeze/cough during or after exertion; pre-treat with a SABA and ensure good baseline control.
- Cough-variant asthma — persistent dry cough (often nocturnal) as the only symptom.
💊KEY DRUG DOSES (viva)- Salbutamol MDI 2–6 puffs (100 µg each) via spacer, or nebs 0.15 mg/kg (2.5 mg < 5 yr, 5 mg older).
- Prednisolone 1–2 mg/kg/day (max 40 mg) × 3–5 days; or IV hydrocortisone 4 mg/kg.
- Ipratropium 250 µg (<5 yr) / 500 µg neb.
- IV magnesium sulfate 25–50 mg/kg (max 2 g) over 20 min (severe).
- Controller: inhaled corticosteroid (low-dose budesonide/fluticasone).
🔑KEY POINTS TO REMEMBER- Asthma = chronic airway inflammation with reversible obstruction & hyper-responsiveness.
- Viral infections are the commonest trigger of exacerbations in children.
- Diagnosis clinical; spirometry shows reversibility (FEV1 ↑ ≥ 12% post-bronchodilator).
- Acute: O2 + SABA + ipratropium + systemic steroids (± IV magnesium).
- Controller = inhaled corticosteroid (stepwise GINA); check inhaler technique & action plan.
📝CLINICAL / APPLIED POINTS- Recurrent, reversible, triggered wheeze/cough with atopy suggests asthma.
- Spirometry reversibility (FEV1 ↑ ≥ 12%) supports the diagnosis in older children.
- Acute: O2 + repeated SABA + ipratropium + early systemic steroids; add IV magnesium if severe.
- ICS is the controller cornerstone; step up/down by control.
- Educate on inhaler technique, triggers and a written action plan.
📚SOURCES: GINA guidelines; Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; IAP respiratory guidelines.DEFINITION
Pneumonia is an acute inflammation of the lung parenchyma (alveoli), usually infective, presenting with cough, fever and fast/difficult breathing. It is a leading cause of under-5 mortality worldwide and in India.
ETIOLOGY (varies with age)
- Neonates: Group B Streptococcus, E. coli, Klebsiella, Listeria.
- Infants & young children: viruses are commonest (RSV, influenza); the leading bacterium is Streptococcus pneumoniae, then H. influenzae type b and Staphylococcus aureus.
- Older children (> 5 yr): Mycoplasma pneumoniae (atypical), S. pneumoniae, Chlamydophila.
- Special settings — Staph aureus (post-measles, empyema/pneumatocele), TB, Pneumocystis (in HIV).
WHO / IMNCI CLASSIFICATION (cough or difficult breathing)
Category Signs Management No pneumonia (cough/cold) No fast breathing, no chest indrawing Home care, fluids, review Pneumonia Fast breathing only Oral amoxicillin, home treatment Severe pneumonia Chest indrawing OR any danger sign Refer/admit; injectable antibiotics + O2 💡CLINICAL PEARL: Fast-breathing thresholds: < 2 months ≥ 60/min · 2–12 months ≥ 50/min · 1–5 years ≥ 40/min. Danger signs: unable to drink/feed, persistent vomiting, convulsions, lethargy/unconsciousness, stridor at rest, or severe malnutrition.CLINICAL FEATURES
- Fever, cough, and fast/difficult breathing; poor feeding and irritability.
- Signs of respiratory distress — chest indrawing, nasal flaring, grunting, head-nodding, cyanosis.
- Chest signs — reduced air entry, crepitations, bronchial breathing, dullness (if consolidation/effusion).
INVESTIGATIONS
- Often a clinical diagnosis; pulse oximetry to assess hypoxia.
- Chest X-ray — lobar consolidation (bacterial) or diffuse/patchy infiltrates (viral/atypical); detects effusion/empyema.
- CBC, CRP; blood culture in severe cases; sputum/NP aspirate; Mantoux/GeneXpert if TB suspected.
MANAGEMENT
- Pneumonia (fast breathing): home care with oral amoxicillin (the drug of choice) for 5 days; supportive care and review.
- Severe pneumonia: admit, give oxygen (target SpO2 ≥ 90%), IV antibiotics (ampicillin + gentamicin, or ceftriaxone; add cloxacillin/vancomycin for suspected Staph).
- Supportive care — maintain hydration & nutrition, antipyretics, continue breastfeeding, and treat wheeze if present.
- Switch to oral antibiotics once improving; total course guided by severity and organism.
COMPLICATIONS
- Parapneumonic effusion / empyema; lung abscess; pneumatocele and pneumothorax (Staph).
- Respiratory failure; septicaemia and metastatic infection; SIADH.
PREVENTION
- Immunisation — PCV (pneumococcal), Hib, measles, pertussis and influenza vaccines.
- Exclusive breastfeeding, adequate nutrition, vitamin A, zinc; hand hygiene.
- Reduce indoor air pollution (biomass smoke) and overcrowding; avoid tobacco exposure.
PATHOPHYSIOLOGY
Pathogen reaches the alveoli → Inflammatory exudate fills alveoli (consolidation) → Impaired gas exchange (V/Q mismatch) → Hypoxia, fast breathing & work of breathing ↑
TYPES / RADIOLOGICAL PATTERNS
- Lobar pneumonia — consolidation of a lobe (typically pneumococcal).
- Bronchopneumonia — patchy, bilateral infiltrates (common in infants).
- Interstitial / atypical — diffuse pattern (viral, Mycoplasma).
DIFFERENTIAL DIAGNOSIS
- Bronchiolitis and asthma (wheeze-predominant); tuberculosis (chronic course, contact history).
- Foreign-body aspiration (non-resolving/localised); congestive cardiac failure; empyema.
INDICATIONS FOR HOSPITAL ADMISSION
- Severe pneumonia (chest indrawing / any danger sign); hypoxia (SpO2 < 90%).
- Age < 2 months; inability to feed/drink; severe malnutrition or significant comorbidity.
- Failure of oral outpatient therapy; complications (effusion/empyema).
EMPIRICAL ANTIBIOTIC CHOICE
Setting First-line antibiotic Outpatient (non-severe) Oral amoxicillin (high dose) Inpatient / severe IV ampicillin + gentamicin, or ceftriaxone Suspected Staph (empyema/pneumatocele) Add cloxacillin / vancomycin Atypical (older child) Macrolide (azithromycin) SUPPORTIVE CARE
- Oxygen to maintain SpO2 ≥ 90%; antipyretics for fever/comfort.
- Maintain hydration and nutrition; continue breastfeeding; small frequent feeds or IV fluids if unable to feed.
- Clear nasal secretions; treat associated wheeze; monitor for deterioration and complications.
💊KEY DRUG DOSES (viva)- Oral amoxicillin 40–45 mg/kg/dose BD (high dose) — non-severe.
- IV ampicillin 50 mg/kg/dose + gentamicin 5–7.5 mg/kg/day, or ceftriaxone 50–75 mg/kg/day.
- Add cloxacillin 50 mg/kg/dose / vancomycin for suspected Staph.
- Azithromycin 10 mg/kg/day for atypical.
🔑KEY POINTS TO REMEMBER- Pneumonia = alveolar inflammation; leading cause of under-5 deaths.
- Viral commonest overall; S. pneumoniae the leading bacterium.
- WHO/IMNCI: fast breathing = pneumonia; chest indrawing/danger sign = severe.
- Fast-breathing cut-offs: < 2 mo ≥ 60, 2–12 mo ≥ 50, 1–5 yr ≥ 40.
- Oral amoxicillin (non-severe); admit + IV antibiotics + O2 (severe); prevent with PCV/Hib.
📝CLINICAL / APPLIED POINTS- Count the respiratory rate — fast breathing defines pneumonia (WHO/IMNCI).
- Chest indrawing or a danger sign = severe pneumonia → admit + IV antibiotics + O2.
- Non-severe → oral amoxicillin at home with review.
- Suspect Staph with rapid deterioration, empyema or pneumatoceles.
- Prevent with PCV, Hib, measles & pertussis vaccines and good nutrition.
📚SOURCES: WHO/IMNCI pneumonia guidelines; Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Acute bronchiolitis is an acute viral lower respiratory tract infection of infants (usually < 2 years, peak 2–6 months), characterised by inflammation and obstruction of the small airways (bronchioles), producing wheeze and respiratory distress. It typically occurs in winter epidemics.
ETIOLOGY
- Respiratory Syncytial Virus (RSV) — the commonest cause (~70%).
- Others — human metapneumovirus, parainfluenza, influenza, adenovirus, rhinovirus.
- Spread is by droplets and contact; highly contagious (hospital & household spread).
PATHOPHYSIOLOGY
Viral infection of bronchiolar epithelium → Inflammation, oedema & mucus + sloughed cells → Small-airway obstruction (a 'ball-valve' effect) → Air trapping + hyperinflation and patchy collapse → V/Q mismatch → hypoxia and increased work of breathing
CLINICAL FEATURES
- A preceding coryza (runny nose, mild fever) for 1–3 days, then lower-respiratory signs.
- Cough, wheeze, tachypnoea and feeding difficulty (breathlessness interrupts feeds).
- Respiratory distress — chest indrawing, nasal flaring, grunting; a hyperinflated chest.
- Auscultation — fine end-inspiratory crepitations with widespread wheeze.
- Apnoea may be the presenting feature in young/preterm infants.
RISK FACTORS FOR SEVERE DISEASE
- Age < 3 months; prematurity; low birth weight.
- Congenital heart disease, chronic lung disease, immunodeficiency, and neuromuscular disease.
DIAGNOSIS & INVESTIGATIONS
- A clinical diagnosis; investigations are usually unnecessary.
- Pulse oximetry to assess hypoxia; chest X-ray (if atypical) shows hyperinflation, patchy atelectasis.
- Nasopharyngeal aspirate for RSV (rapid antigen/PCR) — mainly for cohorting in hospital.
MANAGEMENT — Mainly Supportive
- Oxygen for hypoxia (SpO2 < 90–92%); gentle nasal suction to clear secretions.
- Maintain hydration & feeding — small frequent feeds; NG or IV fluids if unable to feed.
- Minimal handling; monitor for apnoea and worsening distress.
- Respiratory support (high-flow nasal cannula / CPAP / ventilation) for severe disease.
⚠️DANGER / REMEMBER: Bronchodilators, corticosteroids, antibiotics and nebulised adrenaline are NOT routinely recommended — bronchiolitis is a self-limiting viral illness, and these do not change its course. Antibiotics are added only if there is secondary bacterial infection.COMPLICATIONS & PREVENTION
- Complications: apnoea, respiratory failure, dehydration, secondary bacterial infection; later recurrent wheeze.
- Prevention: hand hygiene and isolation of cases; exclusive breastfeeding; avoid smoke exposure.
- Palivizumab (RSV monoclonal antibody) prophylaxis for selected high-risk infants (preterm, chronic lung/heart disease).
EPIDEMIOLOGY
- Chiefly affects infants < 2 years, peaking at 2–6 months; occurs in winter epidemics.
- A leading cause of infant hospitalisation for respiratory illness.
ASSESSMENT OF SEVERITY
- Mild: feeding well, minimal distress, SpO2 normal.
- Moderate: some feeding difficulty, chest indrawing, tachypnoea.
- Severe: poor feeding, marked distress/grunting, SpO2 < 92%, apnoea, exhaustion.
CRITERIA FOR HOSPITAL ADMISSION
- Poor feeding (< 50% of normal) or dehydration; apnoea.
- Hypoxia (SpO2 < 92%); severe respiratory distress; age < 3 months or high-risk infant.
DIFFERENTIAL DIAGNOSIS
Feature Bronchiolitis Asthma Pneumonia Age < 2 yr (often first episode) Usually > 2 yr, recurrent Any Onset Coryza then wheeze Recurrent, triggered Fever + fast breathing Auscultation Fine creps + wheeze Wheeze Focal creps/bronchial breath Response to bronchodilator Poor Good N/A PROGNOSIS
Most infants recover fully within 1–2 weeks. Some have recurrent viral wheeze in early childhood; severe RSV bronchiolitis in infancy is associated with later wheezing tendency.
CLINICAL COURSE
Illness typically peaks around days 3–5 and then improves over 1–2 weeks; cough may linger longer. Close monitoring during the peak is important, especially in young infants at risk of apnoea.
KEY SUPPORTIVE MEASURES
- Ensure adequate hydration — offer small, frequent feeds; use NG/IV fluids if feeding is inadequate.
- Gentle nasal saline and suction before feeds; nurse with the head slightly elevated.
- Reassess frequently for hypoxia, apnoea and worsening work of breathing.
🔑KEY POINTS TO REMEMBER- Bronchiolitis = viral LRTI of infants < 2 yr; RSV is commonest.
- Coryza → cough, wheeze, fine creps, hyperinflation, feeding difficulty, apnoea.
- Management is mainly supportive (O2, feeds/hydration, suction).
- Bronchodilators, steroids and antibiotics are NOT routinely useful.
- Palivizumab for selected high-risk infants.
📝CLINICAL / APPLIED POINTS- First wheezy episode in an infant < 2 years with coryza suggests bronchiolitis.
- Management is supportive — oxygen, feeding/hydration, nasal suction.
- Bronchodilators/steroids/antibiotics are NOT routinely helpful.
- Watch young infants for apnoea; admit for hypoxia/poor feeding.
- Palivizumab for selected high-risk infants; hand hygiene prevents spread.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; NICE/AAP bronchiolitis guidelines.DEFINITION
Foreign body (FB) aspiration is the inhalation of an object into the airway (larynx, trachea or bronchi). It is a paediatric emergency, most common in children aged 1–3 years, in whom curiosity, incomplete dentition and immature swallowing coordination increase the risk.
COMMON FOREIGN BODIES & SITE
- Organic objects are commonest — groundnuts/peanuts, seeds, pulses; also small toy parts, beads, and pins.
- The right main bronchus is the commonest site of lodgement (it is wider, shorter and more vertical).
- Most FBs are radiolucent (organic), so they are not seen directly on X-ray.
CLINICAL PHASES
- Initial phase — sudden choking, coughing, gagging and wheeze at the time of aspiration (a witnessed 'choking episode' is the key clue).
- Asymptomatic (latent) phase — symptoms settle as the FB lodges; this false reassurance often delays diagnosis.
- Complications phase — persistent cough, recurrent/non-resolving pneumonia, localised wheeze or lung collapse.
CLINICAL FEATURES (by site)
- Laryngeal/tracheal FB: stridor, hoarseness, severe distress — can cause complete obstruction and asphyxia (an emergency).
- Bronchial FB: unilateral wheeze, reduced air entry and a hyper-resonant/dull hemithorax on the affected side.
INVESTIGATIONS
- Chest X-ray — an opaque FB is directly seen; a radiolucent FB shows indirect signs: unilateral obstructive emphysema (air trapping), mediastinal shift away from the affected side, atelectasis, or non-resolving consolidation.
- Inspiratory–expiratory (or lateral decubitus) films highlight air trapping.
- Bronchoscopy — both diagnostic and therapeutic; a normal X-ray does not exclude an FB, so a strong history warrants bronchoscopy.
MANAGEMENT — Acute complete obstruction (choking child)
- Infant (< 1 yr): alternate 5 back blows + 5 chest thrusts (head down).
- Older child: abdominal thrusts (Heimlich manoeuvre).
- If the child becomes unconscious → start CPR and attempt to visualise/remove the FB.
- Do NOT perform blind finger sweeps (risk of pushing the FB deeper).
MANAGEMENT — Definitive
- Rigid bronchoscopy under general anaesthesia is the treatment of choice for removal.
- Antibiotics and physiotherapy for associated infection/atelectasis; treat complications.
COMPLICATIONS & PREVENTION
- Complications: asphyxia/death, recurrent pneumonia, lung abscess, bronchiectasis, atelectasis, pneumothorax.
- Prevention: avoid giving nuts, seeds and small hard foods to children under 3 years; keep small objects out of reach; supervise feeding; parental awareness.
⚠️DANGER / REMEMBER: A witnessed choking episode with sudden cough/wheeze is foreign-body aspiration until proven otherwise — a normal chest X-ray does NOT rule it out, and bronchoscopy should be done on a strong history.WHY CHILDREN ARE PRONE
- The habit of putting objects in the mouth and running/playing while eating.
- Incomplete dentition (poor chewing of nuts) and immature airway-protective (swallowing) coordination.
- Peak age 1–3 years.
DIFFERENTIAL DIAGNOSIS
- Croup and asthma (wheeze/stridor without a choking history); recurrent pneumonia of other cause.
- The key discriminator is a witnessed choking/aspiration episode.
POST-REMOVAL CARE
- Observe for airway oedema/laryngospasm; chest physiotherapy and antibiotics for associated infection/atelectasis.
- Repeat imaging to confirm re-expansion of the lung.
PROGNOSIS
Excellent with early recognition and bronchoscopic removal. Delayed diagnosis leads to recurrent pneumonia, bronchiectasis and lung damage — hence a low threshold for bronchoscopy on a strong history.
FEATURES BY SITE OF LODGEMENT
Site Key features Laryngeal Stridor, hoarseness/aphonia, severe distress — risk of complete obstruction Tracheal Biphasic stridor, audible slap/wheeze, cough Bronchial (commonest) Unilateral wheeze, reduced air entry, recurrent focal pneumonia RADIOLOGICAL SIGNS (radiolucent FB)
- Obstructive emphysema (air trapping) of the affected side — hyperlucent lung.
- Mediastinal shift away from the affected side (more marked on expiration).
- Atelectasis/collapse or persistent, non-resolving consolidation distal to the obstruction.
🔑KEY POINTS TO REMEMBER- FB aspiration commonest at 1–3 yr; groundnut is the classic FB.
- Right main bronchus is the commonest site; most FBs are radiolucent.
- Phases: choking → asymptomatic latent → complications (recurrent pneumonia).
- CXR (radiolucent): obstructive emphysema, mediastinal shift away, atelectasis.
- Rigid bronchoscopy is diagnostic & therapeutic; a normal CXR doesn't exclude it.
📝CLINICAL / APPLIED POINTS- A witnessed choking episode is FB aspiration until proven otherwise.
- Right main bronchus is commonest; most FBs are radiolucent.
- Look for obstructive emphysema and mediastinal shift AWAY on CXR.
- A normal CXR does NOT exclude an FB — bronchoscopy on a strong history.
- Prevent by keeping nuts/small objects away from under-3s.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; paediatric BLS/airway guidelines.DEFINITION
Croup (acute laryngotracheobronchitis) is a common viral infection causing inflammation of the larynx, trachea and bronchi, leading to upper-airway obstruction. It typically affects children aged 6 months to 3 years and is the commonest cause of acute stridor with fever in this age group.
ETIOLOGY
- Parainfluenza virus (types 1 & 3) — the commonest cause.
- Others — RSV, influenza, adenovirus, and (rarely) measles.
- It occurs in autumn/winter; subglottic oedema in a narrow infant airway causes the obstruction.
PATHOPHYSIOLOGY
Viral infection of the larynx & subglottis → Inflammation & oedema of the subglottic region → Narrowing of the already-small infant airway → Turbulent airflow → inspiratory stridor + barking cough
CLINICAL FEATURES
- A preceding coryza and low-grade fever for 1–2 days.
- The classic triad — barking ('seal-like') cough, inspiratory stridor, and a hoarse voice.
- Symptoms are typically worse at night and with crying/agitation.
- Signs of increasing obstruction — stridor at rest, chest indrawing, tachypnoea, restlessness, and (late/ominous) cyanosis, drowsiness or a silent chest.
ASSESSMENT OF SEVERITY (Westley score concept)
- Mild: barking cough, no stridor at rest, no/mild indrawing — the child is playful and feeding.
- Moderate: stridor at rest with chest indrawing, but no agitation.
- Severe: stridor at rest with marked indrawing, agitation/distress.
- Impending respiratory failure: lethargy, decreasing stridor with fatigue, cyanosis.
INVESTIGATIONS
- A clinical diagnosis — avoid distressing the child.
- If done, a neck X-ray (AP) may show the 'steeple sign' (subglottic narrowing).
- Do NOT examine the throat or perform painful procedures if severe obstruction is suspected.
MANAGEMENT
- Keep the child calm (crying worsens obstruction); allow the parent to comfort them.
- Corticosteroids for all — a single dose of oral dexamethasone (0.15–0.6 mg/kg) (or nebulised budesonide) reduces oedema and severity.
- Moderate–severe: add nebulised adrenaline (rapid but temporary relief — observe for rebound for 2–4 hours) and give oxygen.
- Impending failure: senior/anaesthetic help and airway management (intubation) in a controlled setting.
- Maintain hydration; most mild cases are managed and discharged home with advice.
DIFFERENTIAL DIAGNOSIS OF ACUTE STRIDOR
Feature Croup Epiglottitis Foreign body Onset Gradual (1–2 days) Rapid (hours) Sudden (choking) Cough Barking Absent Variable Drooling / dysphagia Absent Present Absent Toxaemia / fever Mild High, toxic Absent Voice Hoarse Muffled Normal/hoarse ⚠️DANGER / REMEMBER: Consider epiglottitis (toxic, drooling, no cough) and foreign body (sudden choking) in any child with stridor — the management differs and epiglottitis is an airway emergency.EPIDEMIOLOGY
- Commonest in children aged 6 months–3 years; occurs in autumn/winter.
- The commonest cause of acute stridor with fever in this age group.
SPASMODIC (RECURRENT) CROUP
A variant with sudden night-time barking cough and stridor without preceding fever/coryza, often recurrent, with an allergic/atopic tendency. It settles quickly and is managed like viral croup.
CRITERIA FOR HOSPITAL ADMISSION
- Stridor at rest, moderate–severe chest indrawing, or hypoxia.
- Poor response to steroids/adrenaline; toxic appearance or diagnostic doubt; young infant or poor social support.
PROGNOSIS
Most croup is mild and self-limiting, resolving in 3–5 days; steroids markedly reduce severity and the need for admission. Serious airway obstruction is uncommon but must be anticipated.
MEDICATIONS AT A GLANCE
Drug Role Dexamethasone (oral, single dose) For ALL severities — reduces oedema & admission Nebulised budesonide Alternative steroid if oral not tolerated Nebulised adrenaline Moderate–severe — rapid but temporary; observe for rebound Oxygen / airway support Severe / impending failure HOME ADVICE (mild croup)
- Keep the child calm and comfortable; ensure adequate fluids.
- Return urgently if there is stridor at rest, chest indrawing, drooling, cyanosis or the child looks unwell.
💊KEY DRUG DOSES (viva)- Dexamethasone 0.15–0.6 mg/kg (single oral dose) — for ALL severities.
- Nebulised adrenaline (1:1000) 0.5 mL/kg (max 5 mL) — moderate–severe (observe 2–4 h for rebound).
- Nebulised budesonide 2 mg if oral not tolerated.
🔑KEY POINTS TO REMEMBER- Croup = viral laryngotracheobronchitis (parainfluenza), 6 mo–3 yr.
- Triad: barking cough, inspiratory stridor, hoarse voice; worse at night.
- 'Steeple sign' on neck X-ray; keep the child calm.
- Dexamethasone for all; nebulised adrenaline for moderate–severe.
- Differentiate from epiglottitis (toxic, drooling, no cough) and foreign body.
📝CLINICAL / APPLIED POINTS- Barking cough + inspiratory stridor + hoarse voice = croup.
- Keep the child calm; give dexamethasone to ALL.
- Nebulised adrenaline for moderate–severe (watch for rebound).
- 'Steeple sign' on neck X-ray; avoid throat examination if severe.
- Always consider epiglottitis and foreign body in the differential.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; croup management guidelines.DEFINITION
Whooping cough (pertussis) is an acute, highly contagious bacterial respiratory infection caused by Bordetella pertussis, characterised by paroxysms of coughing followed by an inspiratory 'whoop'. It is most severe and dangerous in young unimmunised infants.
PATHOGENESIS
- Spread by respiratory droplets; the organism attaches to respiratory cilia and releases pertussis toxin and other toxins → mucosal damage and impaired clearance.
- This produces thick secretions and the paroxysmal cough.
CLINICAL STAGES
- Catarrhal stage (1–2 weeks): coryza, mild cough, low fever — the most infectious phase.
- Paroxysmal stage (2–6 weeks): bursts of rapid coughs ending in a whoop, often with post-tussive vomiting, cyanosis and subconjunctival haemorrhage.
- Convalescent stage: gradual reduction over weeks ('the 100-day cough').
💡CLINICAL PEARL: Young infants may present with apnoea and cyanosis WITHOUT the classic whoop — a high index of suspicion is needed, as they are at greatest risk of severe disease and death.INVESTIGATIONS
- Marked absolute lymphocytosis on the blood count.
- Nasopharyngeal swab for culture or PCR confirms the diagnosis.
MANAGEMENT
- Macrolide antibiotics — azithromycin/erythromycin (reduce infectivity; most effective in the catarrhal stage).
- Supportive care — oxygen, gentle suction, nutrition/hydration, and monitoring for apnoea (admit young infants).
- Isolation and chemoprophylaxis of close contacts.
COMPLICATIONS & PREVENTION
- Complications — pneumonia (commonest cause of death), apnoea, seizures, encephalopathy, hernia.
- Prevention — DPT/pentavalent vaccine (and maternal Tdap); this is the key protective measure.
DIAGNOSIS — SUPPORTING POINTS
- A prolonged cough (> 2 weeks) with paroxysms, whoop or post-tussive vomiting in an under-/partially-immunised child is highly suggestive.
- Contact with a chronic cougher; marked lymphocytosis on CBC.
KEY EXAM POINT
Pertussis is most dangerous in young infants, who may present with apnoea and cyanosis rather than a whoop — always admit and monitor them, and remember that the DPT vaccine is the mainstay of prevention.
💊KEY DRUG DOSES (viva)- Azithromycin 10 mg/kg/day × 5 days (drug of choice), or erythromycin 40 mg/kg/day × 7–14 days.
- Same macrolide for post-exposure prophylaxis of close contacts.
🔑KEY POINTS TO REMEMBER- Pertussis (Bordetella) — catarrhal → paroxysmal (whoop, post-tussive vomiting) → convalescent.
- Infants may present with apnoea/cyanosis without a whoop.
- Marked lymphocytosis; confirm by culture/PCR.
- Macrolide antibiotic + isolation; prevent with DPT vaccine.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; WHO pertussis guidelines.DEFINITION
Acute epiglottitis is a rapidly progressive, life-threatening inflammation of the epiglottis and supraglottic structures that can cause sudden complete airway obstruction. It is a true paediatric airway emergency.
ETIOLOGY
- Classically Haemophilus influenzae type b (Hib) — now rare where Hib vaccination is routine.
- Other causes — Streptococcus pneumoniae, Staphylococcus aureus, group A streptococcus.
CLINICAL FEATURES (the classic picture)
- Rapid onset (over hours) of high fever and a toxic, ill appearance.
- The '4 D's' — Drooling, Dysphagia, Dysphonia (muffled/'hot-potato' voice), and Distress.
- The child sits upright, leaning forward in the 'tripod' position, with soft inspiratory stridor.
- Notably, there is NO barking cough (unlike croup).
⚠️DANGER / REMEMBER: Do NOT examine the throat, lie the child down, or perform painful/upsetting procedures — these can precipitate complete, fatal airway obstruction. Keep the child calm with the parent.INVESTIGATIONS
- Diagnosis is clinical; if a lateral neck X-ray is done it shows the 'thumb sign' (a swollen epiglottis).
- Definitive visualisation is done only in a controlled setting (theatre) during airway management.
MANAGEMENT
- Secure the airway first — call senior anaesthetic/ENT help; intubation (or tracheostomy) under controlled conditions in theatre.
- IV antibiotics — third-generation cephalosporin (ceftriaxone / cefotaxime).
- Oxygen and supportive care; treat close contacts (rifampicin prophylaxis for Hib).
CROUP vs EPIGLOTTITIS (must distinguish)
Feature Croup Epiglottitis Onset Gradual Rapid Cough Barking Absent Drooling No Yes Toxaemia Mild Severe X-ray Steeple sign Thumb sign KEY PRINCIPLE
The priority is a calm child and a secured airway — antibiotics come after the airway is safe.
💊KEY DRUG DOSES (viva)- Ceftriaxone 50–75 mg/kg/day (or cefotaxime) IV.
- Rifampicin prophylaxis for Hib contacts.
🔑KEY POINTS TO REMEMBER- Epiglottitis (Hib) — rapid onset, toxic, high fever.
- 4 D's: Drooling, Dysphagia, Dysphonia, Distress; tripod position; NO cough.
- 'Thumb sign'; do NOT examine the throat or upset the child.
- Secure the airway first, then IV ceftriaxone.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Empyema thoracis is the collection of pus in the pleural cavity. In children it is most often a complication of bacterial pneumonia (a 'parapneumonic effusion' that becomes infected).
ETIOLOGY
- Staphylococcus aureus (classic, especially in infants), Streptococcus pneumoniae, and Streptococcus pyogenes.
- Tuberculosis and Gram-negative organisms in specific settings.
STAGES
- Exudative stage — thin, free-flowing fluid.
- Fibrinopurulent stage — thick pus with fibrin strands and loculations.
- Organising stage — a thick fibrous 'peel' traps the lung.
CLINICAL FEATURES
- Persistent or swinging fever despite antibiotics for pneumonia, with toxaemia.
- Respiratory distress, chest pain, and reduced movement of the affected side.
- Signs — stony dull percussion note, reduced breath sounds and reduced vocal resonance on the affected side; mediastinal shift to the opposite side.
INVESTIGATIONS
- Chest X-ray — homogeneous opacity with a fluid level / obliterated costophrenic angle.
- Ultrasound of the chest — confirms fluid, detects loculations, and guides tapping.
- Pleural fluid aspiration & analysis — frank pus; sent for cell count, biochemistry, Gram stain, culture and AFB/TB testing.
MANAGEMENT
- Appropriate IV antibiotics (covering Staph & pneumococcus) for a prolonged course.
- Drainage — intercostal chest-tube (closed) drainage is the mainstay.
- Intrapleural fibrinolytics for loculated collections; surgery (decortication / VATS) for the organised stage or failed drainage.
- Supportive care — nutrition, oxygen, and treatment of the underlying pneumonia.
EMPYEMA vs SIMPLE EFFUSION
- A simple parapneumonic effusion is thin, sterile fluid; an empyema is frank pus with a low pH and glucose and a high LDH on pleural analysis.
- Ultrasound distinguishes free from loculated fluid and guides drainage.
PROGNOSIS
With timely antibiotics and drainage, most children recover fully with good lung function; delay leads to a thick pleural peel needing decortication.
🔑KEY POINTS TO REMEMBER- Empyema = pus in the pleural space, usually complicating pneumonia (Staph/pneumococcus).
- Persistent/swinging fever, stony dullness, reduced breath sounds.
- USG chest + pleural aspiration (frank pus) confirm it.
- Treat with antibiotics + chest-tube drainage (± fibrinolytics/decortication).
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; BTS pleural infection guidelines.DEFINITION
Status asthmaticus is a severe, prolonged asthma exacerbation that fails to respond to initial bronchodilator therapy and can progress to respiratory failure. It is a medical emergency.
ASSESSMENT OF SEVERITY (look for life-threatening features)
- Inability to complete sentences / feed; SpO2 < 92%; marked accessory-muscle use.
- Silent chest, cyanosis, poor respiratory effort.
- Exhaustion, agitation, drowsiness or confusion (altered sensorium).
- PEFR < 50% of predicted/best (in older children).
MANAGEMENT (stepwise, aggressive)
- Oxygen — high-flow to keep SpO2 ≥ 94%.
- Continuous / back-to-back nebulised salbutamol + ipratropium bromide (driven by oxygen).
- Systemic corticosteroids — early oral prednisolone or IV hydrocortisone/methylprednisolone.
- IV magnesium sulfate for severe/life-threatening cases.
- Consider IV salbutamol / aminophylline and shift to ICU; ventilation if there is respiratory failure or exhaustion.
MONITORING
- Continuous SpO2, heart rate, respiratory effort and mental status.
- Watch for complications — pneumothorax, hypokalaemia (from salbutamol), and worsening fatigue.
- Blood gas if deteriorating — a rising/normalising PaCO2 in a tiring child is an ominous sign.
⚠️DANGER / REMEMBER: A silent chest, cyanosis, exhaustion or a normalising/rising PaCO2 signals imminent respiratory failure — call for senior/ICU help and prepare for ventilation.PRECIPITATING FACTORS
- Poor adherence to controller therapy; a viral respiratory infection; heavy allergen/irritant exposure.
- Under-treatment of a worsening exacerbation at home.
KEY EXAM POINT
Early, aggressive treatment (oxygen + repeated bronchodilators + systemic steroids) and prompt escalation prevent progression to respiratory failure; do not be reassured by a 'quiet' chest — a silent chest is a danger sign.
PREVENTION OF FUTURE ATTACKS
- Optimise long-term controller (ICS) therapy and adherence.
- Provide a written asthma action plan and check inhaler technique.
- Identify and avoid triggers; treat allergic rhinitis; give the influenza vaccine.
💊KEY DRUG DOSES (viva)- Continuous/back-to-back salbutamol nebs + ipratropium; IV magnesium 25–50 mg/kg.
- Systemic steroids — prednisolone 1–2 mg/kg or IV hydrocortisone 4 mg/kg 6-hourly.
- IV salbutamol/aminophylline in ICU for refractory cases.
🔑KEY POINTS TO REMEMBER- Status asthmaticus = severe attack failing initial bronchodilators.
- Danger signs: silent chest, cyanosis, exhaustion, altered sensorium, rising PaCO2.
- O2 + continuous nebulised SABA + ipratropium + systemic steroids + IV magnesium.
- Escalate early to ICU/ventilation; a silent chest is ominous.
📚SOURCES: GINA guidelines; Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Cystic fibrosis (CF) is an autosomal recessive multisystem disorder caused by mutations in the CFTR gene (a chloride channel; ΔF508 is the commonest mutation). Defective chloride transport produces thick, viscid secretions that obstruct exocrine ducts throughout the body.
CLINICAL FEATURES (multisystem)
- Respiratory — chronic cough, recurrent chest infections (Staph, then Pseudomonas), and bronchiectasis.
- Gastrointestinal — meconium ileus in the newborn; pancreatic insufficiency → steatorrhoea, malabsorption and failure to thrive.
- Others — salty sweat, nasal polyps/sinusitis, biliary disease, and infertility (males).
DIAGNOSIS
- Sweat chloride test — chloride > 60 mmol/L is diagnostic (the classic test).
- Genetic testing for CFTR mutations; newborn screening (immunoreactive trypsinogen) where available.
MANAGEMENT (multidisciplinary)
- Respiratory — chest physiotherapy, mucolytics, bronchodilators, and aggressive antibiotics for infections.
- Nutritional — high-calorie diet, pancreatic enzyme replacement, and fat-soluble vitamins (A, D, E, K).
- CFTR modulator drugs in eligible patients; management of complications; and genetic counselling.
💡CLINICAL PEARL: Suspect CF in any child with recurrent chest infections plus failure to thrive/steatorrhoea, meconium ileus at birth, or unusually salty sweat.INHERITANCE & GENETICS
- Autosomal recessive; carrier parents have a 1 in 4 risk with each pregnancy.
- The ΔF508 mutation in the CFTR gene is the commonest; genetic counselling is important.
COMPLICATIONS
- Bronchiectasis and respiratory failure; recurrent Pseudomonas infection.
- Diabetes (CF-related), liver disease, osteoporosis and infertility.
NEWBORN & INFANT CLUES
- Meconium ileus at birth (bilious vomiting, failure to pass meconium) is a classic early presentation.
- Prolonged neonatal jaundice; failure to thrive despite a good appetite; salty taste on kissing the baby.
CFTR MUTATION CLASSES
- Classes I–III — no functional protein → severe (pancreatic-insufficient) disease (ΔF508 is class II, the commonest).
- Classes IV–VI — some residual function → milder phenotype.
- CFTR modulators (e.g. ivacaftor/lumacaftor) target specific mutation classes.
SWEAT CHLORIDE — INTERPRETATION
Sweat chloride Interpretation > 60 mmol/L Diagnostic of CF 30–59 mmol/L Intermediate — needs genetic testing < 30 mmol/L CF unlikely 🔑KEY POINTS TO REMEMBER- CF = autosomal recessive CFTR defect (ΔF508); thick secretions.
- Recurrent chest infections (Pseudomonas), bronchiectasis, pancreatic insufficiency, salty sweat.
- Meconium ileus at birth; failure to thrive with a good appetite.
- Sweat chloride > 60 diagnostic; multidisciplinary care + enzymes + physio.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.PRINCIPLE
The inhaled route is preferred for asthma drugs because it delivers the drug directly to the airways, achieving a rapid effect with a small dose and fewer systemic side-effects. Choosing the right device for the child's age and ensuring correct technique are as important as the drug itself.
TYPES OF DEVICES
- Metered-Dose Inhaler (MDI) — delivers a fixed dose; requires good hand–breath coordination, so it is not ideal alone for young children.
- MDI + Spacer — the device of choice in children; the spacer removes the need for coordination and improves lung deposition. Use with a face mask < 4 years and a mouthpiece in older children.
- Nebuliser — converts liquid drug to a fine mist; useful in acute severe attacks and in very young/uncooperative children.
- Dry-Powder Inhaler (DPI) — breath-actuated; suitable for older children (> 6–8 years) who can generate a strong, fast inspiration.
DEVICE SELECTION BY AGE
Age Preferred device < 4 years MDI + spacer + face mask (or nebuliser) 4–6 years MDI + spacer + mouthpiece > 6 years MDI + spacer or DPI KEY POINTS ON TECHNIQUE
- Shake the MDI, actuate one puff at a time into the spacer, and take several tidal breaths (or a slow deep breath).
- Rinse the mouth after inhaled steroids (prevents oral thrush).
- Check inhaler technique at every visit — poor technique is a common cause of 'treatment failure'.
ADVANTAGES OF THE INHALED ROUTE
- Drug delivered directly to the target (airways) → rapid onset.
- A much smaller dose is needed → fewer systemic side-effects than oral/IV drugs.
COMMON PITFALLS
- Poor coordination with an MDI alone; not using a spacer in young children.
- Not rinsing the mouth after inhaled steroids (oral thrush); using an out-of-date/empty canister.
CHOOSING & TEACHING THE DEVICE
- Match the device to the child's age and ability; demonstrate and have the caregiver demonstrate back.
- Re-check technique at follow-up; provide written/pictorial instructions.
- Ensure the spacer is cleaned correctly and the canister is not empty.
🔑KEY POINTS TO REMEMBER- Inhaled route: direct, rapid, low dose, fewer side-effects.
- MDI + spacer is the device of choice in children (mask < 4 yr).
- Nebuliser for acute/very young; DPI for older children (> 6–8 yr).
- Rinse the mouth after inhaled steroids; check technique at every visit.
📚SOURCES: GINA guidelines; Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Stridor is a harsh, high-pitched noisy sound produced by turbulent airflow through a partially obstructed upper airway (larynx/trachea). Its timing helps localise the obstruction and it is always a sign that needs assessment.
TIMING & LOCALISATION
- Inspiratory stridor → obstruction above/at the larynx (extrathoracic).
- Expiratory stridor / wheeze → intrathoracic (lower trachea/bronchi).
- Biphasic stridor → a fixed obstruction (e.g. subglottic stenosis).
ACUTE CAUSES
- Croup (commonest — barking cough, stridor, hoarse voice).
- Acute epiglottitis (toxic, drooling, no cough — an emergency).
- Foreign body (sudden choking); bacterial tracheitis; retropharyngeal abscess; anaphylaxis/angio-oedema.
CHRONIC / CONGENITAL CAUSES
- Laryngomalacia — the commonest cause of chronic stridor in infants.
- Vocal-cord palsy, subglottic stenosis, subglottic haemangioma, and vascular ring.
LARYNGOMALACIA (the commonest chronic cause)
- Inspiratory stridor from birth/early weeks, worse supine, on feeding and crying, and better prone.
- The infant is otherwise well and thriving; it is due to a floppy, immature larynx.
- Usually self-limiting, resolving by 12–18 months; surgery only if severe (feeding difficulty, failure to thrive, apnoea).
APPROACH
- Assess severity first (stridor at rest, indrawing, cyanosis, feeding) and secure the airway if compromised.
- Identify the cause from the history (onset, fever, cough, choking) and treat accordingly; avoid upsetting a child with severe obstruction.
RED-FLAG (EMERGENCY) FEATURES
- Stridor at rest, severe chest indrawing, cyanosis, drooling or a toxic appearance.
- Rapidly progressive obstruction, exhaustion or altered sensorium — secure the airway urgently.
INVESTIGATION
Guided by the likely cause — most acute stridor is diagnosed clinically; flexible laryngoscopy is used to confirm laryngomalacia and other structural causes of chronic stridor.
🔑KEY POINTS TO REMEMBER- Stridor = harsh sound from upper-airway obstruction.
- Inspiratory = extrathoracic; biphasic = fixed obstruction.
- Acute: croup, epiglottitis, foreign body, anaphylaxis.
- Laryngomalacia = commonest chronic cause (better prone, resolves by 12–18 mo).
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.