Pneumonia in Children

Overview & Definition

Pneumonia in children is inflammation of the lung parenchyma, typically of infectious origin, producing cough, fever, respiratory distress (tachypnoea, indrawing, grunting, nasal flaring, head nodding), and parenchymal infiltrates on imaging.[24]

It is the leading infectious cause of death in children under 5 worldwide, ahead of acute gastroenteritis, malaria, and measles. The disease burden is concentrated in sub-Saharan Africa and South Asia, where access to vaccines, antibiotics, oxygen, and timely care is constrained.[1][2]

Clinical definition. In hospital and high-resource settings, pneumonia is a clinical-radiographic syndrome: fever, cough, tachypnoea, focal respiratory signs (crepitations, dullness, bronchial breathing, wheeze), and a new parenchymal opacity on chest X-ray. In low-resource and primary-care settings, where chest X-ray is unavailable, the WHO operational definition is used:[5]

"Pneumonia = cough or difficulty breathing plus fast breathing for age."[24]

This single bedside rule has underpinned two decades of reduction in pneumonia mortality at first-level facilities and is the framing every NEET-PG/INICET candidate must know.[24]

Aetiological framing. Pneumonia is caused by a wide range of viruses, bacteria, atypical organisms, and (rarely) parasites. The organism varies sharply by age, and the organism dictates the management (typical bacteria need a beta-lactam; atypical organisms need a macrolide; influenza needs a neuraminidase inhibitor if within 48 h).[5]

The disease is preventable in most cases. Pneumococcal conjugate vaccine (PCV10/PCV13), Hib conjugate vaccine, measles vaccination, annual influenza vaccination, exclusive breastfeeding for 6 months, hand hygiene, smoke-free indoors, and reduction of indoor air pollution are the WHO-anchored prevention pillars.[11][12][13]

Classification

Pneumonia in children is classified along three clinically useful axes: severity (the most important for treatment), pathology (lobar vs bronchopneumonia vs interstitial), and aetiology (typical bacterial, atypical, viral).[13]

By severity — WHO (the operational gold standard)

By pathology

By aetiology — typical, atypical, viral

[17]

By age — the most useful clinical axis

Epidemiology & Risk Factors

Global burden

Pneumonia has been the leading infectious killer of children under 5 for decades. The GBD 2019 study estimates ~700,000 under-5 deaths annually attributable to lower respiratory infections (LRIs) — about 14% of all under-5 deaths globally — with the bulk falling in sub-Saharan Africa and South Asia.[2][3]

[5]

Trend over time

Under-5 pneumonia mortality has fallen substantially over the past three decades — from over 2 million/year in 1990 to ~700,000/year by 2019 — driven by:[24]

• Conjugate vaccines — PCV, Hib — the single largest biomedical lever.[11][12][22]
• Expanded oxygen access — universal pulse oximetry and oxygen concentrators at first-level facilities.[24]
• Standardised case management (WHO IMCI/IMNCI) — amoxicillin for WHO pneumonia.[7][8][24]
• Improved nutrition — exclusive breastfeeding for 6 months, micronutrient supplementation, and reduction of severe acute malnutrition.
• Socioeconomic change — urbanisation, clean-fuel cooking, reduced household crowding.

Even so, the burden plateaued in many countries during the COVID-19 era and health-system disruption; the GBD 2021 update shows a rebound of LRIs to levels comparable to pre-pandemic estimates.[3]

Aetiological epidemiology by age

[11]

Vaccine impact

The conjugate vaccines have transformed childhood pneumonia epidemiology. The Watt 2009 Lancet analysis estimated Hib caused ~8% of pneumonia deaths in children under 5 globally (in the pre-vaccine era); after Hib conjugate introduction, Hib disease in vaccinated populations collapsed.[10][14] PCV10/PCV13 has produced parallel drops in invasive pneumococcal disease and radiologically confirmed pneumonia in vaccinated cohorts.[11][12] The Hanquet 2019 Thorax study confirmed a substantial indirect (herd) effect on older unvaccinated cohorts across Europe.[22]

Risk factors

Child-level risk factors:[2]

• Age: peak incidence 2-12 months; mortality highest in 2-12 month age band.
• Prematurity / low birth weight.
• Non-breastfed, or exclusively breastfed under 6 months.
• Severe acute malnutrition (SAM) — multiplies pneumonia mortality.
• Immunodeficiency — congenital, HIV, chemotherapy, transplantation.
• Chronic lung disease of prematurity (BPD).
• Congenital heart disease, especially cyanotic.
• Sickle-cell disease / functional asplenia — risk of pneumococcal sepsis.
• Recurrent aspiration — neurodisability, GERD, neuromuscular disorders.
• Wheezing — concurrent asthma or viral-triggered wheeze.[3]

Household / environmental risk factors:[2]

• Indoor air pollution — solid-fuel cooking (biomass), second-hand tobacco smoke.
• Household crowding.
• Lack of immunisation.
• Lower socioeconomic status — multiple pathways (poor nutrition, crowding, lower care-seeking).[2]

Care-seeking factors:[2]

• Delayed presentation.
• Inadequate access to oxygen and pulse oximetry.
• Self-medication or inappropriate antibiotics.[2]

Pathophysiology

The two archetypes

The behaviour and treatment of childhood pneumonia are dominated by two anatomical-pathological archetypes — alveolar consolidation (typical bacterial) and small-airway/airway-centred interstitial disease (viral and atypical). They have different microanatomy, different physiology, different imaging, and different first-line antibiotic rationale.[7]

Bacterial alveolar consolidation

The S pneumoniae model best illustrates the cascade:[11]

1. Nasopharyngeal colonisation — pneumococcus colonises the upper airways in roughly 20-40% of healthy children at any time. Colonisation is harmless unless the host's defences fail.
2. Micro-aspiration — overflow into the lower respiratory tract occurs physiologically; effective mucociliary clearance and alveolar macrophage function normally contain it.
3. Failure of defence — viral upper-respiratory infection (especially influenza), malnutrition, immune suppression, or no prior immunological experience (infants) allow the organism to establish in alveoli.
4. Alveolar exudate — exudation of neutrophils, fibrin and red cells into the alveolar air space; this consolidates the alveolus and replaces air with fluid/cells.
5. Spread — through the pores of Kohn and canals of Lambert within the lobe (lobar) or via centrilobular airways (bronchopneumonia).
6. Impaired gas exchange — perfusion continues but ventilation drops in consolidated regions → shunting → hypoxaemia.
7. Systemic signs — pyrogens (IL-1, IL-6, TNF) drive fever, rigors, anorexia, tachycardia.[1]

Viral bronchiolitis and viral pneumonia

The RSV model illustrates viral lower respiratory disease:[1]

1. Nasopharyngeal inoculation → viral replication in ciliated epithelial cells.
2. Cellular cytotoxicity and immune response — epithelial necrosis, submucosal oedema, lymphocytic infiltrate.
3. Mucus hypersecretion and peribronchiolar inflammation — combine with exudate in the small airways.
4. Small-airway plugging — produces air trapping and hyperinflation distal to plugs (ball-valve mechanism).
5. Interstitial mononuclear infiltrate — interstitial thickening; alveolar air preserved.
6. Wheeze and crackles — mixed obstruction and inflammation.
7. Hypoxaemia — primarily V/Q mismatch with air-trapping; alveolar collapse in more severe disease.[5]

Viral infection is also the most important risk for secondary bacterial pneumonia: influenza damages airway epithelium and impairs mucociliary clearance, allowing bacterial superinfection (Streptococcus pneumoniae, Staphylococcus aureus) 5-10 days into the illness.[5]

Atypical (interstitial) pneumonia

Mycoplasma pneumoniae binds to sialic acid residues on respiratory epithelium via the P1 adhesin, causes ciliary dysfunction, and produces a subepithelial lymphocytic infiltrate. Bacteria are intracellular and cannot be cultured on routine media, which is why macrolides (which concentrate intracellularly) are required.[16]

The clinical manifestation is subacute: dry cough, low-grade fever, headache, and the x-ray-physical dissociation — interstitial infiltrates on imaging disproportionate to the physical findings.[21]

Necrotising pneumonia — the dangerous complication

Necrotising pneumonia is parenchymal necrosis with multiple thin-walled cavities, pneumatoceles and frequently empyema. It is most commonly caused by:[21]

• Streptococcus pneumoniae serotype 19A (not covered by older PCV7),
• Staphylococcus aureus, particularly Panton-Valentine leukocidin (PVL)-positive strains — epidemic in parts of Europe and elsewhere;[21]
• Less commonly, H. influenzae and Klebsiella.

Complications pathophysiology

Clinical Presentation

The textbook triad is cough, fever, and tachypnoea — but infants often present atypically, and older children may have subtle features. A complete history must establish:[22]

• Onset and tempo — abrupt = typical bacterial; gradual = atypical/viral.
• Cough character — dry, productive; paroxysms ± whoop; post-tussive vomiting (pertussis).
• Fever — height and pattern; rigours suggest typical bacterial.
• Breathing difficulty — fast breathing, indrawing, grunting, nasal flaring, head nodding, accessory muscle use.
• Feeding / hydration — decreased feeding, vomiting, reduced wet nappies, lethargy.
• Immunisation history — RSV, influenza, PCV, Hib, measles, pertussis, BCG.
• Exposure — household illness, daycare, family TB, fumes/biomass cooking.
• Past medical history — prematurity, BPD, congenital heart disease, recurrent pneumonia (immunodeficiency, malformation, aspiration).
• Drugs / allergies, especially prior antibiotic exposure.
• Skin rash — scarlatiniform (S aureus scarlet fever), maculopapular (measles), vesicular (varicella), urticarial.[21]

Cardinal signs of respiratory distress

Typical pattern by aetiology

Chlamydia trachomatis in young infants (4-12 weeks)

Classic profile: afebrile or low-grade, staccato cough (paroxysmal, single-cycle cough), conjunctivitis, tachypnoea, scattered crepitations, normal or mild interstitial CXR, peripheral eosinophilia. History of maternal STI or untreated maternal conjunctivitis. Treatment: oral erythromycin 50 mg/kg/day in 4 divided doses for 14 days (or azithromycin 10 mg/kg/day for 5 days).[24]

Staph aureus pneumonia (and PVL-positive)

• Post-influenza superinfection (5-10 days into influenza).
• Abrupt onset, high fever, pleuritic pain, rapidly progressive.
• Pneumatoceles, empyema, necrotising pneumonia, pyopneumothorax.
• PVL-positive strains in particular progress rapidly with necrotic lung lesions and are highly lethal if not treated aggressively.[21]

Bordetella pertussis

• Paroxysmal cough ending in inspiratory whoop, post-tussive vomiting, subconjunctival haemorrhage.
• Apnoea as the cardinal feature in infants under 6 months.
• Peripheral blood: marked lymphocytosis (often over 20 ×10⁹/L).
• Confirm with nasopharyngeal swab PCR.
• Treat with azithromycin or erythromycin.[7]

Measles pneumonia

• Coryza, cough, conjunctivitis (the 3 Cs) + Koplik spots → maculopapular rash.
• Pneumonia may be measles-virus pneumonitis or secondary bacterial superinfection (S pneumoniae, S aureus, H influenzae).
• Vitamin A 200,000 IU (over 12 months) or 100,000 IU (under 12 months) × 2 days empirically, then repeat in 4 weeks.[13]

Atypical presentations — the examiner's favourites

Examining the chest in a child

1. Look — tachypnoea, indrawing, nasal flaring, head nodding, asymmetry of chest expansion, scars (chest tubes), central cyanosis, clubbing (chronic pneumonia — consider bronchiectasis, immunodeficiency).
2. Feel — tracheal position (push = effusion/mass; pull = collapse), chest expansion (decreased on consolidated side), tactile vocal fremitus (increased over consolidation, decreased over effusion).
3. Percuss — dull (consolidation, effusion); hyper-resonant (pneumothorax, large consolidation with air trapping).
4. Listen — crackles (crepitations) over consolidation; bronchial breathing with increased vocal resonance = consolidation; absent breath sounds and dullness = effusion; wheeze = bronchospasm (viral, foreign body, asthma).[24]

Differential Diagnosis

The "pneumonia" label is potentially applied to many non-pneumonic conditions. A structured differential is mandatory because missing it changes outcome.[7]

Clinical & Bedside Assessment

The WHO approach is the operational gold standard, and every examiner will expect it reproduced verbatim.[24]

[5]

WHO assessment sequence (use this at first-level facilities and in any exam):[24]

1. CHECK FOR DANGER SIGNS — if any, the child has VERY SEVERE pneumonia. Move to emergency care.
2. COUNT respirations over a full minute (a young infant's RR is labile; count again if borderline).
3. Look for chest indrawing — subcostal/intercostal retractions on inspiration with the chest wall visibly sinking between/below the ribs.
4. Listen for grunting — soft, audible expiratory vocalisation in young infants (a sign of impending respiratory failure).
5. Stridor, wheeze, or general danger signs (vomiting everything, convulsions, lethargy/unconsciousness).[24]

WHO severity classification — reproduced exactly

Additional bedside findings that matter

• Pulse oximetry: target 94-98% in non-cardiac children; <90% triggers oxygen supplementation.
• Capillary refill >2 s — coexisting shock, poor perfusion.
• Hydration — sunken eyes, reduced tears, dry mucosa, decreased urine output, weight change.
• Nutritional status — weight, mid-upper-arm circumference (MUAC, SAM if <11.5 cm in 6-59 months).
• Temp — fever >38.5 °C or hypothermia <36 °C.
• Chest signs — see Examining the chest above.[7]

Investigations

Most childhood pneumonia is a clinical diagnosis. Investigations are risk-stratified.[24]

Imaging

[5]

Microbiology

[2]

Bloods

• FBC: leucocytosis with left shift suggests bacterial; lymphocytosis suggests pertussis or atypical.
• CRP / procalcitonin (PCT): CRP>100 mg/L, PCT>2 ng/mL — favours bacterial; PCT more specific. Not discriminative in infants or after antibiotic pretreatment.
• U&E / venous blood gas: hyponatraemia (SIADH with pneumonia), raised creatinine (HUS), metabolic acidosis (severe sepsis).
• Glucose: hypoglycaemia in SAM or sepsis.
• Lactate: >2 mmol/L — sepsis, poor perfusion.
• HIV testing: in severe or recurrent pneumonia, in high-prevalence settings, or if WHO guidance supports.
• Tuberculin test (TST or IGRA / QuantiFERON-TB Gold): when TB pneumonia is suspected — persistent symptoms, contact with TB, malnutrition, inconclusive CXR.
• Blood culture × 1 set minimum before antibiotics.
• Arterial blood gas / capillary gas: when the child is severely hypoxaemic, in impending respiratory failure, or for guiding HFNC/CPAP escalation.[5]

Other

• Urine pneumococcal antigen and Legionella urinary antigen — older child, atypical presentation, outbreak setting.
• Serology — cold agglutinins and Mycoplasma IgM (4-fold rise, or single positive IgM with clinical picture).
• Bronchoscopy with bronchoalveolar lavage (BAL): immunocompromised, ventilator-associated, refractory pneumonia.
• ECG and echocardiogram: when myocarditis or pericardial effusion is considered.
• Sputum AFB and GeneXpert MTB/RIF: when TB is suspected.[17]

Management — Resuscitation

The first minutes of very severe pneumonia are about airway, breathing, and circulation — ABCDE — not antibiotics.[5]

[5]

Oxygen delivery — escalation ladder

[15]

Management — Definitive & Stepwise

The pillars are (1) oxygen, (2) appropriate antibiotic, (3) supportive care, (4) fluids + nutrition, (5) monitoring, and (6) prevention of transmission. For complicated disease, (7) procedural management of empyema, (8) necrotising pneumonia care, and (9) follow-up imaging.[13]

Empirical antibiotic selection — by severity

[7] [8]

Atypical-pathogen consideration

When a school-age child has persistent dry cough, bilateral wheeze or crackles, or inadequate response to a beta-lactam at 48-72 hours, add a macrolide or switch to a macrolide:[16][17][23]

• Azithromycin 10 mg/kg once daily for 3 days — better tolerated than erythromycin.
• Clarithromycin 15 mg/kg/day in 2 divided doses for 7-10 days.
• Erythromycin 50 mg/kg/day in 4 divided doses for 14 days — preferred for pertussis exposure, neonate.[16]

Supportive care — the rest of the bundle

[7]

Complications — when the bundle isn't enough

Pleural effusion and empyema — the most common pneumonia complication.[20]

• Uncomplicated parapneumonic effusion: 7-10 days of IV antibiotics; serial ultrasound; usually resolves.
• Complicated parapneumonic effusion / empyema: aspiration yields pH <7.2, glucose <3.3 mmol/L, LDH >1000 IU/L, pus, or positive culture/Gram stain. Action: chest drain (small-bore 8-14 Fr preferred) ± intrapleural fibrinolysis.
• Intrapleural fibrinolysis (MIST2 regimen): tPA 10 mg + DNase 5 mg intrapleural twice daily for 3 days — improves drainage success over either agent alone or streptokinase.[19]
• VATS (video-assisted thoracoscopic surgery) — if fibrinolysis fails, or if the child is deteriorating; safe and effective in children.[18]

Pneumothorax — needle aspiration (2nd intercostal space mid-clavicular line or 4th-5th intercostal space anterior axillary line for paediatric small-bore drains), then small-bore chest drain in the triangle of safety.[18]

Pneumatocele — usually conservative; serial CXR; intervention only if large and symptomatic.[18]

Lung abscess — prolonged IV antibiotics (4-6 weeks) targeting anaerobes, S aureus, S pneumoniae; percutaneous drainage if persistent.[11]

Necrotising pneumonia — prolonged IV antibiotics (often 4-6 weeks) covering S aureus (incl. PVL — vancomycin/linezolid if MRSA), pneumococcus, anaerobes; supportive management; surgical lobectomy rarely needed.[5]

When to escalate, when to step down

[8]

Vaccination and prevention

Specific Subtypes & Scenarios

Neonatal pneumonia

Staphylococcal pneumonia (PVL-positive and MSSA)

• Often follows influenza, measles, or post-tonsillectomy.
• Pneumatoceles, empyema, pyopneumothorax, necrotising pneumonia.
• Treat: IV anti-staphylococcal beta-lactam (flucloxacillin) ± vancomycin/linezolid if MRSA; chest drain for empyema; prolonged IV course 4-6 weeks.[21]

Mycoplasma pneumoniae — rising

• Commonest pathogen in school-age children with community-acquired pneumonia.[17]
• Can complicate Stevens-Johnson syndrome, cold agglutinin haemolytic anaemia, GBS, polyarthritis.
• Macrolide resistance is rising; consider tetracycline/doxycycline in children >8 years as an alternative.[16][23]

Tuberculous pneumonia

• Subacute presentation (over 2-4 weeks), weight loss, night sweats, persistent CXR opacity with hilar adenopathy.
• Often primary complex: Ghon focus + hilar lymphadenopathy.
• Diagnosis: clinical + CXR + Tuberculin test (or IGRA in older children) + microbiology (gastric aspirate or BAL GeneXpert MTB/RIF).
• Standard 6-month TB regimen (isoniazid + rifampicin × 6 months; pyrazinamide × 2 months; ± ethambutol).[7]

Necrotising pneumonia

• Multiple thin-walled cavitations on CXR, persistent fevers despite appropriate antibiotics.
• Common after pneumococcal serotype 19A or PVL-positive S aureus.[21]
• Management: prolonged IV antibiotics, supportive management, intervention only if severe.

Measles-associated pneumonia

• Direct viral pneumonitis or post-measles bacterial superinfection.
• Treatment: empiric broad-spectrum antibiotics + vitamin A 200,000 IU orally for 2 days; repeat in 4 weeks if SAM or clinical vitamin A deficiency.
• Seek BCG scar; consider TB if symptoms persist.[21]

Recurrent pneumonia

Complications & Pitfalls

[7]

Prognosis & Disposition

Disposition decisions:[1]

• WHO pneumonia: home after first dose observed; follow-up at 48-72 h and 7 days.
• Severe pneumonia: hospital admission, ward care; HFNC if needed.
• Very severe pneumonia: high-dependency or PICU; intubation if indicated.
• Empyema: surgical/medical ICU level of care depending on drainage approach.
• Necrotising pneumonia: PICU.[5]

Safety-net advice at discharge:[24]

• Return immediately if breathing worsens, fever recurs, cannot drink, vomits everything, convulsion, or drowsy.
• Complete the full course of oral antibiotic (typically 5 days for WHO pneumonia; longer if severe).
• Avoid tobacco smoke exposure and indoor air pollution.
• Catch-up immunisations (PCV, Hib, measles, pertussis, influenza) on recovery.
• If recurrent pneumonia, follow-up in clinic with CXR and immunological workup.[8]

Special Populations

Severe acute malnutrition (SAM)

Pneumonia is one of the largest contributors to SAM mortality. The WHO IMCI protocol for SAM provides specific guidance:[6]

• Sign blunting: hypothermia rather than fever; subtle indrawing; cough may be quiet.
• Always check glucose (often <3 mmol/L); treat with 2 mL/kg 10% dextrose.
• Empirical antibiotics: include broad Gram-negative cover (e.g. ampicillin + gentamicin).
• Resomal instead of standard ORS for fluid resuscitation in SAM (high potassium, low sodium).
• Careful fluid resuscitation — avoid overload in the malnourished myocardium.[24]

HIV-infected child

The differential widens substantially:[5]

• Pneumocystis jirovecii pneumonia — typically subacute, diffuse bilateral interstitial CXR ("ground glass"), no wheeze, often afebrile, hypoxaemia disproportionate; treat with co-trimoxazole 80/400 mg/kg/day of trimethoprim/sulfamethoxazole in 4 divided doses for 21 days plus corticosteroids if severe.
• Mycobacterium avium complex, CMV, Bartonella, Cryptococcus, TB.
• Repeat PCRs and BAL if necessary.
• Continue co-trimoxazole prophylaxis when stable.[7]

Immunocompromised (transplant, chemotherapy)

• Pre-test for PJP, CMV, RSV, parainfluenza, adenovirus, RSV; broad respiratory viral PCR and BAL routinely.
• Consider empirical co-trimoxazole + broad-spectrum antibacterial + voriconazole/echinocandin if febrile neutropenic.[1]

Sickle-cell disease

• Pneumococcal sepsis is a major risk (functional asplenia); cover with empirical ceftriaxone ± vancomycin.
• Vaccination: PCV, PPSV23, Hib, influenza annually; daily penicillin prophylaxis <5 years.[22]

Cystic fibrosis

• Recurrent pneumonia with Pseudomonas or Staph aureus.
• Chest CT, sweat test.
• Airway clearance and chronic antibiotics as per CF team.[5]

Neurodisability / aspiration

• Consider positioning, thickened feeds, H2-blockers or PPIs for GERD, swallow assessment.
• Recurrent aspiration with right upper-lobe involvement.[1]

Congenital cyanotic heart disease

• Increased pneumonia risk with poor perfusion; the myocardium is at risk.
• Avoid fluid overload.[5]

Evidence, Guidelines & Regional Differences

Landmark evidence

• Hazir Lancet 2008 (SAT trial): demonstrated high-dose oral amoxicillin 80-90 mg/kg/day for 5 days was equivalent to WHO-recommended injectable ampicillin + gentamicin for severe pneumonia in hospitalised children aged 3-59 months — supporting outpatient treatment of severe pneumonia in low-resource settings.[8] This underpins the modern WHO/IMNCI recommendation.
• Hazir ADC 2007: the double-dose amoxicillin RCT showed standard dose 80-90 mg/kg/day was equivalent to 40-45 mg/kg/day — supporting the upper dose as adequate.[7]
• Mulholland Lancet 1997: the Hib PRP-T Gambian trial — 5 cases prevented per 100 vaccinated, demonstrating Hib conjugate efficacy in a high-burden developing setting.[13]
• Watt Lancet 2009 and Wahl Lancet Glob Health 2018: quantified the Hib and pneumococcal pneumonia burden in unvaccinated vs vaccinated settings.[10][11]
• de Benedictis Lancet 2020: a comprehensive review of complicated pneumonia in children.[21]
• PERCH Lancet 2019 (PERCH): defined the aetiology of severe childhood pneumonia in 7 low- and middle-income sites — RSV most prominent, S pneumoniae a major bacterial contributor, similar across African and Asian sites.[5]
• St Peter 2009 (J Pediatr Surg): VATS vs chest tube + fibrinolysis in pediatric empyema — both effective, VATS shorter hospital stay but higher cost.[18]
• Rahman NEJM 2011 (MIST2): tPA + DNase intrapleural superior to either agent alone in adult empyema; widely extrapolated to children and now accepted as standard for complicated paediatric empyema.[19]
• Waites 2004 Clin Microbiol Rev and Kutty 2019 Clin Infect Dis: comprehensive reviews of Mycoplasma pneumoniae in children — clinical, diagnostic, and treatment considerations.[16][17]
• Roberts BTS 2023 Thorax: full BTS pleural disease guideline including parapneumonic effusion/empyema drainage triggers.[20]
• Nair Lancet 2010: quantified RSV's share of global childhood pneumonia.[4]
• Li Lancet 2022 + GBD 2019/2021 Collaborators: the GBD series as the source of contemporary mortality numbers.[1][2][3]
• Italian Intersociety Consensus (Donà Ital J Pediatr 2024): clinical pathways for mild-to-moderate CAP in previously healthy children.[23]

Guidelines

• WHO Pocket Book of Hospital Care for Children, 2nd ed. 2013 — bedside reference for pneumonia management in hospitals.[24]
• WHO IMCI/IMNCI chart booklet — first-level facility framework.
• BTS adult CAP guideline (Lim Thorax 2009) — adult-specific, but cross-cutting principles apply.[9]
• Italian Pediatric Intersociety Consensus (Dona Ital J Pediatr 2024) — example of national paediatric consensus.[23]

Regional deltas

Controversies

• Corticosteroids in childhood pneumonia — meta-analyses in adults show benefit; paediatric evidence is mixed; not routine, considered for severe hypoxaemic pneumonia on a case-by-case basis.
• Vitamin A supplementation — WHO recommends in measles and severe acute malnutrition; routine supplementation in pneumonia without measles/SAM has limited benefit.
• Duration of antibiotic course — 3 days may be non-inferior to 5 days for non-severe pneumonia (green-IMCI Kenya data); 5-7 days remains the mainstream MBBS/NEET-PG approach.
• Criteria for HFNC vs CPAP vs early IMV in severe pneumonia — under active trial.[7]

Exam Pearls

A high-yield summary designed for last-minute revison.[24]

• Pneumonia is the leading infectious cause of under-5 mortality globally: ~700,000 deaths/year, 14% of all under-5 deaths.[1]
• WHO operational definition: cough or difficulty breathing with fast breathing.
• WHO fast-breathing thresholds: 2-12 months >50/min; 1-5 years >40/min; >5 years >20/min.[24]
• Lower chest wall indrawing = severe pneumonia → hospitalise.
• WHO danger signs = very severe pneumonia: inability to drink, convulsions, vomiting everything, severe malnutrition, grunting → emergency care.
• Leading viral cause under 1 year = RSV.[4][15]
• Leading bacterial cause overall = Streptococcus pneumoniae (still, despite PCV).
• Hib pneumonia has fallen dramatically with the introduction of conjugate vaccine.[10][11][13][14]
• Mycoplasma pneumoniae = most common cause of CAP in school-age (>5 yr) children; macrolide is the antibiotic.[16][17]
• PVL-positive Staph aureus in children: pneumatocele, empyema, necrotising pneumonia; cover with vancomycin/linezolid empirically.[21]
• Oral amoxicillin 80-90 mg/kg/day × 5 days for WHO pneumonia (Hazir evidence).[7][8]
• Severe pneumonia: IV ampicillin 50 mg/kg IV q6h + gentamicin 7.5 mg/kg q24h (or ceftriaxone 50-80 mg/kg/day q24h).
• Very severe pneumonia: as above + add macrolide if atypical, ± vancomycin if MRSA, ± oseltamivir if influenza in 48 h.
• SpO2 <90% triggers oxygen; target 94-98% in non-cardiac children (88-92% in BPD).
• Pleural drainage trigger: pH<7.2, glucose <3.3 mmol/L, LDH >1000, pus, positive culture → chest drain + MIST2.[19][20]
• MIST2 intrapleural fibrinolysis: tPA 10 mg + DNase 5 mg twice daily for 3 days.[19]
• VATS (video-assisted thoracoscopic surgery) if fibrinolysis fails.
• PCV13/PCV10 + Hib + measles + annual influenza are the four most important vaccines.
• Chlamydia trachomatis pneumonia in 4-12 weeks: afebrile, staccato cough, conjunctivitis, eosinophilia → erythromycin/azithromycin.
• RSV bronchiolitis ≠ pneumonia, but both can coexist; treatment of bronchiolitis is supportive.
• Bordetella pertussis in infants: paroxysms, whoop, lymphocytosis, apnoeas → macrolide.
• Staphylococcal pneumonia (post-influenza): pneumatoceles, empyema, necrotising pneumonia.
• Severe acute malnutrition pneumonia: blunted signs, hypothermia, hypoglycaemia, broad-cover antibiotics.
• HIV pneumonia differential widens: Pneumocystis, CMV, MAC, TB.
• Antibiotics NOT routine in viral URTI; only indicated in pneumonia meeting WHO severity criteria.

Exam application bank (NEET-PG / INICET)

One-line answer

Pneumonia in children = inflammation of the lung parenchyma, the single leading infectious cause of under-5 mortality globally, responsible for ~700,000 deaths/year (≈14% of all under-5 deaths). The WHO operational definition is cough or difficulty breathing with fast breathing defined by age (over 50/min at 2-12 months, over 40/min at 12 months-5 years, over 20/min at over 5 years). WHO classifies severity into pneumonia (fast breathing only, treat at home with oral amoxicillin), severe pneumonia (lower chest wall indrawing, hospitalise), and very severe pneumonia (danger signs: inability to drink, convulsions, vomiting everything, severe malnutrition, grunting — IV/IM antibiotics urgently). Leading viral cause under 1 year = RSV. Leading bacterial cause = Streptococcus pneumoniae; Hib pneumonia has fallen dramatically with conjugate vaccination. Empirical treatment: oral amoxicillin 80

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard.[7]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes.[21]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change.[12]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each.[24]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory.[24]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Pneumonia in Children.

References

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