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Diagnosis: Community-Acquired Pneumonia (CAP)

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Most Likely Causative Organisms (Age 2-5 Years)

"In children between 2 and 5 years of age, most community-acquired pneumonia is caused by respiratory viruses, notably respiratory syncytial virus, human rhinovirus, and human metapneumovirus. Other notable pathogens in this age group include Streptococcus pneumoniae, H. influenzae type b, and nontypeable H. influenzae. Mycoplasma pneumoniae and Chlamydophila pneumoniae are thought to be less common in children <5 years old."

• Tintinalli's Emergency Medicine, p. 853

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Clinical Features Explained

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Pathophysiology

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Workup

• Chest X-ray - lobar/segmental consolidation favors bacterial; bilateral interstitial infiltrates favor viral/atypical
• CBC - leukocytosis with neutrophilia suggests bacterial etiology
• Blood culture - in hospitalized children (yield ~3-7% but useful when positive)
• Nasopharyngeal swab for rapid viral panel (RSV, influenza, rhinovirus, metapneumovirus)
• Pulse oximetry and respiratory rate - key severity markers
• CRP / Procalcitonin - procalcitonin >0.25 ng/mL supports bacterial etiology

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Treatment

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Physical Examination Findings in Pulmonary Consolidation

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Summary Table (from Murray & Nadel's Respiratory Medicine)

Murray & Nadel's Textbook of Respiratory Medicine, Table 18.4

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Finding-by-Finding Breakdown

1. Inspection

• Chest wall lag / splinting on the affected side - the patient subconsciously limits expansion of the painful/consolidated side
• Tachypnea - increased respiratory rate is one of the most sensitive early signs
• Use of accessory muscles in severe disease

2. Palpation - Increased Tactile Fremitus

• Ask the patient to say "99" or "one, one, one" and feel chest wall vibrations with the ulnar edge of the hand
• Consolidated (solid) lung transmits low-frequency sound vibrations better than air-filled lung, so vibration is felt more strongly over the affected area
• Contrast: over a pleural effusion, fremitus is decreased (fluid insulates the chest wall from vibration)

"Tactile fremitus increases over an area of consolidation related to pneumonia." - Frameworks for Internal Medicine

3. Percussion - Dullness

• Consolidated lung is solid, not air-filled, so percussion produces a dull (not resonant) note over the affected area
• A very large effusion produces a "stony dull" or flat note
• Dullness to percussion is consistent with both consolidation and pleural effusion - differentiate by fremitus (increased in consolidation, decreased in effusion)

"Dullness to percussion is consistent with consolidation or a pleural effusion." - Goldman-Cecil Medicine

4. Auscultation - Multiple Signs

• Normally, vesicular (soft, rustling) breath sounds are heard over the lung periphery
• In consolidation, large-airway sounds (normally only heard over the trachea/mainstem bronchi) are transmitted through the solid lung to the chest wall - heard as loud, hollow, bronchial sounds with an audible expiratory phase equal to or longer than inspiration

• Late inspiratory crackles (fine crackles/crepitations) over the affected area
• Caused by the explosive reopening of small airways and alveoli that have collapsed due to fluid/exudate
• Heard classically at the end of inspiration

• Ask patient to say "99" - words are transmitted with abnormally increased clarity and volume over consolidated lung
• Normal aerated lung filters and muffles spoken words; solid lung transmits them sharply

• Ask patient to say "eee" - over consolidation, it is heard through the stethoscope as "ayyy"
• The word "egophony" means "goat sound" (Greek: ego = goat) - the bleating, nasal quality is characteristic
• Mechanism: consolidated lung selectively filters lower frequencies, causing the "ee" vowel to shift upward in pitch to sound like "ay"
• Most common when consolidation and pleural fluid coexist; also heard in uncomplicated lobar pneumonia and pulmonary infarction

"When bronchophony is extreme, spoken words assume a nasal or bleating quality (egophony) and the sound 'ee' is heard through the stethoscope as 'ay'." - Fishman's Pulmonary Diseases and Disorders

• Ask patient to whisper a phrase (e.g., "66 whiskeys, please")
• Normal aerated lung acts as a filter - whispered words are garbled and indecipherable
• Over consolidation, whispered words are heard clearly and distinctly
• Pectoriloquy = "chest speaking" (Latin: pectus = chest, loqui = to speak)
• Has the same significance as bronchophony; indicates non-aerated lung (consolidation, tumor, or compressed lung)

"Normal, aerated lung acts as a filter, making these whispered words garbled and undecipherable. If the words are clearly discernible, then pectoriloquy is present and indicative of underlying nonaerated lung." - Frameworks for Internal Medicine

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Why These Signs Occur - The Unifying Mechanism

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Important Caveat

"None of these findings on physical examination is sufficiently sensitive or specific to avoid the need for imaging for radiographic validation."

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Radiology Correlation

• Goldman-Cecil Medicine, Figure 35-1

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Differentiating Consolidation from Pleural Effusion on Physical Examination

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Head-to-Head Comparison Table

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The Pivotal Finding: Tactile Fremitus

"Tactile fremitus is increased over an area of consolidation, whereas it is decreased (often absent) over an effusion. The area of compressed lung just above an effusion is sometimes associated with a thin band of increased tactile fremitus and other signs of consolidation."

• Frameworks for Internal Medicine

"Vocal fremitus and tactile fremitus are increased in lung consolidation but decreased in pleural effusion."

• Textbook of Family Medicine 9e

"Vocal fremitus is increased over regions of lungs where there is increased transmission of sound, for example, consolidation from pneumonia. Conversely, fremitus is decreased in conditions in which sound transmission is impaired, for example, pleural effusion."

• Murray & Nadel's Textbook of Respiratory Medicine

• In consolidation, the lung is solid and directly contiguous with the chest wall - it conducts low-frequency vocal vibrations better than normal
• In pleural effusion, fluid sits between the visceral pleura and the chest wall - it acts as an acoustic insulator, blocking vibrational transmission to the examining hand

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The Egophony Trap

"Localized egophony ('e-to-a' changes) indicates consolidation of that segment or lobe of the lung; it is NOT present in pleural effusion except in a small band just above the upper edge of the effusion."

• Textbook of Family Medicine 9e

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Mediastinal Shift - An Extra Clue for Large Effusions

"The distinction between pleural effusion and atelectasis can be made on physical examination by determining whether the heart and mediastinal contents shift toward or away from the abnormal side."

• Murray & Nadel's Textbook of Respiratory Medicine

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Complete Differential: Three Dull Conditions Side by Side

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Practical Memory Aid

• Consolidation = solid lung = everything conducted/amplified (fremitus up, bronchial breathing, egophony, pectoriloquy)
• Pleural effusion = fluid barrier between lung and chest wall = everything blocked/silenced (fremitus down, no breath sounds, no voice signs)

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Diagnosis: Bronchiolitis

Causative Organism: Respiratory Syncytial Virus (RSV)

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Why This Case = Bronchiolitis

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The Organism: Respiratory Syncytial Virus (RSV)

"RSV is the most common infectious agent [in bronchiolitis], although influenza virus, adenovirus, parainfluenza virus, human metapneumovirus, coronavirus, and human bocavirus also cause bronchiolitis."

• Swanson's Family Medicine Review

Other causative organisms (in decreasing order of frequency):

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Pathophysiology

"Pathophysiologic features of bronchiolitis include inflammation, edema, and necrosis of the epithelial linings of the small airways. Increased production of mucus and bronchospasm are seen in conjunction with wheeze, cough, accessory muscle use, tachypnea, and rhinorrhoea."

• Swanson's Family Medicine Review

1. RSV infects and destroys bronchiolar epithelium
2. Inflammatory edema + increased mucus secretion narrow the small airways
3. Partial airway obstruction creates air trapping (wheeze on expiration, hyperinflation on CXR)
4. Complete obstruction of some bronchioles causes atelectasis (patchy collapse)
5. Ventilation-perfusion mismatch leads to hypoxemia and, in severe cases, hypercapnia

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Clinical Features in Detail

Symptoms

• Prodrome (days 1-3): rhinorrhoea, low-grade fever, mild cough - indistinguishable from a common cold
• Lower tract phase (days 3-5): worsening cough, rapid breathing, wheeze, feeding difficulty
• Peak severity: around day 3-5; total illness duration typically 10-14 days

Signs on Examination

• Tachypnea (RR > 50-60/min in infants) - most sensitive sign of severity
• Subcostal/intercostal retractions - increased work of breathing
• Nasal flaring
• Hyperinflation - barrel-shaped chest; liver pushed down (due to air trapping)
• Widespread fine end-expiratory crackles and wheeze (expiratory > inspiratory)
• Hypoxia (SpO2 < 92% in severe disease)
• Poor feeding / dehydration
• Fever is variable - often low-grade or absent

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Chest X-Ray Findings

• Bilateral hyperinflation (flat diaphragms, increased AP diameter, >9 posterior ribs visible)
• Peribronchial cuffing (thickened bronchial walls)
• Patchy atelectasis (often right upper lobe - due to small right upper lobe bronchus easily blocked)
• Bilateral interstitial infiltrates
• Note: CXR is NOT routinely recommended - clinical diagnosis is sufficient in typical cases

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Diagnosis

• Clinical diagnosis in most cases - no investigations routinely needed
• Rapid antigen test / RT-PCR nasopharyngeal swab can confirm RSV (useful for cohorting in hospital, not to change management)
• Multiplex respiratory panel (e.g., BioFire) detects RSV, hMPV, parainfluenza, and 14-19 other pathogens simultaneously

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Management (Evidence-Based)

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High-Risk Groups (Severe/Fatal Disease)

"The fatality rate among hospitalized infected infants is estimated to be 0.5%-1%; however, this rises higher in children receiving cancer chemotherapy, infants with congenital heart disease, and those with severe immunodeficiency."

• Sherris & Ryan's Medical Microbiology

• Premature infants (especially < 32 weeks gestation)
• Congenital heart disease (haemodynamically significant)
• Chronic lung disease (e.g., bronchopulmonary dysplasia)
• Immunodeficiency
• Age < 3 months

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Prevention

Recent 2025 ALAT Consensus [PMID: 41714249] and 2025 Australasian Bronchiolitis Guideline [PMID: 40685806] confirm supportive care remains the cornerstone of management.

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Diagnosis: Severe Dehydration secondary to Acute Gastroenteritis

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Clinical Reasoning

• Abnormal mental status (drowsy)
• Oliguria/anuria
• Weakness
• Refusal of oral intake

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Causative Organisms

"Rotavirus is a common etiology of gastroenteritis leading to hospitalization of children from dehydration and lethargy."

• Yamada's Textbook of Gastroenterology

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Dehydration Assessment (Degree in This Child)

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Treatment

Step 1 - Immediate IV Resuscitation (Emergency)

"Standard therapy involves 20-mL/kg boluses of NS or lactated Ringer's solution infused over a 60-minute period each, until normalization of pulse, perfusion, and mental status occurs."

• Roberts & Hedges' Clinical Procedures in Emergency Medicine

• IV access - establish immediately (two large-bore cannulas or intraosseous if IV fails)
• Fluid bolus: 20 mL/kg of Normal Saline (0.9% NaCl) or Lactated Ringer's over 15-60 minutes
• Repeat boluses of 20 mL/kg as needed, reassessing after each bolus (pulse, CRT, mental status, urine output)
• A 4-year-old is typically ~16-18 kg, so first bolus = ~320-360 mL

Step 2 - Urgent Investigations

Step 3 - Maintenance Fluids (After Stabilisation)

• 100 mL/kg for first 10 kg = 1000 mL
• 50 mL/kg for next 10 kg = 500 mL
• 20 mL/kg for remaining weight

Step 4 - Antiemetic

• Ondansetron 0.15 mg/kg IV - reduces vomiting, reduces need for IV hydration, NNT = 5
• For a ~17 kg child: 4 mg IV/oral
• Caution: prolongs QTc by 10-17 ms (generally safe in healthy children)

Step 5 - Transition to Oral Rehydration

• Transition to Oral Rehydration Solution (ORS) - WHO formula: 75 mEq/L sodium, 20 g/L glucose
• Start small volumes: 5-10 mL every 5 minutes, increasing slowly
• ORS is equivalent to IV therapy in mild-moderate dehydration (Cochrane evidence)

Step 6 - Specific Interventions

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Admission Criteria

• Severe dehydration with altered mental status
• Oliguria/anuria
• Unable to tolerate oral fluids
• IV rehydration needed

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Prevention (Rotavirus)

• Rotavirus oral vaccine (Rotarix or RotaTeq) - given at 6-10-14 weeks of age; reduces severe gastroenteritis hospitalisations by ~85%
• Hand hygiene, safe water, food hygiene

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Immunological Causes of Glomerulonephritis and Their Mechanisms

1. Immune complex deposition (circulating or in situ)
2. Anti-GBM antibody disease
3. ANCA-mediated (pauci-immune) vasculitis
4. Complement dysregulation (alternative pathway)
5. Cell-mediated immunity (T-cell driven) - supporting role

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The Immunological Deposit Location Diagram

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Mechanism 1: Immune Complex-Mediated GN

How immune complexes form in the glomerulus:

• Antigen-antibody complexes form in the bloodstream and become trapped in the glomerular filtration barrier
• Favored by: large amounts of antigen, low-avidity antibodies, impaired reticuloendothelial clearance
• Factors governing deposition site: charge, size of complexes, glomerular hemodynamics, mesangial function

• Circulating antigen "plants" in the glomerulus first; antibody then binds to it in situ
• Classic example: Heymann nephritis (experimental model of membranous nephropathy) - megalin/PLA2R antigen in the podocyte foot process is the target

Two root causes of immune complex accumulation:

"Two major mechanisms account for the presence of immune complexes in glomerular diseases. There may be ineffectual clearance of an antigen from an impaired immune response, as in chronic viral infections caused by hepatitis B or hepatitis C virus... More often, glomerular disease results from autoimmunity."

• Comprehensive Clinical Nephrology, 7th Edition

Location determines the inflammatory response:

"The presence of glomerular inflammation is largely determined by the site of immune deposits. Immune deposits with direct access to the circulation (subendothelial and intrabasement membrane locations) are usually associated with leukocyte accumulation. Mesangial deposits elicit an intermediate response, whereas immune deposits in the subepithelial space generally are not associated with inflammatory cells."

• Comprehensive Clinical Nephrology, 7th Edition

"Subendothelial immune complexes provoke leukocyte infiltration and glomerular crescent formation... In contrast, subepithelial immune complexes are shielded from the circulation by the GBM and do not induce inflammatory responses."

• Robbins & Cotran Pathologic Basis of Disease

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Mechanism 2: Anti-GBM Antibody Disease (Goodpasture Disease)

1. Autoantibodies (IgG, usually IgG1/IgG3) are produced against α3(IV)NC1
2. These bind directly and uniformly along the entire GBM → linear IgG pattern on immunofluorescence (distinguishes this from all immune complex diseases, which show granular deposits)
3. Complement activation (classical pathway via C1q binding to IgG)
4. Neutrophil recruitment via Fc-receptor engagement and C5a generation
5. Severe GBM disruption → crescentic (rapidly progressive) GN + alveolar haemorrhage (if lung BM also attacked)
6. HLA-DR2 (DRB1*1501) is strongly associated with susceptibility

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Mechanism 3: ANCA-Associated (Pauci-Immune) GN

• c-ANCA (cytoplasmic) → anti-PR3 (proteinase 3) → Granulomatosis with polyangiitis (GPA, Wegener's)
• p-ANCA (perinuclear) → anti-MPO (myeloperoxidase) → Microscopic polyangiitis, Eosinophilic GPA (Churg-Strauss)

1. ANCAs (IgG) are produced against neutrophil granule proteins (PR3 or MPO)
2. Primed neutrophils (by cytokines like TNF, IL-8 from infection/inflammation) surface-express PR3/MPO
3. ANCAs bind surface-expressed antigen → neutrophil activation
4. Activated neutrophils release proteases, reactive oxygen species (ROS), and extracellular traps (NETs)
5. These directly damage the glomerular endothelium and GBM
6. GBM rupture → fibrin leaks into Bowman's space → crescent formation
7. Minimal/no immune deposits on IF (pauci-immune) because no antigen is planted in the glomerulus

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Mechanism 4: Complement-Mediated GN (C3 Glomerulopathy)

• Normally, Factor H inhibits C3b amplification; Factor I cleaves and inactivates C3b
• In C3 glomerulopathy: mutations in Factor H, Factor I, CD46, or C3; or autoantibodies against Factor H or C3 convertase (C3 nephritic factor)
• C3 convertase (C3bBb) becomes hyperactive and continuously cleaves C3
• C3b fragments deposit massively in the mesangium and GBM
• C5a generated → neutrophil recruitment → glomerular injury

• Dense deposit disease (MPGN type II): extremely electron-dense intramembranous deposits (sausage-shaped)
• C3 glomerulonephritis: mesangial and subendothelial C3 deposits
• IF shows C3 alone (no IgG/IgM)

"Alternative complement pathway activation occurs in the clinicopathologic entity called C3 glomerulopathy, which encompasses the entities of dense deposit disease and C3 glomerulonephritis."

• Robbins & Cotran Pathologic Basis of Disease

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The Complement System in GN

• C3a/C5a: anaphylatoxins - increase vascular permeability and recruit neutrophils/monocytes
• C5b-9 (MAC): directly lyses glomerular endothelial cells and podocytes
• C1q: bridges immune complexes to the classical pathway
• Loss of complement in serum (low C3, C4) is a diagnostic clue to immune complex disease (SLE, post-streptococcal GN, MPGN)

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Mechanism 5: Cell-Mediated (T-Cell) Immunity

"T cells likely have a role in crescentic nephritis, becoming sensitized to endogenous or exogenous antigen and then recruiting macrophages that mediate crescent formation."

• Comprehensive Clinical Nephrology, 7th Edition

• Regulatory T cells (Tregs, CD4+/CD25+) normally suppress autoreactive responses; their failure allows GN to develop
• Activated T cells and macrophages release cytokines (IL-1, TNF-α, IFN-γ) and TGF-β that drive proliferation and fibrosis
• Minimal change disease (MCD): thought to be a T-cell disorder - a soluble factor (possibly CD80 or a suPAR-like molecule) produced by T cells damages podocyte foot processes directly, without immune deposits

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Effector Cells and Mediators - Downstream Injury

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Crescent Formation - The Final Common Pathway in Severe GN

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Summary Table: Immunological Mechanisms by Disease

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Investigations Required Before Starting Hemodialysis

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1. Confirm & Quantify Renal Failure

KDOQI (2015) recommends: "The decision to initiate maintenance dialysis should be based primarily on an assessment of attributable complications of kidney failure, including signs/symptoms of uremia, protein-energy wasting, and development of metabolic or volume disturbances refractory to medical therapy - rather than a specific GFR level."

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2. Identify the Underlying Cause of CKD

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3. Haematological Investigations

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4. Metabolic / Biochemical Panel

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5. Infection Screening (MANDATORY - for safe unit cohorting)

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6. Cardiovascular Assessment

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7. Vascular Access Investigations

Per KDOQI: An AV fistula should ideally be placed at least 6 months before anticipated start of hemodialysis to allow adequate time for maturation. Patients who reach CKD stage 4 (GFR < 30 mL/min) should begin access planning.

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8. Nutritional Assessment

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9. Immunological / Transplant-Related (If Transplant Anticipated)

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Summary Checklist

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Management of Acute Atypical Pneumonia

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What is "Atypical" Pneumonia?

• Cannot be cultured on standard blood/chocolate agar
• Do not respond to beta-lactam antibiotics (penicillins, cephalosporins) - they either lack a cell wall or have intracellular survival
• Produce a clinical picture of gradual onset, dry/hacking cough, low-grade fever, and extrapulmonary features disproportionate to the chest findings ("walking pneumonia")
• Show interstitial (rather than lobar) infiltrates on CXR

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Causative Organisms

"Levofloxacin or azithromycin are preferred for treatment [of Legionella]."

• Sherris & Ryan's Medical Microbiology 8th Edition

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Clinical Features of Atypical Pneumonia (vs. Typical)

Extrapulmonary Manifestations of Mycoplasma Pneumoniae:

• Haemolytic anaemia (cold agglutinins)
• Stevens-Johnson syndrome
• Erythema multiforme
• Meningoencephalitis, Guillain-Barré syndrome, transverse myelitis
• Myopericarditis
• Arthritis, rhabdomyolysis

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Diagnosis

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Antibiotic Treatment

Treatment by Clinical Setting

A. Outpatient - Mild Atypical Pneumonia (no comorbidities)

Per IDSA 2019: "For healthy outpatient adults without comorbidities, we recommend amoxicillin 1 g TDS, or doxycycline 100 mg BD, or a macrolide (only in areas with pneumococcal resistance <25%)."

B. Outpatient - With Comorbidities (diabetes, CKD, cardiac/lung disease, smoker)

C. Inpatient - Non-Severe (ward admission)

Recent meta-analysis [PMID: 37385561, 2023]: Respiratory fluoroquinolone monotherapy vs β-lactam + macrolide combination showed comparable outcomes in hospitalised CAP - supports guideline flexibility.

D. Inpatient - Severe CAP / ICU Admission (at least 1 major criterion: septic shock OR mechanical ventilation)

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Organism-Specific Treatment

Mycoplasma pneumoniae

Chlamydophila (Chlamydia) pneumoniae

Legionella pneumophila (Legionnaires' Disease)

"Levofloxacin or azithromycin are preferred for treatment [of Legionella]."

• Sherris & Ryan's Medical Microbiology 8th Edition

Coxiella burnetii (Q Fever)

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Supportive Management

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Duration of Treatment and Step-Down

• Minimum 5 days for non-severe CAP (IDSA/ATS 2019)
• Patient must be afebrile for ≥48 hours and clinically stable before stopping
• IV to oral switch when: haemodynamically stable + tolerating oral intake + improving clinically (same-day switching is now endorsed in guidelines)
• Macrolide-resistant Mycoplasma (increasing in Asia): switch to doxycycline or respiratory fluoroquinolone

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Severity Assessment (PSI / CURB-65)

• Confusion
• Urea > 7 mmol/L
• Respiratory rate ≥ 30/min
• BP systolic < 90 or diastolic ≤ 60 mmHg
• 65 years or older

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Summary Antibiotic Algorithm

Atypical CAP suspected
         │
         ▼
  Severity assessment
  (CURB-65 / PSI)
         │
   ┌─────┴──────┐
   │            │
Outpatient   Inpatient
   │            │
   ▼        ┌───┴────────┐
Doxycycline │            │
100mg BD  Non-severe   Severe/ICU
  OR        │            │
Azithromycin│    β-lactam + │  β-lactam + 
500/250mg  Azithromycin  │  IV azithromycin
  OR        OR β-lactam +│  OR
Respiratory │  doxycycline│  β-lactam +
 FQL        OR FQL mono   │  IV levofloxacin
  5 days    5 days        5-14 days

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