• M/35, chronic smoker, good past health
• URTI symptoms (sore throat, running nose) 10 days ago ← the preceding viral illness
• Increasing cough and greenish sputum over past 5 days
• Progressive SOB with right pleuritic chest pain for 3 days
• High swinging fever with chills and rigor for 3 days
• Seen by GP → oral antibiotics + paracetamol → worsening → A&E

• Respiratory distress, mentally alert
• Chest: dullness, bronchial breath sound, and coarse inspiratory crackles over right lower chest
• BP 90/50 mmHg (hypotension → urgent sepsis/haemodynamic assessment; this alone does not define septic shock)
• SpO₂ 92% on room air (hypoxaemia)

Why this is CAP and not something else:

• Onset in the community (not hospitalised)
• Preceded by URTI → secondary bacterial infection is classic
• Consolidation signs (dullness + bronchial breath sounds + crackles) = lobar consolidation
• Systemic toxicity (high swinging fever, chills, rigor)

Why is he sick?

• Hypotension (BP 90/50) raises concern for sepsis with haemodynamic compromise; septic shock requires assessment after initial resuscitation (including vasopressor requirement and lactate), not BP alone
• Hypoxaemia (SpO₂ 92%) suggests significant parenchymal involvement
• These features push him into the "severe CAP" category

Slide 6 CXR read: the film shows dense right mid-to-lower-zone air-space opacity, in keeping with the bedside right-sided consolidation signs. Always read the whole image systematically: side marker and technical quality, lobar distribution/silhouette signs, air bronchograms, pleural fluid, cavitation, additional lobes and any obstructing lesion.

Inflammation of lung parenchyma, commonly due to infective agents (bacteria, viruses or fungi). ^[1]

This is important: pneumonia = parenchymal inflammation. Bronchitis = airway inflammation. That's why you see consolidation on CXR in pneumonia but not in bronchitis.

The slide quotes 2021–2022 figures and a 2007 mortality chart. Treat these as dated teaching snapshots rather than current denominators. The current official HealthyHK dataset reports that pneumonia remained the second leading cause of death in 2024, with 11,395 deaths (21.8% of registered deaths) and 80,485 inpatient discharges and deaths (3.4% of all inpatient discharges and deaths). ^[9]

2007 Mortality Breakdown (pie chart from lecture slide): ^[1]

Source shown on the slide: Hospital Authority and Department of Health, HKSAR. ^[1] These historical percentages should not be directly interpreted as a trend without checking changes in coding, population age structure and denominators.

Cough, sputum, haemoptysis, dyspnoea, pleuritic chest pain; fever, chills, rigor; confusion, constitutional or systemic symptoms.

Why each symptom occurs:

• Cough + sputum: inflammatory exudate in alveoli stimulates cough reflex; purulent sputum = neutrophilic response to bacterial infection
• Haemoptysis: necrosis of alveolar tissue or inflamed bronchial mucosa
• Pleuritic chest pain: inflammation reaching the visceral/parietal pleura → sharp, stabbing pain worse with inspiration
• Fever/chills/rigor: systemic inflammatory response; rigor (uncontrollable shaking) suggests bacteraemia
• Confusion: especially in elderly; marker of severe disease (the "C" in CURB-65)

Chest: percussion dullness, bronchial breath sound, coarse crackles, increased vocal resonance. Vital signs: BP, SpO₂; mental state.

Why these signs occur — from first principles:

• Percussion dullness: consolidated (solid) lung transmits percussion energy poorly → dull note (vs resonant normal air-filled lung)
• Bronchial breath sounds: normally heard only over trachea. When lung is consolidated, it conducts sound from central airways to the chest wall without filtering → harsh, hollow quality heard peripherally
• Coarse crackles: secretions in airways "pop" open during inspiration
• Increased vocal resonance (including whispering pectoriloquy and aegophony): consolidated lung transmits voice sounds more efficiently than air-filled lung

Travel, Occupation, Contact, Clustering

This is crucial for identifying atypical pathogens and notifiable diseases:

• Travel: Legionella (contaminated water systems, hotels), TB (endemic areas), MERS (Middle East)
• Occupation: healthcare workers (TB, influenza), farmers (Q fever, melioidosis)
• Contact: household contacts with similar illness → viral, TB
• Clustering: outbreak → influenza, COVID-19, Legionella

Usually refers to M. pneumoniae, C. pneumoniae, L. pneumophila. Syndrome of pneumonitis, fever, and a relatively normal WBC, without identifiable bacterial pathogens. Prominent systemic complaints.

Why "atypical"?

• These organisms don't grow on standard blood agar/chocolate agar (hence "without identifiable bacterial pathogens")
• They cause interstitial rather than alveolar inflammation → less sputum production
• Systemic symptoms (headache, myalgia, malaise) are disproportionately prominent vs respiratory symptoms
• WBC is typically normal (unlike typical bacterial pneumonia where WBC is elevated)
• CXR often shows patchy/interstitial infiltrates rather than dense lobar consolidation

Compatible respiratory symptoms and signs + Chest X-ray: consolidations in lobar pneumonia; patchy infiltrates in bronchopneumonia.

In hospital, obtain a chest X-ray promptly to confirm suspected pneumonia. In community care, pneumonia can be diagnosed clinically when imaging is unavailable, and an initially normal film does not absolutely exclude early, dehydrated or immunocompromised pneumonia. Reassess and repeat or escalate imaging when clinical suspicion remains high. NICE also recognises lung ultrasound as an adjunct where trained expertise is available. ^[9]

The slide's investigation list:

• Complete blood counts (total WBC and differential counts)
• Electrolytes, liver and renal function tests
• Arterial blood gases
• Atypical pneumonia serology
• Nasopharyngeal aspirate if influenza or atypical pneumonia suspected
• Urinary antigen test for Legionella and pneumococcus
• Sputum and blood cultures

Why each investigation matters:

Microbiological diagnosis is retrospective. Initial management is based on clinical setting and host factors: co-morbidities, immunocompetent vs immunocompromised status, and previous antibiotic use. ^[1]

This is a critical teaching point: you almost never know the pathogen when you start treatment. You must use clinical context to make your best guess and start empirical therapy.

Need to cover Streptococcus pneumoniae in ALL cases of CAP. Need to cover Legionella pneumophila in SEVERE cases of CAP.

Why cover Legionella in severe CAP?

• Legionella causes severe disease with multi-organ involvement
• It is an intracellular pathogen → beta-lactams alone won't work
• It requires an active non-beta-lactam agent, commonly a macrolide or respiratory fluoroquinolone in guideline regimens
• This is why severe-CAP protocols include appropriate atypical/Legionella coverage; follow the current local regimen rather than adding a drug ad hoc

CURB-65:

• C — Confusion
• U — Urea > 7 mmol/L
• R — Respiratory rate ≥ 30/min
• B — Blood pressure (SBP < 90 mmHg OR DBP ≤ 60 mmHg)
• 65 — Age ≥ 65

Apply to the case: The 35-year-old man scores 1 from the supplied data (DBP 50; the respiratory rate and urea are not given). SpO₂ 92% does not earn a CURB-65 point. Nevertheless, hypotension, hypoxaemia and respiratory distress mandate hospital management and urgent sepsis/critical-care assessment. This illustrates why CURB-65 supplements rather than replaces clinical judgement. ^[9]

Lecture poor-prognosis list: old age, hypoxaemia (PaO₂ < 8 kPa), high (> 11 × 10⁹/L) or low WBC (< 4 × 10⁹/L), high urea (> 8 mmol/L), multilobar involvement, bacteraemia. ^[1]

The unit on slide 18 should be ×10⁹/L, not ×10⁹/mL.

Lecture-era rule: administer appropriate antibiotics within 6–8 hours.

Current NICE guidance is more specific: start antibiotics as soon as possible after the diagnosis is established and within 4 hours of hospital presentation; suspected sepsis or shock follows the urgent sepsis pathway. Review IV therapy by 48 hours and narrow/switch to oral therapy when possible. ^[9]

Lecture-era example: a beta-lactam/beta-lactamase inhibitor ± macrolide or tetracycline; duration 7–10 days.

Do not memorise this as a universal prescription. Choose the agent and route from the current local antimicrobial guideline, illness severity, allergies, renal/hepatic function, recent antibiotics, local resistance and prior microbiology. For uncomplicated clinically stable adult CAP, NICE recommends stopping after 5 days unless microbiology requires longer treatment or instability persists. ^[9]

Why this combination?

• Amoxicillin-clavulanate (Augmentin): covers S. pneumoniae, H. influenzae (including beta-lactamase producing strains), and many Gram-negatives. The clavulanate inhibits beta-lactamase enzymes that would otherwise destroy amoxicillin.
• Macrolide (clarithromycin/azithromycin) or doxycycline: covers atypical pathogens (Mycoplasma, Chlamydophila, Legionella) which are intracellular and not covered by beta-lactams. Added especially in severe CAP to cover Legionella.

The slide lists recent antibiotics/hospitalisation, nursing-home residence and immunosuppression as MDR risks. ^[1]

The old “healthcare-associated pneumonia” shortcut has been abandoned. Nursing-home residence alone does not mandate broad-spectrum therapy. Stronger triggers for MRSA or Pseudomonas evaluation include prior respiratory isolation/colonisation and recent hospitalisation with parenteral antibiotics; severe CAP increases the consequence of missing these organisms. Obtain cultures, use locally validated risks and de-escalate promptly when results permit. ^[10]

The slide lists O₂/ventilatory support, chest physiotherapy, fluids, COPD bronchodilators and arrhythmia control.

• Prescribe oxygen to a target: commonly 94–98%, or 88–92% pending blood gases when hypercapnic respiratory failure is a risk. ^[16]
• Give fluids according to haemodynamics and the sepsis pathway; avoid indiscriminate loading in cardiac/renal dysfunction.
• Routine chest physiotherapy is not required for uncomplicated pneumonia; use respiratory physiotherapy/airway-clearance techniques for retained secretions or coexisting suppurative airway disease.
• Treat bronchospasm and organ complications on their own indications.

Why AF in pneumonia?

• Infection → systemic inflammation → autonomic imbalance + hypoxia + fever → triggers atrial fibrillation, especially in elderly patients
• AF with rapid ventricular response can worsen haemodynamic status
• Usually reverts with treatment of the underlying infection

Pneumonia occurring > 48 hours after hospitalization.

This time threshold is critical — it distinguishes HAP from CAP that was incubating at the time of admission.

Mostly related to aspiration of oropharyngeal secretions colonized by hospital-acquired organisms.

Why hospitals are different: The oropharynx becomes colonized with Gram-negative bacilli and resistant organisms within 48 hours of hospital admission (due to altered mucosal defences, exposure to antibiotics, supine positioning, and invasive devices).

General debility and old age, cigarette smoking, COPD, aspiration, post-GA, H₂ blockers or antacids, nasogastric tube, mechanical ventilation (VAP).

Why H₂ blockers/antacids? They raise gastric pH → allow bacterial colonization of the stomach → retrograde colonization of the oropharynx → aspiration. This is a classic exam question.

The slide proposes broad Gram-positive, Gram-negative, MRSA, antipseudomonal, ESBL and anaerobic coverage, with piperacillin-tazobactam or meropenem as examples.

That list is not a blanket contemporary regimen. Base initial therapy on the hospital's HAP antibiogram, prior respiratory cultures, illness severity and recent IV antibiotic exposure. Empiric MRSA coverage is reserved for recognised MRSA risk or high mortality risk; dual antipseudomonal therapy is likewise reserved for selected high-risk cases. Obtain respiratory cultures, narrow therapy when susceptibilities return, and avoid routine anaerobic or carbapenem coverage without an indication. A 7-day course is generally recommended for HAP/VAP, adjusted to clinical, radiological and laboratory response. ^[11]

Altered consciousness, alcoholism, vomiting, dysphagia and oesophageal diseases, neurological disorders (bulbar palsy), nasogastric tube feeding, severe dental or URTI, terminal illness, drowning.

Common thread: All these conditions impair airway protective reflexes (gag, cough, swallowing coordination) → aspiration of oropharyngeal or gastric contents into the lower respiratory tract.

Usually affects dependent parts of lungs:

• Lower lobes (especially on the right)
• Posterior segments of upper lobes (in those mostly recumbent)

Distribution follows body position at aspiration: upright aspiration favours basal lower-lobe segments (often right-sided); supine aspiration favours posterior upper-lobe and superior lower-lobe segments. The right main bronchus makes right-sided involvement common, but left-sided disease does not exclude aspiration.

Videofluoroscopic swallowing test (VFSS) — to confirm swallowing dysfunction and guide feeding strategy.

Slide 27 image: the radiograph demonstrates radiopaque contrast tracking into the right tracheobronchial tree and dependent lung after a swallow study—direct visual evidence of aspiration. VFSS should identify the phase/mechanism of dysphagia and test compensatory strategies, not merely label aspiration present or absent.

First distinguish:

• Aspiration pneumonitis: chemical injury after a witnessed macroaspiration, often abrupt; provide supportive care and reassess. Prophylactic antibiotics are not routinely indicated unless bacterial infection subsequently becomes likely.
• Aspiration pneumonia: established infection after aspiration; treat according to the current local pneumonia guideline and setting. Do not routinely add anaerobic coverage unless lung abscess or empyema is suspected. ^[10]

Reduce recurrence with multidisciplinary swallow assessment, appropriate positioning and feeding assistance, oral hygiene, medication/sedation review and treatment of reversible causes. Slide 28 shows a PEG tube, but PEG does not eliminate aspiration risk (oropharyngeal secretions and reflux can still be aspirated); tube feeding decisions require goals-of-care and nutritional assessment.

• Severe pneumonia → widespread alveolar consolidation → V/Q mismatch → hypoxaemia
• May progress to ARDS if overwhelming inflammation

• Bacteraemia → sepsis → septic shock → organ dysfunction (renal, hepatic, coagulopathy)

Air-fluid level/cavity; may be polymicrobial. The slide suggests 4–6 weeks of antibiotics and no percutaneous drainage in most cases.

Visual pattern: a thick-walled intraparenchymal cavity containing an air–fluid level suggests lung abscess, but CT is useful when the diagnosis, anatomy, underlying obstruction or alternative cavitating disease is uncertain.

Treatment duration is guided by clinical and radiological response rather than an automatic fixed number. Most abscesses drain through the bronchial tree; percutaneous/endoscopic/surgical drainage is reserved for selected cases such as failure of appropriate therapy, poor spontaneous drainage or an obstructing lesion.

• Reactive pleural effusion adjacent to pneumonia
• Initially sterile (simple parapneumonic effusion) → may become infected → complicated effusion → empyema

The slide defines empyema by pleural pus or positive Gram stain/culture and prescribes prolonged antibiotics plus pleural drainage.

Current BTS guidance adds a practical decision pathway: use thoracic ultrasound to confirm a safely accessible collection and sample it. Frank pus requires drainage. If the aspirate is not purulent, measure pleural pH promptly: pH ≤7.2 indicates high-risk complicated parapneumonic effusion/pleural infection and supports intercostal drainage; pH 7.2–7.4 requires LDH plus the clinical and imaging context. Antibiotic duration is individualised to source control and response rather than fixed at 4–6 weeks for every patient. ^[17]

Key difference from lung abscess: Empyema = pus in the pleural space (needs drainage). Lung abscess = pus in the lung parenchyma (usually drains via bronchi, no external drainage needed).

Electrolyte abnormalities e.g. hypoNa due to SIADH; acute myocardial infarction; cardiac arrhythmia (AF).

Hyponatraemia in pneumonia may reflect non-osmotic ADH release, volume depletion, renal dysfunction or medication effects. It is associated with Legionella but is not organism-specific; assess serum/urine osmolality and volume status before diagnosing SIADH.

Influenza A and B. Immunogenic surface antigens: Haemagglutinin (H) and Neuraminidase (N).

Why H and N matter:

• Haemagglutinin (H): binds sialic acid on host respiratory epithelial cells → mediates viral entry
• Neuraminidase (N): cleaves sialic acid → releases progeny virus from infected cells → allows spread

Mechanism of neuraminidase activity and inhibition (adapted from NEJM 2005;353:1363–1373): ^[1]

The slide describes antigenic shift as a major antigen change and drift as a minor change. Antigenic drift: minor changes in antigens. It links pandemics to a novel virus and little population immunity. ^[1]

Important correction: antigenic shift is a mechanism of influenza A, not B, and a subtype switch such as “H3N2 to H1N1” is not itself proof that shift occurred. Novel antigenicity alone also does not guarantee either high pathogenicity or a pandemic—efficient sustained human transmission is required.

In Hong Kong, influenza is more common from January to March and from July to August.

This remains a useful HK pattern: CHP describes increased activity usually from January to March/April and July to August, although influenza circulates year-round and actual season timing varies. ^[14]

Slide 34 graph: the bars are monthly influenza isolates in 2004, not a current surveillance curve. It visually shows an H3N2-dominant peak around March and another around July, while the consultation-rate line varies much less. Use live CHP surveillance—not the 2004 graph—to infer the current circulating subtype or epidemic intensity.

URTI symptoms: running nose, sore throat, cough and sputum. Fever, myalgia, arthralgia. Lower respiratory tract or systemic involvement.

Distinguishing influenza from common cold: Influenza has prominent systemic symptoms (high fever, myalgia, prostration) that are disproportionate to respiratory symptoms. Common colds have predominant nasal symptoms with mild or no systemic upset.

The slide lists rapid antigen testing on NPA, RT-PCR, viral culture and serology.

• Rapid antigen test: fast but less sensitive; a negative result does not reliably exclude influenza when prevalence or suspicion is high
• Molecular assay (for example RT-PCR): preferred for hospitalised patients because of its higher sensitivity and specificity
• Viral culture: takes days; mainly for epidemiological surveillance
• Serology: retrospective (paired sera); not useful for acute management

Test all patients admitted with suspected influenza using a molecular assay. If a critically ill ventilated patient has a negative upper-respiratory molecular test but suspicion remains, test a lower-respiratory specimen. Do not delay empiric antiviral treatment in priority groups while waiting for the result. ^[13]

Personal hygiene, symptomatic treatment, specific antivirals.

Pathological dilatation of bronchi. Generalized or localized. Cause: mostly idiopathic (needs to exclude other causes e.g. post-infection, TB).

Why does bronchiectasis develop? The "vicious cycle" hypothesis: infection → inflammation → structural damage to bronchial walls → impaired mucociliary clearance → mucus pooling → further infection → more damage. The end result is irreversible dilation of bronchi.

Causes to exclude:

• Post-infectious: childhood measles/pertussis/severe pneumonia, TB
• Immunodeficiency: hypogammaglobulinaemia, HIV
• Cystic fibrosis (sweat test)
• Primary ciliary dyskinesia (specialist pathway based on compatible lifelong history; nasal nitric oxide and confirmatory ciliary/genetic testing)
• Aspiration/GORD (barium studies/pH monitoring)
• Allergic bronchopulmonary aspergillosis (ABPA)
• Autoimmune: RA, SLE

Symptoms:

Chronic sputum production and cough, infective exacerbations, haemoptysis (usually infective), weight loss, fatigue, chest pain, dyspnoea.

Signs:

Cachexia, clubbing, coarse crackles, associated COPD, respiratory failure.

Why clubbing? Chronic suppurative lung disease → likely related to circulating growth factors (VEGF, PDGF) from chronically inflamed tissue → nail bed vasodilation and connective tissue proliferation.

Progressive lung damage, lung abscesses, empyema, brain abscesses.

Brain abscess is a rare metastatic complication of chronic suppurative infection. Its presence should prompt a search for bacteraemia, endocarditis and a right-to-left shunt rather than assuming bronchiectasis alone explains it.

The slide lists CXR/HRCT, immunoglobulins, autoantibodies, aspiration/reflux studies, ciliary/sperm analysis, sputum culture/AFB, neutrophil testing and sweat testing.

Use a minimum aetiology panel for everyone, then phenotype-directed tests rather than ordering the entire historical slide list. A cause can change treatment (for example immunoglobulin replacement, ABPA therapy, CF/PCD care or aspiration management). ^[15]

• Sputum Gram stain and culture: a good quality specimen should have > 25 PMNs and < 10 squamous epithelial cells per low-power field
• When blood cultures are indicated, obtain appropriate sets from separate venepunctures before antibiotics if this does not delay urgent treatment
• MALDI-TOF mass spectrometry increasingly replacing traditional culture for rapid pathogen identification

• Fever = core temperature ≥38.0°C (oral ≥37.5°C)
• Swinging/hectic fever pattern: suggestive of abscess or empyema (wide temperature fluctuations)

• CXR for pneumonia: look for consolidation, air bronchograms, pleural effusion, cavity/air-fluid level
• CT thorax: for complications (abscess, empyema, underlying tumour) and for bronchiectasis diagnosis (HRCT)

• From respiratory DI sessions ^[8]: Interpreting ABG in the context of pneumonia:
  • Type 1 respiratory failure: low PaO₂, normal/low PaCO₂ (pneumonia)
  • Type 2 respiratory failure: low PaO₂, high PaCO₂ (severe pneumonia with exhaustion, or underlying COPD)