Pneumonia

Acute infection of the lung parenchyma causing inflammation and consolidation of alveolar spaces, typically bacterial, viral, or (less commonly) fungal in etiology.

Classified by acquisition setting (guides likely pathogens and empirical treatment):

Community-acquired pneumonia (CAP): acquired outside healthcare settings; typical pathogens : Streptococcus pneumoniae (most common), Haemophilus influenzae, Mycoplasma pneumoniae, Chlamydophila pneumoniae, Legionella pneumophila, respiratory viruses (influenza, RSV, now including SARS-CoV-2)
Hospital-acquired pneumonia (HAP): onset ≥48 hours after admission; broader/more resistant pathogen spectrum ; gram-negatives (Pseudomonas, E. coli, Klebsiella), S. aureus (including MRSA)
Ventilator-associated pneumonia (VAP): subset of HAP in mechanically ventilated patients
Aspiration pneumonia: anaerobes and mixed oral flora, in patients with impaired swallow/consciousness

Fever, productive cough (purulent sputum), dyspnea, pleuritic chest pain
Rigors, malaise, fatigue; in elderly may present atypically; confusion, falls, non-specific decline without prominent fever/respiratory symptoms
Examination: tachypnea, tachycardia, reduced oxygen saturation, focal chest signs — dullness to percussion, bronchial breathing, coarse crackles, increased vocal fremitus/resonance over consolidated area
Atypical pneumonia (Mycoplasma, Chlamydophila, Legionella): more gradual onset, extrapulmonary symptoms (headache, myalgia, GI symptoms, relative bradycardia with Legionella), dry cough, chest exam may be relatively unremarkable despite CXR changes ("walking pneumonia")
Legionella-specific clues: hyponatremia, deranged LFTs, GI symptoms, confusion, recent travel/water exposure (air conditioning, hot tubs)
Complications: parapneumonic effusion/empyema (persistent fever despite antibiotics, pleuritic pain), lung abscess (cavitation, foul-smelling sputum; aspiration risk), sepsis/septic shock, respiratory failure

Clinical + radiographic: CXR showing new consolidation confirms diagnosis (though may lag behind clinical presentation, especially if dehydrated, or in early disease)

Severity assessment: CURB-65 score (guides site of care/treatment intensity): Confusion, Urea >7mmol/L, Respiratory rate ≥30/min, Blood pressure (SBP<90 or DBP≤60), Age ≥65 : 1 point each

0-1: low risk, outpatient management
2: moderate risk, consider hospital admission
≥3: high risk, hospital admission, consider ICU/HDU

Labs: FBC (leukocytosis), U&E (urea for CURB-65, renal function), CRP (trend to monitor response), LFTs, blood cultures (before antibiotics if moderate-severe/hospitalized), sputum culture and Gram stain

Pulse oximetry/ABG if hypoxic or severe

Urinary antigen testing: pneumococcal and Legionella antigen (particularly for moderate-severe CAP, or specific clinical suspicion for Legionella)

Atypical serology/PCR (Mycoplasma, Chlamydophila) if suspected based on clinical picture

Pleural ultrasound/CT chest: if complicated pneumonia suspected (effusion, empyema, abscess, non-resolving pneumonia)

Consider influenza/COVID/respiratory viral panel per seasonal/clinical context

Differentials: acute bronchitis (no focal consolidation, milder illness), pulmonary embolism (pleuritic pain, dyspnea, risk factors — can mimic/coexist), heart failure/pulmonary edema (bilateral, cardiac history), lung malignancy (especially if non-resolving/recurrent pneumonia in same location — warrants follow-up imaging), TB (chronic symptoms, risk factors, apical changes), COVID-19 pneumonia.

Empirical antibiotic therapy (per severity, adjust to local guidelines/resistance patterns and culture results once available):

Low severity CAP (CURB-65 0-1, outpatient): amoxicillin 500mg-1g tds for 5 days; penicillin-allergic; doxycycline 200mg loading then 100mg od, or clarithromycin 500mg bd
Moderate severity (CURB-65 2): amoxicillin + clarithromycin (dual cover for atypicals), or doxycycline alone; duration typically 5-7 days
High severity (CURB-65 ≥3, or ICU): broad-spectrum beta-lactam (co-amoxiclav or ceftriaxone/cefotaxime) + macrolide (clarithromycin/azithromycin) covering atypicals; consider longer duration (7-10 days), IV initially transitioning to oral once clinically stable (afebrile 24h, improving)
Aspiration pneumonia: cover anaerobes ; co-amoxiclav, or clindamycin if penicillin-allergic
Hospital-acquired pneumonia: broader gram-negative/MRSA cover based on local resistance patterns and risk factors; e.g., piperacillin-tazobactam ± vancomycin/linezolid if MRSA risk
Suspected Legionella: fluoroquinolone (levofloxacin) or macrolide, often requires longer duration and higher clinical suspicion for atypical/severe course

Supportive care:

Oxygen therapy (titrate to target saturation 94-98%, or 88-92% if COPD/CO2 retention risk)
IV fluids if dehydrated/septic, analgesia for pleuritic pain, antipyretics
Chest physiotherapy for sputum clearance if indicated
VTE prophylaxis for hospitalized patients (reduced mobility risk)
Early mobilization

Sepsis/severe pneumonia: sepsis six/bundle care; cultures, lactate, IV fluids, oxygen, antibiotics within 1 hour, escalate to ICU if shock/respiratory failure requiring vasopressor/ventilatory support.

Complications management:

Parapneumonic effusion/empyema: pleural fluid analysis (pH <7.2, low glucose, high LDH suggests empyema/complicated effusion) ; chest drain insertion if empyema or complicated effusion, prolonged antibiotics
Lung abscess: prolonged antibiotic course (weeks), drainage rarely needed unless large/not responding

Follow-up: repeat CXR at 6 weeks post-treatment in smokers, older patients, or persistent symptoms to confirm resolution and exclude underlying malignancy; earlier follow-up for clinical response assessment (48-72 hours).

Prevention: pneumococcal vaccination (high-risk groups ; elderly, chronic disease, immunosuppressed, asplenia), annual influenza vaccination, smoking cessation.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Respiratory Acidosis

Also known as: Hypercapnia, Hypercapnic respiratory failure

Respiratory acidosis is a primary rise in PaCO₂ producing a fall in pH, resulting from alveolar hypoventilation: the lungs failing to clear CO₂ at the rate it is produced.

Renal compensation retains bicarbonate, but this takes 3–5 days to become fully established, which is why the distinction between acute and chronic matters so much.

Acute respiratory acidosis shows a markedly low pH with only a small rise in bicarbonate (roughly 1 mmol/L per 10 mmHg rise in PaCO₂), because compensation has not had time to develop.

Chronic respiratory acidosis shows a near-normal pH with a substantially raised bicarbonate (roughly 3.5–4 mmol/L per 10 mmHg), reflecting established renal compensation.

Causes include central respiratory depression (opioids, sedatives, brainstem pathology), neuromuscular disease (Guillain-Barré, myasthenia, motor neurone disease), chest wall and pleural disease, and airways and parenchymal disease, principally COPD, severe asthma and obesity hypoventilation.

Blood gas showing low pH with raised PaCO₂. An arterial sample is preferred where precise PaCO₂ matters, though venous CO₂ correlates well enough for screening
Distinguish acute from chronic by the bicarbonate, using the compensation rules above. A patient with PaCO₂ of 70 mmHg and bicarbonate of 26 is acutely decompensated and in danger; the same PaCO₂ with a bicarbonate of 38 reflects chronic adaptation. Mistaking chronic compensated hypercapnia for acute failure leads to unnecessary intervention, and mistaking acute failure for chronic leads to dangerous delay
Acute-on-chronic is common and is identified by a bicarbonate that is raised but insufficient for the degree of hypercapnia
Identify the cause: chest examination and imaging, drug chart review for opioids and sedatives, neurological assessment for neuromuscular weakness, and assessment for airway obstruction
Serial gases are more informative than a single measurement, since the trajectory determines management
In neuromuscular disease, forced vital capacity predicts respiratory failure earlier and more reliably than blood gases, which can remain normal until decompensation is imminent

Treat the underlying cause, which is the priority: bronchodilators, steroids and antibiotics for COPD exacerbation; naloxone for opioid-induced respiratory depression; treatment of the neuromuscular disorder
Controlled oxygen therapy in patients at risk of CO₂ retention, targeting saturations of 88–92% rather than normal values. The concern is real but is often misunderstood: the mechanism is principally increased ventilation-perfusion mismatch and the Haldane effect rather than simple loss of hypoxic drive. Critically, hypoxia kills before hypercapnia does, so oxygen should never be withheld from a hypoxic patient for fear of retention; it should be titrated
Non-invasive ventilation (BiPAP) is the key intervention in acute hypercapnic respiratory failure, particularly in COPD, where it has clear mortality benefit. Indications include a pH below 7.35 with PaCO₂ above roughly 45–50 mmHg persisting despite initial medical therapy
Invasive ventilation where non-invasive ventilation fails or is contraindicated: reduced consciousness with an unprotected airway, haemodynamic instability, copious secretions, facial trauma, or vomiting
Avoid over-correcting chronic hypercapnia: rapidly normalising PaCO₂ in a chronically compensated patient produces a post-hypercapnic metabolic alkalosis, since the raised bicarbonate persists after the CO₂ has fallen
Stop or reverse contributing sedatives and opioids
Discuss ceiling of care early in patients with advanced chronic lung disease, since decisions about escalation to invasive ventilation are best made before the patient deteriorates rather than during a crisis

Referral: respiratory medicine and critical care for acute hypercapnic failure; neurology for neuromuscular causes, with early critical care involvement given the speed of decompensation.

Pneumonia

Overview

Clinical Features

Diagnosis

Management

Overview

Diagnosis

Management