Lobar Pneumonia

Definition

FIG. 11.29 — Anatomic contrast: patchy bronchopneumonia (left) vs. lobar consolidation (right). — Robbins & Kumar Basic Pathology

Etiology / Common Organisms

Pathology — The Four Classic Stages

1. Congestion

• Lung is heavy, boggy, and red
• Vascular engorgement, intraalveolar edema fluid with few neutrophils
• Bacteria often numerous

2. Red Hepatization

• Massive confluent exudation: neutrophils + red blood cells + fibrin fill alveolar spaces
• Gross: lobe is red, firm, airless, with liver-like consistency (hence "hepatization")

3. Gray Hepatization

• Progressive disintegration of red cells
• Persistence of fibrinopurulent exudate
• Color shifts to grayish-brown

4. Resolution

• Exudate is broken down by enzymatic digestion → granular, semifluid debris
• Debris is resorbed, ingested by macrophages, expectorated, or organized by fibroblasts
• If extension to pleura → fibrinous pleuritis; may leave fibrous thickening or adhesions

FIG. 11.30 — Lobar pneumonia with gray hepatization. The lower lobe is uniformly consolidated. — Robbins & Kumar Basic Pathology

(A) Red hepatization — congested capillaries, massive neutrophilic exudate in alveoli. (B) Gray hepatization / early organization — exudate streaming through pores of Kohn (arrow). (C) Advanced organizing pneumonia — fibromyxoid masses with macrophages and fibroblasts. — Robbins & Kumar Basic Pathology

Clinical Features

• Abrupt onset of high fever, shaking chills
• Productive cough with mucopurulent sputum (may be rust-colored/hemoptysis in pneumococcal disease)
• Pleuritic chest pain and pleural friction rub when pleuritis is present
• In the elderly, classic features may be absent; may mimic CHF, PE, or malignancy

Radiology

• Homogeneous, nonsegmental consolidation confined to one lobe
• Entire lobe is radiopaque in lobar pneumonia (vs. focal opacities in bronchopneumonia)
• Air bronchogram — airways made visible by surrounding alveolar filling — is characteristic
• Volume loss is absent or minimal in the acute stage; minor atelectasis may develop from bronchial obstruction by exudate
• Pleural effusion in up to 50% of cases (highly suggestive of bacterial process when large)

• Dense parenchymal consolidation with air bronchograms
• The CT angiogram sign — enhancement of branching pulmonary vessels within a homogeneous low-attenuation consolidation — can occur in lobar pneumonia (originally described in lepidic adenocarcinoma)
• Klebsiella: bulging fissure sign, early necrosis/abscess

Fig. 5.7 — CT of lobar pneumococcal pneumonia. Dense consolidation with air bronchogram (white arrows) and CT angiogram sign (black arrow). — Grainger & Allison's Diagnostic Radiology

Complications

1. Lung abscess — tissue destruction/necrosis (especially Klebsiella, Staphylococcus)
2. Empyema — spread of infection to the pleural space → intrapleural fibrinopurulent reaction
3. Bacteremic dissemination → endocarditis, meningitis, brain/renal/splenic abscesses, suppurative arthritis, pericarditis

Treatment

• Effective antibiotics markedly alter the clinical course; treated patients often become afebrile within 48–72 hours
• Identification of the causative organism and antibiotic sensitivity testing are the keystones of therapy
• Mortality in hospitalized patients is <10%; most deaths result from complications (empyema, meningitis, endocarditis) or underlying debility/alcoholism

Arterial Blood Gas (ABG) — Harrison's Principles of Internal Medicine (22nd Ed., 2025)

1. Normal Acid-Base Homeostasis

• Extracellular and intracellular chemical buffering
• Respiratory regulation of PaCO₂ (CNS control)
• Renal regulation of plasma HCO₃⁻

2. Normal ABG Values

In clinical laboratory reporting, pH and PaCO₂ are directly measured; HCO₃⁻ is calculated from the Henderson-Hasselbalch equation. This calculated HCO₃⁻ must match the measured total CO₂ on the electrolyte panel within ±2 mmol/L. A discrepancy suggests simultaneous sampling error or laboratory error.

3. Stepwise Approach to ABG Interpretation

1. Obtain ABG and venous electrolytes simultaneously (before therapy)
2. Compare calculated HCO₃⁻ (from ABG) with measured HCO₃⁻ (electrolyte panel) — should agree within ±2 mmol/L
3. Assess the Anion Gap (AG) — correct for albumin if hypoalbuminemia present; high AG if >10 mEq/L
4. Identify causes of high-AG acidosis (ketoacidosis, lactic acidosis, renal failure, toxic alcohols)
5. Identify causes of non-gap acidosis (GI bicarbonate loss, renal tubular acidosis)
6. Estimate predicted compensatory response (Table below)
7. Compare delta values (ΔAG vs. ΔHCO₃⁻)
8. Compare change in [Cl⁻] with change in [Na⁺] on the electrolyte panel

4. The Four Primary Acid-Base Disorders

A. Metabolic Acidosis

• ↓ pH, ↓ HCO₃⁻, ↓ PaCO₂ (respiratory compensation)
• Causes: increased endogenous acid production (lactate, ketoacids), HCO₃⁻ loss (diarrhea), or failure of renal acid excretion (CKD)
• Effects: increased ventilation, myocardial depression, peripheral vasodilation, CNS depression (headache, lethargy, coma), glucose intolerance

B. Metabolic Alkalosis

• ↑ pH, ↑ HCO₃⁻, ↑ PaCO₂ (hypoventilation as compensation)

C. Respiratory Acidosis

• ↓ pH, ↑ PaCO₂, ↑ HCO₃⁻ (renal compensation)
• Acute vs. chronic (degree of HCO₃⁻ rise differs)

D. Respiratory Alkalosis

• ↑ pH, ↓ PaCO₂, ↓ HCO₃⁻ (renal compensation)
• Exception: Chronic respiratory alkalosis may return pH fully to normal — the only disorder where full compensation to normal pH occurs

5. Predicted Compensatory Responses (Harrison's Table 58-1)

Key rule: Compensatory responses move PaCO₂ and HCO₃⁻ in the same direction as the primary change. If PaCO₂ and HCO₃⁻ move in opposite directions, a mixed disorder is present.

FIGURE 58-1 — Acid-base nomogram. The 90% confidence limits for normal compensatory responses to all primary acid-base disturbances. Points falling outside these bands suggest a mixed disorder. — Harrison's Principles of Internal Medicine, 22E

6. The Anion Gap (AG)

• Normal AG: 6–12 mmol/L (average ~10 mmol/L)
• Normal unmeasured anions: albumin, phosphate, sulfate, organic anions

• Accumulation of acid anions (lactate, ketoacids, uremic acids, toxic alcohols, salicylates)

• ↑ unmeasured cations (lithium, calcium, magnesium, cationic immunoglobulins)
• ↓ albumin (nephrotic syndrome, liver disease, malabsorption)
• Hyperviscosity / severe hyperlipidemia

For every 1 g/dL albumin below 4.5 g/dL, add 2.5 mmol/L to the measured AG. Example: albumin 2.5 g/dL (2 below normal), uncorrected AG 15 → corrected AG = 15 + (2 × 2.5) = 20 mmol/L

High-AG Metabolic Acidosis — Causes (MUDPILES):

7. Delta-Delta (Δ/Δ) Ratio — Detecting Mixed Disorders

• ΔAG = patient's AG − 10 (normal AG)
• ΔHCO₃⁻ = 25 − patient's HCO₃⁻

• ΔAG >> ΔHCO₃⁻ → concurrent metabolic alkalosis masking the acidosis
• ΔAG << ΔHCO₃⁻ → concurrent non-gap acidosis (e.g., RTA + lactic acidosis)

8. Mixed Acid-Base Disorders (Harrison's Table 3-2)

Changes in PaCO₂ and HCO₃⁻ in opposite directions always indicate a mixed disorder.

9. Treatment Principle