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Pleural Effusion & Lung Abscess

Harrison's Principles of Internal Medicine, 22e


PART I: PLEURAL EFFUSION

Definition & Pathophysiology

A pleural effusion is excess fluid in the pleural space. Normally, fluid enters from parietal pleural capillaries and exits via parietal pleural lymphatics (which can absorb 20x normal fluid load). An effusion forms when hydrostatic-oncotic imbalance overwhelms lymphatic drainage. ~1.5 million Americans are affected per year. Presenting symptoms: dyspnea and pleuritic chest pain.

Transudate vs. Exudate: Light's Criteria

An effusion is an exudate if it meets ANY of the following (otherwise transudate):
CriterionThreshold
Pleural fluid protein / serum protein>0.5
Pleural fluid LDH / serum LDH>0.6
Pleural fluid LDH>2/3 upper normal serum limit
Pseudoexudates: Light's criteria misidentify ~25% of transudates as exudates (often "diuresed transudates"). If clinical suspicion favors a transudate, use: Serum-PF protein gradient >3.1 g/dL OR serum-PF albumin gradient >1.2 g/dL - these identify pseudoexudates with ~99-100% sensitivity.

Diagnostic Algorithm

FIGURE 305-1 Approach to diagnosis of pleural effusions
Fig. 305-1: Diagnostic approach to pleural effusions. Transudate → treat underlying cause. Exudate → further workup including glucose, cytology, cultures, TB markers.

Causes

Transudates
  • Congestive heart failure (most common)
  • Cirrhosis
  • Nephrotic syndrome
  • Peritoneal dialysis
  • Superior vena cava obstruction
  • Myxedema, Urinothorax
Exudates
  • Bacterial pneumonia / parapneumonic (most common exudative cause in USA)
  • Malignancy (lung, breast, lymphoma = 75% of malignant effusions)
  • Tuberculosis (most common cause worldwide)
  • Pulmonary embolism (most commonly overlooked)
  • Viral infections
  • Collagen vascular disease (RA, SLE)
  • GI disease (esophageal perforation, pancreatitis, intra-abdominal abscess)
  • Chylothorax, hemothorax

Key Specific Effusions

Parapneumonic Effusion (PPE)
  • Occurs in up to 50% of community-acquired pneumonia
  • Usually reactive (sterile cultures)
  • 10% progress to complicated PPE or empyema (fibrinopurulent or grossly purulent fluid)
  • Indicators requiring drainage (chest tube or intervention):
    • Loculated fluid
    • pH <7.20
    • Glucose <3.3 mmol/L (<60 mg/dL)
    • Positive Gram stain or culture
    • Gross pus (empyema)
    • PF LDH >900 IU/L
Malignant Effusion
  • Second most common exudate; poor prognosis (<6-month survival)
  • Lung, breast, lymphoma = ~75%
  • Usually exudate; reduced glucose if high tumor burden
  • Diagnosis: cytology. If negative x2, consider thoracoscopic biopsy
  • Treatment: therapeutic thoracentesis, indwelling pleural catheter (IPC), or pleurodesis with talc
Tuberculous Pleuritis
  • Predominantly lymphocytic exudate
  • Markers: adenosine deaminase >40 IU/L or IFN-γ >140 pg/mL
  • Diagnosis: pleural biopsy culture (higher yield than fluid); thoracoscopy
Chylothorax
  • Thoracic duct disruption (trauma/surgery or mediastinal tumor)
  • Milky fluid; triglycerides >1.2 mmol/L (110 mg/dL)
  • Treatment: chest tube + octreotide + eliminate enteral fat; if refractory - percutaneous thoracic duct blockage or ligation
Hemothorax
  • PF hematocrit >50% of peripheral blood hematocrit
  • Most from trauma; treat with tube thoracostomy
  • If bleeding >200 mL/h: consider angiographic embolization or surgery

Imaging of Pleural Effusion

FIGURE 305-2 CT and ultrasound of pleural effusions
Fig. 305-2: A - Simple (free-flowing) effusion on CT. B - Loculated effusion on CT (two pockets). C - Simple effusion on ultrasound. D - Complex effusion with loculations and septations on ultrasound.

Empyema CT

FIGURE 305-3 CT of empyema
Fig. 305-3: Empyema on CT - note thick, contrast-enhancing pleural rind (red arrows).

Management of Parapneumonic Effusion/Empyema

  1. Simple PPE - antibiotic treatment of pneumonia; no drainage needed
  2. Complicated PPE (criteria above) - chest tube drainage
  3. Fibrinopurulent stage (cannot fully drain) - intrapleural tPA (10 mg) + DNase (5 mg), or VATS/thoracoscopy to break adhesions
  4. Organized stage (pleural peel) - surgical decortication
  5. Trapped lung - pleural manometry; decortication if needed


PART II: LUNG ABSCESS

Definition

Necrosis and cavitation of lung parenchyma due to microbial infection. Usually a single dominant cavity >2 cm. Can be single or multiple.

Classification

TypeDescription
Primary (~80%)Aspiration-related; anaerobic organisms; no underlying condition
Secondary (~20%)Underlying condition: obstruction (tumor, foreign body), immunocompromise
Acute<4-6 weeks
Chronic (~40%)>4-6 weeks duration

Epidemiology & Risk Factors

  • More common in middle-aged men
  • Major risk factor: aspiration
  • At-risk groups: altered mental status, alcoholism, drug overdose, seizures, bulbar dysfunction, stroke, neuromuscular disease, esophageal dysmotility/obstruction, GERD
  • Periodontal disease / gingivitis - anaerobic colonization of gingival crevices is critical; lung abscess is extremely rare in edentulous patients

Microbiology (Table 132-1)

Clinical SettingPathogens
Primary (aspiration)Anaerobes: Peptostreptococcus, Prevotella, Bacteroides, milleri group streptococci; microaerophilic streptococci
Secondary (immunocompromise)S. aureus, Gram-negatives (Pseudomonas, Enterobacteriaceae), Nocardia, Aspergillus, Mucorales, Cryptococcus, Legionella, Rhodococcus equi, PCP
Embolic lesionsS. aureus (endocarditis), Fusobacterium necrophorum (Lemierre's syndrome)
Endemic fungi/TBM. tuberculosis, Coccidioides, Histoplasma, Blastomyces; parasites (E. histolytica, Paragonimus)
Post-viralS. aureus after influenza; Actinomyces

Pathogenesis

Primary: Aspirated anaerobes from gingival crevices → pneumonitis (worsened by gastric acid) → over 7-14 days → parenchymal necrosis and cavitation. Polymicrobial synergy worsens tissue destruction.
Secondary: Depends on predisposing factor (e.g., bronchial obstruction → distal infection; hematogenous seeding in immunocompromise).

CT of Lung Abscess

FIGURE 132-1 CT chest showing lung abscess
Fig. 132-1: CT chest showing lung abscess - early consolidation (left, black arrow) progressing to cavitation with an air-fluid level (right, white arrow).

Clinical Features

  • Subacute presentation is typical for primary (anaerobic): weight loss, low-grade fever, mild anemia, leukocytosis, history of aspiration risk
  • Putrid-smelling sputum = virtually diagnostic of anaerobic infection
  • Pleuritic chest pain and productive cough
  • Large effusion with minimal infiltrate may occur (especially anaerobic)

Differential Diagnosis of Cavitary Lung Lesion

  • Lung infarction
  • Malignancy (cavitating tumor)
  • Pulmonary sequestration
  • Cryptogenic organizing pneumonia
  • Sarcoidosis, vasculitis (GPA/Wegener)
  • Lung cysts/bullae with fluid
  • Septic emboli (tricuspid endocarditis)

Diagnosis

  • Chest X-ray: thick-walled cavity with air-fluid level
  • CT chest: better definition; earlier cavitation; identifies underlying cause (malignancy); distinguishes peripheral lung abscess from empyema (critical distinction for treatment)
  • Sputum: Gram stain + culture (may miss anaerobes; likely polymicrobial)
  • Molecular methods (16S rRNA gene amplification) - increasingly used
  • Secondary abscesses / failed empirical therapy: sputum + blood cultures, serology for fungi/viruses, bronchoscopy with BAL or protected brush, CT-guided needle aspiration (risks: contralateral spillage, pneumothorax, bronchopleural fistula)
  • Bronchoscopy early if bronchial obstruction suspected

Treatment

Antibiotics (primary treatment):
RegimenDetails
Clindamycin (preferred)600 mg IV TID → when afebrile: 300 mg PO QID
IV β-lactam/β-lactamase inhibitore.g., ampicillin-sulbactam → then oral amoxicillin-clavulanate
Moxifloxacin400 mg/d PO (evidence: as effective as ampicillin-sulbactam)
Why clindamycin over penicillin? - Oral anaerobes can produce β-lactamases; clindamycin proved superior to penicillin in clinical trials.
Duration: Continue until imaging shows resolution or small scar.
  • Typically 3-4 weeks to 14 weeks
  • At least 6 weeks may be associated with better outcomes
  • Chronic abscesses may need longer courses
Drainage:
  • Spontaneous drainage via bronchial tree is most common
  • Percutaneous CT-guided catheter drainage - systematic reviews support use for selected cases; consider when medical therapy fails or if patient is a poor surgical candidate
  • Surgery (lobectomy/segmentectomy) - reserved for: failed medical therapy, massive hemoptysis, suspected malignancy, bronchopleural fistula, or inability to rule out cancer

Source: Harrison's Principles of Internal Medicine, 22e (2025) - Chapter 132: Lung Abscess; Chapter 305: Pleural Effusion
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