Pleuritis

Pleuritis, also known as pleurisy, is an inflammation of the visceral and parietal layers of the pleural membranes of the lungs. The condition can be primary or secondary and results in sudden, sharp, and intense chest pain on inhalation and exhalation.  Etiologies include infection, trauma, cardiac ischemia, and lung cancer. The most common primary infectious cause is a viral infection, and underlying lung infections account for the majority of secondary infectious causes. Management consists of pain control and the treatment of the underlying condition.

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Etiology

  • Infectious causes: (viral causes are often associated with transudative pleural effusions, and the others often have exudative pleural effusions)
    • Viral (e.g., coxsackie, cytomegalovirus, Epstein-Barr virus, influenza): often associated with a transudative pleural effusion
    • Bacterial (e.g., pneumonia [50% develop pleuritis], tuberculosis, Legionnaires disease, rickettsia)
    • Parasitic (e.g., amebiasis)
    • Fungal infections
    • Liver or splenic abscesses
  • Systemic causes: (often with transudative pleural effusions)
    • Autoimmune disorders: rheumatoid arthritis (5% have pleuritis) or systemic lupus erythematosus (50% have pleuritis), others
    • Inflammatory bowel disease
    • Lung cancer, mesothelioma (from asbestos exposure), other malignancies involving the pleura
    • Lymphoma
    • Cystic fibrosis
    • Cardiac problems (ischemia, pericarditis)
    • Pancreatitis
  • Traumatic or mechanical causes: (trauma often associated with hemothorax)
    • Pneumothorax (90% develop pleuritis)
    • Pulmonary embolism (5%–20% associated with pleuritis)
    • Chest injuries (blunt or penetrating):
    • Rib fracture
    • Aortic dissection
    • Disruption or obstruction of the thoracic duct, leading to accumulation of lymph in the pleural space (chylothorax)
  • Medications:
    • Amiodarone, bleomycin, bromocriptine, cyclophosphamide, methotrexate, procarbazine, hydralazine, procainamide, quinidine, etc.

Pathogenesis

  • Anatomical pathology considerations:
    • Pleural space: a potential space lined by a single layer of mesothelial cells supported by connective tissue
    • Inflammation can cause inflammatory mediators to infiltrate the pleural space, causing the production of pleural fluid, which can be transudative or exudative; if frank pus is within the space, then it is called an “empyema,” which is different from an abscess because the neutrophils accumulate in a pre-formed space.
    • Blood, air, or chyle can also enter the pleural space.
  • Pain receptors
    • Present on the parietal pleura
    • Peripheral and lateral hemidiaphragm pleural membranes are innervated by intercostal nerves that also have cutaneous distributions.
    • Peripheral and lateral hemidiaphragm pleural membranes are innervated by intercostal nerves that also have cutaneous distributions.
    • Central diaphragm pleura is innervated by the phrenic nerve and can refer pain to the ipsilateral neck and shoulder.
    • Pain is transmitted by fast-conducting A-delta fibers → sharp and well-localized pain

Clinical Presentation

  • Sharp, sudden chest pain (i.e. pleuritic pain) upon inhalation and exhalation
    • Worsens with increased intrathoracic pressure (e.g., deep respiration, coughing, sneezing, body trunk movement)
    • Other common descriptors: dull, burning, catching, stabbing
    • Can be alleviated when the pleural cavity fills with fluid, as in pleural effusion
  • Dry cough
  • Sneezing
  • Dyspnea and rapid, shallow breathing
  • Fever and/or chills if infectious
  • Other signs and symptoms which present will depend on the underlying cause

Diagnosis

  • Blood tests
    • Test for presence of infection via elevated WBC on CBC with differential
    • Antibodies can be tested to determine/rule out autoimmune conditions:
      • Rheumatoid arthritis
      • Systemic lupus erythematosus
    • D-dimer elevation can suggest pulmonary embolism.
    • Cardiac troponin is suggestive of myocardial infarction.
  • Physical examination 
    • Pleural friction rub upon auscultation
    • May also reveal other abnormal sounds if concomitant lung disease is present, such as crackles and decreased breath sounds in pneumonia
  • Imaging
    • Chest X-ray: may show air or fluid in the pleural space, and suggest a cause (e.g., fractured rib, malignancy)
      • Consolidation can represent pneumonia.
      • Pneumothorax
      • A widened mediastinum is indicative of aortic dissection.
      • Cardiomegaly can represent pericarditis.
      • Lymphadenopathy or cavitation may suggest tuberculosis.
    • CT scan: may show signs of pneumonia or the presence of a causative abscess, tumor, or blood clot within the lung with angiography
    • Ultrasound: can be used to confirm pleural effusion at bedside
  • Electrocardiogram: used to help diagnose cardiac causes including myocardial infarction, and pericarditis
  • Diagnostic procedures
    • Sputum testing: test for infectious causes, especially tuberculosis
    • Thoracentesis: Fluid is aspirated for laboratory analysis.
      • Exudative pleural fluid shows elevated pleural fluid protein, elevated lactate dehydrogenase, or leukocytosis.
      • Use Light’s criteria (see table below) to determine etiology.
    • Thoracoscopy: direct visualization of the lungs and pleural cavity to visualize abnormalities and obtain a tissue sample for pathologic examination and possible microbiologic culture
Light’s criteria for pleural effusions
TransudateExudate
Protein (pleural/serum) ≤ 0.5> 0.5
LDH (pleural/serum) ≤ 0.6> 0.6
Pleural LDH ≤ two-thirds upper limit of normal serum LDHPleural LDH > two-thirds upper limit of normal serum LDH
Common causes
  • Hypoalbuminemia (cirrhosis, nephrotic syndrome)
  • Congestive heart failure
  • Constrictive pericarditis
  • Autoimmune disease (lupus, rheumatoid arthritis)
  • Esophageal rupture
  • Infection (parapneumonic, tuberculosis, fungal, empyema)
  • Malignancy
  • Pancreatitis
  • Post-CABG
  • Pulmonary embolism

Natural History

  • If inflammation resolves promptly, the pleural surfaces return to normal with no sequelae.
  • If inflammation prolonged, then fibrosis with adhesions and anatomical distortions occur.

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