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Author: Angie Warner, D.V.M.,D.Sc.
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1. Learning Objectives:

  • Be able to define terms for different types of fluid accumulation in the pleural space, and be able to explain the pathophysiology of each.
  • Be able to compare a pneumothorax and a pneumomediastinum in terms of how they can occur and how they are diagnosed.
  • Understand how a thoracocentesis is performed.

2. Introduction

2.1. Anatomy and Physiology

  • The pleural membranes are a single layer of mesothelial cells, with fat, elastin, lymphatics and vessels. There is a 10-20 µm space between the visceral and parietal pleurae. Mesothelial cells have microvilli, and there are openings (stomata) between parietal mesothelial cells.
  • Pleural fluid is normally only a small film (0.1-0.2 ml/kg) that facilitates pleural membrane sliding during ventilation. Fluid balance is maintained between transudation from vessels and drainage via lymphatics. Protein content is normally around 1.5 g/dl.
    • Lymphatic drainage via the stomata normally removes excess fluid, protein and red cells
  • The mediastinum separates the right and left pleural cavities and contains the thymus, lymph nodes, esophagus, large thoracic vessels and heart. A complete mediastinum can be easily disrupted during thoracic disease.
  • The mediastinal space potentially communicates with the subcutaneous space via facial planes. Thus a pneumomediastinum can lead to subcutaneous emphysema.

2.2. Pleural Disease

2.2.1. Definitions

  • Pleural effusion is increased fluid of any sort in the pleural space:
    • hydrothorax: non inflammatory transudate (more likely with cardiac failure)
    • pyothorax or empyema: purulent effusion (infection or neoplasia). Serous pleuritis implies fewer cells and less protein in the fluid
    • hemothorax: blood
    • chylothroax: fluid and chylomicrons (pleural effusion with thoracic and intestinal lymph)
  • Pleuropneumonia is a respiratory disease extending from the airways and parenchyma into the pleural membranes and space. It implies a common infectious agent.
  • Fibrinous pleuritis is thickening of the pleura without effusion. Dry pleuritis implies only pleural inflammation and can precede purulent pleuritis or follow longstanding effusion.
    • Pleural friction rubs are heard on auscultation
    • Pleural inflammation is very painful; there is shallow, rapid breathing and a restrictive disease pattern
  • Etiology of Pleural Effusion
    • Pleural transudation occurs due to an imbalance in hydrostatic and oncotic pressures. Cardiac failure could be a cause.
    • Pleural exudation is caused by pleural inflammation (increased vascular permeability) and impaired lymphatic drainage of fluid and protein
    • Most pleural disease is secondary, and demonstration of a pleural effusion should spur a search for an underlying cause.
    • Serous pleuritis is seen with bacterial and viral infections of the feline respiratory disease complex. Parasites such as Aleurostrongylus may also cause serous pleuritis.
    • Hemothorax is usually seen after thoracic trauma or surgery, but can occur with a coagulation defect
  • Pyothorax or Pleural Empyema
    • Pyothorax is purulent exudate in pleural fluid. It is seen as a complication of primary pneumonia (occurs relatively commonly in the horse) or pulmonary abscess. It may also follow trauma such as bite wounds or esophageal perforation.
    • Pleuropneumonia in horses is a devastating complication of pneumonia or pulmonary abscesses. Following inflammation and fluid exudation into pleural space, bacterial colonization of the fluid from contiguous pneumonic lung or pulmonary abscesses occurs, bringing an influx of neutrophils. Risk factors in horses include long distance transportation and prior viral respiratory infection.
      • Transportation in a confined environment enhances exposure to potential pathogens. Viral infection can impair mucociliary clearance, allowing bacterial colonization.
    • In the horse, the bacterial species isolated will be the same as those causing the underlying pneumonia (often Streptococcus zooepidemicus +/ E. coli +/- anarobes).
    • In dogs and cats, many common respiratory pathogens plus Nocardia sp. have been isolated.
  • Chylothorax
    • Chylothorax is pleural effusion with a mixture of intestinal and thoracic lymph; thus it is milky white and contains chylomicrons.
    • It is seen in dogs and cats after traumatic or surgical thoracic duct rupture, or less commonly neoplasia with thoracic duct obstruction, dilation and rupture.
    • Chylothorax can be idiopathic in cats and dogs, especially Afghans and Borzois.
    • Clinical signs are due to physiologic effects of pleural effusion (restrictive disease pattern), but repeated drainage can lead to weight loss and deficiency of fat soluble vitamins.
    • Lymph contains bacteriostatic lecithin, so secondary infections of the accumulated pleural fluid are uncommon.
    • A pseudochylous effusion containing cholesterol crystals, but not lymph, has been reported.
  • Pneumothorax
    • Air can enter the pleural space from the lungs or outside the chest wall. Spontaneous pneumothorax is rupture of a small bleb on the visceral pleural surface.
    • When air enters the pleural space, the lungs collapse and the rib cage springs out. Radiographic signs are lung collapse, over expansion of the rib cage, and mediastinal shift.
    • Clinical signs are pain and dyspnea. There are reduced lung sounds on auscultation.
    • Tension pneumothorax occurs when air enters the pleural space during inspiration but cannot escape during expiration. Increasing positive pressure develops in the pleural space. Clinical signs are increasing respiratory distress and tachycardia, with mediastinal shift and tracheal deviation radiographically.
    • Flail chest occurs when there are 2 rib fractures causing an unstable segment of the thoracic wall. The flail segment moves paradoxically during spontaneous ventilation.
  • Pleural Neoplasia
    • Primary pleural tumors are mesotheliomas arising from either visceral or parietal pleura. These can be mesenchymal (fibroma like) or epithelial (carcinoma like).
    • Primary mesothelioma in humans is linked with occupational asbestos exposure. There is often a 25-45 year latent period between exposure and development of tumor. The tumor is progressive and has a guarded poor prognosis.
      • Asbestos association has not been clearly seen with mesothelioma in dogs, but lack of correlation may be related to time between exposure and development of the tumor.
    • Secondary pleural tumors can develop from spread of primary lung tumor.
    • Extrapleural masses are defined as those arising in the potential space between the pleura and thoracic wall. These may be undetected for extended periods until a pleural effusion develops.
  • Diagnostic Techniques: Thoracocentesis and Pleural Fluid Evaluation
    • Pleural fluid is obtained by thoracocentesis direct puncture into the pleural space with a blunt trocar. The optimal site varies with species (usually 7 - 8th intercostal space). Ultrasound guidance for site selection is helpful
    • The skin stab incisions and site of parietal pleural puncture are offset to help prevent pneumothorax.
    • Pleural fluid is normally very small in volume and straw colored.
      • Normal cytology: <10,000/ul WBC and < 3.5 g/dl protein
      • PMN may be up to 68% of nucleated cells normally
      • Normal pleural fluid cultures negative for both aerobes and anaerobes.
    • Culture and cytologic examination for neoplastic cells should be performed whenever pleural fluid volume is increased.
    • Pleural fluid drainage can be therapeutic as well as diagnostic. An indwelling tube with a one way valve (Heimlich valve) can be placed for repeated drainage. Maintenance of sterility is essential and difficult.
  • Pathophysiology
    • Pleural effusion and the pain of pleural inflammation create a restrictive disease pattern, with V/Q inequality, reduced lung volumes and atelectatic lobes.
      • Patients may experience orthopnea difficulty breathing in lateral recumbency
    • Dyspnea and thoracic pain are characteristic.
    • Pleural effusion causes muffling of lung sounds ventrally and a horizontal fluid line on percussion of the thorax.
      • Pleural fluid can also be loculated (encapsulated) due to organizing fibrin
    • Radiographically, fluid outlining the visceral pleura of adjacent lung lobes causes the image of interlobar pulmonary fissures.
    • Ultrasound offers good visualization of the pleural space and characterization of any effusion (loculated, fibrin containing). It can detect small volumes of fluid in the pleural space.

2.3. Abnormalities of the Mediastinum

2.3.1. Etiology and Pathophysiology

  • Mediastinal disease is usually not primary but a sequela of systemic, thoracic or cervical disorders.
  • The signs are often absent or vague during the early phase, and disease may go undiagnosed for long periods.
  • Mediastinal diseases are often space occupying, causing airway or esophageal compression, compression of large vessels, Horner's syndrome, or lymphatic obstruction.

2.3.2. Pneumomediastinum

  • Gas can accumulate in the mediastinum after migration from deep neck wounds, esophageal or tracheal rupture, sequela of transtracheal aspirate, or bronchial rupture with peribronchial air that migrates to the hilus.
  • Sequelae of pneumomediastinum include generalized subcutaneous emphysema, and accumulation of air along the aorta or in the retroperitoneal space. These events are generally harmless and self limiting, and the gas migration decompresses the mediastinum.
    • Penumomediastinum can progress to pneumothorax, but the reverse is unlikely

2.3.3. Mediastinal Space Occupying Masses

  • More common entities are lipoma, abscesses, lymphoma and granuloma. Less common are thymoma, aortic body tumor and primary mediastinal tumor.

2.3.4. Mediastinitis

  • Infection causes inflammation, with thoracic pain, difficult respiration and a restrictive pattern.
  • Direct infection of the mediastinal space can occur as contaminated material escapes from a perforated esophagus.

3. References

  • Chaffin MK, and Carter GK. Equine bacterial pleuropneumonia I. Epidemiology, pathophysiology, and bacterial isolates. Compend Cont Ed Pract Vet 15:1642-1650, 1993.
  • Rogers KS, Walker MA. Disorders of the mediastinum. Compend Cont Ed Pract Vet 19:69-82, 1997
  • Tillson DM. Thoracostomy tubes I and II. Compend Cont Ed Pract Vet 19:1258-1267 and 1331-1338, 1997.