Pleural space/mediastinal disease (Proceedings)


Air within the mediastinum may be the result of spontaneous rupture, trauma, or the result of diagnostic or therapeutic interventions.


Air within the mediastinum may be the result of spontaneous rupture, trauma, or the result of diagnostic or therapeutic interventions. Iatrogenic causes include surgical trauma, mechanical ventilation and transtracheal aspiration biopsy. Any trauma to the cervical trachea can result in pneumomediastinum. Pneumomediastinum is often asymptomatic and diagnosed only as the result of thoracic radiographs. Dyspneic animals usually have accompanying pneumothorax and treatment is directed at the pleural space disease.


Mediastinitis is either acute or chronic and usually is the result of an infectious process. Acute causes are usually due to perforation of the esophagus or trachea with leakage into the mediastinum. These cases are usually surgical emergencies to fix the perforated organ and lavage the surrounding tissue. Granulomatous mediastinitis is occasionally the result of fungal disease. Agents implicated in these chronic cases include Histoplasma, Crytococcus, Coccidioides, Actinomycoses and Nocardia species.


Pneumothorax is an accumulation of air in the pleural space and can develop secondary to pathologic or iatrogenic causes. Trauma commonly causes pneumothorax. Spontaneous pneumothorax occurs secondary to underlying pulmonary disease or to rupture of an air-containing space such as a pulmonary bulla or bleb. Spontaneous pneumothorax is classified as closed pneumothorax (no communication with the atmosphere). Close pneumothorax develops due to diseases of trachea, bronchi, lungs, or esophagus. Tension pneumothorax develops when there is a defect in the pleura that allows accumulation of air in the pleural space during inspiration but the air does not escape during expiration. Iatrogenic pneumothorax can develop secondary to diagnostic procedures that cross the pleural space (transthoracic aspiration, transthoracic biopsy, pericardiocentesis), intrathoracic surgery, tracheal intubation, and excessive positive pressure ventilation.

Animals with pneumothorax present with some degree of increased respiratory rate, dyspnea, exercise intolerance, restrictive (rapid, shallow) breathing pattern, cyanosis and poor capillary refill time. Abnormalities are due primarily to hypoventilation resulting in hypoxia. Ventilation-perfusion mismatching and decreased cardiac output also contribute to clinical disease. Diagnosis is based on history, signalment, physical examination findings, thoracocentesis, and thoracic radiographic findings. Traumatic and iatrogenic pneumothorax can usually be managed with intermittent thoracocentesis or continuous suction via chest tube. Spontaneous pneumothorax may need to be managed surgically depending on the primary etiology. Primary spontaneous pneumothorax secondary to bulla or blebs often recurs and so some authors recommend surgical intervention.

Pleural effusions

Table 1. Differential diagnoses of pleural effusions based on cell number and protein content.


Pyothorax is diagnosed by cytology. Pleural lavage is the treatment of choice. Because the disease usually affects both hemi thoraces bilateral chest tubes are usually necessary. The pleural space is lavaged 2-3 times daily with approximately 20 ml/kg of warmed 0.9% saline or Ringer's solution. The lavage fluid should be instilled slowly; the injection should be discontinued if respiratory distress occurs. The lavage fluid remains in the pleural space for 30-60 minutes unless the animal becomes dyspneic. The patient will absorb approximately 25% of the initial lavage volume. Clinical findings, thoracic radiographs and cytology of the pleural effusion are used monitor clinical progress. Most animals with successful pleural lavage will have a decrease in fever and improvement in general attitude within the first 48 hours. Radiographic re-evaluation should be performed 48 hours after tube placement and following the complete removal of all lavage fluid. Assess the radiographs for pleural space fluid volume, atelectasis, and areas of encapsulated fluid. Cytology of pleural fluid is generally performed prior to lavage. Numbers of neutrophils, macrophages and bacteria as well as the percentage of degenerate neutrophils are estimated. Most cases with pyothorax will have a gradual decrease in inflammatory cell numbers over 3-5 days.

Thoracic radiographs are generally suggested at 7 and 28 days following tube removal. The combination of pleural lavage and antibiotic therapy has been reported to successfully resolve pyothorax in 53% of dogs and 60% of cats. Surgical exploration is indicated when pleural lavage does not result in a rapid resolution of clinical signs.


Large volumes of blood in the thoracic cavity may be the result of trauma or a coagulopathy. Patients with acute acquired coagulopathies may present with large intracavitary hemorrhage. Anticoagulant rodenticide intoxication is the most common cause of pleural hemorrhage. Activated clotting time and partial thromboplastin times will be prolonged. Thoracocentesis is dangerous with clotting disorders, as iatrogenic hemorrhage is likely. When possible the patient is supported with oxygen while fresh clotting factors are replaced. Therapy with fresh frozen plasma or fresh whole blood with help stop the hemorrhage while vitamin K replacement is begun.


The accumulation of chyle within the thoracic cavity can be caused by numerous primary problems including traumatic rupture of the thoracic duct, neoplasia, and heart disease. A primary etiology may not be determined though the chylous effusion persists. The fluid has a milky appearance with high triglyceride content. The effusion may become pink with blood following trauma or multiple chest taps. Conservative treatment includes thoracocentesis as needed and a reduced fat diet to slow chyle formation. When possible treatment of the underlying disease should be attempted. Many surgical treatments have been proposed including thoracic duct ligation, pleurodesis and pleuroperitoneal shunts. Long-term prognosis is poor for chronic idiopathic chylous effusions in dogs and cats. They frequently develop fibrosing pleuritis causing permanent restriction of the lung lobes. Potential drug therapies include statins and therapy aimed at decreasing lymph production.

Neoplastic pleural effusion

Most pleural neoplasia is metastatic. Malignant effusions can be due to obstruction of pleural lymphatics, obstruction of major mediastinal lymph nodes or the thoracic duct. Pleural irritation and inflammation can lead to increased fluid production and increased vascular permeability. Neoplastic effusions tend to return rapidly after thoracocentesis. Cytopathologic examination of the fluid may yield neoplastic cells but is often non-diagnostic. Ultrasound of the thorax before thoracocentsis may help localize mass lesions. Radiographs should be taken after the fluid is evacuated to evaluated cardiac size and shape and mediastinal structures to help determine the cause of the effusion. Long-term therapy includes treatment of the underlying neoplasia (surgical or medical), thoracocentesis as needed and pleurodesis.

Miscellaneous causes of pleural effusion

Diaphragmatic hernia, lung lobe torsion, pancreatitis, renal failure, pulmonary thromboembolism, hyperthyroidism, postpartum and pyometra have all been associated with pleural effusion. Right-sided heart failure can produce a modified transudate. Abdominal surgery with large volumes of lavage and peritoneal dialysis are two reported iatrogenic causes of pleural effusion.

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