Many disease processes can cause pleural effusion. Symptoms caused by the effusion may be the major presenting complaint or the effusion may be discovered incidentally during diagnostic tests. Determining the cause of the effusion is sometimes challenging, requiring ongoing stabilisation of the patient and potentially invasive diagnostic and therapeutic procedures, so a logical approach is essential.

History

Following triage and any appropriate emergency stabilisation of the patient, a thorough history is no more or less important than with any other serious medical disorder. For example, weight loss, exercise intolerance, other recent respiratory symptoms or injuries and potential for unwitnessed trauma or toxin access may all prove relevant in determining the underlying cause of the effusion.

Physical Examination

Pleural effusions restrict the excursions of the lungs. Most animals do not show symptoms until the ability to expand the lungs is significantly impaired, causing a breathing pattern characterised by a small tidal volume, hence shallow inspiration and an increased respiratory rate. This normally occurs when 30-60 ml/kg body weight of fluid has accumulated. Open-mouth breathing and cyanosis may be present. Following prolonged dyspnoea, respiratory muscle fatigue/failure may lead to paradoxical breathing, characterised by opposing movements of the chest and abdominal wall in inspiration and expiration. Auscultation reveals unilateral or bilateral ventral muffling of the normal bronchovesicular sounds, with normal or increased sounds dorsal to the fluid line. The resonance on percussion of the chest reflects the auscultation findings, with a dull note of percussion below the fluid line (more useful in larger patients).

Abnormal heart sounds and rhythms may be auscultated in animals with cardiogenic effusions. Jugular vein distension is present in some patients with right-sided heart failure, but in cats large pleural effusions of any cause may compress intrathoracic vessels and impede venous return sufficiently to lead to some extrathoracic jugular distension. Further findings that may help determine the cause of the effusion include reduced compressibility of the cranial thorax in cats with a mediastinal mass, pyrexia in animals with pyothorax, focally dull lung sounds in patients with a pulmonary mass and borborygmi in patients with a ruptured diaphragm.

Initial Stabilisation and Diagnostic Work-Up

The choice and order of procedures is dictated by the physical status and temperament of the patient. Thoracocentesis is indicated both for diagnostic and therapeutic purposes in any patient with a pleural effusion showing respiratory compromise. Fluid should be analysed for protein content, nucleated and red cell counts and cytological appearance. More detailed biochemical analysis may be appropriate depending on initial results. Transudates and modified transudates are generally sterile. Bacterial culture should always be performed for exudates. Not all cases require thoracocentesis: non-dyspnoeic patients in which the likely cause of the effusion may be determined from the clinical presentation and other non-invasive tests may have thoracocentesis postponed while response to initial therapy is followed. Small to moderate effusions or those remaining after partial drainage can enhance visualisation of intrathoracic structures on ultrasonography without jeopardising the patient. However, more complete drainage is desirable prior to radiographic assessment. Rapid complete removal of long-standing effusions risks re-expansion pulmonary oedema, a complex condition characterised by accumulation of protein-rich fluid in the alveoli.

Thoracocentesis is performed at the seventh or eighth intercostal space at or above the costochondral junction (unless ultrasound guidance is used to direct the clinician to a larger fluid pocket), with the animal in sternal recumbency. A 21-gauge butterfly needle attached to a three-way stopcock and a 20 ml syringe are used for cats and small dogs. Large-bore over-the needle catheters with a large-bore extension set, three-way stopcock and 50 ml syringe are used for larger dogs. When larger-bore catheters are used, local anaesthetic is infiltrated into the intercostal space, a small nick is made in the skin and one or two side holes are cut towards the end of the catheter. Oxygen is administered via a face mask if tolerated. The author does not hesitate to sedate poorly cooperative dyspnoeic patients; the need to minimise the risk of creating pneumothorax or haemothorax in a struggling patient outweighs theoretical concerns regarding pharmacological cardiorespiratory depression if efficient removal/ reduction of a large effusion can be achieved. Often aspiration of one side of the thorax will drain the other side because of fluid movement across the mediastinum, although fenestrations in the mediastinum may become occluded in very inflammatory conditions such as pyothorax. Repeat auscultation and/or ultrasonography are useful in determining the need for bilateral drainage.

Rapid recurrence of effusion, development of pneumothorax or the presence of a very viscous effusion or pyothorax are potential indications for placement of thoracostomy tubes. A recent case series questions the need for routine thoracostomy tube placement in canine pyothorax.

Radiography

Small effusions obscure the ventral cardiac silhouette and diaphragmatic shadow on a lateral projection. An apparent increase in space between the lung and the spine in the dorsocaudal lung fields may be present but must be distinguished from the quadratus lumborum muscle (especially in cats). On a dorsoventral view, small effusions may obscure the cardiac silhouette and create fissure lines between lung lobes. A ventrodorsal projection may increase the chances of detecting small effusions and the cardiac silhouette and mediastinum may be clearer. With moderate effusions, edges of lung lobes are more clearly separated from the thoracic wall and become scalloped along the sternal border on lateral views. Pleural fissure lines are visible. Most of the heart and diaphragm are obscured and the mediastinum appears widened. With severe effusions, lobes are dorsally compressed and leaf-like. With chronicity or severe inflammation, extensive accumulation of fibrin on the visceral pleura reduces elasticity of the lung lobes, leading to a more rounded and irregular appearance. Horizontal beam techniques may help detect encapsulated effusions (for example, within a bulla) or move fluid away from suspected mediastinal masses if the forelegs are elevated.

Ultrasonography

Ultrasonography is a sensitive method of confirming the presence of fluid when in doubt, and helpful for guiding needles to obtain diagnostic aspirates of small volume effusions and percutaneous aspirates of abnormal structures. The echogenicity of the effusion often reflects the cellularity. The normal mediastinum cannot be imaged by ultrasound, but it may be imaged if pleural effusion displaces the aerated lung normally present between the mediastinum and the thoracic wall and a widened mediastinum may be imaged if it contacts the thoracic wall. Echocardiography is indicated to determine cardiac size and function whenever a transudate, modified transudate or chylothorax is documented.

Computed Tomography and Magnetic Resonance Imaging

The inherently better contrast resolution of computed tomography (CT) compared with radiography may allow the operator to distinguish soft tissue from pleural effusion, although this can often be achieved with ultrasonography. CT may also help distinguish pulmonary from large thoracic wall masses, detect small metastases and assist surgical planning. Magnetic resonance imaging (MRI) currently has fewer thoracic imaging indications due to the longer time taken to acquire the sequences and hence the increased chance of motion blur due to respiratory movement. However, the author has found it useful for imaging relatively fixed intrathoracic structures (large mediastinal and oesophageal masses).

Classification of Effusions

Pleural effusions are often classified as shown in Figure 1.

Figure 1. Classification of pleural effusions.

Transudates and modified transudates contain predominantly monocytes, small lymphocytes and mesothelial cells. With time, irritation of the pleural lining by the presence of fluid recruits increasing numbers of inflammatory cells and free water is absorbed, leading to concentration of cells and fluid and overlap between categories of effusion. Exudates are much more likely to contain degenerate neutrophils, activated macrophages and mixed lymphoid populations and they may be sterile or septic. Neoplastic effusions may fall into any category. Other types of fluid treated as distinct entities include chyle (chylothorax), pus (pyothorax) and blood (haemothorax). The large numbers of disorders that may produce modified transudates have led one investigator to abandon this category and adapt a human classification system for use in feline (but not canine) patients: fluids are classified as transudates or exudates based on their lactate dehydrogenase content and exudates are further analysed by measuring pH, glucose levels and cell content to determine the likelihood of infection or malignancy.

An exhaustive list of causes of effusion is beyond the scope of these notes but the following points are worth considering:

 Pleural fluid formation is a balance of Starlings forces favouring fluid production (net hydrostatic pressure gradient between the parietal and visceral pleural capillaries and negative atmospheric pressure in the pleural space) and those favouring resorption (oncotic pressure in the capillaries), with further fluid removal by the parietal pleural lymphatics. Fluid flow also varies with the integrity/permeability of the capillary and lymphatic walls.

 Increased vascular permeability allows protein and cells to leak into the pleural fluid, causing modified transudates and exudates. This phenomenon is hard to quantify and probably underdiagnosed. Conditions associated with vascular leak include sepsis, pancreatitis and immune-mediated haemolytic anaemia.

 Transudates occur due to increased hydrostatic pressure (congestive heart failure, vascular obstruction, systemic hypertension or excessive fluid administration) or severe hypoproteinaemia (hepatopathy, protein-losing nephropathy or enteropathy or chronic haemorrhage).

 Increased lymphatic pressure or impaired lymphatic drainage usually causes chylous effusions but modified transudates are also possible.

 Some events (for example, lung lobe torsion or pulmonary thromboembolism) can trigger unpredictable and complex haemodynamic and pathological change in affected and surrounding tissue making the composition of any resultant effusion hard to predict.

 Haemorrhagic effusions (packed cell volume (PCV) of fluid 1-5%) are more common than true haemothorax (PCV of the fluid >25% of that in peripheral blood) and more likely to require drainage due to respiratory compromise. Haemothorax results from a chest bleed. Symptoms of vascular collapse and hypovolaemic shock are likely before sufficient blood has been lost into the thorax to cause respiratory compromise. In determining how much to remove, the clinician should consider that erythrocytes in the thorax are readily resorbed into the circulation within a few days.

References

1.  Gookin JL, Atkins CE. Evaluation of the effect of pleural effusion on central venous pressure in cats. Journal of Veterinary Internal Medicine 1999; 13: 561-563.

2.  Johnson MS, Martin MWS. Successful medical treatment of 15 dogs with pyothorax. Journal of Small Animal Practice 2007; 48: 12-16.

3.  Padrid PA. Canine and feline pleural disease. In: Veterinary Clinics of North America: Small Animal Practice: Respiratory Medicine and Surgery. Philadelphia: WB Saunders, 2000; 30: 1295-1307.

4.  Sanders NA, Sleeper M. Pleural transudates and modified transudates. In: King, LG. ed. Textbook of respiratory disease in dogs and cats. St Louis: Saunders, 2004; 587-597.