PLEURAL SPACE

The pleural space is a potential space formed by the parietal and visceral pleura. It normally contains a minimal amount (few milliliters) of serous fluid to facilitate motion of the lungs in relation to the thoracic cavity and to each other.¹ The pleura is a thin epithelium formed of mesothelial cells overlying a thin basal membrane. The pleura contain a superficial network of lymphatic ducts, blood vessels, and rare nerves.² The partition between the right and left hemithoraces is incomplete in small animals, but unilateral or unevenly distributed disease is common.³

Physiologic fluid flux in the pleural space is governed by Starling’s law (Box 30-1). Hydrostatic pressure favors fluid accumulation within the pleural cavity (where pressure is subatmospheric), and the parietal pleura (systemic circulation) has greater filtration capacity than the visceral pleura (pulmonary circulation). However, oncotic pressure favors reabsorption of fluid from both pleura because the colloid osmotic pressure of the pleural space is 3.2 cm H₂O in dogs (compared with 24.5 to 27 cm H₂O in the vascular space). The visceral pleura assumes a larger role in determining the net pressure and favors reabsorption of fluid from the pleural space, where a greater vascular supply and lower hydrostatic pressure exist. Pleural lymphatic vessels are also an important component of fluid and blood reabsorption from the thorax.³

There is an average pleural pressure of −5 cm H₂O, representing the difference between the lung recoil and the thoracic cavity expanding forces, at rest.⁴ Air, fluid, or soft tissue within the pleural space can cause the lungs to collapse and the chest wall to spring out by increasing the subatmospheric pressure within the thorax.⁵ Pleural pathologies such as these subsequently lead to a decrease in tidal volume, total vital capacity, and functional residual capacity.⁶ The resulting atelectasis can lead to both hypoxemia and hypoventilation.

CLINICAL EVALUATION

Clinical signs of pleural disease may include tachypnea, open-mouth breathing, extended head and neck, crouched sternal recumbency with elbow abduction (orthopnea), cyanosis, and short, shallow breathing with an increased abdominal component. The degree of dyspnea will vary depending on the amount of fluid, rate of fluid accumulation, and concurrent respiratory and metabolic disturbances. Auscultation reveals muffled breath sounds ventrally (fluid or tissue) or dorsally (air). Thoracic percussion reveals a low-pitched (fluid) or high-pitched (air) resonance of the affected area. The heart sounds may be muffled by fluid or tissue, or abnormally loud or displaced with unilateral or focal disease.

Thoracic radiographs are extremely helpful in diagnosing and quantifying pleural space disease and other intrathoracic pathology. Repeat radiographs after thoracentesis can be of diagnostic utility but were found to rarely be beneficial in providing additional diagnostic information in one human study.⁷ Routine radiographs after thoracentesis are considered unnecessary for stable patients in the absence of suspicion, clinical indication, or risk factors for complications (mostly pneumothorax)^7,8 (Figure 30-1). Because the shape of the canine and feline chest is much different from that of humans, it is possible that dorsoventral radiographs in animals with pleural effusion (following thoracentesis) may still have improved diagnostic utility for evaluating the dorsal lung fields. Ultrasonographic examination is very helpful for rapid identification of pleural fluid in the emergency setting. In human medicine, indications for use of ultrasonographically guided thoracentesis include a small-volume effusion, inability to properly position the patient, failure of fluid to layer out on radiographs, and coagulopathy.⁹ “In veterinary medicine, ultrasound guidance is used routinely to confirm the ideal point of needle insertion for thoracentesis, mostly in patients with a small volume of effusion, fluid pockets or those at increased risk for complications.”

Figure 30-1 Cats with pleural space disease. A, Moderate volume of malignant effusion secondary to bronchogenic adenocarcinoma. B, Pneumothorax after thoracentesis in the patient shown in A. C, Traumatic pneumothorax from high-rise syndrome. D, Spontaneous pneumothorax from diffuse pulmonary metastasis of salivary gland adenocarcinoma.

Thoracic ultrasonography may reveal underlying pathology such as a diaphragmatic hernia, neoplastic process, or lung lobe torsion.^10,11 Echocardiography will permit a diagnosis of cardiac disease, heart base tumor, and pericardial disease. Ultrasonography may also identify a pneumothorax by identifying the presence or absence of “lung sliding” (normal respiratory movement) at the lung surface.¹² Computed tomography is commonly used to characterize pleural and pulmonary lesions.¹⁰ Thoracic scintigraphy is used mostly in small animal practice to identify pulmonary thromboembolism.¹⁰ Thoracoscopy is another useful diagnostic and therapeutic tool in patients with pleural effusion and other intrathoracic pathology.¹³

Thoracentesis is an invaluable diagnostic, and often therapeutic, tool (see Chapter 31, Thoracentesis). Its indications include (1) the presence of any undiagnosed pleural effusion and (2) therapeutic thoracentesis to relieve respiratory signs caused by large amounts of air or fluid. However, if the etiology of the effusion is known and the patient is not dyspneic, the procedure may be delayed and the clinical signs followed.¹⁴ Fluid analysis has great diagnostic utility in patients with pleural effusion of an undetermined etiology.^14,15

PLEURAL EFFUSION

Pure Transudate and Modified Transudate

Transudative pleural effusion, or hydrothorax, is the result of variations in the Starling forces that govern pleural fluid flux (see Box 30-1). Pure transudates are characterized by a low total protein and total nucleated cell count (Table 30-1). Hydrothoraces generally develop secondary to decreased oncotic pressure within the vasculature and are commonly associated with hypoalbuminemia, although it also may be secondary to an increased hydrostatic pressure or neoplasia. Modified transudates are associated with an increased hydrostatic pressure (i.e., heart failure) or vascular permeability (e.g., vasculitis, lung lobe torsion, diaphragmatic hernia) causing leakage of a higher protein ultrafiltrate.¹⁶ However, in animals with chronic effusion, irritation of the pleura may cause an increased nucleated cell count and water can be reabsorbed in excess of protein and cells.⁶ Translocation of abdominal effusion, neoplastic effusion, and chylothorax are other causes of transudates.

Table 30-1 Fluid Type and Characteristics¹⁶