Pleural Effusions
World Small Animal Veterinary Association World Congress Proceedings, 2004
Eric Monnet, DVM, PhD, FAHA, DACVS, ECVS
College of Veterinary Medicine, Colorado State University
Fort Collins, CO, USA

The thoracic cavity is lined entirely by a serous membrane known as pleura. The pleura is divided into visceral pleura which covers the lungs and parietal pleura which covers the remaining thoracic cavity. The pleura is composed of a single layer of mesothelial cells supported by a delicate network of elastic connective tissue. The visceral and parietal pleura contain a rich capillary network that originates from the pulmonary and systemic circulations, respectively. In addition, the parietal pleura contains a rich lymphatic network responsible for lymphatic drainage of the pleural space. Under normal conditions, the pleural space is only a potential cavity. Liquid coupling between the thoracic wall and lungs provides instantaneous transmission of thoracic volume changes to the lungs, and yet allows low friction sliding between the pleural surfaces.

Because high pleural permeability causes the pleural space to be continuous with the interstitial fluid of the thoracic wall, the dynamics of pleural fluid formation and absorption are controlled by Starling's forces.

HYDROTHORAX

Hydrothorax is the result of transudative effusion caused by a disturbance in the balance of Starling forces responsible for pleural fluid formation and absorption. Hypo-albuminemia, congestive heart failure, right sided heart failure are the most common causes of hydrothorax.

Diagnosis of hydrothorax is based on identification of an effusion as a transudate or modified transudate (Table 1). As a transudative effusion becomes longstanding, mesothelial cells degenerate and attract neutrophils to the pleural space. Total nucleated cell counts may approach 5 X 103 cells/ul with a significant percentage of the cells being neutrophils. These effusions are termed modified transudates. Effusions associated with obstructive phenomenon such as lung lobe torsion or liver incarceration will have a total protein of 1.5 to 5 gm/dl. Pleural effusions with these characteristics are termed high-protein modified transudates or obstructive effusions. The treatment of hydrothorax consists of pleural drainage if respiratory distress is present and correction of its underlying cause if possible.

PLEURITIS AND PYOTHORAX

Purulent pleuritis, also referred to as pyothorax or empyema, is invariably the result of bacterial or fungal sepsis of the pleural space. Sources of bacterial contamination include penetrating thoracic wounds, extension of bacterial pneumonia, migrating foreign bodies, esophageal perforations, extension of cervical, lumbar or mediastinal infections, and hematogenous spread. Thoracic bite wounds are frequently implicated in feline pyothorax. Inhalation and migration of a grass awn often is suspected in field dogs with pyothorax. Anaerobic bacteria and Nocardia asteroides are isolated most often from dogs with pyothorax. Pasteurella multocida and anaerobes are the most prevalent isolates in cats.

Table 1. Differentiation of Transudates, modified Transudates, Exudates, and Chylous effusion

Transudate

Modified
Transudate

Exudate

Chylous

Specific gravity

<1.017

1.017-1.025

>1.025

1.017-1.025

Total protein (gm/dl)

<2.5

2.5-5.0

>3.0

2.5-5.0

Nucleated cells (per mm3)

<1000

500-10,000

>5000

500-20,000

Predominant cell types

Mononuclear
Mesothelial

Lymphocytes
Monocytes
Mesothelial RBCs

Neutrophils
Mononuclear
RBCs

Lymphocytes
Neutrophils
Mesothelial

Biochemistry

High triglycerides
Low cholesterol

Bacteria

Absent

Absent

Variable

Absent

Pleuritis and pyothorax frequently have an insidious course and presentation may be delayed. Moderate to severe respiratory distress usually is present. The patient also shows signs of systemic infection characterized by anorexia, weight loss, malaise, and fever. Physical and radiographic findings are those of pleural effusion. Inflammatory exudates typically exhibit a total protein greater than 3.0 gm/dl, a specific gravity greater than 1.018, and a total cell count greater than 30 X 103 cells/ul. Inflammatory exudates may be nonseptic or septic (Table 1). Degenerate neutrophils predominate and bacteria are often visualized. Gram stains may give an early indication of the types of bacteria present. Fluid should be cultured for aerobic and anaerobic bacteria. Macrophages and plasma cells increase as an exudative process becomes longstanding.

Treatment of pyothorax must be prompt and aggressive. The prognosis is guarded but not hopeless. The initial goal of therapy is to relieve respiratory embarrassment by thoracocentesis, preferably under minimal restraint with the patient sternal or standing. Supportive care with intravenous fluids is necessary to correct dehydration, acid-base and electrolyte imbalance. Systemic antibiotic therapy should be initiated immediately, and then adjusted based on culture and sensitivity results if necessary. Due to the high incidence of anaerobic infections, antibiotics with an anaerobic spectrum should be started upon diagnosis of pyothorax and continued throughout the course of disease. Many animals with pyothorax will have bacteremia or septicemia so intravenous antibiotics are indicated in the initial treatment period. Once the patient is stable, a thoracostomy tube should be placed utilizing local anesthesia and sedation. After complete evacuation of the pleural space, pleural lavage is initiated. The pleural space should be lavaged twice daily with approximately 20 ml/kg of warmed 0.9% saline or Ringer's solution. Efficacy of treatment is monitored by clinical findings, thoracic radiographs, and cytology of the pleural effusion. Most animals with successful treatment will have a decrease in fever and improvement in general attitude within the first 48 hours. Cytology of pleural fluid can be used to assess the response to therapy. Neutrophils, both total number and percentage of degenerate cells, and bacteria should gradually subside over three to five days.

Lack of significant clinical improvement within 48 to 72 hours or radiographic demonstration of undrained encapsulated fluid are indications to surgically explore the thoracic cavity. Radiographic evidence of lung lobe consolidation and pneumothorax suggest the possibility of a ruptured pulmonary abscess and is a relative indication for surgery. Exploratory thoracotomy should be undertaken by medium sternotomy which gives access to both hemithoraces. Mediastinotomy often is necessary since the ventral mediastinum is invariably thickened and filled with small abscesses. The pericardium also may require excision if it is thickened and abscessed. Consolidated lung lobes which cannot be inflated should be excised by partial or complete lobectomy. Before closure, the thoracic cavity is vigorously lavaged with copious amounts of warm isotonic crystalloid solution. Closed pleural lavage should be continued postoperatively for at least two to three days. The probability of success with surgical management of refractory pyothorax is better for dogs than for cats.

Constrictive pleuritis is a serious sequela to longstanding pyothorax that is suggested by an inability to re-expand the lungs following resolution of the pyothorax. If the constriction is diffuse, then surgical decortication of the fibrous peel from the visceral pleura is necessary.

CHYLOTHORAX

Chylothorax results when chyle from the cisterna chyli-thoracic duct system gains access to the pleural space. In the dog, the caudal thoracic duct courses dorsal and to the right of the aorta, lateral to the intercostal arteries, and ventral to the azygos vein. The duct crosses to the left side of the aorta ventral to the body of the fifth thoracic vertebra and continues cranioventral across the left side of the esophagus to empty at the junction of the left jugular vein and cranial vena cava. In the cat, the caudal thoracic duct typically courses dorsal and to left of the aorta.

The etiology of chylothorax is poorly understood in the dog and cat. The incidence of chylothorax in Afghan is inordinately high, but it is unknown if this predisposition is hereditary. Trauma and obstruction of the thoracic duct might be causes of chylous effusion. It is speculated that lymphangiectasia may allow extravasation of chyle through the lymphatic vessel wall. Malignancies or thrombosis that occludes the cranial vena cava might induce chylothorax by such a mechanism. Elevations in systemic venous pressure secondary to congestive heart failure likely explain why chylothorax occurs with cardiomyopathy, tricuspid dysplasia, and heartworm disease. Lymphangiectasia of unknown origin has been demonstrated in dogs and cats with spontaneous chylothorax.

Debilitation associated with chylothorax is caused primarily by loss of chyle from the body after pleural drainage is instituted. Water and electrolyte losses can be sufficient to cause dehydration and electrolyte imbalance. Loss of lipid and protein can lead to protein-calorie malnutrition and hypoproteinemia. Malnutrition is compounded by the loss of fat soluble vitamins. Immunocompetence becomes impaired due to loss of antibodies, lymphopenia, and malnutrition.

Diagnosis of chylothorax is based on recognition of characteristic clinical and radiographic findings of pleural effusion and by demonstration of chyle on fluid analysis (Table 1). Chylous fluids typically show triglyceride levels that are 12 to 100 times greater than levels measured in the serum. Cholesterol levels in chylous effusions are not elevated when values are compared to values from serum. Anorectic animals with chylous effusion may have greatly reduced levels of chylomicrons. Pleural fluid from such animals may easily be mistaken for a modified transudate or obstructive effusion. Feeding a fatty meal is often necessary to demonstrate the chylous nature of a pleural effusion in these animals. Pleural effusions high in cholesterol or lecithin-globulin complexes appear grossly similar to chylous effusions, but are due to degenerating cells associated with chronic inflammatory or malignant processes. These effusions are termed pseudochylous effusions. Pseudochylous effusions will be low in triglycerides and may have a high cholesterol level.

Once chylothorax is diagnosed, an attempt to determine its cause should be undertaken. Owners should be questioned regarding the possibility of recent trauma. Thoracic radiographs taken after complete pleural drainage should be evaluated for the presence of masses particularly in the cranial mediastinum. Echocardiography and ultrasound examination of the mediastinum also can be undertaken. Animals with chylothorax should be evaluated for dirofilariasis using microfilaria concentration techniques or serum adult antigen detection tests, or both. Cytologic examination of the chylous effusion for the presence of neoplastic cells helps rule out neoplasia. Often, a cause for chylothorax is not found and the clinician is left with a diagnosis of idiopathic chylothorax. Direct lymphangiography may provide information on the etiology of idiopathic chylothorax (i.e., rupture versus lymphangiectasia), but generally is of academic interest only since it usually does not change the therapeutic plan.

Treatment of chylothorax may be medical or surgical. Medical management is directed at draining the pleural space and reducing the formation of chyle. Pleural drainage is indicated to relieve respiratory distress and may either be intermittent or continuous. Low-fat diets decrease the triglyceride content of chyle, but there is no evidence that the volume of chyle is similarly decreased. Animals with chylothorax should receive aggressive nutritional support and be supplemented with fat soluble vitamins.

Absolute indications for surgical intervention are not established in animals. The following indications for surgery are suggested: 1) failure to significantly diminish the flow of chyle after 5 to 10 days of medical management; 2) losses of chyle exceeding 20 ml/kg/day over a five day period; or 3) protein-calorie malnutrition and hypoproteinemia. Transthoracic ligation of the thoracic duct is accomplished through a right ninth or tenth intercostal thoracotomy in the dog. Failure to ligate all collateral branches of the caudal thoracic duct is thought to be a most common cause of operative failure. For this reason, en bloc ligation of all structures in the caudal mediastinum dorsal to the aorta is recommended. Intraoperative lymphangiograms performed to ensure complete ligation of the thoracic duct have been advocated, however this approach substantially increases operative time and requires facilities for taking intraoperative radiographs. The success rate for surgical management of chylothorax alone is generally less than 60%. Combined mechanical pleural pleurodesis and thoracic duct ligation, both performed via median sternotomy, is recommended. Omentalization of the thoracic cavity is an alternative to pleurodesis. Placement of pleurovenous shunts have also been evaluated.

Despite vigorous attempts at medical and surgical management, a significant number of animals with chylothorax will fail to respond to therapy. Chronic chylothorax can cause a constrictive pleuritis that may require decortication.

HEMOTHORAX

The most common cause of hemothorax is trauma, either accidental and surgical. Coagulopathies including thrombocytopenia or warfarin toxicity also can manifest with hemothorax as a primary finding. Neoplasia or parasites, e.g., Spirocerca lupi and Dirofilaria immitis, can cause rupture of thoracic vessels and spontaneous hemothorax.

Diagnosis of hemothorax is based on demonstration of blood in the pleural space. Specific gravity, total protein, total cell counts, and cytologic findings of hemorrhagic effusions are similar to values in the peripheral blood. The myeloid-erythroid ratio is approximately 1 to 100, similar to peripheral blood. Hemorrhagic effusions generally will have a hemoglobin level of at least 25% of the blood level, whereas serosanguineous effusions rarely have hemoglobin values exceeding 1 gm/dl. Hemorrhage within the pleural space generally does not clot due to mechanical defibrination and activation of fibrinolytic mechanisms. Clotting also is impaired by the disappearance of platelets within eight hours following hemorrhage.

Diagnostic evaluation of coagulation parameters is indicated in animals with hemothorax, especially in the absence of obvious trauma. A platelet count and activated clotting time should be performed. If a platelet count and activated clotting time are normal but coagulopathy is still suspected, a mucosal bleeding time should be performed to assess platelet function particularly in breeds that commonly have von Willebrand's disease. A citrated blood sample should be collected before blood transfusion, centrifuged immediately, and frozen for future assessment of specific factor deficiencies if needed.

Hemothorax is a common injury associated with thoracic trauma. Hemorrhage can originate from internal structures such as the heart, great vessels, or lungs, or from laceration of intercostal or internal thoracic arteries. Treatment of hemothorax depends on the volume and flow of hemorrhage in the pleural space. Therefore, mild hemothorax that does not induce significant respiratory distress should be managed conservatively to allow resorption of pleural blood. Occasionally, pleural hemorrhage is sufficient to require pleural drainage for relief of respiratory embarrassment. Animals with substantial blood loss from the pleural space may require blood transfusion in addition to crystalloid volume replacement to maintain an adequate packed cell volume. Autotransfusion of autogenous blood removed by pleural drainage provides a readily available source of compatible blood in patients with severe hemothorax. Rarely pleural hemorrhage will be such that pleural drainage and autotransfusion cannot keep ahead of accumulation. In this case, exploratory thoracotomy is indicated in an attempt to repair the site of hemorrhage. Exploratory thoracotomy should be undertaken by a median sternotomy approach.

NEOPLASTIC EFFUSION

Pleural effusion can result from primary or metastatic neoplasia involving the thoracic cavity. Lymphosarcoma, pulmonary carcinoma, metastatic carcinomas, and hemangiosarcomas have all been reported to cause neoplastic effusions. Mesotheliomas are rare in all species, but are associated with pleural effusion when present.

Neoplastic effusions are suspected when physical, radiographic, and laboratory findings suggest the presence of a thoracic neoplasm. Neoplastic effusions may have either a exudative or transudative fluid pattern and are identified by the presence of neoplastic cells on cytological examination. Thymic lymphosarcoma is the most common cause of neoplastic effusions in cats. Neoplastic lymphocytes are usually prolymphocytes or lymphoblasts. These cells are large, variable in size, and have intensely basophilic cytoplasm and multiple nucleoli. Metastatic carcinomas and occasionally sarcomas will produce neoplastic effusions. Differentiation of neoplastic cells from reactive mesothelial cells is difficult even for experienced cytologists. Therefore, care must be used in diagnosing neoplasia on cytologic examination alone. Cytologic findings should be correlated with other clinical findings. A punch biopsy of the pleura is indicated when pleural neoplasia such a mesothelioma is suspected.

Treatment of a neoplastic pleural effusion is directed at the causative neoplasm. The prognosis for animals with neoplastic effusions is poor with the exception of effusions associated with lymphosarcoma. Intermittent pleural drainage gives temporary relief from respiratory distress. Intracavitary chemotherapy or radionucleotides have been used in the management of neoplastic effusions in dogs. Pleurodesis also may be considered for palliation of neoplastic effusions.

Speaker Information
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Eric Monnet, DVM, PhD, FAHA, DACVS, ECVS
College of Veterinary Medicine, Colorado State University
Fort Collins, CO


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