Pleural effusion

Etiology

Transudates and modified transudates

• Hypoproteinemia (< 2g/dl albumin):
  • Protein-losing enteropathy Protein-losing enteropathy Inflammatory bowel disease: overview.
  • Protein-losing glomerulonephropathy Glomerulonephritis.
  • Amyloidosis Amyloidosis.
  • Hepatic failure Liver: failure.
  • Starvation.
  • Intestinal parasitism.
  • Malabsorption.
• Congestive heart failure   →   raised systemic venous pressures (right-sided), or left sided failure Heart: congestive heart failure:
  • Cardiomyopathy Heart: dilated cardiomyopathy (DCM).
  • Congenital cardiac defects.
• Neoplasia and pleural adhesions   →   obstruction of venous and lymphatic flow.
• Ruptured diaphragm   →   pressure on pleural venous and lymphatic drainage and protein leakage from herniated abdominal contents Diaphragm: hernia.
• True transudates rarely recognized   →   modified transudates (by addition of increased protein and cellular elements   →   increased opacity and yellow/pink color).

Exudates

• Bacterial invasion by aerobes and anaerobes, eg Streptococcus, Staphylococcus, Proteus and Pasturella spp and Escherichia coli, following puncture of chest wall, eg by a bite wound, migrating foreign body   →   inflammation Pyothorax.
• Feline infectious peritonitis Feline infectious peritonitis.
• Chest trauma   →   lung contusion or lung lobe torsion.
• Extension of mediastinal diseases.
• Neoplasia.

Hemothorax

• Severe intrapulmonary hemorrhage.
• Trauma.
• Blood vessel erosion (neoplasia), rupture of blood vessels in pleural adhesions.
• Coagulopathies:
  • Ingestion of coumarin-based rodenticides Anticoagulant rodenticide poisoning.
  • Inherent coagulation disorders (clotting factor deficiency, thrombocytopenia: more usually causes petechiation/echymosis), although bleeding into the lungs is more likely Lung: pulmonary hemorrhage.
  • Lung lobe torsion.

Chyle  

• Chylothorax. 
• Congestive heart failure Heart: congestive heart failure.
• Neoplasia Lymphoma, often mediastinal lymphoma.
• May not be identified.
• Thoracic duct erosion by inflammatory processes and neoplasia.
• Heart worm disease.
• Coughing and vomiting.

Pathophysiology

• Fluid accumulation in pleural space   →   lung lobes unable to expand   →   dyspnea.

• True transudates associated with hypoproteinemia. Plasma albumin <2 g/dl may   →   plasma leakage, levels <1.5 g/dl usually required for significant development of pleural effusion. Protein-losing glomerulonephropathy, amyloidosis, protein-losing enteropathies and reduced albumin production by liver are most common causes of hypoproteinemia. Reduction in plasma oncotic pressure   →   effusion.
• True transudates are rarely recognized as they soon become modified, ie have increased protein content and added cellular elements. Modified transudates are yellow to pink in color and more opaque than true transudates.
• Modified transudates are found with right-sided congestive heart failure, obstruction to lymphatic drainage by tissue adhesions in pleural space, neoplasms and abdominal contents herniating through the diaphragm.
• Exudates are associated with active inflammatory processes in pleural space, infections with bacteria penetrating wounds of chest wall, microerophilic agents such as Nocardia spp and Actinomyces spp, neoplasia, thoracic trauma and mediastinal disease.
• Hemothorax is found with coagulopathies, trauma and blood vessel erosion associated with neoplasms or destruction of pleural adhesions by inflammation or neoplastia.
• Chyle leaks from lymphatics in chest into pleural space. The etiology is usually unknown, but heart failure, lymphoma, heart worm infection and lymphangiectasia are sometimes implicated.

Timecourse

• Acute.
• Insidious and progressive.