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Summary Table

Category	Details
Risk Factors	Heart failure (most common cause of transudative), pneumonia, malignancy, liver cirrhosis, nephrotic syndrome, pulmonary embolism, tuberculosis, autoimmune disease (SLE, RA), pancreatitis, post-cardiac surgery
Etiology	Imbalance between pleural fluid production and absorption; transudative effusions result from altered hydrostatic/oncotic pressures; exudative effusions result from increased capillary permeability, impaired lymphatic drainage, or direct pleural inflammation/invasion
Patient Presentation	Progressive dyspnea, pleuritic chest pain (especially exudative), dry cough that worsens when lying on the unaffected side; large effusions present with orthopnea and respiratory distress
Classic Physical Exam	Decreased or absent breath sounds over the effusion, dullness to percussion, decreased tactile fremitus, tracheal deviation away from the affected side (in large effusions), egophony at the superior border of the effusion
Key Diagnostic Results	Blunting of the costophrenic angle on upright chest X-ray (requires ~200-300 mL of fluid); lateral decubitus film to confirm free-flowing fluid; thoracentesis with Light's criteria to classify; CT for loculated effusions or underlying mass
Management	Treat the underlying cause; therapeutic thoracentesis for symptomatic relief; chest tube drainage for empyema or complicated parapneumonic effusion; pleurodesis for recurrent malignant effusion
Keywords	"Dullness to percussion," "decreased breath sounds," "meniscus sign," "costophrenic angle blunting," "straw-colored fluid," "Light's criteria," "fluid layering on decubitus film"

1. Pathophysiology

The pleural space normally contains approximately 5 to 15 mL of fluid that acts as a lubricant between the visceral and parietal pleura. This fluid is maintained by a balance between hydrostatic pressure (pushing fluid into the space), oncotic pressure (pulling fluid back into the vasculature), and lymphatic drainage (removing excess fluid and protein from the pleural space). A pleural effusion develops when any of these mechanisms is disrupted, leading to net fluid accumulation.

Transudative effusions occur when systemic factors alter the hydrostatic-oncotic balance without directly affecting the pleural membrane. In congestive heart failure, elevated pulmonary venous pressure increases the hydrostatic gradient, pushing fluid into the pleural space. In cirrhosis, ascitic fluid migrates through diaphragmatic defects (called hepatic hydrothorax), and the low serum albumin further reduces plasma oncotic pressure. In nephrotic syndrome, the primary driver is hypoalbuminemia reducing the oncotic gradient. The pleura itself is healthy in all these cases, which is why the fluid is protein-poor and cell-poor.

Exudative effusions arise from local pathology affecting the pleura directly. In pneumonia, bacterial infection triggers an inflammatory cascade that increases capillary permeability, allowing protein-rich fluid and inflammatory cells to leak into the pleural space (parapneumonic effusion). If bacteria invade the pleural space itself, the result is empyema, characterized by frank pus, very low pH, and very low glucose. In malignancy, tumor cells can directly implant on the pleural surface, obstruct lymphatic drainage, or both, leading to protein-rich, often bloody fluid. In tuberculosis, a delayed-type hypersensitivity reaction causes granulomatous inflammation of the pleura with a lymphocyte-predominant exudate.

The clinical symptoms are a direct consequence of the fluid's mechanical effects. As fluid accumulates, it compresses the underlying lung parenchyma, reducing functional residual capacity and causing dyspnea. Pleuritic chest pain occurs when the inflamed parietal pleura (which is innervated, unlike the visceral pleura) is stretched or irritated. Large effusions shift the mediastinum toward the contralateral side, potentially compressing the opposite lung and causing tracheal deviation.

2. Classification and Clinical Manifestation

Light's Criteria

An effusion is classified as exudative if it meets any one of the following criteria. If none are met, it is transudative.

Light's Criteria Parameter	Exudative Threshold
Pleural fluid protein / Serum protein	> 0.5
Pleural fluid LDH / Serum LDH	> 0.6
Pleural fluid LDH	> 2/3 the upper limit of normal for serum LDH

Common Causes by Category

Category	Causes	Characteristic Features
Transudative	Congestive heart failure	Bilateral effusions (right > left), BNP elevated in pleural fluid, responds to diuresis
	Hepatic cirrhosis (hepatic hydrothorax)	Right-sided predominance (~70%), associated with ascites, transdiaphragmatic migration
	Nephrotic syndrome	Bilateral, low serum albumin (< 2.5 g/dL)
	Atelectasis	Small, ipsilateral to the atelectatic lung
Exudative	Parapneumonic effusion / Empyema	Associated with pneumonia; complicated if pH < 7.2, glucose < 60, or positive Gram stain
	Malignancy	Bloody fluid common, cytology positive in ~60% on first tap, lymphocyte-predominant
	Tuberculosis	Lymphocyte-predominant, elevated adenosine deaminase (ADA > 40 U/L), low glucose
	Pulmonary embolism	Can be either transudative or exudative; small, unilateral, often bloody
	Autoimmune (SLE, RA)	SLE: bilateral, ANA-positive fluid. RA: very low glucose (< 30), low pH
	Pancreatitis	Left-sided, elevated pleural fluid amylase
	Esophageal rupture (Boerhaave syndrome)	Left-sided, elevated pleural fluid amylase (salivary isoenzyme), very low pH, particulate matter
	Chylothorax	Milky white fluid, elevated triglycerides (> 110 mg/dL), caused by thoracic duct injury
	Hemothorax	Pleural fluid hematocrit > 50% of peripheral blood hematocrit

Clinical Manifestation by Effusion Size

Size	Approximate Volume	Symptoms and Signs
Small	< 300 mL	Often asymptomatic; may have mild pleuritic pain; CXR may appear normal on PA view
Moderate	300 to 1000 mL	Dyspnea on exertion, dullness to percussion, decreased breath sounds
Large	> 1000 mL	Dyspnea at rest, orthopnea, tracheal deviation to the contralateral side, absent breath sounds, contralateral mediastinal shift

3. Diagnostic Workup

Test	Role	Key Findings
Upright PA chest X-ray	Best initial test	Blunting of costophrenic angle (meniscus sign); requires ~200-300 mL to detect
Lateral decubitus X-ray	Confirms free-flowing fluid	Fluid layers dependently; detects as little as ~50 mL; free layering > 10 mm suggests safe thoracentesis
Chest ultrasound (point-of-care)	Guides thoracentesis, detects small/loculated effusions	Anechoic space (simple); septations or echogenic debris (complex/empyema); most sensitive bedside modality
CT chest with contrast	Evaluates underlying etiology	Identifies loculations, pleural thickening/enhancement, lung masses, lymphadenopathy, mediastinal pathology
Thoracentesis with fluid analysis	Most important diagnostic step	Light's criteria, cell count/differential, glucose, pH, LDH, cytology, Gram stain/culture, amylase, triglycerides as indicated
Pleural biopsy	When thoracentesis is non-diagnostic	Gold standard for tuberculous pleuritis and mesothelioma; sensitivity ~80% for TB, higher with CT-guided or thoracoscopic biopsy

The workup begins with an upright posteroanterior (PA) chest X-ray, which is the best initial test. The classic finding is blunting of the costophrenic angle with a meniscus-shaped opacity that curves upward laterally. A completely opacified hemithorax with contralateral mediastinal shift indicates a large effusion, while ipsilateral shift (or no shift) with complete opacification should raise suspicion for an obstructive process such as a central bronchial mass causing atelectasis with concurrent effusion.

If there is uncertainty about whether the opacity represents fluid versus consolidation or a mass, a lateral decubitus film (patient lying on the affected side) is the next step. Free-flowing fluid will layer along the dependent chest wall. If the layering measures greater than 10 mm, the effusion is large enough to safely perform a diagnostic thoracentesis. If the fluid does not layer, it is either loculated or not truly an effusion.

Point-of-care ultrasound has increasingly replaced the lateral decubitus film in clinical practice and is considered the most sensitive bedside tool for detecting pleural effusions. It can detect volumes as small as 20 mL, identify septations or loculations, and guide safe needle placement for thoracentesis. Exam questions may test the utility of ultrasound guidance to reduce complications such as pneumothorax.

Thoracentesis is the most important diagnostic step and should be performed on virtually all new, clinically significant effusions unless the clinical picture strongly suggests a transudative cause that will respond to treatment (e.g., bilateral effusions in a patient with known decompensated heart failure). The fluid is sent for protein, LDH, glucose, pH, cell count with differential, Gram stain, culture, and cytology. Additional studies such as amylase (pancreatitis, esophageal rupture), triglycerides (chylothorax), and adenosine deaminase/ADA (tuberculosis) are ordered based on clinical suspicion.

Light's criteria are then applied to classify the effusion. One important caveat: patients with heart failure on chronic diuretic therapy may have a transudative effusion that is misclassified as exudative because diuresis concentrates the pleural fluid protein and LDH. In this scenario, the serum-to-pleural-fluid albumin gradient should be calculated. If the gradient is greater than 1.2 g/dL, the effusion is likely transudative despite meeting Light's exudative criteria.

For exudative effusions, the pleural fluid pH and glucose are critical for decision-making. A parapneumonic effusion with a pH < 7.2, glucose < 60 mg/dL, positive Gram stain, or frank pus is classified as a complicated parapneumonic effusion or empyema and requires chest tube drainage rather than antibiotics alone.

If cytology is negative after two thoracenteses in a patient with a high suspicion for malignancy, the next step is thoracoscopy (medical or video-assisted thoracoscopic surgery/VATS) with pleural biopsy. This is the gold standard for confirming malignant pleural disease and mesothelioma. For suspected tuberculous pleuritis, pleural biopsy showing caseating granulomas is the most accurate confirmatory test, though a markedly elevated pleural fluid ADA (> 40 U/L) in a lymphocyte-predominant exudate is highly suggestive in endemic areas.

4. Management and Treatment

Clinical Scenario	Treatment	Key Details
Transudative (CHF)	Diuresis with furosemide; treat underlying heart failure	Loop diuretics (e.g., furosemide 40 mg IV, titrate to response); no thoracentesis needed unless dyspnea is refractory
Transudative (cirrhosis)	Sodium restriction, diuretics (spironolactone + furosemide), consider TIPS	Avoid repeated large-volume thoracentesis; treat the ascites
Uncomplicated parapneumonic	Antibiotics alone	Small, free-flowing, pH > 7.2, glucose > 60, Gram stain and culture negative
Complicated parapneumonic	Antibiotics + chest tube drainage	pH < 7.2, glucose < 60, positive Gram stain, or loculated on imaging
Empyema	Antibiotics + chest tube drainage; consider intrapleural fibrinolytics or VATS if drainage is inadequate	Frank pus on thoracentesis; fibrinolytics: tPA (10 mg) + DNase (5 mg) intrapleurally twice daily for 3 days
Malignant effusion	Therapeutic thoracentesis for symptom relief; pleurodesis (talc) for recurrence; indwelling pleural catheter (IPC) for trapped lung	Talc pleurodesis via thoracoscopy is most effective (~90% success); IPC for patients with poor performance status or trapped lung
Tuberculous	Standard anti-TB therapy (RHZE regimen) for 6 months; corticosteroids are sometimes used but evidence is mixed	Isoniazid + Rifampicin + Pyrazinamide + Ethambutol for 2 months, then Isoniazid + Rifampicin for 4 months
Chylothorax	NPO or medium-chain triglyceride (MCT) diet; thoracic duct ligation if conservative measures fail	MCT diet bypasses the thoracic duct (absorbed directly into portal circulation); octreotide may reduce chyle flow
Hemothorax	Chest tube (large-bore, 28-36 Fr); thoracotomy if initial output > 1500 mL or > 200 mL/hr for 2-4 hours	Autotransfusion should be considered; surgical exploration for ongoing bleeding

The foundational principle is to treat the underlying cause. A transudative effusion from heart failure does not require thoracentesis unless the patient has refractory dyspnea despite adequate diuresis. The initial management is aggressive volume management with intravenous furosemide (starting at 40 mg IV, doubling the dose if urine output is inadequate). For hepatic hydrothorax, the target is the ascites: sodium restriction (< 2 g/day) and dual diuretic therapy with spironolactone (100 mg/day) and furosemide (40 mg/day), titrated in a 100:40 ratio. TIPS (transjugular intrahepatic portosystemic shunt) is considered for refractory cases.

For parapneumonic effusions, the distinction between uncomplicated and complicated determines management. An uncomplicated parapneumonic effusion (small, free-flowing, pH > 7.2, glucose > 60, negative cultures) resolves with antibiotics directed at the underlying pneumonia and does not need drainage. A complicated parapneumonic effusion (pH < 7.2, glucose < 60, positive Gram stain or culture, or loculated fluid) requires prompt chest tube insertion in addition to antibiotics. Failure to drain a complicated effusion leads to organization, fibrous peel formation, and potentially the need for decortication surgery.

Empyema (frank pus or positive culture from the pleural space) always requires drainage plus antibiotics. If the effusion is loculated and draining poorly, intrapleural fibrinolytic therapy with tissue plasminogen activator (tPA, 10 mg) combined with deoxyribonuclease (DNase, 5 mg) given intrapleurally twice daily for 3 days has been shown to improve drainage and reduce the need for surgery. If this fails, VATS decortication is the next step.

For malignant pleural effusions, the goal is palliation. Initial management is a large-volume therapeutic thoracentesis (up to 1000 to 1500 mL, stopping if the patient develops chest tightness, cough, or if pleural pressure drops significantly). If the effusion recurs rapidly (which is common in malignancy), chemical pleurodesis with talc slurry via chest tube or talc poudrage via thoracoscopy is performed to obliterate the pleural space and prevent reaccumulation. For patients with trapped lung (the lung cannot re-expand to appose the chest wall), pleurodesis will not work, and an indwelling pleural catheter (IPC) is the preferred approach, allowing the patient to drain fluid at home.

For chylothorax, initial management is conservative: nil per os (NPO) or a diet restricted to medium-chain triglycerides (MCT). MCTs are absorbed directly into the portal venous system, bypassing the thoracic duct entirely and reducing chyle production. If conservative management fails after 2 weeks, or if output exceeds 1.5 L/day, thoracic duct ligation (surgical or interventional) is indicated.

5. Differential Diagnosis and Distractors

Differential	Why It Is Similar	Key Discriminator
Pneumonia/Consolidation	Both cause dullness to percussion, decreased breath sounds, and opacification on CXR	In consolidation, tactile fremitus is increased (vs. decreased in effusion); bronchial breath sounds and egophony are heard over the consolidation; no fluid layering on decubitus film
Atelectasis	Opacification on CXR, decreased breath sounds	Mediastinal shift is toward the affected side in atelectasis (vs. away in large effusion); volume loss on the affected side
Pneumothorax	Dyspnea, decreased breath sounds	Pneumothorax has hyperresonance to percussion (vs. dullness); absent tactile fremitus in both, but percussion is the key differentiator
Lung mass/tumor	Opacification on CXR	Mass does not layer on decubitus; no meniscus sign; CT shows a discrete lesion rather than free fluid
Diaphragmatic elevation	Apparent costophrenic blunting, especially on the left	Lateral decubitus film shows no layering fluid; ultrasound confirms no fluid above the diaphragm
CHF effusion vs. malignant effusion	Both can be large and bilateral	CHF effusion is transudative (fails Light's criteria), bilateral, responds to diuresis; malignant effusion is exudative, often unilateral, bloody, cytology-positive
Parapneumonic effusion vs. empyema	Both occur alongside pneumonia	Uncomplicated parapneumonic: pH > 7.2, glucose > 60, culture-negative. Empyema: frank pus, pH < 7.2, glucose < 40, positive Gram stain/culture. This distinction determines whether a chest tube is needed.
Mesothelioma vs. metastatic pleural disease	Both cause exudative, often bloody effusions	Mesothelioma: occupational asbestos exposure, pleural thickening/calcification on CT, calretinin-positive on immunohistochemistry. Metastatic disease: history of primary malignancy (lung, breast), nodular pleural enhancement on CT
Tuberculous effusion vs. malignant effusion	Both are lymphocyte-predominant exudates	TB effusion: ADA > 40 U/L, young patient in endemic area, positive PPD/IGRA, caseating granulomas on biopsy. Malignant: cytology-positive, older patient, no fever, weight loss pattern may differ

6. Traps and High-Yield Pearls

The single most common trap with pleural effusion questions is failing to apply Light's criteria correctly. Students often memorize the thresholds but forget that meeting any one of the three criteria classifies the effusion as exudative. The exam will present a case where only one parameter barely crosses the threshold, and the correct answer hinges on recognizing that a single positive criterion is sufficient.

The second major trap involves the diuretic pitfall. A patient with known heart failure on chronic furosemide therapy undergoes thoracentesis, and the fluid meets Light's criteria for an exudate. The unwary student selects an exudative workup. The correct approach is to calculate the serum-to-pleural-fluid albumin gradient. If it exceeds 1.2 g/dL, the effusion is a "pseudo-exudate," and the patient should be managed as transudative (continued diuresis, not a biopsy or CT-guided drainage).

Another frequently tested concept is the decision to place a chest tube in parapneumonic effusions. The exam will present a patient with pneumonia and a new effusion, then ask for the next best step. The answer depends entirely on the thoracentesis results: pH < 7.2 or glucose < 60 mg/dL mandates drainage, even if the fluid looks clear. Students who skip ahead to "antibiotics alone" without checking the pleural fluid pH will miss this.

Finally, remember that pulmonary embolism can cause either a transudative or an exudative effusion, making it a diagnosis that does not fit neatly into the Light's criteria framework. When a vignette describes a small, unilateral, bloody effusion in a patient with risk factors for DVT (recent surgery, immobilization, oral contraceptive use), the intended diagnosis is PE, and the next best step is CT pulmonary angiography, not repeated thoracentesis.

The core competency being tested across all pleural effusion questions is the ability to systematically classify the effusion, interpret thoracentesis results in clinical context, and match the management to the category and severity of the effusion rather than reflexively treating all effusions the same way.

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