Introduction There is normally a very thin layer of fluid (from 2 to 10 µm thick) between the two pleural surfaces, the parietal pleura and visceral pleura. The pleural space and the fluid within it are not under static conditions. During each respiratory cycle the pleural pressures and the geometry of the pleural space fluctuate widely. Fluid enters and leaves the pleural space constantly.
The serous membrane covering the lung parenchyma is called the visceral pleura . The remainder of the lining of the pleural cavity is the parietal pleura. The parietal pleura receives its blood supply from the systemic capillaries . The visceral pleura is supplied predominantly by branches of the bronchial artery in humans
The lymphatic vessels in the parietal pleura are in direct communication with the pleural space by means of stomas. These stomas are the only route through which cells and large particles can leave the pleural space . Although there are abundant lymphatics in the visceral pleura, these lymphatics do not appear to participate in the removal of particulate matter from the pleural space.
Mechanism of pleural fluid turnover Dependent on the hydrostatic and oncotic pressures across membranes. When the capillaries in the parietal pleura are considered, it can be seen that the net hydrostatic pressure favoring the movement of fluid from these capillaries to the pleural space is the systemic capillary pressure (30cm H 2 O) minus the negative pleural pressure (-5cm H 2 O) or 35cm H 2 O. Opposing this is the oncotic pressure in the blood ( 34cm H 2 O ) minus the oncotic pressure in the pleural fluid (5 cm H 2 O ), or 29cm H 2 O. The resulting net pressure differences of 6 cm H 2 O (35-29) favors movement of fluid from the parietal pleura into the pleural space .
Pathophysiology Pleural fluid will accumulate when the rate of pleural fluid formation is greater than the rate of pleural fluid removal by the lymphatics . Pleural effusions have classically been divided into Transudative Exudative
A transudative pleural effusion occurs when alterations in the systemic factors that influence pleural fluid movement result in a pleural effusion . Ex. Heart failure, nephrotic syndrome, hepatic cirhosis . Exudative pleural effusions occur when the pleural surfaces are altered . Ex. Pleurisy.
Clinical features Many patients have no symptoms due to the effusion when effusion is small . Pleuritic chest pain is the usual symptom of pleural inflammation. Irritation of the pleural surfaces may also result in a dry, nonproductive cough . With larger effusions, dyspnea results from lung compression.
Physical examination Signs are proportional to amount of effusion. Fullness of intercostal spaces. Decreased or absent tactile fremitus . Dullness to percussion. Diminished breath sounds over the site of the effusion. Change in findings with change in position. Signs of pneumonia like bronchial breathing,crackles etc.
Chest xray The first fluid accumulates in the lowest portion of the thoracic cavity, which is the posterior costophrenic angle. The earliest radiologic sign of a pleural effusion is blunting of the posterior costophrenic angle on the lateral chest radiograph. If a posteroanterior radiograph is obtained with the patient lying on the affected side, free pleural fluid will gravitate inferiorly and a pleural fluid line will be visible.
Pleural fluid is loculated when it does not shift freely in the pleural space as the patient’s position is changed. Loculated pleural effusions occur when there are adhesions between the visceral and parietal pleurae. Both ultrasound and computed tomography (CT) have useful in making this differentiation.
USG thorax
CT chest
Should thoracentesis be performed? If thoracentesis is done Is the fluid a transudate or exudate ? If the fluid is an exudate What is the etiology?
Should thoracentesis be performed ? Most patients should be tapped Newly recognized effusion. Two exceptions Small Effusions ( < 1 cm on decubitus ) Congestive Heart Failure Thoracentesis only if bilateral effusions not equal. Fever. Pleuritic chest pain. Impending respiratory faillure .
Is The Fluid A Transudate Or Exudate ? Transudative Effusions Mechanical No capillary leak or cytokine activation Excessive formation or impaired absorption Limits the differential with no additional workup CHF, Cirrhosis, or Nephrotic Syndrome If Exudative , more investigation required Method: LIGHT’s Criteria
Light’s Criteria ( Exudate ) Pleural fluid total protein/ serum protein >0.5 Pleural total protein > 3g/dl. Pleural fluid LDH/serum LDH > 0.6 Pleural fluid LDH > 200 IU/l. Pleural fluid LDH level > 2/3 of upper normal level of serum LDH.
Parapneumonic effusion Any pleural effusion associated with bacterial or viral pneumonia Loculated parapneumonic effusion Not free flowing Multiloculated parapneumonic effusion Noncommunicating compartments Empyema ( fibrosuppurative exudate ) Pus in the pleural space . pH < 7.2, Glucose < 60 mg/ dL , High LDH.
Empyema Empyema is an accumulation of pus in the pleural space. It is most often associated with pneumonia. It can also be produced by : Rupture of a lung abscess into the pleural space. Contamination introduced from trauma or thoracic surgery. Mediastinitis or the extension of intra-abdominal abscesses.
Natural History Empyema Exudative stage Rapid accumulation of inflammatory fluid Normal pH, Glucose, and LDH level Antibiotics effective Fibropurulent stage PMN’s, Fibrin deposition, loculations occur Low pH and glucose, high LDH Organization stage ( fibrothorax ) Fibroblast proliferation between pleural layers Pleural peel develops, decortication required
Clinical features Primary signs & symptoms of pneumonia. Most patients are febrile, develop increased work of breathing or respiratory distress, and often appear more ill. Physical findings are similar to effusion.
Diagnosis Similar to other effusion radiologically . Pleural fluid analysis is must to differentiate. Characteristic of pus : Bacteria are present on Gram staining. pH is < 7.20. >100,000 neutrophils /µL. Pleural fluid culture & PCR analysis to identify organism.
Treatment Systemic antibiotics. Depends on culture & sensitivity report. 2 weeks of IV antibiotics.(in staphylococci infection response is very slow so required for 3-4wks.) Closed tube drainage. VATS Open decortication .
Treatment In the child who remains febrile and dyspneic >72 hr after initiation of therapy with intravenous antibiotics and thoracostomy tube drainage, surgical decortication via VATS or open thoracotomy may speed recovery . If pneumatoceles form, no attempt should be made to treat them surgically or by aspiration, unless they reach cause respiratory embarrassment or become secondarily infected.
Complications Local Bronchopleural fistula. Pyopneumothorax . Purulent pericarditis . Pulmonary abscesses. Peritonitis from extension through the diaphragm. Osteomyelitis of the ribs . Systemic Septicemia . Meningitis Arthritis. Osteomyelitis .