There is normally a very thin layer of fluid (from 2 to 10 m 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 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.
Anatomy of the Pleural Space Dr. Canmao xie SC: Systemic capillaries PC: Pulmonary capillaries
Figure 1. Anatomy of the pleural space SC: Systemic capillaries PC: Pulmonary capillaries Dr. Canmao xie
Figure 2. pleural fluids turnover PF enter the pleural space through parietal & visceral pleurae, And leave pleural space through lymphatics in parietal pleura Dr. Canmao xie
The passage of protein-free liquid across the pleural membranes is dependent on the hydrostatic and oncotic pressures across them.
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.
Mechanism of pleural fluids turnover Dr. Canmao xie
Figure. Diagrammatic representation of the pressures involved in the formation and absorption of pleural fluid. Parietal Pleura Visceral Pleura Space Pleura Hydrostatic Pressure + 30 - 5 + 24 35 29 6 0 Net 29 29 + 34 + 5 +34 Oncotic Pressure Dr. Canmao xie
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 and exudative pleural effusions.
A transudative pleural effusion occurs when alterations in the systemic factors that influence pleural fluid movement result in a pleural effusion. Examples are elevated visceral pleural capillary pressure with left heart failure, elevated parietal pleural capillary pressure with right heart failure, and decreased serum oncotic pressure with the nephrotic syndrome, hepatic cirrhosis.
In contrast, exudative pleural effusions occur when the pleural surfaces themselves are altered. Inflammation of the pleura, leading to increased protein in the pleural space, is the most common cause of exudative pleural effusions.
The first fluid accumulates in the lowest portion of the thoracic cavity, which is the posterior costophrenic angle. Therefore, 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 said to be 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 proved useful in making this differentiation.
Dr. Canmao xie
A posteroanterior and lateral chest radiograph of pleural effusion blunting of the posterior costophrenic angle Dr. Canmao xie
If the patient possibly has a transudative pleural effusion, it is most cost-effective to only measure the pleural fluid protein and LDH levels initially.
If the effusion is transudative, additional tests provide no additional information and sometimes produce misleading positive results.
Additional tests to consider ordering on exudative pleural fluids include smears and cultures for bacteria, cell count with differential, glucose levels, a pleural fluid markers for tuberculosis and pleural fluid cytology.
Although the pleural fluid LDH does not help differentiate various exudative pleural effusions, it is an indicator of the degree of pleural inflammation and should be measured each time pleural fluid is sampled from an undiagnosed pleural effusion.
Pleural LDH>500u/L indicates a possibility of neoplastic pleural disease or secondary pleural bacterial infection.
If the patient has a parapneumonic or a malignant pleural effusion, a pleural fluid pH (using a blood gas machine) is indicated.
A pleural fluid pH below 7.20 in patient with a parapneumonic effusion is an indicator for drainage of the effusions.
A pleural fluid pH below 7.20 in a patient with a malignant pleural effusion indicates that the patient’s life expectancy is only about 30 days and that chemical pleurodesis is likely to be ineffective.
Cytologic examination of the pleural fluid is a fast, efficient and minimally invasive means by which this diagnosis can be established.
There have been many studies evaluating the utility of tumor markers such as CEA, CA 15-3, CA 19-9, and ENOLAS
If cutoff set high enough, there is no false positives, then it is very insensitive.
In order to be useful, the tumor marker must be complimentary to the pleural fluid cytology – The diagnostic GOLD standard for malignant pleural effusion.
Since a blind needle biopsy of the pleura adds little to cytology in diagnosing pleural malignancy, thoracoscopy is the procedure of choice for the patient with suspected malignancy and negative cytology.
If tuberculous pleuritis is not treated, the effusion will resolve but pulmonary or extrapulmonary tuberculosis subsequently develops in more than 50%.
Since less than 40% of patients with tuberculous pleuritis have positive pleural fluid cultures, alternative means such as the level of adenosine deaminase (ADA), gamma interferon or polymerase chain reaction (PCR) are used to establish the diagnosis.
The pleural fluid ADA level above 45 IU/L is significant in establishing the diagnosis of tuberculous pleuritis.
At the onset of tuberculous pleuritis, most patients also have pleuritic chest pain.
Tuberculosis toxic syndrome– dry cough, low grade fever, night sweat and losing body weight.
With a positive tuberculin skin test (PPD) and significantly high ADA level in pleural effusion.
The fluid is invariably an exudate. Frequently the pleural fluid protein is over 50 g/L and this finding is very suggestive of tuberculous pleuritis. The differential white cell count reveals more than 80% lymphocytes.
Pleural biopsy has its greatest utility in establishing the diagnosis of tuberculous pleuritis. The demonstration of granuloma in the parietal pleura is highly suggestive of tuberculous pleuritis. Caseous necrosis or acid-fast bacilli need to be demonstrated.
Anti-tuberculosis chemotherapy: Adequate therapy for tuberculous pleuritis is a 9--month course of isoniazid and rifampin daily.
The performance of the therapeutic thoracentesis is highly recommended as soon as the diagnosis is confirmed.
The administration of corticosteroids will rapidly relieve the patient's symptoms of pleuritic chest pain, malaise, and fever and does not seem to lead to dissemination of the tuberculosis. Markedly symptomatic patients should be started on prednisone 40 mg/day and then gradually tapered over several weeks.
Therapeutic thoracentesis with or without a chest tube.
Mechanisms of pleurodesis not clearly understood. In general, an inflammation producing agent is injected into the pleural space. Resulting inflammatory reaction leads to pleural fibrosis such that the visceral and parietal pleurae fuse.
Talc, Tetracycline Derivatives (Tetracycline, Doxycycline), Antineoplastic drugs (Bleomycin, Mitoxantrone, Nitrogen mustard) are the choice of pleurodesis agents.