Carlos R. Salvarezza
The pleural sheets limit a space that contains a small amount of fluid that allows a smooth gliding of the lungs when moving. When the fluid volume increases, it causes the pleural syndrome.
The pleural cavity is limited by the visceral pleura, which covers the lung surface except for the hilum, and by the parietal pleura, which lines the wall that contains the lung (gums, mediastinum and diaphragm) .The mediastinal parietal pleura is reflected around the hilum continuing with the visceral and extending towards the diaphragm or its vicinity (pulmonary ligament). The right and left cavities are separated.
The pleural sheets are made up of five layers; the mesothelial cells of the innermost cells would synthesize hyaluronic acid that reduces the friction between the lung and the thoracic wall.
The visceral pleura is supplied by the bronchial artery and by some branches of the pulmonary artery, while the parietal one receives blood from the intercostal and internal mammary arteries.
The parietal pleura is drained by the bronchial veins that flow into the azygous and hemiazygous veins, and the visceral through the pulmonary veins. length of the mammary artery and internal intercostals and in the anterior and posterior mediastinal nodes.The parietal pleura and the lymphatics are connected by communications that measure between 2 and 12 microns in length, most of which are located in the cribriform membrane and in a dilation called the lymphatic lagoon.
Physiopathology of fluid transport through the pleura . The capillaries of the parietal pleura receive blood from the inercostal and internal mammary arteries, which develop a hydrostatic pressure of 30 cmm H2O and an oncotic pressure of 34 cm H2O. The hydrostatic pressure of the cavity is -5 cm H2O and the oncotic pressure is 5 cm H2O. Due to the pressure difference, a pressure of 6 cm H2O is generated that favors the passage of the parietal pleura into the pleural space.
The hydrostatic pressure of the capillaries of the visceral pleura is 11 cm H2O and the oncotic pressure is 34 cm H2O. A pressure of 13 cm H2O is created that directs the liquid from the cavity to the visceral leaf.
Another mechanism of fluid transport through the pleuta is that of the communications between the pleural cavity and the lymphatic channels and the lymphatic lagoon. These lymphatics have valves that act synchronously with respiratory movements, removing fluid and particles from the pleural cavity to the lymphatic lagoon. The contents of the lagoon are propelled to the proximal lymphatics by a similar mechanism.
Characteristics of the pleural fluid . The thickness of the liquid layer is 10 to 25 microns. The amount is difficult to establish, but the volume drawn from healthy volunteers was approximately 1ml. Production is estimated to be 100 ml per hour and absorption can reach 300 ml per hour.
The number of cells is 1500 to 4500 per milliliter, of which 60 to 70% are monocytes. Macrophages, lymphocytes and mesothelial cells are found in a variable percentage; Neutrophils are rarely detected.
The protein content varies between 1 and 2 g / 100 ml, and the pH is 7.64. the remaining elements were dosed in experimental animals and not in people.
Pleural fluid pathophysiology
Many diseases alter the normal mechanisms that maintain the low amount of pleural fluid constant, varying the volume and content. Schematically, pleural effusions are divided into transudates and exudates.
Transudated . They originate from increased hydrostatic pressure, decreased oncotive pressure, difficulty in bordering drainage, and passage of fluid from the peritoneum to the pleural cavity through the lymphatics that cross the diaphragm or through defects in it.
The protein content of the liquid is less than 3g / 100 ml, and the density is less than 1.016. the ratio between the concentration of pleutal and serum proteins is less than 0.5 and the concentration of the enzyme lactic dehydrogenase (LDH) is less than 200 IU / 100 ml; the relationship between pleural and serum LDH concentration is less than 0.6. the white blood cell count is less than 1000 per mm3 the alkaline pH.
The sediment is scarce and the liquid does not coagulate; it is colorless or slightly yellow and odorless.
The first five parameters are the most important.
Exudates . They are caused by increased cpaillary permeability of the visceral pleura, obstruction of lymphatic drainage, bronchopleural fistula, mediastinitis with or without rupture of the mediastinal pleura, direct communication between the pancreas and the pleural cavity, increased permeability of the capillaries of the diaphragmatic parietal peura, and tumor invasion of the pleural cavity.
The protein content of the liquid is greater than 3g / 100 ml and the density is greater than 1.016. the ratio between pleural and serum proteins is greater than 0.5 and LDH shows values above 200 IU; the relationship between pleural and serum LDH concentration is greater than 0.6 and the leukocyte count is greater than 1000 mm3. PG is weakly alkaline or acidic (relative to blood) and sediment is abundant. The liquid generally coagulates; It is colored and sometimes has an odor.
Pathophysiology of the different causes.
Transudated . Congestive heart failure is the most common cause of transudate. Left ventricular failure originates venocapillary hypertension with increased hydrostatic pressure of the visceral pleural capillaries. Right ventricular failure produces systemic venous hypertension that hinders lymphatic drainage and / or increases the hydrostatic pressure of the capillaries of the parietal pleura.
In constrictive pericarditis, the transudate is caused by heart failure. The etiology of pericarditis is multiple: tuberculosis, neoplasms, thoracic irradiation, trauma.
The effusion of liver cirrhosis with asccitis originates from the passage of fluid from the peritoneum to the pleural cavity through diaphragmatic defects and / or transdiaphragmatic lymphatics, possibly due to negative pleutal pressure. Hypoproteinemia in cirrhotics is a minor mechanism in the production of pleural fluid.
The nephrotic syndrome generates effusion in advanced stages of the disease, when the patient has generalized edema and ascites. The mechanism would be twofold: oncotica decreased by hypoproteinemia.
40% of pulmonary embolisms present with effusion and 25% of these are transudate. The cause is right heart failure that occasionally produces pulmonary embolism.
Other diseases that rarely cause transudate are acute glomerulonephritis, ovarian tumors, urinary tract obstructions, and myxedema.
Exudates . Paraneumonic effusion may or may not present pus (empyema), and is generally associated with pneumonia, abscesses, and abscessed bronchitis. The microorganisms that predominate in the pleural fluid of parapneumic effusions are streptococci, pneumococci, Haemophilus influenzae, staphylococci, viruses and mycoplasmas; anaerobes and gram-negative empyemas. The fluid accumulates in the pleura due to an alteration of the capillaries and / or rupture of the visceral plura. Neutrophils are mostly in the pleural fluid.
In tuberculosis, exudates are formed due to an increase in the permeability of the visceral pleura or due to tupture of a peripheral parenchymal focus (bronchopleural fistula). Neutrophils predominate in the early stages, but later lymphocytes.
Pulmonary embolism produces pleural effusion due to alteration of the permeability of the capillaries of the visceral pleura. Most of the elements of the pleural fluid are lymphocytes and red blood cells.
Secondary pleural carcinoma is much more frequent than the primary one. Regarding the secondary ones, the tumors that most often generate metastases in the pleura are bronchogenic carcinomas in men and breast carcinomas in women. The fluid accumulates due to decreased lymphatic drainage (neoplastic pleural thickening) or due to invasion of lymph nodes that compress the thoracic duct. Among the primary neoplasms, the variety called diffuse msothelioma is the one that presents with pleural effusion. The fluid originates from decreased lymphatic drainage due to thickening of the pleural leaves.
Lymphocytes and red blood cells predominate in both varieties.
Regarding acute pancreatitis, it must be remembered that the tail of the pancreas directly contacts the diaphragm, so that when this organ becomes inflamed, it produces an exudate rich in enzymes that penetrates the lymphatics that cross the diaphragm and the parietal pleura to that level, reaching the pleural space. Effusion increases because as the diaphragm becomes inflamed, the permeability of the parietal pleura increases.
In chronic pancreatitis, the liquid collections of the organ (pseudocysts) form paths between the pancreas and the pleural space; other times the pancreatic fluid passes through the esophageal and / or aortic hiatuses and reaches the mediastinum, where it breaks the mediastinal pleura, causing one or bilateral pleurisy. In pancreatopathy with ascites, the same occurs as in cirrhotics with ascites. Neutrophils and red blood cells predominate in all varieties.
Subphrenic abscesses originate liquid collections located below the diaphragm, which they inflame, increasing the permeability of the capillaries of the parietal pleura. Another mechanism in the formation of pleural fluid is the passage of fluid through diaphragmatic defects. Most elements of the pleural fluid are neutrophils.
The most common pulmonary vasculitis are rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), progressive systemic sclerosis, dermatomyositis, and Wegener's granulomatosis. Some of them (RA and SLE) generate effusion due to increased permeability of the capillaries of the visceral pleura. Lymphocytes predominate, although neutrophils may be the majority in the acute phase.
Perforation of the esophagus causes esophagoscopy, trauma, or spontaneously. It causes an infectious mediastinitis that ruptures the mediastinal pleura and gives rise to a pleurasia in whose fluid neutrophils predominate.
Postcardiac injury syndrome is caused by myocardial infarction, cardiac surgery, thoracic trauma, pacemaker implantation, or transcutaneous left ventricular puncture. The lung, pleura, and pericardium are involved. The effusion is generated by increased permeability of the capillaries of the visceral pleura; in the liquid the neutrophils prevail in the first days and then the lymphocytes.
Exceptionally, pleural effusion is observed in actinomycosis, nocardiasis, sarcoidosis and intrahepatic abscesses.
Symptoms and signs.
Symptoms depend on the amount of fluid accumulated, the rate of production, the previous ventilatory function, and the disease that caused the syndrome.
Pain is one of the most frequent symptoms. It is located in the affected hemithorax, although it can radiate to the abdomen, neck and shoulder. Like most chest pain, it increases in intensity with breathing movements and coughing. The pain disappears when the pleural sheets separate due to the accumulation of fluid, and is generally lacking in the transudates. The dyspnea is permanent or exertional, while the cough is dry and of variable intensity; usually transudates do not generate it.
The patient is usually positioned laterally on the affected hemithorax to allow better expansion of the healthy lung. In the altered area, a decrease in mobility can be observed.
Palpation detects diminished or abolished vocal vibrations in the area of the effusion. Above these, they are normal or are increased because the lung parenchyma is condensed by the effusion. Occasionally a pleural fremitus is palpated.
On percussion, submatidity or dullness is noted in the area corresponding to that occupied by the effusion and in the adjacent spinal column. In medium-volume liquid collections, the upper percutory limit of dullness is at the level of the scapula and the lower one at the vertebral column. A concave curve is formed upwards and inwards (Damoiseau's parabolic curve or Ellis's line). This curve is usually missing in transudates and empyemas.
The percutaneous slope sign is the most important semiological maneuver to detect pleural fluid collections of medium and small volume. It is investigated by percussion of the anterior or posterior part of the affected hemithorax (preferably the posterior area, since the posterior cul-de-sac is the deepest) while the patient is seated. The upper limit of dullness is marked, then the patient is laid on his stomach, waiting a few minutes for the liquid to move and percuss again. If the cavity contains fluid, it moves to the front of the chest and the dullness clears.
Auscultation confirms a decrease or abolition of respiratory sound in the area of the effusion, a sound that is normal or is increased in intensity above. A bronchial sound is usually found at the upper limit of medium volume effusions. Occasionally a pleural rub may be heard.
A pleural effusion can be diagnosed when the patient consults for chest pain, dyspnea, and dry cough, and the physical examination reveals percutaneous dullness, positive signs of unevenness, absence of respiratory sound, and a bronchial sound. Usually not all the elements of the syndrome are found and then other diagnostic methods are used to confirm the suspicions and certify the etiology of the pleural effusion.
Radiological examination . The chest X-ray from the front shows a homogeneous density opacity that blurs the diaphragm and the corresponding cardiac border, occupying the costophrenic and cardiophrenic cul-de-sac. The upper limit is concave upward and inward in medium-volume effusions, while in transudates and empyemas it is usually horizontal.
When it is voluminous, the opacity occupies the entire hemithithorax and displaces the mediastinum to the opposite hemithorax. Small liquid collections are not detected or are only externalized by an occupied costophrenic cul-de-sac and / or by a thickening of the parietal pleura.
In the profile radiograph , the opacity observed is of lower density and extends from the rib cage to the vertebral column, erasing the corresponding hemidiaphragm and the anterior and posterior costophrenic cul-de-sac.
The CT scan to diagnose small spills that are not detected on chest radiographs conventional front-profile. Its indication is limited. Thoracic ultrasound is exceptionally indicated to study pleural effusions.
The scintigraphy and pulmonary arteriography are used to investigate a pulmonary embolism as a probable cause of pleural effusion. The echocardiography is performed as suspected pleural liquid is related to congestive heart failure or pericarditis.
Thoracentesis . It is a simple and easy method to perform that allows to certify the presence of fluid in the pleural cavity and study its characteristics, in order to reach the diagnosis. Another indication for pleutal puncture is the removal of large volumes of fluid to relieve dyspnea in large effusions. Once the liquid is extracted, it is examined macroscopically and microscopically.
Macroscopic examination of the pleural fluid . Observe the color and odor, and if the puncture is evacuating, the amount extracted. This test generally orients towards the etiological diagnosis.
Color . It can be light yellow in the serofibrinous exudates that are frequently caused by tuberculosis, vasculitis, neoplasms, pulmonary embolism; colorless or slightly yellow in the transudates; cloudy in parapneumonic effusions of bacterial origin; purulent in empyemas also generated by some bacteria; serohematico, in the effusions produced by tuberculosis, neoplasia, lung infarction, acute pancreatitis; hematic in thoracic trauma; milky in chylothorax and pseudokylothorax; and chryslatin in hydatid pleurisy.
Smell . Anaerobic empyemas can be fetid because the metabolism related to these germs gives rise to short-chain fatty acids such as valeric and butyric.
Quantity . It is generally rare in pulmonary embolism, vasculitis, subphrenic abscesses, and postcardiac injury syndrome. Fluid collections are usually large in neoplasms, large-cavity empyemas, and chylothorax.
Microscopic examination of the pleural fluid . The liquid is divided and sent for various tests.
Microbiological. Look for aerobic and anaerobic bacteria (parapneumonic effusions and empyemas) and acid-fast bacilli (tuberculosis).
Mycological. The presence of histoplasma, coccidioides, blastomyces, cryptococcus is investigated.
Anatomopathological. Neoplastic cells are researched.
Cytological. In this test, the following are investigated: a) concentration of red blood cells: when it is greater than 100,000 per mm3, the etiology is pleural carcinoma, thromboembolism or thoracic trauma; b) leukocyte concentration: less than 1000 per mm3 orients towards a transudate, greater than 1000 mm3 is an indication of exudate; c) leukocyte formula: lymphocytes predominate in tuberculosis, pleural carcinoma, vasculitis and postcardiac injury syndrome; Neutrophils are the majority in bacterial and pancreatic effusions and those produced by subphrenic abscesses and esophageal perforation; An eosinophil concentration greater than 10% can be detected in hydropneumothorax, pulmonary eosinophilia, hydatidosis, tuberculosis, and pleural carcinoma; d) LE cells are occasionally found in systemic lupus erythematosus.
Physiochemical examination . Density, protein concentration, and LDH figures are useful for differentiating transudates from exudates.
Low glucose values relative to serics (less than half) are found in rheumatoid arthritis, bacterial effusions, pleural carcinomas, and tuberculosis.
The pH is low in bacterial pleurisy, pleural carcinomas, rheumatoid arthritis, and systemic lupus erythematosus.
Amylase concentration is elevated in pleural fluids in acute pancreatitis and in perforated esophagus.
Complements, immune complexes, chylomicrons, cholesterol, hyaluronic acid, minerals, etc. can also be investigated.
Pleural needle biopsy . Parietal pleural portions are obtained with the COPE and Abrams needles. They are sent to the bacteriologist for direct examination and culture of acid-fast bacteria and bacilli, and to the pathologist to look for neoplastic tissues. It is indicated in all effusions without etiological diagnosis.
Fiberoptic bronchoscopy . It is carried out in all effusions in which the etiological diagnosis has not been established with the previous procedures. Positivity is killer when pleiresias are associated with parenchymal abnormalities.
Laparoscopic hepaticam puncture, abdominal computed tomography. They are performed in patients with liver or pancreatic diseases that present with pleural effusions.
Explorer thoracotomy. This procedure is indicated exceptionally since with the methods previously analyzed, the etiological diagnosis of pleural effusions is reached in most cases.
Pleurisy . It is the name given to pleural effusions when the liquid is an exudate.
Hydrothorax . It is the name of pleural effusions when the liquid is transudated.
Encysted pleurisy . It is one in which the pleural cavity is blocked by adhesions that isolate the liquid collection from the rest of the cavity. The etiology is usually infectious.
Non-cystic pleurisy of selective location . The pleural effusion simulates a raised diaphragm or an enlarged cardiac image or suspended opacities. The cause of the location of the fluid in the diaphragmatic, mediastinal and fissural pleura is unknown.
Quilothorax . It is the accumulation of liquid with abundant chylomicrons. The etiology can be neoplastic (carcinomas, lymphomas), traumatic or idiopathic.
Pseudochylothorax or cholesterin pleurisy . In this pleural effusion, the cholesterol content is very high. The most common causes are tuberculosis and rheumatoid arthritis.