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Access myPennMedicine For Patients and Visitors. Patient Information. Conditions Treated A-Z. Pleural Effusion. Tuberculous pleuritis is thought to represent primarily a hypersensitivity reaction to tuberculous protein, and the bacillary burden in the pleural space is low.
Patients usually present with an acute illness. The most frequent symptoms are cough, which is nonproductive and associated with chest pain, which is usually pleuritic in nature. The pain usually precedes the cough. Effusions are usually unilateral and can be of any size. On rare occasions, pleural tuberculosis can present with pleural-based nodules and thickening. The fluid is serous or hemorrhagic with formation of coagulum.
Pleural fluid glucose may be reduced, but is usually similar to the serum level. The pH is usually above 7. The lactate dehydrogenase level in pleural fluid is usually higher than that in serum. Presence of eosinophils or mesothelial cells is unlikely.
Intense lymphocytic infiltration covers both pleural surfaces and prevents the mesothelial cells from entering the pleural space. However, these are superior to adenosine deaminase in the diagnosis of tuberculous pleuritis and can be used as a routine test in the diagnostic workup of patients with pleural effusions in areas with a high prevalence of tuberculosis.
More than 8 weeks after the development of symptoms, the skin test is almost always positive. The skin test may become negative in patients with immunosuppression and HIV infection. Without treatment, tuberculous pleuritis usually resolves spontaneously, but the patient frequently develops active tuberculosis at a later date. An empyema or empyema-like fluid occurs due to bacterial infection in the pleural space.
An effusion is called an empyema when the concentration of leucocytes becomes macroscopically evident as a thick and turbid fluid, ie, pus. Accumulation of exudative pleural fluid associated with an ipsilateral pulmonary infection that does not look like pus but satisfies the above is called empyema-like fluid.
Adenosine deaminase is elevated and its activity in tuberculous empyema is determined by isoenzyme ADA Patients usually suffer from an acute febrile illness, anemia, and digital clubbing. Anerobic infections tend to present with a more subacute or chronic condition. Loculated effusions can be confirmed by lateral decubitus X-ray or ultrasonography.
The American Thoracic Society delineates three progressive phases of empyema, ie, an early exudative phase, an intermediate fibrinopurulent phase, and a late organizing phase. When pleural inflammation is intense, its resolution may be associated with deposition of a thick layer of dense fibrous tissue on the visceral pleura, a condition known as fibrothorax. As a result of marked pleural thickening, the hemithorax becomes contracted and its mobility is reduced.
As it progresses, the intercostal spaces narrow and the mediastinum may be displaced ipsilaterally. Radiologically this presents as opaque minihemithorax, perhaps with calcification on the inner aspect of peel. A bronchopleural fistula can be detected early if there is continuous air leak through an intercostal drainage tube and amphoric breathing on auscultation.
The diagnosis can be confirmed by the methylene blue test Figure 11 , bronchoscopy, and CT thorax with maximum intensity projection images for demonstration of a fistula.
Bronchoscopy may be useful for therapeutic closure of a proximal fistula or to ascertain the condition of the bronchi. CT thorax helps to confirm the diagnosis and in detection of a mass or foreign body in the vicinity, which may be helpful in the preoperative assessment if the patient needs closure of a bronchopleural fistula.
Malignant pleural effusion can result from primary malignancies of the pleurae or with intrathoracic and extrathoracic malignancies that reach the pleural space by hematogenous, lymphatic, or contiguous spread. It is defined by the presence of malignant cells in the pleural space; for which fluid needs to be sent for cytology units of heparin in 20 mL of fluid.
Patients with cancer can develop pleural effusion as an indirect effect of cancer, even when cancer cells are absent from the pleural space. These effusions are known as paraneoplastic or paramalignant pleural effusions. They can result from mediastinal lymph node tumor infiltration, bronchial obstruction, radiochemotherapy, pulmonary embolism, superior vena cava syndrome, 79 or decreased oncotic pressure.
Chest radiography showing massive pleural effusion increases the probability of a malignant etiology. Radiographic signs of a malignant pleural effusion include circumferential lobulated pleural thickening, crowding of the ribs, and elevation of the hemidiaphragm or ipsilateral mediastinal shift consistent with lung atelectasis due to airway obstruction by a tumor. Management of malignant pleural effusions begins with therapeutic thoracocentesis. If symptoms do not improve with large-volume thoracocentesis, alternative causes of dyspnea should be considered.
These could be microtumor emboli, lymphangitic cancer, the effects of chemotherapy or radiotherapy, or pulmonary thromboembolism. The removal of a large volume of pleural fluid could rapidly expand atelectatic lung regions beyond their capacity to reinflate and cause alveolar capillary injury, resulting in re-expansion pulmonary edema.
Immunocytochemistry, as an adjunct to cell morphology, is becoming increasingly helpful in distinguishing benign from malignant mesothelial cells and mesothelioma from adenocarcinoma. Fluid is generally serous or turbid, and exudative with lymphocytic predominance. Polymorphonuclear predominance is seen in the early stages.
Distinction between rheumatoid effusions and empyema becomes difficult, but findings of elevated pleural fluid rheumatoid factor titer and low C 4 complement levels 0.
These effusions are self-limiting over several weeks. Sometimes pleural thickening with fibrothorax develops and requires decortication. These complement fragments increase vascular permeability, allowing fluid and proteins to escape into the pleural space. The pathogenesis of amebic pleural effusion is related to diaphragmatic irritation resulting in sympathetic effusion or rupture of an amebic hepatic abscess through the diaphragm into the pleural space.
Chest radiography shows an elevated right hemidiaphragm, plate-like atelectasis, and small right pleural effusion. Usually it is right-sided effusion and the fluid is the color of anchovy sauce, exudative, and with polymorphonuclear predominance.
Ultrasonography is diagnostic, showing abscess in the liver with disruption of the diaphragm. Entamoeba histolytica can be isolated from the fluid. Hydatid cyst disease is caused by the larval stage of Echinococcus granulosus. Extrapleural hydatid cysts are rare and can be located in the fissures, pleural cavity, chest wall, mediastinum, myocardium, and diaphragm.
CT scanning is the main diagnostic tool for thoracic hydatidosis. Pancreatitis-related pleural effusions are largely due to the close proximity of the pancreas to the diaphragm. Effusions can occur with either acute or chronic pancreatitis with different clinical presentation, management, and prognosis.
Mechanisms involved in the pathogenesis include direct contact of pancreatic enzymes with the diaphragm, giving rise to sympathetic effusion, transfer of ascitic fluid via transdiaphragmatic lymphatics or diaphragmatic defects, communication of a fistulous tract between a pseudocyst and pleural space, and retroperitoneal movement of fluid into the mediastinum with mediastinitis or rupture into the pleural space.
Fluid is a hemorrhagic exudate with polymorphonuclear predominance. The pH is 7. In acute pancreatitis, effusions are small, with an increase in both serum and pleural fluid amylase. These effusions resolve rapidly once the pancreatitis resolves. There is massive effusion in chronic pancreatitis due to rupture of pseudocyst with pancreaticopleural fistula. There is also an increase in pleural fluid amylase in chronic pancreatitis, but serum amylase is normal.
Patients typically present with a history of repeated episodes of alcoholic pancreatitis. Pancreatic calcifications on ultrasonographic or CT scans are diagnostic. These are usually small effusions and are immunological in origin.
Fluid is dark, with yellow exudates and a small number of lymphocytes. Pleural fluid amylase is low and glucose is similar to blood glucose. Hepatitis B surface antigen and e antigen can be detected in the fluid. Effusion generally resolves prior to resolution of hepatitis. The pleural fluid findings in spontaneous esophageal rupture will depend on the degree of perforation and the timing of thoracocentesis in relation to the injury.
Early thoracocentesis without mediastinal perforation will show sterile serous exudates with polymorphonuclear predominance. Pleural fluid amylase and pH will be normal. Once the mediastinal pleura tears, amylase of salivary origin will appear with higher concentration. As the pleural space is seeded with anerobes from the mouth, the pH may reduce to approximately 6. Squamous epithelial cells and food particles will be present. A pleural effusion that contains chyle is known as a chylothorax.
DeMeester classified chylothorax into congenital, traumatic, neoplastic, and miscellaneous. Pleuritic chest pain and fever are uncommon because chyle is not irritating to the pleural surface. The severity of symptoms depends on the size of the chylothorax. The course of the thoracic duct explains why injury to the duct above the level of the fifth thoracic vertebra usually produces left-sided chylothorax and injury below that level produces a right-sided chylothorax. A chylothorax is an odorless exudate with a predominance of lymphocytes.
Electron microscopy shows chylomicrons. Chylomicrons stain with Sudan III stain. Chylothorax needs to be differentiated from pseudochylothorax. Pseudochylothorax is more likely to result from long-standing pleural effusion. High cholesterol levels are typical of a pseudochylous pleural effusion. Rheumatoid arthritis and trapped lung are rare causes. In the event of pseudochylothorax, there will be clearing of fluid as a result of dissolution of cholesterol with ether.
In , Meigs and Cass reported seven patients with ovarian fibroma associated with ascites and hydrothorax. This syndrome can occur with other tumors of the ovary. The fluid moves into the pleural space through small diaphragmatic lymphatics, because of the pressure gradient across the diaphragm. The fluid is a yellow-colored exudate with a paucity of mononuclear cells.
Radiation therapy can cause pleural effusion by two mechanisms, ie, radiation pleuritis and systemic venous hypertension or lymphatic obstruction from mediastinal fibrosis. Bachman and Macken have reported patients with carcinoma of the breast who developed ipsilateral pleural effusions due to radiation pleuritis. Patients are either asymptomatic or complain of pleuritic chest pain. The effusion is usually hemorrhagic with multiple reactive mesothelial cells.
Pleural effusions can result from radiation therapy not associated with radiation pleuritis. These effusions tend to occur 1—2 years following completion of intensive mediastinal radiation. Mechanisms for development of pleural effusion as a late complication of radiation therapy include constrictive pericarditis, superior vena cava obstruction, and lymphatic obstruction. A trapped lung occurs when a fibrous membrane covers a portion of the visceral pleura, preventing that part of the lung from expanding to the chest wall.
The diagnosis should be suspected in an asymptomatic individual with a chronic unilateral effusion that recurs rapidly following thoracocentesis. The effusion is a serous transexudate with a small number of mononuclear cells. CT scan shows the split pleura sign, confirming the diagnosis.
Patients with congestive heart failure and pleural effusion present with orthopnea, paroxysmal nocturnal dyspnea, and on examination have fine crackles. Chest X-ray shows cardiomegaly and bilateral pleural effusions, generally the right effusion being larger than the left.
These are transudative effusions but may present with transexudates in patients who are on diuretic therapy. The pleural to serum-effusion albumin gradient will be greater than 1.
Hence they are of high diagnostic value in the diagnosis of heart failure-related pleural effusion. Therapeutic tapping is needed only if the patient has respiratory embarrassment. In patients with clinical or radiological evidence of congestive heart failure, investigation of the effusion need not go any further. Hepatic hydrothorax is a pleural effusion that develops in a patient with pulmonary hypertension in the absence of cardiopulmonary disease. Effusion is caused by passage of ascitic fluid from the peritoneal cavity into the pleural space through diaphragmatic defects.
It is usually a serous or hemorrhagic transudate, with predominantly lymphocytes and mesothelial cells. Pleural fluid and ascitic fluid show similar biochemistry. Increasing effusion is often associated with a decrease in ascitic fluid.
Peritoneal dialysis is frequently associated with small bilateral pleural effusions, but occasionally massive right pleural effusions are seen.
Fluid is serous and generally resembles dialysate. Rapid movement of radiolabeled tracer from the peritoneal to pleural cavity confirms the diaphragmatic defect if there is doubt about diagnosis. Alternative hemodialysis should be used. Pleural effusion secondary to obstructive uropathy is known as urinothorax.
Pleural fluid can be right-sided or left-sided, depending on the side of obstructive hydronephrosis. Urinothorax occurs due to perinephric urine leak, which passes through diaphragmatic defects to pleura.
It smells like urine. Effusion resolves with treatment of the primary problem. These are self-limiting effusions where diagnostic thoracocentesis is not required. Patients present with acute symptoms of febrile illness, dry cough, and chest pain. Radiological findings may show associated pneumonia. These are small effusions, ie, serous exudates with few mononuclear cells.
However, acute viral pleurisy may present with polymorphonuclear predominance. Effusions are self-limiting, and usually resolve within 2 weeks. Postcardiac injury syndrome was first described in the s in patients undergoing mitral commissurotomy and other cardiac surgeries.
The cause of postcardiac injury syndrome is still unclear, although there is some evidence to support an immunological or viral origin. The degree of myocardial damage does not correlate directly with the development of postcardiac injury syndrome, which also implies an immunological basis for the syndrome.
Small effusions resolve spontaneously. Salicylates, other nonsteroidal anti-inflammatory drugs, or corticosteroids should be used for the symptomatic patient or those with large-to-moderate symptomatic pleural effusion. These effusions are seen in postoperative patients especially following upper abdominal surgery and in patients in medical intensive care units.
Patients may present with fever and breathlessness. Effusion is transudative, but over a time it may change to exudate. They are self-limiting effusions for a short period when the underlying cause is treated. Effusions occur due to asbestos exposure. Prevalence is dose-related and varies from 0. Pleural effusion can be early, occurring in the first year or can be late, occurring after 20 years. The majority of patients are asymptomatic, and are discovered usually on routine chest radiography.
Pleural biopsy is frequently required to rule out other causes of pleural effusions, including mesothelioma. The usual pathological findings are a chronic fibrous pleurisy with minimal cellularity. Effusions resolve without treatment within a month to a year, with a mean duration of 3—4 months, and recurrence is common.
A long-term follow up of 3 years is required to exclude malignancy for a fully established diagnosis of benign nature. The effusions are transudative and could be related to left ventricular dysfunction and congestive heart failure.
Effusions are incidental findings and resolve spontaneously. Patients with hypothyroidism develop pleural effusions from other causes or related to their state of reduced thyroid function, such as pericardial fluid, congestive heart failure, or ascites.
Normal pregnancy could promote transudation of fluid into the pleural space because of increased hydrostatic pressure in the systemic circulation, increased blood volume, and decreased colloid osmotic pressure.
Atelectasis from a gravid uterus could also lead to accumulation of pleural fluid. Treatment of the specific cause, drainage of fluid, pleurodesis, and surgical management are the therapeutic options for pleural effusion. The specific treatment of pleural effusion depends on the etiology. Treatment of the underlying cause helps resolve most transudative effusions. Effusions associated with connective tissue disorders like rheumatoid arthritis and systemic lupus erythematosus are treated with steroids, and resolution may occur within 2 weeks.
Tuberculous pleural effusions are treated with short-course antituberculosis therapy, ie, 2 months of isoniazid, rifampicin, pyrazinamide, and ethambutol, followed by 4 months of isoniazid and rifampicin. Controlled trials have shown no benefit of using steroids along with antituberculosis therapy. Amebic pleural effusions are treated with metronidazole mg three times daily for 5—10 days followed by diloxanide furoate mg three times daily for 10 days.
Pleural hydatidosis needs surgical management with excision of cysts and decortication, along with albendazole mg once daily for one month prior to surgery.
At the time of opening of the parietal pleura, care should be taken to avoid accidental incision over a cyst, because the intrapleural cysts lie immediately below the parietal pleura. This article will look at what happens in pleural effusion, why it occurs, and some options for resolving it. When a person has pleural effusion, it means that fluid has collected in the space between their lungs and chest cavity, or pleural cavity.
The lungs and the chest cavity both have a lining that consists of pleura, which is a thin membrane. In healthy lungs, these membranes ensure that a small amount of liquid is present between the lungs and chest.
This prevents friction as the lungs expand and contract during breathing. Anyone who may have pleural effusion needs immediate medical attention, as it can be life threatening without treatment. Pleural effusion always results from another condition.
Many conditions can cause it. Here are some of the most common causes :. Some people do not experience any symptoms of pleural effusion.
If symptoms do occur, they typically start to appear as fluid fills the chest cavity. Persistent hiccups may also be a symptom of pleural effusion. Some people only find out they have pleural effusion when they undergo a test for another condition. Also, it is important to note that the symptoms of pleural effusion can resemble those of other lung conditions.
A person needs prompt medical help if they experience any of these symptoms. Explore the model using your mouse pad or touchscreen to learn more about this condition. It can be challenging to diagnose pleural effusion , as the symptoms may overlap with those of many other conditions. The healthcare professional will also need to determine whether the effusion is transudate or exudate. The sections below will look at these types in more detail.
To further help with diagnosis, a doctor may extract a sample of the excess fluid to be tested to determine the cause. The best way is to treat the cause of the effusion.
If the cause is pneumonia, a doctor will likely prescribe antibiotics to treat the infection, which may also cause the fluid to go away. If fluid build-up has been caused by congestive heart failure, a physician will likely prescribe diuretics, such as Lasix, for treatment.
For large pleural effusions, or for those with an unknown cause, the fluid will need to be drained through a procedure called thoracentesis. This involves inserting a needle in the space between the lung and the chest wall and draining the liquid. In these cases, a doctor may also send a sample of fluid to be tested for other causes, such as lung cancer, for example. Some patients may require a pleural drain that is inserted through the skin so that the buildup of fluid can be drained repeatedly without the need for repeated thoracentesis.
For lung cancer patients, he explains, the buildup is likely to occur again.
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