CHAPTER 10 The pleura is a thin, serous membrane comprising of the visceral pleura, which covers the lungs and the mediastinum, and the parietal pleura which lines the inside of the thoracic cage and diaphragm. Chapter 2 has more details on the anatomy and physiology of the lung. Pleural fluid is filtered from blood in the capillaries supplying the parietal pleura down a pressure gradient into the pleural space. Pleural fluid drains out of the pleural space through stomata in the parietal lymphatics which lie between the parietal mesothelial cells. These stomata merge into small lymphatic channels which form larger vessels which connect areas of the parietal, mediastinal and diaphragmatic pleura, ultimately draining into the mediastinal lymph nodes. In health, there is a thin layer of pleural fluid in the pleural space, approximately 1–5 ml and 10 μm thick, which acts as a lubricant, allowing expansion of the lungs without friction. There is a turnover of 1–2 L of pleural fluid each day. More pleural fluid is secreted at the apices of the lungs and more fluid is resorbed at the bases as there are a greater number of parietal lymphatics in the diaphragm and mediastinum. In health, pleural fluid contains the same amount of protein and glucose as interstitial fluid, but a lower amount of sodium and a greater amount of lactate dehydrogenase (LDH). Pleural fluid also contains mesothelial cells, macrophages, and lymphocytes. The pH of healthy pleural fluid is 7.6. Water and small molecules move passively between the layers while larger particles are transported across by cytoplasmic transport mechanisms. A pleural effusion is fluid in the pleural cavity. A pleural effusion occurs if more fluid is produced than is resorbed. A pleural effusion can be unilateral or bilateral. Analysis of pleural fluid and applying Light’s criteria can differentiate between an exudate and a transudate. Box 10.4 summarises what constitutes an exudate and a transudate. There are many different causes for an exudative and transudative pleural effusion. The main symptom associated with a pleural effusion is breathlessness. The patient may also complain of chest pain and other symptoms depending on the cause of the effusion. It is important to elicit the following information from the history: (Boxes 10.1 and 10.2). Figure 10.1 shows the BTS diagnostic algorithm for investigation of a unilateral pleural effusion. There are several clinical signs that indicate a pleural effusion (Box 10.3). Figure 10.1 BTS diagnostic algorithm for investigation of a unilateral pleural effusion. Chest X‐ray (CXR): A pleural effusion with more than 300 ml fluid can be seen on a postero‐anterior (PA) CXR as an area of whiteness. The fluid accumulates at the lung base because of gravitational forces, so the costophrenic angle is usually obliterated first. If the effusion is extensive, the CXR can show as a complete ‘white‐out’ of the hemithorax. A small effusion, with only 50 ml of fluid, may be detected on a lateral decubitus CXR (Figure 10.2). A pleural effusion may be difficult to detect on a CXR taken when the patient is supine, for example, on the intensive care unit (ICU), as the fluid lies posteriorly. An ultrasound may be better at detecting fluid under these circumstances. Figure 10.2 CXR showing a unilateral (right‐sided) pleural effusion. In a patient with congestive cardiac failure (CCF), bilateral pleural effusions can occur and there may be other radiological evidence of heart failure, such as an enlarged heart, Kerley B lines and fluid in the horizontal fissure. Thoracic ultrasound is an essential investigation in the management of a pleural effusion as it is more sensitive than a CXR at identifying small effusions, including sub‐pulmonic effusions (Figure 10.3). Thoracic ultrasound is also better at differentiating between pleural fluid and pleural thickening. Features such as septation seen on thoracic ultrasound may help distinguish between an exudate and a transudate and between a malignant and a benign pleural effusion with greater sensitivity than a contrast CT scan. Thoracic ultrasound is also essential for successful and safe thoracocentesis. Figure 10.3 Thoracic ultrasound scan showing a pleural effusion with underlying lung atelectasis. CT thorax with contrast should be conducted if the fluid is an exudate and if there are other abnormalities on the chest X‐ray, such as a mass (Figure 10.4). Ideally, the CT scan should be done before the pleural fluid is completely drained. Septation, due to fibrin deposition, appears as suspended air bubbles. Contrast CT can reliably distinguish between an empyema and a lung abscess, as the former appears as a lenticular opacity with pleural enhancement around it. Contrast enhancement of the pleura can distinguish between benign and malignant pleural thickening, with malignant pleura showing areas of pleural nodularity. Mediastinal, parietal, and circumferential pleural thickening of >1 cm suggests a malignant process. Pleural enhancement can also occur when there is inflammation of the pleura secondary to infection. A CT thorax with contrast is essential if a surgical pleural biopsy is required and in the management of complicated pleural infections, including empyema. Figure 10.4 CT thorax showing a unilateral (right‐sided) pleural effusion. An MRI is not routinely required in the management of a pleural effusion but can distinguish between a malignant and a benign pleural effusion when CT with contrast is contraindicated. An MRI can also give anatomical information about chest wall and diaphragmatic involvement when the effusion is secondary to malignancy, especially if surgery is being contemplated. A PET‐CT is not routinely used in the management of a pleural effusion as there are many false positives but, as with MRI, can be occasionally used for staging when there is a malignant pleural effusion. This is an essential investigation in the diagnosis of a pleural effusion and should be conducted using direct ultrasound guidance as this increases the chance of successful aspiration, reduces the need for repeated aspiration, and reduces the risk of pneumothorax and injury to the heart, liver, and spleen. A 21G fine bore needle attached to a 50 ml syringe should be used. Appendix 10.A describes the methodology of pleural fluid collection. Table 10.1 describes the analysis of pleural fluid. Table 10.1 Analysis of pleural fluid from thoracocentesis. Classification of the fluid into either an exudate or a transudate is essential for diagnosis and further management. This can be done by applying Light’s criteria (Box 10.4). Histological and microbiological analysis of pleura is essential in the management of an exudate as this can usually distinguish between malignancy, infection, and benign pleural fibrosis. Pleural biopsy can be obtained through an Abram’s needle, with a CT‐guided biopsy or a VATS biopsy. An Abrams needle biopsy with a local anaesthetic is only recommended if mycobacterium tuberculosis is strongly suspected, if there is diffuse pleural enhancement on a contrast CT scan, and alternative methods of obtaining tissue are not feasible. Generally, this method of obtaining pleural tissue has a low yield and a high complication rate and is done much less now than it was a few years ago. A CT‐guided percutaneous pleural biopsy, which is less invasive than a surgical biopsy, can be performed if there is obvious pleural disease on imaging and if the patient is not fit for surgery. This has a better yield than an Abram’s blind biopsy and is much safer. A CXR is required after any invasive procedure to ensure that there is no iatrogenic pneumothorax. A thoracoscopic pleural biopsy has the best yield and is a safe procedure. A therapeutic pleurodesis can be carried out at the same time if indicated, for example, for a malignant pleural effusion, avoiding two separate procedures. A medical thoracoscopic pleural biopsy with local anaesthetic and sedation can be carried out by a trained respiratory physician and is a safer procedure than a blind pleural biopsy, with a reasonable yield of 92% in experienced hands. The main complications are infection and haemorrhage. A VATS pleural biopsy, carried out by a thoracic surgeon, is the investigation of choice for a patient with an exudate, so long as they can tolerate a general anaesthetic. The pleura can be directly visualised, and this gives the best yield of 95%, with a low complication rate. If there is a trapped lung, this can be freed, and a talc pleurodesis can be conducted at the same time as the biopsy. Bronchoscopy is indicated if the patient with an exudative pleural effusion presents with haemoptysis, if aspiration pneumonia or inhalation of a foreign body is suspected, or if there are radiological changes suggestive of an endobronchial lesion. A transudate occurs either due to an increase in the hydrostatic pressure in the parietal pleura or due to reduced oncotic pressure of the fluid, usually from hypoalbuminaemia. Table 10.2 lists the differential diagnosis of a transudate. Table 10.2 Differential diagnosis of a transudate. Management of a transudate is that of the underlying condition. Bilateral pleural effusions are usually transudates, most commonly secondary to CCF. The BTS guidelines do not recommend pleural aspiration in this situation unless there are atypical features, or the effusion does not respond to diuretics. CT thorax and pleural biopsy are not required in most cases of a transudate. An exudate occurs when there is increased permeability of the capillaries, usually due to inflammation, with reduced fluid resorption. Table 10.3 lists the differential diagnosis of an exudate. Table 10.3 Differential diagnosis of an exudate. Malignant cells reach the visceral pleura either haematogenously or through the lymphatic network and spread to the parietal pleural through pleural adhesions. Malignant cells, cytokines, and vascular endothelial growth factor (VEGF) increase endothelial permeability, disrupt the lymphatic network, and promote angiogenesis, thereby causing accumulation of fluid, which is often blood‐stained. Involvement of the regional lymph nodes is usually associated with the presence of a pleural effusion. The presence of malignant cells in the pleura or pleural fluid suggests advanced metastatic disease with a median survival of 3–12 months, depending on the cancer. The commonest cause of a malignant pleural effusion in men is lung cancer (40%) and in women is breast cancer (17%). Other causes of a malignant pleural effusion include lymphoma, tumours of the gastrointestinal system, and tumours of the genitourinary system. In 10% of cases of a malignant pleural effusion, no primary malignancy is identified. A large pleural effusion is most likely to be malignant, but in 25% of cases of a malignant pleural effusion, the patient is asymptomatic. Overall, 60% of malignant effusions can be diagnosed by pleural fluid cytology, with a greater diagnostic rate for adenocarcinoma of the lung than for mesothelioma or other types of lung cancers. Measurement of tumour markers in pleural fluid is not routinely done for lung cancer. Mesothelin levels may be elevated in epithelioid mesothelioma. A pH < 7.3 in a malignant pleural effusion confers a worse prognosis and a lower chance of successful pleurodesis. Malignant pleural effusions recur within weeks after drainage and repeated aspirations are not ideal in most cases. There are several therapeutic options which will depend on the fitness of the patient and their overall prognosis. Patients who are relatively asymptomatic from their effusion can be observed. In symptomatic patients who have a poor performance status and life expectancy of only a few weeks, repeated pleural aspirations can be carried out as a palliative procedure to remove some fluid to improve breathlessness. Patients who are not surgical candidates should have a small bore intercostal chest drain inserted to remove 500 ml to 1.5 L of fluid in a controlled way to avoid re‐expansion pulmonary oedema. A low‐pressure, high‐volume suction device and regular flushing may be helpful. Chemical pleurodesis using talc, bleomycin or tetracycline should be considered as this will reduce the chance of recurrence, even if the effusion cannot be completely drained because of a trapped lung. Patients who have a reasonable performance status and life expectancy of at least several months should have a VATS pleurodesis, as any trapped lung can be freed and the outcome is better, with fewer complications. A systematic review of 46 randomised controlled trials (RCTs) with 2053 patients concluded that talc pleurodesis was associated with fewer recurrences than bleomycin or tetracycline and that a thoracoscopic pleurodesis was better than a pleurodesis done via an intercostal chest drain. Patients with a recurrent malignant pleural effusion who cannot have a medical or surgical pleurodesis because of poor performance status or a trapped lung, should have a tunnelled pleural catheter (PleurX) inserted. This will improve symptoms and allow the patient to go home. Rarely, when pleurodesis fails, a pleuroperitoneal shunt can be considered. Pleural infection is an infection in the pleural space. Empyema is frank pus in the pleural space. The annual incidence of pleural infection in the UK and the USA is 80 000 cases. Pleural infections are commoner in the very young, the elderly, and commoner in men compared to women. The morbidity and mortality of pleural infection are high, especially for empyema, which has a mortality of 20%. Prompt diagnosis and management by an expert reduce the morbidity and mortality. Box 10.5 lists the risk factors for developing pleural infections and empyema. Most pleural infections result from sub‐optimally treated pneumonia, with progression of a parapneumonic effusion to frank empyema. Over 50% of patients with community acquired pneumonia (CAP) develop a parapneumonic effusion which usually resolves over a few weeks with prompt antibiotic treatment. If there is a delay in treatment or if there are underlying risk factors, some parapneumonic effusions can progress to pleural infection and empyema. Iatrogenic causes of pleural infection include any pleural intervention, especially repeated aspirations, thoracic surgery, oesophageal surgery, and oesophageal perforation. Although the majority of parapneumonic effusions resolve with antibiotic treatment, some can progress through a fibrinopurulent stage to an empyema. Pro‐inflammatory cytokines increase capillary vascular permeability resulting in fluid entering the pleural cavity. If the patient does not receive prompt antibiotics at this stage, then bacteria invade the pleural cavity, followed by neutrophils. There is activation of the coagulation cascade with deposition of fibrin, causing septation. The increased metabolic activity in the pleural space results in an increase in LDH, a decrease in the glucose content of the fluid, a lactic acidosis, and a decrease in the fluid pH. There is gradual organisation of the fluid with fibroblast proliferation and the formation of a pleural peel, which can encase the lung and reduce lung expansion. Hypoalbuminaemia (<30 g l−1), thrombocytosis (platelet count >400 × 10 9 l−1) and hyponatraemia (sodium <130 mmol/L) predispose to the development of an empyema. Pleural infection should be suspected in any patient with a pneumonia who fails to improve after 3 days of antibiotic treatment, with continuing fever and high CRP. Table 10.4 describes the process whereby a simple parapneumonic effusion becomes an empyema. Table 10.4 Pathophysiology of pleural infection. Appendix 10.A describes how pleural fluid should be collected for analysis. Pleural infections can be complicated, have a high morbidity and mortality, and should be managed by a respiratory physician and a thoracic surgeon. Poor prognostic factors include older age, co‐morbid disease, poor nutrition, and a serum albumin of less than 30 g l−1. Pleural fluid should be sent in a blood culture bottle as this increases the diagnostic yield of anaerobic infections. Samples will be culture positive in 60% of cases and this guides antibiotic treatment. When pleural fluid cultures are negative, blood cultures may be helpful in 15% of cases. Pleural fluid samples should always be stained for acid‐fast bacilli (Ziehl‐Neelsen stain) and sent for Mycobacterium tuberculosis culture. Community acquired pleural infections are usually secondary to community acquired pneumonia. The commonest infections are Gram positive organisms, such as Streptococcus milleri and Staphylococcus aureus, which account for 65% of cases. Co‐infection with anaerobic infections occurs in up to 76% of cases, often associated with aspiration pneumonia or poor dental hygiene and can have a more insidious onset. Gram‐negative organisms, such as Enterobacteriaceae, Escherichia coli and Haemophilus influenza, can occur in patients with co‐morbidities. Hospital acquired pleural infections are often associated with pleural or other interventions. Staphylococcus aureus and methicillin‐resistant Staphylococcus aureus (MRSA) infections account for two‐thirds of these cases. Gram‐negative infections, such as Escherichia coli, Enterobacter Spp and Pseudomonas Spp occur in older, immunocompromised patients and have a high morbidity and mortality. Fungal empyema, which is usually due to candida, is uncommon (<1%) and occurs in the immunocompromised. Prompt antibiotics should be prescribed for empyema after discussion with the microbiologist, taking note of local prescribing guidelines and resistance patterns. Penicillin antibiotics with beta lactamase inhibitors, metronidazole and cephalosporins, which have good penetration into the pleural space, are usually the first choice. Patients with a penicillin allergy should be prescribed clindamycin. Macrolides are not usually required and aminoglycosides do not penetrate the pleural space well. Intravenous antibiotics should be given for at least 48 hours followed by oral antibiotics for up to 6 weeks, until there is complete resolution of symptoms, normalisation of inflammatory markers and radiological improvement. Intra‐pleural antibiotics are not recommended. A chest drain should be considered in all patients who show no clinical improvement after 3 days of treatment with antibiotics, with continuing fever, high respiratory rate, and high CRP (Figure 10.5). Indications for a chest drain include pleural fluid pH < 7.2, frank pus in the pleural cavity, pleural fluid glucose of <2.2 mmol/L, and features of a complicated effusion on thoracic ultrasound, such as septation and loculation. Figure 10.5 CT thorax showing right‐sided empyema with inserted drain. The BTS and the National Patient Safety Agency (NPSA) recommend that a small bore (10–14F) chest drain is inserted using thoracic ultrasound guidance (Figure 10.6). Regular flushing with 20–30 ml of normal saline every 6 hours, together with suction of −20 cm H2O, is recommended. Figure 10.6 Thoracic ultrasound scan of empyema with air‐bubbles post aspiration. There are no clear, evidence‐based guidelines as to when a patient with an infective pleural effusion should be referred for surgery, although there is some evidence that surgery may have better long‐term outcome than more conservative approaches. Patients who have clinical evidence of persistent sepsis and radiological evidence of infection despite antibiotics and a chest drain for more than 4 or 5 days should be discussed with a thoracic surgeon. A patient who is compromised because of a fibrinous peel causing compression of the lung may also warrant surgical decortication. The thoracic surgeon will need to decide between a VATS procedure and a thoracotomy with decortication depending on the fitness of the patient, their co‐morbidities, and the extent of the pleural disease. The use of intrapleural fibrinolytic drugs in the management of pleural infection is controversial. A large British RCT did not find any long term benefit with intrapleural streptokinase, with no reduction in the need for surgical intervention, length of stay or mortality, but with significant side effects of fever and malaise. Some argue that this was because a heterogeneous group of patients, at various stages of organisation of the pleural fluid, were included. Several smaller RCTs using streptokinase and urokinase have reported benefits, with increased volume of fluid drained and reduced need for surgical decortication compared to placebo. A Cochrane meta‐analysis with a small number of trials also concluded that intrapleural fibrinolytic drugs reduced the hospital stay, and resulted in radiological and symptomatic improvement. The BTS recommendation is that intrapleural fibrinolytic drugs should not be given routinely to patients with pleural infection. However, fibrinolytic drugs could be used by experienced physicians in selected patients, for example, in elderly patients who have a complex, loculated effusion who are unfit for surgery. Some 13% of patients with a pleural infection and empyema develop pleural thickening which can, over time, become calcified. In rare cases, a bronchopleural fistula can develop. An extensive fibrothorax can cause breathlessness and a restriction in breathing. If severe, patients may require surgical decortication. Empyema necessitans results from a disruption of the parietal pleura, with spontaneous discharge of the pleural contents into the subcutaneous tissue of the chest wall. The commonest cause is Mycobacterium tuberculosis. Actinomycosis and aspergillus can also be the causative organisms. A CXR will show a soft tissue density. Management is surgical drainage and a prolonged course of antibiotics. An exudative pleural effusion with a high lymphocyte count and low glucose is a common presentation of mycobacterium tuberculosis infection. The number of organisms in the fluid is very low, and acid‐fast bacilli will be detected in less than 5% of cases. The pleural fluid culture has a slightly better yield of 10–20%. If a tuberculous effusion is suspected, it is essential to obtain pleural biopsies for microbiological staining and culture. This will be positive in 70% of cases and will give information about drug sensitivities and resistance, thus dictating therapy. If TB is suspected, the pleural fluid should be sent for adenosine deaminase testing, an enzyme present in lymphocytes, which is elevated (>45 U l−1) and has a sensitivity of 92% and specificity of 90%. This test may be a particularly useful in those with HIV or those who are immunosuppressed. Pleural fluid should also be sent for unstimulated interferon‐gamma levels and PCR. Interferon‐gamma release assays (IGRA) are more expensive and have not been validated for the diagnosis of pleural TB. TB is discussed in more detail in Chapter 8. Although rheumatoid arthritis is commoner in women compared to men, pleural effusion associated with rheumatoid arthritis is commoner in men. Acute rheumatoid pleurisy can occur in 50% of cases and the exudate will have a very low glucose of <1.6 mmol/L, a high lymphocyte count, and low C4 complement levels. A chronic rheumatoid effusion may present as a pseudochylous effusion with a high cholesterol level and the presence of cholesterol crystals. A third of patients with a pulmonary embolus will develop either a unilateral, or bilateral small exudates. Pulmonary emboli should be suspected in patients whose symptoms of breathlessness are out of proportion to the size of the effusion. Thromboembolic disease is discussed in Chapter 11. Chylothorax is the accumulation of chyle, which is lymphatic fluid of intestinal origin, in the pleural cavity. It appears as a milky pleural fluid which remains milky after centrifuging. It occurs as the result of damage to the thoracic duct, often after thoracic surgery (particularly oesophageal), malignancy or disorders of the lymphatic system. The diagnosis is confirmed by the presence of chylomicrons in the pleural fluid or elevated triglyceride levels of >1.24 mmol/L. Lymphangiography and a CT scan are essential to identify where the lymph is coming from. Management depends on the cause and includes conservative management, drainage of chyle with pleurodesis, a period of fasting, a high protein‐low fat diet supplemented by medium chain triglycerides, octreotide analogues, such as somatostatin, and surgical repair of the thoracic duct. Pseudo chylothorax can occur in rheumatoid arthritis and with mycobacterium tuberculosis infection. The fluid appears milky, as with a chylothorax, but there are cholesterol crystals in the fluid. This condition, unlike the other asbestos‐related pleural diseases, has a much shorter latency period, occurring 10–20 years after asbestos exposure. It is also dose‐related, so more likely to occur with a greater exposure to asbestos. The patient is usually asymptomatic and presents with a small, unilateral, bloody, effusion, which resolves within 6–12 months, leaving diffuse pleural thickening. As the differential diagnosis for this presentation includes mesothelioma, patients will require surgical pleural biopsies, perhaps several, and long term follow‐up before mesothelioma can be excluded. In about 8% of cases no obvious cause for the effusion is identified. Most of these will resolve spontaneously. A pneumothorax is air in the pleural space, either from air leaking through a hole in the lung or from a penetrating chest injury. The sudden entry of air into the pleural space causes collapse of the underlying lung. The incidence of primary spontaneous pneumothorax is 10/100 000/year, with a male to female ratio of 5 : 1. PSP occurs in patients with apparently normal lungs, although high resolution CT scan shows apical sub‐pleural blebs and bullae in 90% of cases (Box 10.6). The aetiology of these blebs is unclear.
Pleural disease
Abbreviations
Normal pleura and pleural fluid
Pleural effusion
Definition
Aetiology of pleural effusion
Clinical assessment of a patient presenting with a pleural effusion
Diagnostic pathway for management of a unilateral pleural effusion
Investigations for a pleural effusion
Pleural Aspiration (Thoracocentesis)
Measurement
Result of pleural fluid analysis
Appearance
Serous (clear)
Turbid suggests infection or empyema
Pus suggests empyema
Milky suggests chylothorax or pseudo chylothorax
Blood‐stained suggests malignancy, mesothelioma, pulmonary embolus with infarction, trauma, or post‐cardiac surgery
Bloody: if the pleural fluid haematocrit is >50% of the blood haematocrit, then it is classified as a haemothorax.
Odour
Malodour suggests anaerobic infection
Biochemistry
Pleural fluid protein and pleural fluid protein/serum protein ratio
Pleural fluid lactate dehydrogenase (LDH) and pleural fluid LDH/serum LDH ratio
Pleural fluid glucose will be low (<3.3 mmol/L) in a chronic effusion with a pleural fluid/serum glucose ratio < 0.5.
Common causes of a low fluid glucose include empyema, malignancy, or mycobacterium tuberculosis infection.
Rheumatoid arthritis is associated with a very low fluid glucose level < 1.6 mmol/L
Cytology
Malignant cells may be detected in 60% of malignant effusions
Differential cell count may be helpful, but is very non‐specific and not diagnostic
Neutrophilia (>50%) suggests an acute process. This includes parapneumonic effusions secondary to a bacterial infection, pulmonary embolus, acute mycobacterium tuberculosis infection or benign asbestos pleural effusion
Lymphocytosis (>50%) suggests a chronic effusion secondary to mycobacterium tuberculosis infection or malignancy. Significant lymphocytosis (>80%) suggests mycobacterium tuberculosis infection, lymphoma, sarcoidosis, chronic rheumatoid pleurisy, or post‐cardiac bypass surgery.
Eosinophilia (>10%) is usually due to air or blood in the pleural space but could indicate parapneumonic effusions, eosinophilic granulomatosis with polyangiitis, lymphoma, drugs, parasitic infestation, pulmonary infarction, or benign asbestos pleural effusion
Mesothelial cells predominate in transudates
Microbiology
Gram stain
Ziehl‐Neelsen stain
Microscopy, culture, and sensitivity, including TB culture
pH
Normal pleural fluid pH is 7.6
pH can vary significantly between locules in a complicated effusion
pH < 7.3 in chronic malignant effusions, rheumatoid arthritis, mycobacterium tuberculosis infection and oesophageal rupture
pH < 7.2 is the best indicator of an empyema and the need for a chest drain
pH > 7.6 when there is infection with proteus spp. which produces ammonia
Other tests as indicated
Adenosine deaminase if TB suspected (>45 IU l−1)
Polymerase chain reaction (PCR) for Mycobacterium tuberculosis
Interferon‐gamma assay for Mycobacterium tuberculosis
Pancreatic amylase if pancreatitis is suspected or salivary amylase for oesophageal rupture
Chylomicrons will be seen with a chylothorax (milky effusion)
Pleural fluid triglyceride level will be >110 mg dl−1 in a chylothorax
Pleural fluid cholesterol will be elevated in a pseudo chylothorax
Pleural biopsy
Differential diagnosis of a transudate
Management of a transudate
Differential diagnosis of an exudate
Management of malignant pleural effusion
Pleural infection and empyema
Definitions
Aetiology of pleural infection
Pathophysiology of pleural infection
Diagnostic tests
Simple parapneumonic effusion
Fibrinopurulent effusion
Empyema
Appearance of fluid
Clear
Turbid
Pus
Appearance on ultrasound
Fluid
Echogenic with septation and loculation
Fibrous pleural peel, multi‐loculated with numerous septation
Appearance on CT scan
No pleural thickening
Pleural thickening in 56%
Pleural thickening in 86–100%
Split pleura sign with enhancement of visceral and parietal pleura
Protein
>30 g l−1
>30 g l−1
>30 g l−1
LDH
50% of serum LDH
Raised
Markedly raised
Glucose
Normal
<2.2 mmol/L
<2.2 mmol/L
pH
7.6
<7.2
Unable to analyse
Differential cell count
Normal
Predominantly neutrophils
Predominantly neutrophils. If lymphocytes predominate, suspect mycobacterium tuberculosis infection
Organisms
None
Positive in 60%
Positive in 60%
Management
Antibiotics
Antibiotics and chest drain
Antibiotics and chest drain. Surgery for debridement and pleurodesis may be required
Management of pleural infection
Management
Antibiotics for pleural infection
Indications for chest drain insertion in pleural infection
Indications for surgery for pleural infection
Intrapleural fibrinolytic drugs
Long term sequelae of pleural effusion secondary to pleural infection
Mycobacterium tuberculosis pleural effusion (tuberculous effusion)
Rheumatoid arthritis pleural effusion
Pulmonary emboli and pleural effusion
Chylothorax
Benign asbestos pleural effusion
Idiopathic pleural effusion
Pneumothorax
Definition
Primary spontaneous pneumothorax (PSP)
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