Pleural effusion

Pleural effusion

1. ETIOPATHOGENESIS AND DIAGNOSTIC APPROACH TO PLEURAL EFFUSION Chairperson –Dr. Chandrashekar K Student- Dr. Vinod Kumar L

2. ANATOMY OF THE PLEURA The pleura is the serous membrane that covers the lung parenchyma, the mediastinum, the diaphragm, and the rib cage. This structure is divided into the visceral pleura and the parietal pleura. Visceral and the parietal pleura meet at the lung root.

3. A film of fluid (pleural fluid) is normally present between the parietal and the visceral pleura. This thin layer of fluid acts as a lubricant and allows the visceral pleura covering the lung to slide. The space, or potential space, between the two layers of pleura is designated as the pleural space. (18-20micron) The mediastinum completely separates the right pleural space from the left in humans.

4. HISTOLOGY OF THE PLEURA The parietal pleura is composed of loose, irregular connective tissue covered by a single layer of mesothelial cells. Blood, lymph vessels and nerves are located in the connective tissue. Visceral pleura is composed of two layers: the mesothelium and connective tissue. Blood, lymph vessels and nerves are located in the connective tissue.

5. PARIETAL PLEURA

6. PLEURAL FLUID Volume The total pleural fluid volume in humans is around 0.26 mL/kg Rate of production – 0.01ml/kg/hr Maximum rate of absorption – 0.2ml/kg/hr

7. PHYSICOCHEMICAL FACTORS Small amount of protein is normally present in the pleural fluid - 1 to 1.5 g/dL Ionic concentrations in pleural fluid differ significantly from those in serum. Bicarbonate concentration is increased by 20% to 25% relative to that in plasma whereas the major cation (Na•) is reduced by 3% to 5%, and the major anion (Cl-) is reduced by 6% to 9%. The concentration of K• and glucose in the pleural fluid and plasma appears to be nearly identical.

8. BLOOD SUPPLY TO THE PLEURA The parietal pleura receives its blood supply from the systemic capillaries. The venous drainage of the parietal pleura is primarily by the intercostal veins, which empty into the inferior vena cava or the brachiocephalic trunk.

9. In general, the blood supply to the visceral pleura originates from the systemic circulation through the bronchial arteries. Bronchial artery supplies most of the visceral pleura and a small portion is through the pulmonary artery . The venous drainage of the visceral pleura is through the pulmonary veins.

10. PLEURAL LYMPHATICS The lymphatic vessels of the costal pleura drain ventrally toward nodes along the internal thoracic artery and dorsally toward the internal intercostal lymph nodes near the heads of the ribs. The lymphatic vessels of the mediastinal pleura pass to the tracheobronchial and mediastinal nodes, whereas the lymphatic vessels of the diaphragmatic pleura pass to the parasternal, middle phrenic, and posterior mediastinal nodes.

11. The lymphatic vessels in the parietal pleura have many branches. Some submesothelial branches have dilated lymphatic spaces called lacunas .Stomas are found only over the lacunas. At the stoma, the mesothelial cells with their microvilli are in continuity with the endothelial cells of the lymphatic vessels. These stomas with their associated lacunas and lymphatic vessels are thought to be the main pathway for the elimination of particulate matter from the pleural space .

12. No stomas are seen in the visceral pleura, and the lymphatic vessels of the visceral pleura are separated from the mesothelial cells by a layer of connective tissue. The lack of stomas in the visceral pleura explains that fluid from the pleural space does not enter the lymphatics in the visceral pleura in humans.

13. INNERVATION OF THE PLEURA Sensory nerve endings are present in the costal and diaphragmatic parietal pleura. The intercostal nerves supply the costal pleura and the peripheral part of the diaphragmatic pleura. When either of these areas is stimulated, pain is perceived in the adjacent chest wall.

14. In contrast, the central portion of the diaphragm is innervated by the phrenic nerve. Stimulation of this pleura causes the pain to be perceived in the ipsilateral shoulder. The visceral pleura contains no pain fibers.

15. PHYSIOLOGY OF THE PLEURAL SPACE PLEURAL FLUID FORMATION Fluid that enters the pleural space can originate in the pleural capillaries, the interstitial spaces of the lung, the intrathoracic lymphatics, the intrathoracic blood vessels, or the peritoneal cavity.

16. Pleural Capillaries The movement of fluid between the pleural capillaries and the pleural space is believed to be governed by Starling's law of transcapillary exchange

17. Normally the fluid in pleural space due to capillaries is governed by starling forces. But in disease states more fluid can accumulate from interstitium . With increasing levels of interstitial fluid, it has been shown that the subpleural interstitial pressure increases.

18. The barrier to the movement of fluid across the visceral pleura appears to be weak, even though the visceral pleura is thick. Therefore, once the subpleural interstitial pressure increases, it follows that fluid will traverse the visceral pleura to the pleural space.

19. Peritoneal Cavity Pleural fluid accumulation can occur if there is free fluid in the peritoneal cavity and if there are openings in the diaphragm. Under these conditions, the fluid will flow from the peritoneal space to the pleural space because the pressure in the pleural cavity is less than the pressure in the peritoneal cavity.

20. Thoracic Duct or Blood Vessel Disruption If the thoracic duct is disrupted, lymph will accumulate in the pleural space, producing a chylothorax . The rate of fluid accumulation with chylothorax can be more than 2500 mL/day. In a like manner, when a large blood vessel in the thorax is disrupted owing to trauma or disease, blood can accumulate rapidly in the pleural space, producing a hemothorax.

21. PLEURAL FLUID ABSORPTION Lymphatic Clearance The pleural space is in communication with the lymphatic vessels in the parietal pleura by means of stomas in the parietal pleura. No such stomas are present in the visceral pleura. Proteins, cells, and all other particulate matter are removed from the pleural space by these lymphatics in the parietal pleura .

22. Clearance through Capillaries in Visceral Pleura Several hundred milliliters of water probably traverse the pleural membranes each day, but the net movement is of only a few milliliters because the osmolarity is nearly identical on each side of the membrane.

23. Transudate vs Exudate Light's criteria : 1 . Pleural fluid protein divided by serum protein greater than 0.5 2. Pleural fluid LDH divided b y serum LDH greater than 0.6 3 . Pleural fluid LDH greater than two thirds of the upper limit of normal serum LDH

24. DIAGNOSTIC APPROACH

25. Pleural transudates Increased hydrostatic pressure Congestive cardiac failure Constrictive pericarditis Pericardial effusion Constrictive cardiomyopathy Massive pulmonary embolism Decreased capillary oncotic pressure Cirrhosis Nephrotic syndrome Malnutrition Protein-losing enteritis Small bowel disease

26. Transmission from peritoneum Any cause of ascites Peritoneal dialysis Liver transplantation Increased capillary permeability Small pulmonary emboli Myxoedema Obstructed lung lymphatics Lung transplantation

27. Pleural exudates Neoplasms Mesothelioma, very rarely pleural sarcoma Metastases Lymphoma Infections Pneumonia, abscess Tuberculosis AIDS Hantavirus syndrome Fungal and actinomycotic disease Subphrenic abscess Hepatic amoebiasis

28. Immune disorders Post-myocardial infarct/cardiotomy syndrome Rheumatoid disease Systemic lupus erythematosus Wegener’s granulomatosis Rheumatic fever Abdominal diseases Pancreatitis Uraemia Other causes of peritoneal exudates

29. Pulmonary embolism and infarction Other causes Sarcoidosis Drug reactions Radiation therapy Asbestos exposure Recurrent polyserositis Yellow nails syndrome Oesophageal rupture

30. Chest film showing left pleural effusion

31. PLEURAL TRANSUDATES Most common cause is cardiac failure This effusion is often unilateral initially, usually on the right side In severe cases, bilateral Mechanism - increased pulmonary interstitial pressure increased capillary pressure transudation of fluid from the lung.

32. Pulmonary embolism Transudative, but blood staining occurs in ¼ of cases These are often bilateral and small Associated with dome shaped or linear pulmonary shadows

33. Hypoproteinemia Cirrhosis Nephrotic syndrome and Protein malnutrition Constrictive pericarditis ( old TB, Rheumatoid disease, malignant infiltration of the pericardium) and constrictive cardiomyopathies are usualy associated with ascitis This fluid tracks up into the right pleural space through small defects in the diaphragm producing a large unilateral effusion.

34. Meigs syndrome Benign ovarian fibroma Ascitis right sided pleural effusion Myxoedema Consequence of ascitis or pericardial effusion Rarely direct effect on pleural capillary permeability

35. PLEURAL EXUDATES Neoplasms Mesothelioma Mets from bronchial, breast, stomach and ovarian Ca Malignant effusions are usually but not always blood stained

36. Infections Bacterial pneumonia is associated with effusion in 40% of cases Tuberculosis Viral and mycoplasma

37. PARAPNEUMONIC EFFUSIONS AND EMPYEMA Any pleural effusion associated with bacterial pneumonia, lung abscess, or bronchiectasis is a parapneumonic effusion . An empyema , by definition, is pus ( thick, purulent )in the pleural space

38. PATHOPHYSIOLOGIC FEATURES divided into three stages exudative stage fibropurulent stag organization stage

39. BACTERIOLOGIC FEATURES Aerobic organisms are isolated slightly more frequently than anaerobic organisms S. aureus and S. pneumoniae account for approximately 70% of all aerobic gram-positive isolates. When there is a single aerobic gram-positive organism in the pleural fluid, it almost always is S. aureus , S. pneumoniae , or Streptococcus pyogenes .

40. gram-positive aerobic organisms are isolated approximately twice as frequently as are gram-negative aerobic organisms. Escherichia coli is the most commonly isolated gram-negative aerobic organism, Klebsiella sp, Pseudomonas sp, and Hemophilus influenzae are the next three most commonly isolated aerobic gram-negative organisms, and these three organisms account for approximately 75% of all aerobic gram negative empyemas with a single organism.

41. Bacteroides sp and Peptostreptococcus are the two most commonly isolated anaerobic organisms from infected pleural fluid. it is uncommon for a single anaerobic organism to be isolated from pleural fluid. In patients with community-acquired pneumonia, the organisms most commonly responsible were Streptococcus intermedius- anginosus - constellatus ( milleri ) group , S. pneumoniae, and other streptococcus species , S. aureus ( methicillin resistant Staphylococcus aureus [MRSA]), gram negatives , and anaerobes

42. In patients with hospital acquired parapneumonic effusions, the most common organism was S. aureus ( MRSA ). Streptococcus intermediusanginosus-constellatus ( milleri ) was also the most common organism isolated in culture positive complicated parapneumonic effusions. In the intensive care unit, gram-negative aerobic organisms are most likely to be responsible, with K.pneumonia being the most common organism .

43. TUBERCULOUS PLEURAL EFFUSIONS When a tuberculous pleural effusion occurs in the absence of radiologically apparent TB, it may be the sequel to a primary infection 6 to 12 weeks previously or it may represent reactivation TB. The tuberculous pleural effusion is thought to result from rupture of a subpleural caseous focus in the lung into the pleural space . DELAYED HYPERSENSITIVITY plays a large role in the pathogenesis of tuberculous pleural effusion.

44. Extensive right pleural calcification following tuberculosis effusion

45. Fatal left pyopneumothorax due to extensive pulmonary tuberculosis

46. IMMUNE DISORDERS Rheumaoid arthritis- within 5 yrs of start of disease Straw colored or turbid Low glucose and pH and high LDH Rheumatoid factor and immune Complexes may be found at higher titres than blood Thoracoscopy shows highly characteristic granular appearance

47. Systemic lupus erythematosis Bilateral small effusions Lupus cell High titre of antinuclear antibodiesin the fluid is diagnostic Fluid blood stained with normal glucose and low LDH

48. ABDOMINAL DISEASES Acute pancreatitis Transmission of inflammation through adjacent diaphragm and of fluid through diaphragmaic lymphatics . High amylase levels more than serum.

49. YELLOW NAILS SYNDROME Hypoplasia of lymphatic vessels Lymphedema Dystrophic changes in nails Intractable pleural effuusion Complicated by bronchiectasis , sinusitis or protein losing enteropathy .

50. DRUGS Practolol sulphonamides Salicylates Β blockers Para aminosalicylic acid Methylsergide Nitrofurantoin

51. CLINICAL FEATURES Symptoms Small effusions are often symptomless Very large effusions – pleuritic chest pain shortness of breath recurrent dry cough if fluid has accumulated quickly

52. Signs Since most effusions are on the dependent part of pleural space, diminished movements, dull note on percussion and absent breath sounds are found here. bronchial breath sounds or aegophony may be heard immediately above the effusion Large effusions displace the mediastinum to the opposite side

53. Investigations Pleural aspiration and biopsy Imaging Examination of the fluid

54. ABRAM’S NEEDLE

55. Macroscopic appearances Transudate- clear and pale straw-coloured Exudate –amber-coloured and may be turbid if the cell count is high. Uniform blood-staining, of a red or brown colour , frequently indicates pleural tumour , although infarction, rheumatoid, leukaemic and tuberculous effusions may be haemorrhagic. Milky fluid is usually due to chyle (see Purulent fluid in cases of frank empyema from that due to a high cell content. A fluid with a shimmering sheen may contain high levels of cholesterol

56. Microscopic appearances Infective cause in lung or pleura, other than tuberculosis- polymorphs are predominant. Tuberculosis – lymphocytes are predominant Pulmonary eosinophilia, polyarteritis nodosa, tropical eosinophilia, filariasis and Hodgkin’s- eosinophils are predominant Examination of the fluid for malignant cells

57. Biochemical tests protein content of pleural fluid 30g/L being taken as the dividing line between transudate and exudate cholesterol content is usually less than 55mg/dL and the fluid–blood ratio is 0.3 or below in transudates Glucose content may be low (<1.7mmol/L or 30 mg/dL) in infected effusions and rheumatoid disease Lactate dehydrogenase is raised in exudates above the serum level Amylase levels may be very high (>1000 u/L) in effusions due to pancreatitis and oesophageal rupture

58. Further diagnostic tests Ultrasound. CT scan. Thoracoscopy can be carried out using a rigid thoracoscope or video-assisted techniques with biopsy of any pleural lesions seen.

59. MANAGEMENT The management of pleural effusion depends on the cause. Infective effusions should be treated with the appropriate antibiotics and tube drainage may be necessary. Tuberculous effusions require antituberculosis and it is usual to add corticosteroids (prednisolone 20mg daily or 2–3 weeks, reducing over a further 2–4 weeks, speeds reabsorption and prevents pleural fibrosis, Corticosteroids- sarcoidosis, systemic lupus erythematosus, the post-cardiac injury syndrome and rheumatoid disease.

60. Large malignant pleural effusion-Promote pleurodesis, To prevent lung compression by instillation of 1. nitrogen mustard 2. radioactive colloidal gold 3. tetracycline SUCCESS RATE 60% 4. doxorubicin 5. quinacrine Use of Corynebacterium parvum

61. Pleural manifestations of asbestosis Pleural disease is the most common manifestation of asbestos exposure 1. pleural plaques 2. diffuse pleural thickening 3. rounded atelectasis 4. Asbestos related pleural effusion

62. Pleural plaques Focal round irregular white lesions found on parietal and rarely visceral pleura Asbestos fibers scratch, irritate and injure pleural surface leading to hemorrhage, inflammation and eventually fibrosis Most cases are asymptomatic but can result in decreased vital capacities in later stages

63. Imaging- Chest x-ray and CT CT scanning increases plaque detection rates Treatment- No specific treatment required They are markers of asbestos exposure and they identify

64. Diffuse pleural thickening Mechanisms – Confluence of large pleural plaques Extension of subpleural fibrosis to visceral pleura Fibrotic resolution of a benign pleural effusion Clinical features- Dyspnea on exertion Chronic dry cough Chest pain

65. Rounded atelectasis Rare complication Scarring of visceral and parietal pleuraand the adjacent lung Pleural surfaces fuse to one other and trap the underlying lung causing atelectasis Chest x ray- mass lesion which mimics lung cancer is seen. HRCT- diffuse pleural thickening , volume loss, comet tail of vessels and bronchi sweeping into wedge shaped mass.

66. Other complications Acute benign pleural effusion 2. Malignant mesothelioma 3. Lung cancer- all histologic types can occur but adenocarcinoma is the most common

67. Post radiation lung injury Mechanism Transient increase in reactive oxygen and nitrogen species Macrophage infiltration and proliferation Oxidative stress and Induction of interstitial fibrosis with regional tissue hypoxia.

68. Acute manifestation Erythematous mucosa with thickened secretions Irritative dry cough Resolution of symptoms within several weeks Chronic manifestations Pneumonitic process 6 weeks to 6 months following radiation Fever, cough congestion Hemoptysis , dyspnea , respiratory distress in severe cases

69. Diagnosis - bronchoscopy and lung biopsy Treatment- Asymptomatic- observation and symptomatic treatment Severe cases- antibiotics with glucocorticoids tailored to the severity of symptoms To be tapered slowly after patient is stabilized Response rate-20 to 100%

70. Complications of Pleural Effusion Empyema Pleural Fibrosis Pleural Thickening

71. REFERENCES CROFTON AND DOUGLAS’S RESPIRATORY DISEASES, 5 TH EDITION HARRISON’S PRINCIPLES OF INTERNAL MEDICINE, 20 TH EDITION. LIGHT’S PLEURAL DISEASES 6 TH EDITION

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