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  1. 1. PLEURESY Aiyub medicine
  2. 2. Anatomy • parietal pleura - covers the inner surface of the thoracic cavity, including the mediastinum, diaphragm, and ribs. • visceral pleura - envelops all lung surfaces, including the interlobar fissures.
  3. 3. Anatomy • pleural space - coupling the movement of the chest wall with that of the lungs – relative vacuum in the space keeps the visceral and parietal pleurae in close proximity. – small volume of pleural fluid (0.13 mL/kg of body weight) serves as a lubricant – the volume of fluid is maintained through the balance of hydrostatic and oncotic pressure and lymphatic drainage.
  4. 4. Pleural syndromes • Dry pleuresy (pleuritis) • Pleuresy with effusion (hydrothorax, liquid pleural sdr.) • Pneumothorax (aeric pleural syndrome) • Hydropneumotorax (mixed pleural syndrome) • Fibrothorax (pahipleuritis)
  5. 5. DRY PLEURISY • Causes: – TB, RA, sarcoidosis, uremia, viruses (Coksackie) • Symptoms: – chest pain (a characteristic symptom )which becomes stronger during breathing and coughing. – Cough (is usually dry) – general indisposition; – the temperature (subfebrile)
  6. 6. DRY PLEURISY Physical signs • Respiration is superficial (deep breathing intensifies friction of the pleural membranes to cause pain). • Lying on the affected side lessens the pain. Inspection of the patient can reveal unilateral thoracic lagging during respiration. • Percussion fails to detect any changes except decreased mobility of the lung border on the affected side. • Auscultation determines pleural friction sound over the inflamed site.
  7. 7. Pleural effusion • Pleural effusion - is an abnormal collection of fluid in the pleural space resulting from excess fluid production or decreased absorption. • Pleural effusion is an indicator of an underlying disease process that may be pulmonary or nonpulmonary in origin and may be acute or chronic.
  8. 8. Ethiology • Altered permeability of the pleural membranes (eg, inflammation, malignancy, pulmonary embolus) • Reduction in intravascular oncotic pressure (eg, hypoalbuminemia, cirrhosis) • Increased capillary permeability or vascular disruption (eg, trauma, malignancy, inflammation, infection, pulmonary infarction, drug hypersensitivity, uremia, pancreatitis) • Increased capillary hydrostatic pressure in the systemic and/or pulmonary circulation (eg, congestive heart failure, superior vena cava syndrome)
  9. 9. Ethiology • Reduction of pressure in the pleural space, preventing full lung expansion (eg, extensive atelectasis, mesothelioma) • Decreased lymphatic drainage or complete blockage, including thoracic duct obstruction or rupture (eg, malignancy, trauma) • Increased peritoneal fluid, with migration across the diaphragm via the lymphatics or structural defect (eg, cirrhosis, peritoneal dialysis) • Movement of fluid from pulmonary edema across the visceral pleura • Persistent increase in pleural fluid oncotic pressure from an existing pleural effusion, causing further fluid accumulation
  10. 10. Epidemiology • The estimated prevalence of pleural effusion is 320 cases per 100,000 people in industrialized countries, with a distribution of etiologies related to the prevalence of underlying diseases
  11. 11. Epidemiology • In general, the incidence is equal between the sexes. • Certain causes have a gender predilection. – About two thirds of malignant pleural effusions occur in women. Malignant pleural effusions are significantly associated with breast and gynecologic malignancies. – Pleural effusion associated with systemic lupus erythematosus is also more common in women than in men. – Pleural effusions associated with chronic pancreatitis are more common in males, with the majority of male cases having alcoholism as the etiology. – Rheumatoid effusions also occur more commonly in males than in females.
  12. 12. Clinical presentations (symptoms) • Progressive dyspnea – the most common symptom associated with pleural effusion – is related more to distortion of the diaphragm and chest wall during respiration than to hypoxemia – may be caused by the condition producing the pleural effusion, rather than by the effusion itself • Cough – often mild and nonproductive – purulent or bloody sputum suggests an underlying pneumonia or endobronchial lesion
  13. 13. Clinical presentations (symptoms) • Pleuritic chest pain – raises the likelihood of an exudative etiology – may be mild or severe – localized to the chest wall or referred to the ipsilateral shoulder or upper abdomen, usually because of diaphragmatic involvement • Other symptoms could be suggestive for the underlying disease – increasing lower extremity edema, orthopnea, and paroxysmal nocturnal dyspnea – night sweats, fever, hemoptysis, and weight loss – acute febrile episode, purulent sputum production – hemoptysis
  14. 14. Clinical presentations (signs) • are variable and depend on the volume of the effusion. • no physical findings for effusions smaller than 300 mL.
  15. 15. Clinical presentations (signs) • Mediastinal shift away from the effusion - this is observed with effusions of greater than 1000 mL • Asymmetrical chest expansion, with diminished or delayed expansion on the side of the effusion
  16. 16. Clinical presentations (signs) • Decreased tactile fremitus, • Dullness to percussion, • Diminished or inaudible breath sounds • Egophony ("e" to "a" changes) at the most superior aspect of the pleural effusion • Pleural friction rub
  17. 17. Clinical presentations (signs) • Other physical findings suggestive for the underlying cause of the pleural effusion: – Peripheral edema, distended neck veins, and S3 gallop suggest congestive heart failure. – Edema may also be a manifestation of nephrotic syndrome; pericardial disease; – Cutaneous changes with ascites suggest liver disease – Lymphadenopathy or a palpable mass suggests malignancy.
  18. 18. Chest Radiography • homogenous increase in density spread over the lower lung fields • Apparent elevation of the hemidiaphragm, lateral displacement of the dome of the diaphragm, or increased distance between the apparent left hemidiaphragm and the gastric air bubble suggests subpulmonic effusions
  19. 19. Chest Radiography • Lateral decubitus films more reliably detect smaller pleural effusions. • Layering of an effusion on lateral decubitus films defines a freely flowing effusion and, if the layering fluid is 1 cm thick, indicates an effusion of greater than 200 mL that is amenable to thoracentesis. • Failure of an effusion to layer on lateral decubitus films indicates the presence of loculated pleural fluid or some other etiology causing the increased pleural density.
  20. 20. Minimal pleural effusion. Bounded left sinus
  21. 21. Moderate pleural effusion
  22. 22. Radiograma de faţă şi profilul drept. Incidenţa AP - opacitate neomogenă în câmpul pulmonar inferior pe dreapta,caracterul căreia se poate defini din imaginea de profil - pleurezie încarcerată în scizura interlobară oblică cu aspect de lentilă biconcavă.
  23. 23. Diverse aspecte radiografice la pacienţi cu pleurezii încarcerate. A - profil drept; colecţia lichidiană încarcerată în scizura interlobară orizontală prezintă o opacitate ovală;opacitatea inferioară atestă lichid liber în marea cavitate. B - radiogramă în poziţie oblică, pleurezia parietală încarcerată se prezintă ca opacitate ovoidă, bine delimitată în câmpul inferior stâng.
  24. 24. Empiem pleural 25
  25. 25. Analysis of pleural fluid Normal pleural fluid • Clear ultrafiltrate of plasma that originates from the parietal pleura • pH of 7.60-7.64 • Protein content of less than 2% (1-2 g/dL) • Fewer than 1000 white blood cells (WBCs) per cubic millimeter • Glucose content similar to that of plasma • Lactate dehydrogenase (LDH) less than 50% of plasma
  26. 26. Gross characteristics • Frankly purulent fluid indicates an empyema • A putrid odor suggests an anaerobic empyema • A milky, opalescent fluid suggests a chylothorax, resulting most often from lymphatic obstruction by malignancy or thoracic duct injury by trauma or surgical procedure • Grossly bloody fluid may result from trauma, malignancy, postpericardiotomy syndrome, or asbestos-related effusion and indicates the need for a spun hematocrit test of the sample; a pleural fluid hematocrit level of more than 50% of the peripheral hematocrit level defines a hemothorax, which often requires tube thoracostomy
  27. 27. Exsudate vs Transudate Light cretiria • Ratio of pleural fluid to serum protein greater than 0.5 • Ratio of pleural fluid to serum LDH greater than 0.6 • Pleural fluid LDH greater than two thirds of the upper limits of normal serum value Clinical judgment is required when pleural fluid test results fall near the cutoff points
  28. 28. Exsudate vs Transudate • The criteria from Light et al and these alternative criteria identify nearly all exudates correctly, but they misclassify approximately 20-25% of transudates as exudates, usually in patients on long-term diuretic therapy for congestive heart failure (because of the concentration of protein and LDH within the pleural space due to diuresis). • Using the criterion of serum minus pleural protein concentration level of less than 3.1 g/dL, rather than a serum/pleural fluid ratio of greater than 0.5, more correctly identifies exudates in these patients.[24] • Although pleural fluid albumin is not typically measured, a gradient of serum albumin to pleural fluid albumin of less than 1.2 g/dL also identifies an exudate in such patients.
  29. 29. Pleural Fluid Cell Count Differential • Pleural fluid lymphocytosis, – lymphocyte values greater than 85% of the total nucleated cells, suggests TB, lymphoma, sarcoidosis, chronic rheumatoid pleurisy, yellow nail syndrome, or chylothorax. – Pleural lymphocyte values of 50-70% of the nucleated cells suggest malignancy.
  30. 30. Pleural Fluid Cell Count Differential • Pleural fluid eosinophilia (PFE) – most often caused by air or blood in the pleural space. – pulmonary embolism with infarction or benign asbestos pleural effusion. – parasitic disease (especially paragonimiasis) – fungal infection (coccidioidomycosis, cryptococcosis, histoplasmosis) – medications. – PFE does not exclude a malignant effusion – PFE makes tuberculous pleurisy unlikely – makes the progression of a parapneumonic effusion to an empyema unlikely.
  31. 31. Pleural Fluid Cell Count Differential • Mesothelial cells greater than 5% of total nucleated cells makes a diagnosis of TB less likely. • Markedly increased numbers of mesothelial cells, especially in bloody or eosinophilic effusions, suggests pulmonary embolism as the cause of effusion.
  32. 32. Pleural fluid cytology • The reported diagnostic yields in cytology vary from 60-90%, depending on the extent of pleural involvement and the type of primary malignancy. • Cytology findings are positive in 58% of effusions related to mesothelioma.
  33. 33. Other tests for pleural fluid • Amylase • Triglyceride, cholesterol • Immunological markers (RF, DNA anti-body, etc.) • ADA • IGRA • Microbiological examination • Biopsy
  34. 34. Treatment • Transudative effusions are usually managed by treating the underlying medical disorder. • However, whether transudates or exudates, large, refractory pleural effusions causing severe respiratory symptoms, even if the cause is understood and disease-specific treatment is available, can be drained to provide relief.
  35. 35. Treatment • The management of exudative effusions depends on the underlying etiology of the effusion. Pneumonia, malignancy, or TB causes most diagnosed exudative pleural effusions, with the remainder typically deemed idiopathic. • Complicated parapneumonic effusions and empyemas should be drained to prevent development of fibrosing pleuritis. • Malignant effusions are usually drained to palliate symptoms and may require pleurodesis to prevent recurrence.
  36. 36. Treatment • Medications cause only a small proportion of all pleural effusions and are associated with exudative pleural effusions. • However, early recognition of these iatrogenic causes of pleural effusion avoids unnecessary additional diagnostic procedures and leads to definitive therapy, which is discontinuation of the medication. • Implicated drugs include medications that cause drug- induced lupus syndrome (eg, procainamide, hydralazine, quinidine), nitrofurantoin, dantrolene, methysergide, procarbazine, and methotrexate.
  37. 37. Prognosis • Morbidity and mortality of pleural effusions are directly related to cause, stage of disease at the time of presentation, and biochemical findings in the pleural fluid. • Morbidity and mortality rates in patients with pneumonia and pleural effusions are higher than those in patients with pneumonia alone. – Parapneumonic effusions, when recognized and treated promptly, typically resolve without significant sequelae. – However, untreated or inappropriately treated parapneumonic effusions may lead to empyema, constrictive fibrosis, and sepsis.
  38. 38. Prognosis • Development of a malignant pleural effusion is associated with a very poor prognosis, . – The most common associated malignancy in men is lung cancer, and the most common associated malignancy in women is breast cancer. – Median survival ranges from 3-12 months, depending on the malignancy. • A lower pleural fluid pH is often associated with a higher tumor burden and a worse prognosis.
  40. 40. ILD Associated with Connective Tissue Disorders • Clinical findings suggestive of a CTD should be sought in any patient with ILD • musculoskeletal pain, weakness, fatigue, fever, joint pains or swelling, photosensitivity, Raynaud's phenomenon, pleuritis, dry eyes, dry mouth) • The CTDs may be difficult to rule out since the pulmonary manifestations occasionally precede the more typical systemic manifestations by months or years.
  41. 41. Rheumatoid Arthritis
  42. 42. 2010 ACR/EULAR Classification Criteria for RA JOINT DISTRIBUTION (0-5) 1 large joint 0 2-10 large joints 1 1-3 small joints (large joints not counted) 2 4-10 small joints (large joints not counted) 3 >10 joints (at least one small joint) 5 SEROLOGY (0-3) Negative RF AND negative ACPA 0 Low positive RF OR low positive ACPA 2 High positive RF OR high positive ACPA 3 SYMPTOM DURATION (0-1) <6 weeks 0 ≥6 weeks 1 ACUTE PHASE REACTANTS (0-1) Normal CRP AND normal ESR 0 Abnormal CRP OR abnormal ESR 1 ≥6 = definite RA What if the score is <6? Patient might fulfill the criteria…  Prospectively over time (cumulatively)  Retrospectively if data on all four domains have been adequately recorded in the past
  43. 43. RA • Pulmonary Involvement is more common in male (3/1) • Ocasional is the first manifestation 1)PLURISY with or without pleural effusion – low GLU, high LDH, low Ph, – RF may be positive, WBC is more LYM. 2)PULMONARY NODULE multiple, in periphery, – Can cause PTX, hemoptysis and may became infected. – In CWP diffuse nodular fibrotic proces (Caplan sdr).
  44. 44. Nodular Lung Disease
  45. 45. Nodular Lung Disease
  46. 46. Nodular Lung Disease
  47. 47. RA 2)PULMONARY FIBROSIS: more in base of lung 3)BRONCHIOLITIS OBLITERANS: granulation and fibrosis of bronchioles. it cause symptoms of asthma. in spirometry : obstructive pattern. not responsive to treatment. 4)BOOP: diffuse infiltration in CXR, restrictive pattern, good response to steroid.
  48. 48. 51 Radiografia unei paciente cunoscută cu AR de 24 ani (tratament de fond administrează ultimii 2 ani Metotrexat 10 mg săptămânal) prezintă leziuni minime manifestate prin reticulaţie fină în câmpurile pulmonare inferioare, dar afectarea articulară este mult mai severă.
  49. 49. 52 Radiografia unui pacient cu AR cu leziuni pulmonare severe, distorsionare pronunţată a arhitectonicii pulmonare, modificări fibrochistice cu aspect de „fagure de miere” mai exprimate bazal bilateral, cu tendinţă de extindere pe toată aria pulmonară. Tomografia plană (8 cm) confirmă prezenţa fagurelui prepoderent periferic şi nu atestă infiltraţii pulmonare, deşi la aceşti pacienţi este foarte dificil a exclude pneumonia.
  50. 50. 53 Deformările articulare nu impresionează, dar acest pacient a avut factori de risc importanţi pentru dezvoltarea leziunilor pulmonare interstiţiale: -sexul masculin, -tabagismul, -prezenţa nodulilor reumatoizi subcutani, -titre înalte de factor reumatoid.
  51. 51. 54 Artrita reumatoidăArtrita reumatoidă HRCT demonstrează prezenţa leziunilor interstiţiale atât la pacienţii simptomatici (69- 80%) cât şi la asimptomatici (20-29%) Semnele sunt cele tipice pentru pneumonitele interstiţiale idiopatice Distinctiv la HRCT se determină “fagure de miere” progresiv de la bazele pulmonare spre apexuri Poate fi prezent şi emfizemul pulmonar în asociere cu bronşiectazii, inclusiv la cei nefumători .
  52. 52. 55 Radiografia în incidenţă PA la o pacientă cu istoric de AR de 17 ani (A) evidenţiază în câmpul pulmonar inferior drept şi stâng opacităţi "în voal" (de intensitate foarte slabă), care au fost eronat interpretate drept infiltraţie pulmonară. La examenul în incidenţă laterală dreaptă (B) se confirmă etiologia pleurală (îngroşări pleurale).
  53. 53. 56 • RadiograRadiografia în incidenţă PAfia în incidenţă PA la ola o paciepacientă cu AR de ... ani, evidenţiază în câmpul pulmonar inferiorntă cu AR de ... ani, evidenţiază în câmpul pulmonar inferior drept şi stâng opacităţi “în voal” (de intensitate foarte slabă), care au fost eronat interpretate dreptdrept şi stâng opacităţi “în voal” (de intensitate foarte slabă), care au fost eronat interpretate drept infiltraţie pulmonară, dar la examenul în incidenţă laterală este confirmată etiologia pleuralăinfiltraţie pulmonară, dar la examenul în incidenţă laterală este confirmată etiologia pleurală (îngroşări pleurale).(îngroşări pleurale).
  54. 54. 57
  55. 55. 58 Radiografia mâinii şi plantelor confirmă leziuni caracteristice din artrită reumatoidă: chisturi, eroziuni, îngustarea spaţiilor articulare cu subluxaţii
  56. 56. 59 Radiografia cutiei toracice evidenţiază leziuni fibrotice în ambele câmpuri pulmonare inferioare, modificări fibrochistice cu aspect de "fagure de miere", confirmate la HRCT pulmonar
  57. 57. 60
  58. 58. Radiografia de faţă la un pacient cu artrită reumatoidă. Pneumonită bilaterală (infiltraţie în cîmpul pulmonar inferior şi mediu pe stînga şi în cîmpul superior şi mediu pe dreapta). (Colecţia doctor în medicină, conferenţiar Matcovshi S.)
  59. 59. Systemic Lupus Erythematosus
  60. 60. 1. Malar rash: Fixed erythema over malar areas, sparing nasolabial folds 2. Discoid rash: Erythematous raised patches with keratotic scaling and follicular plugging 3. Photosensitivity: Skin rash after exposure to sunlight, history or physical exam 4. Oral ulcers: Oral or nasopharyngeal, painless, by physical exam 5. Arthritis:Tenderness, swelling, effusion in 2 or more peripheral joints 6. Serositis: A) pleuritis or B) pericarditis 7. Renal disorder A) proteinuria>0.5g/24hour or 3+ or B) cellular casts 8. Neurological disorder: A) seizures or B) psychiatric disorder (having excluded other causes, e.g. drigs) 9. Haematological disorder: A) haemolytic anaemia or B) leucopenia or C) thrombocytopenia 10. Immunologic disorder: A) positive LE cells or B) raised anti-native DNA antibdy binding or C) anti-Sm antibody or D) false positive serological test for syphilis. 11. Positive antinuclear antibody: Criteria of the ARA for the classification of SLE
  61. 61. SLE • In the course of disease 60-70% develop pleural or pulmonary disease. • It can be primary , secondary (drug) or infection. • The most common cause of pulmonary infilteration in SLE is infection. • Pulmonary function testing, particularly DLCO, reveals abnormalities in many patients with SLE.
  62. 62. PATTERN OF INVOLVEMENT 1) LUPUS PNEUMONITIS (acute, chronic) • Acute it is due to activation of immune mechanism, mimic infection) • Chronic form progress to pulmonary fibrosis (uncommn). 2)PULMONARY HTN (vasoconstriction, emboli, capilaritis) • vasoconstriction is associted with Raynaud and emboli associted with LA, APLA
  63. 63. 3) PLEURITIS WITH OR WITHOUT PLEURAL effusion is the most common pulmonary manifestation: it may be unilateral or bilateral • It is exudative with normal glucose and low LDH, low C3 and C4, ANA and LE cell may be positive, WBC may be predominantly PMN or LYM. • Diferential with infection, emboli 4) Other lung manifestations include the following: atelectasis, diaphragmatic dysfunction with loss of lung volumes, pulmonary vascular disease, pulmonary hemorrhage, uremic pulmonary edema, infectious pneumonia, and BOOP. PATTERN OF INVOLVEMENT
  64. 64. Radiogramă de faţă în LES. Bilateral bazal atelectazii discoide. Sinusurile costodiafragmale opacifiate (colecţie lichidiană pleurală minimă bilateral).(Colecţia doctor Elena Volcovski)
  65. 65. Radiogramă de faţă şi tomografie convenţională (secţia 7 cm) în lupusul eritematos sistemic. Bilateral infiltraţie în cîmpurile pulmonare superioare - pneumonită lupică. Configuraţie mitrală a cordului, bombarea conului pulmonar. Diafragmul elevat. (Colecţia doctor în medicină, conferenţiar Matcovshi S.)
  66. 66. Scleroderma
  67. 67. Scleroderma
  68. 68. Scleroderma Diagnostic Criteria • One major criterion: scleromatous skin changes proximal to the metacarpal- phalangeal joints • Two of three minor criteria: sclerodactyly, digital pitting scars, bi-basilar pulmonary fibrosis on CXR
  69. 69. SCLERODERMA • Clinical evidence of ILD is present in about one-half of patients. • Pulmonary function tests show a restrictive pattern and impaired diffusing capacity, often before any clinical or radiographic evidence of lung disease appears. • LEADING CAUSE OF DEATH .
  70. 70. SCLEODERMA 1)PULMONARY FIBROSIS: more in base of lung, ILD pattern, dry cough, dyspnea at exertion and then at rest, restrictive pattern, low DLCO. 2)Superimposision of lung cancer (Adenocarcinoma) 3)PULMONARY HTN: more common in CREST than systemic form (in systemic form pulmonary fibrosis is more common). 4)PLURAL INVOLVEMENT & ASPIRATI0N PNEUMONIA
  71. 71. 74 Radiograma de faţă (A) şi profilul drept (B) la o pacientă cu scleroză sistemică prezintă opacităţi "în sticlă mată" şi multiple opacităţi reticulonodulare bilateral, în câmpurile pulmonare inferioare se conturează imaginea "în fagure de miere".
  72. 72. 75 La CT pulmonar (C) se determină leziuni fibrotice avansate cu îngroşarea septurilor, zone de pneumoscleroză şi dezvoltarea fagurelui subpleural. De notat, predilecţia leziunilor subpleural şi în lobii inferiori.
  73. 73. Polymiositis/Dermatomyositis
  74. 74. ACR Diagnostic Criteria • 1. Symmetrical weakness – Limb-girdle and neck flexors, with or without dysphagia/respiratory sx • 2. Biopsy • 3. Elevation of muscle enzymes in serum – CK, aldolase, LDH, AST, ALT • 4. EMG evidence • 5. Dermatologic features – Gottron’s sign, heliotrope rash, shawl sign, etc. Polymyositis 4 criteria, no rash 3 criteria, no rash 2 criteria, no rash Dermatomyositis Rash + 3 criteria Rash + 2 criteria Rash + 1 criteria Definite Probable Possible
  75. 75. POLYMYOSITIS • ILD IN 10% OF PATIENT • Diffuse reticular or nodular opacities with or without an alveolar component occur radiographically, with a predilection for the lung bases. • ASPIRATION PNEUMONIA (due to pharyngeal muscle involvement) • HYPOVENTILATION (due to resp muscle weakness) • PLEURAL INVOLVEMENT IS RARE. • ANTI JO1 (antihistidyl t RNA synthetase) is present in patient with lung involvement.
  76. 76. Wegener’s Granulomatosis
  77. 77. Wegener’s Granulomatosis • General – necrotizing granulomas of upper airway, lower airway, kidney – bilateral pneumonitis 95% – chronic sinusitis 90% – mucosal ulceration of nasopharynx 75% – renal disease 80% – hallmark pathologic lesion • necrotizing granulomatous vasculitis
  78. 78. Wegener’s Granulomatosis antineutrophil cytoplasmic antibody (c-ANCA) sensitivity 65-90% high specificity need to confirm diagnosis • often 3-4 biopsies necessary • nasopharynx commonly involved good site • open pulmonary biopsy occasionally needed • untreated mortality of 90% at two years
  79. 79. Granulomatoza Wegener Opacităţi multiple macronodulare cu margini mprecise, bilaterale cu evoluţie spre excavare. Radiografia toracelui repetată după 2,5 luni tratament cu prednisolon şi ciclofosfamidă arată reducerea dramatică a infiltraţiei pulmonare.
  80. 80. 83 Granulomatoza Wegener CT pulmonar