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PLEURAL EFFUSION, PYOTHORAX & PNEUMOTHORAX Dr Sarika Gupta, Asst. Professor.

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Presentation on theme: "PLEURAL EFFUSION, PYOTHORAX & PNEUMOTHORAX Dr Sarika Gupta, Asst. Professor."— Presentation transcript:

1 PLEURAL EFFUSION, PYOTHORAX & PNEUMOTHORAX Dr Sarika Gupta, Asst. Professor

2 DEFINITION  Pleural effusion: inflammation of the pleura, accompanied by collection of fluid in the pleural space.  Normal Pleural fluid: 0.3 ml/kg BW  Protein: 1.5 g/dL  pH: alkaline (7.60)  Cells: 1700 cells/ml (75% macrophages, 23% lymphocytes & 2% mesothelial cells)

3 Pleural space should be virtually fluid free Pleural fluid is produced by the parietal pleura and absorbed by the visceral pleura as a continuous process

4  Intrapulmonary pressure -the pressure within the alveoli -as the chest expands on inspiration the intrapulmonary pressure becomes more negative, which causes air to be sucked into the lungs.  Intrapleural pressure -Negative pressure is created in the pleural space as the thoracic cage enlarges and the lungs recoil during normal inspiration -negative pressure may be lost if fluid collects in the pleural space, making the lung unable to expand fully.

5  Fluid accumulates in the pleural space by three mechanisms:  increased drainage of fluid into the space  increased production of fluid by cells in the space  decreased drainage of fluid from the space

6  Development of Pleural Effusion  pulmonary capillary pressure (CHF)  capillary permeability (Pneumonia)  intrapleural pressure (atelectasis)  plasma oncotic pressure (hypoalbuminemia)  pleural membrane permeability (malignancy)  lymphatic obstruction (malignancy)  diaphragmatic defect (hepatic hydrothorax)  thoracic duct rupture (chylothorax)

7 CAUSES EXUDATIVE (usually unilateral) Parapneumonic effusion Tuberculosis Connective tissue disorders Malignancy Pancreatitis Subphrenic abscess Severe dengue Radiation pleuritis TRANSUDATIVE (usually bilateral ) Congestive heart failure Cirrhosis Nephrotic syndrome Constrictive pericarditis Peritoneal dialysis CHYLOUS Congenital chylothorax Post-traumatic HEMOTHORAX Blunt trauma Malignancy

8 CLINICAL FEATURES History:  Small pleural effusion: asymptomatic  Large pleural effusion: pleuritic chest pain, abdominal pain, pain during inspiration or coughing  The child may prefer to lie on the affected side (to decrease respiratory excursions)  Cough  Fever  Respiratory distress, dyspnea, orthopnea, or cyanosis

9 CLINICAL FEATURES Examination:  Tracheal deviation to the opposite side  Bulging chest wall on the affected side with reduced movement  Decreased vocal fremitus  Dullness to percussion  Decreased or absent breath sounds  Diminished whispering pectoriloquy & decreased vocal resonance  Egophony-audible at the upper level of pleural effusion due to prtially collapsed underlying lung

10 CLINICAL FEATURES Examination:  Pleural friction rub:  Inflamed parietal & visceral pleurae rub against each other  leathery, rough in character  Heared in both inspiration and expiration  Disappears rapidly as the size of effusion increases  If a child remains pyrexial or unwell 48 hours after admission for pneumonia, parapneumonic effusion/empyema must be excluded.

11 DIAGNOSIS  Chest radiograph (x-ray) -able to distinguish >200ml of fluid (blunted costophrenic angles) -Chest radiographs acquired in the lateral decubitus position are more sensitive and can pick up as little as 50 ml of fluid.  Pleural fluid analysis  Chest ultrasound -locates small amounts or isolated loculated pockets of fluid -able to give precise position of accumulation  Computed Tomography (CT) scan -Differentiates between fluid collection, lung abscess, or tumor

12 PLEUAL EFFUSION  Created by an abnormal collection of fluid in the pleural space  Seen in chest X-ray with presence of about 200ml pleural fluid  Fluid in X-ray seen as a dense, white shadow with a concave upper edge (fluid level)

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14 CT scan of chest showing loculated pleural effusion in left side. Some thickening of pleura is also noted.

15 Pleural fluid analysis 1. Routine tests  Gross examination  Pleural fluid/serum protein ratio  Pleural fluid/serum LDH ratio  Cytology and culture

16 Pleural fluid analysis 2. Tests in selected cases  Pleural fluid cholesterol  Pleural fluid/serum cholesterol ratio  Lactate  Enzymes  Interferon  CRP  Tumor markers

17 Gross examination  Transudates: typically clear, pale yellow to straw-colored, odorless & do not clot.  Exudates: show variable degrees of cloudiness or turbidity & they often clot if not heparinized  A feculent odor may be detected in anaerobic infections

18 Gross examination  A bloody pleural effusion (hematocrit >1%) suggests trauma, malignancy, or pulmonary infarction.  A pleural fluid hematocrit greater than 50% of the blood hematocrit is good evidence for a hemothorax  Turbid, milky, and/or bloody specimens should be centrifuged and the supernatant examined. If the supernatant is clear, the turbidity is most likely due to cellular elements or debris. If the turbidity persists after centrifugation, a chylous effusion is likely

19 Differential Leukocyte Count and Cytology Cytological analysis will establish the diagnosis of metastatic carcinoma in 70% or more of cases

20 Chemical analysis Light’s Criteria (Sensitivity 99%, Specificity 98%) ) CriteriaTransudateExudate Pleural fluid protein:serum protein ratio ≤0.5> 0.5 Pleural fluid LDH:serum LDH ≤0.6> 0.6 Pleural fluid LDH≤200>200

21 Microbiological examination:  The sensitivity of the Gram stain is approximately 50%  For patients with suspected M. tuberculosis, direct staining of tuberculous effusions for acid-fast bacteria has a sensitivity of 20%–30% and positive cultures are found in 50%–70% of cases

22 Chemical analysis Glucose:  The glucose level of normal pleural fluid, transudates, and most exudates is similar to serum levels  Decreased pleural fluid glucose, accepted as a level below 60 mg/dL (3.33 mmol/L) or a pleural fluid/serum glucose ratio less than 0.5, is most consistent and dramatic in rheumatoid pleuritis and grossly purulent parapneumonic exudates

23 Lactate:  Pleural fluid lactate levels: useful adjunct in the rapid diagnosis of infectious pleuritis  Levels are significantly higher in bacterial and tuberculous pleural infections than in other pleural effusions  Values greater than 90 mg/dL (10 mmol/L) have a positive predictive value for infectious pleuritis of 94% and a negative predictive value of 100%

24 Amylase:  Elevations above the serum level (usually 1.5–2.0 or more times greater) indicate the presence of pancreatitis, esophageal rupture, or malignant effusion  Elevated amylase derived from esophageal rupture or malignancy is the salivary isoform, which differentiates it from pancreatic amylase

25 Lactate dehydrogenase:  Pleural fluid LD levels rise in proportion to the degree of inflammation  In addition to their use in separating exudates from transudates, declining LD levels during the course of an effusion indicate that the inflammatory process is resolving  Conversely, increasing levels indicate a worsening condition requiring aggressive workup or treatment

26 Adenosine deminase:  >40 unit/l  Tuberculosis Interferon-γ:  Pleural fluid interferon (IFN)-γ levels are significantly increased in the pleural fluid of patients with tuberculous pleuritis  The sensitivity of levels of 3.7 IU/L or greater is 99%, and the specificity is 98%  Consider when ADA is unavailable or nondiagnostic

27 pH:  Pleural fluid pH measurement has the highest diagnostic accuracy in assessing the prognosis of parapneumonic (pneumonia-related) effusions  A parapneumonic exudate with a pH greater than 7.30 generally resolves with medical therapy alone  A pH less than 7.20 indicates a complicated parapneumonic effusion (loculated or associated with empyema), requiring surgical drainage.  A pH below 6.0 is characteristic of esophageal rupture, although the pH in severe empyema may be 6.0 or less

28 Lipids:  Helpful in identifying chylous effusions  Pleural fluid triglyceride levels > 110 mg/dL indicate a chylous effusion  values from 60–110 mg/dL require lipoprotein electrophoresis to confirm a chylothorax  Nonchylous effusions : triglyceride levels <50 mg/dL & no chylomicrons on electrophoresis

29 Cholesterol:  Cholesterol measurements may be useful in separating transudates from exudates, especially when there is a question regarding Light’s criteria  A total cholesterol value of 54 mg/dL or more and a pleural fluid/serum cholesterol ratio of 0.32 or higher have sensitivity and specificity values similar to Light’s criteria

30 Immunologic studies:  Approximately 5% of patients with RA and 50% with SLE develop pleural effusions  RF is commonly present in pleural effusions associated with seropositive RA  ANA titers may be useful in the diagnosis of effusion due to lupus pleuritis

31 TREATMENT 1. Therapy should be aimed at the underlying disease  Transudative effusion by fluid overload as in cardiac or renal failure: diuretics & fluid management  Nephrotic syndrome and cirrhosis of liver: Albumin infusion  Tubercular pleural effusion: Anti-tubercular drugs

32 TREATMENT  Chylous pleural effusion:  Thoracocentesis or placement of ICD tube followed by feeding with MCT  Continuous development: discontinuation of oral feeds and TPN  Somatostatin & Octreotide  Traumatic hemothorax: drainage of blood with proper replacement  Recurrent pleural effusion due to malignancies: prolonged placement of catheter or pleurodesis

33 TREATMENT Parapneumonic effusion Analgesia Supplemental oxygen Systemic antibiotics  based on the in vitro sensitivities of the responsible organism (Staphylococcus, S. pneumoniae, and H. influenzae)  Duration: 2 wk. With staphylococcal infections: systemic antibiotic therapy for 3-4 wk; anaerobic empyema-6-12 weeks  Instillation of antibiotics into the pleural cavity does not improve results

34 TREATMENT Parapneumonic effusion 1. Tube thoracostomy is considered necessary if the pleural fluid pH is <7.20 or the pleural fluid glucose level is <50 mg/dL 2. If the fluid is clearly purulent, tube drainage with thrombolytic therapy or video-assisted thoracoscopic surgery (VATS) or open decortication

35 TREATMENT Thoracentesis  Diagnostic thoracentesis  A needle is inserted into the chest wall to remove the collection of fluid  ml of fluid is sent for analysis; Determines the type of fluid (transudate or exudate)  temporarily relieve symptoms  Potential complications: bleeding, infection & pneumothorax

36 TREATMENT  BUT if sufficient fluid reaccumulates to cause respiratory embarrassment, chest tube drainage should be performed  Rapid removal of ≥1 L of pleural fluid may be associated with the development of reexpansion pulmonary edema Chest tube drainage

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38 TREATMENT  Thrombolytic therapy  Promote drainage, decrease fever, lessen need for surgical intervention & shorten hospitalization  Streptokinase 15,000 U/kg in 50 mL of 0.9% saline daily for 3-5 days and urokinase 40,000 U in 40 mL saline every 12 hr for 6 doses  Anaphylaxis with streptokinase & both drugs can be associated with hemorrhage

39 TREATMENT  Video-assisted thoracoscopic surgery (VATS) or Open decortication  The child who remains febrile & dyspneic >72 hr after initiation of therapy with intravenous antibiotics and thoracostomy tube drainage, surgical decortication via VATS or, less often, open thoracotomy may speed recovery  If pleural fluid septa are detected on ultrasound, immediate VATS can be associated with a shortened hospital course

40 EMPYEMA

41 DEFINITION  Empyema or Purulent Pleurisy: Empyema is an accumulation of pus in the pleural space  Most often associated with pneumonia due to Staphylococcus aureus & Streptococcus pneumoniaea  The relative incidence of Haemophilus influenzae empyema has decreased (Hib vaccination)  Also produced by rupture of a lung abscess into the pleural space, by contamination introduced from trauma or thoracic surgery or by mediastinitis or the extension of intra- abdominal abscesses

42 EPIDEMIOLOGY  Most frequently encountered in infants & preschool children  Predisposing factors: preceding history of pustules, blunt trauma to the chest, viral infection, severe malnutrition, contiguous extension

43 PATHOLOGY  Empyema has 3 stages: exudative, fibrinopurulent, and organizational  Exudative stage: 1-3 days  Fibrinopurulent stage: 4-14 days  Organizational stage: After 14 days

44 PATHOLOGY  Exudative stage: fibrinous exudate forms on the pleural surfaces  Fibrinopurulent stage: fibrinous septa form, causing loculation of the fluid & thickening of the parietal pleura  If the pus is not drained, it may dissect through the pleura into lung parenchyma, producing bronchopleural fistulas and pyopneumothorax, or into the abdominal cavity or through the chest wall (empyema necessitatis)  Organizational stage: fibroblast proliferation; pockets of loculated pus develop into thick-walled abscess cavities or the lung may collapse & become surrounded by a thick, inelastic envelope (peel)

45 CLINICAL MANIFESTATIONS  The initial signs & symptoms are primarily those of bacterial pneumonia  Children treated with antibiotic agents may have an interval of a few days between the clinical pneumonia phase & the evidence of empyema  Most patients are febrile (fever may be absent in immunocompromised patients), develop increased work of breathing or respiratory distress & often appear more ill  Physical findings are identical to those for uncomplicated parapneumonic effusion & the 2 conditions are differentiated only by thoracentesis

46 DIAGNOSIS  The effusion is empyema if bacteria are present on Gram staining, the pH is 1000 IU/L and there are >100,000 neutrophils/µL  Cultures of the fluid must always be performed  Blood cultures also have a high yield

47 DIAGNOSIS  Tuberculous empyema can be confirmed by stains for AFB in fewer than 25% of cases but pleural biopsy and culture can dignose more than 90% cases, ADA (>70 U/L)

48 COMPLICATIONS 1. Bronchopleural fistulas  Usually respond to adequate drainage, nutritional support & sealing of the open communication over the lung surface  Prolonged bronchopleural fistulas (>2-3 weeks) requires decortication, lobectomy or thoracoplasty

49 COMPLICATIONS 2. Pyopneumothorax 3. Purulent pericarditis & pulmonary abscesses 4. Peritonitis from extension through the diaphragm & osteomyelitis of the ribs 5. Septic complications: meningitis, arthritis 6. Septicemia is often encountered in H. influenzae and pneumococcal infections 7. Peel: may restrict lung expansion and may be associated with persistent fever and temporary scoliosis 8. Empyema necessitans 9. Gastropleural fistula

50 COMPLICATIONS 8. Diaphragmatic palsy 9. Horner’s syndrome

51 TREATMENT  Systemic antibiotics  Staphylococcus aureus: cloxacillin & aminoglycoside or 3 gen cephlosporin & aminoglycoside  Gram-ve organism: cefotaxim & aminoglycoside  Gram stain inconclusive: cefotaxim & cloxacillin  Resistant Staphylococcus: vancomycin, teicoplanin & linezolid  Thoracentesis

52 TREATMENT  Chest tube drainage with or without a fibrinolytic agent Indications for surgical treatment: a) Pleural thickening b) Loculated empyema c) Non-expansion of lungs with intercostal drainage d) Bronchopeural fistula 1. Video-assisted thorascopic surgery: effective in lysis of adhesions in multiloculted effusions & removal of fibrinous material from pleural cavity 2. Open decortication: significant pleural thickening

53 TREATMENT  The long-term clinical prognosis for adequately treated empyema is excellent & follow-up pulmonary function studies suggest that residual restrictive disease is uncommon, with or without surgical intervention

54 PNEUMOTHORAX

55 DEFINITION  Accumulation of extra pulmonary air within the chest, most commonly from leakage of air from within the lung PNEUMOTHORAX CLOSED-air entry into the pleural space by disruption of pulmonary parenchyma OPEN-due to disruption in the integrity of chest wall & parietal pleura

56 ETIOLOGY Closed pneumothorax -Pulmonary disease  Foreign body  RDS  Respiratory infections  Bronchial asthma  Cystic fibrosis  Chemical pneumonitis  Diffuse lung disease  Tumors -Iatrogenic  Mechanical ventilation  Central venous catheterization Open pneumothorax  Invasive pleural & pulmonary procedures  Chest trauma Spontaneous pneumothorax  Idiopathic (ruptured subpleural blebs)  Familial

57 PATHOGENESIS  The tendency of the lung to collapse is balanced in the normal resting state by the inherent tendency of the chest wall to expand outward, creating negative pressure in the intrapleural space  When air enters the pleural space, the lung collapses  In simple pneumothorax, intrapleural pressure is atmospheric, and the lung collapses up to 30%.  In complicated, or tension pneumothorax, continuing leak causes increasing positive pressure in the pleural space, with further compression of the lung, contralateral shift of mediastinal structures & decreases in venous return and cardiac output

58 CLINICAL MANIFESTATIONS  Sudden onset  Dyspnea, pain, & cyanosis  Trachea & heart may be shifted toward the unaffected side  Hyperinflation & reduced movements on affected side  Respiratory distress with retractions  Decreased vocal fremitus & vocal resonance  Markedly decreased breath sounds and a tympanitic percussion note over the involved hemithorax  When fluid is present, there is usually a sharply limited area of tympany above a level of flatness to percussion

59 CLINICAL MANIFESTATIONS  Succussion splash: to rule out hydropneumothorax  Coin test  Friction test

60 Because the ratio of extrapulmonary gas to solid tissue increases in a pneumothorax, hyperresonant percussion notes are produced over the affected area.

61 Breath sounds diminish as gas accumulates in the intrapleural space.

62 As gas accumulates in the intrapleural space, the chest diameter increases on the affected side in a tension pneumothorax.

63 Time and Progression of Disease Pa O Alveolar Hyperventilation Point at which PaO 2 declines enough to stimulate peripheral oxygen receptors Pa CO 2 Acute Ventilatory Failure Disease Onset Point at which disease becomes severe and patient begins to become fatigued Pa 0 2 or Pa C0 2 PaO 2 and PaCO 2 trends during acute ventilatory failure (Large pneumothorax)

64 DIAGNOSIS  By radiographic examination  When the possibility of diaphragmatic hernia is being considered, a small amount of barium may be necessary to demonstrate that it is not free air but is a portion of the gastrointestinal tract that is in the thoracic cavity  Ultrasound can also be used to establish the diagnosis

65 TREATMENT  Extent of the collapse & nature and severity of the underlying disease  A small (<5%) or even moderate-sized pneumothorax in an otherwise normal child may resolve without specific treatment, usually within about 1 wk  Needle aspiration: tension pneumothorax & primary spontaneous pneumothorax  If the pneumothorax is recurrent, secondary or under tension or there is >5% collapse: chest tube drainage  Pneumothorax complicating malignancy: chemical pleurodesis or surgical thoracotomy

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67 TREATMENT  Closed thoracotomy: adequate to reexpand the lung in most patients  Chemical pleurodesis: recurrent pneumothoraces; introduction of talc, doxycycline, or iodopovidone into the pleural space  Open thoracotomy: plication of blebs, closure of fistula, stripping of the pleura and basilar pleural abrasion; Stripping and abrading the pleura leaves raw, inflamed surfaces that heal with sealing adhesions  VATS: preferred therapy for blebectomy, pleural stripping, pleural brushing and instillation of sclerosing agents; less morbidity than with open thoracotomy


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