282791124-Pleural-Effusion.pptx raafat.pptx

Nursing school

1. pneumothorax & Hemothrax Dr Raafat Al-Awadhi

2. Anatomy of the lung Lung Diaphragm

3. Pneumothorax Definition: It is a potential medical emergency caused by accumulation of air or gas in the pleural cavity, occurring as a result of disease or injury, or spontaneously.

4. Type of pneumothorax Closed Pneumothorax Open Pneumothorax Tension Pneumothorax

5. Type of pneumothorax Closed Pneumothorax It is entering of air in to the pleural cavity from a puncture or tear in an internal respiratory structure such as bronchus, bronchioles, or alveoli. May be spontaneous The chest wall is intact C/P : the condition maybe symptomless or present by mild chest pain and mild dyspnea Minimal amount of air without dyspnoea : spontaneous absorption of air take place Marked dyspnoea with lung collapse: insertion of intercostals tube until full lung expansion.

6. Blunt traumas Causes of Blunt Traumas: - Motor Vehicular Accident - Fall or physical abuse Iatrogenic causes - Mechanical ventilation -Mechanical Ventilation (PEEP)
-Subclavian CVC -Thoracentesis
-Pleural Biopsy

7. Type of pneumothorax Open Pneumothorax It is entering of air in to the pleural cavity by a hole in chest wall or diaphragm causes a passage between outside air and the intrapleural space. Result from surgery on the chest or trauma to the chest wall (e.g. stab wound, gun shot or penetrating traumas)

8. Causes the lung to collapse due to increased pressure in pleural cavity C/P there is moderate dyspnea and Cyanosis, Intial treatment is occlusive dressing fixed at 3 sides only. Definitive treatment is insertion of chest tube in the 5 th intercostals space just in front of mid-axillary line connected to under water seal

9. Tension Pneumothorax It happens when the opening to the intrapleural space creates a one-way valve where air collects into the space but never leaves. causes major compression on the lungs and heart. C/P : sever sharp and staping chest pain , severe progressive dyspnea and cyanosis followed by respiratory arrest - there is tracheal and mediastinal shift to unaffected side

10. Initial treatment insertion of wide bore needle in the 2 nd intercostal space in the mid-clavicular line to decompress the chest ( life saving) It is temporary measure until the definitive treatment is available. Definitive treatment is insertion of chest tube in the 5 th intercostal space just in front of mid-axillary line connected to under water seal Continuous bubbling of air through the intercostal tube indicate broncho -pleural fistula which need thoracotomy to close it.

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

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

13. 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

14. 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

15. 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%

16. 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

17. 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

18. 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

19. 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

20. 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

21. 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

22. 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

23. TREATMENT 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

24. 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

25. 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

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

27. TREATMENT Thoracentesis Diagnostic thoracentesis A needle is inserted into the chest wall to remove the collection of fluid 50-100ml of fluid is sent for analysis; Determines the type of fluid (transudate or exudate) temporarily relieve symptoms Potential complications: bleeding, infection & pneumothorax

28. 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

29. Chest tube drainage

30. 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

31. 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

32. EMPYEMA

33. 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

34. 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

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

36. 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)

37. 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

38. DIAGNOSIS The effusion is empyema if bacteria are present on Gram staining, the pH is <7.20, glucose<40 mg/dl and LDH>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

39. 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)

40. COMPLICATIONS 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

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

42. COMPLICATIONS Diaphragmatic palsy Horner’s syndrome

43. 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

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

45. 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

46. PNEUMOTHORAX PNEUMOTHORAX

47. DEFINITION Accumulation of extra pulmonary air within the chest, most commonly from leakage of air from within the lung

48. 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

49. 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