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Posttraumatic Pulmonary Insufficiency

Posttraumatic Pulmonary Insufficiency. Bradley J. Phillips, M.D. Burn-Trauma-ICU Adults & Pediatrics. Definition. Clinical state in which gas exchange in the lungs is inadequate to maintain body function without mechanical support. Incidence. Pulmonary complications 11% ( Hoyt, 1993)

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Posttraumatic Pulmonary Insufficiency

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  1. Posttraumatic Pulmonary Insufficiency Bradley J. Phillips, M.D. Burn-Trauma-ICU Adults & Pediatrics

  2. Definition Clinical state in which gas exchange in the lungs is inadequate to maintain body function without mechanical support

  3. Incidence • Pulmonary complications 11% ( Hoyt, 1993) • Pneumonia 7.5% • Atelectasis 3.4% • ARDS 2.8% • Aspiration 1.5% • PE 0.7%

  4. Predictors • Injury Severity Score > 16 • Blunt trauma • Shock on admission • Chest surgery • Pedestrian vs MVC • Head injury • Age > 55 years

  5. Disease-related Shock Pulmonary contusion Fat emboli CNS injuries Sepsis PE Smoke inhalation Iatrogenic Fluid overload Massive blood transfusion Ventilator-induced Causes

  6. Pulmonary contusion • Evident on CXR within 24 hours • Worsen within 24-48 hrs • Increased risk of infection • Flail chest induced hypoxia result of contusion

  7. Fat Embolism • Syndrome characterized by cerebral and pulmonary dysfunction after long bone injury • asymptotic 12-48 hrs post injury • increasing tachypnea, restlessness, and confusion • “full blown” - severe hypoxia/coma mortality 10-20% • Assume in all patient with pelvic and long bone fractures • quantified by platelet count and A-a gradient

  8. Fat Embolism • Origin • long bone • in situ blood formation with increased lipolysis • Platelet adhere to fat particles • thrombocytopenia • petechiae on chest/conjunctiva/axilla • Increased risk with immobilized fracture • Early fixation recommended

  9. CNS Injuries • Greatly increased risk • aspiration • atelectasis • prolonged ventilation • Neurogenic pulmonary edema • frequently pre-mortem spinal cord/head injury • increased pulmonary tone • increased capillary leak

  10. Pneumonitis • Risk in ventilated patients 1-4% per day • Diagnosis • Fever ( > 101) • Leukocytosis ( > 12 K) • New infiltrate • Sputum with PMN’s • Bacteria on gram stain and culture • Stress ulcer prophylaxis • no difference in ventilated patients on sulcrafate, antiacids, or ranitidine

  11. Pulmonary Embolism • Significant risk in trauma patients • Risk assessment profile of thromoembolism (RAPT) by Greenfield • 5 or more (out of 14) increases risk 3 times • Underlying condition • Obses, malignancy, hx of thromboembolism • Iatrogenic factors • CVL, operations > 2 hrs, major venous repair • Injury-related factor • Spinal factures, coma, pelvic fx, plegia • Age • > 40 (highest risk > 75)

  12. Other Causes • Shock • decreases ciliary function and surfactant • hypotension alone ARDS • Fluid Overload • increased interstitial edema • Massive blood transfusions • controversial • main risk is increased infections

  13. Other Causes • Smoke inhalation injury • 36 hrs2-6 days1-2 weeks • bronchospasms pulmonary edema bronchopneumonia • airway edema airway cast formation • bronchitis • Ventilator-induced injury • Volumenot pressure etiology • Sepsis • increased risk of ARDS • severe persistent infections

  14. Adult Respiratory Disease Syndrome • First described in 1967 (12 patients) • cyanosis refractory to oxygen • decreased lung compliance • diffuse infiltrates on CXR • Modern definition (1994) • Acute onset • Bilateral infiltrates on CXR • Wedge < 18 mmHG or absence of L atrial HTN • PaO2/FiO2 < 200 ( if > 200, acute lung injury) • Not predictive of outcome within 24-72 hrs

  15. ARDS • Incidence • 15- 75 /100,000 • depends on definition • prospective study underway • Phases of Pathophysiology • Acute (0-6 days) • Proliferative (4-10 days) • Chronic or fibrosis (8-14 days)

  16. Direct Common Pneumonia Aspiration Less common Pulmonary contusion Fat emboli Near drowning Inhalation injury Reperfusion injury Indirect Common Sepsis Severe trauma with shock and transfusions Less common Cardiopulmonary bypass Drug overdose Acute pancreatitis Transfusion of blood products Risk Factors

  17. Mediators of Injury • Vasoactive substances • Leukocyte activation • oxygen radicals • neutrophil proteases • arachidonic acid metabolites • Complement activation • Platelets • Cytokines • TNF, IL-1, IL-8

  18. Anatomical Consequences • Capillary endothelium • gap junctions wider • “leaky” = fluid and protein interstitium • Proliferation of type II pneumocytes • Vascular occlusion • capillaries and small vessels • 75-80% occlusion for increase in PA pressures (moderate-severe ARDS) • poor prognosis • Pulmonary fibrosis (late)

  19. Gas Exchange • Hypoxemia • V/Q abnormalities • atelectasis and alveolar flooding • shunting (20%) • most sensitive for impending early respiratory failure • Increased dead space • dead space fraction of .6-.65 = severe dysfunction

  20. Physiologic Changes • Most consistent and frequent hemodynamic evidence of poor prognosis after trauma • early secondary to neurohumoral activity • late secondary to microemboli and edema • Decreased compliance (< 50 ml/cm H2O) • interstitial and alveolar edema • tachypnea is usually first sign • if not correctable = poor prognosis • TV and PEEP adjusted to provide best static compliance

  21. Treatment • Eradicate all underlying infection • General supportive measures • frequent position changes • elevation of head/chest • chest physiotherapy • pain control • relief of gaseous distension • reduce O2 requirements

  22. Treatment • Fluids • maintain adequate perfusion • excessive fluid greatly aggravates tendency toward ARDS • Central venous monitoring • ? Role of colloid ( risk of leaking into interstitium) • maintain hemoglobin • accept > 10 g/dl • trend in survival if Hgb > 12 g/dl

  23. Treatment • Optimizing DO2 and VO2 • Shoemaker (1988) reduced incidence of pulmonary complications in high-risk surgery for 27% to 4% • Fleming (1992) fewer deaths (14% vs 44 %) and respiratory failure (39% vs 68%) • supranormal CI (>4.5) • DO2 (> 670 ml/min/m2) • VO2 (160 ml/min/m2)

  24. Treatment • Nutrition • early, aggressive enteral nutrition • ? enteral vs no feeding • ? benefit of fish oil, arginine, glutamine • Drugs • bronchodilators • inotropics • diuretics

  25. Ventilatory Support • Oxygenation • > 60% usually required • oxygen toxicity not an issue if PaO2 < 50 • PEEP • ability to reduce oxygen • risks • CO2 retention • high airway pressures/ • hemodynamic instability

  26. Ventilatory Support Type Year Type Outcome High PEEP 1975 Observe High PTX ECMO 1979 Phase III No benefit Jet Vent 1983 Phase III No benefit PC/Inverse 1994 Observe Inconclusive Liquid 1996 Observe Safe, ? Benefit Oscillatory 1997 Observe Safe, ? Benefit Prone 1997 Observe Inconclusive Prone 2000 Observe Inconclusive Open Lung 1998 Phase III dec. 28 day mortality Low tidal 1999-2000 Phase III No benefit/dec. mortality

  27. Problems • High airway pressures • sedation and/or paralytics • pressure control ventilation • permissive hypercapnea • reduce tidal volume (5-7 ml/kg) • in general maintain pH > 7.2 • ? permissive hypoxemia • Hypoxia • acidemia • reverse I:E ratio

  28. Recommendation • Minimize FiO2 and PEEP to maintain PaO2 > 60 • Low tidal volumes (5-7 ml/kg) • Pressure regulated or control ventilation • PIP < 30 • Permissive hypercapnea • Reverse I:E ratio

  29. Other Therapies • Steroids • possible benefit in late ARDS with difficulty weaning • Nitric Oxide • no benefit • Surfactant replacement • successful in neonates only • Triiodothyronine • experimental in animals • improved compliance, histologic integrity, and surfactant

  30. Other Therapies Treatment Year Type Findings Steroids (acute) 1987 Phase III No benefit Steroids (acute) 1988 Phase III No benefit Steroids (late) 1998 Phase III dec. mortality Surfactant 1996 Phase III No benefit Nitric Oxide 1998 Phase II No benefit Nitric Oxide 1999 Phase III No benefit Ketoconazole 2000 Phase II No benefit

  31. Nonconventional Methods • Unilateral pulmonary insufficiency (isolated pulmonary contusions or aspiration pneumonitis) • “Down with the good lung” • Independent lung ventilation • Bilateral pulmonary insufficiency • Permissive hypercapnia • I:E reversal • High –frequency Ventilation • Prone positioning • ECMO

  32. Unilateral Pulmonary Insufficiency • Lateral positioning • Allow redistribution of V/Q mismatch • Good lung down – increased blood flow to normal lung parenchyma • Independent lung ventilation • Two separate ventilators using double lumen ET • Deliver TV to each lung based on pathology • Numerous disadvantages • Monitoring tube position (tube dislogdes often) • Heavy sedation/paralysis • Increased cost

  33. Bilateral Pulmonary Insufficiency • Permissive hypercapnia • Minimize peak inspiratory pressure with low TV while maintaining acceptable oxygenation • Acceptance of hypoventilation/hypercapnia • Slow increase in CO2 tolerated very well • Often maintain pH 7.10 to 7.20 range • ? Use of bicarb to buffer pH • Contraindicated in head injury

  34. Bilateral Pulmonary Insufficiency • I:E reversal • Normal I:E is 1:2 TO 1:4 • Allows more time for recruitment of alveoli and oxygen diffusion • Disadvantages • Often leads to permissive hypercapnia • Auto-PEEP • High-frequency ventilation • Small TV (1-3 ml/kg) at 100-3000/min) • Adequate oxygenation with reduced airway pressures • Disadvantages • Necrotizing tracheobronchitis • No difference in outcomes compared to conventional methods

  35. Bilateral Pulmonary Insufficiency • Prone positioning • Physiology • Better V/Q matching anteriorly • Disadvantages • More intensive nursing care • Risk of tube and line dislodgement • ? Increase skin breakdown • Cannot use in open abdomens, spinal fractures etc • Outcomes • Reduced FiO2 and PEEP • > 2/3 of patients • PaO2/FiO2 improved by 50% • Reduced shunt 50% to 34% • ? Improved mortality • Small studies show increased survival using combined prone ventilation, low tidal volumes, and permissive hypercapnia

  36. Ventilatory Strategies Hirvela, E, Archives of Surgery, 2000.

  37. Volume-Pressure Curve

  38. Outcomes • Mortality rates 40-60% (Historical) • sepsis • MSOF • not usually primary respiratory causes • Mortality rates 30-40 %(recent) • ? more effective treatments of sepsis • changes in mechanical ventilation • improvement in supportive care • Risk factors for death • chronic liver disease, sepsis, age, MSOF • failure to improve in first week

  39. ARDS Consequences • After 1 year, most not restricted in activities • Permanent restrictive changes and pulmonary HTN develop if prolonged need for oxygen > 60%

  40. Questions…?

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