1. Trauma Patients and Acute Respiratory Distress Syndrome

2. Definition
A syndrome of acute respiratory failure characterized by non-cardiac pulmonary edema and manifested by refractory hypoxemia caused by intrapulmonary shunt and diffusion barrier

3. Direct Injury Chest trauma – pulmonary contusion Near-drowning
Hypervolemia – pulmonary edema
Inhalation of toxic gases and vapors
Pulmonary embolism
Pneumonia (viral, bacterial or fungal)

4. Indirect Injury Sepsis Shock or prolonged hypotension
Multi-system trauma, especially multiple fractures
Burns
DIC
Acute pancreatitis
Head Injury
Abdominal trauma
Multiple blood transfusions

5. Pathophysiology
Onset of symptoms is usually 12 – 48 hours after time from acute injury
Has acute and chronic phases

6. Acute phase
Acute lung injury Reduces normal perfusion to the lungs Causes platelet aggregation and stimulation of the inflammatory-immune system

7. Acute phase
Release of mediators of the inflammatory process Mediators activate neutrophils, macrophages and other cells to release toxic substances that cause microvascular injury

8. Acute phase
Acute and diffuse injury to endothelium and epithelium surface of lung occur Damage to pulmonary capillary membrane and increase in capillary permeability occurs

9. Acute phase
Capillary leak allows proteins and fluids to spill into the interstitium and alveolar spaces Pulmonary lymphatic drainage capacity is overwhelmed and alveolar flooding occurs

10. Acute phase
Pulmonary edema results and causes interference with oxygen diffusion and inactivation of surfactant Alveolar collapse and massive atelectasis occur and decrease functional residual capacity and lung compliance

11. Acute phase
Profound hypoxemia related to extensive shunting (V/Q mismatch) Vasoconstrictive mediators cause increased pulmonary vasoconstriction and pulmonary hypertension

12. Chronic phase
Type I pneumocytes are destroyed and replaced by type II pneumocytes which proliferate Interstitial space expands by edema fluid, fibers and proliferating cells Hyaline membranes are formed which increase the thickness of the alveolar-capillary membrane Pulmonary fibrosis may occur

13. Clinical Presentation
Presence of a predisposing condition
Severe oxygenation defect – hypoxemia is the hallmark of ARDS
PaO2 < 60 mmHg on FiO2 > 50%
PaO2/FiO2 ratio < or = to 200
CXR: diffuse bilateral parenchymal infiltrates
PAOP: < 18 mm Hg.

14. Clinical Presentation
Elevated PAP with normal PAOP (cardiac pulmonary edema causes elevated PAP and PAOP)
Pulmonary vascular resistance (PVR) is increased because of hypoxemic pulmonary vasoconstriction
ABG: Refractory hypoxemia

15. Pulmonary function studies
Lung volumes decreased:
Tidal volume /vital capacity
Functional residual capacity decreased
Static and dynamic compliance decreased

16. Chest x-ray findings
Bilateral diffuse interstitial and alveolar infiltrates
Ground glass appearance
“White-out” due to massive atelectasis
Heart size is normal (unusual in cardiac pulmonary edema)

17. Ventilatory management
Modes: pressure control / inverse ratio ventilation or high-frequency jet ventilation may be used
Tidal volume: limitation of peak inspiratory pressure and reduction of regional lung overdistension by the use of low tidal volumes with permissive hypercapnia.

18. Ventilatory management
“Baby-lung” treatment: TV should be 4-8 ml/kg. - excessive volume forced into a small aerated lung can cause volutrauma
PaCO2 is allowed to gradually increase as minute ventilation is reduced – bicarbonate may be used in pH is less than 7.15
Hypercapnia contraindicated with
concurrent head injury

19. Ventilator management
CPAP or PEEP
Decreases surface tension: keeps alveoli open
Aids in reopening collapsed alveoli
Reduces intrapulmonary shunt and increases functional residual volume
Obtain higher PaO2 with same or lower FIO2
Usual level 5-15 cm H2O – may be higher

20. Ventilator management
FIO2 should be maintained as low as possible to prevent oxygen toxicity
Need nitrogen to keep alveoli inflated
CPAP may be administered via mask prior to intubation
Patients very PEEP dependent and will quickly desaturate when temporarily discontinued
Utilize transport ventilator when moving patient
May require sedation and/or paralysis to maintain PEEP

21. Intraalveolar fluid
CPAP or PEEP increases intraalveolar pressure – prevents further fluid sequestration into the alveoli
Diuretics may be considered - maintain PAOP at ~ 12 mmHg
Colloids leak across the alveolar-capillary membrane as readily as crystalloids

22. Hemodynamics Inotropes as indicated by cardiac index/output
Dobutamine is usually the first choice
Best PEEP = in PaO2 and SaO2 but
does not cardiac output

23. Other therapies
Nitric oxide: Synthesized by vascular endothelium and acts as a natural local vasodilator when inhaled – it dilates vessels only to ventilated areas and acts as a potent bronchdilator More effective when used during early stages

24. Other therapies
Corticosteriods: May be helpful during the fibroprofilerative phase
Nutritional support: To prevent respiratory muscle atrophy and translocation of bacteria from GI tract

25. Complications Nosocomial pneumonia Sepsis Shock
Multiple organ dysfunction syndrome (MODS)
DIC
Airway trauma
Dysrhythmias
Pulmonary embolism
Pulmonary fibrosis
Barotrauma
GI hemorrhage
Renal failure

26. ARDS vs. Pulmonary Contusion
Pulmonary contusion is usually localized and occurs near the site of external trauma
ARDS causes diffuse bilateral changes
CXR with contusions show increased density reflecting intraalveolar hemorrhage

27. Questions ?