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Trauma Patients and Acute Respiratory Distress Syndrome

Lynn Kemp, R.N. Trauma Coordinator St. Barnabas Hospital

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

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

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

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

Acute phase
Acute lung injury

Reduces normal perfusion to the lungs

Causes platelet aggregation and stimulation of the inflammatory-immune system

Acute phase
Release of mediators of the inflammatory process

Mediators activate neutrophils, macrophages and other cells to release toxic substances that cause microvascular injury

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

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

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

Acute phase
Profound hypoxemia related to extensive shunting (V/Q mismatch)

Vasoconstrictive mediators cause increased pulmonary vasoconstriction and pulmonary hypertension

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

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.

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

Pulmonary function studies

Lung volumes decreased: Tidal volume /vital capacity
Functional residual capacity decreased

Static and dynamic compliance decreased

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)

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.

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

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

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

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

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

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

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

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

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