Trauma Patients and

Acute Respiratory Distress Syndrome

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

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

Pathophysiology

• 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

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

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

Complications

• 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

Questions

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