ARDS is characterized by:


Acute tachypnea (&dyspnea)
Bilateral infiltrates on chest radiograph
Pulmonary artery wedge pressure < 18 mmHg (obtained by pulmonary artery catheterization), if this information is available; if unavailable, then lack of clinical evidence of left ventricular failuresuffices
if PaO2:FiO2 < 200 mmHg
(if PaO2:FiO2 < 300 mmHg acute lung injury (ALI) is considered to be present if PaO2:FiO2 < 300 mmHg acute lung injury (ALI) is considered to be present



No specific treatment is currently available for ARDS. Management is based on recognizing patients at risk, minimizing initiating factors, such as sepsis, and providing respiratory support. ARDS should be suspected in a patient with a history of recent shock who develops respiratory alkalosis and increasing dyspnea that does not respond to supplemental oxygen. Unless the precipitating condition is eliminated, ARDS progresses with increased intrapulmonary shunting and accumulation of protein-rich fluid in the alveoli. When hypoxia and the effort of breathing increase, assisted ventilation becomes necessary. Many patients require prolonged ventilation. As ARDS is a highly dynamic process, vigilant monitoring is essential with continuous modification of treatment.

Predisposing Factors – ARDS

Direct Injury
Inhalation Injury (i.e. Burns)
Aspiration (i.e. chemical pneumonitis)

Indirect Injury
Bacterial Sepsis (i.e. endotoxemia)
Pancreatitis

Some info from review of emergency care online
Management:

Diagnostic Studies: The CXR
The CXR may be “normal” for a period of time (hours - days) following the precipitating event [e.g. sepsis]

Full progression to diffuse, bilateral alveolar infiltrates ordinarily takes place within 4 - 24 hours after the first abnormal radiographic signs appear

The shadows within the lung parenchyma may be very similar to those identified in CHF

As alveolar filling continues, more of the lung parenchyma is involved - leading at times to a near-total “white-out” of both fields

CXR's are strongly influenced by the effects of therapy

IV Fluids can increase alveolar content
Diuretic agents may decrease total content
PEEP increases lung inflation thereby reducing regional lung density
Remember... your treatment may produce the appearance of radiographic improvement despite continued severe abnormalities in gas exchange !

Despite what appears to be a UNIVERSAL involvement of all lung fields on standard CXR, C.T. will often reveal patchy areas of infiltrate interspersed with normal-appearing lung ! Degree of lung involvement on C.T. correlates with the efficiency of gas exchange and underlying lung compliance (Gattioni et al. 1988) C.T. can also reveal Barotrauma or localized infection
i.e. loculated empyema or abscess

The efficiency of gas exchange [PaO2/FiO2] at the onset of A.R.D.S., has correlated to patient outcome
Bone et al. 1989

Dead-space ventilation is markedly increased in patients with ARDS.

Measuring” Membrane Permeability:
Analyze the Protein Content within the Alveolus or you can measure the flux of radiolabeled proteins

When this is done, the pulmonary edema that we see in ARDS appears to be noncardiogenic in etiology!
Drake & Lane 1988

The amount of extravascular water within the lungs can also be measured

Thermal Indocyanine Green Technique
Rarely done in the clinical setting

How much fluid do we normally have in our lungs ?
Upper-limit of Normal: 500 cc's
The “average” ARDS patient: 1500 cc's

Bronchoalveolar Lavage:
Usually employed to document nosocomial infection
can be safely performed in A.R.D.S. patients
has never been prospectively validated
can identify opportunistic lung infections presenting as ARDS

Treatment of ARDS:
Nonpharmacologic Therapy.................................Pharmacolo gic Therapy
Currently, specific measures to correct the abnormality in vascular permeability or to limit the degree of inflammatory reaction present in ARDS, do not exist.

Clinical management involves primarily supportive measures aimed at maintaining cellular and physiologic function, while the acute lung injury resolves.

What cellular functions are you trying to maintain ?
Alveolar Gas Exchange
Organ Perfusion
Aerobic Metabolism

Nonpharmocological Approaches
Mechanical Ventilation: Pressure vs. Volume

Goals in providing support:
Preserve Arterial Oxygen Saturation
Prevent complications from elevated airway pressures
i.e. Peak Airway Pressures > 40 cmH2O
Minimize “oxygen toxicity” [FiO2 < 0.6]

Tidal Volume

large volumes & high airway pressures have been implicated as causes of gross lung injury & direct injury to the alveolar-endothelial membrane
Dreyfuss et al. 1988
12 - 15 ml/kg : “old surgical dogma”
6 - 10 ml/kg [6 - 8 ml/kg]: “new surgical dogma”

PEEP:
Theory: increases lung volume by limiting the degree of alveolar closure

Problem: there are no prospective studies of how or when PEEP should be used in A.R.D.S.

Prophylactic-PEEP: will NOT prevent ARDS in patients at risk
Pepe et al. 1984

Routine Low-Level PEEP [5 cmH2O]

May limit atelectasis
May improve arterial oxygenation
Has never been proven harmful

Permissive Hypercapnea

Theory: controlled hypoventilation with subsequent hypercapnea avoid detrimental increases in peak airway pressure
Gradual increases of PaCO2 are well tolerated (up to 100 mmHg) - and marked acidosis (pH < 7.25) can be corrected with sodium bicarbonate
Inverse Ratio Ventilation

Theory: by prolonging inspiration time, mean airway pressure is increased (allowing a subsequent increase in oxygen diffusion) while maintaining acceptable peak airway pressures


Patient Repositioning:
West Zone's of the Lung

Lung infiltrates are not uniformly distributed in A.R.D.S.

Changes in position can improve oxygenation by altering the distribution of perfusion to ventilated areas (Piehl & Brown 1976)
The Prone Position
Complicated
Logistic Nightmare - but the theory is sound !
Prone = “Dimensional Ventilation”

Oxygen Transport:

Fluid Management in ARDS:
In A.R.D.S., the primary problem is vascular permeability - however, increased hydrostatic forces can still worsen alveolar content
Goal of Therapy
to achieve the lowest possible PA-Occlusion Pressure consistent with an “adequate” cardiac output - (especially during the first few days after onset) while correcting any compromise in end-organ function (the benefit of this for more than 3 -4 days is unclear)

Diuretics & Fluid Restrictions can help to reduce total lung water

[which would work with Hydrostatic Pulmonary Edema]

ARDS is an INFLAMMATORY CONDITION & these methods are not as effective
Pharmacologic Treatment:
Exogenous Surfactant
Corticosteroids
Antioxidants
Vasodilators
Antiendotoxin
Ketoconazole
Nitric Oxide
Eicosanoid Inhibitors
Vasoconstrictors
Pentoxifylline

Management: of ARDS: The Recovery Phase
Most patients who die of ARDS, do so within the first two weeks of their illness

For those who survive, “recovery” takes weeks to months

General Supportive Care Issues:

Ventilatory Support (i.e. Barotrauma / Tracheostomy)
Nutritional Support (i.e. PEG vs. Jejunostomy)
Nosocomial Infections (Pneumonia / UTI's...)
“Stress-related” GI Bleeding