III_C.  ADULT RESPIRTORY DISTRESS  SYNDROME (Low Pressure Pulmonary Edema)

Pathophysiology:

ARDS is the name given to the clinical manifestation of a number of indirect lung injury states characterized by dyspnea, severe hypoxemia, and decreased lung compliance with radiographic evidence of diffuse bilateral pulmonary infiltrates.^118-120 Alveolar consolidation with fluid, protein, and inflammatory cells in the presence of a normal capillary or wedge pressure is also a characteristic finding, i.e., low pressure pulmonary edema. The altered permeability results in a rapid movement of fluid from plasma to interstitial space with even a normal capillary (wedge) pressure. The causes and differential diagnosis of ARDS are presented.  The ARDS in a burn patient has a very high mortality rate with death usually due to multiple organ failure.^119-121

Pathophysiology & Diagnosis

The most common period to see ARDS is in the inflammatory phase of burn injury during the sepsis syndrome.^121-123  The lung damage is the result of a systemic process initiated by burn tissue, infection or inflammation rather than a direct lung injury. However, the term "ARDS" is commonly but inappropriately used to describe direct lung injury processes, such as an inhalation injury. There are probably several distinct ARDS state, each with a different cause. Although the pathophysiology may be extremely complex and the etiologic agents varied, the presenting signs and symptoms for the ARDS states are nearly identical. The hypoxemia produced is characteristically refractory to an increase in fractional inspired oxygen, indicating increased shunting. In addition, the degree of shunt is not directly correlated with the degree of increased water content, as is the case with cardiogenic edema.

 Figure 2:  Severe Established ARDS

Bilateral alveolar consolidation is evident

There is a decrease in dynamic compliance and functional residual capacity resulting in increased ventilation to perfusion mismatch probably due to mediator-induced bronchoconstriction.  The pathophysiologic abnormalities produced by this inflammatory process can be divided into four phases.^118-122

Phase One:

In the first, or initial phase dyspnea and tachypnea are noted, with a relatively normal arterial oxygen tension and a hyperventilation-induced respiratory alkalosis.  Lung findings are absent on physical examination or radiographs. The prodome is mediator-induced.  Initial treatment should focus on finding the source of the lung response, i.e., a septic focus, necrotic tissue, an area of inflammation.  Pulmonary emboli need to be considered as well.

Phase Two:

The second phase, usually beginning with 12 to 24 hours of the early symptoms, is characterized by physiologic and pathologic evidence of lung injury.  Initial parenchymal changes are patchy and not homogenous, appearing initially in the dependent lung field.  Hypoxemia is now evident, along with continuing dyspnea. An increasing shunt fraction or venous admixture is primarily responsible, since little effect is noted by increasing the fractional inspired oxygen.  The dynamic and static compliance decreases modestly, as does functional residual capacity, reflecting the stiff lung.  Minor auscultatory findings are present that consist mostly of signs of early patchy consolidation.

Early pathogenic findings consist of interstitial edema, focal hemorrhage, and atelectasis, with pulmonary microvascular congestion.  This progresses to intra-alveolar edema and hemorrhage with severe congestion and atelectasis.  Hyaline membranes are seen in the alveoli. The mechanism of the acute injury process is not totally defined, but the initiating event is an injury to the circulatory side of the alveolar capillary membrane.  At this stage, the ARDS process is reversible if the initiating factor is controlled.

Phase Three:

Progression to phase three is manifested by the onset of acute respiratory failure, as previously outlined, necessitating mechanical ventilation.  The lungs become more diffusely involved and more stiff.  The shunt fraction increases as a result of patchy atelectasis from surfactant denaturation and focal alveolar consolidation due to increased permeability.  The increase in carbon dioxide production during this postburn period can also lead to hypercapnia when the lung is damaged.  A hyperdynamic state frequently evolves with an increase in cardiac output, evidence of lactic acidosis, and a characteristic decrease in oxygen extraction from hemoglobin, in order to compensate for increased oxygen needs, is a characteristic of the sepsis syndrome when ARDS is present.  The mechanism may be related to impaired metabolic function of the lung, which normally removes vasodilator agents released from inflammation.

Phase Four:

The fourth phase is one of progressive pulmonary fibrosis and recurrent pneumonias.  Areas of lung infection become evident due to impaired bacterial clearance.  Areas of the lung become relatively acellular, being replaced by fibrous tissue.  The process becomes much less reversible at this stage. The progression of single organ lung failure to a multisystem failure (with liver, gastrointestinal tract, and kidney dysfunction) commonly occurs with late ARDS.  Further lung insults need to be avoided if the fibrosis is to resolve.  Mortality rate is more than 90%, once burn patients enter this phase. Typically a burn patient will enter the multisystem organ failure process instead of the progressive pulmonary fibrosis process.

Treatment:

Mortality rate of ARDS caused by burn inflammation and infection is extremely high.^120,128  The major reason for the lethal nature of the process is that resolution will not occur until the initiating process is removed: the wound especially in the large burn, cannot be readily excised and closed at this stage of the postburn process.  The most important early treatment is prevention, i.e., early removal of as much of the potential source of the systemic inflammatory response as is feasible.^118,124

A variety of new low pressure ventilation systems are available for management, which appear to be effective.^127-129

 ARDS Treatment Summary

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