The most common etiologies of ALI/ARDS, grouped according to the pathogenetic pathway (i.e. direct versus indirect insult), are summarized in Tab]eJ... Traditionally, ALI/ARDS is considered to be a terminal event which is independent of the pathogenetic pathway. However, there is increasing experimental and clinical evidence that direct insult (via airways) and indirect insult (via bloodstream) may lead to different lung pathologies, with intra-alveolar damage being dominant if the insult is direct, as in diffuse pneumonia, and microvessel congestion and interstitial edema being dominant, with alveolar collapse, if the insult is indirect, as in peritonitis (Gattinoni et al. 1998).
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Table 1 Etiologies associated with ALI/ARDS
The etiologies leading to direct or indirect insult account for more than 80 per cent of ALI/ARDS occurring in the ICU. However, ALI/ARDS may occur in another setting, i.e. pulmonary embolism, pulmonary thrombosis, or pulmonary vasculitis.
Thus, when confronted with severe hypoxemia, it is mandatory to identify the etiology from the history, clinical signs, and laboratory findings. Understanding the etiology allows the patient to be assigned to one of three main pathogenetic categories:
1. direct insult (consolidation);
2. indirect insult (edema/collapse);
3. vascular disease (embolism, thrombosis, and vasculitis), frequently with a near-normal chest radiograph and severe hypoxemia. Underlying pathology
Traditionally, ALI/ARDS was considered as a diffuse inflammation of the lung parenchyma. However, CT scanning has revealed that the alterations in the lung parenchyma are not homogeneously distributed, as the CT densities are more concentrated in the dependent lung regions. These observations led to the 'baby lung'
model, which encompasses two concepts.
1. As little as 20 or 30 per cent of the normal lung volume has near-normal aeration.
2. The functional baby lung is located in the non-dependent regions of the lung.
Understanding of the functional anatomy of the ALI/ARDS lung has been improved further by quantitative regional CT scan analysis. In fact, the inflammatory edema is quite evenly distributed throughout the lung parenchyma, from sternum to vertebra. The increased lung weight ('wet sponge' model) leads to 'compression' of the most dependent regions, in which the increased densities are not due to greater edema but to reduced aeration as a result of 'compression atelectasis'.
The sponge model is valid for severe ALI/ARDS where the dominant pathology is represented by diffuse edema (increased lung weight) compression atelectasis. However, this model does not describe other ALI/ARDS conditions, in which the dominant underlying pathology is represented not by diffuse interstitial edema but by intra-alveolar lesions, as in diffuse pneumonia. For example, it has recently been shown that, in ALI/ARDS due to diffuse Pneumocystis carinii pneumonia, the CT densities are more homogeneously distributed than predicted by the sponge model. Although no specific studies have been performed, it can also be predicted that the sponge model does not describe early-phase pulmonary embolism, thrombosis, or vasculitis.
As the response to positive pressure may be different for intra-alveolar lesions (consolidation), compression ateletasis (collapse), or vascular disease, it is important to establish which is dominant. Unfortunately, the CT scan may not discriminate between collapse and consolidation. However, it may be possible to infer the dominant damage from the respiratory mechanics and imaging. The goal of the maneuvers described below is to establish, in a given patient, the potential for lung recruitment when applying positive pressure, i.e. to differentiate between consolidation and compression atelectasis.
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