The SIRS/ARDS relationship. (rocky though it is)
In the SIRS response, there is ultimately vascular permiability, stipulated from over production of NO. Some leakage of either lipopolysaccharide (LPS) or vascularly disseminated organism into the lung. (preferentially it localizes to the lung and liver, where there are supposed to be exchanges taking place)
ARDS
At that point the neutrophyilic response to/from the LPS directly damages the alveolar walls. As part of this reaction there is a fibrin deposition. (part of DIC mediated by IL1 and TNF) type II pneumocyyes then try to reproduce in order to clear this fibrin/cellular remnants (cytoplasm&lipid) More often than not, instead of clearing these products, the fibrin undergoes organization, with the end stage of alveolar fibrosis.
As the septal thickening increases, interstitial cells produce and deposite collagen further adding a layer(s) limiting gas diffusion.
Even without direct tissue invasion or damage, large amounts of systemic or direct NF-K-B can cause a proinflammatory response, which again, the lungs and liver are most suseptable to. Toll-like receptors (TLRs) can also stimulate the pathway.
The combination of IL1, TNF, and IL8 leads to attraction and activation of neutrophils.
So what I think your dilemma is centered around is the progressions of SIRS to ARDS vs. the direct injury and resultant acute ARDS?
From the systemic infection standpoint, it will take longer for there to be lung tissue involvement than if there is direct tissue injury.
From the practical point, the management is going to be similar.
For the record, there are 4 causes that together make up more than 50% of ARDS development.
Sepsis, diffuse pulmonary infections, gastric aspiration, and trauma.
The leading cause of sepsis is still infection from indwelling urinary catheters.
I think the big problem you spoke of in PM is that pulmonary edema is transudate and does not organize. Exudate caused by necrotic pneumocytes has more than just a liquid component and does organize, the whole fluid argument is a bit flawed, because there is a big difference between what is basically just serum, and serum with all kinds of floaty things. Obviously total fluid going into the lung would be an issue, but if you are trading cardiovascular collapse in exchange for alveolar fluid limitation, there is going to be an issue there.
The beauty of CC medicine, more than one pathologic process in which one treatment directly contradicts another.
Personally I always advocated pressors prior to or concurrently with fluid in septic shock, because I see absolutely no point in adding fluid without correcting the vascular permiability issues. You are basically just making cool aide again, since there is far more vasculature to fill than blood to do it with.
Increasing PVR helps keep blood in the core and raises renal perfusion with blood, water doesn't do S*** for renal medulary oxygen demand.
If you are trying to manage cardiovascular collapse, the loss of the kidney and the RAA cycle will definately make it harder. Decrease in erythropoeitin over the long term will not do much for anemia either.
With a respiratory focus, direct diffuse lung damage makes ARDS more likely than sepsis, which while preferentially affecting lungs and liver, still has to go through a progression to get to that point. Whether or not that is a clinically significant amount of time depends on the organism and host defense. Probably sometimes "yes" and sometimes "no."
Indirect injury: Sepsis->DIC->ARDS
Direct injury can start with ARDS
). The big ARDS kicker is mechanical ventilation. That's why lung protective strategies have become so important.