I actually was recently first author on a paper about post-ARDS restrictive lung disease. Assuming that COVID ARDS is not different from regular old ARDS, then this is the deal ( @
ccmdfd should jump in and correct me if I am off the mark):
Fibroproliferative ARDS - that is, the fibrotic "scarring" that occurs in, depending on who you read, something like 25% of ARDS survivors, based on evidence of restrictive lung physiology 180 days after discharge that correlates with reticular pulmonary infiltrates on HRCT scan. (
source). Taken together, this is evidence of residual 'scarring' in a significant proportion of ARDS survivors.
However, if you read closely, the authors use median - not mean - % expected value. In reality, the mean is much higher, and the residual dysfunction measured by these tests are heavily weighted by an even smaller subset of survivors with significant residual scarring. Furthermore, aside from PFTs, the only other ways we have to measure lung fibrosis (not including direct biopsy) are CT scans and health questionnaires. However, 1) patient questionnaires, for lots of hopefully obvious reasons, are a fairly flawed measurement tool, and 2) imaging often does not necessarily reflect underlying organ function (the COVID Xrays are a great example - blown TF up on plain film but standing, walking, talking).
So, to put it all together, there are clearly a subset of ARDS patients (and, I imagine, also a subset of COVID ICU patients) who will develop fibroproliferative disease with significant long term consequences for lung function. However, this isn't going to be most people, and even then, for most with measurable residual deficits in lung function, it will not be an enormous change from baseline.
It's still unclear if COVID ARDS is really that different from "regular" ARDS. That is an extremely active discussion and I don't honestly know enough to weigh in. Will likely take some time for the smoke to clear.