Sepsis and Acute Respiratory Distress Syndrome

[Smash]

Right, clever people, riddle me this: If your patient has sepsis is he/she more likely to develop Acute Respiratory Distress Syndrome (ARDS) if the focus is respiratory as compared to a different focus (eg uro-sepsis)

Humour me, and pretend that the government has shut down Google so I can't look this up myself.

 

[firetender]

Humour me, and pretend that the government has shut down Google so I can't look this up myself.

Sepsis is a generalized, systemic reaction, as likely to localize symptomatically here as it can localize there. It's a whole body thing by definition.

 

[blindsideflank]

hmm interesting. if ARDS was secondary to a systemic infection (wouldnt it always be systemic at this point?) it is obviously bad news bears. If you have a pathology in the lungs/infection it may be possible to develop it earlier and therefore if would have less of a systemic effect and not be as advanced?

just thinking out loud

you can obviously develop it by both but i have no idea if its "easier" to get one way or another. i guess when you think about the patho if infiltrates can reach the chest faster(by already being there) then you would dvelop it more quickly.

the resulting responses and inflammation will have to take place there to develop ards. the lungs as a the primary site would be the quickest way.
although i am very unclear on the definition of ARDS, as it seems to be a set of symptoms more than a set physiological state.

enough of me talkin out of my butt, let the smart fellers in here to correct me

 

[Veneficus]

Right, clever people, riddle me this: If your patient has sepsis is he/she more likely to develop Acute Respiratory Distress Syndrome (ARDS) if the focus is respiratory as compared to a different focus (eg uro-sepsis)

Humour me, and pretend that the government has shut down Google so I can't look this up myself.

so what are you asking exactly?

 

[usalsfyre]

I'm wanting to say it's slightly more likely in pneumococcal infection than say urosepsis (or eurosepsis as my intern wrote the other day, who knew being European was so deadly ). The big ARDS kicker is mechanical ventilation. That's why lung protective strategies have become so important.

 

[Smash]

I hope he publishes on the scourge of Eurosepsis!

I understand the seductiveness of thinking that a respiratory focus of sepsis would mean that the patient is more likely to develop ARDS, but my feelings are in line with firetender's: SIRS (leading to ARDS) is, by definition, systemic, so it shouldn't matter where the initial infection came from. SIRS of course doesn't even need a pathogen to get underway anyway, and patients can still develop ARDS.
The trouble is, I'm struggling to find data to support either train of thought.

 

[Veneficus]

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

 

[Smash]

Thanks, that about covers it!

 

[Veneficus]

I should have been more clear.

The neutrophil reaction causes necrosis of type I and type II pneumocytes which undergoes an attempt at fibrous repair. (scarring)

Sorry. Sometimes my thinking and typing to not always sync up.

 

[Smash]

No, that's ok, the general patho of ARDS I think I'm moderately ok with, although all the IL1s and 4s and TNF and so forth gets me tied up sometimes.

Type I cells damaged --> increased permeability (exudative phase)
Type II cells damaged (tougher than type I) --> decreased surfactant production, alveolar collapse and decreased compliance with increased fibroblasts and fibrosis (Proliferative phase)
And then Fibrosis with destruction of vascular or resolution (Fibrotic phase)

Is that kind of the major steps in a nutshell? I know it is vastly more complicated than this, but for a bear of little brains I try my best!

 

[johnmedic]

This is all a bit out of my scope of knowledge.. sorry if it's irrelevant but here it is.

"Cytokines [...] also are important in the development of ARDS. An imbalance of proinflammatory and anti-inflammatory cytokines is thought to occur after an inciting event, such as sepsis."

Source: http://emedicine.medscape.com/article/165139-overview

 

[8jimi8]

And a tiny follow up with Early goal directed therapy.



From the research I have done, draw your labs and cultures, fluid resuscitation, broad spectrum ABX coverage, then pressors. Central line placement, and serial lactates / scvo2. And don't forget the lung protective ventilator strategies.

 

[johnmedic]

Oh damnit.. I'm sorry, usually I'm good at browsing back & not responding to old threads. Sorry. :|

 

[HappyParamedicRN]

Not sure if this helps,but...

I had a 32 year old patient present in cold septic shock with ARDS - source of her infection was an obstructing kidney stone. It only took 48 hours from initial onset of symptoms to get to her presenting condition. No other infection source was present.. Thankfully a urologist came in emergently and dislodged the stone. She spent about a week on a vent and on pressors and of course antibiotics in the ICU, but evemtually made a full recovery.

Happy