I'm gonna talk to you now about a really important topic
that every emergency physician needs to understand
and that is severe sepsis and septic shock.
So what is sepsis?
Sepsis definitions where rewritten recently by an international consortium
and sepsis is now defined as a life threatening organ dysfunction
caused by a disregulated host response to infection.
It's a lot of fancy terminology.
We're gonna breakdown exactly what that means in just a minute.
Septic shock on the other hand is a sub-set of sepsis.
So not every patient with sepsis will have septic shock.
And in the case of septic shock,
you will have circulatory and cellular metabolic dysfunction,
which in turn leads to a high risk of mortality.
So what is all of that really mean?
Well, the bottom-line is that in sepsis you develop an infection,
your body’s immune response attempts to fight it
and that immune response causes injury to any of a variety of organ systems.
So in sepsis the circulatory system can be affected,
you’ll see myocardial depression and vasodilation which is what leads to shock.
The lungs are often affected leading to ARDS.
The GI tract can be affected causing dysmotility.
Shock liver is quite common in which you'll see transaminitis
and problems with hepatic synthetic dysfunction.
The kidneys can be affected leading to oliguria,
anuria, or acute kidney injury.
And the CNS is very commonly involved
with altered mental status being a common presenting complaint associated with sepsis.
So the bottom-line is that septic shock occurs when sepsis impairs circulation
which in turn leads to cellular hypoxia, cell death, and anaerobic metabolism.
So sepsis can affect any organ,
but when it affects the circulatory system
and impairs normal cellular oxygen delivery,
that is when you see septic shock.
So how does this all work physiologically?
Well, very simply, it starts with an infection.
It's a normal physiologic process for your body to fight infection.
So the infection stimulates normal physiologic release of inflammatory mediators.
However, in sepsis,
this process becomes sort of self-stimulating and turns into a vicious cycle.
So you get inflammatory mediators released,
those mediators recruit all of white blood cells that are in your body to fight infection
and those white blood cells will destroy healthy tissue.
Now this in turn is gonna take us back to step one,
when healthy tissues start breaking down, the body is like—
Whoa! That's wrong!
And will further release inflammatory mediators
which causes even more recruitment of white blood cells
which causes even more tissue damage, etc.
So it's a vicious cycle that's self-perpetuating
that basically leads the body’s own immune system
to not only fight the infection that's present
but also to fight the body itself.
This loss of normal homeostasis,
the body’s inability to shut down the inflammatory process,
is what ultimately leads to organ damage and failure.
And it's important to remember that this organ failure
is not just caused by circulatory insufficiency.
We all used to think 20 years ago that vasodilation and shock
is what lead to all of the downstream complications of sepsis
and we now know
that it is actual tissue damage being caused by the immune system itself,
not just circulatory failure.
Now, we've all heard of SIRS,
and the SIRS criteria were used to define sepsis for many years.
However, we have new definitions now
that were just postulated by the International Workgroup On Sepsis in 2016.
So now when we talked about how to define sepsis clinically,
we use the SOFA criteria.
That stands for Sequential Organ Failure Assessment.
It's a very reliable and valid assessment scheme
but it's really designed to be used sequentially over time
in an intensive care unit setting.
So it's not terribly helpful in the Emergency Department setting
because we don’t even have access to all of the data that you need
to calculate the SOFA right upfront.
So in the ED, we use the qSOFA,
where the q stands for quick.
The qSOFA is very easy to remember,
it's only got three parameters.
Altered mental status which is defined as a GCS of anything less than 15.
Tachypnea which is defined as a respiratory rate greater than 22.
And hypotension, which is defined as a systolic blood pressure of less than 100.
If you have any two of these three criteria in the setting of an infection,
you have an increase risk of death or prolonged hospitalization.
This is a clinically validated tool that reliably predicts
who's gonna do well
and who's not gonna do as well in the setting of infection.
So it's very useful for us prognosticating in the Emergency Department setting.
So, when do you move from sepsis to septic shock?
In order to diagnose septic shock,
you first and foremost have to provide adequate fluid resuscitation.
And septic shock is said to exist when despite adequate resuscitation
you have persistent hypotension requiring use of vasopressors,
and or an elevated lactate level which is greater than 2 mmol/L.
The mortality of septic shock is greater than 40%.
So when you move from sepsis to septic shock
you should recognize that you're also moving into a domain
where your patient’s outcomes are much, much more likely to be adverse
and you really need to be very aggressive and meticulous in how you treat them.
The definition sounded simple enough,
but there actually aren't clearly defined parameters
for what constitutes adequate fluid resuscitation
or the need for a vasopressor.
These are gonna vary according to what's going on with your patient,
What their comorbidities are?
What factors there are regarding their presentation?
Have they had vomiting?
Have they not been taking PO?
Have they been really febrile?
Are they debilitated and unable to feed and hydrate themselves?
All of these things are gonna influence how much volume they need
and when you're gonna transition from fluids to vasopressors.
But in general, the criteria that we apply is about 30 cc/k.
If you need more than that we should probably be at least thinking about
the possibility that vasoconstrictor should be in your future.