As a senior resident, I thought I had a pretty strong understanding of sepsis and septic shock.
But after doing a deep dive, I realized there's so much nuance.
Here's my approach to workup and management, along with some key pearls and lessons.
- Thread -
Check out the @pointofcaremed digital resources on sepsis and septic shock for use at the point of care!
They include templates with admission checklists, sample dotphrases for the EHR, and key clinical pearls, along with a podcast and YouTube video with slides.
First of all, how do we even know if someone has sepsis?
Some history:
In 1991, SIRS criteria were established to identify those at high risk of sepsis-related death.
- HR >90
- RR >20
- WBC >12 or <4
- T >100.4 or <96.8
Sepsis was defined as 2/4 SIRS + e/o infection
However, the broad nature of SIRS commonly leads to misclassification.
For example, if I were to walk up a flight of stairs with my team on rounds, I very well might meet 2/4 SIRS criteria!
SIRS is sensitive but not specific.
In 2001, Sepsis-2 expanded and clarified the definitions but did not completely overhaul the system.
Sepsis was still SIRS + infection
Severe sepsis was sepsis with organ dysfunction
Septic shock was severe sepsis with hypotension unresponsive to fluids.
Between 2014-2016, Sepsis-3 got rid of "SIRS" and "severe sepsis" and made new definitions.
Sepsis:
"Life-threatening organ dysfunction caused by a dysregulated host response to infection"
Septic Shock:
"Sepsis PLUS pressor need and lactate >2 without hypovolemia"
Based on these, the SOFA score was introduced to focus on organ dysfunction.
However, SOFA is a bit cumbersome for use at the point of care (just look it up), so qSOFA was suggested as a more specific criterion for sepsis.
- RR >22
- systolic BP <100
- AMS
The pathophys of sepsis put VERY simply is an immune response to a pathogen leading to:
- vessel dilation + capillary leak
- microvascular thrombosis
- tissue ischemia
- acidosis
All resulting in organ dysfunction, often presenting as hypotension and respiratory distress.
Note that the core problem in sepsis is NOT hypovolemia, but rather vasodilation and poor perfusion.
Thus, aggressive fluid is not going to fix everything, and may in fact cause harm.
Be wary of just reacting to high lactate and low UOP - there are many reasons for each.
This in mind, here's a checklist when admitting a patient with suspected sepsis.
Key questions:
- Need for pressor?
- Need intubation?
- High risk of overload or pulm edema?
- Source?
- Source control?
- Prior culture data?
Here's a sample plan for sepsis.
The most important parts:
- 2x peripheral BCx + any indwelling line
- UA/UCx, CXR, lactate
- Broad-spectrum antibiotics
- Fluid to achieve euvolemia
- Pressor and steroid if persistently hypotensive
- Address severe acidosis
Antibiotics will almost always start broad with vancomycin and a beta-lactam (commonly cefepime or pip-tazo).
However, maintain a broad differential necessitating different tx, including:
- Atypical PNA
- C Diff
- Toxic shock or nec fasc
- Anaplasmosis
- Fungal
- Mimics
Some extra considerations for workup:
- Procalcitonin if equivocal
- Fungal markers if immunocompromised
- CT pan-scan if source unknown - consider source control
Trend:
- Daily CBC, CMP, coags
- Urine output via strict I/O's
- MAP
- Capillary refill, goal < 3 seconds
Some other pearls on workup and monitoring:
- PNA is the most common cause of sepsis
- Look out for ARDS, cholestasis, AKI, hepatic dysfunction, and DIC
- Good UOP is reassuring, but low UOP is nonspecific
Lactate is most commonly attributed to hypoperfusion and is viewed as something to be corrected.
However, it can instead be thought of as a reflection of endogenous epinephrine production.
Still, persistent elevation should draw extra attention to your management.
DDx for lactatemia:
Type A (tissue hypoxia)
- hypovolemia
- shock
- local ischemia (mesenteric, limb)
- decreased oxygenation
- anemia
Type B
- increased adrenergic state (albuterol, cocaine, epinephrine)
- decreased krebs (thiamine deficiency, EtOH)
- liver dysfunction
Procalcitonin is a measure of inflammation sensitive to bacteria, notably gram-negatives.
Though it's validated for ruling out HAP to discontinue abx in the ICU setting, if < 0.5, it's reasonable to say the etiology is less likely to be sepsis 2/2 a bacterial source.
Some pearls on fluid resuscitation:
- focus on euvolemia, MAP, and cap refill
- a good deal of fluid will leak out of vessels - much more than 2-3L (30cc/kg) of LR is rarely helpful
- low UOP or AKI may not be prerenal but rather ATN and will not improve with fluid
When it comes to pressors, many are taught:
norepi -> vaso -> epi
This often works well, but
- Norepi can lead to arrhythmias
- Vaso can be used first, but can't be given peripherally
- Epi is good in reduced EF or low HR
- Phenylephrine is ideal in AFib or AS
Here's a table for use at the point of care with some high-yield information for the commonly used vasopressors in sepsis.
MAP is the most reliable parameter for assessing response to therapy.
The goal is commonly MAP >65
The primary concern with low MAP is renal and cerebral injury.
In certain cases (i.e. dialysis), it may be okay to lower this goal and lower pressor needs.
Acidosis can worsen hypotension and respiratory distress via:
- Myocardial depression
- Decreased pressor efficacy
- Inceased arrythmia risk
- Compensatory increased RR
If pH < 7.1, consider bicarbonate
Just note that bicarb turns to pCO2 and must be ventilated off
The use of steroids in sepsis is a topic of debate.
Sepsis may lead to "relative adrenal insufficiency".
In general, if shock is refractory to low-med dose pressor, it's likely worth starting hydrocort 50mg q6.
Fludrocort is unlikely to add additional benefit.
Here's an approach to the daily presentation for patients with sepsis or septic shock I learned while in the ICU.
It helps you to keep track of all the moving parts while remaining thorough with your assessment and plan.
Here are some trials related to the management of sepsis and septic shock.
SMART - LR > NS in critically ill patients
SOAP II - dopamine increases risk of arrythmia vs norepi
CORTICUS Trial - hydrocort speeds up reversal of shock but does not reduce mortality
If you remember nothing else:
- Obtain cultures and promptly start antibiotics
- Source control
- Fluids are important but don't overdo it
- Don't delay starting pressor if MAP is < 65
- Watch MAP and cap refill, be cautious of responding only to UOP and lactate
For making it this far, here's a downloadable PDF with the checklist, differential, and sample EHR dotphrase for admitting a patient with sepsis and septic shock!