Septic Shock
Summary
TLDRThis ICU curriculum session focuses on defining sepsis and septic shock, outlining their clinical manifestations, and detailing treatment protocols. It emphasizes the importance of early recognition and management, including prompt administration of broad-spectrum antibiotics, fluid resuscitation with lactated ringers, and vasopressors like norepinephrine and vasopressin. The session also discusses the role of corticosteroids in refractory septic shock and the significance of source control. A case study illustrates the application of these principles in managing a patient with suspected pyelonephritis.
Takeaways
- π The session focuses on defining sepsis and septic shock according to the Sepsis-3 definitions.
- π©Ί Septic shock is a subset of sepsis characterized by underlying circulatory and cellular metabolic abnormalities that significantly increase mortality.
- π‘ Clinically, septic shock is identified by sepsis plus hypotension that does not improve despite fluid resuscitation, and a serum lactate level >2 mmol/L.
- π¨ Sepsis is a time-sensitive medical emergency requiring prompt recognition and management to improve patient outcomes.
- π Early administration of broad-spectrum antibiotics is crucial in the treatment of septic shock, with each hour's delay increasing the risk of in-hospital mortality.
- π§ The initial fluid resuscitation for sepsis or septic shock involves a 30 mL/kg bolus of intravenous fluid, typically lactated Ringer's solution.
- π Vasopressors are used to maintain a mean arterial pressure (MAP) β₯65 mmHg, with norepinephrine being the first-line agent.
- π Source control, including broad cultures and imaging, is essential in managing septic shock to identify and treat the infection site.
- π©Ή Corticosteroids, such as hydrocortisone, are considered for patients with vasopressor-refractory septic shock to improve vasopressor responsiveness.
- π The session emphasizes the importance of continuous assessment and monitoring of patients in septic shock, including mental status, perfusion, urine output, and lab trends.
Q & A
What are the objectives of the fifth session in the ICU curriculum?
-The objectives are to define sepsis and septic shock according to Sepsis-3 definitions, describe the pathophysiologic abnormalities and clinical manifestations of septic shock, and to describe the treatment principles for a patient in septic shock including appropriate antibiotics, fluid resuscitation, and vasopressors.
How is sepsis defined according to the Sepsis-3 task force definition from 2016?
-Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection.
What are the clinical criteria used to identify sepsis before the Sepsis-3 definition?
-Before the Sepsis-3 definition, sepsis was identified using the SIRS criteria, which include temperature greater than 38 or less than 36 degrees Celsius, heart rate greater than 90 beats per minute, respiratory rate greater than 20 breaths per minute, and white blood cell count greater than 12,000 or less than 4,000 or greater than 10 percent bands.
What is the qSOFA score and how is it used?
-qSOFA stands for quick Sequential Organ Failure Assessment and is used to identify patients with suspected infection likely to have sepsis or patients with sepsis at high risk of deterioration or poor outcome. It is composed of three variables: systolic hypotension less than 100 mmHg, respiratory rate greater than 22 breaths per minute, and altered mental status.
What is the clinical definition of septic shock according to the Sepsis-3 guidelines?
-Septic shock is defined as sepsis with persistent hypotension requiring vasopressors to maintain a mean arterial pressure (MAP) of at least 65 mmHg and a serum lactate greater than 2 mmol/L despite adequate fluid resuscitation.
What types of infections are most commonly associated with sepsis?
-Sepsis is most commonly caused by infections of the respiratory system, followed by infections of the gastrointestinal and genitourinary systems.
What are the clinical manifestations of septic shock?
-Clinical manifestations of septic shock include hypotension, tachycardia, altered mental status, and signs of poor perfusion such as mottling or oliguria.
What are the four main principles in the management of septic shock?
-The four main principles in the management of septic shock are early antibiotics, fluid resuscitation, vasopressors, and source control.
What is the recommended initial fluid resuscitation for patients with sepsis or septic shock?
-Patients with sepsis or septic shock should receive a bolus of 30 mL/kg of intravenous fluid for initial volume resuscitation.
Which vasopressor is typically used first in the treatment of septic shock, and why?
-Norepinephrine is typically used first in the treatment of septic shock because it is a predominant alpha-1 agonist with some additional beta agonist effects, and it has been shown to be effective in maintaining blood pressure without increasing the risk of arrhythmias compared to other vasopressors like dopamine.
What is the role of corticosteroids in the treatment of septic shock?
-Corticosteroids are typically reserved for patients in vasopressor-refractory septic shock. They may improve vasopressor responsiveness and have been associated with faster resolution of shock, more ventilator-free days, and decreased ICU length of stay.
Outlines
π Introduction to Sepsis and Septic Shock
This paragraph introduces the fifth session of the ICU curriculum, focusing on sepsis and septic shock. The session aims to define sepsis and septic shock according to the Sepsis-3 definitions, describe the physiological abnormalities and clinical manifestations, and outline the treatment principles. A case study of a 65-year-old woman with diabetes and symptoms of sepsis is presented. The patient exhibits signs of septic shock, including fever, hypotension, and tachycardia. The importance of recognizing and promptly managing sepsis and septic shock is emphasized due to their time-sensitive nature.
π¬ Understanding Sepsis and Septic Shock
The paragraph delves into the clinical definitions of sepsis and septic shock. Sepsis is defined as life-threatening organ dysfunction due to a dysregulated host response to infection. Septic shock is a subset of sepsis characterized by underlying circulatory and cellular metabolic abnormalities that significantly increase mortality. The clinical manifestations of septic shock include hypotension, elevated lactate levels, and altered mental status. The paragraph also discusses the evolution of sepsis definitions and the use of the qSOFA score to identify patients at risk of deterioration.
π©Ί Pathophysiology and Treatment of Septic Shock
This section discusses the pathophysiology of septic shock, highlighting the immune response to infection and the cascade of inflammatory reactions that can lead to organ dysfunction and death. The paragraph outlines the clinical manifestations of septic shock, including effects on the brain, respiratory system, cardiovascular system, and other organs. The treatment principles for septic shock are also detailed, emphasizing the importance of early and appropriate antibiotics, fluid resuscitation, vasopressors, and source control. The use of lactated ringers and the choice of vasopressors are specifically addressed.
π Management Strategies for Septic Shock
The final paragraph summarizes the management strategies for septic shock, including the administration of broad-spectrum antibiotics, fluid resuscitation with lactated ringers, and the use of vasopressors. It also touches on the role of corticosteroids in treating vasopressor-refractory septic shock and the importance of source control. The paragraph concludes by reiterating the critical nature of early intervention and the need for continuous assessment and monitoring of patients with septic shock.
Mindmap
Keywords
π‘Sepsis
π‘Septic Shock
π‘SIRS Criteria
π‘qSOFA
π‘Lactate
π‘Fluid Resuscitation
π‘Vasopressors
π‘Broad-Spectrum Antibiotics
π‘Source Control
π‘Corticosteroids
π‘Cardiac Output
Highlights
Definition of septic shock according to Sepsis-3 guidelines.
Clinical manifestations and treatment principles for septic shock.
The importance of early recognition and management of sepsis and septic shock.
The evolution of sepsis definitions and the current Sepsis-3 criteria.
The clinical signs of sepsis using the SOFA score for severity assessment.
The distinction between sepsis and septic shock in terms of circulatory and cellular metabolism abnormalities.
The pathophysiology of septic shock, including the role of nitric oxide and mitochondrial dysfunction.
The types of infections that commonly cause sepsis and their clinical presentations.
The end-organ effects of septic shock, including encephalopathy, ARDS, and cardiovascular dysfunction.
The four main principles in the management of septic shock: early antibiotics, fluid resuscitation, vasopressors, and source control.
The significance of early and appropriate antibiotic therapy in septic shock.
The role of fluid resuscitation with lactated ringers in the initial management of septic shock.
The choice of vasopressors in septic shock, with a focus on norepinephrine and vasopressin.
The use of corticosteroids in vasopressor-refractory septic shock and their impact on outcomes.
The importance of source control in the management of septic shock.
The continuous assessment and monitoring of patients in septic shock, including vasopressor requirements and lab trends.
A checklist of high-yield management principles for septic shock.
Transcripts
welcome to the fifth session in the ICU
curriculum in this session will cover
septic shock our objectives for the
session include to define sepsis and
septic shock
according to sepsis three definitions
describe the path of physiologic
abnormalities and clinical
manifestations of septic shock and to
describe the treatment principles for a
patient in septic shock including
appropriate antibiotics fluid
resuscitation and vasopressors as a
reminder in our prior session on shock
we introduced the shock and awe physical
exam based approach for going through
the shock differential at the bedside
for an undifferentiated patient in
today's session we will be talking about
the first part of this approach let's
start with a case
the patient is a 65 year old woman with
diabetes presenting with a three day
history of dysuria and right flank pain
this morning she became lightheaded
dizzy and developed shaking chills in
the ER she has febrile to 39.5
hypotensive to 70 over 40 and
tachycardic to 140 on exam she is pale
lethargic and has super pubic and
right-sided CVA tenderness after
approximately two liters of IV fluid her
blood pressure remains 75 over 40 labs
return and she is a white blood cell
count of 17 creatinine of 2.5 and
lactate of 6 she is admitted to the ICU
for further management
it appears the patient is septic likely
from pyelonephritis and perhaps
gram-negative bacteria given her ragas
but is she in septic shock and if so how
are we going to treat her when she
arrives to the ICU sepsis is a
time-sensitive medical emergency in the
same way that stem ease and CBA's are
emergencies therefore it is important
that every doctor be able to recognize
sepsis and septic shock and initiate
evaluation and management promptly in
order to recognize sepsis and septic
shock we first need to be able to define
both terms clinically
to define septic shock you first need to
be able to recognize and define sepsis
the definition for sepsis has evolved
over the years we are currently using
the sepsis 3 task force definition from
2016 which defines sepsis as
life-threatening organ dysfunction
caused by a dysregulated host response
to infection what a sepsis look like
clinically from 1991 to 2016 sepsis was
defined as two out of four service
criteria plus a suspected site of
infection as a review the service
criteria include temperature greater
than 38 or less than 36 degrees Celsius
heart rate greater than 90 beats per
minute
respiratory rate greater than 20 breaths
per minute and white blood cell count
greater than 12,000 or less than 4000 or
greater than 10 percent bands the
problem with serves is that it is not
specific enough for recognizing sepsis
as a number of common inpatient medical
problems can cause at least two of the
after mentioned abnormalities what else
can we use then to identify the sickest
patients with sepsis the answer q sofa Q
sofa stands for quick sequential organ
failure assessment it was created to
identify patients with suspected
infection likely to have sepsis or
patients with sepsis at high risk of
deterioration or poor outcome outside of
the ICU for example patients on the
floor or in the emergency room Q sofa is
composed of three variables systolic
hypotension less than 100 millimeters of
mercury respiratory rate greater than 22
breaths per minute an altered mental
status as discussed in previous sessions
to Kipp Nia and respiratory alkalosis
are often the body's compensatory
response to the worsening metabolic
acidosis in sepsis or septic shock one
point is given for each variable present
scores greater than or equal to two or
predictive of worsened outcomes and
increased in hospital mortality so in a
patient with either unknown or suspected
infection two out of three Q sofa
variables should prompt consideration of
sepsis and/or escalation of care to the
ICU note the term severe sepsis has
largely fallen out of favor
moving on to septic shock sepsis three
define septic shock as a subset of
sepsis and which underlying circulatory
and cellular metabolism abnormalities
are profound enough to substantially
increase mortality
clinically septic shock is defined as
sepsis plus phase oppressors needed to
maintain a map greater than or equal to
65 and a serum lactate greater than two
despite adequate fluid resuscitation
here defined as 30 CC's per kilogram of
body weight basically septic shock is
sepsis plus hypotension after
appropriate fluid resuscitation know
from the sepsis three guidelines meeting
all of these criteria is associated with
greater than 40 percent hospital
mortality so we have defined sepsis and
septic shock next let's describe the
pathophysiologic abnormalities and
clinical manifestations of septic shock
at its most basic sepsis represents the
body's immune response to infection an
infection triggers a cascade of
inflammatory and immune responses that
can potentially lead to multi organ
dysfunction and death what types of
infections cause sepsis prior to the
1980s gram-negative infections
predominated in a gram-negative
infection lipopolysaccharide or LPS of
the bacterial cell wall triggers the
inflammatory response since the 1980s
gram-positive infections have been the
most common cause of sepsis
gram-positive infections namely staph
aureus and strep pyogenes trigger
inflammation via exotoxin sepsis is most
commonly caused by infections of the
respiratory system and then by
infections of the GI and GU systems next
what are the clinical manifestations of
septic shock as discussed in the shock
session the equation mean arterial
pressure equals cardiac output times
systemic vascular resistance defines
much of the physiology encountered
within the ICU in shock the mean
arterial pressure decreases therefore
there are two ways to achieve a low mean
arterial pressure either a decrease in
the cardiac output or systemic vascular
resistance septic shock Falls him to the
broad category of distributive shock and
is characterized by a decrease in the
systemic vascular resistance and often a
compensatory increase in the cardiac
output why does the decrease in SVR
occur the answer excessive an
uncontrolled release of nitric oxide via
an inducible nitric oxide synthase
excess nitric oxide caused a systemic
baser dilation and decreases vascular
tone for this reason patients with
septic shock rough and warm and flushed
there is also a mitochondrial damage
which impairs cellular oxygen
utilization the peripheral tissues and
vital organs what are the end organ
effects of pathologic vasodilation and
cellular hypoxia on the screen is a
figure used in the shock session we will
again use this figure to discuss
clinical effects and end organ
dysfunction and septic shock in a
head-to-toe fashion in the brain septic
shock causes encephalopathy and delirium
in part due to decreased cerebral
perfusion referring back to earlier in
the session
remember that altered Mental Status is
also one of the cue sofa criteria from a
respiratory standpoint septic shock can
cause the acute respiratory distress
syndrome or a RDS a RTS is one of the
most important and organ effects of
septic shock and is associated with the
significant amount of
immortality of present pictured in this
x-ray are the characteristic bilateral
alveolar infiltrates of a RDS within the
cardiovascular system septic shock can
cause ventricular dysfunction there are
multiple GI FX of septic shock
including bowel ischemia due to
hypoperfusion ileus shock liver and
cholestasis in a calculous cholecystitis
approximately 50% of patients with
septic shock will develop acute kidney
injury secondary to acute tubular
necrosis or a TN patients may also
develop relative adrenal insufficiency
disseminated intravascular coagulation
and thrombocytopenia at this point we've
discussed definitions of sepsis and
septic shock
clinical manifestations and end organ
damage the CEM result next how do we
treat septic shock in order to minimize
the chance of all these horrible things
happening we stated at the beginning of
the session that septic shock is a
medical emergency requiring immediate
treatment there are four main principles
in the management of septic shock early
antibiotics fluid resuscitation
vasopressors and source control let's go
through each of these principles one by
one first antibiotics the life-saving
intervention in sepsis and septic shock
from a study in 2014 for every one hour
delay in antibiotics and septic shock
there is a three to seven percent
increase in the odds of in hospital
death what is an appropriate initial
antibiotic regimen the initial regimen
should include broad gram-negative
coverage plus Pseudomonas as well as
methicillin-resistant Staph aureus or
Mrs a coverage for gram-negative
coverage possible options include
piperacillin Tazo back dam cefepime plus
metronidazole and meropenem
metronidazole is included with cefepime
for improved anaerobic coverage for mrs
a coverage possible options include
vancomycin and lynnae's illud
antibiotics need time to work therefore
we need to support the patient's blood
pressure and profuse the vital organs
while the antibiotics kick in we
accomplish this with fluid resuscitation
and vasopressors first fluid
resuscitation
patients with sepsis or septic shock
should receive a bolus of 30 CC's per
kilogram of intravenous fluid for
initial volume resuscitation nope fluid
resuscitation and sepsis and septic
shock is currently under further
investigation with numerous ongoing RCTs
at this time guidelines continue to
recommend an initial 30 CC per kilogram
bolus within the first three hours and
management this guideline is from the
surviving sepsis campaign report of 2016
and is a strong recommendation with low
quality evidence so we've decided to
give our patient 30 CC's per kilogram of
IV fluid should the patient receive
crystalloid meaning lactated ringers and
normal saline or colloid meaning albumin
or starches
the answer crystal a Cochrane review
from 2018 found no difference in
outcomes including mortality and need
for renal replacement therapy between
crystalloid and colloid with
crystalloids being cheaper and more
readily available so we decided to give
our patient of 30 cc per kilogram bolus
of crystalloid for our crystalloid
should we choose lactated ringers or
normal saline the answer lactated
ringers the smart med trial from
Vanderbilt in 2018 enrolled more than
15,000 patients and compared LR to NS
for initial volume resuscitation and
critically ill adults admitted to the
ICU the study found the LR reduced death
from any cause need for new renal
replacement therapy or persistent renal
dysfunction
therefore LR should be the choice in
almost all situations for initial volume
resuscitation in critically ill adults
finally it is important to keep in mind
that each patient is different and some
patients may require additional fluid
after the initial 30 CC per kilogram
bolus fluid administration at that time
should be based upon objective measures
of fluid responsiveness including
passive straight leg raise bedside
ultrasound etc so we've administered
broad-spectrum antibiotics and the
patient has received their initial 30 cc
per kilogram bolus of lactated ringers
however as in our example from the
beginning of the session the patient
remains hypotensive with an elevated
lactate what do we do next the answer ad
vasopressors our goal with Basel
pressors is to maintain a mean arterial
pressure greater than or equal 65
millimeters of mercury in order to
maintain perfusion of the vital organs
the main bays opressors available in the
ICU are norepinephrine epinephrine
phenol Efren and vasopressin of these
which phase opressor do we reach for
first typically our first phase
oppressor is norepinephrine
norepinephrine is a predominant alpha-1
agonist with some additional beta
agonist why norepinephrine soap 2 was a
large RCT in 2010 that compared
norepinephrine to dopamine for treatment
of septic shock the study found no
difference in 28-day mortality but an
increased risk of arrhythmias with
dopamine compared to norepinephrine
therefore norepinephrine became the
first pressure of choice so we add
norepinephrine
but unfortunately the patient's mean
arterial pressure remains less than 65
on increasing doses of norepinephrine
what pressor do we typically add next
the answer
vasopressin vasopressin unsurprisingly
acts on the vasopressin receptors
vasopressin has given it a fixed dose of
point zero 3 or point zero four units
per minute because dose is greater than
point zero 4 it increased the risk of
coronary and mesenteric ischemia
why add vasopressin to norepinephrine
the vast trial in 2008 compared adding
additional norepinephrine to vasopressin
for patients with septic shock who were
already receiving norepinephrine well
the study found no mortality benefit
from vasopressin vasopressin use did
allow for decreased dosages of
norepinephrine therefore for patients
with norepinephrine refractory shock
vasopressin is an appropriate second
agent to add
unfortunately after adding vasopressin
the patient remains hypotensive with the
map less than 65 while trying to figure
out why the patient is deteriorating we
can add fennel Efren and or epinephrine
for blood pressure support fennel Efrain
is a pure alpha one agonist it is
typically the third vasopressor added
after norepinephrine and vasopressin
but can also be used as a primary base
oppressor for patients that develop
tachyarrhythmias like a fib with rbr or
SVT from the beta agonizing HEPA nephron
works via the alpha 1 and beta receptors
no it has more beta agonizing than
norepinephrine it is typically the third
or fourth phase of pressure added if
needed take a second again to review the
receptors on which the various phase
oppressors act
as antibiotics fluids and BAE's
oppressors are infusing it's important
to go looking for the source of
infection with broad cultures and
imaging if possible
what about corticosteroids for example
hydrocortisone in the treatment of
septic shock corticosteroids are
typically reserved for patients in
vasopressor refractory shock vasopressor
refractory shock is typically defined as
shock requiring both norepinephrine and
vasopressin to maintain a map greater
than 65 if a patient is requiring both
norepinephrine and vasopressin we can
add on hydrocortisone
at a dose of either 50 milligrams every
six hours or 100 milligrams every eight
hours as discussed earlier patients in
septic shock may have relative adrenal
insufficiency and corticosteroids may
improve vasopressor responsiveness there
have been numerous landmark studies over
the last two decades evaluating the role
of corticosteroids in septic shock to
name a few there has been the French
trial otherwise known as the anon trial
in 2002 cortico sand 2008 and adrenal
and approaches in 2018 these studies
have demonstrated mixed mortality
outcomes the French trial and approaches
both demonstrated mortality benefit from
corticosteroids while QWERTY kisum
adrenal do not demonstrate a mortality
benefit however all of these landmark
studies demonstrate that corticosteroids
are associated with faster resolution of
shock more ventilator free days and
decreased ICU length of stay all of
which are objectively good things but
what about corticosteroids for patients
with sepsis without shock the high press
trial in 2016 found no role for
hydrocortisone and patients with sepsis
without shock
in summary corticosteroids represent an
evidence-based Salvage therapy for
patients with vasopressor refractory
septic shock we discussed the importance
of early antibiotics IV fluid
resuscitation phase opressors
corticosteroids and source control you
know these interventions are working by
continuously assessing the patient's
exam including mentation perfusion
status urine output etc their
vasopressin requirements and by trending
labs every four to six hours
on this page is a checklist highlighting
the high yield management principles
just discussed
in summary in this session we define
sepsis and septic shock
according to sepsis three definitions we
describe the pathophysiologic
abnormalities and clinical
manifestations of septic shock and
finally describe the treatment
principles for a patient in septic shock
including early broad-spectrum
antibiotics fluid resuscitation with
lactated ringers and bayes oppressors
thank you for your participation
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