Septic shock initial 1 hour EM | Jean-Louis Vincent at TBS23

Jean-Louis Vincent, MD, PhD
Professor of intensive care medicine
(University of Brussels)
Past-President, European Society of Intensive Care Medicine
Past-President, World Federation of Intensive and Critical Care Societies
SEPSIS
INITIAL RESUSCITATION
IN THE EMERGENCY DEPT

I HAVE
NO CONFLICT OF INTEREST

Definition
Criteria
(scientific publication)
Definition

✓Circulatory
✓Respiratory
✓Renal
✓Hepatic
✓Neurological
✓Hematological
SEPSIS ?
ACUTE CHANGES IN ORGAN FUNCTION
hypotension, tachycardia
hyperlactatemia
disorientation, confusion
tachypnea, hypoxemia (low SpO2)
oliguria
increased creatinine levels
Icterus,
hyperbilirubinemia
low platelet count
If these acute changes are not well explained

quickSOFA (qSOFA)
✓ Tachypnea (RR ≥ 22 breaths/min)
✓ Hypotension (systolic BP ≤100 mmHg)
✓ Altered Mentation
ALARM SIGNAL
to identify infected patients with poor outcomes
- additional tests to evaluate organ function
- prompt intervention
- increased surveillance / transfer to ICU?

✓Circulatory
✓Respiratory
✓Renal
✓Hepatic
✓Neurological
✓Hematological
SEPSIS ?
hyperlactatemia
oliguria
Icterus,
hyperbilirubinemia
low platelet count
If these acute changes are not explained by other factors than an infection

✓Circulatory
✓Respiratory
✓Renal
✓Hepatic
✓Neurological
✓Hematological
SEPSIS ?
hyperlactatemia
oliguria
Icterus,
hyperbilirubinemia
low platelet count
If these acute changes are not explained by other factors than an infection
hypotension
tachypnea
altered
mentation
qSOFA

qSOFA SEPSIS INFECTION

qSOFA SEPSIS INFECTION
qSOFA is NOT specific for sepsis
It could be severe heart failure, hypovolemia, pulmonary embolism…

Risk assessment of the blunt trauma victim:
The role of the quick Sequential Organ Failure
Assessment Score (qSOFA)
Jawa et al

HEMODYNAMIC
STABILIZATION
INFECTION
CONTROL
MODULATION
OF THE
HOST RESPONSE
IV fluids Vasoactive
agents Antibiotics Source
control
MANAGEMENT OF SEPSIS

INFECTION
IF
antibiotics are effective
THEN
antibiotic therapy 1) should be started early
2) should be adequate

INFECTION
IF
antibiotics are effective
THEN
antibiotic therapy 1) should be started early
2) should be adequate
Very important
in severe cases

ANTIBIOTIC THERAPY IN SEPSIS
Timing
Choice

e.g. septic shock
meningococcemia
e.g. possible
lung infection
(+ moderate OF)
SEVERITY
1
12
2
3
4
5
6
7
8
9
10
11
No waste
of time

e.g. septic shock
meningococcemia
e.g. possible
lung infection
(+ moderate OF)
SEVERITY
Urgently Very early Early
1
12
2
3
4
5
6
7
8
9
10
11
No waste
of time

e.g. septic shock
meningococcemia
e.g. possible
lung infection
(+ moderate OF)
SEVERITY
Urgently Very early Early
1
12
2
3
4
5
6
7
8
9
10
11
No waste
of time
Additional tests?
(BAL?)
Advise?

2021
nationwide VA hospitals (N = 111,385 pts)
30 d mortality 12.4%
time-to-antibiotics for sepsis has declined over time

3035 patients (20% septic shock)
19 hospitals (Sept 2019 – Dec 2020)
2022

2021
24,093 cases - 12 hospitals
OR for mortality
Recognition delay
Administration delay

What I tell the nurse
Give antibiotics without delay
in severe cases
How I treat septic shock
I motivate the team!

Conclusion:
Among patients with severe manifestations of sepsis,
initiation of empirical antimicrobial therapy significantly reduces
the sensitivity of blood cultures drawn shortly after treatment initiation.
Preantimicrobial blood cultures were positive in 102 of 325 (31.4%) patients.
Postantimicrobial blood cultures were positive in 63 of 325 (19.4%) patients
Adults with severe manifestations of sepsis,
(systolic BP< 90 mm Hg or serum lactate level > 4 mmol/L)
Intervention:
Blood cultures obtained before and within 120 min after initiation of antimicrobial treatment.
2019

URGENT
Broad spectrum
antibiotics
EARLY
Evaluate – discuss
- Other tests?
1
12
2
3
4
5
6
7
8
9
10
11
No waste
of time

MICROBIAL RESISTANCE IN SEPSIS
Sepsis
Need to cover for all
responsible microorganisms
Rapid action

Sepsis
Rapid action
Medico-legal
pressure

Sepsis
Use of broad spectrum
antibiotics
Rapid action
Medico-legal
pressure

Sepsis
Use of broad spectrum
antibiotics
Increase in microbial
resistance
Rapid action
Medico-legal
pressure

2023
Severe Sepsis/Septic Shock Early Management Bundle (SEP-1).
SEP-1 requires hospitals to report adherence to the bundle.

2023
Including broad-spectrum antibiotics within 3 hours +
at least 30 mL/kg of crystalloids for hypotension or hyperlactatemia.
Hospitals receive credit only if all components are performed
or contraindications documented.

2023
Four large, rigorous, multicenter time-series analyses document
the disappointing real-world impact of SEP-1 across hundreds of US hospitals.
No change in mortality.
Benefit only in SEP-1–compliant vs noncompliant care (different populations).
Pakyz et al. Clin Infect Dis. 2021;
Rhee et al. JAMA Open. 2021
Barbash et al. Ann Intern Med. 2021
Anderson et al. Clin Infect Dis. 2022

2023
The use of broad-spectrum antibiotics increased. Aggressive fluid resuscitation.

2023
The use of broad-spectrum antibiotics increased. Aggressive fluid resuscitation.
it focuses exclusively on the initial hours of care and lacks incentives
to optimize subsequent care.

I give antibiotics as soon as possible….
the more severe the clinical presentation
the more urgent the antibiotic administration
Antibiotic therapy should cover all likely pathogens
Not less – not more!
ANTIBIOTICS

Possible infection
(fever?)
Take
bacteriological samples
Is the patient critically ill?
General
strategy

Possible infection
(fever?)
Take
No
Evaluate
Withhold
antibiotics
‘reasonable’
antibiotic
therapy
Yes
General
strategy

Possible infection
(fever?)
Take
No
Evaluate
Withhold
antibiotics
‘reasonable’
antibiotic
therapy
Yes
In shock?
Yes
No
Urgent
Broad spectrum
antibiotics
General
strategy

Possible infection
(fever?)
Take
No
Evaluate
Withhold
antibiotics
‘reasonable’
antibiotic
therapy
Yes
In shock?
Yes
No
Urgent
Broad spectrum
antibiotics
Reevaluate
General
strategy

HEMODYNAMIC
STABILIZATION
INFECTION
CONTROL
MODULATION
OF THE
HOST RESPONSE
agents Antibiotics
Source
control

SOURCE OF SEPSIS ?
The big five

SOURCE OF SEPSIS ?
The big five
Lungs
Abdomen
Urine
Skin
Catheter

This patient needs
to go to the OR
immediately !
RAPID SOURCE CONTROL

This patient needs
to go to the OR
immediately !
Yes, the
anesthesiologist
is on his way

This patient needs
to go to the OR
immediately !
Yes, the
anesthesiologist
is on his way
The surgeon
is quickly evaluating
another patient
first

This patient needs
to go to the OR
immediately !
Yes, the
anesthesiologist
is on his way
They will call us
as soon as
the OR is ready
The surgeon
another patient
first

This patient needs
to go to the OR
immediately !
Yes, the
anesthesiologist
is on his way
They will call us
as soon as
the OR is ready
Shouldn't we
have another CT
first ?
The surgeon
another patient
first

Control the source when indicated,
and as soon as possible
I motivate the team!

Ventilate
Infuse
Pump
The VIPrule
(Weil and colleagues)
Oxygen administation
mechanical ventilation ?
IV fluids
Blood transfusions ?
Vasopressor agents ?
Dobutamine ?

High flow oxygen
Non-invasive ventilatiion
In shock states
In shock states

Ventilate Oxygen administation
When to intubate the trachea ?
Answer : When the question is raised…
Question :
What are the benefits of mechanical ventilation ?
Question :
Answer : Improved gas exchange
Decreased oxygen requirements (of the respiratory muscles)
(Unloading of the left ventricle)
Severe hypoxemia and/or elevated work of breathing

Endotracheal intubation : optimal timing
TIME
Is intubation
avoidable?
Respiratory
arrest
When is
the right time?

Endotracheal intubation : optimal timing
TIME
Is intubation
avoidable?
Respiratory
arrest
Dyspnea
RR
Gas exchange
Speech
Consciousness
When is
the right time?

SURVIVAL
DAYS
Early
intubation
Late
intubation
2022
735 pts – 78 x 2

The new SSC guidelines offer little leeway for adapting
the recommendations to the idiosyncrasies of each and every patient.
Some allowance for breaking the “one size fits all” guideline mold
that has taken root in the last two decades
would have been a daring but welcome and timely change.
2021

We recommend individualizing the need for and timing of tracheal intubation,
based on careful clinical assessment, including level of consciousness, respiratory
rate and work of breathing, hemodynamic status, and assessment of gas exchange.
Delaying tracheal intubation may lead to respiratory and even cardiac arrest, with
dire consequences,
yet premature use of invasive mechanical ventilation can expose the patient to
ventilator-induced lung injury, distant organ complications, and increased risk of
nosocomial lung infection.
2021

PaO2/FiO2
Very low Low
Endotracheal intubation?
AI in medicine

PaO2/FiO2
Very low Low
Neurological
status
Coma Conscious state
AI in medicine

PaO2/FiO2
Very low Low
Neurological
status
PCO2
Acidemia
(hypercapnic acidosis)
Normal pH
AI in medicine

PaO2/FiO2
Very low Low
Neurological
status
PCO2
Acidemia
Normal pH
Hemodynamic
status
Altered
tissue perfusion
Normal
tissue perfusion
AI in medicine

PaO2/FiO2
Very low Low
Neurological
status
PCO2
Acidemia
Normal pH
Hemodynamic
status
Altered
tissue perfusion
Normal
tissue perfusion
Muscle function
Muscle weakness
Use of accessory muscles
Normal strength
AI in medicine

PaO2/FiO2
Very low Low
Neurological
status
PCO2
Acidemia
Normal pH
Hemodynamic
status
Altered
tissue perfusion
Normal
tissue perfusion
Muscle function
Muscle weakness
Use of accessory muscles
Normal strength
Plans for
major surgery
Yes No
AI in medicine

When to intubate the trachea ?

A recommendation to keep SpO2within the low-normal range of 92–96%
in all critically ill patients
is easily achievable with minimum effort and little cost.

Ventilate
Infuse
Pump
The VIPrule
(Weil and colleagues)
Oxygen administation
IV fluids
Blood transfusions ?
Vasopressor agents ?
Dobutamine ?

HEMODYNAMIC
STABILIZATION
INFECTION
CONTROL
MODULATION
OF THE
SEPSIS RESPONSE
agents
Antibiotics Source
control
SEPSIS MANAGEMENT

Normal
Fluid requirement is more than correction of hypovolemia

Normal
Hypovolemia

Normal
Blood volume
in the critically ill
(sepsis, surgery, trauma,…)
Hypovolemia
Vasodilation

Normal
Blood volume
Hypovolemia
Vasodilation
Capillary
leak

Normal
Blood volume
Hypovolemia
Vasodilation
Hyperdynamic
state
CARDIAC
OUTPUT
FILLING
Capillary
leak

RESTRICTED
FLUID
ADMINISTRATION
LIBERAL
FLUID
ADMINISTRATION

"critically ill"
"ARDS"
"sepsis"
More IV fluids
Less IV fluids
RANDOMIZATION
CLINICAL TRIALS IN THE ICU

"critically ill"
"ARDS"
"sepsis"
More IV fluids
Less IV fluids
RANDOMIZATION
No difference in outcome

Benefit
Harm
"critically ill"
"ARDS"
"sepsis"
More IV fluids
Less IV fluids
RANDOMIZATION
Benefit
Harm

INCREASE IN
CARDIAC OUTPUT
INCREASE IN AP
IMPROVED TISSUE PERFUSION
INCREASED URINE OUTPUT
FLUIDS VASOPRESSORS

INCREASE IN
VENOUS PRESSURES
EXCESSIVE
EDEMA
FORMATION
INCREASE IN
CARDIAC OUTPUT
INCREASE IN AP
FLUIDS VASOPRESSORS

INCREASE IN
VENOUS PRESSURES
EXCESSIVE
EDEMA
FORMATION
INCREASE IN
CARDIAC OUTPUT
INCREASE IN AP
FLUIDS VASOPRESSORS
INCREASE IN
ARTERIAL PRESSURE

INCREASE IN
VENOUS PRESSURES
EXCESSIVE
EDEMA
FORMATION
INCREASE IN
CARDIAC OUTPUT
INCREASE IN AP
FLUIDS VASOPRESSORS
VASOCONSTRICTION
IMPAIRED OXYGEN AVILABILITY
DECREASED CARDIAC OUTPUT
INCREASE IN
ARTERIAL PRESSURE

FLUIDS Nepi
BAD BAD
FLUIDS and / or VASOPRESSORS
amount amount

250 to 500 ml allowed only in severe hypoperfusion
(lactate >4 mMol/L, MAP < 50 mmHg despite vasopressors, mottling, UO < 0.1 ml/kg/h)
& to ensure a total daily fluid intake of 1 liter.
fluids in fluid – responsive patients
2022
Restrictive
Standard
CLASSIC trial – 1554 patients

250 to 500 ml allowed only in severe hypoperfusion
(lactate >4 mMol/L, MAP < 50 mmHg despite vasopressors, mottling, UO < 0.1 ml/kg/h)
& to ensure a total daily fluid intake of 1 liter.
fluids in fluid – responsive patients
2022
Restrictive
Standard
No difference in any outcome
CLASSIC trial – 1554 patients

2 possible explanations
➢Fluids vs. vasopressors: it does not matter
(you do not need intelligence)
➢Treatment should be personalized
(you do need intelligence)
2023
NO DIFFERENCE

2021
p
(PROPENSITY SCORE MATCHING)
Immediate
(<1 hour)
Delayed
(>1 hour)
16 hospitals in Korea
vasopressor therapy

2021
Higher SOFA score and
Higher blood lactate level
on ICU day 3
p
Immediate
(<1 hour)
Delayed
(>1 hour)
vasopressor therapy

2021
Say YES to early vasopressor use
but this should not limit fluid administration!
Higher SOFA score and
Higher blood lactate level
on ICU day 3
p
Immediate
(<1 hour)
Delayed
(>1 hour)
vasopressor therapy

Fluid restriction will always reduce edema
(cerebral, pulmonary, cutaneous…)
Fluid restriction may decrease oxygen availability
Fluid restriction may impair healing
Fluid restriction may result in multiple organ failure
FLUID RESTRICTION IS DANGEROUS

The mean volume infused as boluses on day 1 was
1162 mL (916 mL) for slower infusion vs
1252mL (1009mL) for control infusion rate
Outcomes Comparing Slower (333 mL/h) vs Control (999 mL/h) Infusion Speed
2021

Conditional Treatment Effect Analysis of Two Infusion Rates
in Critically Ill Patients: BaSICS Trial
FG Zampieri et al., Ann Am Thorac Soc.
2023
10,465 pts
Model trained in 5230 pts
Model tested in 5235 pts

2023
81%
No recommendation
5%
333 mL/h
14%
999 mL/h
10,465 pts
Recommendation

2023
81%
No recommendation
5%
333 mL/h
14%
999 mL/h
10,465 pts
36 years
APACHE II 7
RRT 3.6%
Mortality 7.9%
Recommendation

2023
81%
No recommendation
5%
333 mL/h
14%
999 mL/h
10,465 pts
36 years
APACHE II 7
RRT 3.6%
Mortality 7.9%
79 years
APACHE II 17
RRT 12%
Mortality 46%
Recommendation

AN EDEMATOUS PATIENT
MAY BE HYPOVOLEMIC

AN EDEMATOUS PATIENT
MAY BE HYPOVOLEMIC
Beware of the terms
➢ Hypervolemia
➢ Fluid overload

How do you call it?
Fluid overload? Hypervolemia? Edema
Edema does not exclude hypovolemia!

2018
The terms hypervolemia and fluid overload are often used interchangeably,
yet they do not have the same meaning.
“Fluid overload” may vaguely refer
to excess total body water content associated with edema,
but it would be better if the term were avoided completely.
The word “hypervolemia” is sufficient to indicate an excess in circulating
blood volume and, if present, needs to be properly documented before a
strategy of fluid restriction and/or diuretics is applied.

How much fluids?
By formula
Fluid balance / presence of edema
Individualized / Monitoring

SOSD
Rapid fluid
administration
(1 liter fast)
Individualize
(fluid challenge)
Limit fluid
infusion
no need for
fluid challenges
Minimal fluid
infusion
Diuretics
Ultrafiltration?

INITIAL RESUSCITATION
(salvage)

Does this patient need IV fluid ?

Central venous pressure 6 mmHg maybe

Arterial pressure 85/45 mmHg maybe

Heart rate 117 / min maybe

Cardiac output 3.9 L/min maybe

Urine output 10 mL/h maybe

ScvO2 60 % maybe

ScvO2 60 % maybe
Lactate 3.1 mEq/L maybe

Static
vs.
Dynamic
measurements
a CVP level
a EDV level
cardiac chamber size
PPV / SSV when applicable
Fluid challenge
Passive leg raising

Static
vs.
Dynamic
measurements
a CVP level
a EDV level
cardiac chamber size
PPV / SSV when applicable
Fluid challenge
Passive leg raising
preferable

MORE FLUIDS ?
Pulse Pressure Variation (PPV)
Stroke Volume Variation (SVV)
Anesthetized or
Deeply sedated/paralyzed
Spontaneous breathing
(with or without mechanical ventilation)
Fully controlled
mechanical ventilation
End-expiratory pause
Sigh

AIRWAY
PRESSURE
ARTERIAL
PRESSURE
FLUID RESPONSIVENESS
Transient increase in
intrathoracic pressure
Transient decrease in venous return
(+ reduced RV ejection)
Decreased RV stroke volume
Decreased LV stroke volume
(after a few beats)
Transient decrease
in pulse pressure

Pulse Pressure Variation
(PPV)
Stroke Volume Variation
(SVV)
AP monitoring
CO monitoring
ONLY
During mechanical ventilation
With deep sedation / anesthesia
(without major arrhythmia)

END-DIASTOLIC VOLUME
STROKE
VOLUME

Sedative agents?
Shock No shock
Adverse
hemodynamic
effects
Delirium
Weakness
Cognitive alterations

No routine sedation for comfort
Use sedative agents only when absolutely required
Sedative agents can have adverse hemodynamic effects
SEDATIVE AGENTS

I AVOID SEDATIVE AGENTS
Decreased vascular tone
Decreased myocardial contracility
Risk of delirium
Long term weakness

MORE FLUIDS ?
Fluid
challenge
Pulse Pressure Variation (PPV)
Stroke Volume Variation (SVV)
Anesthetized or
Deeply sedated/paralyzed
Spontaneous breathing
(with or without mechanical ventilation)
Fully controlled
mechanival ventilation
End-expiratory pause
Sigh

ECHOCARDIOGRAPHY
All cardiac measurements
All diagnosis
Large pericardial effusion / tamponade
Severe valvular dysfunction
LV failure
RV dilatation
Any
medical
doctor
cardiologist
ICU / ER
doctor

ECHOCARDIOGRAPHY
All cardiac measurements
All diagnosis
Quantitative assessment of LV function
Mild/moderate valvular dysfunction
Assessment of cardiac output
and pulmonary artery pressures
Reliable assessment of VTI
Large pericardial effusion / tamponade
Severe valvular dysfunction
LV failure
RV dilatation
Any
medical
doctor
cardiologist
ICU / ER
doctor

Fluid
challenge
Dobutamine
challenge
Vasopressor
challenge
THE CHALLENGES

The goal of fluid administration
Increase
in DO2
Improved
tissue perfusion
Increase
in cardiac output

The goal of fluid administration
Increase
in DO2
No increase
in edema
Improved
tissue perfusion
Minimal increase
in cardiac filling pressures
Increase
in cardiac output

CVP / PAOP
EDV
CARDIAC
OUTPUT
CARDIAC FILLING PRESSURES/VOLUMES
AS INDICATORS OF FLUID RESPONSIVENESS
FRANK-STARLING RELATION

CVP / PAOP
EDV
CARDIAC
OUTPUT
CARDIAC FILLING PRESSURES/VOLUMES
AS INDICATORS OF FLUID RESPONSIVENESS
Likely to
respond
?
FRANK-STARLING RELATION

COST
BENEFIT
MORE IV FLUIDS ?
Major increase
in filling
No significant increase
in cardiac output
Minor increase
in filling
Significant increase
in cardiac output

COST
BENEFIT
MORE IV FLUIDS ?
Major increase
in filling
No significant increase
in cardiac output
Minor increase
in filling
Significant increase
in cardiac output
CARDIAC
OUTPUT
CARDIAC
FILLING

CENTRAL VENOUS CATHETER
Treatment
Monitoring
Rapid and safe fluid administration
Safe administration of vasopressors
CVP
ScvO2
Easy blood sampling
(if no arterial catheter)

FLUID ADMINISTRATION
Fluid challenge
PRACTICALLY ?

>20 min
in
at least 50%
of the studies
2022
Positive response:
> 15% increase in CO
124 studies

TIME should be LIMITED
for two reasons
1- to avoid giving much fluid
in the patient who does not benefit
2- to avoid interferences
from other interventions
Fluid challenge
Vincent JL & Weil MH, Crit Care Med 34: 1333-7, 2006
Vincent JL, Cecconi M, De Backer D, Crit Care 2020

TIME, min
CO
Too slow / too long Too small effect
Other influences
on cardiac output
30 min
Fluid challenge

TIME, min
CO
Too slow / too long Too small effect
Other influences
on cardiac output
Optimal? (ER/ICU)
CO
5-10 min
30 min
Fluid challenge

Fluid challenge
assess assess
Do not change anything (vasoactive agents, …)
Do not suction the trachea…
Do not stimulate the patient…
Do not touch the patient !
Baseline 5-10 min
100 – 200 mL

Fluid challenge
assess assess
Do not change anything (vasoactive agents, …)
Do not suction the trachea…
Do not stimulate the patient…
Do not touch the patient !
Baseline 5-10 min
100 – 200 mL
assess
5-10 min
100 – 200 mL

1 liter in 30 min
What is a
fluid challenge?

1 liter in 30 min
What is a
fluid challenge?
200 mL in 5-10 min

1 liter in 30 min
What is a
fluid challenge?
200 mL in 5-10 min
200 mL in 5-10 min
Repeat?

1 liter in 30 min
What is a
fluid challenge?
200 mL in 5-10 min
200 mL in 5-10 min
200 mL in 5-10 min
Repeat?
Repeat?

100 mL HES in 1 min
Anesthesiology, 2011

TIME, min
CO
Too slow / too long
EFFECTS OF FLUID BOLUSES
Too small effect
Other influences
on cardiac output
Optimal? (ER/ICU)
CO
5-10 min
30 min

TIME, min
CO
Too slow / too long
Too small effect
Other influences
on cardiac output
Short time (OR)
CO
Optimal? (ER/ICU)
CO
1 min
5-10 min
30 min

Too short time
CO
TIME, min
CO
Too slow / too long
positive response
in any individual
Too small effect
Other influences
on cardiac output
Short time (OR)
CO
Optimal? (ER/ICU)
CO
< 1 min
1 min
5-10 min
30 min

Arterial
Pressure
Cardiac output
Increased vascular tone
Low vascular compliance
Decreased vascular tone
High vascular compliance
HEMODYNAMIC EFFECTS OF FLUID ADMINISTRATION
IN FLUID RESPONDERS

VTI
Velocity time integral
Velocity cm/sec
Time sec
in cm

2022
Automatic echo measurement of sub-aortic VTI from a transthoracic apical 5-chamber view.
Correct positioning of the probe + optimal Doppler signal in the left ventricular outflow tract (LVOT): green
VTI

Averaging three measurements within one TTE examination
enough for VTI in patients in sinus rhythm
(not in atrial fibrillation).
Between two TTE examinations performed by the same operator,
significant changes in VTI with assessment
of the effects of a 500-mL fluid infusion.
2019

Can this patient benefit from fluids ?
Yes, definitely Maybe
Give
fluids
The clinical scenario
e.g. acute bleeding
Fluid loading

Give
fluids
Fluid
challenge
e.g. acute bleeding
Fluid loading
Positive
response
Negative
response

Give
fluids
Fluid
challenge
Do not give
fluids
e.g. acute bleeding
Fluid loading
Positive
response
Negative
response

143 patients
11 French ICUs
500 mL crystalloids
over 10 min
>15%
increase in VTI 76 (53%)
Fluid responders
37
transient
39
persistent
2019

PASSIVE LEG RAISING
Is there a transient increase in stroke volume?
yes no
FLUID RESPONSIVENESS NO FLUID RESPONSIVENESS

PASSIVE LEG RAISING
I just
raise the legs…
?
?
?
?
?
?
?
?
What do you mean ?
?
?

How to do a
PASSIVE LEG RAISING TEST

First, PLR should start from the semi-recumbent and not the supine position.
Second, the PLR effects must be assessed by a direct measurement of
cardiac output and not by the simple measurement of blood pressure.
Third, the technique used to measure cardiac output during PLR
must be able to detect short-term and transient changes
since the PLR effects may vanish after1 minute.
Fourth, cardiac output must be measured not only before and during PLR
but also after PLR when the patient has been moved back
to the semi-recumbent position, in order to check that it returns to its baseline.
Fifth, pain, cough, discomfort, and awakening could provoke adrenergic stimulation,
resulting in mistaken interpretation of cardiac output changes.
Some simple precautions must be taken to avoid these confounding factors.
PLR must be performed by adjusting the bed and
not by manually raising the patient’s legs.

Can the patient
benefit from IV fluids?
Internal
(Passive Leg Raising)
Fluid
Challenge
External
(200 mL in 10 min)

Can the patient
Internal
Fluid
Challenge
Increase in stroke volume / cardiac output ?
External
(200 mL in 10 min)

Can the patient
Internal
Fluid
Challenge
Increase in stroke volume / cardiac output ?
External
(200 mL in 10 min)
Yes No
Do not give
more fluids

Type of fluid ?
CRYSTALLOIDS
NaCl 0.9 %
Ringer's lactate
Plasmalyte
…
FLUIDS FOR RESUSCITATION
COLLOIDS
Albumin
HES
Gelatins
…

THE DIFFERENT CRYSTALLOID SOLUTIONS

Na Cl
HCO3
K
ELECTROLYTES
Ca 5
Mg 2
Prot 15
Organ ac 4
Phosph 2
Sulf 2
Na Cl
154 154
0.9 % NaCl
("physiologic" ??)
Our blood

1999
Approximately 1 liter/hour for 2 hours
Time, min Time, min Time, min

ANY abnormality is associated with worse outcomes

hypertension
hypernatremia
hyponatremia
hypoglycemia
tachycardia
uremia
high creatinine
hypercholesterolemia
low creatinine
hypochloremia
hypotension
hypoalbuminemia
hypothermia
fever
hyperglycemia
increased SGOT
metabolic acidosis metabolic alcalosis
hypocholesterolemia
increased WBC
anemia
hyperammoniemia
hyperglobulism
bradycardia
leukopenia
elevated CRP
elevated sedimentation rate
hyperkaliemia
hypokaliemia
tachypnea
bradypnea

hypertension
hypernatremia
hyponatremia
hypoglycemia
tachycardia
uremia
high creatinine
hyperchloremia
hypercholesterolemia
low creatinine
hypochloremia
hypotension
hypoalbuminemia
hypothermia
fever
hyperglycemia
increased SGOT
metabolic acidosis metabolic alcalosis
hypocholesterolemia
increased WBC
anemia
hyperammoniemia
hyperglobulism
bradycardia
leukopenia
elevated CRP
elevated sedimentation rate
hyperkaliemia
hypokaliemia
tachypnea
bradypnea

HYPERCHLOREMIC ACIDOSIS
Hyperchloremia induces renal vasoconstriction
Wilcox et al, J Clin Invest 71: 726-35, 1983

Na Cl
HCO3
K
ELECTROLYTES
Ca 5
Mg 2
Prot 15
Organ ac 4
Phosph 2
Sulf 2
Na Cl
Balanced
solutions

Not more than one glass of wine a day, OK ?

major adverse kidney events
within 30 days
creatinine
974 patients
SALT

We are not dealing here with a new drug or procedure whose effects need further
exploration in humans. Rather, we are dealing with intravenous solutions whose composition is quite
simple and well known. No-one would dispute that giving large amounts of a solution including 154
mEq/L of chloride will result in hyperchloremia, which cannot be good for the patient. Even without
reviewing in detail all the potentially harmful effects of hyperchloremia, anyone can appreciate that
any electrolyte abnormality can have harmful effects. From the opposite perspective, no-one has
ever suggested that hyperchloremia could be beneficial in any situation.
Giving any kind of fluid in small amounts cannot be very toxic. Saline solutions are cheap and
there is no reason to entirely prohibit their use in all patients. They also have a specific indication in
the management of metabolic alkalosis or hyponatremia. However, it is not good medical practice to
continue to give 0.9% saline solutions when chloride levels increase above the normal range. One
would not do a study comparing crystalloids with or without potassium chloride without monitoring
potassium levels. More generally, one would not give any electrolyte supplementation when levels of
that electrolyte are more than adequate. Any biochemical abnormality is associated with worse
outcomes; why would this be different for chloride? Such RCTs therefore raise ethical questions, as
equipoise is no longer present when patients who have developed hyperchloremia continue to
receive chloride. We would not want to be randomized to that group, as the treatment offered
would represent poor clinical management.
The authors of the SALT trial call for a larger trial on this question: they would be wise to
abandon their plans and, instead, start to monitor chloride levels in their patients.
2017

SMART
More major adverse kidney events
2018

THE MESSAGE
We must measure
the serum chloride levels !

< 105 mMol/L
Chloride
> 110 mMol/L
and/or
severe metabolic acidosis
(pH < 7.32 and PaCO2 < 40 mmHg)
0.9% saline
is OK
Acute neurological problem?
yes
no
Plasmalyte
Ringer’s lactate
(Hartmann solution)
Fluid resuscitation: which crystalloid?

De Backer et al, N Engl J Med 362: 779-89, 2010
Dopamine vs norepinephrine in shock states
SURVIVAL

TREAT SEVERE HYPOTENSION
IMMEDIATELY
THE PROBLEM OF HYPOTENSION

VASOPRESSOR SUPPORT IN SEPTIC SHOCK
" Vasopressor support is added
when hypotension persisted
despite fluid administration."

Not ideal

Not ideal
If hypotension is severe,
vasopressor therapy
should be started immediately,
together with fluid administration.

2020
MAKE = major adverse kidney events
302 patients – 9 ICUs
>4 hours of vasopressor support for nonhemorrhagic shock

Increased survival
Retrospective – 478 patients (143 Norepi)
Early nepi: lower MAP initially – same MAP at hospital admission
2022

Target
65-70 mmHg
Target
80-85 mmHg

"critically ill"
"ARDS"
"sepsis"
Higher arterial pressure
Lower arterial pressure
RANDOMIZATION

Benefit
Harm
"critically ill"
"ARDS"
"sepsis"
Higher arterial pressure
Lower arterial pressure
RANDOMIZATION
Benefit
Harm

Target
65-70 mmHg
Target
80-85 mmHg
2014

In patients with chronic arterial hypertension:

THE MESSAGE
A MAP > 75 mmHg
may be optimal in some patients
(history of hypertension)
A MAP of 65 mmHg for all?
It can be the INITIAL target

60-65mmHg (permissive hypotension) (n = 1291)
usual care (n = 1307).
MAP target:
2020

60-65mmHg (permissive hypotension) (n = 1291)
usual care (n = 1307).
MAP target:
2020
NO DIFFERENCE
IN MORTALITY

THE MESSAGE
A MAP >75 mmHg
may be optimal in some patients
(history of hypertension)
A MAP of 65 mmHg for all?
A MAP <65 mmHg
may be acceptable in some patients
(even if older than 65 years)
It can be the INITIAL target

0 25 50 75 100 125 150
PRESSURE, mmHg
FLOW
Chronic
hypertension
AUTOREGULATION OF BLOOD FLOW

RBF by retrograde thermodilution + renal excretion of 51Cr-EDTA

Optimal arterial pressure in septic shock : always 65 mmHg ?
Thooft et al, Crit Care 15: R222, 2011

Vasopressor therapy
2021
Quid thereafter?

We recommend
an initial target mean arterial pressure (MAP) of 65 mm Hg
in patients with septic shock requiring vasopressors.
Grade 1 B
SEPSIS
SURVIVING CAMPAIGN
2016
Crit Care Med 2017
Intensive Care Med 2017
VASOPRESSOR AGENTS

We recommend
an initial target mean arterial pressure (MAP) of 65 mm Hg
in patients with septic shock requiring vasopressors.
Grade 1 B
SEPSIS
SURVIVING CAMPAIGN
2016
Crit Care Med 2017
Intensive Care Med 2017
VASOPRESSOR AGENTS
Remarks:
If initiated, vasopressor dosing should be titrated
to an end point reflecting perfusion…

We recommend individualizing arterial blood pressure levels.
Although a mean value of 65 mmHg may be recommended as an
initial goal, the optimal level may be higher in patients with a
history of hypertension, atherosclerosis or chronic kidney disease.
Conversely it may be lower in younger patients without previous
vascular problems, in those with chronically low arterial pressure,
or in whom adequate tissue perfusion is maintained.
2021

INDIVIDUALIZE THE TARGETS

What is the target blood pressure in shock ?
60
70
80
90
?
Young,
No atherosclerosis
Chronically low blood pressure
Elderly
Atherosclerosis
Chronic hypertension
Mean
arterial
pressure
INITIAL target = 65 mmHg
then REASSESS

60
70
80
90
?
Young,
No atherosclerosis
Chronically low blood pressure
Elderly
Atherosclerosis
Chronic hypertension
Diuresis ?
Mental status ?
Skin perfusion ?
+
cardiac output?
SvO2? Lactate?
Mean
arterial
pressure
INITIAL target = 65 mmHg
then REASSESS

60
70
80
90
Arterial
pressure
100
50
40

60
70
80
90
Arterial
pressure
100
50
40
Vasopressors
are probably needed
Vasopressors
may or may not be needed

Fluid
challenge
Dobutamine
challenge
Noradrenaline
challenge
THE CHALLENGES

BEWARE OF VASOCONSTRICTION

The patient is getting worse and worse....
I have no other choice
than to increase the doses of norepinephrine...

The patient is getting worse and worse....
I have no other choice
than to increase the doses of norepinephrine...
Let us consider
all options

Capillary refill time
2 sec max

Arterial pressure = cardiac output x resistance
THE DANGERS OF VASOPRESSOR THERAPY

ADRENERGIC AGENTS
Isoproterenol
Dopexamine
Dobutamine
Dopamine
Epinephrine
Norepinephrine
Phenylephrine
b
a

VASOPRESSOR AGENTS
No
inotropic effect
Some
inotropic effect
Phenylephrine
Metaraminol
Mephentermine
Vasopressin
Angiotensin
(LNMMA)
Methylene blue
….

VASOPRESSOR AGENTS
No
inotropic effect
Some
inotropic effect
Phenylephrine
Metaraminol
Mephentermine
Vasopressin
Angiotensin
(LNMMA)
Methylene blue
….
Norepinephrine

ARTERIAL PRESSURE = BLOOD FLOW x VASCULAR TONE

low blood flow
(high vascular tone)
VASOPRESSORS FOR HYPOTENSION
vasoconstriction vasoplegia
high blood flow
(low vascular tone)
harmful beneficial
ARTERIAL PRESSURE = BLOOD FLOW x VASCULAR TONE

VASOPRESSIN
DOSES
Increased urine output (?)
Less edema formation
Maybe ?
0.05 U/min
0.10 U/min

VASOPRESSIN
DOSES
Maybe ?
No !
0.05 U/min
0.10 U/min
Decreased cardiac output
Excessive vasoconstriction
Impaired hepato-splanchnic perfusion
Reduced coronary blood flow
Pulmonary hypertension

VASOPRESSIN
DOSES
Maybe ?
No !
0.05 U/min
0.10 U/min
HYPERKINETIC STATE
Decreased cardiac output
Excessive vasoconstriction
Impaired hepato-splanchnic perfusion
Reduced coronary blood flow
Pulmonary hypertension

Need for vasopressors
Oliguria / altered mentation/cutaneous vasoconstriction
Increased lactate levels
CI < 3 L/min.M²
ScvO2 < 70%
CI > 3 L/min.M²
ScvO2 > 70%
SHOCK

CI < 3 L/min.M²
ScvO2 < 70%
CI > 3 L/min.M²
ScvO2 > 70%
Fluid challenge
SHOCK

CI < 3 L/min.M²
ScvO2 < 70%
CI > 3 L/min.M²
ScvO2 > 70%
Fluid challenge
Increase in CI
No major Increase in filling
OK ?
SHOCK

CI < 3 L/min.M²
ScvO2 < 70%
CI > 3 L/min.M²
ScvO2 > 70%
Fluid challenge
No increase in CI
Increase in filling
Increase in CI
No major Increase in filling
Dobutamine
Vasodilators ?
Transfusion ?
OK ?
SHOCK

CONTRACTILITY
HEART RATE
PRELOAD
AFTERLOAD
CARDIAC OUTPUT
FLUIDS PACEMAKER
DOBUTAMINE VASODILATORS

2021
ESICM survey - 839 doctors - 82 countries

Fluid
challenge
Dobutamine
challenge
Norepinephrine
challenge
THE CHALLENGES

In the recent trials
Less severely ill
Higher initial ScvO2 (already in the target range)
Improved early resuscitation?
Higher patient selection
Less commonly treated by mech. ventilation
Lower mortality rate
Not all needed ICU admission
Enrolment primarily during office hours
(but greater benefit outside these hours?)

The end of early goal directed therapy ?

THE MESSAGE
Systematic maintenance of SvO2 above 70% (EGDT)
is naïve and potentially harmful
(too much fluids, transfusions, dobutamine)
SvO2 measurements can be helpful
BUT

THE MESSAGE
Systematic maintenance of SvO2 above 70% (EGDT)
is naïve and potentially harmful
(too much fluids, transfusions, dobutamine)
in prolonged septic shock
after resuscitation
(when you become short of ideas)
SvO2 measurements can be helpful
BUT

ScvO2 < 70%
SaO2
low
Consider
transfusion
Correct
hypoxemia
Fluid
challenge
normal
low
Hb
normal
Dobutamine
infusion
Inadequate
cardiac output
Possibility of
fluid responsiveness
Myocardial
depression

SvO2
75 %
70 %
65 %
60 %
55 %
Fluids
Transfusion
Dobutamine
Vasopressors
(primarily)

WEAN FROM VASOPRESSORS
AS SOON AS POSSIBLE

HEMODYNAMIC
STABILIZATION
INFECTION
CONTROL
MODULATION
OF THE
HOST RESPONSE
agents
Antibiotics Source
control
Hydrocortisone?
Vasopressin ?
Gamma-globulins ?
Thrombomodulin
Blood purification ?

Endotracheal
intubation?
SpO2 95-98%
Oxygen
Ventilate Infuse Pump

Endotracheal
intubation?
SpO2 95-98%
Saline
If no severe acidemia
If hyponatremia
Oxygen
Balanced
solution
If severe acidemia
If hypernatremia
If hyperchloremia
1 liter
fast

Endotracheal
intubation?
SpO2 95-98%
Saline
If hyponatremia
Measure Cl
If < 105 mEq/L If > 105 mEq/L
Oxygen
Balanced
solution
If severe acidemia
If hypernatremia
If hyperchloremia
1 liter
fast

Endotracheal
intubation?
SpO2 95-98%
Saline
If hyponatremia
Measure Cl
If < 105 mEq/L If > 105 mEq/L
Oxygen
Balanced
solution
If severe acidemia
If hypernatremia
If hyperchloremia
1 liter
fast
Albumin
If edema
If hypoalbuminemia

Endotracheal
intubation?
SpO2 95-98%
Oxygen
1 liter
fast
To be repeated?

Endotracheal
intubation?
SpO2 95-98%
Oxygen
Insert
a CVC
1 liter
fast
To be repeated?

Endotracheal
intubation?
SpO2 95-98%
Oxygen
Insert
a CVC
1 liter
fast
To be repeated?
Insert
an
arterial
catheter
Norepinephrine
Start early
if profound
hypotension

Endotracheal
intubation?
SpO2 95-98%
Oxygen
Insert
a CVC
1 liter
fast
To be repeated?
Insert
an
arterial
catheter
If profound
sedation
Look at
PPV / SVV
Norepinephrine
Start early
if profound
hypotension

Endotracheal
intubation?
SpO2 95-98%
Oxygen
Insert
a CVC
1 liter
fast
To be repeated?
Insert
an
arterial
catheter
If profound
sedation
Fluid
challenge
PLR test
Measure
SV/CO
Look at
PPV / SVV
Use a
cardiac output
monitor
Norepinephrine
Start early
if profound
hypotension

Endotracheal
intubation?
SpO2 95-98%
Oxygen
Insert
a CVC
1 liter
fast
Fluid
challenge
Excessive
vasoconstriction?
Dobutamine
3-5 mcg/kg/min
ScvO2 >70%?
Need for transfusion? (check Hb)
Is lactate level decreasing?
To be repeated?
Norepinephrine
Start early
if profound
hypotension

Blood lactate
is
NOT
a sepsis marker

Blood lactate
is
NOT
a sepsis marker
It is a marker of
altered tissue perfusion
(shock)

Distributive
Sepsis
Infection
SEVERITY
Hypovolemic
Hypovolemia
Cardiogenic
Heart
failure
Obstructive
Pulm.
embolism
Pericardial
effusion
Arrhythmias

Distributive
Sepsis
Infection
SEVERITY
Hypovolemic
Hypovolemia
Cardiogenic
Heart
failure
Obstructive
CIRCULATORY SHOCK
Pulm.
embolism
Pericardial
effusion
Arrhythmias
ELEVATED LACTATE

0
10
20
30
40
50
60
70
80
90
100
<1.2 1.2-1.5 1.5-2.0 2.0-4.0 4.0-6.0 >6.0
172,723 blood lactate measurements
in 7,155 critically ill patients (4 hospitals)
Hospital mortality, %
Initial
lactate
levels

6
5
4
3
2
1
0
TIME
mEq/L
or
mMol/L
LACTATE
Single
measurement

6
5
4
3
2
1
0
TIME
mEq/L
or
mMol/L
LACTATE

This is NOT ONLY about lactate clearance
2016

Conclusions:
Better outcome associated with decreasing blood lactate concentrations
- consistent throughout the clinical studies
- not limited to septic patients
- valid regardless of the initial value
- in all groups, changes relatively slow, so that
lactate measurements every 1–2 hrs are probably sufficient
in most acute conditions.
2016

TIME
SvO2
lactate
RESUSCITATION
LACTATE vs. SvO2

We must monitor blood lactate levels
(every hour in critical periods)
SEPSIS MANAGEMENT
Practical aspects
(not to GUIDE therapy)
To make sure we are on the right track

HEMODYNAMIC STABILIZATION
Adequate MAP without vasopressors
The three windows of tissue perfusion
Lactate levels normal or decreasing
Normal skin perfusion
Urine output > 0.5 mL/kg/h
Preserved mental status
The goals

HEMODYNAMIC
STABILIZATION
INFECTION
CONTROL
MODULATION
OF THE
SEPSIS RESPONSE
agents
Antibiotics Source
control
SEPSIS MANAGEMENT
blood cultures
other specimens
X rays
CT-scan

HEMODYNAMIC
STABILIZATION
INFECTION
CONTROL
MODULATION
OF THE
SEPSIS RESPONSE
agents
Antibiotics Source
control
SEPSIS MANAGEMENT
blood cultures
other specimens
X rays
CT-scan
Arterial pressure
CVP / PAOP
lactate
ScvO2
cardiac output

EARLY RESUSCITATION
RAPID TRANSPORTATION
INITIAL WORK-UP
EARLY SURGERY
FULL RESUSCITATION
COMPREHENSIVE WORK-UP
TRAUMA

Captain
Nurse
Doctor
Trauma team
gives orders
receives
informations
Nurse
Nurse
Nurse
Doctor
Doctor
TRAUMA

TRAUMA
Insert
a central venous catheter
Insert
a Foley catheter
Order blood
Send blood
for coagulation tests
Call the surgeon
Let us go
to the CT-scanner
Do an echo
Call for imaging
Call the OR
Insert
a NG tube
Ask for
a head CT-scan
Send
other lab tests
Give another liter
of RL solution
Give another unit
of RBC
Intubate
the trachea
Call
the orthopedist surgeon
!
!
!
!
!
!
! !
!
!
!
!
!
!
!
!
!
!
!
!
!

TRAUMA
Insert
a central venous catheter
Insert
a Foley catheter
Order blood
Send blood
for coagulation tests
Call the surgeon
Let us go
to the CT-scanner
Do an echo
Call for imaging
Call the OR
Insert
a NG tube
Ask for
a head CT-scan
Send
other lab tests
Give another liter
of RL solution
Give another unit
of RBC
Intubate
the trachea
Call
the orthopedist surgeon
!
!
!
!
!
!
! !
!
!
!
!
!
!
!
!
!
!
!
!
!
SEPSIS

The 5 tubes
central venous
catheter
arterial catheter
Foley catheter
gastric tube
endotracheal
tube
TRAUMA

The 5 tubes
central venous
catheter
arterial catheter
Foley catheter
gastric tube
endotracheal
tube
TRAUMA
SEPSIS

The 5 tubes
central venous
catheter
arterial catheter
Foley catheter
gastric tube
endotracheal
tube

The 5 tubes
central venous
catheter
arterial catheter
Foley catheter
gastric tube
endotracheal
tube
echography
Diagnostic
techniques
chest
X ray
call for
CT-scan

The 5 tubes
central venous
catheter
arterial catheter
Foley catheter
gastric tube
endotracheal
tube
echography
Diagnostic
techniques
chest
X ray
Blood
tests
ABG – lactate
cell count
urea/BUN - creatinine
coagulation panel…
call for
CT-scan

The 5 tubes
central venous
catheter
arterial catheter
Foley catheter
gastric tube
endotracheal
tube
echography
Diagnostic
techniques
chest
X ray
Blood
tests
ABG – lactate
cell count
Microbiology
blood cultures urine
culture
sputum
drainage
fluid
call for
CT-scan

The 5 tubes
central venous
catheter
arterial catheter
Foley catheter
gastric tube
endotracheal
tube
echography
cardiac
output
Diagnostic
techniques
chest
X ray
Blood
tests
ABG – lactate
cell count
Microbiology
culture
sputum
drainage
fluid
CVP
call for
CT-scan
Monitoring
arterial pressure
echography

The 5 tubes
central venous
catheter
arterial catheter
Foley catheter
gastric tube
endotracheal
tube
echography
cardiac
output
Diagnostic
techniques
chest
X ray
Blood
tests
ABG – lactate
cell count
Microbiology
culture
sputum
drainage
fluid
antibiotics
fluids
noradrenaline
CVP
Treatment call the surgeon
call for
CT-scan
Monitoring
arterial pressure
echography
dobutamine

SEPSIS TEAM
TRAUMA TEAM
SEPSIS TEAM

TIME…..
TRAUMA
MYOCARDIAL INFARCTION
STROKE
SEPSIS

TIME…..
TRAUMA
STROKE
SEPSIS
Every minute counts !

I involve a resuscitation team
at all times (24/365)

CPR
Polytrauma
Intoxications
Shock
Stroke
…
Abdominal pain
Infections
Febrile child
Minor trauma
Ophtalmology
…
Emergency medicine Critical care medicine
General
practice
ARDS
Acute renal failure
SAH
Nosocomial infections
Persisting shock
…

SEPSIS TEAM
Université Libre
de Bruxelles

SHOCK LAB
4 3 2 1
Dept
of
Intensive Care
Dept
of
Emergency
Medicine
Erasme Univ. Hospital
Piagnerelli M, Vannuffelen M, Maetens Y, Lheureux P, Vincent JL
Anaesth Intensive Care 37: 426-31, 2009

SHOCK LAB
4 3 2 1
Dept
of
Intensive Care
Dept
of
Emergency
Medicine
Erasme Univ. Hospital
STAFF

SHOCK LAB

Trauma
Myocardial infarction
Stroke
Sepsis
S/P CPR
…..
TIME
ONSET ADMISSION

Have adequate facilities to manage
these complex patients
SEPSIS MANAGEMENT
Practical aspects

“golden hour”
R. Adams Cowley,
Founder of the Trauma Institute, Baltimore
(1975)
“the first hour after injury will largely determine
a critically injured person's chances for survival”
TRAUMA

You have not
done much
in the last 55 min!
… but I still have
5 min !
EVERY MINUTE COUNTS !
The GOLDEN hour??

TIME IS ESSENTIAL…
TRAUMA
STROKE
SEPSIS

TIME IS ESSENTIAL…
TRAUMA
STROKE
SEPSIS
Every minute counts !

Septic shock initial 1 hour EM | Jean-Louis Vincent at TBS23

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