By : Mohd Ekhwan Bin Darus

Jabatan Kecemasan dan Trauma

Hospital Yan
FEB 2018
Outline
 Introduction
 Definition
 qSOFA
 Management
 Summary
 Problem in diagnosing sepsis
 PREVIOUS SURVIVING SEPSIS
CAMPAIGN DEFINITION
 Systemic inflammatory response syndrome (SIRS)
requires 2 or more of the following (the definition
differs for children):
1. T >38 C or <36 C
2. P >90/min
3. RR >20/min or PaCO2 <32 mmHg
4. WCC >12 or >10% immature band forms
 Sepsis
 Sepsis is SIRS + confirmed or presumed infections mortality:
10-15%
 Severe Sepsis
 Severe Sepsis is sepsis with organ dysfunction includes:
 SBP <90 mmHg or MAP < 65 mmHg or lactate > 2.0
mmol/L (after initial fluid challenge)
 INR >1.5 or a PTT >60 s
 Bilirubin >34 µmol/L
 Urine output <0.5 mL/kg/h for 2 h
 Creatinine >177 µmol/L
 Platelets <100 ×109/L
 SpO2 <90% on room air
 mortality: 17-20%
 Septic Shock
 Septic shock is defined as sepsis with
refractory hypotension
 hypotension is defined as SBP <90 mmHg or
MAP <70 mmHg
 refractory means that hypotension persists
after 30 mL/kg crystalloid; i.e. vasopressor
dependence after adequate volume
resuscitation
 mortality: 43-54%
 2016
Sepsis-3
So What is Sepsis Then?
 Sepsis – now defined as life-threatening organ
dysfunction caused by a dysregulated host response to
infection. This is a clinical diagnosis. Note that
“Severe sepsis” (previously used for sepsis with
organ dysfunction) is no longer recognized since
it would be redundant.

 Septic Shock – a subset of Sepsis with circulatory and

cellular/metabolic dysfunction associated with a
higher risk of mortality. This is a clinical diagnosis.
JAMA. 2016;315(8):801-810. doi:10.1001/jama.2016.0287
 Sepsis and Septic Shock are medical emergencies
and it is recommended that treatment and
resuscitation begin immediately

(Best Practice Statement).

 Sepsis clinical criteria: organ dysfunction is
defined as an increase of 2 points or more in the
Sequential Organ Failure Assessment (SOFA)
score
 for patients with infections, an increase of 2
SOFA points gives an overall mortality rate of
10%
 Patients with suspected infection who are likely
to have a prolonged ICU stay or to die in the
hospital can be promptly identified at the
bedside with qSOFA (“HAT”); i.e. 2 or more of:
 Hypotension: SBP less than or equal to 100
mmHg
 Altered mental status (any GCS less than 15)
 Tachypnoea: RR greater than or equal to 22
 Septic shock is a subset of sepsis in which
underlying circulatory and cellular/metabolic
abnormalities are profound enough to
substantially increase mortality.
 Septic shock clinical criteria: Sepsis and (despite
adequate volume resuscitation) both of:
 Persistent hypotension requiring vasopressors to
maintain MAP greater than or equal to 65 mm Hg, and
 Lactate greater than or equal to 2 mmol/L
 With these criteria, hospital mortality is in excess
of 40%
 Not that the term “severe sepsis” is no longer in
use.
MANAGEMENT
1.DETECT
Identify Sepsis Earlier
 Early identification is paramount – both at first contact and later,
since sepsis can develop during care.
 Failing to recognize sepsis and septic shock leads to delays in therapy –
especially resuscitation and antibiotics – and can worsen outcomes.1,2
 Routine screening, including at triage and by nurses, can increase early
identification.2
 Suspect sepsis/septic shock in obvious cases such as those with fever,
leukocytosis, and hypotension.
 Outside classic presentations, suspect sepsis for unexplained altered
mental status, tachypnea with a clear chest and normal oxygenation, or
if clinical instinct suggests something is “not right” in a patient with a
seemingly routine infection or suspected infection.
 Pause and consider sepsis when ordering cultures or antibiotics.
 Reassess after initial evaluation. Some patients will develop sepsis after
the initial assessment when it might not have been present.
Measure lactate
 Patients with a suspected or diagnosed infection and a high lactate are at
increased risk of adverse outcomes.1
 Get a venous or arterial blood lactate level early in patients with suspected
infection and sepsis but normal or mildly abnormal vital signs.2
 Also, get a lactate level if uncertain about the presence of shock to detect occult
cases.
 Elevated blood lactate is associated with higher risk for the development of
overt septic shock and poor outcome.
 Lactate greater than 2 mmol/L is abnormal, and levels above 4 mmol/L
often mean occult hypoperfusion and should trigger resuscitation.
 Patients with a history of cirrhosis or renal failure can have a slightly higher
baseline blood lactate, but elevated lactate is still an important measurement
in these populations.
 If lactate is elevated initially, a primary goal should be achievement of a
relative lactate clearance of at least 10%.3
 Epinephrine infusion or large-volume Lactated Ringer’s solution can impair
clearance and hinder remeasurement assessments.
2.ACT
Fluid Therapy
 Give more fluids in 500-mL to 1,000-mL increments based
on the clinical response.
 The recommended target volume of initial fluid in the first
hour is 30 mL/kg, followed by maintenance fluids if
improved, otherwise continue bolus therapy.1-6
 A history of heart failure, liver failure, or renal failure
is not a contraindication to fluid resuscitation. These
patients might need less total fluid or smaller boluses with
more frequent reassessment of intravascular volume status.
 Using adequate, large peripheral intravenous access for
early resuscitation might prevent the need for central
venous catheterization due to the ability to rapidly deliver
fluids.2-4
 A central venous catheter above the diaphragm is
optimal, allowing venous pressure or oxygenation
assessment if needed.
 0.9% saline or balanced plasma solutions (Plasma-
Lyte or Ringer’s) are equally effective, recognizing high
volumes of saline might induce acidosis and renal
dysfunction.5
 There is not a routine role for colloid solutions or
blood products for shock therapy alone. Consider red
cell transfusion for those with Hgb 7 g/dL or less.7
 DO NOT DELAY fluid and vasopressor
therapy. Prompt resuscitation of ED septic shock
patients is associated with more rapid resolution and
improved survival rates.5,8,9
 Vasopressors
 Useful in patients who remain hypotensive despite
adequate fluid resuscitation
 Target mean arterial pressure (MAP) of 65mmHg
 First line vasopressor: norepinephrine
 Dose: start 2-12 mcg/min (no true maximum dose)
 Administer vasopressin (up to 0.03) and epinephrine as
add-on therapies if not at target MAP or to decrease
norepinephrine dose
 Consider inotropes in low cardiac output states i.e.
septic cardiomyopathy, which can be common in these
patients
Start Antibiotic Early
 Obtain appropriate cultures before antibiotics are initiated, but do
not delay antibiotic administration solely to complete this
task.Urine and blood cultures are commonly and easily obtained.
 Microbiologic samples allow for later tailoring of antibiotics.
 To optimize the identification of causative organisms, obtain at least
two blood cultures before antibiotics, but do not delay antibiotic
administration.
 Culture other sites, tissues, or fluids (cerebrospinal fluid, wounds,
respiratory secretions) that might be the source of infection; these do
not sterilize quickly and can be sampled as antibiotics are given.
 Adequate soft tissue and respiratory samples are often hard to obtain in
the ED.
 Surrogate tests for bacterial infection and inflammation (C-reactive
protein and procalcitonin) often show elevated levels but cannot
currently effectively guide ED care in adult patients with sepsis or
septic shock.3
 Give early appropriate antibiotics, ideally within
the first hour of recognition.
 Delays in appropriate antibiotics can increase
mortality rates.4,5
 Choose based on suspected site and local patterns
and evidence-based guidelines for specific types
of infections.6
 Broader antimicrobial therapy including antifungals
might help in patients with immunosuppression or
neutropenia.
 Consider removing an intravascular device if suspected
as the source of infection.
 Obtain appropriate consults (surgical or interventional
radiology) when needed for source control.
 Antibiotic Regimen
 Begin with broad spectrum coverage when the potential
pathogen is not immediately obvious
 Narrow once pathogen identification and sensitivities are
established
 Vancomycin
 Goal to achieve a trough of 15-20mg/L
 IV loading dose of 25-30mg/kg in septic shock
 For β-lactams, achieve higher Time-Dependent Killing (T>MIC)
by increasing frequency of dosing
 Fluoroquinolones should be given at their optimal nontoxic dose
 Aminoglycosides should be dosed using once-daily dosing
 Average duration: 7-10 days is recommended in most patients
3.REASSES
Re-measure Lactate Level
 Re-measure lactate at least 1 to 2 hours (too soon does
not help) after starting resuscitation in patients with
initially abnormal lactate to help gauge progress.
 Persistence of elevated lactate, even in the absence of
hypotension, is associated with poor outcomes; ongoing
resuscitation is optimal.1
 If lactate was elevated initially, a primary goal should
be achievement of a relative lactate clearance of at
least 10%.2
 Epinephrine infusion or large-volume Ringer’s solution can
impair clearance and hinder remeasurement assessments.
Re-evaluate Fluid Resusitation
 It is best to use more than one method to assess
resuscitation adequacy. Methods to measure
intravascular volume or fluid responsiveness include the
following1:
 Bedside vital sign assessment (including shock index); and
 Clinical examination to assess perfusion and volume
status; or ANY TWO of the following:
 Passive leg raises, pulse pressure variation >/= 13% (if arterial line
placed) or heart rate variability to assess volume responsiveness2; or
 Ultrasound assessment of vascular filling; or
 Stroke volume variation3; or
 Central venous pressure measurement (target 8-12 mm Hg while
recognizing a trend is more important than one absolute value) or
central venous oximetry (targeting 70%); or
 Repeat serum lactate level if elevated initially (should drop by 10% or
more in 1 to 2 hours if resuscitation is adequate)7,8
 Again, DO NOT DELAY fluid and vasopressor
therapy. Prompt resuscitation of ED septic shock
patients is associated with more rapid resolution and
improved survival rates.1,7,9
 Repeat vital signs. Check blood pressure, heart rate,
shock index – look for changes.
 Look for signs of adequate fluid resuscitation or any
complications from volume therapy.1,2
 There is no singular ideal total fluid target, but
commonly 4 to 6 L of total IV crystalloid solution
is needed during the first 6 hours.3-6
 Early titrated but aggressive fluid resuscitation is
more important than any specific prescribed method
of delivering or reassessing therapy.
4.TITRATE
 Titrate further fluids/ pressors to patient response.
 Vasopressors are often needed.
 In PATIENTS WITH PROFOUND OR ONGOING
HYPOTENSION after fluid resuscitation or those who have
signs of volume overload and signs of shock, USE
CONTINUOUS IV NOREPINEPHRINE, targeting a mean
arterial pressure of 65 mm Hg.1,2
 A well-secured large-bore peripheral catheter may be used
to initiate therapy for the short term until central venous
access is secured.
 Epinephrine is an option but can have more complications and
less effect than norepinephrine.
 Higher blood pressure targets (MAP >65 mm Hg) do not confer a
better outcome.
Summary
THANK YOU