Download Severe Sepsis and Septic Shock

“Do you know 47 out of 53
patients admitted from South
Surgical Ward in year 2015 in
Surgical ICU died of Severe
Sepsis?”
“Do you know 47 out of 53
patients admitted from South
Surgical Ward in year 2015 in
Surgical ICU died of Severe
Sepsis?”
A mortality rate of 88%
Want to know why ?
Lets know what’s it all about ?
SEPSIS
“Is a systemic, harmful ( deleterious) host response to infection”.
SEPSIS
“Is a systemic, deleterious host response to infection”.
leading to
Severe Sepsis
(acute organ dysfunction secondary to documented or suspected infection)
Severe Sepsis
(acute organ dysfunction secondary to documented or suspected infection)
Dysfunction of organ(s) distant from the site of infection
leading to
SEPTIC SHOCK
(severe sepsis plus hypoperfusion or hypotension not reversed
with fluid resuscitation).”
INFECTION
INFECTION
Presence of microorganisms in a normally sterile site
INFECTION
Presence of microorganisms in a normally sterile site
Do Not confuse with “colonization,” which is the presence of
microorganisms on an epithelial surface
Bacteremia
Bacteremia
Cultivatable bacteria in the bloodstream
May be transient and inconsequential;
Systemic
inflammatory
response
syndrome
(SIRS)
Systemic
inflammatory
response
syndrome
(SIRS)
Early Host Responses to Infection
Local Defenses: Walling Off and Killing
Invading Microbes
Early Systemic Responses:
Keeping Infection and
Inflammation Localized
Early Systemic Responses: Keeping
Infection and Inflammation Localized
Acute-Phase Responses (Categorized According to Possible Roles in Defense)
Anti-infective
Increases synthesis of complement factors, microbe pattern-recognition molecules
(mannose-binding lectin, LBP, CRP, CD14, others)
Sequesters iron (lactoferrin, hepcidin) and zinc (metallothionein)
Anti-inflammatory
Releases anti-inflammatory neuroendocrine hormones (cortisol, ACTH, epinephrine, αMSH)
Increases synthesis of proteins that help prevent inflammation within the systemic
compartment
Cytokine antagonists (IL-1Ra, sTNF-Rs)
Anti-inflammatory mediators (e.g., IL-4, IL-6, IL-6R, IL-10, IL-13, TGF-β)
Protease inhibitors (e.g., α1-antiprotease)
Antioxidants (haptoglobin)
Reprograms circulating leukocytes (epinephrine, cortisol, PGE 2 , ? other factors)
Procoagulant
Metabolic
Thermoregulatory
Walls off infection, prevents systemic spread
Increases synthesis or release of fibrinogen, PAI-1, C4b
Decreases synthesis of protein C, antithrombin III
Preserves euglycemia, mobilizes fatty acids, amino acids
Epinephrine, cortisol, glucagon, cytokines
Inhibits microbial growth
Fever
Harmful Responses to Infection:
Severe Sepsis and Septic Shock
“Hypofunction” implies an inadequate level of activity, whereas
“dysfunction” suggests that organ performance is in some way abnormal.
Develop when normally adaptive stress responses are pushed
beyond their ability to be protective.
CONCEPTs
1.Microvascular derangement
TWO Theories
2.Mitochondrial dysfunction.
• An extension of the body's normal neuroendocrine responses to
stress
• An exhaustion of ATP in critical organs
• when the inflammatory stimulus is too strong or too prolonged.
• Cytokines circulate via the blood and induce injury to the vascular
endothelium and/or microcirculation in different organs.
• An extension of the body's normal neuroendocrine responses to
stress
• An exhaustion of ATP in critical organs
• when the inflammatory stimulus is too strong or too prolonged.
Septic Shock
Opportunistic commensal bacteria typically invade across
disrupted epithelia.
Hosts in whom immunosuppressive acute-phase responses are
already occurring because of illness, injury, or infection.
Host is unable to kill the bacteria because of mechanical failure
(obstructed drainage pathway), immunosuppression
(neutropenia, “endogenous immunosuppression”)
• These bacteria invade the bloodstream when local defenses are
unable to kill or contain them; bacteremia.
• Locally-produced mediators act as trigger for severe sepsis and
septic shock
• Outcome is strongly related to the patient's underlying
physiologic fitness.
• Pathogenic microbes/virus that can survive and multiply in
previously healthy humans.
• the microbes/viruses may enter the bloodstream, infect vascular
endothelial cells and/or blood cells, and release toxins.
• The circulating microbes may provoke both shock and
profound coagulopathy that not uncommonly results in
hemorrhage and/or arterial thrombosis
DIAGNOSTIC CRITERIA
Initial Resuscitation and Infection Issues
A. Initial Resuscitation (Goals during the first 6 hrs of resuscitation)
1. Hypotension persisting after initial fluid challenge or blood lactate
concentration ≥ 4 mmol/L
a) Central venous pressure 8–12 mm Hg
b) Mean arterial pressure (MAP) ≥ 65 mm Hg
c) Urine output ≥ 0.5 mL/kg/hr
d) Central venous (superior vena cava) or mixed venous oxygen
saturation 70% or 65%, respectively
B. Diagnosis
• Cultures as clinically appropriate before antimicrobial therapy if no
significant delay (> 45 mins) in the start of antimicrobial(s)
• At least 2 sets of blood cultures (both aerobic and anaerobic bottles) be
obtained before antimicrobial therapy
• Imaging studies performed promptly to confirm a potential source of
infection (UG).
C. Antimicrobial Therapy
• Administration of effective intravenous antimicrobials within the first hour
of recognition of septic shock and severe
• sepsis without septic shock as the goal of therapy.
• Initial empiric anti-infective therapy of one or more drugs that have activity
against all likely pathogens
• Antimicrobial regimen should be reassessed daily for potential
deescalation.
• Use of low procalcitonin levels in the discontinuation of empiric antibiotics
• Combination empirical therapy for neutropenic respiratory failure and
septic shock,
TO BE COMPLETED WITHIN 3 HOURS OF TIME OF
PRESENTATION*:
1. Measure lactate level
2. Obtain blood cultures prior to administration of antibiotics
3. Administer broad spectrum antibiotics
4. Administer 30ml/kg crystalloid for hypotension or lactate
≥4mmol/L
TO BE COMPLETED WITHIN 6 HOURS OF TIME OF
PRESENTATION:
5. Apply vasopressors (for hypotension that does not respond to
initial fluid resuscitation) to maintain a mean arterial pressure
(MAP) ≥65mmHg
6. In the event of persistent hypotension after initial fluid
administration (MAP < 65 mm Hg) or if initial lactate was ≥4
mmol/L, re-assess volume status and tissue perfusion 7. Remeasure lactate if initial lactate elevated.
Fluid Therapy of Severe Sepsis
• Crystalloids as the initial fluid of choice
• Against the use of hydroxyethyl starches
• Albumin when substantial amounts of crystalloids (grade 2C).
• Initial fluid challenge a minimum of 30 mL/kg of crystalloids (a portion of
this may be albumin equivalent).
• Fluid challenge technique be applied
Change in pulse pressure,
Stroke volume variation)
Arterial pressure, Heart rate
Vasopressors
• Vasopressor therapy initially to target a mean arterial pressure (MAP) of 65 mm Hg
• Norepinephrine as the first choice vasopressor.
• Epinephrine (added to and potentially substituted for norepinephrine) when an additional
agent is needed to maintain adequate blood pressure (grade 2B).
• Vasopressin 0.03 units/minute can be added to norepinephrine (NE) with intent of either
raising MAP or decreasing NE dosage .
• Low dose vasopressin is not recommended as the single initial vasopressor for treatment
of sepsis-induced hypotension and vasopressin doses higher than 0.03-0.04 units/minute
should be reserved for salvage therapy (failure to achieve adequate MAP with other
vasopressor agents) .
• Dopamine as an alternative vasopressor agent to norepinephrine only in highly selected
patients (eg. patients with low risk of tachyarrhythmias and absolute or relative
bradycardia).
Hemodynamic Support and Adjunctive Therapy
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Inotropic Therapy
Corticosteroids
Blood Product Administration.
Immunoglobulins
Mechanical Ventilation of Sepsis-Induced ARDS
Sedation, Analgesia, and Neuromuscular Blockade in Sepsis
Glucose Control
Renal Replacement Therapy
Bicarbonate Therapy
Deep Vein ThrombosisProphylaxis
Nutrition
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