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Septic shock; latest update

The document provides a comprehensive overview of septic shock, its incidence, symptoms, and pathophysiology, emphasizing its prevalence as a leading cause of mortality in intensive care units. It details the diagnostic criteria for sepsis syndromes and outlines management strategies, including early recognition, antibiotic therapy, hemodynamic resuscitation, and continuous monitoring of vital signs to improve patient outcomes. The document also describes the various complications associated with septic shock and emphasizes the importance of source control and fluid management in treatment.

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‫الرحيم‬ ‫الرحمن‬ ‫هللا‬ ‫بسم‬
Management of Septic Shock Dr. Ramadan Arafa; MSc, MRCPI Physician; Fujairah Hospital
OVERVIEW • Septic shock is the most common cause of mortality in the intensive care units. • An analysis of a large sample from major US medical centers reported the incidence of severe sepsis is 3 cases/1000 population and 2.26 cases per 100 hospital discharges. Of these patients, 51.1% were admitted to ICU, and 17.3% were in an intermediate care or CCU (Angus 2001). • The incidence of severe sepsis doubled over a 6- year period (2004-2009) (Gaieski 2013).
Etiology Pathophysiology How To Diagnose? How To Manage? Sepsis syndromes Objectives
Sepsis syndromes SIRS Sepis Severe sepsis-SIRS Septic shock MODS
(Systemic Inflammatory Response Syndrome) is a systemic inflammatory response to non specific insults. SIRS SIRS is either due to Infection or others Clinically: 1. hyperthermia >38°C or hypothermia <36°C 2. tachycardia > 90 bpm 3. tachypnea > 20 r.p.m. or PaCO2 <4.3 kPa 4. neutrophilia >12000 or neutropenia <4000/uL or more than 10% immature forms
Venn Diagram; Andre Kalil; septic shock 2015
Clinically?! • Known or suspected infection, plus • >2 SIRS Criteria. Sepsis The systemic inflammatory response to infection. Severe sepsis-SIRS • Severe sepsis resulting in at least one organ failure Clinically?! • Sepsis plus >1 organ dysfunction.
Septic shock •Sepsis induced shock with hypotension (SBP <90 mmHg or decreased > 40 mmHg from baseline readings) despite adequate resuscitation plus; presence of perfusion abnormalities which may include lactic acidosis, oliguria, or an acute alteration in mental status.
• Shock = inadequate tissue perfusion –Decreased O2 delivery and decreased removal of metabolites • Tissue perfusion is determined by: –Cardiac output (CO) = HR x SV SV = function of preload, afterload, contractility –Systemic vascular resistance (SVR)
MODS (multiple organ dysfunction syndrome) The presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention.
SIRS systemic inflammatory response syndrome SEPSIS SIRS with a presumed or confirmed infectious process Severe sepsis Sepsis with ≥1 sign of organ failure Septic shock SIRS + Infection + Organ Failure + Refractory Hypotension
Etiology Pathophysiology How To Diagnose? How To Manage? Sepsis syndromes Objectives
Etiology Caustive organisms •Gram –ve the commonest •Staph •Candida Sources of infection • Endogenus source 1. Peritonitis 2. Perforated viscous 3. Gangrenous bowel 4. Genitourinary infection • Exogenus source  Infected CVP Predisposing factors • Old age • DM • Corticosteroid therpy • Malignancy • Major surgery
Etiology Pathophysiology How To Diagnose? How To Manage? Sepsis syndromes Objectives
It is not precisely understood, but it involves a complex interaction between the pathogen and the host's immune system. Physiological response to localized infection: o Influx of activated PMN leukocytes & monocytes  release of inflammatory mediators o Local vasodilatation & increased endothelial permeability o Activation of the coagulation cascade. Pathophysiology
• The same occurs in septic shock but at a systemic level. 1. Diffuse endothelial disruption 2. Increased vascular permeability 3. Vasodilatation 4. Thrombosis of end organ capillaries
Infection Inflammatory Mediators Endothelial Dysfunction Vasodilation Hypotension Vasoconstriction Edema Maldistribution of Microvascular Blood Flow Organ Dysfunction Microvascular Plugging Ischemia Cell Death
Inadequate Resuscitation Preoperative Illness Trauma or Operation Tissue Injury optimal oxygen delivery and support Recovery Excessive Inflammatory Response SIRS/MODS Pathogenesis of SIRS/MODS in surgical patients
Identifying Acute Organ Dysfunction as a Marker of Severe Sepsis Tachycardia Hypotension  CVP  PAOP Jaundice  Enzymes  Albumin  PT Altered Consciousness Confusion Psychosis Tachypnea PaO2 <70 mm Hg SaO2 <90% PaO2/FiO2 300 Oliguria Anuria  Creatinine  Platelets  PT/APTT  Protein C  D-dimer Rhabdomyolysis Addison’s disease Polyneuropathy
Etiology Pathophysiology How To Diagnose? How To Manage? Sepsis syndromes Objectives
How To Diagnose? • When you suspect sepsis in patient with predisposing factors, do not wait for septic shock • The diagnosis of sepsis requires the taking of an EXCELLENT history, physical examination, appropriate laboratory tests, and a close follow- up of hemodynamic status • Early recognition is live saving in such rapid overwhelming situation
Hyperdynamic- Warm- Early Septic Shock Restlness & confusion Vitals 1. fever more than 38 chills 2. Mild decrease ABP 3. Tachycardia 4. Tachypnea Skin warm ,dry ,flushed High cardiac output Hypodynamic- Cold- Late Septic Shock  Semicomatosed  Vitals 1. Temperature decreased 2. Tachycardia 3. Tachypnea 4. SBP<90mmHg  Oliguria & low COP  Multiorgan failure start at this stage
Work up… Laboratory studies o CBC o Coagulation studies o Blood, sputum, body fluids & urine cultures o LFT, Renal and electrolytes o Serum lactate Imaging studies o Chest radiography o Abdominal radiography o Others according to the suspected cause.
Complications of septic shock • ARDS: starts 12-48 hours of the inciting event. – Mild (mortality: 27%) – moderate (mortality: 32%) – severe (mortality: 45) (JAMA 2012) • AKI: affects 40-70% of critically ill patients • Chronic renal insufficiency • DIC • Mesentric ischemia • Myocardial dysfunction and MI • Liver failure
Etiology Pathophysiology How To Diagnose? How To Manage? Sepsis syndromes Objectives
How To Manage?
How To Manage? Goals: Septic •Identify and manage Infection Source Shock •Adequate Resuscitation MODS •Support Dysfunctional Systems & Monitoring
Management principles • Early recognition • Early and adequate antibiotic therapy • Source control • Early hemodynamic resuscitation and continued support • Proper ventilator management with low tidal volume in patients with ARDS
General measures • Venous access • Crystalloid infusion • Central venous line insertion ? • Urinary catheterization • Oxygenation and ventilation. Low tidal volume ventilation is associated with better outcome
• Within 6 hours of presentation to ER, intensive monitoring of specific circulatory parameters with the aggressive management of 5 key parameters to specified targets to optimise oxygen delivery to tissues and maintain hemodynamic stability. (Rivers 2001) Early goal directed therapy (EGDT)
Effective Sepsis Management for Quality Patient Outcomes • EGDT have been shown to be effective at improving patient costs and outcomes, including significant reductions in sepsis- related mortality. • EGDT with the PreSep oximetry catheter has been shown to: – Reduce sepsis-related mortality by 46% – Reduce hospital length-of-stay by 5 days – Reduce hospital charges by $5,882 per patient – Guide therapy and enable early intervention
Continuous ScvO2 Monitoring, PreSep Oximetry Catheter The Vigileo monitor works with the PreSep catheter The PreSep catheter is a triple lumen central venous oximetry catheter with an added capability for continuously monitoring ScvO2.
• Parameters – CVP 8-12 mmHg – MAP > 65mmHg and / or SBP > 90 mmHg – Urine output > 0.5 ml/kg/hr – Mixed venous oxygen saturation >65% / ScvO2 >70% – Haematocrit >30% • Interventions – Reduce work of breathing by early use of mech. Vent – Fluid resuscitation – Use of vasoactive agents: noradrenaline, dobutamine – Transfusion
ScvO2 O2 delivery Cardiac output HR SV preload Bleeding Fluid shift afterload Vascular resistance contractility Heart disease Hb Bleeding Hemodilution Anemia Oxygenation SaO2 FiO2 Vent O2 consumption Metabolic demands Fever Anxiety Pain Shivering Muscle activitySt joseph 2008
• In critically ill patients, it is crucial to maintain the balance between oxygen consumption and oxygen delivery
International guidelines for management of severe sepsis and septic shock 2012 The Society of Critical Care Medicine The European Society of Intensive Care Medicine 2013
Initial Resuscitation and Infection Issues A. Initial Resuscitation: 1. We recommend the protocolized, quantitative resuscitation of patients with sepsis- induced tissue hypoperfusion (defined in this document as hypotension persisting after initial fluid challenge or blood lactate concentration ≥ 4 mmol/L). This protocol should be initiated as soon as hypoperfusion is recognized and should not be delayed pending ICU admission.
During the first 6 hr of resuscitation, the goals of initial resuscitation of sepsis-induced hypoperfusion should include all of the following (grade 1C): a) CVP 8–12 mm Hg b) MAP ≥ 65 mm Hg c) Urine output ≥ 0.5 mL/kg/hr d) ScvO2 or SvO2 70% or 65%, respectively. 2. We suggest targeting resuscitation to normalize lactate in patients with elevated lactate levels
B. Screening for Sepsis and Performance Improvement 1. Routine screening of potentially infected seriously ill patients for severe sepsis to allow earlier implementation of therapy (grade 1C). 2. Hospital–based performance improvement efforts in severe sepsis (UG).
C. Diagnosis 1. Cultures as clinically appropriate before antimicrobial therapy if no significant delay (> 45 mins) in the start of antimicrobial(s) (grade 1C). At least 2 sets of blood cultures to be obtained before antimicrobial therapy with at least 1 drawn percutaneously and 1 drawn through each vascular access device, unless the device was recently (<48 hrs) inserted (grade 1C). 2. Invasive candidiasis should be in differential diagnosis of cause of infection. 3. Imaging studies performed promptly to confirm a potential source of infection (UG).
D. Antimicrobial Therapy 1. Administration of effective IV antimicrobials within the first hour of recognition of septic shock (grade 1B) and severe sepsis without septic shock (grade 1C) as the goal of therapy. 2. - 2a. Initial empiric anti-infective therapy of one or more drugs that have activity against all likely pathogens (bacterial and/or fungal or viral) and that penetrate in adequate concentrations into tissues presumed to be the source of sepsis (grade 1B). – 2b. Antimicrobial regimen should be reassessed daily for potential de-escalation (grade 1B).
3. Use of low procalcitonin levels or similar biomarkers to assist the clinician in the discontinuation of empiric antibiotics in patients who initially appeared septic, but have no subsequent evidence of infection (grade 2C). 4a. Combination empirical therapy for neutropenic patients with severe sepsis (grade 2B) and for patients with difficult-to- treat, multi-drugresistant bacterial pathogens such as Acinetobacter and Pseudomonas spp. (grade 2B). For patients with severe infections associated with respiratory failure and septic shock, combination therapy with an extended spectrum beta-lactam and either an aminoglycoside or a fluoroquinolone is for P. aeruginosa bacteremia (grade 2B). A combination of beta-lactam and macrolide for patients with septic shock from bacteremic Streptococcus pneumoniae infections (grade 2B).
4b. Empiric combination therapy should not be administered for more than 3–5 days. De-escalation to the most appropriate single therapy should be performed as soon as the susceptibility profile is known (grade 2B). 5. Duration of therapy typically 7–10 days; longer courses may be appropriate in patients who have a slow clinical response, undrainable foci of infection, bacteremia with S. aureus; some fungal and viral infections or immunologic deficiencies, including neutropenia (grade 2C). 6. Antiviral therapy initiated as early as possible in patients with severe sepsis or septic shock of viral origin (grade 2C). 7. Antimicrobial agents should not be used in patients with severe inflammatory states determined to be of noninfectious cause (UG).
E. Source Control 1. A specific anatomical diagnosis of infection requiring consideration for emergent source control be sought and diagnosed or excluded as rapidly as possible, and intervention be undertaken for source control within the first 12 hr after the diagnosis is made, if feasible (grade 1C). 2. When infected peripancreatic necrosis is identified as a potential source of infection, definitive intervention is best delayed until adequate demarcation of viable and nonviable tissues has occurred (grade 2B).
3. When source control in a severely septic patient is required, the effective intervention associated with the least physiologic insult should be used (eg, percutaneous rather than surgical drainage of an abscess) (UG). 4. If intravascular access devices are a possible source of severe sepsis or septic shock, they should be removed promptly after other vascular access has been established (UG).
F. Infection Prevention 1a. Selective oral decontamination and selective digestive decontamination should be introduced and investigated as a method to reduce the incidence of VAP; This infection control measure can then be instituted in health care settings and regions where this methodology is found to be effective (grade 2B). 1b. Oral chlorhexidine gluconate be used as a form of oropharyngeal decontamination to reduce the risk of VAP in ICU patients with severe sepsis (grade 2B).
G. Fluid Therapy of Severe Sepsis 1. We recommend against using hydroxymethyl starch for fluid resuscitation in severe sepsis and septic shock (grade1B). 2. We suggest the use of albumin in the fluid resuscitation of severe sepsis and septic shock when patients require substantial amounts of crystalloids (grade 2C).
4. Initial fluid challenge in a minimum of 30 mL/kg of crystalloids (a portion of this may be albumin equivalent). More rapid administration and greater amounts of fluid may be needed in some patients (grade 1C). 5. Fluid challenge technique be applied wherein fluid administration is continued as long as there is hemodynamic improvement either based on dynamic or static variables (UG).
H. Vasopressors 1. Vasopressor therapy initially to target a MAP of 65 mm Hg (grade 1C). 2. Norepinephrine as the first choice vasopressor (grade 1B). 3. Epinephrine (added to and potentially substituted for norepinephrine) when an additional agent is needed to maintain adequate blood pressure (grade 2B). 4. Vasopressin 0.03 units/minute can be added to norepinephrine (NE) with intent of either raising MAP or decreasing NE dosage (UG).
5. 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) (UG). 6. 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) (grade 2C).
7. Phenylephrine is not recommended in the treatment of septic shock except in circumstances where (a) norepinephrine is associated with serious arrhythmias, (b) cardiac output is known to be high and blood pressure persistently low or (c) as salvage therapy when combined inotrope/vasopressor drugs and low dose vasopressin have failed to achieve MAP target (grade 1C).
8. Low-dose dopamine should not be used for renal protection (grade 1A). 9. All patients requiring vasopressors have an arterial catheter placed as soon as practical if resources are available (UG).
I. Inotropic Therapy 1. Dobutamine infusion up to 20 mcg/kg/min be administered or added to vasopressor (if in use) in the presence of (a) myocardial dysfunction as suggested by elevated cardiac filling pressures and low cardiac output, or (b) ongoing signs of hypoperfusion, despite achieving adequate intravascular volume and adequate MAP (grade 1C).
J. Corticosteroids 1. Not using IV hydrocortisone to treat adult septic shock patients if adequate fluid resuscitation and vasopressor therapy are able to restore hemodynamic stability . In case this is not achievable, we suggest IV hydrocortisone at a dose of 200 mg/ day (grade 2C). 2. Not using the ACTH stimulation test to identify adults with septic shock who should receive hydrocortisone (grade 2B).
3. In treated patients hydrocortisone tapered when vasopressors are no longer required (grade 2D). 4. Corticosteroids not be administered for the treatment of sepsis in the absence of shock (grade 1D). 5. When hydrocortisone is given, use continuous flow (grade 2D). 6. Steroids may be indicated in the presence of a history of steroid therapy or adrenal dysfunction !!
K. Blood Product Administration 1. Once tissue hypoperfusion has resolved and in the absence of extenuating circumstances, such as myocardial ischemia, severe hypoxemia, acute hemorrhage, or ischemic coronary artery disease, we recommend that RBCs transfusion occur when the Hb concentration decreases to < 7.0 g/dL to target a Hb concentration of 7.0 to 9.0 g/dL in adults (grade 1B).
2. We recommend not using erythropoietin as a specific treatment of anemia associated with severe sepsis (grade 1B). 3. We suggest that FFP not be used to correct laboratory clotting abnormalities in the absence of bleeding or planned invasive procedures (grade 2D). No studies suggest that correction of more severe coagulation abnormalities benefits patients who are not bleeding. 4. We recommend against antithrombin administration for the treatment of severe sepsis and septic shock (grade 1B).
5. In patients with severe sepsis, we suggest that platelets be administered prophylactically when: – counts are ≤ 10,000/mm3 in the absence of apparent bleeding – counts are ≤ 20,000/mm3 if the patient has a significant risk of bleeding. – platelet counts ≥ 50,000/mm3 if the patient has active bleeding, surgery, or invasive procedures (grade 2D).
L. Immunoglobulins 1. We suggest not using IV immunoglobulins in adult patients with severe sepsis or septic shock (grade 2B). Large RCTs found no benefit M. Recombinant activated protein C 1. It is no longer available for treating patients with severe sepsis or septic shock
N. Glucose Control 1. We recommend a protocolized approach to blood glucose management in ICU patients with severe sepsis, commencing insulin dosing when two consecutive RBS levels are > 180 mg/dL. This approach should target an upper blood glucose level ≤ 180 mg/dL rather than an upper target blood glucose ≤ 110 mg/dL (grade 1A). 2. We recommend blood glucose values be monitored every 1-2 hrs until glucose values and insulin infusion rates are stable, then every 4 hrs thereafter (grade 1C).
3. We recommend that capillary glucose levels to be interpreted with caution, as such measurements may not accurately estimate arterial blood or plasma glucose values (UG).
O. Renal Replacement Therapy 1. Continuous RRT and intermittent hemodialysis are equivalent in patients with severe sepsis and acute renal failure (grade 2B). 2. Use continuous therapies to facilitate management of fluid balance in hemodynamically unstable septic patients (grade 2D). P. Bicarbonate Therapy 1. Not using sodium bicarbonate therapy for the purpose of improving hemodynamics or reducing vasopressor requirements in patients with hypoperfusion-induced lactic acidemia with pH ≥7.15 (grade 2B).
Q. Deep Vein Thrombosis Prophylaxis 1. Patients with severe sepsis receive daily pharmacoprophylaxis against VTE (grade 1B). Daily SC LMWH is more preferred than twice daily UFH or three times daily UFH. If creatinine clearance is <30 mL/min, use dalteparin (grade 1A) or another form of LMWH that has a low degree of renal metabolism (grade 2C) or UFH (grade 1A). 2. Patients with severe sepsis be treated with a combination of pharmacologic therapy and intermittent pneumatic compression devices whenever possible (grade 2C).
3. Septic patients who have a contraindication for heparin use not receive pharmacoprophylaxis (grade 1B), but receive mechanical prophylactic treatment, such as graduated compression stockings or intermittent compression devices (grade 2C), unless contraindicated. When the risk decreases start pharmacoprophylaxis (grade 2C).
R. Stress Ulcer Prophylaxis 1. Stress ulcer prophylaxis using H2 blocker or PPI be given to patients with severe sepsis/septic shock who have bleeding risk factors (grade 1B). 2. When stress ulcer prophylaxis is used, PPIs rather than H2RA (grade 2D) 3. Patients without risk factors do not receive prophylaxis (grade 2B).
Thank you
Questions ???

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Septic shock; latest update

  • 1.
  • 2.
    Management of SepticShock Dr. Ramadan Arafa; MSc, MRCPI Physician; Fujairah Hospital
  • 3.
    OVERVIEW • Septic shockis the most common cause of mortality in the intensive care units. • An analysis of a large sample from major US medical centers reported the incidence of severe sepsis is 3 cases/1000 population and 2.26 cases per 100 hospital discharges. Of these patients, 51.1% were admitted to ICU, and 17.3% were in an intermediate care or CCU (Angus 2001). • The incidence of severe sepsis doubled over a 6- year period (2004-2009) (Gaieski 2013).
  • 4.
    Etiology Pathophysiology How To Diagnose? HowTo Manage? Sepsis syndromes Objectives
  • 5.
  • 6.
    (Systemic Inflammatory ResponseSyndrome) is a systemic inflammatory response to non specific insults. SIRS SIRS is either due to Infection or others Clinically: 1. hyperthermia >38°C or hypothermia <36°C 2. tachycardia > 90 bpm 3. tachypnea > 20 r.p.m. or PaCO2 <4.3 kPa 4. neutrophilia >12000 or neutropenia <4000/uL or more than 10% immature forms
  • 7.
    Venn Diagram; AndreKalil; septic shock 2015
  • 8.
    Clinically?! • Known orsuspected infection, plus • >2 SIRS Criteria. Sepsis The systemic inflammatory response to infection. Severe sepsis-SIRS • Severe sepsis resulting in at least one organ failure Clinically?! • Sepsis plus >1 organ dysfunction.
  • 9.
    Septic shock •Sepsis inducedshock with hypotension (SBP <90 mmHg or decreased > 40 mmHg from baseline readings) despite adequate resuscitation plus; presence of perfusion abnormalities which may include lactic acidosis, oliguria, or an acute alteration in mental status.
  • 10.
    • Shock =inadequate tissue perfusion –Decreased O2 delivery and decreased removal of metabolites • Tissue perfusion is determined by: –Cardiac output (CO) = HR x SV SV = function of preload, afterload, contractility –Systemic vascular resistance (SVR)
  • 11.
    MODS (multiple organ dysfunctionsyndrome) The presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention.
  • 12.
    SIRS systemic inflammatory response syndrome SEPSIS SIRS with apresumed or confirmed infectious process Severe sepsis Sepsis with ≥1 sign of organ failure Septic shock SIRS + Infection + Organ Failure + Refractory Hypotension
  • 14.
    Etiology Pathophysiology How To Diagnose? HowTo Manage? Sepsis syndromes Objectives
  • 15.
    Etiology Caustive organisms •Gram –ve the commonest •Staph •Candida Sourcesof infection • Endogenus source 1. Peritonitis 2. Perforated viscous 3. Gangrenous bowel 4. Genitourinary infection • Exogenus source  Infected CVP Predisposing factors • Old age • DM • Corticosteroid therpy • Malignancy • Major surgery
  • 16.
    Etiology Pathophysiology How To Diagnose? HowTo Manage? Sepsis syndromes Objectives
  • 17.
    It is notprecisely understood, but it involves a complex interaction between the pathogen and the host's immune system. Physiological response to localized infection: o Influx of activated PMN leukocytes & monocytes  release of inflammatory mediators o Local vasodilatation & increased endothelial permeability o Activation of the coagulation cascade. Pathophysiology
  • 18.
    • The sameoccurs in septic shock but at a systemic level. 1. Diffuse endothelial disruption 2. Increased vascular permeability 3. Vasodilatation 4. Thrombosis of end organ capillaries
  • 19.
    Infection Inflammatory Mediators Endothelial Dysfunction Vasodilation Hypotension Vasoconstriction Edema Maldistributionof Microvascular Blood Flow Organ Dysfunction Microvascular Plugging Ischemia Cell Death
  • 20.
    Inadequate Resuscitation Preoperative Illness Trauma or Operation Tissue Injury optimaloxygen delivery and support Recovery Excessive Inflammatory Response SIRS/MODS Pathogenesis of SIRS/MODS in surgical patients
  • 21.
    Identifying Acute OrganDysfunction as a Marker of Severe Sepsis Tachycardia Hypotension  CVP  PAOP Jaundice  Enzymes  Albumin  PT Altered Consciousness Confusion Psychosis Tachypnea PaO2 <70 mm Hg SaO2 <90% PaO2/FiO2 300 Oliguria Anuria  Creatinine  Platelets  PT/APTT  Protein C  D-dimer Rhabdomyolysis Addison’s disease Polyneuropathy
  • 22.
    Etiology Pathophysiology How To Diagnose? HowTo Manage? Sepsis syndromes Objectives
  • 23.
    How To Diagnose? •When you suspect sepsis in patient with predisposing factors, do not wait for septic shock • The diagnosis of sepsis requires the taking of an EXCELLENT history, physical examination, appropriate laboratory tests, and a close follow- up of hemodynamic status • Early recognition is live saving in such rapid overwhelming situation
  • 24.
    Hyperdynamic- Warm- Early SepticShock Restlness & confusion Vitals 1. fever more than 38 chills 2. Mild decrease ABP 3. Tachycardia 4. Tachypnea Skin warm ,dry ,flushed High cardiac output Hypodynamic- Cold- Late Septic Shock  Semicomatosed  Vitals 1. Temperature decreased 2. Tachycardia 3. Tachypnea 4. SBP<90mmHg  Oliguria & low COP  Multiorgan failure start at this stage
  • 26.
    Work up… Laboratory studies oCBC o Coagulation studies o Blood, sputum, body fluids & urine cultures o LFT, Renal and electrolytes o Serum lactate Imaging studies o Chest radiography o Abdominal radiography o Others according to the suspected cause.
  • 27.
    Complications of septicshock • ARDS: starts 12-48 hours of the inciting event. – Mild (mortality: 27%) – moderate (mortality: 32%) – severe (mortality: 45) (JAMA 2012) • AKI: affects 40-70% of critically ill patients • Chronic renal insufficiency • DIC • Mesentric ischemia • Myocardial dysfunction and MI • Liver failure
  • 28.
    Etiology Pathophysiology How To Diagnose? HowTo Manage? Sepsis syndromes Objectives
  • 29.
  • 30.
    How To Manage? Goals: Septic •Identifyand manage Infection Source Shock •Adequate Resuscitation MODS •Support Dysfunctional Systems & Monitoring
  • 31.
    Management principles • Earlyrecognition • Early and adequate antibiotic therapy • Source control • Early hemodynamic resuscitation and continued support • Proper ventilator management with low tidal volume in patients with ARDS
  • 32.
    General measures • Venousaccess • Crystalloid infusion • Central venous line insertion ? • Urinary catheterization • Oxygenation and ventilation. Low tidal volume ventilation is associated with better outcome
  • 33.
    • Within 6hours of presentation to ER, intensive monitoring of specific circulatory parameters with the aggressive management of 5 key parameters to specified targets to optimise oxygen delivery to tissues and maintain hemodynamic stability. (Rivers 2001) Early goal directed therapy (EGDT)
  • 34.
    Effective Sepsis Managementfor Quality Patient Outcomes • EGDT have been shown to be effective at improving patient costs and outcomes, including significant reductions in sepsis- related mortality. • EGDT with the PreSep oximetry catheter has been shown to: – Reduce sepsis-related mortality by 46% – Reduce hospital length-of-stay by 5 days – Reduce hospital charges by $5,882 per patient – Guide therapy and enable early intervention
  • 35.
    Continuous ScvO2 Monitoring,PreSep Oximetry Catheter The Vigileo monitor works with the PreSep catheter The PreSep catheter is a triple lumen central venous oximetry catheter with an added capability for continuously monitoring ScvO2.
  • 36.
    • Parameters – CVP8-12 mmHg – MAP > 65mmHg and / or SBP > 90 mmHg – Urine output > 0.5 ml/kg/hr – Mixed venous oxygen saturation >65% / ScvO2 >70% – Haematocrit >30% • Interventions – Reduce work of breathing by early use of mech. Vent – Fluid resuscitation – Use of vasoactive agents: noradrenaline, dobutamine – Transfusion
  • 37.
    ScvO2 O2 delivery Cardiac output HR SV preload Bleeding Fluidshift afterload Vascular resistance contractility Heart disease Hb Bleeding Hemodilution Anemia Oxygenation SaO2 FiO2 Vent O2 consumption Metabolic demands Fever Anxiety Pain Shivering Muscle activitySt joseph 2008
  • 38.
    • In criticallyill patients, it is crucial to maintain the balance between oxygen consumption and oxygen delivery
  • 41.
    International guidelines for managementof severe sepsis and septic shock 2012 The Society of Critical Care Medicine The European Society of Intensive Care Medicine 2013
  • 42.
    Initial Resuscitation andInfection Issues A. Initial Resuscitation: 1. We recommend the protocolized, quantitative resuscitation of patients with sepsis- induced tissue hypoperfusion (defined in this document as hypotension persisting after initial fluid challenge or blood lactate concentration ≥ 4 mmol/L). This protocol should be initiated as soon as hypoperfusion is recognized and should not be delayed pending ICU admission.
  • 43.
    During the first6 hr of resuscitation, the goals of initial resuscitation of sepsis-induced hypoperfusion should include all of the following (grade 1C): a) CVP 8–12 mm Hg b) MAP ≥ 65 mm Hg c) Urine output ≥ 0.5 mL/kg/hr d) ScvO2 or SvO2 70% or 65%, respectively. 2. We suggest targeting resuscitation to normalize lactate in patients with elevated lactate levels
  • 44.
    B. Screening forSepsis and Performance Improvement 1. Routine screening of potentially infected seriously ill patients for severe sepsis to allow earlier implementation of therapy (grade 1C). 2. Hospital–based performance improvement efforts in severe sepsis (UG).
  • 45.
    C. Diagnosis 1. Culturesas clinically appropriate before antimicrobial therapy if no significant delay (> 45 mins) in the start of antimicrobial(s) (grade 1C). At least 2 sets of blood cultures to be obtained before antimicrobial therapy with at least 1 drawn percutaneously and 1 drawn through each vascular access device, unless the device was recently (<48 hrs) inserted (grade 1C). 2. Invasive candidiasis should be in differential diagnosis of cause of infection. 3. Imaging studies performed promptly to confirm a potential source of infection (UG).
  • 46.
    D. Antimicrobial Therapy 1.Administration of effective IV antimicrobials within the first hour of recognition of septic shock (grade 1B) and severe sepsis without septic shock (grade 1C) as the goal of therapy. 2. - 2a. Initial empiric anti-infective therapy of one or more drugs that have activity against all likely pathogens (bacterial and/or fungal or viral) and that penetrate in adequate concentrations into tissues presumed to be the source of sepsis (grade 1B). – 2b. Antimicrobial regimen should be reassessed daily for potential de-escalation (grade 1B).
  • 47.
    3. Use oflow procalcitonin levels or similar biomarkers to assist the clinician in the discontinuation of empiric antibiotics in patients who initially appeared septic, but have no subsequent evidence of infection (grade 2C). 4a. Combination empirical therapy for neutropenic patients with severe sepsis (grade 2B) and for patients with difficult-to- treat, multi-drugresistant bacterial pathogens such as Acinetobacter and Pseudomonas spp. (grade 2B). For patients with severe infections associated with respiratory failure and septic shock, combination therapy with an extended spectrum beta-lactam and either an aminoglycoside or a fluoroquinolone is for P. aeruginosa bacteremia (grade 2B). A combination of beta-lactam and macrolide for patients with septic shock from bacteremic Streptococcus pneumoniae infections (grade 2B).
  • 48.
    4b. Empiric combinationtherapy should not be administered for more than 3–5 days. De-escalation to the most appropriate single therapy should be performed as soon as the susceptibility profile is known (grade 2B). 5. Duration of therapy typically 7–10 days; longer courses may be appropriate in patients who have a slow clinical response, undrainable foci of infection, bacteremia with S. aureus; some fungal and viral infections or immunologic deficiencies, including neutropenia (grade 2C). 6. Antiviral therapy initiated as early as possible in patients with severe sepsis or septic shock of viral origin (grade 2C). 7. Antimicrobial agents should not be used in patients with severe inflammatory states determined to be of noninfectious cause (UG).
  • 49.
    E. Source Control 1.A specific anatomical diagnosis of infection requiring consideration for emergent source control be sought and diagnosed or excluded as rapidly as possible, and intervention be undertaken for source control within the first 12 hr after the diagnosis is made, if feasible (grade 1C). 2. When infected peripancreatic necrosis is identified as a potential source of infection, definitive intervention is best delayed until adequate demarcation of viable and nonviable tissues has occurred (grade 2B).
  • 50.
    3. When sourcecontrol in a severely septic patient is required, the effective intervention associated with the least physiologic insult should be used (eg, percutaneous rather than surgical drainage of an abscess) (UG). 4. If intravascular access devices are a possible source of severe sepsis or septic shock, they should be removed promptly after other vascular access has been established (UG).
  • 51.
    F. Infection Prevention 1a.Selective oral decontamination and selective digestive decontamination should be introduced and investigated as a method to reduce the incidence of VAP; This infection control measure can then be instituted in health care settings and regions where this methodology is found to be effective (grade 2B). 1b. Oral chlorhexidine gluconate be used as a form of oropharyngeal decontamination to reduce the risk of VAP in ICU patients with severe sepsis (grade 2B).
  • 52.
    G. Fluid Therapyof Severe Sepsis 1. We recommend against using hydroxymethyl starch for fluid resuscitation in severe sepsis and septic shock (grade1B). 2. We suggest the use of albumin in the fluid resuscitation of severe sepsis and septic shock when patients require substantial amounts of crystalloids (grade 2C).
  • 53.
    4. Initial fluidchallenge in a minimum of 30 mL/kg of crystalloids (a portion of this may be albumin equivalent). More rapid administration and greater amounts of fluid may be needed in some patients (grade 1C). 5. Fluid challenge technique be applied wherein fluid administration is continued as long as there is hemodynamic improvement either based on dynamic or static variables (UG).
  • 54.
    H. Vasopressors 1. Vasopressortherapy initially to target a MAP of 65 mm Hg (grade 1C). 2. Norepinephrine as the first choice vasopressor (grade 1B). 3. Epinephrine (added to and potentially substituted for norepinephrine) when an additional agent is needed to maintain adequate blood pressure (grade 2B). 4. Vasopressin 0.03 units/minute can be added to norepinephrine (NE) with intent of either raising MAP or decreasing NE dosage (UG).
  • 55.
    5. Low dosevasopressin 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) (UG). 6. 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) (grade 2C).
  • 57.
    7. Phenylephrine isnot recommended in the treatment of septic shock except in circumstances where (a) norepinephrine is associated with serious arrhythmias, (b) cardiac output is known to be high and blood pressure persistently low or (c) as salvage therapy when combined inotrope/vasopressor drugs and low dose vasopressin have failed to achieve MAP target (grade 1C).
  • 58.
    8. Low-dose dopamineshould not be used for renal protection (grade 1A). 9. All patients requiring vasopressors have an arterial catheter placed as soon as practical if resources are available (UG).
  • 59.
    I. Inotropic Therapy 1.Dobutamine infusion up to 20 mcg/kg/min be administered or added to vasopressor (if in use) in the presence of (a) myocardial dysfunction as suggested by elevated cardiac filling pressures and low cardiac output, or (b) ongoing signs of hypoperfusion, despite achieving adequate intravascular volume and adequate MAP (grade 1C).
  • 60.
    J. Corticosteroids 1. Notusing IV hydrocortisone to treat adult septic shock patients if adequate fluid resuscitation and vasopressor therapy are able to restore hemodynamic stability . In case this is not achievable, we suggest IV hydrocortisone at a dose of 200 mg/ day (grade 2C). 2. Not using the ACTH stimulation test to identify adults with septic shock who should receive hydrocortisone (grade 2B).
  • 61.
    3. In treatedpatients hydrocortisone tapered when vasopressors are no longer required (grade 2D). 4. Corticosteroids not be administered for the treatment of sepsis in the absence of shock (grade 1D). 5. When hydrocortisone is given, use continuous flow (grade 2D). 6. Steroids may be indicated in the presence of a history of steroid therapy or adrenal dysfunction !!
  • 62.
    K. Blood ProductAdministration 1. Once tissue hypoperfusion has resolved and in the absence of extenuating circumstances, such as myocardial ischemia, severe hypoxemia, acute hemorrhage, or ischemic coronary artery disease, we recommend that RBCs transfusion occur when the Hb concentration decreases to < 7.0 g/dL to target a Hb concentration of 7.0 to 9.0 g/dL in adults (grade 1B).
  • 63.
    2. We recommendnot using erythropoietin as a specific treatment of anemia associated with severe sepsis (grade 1B). 3. We suggest that FFP not be used to correct laboratory clotting abnormalities in the absence of bleeding or planned invasive procedures (grade 2D). No studies suggest that correction of more severe coagulation abnormalities benefits patients who are not bleeding. 4. We recommend against antithrombin administration for the treatment of severe sepsis and septic shock (grade 1B).
  • 64.
    5. In patientswith severe sepsis, we suggest that platelets be administered prophylactically when: – counts are ≤ 10,000/mm3 in the absence of apparent bleeding – counts are ≤ 20,000/mm3 if the patient has a significant risk of bleeding. – platelet counts ≥ 50,000/mm3 if the patient has active bleeding, surgery, or invasive procedures (grade 2D).
  • 65.
    L. Immunoglobulins 1. Wesuggest not using IV immunoglobulins in adult patients with severe sepsis or septic shock (grade 2B). Large RCTs found no benefit M. Recombinant activated protein C 1. It is no longer available for treating patients with severe sepsis or septic shock
  • 66.
    N. Glucose Control 1.We recommend a protocolized approach to blood glucose management in ICU patients with severe sepsis, commencing insulin dosing when two consecutive RBS levels are > 180 mg/dL. This approach should target an upper blood glucose level ≤ 180 mg/dL rather than an upper target blood glucose ≤ 110 mg/dL (grade 1A). 2. We recommend blood glucose values be monitored every 1-2 hrs until glucose values and insulin infusion rates are stable, then every 4 hrs thereafter (grade 1C).
  • 67.
    3. We recommendthat capillary glucose levels to be interpreted with caution, as such measurements may not accurately estimate arterial blood or plasma glucose values (UG).
  • 68.
    O. Renal ReplacementTherapy 1. Continuous RRT and intermittent hemodialysis are equivalent in patients with severe sepsis and acute renal failure (grade 2B). 2. Use continuous therapies to facilitate management of fluid balance in hemodynamically unstable septic patients (grade 2D). P. Bicarbonate Therapy 1. Not using sodium bicarbonate therapy for the purpose of improving hemodynamics or reducing vasopressor requirements in patients with hypoperfusion-induced lactic acidemia with pH ≥7.15 (grade 2B).
  • 69.
    Q. Deep VeinThrombosis Prophylaxis 1. Patients with severe sepsis receive daily pharmacoprophylaxis against VTE (grade 1B). Daily SC LMWH is more preferred than twice daily UFH or three times daily UFH. If creatinine clearance is <30 mL/min, use dalteparin (grade 1A) or another form of LMWH that has a low degree of renal metabolism (grade 2C) or UFH (grade 1A). 2. Patients with severe sepsis be treated with a combination of pharmacologic therapy and intermittent pneumatic compression devices whenever possible (grade 2C).
  • 70.
    3. Septic patientswho have a contraindication for heparin use not receive pharmacoprophylaxis (grade 1B), but receive mechanical prophylactic treatment, such as graduated compression stockings or intermittent compression devices (grade 2C), unless contraindicated. When the risk decreases start pharmacoprophylaxis (grade 2C).
  • 71.
    R. Stress UlcerProphylaxis 1. Stress ulcer prophylaxis using H2 blocker or PPI be given to patients with severe sepsis/septic shock who have bleeding risk factors (grade 1B). 2. When stress ulcer prophylaxis is used, PPIs rather than H2RA (grade 2D) 3. Patients without risk factors do not receive prophylaxis (grade 2B).
  • 72.
  • 73.