Approach in the
 Management of Septic Shock




Esteban Osorio Salazar
Resident of Anesthesiology
HUAV
July -2012


                             “The sick girl” by Gabriel Metsu (1658)
Questions/objectives.
1.        Introduction.
2.        Definition.
3.        Pathophysilogy of sepsis.
4.        Management of septic shock.
     1.    Stabilize respiration.
     2.    Therapeutic priorites (monitoring andr initial resuscitation)
     3.    Diagnosis-AB therapy- Source Control.
     4.    Fluid Therapy.
     5.    Vasopressors and Inotropic Therapy.
     6.    Additional therapies.
1. Introduction.

   450.000-500.000 cases of sepsis/year in EU.
   80.000 cases in SPAIN.
   Mortality Index 4-5 deaths/100.000/year.
   Hospital admission of sepsis : 3.4-28 cases/1000
    admission.
   Incidence of Severe sepsis in ICU.
2. Definition.
Septic Shock                       Severe sepsis +:
                                   *SMBP of <60 mm Hg (<80 mm Hg if
                                   hypertension) after 20 to 30 mL/kg starch or
                                   40 to 60 mL/kg saline solution.
                                   *PCWP between 12 and 20 mm Hg
                                                    +
                                   *Dopamine of >5 mcg/kg/min
                                   *Norepinephrine or epinephrine of <0.25
                                   mcg/kg/min.
Refractory Septic Shock            *Dopamine at >15 mcg/kg/min
                                   *Norepinephrine or epinephrine at >0.25
                                   mcg/kg/min




     Mean BP at >60 mm Hg (80 mm Hg if previous hypertension



    Schmidt Gregory A, MD, Mandel Jess, MD. Management of severe sepsis and septic shock in
    adults.Wolters Kluwer Healt and Uptodate, May 2012.
3. Pathophysiology of Sepsis.




    Richard S. Hotchkiss, M.D., and Irene E. Karl, Ph.D.The Pathophysiology and Treatment of Sepsis.
    N Engl J Med 2003 348;138-150.
3. Pathophysiology of Sepsis.




  Richard S. Hotchkiss, M.D., and Irene E. Karl, Ph.D.The Pathophysiology and Treatment of Sepsis. N
  Engl J Med 2003 348;138-150.
3. Pathophysiology of Sepsis




   Emanuel P. Riversa, Anja Kathrin Jaehne, Laura Eichhorn-Wharry, Samantha Brown and David
   Amponsah. Fluid therapy in septic shock. Current Opinion in Critical Care 2010,16:001–012.
3. Pathophysiology of Sepsis




  Emanuel P. Riversa, Anja Kathrin Jaehne, Laura Eichhorn-Wharry, Samantha Brown and David
  Amponsah. Fluid therapy in septic shock. Current Opinion in Critical Care 2010,16:001–012.
4. Management of Septic Shock.
4.1.Stabilize respiration
    Supplemental oxygen to all patients and monitored continuously with
     pulse oximetry.
    Intubation and mechanical ventilation (may be required).
    Chest Rx
    Sedative and induction agents.
    Target in Mechanical ventilation of sepsis-induced ALI/ARDS

    *Tidal volume of 6 mL/kg (predicted).
    *Initial upper limit plateau pressure <30 cm H2O.
    *PEEP for prevent lung collapse in ALI/ARDS.
    *Prone position for ARDS patients with max FiO2/Pp? (2C)
    *Mild to moderate hypoxemic respiratory failure: NIMV.
    *
    Target in sedative, inductive agents and NMB in sepsis

    *Sedation protocols.
    *Intermittent bolus sedation or continuous infusion sedation (1C).
    *Avoid NMB where possible. Train-of-four when using continuous
    infusions(1B).
     *Dellinger RP, Levy MM, Carlet JM, et al: Surviving Sepsis Campaign: International guidelines for
     management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296–327.
     *Schmidt Gregory A, MD, Mandel Jess, MD. Management of severe sepsis and septic shock in
     adults.Wolters Kluwer Healt and Uptodate, May 2012.
4. Management of Septic Shock.
4.1.Stabilize respiration




      Murray MJ, Cowen J, DeBlock H, et al. Clinical practice guidelines for sustained neuromuscular
      blockade in the adult critically ill patient. Crit Care Med 2002; 30:142-156.
4. Management of Septic Shock.
4.2.Therapeutic Priorities
Monitoring and Initial Resuscitation
Monitoring
Assess perfusion:
*Arterial catheter.
*Signs of Hypoperfusion (cold, VC skin, olig/anuria and lactate>4mmol/l.


Catheters:
*Central venous catheter
*Avoid PACs (SvO2 = ScvO2) + PAOP
*Radial artery pulse pressure
                                     x           Static Hemod. Measures


*Aortic blood flow peak velocity                 Dynamic Hemod.Measures
*brachial artery blood flow velocity



     Schmidt Gregory A, MD, Mandel Jess, MD. Management of severe sepsis and septic
     shock in adults.Wolters Kluwer Healt and Uptodate, May 2012.
4. Management of Septic Shock.
4.2.Therapeutic Priorities
Monitoring and Initial Resuscitation
Initial Resuscitation




    Matthew R.Morrell, MD, Scott T.Micek, PharmD,Marin H. Kollef, MD. The Management of Severe
    Sepsis and Septic Shock. Infect Dis Clin N Am 23 (2009) 485–501.
4. Management of Septic Shock.
4.2.Therapeutic Priorities
Monitoring and Initial Resuscitation
4. Management of Septic Shock.
4.3. Diagnosis-AB therapy- Source Control.
  Diagnosis
  *Obtain ≥ 2 BCs one drawn percutaneosuly.
  *Obtain ≥1 BCs of vascular access devices.
  *Obtain culture of other sites clinically indicated

   Antibiotics therapy




                                                                             1º Appropiate
                                                                             antibiotics




Matthew R.Morrell, MD, Scott T.Micek, PharmD,Marin H. Kollef, MD. The Management of Severe Sepsis and
Septic Shock. Infect Dis Clin N Am 2009;23:485–501.
Dellinger RP, Levy MM, Carlet JM, et al: Surviving Sepsis Campaign: International guidelines for management of
severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296–327.
4. Management of Septic Shock.
4.3. Diagnosis-AB therapy- Source Control.
Antibiotics therapy



                                                                       2º Early therapy (First
                                                                       hour of onset the
                                                                       hypotension)




 Anand Kumar, MD; Daniel Roberts, MD; Kenneth E. Wood, DO; Bruce Light, MD; Joseph E. Parrillo, MD;
 Satendra Sharma, MD; Robert Suppes, BSc; Daniel Feinstein, MD; Sergio Zanotti, MD; Leo Taiberg, MD; David
 Gurka, MD; Aseem Kumar, PhD; Mary Cheang, MSc. Duration of hypotension before initiation of effective
 antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med 2006
 ;34:1589-1596.
4. Management of Septic Shock.
  4.3. Diagnosis-AB therapy- Source Control
  Antibiotics therapy


                                                                           3ºApproach of
                                                                           antibiotics therapy




Matthew R.Morrell, MD, Scott T.Micek, PharmD,Marin H. Kollef, MD. The Management of Severe Sepsis
and Septic Shock. Infect Dis Clin N Am 2009;23:485–501.
4. Management of Septic Shock.
      4.3. Diagnosis-AB therapy- Source Control.


Source Control
*the drainage of infected fluids.
*Removal of infected devices.
*Debridement of infected soft tissues.
*Definitive measures to correct anatomic
derangement      resulting    in  ongoing
antimicrobial contamination.




    *Matthew R.Morrell, MD, Scott T.Micek, PharmD,Marin H. Kollef, MD. The Management of Severe Sepsis
    and Septic Shock. Infect Dis Clin N Am 2009;23:485–501.
    *Dellinger RP, Levy MM, Carlet JM, et al: Surviving Sepsis Campaign: International guidelines for
    management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296–327.
4. Management of Septic Shock.
4.4. Fluid Therapy
     1000 mL of crystalloids or 300–500 mL of colloids over 30
      mins.

     More rapid and larger volumes in tissue hypoperfusion.

     If there are not improvement in the hemodinamics
      paramethers, the rate of fluid administration should be
      reduced.




*Emanuel P. Rivers, Anja Kathrin Jaehne, Laura Eichhorn-Wharry, Samantha Brown and David
Amponsah. Fluid therapy in septic shock. Current Opinion in Critical Care 2010;16:001–012.
*Dellinger RP, Levy MM, Carlet JM, et al: Surviving Sepsis Campaign: International guidelines for
management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296–327.
4. Management of Septic Shock.
   4.4. Fluid Therapy
        Target a CVP of 8 mm Hg (12mmHg MV).




Design: Retrospective review of the use of intravenous fluids during the first
4 days of care.
Setting: Multicenter randomized controlled trial.
Patients: The Vasopressin in Septic Shock Trial (VASST) study enrolled 778
patients who had septic shock and who were receiving a minimum of 5 ug
NA/min
The VASST patient database included daily fluid intake and urine output for
the first 4days of treatment, CVP and (APACHE) II score.

 John H. Boyd, MD, FRCP(C); Jason Forbes, MD; Taka-aki Nakada, MD, PhD; Keith R. Walley, MD, FRCP(C);
 James A. Russell, MD, FRCP(C).Fluid resuscitation in septic shock: A positive fluid balance and elevated central
 venous pressure are associated with increased mortality. Crit Care Med 2011 Vol. 39, No. 2
4. Management of Septic Shock.
  4.4. Fluid Therapy
       Target a CVP of 8 mm Hg (12mmHg MV).




John H. Boyd, MD, FRCP(C); Jason Forbes, MD; Taka-aki Nakada, MD, PhD; Keith R. Walley, MD, FRCP(C);
James A. Russell, MD, FRCP(C).Fluid resuscitation in septic shock: A positive fluid balance and elevated central
venous pressure are associated with increased mortality. Crit Care Med 2011 Vol. 39, No. 2
4. Management of Septic Shock.
  4.4. Fluid Therapy
      Colloids vs Crystalloids??




Colloids versus crystalloids for fluid resuscitation in critically ill patients.
Roberts I, Alderson P, Bunn F, Chinnock P, Ker K, Schierhout G.
Update in Cochrane Database Syst Rev. 2007;(4):CD000567.
“There is no evidence from randomised controlled trials that resuscitation
with colloids reduces the risk of death, compared to resuscitation with
crystalloids”




    Emanuel P. Rivers, Anja Kathrin Jaehne, Laura Eichhorn-Wharry, Samantha Brown and David
    Amponsah. Fluid therapy in septic shock. Current Opinion in Critical Care 2010;16:001–012.
4. Management of Septic Shock.
4.4. Fluid Therapy




  Anders Perner, Nicolai Haase, Anne B. Guttormsen, Jyrki Tenhunen, Gudmundur Klemenzson, Anders
  Åneman, Kristian R. Madsen, Morten H. Møller, , Jeanie M. Elkjær, Lone M. PoulsenAsger BendtsenRobert
  WindingMorten SteensenPawel Berezowicz, Peter Søe-JensenMorten BestleKristian StrandJørgen Wiis,
  Jonathan O. White, Klaus J. Thornberg, Lars Quist, Jonas Nielsen, Lasse H. Andersen, Lars B. Holst, Katrin
  ThormarAnne-Lene Kjældgaard, Maria L. Fabritius., Frederik Mondrup, Frank C. PottThea P. MøllerPer
  Winkel, Jørn Wetterslev.Hydroxyethyl Starch 130/0.4 versus Ringer's Acetate in Severe Sepsis. N Engl J
  Med 2012 .
4. Management of Septic Shock.
4.5.Vasopressors and inotropes therapy




   Alpha 1 Receptor stimulation px VC
   Alpha 2 Receptor stimulation px VD by endothelial NO production
Christopher B. Overgaard, MD; Vladimír Dzˇavík, MD. Inotropes and Vasopressors Review of Physiology and
Clinical Use in Cardiovascular Disease.Circulation 2008,118:1047-1056.

Timothy J. Ellender,MD, Joseph C. Skinner,MD.The Use of Vasopressors and Inotropes in the Emergency
Medical Treatment of Shock. Emerg Med Clin N Am 26 (2008) 759–786.
4. Management of Septic Shock.
    4.5.Vasopressors and inotropes therapy




   Beta1 receptor produces inotropic and chronotropic effect by sinoatrial
    nodal conduction. Also Dromotrophic effect (A/V nodal conduction)
   Beta2 receptor px relaxation of smooth muscle and VD

    Christopher B. Overgaard, MD; Vladimír Dzˇavík, MD. Inotropes and Vasopressors Review of Physiology and
    Clinical Use in Cardiovascular Disease.Circulation 2008,118:1047-1056.

    Timothy J. Ellender,MD, Joseph C. Skinner,MD.The Use of Vasopressors and Inotropes in the Emergency
    Medical Treatment of Shock. Emerg Med Clin N Am 26 (2008) 759–786.
4. Management of Septic Shock.
4.5.Vasopressors and inotropes therapy
NOREPINEPHRINE
•NT and potent alpha 1 adrenergic receptor agonist.
•Modest beta agonist effect.
•Powerful VC
•Increase systolic and diastolic pressures (coronary flow).
•Direct toxicity in continue infusion (apoptosis)

•NE doesn´t improve sublingual microcirculatory perfusion,
intestinal [pCO2] or arterial lactate levels.




   *E. Christiaan Boerma.The role of vasoactive agents in the resuscitation of microvascular perfusion and
   tissue oxygenation in critically ill patients. Intensive Care Med (2010) 36:2004–2018.
   *Christopher B. Overgaard, MD; Vladimír Dzˇavík, MD. Inotropes and Vasopressors Review of Physiology
   and Clinical Use in Cardiovascular Disease.Circulation 2008,118:1047-1056.
4. Management of Septic Shock.
4.5.Vasopressors and inotropes therapy




             n?
                    Critical Care 2008, 12:R143 (doi:10.1186/cc7121)
4. Management of Septic Shock.
 4.5.Vasopressors and inotropes therapy
DOPAMINE
•Inmediate precursor to NE
•Low doses
    * D1: renal, coronary, mesenteric, cerebral beds
    * D2: vasculature and renal tissues.(natriuretic
effects). RENAL DOSE???
•Medium doses
    * B1: inotropy and chronotropy effect with mild VC
•High doses
    * A1:VC




      *E. Christiaan Boerma.The role of vasoactive agents in the resuscitation of microvascular perfusion and
      tissue oxygenation in critically ill patients. Intensive Care Med (2010) 36:2004–2018.
      *Christopher B. Overgaard, MD; Vladimír Dzˇavík, MD. Inotropes and Vasopressors Review of Physiology
      and Clinical Use in Cardiovascular Disease.Circulation 2008,118:1047-1056.
4. Management of Septic Shock.
  4.5.Vasopressors and inotropes therapy


•58 RCTs studies (2,149 patients)/ 33 years.
•Dopamine did not prevent mortality, the onset of acute renal
failure, or the need for dialysis.
•Sufficient statistical power to exclude any large effect of
dopamine on the risk of acute renal failure or the need for dialysis.
•“There is no evidence to support the use of low-dose dopamine to
prevent or treat acute renal failure, and, therefore, dopamine
should be eliminated from routine clinical use for this indication.”




   *E. Christiaan Boerma.The role of vasoactive agents in the resuscitation of microvascular perfusion and tissue
   oxygenation in critically ill patients. Intensive Care Med (2010) 36:2004–2018.
4. Management of Septic Shock.
4.5.Vasopressors and inotropes therapy
DOBUTAMINE
•Beta1: Beta2 (3:1).
•Low doses (<5 ug/kg/min):
      * VD(beta2) vs VC(alpha1)
•High doses (>15ug/kg/min):
      * VC>VD.
•Increase myocardial oxygen consumption.




   *E. Christiaan Boerma.The role of vasoactive agents in the resuscitation of microvascular perfusion and
   tissue oxygenation in critically ill patients. Intensive Care Med (2010) 36:2004–2018.
   *Christopher B. Overgaard, MD; Vladimír Dzˇavík, MD. Inotropes and Vasopressors Review of Physiology
   and Clinical Use in Cardiovascular Disease.Circulation 2008,118:1047-1056.
4. Management of Septic Shock.
 4.5.Vasopressors and inotropes therapy

Vasopressors therapy
•Maintain MAP 65 mm Hg.
•NE and DO are the initial vasopressors of choice (1C)
•Epinephrine, phenylephrine, or vasopressin should not be administered as
the initial
vasopressor in septic shock .
•Use epinephrine if blood pressure is poorly responsive to norepinephrine or
dopamine.
•Do not use low-dose dopamine for renal protection.
Inotropes therapy
•Dobutamine is the firstchoice inotrope for patients low cardiac output in
adequate left ventricular filling pressure and adequate mean arterial
pressure.




       *Dellinger RP, Levy MM, Carlet JM, et al: Surviving Sepsis Campaign: International guidelines
       for management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296–327.
       *Matthew R.Morrell, MD, Scott T.Micek, PharmD,Marin H. Kollef, MD. The Management of
       Severe Sepsis and Septic Shock. Infect Dis Clin N Am 2009;23:485–501.
4. Management of Septic Shock.
    4.6.Additional Therapies
CORTICOIDS
   Consider intravenous hydrocortisone for adult septic shock when hypotension
    responds poorly to adequate fluid resuscitation and vasopressors.
   ACTH stimulation test is not recommended.
   Hydrocortisone is preferred to dexamethasone.
   Fludrocortisone (50 g vo/d) if an alternative to hydrocortisone (IF lacks significant
    mineralocorticoid activity.
    *Dellinger RP, Levy MM, Carlet JM, et al: Surviving Sepsis Campaign: International guidelines for
    management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296–327.




       Kaufman, David,MD, Mancebo, Jordi,MD.Corticosteroid therapy in septic shock . Wolters Kluwer
       Healt and Uptodate, April 2012.
4. Management of Septic Shock.
4.6.Additional Therapies
METHODS
    Muticenter RCT, double-bind, placebo-controlled.
    250 pts to receive 50 mg HCT ev and 248 pts to receive placebo every 6 hours
     for 5 days.
    At 28 days: primary outcomes were death among patients who did not have
     response to corticotropin test.
RESULTS
    At 28 days, there was no significant difference in mortality between patients in
     the two study groups who did not have a response to corticotropin (39.2% HCT vs
     36.1% PCB,P=0.69).
CONCLUSIONS
    Hydrocortisone did not improve survival or reversal of shock in patients with
     septic shock.




    Charles L. Sprung,Djillali Annane,Didier Keh,Rui Moreno,Mervyn Singer, Klaus Freivogel,Yoram G. Weiss,Julie
    Benbenishty,Armin Kalenka, Helmuth Forst,Pierre-Francois Laterre, Konrad Reinhart,Brian H. Cuthbertson,Didier
    Payen,Josef Briegel for the CORTICUS Study Group.Hydrocortisone Therapy for Patients with Septic Shock.N
    Engl J Med 2008;358:111-24.
Thanks!!

Management of septic shock

  • 1.
    Approach in the Management of Septic Shock Esteban Osorio Salazar Resident of Anesthesiology HUAV July -2012 “The sick girl” by Gabriel Metsu (1658)
  • 2.
    Questions/objectives. 1. Introduction. 2. Definition. 3. Pathophysilogy of sepsis. 4. Management of septic shock. 1. Stabilize respiration. 2. Therapeutic priorites (monitoring andr initial resuscitation) 3. Diagnosis-AB therapy- Source Control. 4. Fluid Therapy. 5. Vasopressors and Inotropic Therapy. 6. Additional therapies.
  • 3.
    1. Introduction.  450.000-500.000 cases of sepsis/year in EU.  80.000 cases in SPAIN.  Mortality Index 4-5 deaths/100.000/year.  Hospital admission of sepsis : 3.4-28 cases/1000 admission.  Incidence of Severe sepsis in ICU.
  • 4.
    2. Definition. Septic Shock Severe sepsis +: *SMBP of <60 mm Hg (<80 mm Hg if hypertension) after 20 to 30 mL/kg starch or 40 to 60 mL/kg saline solution. *PCWP between 12 and 20 mm Hg + *Dopamine of >5 mcg/kg/min *Norepinephrine or epinephrine of <0.25 mcg/kg/min. Refractory Septic Shock *Dopamine at >15 mcg/kg/min *Norepinephrine or epinephrine at >0.25 mcg/kg/min Mean BP at >60 mm Hg (80 mm Hg if previous hypertension Schmidt Gregory A, MD, Mandel Jess, MD. Management of severe sepsis and septic shock in adults.Wolters Kluwer Healt and Uptodate, May 2012.
  • 5.
    3. Pathophysiology ofSepsis. Richard S. Hotchkiss, M.D., and Irene E. Karl, Ph.D.The Pathophysiology and Treatment of Sepsis. N Engl J Med 2003 348;138-150.
  • 6.
    3. Pathophysiology ofSepsis. Richard S. Hotchkiss, M.D., and Irene E. Karl, Ph.D.The Pathophysiology and Treatment of Sepsis. N Engl J Med 2003 348;138-150.
  • 7.
    3. Pathophysiology ofSepsis Emanuel P. Riversa, Anja Kathrin Jaehne, Laura Eichhorn-Wharry, Samantha Brown and David Amponsah. Fluid therapy in septic shock. Current Opinion in Critical Care 2010,16:001–012.
  • 8.
    3. Pathophysiology ofSepsis Emanuel P. Riversa, Anja Kathrin Jaehne, Laura Eichhorn-Wharry, Samantha Brown and David Amponsah. Fluid therapy in septic shock. Current Opinion in Critical Care 2010,16:001–012.
  • 9.
    4. Management ofSeptic Shock. 4.1.Stabilize respiration  Supplemental oxygen to all patients and monitored continuously with pulse oximetry.  Intubation and mechanical ventilation (may be required).  Chest Rx  Sedative and induction agents. Target in Mechanical ventilation of sepsis-induced ALI/ARDS *Tidal volume of 6 mL/kg (predicted). *Initial upper limit plateau pressure <30 cm H2O. *PEEP for prevent lung collapse in ALI/ARDS. *Prone position for ARDS patients with max FiO2/Pp? (2C) *Mild to moderate hypoxemic respiratory failure: NIMV. * Target in sedative, inductive agents and NMB in sepsis *Sedation protocols. *Intermittent bolus sedation or continuous infusion sedation (1C). *Avoid NMB where possible. Train-of-four when using continuous infusions(1B). *Dellinger RP, Levy MM, Carlet JM, et al: Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296–327. *Schmidt Gregory A, MD, Mandel Jess, MD. Management of severe sepsis and septic shock in adults.Wolters Kluwer Healt and Uptodate, May 2012.
  • 10.
    4. Management ofSeptic Shock. 4.1.Stabilize respiration Murray MJ, Cowen J, DeBlock H, et al. Clinical practice guidelines for sustained neuromuscular blockade in the adult critically ill patient. Crit Care Med 2002; 30:142-156.
  • 11.
    4. Management ofSeptic Shock. 4.2.Therapeutic Priorities Monitoring and Initial Resuscitation Monitoring Assess perfusion: *Arterial catheter. *Signs of Hypoperfusion (cold, VC skin, olig/anuria and lactate>4mmol/l. Catheters: *Central venous catheter *Avoid PACs (SvO2 = ScvO2) + PAOP *Radial artery pulse pressure x Static Hemod. Measures *Aortic blood flow peak velocity Dynamic Hemod.Measures *brachial artery blood flow velocity Schmidt Gregory A, MD, Mandel Jess, MD. Management of severe sepsis and septic shock in adults.Wolters Kluwer Healt and Uptodate, May 2012.
  • 12.
    4. Management ofSeptic Shock. 4.2.Therapeutic Priorities Monitoring and Initial Resuscitation Initial Resuscitation Matthew R.Morrell, MD, Scott T.Micek, PharmD,Marin H. Kollef, MD. The Management of Severe Sepsis and Septic Shock. Infect Dis Clin N Am 23 (2009) 485–501.
  • 13.
    4. Management ofSeptic Shock. 4.2.Therapeutic Priorities Monitoring and Initial Resuscitation
  • 14.
    4. Management ofSeptic Shock. 4.3. Diagnosis-AB therapy- Source Control. Diagnosis *Obtain ≥ 2 BCs one drawn percutaneosuly. *Obtain ≥1 BCs of vascular access devices. *Obtain culture of other sites clinically indicated Antibiotics therapy 1º Appropiate antibiotics Matthew R.Morrell, MD, Scott T.Micek, PharmD,Marin H. Kollef, MD. The Management of Severe Sepsis and Septic Shock. Infect Dis Clin N Am 2009;23:485–501. Dellinger RP, Levy MM, Carlet JM, et al: Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296–327.
  • 15.
    4. Management ofSeptic Shock. 4.3. Diagnosis-AB therapy- Source Control. Antibiotics therapy 2º Early therapy (First hour of onset the hypotension) Anand Kumar, MD; Daniel Roberts, MD; Kenneth E. Wood, DO; Bruce Light, MD; Joseph E. Parrillo, MD; Satendra Sharma, MD; Robert Suppes, BSc; Daniel Feinstein, MD; Sergio Zanotti, MD; Leo Taiberg, MD; David Gurka, MD; Aseem Kumar, PhD; Mary Cheang, MSc. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med 2006 ;34:1589-1596.
  • 16.
    4. Management ofSeptic Shock. 4.3. Diagnosis-AB therapy- Source Control Antibiotics therapy 3ºApproach of antibiotics therapy Matthew R.Morrell, MD, Scott T.Micek, PharmD,Marin H. Kollef, MD. The Management of Severe Sepsis and Septic Shock. Infect Dis Clin N Am 2009;23:485–501.
  • 17.
    4. Management ofSeptic Shock. 4.3. Diagnosis-AB therapy- Source Control. Source Control *the drainage of infected fluids. *Removal of infected devices. *Debridement of infected soft tissues. *Definitive measures to correct anatomic derangement resulting in ongoing antimicrobial contamination. *Matthew R.Morrell, MD, Scott T.Micek, PharmD,Marin H. Kollef, MD. The Management of Severe Sepsis and Septic Shock. Infect Dis Clin N Am 2009;23:485–501. *Dellinger RP, Levy MM, Carlet JM, et al: Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296–327.
  • 18.
    4. Management ofSeptic Shock. 4.4. Fluid Therapy  1000 mL of crystalloids or 300–500 mL of colloids over 30 mins.  More rapid and larger volumes in tissue hypoperfusion.  If there are not improvement in the hemodinamics paramethers, the rate of fluid administration should be reduced. *Emanuel P. Rivers, Anja Kathrin Jaehne, Laura Eichhorn-Wharry, Samantha Brown and David Amponsah. Fluid therapy in septic shock. Current Opinion in Critical Care 2010;16:001–012. *Dellinger RP, Levy MM, Carlet JM, et al: Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296–327.
  • 19.
    4. Management ofSeptic Shock. 4.4. Fluid Therapy  Target a CVP of 8 mm Hg (12mmHg MV). Design: Retrospective review of the use of intravenous fluids during the first 4 days of care. Setting: Multicenter randomized controlled trial. Patients: The Vasopressin in Septic Shock Trial (VASST) study enrolled 778 patients who had septic shock and who were receiving a minimum of 5 ug NA/min The VASST patient database included daily fluid intake and urine output for the first 4days of treatment, CVP and (APACHE) II score. John H. Boyd, MD, FRCP(C); Jason Forbes, MD; Taka-aki Nakada, MD, PhD; Keith R. Walley, MD, FRCP(C); James A. Russell, MD, FRCP(C).Fluid resuscitation in septic shock: A positive fluid balance and elevated central venous pressure are associated with increased mortality. Crit Care Med 2011 Vol. 39, No. 2
  • 20.
    4. Management ofSeptic Shock. 4.4. Fluid Therapy  Target a CVP of 8 mm Hg (12mmHg MV). John H. Boyd, MD, FRCP(C); Jason Forbes, MD; Taka-aki Nakada, MD, PhD; Keith R. Walley, MD, FRCP(C); James A. Russell, MD, FRCP(C).Fluid resuscitation in septic shock: A positive fluid balance and elevated central venous pressure are associated with increased mortality. Crit Care Med 2011 Vol. 39, No. 2
  • 21.
    4. Management ofSeptic Shock. 4.4. Fluid Therapy  Colloids vs Crystalloids?? Colloids versus crystalloids for fluid resuscitation in critically ill patients. Roberts I, Alderson P, Bunn F, Chinnock P, Ker K, Schierhout G. Update in Cochrane Database Syst Rev. 2007;(4):CD000567. “There is no evidence from randomised controlled trials that resuscitation with colloids reduces the risk of death, compared to resuscitation with crystalloids” Emanuel P. Rivers, Anja Kathrin Jaehne, Laura Eichhorn-Wharry, Samantha Brown and David Amponsah. Fluid therapy in septic shock. Current Opinion in Critical Care 2010;16:001–012.
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    4. Management ofSeptic Shock. 4.4. Fluid Therapy Anders Perner, Nicolai Haase, Anne B. Guttormsen, Jyrki Tenhunen, Gudmundur Klemenzson, Anders Åneman, Kristian R. Madsen, Morten H. Møller, , Jeanie M. Elkjær, Lone M. PoulsenAsger BendtsenRobert WindingMorten SteensenPawel Berezowicz, Peter Søe-JensenMorten BestleKristian StrandJørgen Wiis, Jonathan O. White, Klaus J. Thornberg, Lars Quist, Jonas Nielsen, Lasse H. Andersen, Lars B. Holst, Katrin ThormarAnne-Lene Kjældgaard, Maria L. Fabritius., Frederik Mondrup, Frank C. PottThea P. MøllerPer Winkel, Jørn Wetterslev.Hydroxyethyl Starch 130/0.4 versus Ringer's Acetate in Severe Sepsis. N Engl J Med 2012 .
  • 23.
    4. Management ofSeptic Shock. 4.5.Vasopressors and inotropes therapy  Alpha 1 Receptor stimulation px VC  Alpha 2 Receptor stimulation px VD by endothelial NO production Christopher B. Overgaard, MD; Vladimír Dzˇavík, MD. Inotropes and Vasopressors Review of Physiology and Clinical Use in Cardiovascular Disease.Circulation 2008,118:1047-1056. Timothy J. Ellender,MD, Joseph C. Skinner,MD.The Use of Vasopressors and Inotropes in the Emergency Medical Treatment of Shock. Emerg Med Clin N Am 26 (2008) 759–786.
  • 24.
    4. Management ofSeptic Shock. 4.5.Vasopressors and inotropes therapy  Beta1 receptor produces inotropic and chronotropic effect by sinoatrial nodal conduction. Also Dromotrophic effect (A/V nodal conduction)  Beta2 receptor px relaxation of smooth muscle and VD Christopher B. Overgaard, MD; Vladimír Dzˇavík, MD. Inotropes and Vasopressors Review of Physiology and Clinical Use in Cardiovascular Disease.Circulation 2008,118:1047-1056. Timothy J. Ellender,MD, Joseph C. Skinner,MD.The Use of Vasopressors and Inotropes in the Emergency Medical Treatment of Shock. Emerg Med Clin N Am 26 (2008) 759–786.
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    4. Management ofSeptic Shock. 4.5.Vasopressors and inotropes therapy NOREPINEPHRINE •NT and potent alpha 1 adrenergic receptor agonist. •Modest beta agonist effect. •Powerful VC •Increase systolic and diastolic pressures (coronary flow). •Direct toxicity in continue infusion (apoptosis) •NE doesn´t improve sublingual microcirculatory perfusion, intestinal [pCO2] or arterial lactate levels. *E. Christiaan Boerma.The role of vasoactive agents in the resuscitation of microvascular perfusion and tissue oxygenation in critically ill patients. Intensive Care Med (2010) 36:2004–2018. *Christopher B. Overgaard, MD; Vladimír Dzˇavík, MD. Inotropes and Vasopressors Review of Physiology and Clinical Use in Cardiovascular Disease.Circulation 2008,118:1047-1056.
  • 26.
    4. Management ofSeptic Shock. 4.5.Vasopressors and inotropes therapy n? Critical Care 2008, 12:R143 (doi:10.1186/cc7121)
  • 27.
    4. Management ofSeptic Shock. 4.5.Vasopressors and inotropes therapy DOPAMINE •Inmediate precursor to NE •Low doses * D1: renal, coronary, mesenteric, cerebral beds * D2: vasculature and renal tissues.(natriuretic effects). RENAL DOSE??? •Medium doses * B1: inotropy and chronotropy effect with mild VC •High doses * A1:VC *E. Christiaan Boerma.The role of vasoactive agents in the resuscitation of microvascular perfusion and tissue oxygenation in critically ill patients. Intensive Care Med (2010) 36:2004–2018. *Christopher B. Overgaard, MD; Vladimír Dzˇavík, MD. Inotropes and Vasopressors Review of Physiology and Clinical Use in Cardiovascular Disease.Circulation 2008,118:1047-1056.
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    4. Management ofSeptic Shock. 4.5.Vasopressors and inotropes therapy •58 RCTs studies (2,149 patients)/ 33 years. •Dopamine did not prevent mortality, the onset of acute renal failure, or the need for dialysis. •Sufficient statistical power to exclude any large effect of dopamine on the risk of acute renal failure or the need for dialysis. •“There is no evidence to support the use of low-dose dopamine to prevent or treat acute renal failure, and, therefore, dopamine should be eliminated from routine clinical use for this indication.” *E. Christiaan Boerma.The role of vasoactive agents in the resuscitation of microvascular perfusion and tissue oxygenation in critically ill patients. Intensive Care Med (2010) 36:2004–2018.
  • 29.
    4. Management ofSeptic Shock. 4.5.Vasopressors and inotropes therapy DOBUTAMINE •Beta1: Beta2 (3:1). •Low doses (<5 ug/kg/min): * VD(beta2) vs VC(alpha1) •High doses (>15ug/kg/min): * VC>VD. •Increase myocardial oxygen consumption. *E. Christiaan Boerma.The role of vasoactive agents in the resuscitation of microvascular perfusion and tissue oxygenation in critically ill patients. Intensive Care Med (2010) 36:2004–2018. *Christopher B. Overgaard, MD; Vladimír Dzˇavík, MD. Inotropes and Vasopressors Review of Physiology and Clinical Use in Cardiovascular Disease.Circulation 2008,118:1047-1056.
  • 30.
    4. Management ofSeptic Shock. 4.5.Vasopressors and inotropes therapy Vasopressors therapy •Maintain MAP 65 mm Hg. •NE and DO are the initial vasopressors of choice (1C) •Epinephrine, phenylephrine, or vasopressin should not be administered as the initial vasopressor in septic shock . •Use epinephrine if blood pressure is poorly responsive to norepinephrine or dopamine. •Do not use low-dose dopamine for renal protection. Inotropes therapy •Dobutamine is the firstchoice inotrope for patients low cardiac output in adequate left ventricular filling pressure and adequate mean arterial pressure. *Dellinger RP, Levy MM, Carlet JM, et al: Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296–327. *Matthew R.Morrell, MD, Scott T.Micek, PharmD,Marin H. Kollef, MD. The Management of Severe Sepsis and Septic Shock. Infect Dis Clin N Am 2009;23:485–501.
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    4. Management ofSeptic Shock. 4.6.Additional Therapies CORTICOIDS  Consider intravenous hydrocortisone for adult septic shock when hypotension responds poorly to adequate fluid resuscitation and vasopressors.  ACTH stimulation test is not recommended.  Hydrocortisone is preferred to dexamethasone.  Fludrocortisone (50 g vo/d) if an alternative to hydrocortisone (IF lacks significant mineralocorticoid activity. *Dellinger RP, Levy MM, Carlet JM, et al: Surviving Sepsis Campaign: International guidelines for management of severe sepsis and septic shock: 2008. Crit Care Med 2008; 36:296–327. Kaufman, David,MD, Mancebo, Jordi,MD.Corticosteroid therapy in septic shock . Wolters Kluwer Healt and Uptodate, April 2012.
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    4. Management ofSeptic Shock. 4.6.Additional Therapies METHODS  Muticenter RCT, double-bind, placebo-controlled.  250 pts to receive 50 mg HCT ev and 248 pts to receive placebo every 6 hours for 5 days.  At 28 days: primary outcomes were death among patients who did not have response to corticotropin test. RESULTS  At 28 days, there was no significant difference in mortality between patients in the two study groups who did not have a response to corticotropin (39.2% HCT vs 36.1% PCB,P=0.69). CONCLUSIONS  Hydrocortisone did not improve survival or reversal of shock in patients with septic shock. Charles L. Sprung,Djillali Annane,Didier Keh,Rui Moreno,Mervyn Singer, Klaus Freivogel,Yoram G. Weiss,Julie Benbenishty,Armin Kalenka, Helmuth Forst,Pierre-Francois Laterre, Konrad Reinhart,Brian H. Cuthbertson,Didier Payen,Josef Briegel for the CORTICUS Study Group.Hydrocortisone Therapy for Patients with Septic Shock.N Engl J Med 2008;358:111-24.
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