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SEPSIS
DR SAMRA AHMAD
PGR MS ANESTHESIA
SUPERVISOR AP DR SAAMIA YOUSAF
SEPSIS
 A life-threatening organ dysfunction caused by a dysregulated
host response to infection .
SEPTIC SHOCK
 OLD DEFINITION:
Septic shock describes sepsis with hypotension despite adequate fluid
resuscitation.
 NEW DEFINITION:
 A subset of sepsis in which underlying circulatory and cellular/metabolic
abnormalities are profound enough to substantially increase mortality.
 Persisting hypotension requiring vasopressors to maintain MAP ≥65 mm Hg
 Blood lactate >2 mmol/L despite adequate volume resuscitation
New Definitions
Systemic inflammatory response syndrome
(SIRS)
 Old terminology
 Replaced the previous term 'sepsis syndrome'.
 This is the body's response to a variety of severe clinical insults. It is characterised by
the presence of two or more of:
 Temperature >38°C or <36°C,
 Heart rate > 90/min,
 Respiratory rate > 20/min or PaCO2 <4.3kPa,
 White cell count > 12 x 109/l, < 4 x 109/l or greater than 10% immature neutrophils.
 Sepsis is defined as SIRS in response to infection.(OLD)
Q SOFA
 The new diagnostic tool for sepsis : quickSOFA (qSOFA),
 Sequential Organ Failure Assessment (SOFA) scoring
 3 indicators below each carry 1 point:
 An alteration in mental status
 A decrease in systolic blood pressure of less than 100 mm Hg
 A respiration rate greater than 22 breaths/min
 The score ranges from 0 to 3 points.
 The presence of 2 or more qSOFA points near the onset of infection is associated with
a greater risk of death or prolonged intensive care unit stay.
Q SOFA
SOFA SCORE
SOFA score 1 2 3 4
 Respiration
PaO2/FIO2 (mm Hg) <400 <300 <220 <100
SaO2/FIO2 221-301 142-220 67-141 <67
 Coagulation
Platelets ×103/mm3 <150 <100 <50 <20
 Liver
Bilirubin (mg/dL) 1.2-1.9 2.0-5.9 6.0-11.9 >12.0
 Cardiovascular
Hypotension MAP <70 Dopamine ≤5 or
dobutamine (any)
Dopamine >5 or
norepinephrine ≤0.1
Dopamine >15 or
norepinephrine >0.1
 CNS
Glasgow Coma Score 13-14 10-12 6-9 <6
 Renal
Creatinine (mg/dL) or
urine output (mL/d)
1.2-1.9 2.0-3.4 3.5-4.9 or <500 >5.0 or <200
SOFA SCORE INTERPRETATION
ONE HOUR BUNDLE
INITIAL RESUSCITATION
 Quantitative resuscitation of patients with sepsis- induced tissue
hypoperfusion (hypotension persisting after initial fluid challenge or blood
lactate concentration ≥ 4 mmol/L) .
 GOALS DURING THE FIRST 6 HOURS OF RESUSCITATION
 Central venous pressure (CVP) 8–12 mm Hg
 Mean arterial pressure (MAP) ≥ 65 mm Hg
 Urine output ≥ 0.5 mL/kg/hr
 Central venous or mixed venous oxygen saturation 70% or 65%, respectively
In patients with elevated lactate levels targeting resuscitation to normalize
lactate
SCREENING FOR SEPSIS
 Routine screening of potentially infected seriously ill patients
should be done .
 Hospital–based performance improvement efforts in severe
sepsis.
DIAGNOSIS
 Send Cultures before starting antimicrobial therapy if no significant delay (>
45 mins ) in the start of antimicrobials
 2 sets of blood cultures (both aerobic and anaerobic bottles) 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
 Use 1,3 beta-D-glucan assay , mannan and anti-mannan antibody assays, if
available and invasive candidiasis is in differential diagnosis of cause of
infection.
 Imaging studies to confirm a potential source of infection .
ANTIMICROBIAL THERAPY
 Administer Broad spectrum intravenous antimicrobials within the first hour
 Antimicrobial regimen should be reassessed daily for potential de-escalation.
 Use low Procalcitonin levels or similar biomarkers in patients who appear septic,
but have no evidence of infection .
 For 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.
 combination of beta-lactam and macrolide for Streptococcus pneumoniae
infections .
 Duration 7–10 days
 Antiviral therapy
SOURCE CONTROL
 A specific anatomical diagnosis of infection source should be done within the first 12
hr of sepsis.
 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).
 intravascular access devices or indewelling catheters can be a possible source of
sepsis
INFECTION PREVENTION
 Selective oral decontamination and selective digestive
decontamination should be introduced to reduce the incidence
of ventilator-associated pneumonia.
 Oral chlorhexidine gluconate for oropharyngeal
decontamination
FLUID THERAPY
 Crystalloids as the initial fluid of choice
 Avoid Hetastarch or Hespan compounds
 Use Albumin in patients who require substantial amounts of crystalloids
 Initial fluid challenge in patients with sepsis induced tissue hypoperfusion
with suspicion of hypovolemia give of 30 mL/kg of crystalloids.
 More rapid administration and greater amounts of fluid may be needed in
some patients
 Fluid challenge technique be applied where in fluid administration is
continued as long as there is hemodynamic improvement
VASOPRESSORS
 Vasopressor therapy initially to target a mean arterial pressure
(MAP) of 65 mm Hg
 Norepinephrine as the first choice vasopressor.
 All patients requiring vasopressors should have an arterial
catheter placed.
IONOTROPIC THERAPY
 A trial of dobutamine infusion up to 20 micrograms/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,
(b) Ongoing signs of hypoperfusion, despite achieving adequate
intravascular volume and adequate MAP .
CORTICOSTEROIDS
 Indicated with persistent hemodynamic instability
 Hydrocortisone 50mg IV every 6 hours. OR Hydrocortisone 100mg IV every
8 hours
 DO NOT use the ACTH stimulation test
 taper off hydrocortisone when vasopressors are no longer required
 Corticosteroids not to be administered for the treatment of sepsis in the
absence of shock
 Multiple studies have shown decreased time on vasopressors. No mortality
benefit.
BLOOD PRODUCTS ADMINISTRATION
 Red blood cell transfusion if Hg <7.0 g/dL .Target Hg of 7.0 –9.0 g/dL in adult.
 DO Not use erythropoietin as a specific treatment of anemia
 Do not use Fresh frozen plasma to correct laboratory clotting abnormalities in the
absence of bleeding or planned procedure.
 Do not use Anti thrombin for the treatment of severe sepsis and septic shock.
 Platelets Prophylaxis
 Platelets prophylaxis when counts are <10,000/mm3 (10 x 109/L) in the absence of
apparent bleeding.
 prophylactic platelet transfusion when counts are < 20,000/mm3 (20 x 109/L) if the
patient has a significant risk of bleeding.
 Higher platelet counts (≥50,000/mm3 [50 x 109/L]) are advised for active bleeding,
surgery, or invasive procedures.
Mechanical ventilation
 Target a tidal volume of 6 mL/kg predicted body weight.
 Plateau pressures be ≤30 cm H2O
 Positive end-expiratory pressure (PEEP)
 Recruitment maneuvers be used in sepsis patients with severe refractory hypoxemia
 Prone positioning be used in sepsis-induced ARDS patients with a Pao2/Fio2 ratio ≤
100 mm Hg .
 head of the bed elevated to 30-45 degrees
 Weaning criteria : a) arousable b) hemodynamically stable without vasopressor agents
c) no new potentially serious conditions d) low ventilatory and end-expiratory pressure
requirements; and e) low Fio2, consider for extubation .
 In the absence of specific indications such as bronchospasm, do not use beta 2-
agonists for treatment of sepsis-induced ARDS .
SEDATION, ANALGESIA & NMB
 Continuous or intermittent sedation be minimized
 Neuromuscular blocking agents (NMBAs) be avoided .use intermittent bolus.
 NMBA should not be used greater than 48 hours for patients with early sepsis-induced
ARDS and a Pao2/Fio2 < 150 mm Hg
GLUCOSE CONTROL
 Start insulin dosing when 2 consecutive blood glucose levels are >180 mg/dL
 Target blood glucose ≤180 mg/dL rather than blood glucose ≤ 110 mg/dL
 Blood glucose values be monitored every 1–2 hrs until glucose values until
insulin infusion rates are stable and then every 4 hrs.
RRT
 Continuous renal replacement therapies and intermittent hemodialysis to be
done in patients with severe sepsis and acute renal failure.
 Use continuous therapies to facilitate management of fluid balance in
hemodynamically unstable septic patients
BICARBONATE THERAPY
DO NOT use sodium bicarbonate therapy for the purpose of improving
hemodynamics or reducing vasopressor requirements in patients with
hypoperfusion-induced lactic acidemia with pH ≥7.15
DVT PROPHYLAXIS
 Daily subcutaneous low molecular weight heparin (LMWH) .
 If creatinine clearance is <30 mL/min, use dalteparin or another form of
LMWH that has a low degree of renal metabolism or UFH .
 Use intermittent pneumatic compression devices.
 mechanical prophylactic treatment, such as graduated compression stockings
or intermittent compression devices should be used unless contraindicated.
STRESS ULCER PROPHYLAXIS
 H2 blocker or proton pump inhibitor be given to patients with severe sepsis/septic
shock who have bleeding risk factors.
NUTRITION
 Administer oral or enteral feedings, as tolerated, rather than either complete fasting
or provision of only intravenous glucose within the first 48 hours after a diagnosis of
severe sepsis/septic shock
 start low dose feeding (eg, up to 500 calories per day).
 Use intravenous glucose and enteral nutrition rather than total parenteral nutrition
(TPN) alone or parenteral nutrition in conjunction with enteral feeding in the first 7
days .
 Use nutrition with no specific immunomodulating supplementation
GOALS OF CARE
 Discuss goals of care and prognosis with patients and families
 Incorporate goals of care into treatment and end-of-life care planning,
utilizing palliative care principles.
 Address goals of care as early as feasible.
NO QUESTIONS PLEASE THANK YOU
DR SAMRA AHMAD

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Sepsis dr samra

  • 1. SEPSIS DR SAMRA AHMAD PGR MS ANESTHESIA SUPERVISOR AP DR SAAMIA YOUSAF
  • 2.
  • 3. SEPSIS  A life-threatening organ dysfunction caused by a dysregulated host response to infection .
  • 4. SEPTIC SHOCK  OLD DEFINITION: Septic shock describes sepsis with hypotension despite adequate fluid resuscitation.  NEW DEFINITION:  A subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality.  Persisting hypotension requiring vasopressors to maintain MAP ≥65 mm Hg  Blood lactate >2 mmol/L despite adequate volume resuscitation
  • 6. Systemic inflammatory response syndrome (SIRS)  Old terminology  Replaced the previous term 'sepsis syndrome'.  This is the body's response to a variety of severe clinical insults. It is characterised by the presence of two or more of:  Temperature >38°C or <36°C,  Heart rate > 90/min,  Respiratory rate > 20/min or PaCO2 <4.3kPa,  White cell count > 12 x 109/l, < 4 x 109/l or greater than 10% immature neutrophils.  Sepsis is defined as SIRS in response to infection.(OLD)
  • 7. Q SOFA  The new diagnostic tool for sepsis : quickSOFA (qSOFA),  Sequential Organ Failure Assessment (SOFA) scoring  3 indicators below each carry 1 point:  An alteration in mental status  A decrease in systolic blood pressure of less than 100 mm Hg  A respiration rate greater than 22 breaths/min  The score ranges from 0 to 3 points.  The presence of 2 or more qSOFA points near the onset of infection is associated with a greater risk of death or prolonged intensive care unit stay.
  • 9. SOFA SCORE SOFA score 1 2 3 4  Respiration PaO2/FIO2 (mm Hg) <400 <300 <220 <100 SaO2/FIO2 221-301 142-220 67-141 <67  Coagulation Platelets ×103/mm3 <150 <100 <50 <20  Liver Bilirubin (mg/dL) 1.2-1.9 2.0-5.9 6.0-11.9 >12.0  Cardiovascular Hypotension MAP <70 Dopamine ≤5 or dobutamine (any) Dopamine >5 or norepinephrine ≤0.1 Dopamine >15 or norepinephrine >0.1  CNS Glasgow Coma Score 13-14 10-12 6-9 <6  Renal Creatinine (mg/dL) or urine output (mL/d) 1.2-1.9 2.0-3.4 3.5-4.9 or <500 >5.0 or <200
  • 12.
  • 13.
  • 14. INITIAL RESUSCITATION  Quantitative resuscitation of patients with sepsis- induced tissue hypoperfusion (hypotension persisting after initial fluid challenge or blood lactate concentration ≥ 4 mmol/L) .  GOALS DURING THE FIRST 6 HOURS OF RESUSCITATION  Central venous pressure (CVP) 8–12 mm Hg  Mean arterial pressure (MAP) ≥ 65 mm Hg  Urine output ≥ 0.5 mL/kg/hr  Central venous or mixed venous oxygen saturation 70% or 65%, respectively In patients with elevated lactate levels targeting resuscitation to normalize lactate
  • 15. SCREENING FOR SEPSIS  Routine screening of potentially infected seriously ill patients should be done .  Hospital–based performance improvement efforts in severe sepsis.
  • 16. DIAGNOSIS  Send Cultures before starting antimicrobial therapy if no significant delay (> 45 mins ) in the start of antimicrobials  2 sets of blood cultures (both aerobic and anaerobic bottles) 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  Use 1,3 beta-D-glucan assay , mannan and anti-mannan antibody assays, if available and invasive candidiasis is in differential diagnosis of cause of infection.  Imaging studies to confirm a potential source of infection .
  • 17. ANTIMICROBIAL THERAPY  Administer Broad spectrum intravenous antimicrobials within the first hour  Antimicrobial regimen should be reassessed daily for potential de-escalation.  Use low Procalcitonin levels or similar biomarkers in patients who appear septic, but have no evidence of infection .  For 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.  combination of beta-lactam and macrolide for Streptococcus pneumoniae infections .  Duration 7–10 days  Antiviral therapy
  • 18. SOURCE CONTROL  A specific anatomical diagnosis of infection source should be done within the first 12 hr of sepsis.  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).  intravascular access devices or indewelling catheters can be a possible source of sepsis
  • 19. INFECTION PREVENTION  Selective oral decontamination and selective digestive decontamination should be introduced to reduce the incidence of ventilator-associated pneumonia.  Oral chlorhexidine gluconate for oropharyngeal decontamination
  • 20. FLUID THERAPY  Crystalloids as the initial fluid of choice  Avoid Hetastarch or Hespan compounds  Use Albumin in patients who require substantial amounts of crystalloids  Initial fluid challenge in patients with sepsis induced tissue hypoperfusion with suspicion of hypovolemia give of 30 mL/kg of crystalloids.  More rapid administration and greater amounts of fluid may be needed in some patients  Fluid challenge technique be applied where in fluid administration is continued as long as there is hemodynamic improvement
  • 21. VASOPRESSORS  Vasopressor therapy initially to target a mean arterial pressure (MAP) of 65 mm Hg  Norepinephrine as the first choice vasopressor.  All patients requiring vasopressors should have an arterial catheter placed.
  • 22. IONOTROPIC THERAPY  A trial of dobutamine infusion up to 20 micrograms/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, (b) Ongoing signs of hypoperfusion, despite achieving adequate intravascular volume and adequate MAP .
  • 23. CORTICOSTEROIDS  Indicated with persistent hemodynamic instability  Hydrocortisone 50mg IV every 6 hours. OR Hydrocortisone 100mg IV every 8 hours  DO NOT use the ACTH stimulation test  taper off hydrocortisone when vasopressors are no longer required  Corticosteroids not to be administered for the treatment of sepsis in the absence of shock  Multiple studies have shown decreased time on vasopressors. No mortality benefit.
  • 24. BLOOD PRODUCTS ADMINISTRATION  Red blood cell transfusion if Hg <7.0 g/dL .Target Hg of 7.0 –9.0 g/dL in adult.  DO Not use erythropoietin as a specific treatment of anemia  Do not use Fresh frozen plasma to correct laboratory clotting abnormalities in the absence of bleeding or planned procedure.  Do not use Anti thrombin for the treatment of severe sepsis and septic shock.  Platelets Prophylaxis  Platelets prophylaxis when counts are <10,000/mm3 (10 x 109/L) in the absence of apparent bleeding.  prophylactic platelet transfusion when counts are < 20,000/mm3 (20 x 109/L) if the patient has a significant risk of bleeding.  Higher platelet counts (≥50,000/mm3 [50 x 109/L]) are advised for active bleeding, surgery, or invasive procedures.
  • 25. Mechanical ventilation  Target a tidal volume of 6 mL/kg predicted body weight.  Plateau pressures be ≤30 cm H2O  Positive end-expiratory pressure (PEEP)  Recruitment maneuvers be used in sepsis patients with severe refractory hypoxemia  Prone positioning be used in sepsis-induced ARDS patients with a Pao2/Fio2 ratio ≤ 100 mm Hg .  head of the bed elevated to 30-45 degrees  Weaning criteria : a) arousable b) hemodynamically stable without vasopressor agents c) no new potentially serious conditions d) low ventilatory and end-expiratory pressure requirements; and e) low Fio2, consider for extubation .  In the absence of specific indications such as bronchospasm, do not use beta 2- agonists for treatment of sepsis-induced ARDS .
  • 26. SEDATION, ANALGESIA & NMB  Continuous or intermittent sedation be minimized  Neuromuscular blocking agents (NMBAs) be avoided .use intermittent bolus.  NMBA should not be used greater than 48 hours for patients with early sepsis-induced ARDS and a Pao2/Fio2 < 150 mm Hg
  • 27. GLUCOSE CONTROL  Start insulin dosing when 2 consecutive blood glucose levels are >180 mg/dL  Target blood glucose ≤180 mg/dL rather than blood glucose ≤ 110 mg/dL  Blood glucose values be monitored every 1–2 hrs until glucose values until insulin infusion rates are stable and then every 4 hrs.
  • 28. RRT  Continuous renal replacement therapies and intermittent hemodialysis to be done in patients with severe sepsis and acute renal failure.  Use continuous therapies to facilitate management of fluid balance in hemodynamically unstable septic patients
  • 29. BICARBONATE THERAPY DO NOT use sodium bicarbonate therapy for the purpose of improving hemodynamics or reducing vasopressor requirements in patients with hypoperfusion-induced lactic acidemia with pH ≥7.15
  • 30. DVT PROPHYLAXIS  Daily subcutaneous low molecular weight heparin (LMWH) .  If creatinine clearance is <30 mL/min, use dalteparin or another form of LMWH that has a low degree of renal metabolism or UFH .  Use intermittent pneumatic compression devices.  mechanical prophylactic treatment, such as graduated compression stockings or intermittent compression devices should be used unless contraindicated.
  • 31. STRESS ULCER PROPHYLAXIS  H2 blocker or proton pump inhibitor be given to patients with severe sepsis/septic shock who have bleeding risk factors.
  • 32. NUTRITION  Administer oral or enteral feedings, as tolerated, rather than either complete fasting or provision of only intravenous glucose within the first 48 hours after a diagnosis of severe sepsis/septic shock  start low dose feeding (eg, up to 500 calories per day).  Use intravenous glucose and enteral nutrition rather than total parenteral nutrition (TPN) alone or parenteral nutrition in conjunction with enteral feeding in the first 7 days .  Use nutrition with no specific immunomodulating supplementation
  • 33. GOALS OF CARE  Discuss goals of care and prognosis with patients and families  Incorporate goals of care into treatment and end-of-life care planning, utilizing palliative care principles.  Address goals of care as early as feasible.
  • 34.
  • 35. NO QUESTIONS PLEASE THANK YOU DR SAMRA AHMAD