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COMPILED BY MODERATOR
Dr. Bharat Arora Dr. Abhijit Tarat
PG Trainee Associate Professor
Department Of Anesthesiology And C...
• The condition characterized by signs of systemic
Inflammation(eg . fever & leucocytosis) is called
Systemic Inflammatory...
Diagnostic Criteria For SIRS
 The diagnosis of SIRS requires at least 2 of the
following:
1)Temperature > 380 C or < 360 ...
1)Infections in the aged and malnourished
2)Inadequate immune response due to hepatic or renal
failure, diabetes mellitus,...
Severe SEPSIS :
 Sepsis accompanied by hypo-perfusion or
organ dysfunction.
 Cardiovascular :
 SBP<90mmhg/MAP<70 for at...
 Gastrointestinal :
 Hepatic dysfunction
(hyperbilirubinemia, Elevated
transaminases
 CNS :
 Alteration in Mental stat...
BASIC
PATHOPHYSIOLOGY
Nidus of infection
Blood stream
invasion
Release of
mediators
Peripheral
vascular
effects
Myocardial
depression Cellular I...
 Classically septic shock is due to endotoxins
released by gram negative bacteria though it
can occur with fungal and pro...
 Endotoxins also activates neutrophils with the
release of proteases and oxidants which promote
endothelial cell damage.
...
 Endotoxins also activates the coagulation
factors in the serum stimulating the
coagulation pathway.
 Fibrinolysis norma...
 In summary, invasion by microorganisms
and their toxins elicit a strong response from
the host defenses, which is charac...
• If the host defense system is disorganized
, un-orchestrated , unbalanced and
unchecked it fails to defend the host and
...
Infection
Endotoxin
(LPS)
Cellular activation
Direct cell
injury
Plasma
protein
system
PMN Macrophage Lymphocyte Monocyte ...
• The typical result is a high output hyper dynamic
circulatory state with tachycardia and
hypotension.
• Septic shock in ...
1)Arterial and venous tone markedly decreases
-venous and arteriolar dilatation
- fall in peripheral vascular resistance
-...
3)Combined effect of 1 & 2 leads to
hypovolemia which may mask the hyper
dynamic state.
4)Pattern of blood flow distributi...
Myocardial depression occurs in all patients.
Decreased compliance with decreased left
ventricular diastolic function.
L...
Pulmonary hypertension due to increased
pulmonary vascular resistance can occur when septic
shock produces ARDS.
When pu...
1)Early stage:-Tachycardia , hypotension , low PCWP,
high CI , low SVR
2)With progression and deteriorating cardiac functi...
• Early and evolving phase of sepsis and septic shock
is characterized by increase in DO2 and VO2.
• In spite of increased...
• Reasons are:-
1)Damaged endothelial cells in capillaries ,get
edematous resulting in increased distance necessary
for di...
 4) There is persistent hypotension following
ischemic insult to an organ. This can be explained
due to calcium influx wi...
General Sign and Symptoms
 Rigor – fever (sometimes hypothermia)
 Tachypnea /respiratory alkalosis
 Positive fluid bala...
 Decreased urine output
 Hyperlactatemia – increased base deficit
 Signs of organ dysfunction
 Hypoxemia
 Coagulation...
MODS
 Multiple organ dysfunction syndrome (MODS)-
failure of two or more organ systems
 Homeostasis cannot be maintained...
 Recovery from Sepsis is associated with near complete
recovery of organ function, even in organs whose cells
have poor r...
PATHOPHYSIOLOGY OF MODS
 MITOCHONDRIAL DYSFUNCTION
 INCREASED CELLULAR APOPTOSIS
 ENDOTHELIAL AND EPITHILIAL DYSFUNCTIO...
MANAGEMENT
1)Leucocytosis or leucopenia.
2)Deranged coagulation profile which includes
elevated PT , thrombocytopenia , decreased
fib...
5)Increase in urinary urea or urinary nitrogen
over 24 hrs and a negative nitrogen balance.
6)Low arterial pH due to prese...
Principles of Therapy
1)To find out and eradicate the infection or sepsis
responsible for the state of septic shock.
2)To ...
• Both eradication of infection and shock reversal
are set into motion together . In severe shock
, resuscitation takes pl...
SEPSIS RESUSCITATION BUNDLE
TO BE COMPLETED WITHIN 3 HOURS:
 1) Measure lactate level
 2) Obtain blood cultures prior to...
 TO BE COMPLETED WITHIN 6 HOURS:
 5) Apply vasopressors (for hypotension that does
not respond to initial fluid resuscit...
1)Management of severe sepsis(EGDT)
A) Initial Resuscitation(first 6 hours)
 Begin resuscitation immediately in pts with
...
If venous oxygen saturation target is not achieved:-
Consider further fluid
Transfuse packed red blood cells if required...
 Use of 1,3 beta D glucan assay , mannan and anti-
mannan antibodies for diagnosis of invasive
candidiasis and fungal inf...
• Consider combination empiric therapy in
neutropenic patients
• Combination therapy ≤ 3-5 days and de-escalation
followin...
D)Source identification and control
A specific anatomic site of infection must be must be
established within first 6 hrs ...
E)Fluid Therapy
Fluid resuscitation using crystalloid, the fluid of choice.
Target a CVP of 8mm of Hg( ≥12 mm of Hg if
m...
F)Vasopressors:
Maintain MAP ≥ 65 mm of Hg
Nor epinephrine and dopamine administered centrally are
the initial vasopress...
G)Inotropic therapy:
Use dobutamine in patients with myocardial dysfunction
as supported by elevated cardiac filling pres...
I)Recombinant human activated protein C
Once Considered the use of rh -APC in adult patients
with sepsis induced organ dy...
Supportive Therapy Of
Severe Sepsis
J)Blood Product Administration:
RBC’s to be administered when Hb<7 gm/dl to target Hb at
7-9gm/dl . A higher level may be...
K) Mechanical ventilation of sepsis induced ALI/ARDS
Target a tidal volume of 6ml/kg body weight
Target an initial upper...
Use a weaning protocol and an SBT to evaluate the
potential for discontinuing mechanical ventilation.
SBT options include...
Sedation , analgesia and neuromuscular blockade in sepsis.
Use either intermittent bolus sedation or continuous infusion
...
Glucose Control
Use intravenous insulin to control hyperglycemia in
patients with severe sepsis following stabilization i...
Renal replacement
Intermittent hemodialysis and CRRT are considered
equivalent.
CRRT offers easier management in haemody...
Deep vein thrombosis prophylaxis
 Use either low dose UFH or LMWH , unless
contraindicated.
Use either a mechanical prop...
NUTRITION:
•Administer oral/ enteral feed ,amount as tolerated.
•Avoid mandatory full caloric feeds, suggesting low
calori...
1)Central venous pressure monitoring is done through a
central venous line.
2)Arterial pressure to be monitored through a ...
•Arrhythmias can occur in septic hypotensive patients
who are on inotropic support and who have indwelling
intracardiac ca...
 THOUGH THESE GUIDELINES ARE HELPFUL,
RECOMMENDATIONS FROM THESE
GUIDELINES CANNOT REPLACE THE CLINICIAN
DECISION MAKING ...
Thank
You
Sepsis – pathophysiology and management
Sepsis – pathophysiology and management
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Sepsis – pathophysiology and management

  1. 1. COMPILED BY MODERATOR Dr. Bharat Arora Dr. Abhijit Tarat PG Trainee Associate Professor Department Of Anesthesiology And Critical Care Silchar medical college And Hospital, Silchar
  2. 2. • The condition characterized by signs of systemic Inflammation(eg . fever & leucocytosis) is called Systemic Inflammatory response syndrome (SIRS). •When SIRS is the result of an infection, the condition is called Sepsis. •When sepsis is accompanied by dysfunction of one or more vital organs, the condition is called Severe sepsis. •When sepsis is accompanied by hypotension that is refractory to volume infusion, the condition is called Septic shock.
  3. 3. Diagnostic Criteria For SIRS  The diagnosis of SIRS requires at least 2 of the following: 1)Temperature > 380 C or < 360 C 2)Heart rate > 90 beats/ min 3)Respiratory rate > 20 breaths/ min or Arterial PCO2< 32 mm of Hg 4)WBC count > 12,000/mm3 or <4000 mm3 or >10 % immature (band ) forms
  4. 4. 1)Infections in the aged and malnourished 2)Inadequate immune response due to hepatic or renal failure, diabetes mellitus, malignancy, HIV infection, lymphoma. 3)Iatrogenic infections 4)Virulent gram negative and gram positive infections 5)Oppurtunistic infections (fungal, viral)following organ transplants, HIV infections and lymphoma. 6)Fulminant tetanus 7)Disseminated haematogenous tuberculosis 8)Severe Pl. falciparum infections 9)Fulminant B. typhosus, salmonella, amoebic infection 10) Trauma , crush injuries, burns, pancreatitis.
  5. 5. Severe SEPSIS :  Sepsis accompanied by hypo-perfusion or organ dysfunction.  Cardiovascular :  SBP<90mmhg/MAP<70 for at least 1 hr despite adequate volume resuscitation or the use of vasopressors to achieve the same goals.  Renal :  Urine output <0.5ml/kg/hr or Acute Renal Failure.  Pulmonary :  PaO2/FiO2 <250if other organ dysfunction is present or <200 if the lungs is the only dysfunctional organ.
  6. 6.  Gastrointestinal :  Hepatic dysfunction (hyperbilirubinemia, Elevated transaminases  CNS :  Alteration in Mental status (delirium)  Hematologic :  Platelet count of <80,000/mm3 or decreased by 50% over 3 days/DIC  Metabolic :  PH<7.30 or base deficit >5.0mmol/L  Plasma lactate >1.5 upper limit of normal.
  7. 7. BASIC PATHOPHYSIOLOGY
  8. 8. Nidus of infection Blood stream invasion Release of mediators Peripheral vascular effects Myocardial depression Cellular Injury Poor tissue perfusion and metabolic acidosis Multiple organ dysfunction Death
  9. 9.  Classically septic shock is due to endotoxins released by gram negative bacteria though it can occur with fungal and protozoal infections. Endotoxin is a lipopolysaccharide component of the outer membrane of the bacterial cell. It contains Lipid A which is highly antigenic and is responsible for features of sepsis syndrome.  Endotoxin interacts with normal host defense system and triggers release of numerous mediators notably cytokines like TNF from mononuclear cells.
  10. 10.  Endotoxins also activates neutrophils with the release of proteases and oxidants which promote endothelial cell damage.  Arachidonic acid in the cell wall undergoes degradation through phospholipase leading to formation of prostaglandins, leucotrienes and thromboxanes.  Phospholipase A2 release membrane bound phospholipids which are converted to platelet activating factor which increases vascular permeability, produces free radicals and activates platelets and phagocytes.
  11. 11.  Endotoxins also activates the coagulation factors in the serum stimulating the coagulation pathway.  Fibrinolysis normally counters procoagulant factors but is suppressed in sepsis due to increased levels of plasminogen activator inhibitor-1(PAI-1), thrombin activatable fibrinolysis inhibitor(TAF.1a)and decreased levels of Protein C.  This haemostatic mechanism prevailing in sepsis is believed to lead to micro-vascular thrombi in various organ system.
  12. 12.  In summary, invasion by microorganisms and their toxins elicit a strong response from the host defenses, which is characterized by activation of cellular elements and the plasma protein system. The cells activated are mononuclear cells , macrophages, neutrophils and endothelial cells. These activated cells produce numerous cytokines and mediators . The host defense system also activates the complement , coagulation cascades and the kallikrein-kinin system
  13. 13. • If the host defense system is disorganized , un-orchestrated , unbalanced and unchecked it fails to defend the host and paradoxically enough inflicts injury on the host . • This injury is widespread because of the toxic effect of numerous mediators , and also because of endothelial cell damage and the dominance of procoagulant factors leading to micro vascular thrombi in various organ systems.
  14. 14. Infection Endotoxin (LPS) Cellular activation Direct cell injury Plasma protein system PMN Macrophage Lymphocyte Monocyte Endothelial cell Pro inflammatory mediators Activation of complement coagulation cascade& kallikrein kinin TNF IL-6, IL-1 Leucotrienes, Prostaglandin Superoxide, H2O2,OH- G-CSF Selectins, ICAMS NO Cell injury Organ failure
  15. 15. • The typical result is a high output hyper dynamic circulatory state with tachycardia and hypotension. • Septic shock in addition is characterized by SBP≤ 90 mm of Hg not responding to fluid replenishment. It is associated with evidence of hypo perfusion and/or organ dysfunction. • This state may be a compensatory response to increased tissue metabolism.
  16. 16. 1)Arterial and venous tone markedly decreases -venous and arteriolar dilatation - fall in peripheral vascular resistance - fall in SBP. Vasodialating substances :- TNF,IL-1,NO,EDRF and PAF. Catecholamine receptor down regulation may also occur and causes poor response to vasopressors. 2) Generalized increase in vascular permeability - increase in interstitial fluid and -tissue edema. Peripheral pooling , hepatosplanchnic pooling and loss from GIT leads to low circulatory volume.
  17. 17. 3)Combined effect of 1 & 2 leads to hypovolemia which may mask the hyper dynamic state. 4)Pattern of blood flow distribution changes . Some organs receive supernormal O2 supply and some get ischemic .Especially the splanchnic circulation is affected . Hepatovenous desaturation has been reported in septic patients.
  18. 18. Myocardial depression occurs in all patients. Decreased compliance with decreased left ventricular diastolic function. Left ventricular systolic dysfunction also occurs evidenced by dilated cardiomyopathy with low ejection fraction. Cardiac output increases because of marked tachycardia. Beta receptor downgrading occurs and causes a poor response to inotropic drugs.
  19. 19. Pulmonary hypertension due to increased pulmonary vascular resistance can occur when septic shock produces ARDS. When pulmonary hypertension is significant , right ventricular function may be markedly affected due to an increased after load.
  20. 20. 1)Early stage:-Tachycardia , hypotension , low PCWP, high CI , low SVR 2)With progression and deteriorating cardiac function hypotension , high PCWP , normal or slightly low CI , normal to rising SVR 3) Late (pre terminal stage):-hypotension , high PCWP, low and progressively decreasing CI and increased SVR 4) Rarely very low CI , high PCWP and high SVR is seen at the start of fulminant septic shock.
  21. 21. • Early and evolving phase of sepsis and septic shock is characterized by increase in DO2 and VO2. • In spite of increased O2 consumption , tissue needs may not be satisfied and tissue hypoxia may occur. • In late phase of septic shock,O2 consumption may fall even though DO2 is satisfactory resulting in a low O2 extraction ratio causing hypoxia and acidosis. • Critical threshold of oxygen delivery
  22. 22. • Reasons are:- 1)Damaged endothelial cells in capillaries ,get edematous resulting in increased distance necessary for diffusion of O2 into tissue cells. 2) Damaged tissue cells find it difficult to utilize O2 for their metabolic needs. 3)Tissue oxygenation may not be impaired at all in sepsis as PO2 is increased in sepsis . Defect may be in the O2 utilization in the mitochondria which challenges aerobic metabolism. The culprit may be endotoxin ,which blocks the enzyme pyruvate dehydrogenase which moves pyruvate into mitochondria . Pyruvate accumulates in the cytoplasm where it is converted into lactate.
  23. 23.  4) There is persistent hypotension following ischemic insult to an organ. This can be explained due to calcium influx within the vascular smooth muscles during hypoxia, which leads to persistent vasoconstriction even after CO and BP are restored to normal, leading to progressive multi-organ dysfunction.  5) Reperfusion Injury  6)Oxygen debt leading to Hyper carbonic acidosis in tissues.  7)Assessment of Stress by Gastric tonometry .
  24. 24. General Sign and Symptoms  Rigor – fever (sometimes hypothermia)  Tachypnea /respiratory alkalosis  Positive fluid balance – edema  General inflammatory reaction  Altered white blood cell count  Increased CRP, IL-6, PCT concentrations  Hemodynamic alterations  Arterial hypotension  Tachycardia  Increased cardiac output/low SVR/high SvO2  Altered skin perfusion
  25. 25.  Decreased urine output  Hyperlactatemia – increased base deficit  Signs of organ dysfunction  Hypoxemia  Coagulation abnormalities  Altered mental status  Hyperglycemia  Thrombocytopenia, DIC  Altered liver function (hyperbilirubinemia)  Intolerance to feeding (altered GI motility)
  26. 26. MODS  Multiple organ dysfunction syndrome (MODS)- failure of two or more organ systems  Homeostasis cannot be maintained without intervention-Results from SIRS  SIRS and MODS represent ends of a continuum  Transition from SIRS to MODS DOES NOT occur in a clear-cut manner  MODS occurs late and is the most common cause of death in patients with Sepsis.  Lactic acidosis led investigators to think that this is due to tissue ischemia.
  27. 27.  Recovery from Sepsis is associated with near complete recovery of organ function, even in organs whose cells have poor regenerative capacity.
  28. 28. PATHOPHYSIOLOGY OF MODS  MITOCHONDRIAL DYSFUNCTION  INCREASED CELLULAR APOPTOSIS  ENDOTHELIAL AND EPITHILIAL DYSFUNCTION  LATE ACTING MEDIATORS OF INFLAMMATION like MIF.
  29. 29. MANAGEMENT
  30. 30. 1)Leucocytosis or leucopenia. 2)Deranged coagulation profile which includes elevated PT , thrombocytopenia , decreased fibrinogen and increased FDP . 3)Hyperglycemia is common . Hypoglycemia may also occur in pre terminal or terminal stage signifying hepatic dysfunction. 4)Slight rise in bilirubin , SGOT,SGPT and alk.phosphatase.
  31. 31. 5)Increase in urinary urea or urinary nitrogen over 24 hrs and a negative nitrogen balance. 6)Low arterial pH due to presence of metabolic acidosis 7)Recently cytokines (esp. IL-6 and IL-8), C-reactive proteins and Procalcitonin (PCT) levels have been noted to rise significantly following sepsis.PCT is reported to be superior to other markers in the diagnosis of a bacterial focus complicated by symptoms of severe sepsis and septic shock ( more than 2SD above normal values).
  32. 32. Principles of Therapy 1)To find out and eradicate the infection or sepsis responsible for the state of septic shock. 2)To reverse shock using volume infusion and inotropic support. 3)Ventilator support to all critically ill patients 4)To use recombinant human activated protein C in selected patients with severe sepsis. 5)Provide support to other organ systems 6)Provide nutritional support 7)Provide metabolic support 8)Prophylaxis for DVT and stress ulcers.
  33. 33. • Both eradication of infection and shock reversal are set into motion together . In severe shock , resuscitation takes place of prime , yet resuscitation would come to a standstill if prompt use and continuation of antibiotics are delayed , or if a pocket of pus remains undetected and not drained. • Septic shock needs to be urgently treated and reversed . Though the patient should be urgently shifted to ICU , treatment should commence wherever the patient is at the time of diagnosis(in the ambulance , emergency dep't. or ward)
  34. 34. SEPSIS RESUSCITATION BUNDLE TO BE COMPLETED WITHIN 3 HOURS:  1) Measure lactate level  2) Obtain blood cultures prior to administration of antibiotics  3) Administer broad spectrum antibiotics  4) Administer 30 mL/kg crystalloid for hypotension or lactate 4mmol/L
  35. 35.  TO BE COMPLETED WITHIN 6 HOURS:  5) Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation)  to maintain a mean arterial pressure (MAP) 65 mm Hg  6) In the event of persistent arterial hypotension despite volume resuscitation (septic shock) or initial lactate 4 mmol/L (36 mg/dL):  - Measure central venous pressure (CVP)  - Measure central venous oxygen saturation (ScvO2)  7) Re measure lactate if initial lactate was elevated
  36. 36. 1)Management of severe sepsis(EGDT) A) Initial Resuscitation(first 6 hours)  Begin resuscitation immediately in pts with hypotension and elevated lactate(>4 mmol/l).Do not delay pending ICU admission.  Resuscitation goals CVP 8-12 mm of Hg MAP≥65 mm of Hg Urine output ≥ 0.5 ml/kg/hr Central venous(superior vena cava)oxygen saturation ≥ 70% or mixed venous saturation ≥ 65%
  37. 37. If venous oxygen saturation target is not achieved:- Consider further fluid Transfuse packed red blood cells if required to a haematocrit of ≥ 30% Start dobutamine infusion , maximum 20 mcg/kg/min B)Diagnosis  Obtain appropriate cultures before starting antibiotics provided it does not significantly delay antibiotic administration.  Obtain two or more blood cultures 1) One or more blood cultures may be percutaneous 2) One blood culture from each vascular access device  in place > 48 hrs.  Culture other sites as clinically indicated like urine CSF , wounds, respiratory secretions etc.  Perform imaging studies if safe to do so
  38. 38.  Use of 1,3 beta D glucan assay , mannan and anti- mannan antibodies for diagnosis of invasive candidiasis and fungal infections.(If Available) C)Antibiotic Therapy  Begin i.v. antibiotic therapy as early as possible and always within the first hour of recognizing severe sepsis and septic shock.  Broad spectrum: one or more agents active against likely bacterial/fungal pathogens and with good penetration in the presumed source. Reassess antimicrobial regimen daily to optimize efficacy , prevent resistance , avoid toxicity and minimize costs. • Consider combination therapy in Pseudomonas infection.
  39. 39. • Consider combination empiric therapy in neutropenic patients • Combination therapy ≤ 3-5 days and de-escalation following susceptibilities. Duration of therapy typically limited to 7-10 days, longer if response is slow or there are an un-drainable foci of infection or immunologic deficiencies.
  40. 40. D)Source identification and control A specific anatomic site of infection must be must be established within first 6 hrs of presentation. Formally evaluate a patient for a focus of infection amenable to source control measures(eg. abscess drainage , tissue debridement) Implement source control measure soon after resuscitation.(except infected pancreatic necrosis). Choose source control measure with maximum efficacy and minimum physiological upset Remove i.v. access devices if potentially infected. Infection prevention by oral decontamination using chlorhexidine gluconate solution.
  41. 41. E)Fluid Therapy Fluid resuscitation using crystalloid, the fluid of choice. Target a CVP of 8mm of Hg( ≥12 mm of Hg if mechanically ventilated) Give fluid challenges of 1000 ml of crystalloids or 30 ml/ kg. More rapid and larger volumes needed in sepsis induced tissue hypo perfusion Rate of fluid administration should be reduced if cardiac filling pressures increase without concurrent hemodynamic improvement. Against the use of heta starch for resuscitation. Albumin can be used if patient require substantial amount of crystalloids.
  42. 42. F)Vasopressors: Maintain MAP ≥ 65 mm of Hg Nor epinephrine and dopamine administered centrally are the initial vasopressors of choice. Vasopressin (0.03 units/min) may be subsequently administered with the anticipation of an effect equivalent to nor epinephrine alone. Use epinephrine as the first alternative agent when blood pressure is poorly responsive to nor epinephrine or dopamine Do not use low dose dopamine for renal protection Insert an arterial line as soon as practical
  43. 43. G)Inotropic therapy: Use dobutamine in patients with myocardial dysfunction as supported by elevated cardiac filling pressures and low cardiac output. Do not increase cardiac index to predetermined supernormal levels H)Steroids:  i.v. hydrocortisone to be considered in hypotension not responding to fluids and vasopressors. ACTH stimulation is not recommended for identifying which patients should receive hydrocortisone. Hydrocortisone is preferred to dexamethasone Fludrocortisone (50μg orally OD)may be used if an alternative to hydrocortisone is used lacking mineralocorticoid activity. Hydrocortisone dose should be ≤ 300 mg/day Should not be used in absence of shock unless the endocrine or corticosteroid history warrants it
  44. 44. I)Recombinant human activated protein C Once Considered the use of rh -APC in adult patients with sepsis induced organ dysfunction with high risk of death(APACHE II ≥25 or MODS) if there are no contraindications. Adult patients with severe sepsis and low risk of death(APACHE II ≤ 20 or one organ failure) should not receive rhAPC PROWESS SHOCK Trail in 2011 shows no benefit of rhAPC in patients with septic shock, following which it was withdrawn from the market.
  45. 45. Supportive Therapy Of Severe Sepsis
  46. 46. J)Blood Product Administration: RBC’s to be administered when Hb<7 gm/dl to target Hb at 7-9gm/dl . A higher level may be required in conditions like MI , severe hypoxemia , hemorrhage, cyanotic heart diseases or lactic acidosis. Do not use erythropoietin Do not use FFP to correct clotting defects unless there is bleeding or planned invasive procedures Do not use antithrombin therapy Administer platelets when: • Counts < 10000/mm3 • Counts <20000 and there is significant bleeding risk • Higher platelet counts(>50000) are required for surgery or invasive procedures
  47. 47. K) Mechanical ventilation of sepsis induced ALI/ARDS Target a tidal volume of 6ml/kg body weight Target an initial upper limit plateau pressure ≤ 30 cm H2O.Chest wall compliance to be considered. Allow PACO2 to rise above normal , if needed to minimize plateau pressures and tidal volume. Set PEEP to avoid excessive lung collapse. Consider prone position for patients requiring potentially injurious levels of FIO2 Maintain mechanically ventilated patients in semi- recumbent position between 30o-45o Noninvasive ventilation may be considered in minority of patients with ALI/ARDS. Recruitment maneuvers, beta agonists only if required.
  48. 48. Use a weaning protocol and an SBT to evaluate the potential for discontinuing mechanical ventilation. SBT options include a low level of pressure support with continuous CPAP of 5 cm of H2O or a T-piece. Before SBT patients should be:- •Be arousable •Be haemodynamically stable without vasopressors •Have no new potentially serious conditions •Have low ventilatory and end expiratory requirements •Require FIO2 levels that can be safely delivered through face mask or nasal cannula. Use a conservative fluid management strategy for patients who do not have evidence of tissue hypoperfusion
  49. 49. Sedation , analgesia and neuromuscular blockade in sepsis. Use either intermittent bolus sedation or continuous infusion sedation to predetermined end points(sedation scales) with daily interruptions/ lightening to produce awakening . Re-titrate if necessary. Avoid neuromuscular blockade whenever possible. Monitor depth of blockade whenever with TOF when using continuous infusions.
  50. 50. Glucose Control Use intravenous insulin to control hyperglycemia in patients with severe sepsis following stabilization in ICU. Aim to keep blood glucose levels < 180 mg/dl using a validated protocol for insulin dose adjustment. Provide a glucose calorie source and monitor blood glucose values every 1-2 hours(4 hours when stable) in patients receiving i.v. insulin.
  51. 51. Renal replacement Intermittent hemodialysis and CRRT are considered equivalent. CRRT offers easier management in haemodynamically unstable patients. Bicarbonate Therapy Do not use bicarbonate therapy to improve haemodynamics or reduce vasopressor requirements when treating hypoperfusion induced lactic acidemia with pH ≥ 7.15
  52. 52. Deep vein thrombosis prophylaxis  Use either low dose UFH or LMWH , unless contraindicated. Use either a mechanical prophylactic device , such as compression stockings or an intermittent compression device , when heparin is contraindicated. Use a combination of pharmacologic and mechanical therapy for patients at very high risk for developing DVT. In patients at very high risk , use LMWH rather than UFH. Stress ulcer prophylaxis Provide stress ulcer prophylaxis using H2 blocker or proton pump inhibitor . Benefits of prevention of upper gastrointestinal bleeding must be weighed against the potential for development of ventilator-acquired pneumonia.
  53. 53. NUTRITION: •Administer oral/ enteral feed ,amount as tolerated. •Avoid mandatory full caloric feeds, suggesting low caloric feeds, advancing only as tolerated. •Combine i.v glucose/ enteral nutrition/ par-enteral nutrition as required during 1st week of diagnosis. •No immunomodulating supplementation required. Consideration for limitation of support Discuss advance care planning with patients and families . Describe likely outcomes and set realistic expectations.
  54. 54. 1)Central venous pressure monitoring is done through a central venous line. 2)Arterial pressure to be monitored through a catheter inserted preferably in the radial artery-so that beat to beat pressures are displayed. 3)Septic shock is a prime indicator for use of a Swan- Ganz catheter . The parameters which can be recorded are:- -PvO2 -CI -Svo2 -PAP -CO -PVR -PCWP
  55. 55. •Arrhythmias can occur in septic hypotensive patients who are on inotropic support and who have indwelling intracardiac catheters . Electrolyte disturbances contribute to or often causes dangerous ventricular arrhythmias . So constant monitoring of the cardiac rhythm with ECG is mandatory to recognize and correct these abnormalities.
  56. 56.  THOUGH THESE GUIDELINES ARE HELPFUL, RECOMMENDATIONS FROM THESE GUIDELINES CANNOT REPLACE THE CLINICIAN DECISION MAKING CAPACITY , WHEN HE OR SHE IS PRESENTED WITH PATIENTS UNIQUE SET OF CLINICAL VARIABLES.
  57. 57. Thank You
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