Management of septic shock according to surviving sepsis guidelines

1. Septic Shock
Dr. Shaurya Pratap Singh
SR General Surgery

2. Introduction
 Definitions
 Pathophysiology
 Manifestations
 Markers of Sepsis
 Guidelines for Management

3. Definitions
 SIRS : Based on the following criteria...
1. Temperature : >38°C or <35°C
2. Tachycardia : heart rate >90/min
3. Tachypnea : respiratory rate >20 or PaCO2 <30 on mechanical ventilation
4. TLC
Leukocytosis : WBC >12000/micL or
Leukopenia : WBC<4000/micL or
Bands >10%

4. Definitions
 Sepsis : SIRS and evidence or strong suspicion of infection.
 Or : Life-threatening organ dysfunction caused by dysregulated host response
to infection.

5. Definitions
 Septic Shock : known or suspected infection with 2 or more signs of SIRS,
organ dysfunction, and hypo-tension which is defined as: systolic B/P less
than 90mmHg or MAP less than 65 or 40mmHg decrease in B/P from base line
after a 30mL/Kg fluid bolus
 OR
 Known or suspected infection with 2 or more signs of SIRS, organ dysfunction,
and hypoperfusion evidenced by a lactic acid level greater than or equal to 4.
 OR
 Subset of sepsis with circulatory and cellular/metabolic dysfunction
associated with higher risk of mortality

6. Definitions
 Compensatory Anti-inflammatory Response syndrome :
1. Cutaneous anergy
2. Reduction of lymphocytes by means of apoptosis
3. Decreased cytokine response of monocytes to stimulation
4. Decreased numbers of human leukocyte antigen (HLA) antigen-presenting receptors on
monocytes
5. Expression of cytokines such as IL-10 that suppress TNF expression

7. Definitions
 qSOFA : The qSOFA score (also known as quickSOFA) is a bedside prompt that
may identify patients with suspected infection who are at greater risk for a poor
outcome outside the intensive care unit (ICU).
1. It uses three criteria, assigning one point each for :
2. Low blood pressure (SBP≤100 mmHg),
3. High respiratory rate (≥22 breaths per min), or
4. Altered mentation (Glasgow coma scale<15).
 The score ranges from 0 to 3 points. The presence of 2 or more qSOFA points
near the onset of infection was associated with a greater risk of death or
prolonged intensive care unit stay.

8. Definitions
 Empiric therapy :
Initial therapy started in the absence of definitive microbiologic pathogen
identification. Empiric therapy may be mono-, combination, or broad-spectrum,
and/or multidrug in nature.

9. Definitions
 Targeted/definitive therapy :
Therapy targeted to a specific pathogen (usually after microbiologic
identification). Targeted/ definitive therapy may be mono- or combination, but is
not intended to be broad-spectrum.

10. Definitions
 Broad-spectrum therapy :
The use of one or more antimicrobial agents with the specific intent of
broadening the range of potential pathogens covered, usually during empiric
therapy (e.g., piperacillin/tazobactam, vancomycin, and anidulafungin; each is
used to cover a different group of pathogens). Broadspectrum therapy is typically
empiric since the usual purpose is to ensure antimicrobial coverage with at least
one drug when there is uncertainty about the possible pathogen. On occasion,
broadspectrum therapy may be continued into the targeted/definitive therapy
phase if multiple pathogens are isolated.

11. Definitions
 Multidrug therapy :
Therapy with multiple antimicrobials to deliver broad-spectrum therapy (i.e., to
broaden coverage) for empiric therapy (i.e., where pathogen is unknown) or to
potentially accelerate pathogen clearance (combination therapy) with respect to
a specific pathogen(s) where the pathogen(s) is known or suspected (i.e., for
both targeted or empiric therapy). This term therefore includes combination
therapy.

12. Definitions
 Combination therapy :
The use of multiple antibiotics (usually of different mechanistic classes) with the
specific intent of covering the known or suspected pathogen(s) with more than
one antibiotic (e.g., piperacillin/ tazobactam and an aminoglycoside or
fluoroquinolone for gram-negative pathogens) to accelerate pathogen clearance
rather than to broaden antimicrobial coverage. Other proposed applications of
combination therapy include inhibition of bacterial toxin production (e.g.,
clindamycin with β-lactams for streptococcal toxic shock) or potential immune
modulatory effects (macrolides with a β-lactam for pneumococcal pneumonia).

13. Pathophysiology
 Sepsis is a heterogeneous syndrome with clinical manifestations varying
between patients, underlying etiology and over time. Each response is
determined by many factors, including the virulence of the organism; the size
of the inoculum; and the patient’s coexisting conditions, age, and genetics.
Thus, it is not surprising that the pathogenesis has been difficult to elucidate
and may be protean.

14. Pathophysiology
 Bacterial factors :
All classes of microorganisms, including gram-positive and gram-negative
bacteria, fungi, viruses, and parasites have structural components that interact
with the host immune response. For example, gram-negative bacteria have
endotoxin (lipopolysaccharide, [LPS]), a potent mediator of many of the clinical
manifestations of gram~negative sepsis. Gram-positive bacteria tend to liberate
exotoxins, such as toxic shock syndrome toxin. The importance of these
substances in clinical practice is that they may not be directly neutralized by
antibiotics, thus magnifying the early damage of certain infections.

15. Pathophysiology
 Host response :
1. The host’s response to infection is critical to recovery. The initiation of the
innate immune response occurs with the recognition of typical structural
components of microbes by host cells (e.g., LPS). Toll-like receptors (TLR) are
host’s molecules that can recognize specific bacterial structures and trigger a
protean initial inflammatory cascade, and can be targeted for therapeutic
purposes.
2. The proinflammatory response (adaptive immunity) is mediated by cytokines
such as tumor necrosis factor-a (TNF-a), interleukin-6 (IL6), and IL1-beta. At
various times after the initial proinflammatory state, counterregulatory
cytokines and proinflammatory antagonists are secreted resulting in an anti-
inflammatory state. A state of immuno paralysis can result whereby the host
has inadequate immune responses to microorganisms resulting in subsequent
morbidity and mortality following infection.

16. Pathophysiology
 Cellular iniury :
Failure to generate ATP during sepsis and critical illness may in part be due to
impaired delivery of oxygen to vital tissues secondary to impaired oxygenation
and perfusion. In addition, cytopathic hypoxia, resulting from mitochondrial
dysfunction, may underlie the apparent disconnection between the cellular
oxygen tension, which is usually adequate and the low ATP.

17. Pathophysiology
 Genetics :
Twin studies have suggested a genetic polymorphism in the cytokine response to
sepsis, which may result in differences in mortality.

18. Pathophysiology
 Coagulation cascade :
Inflammation is a procoagulant state. Inflammation and coagulation are both
activated during severe infection, and share common mediators. One of them,
activated protein C, has been successfully targeted for therapy .

19. Pathophysiology
 Epithelial and endothelial dysfunction :
Epithelial cell dysfunction resulting from the deleterious effects of the systemic
inflammatory response can result in impaired barrier function, increased
permeability, and may be a final step in the pathway to sepsis-related MODS.
Endothelial cells play a critical role in systemic inflammation and in maintaining
a balance between coagulation and anticoagulation. Such an imbalance may
result in the development of microvascular thrombosis leading to abnormal
microcirculation and impaired oxygen delivery to tissues. In addition, endotheiial
cells play an active role in recruiting inflammatory cells to sites of infection and
inflammation.

20. Manifestations
 Manifestations :
The early signs of sepsis include tachycardia, hyperventilation, fever, and
disorientation. Later signs can involve any or all organ systems. The mortality
when multiple organs fail is extremely high.

21. Manifestations
 Cardiovascular :
Tachycardia and hypotension are commonly present and may initially be due to
vosodilatation and intravascular hypovolemia.
Sepsis induced myocardial depression can occur early or late in the course,
contributing to the hypotension.

22. Manifestations
 Respiratory :
Hyperventilation is common early in sepsis. Poor oxygenation can be secondary to
leaky alveolar capillaries. Acute lung injury and acute respiratory distress
syndrome are common complications of severe sepsis.

23. Manifestations
 Renal :
Oliguric renal insufficiency can be prerenal due to hypotension, impaired
perfusion, or hypovolemia. Direct damage to the kidneys can lead to acute
tubular necrosis. Oliguria may progress to acute renal failure requiring renal
replacement therapy.

24. Manifestations
 Central nervous system :
Sepsis-induced encephalopathy can range from mild confusion, delirium, and
coma.

25. Manifestations
 Hepatic :
Cholestasis is common. Inflammatory mediators resulting in dysfunction of bile
canaliculi can lead to hyperbilirubinemia. Transaminitis may be mild or severe
secondary to ischemia.

26. Manifestations
 Metabolic :
Catecholamines inhibit insulin release and increase gluconew genesis. Patients
may be hyperor hypoglycemic.

27. Manifestations
 Hematologic :
Consumptive coagulopathy, platelet sequestration, and platelet destruction are
common.

28. Markers of Sepsis
 The diagnosis of sepsis is made with a suspicion of infection and clinical signs
of systemic inflammation. These signs are neither sensitive nor specific for
sepsis, thus there has been a search for biochemical markers of sepsis, which
would lead to earlier more definitive diagnosis. Multiple cytokines, peptides,
receptors, and acute-phase reactants are being studied as possible ideal
markers. Some examples of well studied, clinically available assays include :

29. Markers of Sepsis
 C-reactive protein is an acute-phase protein that is released from hepatic
cells in response to inflammation.
 It is an inexpensive test that suggests the presence of inflammation.
 Its disadvantages include that is nonspecific, has a slow time to peak, and has
no correlation with the severity of inflammation.

30. Markers of Sepsis
 Cytokines such as Il6 and Il8 are primary host response in inflammation.
 They are highly sensitive markers of systemic inflammation, however the
levels are highly variable, level is not correlated with degree of inflammation,
and they have a short half-time in plasma.
 Levels of IL-6 and IL-8 may be useful to distinguish infectious versus
noninfectious causes of neutropenic fever and also in onset of early sepsis in
neonates.

31. Markers of Sepsis
 Procalcitonin (PCT) is a propeptide of calcitonin with a longer half-life.
 Elevated PCT levels are highly specific for severe sepsis and onset of organ
dysfunction.
 It is elevated in inflammatory states that are noninfectious; however, the
plasma levels are not as high as in severe sepsis. Patients with levels more
than 2 ng/mL are at high risk for having severe sepsis. PCT may have utility in
differentiating between an infectious or noninfectious etiology of SIRS. It can
also be helpful in monitoring the efficacy of treatment.

32. Treatment Protocols
 INITIAL RESUSCITATION :
1. Sepsis and septic shock are medical emergencies, and treatment and
resuscitation should begin immediately.
2. In the resuscitation from sepsis-induced hypoperfusion, at least 30 mL/kg of
IV crystalloid fluid be given within the first 3 hours.
3. Following initial fluid resuscitation, additional fluids be guided by frequent
reassessment of hemodynamic status.
4. Reassessment should include a thorough clinical examination and evaluation
of available physiologic variables (heart rate, blood pressure, arterial oxygen
saturation, respiratory rate, temperature, urine output, and others, as
available) as well as other noninvasive or invasive monitoring, as available.

33. Treatment Protocols
 INITIAL RESUSCITATION
1. Further hemodynamic assessment is needed (such as assessing cardiac
function) to determine the type of shock if the clinical examination does not
lead to a clear diagnosis.
2. Dynamic over static variables be used to predict fluid responsiveness, where
available.
3. Aim for an initial target mean arterial pressure of 65 mm Hg in patients with
septic shock requiring vasopressors.
4. Guide resuscitation to normalize lactate in patients with elevated lactate
levels as a marker of tissue hypoperfusion.

34. Treatment Protocols
 SCREENING FOR SEPSIS AND PERFORMANCE IMPROVEMENT
1. Hospitals and hospital systems should have a performance improvement
program for sepsis, including sepsis screening for acutely ill, high risk
patients.

35. Treatment Protocols
 DIAGNOSIS
1. Appropriate routine microbiologic cultures (including blood) should be obtained before
starting antimicrobial therapy in patients with suspected sepsis or septic shock if doing so
results in no substantial delay in the start of antimicrobials.
2. Appropriate routine microbiologic cultures always include at least two sets of blood cultures
(aerobic and anaerobic).
 2012 recommendations were
Cultures as clinically appropriate before antimicrobial therapy if no significant delay (> 45 min) in
the start of antimicrobials (grade 1C). At least 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 (grade 1C).
Use of the 1,3-ß-D-glucan assay (grade 2B), mannan and anti-mannan antibody assays (2C), if
available, and invasive candidiasis in differential diagnosis of cause of infection.3. Imaging
studies performed promptly to confirm a potential source of infection (UG).

36. Treatment Protocols
 ANTIMICROBIAL THERAPY
1. Administration of IV antimicrobials should be initiated as soon as possible
after recognition and within one hour for both sepsis and septic shock (strong
recommendation, moderate quality of evidence).2.
2. Start empiric broad-spectrum therapy with one or more antimicrobials for
patients presenting with sepsis or septic shock to cover all likely pathogens
(including bacterial and potentially fungal or viral coverage).
3. Empiric antimicrobial therapy should be narrowed once pathogen
identification and sensitivities are established and/or adequate clinical
improvement.
4. Don’t use sustained systemic antimicrobial prophylaxis in patients with severe
inflammatory states of noninfectious origin (e.g., severe pancreatitis, burn
injury).

37. Treatment Protocols
 The dosing strategies of antimicrobials should be optimized based on
accepted pharmacokinetic/pharmacodynamic principles and specific drug
properties in patients with sepsis or septic shock.
 Start empiric combination therapy (using at least two antibiotics of different
antimicrobial classes) aimed at the most likely bacterial pathogen(s) for the
initial management of septic shock.
 Combination therapy should not be routinely used for ongoing treatment of
most other serious infections, including bacteremia and sepsis without shock .
This does not preclude the use of multidrug therapy to broaden antimicrobial
activity.
 Don’t use combination therapy for the routine treatment of neutropenic
sepsis/bacteremia. This does not preclude the use of multidrug therapy to
broaden antimicrobial activity.

38. Treatment Protocols
 If combination therapy is used for septic shock,try de-escalation with
discontinuation of combination therapy within the first few days in response
to clinical improvement and/or evidence of infection resolution. This applies
to both targeted (for culture-positive infections) and empiric (for culture-
negative infections) combination therapy.
 An antimicrobial treatment duration of 7 to 10 days is adequate for most
serious infections associated with sepsis and septic shock.
 Longer courses are appropriate in patients who have a slow clinical response,
undrainable foci of infection, bacteremia with Staphylococcus aureus, some
fungal and viral infections, or immunologic deficiencies, including
neutropenia.

39. Treatment Protocols
 Shorter courses are appropriate in some patients, particularly those with
rapid clinical resolution following effective source control of intra-abdominal
or urinary sepsis and those with anatomically uncomplicated pyelonephritis.
 Do daily assessment for de-escalation of antimicrobial therapy in patients
with sepsis and septic shock.
 Measurement of procalcitonin levels can be used to support shortening the
duration of antimicrobial therapy in sepsis patients.
 Procalcitonin levels can be used to support the discontinuation of empiric
antibiotics in patients who initially appeared to have sepsis, but subsequently
have limited clinical evidence of infection.

40. Treatment Protocols
 SOURCE CONTROL
 A specific anatomic diagnosis of infection requiring emergent source control
should be identified or excluded as rapidly as possible in patients with sepsis
or septic shock, and that any required source control intervention should be
implemented as soon as medically and logistically practical after the diagnosis
is made
 There should be prompt removal of intravascular access devices that are a
possible source of sepsis or septic shock after other vascular access has been
established.

41. Treatment Protocols
 FLUID THERAPY
 A fluid challenge technique be applied where fluid administration is continued
as long as hemodynamic factors continue to improve.
 Crystalloids should be the fluid of choice for initial resuscitation and
subsequent intravascular volume replacement in patients with sepsis and
septic shock (strong recommendation, moderate quality of evidence).
 Use balanced crystalloids or saline for fluid resuscitation of patients with
sepsis or septic shock.

42. Treatment Protocols
 Use albumin in addition to crystalloids for initial resuscitation and
subsequent intravascular volume replacement in patients with sepsis and
septic shock, when patients require substantial amounts of crystalloids.
 Don’t use hydroxyethyl starches for intravascular volume replacement in
patients with sepsis or septic shock.
 Use crystalloids over gelatins when resuscitating patients with sepsis or septic
shock.

43. Treatment Protocols
 VASOACTIVE MEDICATIONS
 USE norepinephrine as the first-choice vasopressor
 Use either vasopressin (up to 0.03 U/min) or epinephrine to norepinephrine
with the intent of raising mean arterial pressure to target, or adding
vasopressin (up to 0.03 U/min) to decrease norepinephrine dosage.
 Use dopamine as an alternative vasopressor agent to norepinephrine only in
highly selected patients (e.g., patients with low risk of tachyarrhythmias and
absolute or relative bradycardia).
 Don’t use low-dose dopamine for renal protection
 Use dobutamine in patients who show evidence of persistent hypoperfusion
despite adequate fluid loading and the use of vasopressor agents.

44. Treatment Protocols
 If initiated, dosing should be titrated to an end point reflecting perfusion, and
the agent reduced or discontinued in the face of worsening hypotension or
arrhythmias.
 All patients requiring vasopressors have an arterial catheter placed as soon as
practical if resources are available.

45. Treatment Protocols
 CORTICOSTEROIDS
 Recommendation is against using IV hydrocortisone to treat septic shock
patients if adequate fluid resuscitation and vasopressor therapy are able to
restore hemodynamic stability. If this is not achievable, then IV
hydrocortisone at a dose of 200 mg per day may be initiated.

46. Treatment Protocols
 BLOOD PRODUCTS
 RBC transfusion should curur only when hemoglobin concentration decreases
to < 7.0 g/dL in adults in the absence of extenuating circumstances, such as
myocardial ischemia, severe hypoxemia, or acute hemorrhage.
 Don’t use erythropoietin for treatment of anemia associated with sepsis
 Don’t use fresh frozen plasma to correct clotting abnormalities in the absence
of bleeding or planned invasive procedures.
 Use prophylactic platelet transfusion when counts are < 10,000/mm3 (10 ×
109/L) in the absence of apparent bleeding and when counts are <
20,000/mm3 (20 × 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.

47. Treatment Protocols
 IMMUNOGLOBULIN
 Recommendations are against the use of IV immunoglobulins in patients with
sepsis or septic shock.

48. Treatment Protocols
 BLOOD PURIFICATION
 There are no recommendation regarding the use of blood purification
techniques.

49. Treatment Protocols
 ANTICOAGULANTS
 Don’t use antithrombin for the treatment of sepsis and septic shock.
 No recommendation regarding the use of thrombomodulin or heparin for the
treatment of sepsis or septic shock.

50. Treatment Protocols
 MECHANICAL VENTILATION
 Use a target tidal volume of 6 mL/kg predicted body weight compared with
12 mL/kg in adult patients with sepsis-induced acute respiratory distress
syndrome (ARDS).
 Using an upper limit goal for plateau pressures of 30 cm H2O over higher
plateau pressures in adult patients with sepsis-induced severe ARDS.
 We suggest using higher positive end-expiratory pressure (PEEP) over lower
PEEP in adult patients with sepsis-induced moderate to severe ARDS.
 Use recruitment maneuvers in adult patients with sepsis-induced, severe
ARDS.

51. Treatment Protocols
 Use prone over supine position in adult patients with sepsis-induced ARDS and
a Pao2/Fio2 ratio < 150.
 Don’t use high-frequency oscillatory ventilation in adult patients with sepsis-
induced ARDS.
 There is no recommendation regarding the use of noninvasive ventilation for
patients with sepsis-induced ARDS.
 Use neuromuscular blocking agents for ≤ 48 hours in adult patients with
sepsis-induced ARDS and a Pao2/Fio2 ratio < 150 mm Hg.
 Try a conservative fluid strategy for patients with established sepsis-induced
ARDS who do not have evidence of tissue hypoperfusion.

52. Treatment Protocols
 SEDATION AND ANALGESIA
 Continuous or intermittent sedation should be minimized in mechanically
ventilated sepsis patients, targeting specific titration end points.

53. Treatment Protocols
 GLUCOSE CONTROL
 A protocolized approach to blood glucose management in ICU patients with sepsis,
commencing insulin dosing when two consecutive blood glucose levels are > 180
mg/dL. This approach should target an upper blood glucose level ≤ 180 mg/dL
rather than an upper target blood glucose level ≤ 110 mg/dL.
 The blood glucose values should be monitored every 1 to 2 hours until glucose
values and insulin infusion rates are stable, then every 4 hours thereafter in
patients receiving insulin infusions.
 Glucose levels obtained with point-of-care testing of capillary blood be
interpreted with caution because such measurements may not accurately estimate
arterial blood or plasma glucose values.
 Use arterial blood rather than capillary blood for point-of-care testing using
glucose meters if patients have arterial catheters.

54. Treatment Protocols
 RENAL REPLACEMENT THERAPY
 Use either continuous or intermittent renal replacement therapy (RRT) in
acute kidney injury (weak recommendation, moderate quality of evidence).
 Use continuous therapies to facilitate management of fluid balance in
hemodynamically unstable septic patients.
 Don’t use RRT in patient with sepsis and acute kidney injury for increase in
creatinine or oliguria without other definitive indications for dialysis.

55. Treatment Protocols
 BICARBONATE THERAPY
 Don’t use of sodium bicarbonate therapy to improve hemodynamics or to
reduce vasopressor requirements in patients with hypoperfusion-induced
lactic acidemia with pH ≥ 7.15.

56. Treatment Protocols
 VENOUS THROMBOEMBOLISM PROPHYLAXIS
 Use pharmacologic prophylaxis (unfractionated heparin [UFH] or low-
molecular-weight heparin [LMWH]) against venous thromboembolism (VTE) in
the absence of contraindications to the use of these agents.
 Use LMWH rather than UFH for VTE prophylaxis in the absence of
contraindications to the use of LMWH.
 We may use combination pharmacologic VTE prophylaxis and mechanical
prophylaxis, whenever possible (weak recommendation, low quality of
evidence).
 Use mechanical VTE prophylaxis when pharmacologic VTE is contraindicated.

57. Treatment Protocols
 STRESS ULCER PROPHYLAXIS
 Sress ulcer prophylaxis should be given to patients with sepsis or septic shock
who have risk factors for gastrointestinal (GI) bleeding.
 Use either proton pump inhibitors or histamine-2 receptor antagonists when
stress ulcer prophylaxis is indicated.
 Don’t use stress ulcer prophylaxis in patients without risk factors for GI
bleeding.

58. Treatment Protocols
 NUTRITION
 Recommendations are against the administration of early parenteral nutrition
alone or parenteral nutrition in combination with enteral feedings (but rather
initiate early enteral nutrition) in critically ill patients with sepsis or septic
shock who can be fed enterally.
 We recommend against the administration of parenteral nutrition alone or in
combination with enteral feeds (but rather to initiate IV glucose and advance
enteral feeds as tolerated) over the first 7 days in critically ill patients with
sepsis or septic shock for whom early enteral feeding is not feasible.

59. Treatment Protocols
 Early initiation of enteral feeding rather than a complete fast or only IV
glucose in critically ill patients with sepsis or septic shock who can be fed
enterally.
 Either early trophic/hypocaloric or early full enteral feeding in critically ill
patients with sepsis or septic shock; if trophic/hypocaloric feeding is the
initial strategy, then feeds should be advanced according to patient
tolerance.
 Recommendations are against the use of omega-3 fatty acids as an immune
supplement in critically ill patients with sepsis or septic shock.

60. Treatment Protocols
 Don’t routinely monitor gastric residual volumes in critically ill patients with
sepsis or septic shock.
 However, we suggest measurement of gastric residuals in patients with
feeding intolerance or who are considered to be at high risk of aspiration.
 This recommendation refers to nonsurgical critically ill patients with sepsis or
septic shock.
 We suggest the use of prokinetic agents in critically ill patients with sepsis or
septic shock and feeding intolerance.

61. Treatment Protocols
 We suggest placement of post-pyloric feeding tubes in critically ill patients
with sepsis or septic shock with feeding intolerance or who are considered to
be at high risk of aspiration.
 We recommend against the use of IV selenium to treat sepsis and septic
shock.
 Don’t use arginine to treat sepsis and septic shock.
 Don’t use glutamine to treat sepsis and septic shock.
 No recommendations present about the use of carnitine for sepsis and septic
shock.

62. Treatment Protocols
 SETTING GOALS OF CARE
 Goals of care and prognosis should be discussed with patients and families.
 Goals of care be incorporated into treatment and end-of-life care planning,
utilizing palliative care principles where appropriate.
 Goals of care should be addressed as early as feasible, but no later than
within 72 hours of ICU admission.

63. Thank you…