Sepsis: an overview

1. Submitted to
Mrs.Nadiya Krishnan
Assistant professor
College of nursing
AIIMS Bhubaneswar
seminar
Submitted by
Revathy S
1st year MSc Nursing
College of nursing
AIIMS Bhubaneswar

3. Introduction
 Infection is the most common cause of mortality in critically ill
patients
 SIRS
 Sepsis
 Sepsis syndrome is the systemic host response to infection.
 The incidence of sepsis syndrome is on the rise.
 This condition claims life in very young, very old or
immunocompromised.
 Sep 13

4. Definition
 Sepsis is defined as one or most life-threatening organ
dysfunctions caused by a dysregulated host response to
infection
 Septic shock is a subset of sepsis

6. Non-septic triggers of dysregulated systemic
pro & anti inflammatory responses
 Trauma
 Pancreatitis
 Major burns
 Major surgical procedures
 Hemorrhage
 Ischemic tissue
 Period of inadequate perfusion

8. Risk factors
 Extremes of age
 People with chronic medical conditions – DM, Lung disease,
cancer
 People with weakened immune system
 Sepsis survivors
 Malnutrition
 Drug or alcohol abuse
 Neutropenia
 Splenectomy
 Multiple organ failure

10. Common sites
 The most common sites of infection for severe sepsis varied by
gender. The sites and frequency were:
 Respiratory: 42% men 36% women
 Bacteremia: (site unspecified) 21% men 34% women
 Abdominal: 9% men 10% women
 Genitourinary: 10% men, 9% women
 Wound/soft tissues: 9% men 8% women
 Other sources: 9% men 10% women
 Among older patients, the urinary tract was the most common
source of infection.

12. Clinical manifestation
 Increased heart rate
 Decreased blood pressure
 Wide pulse pressure
 Full, bounding pulse
 Pink, warm, flushed skin

13. Cont.
 Increased respiratory rate (early) or decreased RR (late)
 Crackles
 Change in sensorium
 Decreased urine output
 Increased temperature

14. Bacterial pathogens in sepsis
A final common pathway?
Gram-negative Gram-positive
Cell wall components
Extracellular products
Endotoxin and
other toxins
SEPSIS
INFLAMMATION
e.g. Staphylococcus aureus
Streptococcus pneumoniae
Enterococcus faecalis
e.g. Neisseria meningitidis
Escherichia coli
Host immune response Host immune response

15. Pathophysiology
 Micro organism enters the body
 Stimulate the inflammatory or immune system
 Host pathogen interaction
 Both invading organism and injured tissue release intracellular
protein
 Activates enzyme cascade
 Infection is contained and eradicated

16. When magnitude of the infectious insult
is great
 Patient is physiologically unable to generate a effective host
response.
 Containment fails.
 Systemic release of the pathogen, activated cells, and
mediators including cytokines, which initiates a chain of
complex interaction
 Uncontrolled SIRS

17. Infection
Immune system response
Release of mediators from WBCs and avascular endothelium
Increased
inflammation
Endothelial
damage
Decreased
fibrinolysis
Increased
inflammation
Altered tissue perfusion Microthrombi Capillary leak
Organ system
dysfunction
Edema
formation
Death

18. Cardiovascular alterations
 Septic shock is associated with 3 main pathophysiologic effect on the CVS:
vasodilation, mal-distribution of blood flow and myocardial depression
 Pro-inflammatory cytokines
 Stimulate the release of NO from endothelial cells
 NO is a potent vasodilator
 Potent vasodilation
 Decreased SVR
 Decreased venous return to the heart
 Decreased CO

19. Cont..
 Release of endothelin
 Causes vasoconstriction other vascular bed
 Combination of vasoconstriction and dilation
 Maldistribution of blood flow in all micro circulation

20. Pulmonary alterations
Affect the lung both directly and indirectly
 Activation of SNS and release of epinephrine from the
adrenal medulla causes bronchodilation
 However, inflammatory cytokines override the effect of
epinephrine and causes bronchoconstriction
 Inflammatory mediators and activated neutrophils cause
capillary leak into the pulmonary interstitium- interstitial
edema, area of poor pulmonary perfusion, pulmonary
hypertension, and increased respiratory work

21. CONT..
 As fluid collects in the interstitium, pulmonary compliance is
reduced, gas exchange is impaired, and hypoxemia occurs
 Interstitial fluid also damages the alveolar epithelial barrier,
allowing fluid to accumulate in the alveoli. This further impairs
ventilation and oxygenation

22. HEMOTOLOGICAL ALTERATIONS
 Endotoxin release
 platelet aggregation
 release of more vasoactive substances such as serotonin and
thromboxane A2
 Platelet aggregates in the microvasculature
 Over activation of the coagulation cascade without counter balance
of adequate fibrinolysis
 Overtime clotting factors are depleted
 coagulopathy
 progressing to DIC

23. Metabolic alterations
 Hyper metabolic state
 Increase in resting energy consumption, extensive protein and
fat metabolism, negative nitrogen balance, hyperglycemia and
hepatic gluconeogenesis.
 Excessive catecholamine’s release
 Gluconeogenesis and insulin resistance
 Hyperglycemia in critically ill patient who do not have diabetes

24. Lab findings
 Cultures: blood, sputum, urine, surgical or non-surgical
wounds. Sinuses and invasive catheter
 CBC: WBCs usually will be elevated
 Chemistry panel: hyperglycemia may be evident,
followed by hypoglycemia in later stages
 ABG: metabolic acidosis and compensatory respiratory
alkalosis
 CT scan: to identify site of potential abscesses

25. Cont.
 Chest and abdominal radiographs: reveals infectious processes
 SvO2 or ScvO2: can assist in the assessment of adequacy of
oxygen delivery and consumption
 Lactate level: decrease level indicate aerobic metabolism, elevated
level indicates anaerobic metabolism
 EtCO2: decreased EtCO2 is an early indicator of inadequate
regional and global tissue perfusion

26. For severe sepsis
 Lactate above upper limits laboratory normal
 Urine output <0.5 mL/kg/h for more than 2 h despite adequate fluid
resuscitation
 Acute lung injury with PaO2/FiO2 <250 in the absence of pneumonia as
infection source
 Acute lung injury with PaO2/FiO2 <200 in the presence of pneumonia as
infection source
 Creatinine [2.0 mg/dL
 Bilirubin [2 mg/dL
 Platelet count <100,000 /mic L
 Coagulopathy (international normalized ratio [1.5)

27. Management
 Medical management
 Treatment of a patient in sepsis or septic shock requires a multifaceted
approach
 The goal of treatment is to reverse the pathophysiologic responses,
control the infection, promote metabolic support
 Supporting the CVS
 Enhancing tissue perfusion
 Identifying and treating the infection
 Limiting the systemic inflammatory response
 Restoring metabolic balance
 Initiating nutrition therapy

28. Surviving sepsis campaign (SSC)
 Within the first 3 hour of presentation(3 hour bundle)
 Measure lactate level
 Obtain blood culture before administering antibiotics
 Administer broad spectrum antibiotics
 Administer 30ml/kg crystalloid for hypotension or
lactate≥4mmol/L
 Apply vasopressors if hypotensive during or after fluid
resuscitation to maintain MAP ≥ 65 mmHg

29. Cont.
 Within the first 6 hour of presentation (6 hour bundle)
 Apply vasopressor (for hypotension that does not respond to
initial fluid resuscitation) to maintain MAP ≥65mmHg
 In the event of persistent hypotension that does not respond to
initial fluid administration (MAP <65mmHg) or if initial
lactate was ≥4mmol/L, reassess volume status and tissue
perfusion, and document the findings
 Re-measure lactate if initial lactate elevated


30. Hour 1 bundle
 Measure lactate level
 Obtain blood cultures before administering antibiotics.
 Administer broad-spectrum antibiotics.
 Begin rapid administration of 30mL/kg crystalloid for
hypotension or lactate level ≥ 4 ​mmol/L.
 Apply vasopressors if hypotensive during or after fluid
resuscitation to maintain MAP ≥ 65 mm Hg.
 * Remeasure lactate if initial lactate is elevated (> 2 mmol/L).

31. SSC
 Initial resuscitation
 Screening for sepsis and performance improvement
 Diagnosis
 Antimicrobial therapy
 Source control
 Fluid therapy
 Vasoactive medications

32.  Corticosteroids
 Blood products
 Immunoglobulins
 Blood purification
 Anticoagulants
 Mechanical ventilation
 Sedation and analgesia

33.  Glucose control
 Renal replacement therapy
 Bicarbonate therapy
 Venous thromboembolism prophylaxis
 Stress ulcer prophylaxis
 Nutrition
 Setting goals of care

34. Initial resuscitation
 Target – 30ml/Kg within in first 3 hour, MAP 65mmHg
 Tissue perfusion ᷉ arterial pressure
 Reassessment
 TEMP
 RR
 HR
 BP
 ABG
 Urine output

35. Initial resuscitation
 Sepsis induced hypoperfusion
 Principle –
 Detailed initial assessment
 Ongoing re evaluation
 Assessment of variables
 Fluid responsiveness
 CVP
 PLR
 Pulse pressure variation
 S. Lactate ≥ 4mmol/L
 Lactate guided resuscitation

36. Screening for sepsis and performance
improvement
 Sepsis screening for every
 Acutely ill patients
 High risk patient
 Performance improvement program
 Early recognition
 Improved management
 Improved patient outcome

37. Diagnosis
 Microbiologic culture – at least 2 sets
 Possible sites
 Pan culture
 Culture in correlation with clinical presentation

38. Antimicrobial therapy
 Start in 1 hour of recognition
 Not recommended in SIRS of non infectious orgin
 Delay
 ↑LOS
 AKI
 ALI
 Other organ injury

39. Antimicrobial therapy
 Bolus infusion
 Lengthy infusion
 IM ?
 Imipenem / cilastatin
 Cefepime
 Ceftriaxone
 Ertapenem
 Once culture sent
 Once pathogen identified / clinical improvement

40. Antimicrobial therapy
 How to select broad spectrum??
 Pt history
 Clinical status
 Local epidemiological factors
 Site of infection
 Underlying disease
 Chronic organ failure
 Medication, Indwelling devices
 Immunosuppression
 Recent infection, previous receipt
 Pt location at the time of infection acquisition
• Carbepenem
• β lactamase inhibitor
• 3rd gen cephalosporins
• Multidrug therapy

41. Factors in determining the appropriate
antimicrobial
 Anatomic site of infection
 Prevalent pathogens within the community, hospital, and even
hospital ward
 The resistance patterns of those prevalent pathogens
 The presence of specific immune defects
 Age and patient comorbidities

42. Antifungals
 Candida invasion
 Echinocandin
 Anidulafungin
 Micafungin
 Caspofungin
 Triazoles in hemodynamically stable pt
 L Amp

43. Antimicrobial therapy
 In SIRS – No need of giving sustained antimicrobial
prophylaxis
 As per new studies
 No clinical advantage of prophylactic antibiotic that outweigh their
long term adverse effect
 But – strong suspicion
 Indicated
 Dose
• Aminoglycosides
• Fluoroqunolones
• Vancomycin
• β lactam

46. Antimicrobials
 Antimicrobial treatment duration of 7–10 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
S. aureus, some fungal and viral infections, or immunologic
deficiencies, including neutropenia
 Daily assessment for de-escalation of antimicrobial therapy in
patients with sepsis and septic shock

47. Uncomplicated infection
(1) exclusion of endocarditis
(2) no implanted prostheses
(3) negative results of follow-up blood cultures drawn 2–4 days
after the initial set
(4) defervescence within 72 h after the initiation of effective
antibiotic therapy
(5) no evidence of metastatic infection.
 Procalcitonin levels for de-escalation (diagnose, duration)
 Galacatomannan – to assess invasive aspergillus

48. Source control
 Specific anatomic diagnosis of infection
 Prompt removal of intravascular access devices
 Site of infection
 Control in 6 – 12 hours
 Drain
 Debridement
 Removal
 Least invasive SC should be implemented
 As per indication

49. Fluid therapy
 Crystalloid / colloid
 HES, Gelatin - X
 Cautious fluid therapy
 Avoid hyper chloremia

50. Vasoactive medication
 Vasopressor
 NE
 NE + E, Vasopressin (up to 0.03 U/min)
 Dopamine
 Dobutamine
 Phenylephrine
 Phosphodiesterace inhibitor
 Levosimenden

51. Corticosteroids
 Fluids, Vasopressors X
 IV Hydrocortisone 200 mg/ day
 Adr – hyperglycemia and hypernatremia

52. Blood products
 Hb < 7g/dl –RBC Transfusion
 Erythropoietin - thrombotic events
 FFP - in case of documented deficiency of coagulation factors
 Prophylactic platelet transfusion
 Ab of bleeding, <10000 / mm3
 Risk of bleeding< 20000 / mm3
 Active bleeding ≥50000 / mm3

53. Immunoglobulin
 Suggest against use of immunoglobulins

54. Blood purification
 Not recommended
 Method
 High volume hemofiltration
 Hemoadsorption (sorbents)
 Plasma exchange / plasma filtration
 Coupled plasma filtration adsorption

55. Anti thrombin
 Not recommended
 DIC
 Thrombomodulin
 Heparin

56. Mechanical ventilation
 Target Vt – 12ml / Kg
 With ADRS – 6ml / Kg
 Plateau pressure 30 mmHg in sepsis induced ARDS
 High PEEP
 Recruitment methods +/-
 Prone position
 Do not prefer NIV
 Neuromuscular blockers
 Cisatracurium

57. Mechanical ventilation
 Conservative fluid strategy
 Against β-2 agonist
 Headend elevation
 Spontaneous breathing trials
 Start weaning

58. Sedation and analgesics
 Minimize
 Daily sedation interruption
 Use opioids alone
 Use short acting sedatives

59. Glucose control
 Monitor
 Insulin
 Arterial > capillary
 Should avoid hyperglycemia, hypoglycemia, wide swing in
levels
 With cessation of nutrition
 With balanced nutrition
 Critically ill patients should not be tested with a glucometer

60. RRT
 IRRT
 CRRT
 Hemodynamically unstable patient
 Sepsis + AKI + ↑ creatinine, oliguria = no need of RRT

61. Bicarbonate therapy
 Suggest against use of:
 In pt’s with hypoperfusion induced lactate acidosis (pH ≥7.15)
 Improve hemodynamics
 Helps in limiting tidal volume in ARDS in permissive
hypercapnia

62. Venous thromboembolism prophylaxis
 UFH &LMWH
 LMWH > UHF
 Combination prophylaxis
 Cause – frequent use of vasopressor

63. Stress ulcer prophylaxis
 Recommended in pt with risk of GI bleed
 Disruption of protective mechanism against gastric acid
 Gastric mucosal hypo perfusion
 ↑acid production
 PPI
 H2RA

64. N
u
t
r
i
t
i
o
n
 Parenteral -against
 Parenteral in combination with Enteral – against
 Rather use IV glucose and initiate enteral as per tolerating
 Start with trophic / hypocaloric feed
 Against - Omega 3 fatty acid as an immune supplement
 Against - Monitoring GRV, only in less tolerant pt and high risk of
aspiration
 Prokinetic agents
 Post pyloric feeding tubes - only in less tolerant pt and high risk of
aspiration
 Against - Selenium
 Against - Arginine
 Against - Glutamine

65. Setting goals of care
 Mortality
 Survival
 QOL
 Shared decision- patient and family
 Palliative care

66. Nursing management
 Focus on
 Infection prevention and transmission
 Early recognition and treatment of sepsis and septic
shock
 Supportive nursing care

67. Cont.
 Prevention of sepsis and septic shock is one of the primary
responsibilities of the nurse in the critical care unit.
 Identification of patients at risk and reduction of their risk factors,
including exposure to invading microorganisms
 Handwashing, aseptic techniques, and an understanding of
evidence based practice to reduce nosocomial infection in
critically ill patients are essential components of preventive
nursing care.
 Early identification allows for early treatment and decreases
mortality

68. Nursing interventions
 Early identification of sepsis syndrome
 Administering prescribed fluid, medication and nutrition
 Providing comfort and emotional support
 Preventing and maintaining surveillance for
complications

69. Reference
 1. Jaya kuruvila. Essentials of critical care. 1st edition.
Newdelhi: India: Jaypee: 2007
 2. Suzane M. Burns. Sarah A. Delgado. AACN essentials of
critical care nursing. 4th edition. United states. McGraw-Hill
Education books: 2014
 3.Patrica gonce Morton. Dorrie k fontaine. Critical care nursing
a holistic approach. 11th edition: Wolters Kluwer
 4. Andrew et al. SSC. International guideline for management
of sepsis and septic shock. 2016. conference report and expert
panel. Springer. Intensive care med. 2017