Sepsis Flashcards

1
Q

Incidence and mortality of sepsis

A

-Global incidence and mortality decreasing
-37,000 in UK- third major killers behind CHD and stroke

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2
Q

Sequence of sepsis

A

-Infection
-Bacteraemia
-Sepsis
-Septic shock
-Multiple organ dysfunction
-Death

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3
Q

Definition of infection

A

-Invasion of body tissues by disease causing organisms

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4
Q

Definition of bacteraemia

A

-Presence of viable bacteria in the blood stream

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5
Q

Definition of SIRS

A

-Systemic inflammatory response syndrome (2 or more):
=T: >38* or <36*
=HR: >90 bpm
=RR: >20 breaths per minute
=WBC >12,000 cells/ml or <4000 cells/ml

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6
Q

Definition of sepsis

A

-Life threatening organ dysfunction caused by a dysregulated host response to infection
-Sequential organ-failure assessment score (SOFA):
=Respiration, coagulation, liver, cardiovascular, brain, kidney
=qSOFA: score >2 associated with poor outcomes (RR >22, confusion, systolic BP <100 mmHg)

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7
Q

Definition of septic shock

A

-Subset of sepsis in which circulatory, cellular and metabolic abnormalities are associated with a greater risk of mortality
-Clinically identified by a vasopressor requirement to maintain a mean arterial pressure >65 mmHg and a serum lactate >2mmol/L despite of adequate fluid resuscitation

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8
Q

Risk factors for sepsis

A

-Age
-Bacteraemia
-ICU admission (invasive devices, ventilation)
-Immunosuppression
-Diabetes and obesity
-Cancer
-CAP
-Previous admissions
-Genetic factors (antibody production, lack of T cells, NK cells, complement)

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9
Q

Epidemiology of sepsis

A

-Extremes of age
-Less than 1 year and elderly
-Risk increases around middle ages and beyond
-Incidence in hospitalised 0.3% septic shock, 57% lung
-Gram positive 36%
-Up to a third organism not found

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10
Q

What are PAMPs

A

-Pathogen associated molecular pattern (PAMPs)
=Specific to a micro-organism
=Essential for surviving and pathogenicity
=Molecular signature for pathogens

-Gram negative= LPS
-Gram positive= peptidoglycan- lipoteichoic acid
-Yeast= mannan
-Virus= double stranded RNA
-Mycobacteria= mycolic acid

-Recognised by pattern-recognition receptors (toll-like receptors, NOD and C-type lectin receptors)

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11
Q

What is the innate immune response?

A

-First defence system against pathogens
=Complement (activates cytokine expression, opsonize organism)
=Coagulation (trap with nets)
=Phagocytosis (lyse organism)
=Cytokine expression (signals type and magnitude infection)
=Myelopoiesis (stimuli of bone marrow to produce immune cells)

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12
Q

Pathogenesis of sepsis

A

-Antigen-presenting cells find organism
-Por-inflammatory repsonse
-Cytokines released
-Increased vascular permeability
-Hyperactive immune response
=increased sequestration of fluid
=organ failure
=immune paralysis

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13
Q

Consequences of sepsis

A

-Multiple organ failure
=CV, liver, renal, neuro, resp, haem

-Gut-microbiome
=toxic mediators released from injured gut mucosa are transported and could contribute to dysfunction in other organs

-Endocrinopathy
=Release ACTH- high concentration of cortisol
=High levels of catecholamines
=Insulin resistance

-Neuropathy
=Sepsis associated encephalopathy

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14
Q

Symptoms and signs of septic shock

A

-Hypotension
-Tachycardia
-Peripheral hypoperfusion: cold skin/ cyanosis/ skin blotch
-Purpura
-High RR (hypoxaemia)
-Oliguria
-Altered consciousness
-Fever
-Hypothermia
-Elevated WBC count/ low WBC count
-Low platelet count

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15
Q

Fundamentals of sepsis treatment (Sepsis 6)

A

-To be delivered with 1hr

  1. Deliver high-flow oxygen
  2. Take blood cultures and other cultures, consider source control
  3. Administer empirical IV antibiotics
  4. Measure serum lactate or alternative
  5. Start IV fluid resuscitation using Hartmann’s or equivalent
  6. Commence accurate urine output measurement
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16
Q

Timing of antimicrobial administration

A

-Immediately within 1hr of recognition if sepsis definite or probable and/or shock is present
-Rapid assessment of infectious vs non-infectious causes of acute illness and administer with 3 hours if concern for infection persists when shock is absent and sepsis is possible

17
Q

Antimicrobial combination objectives

A

-Prevent the emergence of MDR (enterobacter, serratia, pseudomonas)
-Increase bactericidal effect during severe infection (endocarditis, neutropenia, bone and joint infections)
-Increase coverage of bacteria (sever sepsis: empiric treatment, intra-abdominal infection, suspected MDR)

18
Q

Source control

A

-Decrease the bacterial burden
=Surgery/ drainage of collections (surgical debridement or amputation in necrotising fasciitis)
=Removal of infected prosthesis

19
Q

Treating hypoperfusion

A

-Fluid resuscitation
-Inotropes/ vasopressors (noradrenaline)

20
Q

Treating organ failure

A

-Respiratory
-Kidney
-Nutrition
-Adrenal insufficiency (hydrocortisone)

21
Q

Monitoring

A

-HR
-BP
-SpO2
-Temp
-Diuresis (per hour)
-GCS
-Arterial catheter
-Central venous pressure
-Cardiac ultrasonography
-CO

22
Q

Triple antibiotics therapy

A

metronidazole, amoxicillin and gentamicin