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Yr 3 Infection > Sepsis and Septic Shock > Flashcards

Sepsis and Septic Shock Flashcards

1
Q

Definition of sepsis? This isnt a clinical definition it is more about how it arises.

A

Systemic illness caused by microbial invasion of normally sterile parts of the body

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2
Q

Within the tradition model of sepsis, SIRS comes first before Sepsis, Severe Sepsis, and Septic shock. To have SIRS you need 2 or more of certain findings. What are these?

A
  • Temp >38 or <36 degrees
  • HR>90
  • RR>20 or PaCO2 <32
  • WBCs >12000 or <4000 or >10% bands
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3
Q

What defines sepsis in the model?

A

SIRS and infection

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4
Q

What defines Severe sepsis in the model?

A

Sepsis and end organ damage

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5
Q

What defines septic shock in the model?

A

severe sepsis and hypotension

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6
Q

what can cause SIRS?

A
  • Pancreatitis
  • Burns
  • Trauma
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7
Q

Clinical definition of sepsis?

A

Life threatening organ dysfunction caused by dysregulated host response to infection
»Organ dysfunction identified as an acute change in total SOFA score >2 points
»SOFA score >2 reflects overall mortality risk of approx 10% in general hospital population with suspected infection

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8
Q

Clinical definition of septic shock?

A

Identified with clinical construct of sepsis with

> > persisting hypotension requiring vasopressors to maintain MAP >65mmHg

> > serum lactate of 2mmol/l despite adequate vol resus

> > hospital mortality of 40%

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9
Q

what 3 criteria constitute qSOFA (quick way of getting SOFA score, at least 2 suggests greater risk of poorer outcome)

A

> > Hypotension systolic BP <100 mmHg
altered mental status
Tachynpoea RR >22/min

Identifies patients likely to have prolonged ICU stay or die in hospital

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10
Q

why is quick intervention key in sepsis?

A

Chance of mortality increases with each hour of delay of antibiotic administering

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11
Q

What intervention is key in reducing mortality and cost?

A

SEPSIS 6

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12
Q

What is the bodys defences against sepsis?

A

> Physical barrier: skin, mucosa, epithelial lining
innate immune system: IgA in GI tract, dendritic cells/macrophages
adaptive immune system - lymphocytes, immunoglobulins

Sepsis originates from breach of host barrier. Organism enters bloodstream creating septic state

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13
Q

Pathophysiology of sepsis?

A

> > uncontrolled inflammatory response
immunosuppression features (loss of delayed hypersensitivity/unable to clear infection/predisposed to nosocomial infection)
Likely change of sepsis syndrome over time
(initial inc. in inflammatory mediators. Later shift towards anti-inflam immunosuppressive phase. Depends on patient health)

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14
Q

what are the 3 phases in pathogenesis of sepsis?

A
  1. release of bacterial toxins
  2. release of mediators
  3. effects of specific excessive mediators
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15
Q

Discuss phase 1: release of bacterial toxins?

A

-bacterial invasion into body tissues is source of dangerous toxins
-may/may not be neutralised and cleared by existing immune system
-commonly released toxins:
>gram -ve (lipopolysaccharide)
>gram +ve (MAMP, superantigens)

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16
Q

Discuss phase 2:release of mediators in response to infection?

A

Effects of infections due to endotoxin release
>LPS needs LPS-binding protein to bind to macrophages. LTA doesnt need a protein

Effects of infections due to exotoxin release
>pro-inflammatory response
>small amount of superantigens will cause lots of mediators to be secreted (cascade effect)

Mediator role on sepsis
>two types of mediators can be released
>pro-inflammatory mediators (eg Neutrophils, prostaglandins, TNF-a) causes inflammatory response that characterises sepsis
>compensatory anti-inflammatory reaction (interleukins, LPS-binding protein) can cause immunoparalysis

17
Q

Discuss phase 3: effects of specific excessive mediators?

A

Pro-inflammatory mediators

  • promote endothelial cell (leukocyte adhesion)
  • release of arachidonic acid metabolites
  • complement activation
  • vasodilatiion of blood vessels by NO
  • inc coagulation by release of tissue factors and membrane coagulants
  • cause hyperthermia

Anti-inflammatory mediators

  • Inhibit TNF alpha
  • augment acute phase reaction
  • inhibit activation of coagulation
  • provide negative feedback mechanisms to pro-inflammatory mediators
18
Q

What can over production of pro-inflammatory mediators lead to?

A

septic shock with multi organ failure and death

19
Q

What can over production of anti-inflammatory mediators lead to?

A

Immunoparalysis with uncontrolled infection and multi organ failure

20
Q

What are some general features of sepsis?

A
  • Fever >38 degrees (chills, rigors, flushes, cold sweats)
  • Hypothermia <36 degrees (esp in elderly/young/immunosuppressed)
  • Tachycardia >90bpm
  • Tachynpoea >20 breaths/min
  • altered mental status (esp in elderly)
  • Hyperglycaemia >8mmol/l in absence of diabetes
21
Q

what are some inflammatory variables in sepsis?

A
  • Leucocytosis (WCC>12000/ml)
  • Leucopenia (WCC<4000/ml)
  • Normal WCC with >10% immature forms
  • high CRP
  • High calcitonin
22
Q

What are some haemodynamic variables in sepsis?

A
  • Arterial hypotension (systolic <90mmHg or MAP <70mmHg)

- SvO2 >70%

23
Q

What are some organ dysfunction variables in sepsis?

A

-Arterial hypoxaemia (PaO2 <50mmHg)
-Oliguria (<0.5ml/kg/h)
-creatinine inc compared to baseline
-coag. abnormalities (PT>1.5/APTT>60s)
-Ileus
-Thrombocytopenia (<150000/ml)
Hyperbilirubinaemia

24
Q

What are some tissue perfusion variables in sepsis?

A
  • High lactate

- skin mottling and reduced capillary perfusion

25
Q

What can affect sepsis presentation in a host?

A
  • Age
  • co-morbidities (COPD, DM etc)
  • Immunosuppression (acquired - HIV/AIDS. Drug induced - steroids/chemo/biologics. Congenital - agammaglobulinaemia/phagocytic defects)
  • previous surgery - splenectomy
26
Q

What aspects of organisms can affect sepsis presentation in a host?

A
  • Gram positive (infections above diaphragm)

- Gram negative (infections below diaphragm)

27
Q

Patient presents with fever nausea, vomiting, abdominal pain. Other than sepsis what could the diagnosis be?

A

Acute pancreatitis

28
Q

What is the SEPSIS6? (remember: take 3 give 3)

A

Take:

  • blood cultures
  • blood lactate
  • measure urine output

Give:

  • Oxygen aim sats 94-98%
  • IV antibiotics
  • IV fluid challenge
29
Q

Why do you take:

  • blood cultures
  • blood lactate
  • low urine output

in SEPSIS6?

A

Blood cultures

  • microbiological diagnosis
  • if temp spike take 2 sets

Blood lactate
-marker of generalised hypoperfusion/severe sepsis/poorer prognosis

Low urine output
-marker of renal dysfunction

30
Q

How do you determine what antibiotics to give patient? and what must you consider?

A
  • Mased on working diagnosis from H+Exam
  • Local antibiotic guidelines

Consider

  • allergy
  • previous MRSA, ESBL, CPE
  • Abx toxicity/interactions
31
Q

What do Type A and B lactate biomarkers indicate?

A

Type A: hypoperfusion

Type B: mitochondrial toxins, alcohol, malignancy, metabolism errors

32
Q

what is the volume of IV fluids given for a fluid challenge?

A

30ml/kg fluid challenge (so 2.1ml for 70kg patient)

33
Q

When do you consider HDU referral?

A
  • low bp responsive to fluids
  • lactate >2 despite fluid resus
  • elevated creatinine
  • oliguria
  • liver dysfunction, bilirubin, PT, platelet count
  • bilateral infiltrates, hypoxaemia
34
Q

When do you consider ITU?

A
  • Septic shock
  • multi organ failure
  • needs sedation, intubation and ventilation

Yr 3 Infection (12 decks)

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