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Flashcards in Sepsis and Septic Shock Deck (29)
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1
Q

Define sepsis

A

Life threatening organ dysfunction caused by dysregulated host response to infection

2
Q

Define septic shock

A

Septic shock can be identified with a clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP >65mmHg and having a serum lactate of >2mmol/l despite adequate volume resuscitation

(sepsis with low blood pressure and high lactate)

3
Q

What is the SOFA score

A

Sequential organ failure assessment score

Used to track a person’s status during the stay in an intensive care unit (ICU) to determine the extent of a person’s organ function or rate of failure

4
Q

What are the systems involved in the sofa score?

A

Respiratory (PaO2)

Nervous system (GCS)

Cardiovascular (MAP or administration of vasopressors required)

Liver (bilirubin)

Coagulation (platelets)

Kidneys (creatinine)

5
Q

What is the qSOFA score?

A

Quick SOFA Score as an initial way to identify patients at high risk for poor outcome with an infection

Only includes three clinical criteria (low blood pressure, high respiratory rate, any altered mental state)

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. These are outcomes that are more common in infected patients who may be septic than those with uncomplicated infection.

qSOFA basically is a good indicator for who is likely to be septic

6
Q

What are the components of the bodyes defence against sepsis?

Physical barrier

Innate immune system

Adaptive immune system

A
  • Physical barrier – skin, mucosa, epithelial lining
  • Innate immune system – IgA in gastrointestinal tract, dendritic cells / macrophages
  • Adaptive immune system – lymphocytes, immunoglobulins
7
Q

How does sepsis arise?

A

Failure of host barrier (physical or immunological)

Organism enters the blod stream creating a septic state

8
Q

Patients with sepsis are said to have features consistent with immunosuppression, what are these features?

A
  • Loss of delayed hypersensitivity
  • Inability to clear infection
  • Predisposition to nosocomial infection
9
Q

What is the probable change of the sepsis syndrome over time?

A
  • Initially there is an increase in inflammatory mediators
  • Later, there is a shift toward an anti-inflammatory immunosuppressive phase
  • Depends on the health of the individual patient
10
Q

What are the three phases in the pathogenesis of sepsis?

A
  1. Release of bacterial toxins
  2. Release of mediators
  3. Effects of specific excessive mediators
11
Q

What are comonly released toxins?

A

•Gram negative:

Lipopolysaccharide (LPS)

•Gram positive:

  • Microbial-associated molecular pattern (MAMP):
  • •Lipoteichoic acid
  • •Muramyl dipeptides

•Superantigens:

  • Staphylococcal toxic shock syndrome toxin (TSST)
  • Streptococcal exotoxins
12
Q

What is the difference between endotoxins and exotoxins?

A

Exotoxins are toxic substances secreted by bacteria and released outside the cell. Pro inflammatory response, small amounts of superantigens will cause a large amount of mediators to be secreted: cascade effect

Endotoxins are bacterial toxins consisting of lipids that are located within a cell. (LPS needs a LPS binding protein to bind to macrophages, LTA (Lipoteichoic acid) does not

13
Q

What are the two types of mediators that can be released in sepsis/?

A
  • Pro-inflammatory mediators – causes inflammatory response that characterises sepsis
  • Compensatory anti-inflammatory reaction – can cause immunoparalysis
14
Q

Name some pro-inflammatory mediators

A

TNF-alpha

IL1b, IL-2, IL-8, IL-15

Neutrophil elastase

IFN-gamma

Prostaglandins, prostacyclin

15
Q

Name some anti-inflammatory mediators

A

IL-1Ra

IL-4

IL-10

IL-13

LPS binding protein

Soluble TNF alpha receptor

Epinephrine phospholipase a2

16
Q

What are the actions of pro-inflammatory mediators?

A

Promote endothelial cell - leukocyte adhesion

Release of arachidonic acid metabolites

Complement activation

Vasodilation of blood vessels by NO

Increase coagulation by release of tissue factors and membrane coagulants

Cause hyperthermia

17
Q

What are the effects of anti-inflammatory mediators?

A
  • Inhibit TNF alpha
  • Augment acute phase reaction
  • Inhibit activation of coagulation system
  • Provide negative feedback mechanisms to pro-inflammatory mediators
18
Q

What is the result of unbalanced pro-inflammaotry and inflammatory mediators?

A

Too much pro-inflammatory = septic shock with multiorgan failure and death

Too much anti-inflammatory = immunoparalysis with uncontrolled infection and multiorgan failure

19
Q

What are the clincal features of sepsis in terms of organ dysfunction?

A

General features:

  • Fever over 38 degrees, presenting as chills, rigors, flushes, cold sweats, night sweats
  • Hypothermia (less than 36 degrees - especially in the elderly and the very young, remember the imunosuppressed)
  • Tachycardia (over 90 bpm)
  • Tachypnoea (rr over 20/min)
  • Altered mental status - especially in the elderly
  • Hyperglycaemia (over 8mmol/l in the absence of diabetes)

Altered consciousness

Confusion

Psychosis

Tachypnoea

PaO2 less than 70mmHg

Sats less than 90%

Jaundice

Increase in liver enzymes

Decrease in albumin

Increase in prothrombin time

Decrease in platelets

Increase in activated partial thromboplastin time

Decrease in protein C (a zymogen, the activated form of which plays an important role in regulating anticoagulation, inflammation, cell death, and maintaining the permeability of blood vessel walls in humans and other animals.)

Increase in D-dimer

Tachycardia

Hypotension

Oliguria

Anuria

Increase in creatinine

20
Q

What are the inflammatory variables in sepsis?

A
  • Leucocytosis (WCC > 12,000/ml)
  • Leucopenia (WCC < 4,000/ml)
  • Normal WCC with greater than 10% immature forms
  • High CRP
  • High procalcitonin
21
Q

What are the haemodynamic variables in sepsis?

A
  • Arterial hypotension (systolic <90mmHg or MAP <70mmHg)
  • SvO2 >70%

Mixed venous oxygen saturation (SvO2) is the percentage of oxygen bound to hemoglobin in blood returning to the right side of the heart. This refects the amount of oxygen “left over” after the tissues remove what they need.

22
Q

What are the organ dysfunction variables in sepsis?

A
  • Arterial hypoxaemia (PaO2/FiO2 < 50mmHg)
  • Oliguria (<0.5ml/kg/h)
  • Creatinine increase compared to baseline
  • Coagulation abnormalities (PT >1.5 or APTT >60s)
  • Ileus
  • Thrombocytopenia (<150,000/ml)
  • Hyperbilirubinaemia
23
Q

What are the tissue perfusion variables in sepsis?

A
  • High lactate
  • Skin mottling and reduced capillary perfusion
24
Q

What can effect the presentation of sepsis?

A
  • Age
  • Co-morbidities (COPD, DM, CCF, CRF, disseminated malignancy)
  • Immunosuppression
  • Acquired – HIV/AIDS
  • Drug-induced – steroids, chemotherapeutic agents, biologics
  • Congenital – agammaglobulinaemia, phagocytic defects, defects in terminal complement component

•Previous surgery - splenectomy

The organism:

  • Gram positive versus Gram negative
  • Virulence factors (example: MRSA, toxin secretion, ESBL, KPC, NDM-1)
  • Bioburden
25
Q

What is the sepsis 6?

A

Take 3 give 3

Take: Blood cultures, blood lactate, measure urine output

Give: Oxygen aim sats 94-98%, IV antibiotics, IV fluid challenge

Lactate is a mrker of generalised hypoperfusion/severe sepsis/poorer prognosis

Low urine output is a marker of renal dysfunction

26
Q

What is the difference between type A and type B lactate?

A
  • Type A - Hypoperfusion
  • Type B – Mitochondrial toxins, Alcohol, Malignancy, metabolism errors
27
Q

When do you consider HDU referral?

A
  • Low BP responsive to fluids
  • Lactate >2 despite fluid resuscitation
  • Elevated creatinine
  • Oliguria
  • Liver dysfunction, Bil, PT, Plt
  • Bilateral infiltrates, hypoxaemia
28
Q

When do you consider ITU?

A

Septic shock

Multi-organ failure

Requires sedation, intubation and ventilation

29
Q

What is treatment of pneumonia based on the CURB65 score?

A

Low severity

CURB65 = 0-1 (amoxicillin)

Moderate severity

CURB65 = 2 (amoxicillin and clarithromycin orally. If oral administration is not possible then amoxicillin IV or benzylpenicillin IV plus clarithromycin)

High Severity

CURB65 = 3-5 (IV co-amoxiclav plus IV clairithromycin, if leigonella strongly suspected, consider adding levofloxacin)

Legionella has diarrhoea, high ALT, hyponatraemia

Detected by urinary antigen