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Y2 infection > sepsis and septic shock > Flashcards

sepsis and septic shock Flashcards

1
Q

what is sepsis

A

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

SIRS + infection

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2
Q

traditional model of sepsis

A

SIRS
sepsis
severe sepsis
septic shock

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3
Q

SIRS

A 
systemic inflammatory response syndrome 
temp >38 or <36
HR >90
RR >20 or PaCO2 <32
WBC >12 000 or <4000 or >10% bands
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4
Q

severe sepsis

A

sepsis + end organ damage

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5
Q

septic shock

A

severe sepsis + hypotension

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6
Q

define sepsis

A

life threatening organ dysfunction caused by dysregulated host response to infection

organ dysfunction - an acute change in total SOFA score >2 points consequent to the infection

SOFA score >2 reflects an overall mortality risk of ~10% in a general hospital pop w/ suspected infection

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7
Q

define septic shock

A

sepsis w/ persisting hypotension requiring vasopressors to maintain MAP >65mmHg and serum lactate >2mmol/L despite adequate volume resus

pts w/ septic shock have a hospital mortality of 40%

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8
Q

what does SOFA stand for

A

sequential (sepsis related) organ failure assessment score

respiration 
coagulation 
LFTs
BP 
GCS 
renal function - creatinine and urine output
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9
Q

qSOFA

A

pts w/ suspected infection who are likely to have a prolonged ICU stay or die in hospital can be promptly identified w/ qSOFA

score ≥2 suggests greater risk of a poor outcome

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10
Q

what observations are measured in qSOFA

A

hypotension - systolic BP <100mmHg
altered mental status
tachypnoea - RR >22/min

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11
Q

importance of sepsis

A

common condition (30% of pts coming through acute medical assessment unit have some form of sepsis)

becoming more common (living longer, more co-morbidities etc)

increased morbidity and mortality

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12
Q

for every hrs delay in administering abx in septic shock, morality increases by …

A

7.6%

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13
Q

what are the body’s defences to sepsis

A

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

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14
Q

origin of sepsis

A

originates from a break of integrity of host barrier (physical or immunological)
organism enters the bloodstream creating a septic state

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15
Q

pathophysiology of sepsis

A

uncontrolled inflammatory response

pts w/ sepsis have features consistent w/ immunosuppression

probable change of the sepsis syndrome over time

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16
Q

what are the features consistent w/ immunosuppression in sepsis pts

A

loss of delayed hypersensitivity
inability to clear infection
predisposition to nosocomial infection

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17
Q

what is the change of the sepsis syndrome over time

A

initial increase in inflammatory mediators
shift towards an anti-inflammatory immunosuppressive phase
depends on the health of the patient

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18
Q

3 phases in pathogenesis of sepsis

A

release of bacterial toxins
release of mediators
effects of specific excessive mediators

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19
Q

release of bacterial toxins

A

bacterial invasion into body tissues is a source of dangerous toxins
may or may not be neutralised and cleared by existing immune system

20
Q

toxins released by gram -ve bacteria

A

lipopolysaccharide (LPS)

21
Q

toxins released by gram +ve bacteria

A

microbial associated molecular pattern (MAMP):
lipoteichoic acid
muramyl dipeptides

superantigens:
staphylococcal toxic shock syndrome toxin (TSST)
streptococcal exotoxins

22
Q

release of mediators in response to infection

A

effects of infections due to endotoxin and exotoxin release

mediator role on sepsis

23
Q

endotoxin release

A

LPS needs an LPS-binding protein to bind to macrophages

LTA don’t require these proteins

24
Q

exotoxin release

A

pro-inflammatory response

small amounts of superantigens will cause a large amount of mediators to be secreted: cascade effect

25
Q

mediator role in sepsis

A

2 types of mediators can be released:
pro-inflammatory mediators - causes inflammatory response that characterises sepsis (too much of pro-inflammatory response can lead to septic shock and multiorgan failure and death)

compensatory anti-inflammatory reaction - can cause immunoparalysis - uncontrolled infection and multi-organ failure

26
Q

examples of pro-inflammatory mediators

A

TNF-alpha
IL1
IFN-gamma

27
Q

examples of anti-inflammatory mediators

A

IL-10
transforming growth factor-beta
LPS-binding protein

28
Q

effects of specific excessive mediators - pro-inflammatory mediators

A

promote endothelial cell - leukocyte adhesion
released of arachidonic acid metabolites
complement activation
vasodilation of blood vessels by NO
increased coagulation by release of tissue factors and membrane coagulants
cause hyperthermia

29
Q

effects of specific excessive mediators - anti-inflammatory mediators

A

inhibit TNF-alpha
augment acute phase reaction
inhibit activation of coagulation system
provide -ve feedback mechanisms to pro-inflammatory mediators

30
Q

what do the clinical features of sepsis depend on

A

host
organism
environment

31
Q

features of organ dysfunction

A

CNS: altered consciousness, confusion, psychosis

haematology: reduced platelets, increased PT/APTT, reduced protein c, increased D dimer
resp: tachypnoea, PaO2 <70mmHg, sats <90%

CVS: tachycardia, hypotension

liver: increased liver enzymes, reduced albumin, increased PT
kidney: oliguria, anuria, increased creatinine

32
Q

general features of sepsis

A

fever >38C - chills, rigor, flushes, cold sweats, night sweats

hypothermia <36C - esp in elderly, very young children and immunosuppressed

tachycardia >90BPM

tachypnoea >20/min

altered mental status - es- elderly

hyperglycaemia >8mmol/L in the absence of diabetes

33
Q

inflammatory variables in sepsis

A 
leucocytosis (WCC >12 000/ml)
leucopenia (WCC <4000/ml)
normal WCC w/ >10% immature forms 
high CRP 
high procalcitonin
34
Q

haemodynamic variables in sepsis

A 
artieral hypotension (systolic <90 or MAP <70)
SvO2 >70%
35
Q

organ dysfunction variables in sepsis

A

arterial hypoxaemia (PaO2/FiO2 <50mmHg)
oliguria (<0.5ml/kg/h)
creatinine increase compared to normal baseline
coagulation abnormalities (PT >1.5 or APTT >60s)
ileus
thrombocytopenia (<150 000/ml)
hyperbilirubinemia

36
Q

tissue perfusion variables in sepsis

A

high lactate

skin mottling and reduced capillary perfusion

37
Q

effect of host on sepsis presentation

A

age
comorbidities (COPD, DM, CCF, CRF, disseminated malignancy)
immunosuppression
previous surgery - splenectomy

38
Q

immunosuppression and sepsis presentation

A

acquired - HIV/AIDS
drug induced - steroids, chemotherapeutic agents, biologics
congenital - agammaglobulinaemia phagocytic defects, defects in terminal complement component

39
Q

effect of organism on presentation of sepsis

A

gram +ve/-ve
virulence factors (e.g. MRSA, toxin secretion, ESBL, KPC, NDM-1)
bioburden

40
Q

effect of environment on presentation of sepsis

A

occupation
travel
hospitalisation

41
Q

Sepsis 6

A

2A2B2C
take 3, give 3

blood cultures
blood lactate
measure urine output

oxygen - aims sats 94-98%
IV abx
IV fluid challenge

42
Q

why do we carry out blood cultures
blood lactate
measure urine output

A

blood cultures - make microbiological diagnosis (30-50% +ve), if spike in temp take 2 sets

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

low urine output - marker of renal dysfunction

43
Q

how to choose what abx to use

A

based on working diagnosis from hx and examination
local abx guidelines

consider: allergy, previous MRSA/ESBL/CPE, abx toxicity/interactions

44
Q

types of lactate

A

type A - hypoperfusion

type B - mitochondrial toxins, alcohol, malignancy, metabolism errors

45
Q

IV fluids

A

30ml/kg fluid challenge

2.1L for 70kg patient

46
Q

when to consider HDU referral

A 
low BP responsive to fluids
lactate >2 despite fluid resus 
elevated creatinine 
oliguria 
liver dysfunction - Bil, PT, Plt
bilateral infiltrates, hypoxaemia
47
Q

when to consider ITU

A

septic shock
multi-organ failure
requires sedation, intubation and ventilation

Y2 infection (15 decks)

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