SEPSIS Flashcards

1
Q

What is sepsis

A

Life threatening organ dysfunction due to dysregulated host response to infection
SIRS / qSOFA + evidence of infection
SIRS now not really used

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2
Q

What is septic shock

A

Sepsis +
Persisting hypotension requiring vasopressors to maintain MAP >65 (hypo after 20ml/kg fluid)
or BP <90 or <40 below normal
Serum lactate >2mm (anaerobic respiration due to hypo-perfusion)

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3
Q

What is SIRS

A
2 of: 
Hypo / hyperthermia 
Tachycardia
Tachypnooea 
PaCO2 <32
WBC <4000 or >12000
Altered mental state
BG >7.7 with DM 
Sats <90 or PaO2 <70
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4
Q

What causes SIRS

A

Sepsis
Bruns
Pancreatitis
Trauma

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5
Q

What do you do if evidence of infection + 2+ qSOFA

A

SEPSIS 6
Assess frequently in 1st house
Look for septic shock / end organ dysfunction

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6
Q

What are red flags (Start sepsis 6)

A
Responding only to pain or voice
Acute confusion
SBP <90
HR >130
RR >25
O2 <92
Non-blanching / rash / mottled / cyanosis 
Not passed urine 18 hours
Lactate >2 even if apyrexial
Chemotherapy
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7
Q

What are RF for sepsis

A
Any condition that impacts on the immune system 
Age
Co-morbid - COPD / DM 
Immunosuppresion - chemo / steroids 
Previous surgery / recent trauma e.g. burns 
Pregnancy 
Indwelling medical devices 
Virulence of organism
Occupation
Travel
Hospital
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8
Q

What is qSOFA

A

Hypotension <100 or <40 below normal
Altered mental status
Tachypnoea >22

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9
Q

What is SEPSIS 6

A

WIRHIN 1 hour
Blood culture (2 sets A+An)
Blood lactate + bloods (easiest with VBG or ABG)
Urine output / catheter to get hourly urine output

Oxygen - 94-98%
IV Antibiotics
IV fluid

Inotropes / vasopressor in ITU if needed if BP is not responding

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10
Q

When should you do blood cultures

A
Fever
Hypothermia 
Leucocytosis 
Neutropenia
Unexplained organ dysfunction
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11
Q

What do you send lab tests of as

A

Emergency

Get results in 1 hour

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12
Q

How much fluid

A

Bolus 500ml over 15 minus

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13
Q

What Ax do you give

A

Cephalosporin + amox
Add vancomycin if resistant
Add metronidazole if GI

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14
Q

What is mortality from sepsis and septic shock

A

Sepsis - 10%
Septic shock - 40%
Mortality increases by 7.6% for each delay

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15
Q

What has different protocol

A

Neutropenic sepsis

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16
Q

What do you get ASAP

A

Senior input

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17
Q

When do you go to HDU

A
Low BP even with fluid
High lactate >2 with fluid
Increased creatinine
Oliguria
Liver dysfunction 
Bilateral. infiltrates
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18
Q

How do you get into ITU

A

Septic shock requiring vasopressor
Multi-organ failure
Incubation required

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19
Q

What are signs of end organ dysfunction / severe sepsis

A
Arterial hypoxaemia
Hyptension BP <90 / MAP <65
Lactate >2
Oliguria <0.5ml/kg/hr for 2 hours
AKI  
Coag abnormalities - raised PT / APTT
Thrombocytopenia
Hyperbilirubin 
Paralytic ileus
Confusion as brain not perfused
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20
Q

What are inflammatory variables

A
Leucocytosis
Leucopenia
Normal WCC 
High CRP
High procalcitonin
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21
Q

What are haemodynamic variables

A

Arterial hypotension
SvO2 >70%
Sats <90%

22
Q

What shows poor perfusion

A

High lactate
Reduce perfusion
SKin mottling

23
Q

What are signs of systemically unwell

A

N+V
Rigors
Poor appetite

24
Q

What do you do if vomiting

A

U+E
ECG
AXR if think obstruction

25
Q

What are amber flags

A
Deterioration
Immunosuppresed
Trauma / surgery <6 weeks
RR 21-25
BP 90-100
HR 90-130
New arrhythmia
Low temp
26
Q

What are features of immunosuppression

A

Loss of delayed hypersensitivity
Inability to clear infection
Predisposed to other

27
Q

When septic what do you become

A

Immunosuppressed as all energy into dealing with infection

28
Q

What is phase 1

A

Release of bacterial toxin

29
Q

What do gram -ve release

A

LPS (endotoxin)

30
Q

What do gram +ve release

A

LTA (endotoxin)

Superantigens which can cause toxin shock syndrome

31
Q

What is phase 2

A

Release of mediators in response to infection

32
Q

What does LPS need

A

Binding protein to bind to macrophage and engulf it

LTA does not

33
Q

What does super antigens (exotoxin) cause

A

Recognised by T cells
Cause large number of mediators to be released
Causes septic shock

34
Q

What is phase 3

A

Effects of specific excessive mediators

35
Q

What two types of mediators

A

Pro-inflammaotry

Anti-inflammatory

36
Q

What are pro-inflammatory

A

TNFa - tumour necrosis factor
Il-1,2 - interleukin
IFN-y

37
Q

What does pro-inflammatory cause

A

WCC adhesion
Increased vessel permeability = reduction in blood volume and hypoperfusion and oedema = reduced O2 to tissue
Release arachidonic acid
Complement activation
Vasodilation by NO
Increased coagulation - compromise perfusion
Increased consumption of platelets / clotting = thrombocytopenia / haemorrhage (DIC)
Hyperthermia

38
Q

What are anti-inflammatory

A

TGF B

IL-1

39
Q

What do anti-inflammatory cause

A

Inhibit TNFa
Inhibit coag
-ve feedback

40
Q

If pro-inflammatory > compensatory

A

Septic shock

41
Q

If compensatory >

A

Immune paralysis

Multi-organ failure

42
Q

What is important to remember with neutropenic patients / immunosuppressed

A

May have normal observations / temp despite being very unwell

43
Q

What bloods and why

A
FBC
U+E
LFT
CRP
Coagulation - look for DIC 
ABG - assess pH, lactate and glucose
44
Q

What additional investigations for source of infection

A

Urine dip and culture
CXR
CT scan if suspect intra-abdominal
LP for meningitis

45
Q

What organisms most common following splenectomy

A

Encapsulated
S.pneumona
H.inlfuena
Meningoccous

46
Q

What do people get following splenectomy

A
Pneumococcal vaccine - 2 WEEKS BEFORE 
Meningococcal vaccine A+C
H.infelunza B vaccine
Annual flu 
Ax prophylaxis offered to all (penicillin or amoxicillin)
47
Q

What is bacteraemia

A

Organism in a sterile site

48
Q

What is infection

A

If bacteraemia causing symptoms

49
Q

If suspect sepsis / red flags

A

999 and ambulance

50
Q

Indications for splenectomy

A
Trauma
Spontaneous rupture e.g. EBV
Hypersplenism - hereditary spheryocytosis
Malignancy
Cyst / abscess
51
Q

What are complications

A

Haemorrhage
Pancreatic fistula
INfection
Thrombocytosis so give aspirn

52
Q

What happens post splenectomy

A

Platelet rise

Howell Jolly form