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3 Sepsis Flashcards

1
Q

Sepsis is a syndrome defined as ?

A

life-threatening organ dysfunction due to the infecting pathogen and a dysregulated host response to infection

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2
Q

What does SIRS stand for ?

A

systemic inflammatory response syndrome

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3
Q

SIRS due to infection is known as what ?

A

sepsis

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4
Q

severe sepsis ?

A

sepsis plus at least one organ failure

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5
Q

septic shock ?

A

sepsis plus haemodynamic instability

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6
Q

SIRS is an inflammatory response to an insult e.g. give 4 examples

A

infection
trauma
infarction
malignancy

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7
Q

SIRS is the presence of 2 or more of what ?

A
  • abnormal body temperature
  • heart rate
  • respiratory rate
  • blood gas
  • white blood cell count
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8
Q

Give the values of the following - that relate to the presence of SIRS
1. HR
2. RR
3. WCC
4. imature neutrophils
5. PaCO2

A
  1. HR > 90
  2. RR > 20
  3. WCC > 12
  4. immature neutrophils > 10%
  5. PaCO2 < 4.3KPa
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9
Q

SIRS = systemic inflammatory response syndrome

Apart from infection what else may SIRS also occur due to other pathophysiological events such as what ?

A

HB TRIP
* Haemorrhage
* Burns
* Trauma
* Reperfusion
* Ischaemia
* Pancreatitis

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10
Q

severe sepsis is an infectious disease state associated with what ?

A

MODS = multiple organ dysfunction syndrome

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11
Q

Severe sepsis is defined as sepsis with ?

A

sepsis-induced organ dysfunction or tissue hypoperfusion (reduced amt blood flow)

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12
Q

Severe sepsis is defined as sepsis with sepsis-induced** organ dysfunction or tissue hypoperfusion** which manifests as what ?

A

THE C between 2L’s & 2R’s

  • thrombocytopenia
  • hypotension
  • elevated lactate levels
  • lung injury
  • liver dysfunction
  • coagulopathy
  • renal dysfunction
  • reduced urine output
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13
Q

Septic shock is severe ……plus persistently……despite the administration of ….fluids

A
  1. sepsis
  2. low blood pressure
  3. intravenous
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14
Q

septic shock = severe sepsis plus the presence of the …….instability such as hypotension despite attempts to correct

A

*haemodynamic

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15
Q

In septic shock:
..1…compensatory mechanisms are overwhelmed resulting in abnormalities of ..2.. and/or ..3… metabolism

A
  1. physiological
  2. circulation
  3. cellular
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16
Q

2 types of septic shock ?

A
  1. compensated
  2. decompensated
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17
Q

Difference between compensated and decompensated septic shock ?

A

compensated = early stage of shock where compensatory mechanisms are still able to maintain tissue perfusion

decompensated = indicates stage where compensatory mechanisms fail, leading to worsening organ dysfunction and haemodynamic instability

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18
Q

Rarely pathogens causing sepsis

A
  • fungal (candida)
  • viral or parasites
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19
Q

Pathophysiology for sepsis involves a collection of responses to infection, one of them being infecting pathogens List 4 more :

A
  • immune system
  • coagulation cascade
  • physiological compensation
  • metabolic compensation
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20
Q

List what the immune response is activated by ?

A
  • Pathogen associated molecular patterns (PAMPS)
  • damage associated molecular patterns (DAMPS)
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21
Q

Give an overview of the inflammatory response

A
  1. insult
  2. trigger
  3. sensors and effector cells
  4. mediators and biomarkers
  5. impact on organ function
  6. outcome
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22
Q
  1. what is blood pressure proportional to ?
  2. BP = calculation?
  3. Cardiac output = calculation?
A
  1. blood pressure is proportional to : (heart rate X stroke volume) and systemic vascular resistance
  2. BP = (HR x SV) x SVR
  3. = HR x SV
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23
Q

Compensatory mechanisms to maintain blood pressure result in 3 increased what ?

A
  • heart rate
  • stroke volume
  • systemic vascular resistance
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24
Q

Compensatory mechanisms to maintain blood pressure:

  • largely driven by ..1.. system (….7.. and ..2.) = speed (3)?
  • ..4…is also important
  • …5..system is slowish
  • …6…. hormone is slowish
A
  1. sympathetic nervous
  2. norepinephrine
  3. quick
  4. cortisol
  5. renin-angiotensin-aldosterone
  6. anti-diuretic
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25
Q

Vascular changes with sepsis ?

A
  • vasodilation
  • vasoconstriction
  • vascular permeability
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26
Q

cellular events with sepsis ?

A
  1. increased adhesion of white blood cells
  2. cellular recruitment and activation of neutrophils
  3. chemical mediators modulate the inflammatory response
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27
Q

In sepsis the balance between what becomes disordered ?

A

pro-inflammatory and anti-inflammatory cytokines

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28
Q

Vasodilation leads to :
* reduced ..1… (peripheral) ..2..resistance
* potentially and eventually leads to fall in ..3…
* recognised by the presence of warm ..4…. (warm shock) (CRT normal)
* skin is …5… but vital organs are ..6….

A
  1. systemic
  2. vascular
  3. BP
  4. peripheries
  5. well perfused
  6. not
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29
Q

vasoconstriction may also occur especially why ?

A

sepsis progresses with sympathetic drive to increase peripheral SVR (lengthened CRT) to “re-direct” blood centrally to maintain vital organ perfusion

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30
Q

Vasodilation results in fall in …1… then compensatory …2… and increased …3… to try to maintain BP

A
  1. SVR
  2. tachycardia
  3. stroke volume
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31
Q

Compensated shock = normal …1.. treat ..2../ preferably well before decompensated shock = ….3… which is difficult to treat

A
  1. BP
  2. now
  3. low BP
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32
Q

Tachycardia will still occur even if there is ….1.. or ..2…

A
  1. vasoconstriction
  2. vasodilation
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33
Q

Pro-inflammatory cytokines damage the …1..endothelium leading to - (..2…syndrome) - …3… hypovolaemia
plus: reduced …4.. and increased …5…losses

A
  1. vascular
  2. capillary leak
  3. intra-vascular
  4. intake
  5. fluid
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34
Q

Intra-vascular hypovolaemia fruther crompromises ..1… , …2…. and …3…. increase to compensate

But reduced ….4…. return compromises ability to increase …5…

Leads to …6… in tissue perfusion lead to tissue …7… and tissue …8… and …9….glycolysis with …..10…acidosis

A
  1. BP
  2. HR
  3. SV
  4. venous
  5. stroke volume
  6. reduction
  7. ischaemia
  8. hypoxia
  9. anaerobic
  10. lactic
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35
Q
  1. In the early stages of sepsis how is cardiac output maintained by?
  2. what is seen ?
A
  1. an increase in HR and myocardial contractility (SV)
  2. ‘hyperdynamic circulation’
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36
Q

Cardiac outpute is maintained by an INC in HR and myocardial contractility …

Further increase in HR shortens …1… during which …2… perfusion occurs and so there is reduced …3…perfusion resulting in ….4… ischaemia and this further reduces ….5..output

A
  1. diastole
  2. diatolic coronary
  3. coronary artery
  4. myocardial
  5. cardiac
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37
Q

In the later stages of sepsis …

what directly impairs myocardial contractiliy , reducing CO further ?

A

pro-inflammatory cytokines in addition to hypoxia and acidosis

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38
Q

How does cardiac output (CO) change as sepsis progresses ?
1. In early stages of sepsis
2. In late stages of sepsis
3. further ….

A
  1. CO maintained due to compensatory increases in HR and SV (hyperdynamic circulation).
  2. Further increases in HR reduce the cardiac filling and coronary perfusion time, resulting in a decreased CO and myocardial ischaemia.
  3. further decrease in CO = The pro-inflammatory cytokines, hypoxia and acidosis all impair myocardial contracility in late sepsis
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39
Q

Summarise the pathophysiology of haemodynamic disturbances

A

1) Vasodilation:
* Reduced systemic vascular resistance
* Reduced/compromised blood pressure.

2) Capillary leak: Intra-vascular hypovolaemia. Reduced vital organ perfusion.

3) Compensatory mechanisms initially effective, then overwhelmed.

4) Intra-vascular hypovolaemia. Reduced venous return. Reduced coronary artery filling. Reduced myocardial
function. Reduced blood pressure. Reduced vital organ perfusion

5) Reduced vital organ perfusion
* Vital organ ischaemia
* Vital organ dysfunction

6) Peripheral vasoconstriction to re-direct blood to vital organs.

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40
Q

Summary of findings from examination / vitals examination

A
  • Tachycardia
  • Warm or cold peripheries (Capillary refill
  • time. CRT)
  • BP maintained (compensated)
  • Low BP, compensatory mechanisms overwhelmed. (Decompensated)
  • Reduced organ perfusion: Tissue hypoxia. Brain, heart, lungs, kidneys and liver.
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41
Q

How can sepsis affect the lungs ?

A

Increased metabolic demand leading to :

P A R R I S

  • Pulmonary oedema
  • Acute respiratory distress syndrome (ARDS)
  • Respiratory failure
  • rapid breathing (hyperventilation)
  • Increased respiratory rate (tachypnoea)
  • Shortness of breath (dyspnea)
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42
Q

Effects on tissues from sepsis ?

A
  • tissue iscaehmia
  • tissue hypoxia
  • inefficient anaerobic respiration in tissues: reduced ATP
  • cell and enzyme dysfunction
  • tissue/organ dysfunction/ necrosis
  • metabolic (lactic) acidosis
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43
Q

effects on renal from sepsis ?

A
  • Reduced intravascular volume
  • Reduced blood pressure
  • Reduced renal blood flow
  • Reduced biochemical homeostasis
  • Acute renal failure
44
Q
  1. What does the brain need for normal cerebral perfusion ?
  2. If not: what happens ?
  3. Good indicator of =
  4. ACVPU = ?
  5. what may occur ?
A
  1. oxygen, CO2 removal, glucose, normal pH, normal chemistry
  2. confusion/ altered level of consciousness, lethargic/ irritable
  3. being unwell
  4. ‘Alert’, ‘Confusion’, ‘Voice’, ‘Pain’, ‘Unresponsive
  5. long term neurological sequelae
45
Q

What does the brain need for normal cerebral perfusion ?

A
  • oxygen
  • carbon dioxide removal
  • normal pH
  • glucose
  • normal chemistry
46
Q

If there is decreased cerebral perfusion what may there be ?

A
  • confusion
  • altered level of consciousness
  • delirium
  • lethargy
  • irritability
47
Q

What damages the vascular endothelium leading to widespread activation of the coagulation system and widespread intra-vascular clot formation ?

A
  • lipopolysaccharides from gram negative bacteria
  • TNF
  • other pro-inflammatory cytokines
48
Q

depletion of clotting factors leads to what ?

A

haemorrhagic tendency

49
Q

coagulation occurs at the same time as what ?

A

haemorrhage

50
Q
  1. Damage to vascular endothelium happens as a result of what ?
  2. this damage leads to widespread activation of what ?
  3. this leads to a depletion of …
A
  1. TNF, LPS and other pro-inflammatory cytokines
  2. the coagulation system and clot formation
  3. clotting factors and haemorrhagic tendency
51
Q

which coagulation pathway is triggered in sepsis ?

A

extrinsic pathway activation (tissue factor pathway )

52
Q

Sepsis pathogenesis summary
1. …I…. the body tissues

  1. ….II..activated with the activation of …III…. and mediators associated with an..IV….response
  2. increased …V…permeability and ..VI… interrupt the body’s ability to provide adequate …VII…, oxygen and nutrients to the tissues and cells
  3. …VIII… and ….IX… cytokines released during the inflammatory response and activate the ..X… system
  4. resulting in ..XI… coagulation and because of ..XII… factors and platelet …XIII.. leading to ..XIV.. coagulation and ..XV… haemorrhage
A

I = microorganisms invade
II = immune response
III = biochemical cytokines
IV = inflammatory
V = capillary
VI = vasodilation
VII = perfusion
VIII / IX = pro-inflammatory / anti-inflammatory
X = coagulation
XI = uncontrolled
XII = clotting factors
XIII = destruction
XIV = intravascular
XV = extravascular

53
Q

PMH of sepsis

A

risk factors such as being immunocompromised

54
Q

TH of sepsis

A

allergy, antiboitic allergy, vaccination status

55
Q

SOH of sepsis

A

contact (eg GAS) , overseas travel

56
Q

List 12 groups of people that woudl be classified as vulnerable patients of patients

A
  • Immunocompromised patients (people with weakened immune systems): Chemotherapy, immuno- modulator therapy, Steroids.
  • people with Chronic conditions e.g. Diabetes, cancer, lung disease, kidney disease
  • Babies and children (children under 1 year)
  • The elderly (adults 65+)
  • Pregnancy
  • Post-operative
  • people with recent severe illness or hospitalisation
  • Pre-existing disease
  • Previous sepsis survivors
  • Indwelling lines and catheters
  • IVDA = intravenous drug abuser
  • People with communication/learning difficulties
57
Q

symptoms of sepsis ?

A
  • Fever. Shivers/rigors. Headaches, muscle aches/pains.
  • Feels generally unwell. Important
  • Carers feel that patient is not their usual self. Subtle but important. * Loss of appetite. Nausea. Vomiting.
  • Rapid breathing
  • Flushed. Warm/cold peripheries, skin mottling, pale.
  • Rash. Non-blanching. (Petechiae/purpura)
  • Altered level of consciousness, irritable, lethargic, convulsions
  • Reduced urine output
  • Systems review to find source/focus
58
Q

What are the key signs and assessments for each component of the ABCDEG approach in evaluating a patient for potential sepsis?

G being don’t ever forget glucose in this situation

A
  • Airway
  • breathing
  • circulation
  • disability
  • exposure / secondary survey
59
Q

In a patient with sepsis what is checked for Airway ?

A

open / obstructed / at risk

60
Q

In a patient with sepsis what is checked for Breathing ?

A
  • tachypnoeic
  • increased work of breathing
  • expiratory grunting
  • low saturations
61
Q

In a patient with sepsis what is checked for Circulation ?

A
  • tachycardia
  • warm/cold peripheries
  • BR
  • CRT (capillary refill time)
  • pale
  • mottled skin
62
Q

In a patient with sepsis what is checked for Disability ?

A
  • ACVPU/GCS (glasgow coma scale)
  • confused etc. urine output
63
Q

What is ACVPU ?

A

‘Alert’, ‘Confusion’, ‘Voice’, ‘Pain’, ‘Unresponsive

64
Q

What is GCS ?

A

Glasgow coma scale = objectively describe the extent of impaired consciousness in all types of acute medical and trauma patients

65
Q

In a patient with sepsis what is checked for Exposure/secondary survey ?

A

for focus of infection eg rash. Head
to toe, back to front. Temperature (low or high)

66
Q

what must not be forgotten to check in sepsis ?

A

glucose:
* ABG (arterial blood gases)
* lactate
* bloods
* cultures

67
Q

Investigations for sepsis

A
    • Blood gas: Glucose, pH, pCO2, lactate, chemistry, Hb.
    • Blood culture and other cultures: CSF. Swabs.
  • Sputum. Covid.
    • Full Blood Count (WCC, neutrophils, platelets)
    • Blood clotting
    • C Reactive Protein
    • Urea and Electrolytes.
    • LFT’s. Amylase.
    • Clotting screen
    • CXR, abdominal ultrasound etc depending upon clinical suspicion
68
Q

When it comes to sepsis , IT’S ABOUT TIME, therefore what should be watched for ?

A

TIME :
TEMPERATURE - higher or lower than normal
INFECTION - may have signs and symptoms of an infection
MENTAL DECLINE - confused, sleepy, difficult to rouse
EXTREMELY ILL - ‘I feel like I must die’ severe pain or discomfort

69
Q

Symptoms in children ?

A
  • Is breathing very fast
  • has a ‘fit’ or convulsion
  • looks mottled, bluish, or pale
  • has a rash that does not fade when you press it
  • is very lethargic or difficult to wake
  • feels abnormally cold to touch
70
Q

What does the acronym SEPSIS stand for as ‘an adult may have sepsis if they show any of these signs’?

A

Slurred speech or confusion
Extreme shivering or muscle pain
Passing no urine (in a day)
Severe breathlessness
It feels like you’re going to die
Skin mottled or discoloured

71
Q
  1. What does NEWS stand for ?
  2. What does it involve ?
A
  1. National early warning score
  2. respiratory, oxygen saturation , temperature, systolic blood pressure, pulse rate, level of consciousness
72
Q

What is scoring system is used to quantify severity or to predict outcome of sepsis ?

A
  • sequential organ failure assessment score (SOFA)
  • SIRS : systemic inflammatory response score
  • qSOFA: quick seqeuntial organ failure assessment
73
Q

what 6 systems are observed when quantifying severity or predicting outcome of sepsis ?

A

respiratory
coagulation
hepatic
cardiovascular
CNS
renal

74
Q

What does the SIRS criteria involve ? (two or more necessary)

A
  • 36 > temperature > 38
  • resp rate > 22/min
  • heart rate > 90 bpm
  • 4000 > white cell count > 12 000
75
Q

What does the qSOFA criteria involve ? (two or more necessary)

A
  • systolic blood pressure < 100mmHg
  • respiratory rate > 20/min
  • glasgow coma scale </= 14
76
Q

What is SOFA score, what is its relevance in sepsis ?

A

Sequential Organ Failure Assessment Score
- 0-24 points
- Higher the score, the worse it is
- In sepsis, organ dysfunction can be identified as an acute change in total SOFA score >2 points due to the infection

77
Q

Management for sepsis involves the sepsis 6 what is this ?

A
  1. Take cultures
  2. Take lactate level
  3. Take urine output measurement
  4. Give O2
  5. Give IV antibiotics
  6. Give IV fluids
78
Q

If any red flag of sepsis is present what should be started in management?

A

Sepsis 6 :
1. give high-flow oxygen
2. take blood cultures
3. give IV antibiotics
4. give a fluid challenge
5. measure lactate
6. measure urine output

all actions must be completed within one hour of sepsis diagnosis

79
Q

what are the 9 red flags for sepsis ?

A
  • objective evidence of new or altered mental state
  • systolic BP < = 90 mmHg (or drop of >40 from normal)
  • heart rate > = 130 per minute
  • respiratory rate > = 25 per minute
  • needs O2 to keep SpO2 > = 92 % (88% in COPD)
  • non-blanching rash/ mottled/ ashen/ cyanotic
  • lactate >= 2 mmol/ L
  • recent chemotherapy
  • not passed uring in 18 hours (less than (<) 0.5ml/kg/hr if catheterised)
80
Q

What shouldn’t be delayed with sepsis ?

A

antibiotics

81
Q

What antibiotics should be given to someone with sepsis ?

A
  • full dose
  • intravenous
  • bactericidal
  • broad spectrum antibiotics based upon likeliest (but at this time unknown) pathogen
  • empirical at first
82
Q

Antibiotics for sepsis if…
community acquired ?

A
  • piperacillin/tazobactam
  • or cefuroxime
  • or ceftriaxone
83
Q

Antibiotics for sepsis if…
MRSA suspected alongside the antibiotics for community acquired

A

add vancomycin

84
Q

Antibiotics for sepsis if…
alongside community acquired if anaerobic infection is suspected what should be added?

A

metronidazole

85
Q
  1. If sepsis is hospital acquired what antibiotics may be used ?
  2. If suspect MRSA
  3. If suspect anaerobic infection
A
  1. a broad-spectrum antipseudomonal beta-lactam antibacterial e.g. Piperacillin/tazobactam or ceftazidimine
  2. vancomycin
  3. metronidazole
86
Q

With sepsis :
1. what should be treated ?
2. who should be kept informed ?

A
  1. pain and other symptoms
  2. patient/family , public health
87
Q

Apart from antibiotics , what other support in terms of airway?

A

monitor and protect if needed

88
Q

Apart from antibiotics , what other support in terms of breathing ?

A
  • oxygen to keep saturation over 92%
  • ventilatory support
89
Q

Apart from antibiotics , what other support in terms of circulation ?

A
  • intravenous boluses of 0.9% (“normal”) saline
  • reassess
  • repeat
  • inotropes
  • ventilatory support
90
Q

Apart from antibiotics , what other support in terms of disability ?

A
  • monitor neurology
  • GCS (glasgow coma scale)
  • urine output
  • acid base
  • chemistry etc
91
Q

Apart from antibiotics , what other support in terms of exposure ?

A

anthying from secondary survey (e.g. systemic examination , temperature)

92
Q

Apart from antibiotics , what other support in terms of DEFglucose ?

A

treat hypoglycaemia / hyperglycaemia

93
Q

9 complications associated with sepsis ?

A
    • Death
    • Organ failure. Lungs, heart, kidneys, liver.
    • Limb loss
    • Malnutrition
    • Immuno-suppression. Reactivation of dormant disease. HSV. VZV.
    • Hospital acquired infections.
    • Ongoing concentration/other neurological sequelae
    • PTSD
    • Chronic pain and fatigue
94
Q

7 methods of prevention for sepsis ?

A
    • Vaccination
    • Hygiene, aseptic technique
    • High index of suspicion and early intervention
    • Recognition of at-risk groups
    • Contact tracing
    • Elimination of nasal carriage
    • Antibiotic stewardship
95
Q

most common infectious cases of sepsis ?

A

pneumonia , urinary tract

96
Q

Why if gram negative bacteria e.g. E.coli the most common cause of developing sepsis?

A

lipopolysaccharide present on GN bacteria activates macrophages and NK cells

97
Q
  1. CRT = ?
  2. It’s the time taken for….after being pressed
  3. it’s a marker of …. that worsens during…..
  4. An abnormal CRT in …. patients after ….. resuscitation has been associated with poor outcome
A
  1. capillary refill time
  2. vessels in the mucous membranes to return to normal
  3. peripheral perfusion , circulatory failure
  4. septic shock, ICU-based
98
Q

What is a common complication of sepsis?
a) Acute kidney injury
b) Hepatic failure
c) Pulmonary hypertension
d) Cerebral haemorrhage
e) None of the above

A

a) Acute kidney injury

99
Q

What symptom is not associated with sepsis?
a) Fever
b) Mottled skin
c) Bradycardia
d) Tachypnoea
e) Delirium/confusion

A

c) Bradycardia

100
Q

What is the recommended time frame for administering antibiotics in sepsis?
a) Within 6 hours of recognition
b) Within 12 hours of recognition
c) Within 24 hours of recognition
d) Within 48 hours of recognition

A

a) Within 6 hours of recognition

101
Q

Which of the following is a common laboratory finding in sepsis?

a) Hypernatremia
b) Hyponatremia
c) Hypoglycaemia
d) Hyperglycaemia

A

d) Hyperglycaemia

102
Q

Which is not a common site of infection leading to sepsis?
a) Urinary tract
b) Respiratory tract
c) Skin and soft tissue
d) Muscular
e) Endocarditis

A

d) Muscular

103
Q

Which of the following does not correctly describe the vascular changes to lipopolysaccharide?
a) Increased heart rate and stroke volume
b) Increased adhesion of white blood cells
c) Increased vascular permeability
d) Vasodilation
e) Reduced viscosity of blood

A

e) Reduced viscosity of blood

104
Q

What is the main reason for the failure of organs in sepsis?
a) Reduced blood flow (ischemia) due to hypotension
b) Direct cellular injury by bacterial toxin
c) Impairment of cellular oxygen utilisation
d) Overactivation of the immune system
e) Upregulated coagulation cascade activation

A

a) Reduced blood flow (ischemia) due to hypotension

105
Q

What causes sepsis-induced effects on the brain by increasing the permeability of the blood brain barrier?
a) Decreased fibrinogen levels
b) Increased C-reactive protein
c) Normal clotting function
d) Prolonged activated partial thromboplastin time
e) Increased platelet count

A

b) Increased C-reactive protein

106
Q

What is the primary mechanism by which sepsis induces vasodilation and hypotension?
a) Increased systemic vascular resistance
b) Enhanced sympathetic tone
c) Overproduction of proinflammatory cytokines
d) Activation of the renin-angiotensin system
e) Stimulation of the parasympathetic nervous system

A

c) Overproduction of proinflammatory cytokines

107
Q

What is the significance of a decreasing platelet count in a patient with sepsis?
a) It indicates that the sepsis is resolving
b) It indicates that the patient is at higher risk for bleeding complications
c) It is a sign of sepsis-induced coagulopathy
d) It is a sign of dehydration
e) It indicates sepsis decompensation

A

c) It is a sign of sepsis-induced coagulopathy

infection (33 decks)

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