Sepsis and Septic Shock Flashcards

1
Q

what is the definition of sepsis?

A

is defined as life-threatening organ dysfunction caused by dysregulated host response to infection

Organ dysfunction can be identified as an acute change in total SOFA score >2 points consequent to the infection

SOFA score >2 reflects an overall mortality risk of approximately 10% in a general hospital population with suspected infection

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2
Q

what is the traditional model of sepsis?

A
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3
Q

what is the definition of septic shock?

A

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
Patients with septic shock have a hospital mortality of 40%

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4
Q

Patients with suspected infection who are likely to have a prolonged ICU stay or die in the hospital can be promptly identified with a ____?

A

qSOFA

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5
Q

what does qSOFA stand for?

A

hypotension systolic bp <100

altered mental state

tachypnea RR >22/min

score of >2 criteri suggests greater risk of poor outcome

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6
Q

what is the sepsis 6?

A
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7
Q

what defences does the body have against sepsis?

A

Physical barrier – skin, mucosa, epithelial lining

Innate immune system – IgA in gastrointestinal tract, dendritic cells / macrophages

Adaptive immune system – lymphocytes, immunoglobulins

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8
Q

describe the pathophysiology of sepsis?

A

Uncontrolled inflammatory response

Patients with sepsis have features consistent with immunosuppression:
Loss of delayed hypersensitivity
Inability to clear infection
Predisposition to nosocomial infection

Probable change of the sepsis syndrome over time
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

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9
Q

what are three phases in the pathogenesis of sepsis?

A

Release of bacterial toxins
Release of mediators
Effects of specific excessive mediators

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10
Q

what is phase one of sepsis?

A

Bacterial invasion into body tissues is a source of dangerous toxins

May or may not be neutralised and cleared by existing immune system

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11
Q

what are commonly released toxins in phase one?

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

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12
Q

what is phase two of sepsis?

A

Release of mediators in response to infection

Effects of infections due to endotoxin release
Effects of infections due to exotoxin release
Mediator role on sepsis

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13
Q

what is endotoxin release?

A

LPS needs an LPS-binding protein to bind to macrophages

LTA do not need such proteins

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14
Q

what is exotoxin release?

A

Pro-inflammatory response

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

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15
Q

what is the role of mediators in sepsis?

A

Two types of mediators can be released - Th1, Th2

Pro-inflammatory mediators – causes inflammatory response that characterises sepsis

Compensatory anti-inflammatory reaction – can cause immunoparalysis

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16
Q

what is phase three of sepsis?

A

Effects of specific excessive mediators

17
Q

what role does pro inflammatory mediators have?

A

Promote endothelial cell – leukocyte adhesion
Release of arachidonic acid metabolites
Complement activation
Vasodilatation of blood vessels by NO
Increase coagulation by release of tissue factors and membrane coagulants
Cause hyperthermia

18
Q

what role do anti-inflammatory mediators have?

A

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

19
Q

why does there need to be a balance between various immune responses?

A
20
Q

what are clinical features of sepsis?

A
21
Q

what are general features of sepsis?

A

Fever >38oC – presenting as chills, rigors, flushes, cold sweats, night sweats, etc
Hypothermia <36oC – especially in the elderly and very young children (remember the immunosuppressed)
Tachycardia >90 beats/min
Tachypnoea >20 /min
Altered mental status – especially in the elderly
Hyperglycaemia >8mmol/l in the absence of diabetes

22
Q

what are 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

23
Q

what are hemodynamic variables in sepsis?

A

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

24
Q

what are 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

25
Q

what are tissue perfusion variables in sepsis?

A

High lactate
Skin mottling and reduced capillary perfusion

26
Q

what effect does the host have on sepsis presentation?

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

27
Q

what effect does an organism have on presentation of sepsis?

A

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

28
Q

55 year old gentleman
History of DM, smoker and IHD
Admitted through Emergency Department with fever, nausea, vomiting and abdominal pain x 4 hours

what examinations would you do?

A

Temp: 38.3oC
Resp rate: 24/ min
Pulse: 120 bpm
BP: 160/85
HS: normal
Chest: Clear
Abdomen: Tenderness in epigastrium, no rebound, BS present

29
Q

Temp: 38.3oC
Resp rate: 24/ min
Pulse: 120 bpm
BP: 160/85
HS: normal
Chest: Clear
Abdomen: Tenderness in epigastrium, no rebound, BS present

what investigations would you do?

A

WCC: 15,600/ml
Platelets: 240,000/ml
INR: 1.2
U&E: Normal
LFT: Bil 80; AAT 20; ALP 35; GGT 40
Lactate 2.2mmol/l
Glucose: 8.8mmol/l
CXR and AXR: normal

30
Q

WCC: 15,600/ml
Platelets: 240,000/ml
INR: 1.2
U&E: Normal
LFT: Bil 80; AAT 20; ALP 35; GGT 40
Lactate 2.2mmol/l
Glucose: 8.8mmol/l
CXR and AXR: normal

what treatment would you give?

A

Sepsis 6
Started on Amoxicillin, Gentamicin and Metronidazole for intra-abdominal sepsis
6 hours later patient failed to improve

31
Q

Sepsis 6
Started on Amoxicillin, Gentamicin and Metronidazole for intra-abdominal sepsis
6 hours later patient failed to improve

why might the patient have failed to improve?

A

Admitted with SIRS
On post-take round another blood test was carried out
Serum amylase 1450
Diagnosed as Acute pancreatitis
Antibiotics stopped and patient transferred to surgery for further management

32
Q

sepsis 6?

A
33
Q

why do we take three in the sepsis 6?

A

lood cultures - make microbiological diagnosis (30-50% positive)
- if spike in temperature, take 2 sets
Lactate – marker of generalised hypoperfusion/severe sepsis/poorer prognosis
Low Urine output – marker of renal dysfunction

34
Q

what antibiotics should a patient with sepsis be given?

A

Based on working diagnosis from History and Examination
Local antibiotic guidelines
BUT consider allergy
BUT consider previous MRSA, ESBL, CPE
BUT consider Abx toxicity/interactions

35
Q

what do different types of lactate show?

A

Type A - Hypoperfusion
Type B – Mitochondrial toxins, Alcohol, Malignancy, metabolism errors
Of available biomarkers, lactate has the most support to identify adverse outcomes

36
Q

how much iv fluids be given?

A

30ml/kg fluid challenge (expert opinion)
2.1L 70kg patient

37
Q

when should hdu referral be considered?

A

lactate >2 despite fluid resuscitation
Elevated creatinine
Oliguria
Liver dysfunction, Bil, PT, Plt
Bilateral infiltrates, hypoxaemia