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Sepsis Flashcards

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1
Q

What does SIRS mean?

A

Systemic inflammatory response syndrome.
Various causes not just infection.

A set of clinical features that may indicate infection.

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2
Q

Symptoms of SIRS

A

Temp >38 or <36
HR >90 bpm
RR >20/min or PaCO2 <4.3 kPa

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3
Q

Sepsis

A

SIRS + infection

Infection with features indicating significant risk of deterioration/death.
Benefit from early antibiotics.

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4
Q

Septic shock

A

Sepsis with hypotension not corrected by fluid resuscitation.

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5
Q

Bacteraemia

A

Circulation of bacteria in the blood.

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6
Q

Septicaemia

A

Blood poisoning, especially that caused by bacteria or their toxins

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7
Q

Clinical syndromes causing sepsis

A

Pneumonia > intra-abdominal > UTI > other

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8
Q

Bugs causing community acquired sepsis

A

Strep. pneumoniae
Strep. pyogenes
Stap. aures
E. coli

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9
Q

Bugs causing healthcare-associated sepsis

A

S. aures

E.coli

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10
Q

Host risk factors for sepsis

A 
Increased risk of acquiring infection.
Impaired immune response.
Pre-existing organ dysfunction.
Extremes of age.
Genetic factors.
Timeliness of treatment.
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11
Q

Environmental factors that increase risk of infection

A

Hygiene

Sanitation

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12
Q

Conditions that increase risk of infection

A

COPD: inc respiratory infections

Lymphoedema: inc soft tissue infections

Urethral catheter: inc urinary tract infections

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13
Q

Factors causing impaired immune response

A

Congenital immunodeficiency syndromes.
HIV/AIDs.
Splenectomy, functional hyposplenism.
Iatrogenic (chemotherapy or immunosuppressant drugs).
Chronic conditions (malignancy, diabeter, malnutrition).

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14
Q

Why are extremes of age vulnerable to sepsis?

A

Old: immune senesence, comorbidity

Yourn: immature immunity, limited physiological reserve

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15
Q

Gender more at risk of sepsis

A

Male

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16
Q

Initiation of innate immune response

A

Pattern recognition receptors (PRRs) on leukocytes recognise PAMPs and DAMPs/alarmins.
PRR activation causes cytokine release (TNFalpha, IL-1, IL-8) which leads to fever, tachycardia, leukocytosis, acute-phase response (high CRP and procalcitonin).

Cascade of leukocyte, complement and coagulation activation.

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17
Q

PAMP

A

Pathogen associated molecular pattern

Structures are highly conserved among microbes.
e.g peptioglycan, LPS, lipoteichoic acid, fermylmethionine, flagellin.

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18
Q

DAMP

A

Damage associated molecular patterns/alarmins

Endogenous molecules released from injured cells (DNA, RNA, histones).
Also released in sterile injury.

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19
Q

What are bacterial ‘super-antigens’

A

Things that directly trigger cytokine release from T-cells.

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20
Q

Examples of bacterial ‘super-antigens’

A

Staphylococcaltoxic shock syndrome from toxic shock syndrome toxin-1 (TSST-1).
Streptococcal toxic shock syndrome with erythrotoxins.
Fulminant septic shock often with erythematous rash.

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21
Q

Causes of acute organ dysfunction associated with sepsis

A 
Tissue hypoperfusion (vasodilation, dysregulated perfusion, hypotension).
Vascular endothelial dysfunction (loss of barrier function, interstitial oedema, intravascular hypovolaemia).
Mitochondrial dysfunction (oxidative stress).
Impaired tissue oxygenation (leads to tissue death and further inflammation released).
Impaired coagulation (tissue factor release, decrease in anti-coagulants, increase in fibrin leading to microvascular thrombosis/DIC).
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22
Q

Mechanism of ARDS

A

Acute respiratory Distress Syndrome

Non-cardiogenic pulmonary oedema.
Increased vascular permeability.
Hypoxaemia and bilateral pulmonary infiltrates.

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23
Q

Mechanism of cardiovascular collapse (spetic shock)

A

Vasodilation (e.g endotoxin).
Hypotension.
Tissue hypoperfusion (inc lactate).
Myocardial damage/impairment (inc troponin).

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24
Q

Mechanism of AKI

A

Acute Kidney Injury

Hypotension +/- hypovolaemia.
Direct inflammatory injury.

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25
GI condition that increases liklihood of sepsis
``` Paralytic ileus (muscles not working) can cause a blockage. Possible leak of organisms/toxins into circulation. ```
26
Clinical presentation of sepsis
``` Shivering, fever, very cold Extreme pain or general discomfort ('worst ever') Pale or discolored skin Sleepy/difficult to wake up, confused I feel like I might die SOB ```
27
Red Flag sepsis signs
INFECTION + one of: - HR >130 - SBP <90 (MAP<65, decrease SBP by >40) - RR >25 - Oxygen sat <92% or need more that 40% FiO2 to maintain it - Lactate >2 - New altered mental state - Purpuric rash, mottled/ashen - Cyanosed skin, lips or tongue - Poor urine output (not passed urine >18hr or <0.5 ml/kg/hr) - Non-blanching rash
28
Sepsis 6
``` Blood cultures Urine output Fluids Antibiotics Lactate Oxygen (keep above 94%) ```
29
False negative
Patient has condition X but test tells you they don't. Sensitivity
30
False positive
Patient doesn't have condition X but test tells you they do. Specificity
31
Positive predictive value
Given a positive test result how likely is the patient to have the disease.
32
Negative predictive value
Given negative test result how likely is the patient not to have disease.
33
Examples of sterile sites
``` CSF Blood/bone marrow Lower respiratory tract Bladder/kidneys Bone/joints Pleura/peritoneum Most surgical specimens ```
34
Examples of non-sterile sites
``` Mouth/nasopharynx Upper respiratory tract Skin GI tract Urethra Female GU tract ```
35
Gram stain
Stain with crystal violet and fix with iodine. Elude the blue stain with acetone for 2 seconds. Thin peptidoglycan wall (gram negative) allows stain to leech out. Counterstain with a red dye, such as neutral red or carbol fuschin.
36
Non-spore forming gram positive
Listeria | Corynebacterium
37
Spore forming gram positive
Clostridium | Bacillus
38
Facultative anaeroes
Prefer aerobic respiration but can switch to anaerobic fermentation. e.g Staphylococcus spp, streptococcus spp, E.coli
39
Obligate aerobes
Require oxygen e.g pseudomonas, mycobacterium tuberculosis
40
Obligate anaerobes
Killed by oxygen. e.g bacteriodes, clostridium spp
41
Microaerophillic
Require small amount of oxygen to survive 2-10%. e.g camphlobacter spp.
42
MacConkey agar
Bile salts (suppress most gram +ves). Lactose (Nutrition source for lactose fermenters-> pH lowers). Peptone (Nutrition source for non-lactose fermenters-> pH increases). Neutral red (Turns pink as pH lowers).
43
Catalase test
hydrogen peroxide turned to water and oxygen within seconds if enzyme present.
44
Coagulase test
Fibrinogen to fibrin (4 hours).
45
Things that Staph. aures causes
Skin and soft tissue infections. Endocarditis Septic arthritis Osteomyelitis
46
First line treatment for MSSA
flucloxacillin
47
First line treatment for MRSA
Vancomycin
48
ESBL
Extended spectrum beta lactamase
49
CPE
Carbapenemase producing enterobacteriacae
50
Enterobacteriacae
Gut commensals, grow on MacConkey agar. e.g E.coli (UTI, biliary sepsis, neonatal meningitis) Klebsiella (UTI, biliary, LRTI) Enterobacter (HAI) Salmonella Non-typhoidal (gastroenteritis, sepsis, osteomyelitis) S.typhi/paratyphi (enteric fever)
51
What causes a green film, HAI?
Pseudomonas aeruginosa
52
acute-phase response markers
high CRP and procalcitonin
53
What does cytokine release cause?
fever tachycardia leukocytosis acute-phase response
54
Definition of severe sepsis
sepsis + end-organ damage
55
Definition of endovascular infection
Infection of vascular endothelium; either arterial or venous
56
Definition of endocarditis
Endovascular infection involving the | heart (either heart valves and/or endocardium)
57
Infective endarteritis
Infection of arterial endothelium, most commonly aorta
58
Risk factors for endocarditis
• Prosthetic heart valves – Increased risk with metal valves and 1st yr after implantation – Overall risk: 1% per patient per year • Congenital / rheumatic heart disease – Not isolated MVP/ASD – Mitral > Aortic > Triscuspid > Pulmonary • Previous history of endocarditis • PWID • Haemodialysis / long lines • Poor dentition
59
PWID
People who use IV drugs
60
Pathological features of endocarditis
``` • Damaged endothelium – Platelet and fibrin deposition – Bacteria in bloodstream may adhere e.g. fibronectin binding of S. aureus • Local damage – Leaky valves – Ruptured chordae – Ring abscesses – ‘Ball-valve’ obstruction • Distant emboli • Sepsis syndrome ```
61
Clinical features of endocarditis
• Often non-specific, ‘grumbling’: malaise, fever/sweats, anorexia, weight loss • Symptoms usually start within 2 weeks of bacteraemia – More acute with Staph aureus • Indolent cases – ‘Subacute bacterial endocarditis’ (SBE) – Usually lower grade pathogens (coagulase negative staphylococci, Strep viridans) • May present acutely with sepsis / cardiac failure / multiorgan failure – Medical and/or surgical emergency • Embolic phenomena (brain, lungs, peripheries) • Vasculitic / immunological phenomena
62
Features of left-sided endocarditis (embolic)
Infarction (stroke) Brain abscess Splinter haemorrhage Janeway lesions (flat, haemorrhagic, painless)
63
Features of right-sided endocarditis (embolic)
Lung abscess | Multiple septic emboli in lungs
64
Investigations for endocarditis
- Multiple sets of blood cultures (off antibiotics) - TTE - TOE
65
What does TTE stand for?
Trans-thoracic echo (TTE): | identifies 50-60% of endocarditis
66
What does TOE stand for?
Trans-oesophageal echo (TOE): | identifies 90% of endocarditis
67
Causitive agents of endocarditis
``` Staphylococci (42%) -S. aureus -Coagulase-negative Staph (CoNS) Streptococci (34%) -Strep viridans (alphaa haem strep) -Streptococcus bovis Enterococci (8%) E. faecalis; E. faecium ‘HACEK’ organisms (3%) Streptococcus pneumoniae (1%) Other bacteria (<1%) Fungi (< 0.5%) Culture negative endocarditis (6%) ```
68
HACEK
``` Haemophilus Actinobacillus / Aggregatibacter Cardiobacterium Eikenella Kingella ```
69
Causes of culture-negative endocarditis
Approx 5% of cases Antibiotics Fastidious/difficult to culture organisms: ``` – Coxiella burnetti (Q fever) – Chlamydia sp – Bartonella sp – Legionella – Mycoplasma ```
70
Treatment of endocarditis caused by viridans streptococci
- 4 weeks of benzylpenicillin (penicillin G) | - together with 2 weeks of gentamicin
71
Treatment of endocarditis caused by enterococci
- 4 weeks of amoxicillin (or vancomycin) | - together with 2 weeks of gentamicin
72
Treatment of endocarditis caused by coagulase-negative staphylococci
6 weeks vancomycin
73
What should you do to monitor for the development of complications of endocartitis?
* Regular ECG * Repeat echocardiogram * Audiometry if receiving regular gentamicin * Renal function / monitor eGFR * LFTs if on high dose beta lactam / rifampicin
74
What is arteritis?
The inflammation of walls of arteries
75
What is infective endarteritis?
Bacterial or other infection of intima layer of arteries.
76
Bacteria causing infective endarteritis
Salmonella and E.coli common in aorta Staphylococcus aures in other vessels

Microbiology (4 decks)

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