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Year 3 Infection > 6. Sepsis > Flashcards

6. Sepsis Flashcards

1
Q

What is sepsis

A

Caused by the microbial invasion of normally sterile parts of the body. Leads to life threatening organ failure due to deregulated host response

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2
Q

What are the stages of sepsis

A

SIRS
Sepsis - SIRS and infection
Severe sepsis- sepsis and organ failure
Septic shock- sepsis and hypotension

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3
Q

What is the clinical criteria for SIRS?

A

temperature >38 or <36
HR>90
RR>20 or paCO2<32
WBC>12,000 or <4,000 or >10% bands

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4
Q

What is septic shock?

A

Persisting vasopressors to maintain MAP>65mmHg and having a lactate>2mmol/l depsite adequate volume resuscitation

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5
Q

What can be used to determine a poor outcome from sepsis?

A

Hypotension systolic blood pressure <100mmHg
Altered Mental Status
Tachypnea RR>22

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6
Q

Why don’t you delay administering antibiotics in sepsis?

A

Every hour delay leads to an increase death rate of 7.6%

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7
Q

What defence does the body have against sepsis

A

Physical barrier- skin, mucosa, epithelial lining
Innate immune system- IgA in GI tract, dendritic cells/macrophages
Adaptive immune system- lymphocytes, immunoglobulins

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8
Q

How does sepsis originate?

A

Breach of integrity of host barrier whether physical or immunological

Organisms enter blood stream causing septic state

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9
Q

What pathophysiological symtoms do people with sepsis have?

A

Features consistent with immunosuppresion (delayed hypersensitivity, inability to clear infection, predisposition to nosocomial infection)

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10
Q

How does sepsis syndrome change over time?

A

phase 1- release of bacterial toxins
Phase two release of mediators
Phase 3. Effects of specific mediators

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11
Q

What is involved in the release of bacterial toxins?

A

bacteria release toxins based on their class:
Gram -ve
Gram +ve
Superantigens- staph. toxic shock syndrome
Strep exotoxins

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12
Q

What occurs in phase two- release of mediators in response to infections?

A

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

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13
Q

How do endotoxins interact with mediators?

A

Depending on what mediators are relased the response can either be pro inflammatory or anti-inflammatory.

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14
Q

What can proinflammatory mediators do in phase 3?

A

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

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15
Q

What can anti-inflammatory mediators do?

A

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

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16
Q

What happens if you have too many pro inflammatory mediators?

A

Septic shock, multi organ failure, death

17
Q

What happens if you have too many Anti inflammatory mediators?

A

Immune paralysis, organ failure and death

18
Q

What effects how you present in sepsis?

A

Age,
co-morbidity,
immunosuppresion (HIV, drug induced, Congential)
Splenectomy

19
Q

What are the general features of sepsis?

A

Fever >38 (chills, rigors, flush, cold sweats, night sweats)
Hypothermia <36 (children, elderly, immune suppressed)
Tachycardia>90bpm
tachypnoea>20
Altered mental state
Hyperglycaemia >8mmol/l in non diabetics

20
Q

What clincical features would you find?

A 
Leucocytosis (WCC>12,000/ml)
Leucopenia (WCC<4,000/ml)
Normal WCC with greater than 10% immature forms
High CRP
High prolactin
hypotension systoic <90mmHg)
Oliguria
Increased creatinine
Ileus
High lactate
Skin mottling and reduced capillary perfusion
21
Q

What are the sepsis 6?

A

Blood cultures
Blood lactate
Measure urine output

Oxygen Aim sats 94-98%
IV antibiotics
IV fluid challenge

Take 3 give 3

22
Q

What could you potentially cram the night before exams?

A

Empirical antibiotic therapy- Slide 70

23
Q

What influnces you rfacotrs when prescribing antibiotic therapy?

A 
based on working diagnosis from history and exam
Local antibiotic guidelines
Consider allergy
Consider previous MRSA, ESBL, CPE
Consider Abx toxicity/interactions
24
Q

When you should consider referrring to HDU?

A 
Low BP responsive to fludis
Lactate>2 despite fluid resus
Elevated creatinine
Oliguria
Liver dysfunction
25
Q

When should you refer to ITU?

A

Septic shock, multi-organ failure, requires sedation, intubation, ventilation

26
Q

What is a good way of managing pneumonia severity?

A 
Confusion
Urea raised
Respiratory rate raised
Blood pressure low
65 and over

0-1 not great
2- intermediate
3-5 oh deary dear

27
Q

How does curb65 affect treatment of pneumonia?

A

Low- home/hospital amoxicillin
moderate- amoxicillin and clarithromycin
High- co-amoxiclav, clarithromycin 500mg

Year 3 Infection (15 decks)

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