6. Sepsis Flashcards
What is sepsis
Caused by the microbial invasion of normally sterile parts of the body. Leads to life threatening organ failure due to deregulated host response
What are the stages of sepsis
SIRS
Sepsis - SIRS and infection
Severe sepsis- sepsis and organ failure
Septic shock- sepsis and hypotension
What is the clinical criteria for SIRS?
temperature >38 or <36
HR>90
RR>20 or paCO2<32
WBC>12,000 or <4,000 or >10% bands
What is septic shock?
Persisting vasopressors to maintain MAP>65mmHg and having a lactate>2mmol/l depsite adequate volume resuscitation
What can be used to determine a poor outcome from sepsis?
Hypotension systolic blood pressure <100mmHg
Altered Mental Status
Tachypnea RR>22
Why don’t you delay administering antibiotics in sepsis?
Every hour delay leads to an increase death rate of 7.6%
What defence does the body have against sepsis
Physical barrier- skin, mucosa, epithelial lining
Innate immune system- IgA in GI tract, dendritic cells/macrophages
Adaptive immune system- lymphocytes, immunoglobulins
How does sepsis originate?
Breach of integrity of host barrier whether physical or immunological
Organisms enter blood stream causing septic state
What pathophysiological symtoms do people with sepsis have?
Features consistent with immunosuppresion (delayed hypersensitivity, inability to clear infection, predisposition to nosocomial infection)
How does sepsis syndrome change over time?
phase 1- release of bacterial toxins
Phase two release of mediators
Phase 3. Effects of specific mediators
What is involved in the release of bacterial toxins?
bacteria release toxins based on their class:
Gram -ve
Gram +ve
Superantigens- staph. toxic shock syndrome
Strep exotoxins
What occurs in phase two- release of mediators in response to infections?
Effects of infections due to endotoxin release
Effects of infections due to endotoxin release
Mediator role on sepsis
How do endotoxins interact with mediators?
Depending on what mediators are relased the response can either be pro inflammatory or anti-inflammatory.
What can proinflammatory mediators do in phase 3?
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
What can anti-inflammatory mediators do?
Inhibit TNF alpha
Augment acute phase reaction
Inhibit coagulation system
Provide negative feedback to pro inflammatory mediators
What happens if you have too many pro inflammatory mediators?
Septic shock, multi organ failure, death
What happens if you have too many Anti inflammatory mediators?
Immune paralysis, organ failure and death
What effects how you present in sepsis?
Age,
co-morbidity,
immunosuppresion (HIV, drug induced, Congential)
Splenectomy
What are the general features of sepsis?
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
What clincical features would you find?
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
What are the sepsis 6?
Blood cultures
Blood lactate
Measure urine output
Oxygen Aim sats 94-98%
IV antibiotics
IV fluid challenge
Take 3 give 3
What could you potentially cram the night before exams?
Empirical antibiotic therapy- Slide 70
What influnces you rfacotrs when prescribing antibiotic therapy?
based on working diagnosis from history and exam Local antibiotic guidelines Consider allergy Consider previous MRSA, ESBL, CPE Consider Abx toxicity/interactions
When you should consider referrring to HDU?
Low BP responsive to fludis Lactate>2 despite fluid resus Elevated creatinine Oliguria Liver dysfunction
