Sepsis Flashcards
What is the definition of sepsis
SEPSIS 3 definition
‘A potentially life threatening organ dysfunction caused by dysregulated host response to infection’
The following terms are no longer used
1. SIRS
2. Severe Sepsis
3. Septicaemia
Hospital mortality in septic shock > 40%
How is Sepsis recognized or suspected in the ward? Sepsis 3 vs SSC Guidelines 2021
SEPSIS 3 2016:
qSOFA (quick SOFA) > 2 of:
- RR > 22
- SBP < 100
- GCS < 15
SSC Guidelines 2021
Recommends against using qSOFA as a single screening tool (leads to missed diagnoses and worse outcomes)
Includes Lactate. Raised lactate should prompt a thorough clinical assessment of the patient.
How is sepsis recognized or suspected in the ICU (why is this different)
SOFA score increase of 2 or more
(More complex patients)
Summarise the SOFA Score
CNS
- GCS 15 (0).
- GCS 13 - 14 (1)
- GCS 10 - 12 (2)
- GCS 6 - 9 (3)
- GCS < 6
CVS
- MAP > 70 (0)
- MAP < 70 no inotropes (1)
- Dopamine < 5 or Dobutamine any dose (2)
- Adrenalin < 0.1 ug/kg/min (3)
- Adrenalin > 0.1 ug/kg/min (4)
RSP
- PF >400 (0)
- PF 300 - 400 (1)
- PF 200 - 300 (2)
- PF 100 - 200 (3)
- PF < 100 (4)
RENAL
- Creat < 110 (0)
- Creat 110 - 170 (1)
- Creat 170 - 300 (2)
- Creat 300 - 440. UO < 500. (3)
- Creat > 440. UO < 200. or on dialysis (4)
LIVER
- TBR < 20 (0)
- TBR 20 - 32 (1)
- TBR 33 - 101 (2)
- TBR 102 - 204 (3)
- TBR > 204 (4)
COAGULATION
- Plts > 150 (0)
- Plts 100 - 150 (1)
- Plts 50 - 100 (2)
- Plts 20 - 50 (3)
- Plts < 20 (4)
Higher score - higher mortality (> 14 = 100%)
Define septic shock (Sepsis 3)
Circulatory, Metabolic and cellular derangement - Subset of sepsis
Vasoconstrictors for MAP < 65 after adequate fluid replacement
AND
Lactate > 2
MOrtality is > 40%
What are the Big 5 most likely sources of sepsis in a patient
- Lungs: “VAP’
- Abdomen
- Wound/Surgical site
- Lines
- Urinary tract
Summarise the pathophysiology of sepsis
Bacteria/Virus/Fungi/Protazoa
Cytokine Storm (TNFa, IL1. IL6)
(All initiated by the innate immune response)
1. Endothelial activation
2. Nitric Oxide generation
3. Microvascular damage with poor perfusion
4. Mitochondrial damage
Innate immune system activation
- Pathogen releases PAMPS (Pathogen associated molecular patterns)
- Recognised by receptors on immune cell surface: PRRs. Pathogen Recognition Receptors
- Genetic variability of the magnitude and pattern of response
- Inflammatory response can be perpetuated by DAMPS (Danger Associated Molecular Patterns) - Dead host cell fragments –> amplify response.
What is the main function of the endothelial glycocalyx
Prevents loss of fluid from the blood vessels
List typical ICU infections with low virulence
Acinetobacter
Stenotrophomonis
Candida
Reactivation of dromant viruses
- HSV
- CMV
Describe Sepsis effects on the CVS
- Hypovolaemia (glycocalyx failure)
- Vasodilatation/Vasoplegia
- Myocardial depression (High CO as low afterload with compensatory tachycardia)
- Receptor down regulation
- Cytokine mediated reduced Calcium movement
Summarise Emmanuel Rivers Early Goal Directed therapy in the treatment of severe sepsis and septic shock 2001.
Early (Emergency department) intervention
- Improve DO2 within 6 hours with IVF/Dobutamine keeping Hct > 30%.
- Noradrenalin for SBP < 90
- Target SvO2 > 70%
- Mortality 30% vs 46%
Name three studies consequent to the Rivers Study that contradicted the findings Rivers and suggest a reason why?
ProCESS 2014
ARISE 2014
ProMISe 2015
These three trials did not favour EGDT. It is possible that in these subsequent studies, that the control patients were also receiving established early resuscitation subsequent to the Rivers trial. i.e. most of these patients were also receiving 30ml/kg within the first 3 hours as ‘usual care’
How does Sepsis affect the respiratory system
- ARDS (Increase permeability of lung capillaries)
- Fluid and neutrophils in alveoli
- V:Q mismatch.
- Respiratory Failure and increase WOB
How are the kidneys affected by sepsis
Later on during ICU –> renal failure develops
Oliguria
ATN
–> Increased mortality!
How is the liver affected by sepsis
Septic shock –> extreme liver ischaemia –> long standing damage to liver–> Raised liver enzymes –> gradual rise in TBR with unresolved sepsis
Cirrhosis with septic shock –> indication to discontinue ICU
How does sepsis affect the brain
Cytokines cross BBB –> delirium.
Incidence is 23 - 71%
Cytokines cross BBB
Brain oedema
Hyperammonaemia
Neurotransmission altered
Long term cognitive dysfunction
Increased mortality
What is critical illness neuro-myopathy in sepsis
Usually starts after about a week
Axonal conduction defect
Neuromuscular junction affected
Myopathy
How does Sepsis 3 2016 and SSC Guidelines 2021 differ with regards to recommendations for initial fluid therapy in sepsis.
Sepsis 3 2016
- 30ml/kg within first 3 hours - strong recommendation
SSC Guidelines 2021
- 30 ml/kg first 3 hours - weak recommendation.
Summarise your initial evaluation of a patient suspected with sepsis/septic shock
INITIAL EVALUATION
- Acknowledgement that although this approach is systematic, in reality, most of the following occur simultaneously
- HHH ABCDE
- ANTIBIOTICS within 1st hour of recognition
- FLUIDS 30ml/kg first 3 hours of recognition
- Simultaneously investigate
1. Blood gas analysis with serum lactate
2. Blood cultures x 2 distinct sites.
3. Routine laboratory studies as per institution
4. Cultures from easily accessible sites (sputum/urine).
5. Imaging of suspected sources (CXR/US/CT/ECHO etc.)
Summarise the initial resuscitation of a patient with sepsis
IV FLUIDS
- Commence within 1st hour
- Complete within 3 hours
- 250 - 500 ml crystalloid (balanced solutions) boluses every 5 - 10 minutes titrated to dynamic parameters (PPV, SVV, CI, PLR), clinical parameters (CRT, MAP) and biochemical parameters (Lactate) and early signs of overload (discontinue at first suspicion of pulmonary oedema).
- Latest recommendation is that colloids are contraindicated in sepsis and septic shock
ANTIBIOTICS
- Empiric broad spectrum within 1 hour of sepsis recognition. If suspected must also cover fungi/viruses.
- If suspected gram negative sepsis: Two agents from different AB classes are recommended to ensure effective treatment of resistant organisms
What factors guide the choice of broad spectrum antibiotics in sepsis
- Patient history
- Comorbidities
- Immune function
- Clinical context
- Suspected site of infection
- Presence of invasive devices
- Gram Stain data
- Local prevalence and resistance patterns
When is an antifungal agent added empirically
In neutropaenic patients