Sepsis and septic shock Flashcards by Sophie C

What is sepsis (Definition)

meaning decay or decomposition.

Systemic illness caused by microbial invasion of normally sterile parts of the body

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What is the traditional model of sepsis and features of

SIRS >38 degrees, HR> 90, RR>20 OR PaCo2<32, WBC> 12,000
Sepsis = SIRS and Infection
Severe sepsis = Sepsis and End organ damage
Septic shock = severe sepsis and hypotension

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Examples of SIRS (3)

Pancreatitis
Burns
Trauma

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What is sepsis (medical)

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

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What is organ dysfunction

What SOFA score reflects an overall mortality risk?

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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What is septic shock (medical)

What values need to be maintained?

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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a qSOFA sepsis score

Hypotension - sys BP <100 mmHg
Altered mental status
Tachypnoea RR >22/min

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Importance of sepsis (4)

Common condition
Becoming more common
Increased morbidity
Increased mortality

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Survival in septic shock is based on

antimicrobial delay

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Features of the septic six?

temp 
HR
WCC
RR
MEN STATE
GLUCOSE

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Body’s defence against sepsis:
physical barrier:
Innate immune system:
Adaptive immune system:

skin, mucosa, epithelial lining
IgA in gastrointestinal tract, dendritic cells / macrophages
– lymphocytes, immunoglobulins

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Origin of sepsis

breach of integrity of host barrier, whether physical or immunological
Organism enters the bloodstream creating a septic state

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Pathophysiology of sepsis

Uncontrolled inflammatory response

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Patients with sepsis have features consistent with immunosuppression: - what are they? (3)

Loss of delayed hypersensitivity
Inability to clear infection
Predisposition to nosocomial infection

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What are the three phases in the pathogenesis of sepsis

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

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Phase 1: Release of bacterial toxins - features

name some commonly released toxins

Bacterial invasion into body tissues is a source of dangerous toxins

- 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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Phase 2: Release of mediators in response to infection - endotoxin release

LPS needs an LPS-binding protein to bind to macrophages

LTA do not need such proteins

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Phase 2: Release of mediators in response to infection - exotoxin release

Pro-inflammatory response

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

Phase 2: Release of mediators in response to infection: iator role in sepsis (Th1 vs Th2)

Two types of mediators can be released
Pro-inflammatory mediators – causes inflammatory response that characterises sepsis
Compensatory anti-inflammatory reaction – can cause immunoparalysis

Phase 3: Effects of specific excessive mediators - give features of pro-inflammatory mediators

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

Phase 3: Effects of specific excessive mediators - give features of anti-inflmmatory mediators

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

Septic shock with multi organ failure has a higher?

Pro-Inflammatory response

Immunoparalysis with uncontrolled infection and multiorgan failure has a higher?

Compensatory anti-inflammatory response

The clinical features of sepsis depends on a number of factors- what are they

Host
Organism
Environment

Organ dysfunction - clinical features

Altered consciousness Confusion Psychosis Tachypnoea PaO2: <70mmHg Sats: <90% Jaundice ↑ Liver enzyment ↓ Albumin ↑ PT ↓ Platelets ↑ PT/APTT ↓ Protein C ↑ D-dimer Tachycardia Hypotension Oliguria Anuria ↑ Creatinine

General features of sepsis and how they present

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

Inflammatory variables in sepsis (5)

``` Leucocytosis (WCC > 12,000/ml) Leucopenia (WCC < 4,000/ml) Normal WCC with greater than 10% immature forms High CRP High procalcitonin ```

Haemodynamic variables in sepsis (2)

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

Organ dysfunction variables in sepsis (7)

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

Tissue perfusion variables in sepsis (2)

High lactate | Skin mottling and reduced capillary perfusion

Effect of host on sepsis presentation (3) + examples

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

Effect of organism on presentation of sepsis

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

The sepsis 6

``` oxygen blood culture antibiotics fluid challenge lactate urine output ```

The sepsis 6 - 2A'S , 2b's and 2'cs

``` Air enriched with o2 Antibes after blood culture blod culture blood gas with lactate crystalloid bolus catheter if sep shock or severe sepsis ```

Why take blood cultures

make microbiological diagnosis (30-50% positive) | - if spike in temperature, take 2 sets

Lactate and low urine output are markers of

Lactate – marker of generalised hypoperfusion/severe sepsis/poorer prognosis Low Urine output – marker of renal dysfunction

What Antibiotics - 5 criteria for prescribing

``` 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 ```

Administer effective intravenous antimicrobials within the first hour of

of septic | shock (Grade 1B) and severe sepsis without septic shock (Grade 1C) as the goal of therapy.

Lactate - type A and B

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

IV fluids in sepsis

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

When to consider HDU referral

``` Low BP responsive to fluids Lactate >2 despite fluid resuscitation Elevated creatinine Oliguria Liver dysfunction, Bil, PT, Plt Bilateral infiltrates, hypoxaemia ```

When to consider ITU

Septic shock Multi-organ failure Requires sedation, intubation and ventilation

Patients with severe sepsis and septic shock may experience ineffective arterial circulation due to?

vasodilatation associated with infection or impaired cardiac output.

Fluid challenges require the definition of four components:- what are they

the type of fluid to be administered; 2) the rate of fluid infusion (e.g., 500 mL to 1,000 mL over 30 minutes); 3) the end points (e.g., mean arterial pressure of >65 mm Hg, heart rate of <110 beats per minute); and 4) the safety limits (e.g., development of pulmonary edema).