Sepsis and septic shock Flashcards

1
Q

define sepsis

A

Sepsis is defined as life-threatening organ dysfunction caused by dysregulated host response to infection, an organism enters the bloodstream creating a septic state.

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2
Q

define septic shock

A

Septic shock can be identified with a clinical construct of sepsis with persisting hypotension requiring vasopressors to maintain MAP >65mmHg and having a serum lactate of >2mmol/l despite adequate volume resuscitation

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3
Q

what does qSOFA consist of?

A

hypotension <100 systolic, altered mental status, tachypnea >22RR. A SCORE OF 2 OR MORE SUGGESTS A GREATER RISK OF A POOR OUTCOME

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4
Q

what is a SOFA score?

A

pao2, GCS, MAP, serum creatinine or urine output, bilirubin, platelet count.

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5
Q

despite adequate fluid resucitation when should you suspect sespis has progressed to septic shock?

A

vassopressors required to maintain MAP over 65mmhg, serum lactate over 2

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6
Q

how much does mortality increase for each hours delay of abx administration in septic shock?

A

7.60%

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7
Q

pathophysiology of sepsis

A

similar to immunosuppression: loss of hypersensitivity, inability to clear infection, predisposition to nosocomial infection

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8
Q

what are the 3 phases in the pathogenesis of sepsis?

A

release of bascterial toxins, release of mediators, effects of specific excessive mediators

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9
Q

describe what happens in phase 1

A

Bacterial invasion into body tissues is a source of dangerous toxins, May or may not be neutralised and cleared by existing immune system

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10
Q

what are commonly released toxins

A

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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11
Q

describe what happens in phase 2

A

effects of infection due to endo/exo toxin release, mediator role on sepsis (endo - LTA don’t need binding proteins to bind to macrophages) (exo - pro-inflammatory response)

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12
Q

what do proinflammatory mediators do? (inflammatory response that characterises sepsis)

A

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

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13
Q

what is a compensatory anti-inflammatory reaction?

A

can cause immunoparalysis

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14
Q

what do anti-inflammatory mediators do?

A

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

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15
Q

what are the Clinical features of sepsis?

A

• Fever >38 degrees – chills, rigors, flushes, cold sweats, night sweats
• Hypothermia < 36 degrees – especially in elderly and children (anti-inflammatory response)
• Tachycardia >90bpm
• Tachypnoea >20/min
• Altered mental state
• Hyperglycaemia >8mmol/l
Arterial hypotension (systolic <90mmHg or MAP <70mmHg)
SvO2 >70%

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16
Q

what are thhe changes in inflammatory variables in sepsis

A
Leucocytosis (WCC > 12,000/ml)
Leucopenia (WCC < 4,000/ml)
Normal WCC with greater than 10% immature forms
High CRP
High procalcitonin
17
Q

what are the changes in organ dysfunction variables in sepsis?

A

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.

18
Q

tissue perfusion variables…

A

high lactate and skin mottling and reduced capillary perfusion

19
Q

factors affecting sy and sx of sepsis…

A

gram of bacteria, age, comorbidities, immunosupression, previous surgery, occupation, travel

20
Q

What is the SEPSIS 6?

A

Take –> blood cultures, blood lactate, measure urine output
Give –> o2 aim for sats off 94-98%, iv abx, iv fluid. (type of empirical ABX given depending on the situation -amox, penc, metrondiazole, if ellegies give vanc)

21
Q

what is lactate a marker of?

A

generalised hypoperfusion, severe sepsis, pooer prognosis. Type a - hypoperfusion, type b - Mitochondrial toxins, Alcohol, Malignancy, metabolism errors

22
Q

how much fluid is appropriate?

A

30ml/kg e.g. 2.1L 70kg patient

23
Q

what to consider when giving abx…

A

allergies, mrsa, esbl, cpe, abx toxicity, interactions.

24
Q

when to consider HDU referral?

A

low bp responsive to fluids, lactate over 2 despite fluids, elevated creatinine, oliguria, liver dysfunction, bilateral infiltrates, hypoxaemia.

25
Q

Case 1

A

55m, DM, smoker, IHD, Admitted through Emergency Department with fever, nausea, vomiting and abdominal pain x 4 hours, riased bp, pulse and resp rate, tender epigastrium, no rebound, BS present, WCC 15,600, tx in a and e - sepsis 6, Started on Amoxicillin, Gentamicin and Metronidazole for intra-abdominal sepsis
6 hours later patient failed to improve
Admitted with SIRS, On post-take round another blood test was carried out, Serum amylase 1450, Diagnosed as Acute pancreatitis, Antibiotics stopped and patient transferred to surgery for further management

26
Q

Case 2

A

68 year old woman admitted with worsening shortness of breath
History of IHD, CVA and bed bound
On examination: Alert, Temp 38oC, Resp rate 26/min, pulse 120/min irreg, BP 85/60, Chest dullness right base
Pneumonia CURB65 score - confusion, >7ureaN2, >30RR, DIASTOLIC <60 SYSTOLIC <90, over 65yo. out of 5, 3/5 is high risk of death.