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Exam 3 clinical > infection: acute sepsis > Flashcards

infection: acute sepsis Flashcards

1
Q

what is sepsis?

A

life-threatening organ dysfunction due to a dysregulated host response to infection

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2
Q

what is septic shock?

A

persisting hypotension requiring treatment to maintain blood pressure DESPITE fluid resuscitation

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3
Q

what is bacteraemia?

A

presence of bacteria in the blood (+/- clinical features)

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4
Q

what is septicaemia?

A

generalised sepsis

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5
Q

how do you recognise sepsis?

A 
using EWS (early warning score):
high RR, 
high HR, 
high temp, 
LOW BP

and clinical features suggesting source e.g. pneumonia, UTI, meningitis etc.

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6
Q

what do you do if the patient has red flag sepsis?

A 
send urgent investigations, inform senior doctor
complete sepsis 6 bundle:
oxygen
IV antibiotics
fluids 
blood cultures
urine output
lactate (anaerobic respiration, from hypoxic, BP drop)
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7
Q

what are the urgent investigations to be carried out if a patient has red flag sepsis?

A 
FBC, U&E
blood sugar
LFT (liver function) - AST & ALT
CRP
ABC - measure pCO2, pO2 etc.
other microbiology samples (CSF, urine)
EDTA bottles for PCR (prevents blood clotting in bottle)
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8
Q

what is the likely diagnosis of red flag sepsis?

A

Meningococcal meningitis (Neisseria meningitidis)
spread by direct contact with resp secretions
most people have harmless colonisation
can be rapidly progressive

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9
Q

what is the structure of Neisseria meningitidis which causes the symptoms?

A
  1. lipopolysaccharide ENDOTOXIN triggers inflammation
  2. PILUS enhances attachment
  3. POLYsaccharide Capsule: promotes adherence & prevents phagocytosis
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10
Q

what is the inflammatory cascade of from infection leading to sepsis?

A
  1. endotoxin binds to macrophages
  2. local effects - inflammatory response (cytokines)
  3. systemic - try to control infection (cytokines circulation)
  4. sepsis - infection not controlled
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11
Q

describe local step of inflammatory cascade

A

cytokines (TNF-a & IL-1) stimulates inflammatory response to promote wound repair & recruit macrophages etc.

INFLAMMATION & WOUND REPAIR

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12
Q

describe systemic step of inflammatory cascade

A

cytokines released into circulation

stimulate GF, macrophages & platelets to try and control infection

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13
Q

what happens in sepsis? (inflammatory cascade from local to systemic)

A

infection NOT controlled
cytokines lead to activation of HUMORAL cascade
Circulatory insult (DIC & organ injury)

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14
Q

describe the relationship between sepsis and coagulation

A
  1. cytokines initiate production of thrombin –> coagulation
  2. cytokines inhibit fibrinolysis (breakdown clot)
  3. coagulation cascade leads to microvascular thrombosis –> organ ischaemia, dysfunction & failure
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15
Q

what is microvascular injury the major cause of?

A

shock & multiorgan failure

coagulation cascade –> microvascular thrombosis –> organ ischaemia –> progress to necrosis

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16
Q

what are the specific treatments of sepsis?

A
  1. antimicrobials

2. surgery - drainage, debridement, dead space removal

17
Q

what are the support treatment of sepsis?

A

symptom relief
physiological restoration
(consider early referral to ITU, sepsis 6, regular monitoring & reassessment)

18
Q

what is the antibiotic treatment used in sepsis?

A

agent that is active against Neisseria meningitides (can penetrate into CSF)
CEFTRIAXONE (a type of ß-lactam, cephalosporin - cell wall)

19
Q

what are the life-threatening complications of sepsis?

A

irreversible hypotension
respiratory failure
AKI
raised intracranial pressure (IV (?) mannitol)
ischaemic necrosis of digits / hands / feet

20
Q

how do you confirm the diagnosis of sepsis?

A

blood culture
PCR of blood
lumbar puncture CSF (IF SAFE) - microscopy & culture of CSF, PCR of CSF - always check contraindications (if harmful to patient)

21
Q

how do you examine the CSF?

A 
urgent transport of CSF to lab - glucose & protein estimation, microscopy, culture
appearance - turbid, colour
microscopy WBC, RBC
gram stain (-ve for N. meningitides)
refer for PCR
22
Q

describe meningococcus

A

Neisseria meningitidis - gram neg Diplococci
lots of serogroups (A, B, C) - based on polysaccharide - mainly B
capsular antigen (evades immune response by preventing phagocytosis)
outer membrane acts as endotoxin - triggering inflammation
spread by aerosols & nasopharyngeal secretions

23
Q

what are the preventions against menigococcus?

A
  1. vaccination (serogroup B)

2. antibiotic prophylaxis (notifiable disease, close contacts can be given antibiotic prophylaxis & vaccination)

Exam 3 clinical (26 decks)

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