Please enable JavaScript.

Coggle requires JavaScript to display documents.

Sepsis and Deterioration - Coggle Diagram

- - - - -improve BP and end organ perfusion
        -30ml/kg in first 3 hours
        -isotonic is recommended, never use glucose
        -adverse: oedema, coagulopathy and hypothermia
    - - -administer in first hour, any delay results in increased mortality
        -initially broad spectrum until M/C/S known, then tailor with narrow spectrum
        -vancomycin and meropenem are nephrotoxic
        -consider antimicrobial stewardship
    - - -O2 admin (hiflow, nasal
        -cellular hypoxia takes time to correct
        -patient positioning to maximise thoracic expansion
        -may require ABGs
    - - -sleep disturbance leading to delirium and fatigue
        -delirium=fluctuating mental status, disordered thought and inattention, increases mortality R/T falls
        -reorientate with books, emotional support, engage with fam, meds review
        -consider safety of patients on ward
        -risk of PTSD
  - - - -will they need enteral or TPN to meet catabolic status?
        -monitor bowel sounds, hypotension may compromise mesenteric artery blood supply
        -need prokinetic agent i.e. metoclopromide to assist w/ enteral?
        -consider constipation
    - - Mobility
        -impaired due to decreased energy
        -DVT risk, sarcopenia
        Integument
        -PU risk, further infection
        -observe new bruising, prolonged bleeding and rashes
    - - Noradrenaline or metaraminol
        -both alpha receptor agonists
        -vasoconstriction to increase BP
        -metaraminol can admin via PIVC, more used in general ward setting
        -Nursing care: monitor BP, HR, UO, peri perfusion
- - - - invading organism -> release of inflammatory mediators -> vasodilation
        
        increases cap permeability and maldistribution of blood volume
        
        CNS and endocrine activation -> hypermetabolic states -> increase O2 demand
        R/T SNS activation (catecholamines), neuroendocrine response (ADH), RAAS (conserve Na and H2O)
    - - compensatory - increase ADH, vasoconstriction, increase HR, low pH
        
        progressive - comp. mechanisms fail. See septic shock S&S.
        
        refractory - profound hypotension and hypoxaemia, exacerbation of anaerobic mechanism. Organ failure
  - - - -mottled or cold peripheries
        -cap refill >3secs
        -SBP <90 MAP <60. MAP=1xSBP and 2xSBP. Clinical hypotension=20% drop from baseline or 40mmHg reduction in SBP
        -tachycardia
        -hyperventilation
        -temperature (cold sepsis possible in immunosuppressed patients)
        -purpuric rash
        -lactate >2mmol/L
        -oliguria
        -hyperglycaemia
        -decreased LOC and delirium
- - - - -sufficient CO
        -uncompromised vascular tone (dilated or constricted?)
        -sufficient blood volume
        -tissues able to utilise oxygen
  - - - -hypersensitiity to substance
        -massive vasodilation, increased permeability, bronchospasm
    - - -heart dysfunction, reduced CO. Decreased filling or arryhthmia
        -narrowed pulse pressure caused by inability to pump blood forward on the systole
        -troponin released in cardiac damage, used as specific marker
        -B-type natriuretic peptide measures stretch of ventricles
    - - -loss of volume, relative or absolute
        -principles=stop bleeding, replace fluids
        -3:1 fluid:blood loss ratio