You are the consultant rostered on at the start of a week in ICU and you are taking handover from another consultant.
The patient being discussed is a 40 year diabetic female admitted to ICU with urosepsis and septic shock 12 hours ago. She is critically ill and still deteriorating despite “aggressive” intensive care.
What are the major actions you would expect to have already been taken for this patient?
This is a stem which asks for the basic management steps as described in the revision summary "Resuscitation of the Septic Shock Patient". In brief:
Pragmatic early steps:
- Large-bore cannulae, whack em in.
- Blood cultures (ideally two sets, from different sites)
- Antibiotic therapy without delay (every hour counts)
- Fluid resuscitation (30ml/kg, so 2-3L in a normal-sized adult- and probably more).
- Arterial line insertion
- Re-assessment of fluid response and either further fluid or vasopressors
- Resuscitation to clinical endpoints including organ perfusion, MAP target,
ICU management steps:
- CVC insertion
- Noradrenaline infusion
- Use dynamic manoeuvres to assess fluid responsiveness (SSG)
- Pulse pressure variation during an expiratory hold manoeuvre (most reliable)
- Passive leg raise autotransfusion (seems reliable if you are measuring cardiac output)
- Stroke volume variation (seems reliable)
- Clinical signs (the only reliable one seems to be capillary refill)
- IVC ultrasonography (probably reliable, but nobody can agree on the cutoff values)
- Pulse pressure variation without expiratory hold (seems unreliable)
- CVP (completely unreliable)
- PAOP (completely unreliable)
- GEDV, GEDVI (completely unreliable)
- Assess adequacy of resuscitation:
- ScvO2 over 70% - recommended by SSG but not supported by the more recent evidence (ProCESS and ARISE)
- Lactate clearance is better than 10% over 2 hours (supported by fairly dodgy evidence)
- Arteriovenous CO2 difference is under 6mmHg (supported by slightly better evidence; in that its main determinant in sepsis is microvascular perfusion, and it seems to relate to an improvement of surrogate outcome measures.)
- Urine output is over 1.0ml/kg (suggested by the SSG but on the basis of expert opinion only)
The patient has two cannulas, one of which is running albumin at 20ml/hr and the other a metaraminol infusion.
What is the rationale for the use of albumin in sepsis?
- Oncotic effects
- Scangenger effects: albumin is able to neutralise toxic compounds
- Anti-NOS effect: albumin may be able to neutralise the vasodilating effect of nitric oxide.
- Extravascular buffer effects: albumin plays a major role as a buffer
- Association with mortality: low albumin levels have been associated with mortality in the critically ill population, in a variety of clinical settings. (JL Vincent, 2003)
- Albumin helps maintain a neutral fluid balance (Dubois et al, 2006)
What are the counter-arguments for the use of albumin in sepsis?
- Allergic reactions.
- Non-essential, as is demonstrated by the excellent health of people in whom it is totally congenitally absent.
- Hypoalbuminaemia of critical illness is not to be viewed as a pathological state. Rather, albumin is a "negative acute phase reactant"
- The normal effect of albumin on oncotic pressure will be completely frustrated by the leakiness of the capillary endothelium in critical illness
- Albumin given to critically ill patients will end up being rapidly cleared from the circulating blood
What is the evidence for the use of albumin in sepsis?
- Slightly superior to saline in terms of mortality (on post-hoc subgroup analysis of the SAFE study)
- Equivalent to saline in terms of mortality (ALBIOS trial)
- Improves mortality of septic shock patients once hemodynamic stability has been achieved (also the ALBIOS trial).
- According to a recent meta-analysis, the results of the available studies support safety, but suggest that albumin is "not robustly effective at reducing all-cause mortality".
The patient is on a metaraminol infusion. Is this a good choice? Why, or why not?
- Metaraminol is peripherally available vasoconstrictor
- It has little risk in terms of extravasation
- Its effects are purely on the α-1 receptors
- It can avert the need for central line insertion
- It may have a sustained indirect sympathomimetic effect
- Metaraminol is an agent of low potency
- Tachyphylaxis phenomena result in diminished effect over time
- Peripheral administration with a sluggish venous circulation may result in erratic drug delivery and difficulty titrating doses
- As a pure α-1 receptor agonist, it can cause bradycardia and has no positive effect on cardiac contractility
What is the rationale for central line insertion in septic shock patients?
- Vasoactive substances can be given centrally without concern for the risk of extravasation
- Highly concentrated or irritant substances can be given (eg. concentrated electrolytes)
- CVP can be measured
- A central venous pressure waveform can be transduced
- It is possible to measure central venous oxygen saturation and central venous CO2.
What is the rationale for the use of SvO2 measurement in septic shock? How would you use it?
- Central venous saturation is one of the methods of assessing the adequacy of tissue oxygen delivery.
- A low ScvO2 suggests that there is poor cardiac output
- A high ScvO2 suggests that there is poor tissue oxygen utilisation
- In combination with other methods of assessment, this may guide the use of fluid resuscitation vasopressors and inotropes
What is the support for this practice in the published literature?
- Rivers famously used an ScvO2 of 70% as one of the goals of early goal-directed therapy
- The first few versions of the Surviving Sepsis guidelines had supported this idea, perhaps at least in part because of the fact that Edwards (a manufacturer of ScvO2 monitors) had sponsored them.
- ProCESS, ARISE and ProMISE studies did not demonstrate any survival benefit from protocolised care, in which the use of ScvO2 was one of the major components.
- Lactate clearance was demonstrated to be equally effective as a resuscitation endpoint (Jones et al, 2010)
You have decided to insert a central line. What is your rationale for your choice of vasopressor agent?
- Noradrenaline is the first choice (SSG) ...
- Perhaps there is no good rationale:
- No better than adrenaline (CATS) though it does not muddle the use of lactate
- No better than phenylephrine (Morelli et al, 2008) - perhaps better for the stroke volume
- No better than vasopressin in terms of mortality (VASST)
- As good as vasopressin at preventing renal failure (VANISH)
- Better than dopamine (SOAP-II) -but who uses dopamine these days?...
The patient's MAP stabilises on 0.20mcg/kg/hr of noradrenaline. However, she suddenly becomes tachycardic and haemodynamically unstable. This ECG is shown to you. What is your interpretation?
This is AF with left bundle branch block. There is no concordance and the rhythm is irregular.
How will you manage this situation?
A variety of answers may be acceptable. A good candidate will give a range of options, which may include:
- Electrical (synchronised DC) cardioversion
- Chemical (amiodarone) cardioversion
- Addition of vasopressin to the vasoactive agents as a noradrenaline-sparing drug, so as to reduce the total β-1 agonist dose
- Electrolyte correction (potassium and magnesium)
- Withdrawal of CVC in case its tip is in the atrium