Lightning rounds 58: Steroids for septic shock with David Janz

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We dive into the common dilemma of when to give stress-dose corticosteroids in septic shock, with Dr. David Janz, pulm/crit intensivist with a Masters of Science in Clinical Investigation, former director of the Clinical Research Unit for the critical care section at LSU, founding member of the Pragmatic Critical Care Research Group, and associate Chief Medical Officer for LCMC.

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Takeaway lessons

1. The purported effect of corticosteroids in septic shock is to increase sensitivity of peripheral catecholamine receptors, either to endogenous or exogenous adrenergic hormones.
2. In the four large RCTs of this topic, two showed a beneficial outcome effect and two did not. The two positive trials also added fludrocortisone to the backbone steroid (usually hydrocortisone), though it seems dubious that this was the key difference (fludro has also been studied separately without effect). Those trials also generally enrolled sicker patients, i.e. on higher doses of pressor and more organ failure.
3. It is probably reasonable to add steroids when on escalating doses of your first-line pressor (e.g. norepinephrine), or when thinking of adding vasopressin, though the SCCM/Surviving Sepsis guidelines now suggest just giving steroids to everyone in septic shock, presumably to simplify decision-making, particularly for non-experts.
4. Most trials have used hydrocortisone 50 mg q6h or thereabouts, or an equivalent dose as a continuous infusion. The latter makes some physiologic sense but has not been shown to be beneficial head-to-head trials. Most likely, the exact dosing strategy is not too important. Alternate steroids are probably also reasonable, i.e. any moderate-dose parenteral corticosteroid probably gets you the desired effect.
5. Many trials continued steroids until the patient left the ICU, even if pressors have been weaned off. Most clinicians would probably stop them sooner than this, although we should acknowledge that their effect in raising blood pressure is reliable (sometimes helping to discontinue pressors as much as several days sooner), so continuing them longer could conceivably help with disposition (i.e. help them leave and stay out of the ICU), which is a good thing for hospitals and probably patients.
6. Dr. Janz stops steroids when the pressors are stopped, with no taper or wean. Some would do a short taper, but the more complex you make the process in a busy ICU, the more likely that someone will forget to discontinue them altogether, and that the patient will stay on steroids for their whole hospitalization (or forever). There is no physiologic suppression of the native steroid production with these durations of steroid therapy (usually 3-4 days, almost always <1 week), and an abrupt halt is what was done in the trials.
7. Etomidate has been repeatedly shown to cause a measurable decrease in cortisol levels, even after single doses (e.g. for intubation). However, this has not been shown to be associated with any negative outcome (most recently in the EVK trial).
8. There is very little data on whether steroids should be used in shock from other etiologies. It may make some sense in other inflammatory states, such as pancreatitis, post-CPB vasoplegia, etc. But we really don’t know. In a mixed shock state where sepsis is present along with something else like cardiogenic shock, Dr. Janz uses steroids; otherwise no.
9. Whether to always augment the home steroid dose in chronic steroid users, even without shock, has shifted—in the past, endocrinology guidelines were to always do this empirically (e.g. in steroid users undergoing surgery or some other stressor), now they still generally favor this but are moving towards increasing the home dose only if signs of adrenal crisis develop.