𝙟𝙤𝙨𝙝 𝙛𝙖𝙧𝙠𝙖𝙨 💊 Profile picture
zentensivist 🧘‍♂️ FOAMite 🌊 diuresis jedi 💦 leader of the rebel alliance ⚔️ resuscitationist 💉 writer with aweful speling 😬 no COI 💰

Mar 18, 2020, 7 tweets

I've been dreading this, but I think we need to reconsider the issue of steroid in COVID-19. This is extremely complicated, especially for two reasons...(1/7)
#COVID19foam

1st level of complication = patients vary a lot!
- Most require minimal care
- Many just need low flow oxygen
- Few develop cytokine storm and multiorgan failure
- Many are somewhere in-between

It may be *impossible* to render any blanket statement for all patients. (2/7)

2nd level of complication = disease goes thru phases in any patient

Initially: viral replication phase w/ weak immune response. Immunosuppression *dangerous* here?

Rarely: later surge of adaptive immunity causes cytokine storm. Immunosuppression potentially good here?? (3/7)

currently best data on COVID-19 is a retrospective series of patients in Wuhan by Wu et al. this study has *lots* of limitations (e.g., single center, variety of different treatments used, most patients not intubated)
(study: bit.ly/33q6Uou)(4/7)

among patients with ARDS, methylprednisolone use correlated with improved survival. this is notable, because generally steroid is used for sicker patients (who will do *worse*). so is steroid actually causing benefit here?? (5/7)

it's impossible to know. this study suggests that it's reasonable to treat patients with ARDS plus systemic inflammation (e.g. markedly elevated CRP) with moderate doses of steroid (e.g. 0.5-1 mg/kg methylprednisolone).
(article: bit.ly/2Uf8tSa)(6/7)

steroid is a nonspecific immunosupressive. more targeted immunomodulators might be superior (e.g. tocilizumab). but for now, this is what we have. dexamethasone could be superior b/c it causes less fluid retention.
(more on steroid in IBCC here: bit.ly/3db51Re)(7/7)

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