more emergency medicine clinicians saying that they can keep COVID-19 patients off intubation with CPAP and HFNC
more stories of "happy hypoxemic" patients who come in with O2 sats in the 40% range who can talk and who can do ok with CPAP and awake proning.
NYC hospitals are seeing shortages of drugs, especially sedatives like propofol & fentanyl. Workarounds are valuable: eg one doctor reports hydromorphone drips being used more.
intensivist gives his experience using convalescent plasma; he did this in collaboration w/ a hematologist & pathologist.
he cites retrospective study in SARS where convalescent plasma associated w/ lower mortality rate: 12% vs 17%.
he cites retrospective study in SARS where convalescent plasma associated w/ lower mortality rate: 12% vs 17%.
getting authorization for emergency use from the FDA and a signoff from the IRB has to be done separately for each medical facility, and it was apparently a saga.
the patient in question was in severe ARDS and also received ECMO; he's now been extubated and is recovering. of course we don't know yet if it was the convalescent plasma that worked.
dr. hopes that blood banks (like the Red Cross) soon scale up a system for collecting & testing convalescent plasma, since it's currently very hard to come by.
on hypercoagulability: 30% DVT rates, clogged lines, arterial ischemia, "outrageous" fibrinogen levels of like 1800. it's a thing. due to intense inflammation and maybe viral infection itself.
ok, so should anticoagulants be given empirically for high d-dimers? dr. says *all* COVID-19 pts should be given prophylactic doses of anticoagulants. and especially high d-dimers should get therapeutic doses.
(to be clear, this means COVID-19 *hospital admissions*, not everyone with the virus, since many are asymptomatic or only mildly ill.)
he's recommending low-molecular-weight heparin, 1 mg/kg as the ideal anticoagulant.
he does *not* recommend thrombolytics like rtPA which have been making the news in some case studies, because they're riskier (can cause hemorrhagic stroke.)
but he's only known one pt who got a hemorrhage after being put on heparin; his experience with COVID19 is that the patients tend to be very "clotty" and rarely do anticoagulants overshoot and make patients overly "bleedy".
your "L-type" patient is someone with profound hypoxia but good lung compliance and not much alveolar collapse. i.e. the "happy hypoxemic." these are hypothesized to be due to V-Q mismatch.
the "H-type" COVID19 patient is more classic ARDS with poor lung compliance & alveolar collapse. Patients often come in as L-type, some get well, some progress to H-type.
when to intubate: watch the work of breathing more than the O2 sat. HFNC + awake proning, let the patient move around instead of lying flat on their back, and *watch* while being ready to intubate at any moment.
transition to CPAP if HFNC isn't working. we're looking at high FiO2 and low PEEP, and also no added fluids. (logic being: lung recruitment isn't the primary problem, so pressure won't help; hypoxemia is severe and hypercapnia pretty rare, so more oxygen is better)
"divorce FiO2 from PEEP" -- at least in type L. this is a *different* ventilatory protocol than ARDSNet, because these aren't typical ARDS patients. If you don't have collapsed alveoli in the first place, extra pressure can cause barotrauma.
does remdesivir work? that recent NEJM study is SUPER USELESS FOR ANSWERING THAT QUESTION. (ed: just what I thought!)
but ok, 57% of remdesivir-treated patients that were intubated got to be extubated, which is a lot higher than typical base rates. but hey, no control group, we don't know what to make of this.
"as many of you have noticed, we have many COVID-positive patients." god i love the gallows humor. Clinical trial recruitment should be a lot easier these days!
should you treat COVID19 pneumonia with antibiotics? dr. laughs, who's gonna send a person with CT evidence of pneumonia home without antibiotics?!
recent evidence says high-dose chloroquine causes cardiac issues & it isn't looking too effective either.
do we want to be giving anti-IL6 receptor antibodies to deal with cytokine storms? like tocilizumab.
retrospective uncontrolled Chinese studies are showing clinical & even mortality benefit from tocilizumab, but as usual, wait for the RCT before jumping to conclusions. (they're enrolling now!)
should we be worried about giving people hardcore immunosuppressants when they have an infectious disease? well you do NOT want to be giving tocilizumab to anyone with mild disease where their immune system might fight it off.
do you want to be neutropenic when you're fighting off a virus? you do NOT.
L-type patients or milder? not good candidates for tocilizumab.
L-type patients or milder? not good candidates for tocilizumab.
is opening up the country with no adequate antibody testing, no prophylactic treatment, no vaccine, and not even knowledge of how long immunity lasts, a good idea? NOPE, says doc.
for heart problems in COVID19: you can't tell myocarditis from STEMI from EKG alone, "take 'em to the cath lab" (ie heart biopsy) because you treat these conditions very differently.
scary thing: the EDs aren't seeing their usual *non* COVID19 cases, their heart attacks and strokes and DKAs, because telling everybody to stay home has worked so well. people are showing up to their GP's office with these emergency conditions.
apparently trying to resuscitate after a non-shockable cardiac arrest has a very poor success rate and can aerosolize the virus, so they're telling people *not* to do chest compressions in COVID19 patients.
(they recommend talking to your patients about end-of-life plans beforehand, and reciprocally it seems like PATIENTS should think about their end-of-life wishes because I can see a lot of people being very disturbed by finding out that the default is not to resuscitate!)
