Thread by @nephrotox

Although propofol can also turn urine green, we gave this patient methylene blue for vasoplegia / refractory shock. Read on for some CCB poisoning discussion. 1/

https://twitter.com/nephrotox/status/1266192234275274757

Severe calcium channel blocker poisoning is a difficult clinical challenge. These patients are profoundly hypotensive and generally receive the kitchen sink re: therapies. @toxiferoustales breaks down the mechanism:
emcrit.org/toxhound/sneak…
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For a superb review of thw two most established effective therapies - vasopressors vs high-dose insulin - look no further than @mbspyres and @jonbcole2 friendly debate:
emcrit.org/toxhound/hdi-v…
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There are a few other options we can pull out when patients have refractory shock: methylene blue, hydroxocobalamin, lipids, or ECLS (mostly ECMO). Note that the definition of "refractory" varies - pressor and HDI insulin doses may get *very* high in profound poisoning.
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Methylene blue "scavenges" nitric oxide by inhibiting nitric oxide synthase. It is intensely colorimetric, which gives you that green urine color (as well as false cyanosis - don't look at peripheral O2 sats for a while!)
pubmed.ncbi.nlm.nih.gov/7679577/
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Hydroxocobalamin - also intensely colorimetric - also "scavenges" nitric oxide by inhibiting nitric oxide synthase. (Expect colorimetric labs like AST and creatinine to be unreliable for hours after).
europepmc.org/article/med/19…
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Both of these drugs have been used for vasoplegia in cardiac surgery, as well as refractory vasodilatory shock in poisoning. For poisoning, they are generally used as last resorts, or just before ECMO.
ccforum.biomedcentral.com/articles/10.11…
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Lipids have been used as well, both for the "lipid sink" effect as well as free fatty acids. They also serve as a substrate for the heart: fatty acid bolus is an inotrope in itself. Watch out for ARDS and pancreatitis.
pubmed.ncbi.nlm.nih.gov/19096109/
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For this patient, with hypotension refractory to HDI and pressors (epi, NE, vaso) as well as evidence of poor perfusion (decreased UOP, cool to touch, lactic acidosis) and volume overload, we considered several options.
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Methylene blue or hydroxocobalamin; further increasing HDI or pressors/inotropes; or ECMO. Ultimately went with MB because ejection fraction was surprisingly OK; it was relatively fast; MB didn't carry much volume with it. Six in one hand...
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Of course, it's possible that simply turning up the insulin would have worked. We ultimately maxed out at 5 u/kg/hr. (We also did other stuff with pressors too). Also got Ca, glucagon earlier w/o response.
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Despite the neat picture, IMO methylene blue actually didn't do that much in this case. I think adding and increasing pressors + later HDI 3 -> 5 u/kg/hr did the trick. UOP increased, lactate dropped, no ECMO needed.
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Speaking of volume, most profoundly ill CCB poisoned patients develop severe volume overload. We concentrate our insulin to 10 U/mL; the previous hospital was unable to do so, and the patient was many liters up. CRRT is commonly employed for volume overload (& was here, too).
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If there was anything I'd want to teach about CCB poisoning: aggressive care saves lives. Go outside your comfort zone with hundreds of units of insulin per hour and high dose pressors. No, they won't die of hypoglycemia (use D20, D70!)
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Despite HDI, 4+ pressors, MB, intubation, CRRT, shock, AKI, etc., this patient is extubated and sitting up, off dialysis with a Cr of <1.5, not on much O2. He'll hopefully be discharged to psychiatric care to start a process for definitive help.
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And ultimately? Most patients who attempt suicide and survive will not die from suicide. This is the real reason to go hard: long-term benefit.
hsph.harvard.edu/means-matter/m…
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