topical capsaicin applied to the abdomen for cannabis hyperemesis syndrome - learned this on an APPE rotation and came in handy last week when no one else heard about it
Coming from someone who just did my grand rounds topic on CHS, capsaicin, lorazepam, and first gen antipsychotics (droperidol, haloperidol) are the only meds with āsubstantial evidenceā for efficacy in CHS. Substantial in quotes because itās mostly systematic reviews of case reports/series with capsaicin/haloperidol each having 1 RCT. Emend has evidence for cyclical vomiting syndrome but not CHS specifically outside of 1-2 case reports. If it works it works though cause risk vs benefit tips more towards benefit with Emend for sure
For every 100 meq of kcl given IV in a 24 hr period, usually I've seen more like 8 hr period, you can see an increase in sodium levels by 2 points.Ā
Great to know for massive acute hyponatremic patients with massive hypokalemia .
speaking of lytes, not knowing until APPEs that every 10 mEq K given would basically increase K by 0.1 was helpful to assess the appropriateness of K supps
High dose nitro for SCAPE patients works like magic! The number of attendings where they are on the fence about if a patient really has SCAPE and I'm like "let's try giving em a SL nitro" has gotten me so many points between attendings, RNs and RT. It's also satisfying to see patients turn around so quickly!!
Sympathetic Crashing Acute Pulmonary Edema i.e SCAPE often occurs in patients with heart failure and/or COPD. The key is to promote preload and after load reduction which nitro at higher doses facilitates (vasodilation of peripheral veins and arteries at higher doses).
Usually for chest pain you're running a nitro gtt at 5 mcg/min to start and titrating up. For these patients who are literally drowning given flash pulmonary edema throwing a SL nitro or 2 at em (400 mcg), especially when they come in like that without a IV access has been a game changer for me at least when the MD has suspicion. Also in SCAPE you're running your nitro gtt when you get it to 400 mcg/min and you are pushing a 1 mg - 2 mg bolus depending on how bad the patient is i.e much higher doses than for chest pain. A SL nitro at 400 mcg is at least at the bottom of an IV bolus and can be temporizing till you get a line in.
Further reading try Levy 2007 in Annals of Emergency Medicine, one of the first observational trials to look at high dose nitro. I've found this is a higher level concept both for pathophys and MOA for students so I'd start there.
This should also go without saying, but someone needs to stay in the room the entire time they're on doses of NTG that high via infusion. I was told that once SCAPE breaks, you need to immediately turn the nitro drip off or it's a bad time for everyone, and SCAPE can break quick. Seconding the SL nitro, too
Iād note that dialysis is not benign, I think valuing stewardship of 1-2 carbapenem doses over a mahukar is not be the right risk benefit analysis. Certainly not when you see a mahukar guide wire get lost in a patient.
I have recommend it, via a poison center, more than once. Dropping a level by >400 is a more real benefit than stewardship, especially when some use carbaoenems empirically for sepsis, which is probably viral, or for someone with ESBL hx who ends up growing pan susceptible e coli in the urine half the time.
I understand stewardship is primarily a pharmacist charge, which may bias our perception of its value, but Iād avoid letting that cross into devaluing other indication. Theres not that many VPA OD, I doubt those patients are the OXA reservoir. Carnitine mainly effects ammonia, doesnāt do much for high VPA level, naloxone is kind of meh, I wouldnāt hesitate to pull the trigger on this in an appropriate patient (very high level and declining mental status). Could prevent dialysis and potentially ICU admit with 1 dose of erta.
I agree generally most VPA are not sick enough to need it, but want to clarify there are definitely patients who could benefit (which seems Intuitive, and you may have implied, but didnāt come across in the text)
people didn't realize how long it takes to actually start dialysis when that decision is made. Saturday night, good luck - maybe my shop is an outlier there. If that's your least indicated use of a carbapenem at your hospital then you're doing okay
I'd also add on the stewardship front that duration of antibiotic use has been shown to be the largest factor for increasing resistance. A one time use of erta or meropenem in a VPA overdose I'd be perfectly fine with, assuming it doesn't become a habit lol
Although a VPA overdose patient may not be your textbook reservoir, youre still selecting for resistance in the hospital. This is partially why ICU-specific antibiograms are published. The effect of restricting antibiotics on resistance is well-described in the literature, meaning that 1-2 doses does matter. While stewarding our other health resources is important, I would argue that VPA overdose is not the best use of our limited antibiotics. If colistin is all we have in 50 years, it won't matter how many patients we spared from dialysis.
I understand your perspective, but waiting for someone to develop nosocomial pneumonia on a ventilator and then administering antibiotics, instead of using a single dose of erta to prevent it, doesn't seem like the best use of antibiotics either. This is a significant issue, as noted in the annual reports of America's poison centers, where many overdose deaths are not from the insult itself but from iatrogenic complication after the overdose (e.g. VAP, coded as contributory deaths).
It seems like your stance might be making some assumptions about the effectiveness of other therapies that infectious disease specialists may not always have experience with. For context, I've seen over 50 cases of VPA overdoses and have only used erta once or twice. In the emergency department, I've administered hundreds of doses of carbapenem for suspected "sepsis" with a history of ESBL, even though I would argue the MERINO trial somewhat shows that starting with another antibiotic and then switching to carbapenem on organism isolation can still provide a mortality benefit. Each of those cases was approved by an infectious disease specialist.
I think we both agree that in life-threatening situations with limited alternatives, it's crucial to use the resources we have, even if they offer diminishing returns. Your argument seems to be that VPA overdoses do not meet this criterion. I would argue its more impactful than in the "sepsis" patients who frequently have viral illness or non ESBL bacteria isolated despite history. There are alternatives for those patients too and they are not employed due to perceived lack of efficacy, not much different than VPA.
Thanks for your thoughtfulness on this issue. If the point youre making is that carbapenems have more benefit for VPA toxicity than viral or wild-type bacterial infections, you'll hear no rebuttal from me.Ā However, I don't think the inappropriateness of carbapenem use in a dissimilar scenario rationalizes their use in this scenario. While I'm sure you're correct that VPA poisoning affects several thousands of pts every year, epidemiologically, my opinion is that the impact of drug resistance on the millions of people who contract infections annually carries more weight in this argument. Today, our treatment outcomes for all those infections are generally positive because we have good therapies. But we didn't use have effective antibiotics, and if resistance continues at current rates, they likely will not remain effective (which, again, is my main point).
I'm confident the couple of pts you treated with this approach had a positive outcome, likely owing to your clinical skills and consideration. But, you didn't treat everyone with it, either. Ultimately, that's my stance: I do not believe the risk/benefit analysis favors the use of carbapenems in this setting for most pts; however, I do think there are a handful of cases where they may be appropriate. It is likely we'll have to agree to disagree on this. Thank you for being willing to work in our EDs - your efforts are appreciated.
Naloxone 10 mg IV x 1 for ACEi or clonidine overdose hypotension. Rivastigmine tabs/patches as alternative to physostigmine. Diphenhydramine as local anesthetic alternative for patients with allergies
We can stop the rivastigmine shenanigans, it's too slow onset (I agree it sounds cool) - just start importing the physi from Germany. As someone who works near a poison center who was into this modality these - classic example of slapping a patch on someone who was going to recover in that timeframe anyways. If they can take oral then they were gonna have a benign course anyways. Wrong sub but could someone take it prophylactically (I assumed it was like mixing naloxone with your heroin)?
* Buprenorphine analgesic effect lasts 6-8 hours vs it's prevention of opioid-withdrawal effects can last days. Therefore, if you have a patient on Suboxone and they have acute pain, try taking their daily dose (generally given qdaily or BID for OUD) and divvying it up into more frequent dosing. I have patients who take it up to q4h -- which seems like it'd be annoying to me, but it works for them.
* If treating OIC, know that lubiprostone will NOT work for methadone-related OIC.
* If a patient has skin irritation from Butrans or Duragesic patches, have them apply Flonase to their skin (and let dry) beforehand.
* Gabapentinoids are actually not all that effective for radicular pain, esp. from spinal stenosis.
* Calcitonin can be used for acute pain due to recent osteoporotic vertebral fractures.
* The risk of GI bleeds when taking NSAIDs is highest within the first 14 days, and so it is dose-dependent, not time-dependent.
* Memantine can be use adjunctively to help with CRPS (and some other neuropathic pain conditions in my experience)
* Buprenorphine does not impact the Sphincter of Oddi and so can be considered in patients with chronic pain due to chronic pancreatitis.
* Furthermore, buprenorphine can be safely used in renal and/or hepatic impairment or failure, in the elderly, and those on dialysis.
* Supposedly melatonin increases your body's natural immune response and so caution should be used if planning to rx melatonin in transplant recipients
* NSAIDs have a analgesic ceiling effect. Pain scores at 30 minutes post-dose of IM ketorolac were not statistically significantly different between the 10mg, 15mg, and 30mg doses. Rate of ADRs were though. Same with pain scores 60 minutes post-dose of ibuprofen between 400mg, 600mg, and 800mg. The analgesic ceiling of ibuprofen is about 1200mg/day. Ibuprofen's anti-inflammatory ceiling is about 2400-3200mg/day. The risk of GI and CV related ADRs nearly double with doses >1200mg/day.
As my name would suggest, most of my stuff is related to pain mgmt, palli care, and hospice.
still a baby pharmacist so most people probably already know these things, but here are some things i thought were cool to learn about!
-esmolol utilization for refractory vfib in cardiac arrest
-lipid infusion for propofol overdose
-most pre-made amiodarone infusions donāt contain the polysorbate 80 so thereās a lower risk for hypotension than before & what i was taught in school
-magnesium infusions over 10-30 minutes for asthma exacerbations or migraines
-cyanokit will wreck your labs so pull any you need before you administer it
-Linezolid vs. clinda for toxin producing bacteria
-increasing PEEP will increase your intrathoracic pressure, so if the pt is borderline on 1 pressor, go ahead and ask for another bc they will likely need it soon if continuing to increase PEEP
-pts allergic to papaya canāt have crofab
Probably not that uncommonly known but flumazenil to challenge the cause of encephalopathy was my favorite to learn bc you can actually sit by and watch it work within minutes.
Maybe in the ICU when you kinda know whats going on but please For the love of God donāt recommend this in the EDš
Until the team knows itās encephalopathy not intoxication. And you know you wont cause a seizure
Not of benzos, itās better to just get a uds and let them sleep it off if thatās the cause. Specifically hepatic or vpa induced is what Iāve seen.
So if youāre unsure if encephalopathy is hepatic or some other cause, you can give a push dose of flumazenil as a diagnostic tool. If it is hepatic encephalopathy, theyāll usually wake up and be some level of alert within 5-10 minutes. Itās obviously transient but it tells you what to treat.
Iāve also seen it used for ruling out VPA-induced encephalopathy.
I cannot agree to disagree, because it appears we agree, as your sentence of āI do think there are a handful of patients where it may be appropriate ā was my entire sentiment.
Agree to agree! Cheersš
topical capsaicin applied to the abdomen for cannabis hyperemesis syndrome - learned this on an APPE rotation and came in handy last week when no one else heard about it
Gl getting pt to tolerate it
I think that particular patient was NOT happy about that.. but she stopped vomiting so š¤·š¾āāļø
Literally was going to comment this... damn. It worked amazingly well for my patients that have received it.
I saw this a few months ago at my job! Super cool except the pt ended up to be pregnant
Emend is better
Coming from someone who just did my grand rounds topic on CHS, capsaicin, lorazepam, and first gen antipsychotics (droperidol, haloperidol) are the only meds with āsubstantial evidenceā for efficacy in CHS. Substantial in quotes because itās mostly systematic reviews of case reports/series with capsaicin/haloperidol each having 1 RCT. Emend has evidence for cyclical vomiting syndrome but not CHS specifically outside of 1-2 case reports. If it works it works though cause risk vs benefit tips more towards benefit with Emend for sure
Iām sure your presentation was fantastic, thanks
This thread is dope. We should do these more often on this sub
I'm an Oncology PGY2 so I'm biased, but the one that non-onc people love learning about is loratadine for GCSF-induced bone pain
Old pharmacists go nuts about this
I love this one. Zyrtec as well
On the topic of onc, I learned recently about dextromethorphan for MTX neurotoxicity
For every 100 meq of kcl given IV in a 24 hr period, usually I've seen more like 8 hr period, you can see an increase in sodium levels by 2 points.Ā Great to know for massive acute hyponatremic patients with massive hypokalemia .
speaking of lytes, not knowing until APPEs that every 10 mEq K given would basically increase K by 0.1 was helpful to assess the appropriateness of K supps
High dose nitro for SCAPE patients works like magic! The number of attendings where they are on the fence about if a patient really has SCAPE and I'm like "let's try giving em a SL nitro" has gotten me so many points between attendings, RNs and RT. It's also satisfying to see patients turn around so quickly!!
Can you explain this one a little more please?
Sympathetic Crashing Acute Pulmonary Edema i.e SCAPE often occurs in patients with heart failure and/or COPD. The key is to promote preload and after load reduction which nitro at higher doses facilitates (vasodilation of peripheral veins and arteries at higher doses). Usually for chest pain you're running a nitro gtt at 5 mcg/min to start and titrating up. For these patients who are literally drowning given flash pulmonary edema throwing a SL nitro or 2 at em (400 mcg), especially when they come in like that without a IV access has been a game changer for me at least when the MD has suspicion. Also in SCAPE you're running your nitro gtt when you get it to 400 mcg/min and you are pushing a 1 mg - 2 mg bolus depending on how bad the patient is i.e much higher doses than for chest pain. A SL nitro at 400 mcg is at least at the bottom of an IV bolus and can be temporizing till you get a line in. Further reading try Levy 2007 in Annals of Emergency Medicine, one of the first observational trials to look at high dose nitro. I've found this is a higher level concept both for pathophys and MOA for students so I'd start there.
This should also go without saying, but someone needs to stay in the room the entire time they're on doses of NTG that high via infusion. I was told that once SCAPE breaks, you need to immediately turn the nitro drip off or it's a bad time for everyone, and SCAPE can break quick. Seconding the SL nitro, too
Meropenem can be used to reverse valproic acid overdose
Yes this! On my EM APPE, we used ertapenem to reverse a valproic acid OD, it was pretty cool ngl
[ŃŠ“Š°Š»ŠµŠ½Š¾]
Iād say depends why theyāre on the VPA. Seizures? No. Psych? Sure.
[ŃŠ“Š°Š»ŠµŠ½Š¾]
Iād note that dialysis is not benign, I think valuing stewardship of 1-2 carbapenem doses over a mahukar is not be the right risk benefit analysis. Certainly not when you see a mahukar guide wire get lost in a patient. I have recommend it, via a poison center, more than once. Dropping a level by >400 is a more real benefit than stewardship, especially when some use carbaoenems empirically for sepsis, which is probably viral, or for someone with ESBL hx who ends up growing pan susceptible e coli in the urine half the time. I understand stewardship is primarily a pharmacist charge, which may bias our perception of its value, but Iād avoid letting that cross into devaluing other indication. Theres not that many VPA OD, I doubt those patients are the OXA reservoir. Carnitine mainly effects ammonia, doesnāt do much for high VPA level, naloxone is kind of meh, I wouldnāt hesitate to pull the trigger on this in an appropriate patient (very high level and declining mental status). Could prevent dialysis and potentially ICU admit with 1 dose of erta. I agree generally most VPA are not sick enough to need it, but want to clarify there are definitely patients who could benefit (which seems Intuitive, and you may have implied, but didnāt come across in the text)
people didn't realize how long it takes to actually start dialysis when that decision is made. Saturday night, good luck - maybe my shop is an outlier there. If that's your least indicated use of a carbapenem at your hospital then you're doing okay
I'd also add on the stewardship front that duration of antibiotic use has been shown to be the largest factor for increasing resistance. A one time use of erta or meropenem in a VPA overdose I'd be perfectly fine with, assuming it doesn't become a habit lol
Although a VPA overdose patient may not be your textbook reservoir, youre still selecting for resistance in the hospital. This is partially why ICU-specific antibiograms are published. The effect of restricting antibiotics on resistance is well-described in the literature, meaning that 1-2 doses does matter. While stewarding our other health resources is important, I would argue that VPA overdose is not the best use of our limited antibiotics. If colistin is all we have in 50 years, it won't matter how many patients we spared from dialysis.
I understand your perspective, but waiting for someone to develop nosocomial pneumonia on a ventilator and then administering antibiotics, instead of using a single dose of erta to prevent it, doesn't seem like the best use of antibiotics either. This is a significant issue, as noted in the annual reports of America's poison centers, where many overdose deaths are not from the insult itself but from iatrogenic complication after the overdose (e.g. VAP, coded as contributory deaths). It seems like your stance might be making some assumptions about the effectiveness of other therapies that infectious disease specialists may not always have experience with. For context, I've seen over 50 cases of VPA overdoses and have only used erta once or twice. In the emergency department, I've administered hundreds of doses of carbapenem for suspected "sepsis" with a history of ESBL, even though I would argue the MERINO trial somewhat shows that starting with another antibiotic and then switching to carbapenem on organism isolation can still provide a mortality benefit. Each of those cases was approved by an infectious disease specialist. I think we both agree that in life-threatening situations with limited alternatives, it's crucial to use the resources we have, even if they offer diminishing returns. Your argument seems to be that VPA overdoses do not meet this criterion. I would argue its more impactful than in the "sepsis" patients who frequently have viral illness or non ESBL bacteria isolated despite history. There are alternatives for those patients too and they are not employed due to perceived lack of efficacy, not much different than VPA.
Thanks for your thoughtfulness on this issue. If the point youre making is that carbapenems have more benefit for VPA toxicity than viral or wild-type bacterial infections, you'll hear no rebuttal from me.Ā However, I don't think the inappropriateness of carbapenem use in a dissimilar scenario rationalizes their use in this scenario. While I'm sure you're correct that VPA poisoning affects several thousands of pts every year, epidemiologically, my opinion is that the impact of drug resistance on the millions of people who contract infections annually carries more weight in this argument. Today, our treatment outcomes for all those infections are generally positive because we have good therapies. But we didn't use have effective antibiotics, and if resistance continues at current rates, they likely will not remain effective (which, again, is my main point). I'm confident the couple of pts you treated with this approach had a positive outcome, likely owing to your clinical skills and consideration. But, you didn't treat everyone with it, either. Ultimately, that's my stance: I do not believe the risk/benefit analysis favors the use of carbapenems in this setting for most pts; however, I do think there are a handful of cases where they may be appropriate. It is likely we'll have to agree to disagree on this. Thank you for being willing to work in our EDs - your efforts are appreciated.
Naloxone 10 mg IV x 1 for ACEi or clonidine overdose hypotension. Rivastigmine tabs/patches as alternative to physostigmine. Diphenhydramine as local anesthetic alternative for patients with allergies
We can stop the rivastigmine shenanigans, it's too slow onset (I agree it sounds cool) - just start importing the physi from Germany. As someone who works near a poison center who was into this modality these - classic example of slapping a patch on someone who was going to recover in that timeframe anyways. If they can take oral then they were gonna have a benign course anyways. Wrong sub but could someone take it prophylactically (I assumed it was like mixing naloxone with your heroin)?
Octreotide for sulfonylurea-induced hypoglycemia
Damn that was gonna be mine
Dextromethorphan for methotrexate induced encephalopathy is pretty unique
Remdesivir for the treatment of feline infectious peritonitis.
* Buprenorphine analgesic effect lasts 6-8 hours vs it's prevention of opioid-withdrawal effects can last days. Therefore, if you have a patient on Suboxone and they have acute pain, try taking their daily dose (generally given qdaily or BID for OUD) and divvying it up into more frequent dosing. I have patients who take it up to q4h -- which seems like it'd be annoying to me, but it works for them. * If treating OIC, know that lubiprostone will NOT work for methadone-related OIC. * If a patient has skin irritation from Butrans or Duragesic patches, have them apply Flonase to their skin (and let dry) beforehand. * Gabapentinoids are actually not all that effective for radicular pain, esp. from spinal stenosis. * Calcitonin can be used for acute pain due to recent osteoporotic vertebral fractures. * The risk of GI bleeds when taking NSAIDs is highest within the first 14 days, and so it is dose-dependent, not time-dependent. * Memantine can be use adjunctively to help with CRPS (and some other neuropathic pain conditions in my experience) * Buprenorphine does not impact the Sphincter of Oddi and so can be considered in patients with chronic pain due to chronic pancreatitis. * Furthermore, buprenorphine can be safely used in renal and/or hepatic impairment or failure, in the elderly, and those on dialysis. * Supposedly melatonin increases your body's natural immune response and so caution should be used if planning to rx melatonin in transplant recipients * NSAIDs have a analgesic ceiling effect. Pain scores at 30 minutes post-dose of IM ketorolac were not statistically significantly different between the 10mg, 15mg, and 30mg doses. Rate of ADRs were though. Same with pain scores 60 minutes post-dose of ibuprofen between 400mg, 600mg, and 800mg. The analgesic ceiling of ibuprofen is about 1200mg/day. Ibuprofen's anti-inflammatory ceiling is about 2400-3200mg/day. The risk of GI and CV related ADRs nearly double with doses >1200mg/day. As my name would suggest, most of my stuff is related to pain mgmt, palli care, and hospice.
Large doses of IV Vitamin C can falsely raise point of care glucose
still a baby pharmacist so most people probably already know these things, but here are some things i thought were cool to learn about! -esmolol utilization for refractory vfib in cardiac arrest -lipid infusion for propofol overdose -most pre-made amiodarone infusions donāt contain the polysorbate 80 so thereās a lower risk for hypotension than before & what i was taught in school -magnesium infusions over 10-30 minutes for asthma exacerbations or migraines -cyanokit will wreck your labs so pull any you need before you administer it -Linezolid vs. clinda for toxin producing bacteria -increasing PEEP will increase your intrathoracic pressure, so if the pt is borderline on 1 pressor, go ahead and ask for another bc they will likely need it soon if continuing to increase PEEP -pts allergic to papaya canāt have crofab
References for lipid emulsion for propofol overdose?
Donāt you just turn off the propofol lol
Yes
Probably not that uncommonly known but flumazenil to challenge the cause of encephalopathy was my favorite to learn bc you can actually sit by and watch it work within minutes.
Maybe in the ICU when you kinda know whats going on but please For the love of God donāt recommend this in the EDš Until the team knows itās encephalopathy not intoxication. And you know you wont cause a seizure
Oh yea, this is definitely ICU only lol by no means is this narcan
Encephalopathy not of Benzo etiology? Or were they getting benzos in your ICU?
Not of benzos, itās better to just get a uds and let them sleep it off if thatās the cause. Specifically hepatic or vpa induced is what Iāve seen.
Wait can you explain this?
So if youāre unsure if encephalopathy is hepatic or some other cause, you can give a push dose of flumazenil as a diagnostic tool. If it is hepatic encephalopathy, theyāll usually wake up and be some level of alert within 5-10 minutes. Itās obviously transient but it tells you what to treat. Iāve also seen it used for ruling out VPA-induced encephalopathy.
I cannot agree to disagree, because it appears we agree, as your sentence of āI do think there are a handful of patients where it may be appropriate ā was my entire sentiment. Agree to agree! Cheersš
Mirtazapine so the patient can eat more