Abilify PRN

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LoKoTe

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Hospital pharmacist here at an academic hospital. I've seen lately quite a few orders for Abilify PO Q8 Hours PRN agitation. The psych team hasn't been able to provide any literature on it. I'm curious, with Abilify's long half life, does this even make sense? Have you seen it? If so, what's the rationale? I'm curious to learn. Thanks.


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Because Abilify IM is approved for acute agitation, some people may be attempting to use the PO form in situations in which they feel uncomfortable giving an injection. In residency we were taught that the onset of action is too slow when absorbed through the gut, and that was the reason only the IM form is used for acute agitation. But then one of our C/L attendings, who was paranoid about QT prolongation and thus only ever wanted to recommend Abilify, one day developed the idea that it was unethical to give a patient an injection without offering them the chance to take a pill first, so she started recommending the PO form for acute agitation.
 
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Wow. Your reply helps a lot. Thank you.


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Also, is IM Abilify still available? (The immediate-acting, not the Maintena.) Last time I tried to order it, about 2 months ago, the pharmacist told me the manufacturer stopped making it.
 
Also, is IM Abilify still available? (The immediate-acting, not the Maintena.) Last time I tried to order it, about 2 months ago, the pharmacist told me the manufacturer stopped making it.
no it was discontinued the beginning of last year. which is not surprising as it was completely useless. who in the world would use abilify IM for a psychiatric emergency?! it agitates more patients than it calms and takes 2 weeks to reach steady state. i am more sad for the discontinuation of the liquid and orodispersible forms.
 
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Absolutely no reason to use it for agitation in a situation where IM is required... I think IM geodon is useless too (though on neuro they LOVE giving it parenterally for migraine). Haldol, Zyprexa, and sometimes Thorazine are the only short acting IMs needed. Again if the patient is delirious and needs non sedating D2 blockade, there is no reason (generally) to not start with Haldol.
 
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Hospital pharmacist here at an academic hospital. I've seen lately quite a few orders for Abilify PO Q8 Hours PRN agitation. The psych team hasn't been able to provide any literature on it. I'm curious, with Abilify's long half life, does this even make sense? Have you seen it? If so, what's the rationale? I'm curious to learn. Thanks.


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The same reason I inherit patients on things like buspar PRN, intuniv tid, and wellbutrin (yes the short-acting) qam...
 
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Because Abilify IM is approved for acute agitation, some people may be attempting to use the PO form in situations in which they feel uncomfortable giving an injection. In residency we were taught that the onset of action is too slow when absorbed through the gut, and that was the reason only the IM form is used for acute agitation. But then one of our C/L attendings, who was paranoid about QT prolongation and thus only ever wanted to recommend Abilify, one day developed the idea that it was unethical to give a patient an injection without offering them the chance to take a pill first, so she started recommending the PO form for acute agitation.

It makes me sad that you had a CL attending so scared of QTc prolongation that he/she would only use Abilify. That is all I have to say. Did the PO form work for acute agitation?

For the original question, no, I've never used prn Abilify. I don't foresee myself ever doing it either.
 
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It makes me sad that you had a CL attending so scared of QTc prolongation that he/she would only use Abilify. That is all I have to say. Did the PO form work for acute agitation?
Well, perhaps I exaggerated a bit. She would use other stuff, but would obsessively check EKGs on everyone and the moment the QTc was over 460/480, would only use Abilify.

As for whether it worked, it's hard to remember specifics. I'm sure there were times when it was given and I didn't get another call about that patient that night. But who knows whether that was because of the Abilify, or just redirection by the nurses, the patient finally getting tired enough to fall asleep, or other confounding factors. That's why we claim we don't "really know" whether something works unless there are double-blind, randomized, placebo-controlled clinical trials.

This thread has been instructive, what with multiple posters scoffing at the idea of PRN Abilify for agitation (even IM.) In my residency, there was a ton of fear of causing an adverse event on a "medically frail" patient. So in addition to the QTc panic, on both the C/L service and the gero unit they would use very low doses. Lots of Seroquel 12.5 mg and Zyprexa 2.5 mg.
 
Well, perhaps I exaggerated a bit. She would use other stuff, but would obsessively check EKGs on everyone and the moment the QTc was over 460/480, would only use Abilify.

As for whether it worked, it's hard to remember specifics. I'm sure there were times when it was given and I didn't get another call about that patient that night. But who knows whether that was because of the Abilify, or just redirection by the nurses, the patient finally getting tired enough to fall asleep, or other confounding factors. That's why we claim we don't "really know" whether something works unless there are double-blind, randomized, placebo-controlled clinical trials.

This thread has been instructive, what with multiple posters scoffing at the idea of PRN Abilify for agitation (even IM.) In my residency, there was a ton of fear of causing an adverse event on a "medically frail" patient. So in addition to the QTc panic, on both the C/L service and the gero unit they would use very low doses. Lots of Seroquel 12.5 mg and Zyprexa 2.5 mg.

Apologies for somewhat thread jacking, but you prefer seroquel/zyprexa over risperdal on gero unit for agitation?

I'm a PGY2 resident, and I'm still trying to figure out what to give for agitation to geriatric patients. So far, my consensus is: seroquel is bad, risperdal is good (like 0.25 qhs or BID at the most).

Your 2 cents?
 
I have seen IM abilify used as a PRN... and I have had a good chuckle about it.

As for QTc prolongation, I think a lot of psychiatrists don't really get it.

Most EKG machines use Bazett's simplified formula which over corrects at heart rates greater than 100. So, an agitated patient with a heart rate in the 130s is going to have a Bazett's QTc print off the EKG machine at 150-200 above the more accurate Framingham formula. Most estimates put QTc prolongation with Haldol around 10. It would take 10 doses of haldol to even begin to approach the error tolerance built into the machine.

Never the less, I see my colleagues toying around with homeopathic doses of second generation agents that cost a bundle and leave the nursing staff begging for standard issue body armor.
 
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Apologies for somewhat thread jacking, but you prefer seroquel/zyprexa over risperdal on gero unit for agitation?

I'm a PGY2 resident, and I'm still trying to figure out what to give for agitation to geriatric patients. So far, my consensus is: seroquel is bad, risperdal is good (like 0.25 qhs or BID at the most).

Your 2 cents?

Seroquel theoretically "bad" because of anticholinergic factors. Probably still not that bad -- actually commonly used, and probably totally OK. Our internists use Seroquel all the time for agitation for geriatric patients. I don't get too hung up on it. Actually nothing is that "good." Admittedly I'm not a geriatric (thank god) or CL psychiatrist.
 
In the elderly, not delirious, non-emergent, agitated patient- stay away from haldol.

Why? Cardiac risks? Our CL attendings loved haldol and used it all the time. Haldol and risperidone are so similar -- why would haldol be much worse? So admittedly I'm lazy and wanting to learn from SDN. Studies?
 
Apologies for somewhat thread jacking, but you prefer seroquel/zyprexa over risperdal on gero unit for agitation?

I'm a PGY2 resident, and I'm still trying to figure out what to give for agitation to geriatric patients. So far, my consensus is: seroquel is bad, risperdal is good (like 0.25 qhs or BID at the most).

Your 2 cents?

1. General guidelines advise avoidance of neuroleptics in the elderly as far as possible, and I think this is good advice. Also bear in mind the risks of stroking out your older patients with atypical neuroleptics, and the sensitivity to dystonia, parkinsonism, NMS particularly with conventional neuroleptics
2. non-pharmacological methods should be used first and this is often forgotten in practice even though everyone knows this is supposed to be the case. Lazy staff or lack of staffing are not appropriate reasons for use of chemical cosh. Even when drugs are needed, the overall burden may be reduced by using additional methods. For example hugs can sometimes be appropriate for older patients. Doll therapy or use of stuffed toys can also be helpful
3. Identifying the causes of agitation is also important and use of non-psychotropic pharmacotherapy first (i.e. analgesia, antibiotics, laxatives) UTI, pneuomonia (often without any clinical signs) constipation, dental problems, pain may be occult and significant drivers of agitation. Demented patients should have dental check ups as appropriate. Sometimes patients cannot communicate their pain. Prescribing scheduled tylenol in patients who you suspect of pain may be helpful. Patients liable to constipation may benefit from scheduled laxatives.
4. Non-neuroleptic psychopharmacological agents are often more effective and reducing bouts of agitation. For example the recent CitAD study showed that citalopram can significantly reduce agitation and carer distress in Alzheimer's disease. Not very helpful for depression. Prazosin has also been used with mixed success for agitation in the setting of dementia. Patients with Lewy Body Disease can experience significant reduction in agitation with rivastigmine. Although acetylcholinesterase inhibitors are fairly useless in Alzheimer's, LBD which involves significant cholinergic deficiency has a somewhat more robust response including reduction of confusion, hallucinations, and agitation driven by the former two.
5.Non-neuroleptic sedatives have been used to in agitated dementia (e.g. trazodone, depakote) but i'm not too impressed with them
6. Remember that neuroleptics do not have great evidence for control of agitation in patient's with Alzheimer's if you read the CATIE-AD study. In that study olanzapine and risperidone had a significantly longer time to discontinuation compared with quetiapine but there was no significant difference in terms of clinical response.
7. Clinical wisdom holds that patient's with psychosis in dementia are better candidates for neuroleptics than simply agitated demented patients. In my experience (and the evidence), psychotic dementia does not respond very well to neuroleptics. Indeed, organic psychosis does not tend to have as robust a response to neuroleptics as primary psychotic illness.
8. Benzodiazepines are not to be forgotten. Though much vilified, and not without risks of falls, paradoxical disinhibition or delirium, they can be invaluable, particularly in involutional melancholia with prominent psychomotor agitation, and excited catatonia. In severe dementia, do not be afraid of benzodiazepines. The brain that has already degenerated cannot fall further into delirium.
9. restless leg syndrome, akathisia, catatonia, and delusional disorders are often overlooked in older patients
10. never forget alcohol withdrawal or other complications of alcoholism in older patients. When the reason for agitation is unclear, do not forget urine toxicology as older patients abuse substances too.
11. remember to look for and correct any nutritional deficiencies including iron, b12, folate, thiamine, and vitamin D
12. In severe cases of agitation - including in the setting of dementia, ECT can be considered taking into consideration the ethical issues. I always feel uncomfortable electrocuting 90 year olds who have no idea why there are in the ECT suite but sometimes the benefits do outweigh the risks. This needs constant re-evaluation.
13. Finally a sobering thought is that if you do nothing, the patient will probably be the same (or better) than if you intervened
 
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Most EKG machines use Bazett's simplified formula which over corrects at heart rates greater than 100. So, an agitated patient with a heart rate in the 130s is going to have a Bazett's QTc print off the EKG machine at 150-200 above the more accurate Framingham formula.
When do you get an EKG prior to medicating a patient who is agitated enough to have a pulse of 130bpm? I just don't see when your post would represent a real life scenario.
 
When do you get an EKG prior to medicating a patient who is agitated enough to have a pulse of 130bpm? I just don't see when your post would represent a real life scenario.

There's a way to calculate the other QTc in patients who are tachycardic that you do by hand after the EKG is obtained. I used to know how to do it and have now forgotten. I spoke to cardiology about it once, and they laughed.
 
Why? Cardiac risks? Our CL attendings loved haldol and used it all the time. Haldol and risperidone are so similar -- why would haldol be much worse? So admittedly I'm lazy and wanting to learn from SDN. Studies?

The APA recommends that in the absence of delirium, if nonemergency antipsychotic
medication treatment is indicated, haloperidol should not be used as a first-line agent.
http://psychiatryonline.org/doi/pdf/10.1176/appi.books.9780890426807


When do you get an EKG prior to medicating a patient who is agitated enough to have a pulse of 130bpm? I just don't see when your post would represent a real life scenario.

I routinely get EKG's on agitated patients prior to administering medications. It would be a good idea to identify the prolonged QRS and large R-waves pathognomonic of TCA overdose before you compound the problem with neuroleptics.
 
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The APA recommends that in the absence of delirium, if nonemergency antipsychotic
medication treatment is indicated, haloperidol should not be used as a first-line agent.
http://psychiatryonline.org/doi/pdf/10.1176/appi.books.9780890426807




I routinely get EKG's on agitated patients prior to administering medications. It would be a good idea to identify the prolonged QRS and large R-waves pathognomonic of TCA overdose before you compound the problem with neuroleptics.


Wow.

Here thats all we give is Haldol for agitation in delirium (in patients below 65). Above 65, I see either Seroquel or Risperdal (but I've been told to lean towards Risperdal for geriatric).
 
I routinely get EKG's on agitated patients prior to administering medications. It would be a good idea to identify the prolonged QRS and large R-waves pathognomonic of TCA overdose before you compound the problem with neuroleptics.

How does this play out, though? If theres a patient acutely agitated enough to the point of chemical sedation, there should be enough lag time from ordering the EKG that the moment has passed or they've escalated completely. Also, "you're agitated enough for an injection but could you be patient and calmly hold still so we can hook all this **** up to you?"
 
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If theres a patient acutely agitated enough to the point of chemical sedation

I should have been more clear. I am not advocating an EKG prior to emergency chemical restraint. I am referring to the more typical agitated patient that responds to persistent deescalation/redirection. The EKG is very seldom the rate limiting step on gathering diagnostics in those cases. The UA on the other hand.... can get messy.
 
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