intravenous olanzapine?

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Interesting.

Never used it. Doubt I will anytime soon. But you never know!
 
Good if you want to kill someone IMO. YOu would never survive the liability if they stopped breathing. How many of those patients that would get agitated and delirious already have gotten benzos or are on other sedating meds like precedex or what not. IM zyprexa already has a warning with giving with IM/iv ativan. The potent sedation and respiratory and circulatory depression with any IV administration would be potentially a lawsuit and dangerous IMO.

Why would you ever need it? Haldol is available and is much safer in all respects, especially given IV, other than EPS risk of course.
 
There is always a time and place for everything. Highly unlikely but it is not impossible. Psychologists can prescribe now.
 
Haldol is available and is much safer in all respects, especially given IV, other than EPS risk of course.

It is alleged that EPS (dystonia) are not an issue with IV haldol (or even non-existent?). I've seen conflicting reports that this may or may not be because it is actually a hepatic reductase metabolite of haldol which ultimately causes EPS, which is avoided via IV administration (no first-pass metabolism).

http://www.ncbi.nlm.nih.gov/pubmed/3597329

Perhaps someone else can more definitively comment on these statements.
 
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we actually had a case of documented torsades soon after IV haloperidol was administered. The patient was critically ill in the CCU and agitated. Resident wrote for IM haldol... nurse gave it IV. That night patient had torsades and died. Since he was in the CCU, the rhythm strips recorded everything. It made for quite a heated M&M that month. Anyway, correlation is not causation.
 
It was 5mg IV. I have no idea what the pre-haldol dose QTc was.
 
Really simple explanation with haldol being related to toursaddes and qtc-its because haldol has been used 1000 times more often and longer than anything else in hospital psychiatry hence most cases of toursades are from haldol but only because of the pure number of uses and not the relative risk being any higher than anything else. Abilify actually is the lowest risk.

And IV haldol definetly has EPS just not as much EPS with IV administration. There is no definitive mechanism for this and several are speculated. I have seen frequent EPS reactions with moderate IV haldol doses and it definetly happens but just at a lower rate.

Also IV haldol has a higher risk of arythmia than oral or even IM. That is the other reason it gets a bad wrap because its the only one available IV. If you gave geodon, risperdal etc IV than they would cause more incidents compared to their oral counterparts. So there is 2 reasons haldol gets the bad name-by far the most use and only one coming in IV which inherently has more potency on cardiac conduction pathways
 
Really simple explanation with haldol being related to toursaddes and qtc-its because haldol has been used 1000 times more often and longer than anything else in hospital psychiatry hence most cases of toursades are from haldol but only because of the pure number of uses and not the relative risk being any higher than anything else.

WS, this is speculative.
 
The papers I've read indicate IV haldol has a dose dependent risk of QTc Prolongation, with higher doses leading to further prolongation. I think I first read that in a BTP issue.
 
WS, this is speculative.

Well of course it is interpreting the available data and making an opinion. But it is a completely reasonable opinion and widely accepted. There are objective data on exact qt prolongation of each antipsychotic. Haldol happens to be right in the middle of the bunch so this would not explain any icreased incidence with haldol. There are the most reported TDP cases from haldol use in the literature (objectively a search will reveal this-not my opinion) and objectively haldol has been used more times over the years than any other. Also objectively no other neuroleptic is used IV in the US anyway for delirium so this is not an opinion.

Of course something that is used much more frequently and used IV which is known to increase effective dose will increase risk of TDP. Nothing is special about IV but the problem it is not dosed correctly for IV, therefore people end up getting much higher relative doses since they often give the same "oral" doses only into the IV. That last part is my speculation. The rest is from pure data
 
Well of course it is interpreting the available data and making an opinion. But it is a completely reasonable opinion and widely accepted. There are objective data on exact qt prolongation of each antipsychotic. Haldol happens to be right in the middle of the bunch so this would not explain any icreased incidence with haldol. There are the most reported TDP cases from haldol use in the literature (objectively a search will reveal this-not my opinion) and objectively haldol has been used more times over the years than any other. Also objectively no other neuroleptic is used IV in the US anyway for delirium so this is not an opinion.

Of course something that is used much more frequently and used IV which is known to increase effective dose will increase risk of TDP. Nothing is special about IV but the problem it is not dosed correctly for IV, therefore people end up getting much higher relative doses since they often give the same "oral" doses only into the IV. That last part is my speculation. The rest is from pure data

Haldol is not "middle of the pack" for risk of QTc prolongation. It has among (if not the absolute) lowest per-dose-equivalent risk of prolonging the QTc of the neuroleptics.
 
Haldol is not "middle of the pack" for risk of QTc prolongation. It has among (if not the absolute) lowest per-dose-equivalent risk of prolonging the QTc of the neuroleptics.

here you are again spewing off incorrect data it is right smack about average for the antipsychotics.
 
here you are again spewing off incorrect data it is right smack about average for the antipsychotics.

I refer you to Table 2 of:

Glassman AH, Bigger JT Jr. Antipsychotic drugs: prolonged QTc interval, torsade de pointes, and sudden death Am J Psychiatry. 2001 Nov;158(11):1774-82
 
QTc prolongation isn't what worries me. I really haven't seen too many problems with geodon. Its that rate of torsades. I don't think IV haldol is lowest in that category. Of course, we don't have a lot of comparison as I don't see a lot of other antipsychotics being given intravenously so its kind of a moot point...unless IV zyprexa is a safer (and available) option.

Also, doesn't zyprexa increase proinsulin c peptide and doesn't that protect against torsades? Not sure if that is correct.
 
For those who are running the old version of Vbulletin and can't actually see what is going on, Wallstreet is dangling awkwardly off the ropes and Doc Sampson has just given his hotel room number to the ring girl and told her to bring her sister.
 
For those who are running the old version of Vbulletin and can't actually see what is going on, Wallstreet is dangling awkwardly off the ropes and Doc Sampson has just given his hotel room number to the ring girl and told her to bring her sister.

:laugh:
 
QTc prolongation isn't what worries me. I really haven't seen too many problems with geodon. Its that rate of torsades. I don't think IV haldol is lowest in that category. Of course, we don't have a lot of comparison as I don't see a lot of other antipsychotics being given intravenously so its kind of a moot point...unless IV zyprexa is a safer (and available) option.

Also, doesn't zyprexa increase proinsulin c peptide and doesn't that protect against torsades? Not sure if that is correct.

So here is where WS might actually have a point. How do we estimate rate of TDP? The denominator for delirious patients receiving IV Haldol worldwide is massively larger than for any other neuroleptic, so just citing the number of reports of TDP with Haldol vs. anything else is inconclusive.

Beyond that - Haldol is a better choice for delirium than any atypical since the goal of treating delirium is to block dopamine and optimize acetylcholine. The anticholinergic load of the atypicals (in comparison to Haldol) makes them a poorer choice. Moreover, the sigma-1 antagonism of Haldol (that none of the atypicals have) have been shown to preserve neuronal stability and prevent cell death in states of oxidative stress (in animal models at least), which may well be the mechanism for the advantages of IV Haldol in delirium beyond 10 mg (which would block 99% of the D2 receptors).

WS - I'd be happy to give you the ref for that if you'd like once I get done with the ring girl and her sister.
 
So here is where WS might actually have a point. How do we estimate rate of TDP? The denominator for delirious patients receiving IV Haldol worldwide is massively larger than for any other neuroleptic, so just citing the number of reports of TDP with Haldol vs. anything else is inconclusive.

Beyond that - Haldol is a better choice for delirium than any atypical since the goal of treating delirium is to block dopamine and optimize acetylcholine. The anticholinergic load of the atypicals (in comparison to Haldol) makes them a poorer choice. Moreover, the sigma-1 antagonism of Haldol (that none of the atypicals have) have been shown to preserve neuronal stability and prevent cell death in states of oxidative stress (in animal models at least), which may well be the mechanism for the advantages of IV Haldol in delirium beyond 10 mg (which would block 99% of the D2 receptors).

WS - I'd be happy to give you the ref for that if you'd like once I get done with the ring girl and her sister.
:laugh::laugh:

good point with sigma 1 recpetors-I did not know that!
 
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