Using an Inhaled Antipsychotic for Agitation

Here is a link to an interesting trial of inhaled loxapine to treat agitation. It looks like it was effective vs. placebo. The comments suggest the chosen analysis was perhaps easier to find a significant effect with.

The idea of this is intriguing.... I would love to hear from any of you that have used/administered this inhaled agent... I certainly have seen loxapine used - just not inhaled... actually it probably would never have been my first choice agent to treat agitation also.

So can anyone out there describe how exactly this agent is used? At what point it kicks in? Is it an inhaler like those used for asthma (i.e. I am sure we can't 'spray' the drug at people... or we'd all be dosed! that might be amusing!)

Is the administration of an inhaled version easier in agitated folks than the shot (I know personally I would prefer most anything to a shot... particularly if onset of action for the drug is equal to or faster than onset IM....)

Here is a link to the summary page I found... I'll have to track down the actual study later...!

http://plus.mcmaster.ca/EvidenceUpdates/NewArticles.aspx?Page=1&ArticleID=38260#Data

Psych APRN Licensure, Certification and Education: Psych CNS & Psych NP

Here is a message I wrote on the APNA Member's Bridge today regarding the dilemmas faced by Psych Mental Health APRN's. I hope you visit the APNA website and become a part of the conversation...

I wanted to share my views about a conversation that has come up sporadically over time...
First I would like to start with a Thank you to the APNA group that examined the issue of advanced practice preparation, and made recommendations regarding our future. I think you tackled one important part of the many questions that have arisen since LACE came out. I agree that an important starting place for Advanced Practice Psychiatric Nursing in the future is to have one base of preparation and certification that is unified, and that prepares nurse clinicians for basic (i.e. beginning) competence and practice in the roles of psychotherapist, pharmacotherapy, and consultation-liaison work. I agree that the education should be across the lifespan if we seek to have a basic level of unified certification. Calling this clinician a Psychiatric Mental Health Nurse Practitioner (PMHNP) is fine with me. I thank the group for finding consensus around this issue.

There are 2 extremely important issues that relate to LACE that require further planning in my view. They are: 1. What happens to already certified, practicing Advanced Practice PMH nurses, particularly those with CNS certification. (but also in the future depending on whether separate 'family' vs. 'adult' PMHNP certifications remain - i.e. whichever certification goes by the wayside, that group could be potentially disenfranchised as well).

2. Who will be deemed eligible to educate, precept, 'train' new Advanced Practice PMH nurses.

In my view APNA needs a very clear plan that is very careful not to disenfranchise all of the highly experienced, practicing Advanced Practice PMH nurses. We need careful planning beyond a statement like,
'in 2015 or 2020 we will have 'enough' PMH NP certified APRN's to educate the new PMHNP's'
'in 2015 or 2020 all of the practicing, certified and licensed CNS's will have retired'
The problem here is that I have not seen a workforce analysis that truly indicates we will ever 'have enough' nursing faculty. I know I currently do not have enough practicing APRN's certified as CNS's and NP's to cover the number of students we would like to admit to our program.
I agree we will have more PMHNP's by 2020, but that does not mean CNS's should retire at that time.
We need some way to use our experienced APRN's in psych that is inclusive of both types of certification.
(and I do not expect that all CNS's should be required to return to school for the 3- P's and 500 clinical hours like I just finished to a cost of between $8000 - $10,000).

We need to issue continued clear statements that in PMH nursing the roles of the CNS and NP are nearly identical (i.e. was it 95% or 98% the same (per the logical job analysis paper by Rice & MOller I believe)).

To not be inclusive of both types of certification will risk that our current expert nurse faculty are out of their jobs... or preceptors will no longer be 'eligible to precept' (who by the way with CNS certification developed the role of PMHNP and educated our current group of PMHNP's... so I suspect they know something about the role and how to teach students to be PMHNP's.)

I do not want to get into a conversation about who is better or which certification is 'better'.
I completely agree that perhaps the better title today is Psych NP.
I do see individuals sharing opinions about who is better or differences in role that are typically state-bound. Meaning that in some states the board of nursing does not allow one kind of certified psych nurse to do the same thing as the other. We need to recognize that this does vary from state to state. Just because CNS's in one state can't prescribe and NP's can prescribe does not mean that in other states both CNS's and NP's can prescribe.

In my view the education and training for CNS's and NP's are (like the role/job) nearly identical. If anything the CNS has more role components in their education. In today's school of nursing, the preparation should be nearly identical. This however does mean that some clinicians can also choose not to prescribe and that is fine with me. Just as some clinicians may not choose to do family therapy. If that role or responsibility is not wanted by a clinician, I don't think we should force them to.

As for who can precept a student being prepared to be a PMHNP. I would hope we keep our heads about this matter too. I believe that the student should be precepted by certified and licensed APRN's in their clinical work. (this means certified as a psych CNS or psych NP) I believe that whoever precepts should be competent to perform and/or supervise the objectives that are part of the course that the student is taking. I believe that that APRN can also call upon other clinicians they work with - whether MD's, psychologists, MSW's, or RN's - to offer experiences that are coordinated and reviewed in the APRN's supervision with the student.
In a state where there is role delineation that does not allow prescribing by a CNS, then I think the faculty should work to be sure that a student is guided to learn the prescribing role either from an NP or MD.

I think we need to be careful to not divide up the PMH Advanced Practice role in a way that is blind to the full areas of practice available at the Advanced Practice level.

My final thought: Let us be very careful to understand that being educated in a lifespan way is very different from being an expert in child or being an expert in adult. That requires specific focus and training. Some programs do offer this (I believe ours is a good example). In my view we also need to be careful in what we are really saying when we identify what we mean by beginning competence, a lifespan approach, and expertise with particular age groups.

Thanks for letting me have my say,

Joanne

Here is a link to the APNA member bridge where this was posted... and where the conversation is continuing... http://community.apna.org/APNA/APNA/eGroups/DigestViewer/Default.aspx?GroupId=7&UserKey=82d60e30-46b4-40dd-b96b-77c0b0f2bd19

Here is the link to APNA's statement on Advanced Practice PMH roles: http://www.apna.org/i4a/pages/index.cfm?pageid=4354

Here is the link to the LACE document that has created controversy regarding roles:
http://www.apna.org/i4a/pages/index.cfm?pageid=3498

I hope you all make your voices heard!!!

Deafness linked to Dementia?

A recent article suggests that those with moderate to severe hearing loss may be at greater risk of dementia. The association was found in the Baltimore Longitudinal Study of Aging, in a prospective study, a group of 795 participants had both hearing and cognitive testing over a five year period from 1990 to 1994, and were free of confirmed or suspected dementia at baseline. The authors suggest a relationship between loss of ability to hear verbal communication and dementia.

The idea that the social isolation due to hearing loss might be harmful is not a new one. However to find such a direct link of hearing loss to something as serious as dementia is interesting. What kinds of things would be important to know about the study? Well, things like: When was the baseline evaluation identifying individuals as free of confirmed or suspected dementia? Was it in 1958 or was it in the 90’s when this evaluation occurred? AND Why was the hearing test done? Was it part of the longitudinal study protocol or was it individuals who also had a test that was then obtained by the study?
So what could this mean? Does it mean that social isolation is harmful? (do other socially isolated people get dementia at higher rates?) Does it mean that some similar mechanism is involved with both hearing loss and dementia? Is it a physiologic process? If so, what might be involved?

Do others with moderate to severe hearing loss have the same association with dementia? (what about those with hearing loss from birth or early in life? What about hearing loss due to accidental injury?) Do those with dementia have a higher rate of moderate to severe hearing loss?

An interesting finding – but one that certainly raises many more questions. I would think several of these questions could be answered in existing cohorts of those with dementia or those with hearing loss.

Here is a link to a report of this study which was originally published in the Archives of Neurology (Lin, 2011, Hearing Loss and incident dementia., Archives of Neurology, 68(2), 214-220).
http://www.medpagetoday.com/Neurology/Dementia/24867?utm_content=GroupCL&utm_medium=email&impressionId=1297757253079&utm_campaign=DailyHeadlines&utm_source=mSpoke&userid=230719

Diet Soda and Cardiovascular Disease

The media is reporting an interesting study by a researcher at the University of Miami, Hannah Gardener (I believe based on an abstract presented at a conference - I cannot find a link to the actual study info). It finds that those who drink diet soda daily have a 61% greater risk of having a heart attack or stroke. (and who knows why in remembering this I'm thinking of diet cola? or a particular brand of diet cola?)

Is this surprising? Well as it is currently being reported by the media - that diet soda 'causes' stroke or heart attack - that is stunning! However we really need to have some more information about that study to appropriately digest it and decide whether it has anything to do with causality or disease outcomes.

As I note, I have not seen the actual study - just a couple of media reports (see links below) - so it is impossible to know... but here is what I would consider:

• At what point in life were people studied? Is it young people drinking diet soda and ending up with strokes or older folks?
• When were measures made of diet soda ‘exposure’ vs. when outcomes were identified?
• How does risk in diet soda drinkers compare to risk in drinkers of ‘regular’ soda?
• Who drinks diet soda? What cardiovascular disease (CVD) risk factors do they have already?
• What other things do diet soda drinkers do that could increase their risk? Is there a tendency for those who are overweight or obese to drink it? Is there a tendency for those who drink diet soda to exercise less? What is the overall health of diet soda drinkers as a group? Do we know that obesity and lack of exercise increase risk for heart attack and stroke? (I think we all know the answer to that)
• What other factors associated with greater risk of heart attack and stroke may be common to diet soda drinkers?
• How were these common risk factors managed in the study - were those with early signs of CVD excluded from the study?
• If all other risk factors were controlled for in the study is it still possible to get an erroneous result (yes, because there is probably great similarity between these factors which tends to result in difficulty modeling things statistically)
• Perhaps most important of all: What would be the proposed mechanism of how diet soda 'causes' heart disease or stroke? Is it additives of some sort? Is it caffeine? Is it artificial sweeteners?

From some of the reports I saw, the researcher was careful to say that all this result meant was that further examination of the role of diet soda was needed... I agree with that… but the media has gone way beyond that in some cases…

It's also interesting to think about how you could design a study to prove/disprove this... would we take a healthy group of people and randomize them to drink diet soda daily vs. some other non-diet 'placebo type drink' (i.e. not regular soda I am certain) and see if there is greater risk at the end of the study? How long would we need to wait to see outcomes?
It is tough to actually know and adequately study this question...

Here are the links... http://www.denverpost.com/nationworld/ci_17345702 or

http://health.usnews.com/health-news/family-health/heart/articles/2011/02/09/can-diet-soda-boost-your-stroke-risk or

http://www.dbtechno.com/health/2011/02/09/diet-soda-increases-your-chance-of-having-a-heart-attack/

Modeling Internet Addiction

Most of us use the internet regularly. It has replaced earlier forms of communication like writing letters, reading news or magazines, phoning, or visiting. Many would agree that it is easier and more convenient than more traditional forms of communication. I also think that the stimulation of using the internet is far more rewarding than other formats offer. I can’t back that up with evidence, but I do know I look forward to checking my email, text messages, etc in much the same way that once a day checking of my mailbox offered (at least until adulthood when bills were often the most frequent arrivals!). Remember the wonderful surprise of finding a letter from a friend addressed to you! We currently have all kinds of places to ‘check’ for stimulation and reward on our computers or other electronic devices.

I am sometimes amazed at myself and others when I see the interest involved in electronic devices… including laptops, ipads, ipods, iphones, androids, and handheld electronic games (like the Nintendo DS). Our internet service was out for a few days this week and we were frustrated and annoyed that we were limited and could not interact with or easily check our devices as usual. It is interesting to reflect on how much we do rely on various forms of electronic communication.

An interesting study was done by Kwon & Chung (2011) studying the use of internet games by adolescents. They applied Baumeister’s escape from self theory (1991) to the phenomenon of pathologic use of internet games. Baumeister’s model has been used to understand other self-destructive behaviors including suicide and addictions to both substances and gambling. This model brings together many of the factors that prior research identifies as associated with internet game addiction, for example depressive symptoms, differences between real and idealized perceptions of self, escape from self, and interpersonal problems involving family and friends.

This model does not directly investigate the role of impulsivity and sensation seeking in internet game addiction. Kwon & Chung (2011) find that differences between real and idealized self perception are associated with depressive mood, which is associated with escape from self and also associated with internet game addiction. The study uses structural equation modeling to identify the strength and type of associations. However this form of modeling does not really offer a cause and effect analysis of events, it is based on cross sectional data which means all factors were present at the same time in participants. But it does establish that these relationships are important in the addiction behavior.

The authors identify that in Korean adolescents, use of internet games begins quite early. I suspect this is also true in other locations. I wonder about the changes that might be taking place in our brains and our children’s brains as we feed ourselves the stimulation readily available from electronic devices today. It is quite different from growing up with TV and radio – which was less satisfying given that you could not find material at any time of day that was personally satisfying and stimulating like we can today. The major factor missing in the study by Kwon is that there is no accounting for potential physiologic effects of electronic stimulation. The immediacy of gratification and plethora of forms of stimuli are so different than for prior experience and generations.

I think I will spend some free time exploring the internet for information about physiologic effects :) (who’s addicted?!) and perhaps I will see if I can buy an electronic version of Baumeister’s book on escape theory! If you know of work that has been done on the physiology let me know- send me a link or do tell about it in the comments!

References:
Kwon, J.H., & Chung, C.S. (2011). The effects of escape from self and interpersonal relationship on the pathological use of internet games. Community Mental Health Journal, 47, 113-121. http://www.ncbi.nlm.nih.gov/pubmed/19701792

Here are references to Baumeister’s model if you are interested:
Baumeister, R.F. (1990). Suicide as escape from self. Psychological Review, 9, 90-113.
Baumeister, R.F. (1991). Escaping the self: Alcoholism, spirituality, masochism, and other flights from the burden of selfhood. New York, NY: Harper Collins.