The Unfortunate Therapeutic Myopia of the EMR

January 19, 2012

There’s a lot you can say about an electronic medical record (EMR).  Some of it is good: it’s more legible than a written chart, it facilitates billing, and it’s (usually) readily accessible.  On the other hand, EMRs are often cumbersome and confusing, they encourage “checklist”-style medicine, and they contain a lot of useless or duplicate information.  But a recent experience in my child/adolescent clinic opened my eyes to where an EMR might really mislead us.

David, a 9 year-old elementary school student, has been coming to the clinic every month for the last three years.  He carries a diagnosis of “bipolar disorder,” manifested primarily as extreme shifts in mood, easy irritability, insomnia, and trouble controlling his temper, both in the classroom and at home.  Previous doctors had diagnosed “oppositional defiant disorder,” then ADHD, then bipolar.  He had had a trial of psychostimulants with no effect, as well as some brief behavioral therapy.  Somewhere along the way, a combination of clonidine and Risperdal was started, and those have been David’s meds for the last year.

The information in the above paragraph came from my single interaction with David and his mom.  It was the first time I had seen David; he was added to my schedule at the last minute because the doctor he had been seeing for the last four months—a locum tenens doc—was unavailable.

Shortly before the visit, I had opened David’s EMR record to review his case, but it was not very informative.  Our EMR only allows one note to be open at a time, and I saw the same thing—”bipolar, stable, continue current meds”—and some other text, apparently cut & pasted, in each of his last 3-4 notes.  This was no big surprise; EMRs are full of cut & pasted material, plus lots of other boilerplate stuff that is necessary for legal & billing purposes but can easily be ignored.  The take-home message, at the time, was that David had been fairly stable for at least the last few months and probably just needed a refill.

During the appointment, I took note that David was a very pleasant child, agreeable and polite.  Mom said he had been “doing well.”  But I also noticed that, throughout the interview, David’s mom was behaving strangely—her head bobbed rhythmically side to side, and her arms moved in a writhing motion.  She spoke tangentially and demonstrated some acute (and extreme) shifts in emotion, at one point even crying suddenly, with no obvious trigger.

I asked questions about their home environment, David’s access to drugs and alcohol, etc., and I learned that mom used Vicodin, Soma, and Xanax.  She admitted that they weren’t prescribed to her—she bought them from friends.  Moreover, she reported that she “had just taken a few Xanax to get out the door this morning” which, she said, “might explain why I’m acting like this.”  She also shared with me that she had been sent to jail four years ago on an accusation of child abuse (she had allegedly struck her teenage daughter during an argument), at which time David and his brothers were sent to an emergency children’s shelter for four nights.

Even though I’m not David’s regular doctor, I felt that these details were relevant to his case.  It was entirely possible, in my opinion, that David’s home environment—a mother using prescription drugs inappropriately, a possible history of trauma—had contributed to his mood lability and “temper dysregulation,” something that a “bipolar” label might mask.

But I’m not writing this to argue that David isn’t “bipolar.”  Instead, I wish to point out that I obtained these details simply by observing the interaction between David and his mom over the course of ~30 minutes, and asking a few questions, and not by reading his EMR record.  In fact, after the appointment I reviewed the last 12 months of his EMR record, which showed dozens of psychiatrists’ notes, therapists’ notes, case manager’s notes, demographic updates, and “treatment plans,” and all of it was generally the same:  diagnosis, brief status updates, LOTS of boilerplate mumbo-jumbo, pages and pages of checkboxes, a few mentions of symptoms.  Nothing about David’s home situation or mom’s past.  In fact, nothing about mom at all.  I could not have been the first clinician to have had concerns about David’s home environment, but if such information was to be found in his EMR record, I had no idea where.

Medical charts—particularly in psychiatry—are living documents.  To any physician who has practiced for more than a decade or so, simply opening an actual, physical, paper chart can be like unfolding a treasure map:  you don’t know what you’ll find, but you know that there may be riches to be revealed.   Sometimes, while thumbing through the chart, a note jumps out because it’s clearly detailed or something relevant is highlighted or “flagged” (in the past, I learned how to spot the handwriting of the more perceptive and thorough clinicians).  Devices like Post-It notes or folded pages provide easy—albeit low-tech—access to relevant information.  Also, a thick paper chart means a long (or complicated) history in treatment, necessitating a more thorough review.  Sometimes the absence of notes over a period of time indicates a period of decompensation, a move, or, possibly a period of remission.  All of this is available, literally, at one’s fingertips.

EMRs are far more restrictive.  In David’s case, the EMR was my only source of information—apart from David himself.  And for David, it seemed sterile, bland, just a series of “check-ins” of a bipolar kid on Risperdal.  There was probably more info somewhere in there, but it was too difficult and non-intuitive to access.  Hence, the practice (adopted by most clinicians) of just opening up the patient’s most recent note—and that’s it.

Unfortunately, this leads to a therapeutic myopia that may change how we practice medicine.  EMRs, when used this way, are here-and-now.  They have become the medical equivalent of Facebook.  When I log on to the EMR, I see my patient’s most recent note—a “status update,” so to speak—but not much else.  It takes time and effort to search through a patient’s profile for more relevant historical info—and that’s if you know where to look.  After working with seven different EMRs in the last six years, I can say that they’re all pretty similar in this regard.  And if an electronic chart is only going to be used for its most recent note, there’s no incentive to be thorough.

Access to information is great.  But the “usability” of EMRs is so poor that we have easy access only to what the last clinician thought was important.  Or better yet, what he or she decided to document.  The rest—like David’s home life, the potential impact of his mother’s behavior on his symptoms, and environmental factors that require our ongoing attention, all of which may be far more meaningful than David’s last Risperdal dose—must be obtained “from scratch.”  If it is obtained at all.

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Do Antipsychotics Treat PTSD?

August 23, 2011

Do antipsychotics treat PTSD?  It depends.  That seems to be the best response I can give, based on the results of two recent studies on this complex disorder.  A better question, though, might be: what do antipsychotics treat in PTSD?

One of these reports, a controlled, double-blinded study of the atypical antipsychotic risperidone (Risperdal) for the treatment of “military service-related PTSD,” was featured in a New York Times article earlier this month.  The NYT headline proclaimed, somewhat unceremoniously:  “Antipsychotic Use is Questioned for Combat Stress.”  And indeed, the actual study, published in the Journal of the American Medical Association (JAMA), demonstrated that a six-month trial of risperidone did not improve patients’ scores in a scale of PTSD symptoms, when compared to placebo.

But almost simultaneously, another paper was published in the online journal BMC Psychiatry, stating that Abilify—a different atypical antipsychotic—actually did help patients with “military-related PTSD with major depression.”

So what are we to conclude?  Even though there are some key differences between the studies (which I’ll mention below), a brief survey of the headlines might leave the impression that the two reports “cancel each other out.”  In reality, I think it’s safe to say that neither study contributes very much to our treatment of PTSD.  But it’s not because of the equivocal results.  Instead, it’s a consequence of the premises upon which the two studies were based.

PTSD, or post-traumatic stress disorder, is an incredibly complicated condition.  The diagnosis was first given to Vietnam veterans who, for years after their service, experienced symptoms of increased physiological arousal, avoidance of stimuli associated with their wartime experience, and continual re-experiencing (in the form of nightmares or flashbacks) of the trauma they experienced or observed.  It’s essentially a re-formulation of conditions that were, in earlier years, labeled “shell shock” or “combat fatigue.”

Since the introduction of this disorder in 1980 (in DSM-III), the diagnostic umbrella of PTSD has grown to include victims of sexual and physical abuse, traumatic accidents, natural disasters, terrorist attacks (like the September 11 massacre), and other criminal acts.  Some have even argued that poverty or unfortunate psychosocial circumstances may also qualify as the “traumatic” event.

Not only are the types of stressors that cause PTSD widely variable, but so are the symptoms that ultimately develop.  Some patients complain of minor but persistent symptoms, while others experience infrequent but intense exacerbations.  Similarly, the neurobiology of PTSD is still poorly understood, and may vary from person to person.  And we’ve only just begun to understand protective factors for PTSD, such as the concept of “resilience.”

Does it even make sense to say that one drug can (or cannot) treat such a complex disorder?  Take, for instance, the scale used in the JAMA article to measure patients’ PTSD symptoms.  The PTSD score they used as the outcome measure was the Clinician-Administered PTSD Scale, or CAPS, considered the “gold standard” for PTSD diagnosis.  But the CAPS includes 30 items, ranging from sleep disturbances to concentration difficulties to “survivor guilt”:

It doesn’t take a cognitive psychologist or neuroscientist to recognize that these 30 domains—all features of what we consider “clinical” PTSD—could be explained by just as many, if not more, neural pathways, and may be experienced in entirely different ways, depending upon on one’s psychological makeup and the nature of one’s past trauma.

In other words, saying that Risperdal is “not effective” for PTSD is like saying that acupuncture is not effective for chronic pain, or that a low-carb diet is not an effective way to lose weight.  Statistically speaking, these interventions might not help most patients, but in some, they may indeed play a crucial role.  We just don’t understand the disorders well enough.

[By the way, what about the other study, which reported that Abilify was helpful?  Well, this study was a retrospective review of patients who were prescribed Abilify, not a randomized, placebo-controlled trial.  And it did not use the CAPS, but the PCL-M, a shorter survey of PTSD symptoms.  Moreover, it only included 27 of the 123 veterans who agreed to take Abilify, and I cannot, for the life of me, figure out why the other 96 were excluded from their analysis.]

Anyway, the bottom line is this:  PTSD is a complicated, multifaceted disorder—probably a combination of disorders, similar to much of what we see in psychiatry.  To say that one medication “works” or another “doesn’t work” oversimplifies the condition almost to the point of absurdity.  And for the New York Times to publicize such a finding, only gives more credence to the misconception that a prescription medication is (or has the potential to be) the treatment of choice for all patients with a given diagnosis.

What we need is not another drug trial for PTSD, but rather a better understanding of the psychological and neurobiological underpinnings of the disease, a comprehensive analysis of which symptoms respond to which drug, which aspects of the disorder are not amenable to medication management, and how individuals differ in their experience of the disorder and in the tools (pharmacological and otherwise) they can use to overcome their despair.  Anything else is a failure to recognize the human aspects of the disease, and an issuance of false hope to those who suffer.


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