Dementia: The Bane of Emergency Medicine?
“Of all the things I’ve lost, I think I miss my mind the most” — Mark Twain
INTRODUCTION
For working clinicians in the ED there are certain presentations that are associated with fear and loathing, and perhaps worse yet, disdain and despair. Whether it is the 45-year-old male with “low back pain” (14 prior visits, requesting narcotics, and allergic to ibuprofen and tramadol), the 62-year-old who is “weak and dizzy” (on 11 medications and no PMD), or the 75-year-old male from home with a suitcase (the tail lights of the family car last seen swiftly departing the ED drop off) with “dementia.” Obviously the EP must guard against negative preconceptions in all of these cases and endeavor to avoid being “locked in” on a diagnosis before an open-minded and genuinely curious evaluation has been undertaken. The focus of this essay is the last of those three cases, with an emphasis on the fact that not all dementia is relentless, chronic and progressive like Alzheimer’s Disease. Nor is all dementia a natural and inevitable part of aging for which the EP has little to offer but a social worker and long term-placement.
A quote about the nature of EM and EPs that I like is relevant here: “Of course it is ‘X,’ after all I’ve never met a conclusion I wouldn’t jump.” Indeed, for much of emergency medicine “fast thinking” and quick conclusion reaching is a very valuable behavioral feature. Pattern recognition is critical to successful and productive (read as 2.5 patients/hour) practice. So I would never advocate that EPs abandon the quick conclusion, fast thinking and acting part of their world (after all, it is this very thing that attracted many of us to EM in the first place). Instead, I am suggesting that there are some situations and some presentations that require a more nuanced approach and dementia, particularly new onset dementia, is one of them. Dementia is among those ED entities that require more attention, more thinking and more diagnostic acumen, because reversible and treatable causes of dementia are out there. As our US population ages and the baby boomers pass the age of 60, the importance of reversible causes of dementia is increasing. Further, I would note that identifying these entities (reversible dementias) can be very satisfying and will profoundly impact those patients’ healthcare trajectories! On the flip side, missing these reversible dementias can sentence these patients to institutionalized care and a predictably miserable end to their life that might take years……..reminding us all that there are worse things than dying!
In this month’s abstracts is a paper titled Frequency of dementia syndromes with a potentially treatable cause in geriatric in-patients: analysis of a 1-year interval, by Marija Djukic et al, in the European Archives of Psychiatry and Clinical Neurosciences (2015) 265:429–438. No doubt you wait at home with anticipation for this very journal, but I chose this paper because I am always harping on the residents regarding the CBC and the red cell indices when evaluating older patients with altered mental status. This paper added further support and found B12 deficiencies to be the second most common treatable, reversible cause of dementia! It’s a darn vitamin, and the data for the diagnosis was there at admission, and yet they had NOT been treated. This also echoes my experiences. Overall, the authors found a treatable cause of dementia in 18% of those with previously known dementia, and a treatable cause of dementia was found in 31% of the new onset cases!! Amazing, and increasingly important (see epi below).
THE AGING OF AMERICA
Look at the graph below which depicts US aging population projections. The rate at which we are aging is astounding and reflects both increased longevity and decreasing birth rates. For some EPs you can go an entire shift without seeing a patient under 60, especially if you have an independent pediatrics track or pod. In some countries it is even worse, notably Japan, where a declining birth rate is shaping policy.
Now, superimpose these data on what is known about the age of onset for dementia. Dementia can begin as early as age 50, but the rate of cases goes up rapidly thereafter. If even 10% of these cases are reversible (estimates are that anywhere from 5–30% are reversible) this is very important. For “new onset” not previously worked-up patients, the number of reversible cases is at the high end (15–30%). Indeed there is ED diagnostic work to be done, and each of these “new onset” cases should be perceived as having about a 1 in 3 chance that we can find something really important to do! Nearly ONE IN THREE!
From these data, it is clear that the thing that is really “booming” among the baby boomers is an epidemic of dementia (which may well exceed the epidemic of CHF). As EPs if we just raise the white flag of intellectual surrender, and fail to identify the reversible causes, the cost to the system will be enormous. SNFs will be chock-a-block full with people in soft restraints being medicated into silence until a benzo-induced pneumonia, an aggressive skin and soft tissue infection, or a PE, mercifully ends it.
SOME ASPECTS OF THE CBC AND B12 DEFICIENCY
Everyone will get the B12 deficient case where the hemoglobin is 5 and the mean corpuscular volume (MCV) is 109. This severe anemia + very big megaloblastic cells does identify B12 deficiency in many cases, but that is not the most common finding on the CBC for these B12 deficient patients. It takes just a little more savvy.
A more common CBC finding is mild anemia (Hgb of 10–12mg/dl) and a normal MCV. You might think it can’t be “megaloblastic” anemia if it is NOT megaloblastic. But remember that the M in MCV stands for “mean”. So a normal MCV could occur with a mixed red cell population where some RBCs were small (microcytic) due to blood loss (maybe from chronic ASA in a 72-year-old), and some red cells were really large (macrocytic) due to B12 deficiency in the same newly demented 72-year-old. The MEAN corpuscular volume will then be normal, which is why another red cell index is provided on the CBC. It is this number that is mostly ignored: the RDW or red cell distribution width. If you have some RBCs with a volume as small as 50, and some as large as 110, the RDW is huge. The normal tight bell curve of RBC volumes has been spread out and the curve might even have TWO peaks in it. Add a low reticulocyte count (<2) and you are DONE. Atrophic gastritis and loss of Intrinsic Factor becomes more common with aging, and these patients often have comorbidities causing other anemias. If B12 levels are indeterminate, a methylmalonic acid level is more sensitive still. My point is that just by understanding the RDW you will identify cases!
In older times this was less of a problem because a hematologist would look at the blood smear with a microscope, and finding of a PMN with a hypersegmented (>5 lobed) nucleus would establish the diagnosis of a B12-deficient anemia. Now a hematologist never looks at a smear unless specifically consulted or a smear analysis is independently ordered (find that one on your CPOE). As you see below, this is not a very subtle finding, and would predictably be found if the smears were to be evaluated, but they aren’t in 2015.
LOOK FOR THYROID DISORDERS
Most EDs now can order a stat TSH with a turn-around time of an hour. Undiagnosed thyroid axis disorders can cause dementia, depression, heart failure and more. While newly available tests like the D-dimer, BNP levels, and Procalcitonin levels have received lots of attention over the last decade, I would posit that rapid TSH testing in the ED has quietly had much greater yield than all of those previously mentioned (and somewhat dubious) tests combined. For those with new-onset dementia, thyroid testing is important because apathetic thyrotoxicosis, hypothyroidism and drug-induced thyroid problems, like amiodarone-induced thyrotoxicosis, are all treatable diseases in which the “dementia” may dramatically resolve. Gan EH et al, in the J Clin Endocrinol Metab 2012 Oct, 97(10):3438–49 noted that “there is a substantial body of evidence to support the association between subclinical hypothyroidism and cognitive impairment,” and clearly this is more true with overt thyroid disease. This reversible entity might impact up to 1 in 20 but falls well below B12 deficiency in importance and also falls below depressive pseudodementia (noted prior).
DEPRESSIVE PSEUDODEMENTIA
In most analyses of reversible treatable dementias, depression is the most common cause (B 12 is number two). Psychiatric treatment and antidepressant medications can result in some remarkable recoveries with benefit lasting for years (although there may ultimately be a higher rate of true dementia further down the road). A good psychiatric assessment of depression is therefore critical in new-onset dementia. The table below helps to differentiate depressive pseudodementia from dementia.
THE DEMENTIA DIFFERENTIAL DIAGNOSIS
For many medical students and residents, a simple mnemonic to remember what to consider and what to order has been created. Sometimes it is useful for the EP to go back in time and refresh these basics, especially when you are faced with an impending epidemic of the disease (as we all age). I offer you two of these tools from my formative years that still seem to meet the challenge.
D = drug-induced
E = emotions (depression especially)
M = metabolic and endocrine issues
E = eyes and ears (sensory problems)
N = nutritional issues (B12 and Vit. D)
T = tumors
I = infections
A = alcohol
S = sleep disorders and rarely seizures
HOW TO WORK IT UP?
(SEND A DEMENTIA 6-PACK!)
1. Head CT (to r/o tumors, etc.)
2. CBC (check MCV+RDW, ?smear) + B12
3. Chem 7 (Na+, Addisonian, Glu, osm)
4. VDRL, poss need for CSF
5. Tox screen with alcohols
6. TSH
The differential can Include many other “zebras,” but unless something specific triggers the further work-up, a diagnostic “safari” (that’s where the zebras live) is not indicated. Obviously, if you think it is non-convulsive status epilepticus, (in the “S” above) get an EEG. Having noted that, a few things become clear when you research this topic further. A huge array of Alzhiemer’s Disease mimics exist and some patients don’t get a diagnosis until autopsy. My limited search found these: Multiple Sclerosis, Hashimoto’s Thyroiditis, Sarcoidosis, Prion Disease, Hyperparathyroidism, Vitamin D disorders, and Restless Leg Syndrome-induced Insomnia. The EP is urged to avoid being locked in early, stay curious, and get as much medical detail and old records as possible before accepting new onset dementia as irreversible!
THE CLOCK DRAWING TEST
This single neurologic test can be rapidly administered, has been validated and yields important clinical information about cognitive impairment. In the paper by Salen, P., et al, J Emerg Med 37(1):8, July 2009 (in the EMA database), a score less than four reliably established cognitive impairment. In another paper by Wilber, S.T., et al, Acad Emerg Med 12(7):612, July 2005, the clock drawing test as part of the Mini-cog test (also adds three random word recall) had a NPV of 93%, and a sensitivity (compared to the 30-minute Mini-Mental Status Exam) of 75%. Knowing this can help you prevent ED bounce-backs among which dementia patients are over-represented (see Gabayan GZ et al, Ann Emerg Med 62(2):136, August 2013).
NOT A REVERSIBLE DEMENTIA: Involve Palliative Care!
The initial “Choosing Wisely” campaign for EM in 2013 included one “big ticket” item which was end-of-life care including palliative care. When the diagnostic search for a reversible cause fails (EM is central to this task) then palliative care options should be explored and EM can be part of initiating this process. EPs perceive many barriers to initiating palliative care in the ED. In the EMA database, a paper by Lamba, S, et al, in J Palliat Med 16(2):143, February 2013 described barriers to palliative care as perceived by EPs. Among the barriers noted were lack of access to a 24/7 consult service, and incomplete access to complete medical records which added to their diagnostic uncertainty (“I don’t know what work-up has been done already?”).
William K. Mallon MD DTMH
Professor of Clinical Emergency Medicine
Department of Emergency Medicine
Stony Brook University Hospital (SUNY)
Stony Brook, New York
