This is a shout out regarding the American Delirium Society Annual Meeting in Nashville which starts today. I’m hoping to catch live tweets about the highlights in the next couple of days. I’m always on duty when the meeting is held. The one I did attend a few years ago was fantastic. There was a ton of practical clinically oriented seminars, thought-provoking research presentations, and I got to hobnob with luminaries like Drs. Alasdair MacLullich, Wes Ely, Sharon Inouye, Joseph Flaherty, and many others too numerous to mention.
See the video above, which is an outstanding general educational production about the critical importance of understanding why it’s so important to prevent delirium.
Look for tweets about this meeting and about the science and practice of preventing delirium. Delirium Awareness Week June 14-21 is also coming up!
I’ve got a sharp medical student, Terrence Wong, on my team who is participating in a new delirium detection study headed by one of my colleagues, Dr. Gen Shinozaki, MD working with surgeon Dr. John Cromwell, MD on using a simplified EEG procedure to detect delirium. It just might help move the clouds away from a path forward toward improving delirium prevention. Recall my post from over a couple of months ago in which I mentioned that I sent a message to the American Delirium Society blog page, asking for feedback about it.
I have been expecting one or two medical students connected with the project to rotate through the general hospital psychiatry consultation service. The leaders of the study want them to get an idea how psychiatric consultants usually assess delirium. The medical student has some background in marketing and has an interest in product development which would reduce waste and increase efficiency in health care.
He’s getting a look at the smokejumper’s view of the general hospital as we rush around putting out fires–getting singed in the process, I might add. I have some thoughts about delirium detection, which I posted back in January .
Anyway, I gave the medical student one of my cheat cards outlining the Confusion Assessment Method (CAM) and the Mini-Cog. So far there hasn’t been a good opportunity for me to demonstrate the usual way I detect delirium using those methods. It’s been pretty hectic and we’ve had to make educated guesses, get collateral history from family members about patients’ baseline behavior and cognition, dodge flailing arms and legs in the process…that kind of thing.
We’ve had an opportunity to actually recommend standard EEG to assess for delirium, which highlighted one of the challenges. How do you tell whether an abnormality would be a patient’s “normal” baseline if the EEG is abnormal? However, it also helped move the medical evaluation further along.
Anyway, here’s a blog post by Terrence on using EEG technology to improve health care for delirium. He’s right on target when he points out the limitations of antipsychotics for delirium .
Delirium silently creeps along during the hospitalization process, only presenting when the condition has erupted to clinical attention. Intervention at that moment is too late, yet currently, the best we can do. When you talk to healthcare providers at the front lines of delirium, you’ll hear the same response echoed over and over again, “Yes when they act crazy, just hit them with some Haldol!” But when you study under a seasoned psychiatrists such as Dr. James Amos, you’ll begin to understand why that perspective is detrimental to patient care. But it doesn’t have to be that way.
Efforts to detect delirium have relied upon two major methods, both which fall short of the practical needs of a modern hospital environment. Screening instruments, largely based upon chart review and patient interview, have been unsuccessful due to challenges implementing these into clinical workflows and in providing ongoing training for healthcare providers to use such instruments. In addition, they exhibit poor sensitivity in routine use.
We believe that there is an enormous opportunity to both improve the quality of care and decrease the cost of care through use of a noninvasive, point-of-care device that accurately predicts, screens, and monitors delirium, yet is simple enough to introduce into existing clinical workflows.
The specialized EEG will be an important and useful delirium screening tool. Our research currently suggests that this may also predict delirium prior to its clinical onset. The key concept here is early detection. The phrase, “an ounce of prevention is worth a pound of cure,” strongly resonates here. If you have ever seen a patient screaming, yelling, and buckling the bed despite restraints, you’ll vividly understand why it is important to prevent this condition.
Modern medicine demands the practice of cost-effective, high-quality healthcare. This clinical research data is currently being collected at University of Iowa Hospital & Clinics (UIHC). Our models predicts significant improvement in quality safety metrics and reduced financial expenditure. The world understands the importance of detecting hyperglycemia and its subsequent treatment. Our goal is to create the glucometer of delirium, establish the proof-of-concept at UIHC, and potentially implement it worldwide.
1.van der Kooi, A. W., et al. (2015). “Delirium detection using eeg: What and how to measure.” Chest 147(1): 94-101.
BACKGROUND: Despite its frequency and impact, delirium is poorly recognized in postoperative and critically ill patients. EEG is highly sensitive to delirium but, as currently used, it is not diagnostic. To develop an EEG-based tool for delirium detection with a limited number of electrodes, we determined the optimal electrode derivation and EEG characteristic to discriminate delirium from nondelirium.METHODS: Standard EEGs were recorded in 28 patients with delirium and 28 age- and sex-matched patients who had undergone cardiothoracic surgery and were not delirious, as classified by experts using Diagnostic and Statistical Manual of Mental Disorders, 4th edition, criteria. The first minute of artifact-free EEG data with eyes closed as well as with eyes open was selected. For each derivation, six EEG parameters were evaluated. Using Mann-Whitney U tests, all combinations of derivations and parameters were compared between patients with delirium and those without. Corresponding P values, corrected for multiple testing, were ranked.RESULTS: The largest difference between patients with and without delirium and highest area under the receiver operating curve (0.99; 95% CI, 0.97-1.00) was found during the eyes-closed periods of the EEG, using electrode derivation F8-Pz (frontal-parietal) and relative δ power (median [interquartile range (IQR)] for delirium, 0.59 [IQR, 0.47-0.71] and for nondelirium, 0.20 [IQR, 0.17-0.26]; P = .0000000000018). With a cutoff value of 0.37, it resulted in a sensitivity of 100% (95% CI, 100%-100%) and specificity of 96% (95% CI, 88%-100%).CONCLUSIONS: In a homogenous population of nonsedated patients who had undergone cardiothoracic surgery, we observed that relative δ power from an eyes-closed EEG recording with only two electrodes in a frontal-parietal derivation can distinguish among patients who have delirium and those who do not.
2.Neufeld, K. J., et al. (2016). “Antipsychotic Medication for Prevention and Treatment of Delirium in Hospitalized Adults: A Systematic Review and Meta-Analysis.” J Am Geriatr Soc: n/a-n/a.
Objectives To evaluate the effectiveness of antipsychotic medications in preventing and treating delirium. Design Systematic review and meta-analysis. Setting PubMed, EMBASE, CINAHL, and ClinicalTrials.gov databases were searched from January 1, 1988, to November 26, 2013. Participants Adult surgical and medical inpatients. Intervention Antipsychotic administration for delirium prevention or treatment in randomized controlled trials or cohort studies. Measurements Two authors independently reviewed all citations, extracted relevant data, and assessed studies for potential bias. Heterogeneity was considered as chi-square P < .1 or I2 > 50%. Using a random-effects model (I2 > 50%) or a fixed-effects model (I2 < 50%), odds ratios (ORs) were calculated for dichotomous outcomes (delirium incidence and mortality), and mean or standardized mean difference for continuous outcomes (delirium duration, severity, hospital and intensive care unit (ICU) length of stay (LOS)). Sensitivity analyses included postoperative prevention studies only, exclusion of studies with high risk of bias, and typical versus atypical antipsychotics. Results Screening of 10,877 eligible records identified 19 studies. In seven studies comparing antipsychotics with placebo or no treatment for delirium prevention after surgery, there was no significant effect on delirium incidence (OR = 0.56, 95% confidence interval (CI) = 0.23–1.34, I2 = 93%). Using data reported from all 19 studies, antipsychotic use was not associated with change in delirium duration, severity, or hospital or ICU LOS, with high heterogeneity among studies. No association with mortality was detected (OR = 0.90, 95% CI = 0.62–1.29, I2 = 0%). Conclusion Current evidence does not support the use of antipsychotics for prevention or treatment of delirium. Additional methodologically rigorous studies using standardized outcome measures are needed.
My wife alerted me to an interesting article about a man arrested for driving while intoxicated who reported that he had auto-brewery syndrome. The most recent article I could find in PubMed which had any credibility cast doubt on the authenticity of the condition and I have to admit I don’t have any confidence in the very limited medical literature .
There is almost the same lack of confidence in the medical literature about Pharmacologic Approaches to Managing Delirium. OK, almost but not quite. The link takes you to the beginnings of a discussion on the American Delirium Society website about the issue and while I’m waiting for my contribution to be reviewed, I’ll copy it below:
“I’m so glad to see this basic information, although it seems inordinately difficult to do more than simply disseminate it to my colleagues in medicine and surgery. Time and time again I’m consulted to help manage delirium and the expectation is that there is some drug (usually an antipsychotic) that will stop or shorten the course or weaken the intensity of the patient’s delirium.
This can happen when the patient has hypoactive delirium, often found late because the behavioral agitation is missing and the patient doesn’t draw attention to herself. We just recently had a case presentation and short literature review on our consultation service from one of our pharmacy trainees about whether or not there is any compelling evidence that pharmacologic treatment of hypoactive delirium makes any difference in the course of the syndrome. The bottom line is there is none, essentially; at least none that would change my practice, https://thepracticalpsychosomaticist.com/2015/12/22/cpcp-pharmacologic-management-of-hypoactive-delirium/”
None of this means that I’m not open to changing my mind in the face of any compelling new evidence if it should appear–and that includes the topic of auto-brewery syndrome.
The remarks of Dr. Karin Neufeld, MD, MPH and Dr. Babar Khan, MD, MS are well taken and Dr. Neufeld’s summary might be something I would consider adding to my usual consultation recommendations:
“There is no evidence for the use of medication to prevent or shorten an episode of delirium.
We need more research in larger groups of patients with the same kinds of conditions and outcomes to see if there are very specific situations where particular medications may be useful (for example: antipsychotics like risperidone in subsyndromal delirium immediately after surgery, melatonin agonists such as Ramelteon in older hospitalized adults, antipsychotics in relation to the patient’s experience of delirium).
And this is a good time to remind you that the American Delirium Society annual meeting is coming up June 1-3, 2016 in Nashville. Here’s the registration link.
My suggestions to consultees and my talks with families revolve around the safest way to help make the patients with delirium as comfortable as possible while facilitating the search for and treatment of the causative medical conditions. It’s usually best to adopt a humble approach and to find a chair and sit down while listening carefully and saying frankly “I don’t know” when that’s called for.
By the way, one way our consultation service has found to promote the development of humility is to take our mascot for a walk about once a week. You have no idea how humbling it can be to walk all the way across the hospital from our office to the gift shop to get Hal recharged with helium. I call it getting small, or cultivating a habit of being more mindful about who we really are and what we can really do for our patients and our colleagues.
Logan, B. K. and A. W. Jones (2000). “Endogenous Ethanol ‘Auto-Brewery Syndrome’ as a Drunk-Driving Defence Challenge.” Medicine, Science and the Law 40(3): 206-215.
The concentration of ethanol in blood, breath or urine constitutes important evidence for prosecuting drunk drivers. For various reasons, the reliability of the results of forensic alcohol analysis are often challenged by the defence. One such argument for acquittal concerns the notion that alcohol could be produced naturally in the body, hence the term ‘auto-brewery’ syndrome. Although yeasts such as Candida albicans readily produce ethanol in-vitro, whether this happens to any measurable extent in healthy ambulatory subjects is an open question. Over the years, many determinations of endogenous ethanol have been made, and in a few rare instances (Japanese subjects with very serious yeast infections) an abnormally high ethanol concentration (<80 mg/dl) has been reported. In these atypical individuals, endogenous ethanol appeared to have been produced after they had eaten carbohydrate-rich foods. A particular genetic polymorphism resulting in reduced activity of enzymes involved in hepatic metabolism of ethanol and a negligible first-pass metabolism might explain ethnic differences in rates of endogenous ethanol production and clearance. Other reports of finding abnormally high concentrations of ethanol in body fluids from ostensibly healthy subjects suffer from deficiencies in study design and lack suitable control experiments or used non-specific analytical methods. With reliable gas chromatographic methods of analysis, the concentrations of endogenous ethanol in peripheral venous blood of healthy individuals, as well as those suffering from various metabolic disorders (diabetes, hepatitis, cirrhosis) ranged from 0–0.08 mg/dl. These concentrations are far too low to have any forensic or medical significance. The notion that a motorist’s state of intoxication was caused by endogenously produced ethanol lacks merit.
This is a shout-out about the American Delirium Society (ADS) 2016 meeting, which will be held in Nashville, Tennessee June 1-3, 2016. The theme is “Improving Care Through the Integration of Science and Policy.” Those interested in presenting can download the call for proposals here. Proposals for symposia, workshops and roundtables should be submitted by September 14, 2015.
I’ll probably be on duty again and will be unable to attend, but I wonder if anyone will be clarifying the role of psychostimulants in the treatment of hypoactive delirium. Most consulting psychiatrists don’t believe this intervention is ready for prime time but the idea comes up occasionally, mainly because of a persisting belief that drugs like methylphenidate can help delirious patients focus their attention, attentional dysfunction being the primary neurocognitive deficit in delirium.
I found at least one paper by W. Breitbart et al which casts doubt on that assumption .
Evidence-Based Treatment of Delirium in Patients With Cancer http://t.co/OuR1qSd1fK Psychostimulants not recommended
And I couldn’t find it mentioned in the APM Delirium Monograph on the Academy of Psychosomatic Medicine web site. Maybe the idea that psychostimulants would be helpful is based in the belief that the mechanism of action in stimulants would be the same for delirium as it is for Attention Deficit Hyperactivity Disorder (ADHD), which is doubtful because of the complexity of the pathophysiology of delirium (it isn’t just dopamine that gets deranged). However, it’s not like there is no literature about it, though it tends to be focused in the cancer patient population [2,3].
The ADS meetings are designed for just these kinds of questions and are not to be missed if you can help it, so get there!
By the way, speaking of Dr. Breitbart, he sent an invitation to many of us to read about the International Psycho-oncology Society (IPOS) new Quality Standards and the IPOS Lisbon Declaration declaring Psychosocial Cancer Care as a Human Right, at link IPOS International Standard of Quality Cancer Care. You can endorse it on line.
It sure would be fantastic to see more signatures!
Breitbart, W. and Y. Alici (2012). “Evidence-based treatment of delirium in patients with cancer.” J Clin Oncol 30(11): 1206-1214.
Delirium is the most common neuropsychiatric complication seen in patients with cancer, and it is associated with significant morbidity and mortality. Increased health care costs, prolonged hospital stays, and long-term cognitive decline are other well-recognized adverse outcomes of delirium. Improved recognition of delirium and early treatment are important in diminishing such morbidity. There has been an increasing number of studies published in the literature over the last 10 years regarding delirium treatment as well as prevention. Antipsychotics, cholinesterase inhibitors, and alpha-2 agonists are the three groups of medications that have been studied in randomized controlled trials in different patient populations. In patients with cancer, the evidence is most clearly supportive of short-term, low-dose use of antipsychotics for controlling the symptoms of delirium, with close monitoring for possible adverse effects, especially in older patients with multiple medical comorbidities. Nonpharmacologic interventions also appear to have a beneficial role in the treatment of patients with cancer who have or are at risk for delirium. This article presents evidence-based recommendations based on the results of pharmacologic and nonpharmacologic studies of the treatment and prevention of delirium.
Gagnon, B., et al. (2005). “Methylphenidate hydrochloride improves cognitive function in patients with advanced cancer and hypoactive delirium: a prospective clinical study.” J Psychiatry Neurosci 30(2): 100-107.
OBJECTIVE: To investigate the clinical improvement observed in patients with advanced cancer and hypoactive delirium after the administration of methylphenidate hydrochloride. METHODS: Fourteen patients with advanced cancer and hypoactive delirium were seen between March 1999 and August 2000 at the Palliative Care Day Hospital and the inpatient Tertiary Palliative Care Unit of Montreal General Hospital, Montreal. They were chosen for inclusion in a prospective clinical study on the basis of (1) cognitive failure documented by the Mini-Mental State Examination (MMSE), (2) sleep-wake pattern disturbances, (3) psychomotor retardation, (4) absence of delusions or hallucinations, and (5) absence of an underlying cause to explain the delirium. All patients were treated with methylphenidate, and changes in their cognitive function were measured using the MMSE. RESULTS: All 14 patients showed improvement in their cognitive function as documented by the MMSE. The median pretreatment MMSE score (maximum score 30) was 21 (mean 20.9, standard deviation [SD] 4.9), which improved to a median of 27 (mean 24.9, SD 4.7) after the first dose of methylphenidate (p < 0.001, matched, paired Wilcoxon signed rank test). One patient died before reaching a stable dose of methylphenidate. In the other 13 patients, the median MMSE score further improved to 28 (mean 27.8, SD 2.4) (p = 0.02 compared with the median MMSE score documented 1 hour after the first dose of methylphenidate). All patients showed an improvement in psychomotor activities. CONCLUSIONS: Hypoactive delirium that cannot be explained by an underlying cause (metabolic or drug-induced) in patients with advanced cancer appears to be a specific syndrome that could be improved by the administration of methylphenidate.
Elie, D., et al. (2010). “[Using psychostimulants in end-of-life patients with hypoactive delirium and cognitive disorders: A literature review].” Can J Psychiatry 55(6): 386-393.
OBJECTIVE: To review the research about psychostimulant effects on cognitive functions in end-of-life patients diagnosed with hypoactive delirium or cognitive disorders. METHOD: The MEDLINE (1966-March 2008), Embase (1974-March 2008), PsycINFO (1806-March 2008), IPA (1970-March 2008), CINAHL (1982-March 2008), ISI Web of Science (1945-March 2008), Current Contents (March 2007-March 2008), Access Medicine (2001-March 2008), and ProQuest Dissertations & Theses (1980-March 2008) databases were searched with keywords related to delirium, cognition, psychostimulants, and palliative care for French or English articles in a dementia-free and hyperactive delirium-free end-of-life population. Cognitive functions had to be assessed before and after initiation of the psychostimulant treatment. Moreover, treatment had to be initiated after the onset of cognitive impairments. RESULTS: A total of 173 studies were screened. Five studies on methylphenidate and 1 study on caffeine met inclusion criteria and were included in this review. Two studies were case reports, 2 were open-label trials, and 2 were double-blind, crossover randomized placebo-controlled trials. Three studies were conducted with hypoactive delirium patients and all studies were conducted in an advanced cancer patient population. CONCLUSIONS: The reviewed studies support the use of methylphenidate to improve end-of-life patient cognitive functions, particularly in the case of hypoactive delirium. Caffeine seems to have beneficial effects on psychomotor activity. Further well-designed studies are needed to consolidate these findings.
I commented although I’m reposting it here until ADS site administrators review it.
I like Jim’s outline. I thought of what Suzuki said about experts, though:
“In the beginner’s mind there are many possibilities, but in the expert’s there are few.”—Shunryu Suzuki
I staff a one man hit-and-run psychiatry consult service and, while psychiatrists are often viewed as the delirium experts, I try to teach medical students and residents rotating on the service that, even as beginners, they’re capable of assessing and managing as well as preventing delirium.
Of course, as beginners they are often under the supervision of non-psychiatric faculty who will insist on calling a psychiatric consultant, sometimes when it’s unnecessary. I let them know that, if they stay on at the University of Iowa and they call me under these circumstances—I will understand.
Change is glacial. Sometimes assembling a team entails taking the long view that such an assembly may well take decades.
Jim’s 3rd step is critical. Offering an alternative intervention in the form of self-improvement programs can lead to corresponding improvements in patient care. One of my residents and I recently made a Maintenance of Certification (MOC) Delirium Performance in Practice (PIP) Assessment Tool, which has gained preapproval by the American Board of Psychiatry and Neurology. Prior to this, there were no MOC tools available for this essential skill. As many readers of my blog know (https://thepracticalpsychosomaticist.com/ ), I have a low opinion of MOC as a vehicle for lifelong learning because of that and other limitations of Part IV of the MOC.
Good listening is an art which takes a long time and a lot of patience to develop. I’m not patient, but I’ve learned over the years (often enough the hard way) that Stephen Covey’s habit “Seek First to Understand, Then to be Understood,” is what stakeholders wish leaders would develop.
Some people thought the news article on delirium, which has been republished a few times, could have gone further to characterize delirium as a life-threatening complication of medical illness. It’s amazing that health care professionals and society in general still seem to struggle to understand this neuropsychiatric condition in terms of its pathophysiology, clinical presentations, and most importantly, prevention.
Every single day, in my role as a psychiatric consultant, I see patients suffering from delirium. Opinions differ about a psychiatrist’s role, but I think my main contribution is to help internists and surgeons identify delirium as quickly as possible in order to propel the health care team away from the notion that it’s a primary psychiatric problem and toward the goal of treating the underlying medical causes of this syndrome which mimics so many mental disorders.
A recent report highlighted the elevated mortality rate of delirious patients, yet omitted the efforts of major groups of researchers and clinicians working to understand delirium better in order to reduce its prevalence.
Over the years I’ve highlighted what I think is the absurdity of calling a psychiatrist first when delirium is an obvious problem when a patient’s mental status abruptly changes in the context of severe medical illness. I teach medical students that delirium should be viewed as a medical emergency, in the hope that the next generation of doctors will improve the recognition and management of this dangerous condition, which can lead to dementia, death, and disability.
There are important groups working diligently on the problem of delirium, including the American Delirium Society and the European Delirium Association to name only two. The latter has a compelling video of a first-person interview of a patient who suffered delirium. And you can also see the video of a ICU delirium survivor’s description of his harrowing experience with delirium and consequent development of PTSD.
The research on delirium continues and probably doesn’t get the press attention it deserves.
All that said, there is still a lot of work to do in order to get a better handle on the pathophysiology of delirium, find reliable pre-operative biomarkers to allow better prediction of which patients are at risk, and preventing this dangerous neuropsychiatric complication of medical illness.