A DSM for Psychiatrists?

 

 

No matter what version - the DSM is clearly a flash point for criticism by psychiatrists and non-psychiatrists alike. There are too many diagnoses.  People don’t like certain diagnoses or complain when some categories are eliminated. There are endless debates about diagnostic criteria, reliability, and validity. Categories are a wrong approach and we need dimensions. Philosophers have a field day imagining what the DSM is and making suggestions.  In an early post on this blog, I responded to the philosophical suggestion that the DSM was supposed to be a blueprint for living. Antipsychiatrists have no problem rejecting the entire volume of course because they are stuck in the 1970s with Szasz and maintain that there are no mental illnesses. The more flexible antipsychiatrists reframe this into everyday problems in living another decades old formulation that did not stand the test of time. Others suggest that the DSM exists to make diagnoses that lead to pharmaceutical treatment and make profits for drug companies.  The more legitimate criticism from psychiatrists is focused on the criteria and whether any diagnostic categories exist. Some of that criticism comes full circle back to why a classification system was needed in the first place. Clinical psychiatrists tend to use a fraction of the available diagnoses and in most practices can recall the diagnostic codes without looking them up. In fact, most psychiatrists use the DSM as a reference, pulling it off the shelf for rarely encountered diagnoses and then typically to look up a diagnostic code for coding and billing purposes. 

The title Diagnostic and Statistical Manual – is the first clue about the original intent of the manual and it antedates the psychiatric profession and the APA in the United States by several decades. The abbreviated history is available on the APA web site and several other Internet sites.  Initially it was to determine numbers of people by diagnosis both in the varied mental illness facilities across the country and later in military service. This function was described as administrative but there was also a consensus building aspect in the early 20^th century as diagnoses shifted from a unitary psychosis model to more nuanced.  The advent of the DSM-III was a turning point because it provided atheoretical definitions of disorders that were subsequently adopted by the ICD-9. Subsequent revisions in the DSM-IV and DSM 5 included revisions based on professionals and professional organizations, assigned work groups and their research, and eventually the general public. The original goal of classification and statistics has remained but it is used for various reasons by non-psychiatrists.

There are many examples of non-psychiatric use.  In the legal and political sphere, most states have rationed services for people with severe mental illnesses who are at high risk for hospitalization and other morbidities. Qualifying for those benefits depends on a  DSM diagnosis.  The same is true for state sponsored services for autism and developmental disabilities. In forensic settings experts are called upon to give diagnoses in an adversarial setting.  Disability, veteran’s benefits, and worker’s compensation are all linked to diagnoses.  All medical billing to insurance companies and government payers depend on DSM equivalent diagnostic codes in the ICD-11. Managed care companies ration care based on many of these codes by refusing to cover them. None of these functions were designed as an original intent for the diagnostic manual.

Heterogeneity – either explicit or implicit is another frequent criticism of the manual. Human biology and the biology of diseases and disorders teaches us that the etiopathogenesis of illnesses is diverse. There are many possible underlying biological and nonbiological causes.  Many genes and lesions can often lead to the same apparent presentation or phenotype.  That lead to the idea of intermediate phenotypes or endophenotypes to get a more consistent population to study but that has only been partially successful. The DSM was never designed to biologically classify mental illnesses, but DSM diagnoses are used for studies of biology and pharmacology. Other systems have been suggested for that purpose – most notably the RDoC system, but so far it has not exhibited any widespread success.  There is no reason to think that a verbally based system will accurately describe biologically based illness whether those descriptions are in the DSM or RDoC.

Apart from classification for statistical, administrative, and planning purposes what good is the DSM to psychiatrists? I recently saw it criticized for not including enough psychopathology. The criticism was bitter and partisan but apart from some very basic definitions the DSM is not a course in psychopathology.  All psychiatric residents need to be taught psychopathology to the point that they are experts in it. That will never happen from reading the DSM. It also doesn’t happen from reading a psychopathology text or taking a college course in psychopathology.  It happens from seminars, reading, and clinical experience – discussing psychopathology with colleagues, supervisors, and instructors.  It happens from learning in treatment relationships with people who have psychopathology not just a list or criteria but experiencing firsthand the interpersonal aspects. The DSM explicitly states that it is for use by trained professionals and that it can be used to facilitate communication between trained professionals.  

The DSM is clearly not a treatment manual of any kind. That is why I have always found the charge that it is a source of prescriptions for the pharmaceutical industry ludicrous.  There are roughly six times as many prescribers of psychiatric drugs as there are psychiatrists and the only medication in that category that is more likely to be prescribed by psychiatrists is lithium. It is easy to speculate that the prescribing patterns of that larger group are not contingent about what is in the DSM.

What about the diagnostic side and what psychiatrists need? Although there was some criticism that the neo-Krapelinians have had too much influence on the manual it is time to acknowledge that verbal descriptions have come to their logical limits. It is also time to acknowledge that psychiatrists need to know a lot more about medical diagnoses in general in order to function in a medical environment. If medical conditions are in the differential diagnosis – how many medical conditions do psychiatrists need to know about and diagnose?  Every psychiatrist I know has stories about medical conditions that were referred to them as a psychiatric disorder where they made the correct medical diagnosis. They are typically conditions from neurology, endocrinology, and infectious disease but also general medical conditions like diabetes mellitus, hypertension, and atrial fibrillation. Approaches I have seen in other specialties include lists of conditions that the trainee or practitioner needs to know about.  That is a useful approach but lists like that in a DSM are likely to raise objections about medicolegal risk and that a larger recipe book is being made for what it takes to be a psychiatrist. There are also many psychiatrists in settings where medical assessments are impossible, where they are referred out, or where the practitioner may feel inadequately trained. I see all of those reasons as being an opportunity to advance the quality of psychiatric treatment.   

A related issue is the diagnostic process in psychiatry as opposed to the rest of medicine.   Nassir Ghaemi, MD had a recent commentary about this on his blog suggesting that the DSM approach prioritizes comorbidities rather than differential diagnosis like the rest of medicine.  He describes the typical pattern matching that occurs early in the process and suggests that the differential diagnosis point, the DSM encourages listing all of the comorbidities rather than going through a differential diagnosis process.  In other words there is a lack of a hierarchical process. 

That has not been my experience. Granted – I may be a more medically oriented psychiatrist than most (but then again had 20 colleagues doing the same work) – but when I see a patient the universe of diagnoses are all possible both in and outside the DSM. The number one priority was making sure that a life threatening medical condition was not misdiagnosed as a psychiatric disorder.  Every physician can recall being taught about differential diagnosis and having to write an exhaustive list for the first few Internal Medicine inpatients. That process illustrated that a lot of the “rule outs” occurred as a mental exercise and really did not need to be written down. By the end of that rotation the differential diagnosis list collapse from the low double digits to the low single digits. There was also a triage element based on the more pressing problem or diagnosis.   A DSM for psychiatrists could make this process explicit, discuss the cognitive aspects of pattern matching and completion necessary for generating hypotheses in the differential diagnosis, the differences between differential diagnosis and comorbidity, and probabilistic considerations in selecting the preferred diagnosis. It would potentially have training implications because in order to optimize the pattern matching required - adequate training experiences need to be supplied to develop those skills. 

A DSM for psychiatrists needs to be much more information intensive in terms of research on validators, psychiatric genetics, multiomics, endophenotyping, drug mechanisms of action, and biological markers for each category.  A typical response to that suggestion is "Well there are no biological markers, labs tests, etc."  I don't find that to be a compelling argument when I think about what is currently being ignored.  We are on the cusp where more of that information is becoming relevant and we are past the point where much relevant information can just be dismissed. Any concern about cost of a more extensive manual can be dealt with by placing it online for subscribers. This may seem like a significant task given the accumulating information, but it is time the APA and research leaders in psychiatry to realize that the task has changed.  Psychiatrists are different from other physicians and other mental health professionals.  Psychiatrists need the technical information to provide quality care and compete against other systems that claim to know more about psychiatry and medicine than they do. Time to adjust to that reality and have the necessary internal debates first.

That concludes my suggestion for a DSM for psychiatrists, but I am open to more suggestions.  And for the record I am suggesting two different publications instead of a general manual full of qualifiers about expertise.  We need a manual for experts and another one like the current version - for everybody else.

 

George Dawson, MD, DFAPA

References:

1:  Horwitz, A.V. (2014). DSM - I and DSM - II . In The Encyclopedia of Clinical Psychology (eds R.L. Cautin and S.O. Lilienfeld). https://doi.org/10.1002/9781118625392.wbecp012

2:  Kim YK, Park SC. Classification of Psychiatric Disorders. Adv Exp Med Biol. 2019;1192:17-25. doi: 10.1007/978-981-32-9721-0_2. PMID: 31705488.

3:  Cooper R, Blashfield RK. Re-evaluating DSM-I. Psychol Med. 2016 Feb;46(3):449-56. doi: 10.1017/S0033291715002093. Epub 2015 Oct 16. PMID: 26470724.

4:  Shorter E. The history of nosology and the rise of the Diagnostic and Statistical Manual of Mental Disorders. Dialogues Clin Neurosci. 2015 Mar;17(1):59-67. doi: 10.31887/DCNS.2015.17.1/eshorter. PMID: 25987864; PMCID: PMC4421901.

5:  Blashfield RK, Keeley JW, Flanagan EH, Miles SR. The cycle of classification: DSM-I through DSM-5. Annu Rev Clin Psychol. 2014;10:25-51. doi: 10.1146/annurev-clinpsy-032813-153639. PMID: 24679178.

6:  Grob GN. Origins of DSM-I: a study in appearance and reality. Am J Psychiatry. 1991 Apr;148(4):421-31. doi: 10.1176/ajp.148.4.421. PMID: 2006685.

Supplementary:

It has been suggested that a hierarchical approach informs the usual differential diagnosis exercise but it may be the application of the parsimony principle. To me there is an open question about how well parsimony works for complex biological systems.

Photo Credit:  Eduardo Colon, MD

 

 

An Outstanding Paper on Atrial Fibrillation

 

I have been fascinated by atrial fibrillation since I was a third-year medical student. I was doing a Medicine rotation and examining a middle-aged man.  Listening to his heart sounds was the first time I heard the irregularly irregular heart rhythm characteristic of atrial fibrillation. It was such an outrageous and unexpected sound compared to what I was used to that I felt a little panicky. Why wasn’t this patient experiencing more symptoms and even more unexplainably – why doesn’t he sense that there is something wrong with his heart beat?  Since then, I have treated hundreds of patients with atrial fibrillation.  I ask them all if they can sense the irregular heart beat and in the people I see about half of them can.  Being a psychiatrist, diagnosing and treating atrial fibrillation is technically not my “job”.  But it is currently such a prevalent condition that a brief examination typically triggered by vital signs and noting a pulse irregularity followed by an electrocardiogram is all that is needed. Atrial fibrillation has considerable mortality and morbidity associated with the most feared complication of stroke. A good friend of mine developed renal failure from a combination of atrial fibrillation and atrial flutter and required ablation procedures to restore normal sinus rhythm.  Two relatives had strokes associated with atrial fibrillation resulting in disability and ultimately death. Both had atrial fibrillation for about 30 years.  One of them was 92 years old, using digoxin for rate control, and not on anticoagulants. The other was 92 years old, using diltiazem for rate control, and on warfarin at therapeutic doses. He had two strokes about 10 years apart on the warfarin and multiple episodes of nuisance bleeding or excessive bleeding from minor injuries due to anticoagulation that did not require medical attention.   Another friend had pulmonary complications from an antiarrhythmic drug that he was taking for a new onset of atrial fibrillation and died as a result of those complications. Sixteen years ago – I developed lone atrial fibrillation while speedskating and have been on antiarrhythmics since that time.

When you see all of those problems associated with a condition and have had it yourself, you tend to read more about it than the average person.  Reading about atrial fibrillation is generally a frustrating task. The evidence base for treating the condition seems to be in a state of flux. For years the research seemed to say that rate control and rhythm control led to equivalent outcomes. When life style measures were included, the rhythm control strategies seemed superior. Even the question of anticoagulation with novel oral anticoagulants of NOACs for stroke prevention based on a scoring system has been called into question recently.

That brings me to the topic of this blog post and that is the single best summary of information about atrial fibrillation that I have seen anywhere - at least for nonspecialists in that area.

The paper was written this year in the New England Journal of Medicine (1). It starts out with a case description of a 63-year-old man with a new onset of atrial fibrillation. The authors discuss the disease in detail and treatment recommendations consistent with their discussion. What I really like about this paper is that they are discussing phenotypes of atrial fibrillation and I do not see that happening very often in real clinical situations. The phenotypes they discuss are paroxysmal atrial fibrillation, persistent atrial fibrillation, and long-standing persistent atrial fibrillation.  They have an excellent figure in their paper that was unfortunately prohibitively expensive for me to try to post here, but the basic idea is that there are distinct anatomical and electrophysiological substrates for each of those phenotypes. In the paper the phenotypes are labeled as “clinical profiles”. His phenotypes have prognostic considerations since the authors make the point that there is a gradation in the likelihood of conversion to normal sinus rhythm and maintaining that rhythm with paroxysmal atrial fibrillation being the most likely to convert and maintain a normal sinus rhythm and long-standing persistent atrial fibrillation being the least likely to convert. Just knowing that much about atrial fibrillation is a significant advance compared with most of the clinical discussions that I hear.

The second feature in this paper that I really like is that atrial fibrillation is not necessarily a benign condition. For years the discussion has been controlling the rate or rhythm and in most cases they have been considered to be equivalent. Many clinicians have their first experience with atrial fibrillation like I had. They are doing a physical examination outpatient for another reason and they notice they are in atrial fibrillation. Depending on physiological factors that patients irregularly irregular heart rate may already be rate controlled. I have talked with many people over the years who knew that their heart rate was irregular because their spouse noticed it and they did not do anything about it for years. Atrial fibrillation is a risk factor for embolic strokes as well as dementia, death, and heart failure. Persistent tachycardia can cause cardiomyopathy and reduced cardiac output can lead to renal failure.  The authors suggest that a heart rate of 110 bpm or greater might lead to cardiomyopathy but they also suggest it can occur at a lower rate. This is an interesting observation because the most recent review in UpToDate on sinus tachycardia suggests it is generally a benign condition, however an irregular tachycardia because of reduced cardiac output is likely a different matter.

In addition, the patient can be symptomatic from reduce cardiac output with lightheadedness, dizziness, fatigue, decreased exercise tolerance, palpitations, hypertension, and an exacerbation of symptoms of underlying coronary artery disease. The lesson for psychiatrists is if you notice that a patient has atrial fibrillation it cannot be approached casually. Atrial fibrillation is associated with significant medical comorbidities such as underlying structural coronary disease, obesity, sleep apnea, hypertension, hyperlipidemia, and diabetes mellitus. If the patient has had limited contact with primary care physicians the comorbid conditions may have gone unnoticed. It makes sense to ask about additional symptoms in the review of systems as well as family history and whether that patient is seen primary care physician or cardiologist recently.  I would have no problem referring a patient with tachycardia, expected symptoms, or risk factors to an emergency department for acute stabilization if I could not get them seen in a primary care clinic.

The authors go into treatment of atrial fibrillation as basically a rate control strategy, a rhythm control strategy, and a strategy to address comorbid medical conditions.  They review rate control with beta-blockers and calcium channel blockers and prefer beta-blockers. They consider a number of antiarrhythmics and the risks and benefits of those medications.  They consider catheter ablation - either radiofrequency pulmonary vein isolation or cryoablation as being more effective for treating and preventing recurrent atrial fibrillation. The recurrence rates are relatively high even after the ablation procedures, so continued antiarrhythmic medications may be necessary.

Once a patient has stable treated atrial fibrillation, the main task for the psychiatrist is to make sure that any prescribed medications do not interfere with the cardiac medications at either the pharmacokinetic or pharmacodynamic level. QTc prolongation is a primary consideration since several of the agents used prolong the QTc interval or affect other cardiac conduction.  At the pharmacokinetic level there is the possible risk of decreased metabolism of beta-blockers and increasing bradycardia and hypotension. If I have any doubts all about medication combinations I am usually in touch with the patient’s cardiologist or primary care physician before making those changes. All of the patients I see with atrial fibrillation also have their blood pressure and pulse taken at every visit along with the description of symptoms and potential medication side effects. That means I never practice in an environment where I can't do that. I will also review how well their comorbid conditions are being treated particularly hypertension, sleep apnea, and diabetes mellitus. I will provide them with concrete advice on how to approach those problems and whether or not they need to be seeing their primary care physician sooner than scheduled.

This is also an opportunity to discuss any comorbid substance use problems. Alcohol is a definite precipitant of atrial fibrillation. I have had patients never experience another episode by stopping alcohol. I have also had patients report that they can tell when their alcohol level reaches a certain point because they will go into atrial fibrillation for several hours until that alcohol is metabolized. Stimulant medications are also a risk because they increase sympathetic tone, increase heart rate, increase blood pressure. All three of those changes can trigger an episode of atrial fibrillation.  Cannabis can have a fairly potent sympathomimetic effect by acutely lowering blood pressure leading to a reflex tachycardia. Atrial fibrillation has been reported as one of several cardiac arrhythmias associated with cannabis use (2). Interestingly, the authors of the NEJM article state that caffeine is not a precipitant. There are no qualifiers on that statement and I think it is based primarily on epidemiological evidence. Caffeine intake is always important to quantify because of its wide variability across the population and general reputation of being a benign compound. There are segments of the population that consume large quantities of caffeinated beverages every day and experience the expected side effects of anxiety (in some cases panic attacks), agitation, insomnia, and hyperadrenergic effects but they seem unaware that these symptoms are related to their caffeine consumption. Certainly consumption at that level can directly or indirectly precipitate an episode of atrial fibrillation.

That is my brief review of the NEJM article in atrial fibrillation. I encourage all psychiatrists to get a copy of this paper, read it, and keep it for reference. I am not suggesting that psychiatrists treat this condition.  I am suggesting that they recognize it - even if it has not been diagnosed and know what to do when that occurs. The reality is that in adult psychiatry no matter what your practice setting there will be a significant number of people with atrial fibrillation and other arrhythmias as well as all of the known comorbidities. You cannot treat those people unless you know about these conditions, the comorbidities, and how to avoid complications.

 George Dawson, MD, DFAPA

 

References:

1:  Michaud GF, Stevenson WG. Atrial Fibrillation. N Engl J Med. 2021 Jan 28;384(4):353-361. doi: 10.1056/NEJMcp2023658. PMID: 33503344.

2:  Richards JR, Blohm E, Toles KA, Jarman AF, Ely DF, Elder JW. The association of cannabis use and cardiac dysrhythmias: a systematic review. Clin Toxicol (Phila). 2020 Sep;58(9):861-869. doi: 10.1080/15563650.2020.1743847. Epub 2020 Apr 8. PMID: 32267189.

Supplementary:

Common and uncommon medications listed in this article used in atrial fibrillation for rate control, antiarrhythmic properties, and anticoagulation.  I added additional warnings and general type of medications that might require avoiding based on pharmacokinetic or pharmacodynamic considerations. Important to keep in mind that all medications vary in their ability to affect these mechanisms as well as therapeutic mechanisms. That includes significant differences between medications in the same class. That leads to qualifiers like "all possible mechanisms leading to complications or serious adverse effects may not be listed" (in this package insert or computerized drug interaction program). Almost every time I am seeing a patient on these medications - it requires a study of the medication combination, even if they are taking a psychiatric medication that appears to be working. Baseline cardiac symptoms related to the arrhythmia also need to be established as well as the patient's plan to obtain assistance if they worsen.

Additional qualifier (if it is not obvious). Psychiatrists prescribe beta blockers (metoprolol, propranolol, pindolol, etc). Psychiatrists can diagnose atrial fibrillation. Psychiatrists do not manage atrial fibrillation but need to know what to do acutely and how to avoid complications of the following medical therapies from drug interactions with psychiatric medications. Practically all of the antiarrhythmics in the following table are prescribed by Cardiologists and subsequently managed by primary care physicians although many patients continue to see Cardiologists in follow up. Like all areas of medicine the limits of technical expertise need to be recognized.  I worked with Cardiologists who became psychiatrists and they restricted their practice to medications prescribed by psychiatrists.  

Graphics Credit:

Bunch TJ, Cutler MJ. Is pulmonary vein isolation still the cornerstone in atrial fibrillation ablation? J Thorac Dis 2015;7(2):132-141. doi: 10.3978/j.issn.2072-1439.2014.12.46

Open Access per this Creative Commons License: https://creativecommons.org/licenses/by-nc-nd/4.0/