The most important thing you can do as a psychiatrist...

 

I won’t build the suspense.  The most important thing you can do as a psychiatrist is to be the medical doctor that you were trained to be.  The second-best thing is to be a good if not great psychiatrist.

I had those thoughts today after reading about a case of misdiagnosed panic disorder (1).  The patient was an athletic 30 yr old women who reported episodic panic attacks, palpitations, light headedness, and shortness of breath.  A Cardiology evaluation was negative.  That was not too surprising since she was asymptomatic during the testing, but given the final diagnosis I would have expected a subtle baseline ECG change.  She was treated with a selective serotonin reuptake inhibitor for presumed panic attacks by her primary care physician.  She is seen in the Emergency Department and an ECG shows an irregular, rapid, wide QRS complex, tachycardia and her usual symptoms. A shortened PR interval with a delta (preexcitation) wave is noted. The entire case description with the associated diagnostic reasoning can be located at this link (1). I am not sure that readers can access it without an account.

The case is an excellent example of the real task of being a psychiatrist. The usual dialogue about what psychiatrists do is typically restricted to criteria in the Diagnostic and Statistical Manual (DSM).  There is a lot of confusion about the importance of the DSM and what it means for psychiatric practice. For example, the popular stereotype is that psychiatrists just sit around and estimate whether people “meet criteria” for a DSM diagnosis and then prescribe an indicated medication.  Life as a psychiatrist is not that simple.  The unique problems of the person in front of you cannot be captured by a crude system of classification.

Using this case as a backdrop, I need to know as much medical detail about this young woman as possible.  More details about the onset of symptoms and associated symptoms. More details about her baseline physical health, associated symptoms, and any cardiology consultation and testing that has occurred.  If I am on the same electronic health record system, I am pulling all of that up including her vital signs over time, lab testing, and cardiac testing.  I am looking at each ECG tracing.  I need to know her detailed family history for cardiac disease, arrhythmias, and sudden cardiac death. How much alcohol, tobacco, and caffeine does she typically use?  Is she using any stimulants?  Does she have an intercurrent illness that could affect her heart rate?

In the next few minutes, I need to be checking her vital signs especially her heart rate and rhythm, respiratory rate, and doing a rapid cardiopulmonary exam. My first decision point is whether she is in a medical emergency or not. This is not always as clear cut as this case where the discussant points out that the patient is treated using the American Heart Association (AHA) Advanced Cardiac Life Support ( ACLS) algorithm and needs electrical or medical cardioversion.

That is where things get tough for a psychiatrist.  Setting is a significant issue.  If I am working in an acute care setting in a hospital – I typically have plenty of back up.  Hospitalists services generally run codes or even have a team for acute care that does not involve codes and I could get them there in a few minutes.  At the other end of the spectrum -  I have worked in a community mental health center with absolutely no access to ECGs and no equipment for cardioversion.  In that case – 911 needs to be called and all medical staff in the facility should be able to perform basic cardiopulmonary resuscitation. 

The main work in this situation is recognizing the medical emergency and getting the patient to the correct setting where she can be stabilized. It is not always black and white.  This patient was eventually diagnosed with atrial fibrillation and Wolf-Parkinson White (WPW) syndrome.  Atrial fibrillation was probably the most frequent cardiac diagnosis that I made as a psychiatrist.  Most people who had it were not aware of it. I happened to pick it up because I noticed an irregularly irregular pulse when checking their vital signs and a pulse deficit on physical exam. It was almost always in a range where the heart rate was not a big problem.  In some cases, it was partially treated by a rate controlling medication like a beta-blocker or calcium channel blocker.  I could typically call the patient’s primary care physician and get them in for a comprehensive evaluation of the problem.  I would have to send some patients to the emergency department or urgent care.     

The issue of cardiac related anxiety is a very interesting issue. Cardiac symptoms can be an associated symptom of anxiety, panic, and other affects like anger.  The symptoms can arise as a sensory phenomenon due to an awareness that the heart is “pounding” or “beating out of my chest”.  Both of those descriptions are very common in people with panic attacks. The sequence of events and what is causing the cardiac phenomenon are wide ranging from an intrinsic cardiac problem to an imbalance in the sympathetic and parasympathetic innervation of the heart. Some electrophysiological experts think that at least some atrial fibrillation is due to overactivity of both autonomic systems.  Even in the absence of a sustained arrhythmias – the autonomic effects can result in premature atrial contractions, premature ventricular contractions, and sustained sinus tachycardia.

There are many other cardiac emergencies that occur in psychiatric settings. I was asked to see an acutely manic woman who was 85 years old.  She was extremely agitated and shouting that her chest hurt.  I was able to get a stat ECG that showed she was having a myocardial infarction and got her transferred to the coronary care unit.  In another case – I was told that a 70-year-old woman was “delusional” about her abdomen.  She clearly had a belief that there were supernatural forces causing her abdominal discomfort.  At the same time, she had a pulsatile mass in her lower abdomen and an abdominal aortic aneurysm on ultrasound.  Both patients survived with timely intervention.

I was a quality reviewer for many years and that job involved reviewing potential quality problems associated with inpatient hospitalizations.  One of those reviews was a patient who was hyperventilating.  He was diagnosed with panic attacks and treated with behavior therapy that did not seem to be effective.  As his condition worsened, he was eventually diagnosed with an acute pulmonary embolism. Since that review, I have seen many ambulatory patients who were short of breath for days due to pulmonary emboli and are not seen in a setting where they can be diagnosed and treated.

There are many more medical problems that crop up in psychiatric outpatients and inpatients that cannot be missed.  They can present as a possible psychiatric disorder and the potentially fatal nature of many mean they cannot be missed.  Many settings are set up to give the appearance that an emergency room physician, hospitalist, primary care physician, or physician extender is medically clearing these patients and that is not the case.  Most frequently that is because the time course of the condition is erratic or communication with a psychiatrist at a more detailed level is necessary.  The only assurance that these patients have no acute problems is if they are acutely symptomatic when they are screened or seeing a psychiatrist who can communicate with them, has no biases against them, and who knows the difference between a medical and a psychiatric problem.

To be very clear, I am not suggesting that psychiatrists initiate care for life threatening medical problems.  They do need to know if there are undiagnosed acute or chronic medical problems and how fast they need to be addressed. They need to be able to recognize the medical causes of signs and symptoms that can be misinterpreted as psychiatric.  They also need to recognize and manage the associated systems problems that in my experience are primarily countertransference driven.  Let me provide a clear example of what I mean.  I was working in an acute care setting and came across a patient leaning against a pool table. He was acutely short of breath, somnolent, and had a history of valvular heart disease. On exam, he was in congestive heart failure. I placed a call to the medical consultant and was told that I should start an IV line and manage the patient myself on an acute care psychiatric unit.  When I suggested that he needed transfer to medicine – I was met with the comment: “Well you know how to start an IV don’t you?”

I most certainly have started hundreds of IVs, but that is not the issue.  My patient had an acute medical problem that needed both medical and nursing expertise to manage in a more medical acute care setting than a psychiatric unit.  I eventually contacted the Chief of Medicine and got the patient transferred where he was subsequently in an ICU setting.  Ideally acute care psychiatrists today can develop good relationships with hospitalists for these kinds of transitions.  The best way to do that is by letting them know you have made a medical assessment and have a good indication for transfer.

Being a good if not great psychiatrist is hard work. My most significant worry was missing a major medical problem and not getting adequate intervention.  That is just the first step. The next steps are a psychiatric formulation, diagnosis, and treatment plan that incorporates state of the art communication and relationship building with the patient.  Hopefully that is followed by a long period of seeing the patient, helping them meet their goals, and providing medical diagnosis and follow up as needed.  In today’s world that is often occurring in a rationed suboptimal environment, overburdened by businesses rationing of both care and medication for profit.

My hat is off to the psychiatrists who are doing this work and probably working way too hard in 2025.

Happy New Year!

 

George Dawson, MD, DFAPA

Supplementary 1:  There is no doubt that I have practiced in settings where there was a high level of concurrent medical and in some cases surgical illness.  There is also no doubt that it was a conscious decision on my part to practice in those settings.  That undoubtedly sharpened my focus on making sure that I had the skills necessary to provide adequate care to those populations. It may be possible to cleanly partition psychiatric work from the rest of medicine but I have not seen that happen for some of the reasons cited in the above essay.  The training of psychiatrists in the past has had a variable relationship with medicine - at one point going to the extreme that much of the medical internship was eliminated.  The best advice I got in medical school was not to use elective time for additional psychiatry rotations because I would be doing psychiatry the rest of my life. I took neurology, neurosurgery, nephrology, endocrinology, cardiology, allergy and immunology, and infectious disease rotations instead. That initial training worked well over my years of practice and I don't regret it.

Some may question the emphasis in this post on the importance of not missing concurrent medical diagnoses and I would offer these additional observations.  Many patients seeing psychiatrists consider them to be their primary care physicians. That should not deter a psychiatrist from clarifying their role, but the fact that psychiatrist is probably seeing the patient much more often than the primary care physician is often a useful reality.  I have called primary care physicians to report what I consider to be an exacerbation of the patient's underlying medical problem.  That collaboration can get more timely care for acute or chronic medical problems.  I have also had the experience hearing from a person that a psychiatrist diagnosed their medical problem when nobody else did.  Many of these scenarios degenerate into who is the better physician.  The focus needs to be on what the patient needs rather than what the physician needs.  Not ignoring or missing a patient's underlying medical problems is a large part of that personalized care. 

 

Reference:

 1:  Hemingway TJ.  An athletic patient who thinks she has panic attacks.  Medscape December 17, 2024 (accessed on December 31, 2024):  https://reference.medscape.com/viewarticle/858516_6

The Prostate Is On The Wrong End - Why Should We Worry?

There is always a lot of news about the prostate these days.  It has become the poster child of the evidence based crowd.  Just last week I saw the headline: "Men are more likely to die in a structure fire than from prostate cancer." This is all part of the political approach to epidemiology that emphasizes that even though most men will develop some type of prostate cancer by the age of 85, they are likely to die of other causes.  Therefore PSA screening is not useful because it leads to more invasive procedures with complications like prostate biopsy and then procedures with even more complications like radical prostatectomy. The sordid aspect of this business has been pointing out the options that several celebrities who made decisions about prostate cancer and therapies.  Depending on the side you take - you will cheer the representative decision.  I noticed that the celebrities who died from prostate cancer including misdiagnosis are omitted from that equation.

In clinical practice, young men with recurrent prostatitis have always been a red flag for me. They often end up on very long courses of antibiotics and seem to have chronic symptoms.  The symptoms don't match descriptions of acute prostatitis that are more similar to an acute urinary tract infection. The anatomy of the male urinary tract often needs to be reviewed, especially the relationship of the prostate and the urethra.  I have treated many young men who were very angry at their Urologists because of these chronic symptoms even though they were not medically explained.  If I see these situations today - I typically call the Urologist and suggest treatment only for a clear cut case of prostatitis and whether they have noticed any changes in the patient's behavior.

My focus in this post is bladder outlet obstruction and all of the associated phenomenon due to benign prostatic hyperplasia.  According to UpToDate (10) it is more common in men and  10% of men greater than the age of 70 and 1/3 of men over the age of 80 will develop it.  Treatment is necessary to prevent renal complications, bladder dysfunction, infection and in severe cases delirium.  I don't intent to focus on the urological treatment - only as required to explain the situation.  I am more interested in what happens with this disorder and how the presentation may appear to be psychiatric.  I think that this is a neglected are in the literature.  Please send me any references that I may have missed.

The neuroanatomy and physiology of micturation is a complicated process.  At the local level, micturation is innervated by both the sympathetic and parasympathetic nerves.  The sympathetic efferent innervation inhibits  β3 adrenoreceptors to relax the detrussor muscle of the bladder and activates α1 receptors at the level of the urethra.  Parasympathetic efferent innervation activates M3 muscarinic receptors in bladder smooth muscle and motor neurons stimulate acetylcholine nicotinic receptors in the external urethral sphincter to cause contraction.  Relaxation of that sphincter muscle is facilitated by postsynaptic parasympathetic neurons that release ATP and nitric oxide.  The efferent arm of micturation requires close coordination of that combination of motor and sympathetic nervous system components.

The afferent side of this function begins at the level of the bladder epithelium.  These cells have complex signalling functions that can lead to local vascular and muscular responses in addition to sensory information being sent to higher centers. Bladder epithelium and underlying myelofibroblasts may function to send a stretch signal as the bladder fills. The actual mechanism that initiates that signal was not clear from the review I read.  A local acetylcholine based mechanism was thought to led to local bladder contractions.  This was thought to be the reason that antimuscarinic agents were used for bladder spasticity.   

This process was not delineated very well until about the past 10-15 years.  A combination of brain imaging during micturation and neuroscience techniques applied to determine the anatomic pathways.  One of those techniques was the application of pseudorabies virus to the wall of the rat  bladder.  This technique leads to retrograde transport of the virus into affected structures.  Viral markers go to structures in both the peripheral and central nervous system. A wide variety of cortical and subcortical structures are involved including the raphe nuclei, locus ceruleus, red nucleus, periaqueductal grey area, pontine micturation center, and cerebral cortex are involved.  The parasympathetic excitatory reflex pathway  is presented in the diagram below (1).

The circuits controlling continence and micturation are shown below. The diagram on the left is the storage reflex consisting of negative feedback to inhibit detrusor contractions and increase urethral sphincter activity. In the voiding phase intense afferent activity in the spinobulbospinal reflex pathways passes the pontine micturation center. That leads to descending parasympathetic activity stimulates detrusor muscle and inhibits urethral sphincter activity at the bladder outlet. Associated structures at the brain level have been suggested by functional imaging studies. The central mechanism suggested is release of tonic inhibition of the micturation center by the frontal cortex. Some of the associated structures are important limbic structures and have connectivity to other organ systems by sympathetic tracts. 

In the case of BPH, there is increased intraluminal pressure in the proximal urethra or bladder outlet. This alters the set point of the system. Voluntary voiding occurs but at higher residual volume and detrussor pressure. That leads to typical symptoms of frequent voiding, decreased urine flow, and small volumes. In extreme cases total obstruction can occur on at least a temporary basis requiring temporary catheter insertion to maintain urine flow. 

Getting back to psychiatry, let me illustrate the relevance of the problem. 

Case 1: JD - a 68 yr old man in fairly good health until about 3 months earlier. At that time he started to experience profound sleep problems. He has obstructive sleep apnea (OSA) and uses CPAP - but his parameters looking at the AHI and air leakage are unchanged. He now has frequent nocturnal panic attacks that awaken him.  Upon waking his heart is pounding and he has palpitations. He purchased a single lead hand held ECG device that takes a 30 second rhythm strip and recorded one ventricular premature contraction in 30 seconds. He consulted both his pulmonologist and cardiologist involved in the original OSA diagnosis. The pulmonologist looks at his CPAP parameters and concludes that he does not need another sleep study. The cardiologist tells him that these VPCs are benign and there is nothing to worry about. JD is concerned because this is a definite change in his health status and neither physician is concerned. 

He went in to see his primary care physician who examines him and jokes about the cardiac-bladder connection. He does a prostate exam and concludes that his prostate is "about the 90th percentile". No further evaluation or treatment is recommended. 

His wife notices that he is sitting up in a chair in the bedroom a lot more at night. He explains that he is having palpitations and is very anxious at night. His wife tells him to see the psychiatrist who is treating her for panic attacks. He makes an appointment and goes in about 2 weeks later. 

The psychiatrist does a complete history and sleep assessment and concludes that these are not typical panic attacks. JD recalls a number of dreams where he is running, exerting himself, or very fearful in the dreams. He awakens with his heart pounding and experiencing the irregular beats. As soon as he is able to void, the tachycardia and palpitations resolve. The psychiatrist thinks they are related to the episodes of urinary frequency and urgency associated with BPH and that therapy targeted to address the bladder outlet obstruction will lead to a resolution of the sleep problems and panic attacks. Since seeing his primary care physician JD has acquired a wrist watch with a vibrating alarm. He uses it to wake himself up at 2AM and 4AM and finds that pre-emptive bladder emptying greatly reduces but does not eliminate the nocturnal panic attacks entirely. The psychiatrist refers JD to a Urologist. He is assessed and treated with tamsulosin - an alpha blocker that relaxes smooth muscle fibers in the bladder neck and prostate. Taking the medication results in a significant improvement but not a normalization of bladder emptying. JD is back to voiding once a night. He has no nocturnal panic attacks or dreams where he is fearful or exerting himself.

The background and case illustrate a few points. Now that micturation is no longer a black box in the brain, the affected structures and the types of symptoms that can be generated need to be considered. It is an easy mistake to treat what seems like a panic attack like a panic attack - especially when previous physicians have not been impressed enough to work up or treat the problem. Nocturnal panic attacks in a 68 year old man with no previous psychiatric history suggests that there are possible medical causes for these symptoms and in this case it was bladder outlet obstruction. The closest syndrome to account for the findings in this case is cystocerebral syndrome - typically delirium in elderly men with acute urinary retention where no other cause can be identified (3-9). Decompressing the bladder typically results in resolution of the acute confusion. That has led several of the authors to postulate that an adrenergic rather than anticholinergic mechanism is involved. I don't not have access to all of these papers and cannot tell if the authors documented some of the problems noted in the case described here (tachycardia, palpitations, VPCs, anxiety and panic) but they are all presumptive hyperadrenergic mechanisms. 

Whether sleep disturbance, panic attacks, and eventual delirium can all occur in the same men with bladder outlet obstruction is not known at this point. That progression of symptoms seems to make sense but it is not well documented and may just be another syndrome waiting for better characterization.  One of the main differences may be the post void residual volume.  In the case presented here that was about 200-300 ml.  In the literature on cystocerebral syndrome there is usually urinary retention and a much larger volume - often 1 liter or more.  

Until then BPH and the associated lower urinary tract symptoms (LUTS) are markers that psychiatrists and sleep medicine specialists need to pay close attention to - especially if it comes with insomnia, panic attacks and palpitations. 

George Dawson, MD, DFAPA

References:

1: Fowler CJ, Griffiths D, de Groat WC. The neural control of micturition. Nat Rev Neurosci. 2008 Jun;9(6):453-66. doi: 10.1038/nrn2401. Review. PubMed PMID: 18490916.

2: Griffiths DJ, Fowler CJ. The micturition switch and its forebrain influences. Acta Physiol (Oxf). 2013 Jan;207(1):93-109. doi: 10.1111/apha.12019. Epub 2012 Nov 16. Review. PubMed PMID: 23164237.

3: Shirvani N, Jimenez XF. Cystocerebral Syndrome: A Case Report and Review of Literature and Mechanisms. J Am Geriatr Soc. 2015 Dec;63(12):2645-2647. doi: 10.1111/jgs.13851. PubMed PMID: 26691712.

4: Washco V, Engel L, Smith DL, McCarron R. Distended bladder presenting with altered mental status and venous obstruction. Ochsner J. 2015 Spring;15(1):70-3. PubMed PMID: 25829883; PubMed Central PMCID: PMC4365850. 

5: Saga K, Kuriyama A, Kawata T, Kimura K. Neurogenic bladder presenting with cystocerebral syndrome. Intern Med. 2013;52(12):1443-4. PubMed PMID: 23774572. 

6: Young P, Lasa JS, Finn BC, Quezel M, Bruetman JE. [Cystocerebral syndrome]. Rev Med Chil. 2008 Nov;136(11):1495-6. Spanish. PubMed PMID: 19301784. 

7: Waardenburg IE. Delirium caused by urinary retention in elderly people: a case report and literature review on the "cystocerebral syndrome". J Am Geriatr Soc. 2008 Dec;56(12):2371-2. doi: 10.1111/j.1532-5415.2008.02035.x. Review. PubMed PMID: 19093953. 

8: Blè A, Zuliani G, Quarenghi C, Gallerani M, Fellin R. Cystocerebral syndrome: a case report and literature review. Aging (Milano). 2001 Aug;13(4):339-42. Review. PubMed PMID: 11695503. 

9: Liem PH, Carter WJ. Cystocerebral syndrome: a possible explanation. Arch Intern Med. 1991 Sep;151(9):1884, 1886. PubMed PMID: 1888260. 8: Blackburn T, Dunn M. Cystocerebral syndrome. Acute urinary retention presenting as confusion in elderly patients. Arch Intern Med. 1990 Dec;150(12):2577-8. PubMed PMID: 2244775.

10: Glen W Barrisford GW, Graeme MS, Steele S. Acute urinary retention.  O'Leary MP, Hockberger, RS Editors. UpToDate. Waltham MA: UpToDate Inc.  http://www.uptodate.com (Accessed on March 30, 2018.)


Graphic Credits

Both neuroanatomy and urology graphics in this post are from reference 1 and posted here:

Reprinted by permission from Nature/Springer: Fowler CJ, Griffiths D, de Groat WC. The neural control of micturition. Nat Rev Neurosci. 2008 Jun;9(6):453-66. doi: 10.1038/nrn2401. Review. PubMed PMID: 18490916. License number  4319020942759

The graphic of the empty sample cup is from Shutterstock per their standard licensing agreement.