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Challenges for Consultation–Liaison Psychiatry in the 21st Century

Received June 26, 2007; revised October 9, 2007; accepted October 9, 2007. From the Mount Sinai School of Medicine Department of Psychiatry, New York, NY 10029, and NY Medical College Department of Psychiatry, Behavioral Health Center Valhalla, NY. Send correspondence and reprint requests to Dr. Strain, Mount Sinai School of Medicine Department of Psychiatry, 1 G.L. Levy Place, New York, NY 10029. e-mail: james.strain{at}mssm.edu
© 2008 The Academy of Psychosomatic Medicine

With the discovery of new, evidenced-based information, the nature and composition of some psychiatric disorders are changing. For example, depression seems no longer purely a mental disorder, but rather a systemic disorder with many somatic ramifications, including its impact on physical illness. This realization raises important challenges for the practice of psychosomatic medicine in the 21st century: 1) issues of diagnosis; 2) content to be taught, to whom, by whom; and 3) which professionals should offer treatment.

The first challenge is how clinical depressive disorders are diagnosed and how accurate (valid) these diagnoses remain. The diagnosis of depression relies on assessment measures that do not take into consideration the contamination of physical symptoms from physical disorders or drugs—for instance, insomnia, anorexia, diminished libido, or decreased energy. Attribution of symptoms remains confounded with psychiatric and medical comorbidity. Unfortunately, there are no current biological markers/mechanisms to enhance validity. In the 1970s, it was believed that the dexamethasone suppression test might be able to predict treatment-responsive depression. However, this postulate was found to be unreliable and now is rarely used.¹ A recent study reports that 25% of the diagnoses of depression may be inaccurate, and these were not necessarily in comorbid conditions.²

The second challenge relates to the nature of the relationship between depression and specific medical illnesses and how this information should be taught to psychiatrists, primary-care physicians, internists, medical students, nurses, and so forth. Depressive symptoms are associated with an increased risk for cardiac morbidity/mortality, poor glycemic control in type 1 or 2 diabetes, increased morbidity with cerebral vascular accidents (CVA), and HIV progression.³ At present, the strongest association appears to be between depression and heart disease. Depression occurs in 16%–23% of patients with cardiovascular disease (CAD), with an even larger proportion experiencing subsyndromal depression.⁴ Frasure-Smith et al. reported depression to be a significant predictor of mortality (p<0.001) 6 months after myocardial infarction (MI).^5,6 There was a threefold greater chance of dying or having a recurrent MI when there was a concurrent major depressive disorder. Multivariate analysis factored out the effects of left-ventricular dysfunction, previous MI, and premature ventricular contractions. An elevated risk was present for major versus minor depression, categorical rated depressions versus dimensional, and new-onset depression in comparison with chronic or recurrent depression. Similar findings have been observed in patients with congestive heart failure.^7–10

Depression is a risk factor for ventricular arrhythmias and sudden cardiac death. Elevated Beck Depression Inventory scores were more powerful predictors of mortality in those patients with 10 premature bpm. Depression is associated with diminished heart rate variability (HRV), a well-known risk factor for mortality in post-MI patients,¹¹ and increases in corticotropin-releasing factor (CRF), ACTH, and beta-endorphin.^12–15 Nemeroff and his coworkers have delineated the somatic changes that occur with the comorbidity of depression and cardiovascular effects via stress mechanisms that affect the HPA axis, the adrenal, cortisol production, the activation of platelets, and their impact on a ruptured plaque.^12–16 (SSRIs may have an effect on platelets independent of depression.¹³)

Hypotheses regarding the relationship of depression and cardiovascular disease include the activation of platelets via stress mechanisms and their impact on damaged cardiac vessels, or perhaps some other mechanism set in motion by depression. Although studies on treating depression with pharmacological agents, such as the Sertraline Antidepressant Heart Attack Randomized Trial (SADHART) study,¹⁷ demonstrated improvement of depression with few adverse side effects, mortality was not altered. Likewise, in the cognitive-behavioral treatment of depression and low perceived social support to increase reinfarction-free survival after a heart attack (the Enhancing Recovery in Coronary Heart Disease [ENRICHD]), there was no observed change in mortality.¹⁸ This may have been related to the fact that both of these studies were underpowered.

Therefore, researchers such as Frasure-Smith and Lesperance are reluctant to use the term "risk factor" for depression and MI because no study has demonstrated that ameliorating a depressive disorder diminishes mortality (personal communication; November 2006; Tucson, AZ). This is despite the fact that Nemeroff et al.¹⁹ state that "... studies have unequivocally identified depression as an independent risk factor for the development of CAD."

Diabetes is another physical disorder in which there is strong evidence relating depression with other manifestations of the physical illness. Patients with diabetes are three times more likely to have depression than those in the general population.²⁰ Comorbidity also significantly compromised performance of activities of daily living and routine social activities.²¹ Depression has been implicated as a risk factor for the development of type 2 diabetes.²⁰ With regard to pathophysiology, depression may have direct effects on the metabolic syndrome; that is, dyslipidemia, hypertension, abdominal obesity, insulin resistance (hyperglycemia).²⁰ Given that patients with depression have demonstrated enhanced levels of inflammatory markers, for example, IL-1-Beta, tumor necrosis factor-alpha, and C-reactive protein,^22,23 there may be important associations between comorbid diabetes and depression.

Data continue to accumulate that depressive disorders have systemic effects on somatic illnesses, which strongly support the concept that they should be regarded as systemic illness, not solely a mental illness. This would signal a requirement for the addition of medical comorbidity to the content taught about depression to psychiatric residents, and the incorporation of this evolving knowledge for primary-care physicians, internists, cardiologists, endocrinologists, and medical students. Currently, this content is not central to either specialty’s curriculum. These data would dictate that patients with CAD should have psychological assessment even before they have an MI.

The World Health Organization (WHO) estimates that, by 2020, the two disorders causing the greatest burden of illness in the world will be CAD and depression.²⁴ A primary prevention model, where depression is diagnosed on routine medical visits much as abnormal blood cholesterol is diagnosed early to prevent heart disease, would be optimal. As we go forward in this century, more and more physical systems will be connected to depression. Also, more psychiatric disorders may be seen as systemic illnesses that must be evaluated and treated with the same rigor as the physical disorder.²⁵

The third challenge is: who should evaluate and treat these patients with psychiatric and somatic comorbidity when the relationship is associated with an increase in morbidity and or mortality from the medical illness? In the psychiatric consultation model, it would require the cardiologist to call a consult on many (if not all) the patients in the coronary care unit for evaluation and/or treatment. The traditional consultation method leaves the decision in the hands of the cardiologist, who may miss many of the nearly one-quarter of the coronary care patients who experience depression.

In the liaison model, a psychiatrist could be assigned to the coronary care unit to screen all patients, treat those with suspected depression, and arrange follow-up visits upon discharge to ensure the continued and appropriate longer-term treatment of the depressive disorder. Departments of psychiatry and medicine may not want to pay for a liaison psychiatrist assigned to the coronary care unit team.

Another model would be to train cardiologists to screen for depression, offer initial treatment, and refer for complicated or refractory depressive disorders. Treatment would have to continue post-discharge either in the cardiologist’s office or through transfer to a psychiatrist. In order to accomplish this, cardiologists would have to want to incorporate this facet into their daily practice. It would require their being trained to diagnose and treat or refer patients having depressive disorders. In a recent national survey of cardiovascular physicians, 49.9% were unaware of depression as an independent cardiac risk factor, and 71.2% asked fewer than half their patients with CAD about depression.²⁶ Primary-care physicians have been trained to adequately detect, diagnose, and treat depression in such settings as that developed by Wayne Katon at the University of Washington.²⁷ It is a comprehensive and intensive training program with considerable input by the psychiatrist to achieve a meaningful outcome for the patient. Random control trials have established that non-psychiatric physicians can identify and treat straightforward depression in the primary-care setting.^27,28 Guidelines could be developed for the cardiologist’s assessment of depression post-MI so that this would become part of the repertoire of their evaluation. As noted above, only a small portion of the post-MI patients are referred to consultation services in our general acute-care hospitals. The majority are not screened for depression.

A depression screening device could be administered by the admitting nurse in the coronary care unit, with the results presented to the physician; or a second depression screening could be used near the time of the patient’s discharge. Both would alert the cardiologist of a potentially depressed patient. It would also lessen the patient’s ambivalence and negativity if the assessment were accomplished by the cardiologist than by a referral to the psychiatrist, which the patient might resist.

With the ever-increasing evidence of depression’s relationship with medical illness, the above approach should be considered for other medical conditions, as well. Should the neurologist routinely evaluate and then treat those stroke patients identified with depression? It has been reported that about 40% of stroke patients are also depressed.²⁹ Post-stroke inpatients with depression diagnosed in the hospital had a mortality rate 3.5 times that of nondepressed patients at a 10-year follow-up.³⁰ A random control study of CVA patients, both depressed and non-depressed, given antidepressants versus placebo and followed for 9 years, demonstrated that those treated with antidepressants were more likely to survive than those on placebo.³⁰

It will be important to observe what data emanate from investigations of patients with HIV, diabetes, multiple sclerosis, systemic lupus erythematosis, and many other illnesses that also have comorbid depression. Some may disagree with the idea of psychiatry training internists to diagnose and treat depression in their medically ill patients and feel that this is the purview of the psychiatrist. (And, it is certainly possible that internists may not want to be trained to take on this additional element as a routine part of their work). Some psychiatrists may regard such an approach as "giving away the store." However, current systems of education, diagnosis, and care are not addressing these serious omissions in the psychological care of medically ill patients as they need to be addressed in the 21st century.

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