uestion:
Choose the most prominent comorbid condition or the last item if none is
present:uestion:
Choose the most prominent comorbid condition or the last item if none is
present:
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Help: If there is more than one comorbid problem, follow the algorithm answering the questions appropriately for each comorbid condition. You will receive several recommendations for treatment. Compare the recommendations. There may be one treatment option that covers several or all of the comorbid conditions. This might be the treatment of choice.
You have reached this point if none of the listed comorbid conditions were present, and if (for non-melancholic depressions) the possible psychopharmacologic implications have been considered for any concomitant Axis II psychopathology. For melancholic depressions, the algorithms for Axis II were skipped because of evidence that pathology on Axis II has little impact on outcome of melancholic or "endogenous" depression.¹
After reconsideration of possible medical causes of this depression that may have been overlooked, precipitating or sustaining psychosocial factors that may be contributing to continued resistance to treatment, and diagnosis, continuation of sequential somatic therapy trials concomitant with psychosocial treatments is reasonable to the extent that reasonably safe and possibly effective alternatives exist. Many factors will influence the order to proceed with the alternatives, including susceptibility to side effects and drug interactions, previous experiences, patient preferences, inpatient vs. outpatient status, etc. The following list of options is offered with the choices not necessarily in the order of preference.
Additional single treatments: Other SSRI's not yet tried. High dose SSRI's. Venlafaxine. Mirtazapine. Clomipramine (if no ischemia). MAOIs (phenelzine, isocarboxazid, tranylcypromine).
Consider ECT, although there is no evidence ECT offers more than optimized pharmacotherapy for non-psychotic depression and the chance of ECT being effective diminishes with each additional adequate pharmacotherapy trial.² However, the APA practice guideline, revised, for major depression puts a more positive spin on the old literature and indicates that ECT may work in more than half of patients who fail on antidepressants.³ New, somewhat troubling data on long term memory loss from ECT, however, supports keeping ECT at the end of the non-psychotic depression somatic therapy algorithm.(4)
Augmentation strategies if not yet tried: lithium (recently reported to augment venlafaxine as well[5], thyroid hormone, pindolol, buspirone, bupropion, stimulants. One case report in a 21 year old chronically and severely (unipolar) depressed patient testified for a robust acute effect from an omega-3 fatty acid preparation (ethyl ester of eicosapentaenoic acid: ethyl-EPA, 4 g per day).(6)
Recommendation #28
¹Andrews G et al. Diagnosis, personality, and the long term outcome of depression. Br J Psychiatry 1990;157:13-18
²Prudic J, Sackheim HA, Davanaud DP. Medication resistance and clinical response to ECT. Psychiatry Res 1990;31:287-296.
³American Psychiatric Association. Practice Guideline for the treatment of patients with major depressive disorder (revision). Am J Psychiatry 2000;157(4):p.30.
(4)Lisanby SH et al. The effects of ECT on memory of autobiographical and public events. Arch Gen Psychiatry 2000;57:581-590.
(5)Hoencamp E et al. Lithium augmentation of venlafaxine: an open-label trial. J Clin Psychopharmacol 2000;20:538-543.
(6)Puri BK et al. Eicosapentaenoic acid in treatment-resistant depression. Arch Gen Psychiatry 2002;59(1):91-92.
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