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Update on Elderly Depression and Suicide

Update on Elderly Depression and Suicide . Dr. E Cheung Associate Consultant Psychogeriatric Team Castle Peak Hospital. Depression in the Elderly. Common Treatable Under-diagnosed & under-treated > 60% treated inappropriately Disease burden Morbidity & mortality.

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Update on Elderly Depression and Suicide

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  1. Update on Elderly Depression and Suicide Dr. E Cheung Associate Consultant Psychogeriatric Team Castle Peak Hospital

  2. Depression in the Elderly • Common • Treatable • Under-diagnosed & under-treated • > 60% treated inappropriately • Disease burden • Morbidity & mortality

  3. Prevalence of elderly depression in different care settings

  4. Prevalence of Depression (2) • In Hong Kong • 1034 elderly aged 70 and above living in Shatin (Chiu et al, 1998): • Major depression 1.54% • Dysthymia 3.66% • Adjustment disorder with depressed mood 1.54%

  5. Global burden of diseases (WHO)

  6. Depression is associated with increased mortality

  7. Risk factors of elderly depression 1. Female gender 2. Being widowed or divorced 3. Medical illness, e.g. stroke, neurological disorders 4. Functional disability 5. Family and personal history of depression 6. Social isolation 7. Life events 8. Medications, e.g. antihypertensives, steroids and antiparkinsonian drugs 9. Caregiving, e.g. carers of people with dementia

  8. Aetiology (1) • Social: reduced social networks, loneliness, bereavement, poverty, physical ill health • Psychological: low self-esteem, lack of capacity for intimacy, physical ill health • Biological: neuronal loss/neurotransmitter loss, genetic risk, physical ill health

  9. Aetiology (2) • Disease: • Direct: CVA, Parkinson's disease, thyroid disease, Cushing's disease, Hungtington's disease • Indirect: pain, disability, chronicity, poor diet, decreased activity

  10. Aetiology (3) • Drugs: • Digoxin, L-dopa, steroid • Beta-blockers, methyldopa • Chronic benzodiazepine use • Phenobarbitone • Neuroleptics in chronic use

  11. Diagnosis • A syndromal diagnosis • Based on eliciting a specific cluster of symptoms through careful history taking and mental state examination, supplemented by relevant physical examination • No confirmatory laboratory tests • ICD-10 or DSM-IV

  12. International Classification of Disease (ICD-10) • Cardinal symptoms: depressed mood, loss of interest (anhedonia), loss of energy (anergia) • Additional symptoms: reduced concentration, reduced self esteem (present), guilty feelings (past), hopelessness and pessimism (future), self harm or suicidal ideas, sleep disturbance, decreased appetite, loss of libido, psychomotor changes

  13. Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) • Depressed mood most of the day • Marked diminished interest or pleasure in normal activities • Significant weight loss or weight gain • Insomnia or hypersomnia • Psychomotor agitation or retardation • Fatigue or loss of energy • Feelings of worthlessness or excessive guilt • Recurrent suicidal thoughts or attempts • Reduced ability to concentrate

  14. Diagnostic difficulties • Primary care physicians could identify no more than 50% of patients with a diagnosable depressive syndrome (Mulsant & Ganguli, 1999) • Presentation of depression in the elderly may be modified by factors associated with old age

  15. Clinical presentation of elderly depression • Compared with young depressives, older people have (Weisman,1991): • Less disturbed sleep (19% vs 25%) • Less appetite disturbance (16% vs 27%) • Less disturbed energy (11% vs 18%) • Less guilt (5% vs 13%) • Less diminished concentration (8% vs 16%) • Fewer thought about death (22% vs 31%)

  16. Peculiar features of elderly depression • Minimisation of sadness (Georgotas, 1983) • Somatisation or disproportionate complaints associated with physical disorder (Sheehanet al, 2003) • "Neurotic" symptoms of recent onset • "Trivial" acts of deliberate self-harm • "Pseudodementia" • Depression superimposed on dementia • Accentuation of premorbid personality traits and recent change in behaviour

  17. Key questions to ask (1) • How is your mood? • Have you lost interest in anything? • Do you get less pleasure from things you usually enjoy? • How long have you had these symptoms? • Have you been diagnosed before with a depressive disorder?

  18. Key questions to ask (2) • Any important health changes within the past year? • Any major changes in your life in the preceding 3 months? • Any symptoms to suggest underlying physical illness? • Have you ever thought you would be better off dead?

  19. Assessment • History • Mental state examination • Use of standardised instruments, e.g. Geriatric depression scale (GDS) • Cognitive assessment • Physical examination • Investigation

  20. Geriatric Depression Scale (GDS) • Validated standardised scales available locally for screening of depression: 15-item Chinese Geriatric Depression Scale Short Form (GDS) (Lee et al, 1993) • Cut-off point of 8/15 • Can be applied by trained non-medical personnel

  21. Principles of management • Monitoring the risk of self-harm • Educating the patient (and care givers) about depression and involving him or her in treatment decisions • Treating the whole person - coexisting physical disorder; attention to sensory deficits and other handicaps; reviewing medication with a view to withdrawing those unnecessary • Treating depressive symptoms with the aim of complete remission (as residual symptoms are a risk factor for chronic depression) • Prompt referral of patients requiring specialist mental health services

  22. When to refer for specialist advice? (WPA, 1999) • When the diagnosis is in doubt (e.g. is this dementia?) • When depression is severe, as evidenced by: • Psychotic depression • Severe risk to health because of failure to eat or drink • Suicide risk • Complex therapy is indicated (e.g. in cases with medical comorbidity) • When first-line therapy fails (although primary care physicians may wish to pursue a second course of an antidepressant from a different class)

  23. Treatment • Physical treatment • Pharmacological treatment • Electroconvulsive therapy • Psychosocial treatment

  24. The Monoamine Hypothesis • The 3 monoamines: noradrenaline, serotonin and dopamine • Depression believed to be the result of a deficiency of monoamine neurotransmitters • All known antidepressants act by increasing the activity of these neurotransmitters in the brain by various mechanisms

  25. Special considerations in the elderly • Pharmacokinetics (change in volume of distribution , metabolism, elimination) • Co-morbid physical illnesses • Drug interactions • Dosing

  26. Pharmacological treatment • Information for patients and carers: • Start low, go slow • Typical side effect • Delay in onset of therapeutic action • Lack of dependence potential • Need for continuation treatment following initial response

  27. The Five “R”s of antidepressant treatment • Response • Remission • Recovery • Relapse • Recurrence

  28. Recovery Remission Mood Response Recurrence Relapse Acute treatment Continuation treatment Maintenance treatment Time

  29. Principles of antidepressant treatment • Ascertain diagnosis • The ultimate aim of treatment is remission • Treatment has to be adequate in dosage, duration and compliance has to be ensured • If there is no response after an adequate trial, switch to another class of antidepressant • If there is partial response, further increase dosage and/or persist for a longer duration or augmentation

  30. Principles of antidepressant treatment • Address psychosocial issues and psychoeducation • Continuation treatment – at least 6 to 9 months after remission, longer for elderly (12 to 24 months) at the same dose • Maintenance treatment – prophylactic treatment for patients with multiple past episodes, serious ill health, chronic social difficulties and very severe depressive symptoms. No consensus on length of maintenance.

  31. Risk factors for recurrence (WHO, 1989) • Comorbidity • Chronic medical conditions • Chronic affective symptoms • Older age of onset of first episode • Severe functional impairment during depression • Psychotic depression • Previous suicide attempt • Family history of suicide and bipolar disorder

  32. Tricyclic antidepressants (TCA) • Nortriptyline (Nortrilen), dothiepine (Prothiaden), amitriptyline • Anticholinergic S/E • Anti-histaminergic S/E • Anti-adrenergic S/E • Cardiotoxicity

  33. Mechanism of action of TCAs Shown here is an icon of a tricyclic antidepressant (TCA). These drugs are actually five drugs in one: (1) a serotonin reuptake inhibitor (SRI); (2) a noradrenaline reuptake inhibitor (NRI); (3) an anticholinergic/antimuscarinic drug (M1); (4) an alpha adrenergic antagonist (alpha); and (5) an antihistamine (H1). Stephen M. Stahl: Essential Psychopharmacology 1996

  34. Therapeutic actions of TCAs The serotonin reuptake inhibitor (SRI) portion of the TCA is inserted into the serotonin reuptake pump, blocking it and causing an antidepressant effect Stephen M. Stahl, Essential Psychopharmacology, 1996

  35. Therapeutic actions of TCAs The noradrenergic portion of the TCA is inserted into the noradrenaline reuptake pump , blocking and causing an antidepressant effect Stephen M. Stahl, Essential Psychopharmacology, 1996

  36. Side effects of TCAs Side effects of the tricyclic antidepressants- part 1. In this diagram, the icon of the TCA is shown with its H1 (antihistamine) portion inserted into histamine receptors, causing the side effects of weight gain and drowsiness. Stephen M. Stahl, Essential Psychopharmacology, 1996

  37. Side effects of TCAs Side effects of the tricyclic antidepressants - part 2. In this diagram, the icon of the TCA is shown with its M1 (anticholinergic/antimuscarinic) portion inserted into acetylcholine receptors, causing the side effects of constipation, blurred vision, dry mouth and drowsiness. Stephen M. stahl, Essential Psychopharmacology, 1996

  38. Side effects of TCAs Side effects of the tricyclic antidepressants- part 3. In this diagram, the icon of the TCA is shown with its alpha(alpha adrenergic antagonist) portion inserted into alpha adrenergic receptors, causing the side effects of dizziness, decreased blood pressure and drowsiness. Stephen M. Stahl, Essential Psychopharmacology, 1996

  39. Dose titration of TCA • Most commonly used TCA: dothiepine (Prothiaden) • Starting dose: 50mg nocte • Then increase in increments of 25 to 50mg depending on side effects every few days aiming at an initial target dose of 150mg • Maximum dose of 225mg nocte

  40. Selective Serotonin Reuptake Inhibitors (SSRIs) • Citalopram (Cipram), sertraline (Zoloft), paroxetine (Seroxat), fluoxetine (Prozac), escitalopram (Lexapro) • GI upset • Anorexia • Headache • Insomnia, anxiety, tremour • Sexual dysfunction • SIADH

  41. Selective Serotonin Reuptake Inhibitor (SSRI) Shown here is the icon of a selective serotonin reuptake inhibitor (SSRI). In this case, 4 out of the 5 pharmacological properties of the TCAs (tricyclic antidepressants; Figure 6-13) are removed. Only the serotonin reuptake inhibitor (SRI) portion remains; thus the SRI action is selective, which is why these agents are called selective SRIs. Includes fluoxetine, fluvoxamine, citalopram, paroxetine, sertraline and escitalopram Stephen M. Stahl, Essential Psychopharmacology,1996

  42. Mechanism of Action of SSRIs In this diagram, the SRI (serotonin reuptake inhibitor) portion of the SSRI molecule is shown inserted in the serotonin reuptake pump, blocking it and causing an antidepressant effect. This is analogous to one of the dimensions of the TCAs. Stephen M. Stahl, Essential Psychopharmacology, 1996

  43. Serotonergic-Noradrenergic Reuptake Inhibitor (SNRI) • Venlafaxine (Efexor/Efexor XR) • Side effects similar to SSRI • May cause hypertension at high doses

  44. Serotonergic-noradrenergic Reuptake Inhibitors (SNRI) Shown here is the icon of a dual reuptake inhibitor which combines the actions of both a serotonin reuptake inhibitor (SRI) and a noradrenaline reuptake inhibitor (NRI). In this case, 3 out of the 5 pharmacological properties of the TCAs (tricyclic antidepressants) were removed. Both the SRI portion and the NRI portion of the TCA remain; however the alpha, antihistamine and anticholinergic portions are removed. These serotonin/noradrenaline reuptake inhibitors are called SNRIs or dual inhibitors. A small amount of dopamine reuptake inhibition (DRI) is also present in some of these agents, especially at high doses. e.g. Venlafaxine Stephen M. Stahl, Essential Psychopharmacology, 1996

  45. Reversible inhibitors of monoamine oxidase A (RIMA) • Moclobemide (Aurorix) • Nausea • Headache • Insomnia • Restlessness • Agitation

  46. Other antidepressants • SARI – nefazodone (Serzone) • Sedation, lack of 5HT2 stimulation S/E • NaSSA – mirtazapine (Remeron) • Sedation, dry mouth, increased appetite, weight gain • NDRI – bupropion (Wellbutrin) • Headache, dry mouth, agitation, nausea, insomnia

  47. Serotonin-2 Antagonist/reuptake Inhibitors (SARI) Shown here are icons for two of the serotonin 2 antagonist/reuptake inhibitors (SARIs). These agents also have a dual action, but the two mechanisms are different from the dual actions of the SNRIs (serotonin noradrenaline reuptake inhibitors). The SARIs act by potent blockade both of serotonin 2 (5HT2) receptors, combined with SRI (serotonin reuptake inhibitor) actions. Nefazodone also has weak NRI (noradrenaline reuptake inhibition) as well as weak alpha adrenergic blocking properties. Trazodone also contains antihistamine properties and alpha antagonist properties, but lacks NRI properties. Stephen M. Stahl, Essential Psychopharmacology, 1996

  48. Noradrenergic and Specific Serotonergic Antidepressant (NaSSA) e.g. Mirtazapine Stephen M. Stahl, Essential Psychopharmacology, 1996

  49. Other antidepressants • Mianserin (Tolvon): • Sedation, aplastic anaemia, agranulocytosis • Trazodone: • Sedation, orthostatic hypotension, priapism

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