As many as 50% of elderly general hospital inpatients are also suffering from an identifiable mental disorder. Most common in this age group are depression, delirium and dementia.1  Depressed elderly patients present in many different ways to healthcare professionals. They may present simply as ‘off legs’ or as a social admission where they may be weak from self neglect and weight loss.  Overdose is another presentation, but unlike younger patients the elderly who overdose are more likely to have a major mental disorder (as opposed to personality difficulties) and to overlap in terms of their demographic and phenomenological characteristics with those who have completed suicide.2

They may present with unexplained physical symptoms (somatisation), the summation of coexistent anxiety (the great mimicker), lowered pain threshold, introspectiveness and negative thinking.Pseudo dementia4 is another presentation and this is an inconsistent picture of cognitive dysfunction (with ‘don’t know’ answers/self-deprecatory answers) and underlying biological symptoms of depression. This presentation seems to be a risk factor for the later development of dementia-depression serving to tip a mild case into a clinical dementia picture.

Another reason is poor rehabilitation5 (due to diminished energy and motivation) and slower recovery (perhaps due to impaired immunological function). Very occasionally, they may present in a catatonic/profoundly psychomotor retarded state.

The above are some of the reasons why knowledge of the major psychiatric disorders forms part of the core curriculum for higher training in geriatrics. Sometimes an elderly depressed patient presents to the district general hospital as a psychiatric and medical emergency. In such cases electroconvulsive therapy (ECT) may be indicated. 

A 78-year-old widow was admitted to a general hospital having been found collapsed on the floor by her home carer one morning. She was found to have hypernatraemia and dehydration and a right basal pneumonia. A week later she was physically better but depressed, bed bound and refusing to eat or drink. Diabetes insipidus had been diagnosed. It had emerged that she had an established diagnosis of bipolar disorder since her student days and that she normally took lithium carbonate. She had become depressed since the death of her pet cat a few weeks ago.

Differential diagnosis
The differential diagnosis of a chronically lethargic, apparently depressed elderly person includes:

  • Severe depression
  • Space occupying lesion—subdural, meningioma
  • Frontal lobe stroke or dementia
  • Metabolic disturbance—hypercalcaemia, hyponatraemia (common complication of SSRIs)
  • Vitamin deficiency—B12, folate
  • Endocrine—hypothyroidism, Addison’s and Cushing’s diseases
  • Iatrogenic—steroids
  • Primary CNS disorder—Parkinson’s, encephalitis.

These are more likely if there is no past history of affective disorder (even post-natal illnesses many decades previously can be significant).

Treatment options
The patient is at imminent risk of the complications of severe depression which include:

  • Malnutrition
  • Dehydration/acute kidney injury—especially in the patient’s case given her diabetes insipidus
  • Bedsores, hypostatic pneumonia
  • Thromboembolic events.


Antidepressant medication eg. venlafaxine (an SNRI) or sertraline (SSRI) are likely to take at least four to six weeks to work.6 Occasionally catatonic patients will respond, within 48 hours, to high dose benzodiazepines.7 The patient is likely to have succumbed to the above complications before medication has worked. ECT is the treatment most likely to produce a rapid response and save her  life.8-11

Limitations of psychiatric units
Unfortunately, most psychiatric units are stand alone facilities and not part of a district general hospital. Psychiatric patients, especially the elderly, are not respecters of this artificial distinction and they frequently have complex healthcare needs. In addition, psychiatric nursing staff receive little general nursing training, on call medical staff are often not resident and (due to modern training schemes) psychiatric juniors may have little general experience. Usually the most that can be offered is subcutaneous fluids.The needs of the vignette patient can only be met in a general hospital. In the first instance, ECT will have to be given in general theatres.

ECT: a brief history12,13
The discovery of the efficacy of ECT in certain severe mental disorders owes much to serendipity. In the beginning of the 20th century the theory of ‘forced normalisation’ held sway. The belief was that patients with psychosis and co-existent epilepsy underwent a diminution of their psychiatric disorder after a run of seizures. Attempts during the 1930s to treat patients by inducing a seizure, first with a solvent (camphor) and then electrically, produced the surprising result that, whilst being ineffective in schizophrenia, it brought about relief of severe depression.

A subsequent study in Edinburgh14 demonstrated a reduction of the death rate amongst depressed inpatients in a post war compared to a pre war group (ECT had been introduced into northern European practice during the war years). Antidepressant medication (an MAOI accidentally produced in the search for a less hepatotoxic form of isoniazid) only became available some years later. Unfortunately, this first truly effective psychiatric treatment fell into disrepute due to overuse (the froth of enthusiasm was not allowed to settle on the cup of knowledge before it was passed on). By the mid 1960s up to 25% of inpatients received ECT, the indications having broadened beyond the evidence base. ECT, like frontal lobotomy, became emblematic of the psychiatric profession’s abuse of vulnerable incapacitated individuals.

From the 1980s,13 the Royal College of Psychiatrists started to look at ECT practice in the UK. An attempt to set standards culminated in a joint venture with the Royal Colleges of Nursing and Anaesthetists—ECT accreditation service. This inspects, triannually, all ECT units against over 200 standards.

The procedure
Patients are kept nil by mouth for six hours before treatment. Anticonvulsant mood stabilisers (valproate, carbamazepine) should be halved in dosage and omitted prior to treatment as should benzodiazepines. All cardio-respiratory drugs should be given with sips of water. If the patient has symptoms of reflux a proton pump inhibitor is prescribed (to reduce the risk from aspiration). Insulin is omitted until the patient is having breakfast upon recovery. Anticoagulants are continued but only with the INR strictly between two and three.

A pre-operative assessment is made of the patient’s mental and cognitive state. Their continuing and freely given consent is verified or a check is made that the relevant Mental Health Act paperwork is in place. Fully clothed, the patient lies down on the trolley. Pulse, blood pressure and temperature having already been recorded. A venflon is inserted and the anaesthetic drugs (an induction agent, methohexitone and a paralysing agent suxamethonium) administered. When the patient is unconscious cardiac monitoring and a two channel EEG are attached. Oxygenation and hyperventilation (which helps lower the seizure threshold) are administered until the suxamethonium has taken full effect. The dose of ECT (measured in millicoloumbs) is determined from a titration schedule; during the first treatment up to three increasing doses are given until the seizure threshold is found. The electrodes are applied in a bilateral (bitemporal) position and the dose discharged. The aim is to produce a generalised but modified convulsion lasting between 20 and 60 seconds. EEG monitoring is continued until the characteristic three per second spike and wave pattern has subsided and there is baseline suppression. Seizures longer than 60 seconds are terminated with propofol.

Evidence base
A meta-analysis15 of trials of ECT, published in 2003, concluded that compared with sham ECT (anaesthetic only) and also with antidepressants, ECT was very effective in the short-term for the treatment of severe depression (effect size in the two comparator groups of -0.9 and -0.8 respectively). The studies did not permit conclusions to be drawn about its use in the elderly. However, at the evidence level of ‘expert opinion’, most UK old age psychiatrists would attest to it being effective, safe and potentially life saving. Most clinics have one or two patients having two to four weekly maintenance treatment—usually elderly patients who have not remained well post ECT. The author has several patients who have been treated in this way for a number of years.

Mechanism of action
The lack of a precise knowledge of the mechanisms of action of ECT has been cited by (usually non-medical) critics as a reason not to use it.15 The riposte is, of course, that penicillin’s action against the bacterial cell wall was only worked out years after it had started to save lives. In fact much is known of the neurophysiological changes that occur during ECT—many of them being the same as those occurring during a successful course of antidepressant medication. For example, monoamine turnover in the brain is increased as evidence by a rise in their major metabolites (5HIAA and HVA) in the CSF. Changes in the expression of certain genes are noted eg. an increase in mRNA coding for brain derived neurotrophic factor (BDNF). The latter results in increased arborisation of dendrites particularly in the medial temporal lobes. This may underpin the improvement in cognitive function seen as depression resolves.

NICE recommendations16

NICE is due to report again soon but in 2003 it recommended the use of ECT for the following conditions:
1. Severe depression that has failed to respond to an adequate trial of pharmacotherapy (undefined) or where there is risk to life (through suicide or neglect of diet/fluids)
2. Mania—with similar caveats
3. Catatonia—the only instance in which ECT is indicated in a form of schizophrenia.

Risks and side effects

  • The absolute contraindications to ECT such as when there is likely to be a fatal outcome are:
  • Raised intra-cranial pressure
  • A leaking aneurysm.
Relative contraindications (relative to the risks of inanition, poor fluids) are those relating to general anaesthesia:
  • Recent myocardial infarction (MI)/CVA
  • Cardiac disease—rhythm disorder, failure, aortic stenosis
  • Respiratory disorder
  • Deep vein thrombosis.

Patients with a ventricular defibrillator must have the device magnetically turned off before ECT lest the electrical discharge is ‘recognised’ as a run of ventricular fibrillation and a shock delivered. Ordinary cardiac pacemakers, provided that they are working, are not a problem. Cochlear implants must be disconnected so that the electrical energy is not conducted to the inner ear.

Common side effects include headache, nausea and myalgia. These can be reduced by giving paracetamol or odansetron before or during the procedure. Most patients will have some transient disorientation and some retrograde amnesia. A service users forum study reported long-term retrograde (autobiographical) amnesia in as many as a third of patients.17 This was based on data gathered before individual titration of electrical dosage became the norm; patients now receive much lower doses using the newer machines. It is likely that the side effect rate is much less. The mortality rate in all patients is said to be 1/50,000.

Risks of untreated depression
Chronic depression,1, 13 is a risk factor for dementia, ischaemic heart disease, poorer outcome in co-existent physical illness (poor compliance with medication/rehabilitation, impaired immune function).
Pre ECT ‘work up’ The local mental health trust will have its ECT care pathway, designed to meet the ECTAS criteria for care. This will provide a comprehensive resume of the patient’s medical history (including details of previous ECTs), a physical examination, blood tests and ECG. 

Anaesthetic issues
An experienced consultant anaesthetist should give anaesthetic for ECT aided by a suitably trained assistant. Ideally there should be a designated consultant who can liaise with the psychiatrists and get to know the procedures.Pre-ECT assessment will help staff identify potential problems such as angina, recent MI, CVA, diabetes, hypertension, hiatus hernia, drug allergies and previous anaesthetic problems. Investigations should include blood pressure, weight, urine, ECG and chest xray if over 55 years or with respiratory problems. Routine bloods should be done and monitoring equipment should include blood pressure, oxygen and EEG. Emergency resuscitation equipment should be easily accessible. Anaesthesia for ECT has a significant effect on its effectiveness. The objective is to achieve the shortest period of unconsciousness necessary to achieve muscle relaxation with a rapid return to full consciousness and orientation. The patient is then taken to a recovery area staffed with fully trained recovery personnel.

Legal issues
The patient’s capacity to consent to treatment is assessed. A capacitated refusal of ECT can only be overridden if their life is at risk. In this situation the patient is assessed and detained under the Mental Health Act and a request for a second opinion appointed doctor’s assessment (SOAD) is made to the Care Quality Commission. If the patient is too ill to wait for the arrival of the SOAD, emergency ECT is given under section 62. All of this is organised by the liaison psychiatry team. An advance directive refusing ECT can be overridden in this way.18

A patient lacking capacity but who is passively accepting treatment can be treated under the Mental Capacity Act after it has been deemed to be in their best interests to do so. This will entail a discussion with the next of kin or, in the case of the ‘unbefriended’, with an independent mental capacity advocate.

Some patient feedback
It can be extremely helpful to share with patients and their families the written testimonies of past patients. In the authors’ experience this can make the difference in helping a patient to accept a course of treatment particularly when the suggestion of ECT is met with an incredulous ‘do they still do that now?’ or conjures up terrifying media portrayals (which are usually greatly at odds with the reality of modern practice). Below are some direct quotes from patients attending our unit:

  • ‘Mum was in a terrible state when she arrived with you and we were unsure as to whether it would be possible for her to ever get back to being independent with a state of mind and wellbeing which she had enjoyed before. The simple fact is she has. ECT has certainly worked for Mum.’
  • ‘I have just visited Mum after her 5th ECT session and she is almost back to her old self after several months of severe depression…she had tried six different antidepressants and none had worked for her and she was extremely poorly.’
  • ‘I want to tell you about the great difference ECT has made to my life. Before treatment I used to spend most of the day in bed with no interest in doing anything. Life was very depressing and I felt unable to tackle the simplest of tasks. Life is very different now. I walk the dog, use the computer, read and do jobs around the house including cooking and entertaining.’

1. Benton T, Staab J, Evans DL. Medical Comorbidity in depressive disorders. Annals of Clinical Psychiatry 2007; 19(4): 289–303
2. Annette L, Beutrais PHD. A case control study of suicide and attempted suicide in older adults. Suicide and Life threatening behaviour 2002; 32(1): 1–9
3. Cimprean D, Drake RE. Treating co-morbid medical conditions and anxiety/depression. Epidemiology and Psychiatric Science 2011; 20: 141–50
4. Kral VA, Emery OB. Long term Follow up of depressive pseudodementia of the aged. Canadian Journal of Psychiatry 1989; 34(5): 445–46
5. DiMatteo Mr Lepper HS, Croghan DW. Depression is a risk factor for non-compliance with medical treatment: Metanalysis on the effects of anxiety and depression on patient adherence. Archives of Internal Medicine 2000; 160(14): 2101–107
6. Bondareff W, Alpert M, Friedhoff AJ, et al. Comparison of sertraline and nortriptyline in the treatment of major depressive disorder in late life. American Journal of Psychiatry 2000; 157: 729–36
7. Ferrier N, Porter R. Emergency treatment of depression. Advances in psychiatric treatment 1995; 5: 3-10
8. Weiner R. ECT in the physically ill. Journal of Psychiatric treatment and evaluation 1983; 5: 457–62
9. Tew JD, Mulsant BH, Haskett RF, et al. The acute efficacy of E.C.T the treatment of major depression in the old–old. Am J Psychiatry 1999; 156: 1865–70
10. Buchan H, Johnstone E, McPherson K, et al. Who benefits from ECT? Combined results of Northwick Park and Leicester trials. BJ Psych 1992; 160: 355–59
11. ECT Review Group. The efficacy and safety of E.C.T. in depressive disorders; a systemic review and meta-analysis U.K. The Lancet 2003; 361(9360): 799–808
12. Shorter E. A history of psychiatry: from the era of the asylum to the age of Prozac 1998 ISBN-10: 0471245313
13. Waite J, Easton A. The ECT handbook 3rd Edition (College report) SBN-10: 190802058X
14. Lansdown J, Gill D. A controlled comparison of simulated and real ECT. BJ Psych 1978; 133: 514–19
15. Rose P, Fleischmann T, Wykes M, et al. Patients` perspectives on electroconvulsive therapy: Systematic review. BMJ 2003: 326
16. NICE technology appraisal {TA 59} April 2003. (accessed 2/2/15)
17. Murphy E. Prognosis of depression in old age. BJ Psych 1983; 142: 111–19
18. MHA code of Practice 1983. (accessed 2/2/15)