Electroconvulsive therapy

When my wife, Ana, suffered a depressive episode in 2001 after thebirth of our daughter,we took it seriously but at first weweren’t excessively worried. Anawas no stranger todepression,havingbeendiagnosedwith it in 1990. The illness had always responded tomedication, and we were both confident it would again. But something in the equation had changed. Drug after drug was tried. We tried to identify what in our lives might be dragging her down, but we couldn’t find anything.Our relationshipwas great, the childrenwere doing well at school, money wasn’t a problem—we should have both been very happy. I watched as Ana, one of the most incredibly active people I’d ever met, shut downbydegrees.We stopped going out forwalks, shopping, andeven just chatting to theneighbours.The situation worsened rapidly until Ana was admitted to hospital inMarch 2003 in such a dire state that she was immediately placed on 15 minute suicide observation. The doctors decided then to put Ana on a programme of electroconvulsive therapy (ECT) to lift her mood. The improvement was rapid and quite profound. It is worth relating what really severe depression is like to live with. Formal medical jargon is specifically designed to be objective and deliberately strips emotive descriptions away to leave a clear picture for the practitioner. But depression affects the emotions; indeed it’s all about emotion. To people with depression and their carers, phrases such as “lowmotivation,” “poor self esteem,” and “persistent low mood” are all miracles of understatement. Tome as a carer, it feels as if some malign, intangible entity has attached itself to my wife, constantly attacking her. Ana and I are very close: I can feel her mood as soon as I enter the same roomas her, andwhen things are bad, the depression is like an oppressive weight that lies on us both. It sucks the colour out of life. I’ve never seen mentioned in any medical text just how truly terrifying depression is. It’s very, very scary, watching the one you love withdraw from life and turn into an inert stranger—and you can never, ever, relax, because you know that the spectre of suicide is always hanging over all your lives. ECT was like a magic wand. Very rapidly Ana picked up before my eyes. Her interest in life was renewed and she began to smile and laugh again. It became safe to speculate about the future. Optimism was reborn and Ana was discharged from hospital. Sadly, the effects of ECT are not permanent. In Ana’s case, although we continued to try different drugs, antidepressantmedicine just wasn’t helping. Psychotherapy carried an 18 month waiting list, and when she reached the top of that list, Ana was told she had not yet achieved sufficient improvement to be able to cope with thetherapyandsoshepromptlyreturnedto thebottomof the list. We struggled through five very long years—a testament to Ana’s willpower, despite the weight of her illness. It wasn’t all bad. Two or three medications produced an improvement that would last three or four months, andwhen things got reallybad,Ana returned for more ECT. The staff in the ECT suite do awonderful job of reassuring new patients and worried carers, because after all, what is this therapy? The process is stigmatised with misunderstanding and scaremongering. My early misconceptions of physical restraints and bulky electric shockpadswere soonbrushedaway.Thepatient receives a general anaesthetic and a muscle relaxant to mitigate

A carer describes the experiences of depression that led his wife to have electroconvulsive therapy and the effect of this treatment on the whole family When my wife, Ana, suffered a depressive episode in 2001 after the birth of our daughter, we took it seriously but at first we weren't excessively worried. Ana was no stranger to depression, having been diagnosed with it in 1990. The illness had always responded to medication, and we were both confident it would again. But something in the equation had changed. Drug after drug was tried. We tried to identify what in our lives might be dragging her down, but we couldn't find anything. Our relationship was great, the children were doing well at school, money wasn't a problem-we should have both been very happy. I watched as Ana, one of the most incredibly active people I'd ever met, shut down by degrees. We stopped going out for walks, shopping, and even just chatting to the neighbours. The situation worsened rapidly until Ana was admitted to hospital in March 2003 in such a dire state that she was immediately placed on 15 minute suicide observation. The doctors decided then to put Ana on a programme of electroconvulsive therapy (ECT) to lift her mood. The improvement was rapid and quite profound.
It is worth relating what really severe depression is like to live with. Formal medical jargon is specifically designed to be objective and deliberately strips emotive descriptions away to leave a clear picture for the practitioner. But depression affects the emotions; indeed it's all about emotion. To people with depression and their carers, phrases such as "low motivation," "poor self esteem," and "persistent low mood" are all miracles of understatement. To me as a carer, it feels as if some malign, intangible entity has attached itself to my wife, constantly attacking her. Ana and I are very close: I can feel her mood as soon as I enter the same room as her, and when things are bad, the depression is like an oppressive weight that lies on us both. It sucks the colour out of life.
I've never seen mentioned in any medical text just how truly terrifying depression is. It's very, very scary, watching the one you love withdraw from life and turn into an inert stranger-and you can never, ever, relax, because you know that the spectre of suicide is always hanging over all your lives.
ECT was like a magic wand. Very rapidly Ana picked up before my eyes. Her interest in life was renewed and she began to smile and laugh again. It became safe to speculate about the future. Optimism was reborn and Ana was discharged from hospital.
Sadly, the effects of ECT are not permanent. In Ana's case, although we continued to try different drugs, antidepressant medicine just wasn't helping. Psychotherapy carried an 18 month waiting list, and when she reached the top of that list, Ana was told she had not yet achieved sufficient improvement to be able to cope with the therapy and so she promptly returned to the bottom of the list. We struggled through five very long years-a testament to Ana's willpower, despite the weight of her illness. It wasn't all bad. Two or three medications produced an improvement that would last three or four months, and when things got really bad, Ana returned for more ECT. The staff in the ECT suite do a wonderful job of reassuring new patients and worried carers, because after all, what is this therapy? The process is stigmatised with misunderstanding and scaremongering. My early misconceptions of physical restraints and bulky electric shock pads were soon brushed away. The patient receives a general anaesthetic and a muscle relaxant to mitigate any physical convulsion. The shock itself is administered through small self adhesive electrodes not dissimilar to those used for pocket TENS (transcutaneous electrical nerve stimulation) machines. After a treatment Ana might forget the way to the local shops or when my birthday is, but she remembers again in most cases before the end of the day. To date, she has never failed to remember who she is or who I am. And that's all there is to it. Ana has far more reticence about visiting the dentist than the ECT suite.
Last year we hit another trough. Ana was recommended for ECT again. It worked, as it always had before, and we-Ana, I, her consultant, and the consultant in charge of ECT-wondered where to go next. I don't think anyone believed that the "right medicine" was still waiting to be found, and psychotherapy still looked like a distant proposition. In Ana's words, she wasn't after perfect recovery, just something she could, quite literally, live with.
It was at this point that the idea of maintenance ECT was suggested. If ECT was the only treatment that consistently worked, why not continue receiving it on an ongoing basis? Initially, treatments might be as frequent as once a fortnight, but over time the frequency is reduced so that the patient receives the minimum number to maintain their mood. Treatment is continued over an extended period-12 months or more. Many of the patients who have undergone this have discovered that in time their better mood seems to persist, as if the brain learns to sustain the effect. The mechanism by which this happens isn't clearly understood but the results are undeniable.
Ana was eager to try maintenance ECT and began it at once. With bated breath, we began to count the weeks as they went by and Ana's mood remained good. Not perfect-the ECT did not effect a complete cure with no sign of depression at all, but it certainly worked well enough for Ana to live life again.
It is now 12 months since Ana started maintenance ECT. It is impossible to convey to anyone who hasn't experienced living with severe depression, just how profound the improvement in our quality of living has been. Not just for Ana, but for the children and me too. We go out as a family now, cautiously maybe, and always with an escape plan so that Ana can retreat any time she wishes. So far she hasn't once done this. The horrible sick feeling I've learnt to live with over the past seven years at seeing my wife in such a dire state has receded. Problems still arise, of course, but I no longer have the constant gut wrenching fear that next time my back is turned Ana will seek to take her own life. That's one hell of an improvement.
And the price? A very acceptable one as far as Ana and I are concerned. We've talked about it a lot. The side effects of ECT are minor and have not constituted any kind of life altering problem. Disorientation and short term memory loss are usually over and done with in a couple of hours. We accept that for slightly more than a day, once every three weeks, we won't be going out anywhere or doing very much-the anaesthetic leaves Ana very sleepy for the day of the therapy, and sometimes the day after. The biggest issue for us is how desirable is it to have a general anaesthetic every three weeks? Ana has had more than 60 treatments in total now. What if the worst did happen? Supposing something went wrong and she died during the procedure?
It's a risk we are both willing to take. The alternative is the almost certain deterioration of her mood until Ana can't fight any more and takes her own life. Instead we accept the slight risk in exchange for living life again-a good quality life-and knowing there is something to live for.
Competing interests: None declared. Provenance and peer review: Not commissioned; not externally peer reviewed. Patient consent obtained.

A DOCTOR'S PERSPECTIVE ON ELECTROCONVULSIVE THERAPY
Administering ECT is a training requirement for all psychiatric trainees. From my experience it is not always easy-technically or emotionally. My anxiety levels were high when I administered my first ECT. On the day, I was left without supervision to muddle my way through the procedure. The patient was offered little explanation of events-I wondered if I was responsible for explaining things but was far too preoccupied with how to work the archaic machine. The anaesthetist and nurse in charge were grumpy at my lack of knowledge, and seven years later I find it difficult to believe that this procedure was left to a junior trainee without adequate training or supervision. The Royal College of Psychiatrists now has guidelines on how ECT training should be undertaken by trusts, and my current trust follows the guidelines impeccably. I hope I am not naive in the belief that juniors no longer experience what I have described above. The evidence base suggests that ECT is a valuable and effective treatment. However, there remains something disturbing to me about being responsible for inducing a seizure in someone who may not be capable of consenting. Patients having ECT deserve dignity in the approach to their treatment, particularly when it is performed without their consent. If the guidelines are followed with regular audit of protocols then I believe dignity and humane treatment can be achieved. The repeated experience of seeing the beneficial effects that ECT can have in patients such as Ana where other treatments have failed, help me to continue administering and advocating ECT.

Indications and administration
The guidance from the National Institute for Health and Clinical Excellence (NICE) recommends that ECT is used to achieve rapid and short term improvement of severe symptoms in individuals with severe depressive illness, catatonia, and a prolonged or severe manic episode. It recommends consideration only after an adequate trial of other treatment options has proved ineffective and/or when the condition is considered to be potentially life threatening (www.nice.org.uk/nicemedia/pdf/59ectfullguidance.pdf) The Royal College of Psychiatrists also recognises that maintenance ECT ( defined as a prophylactic treatment over the first six months of remission) is a treatment option in certain cases (www.rcpsych.ac.uk/publications/collegereports/cr/cr128.aspx). Prescription of ECT requires an assessment of potential risks and benefits of treatment, for which valid consent has been obtained where possible. Risks include those associated with a general anaesthetic, current comorbidities, and anticipated side effects, particularly cognitive impairment. Anterograde and retrograde amnesia surrounding the procedure is a recognised side effect, as is retrograde amnesia affecting longer term memory in some cases. The benefits of the treatment are the improvement or prevention of further deterioration in symptoms and reduction of associated life threatening risks. ECT in the United Kingdom is administered under a general anaesthetic and with a muscle relaxant. Once the patient is anaesthetised, an electrical current is delivered across the brain via placement of electrodes on the skull either unilaterally or bilaterally. A generalised tonic-clonic seizure is induced, which is usually monitored by the use of electroencephalography and electromyography. A typical course would be 6-10 sessions, with two sessions a week.

Atrial fibrillation
Kathryn E Griffith, 1 Maurice Pye 2 A 63 year old man sees your practice nurse for a routine blood pressure check. He has had hypertension for five years and is taking ramipril 10 mg, bendroflumethiazide 2.5 mg, and atenolol 25 mg daily. He has no past history of ischaemic heart disease, stroke, or diabetes. The nurse's electronic sphygmomanometer is unable to produce a recording, and she asks for your advice. You find his pulse to be intermittently irregular.

What issues you should cover
Atrial fibrillation is a recognised cause of error in blood pressure measurement. When atrial fibrillation is an incidental finding and thus asymptomatic, it may be difficult to decide whether it is paroxysmal, persistent, or permanent.
It is important to reach a diagnosis and arrange electrocardiography as soon as possible and to confirm that he has not had an embolic event, particularly a transient ischaemic attack (TIA) with sudden onset of reversible neurological deficit.
Atrial fibrillation can result in symptoms related to abnormal cardiac rate and output or in cerebrovascular symptoms caused by thromboemboli.
Often the onset of atrial fibrillation is difficult to pinpoint. It may follow cardiac surgery or an acute illness such as pneumonia.
Atrial fibrillation is associated with ischaemic heart disease, high alcohol consumption, thyrotoxicosis, obesity, and the use of some illicit drugs such as cocaine. Assess these during the history and examination. Physical examination allows you to assess his heart rate and blood pressure and whether he has cardiac murmurs or heart failure. Your most important treatment decision concerns the use of anticoagulant or aspirin. Rhythm control is recommended for patients who are symptomatic, are younger, who present for the first time with lone atrial fibrillation, who have atrial fibrillation secondary to a treatable cause (such as a chest infection), or who have heart failure or inadequate rate control.
What you should do Arrange electrocardiography-This will confirm the diagnosis, which can then be coded and added to the disease register.
Symptoms-Ask whether he has had palpitations, angina, or symptoms of low cardiac output, such as breathlessness or tiredness. Consider urgent referral to hospital if he has rapid heart rate, hypotension, signs or symptoms of heart failure or has recently had syncope, stroke, or symptoms of TIA.
Cardioversion-Consider rhythm control for younger patients with probable recent onset of atrial fibrillation and thus referral to a specialist for cardioversion. You may wish to review such patients in one week to confirm persistence.
Drug treatment-The first line treatment for rate control is ß blockers. His dosage of atenolol could be increased if he has a tachycardia. Rate limiting calcium channel blockers are used where ß blockers are contraindicated. Digoxin is not recommended in active patients, as it does not control increased heart rate in exercise. To determine the optimum antithrombotic treatment in persistent atrial fibrillation, you can use the stroke risk stratification algorithm at appendix E of the NICE guideline (see Useful Reading). The algorithm shows that although he is aged under the threshold for low risk of stroke (65 years), his hypertension puts him at moderate risk (2-4% a year), unless he has had any embolic complications (high risk). He could therefore be treated with warfarin or aspirin. If he is to have cardioversion he will need warfarin for at least six weeks before the cardioversion. Involve him in the treatment decision and discussion of stroke risk: some patients find regular blood checks and limiting alcohol consumption restrictive. In deciding on treatment you should assess his risk of bleeding: has he a history of gastrointestinal bleeding, excessive alcohol intake, uncontrolled hypertension, or frequent falls? Assess his clinical risk-benefit ratio to make an informed decision.
Echocardiography-Arrange this if he shows evidence of heart failure or a murmur or if you are considering cardioversion. The presence of poor left ventricular function will determine the choice of anti-arrhythmic and antithrombotic treatment. A large left atrium increases the risk of stroke. A rise in concentration of B-type natriuretic peptide in atrial fibrillation may be caused by rapid heart rate, not left ventricular systolic dysfunction.
Future visits-Arrange a baseline thyroid function test, liver and renal function test, full blood count, and international normalised ratio for when you see him next. Review him continually over time to assess control of heart rate and blood pressure and to reassess his stroke risk. If he is initially treated with aspirin, the development of heart failure or diabetes would move him to the high stroke risk category and he would need warfarin.
Competing interests: None declared. Provenance and peer review: Not commissioned; externally peer reviewed. This is part of a series of occasional articles on common problems in primary care. The BMJ welcomes contributions from GPs.

LESSON OF THE WEEK
Rapidly fatal invasive pertussis in young infants -how can we change the outcome? U Theilen, 1 E D Johnston, 2 P A Robinson 1 Prevention of infection may be the only effective intervention against whooping cough for unimmunised infants Although vaccination of infants has greatly reduced morbidity and mortality in children, 1 the incidence of pertussis is rising in the non-paediatric population. 2 In adults persistent cough for more than two weeks is the cardinal feature of pertussis, but with a wide differential and an atypical course, pertussis is often undiagnosed. 3 Infectious adults in a family are the main source of infection for unimmunised infants. 4 We report two fatal cases of invasive pertussis in unvaccinated infants.

Case reports
Case 1 A 1 month old boy presented to a district general hospital with a five day history of cough, runny nose, and difficulty feeding. A working diagnosis of bronchiolitis was made.
Both parents and an older sibling reported coughing episodes for the preceding fortnight. The baby's mother gave a history of vomiting after these spells, and classic bouts with "whoop" were observed. The sibling had been fully vaccinated. The practice searched unsuccessfully for the childhood vaccination status of the parents, but the mother had received a pertussis booster in 1986.
Pertussis was considered and erythromycin was started. Over the next 24 hours the child developed coughing spells with profound apnoeas. He was intubated and transferred to a paediatric intensive care unit.
Initially, adequate ventilation was easily achieved, but over the next 24 hours this became difficult, despite the use of high pressures, up to 100% oxygen, and inhaled nitric oxide. Repeat chest radiography showed complete consolidation of the right lung and evolving consolidation of the left. Ultrasonography confirmed severe parenchymal lung disease.
Circulatory collapse developed rapidly and he failed to respond to fluid resuscitation, maximum doses of inotropes, and support with hydrocortisone and immunoglobulins. Referral to a unit offering paediatric extracorporeal membrane oxygenation was discussed, but circulatory collapse meant that transfer was impossible.
Within 24 hours of admission to paediatric intensive care, the infant died despite maximum treatment. Polymerase chain reaction testing of nasopharyngeal secretions confirmed Bordetella pertussis, and a postmortem examination was not requested. The infant's mother declined to be tested for B pertussis.
Case 2 A 6 week old girl presented to a district general hospital with a five day history of cough and breathlessness. Her mother had had a persistent cough for more than two weeks. The patient's mother was documented as having received all her childhood immunisations including pertussis, but there was no record of the status of pertussis immunisation for her father. On admission the baby had mild recessions and a respiratory rate of 50 with oxygen saturation of 88% in air. Her heart rate was raised (180 beats per minute), but other vital signs were normal. A chest radiograph showed patchy perihilar changes. Her white cell count was high (56 700×10 9 /l (normal 6000-18 000×10 9 /l) with 31 200×10 9 /l lymphocytes (normal 3000-13.5 000 ×10 9 /l). A presumptive diagnosis of bronchiolitis was made, but in view of the leucocytosis, intravenous cefotaxime was started.
Over the next 12 hours, the baby's breathing became more difficult, and she was transferred to paediatric intensive care. Lymphocytic leucocytosis was interpreted as a possible sign of pertussis, and clarithromycin was added.
After 10 hours of stability with little ventilatory support the patient developed rapidly progressive respiratory and cardiovascular failure. She died within 30 hours despite being given maximum treatment, including inhaled nitric oxide and inotropes.
Postmortem examination showed severe pulmonary damage with pneumonic consolidation. Myocardium and liver showed focal ischaemic damage. B pertussis was isolated from the lung. The patient's mother tested positive for B pertussis on nasopharyngeal secretions.

Discussion
This report shows the devastating course of infantile invasive pertussis. This rapidly progressive disease, rarely seen outside paediatric intensive care, mainly affects the respiratory system (parenchymal damage, pulmonary hypertension) and cardiovascular system (overwhelming sepsis, B pertussis toxins blocking the effect of inotropes in animal model). 5 6 Mortality remains high despite the use of extracorporeal membrane oxygenation or pharmacotherapy such as inhaled nitric oxide, sildenafil, or milrinone. 7 Passive transplacental transfer of antibodies does occur, but is insufficient to prevent infection. 8 An age of less than 2 months and massive leucocytosis are strong predictors of poor outcome. 9 In both these cases leucocytosis prompted appropriate antibiotic treatment before paediatric intensive care treatment was started. Despite this timely response, outcome was fatal, suggesting that in an infant infected with B pertussis any action may be ineffective.
The spectrum of pertussis has changed dramatically over the past decades. Vaccination has led to far fewer children being affected. 1 Infants who have not been vaccinated account for most complications, hospitalisations, and deaths related to pertussis. 10 Several countries have reported major increases in infant morbidity, 11 and in the United States the number of infant deaths has increased. 12 Obtaining reliable UK population figures on deaths from pertussis in infants is difficult. The paediatric intensive care audit network (PICANet; a national audit network of UK paediatric intensive care units) had reports of five infants dying from pertussis in an 18 month period. Infant deaths from pertussis may be under-reported and may contribute to cases of sudden infant deaths. 13 Pertussis in infants can be difficult to diagnose clinically, and positive results on a test for respiratory syncytial virus or adenovirus should not preclude the diagnosis. 10 Most infants catch the disease from affected household members-in more than half of the cases the parents. 4 Outbreaks in neonatal units have highlighted the risk of transmission from infected adult carers. 14 In many countries pertussis infections in adolescents and adults are becoming more common. 15 The number of pertussis infections in adolescents and adults in the United States has been estimated to be more than a million cases annually. 16 Several studies in primary care found that pertussis was the cause for prolonged cough in 15-30% of adolescents and adults. 17 The main reason for the changed distribution of pertussis in countries with good vaccination uptake seems to be waning of immunity after vaccination. Although immunity against infection wanes faster than immunity against disease, immunity lasts for about 4-12 years after vaccination. 18 As a consequence, several countries have introduced booster doses for adolescents (Canada, US, Australia, Austria, France, Germany) and some for adults (US, Australia, Austria). 11 While this will reduce the disease burden from pertussis for the adult population, an epidemiological model found that a high coverage rate of adults (>85%) would be required to reduce the number of cases of pertussis in infants. 19 Additionally, France and Germany have recommended a targeted booster for parents and healthcare workers in contact with young children. 20 21 Although the uptake among adolescents is variable in different countries, parents of new babies were particularly motivated to accept vaccination. 22 No outcome data exist to assess the efficacy of these new measures.
What can a general practitioner do to protect vulnerable young infants from pertussis? Cough lasting more than two weeks in adult or adolescent household members is the cardinal symptom and should raise suspicion of pertussis. Nocturnal, paroxysmal cough and post-tussive vomiting increase the likelihood further. Testing is by polymerase chain reaction of nasopharyngeal aspirates or per nasal swabs within three weeks after onset of cough. This sensitive new technique is partly responsible for the increase in reported pertussis cases. After three weeks serology tests for pertussis toxins should be done. Current Left chest radiograph taken when the baby was admitted. It shows central peribronchial thickening only (arrows). The right chest radiograph shows widespread consolidation (confirmed by ultrasonography) less than 24 hours later recommendations support treating infected adults and giving prophylaxis to vulnerable infants with erythromycin for seven days. 23 Infectivity stops after five days of treatment. Studies of chemoprophylaxis for contacts, however, failed to confirm its efficacy. 24 Despite modern paediatric intensive care, mortality remains high for young infants developing invasive pertussis. Even appropriate treatment of symptomatic household contacts that starts after two weeks of cough is unlikely to prevent transmission. The best solution is to prevent infection. Introducing an adolescent pertussis booster, as adopted in several countries, or more targeted vaccination of household contacts of this most vulnerable group should be carefully considered.
Contributors: UT had the idea for the article, identified and managed the cases, and is guarantor. PAR, EDJ, and UT carried out the literature search. UT, EDJ, and PAR wrote the article. Competing interests: None declared. Funding: None received. Patient consent obtained.