Medicine, psychiatry and euthanasia: an argument against mandatory psychiatric review.

Rainer Dziewas and Henning Henningsen, Department ofNeurology, University of Münster, Germany:

In his article ‘Medicine, psychiatry and euthanasia: anargument against mandatory psychiatric review’ MalcolmParker [1] deals with the question whether obligatorypsychiatric examination of patients requesting activeeuthanasia is warranted, while psychiatric examinationis usually not taken into consideration in the context ofpassive euthanasia. The author points out that neither anappeal to the traditional acts and omissions doctrine norto the doctrine of the sanctity of life can help to solve theissue. Rather, the problem should be conceptualized as aconflict between the principle of respect for autonomyand the principle of nonmaleficience. The key questiontherefore is, whether patients who request active eutha-nasia tend to be more impaired in their decision-makingabilities, because of depression, for example, thanpatients who request passive euthanasia. As this matteris not decided at present, the author concludes that therequirement of psychiatric assessment solely in the caseof active euthanasia has neither empirical nor moraljustification. He expresses the fear that such a procedurecould impair the freedom of patients in making decisionsabout their deaths.

While we believe the author’s arguments to be correct,they seem to be incomplete at the same time, making hisconclusions questionable. In the current discussion ofdifferent aspects of euthanasia a lot of attention is paidto slippery-slope arguments. Most prominent is itsso called psychological-sociological version [2], whichexamines the probable impact of making further excep-tions to the rule against killing. It is feared, that if legalrestraints against killing are taken away by moving frompassive to active voluntary euthanasia, for example, anumber of psychological and social forces would pos-sibly make it more difficult to retain the relevant distinc-tions in practice, thereby causing a slide from voluntaryto nonvoluntary or even involuntary euthanasia. Amongothers the following more concrete points have been putforward so far:

Physicians, who are used to disclosing to their patientsnot only ‘pure’ information but to recommend therapeu-tic procedures as well, might start seeing euthanasia asanother therapeutic option and to influence patients inthat direction [3].

Additionally, it is suspected, that a change of theattitude towards the seriously ill could be induced [4].Besides a reduction of sympathy and compassion in theintimate social surrounding of the afflicted person, the

danger is discerned, that changes to the disadvantage ofthe seriously ill – for example confinement of palliativemedical measures – might take place at an institutionallevel [5].

Obviously, these consequences might lead to variousforms of manipulation and coercion, thereby signifi-cantly reducing the voluntariness of the patients’ deci-sions. Although comprehensive empirical evidence insupport of this reasoning is lacking, we think thatslippery-slope arguments constitute a morally relevantdistinction between active and passive euthanasia. Whileit is disputable if a prohibition of active euthanasia canfirmly rest on these arguments, they do justify measuresto enhance and secure patient’s autonomy in the contextof active euthanasia [5]. Mandatory psychiatric review,which does not only serve to diagnose clinical depres-sion but also to identify external manipulation or co-ercion, should be seen as such a suitable measure.

References

1. Parker M. Medicine, psychiatry and euthanasia: an argument against mandatory psychiatric review.

Australian and New Zealand Journal of Psychiatry

2000; 34:318–324.2. Beauchamp TL Childress JF.

Principles of biomedical ethics

4th edn. Oxford: Oxford University Press, 1994.

3. Keown J. Euthanasia in the Netherlands. Sliding down the slippery slope? In: Keown J, ed.

Euthanasia Examined

, Cambridge: Cambridge University Press, 1995.

4. Mayo DJ. Gunderson M. Physician assisted death and hard choices.

Journal of Medicine Philosophy

1994; 19:329–341.5. Battin MP. The least worst death. Oxford: Oxford University

Press, 1994.6. Quante M. Passive, indirect and direct active

euthanasia-descriptive and ethical solid distinctions?.

Ethik Medicine

, 1998; 10:206–226.

Persisting continuous visual perception disorder in a chronic MDMA (‘ecstasy’) user

Torsten Passie, Udo Schneider and Hinderk M. Emrich,Department of Clinical Psychiatry and Psychotherapy,Medical School Hannover (Germany):

A major drug of abuse today is 3,4-Methylenedi-oxymethamphetamine (MDMA or ‘ecstasy’). Seriousmedical complications and neurotoxicity are known tobe caused from its uncontrolled use, but most long-termeffects are still unkown. Neuropsychological studiesshow cognitive deficiencies in chronic users [1].

In March 1999, a 22-year-old man with a 3 yearhistory of drug abuse was admitted to our detoxificationward. Childhood and education were without majorcomplications. He had been taking cannabis since 1996and ‘ecstasy’ tablets almost daily since 1997. He docu-mented in his diary the ingestion of more than 350‘ecstasy’ tablets in 18 months (up to eight tablets at

Correspondence

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weekends; without dancing). He had also consumedLSD 5–7 times in total.

Since his first hospitalization in August 1998 hereported a visual perception disorder which persists con-tinuously until today. He described it as ‘like a snow-storm on a defective TV’. Hundreds of transparent littledots moving chaotically over his whole visual field.When his eyes were open he could see everything indetail, but the whole visual field was overlaid by thisdisturbance. When his eyes were closed, he claimed tosee ‘little coloured dots’. These phenomena were less-ened in sunlight and aggravated in the dark.

A careful ophthalmologic examination showed noabnormality. The disturbances seem to be generatedbeyond the primary visual cortex.

Psychiatric examination showed (according to ICD-10) abuse of cannabis and hallucinogens, sociophobicanxiety disorder with derealization phenomena and adepressive disorder. Toxicological screening was nega-tive for amphetamines, barbiturates, benzodiazepines,opiates, cocaine, phencyclidin and LSD. THC was initi-ally positive. Physical examination, full blood count,HIV-testing, ECG, EEG, cranial CT and MRI and neu-ropsychological performance (attention, short- and long-term memory investigated with a standard computerizedtesting battery) were without abnormalities.

The described disorder remained unchanged in our3 week treatment. When we saw him 6 weeks later therewas still no change and THC-screening was negative.

Chronic administration of MDMA in animals resultedin destruction of serotonergic nerve terminals. Processesof recovery were noted, but showed region-dependenttime-course and degree of recovery with compensatoryre-respectively hyperinnervation [2]. Brain areas that areinvolved in visual perception processes were alsoaffected [3].

We hypothesize that the neuropathological basis ofthis patient’s visual abberations may be an altered re-innervation pattern of neurones responsible for process-ing visual information.

To our knowledge this is the first case described witha persisting continuously visual perception disorderinduced most likely by chronic MDMA use.

References

1. McCann UD, Mertl M, Eligulashvili V, Ricaurte GA. Cognitive performance in (+/-) 3,4-methylenedioxymethamphetamine (MDMA, ‘ecstasy’) users: a controlled study.

Psychopharmacology

1999; 143:417–425.2. Hatzidimitriou G, McCann UD, Ricaurte GA. Altered serotonin

innervation patterns in the forebrain of monkeys treated with (+/-) 3,4-methylenedioxymethamphetamine seven years previously: factors influencing abnormal recovery.

Journal of Neuroscience

1999; 19:5096–5107.

3. Battaglia G, Sharkey J, Kuhar MJ, De Souza EB. Neuroanatomic specifity and time course of alterations in rat brain serotoninergic pathways induced by MDMA (3,4-methylenedioxymethamphetamine).

Synapse

1991; 8:249–260.

Responsible regulation of psychiatric practice

Eleanor M Dawson, Pymble, New South Wales, Australia:

Psychiatrists and their patients require fuller protectionfrom professional regulatory bodies than is currentlyavailable. This includes a more effective way of address-ing complaints in ways to minimize the risk of injusticeto anyone.

I urge the Royal Australian and New Zealand Collegeof Psychiatrists (the College) to become actively involvedin educating, advising and monitoring the statutorysystems. For example, in New South Wales there aretwo relevant authorities, the NSW Medical Board (theBoard) and the Health Care Complaints Commission(the HCCC). The College awaits the outcome of investi-gations and disciplinary inquiries by these agenciesbefore concluding any deliberations of its own.

While a complainant dissatisfied with a finding of aMedical Board Professional Standards Committee appearsto be able to appeal to the Medical Tribunal under theambiguous provisions of the Medical Practice Act [1], inpractice this is not so. The HCCC remains the onlycomplainant with the standing to appeal [2]. Yet theHCCC has also chosen its original advisers, conductedthe investigation, made recommendations to the Board,and decided with the Board whether to make a formalcomplaint and where and how to prosecute that com-plaint at an inquiry.

Psychiatrists on the Peer Review Panel of the HCCCadvise it during investigation of the complaint. They arethen remunerated for reports to the HCCC after reviewof its file and for appearing as witnesses at any resultingcommittee or tribunal inquiry [3]. This inquiry may beheld

in camera

by an ad hoc professional standardscommittee appointed by the Board or in open court by amedical tribunal presided over by a judge.

The reports prepared by the psychiatrists on the PeerReview Panel carry considerable weight, though theymay remain legally privileged and inscrutable. Thismeans that possible deficiencies and biases in the peerreview opinions may remain unchallenged. Furthermore,the criteria by which psychiatrists are selected to theHCCC peer review panel remain quite obscure, as diduntil recently the names of the peer review panellists [4].

I urge our College to take the lead when aware of theoutcome of the current NSW Parliamentary Committee’sInquiry into Procedures followed during HCCC Investi-gations and Prosecutions. There is an urgent need for theCollege to consult with its own membership and to

268 CORRESPONDENCE

develop clear and fair policies and procedures in the areaof professional regulation, particularly in dealing withcomplaints brought against College Fellows.

References

1. NSW Medical Practice Act No 94 1992, Section 87.2. Hidden J, SC NSW, 15 December 1995, Shoulder v NSW

Medical Board and ors.3. Adrian A. Health Care Complaints Commission, Guidelines for

Peer Reviewers, January 2001.4. Hennessy N, Deputy President, NSW Administrative Decisions

Tribunal, General Division, Dawson v Commissioner, Health Care Complaints Commission, 30 July, 1999. www.lawlink.nsw.gov.au/adt

Cerebellar ataxia with intravenous valproate and haloperidol

Sanjeev Ranjan, K. Jagadheesan, S. Haque Nizamie,Central Institute of Psychiatry, Ranchi, India:

Intravenous valproate therapy is getting greater atten-tion in recent times given the fact that it has been foundbeneficial in acute mania and aggressive behaviours [1].Of the typical antipsychotics, chlorpromazine has beenreported to decrease valproate clearance considerably[2]. A clinically significant interaction between halo-peridol and valproate is unknown in the current litera-ture. For its clinical relevance, we report a patient whodeveloped severe ataxia, an uncommon [3] but distress-ing complication of valproate, when haloperidol wasadded to intravenous valproate therapy.

A 30-year-old male with DSM-IV bipolar affectivedisorder was admitted for his fourth manic episode. Forhis refusal to take oral medications and aggressiveness,he was started on intravenous sodium valproate at thedoses of 20 mg/kg/day. His blood investigations includ-ing liver function test and physical examination werenormal at the beginning of valproate therapy. In the first2 days, with the exception of decreased appetite, he didnot have any other adverse effect from valproate. Later,for his persisting aggressive behaviour and manic symp-toms, oral haloperidol 10-mg twice daily was added. Thefirst dose of haloperidol was given at night and from thenext day morning onwards, the patient began feeling asense of imbalance and he started swaying. On examina-tion, he appeared drowsy and had cerebellar ataxia asevidenced by impaired heel-knee test, finger-finger test,finger-nose test and tandem walking. Otherwise, physi-cal examination was unremarkable. Consequently, halo-peridol was discontinued and, within a day, his ataxiahad disappeared completely in spite of continuingvalproate.

To our knowledge, this is the first report indicating asignificant interaction between intravenous valproateand haloperidol. Although we did not monitor serum

valproate levels, the findings that ataxia appeared afteradding haloperidol and it disappeared following dis-continuation of haloperidol hint at the causative role ofhaloperidol in precipitating valproate toxicity. Haloperi-dol has a high protein binding capacity similar to val-proate [4] and it has been found to decrease the clearanceof valproate (400-mg/day) but in an insignificant manner[2]. We believe that both these properties of haloperidolmight have become crucial, particularly when haloperidolis combined with higher doses of intravenous valproatewhich has a greater bioavailability [1], in causing val-proate toxicity. This issue needs further exploration inview of increasing use of intravenous valproate therapy.

References

1. Norton JW, Quarles E. Intravenous valproate in neuropsychiatry.

Pharmacotherapy

2000; 20:88–92.2. Ischizaki T, Chiba K, Saito M, Kobayashi K, Lizuka R. The

effects of neuroleptics (haloperidol and chlorpromazine) on the pharmacokinetics of valproic acid in schizophrenic patients.

Journal of Clinical Psychopharmacology

1984; 4:254–261.3. Gelenberg AJ, Hopkins HS, Delgado PL. Mood stabilizers.

In: Tasman A, Kay J, Liberman JA, eds.

Psychiatry

. Philadelphia: W.B. Saunders, 1997; 1586–1605.

4. Dollery SC.

Therapeutic drugs

. Edinburgh: Churchill Livingston, 1991.

Polydipsia and Risperidone

Nilamadhab Kar, P.S.V.N. Sharma, P. Tolar, K. Pai,R. Balasubramanian, Department of Psychiatry, KasturbaMedical College, India:

Consumption of large quantities of liquids is reportedin 3–39% of chronic psychiatric cases [1]. A number ofpsychotropic drugs such as carbamazepine, thioridazine,amitriptyline, desipramine, haloperidol, chlorpromazine,fluoxetine have been suggested to be associated withprimary polydipsia [2]. The literature on the relationshipof risperidone and polydipsia is scanty. Whitten andRuehter have reported hyponatremia without polydipsiawith risperidone [3]. Many studies [4–8] including thatby Kruse

et al

. [9] have found risperidone beneficial inpolydipsia. In contrast to the above we describe a case ofpolydipsia associated with risperidone therapy.

A 28-year-old male was suffering from schizophreniaof undifferentiated type, with a continuous course of10 years. He did not have any substance abuse or physi-cal illness. He was treated with various oral and inject-able classical antipsychotics and electroconvulsive therapyat different times with minimal improvement. He hadmultiple brief hospitalizations. Over the last 2 years hehad been on risperidone. It was reported that 2 weeksafter starting risperidone, while he was on 8 mg of risp-eridone per day, he started drinking water excessively.The excessive water intake was intermittent. He would

CORRESPONDENCE 269

complain of unbearable thirst and would drink 4–5 L ofwater within a variable period of a few minutes to8 hours. In addition to the water drunk during the poly-dipsia episode he would consume another 1–2 L on thesame day. It was associated with polyuria. The initialfrequency of polydipsia was once every 10–15 days. Itthen became once every 3–4 days and some times twicea day after the dose of risperidone was increased to16 mg per day. Often a period of relative quiescenceincluding staring and unresponsiveness to verbal inter-action preceded the episode of water drinking. Follow-ing excessive water intake he occasionally experiencednausea, vomiting, marked lassitude, slurring of speechand drowsiness. There was no history of muscletwitches, cramps, blurring of vision, fits, delirium orcoma. Due to the improvement of schizophrenic symp-toms with 16 mg of risperidone, that dosage was main-tained. Later the dose of risperidone was graduallydecreased to 8 mg per day. However, there was no fluc-tuation in the frequency of polydipsia episodes. He didnot receive anticholinergic medications during risperi-done therapy. The patient was given lorazepam 2 mg aswhen required to control restlessness during waterintake. He was admitted to our centre for evaluation ofpolydipsia after having been on risperidone for 2 years.He was then on 8 mg of risperidone per day. He wasactively deluded and hallucinated. The content of psy-chotic features was not related to water drinking. He alsohad prominent negative symptoms.

Two episodes of polydipsia were noticed during thefirst week of admission. In the first episode, the patientconsumed 4000 mL of water within 7 h. His weightincreased by 1 kg. Polydipsia was associated with poly-uria. He did not develop hyponatremia. However, serumosmolality decreased from 304mosmol/kg to 279mosmol/kg. His urine osmolality decreased from 483mosmol/kgto 172mosmol/kg. The urine specific gravity decreasedfrom 1.030 (prepolydipsia) to 1.010 (postpolydipsia).His blood pressure increased from 130/80 to 160/100 mmof Hg. There was a marginal increase in his pulse ratefrom 88 to 100/minute. In the second episode he took2800 mL of water in 4 h. The biological parameters weresimilar to the first episode. Electroencephalogram recor-ded before and during the episode was normal. CT scanof the brain showed no abnormality. His blood sugar,thyroid status, urine volume and osmolality were normalwhen he was not in periods of polydipsia.

Risperidone was stopped because of its possible role ininducing polydipsia. The patient was kept drug free for 2weeks. There was no polydipsia during this time. He didnot complain of thirst. He was started on clozapine.There was no report of polydipsia in the follow up periodof 6 months.

The patient did not have polydipsia before initiation ofrisperidone. He complained of increased thirst and con-sumed excess amount of water episodically for short periodsof time. The frequency of such episodes increased withcontinuing treatment with risperidone at and above 8 mgper day. There was no diabetes mellitus or insipidus.He was not on any other medication known to causepolydipsia [1,2]. Though polydipsia is known to be asso-ciated with schizophrenia and some antipsychotic medi-cations it is unlikely to be the case here, as he never hadsuch symptoms in the first 8 years of illness. In addition,an important observation is that polydipsia stopped afterrisperidone was withdrawn. Unlike the report of Whitten

et al

. we did not find hyponatremia in the polydipsiaepisodes we observed [3]. He did not develop features ofwater intoxication. However, a few episodes of poly-dipsia that had occurred at home in the past were associ-ated with nausea, vomiting, marked lassitude, and mighthave been associated with water intoxication. It is knownthat hyponatremia and water intoxication may be causedby psychotropic medications through a mechanism ofsyndrome of inappropriate secretion of antidiuretichormone (SIADH) [2,3]. The presence of SIADH isunlikely in this patient considering the features of poly-uria, urine osmolality decreasing to 172mosmol/kg andabsence of hyponatremia in the episodes of polydipsia.Biochemical features of the possible episodes of waterintoxication that occurred at home are not available.However, all the episodes were associated with signifi-cant polydipsia and polyuria. The remission of polydip-sia during the two-week drug-free period is unlikely tobe spontaneous, as other such remissions did not occurwhile on risperidone. A longer drug free observationperiod could not be maintained for clinical reasons. Theabove observations suggest that risperidone was associ-ated with primary polydipsia in the index patient.

Considering the contradicting reports on efficacy ofrisperidone on polydipsia [6,8]; risperisone itself causinghyponatremia [3]; nonsustenance of improvement ofpolydipsic behaviour by risperidone [9]; and polydipsiaand polyuria in the index case, it seems that the relation-ship of risperidone and polydipsia is far from clear.Variable influences suggest possibility of an indirect andcomplex relationship, which requires further prospectiveexploration.

References

1. de Leon J, Dadvand M, Canuso C

et al.

Polydipsia and water intoxication in a long term psychiatric hospital.

Biological Psychiatry

1996; 40:28–34.2. Assal F, Charcot F. Hyponatremia of therapeutic origin: apropos

of a case.

Encephale

1994; 20:527–529.3. Whitten JR, Ruehter VL. Risperidone and hyponatremia: a case

report.

Annals of Clinical Psychiatry

1997; 9:181–183.

270 CORRESPONDENCE

4. Kern RS, Marshall BD, Kuehnel TG

et al.

Effects of risperidone on polydipsia in chronic schizoprenia patients.

Journal of Clinical Psychopharmacology

1997; 17:432–435.5. Landry P. Effect of risperidone on polydipsia and hyponatremia

in schizophrenia.

Canadian Journal of Psychiatry

1995; 40:566–567.

6. Assouly-Besse F, Seletti B, Lamarque I, Elghozi D, Petitjean F. ‘Polydipsia, intermittent hyponatremia and psychoses’ syndrome: a diagnosis and therapeutic management of a case.

Annals of Medicine Psychological Paris

1996; 154:259–263.7. Buckley PF, Schulz SC. Clozapine and risperidone: refining and

extending their use.

Harvard Review of Psychiatry

1996; 4:184–199.

8. Millson RC, Emes CE, Glckman WG. Self induced water intoxication treated with risperidone.

Canadian Journal of Psychiatry

1996; 41:648–650.9. Kruse D, Pantelis C, Rudd R

et al.

Treatment of psychogenic polydipsia: comparison of risperidone and olanzapine, and the effects of an adjunctive angiotensin-II receptor blocking drug (irbesartan).

Australian and New Zealand Journal of Psychiatry

2001; 35:65–68.

Doubts about HoNOS

Simon Stafrace, Melbourne, Australia:

I wish to comment on 'Measuring mental health out-comes in a private psychiatric clinic: Health of theNation Outcome Scales, Medical Outcomes Short FormSF-36' by Page

et al.

[1]Of the 1360 inpatients assessed, only 1152 (84.7%)

provided questionnaires on admission, and 754 (55.4%)at discharge. The relatively poor completion of question-naires at both points of the admission process occurreddespite ‘regular HoNOS training throughout the studyperiod’ and the fact that the measures were being col-lated as part of a study. This finding raises an importantquestion about the utility of the HoNOS as a routinemeasure in this setting. I am reminded of the point madeby Thornicroft and Slade [2] that though an outcomemeasure may be standardized and acceptable to clini-cians, this does not necessarily mean that it is feasible forroutine use.

The authors state that the data show patients in theirsample were comparable in initial severity and outcometo those in other Australian hospitals and that theHoNOS and the SF-36 provide reliable and valid meas-ures of patient function. The analyses do not allow theseconclusions to be drawn. No evaluation of test-retest orinterrater reliability is provided. The comparison of theHoNOS depression item and the BDI is insufficient todemonstrate construct validity. Further, no statisticalanalysis is used to compare the findings of the studywith those from other Australian hospitals.

Finally, the authors conclude that the HoNOS wassensitive to treatment change, while the SF-36 was not.Again, this does not appear so. The statistical methodused to compare HoNOS and SF-36 scores on admission

and discharge was not described, though P-values wereprovided. These show that changes in the admission anddischarge means of all 12 items of the HoNOS and six ofnine items of the SF-36 were significant to a level ofP < 0.001. In any case, the lack of a significant changeshould not be taken as evidence that the instruments areinsensitive to change without further evidence of signif-icant change using alternative instruments. Thus, a lackof change may be a true finding, and not merely anartefact of the instruments used.

References

1. Page AC, Hooke GR, Rutherford EM. Measuring mental health outcomes in a private psychiatric clinic. Health of the Nation Outcome Scales and Medical Outcomes Short form SF-36.

Australian and New Zealand Journal of Psychiatry

2001; 35:377–381.

2. Thornicroft G, Slade M. Are routine outcome measures feasible in mental health?

Quality in Health Care

2000; 9:84.

Weight gain and hyperglycaemia associated with olanzapine

Gail Riccitelli, Norris Baker, Taranaki Health, New Ply-mouth, New Zealand:

Olanzapine, a thi–obenzodiazepine, is an atypical anti-psychotic frequently prescribed because it is well toler-ated and has a good safety profile. Weight gain is acommonly reported adverse event. We would like toreport a case of olanzapine-associated new onset dia-betes mellitus, probably Type II.

TM is an 18-year-old Caucasian female, who had abaseline weight of 59 kg. She has a probable diagnosisof schizophrenia. TM was initially commenced on ris-peridone, however, this was discontinued as a result ofgalactorrhoea due to hyperprolactinaemia (2549 inter-national units, prolactin). At that time her weight was65 kg, random blood glucose 4.4 mmol/L.

After the apparent remission of her first psychoticepisode, she was weaned off all antipsychotic medi-cation. Three months later her psychosis relapsed andtreatment with olanzapine was begun. This was initially5 mg daily for 1 week and then increased to 10 mg.Despite regular attendance at the gym and a dietitician’ssupervision, her weight increased to 72 kg over 3 monthsand to 86.5 kg 5 months later. A random blood glucosewas now 14.9 mmol/L and her haemoglobin A1C was11.5%.

The patient was admitted to the medical ward fortreatment of diabetes mellitus. She was asymptomatic. Itwas noted that both maternal and paternal grandparentshave diabetes. The olanzapine was discontinued. Herblood glucose levels returned to normal on diet alone.

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Two months later her weight was 74 kg and her HBA1C7.5 and after 6 months her HBA1C was 6.6.

This case example lends further support to the need foridentifying patients at risk for developing diabetes mel-litus (weight gain and positive family history), and insti-tuting closer glucose monitoring [1]. It is also importantto note that the profile of patients at risk is not definedonly by race, gender and baseline weight [2].

References

1. Goldstein LE, Sporn J, Brown S

et al.

New-onset diabetes mellitus and diabetic ketoacidosis associated with Olanzapine treatment.

Psychosomatics

1999; 40:5.2. Fertig MK, Brooks VG, Shelton PS

et al

. Hyperglycaemia associated with Olanzapine (letter).

Journal of Clinical Psychiatry

1998; 59:12.

Outcome measures used by the Mental Health Review Board

Tom Trauer, Cathy Jones, St Vincent’s Mental Health Ser-vice, Melbourne, Australia

We report a case of an involuntary psychiatric out-patient who used outcome measure ratings (in part) toshow that she no longer required a Community Treat-ment Order (CTO), an order made out under the StateMental Health Act [1] that provides for compulsorytreatment in the community.

Victoria (not her real name) is a 43-year-old womanwith schizophrenia. Her 11-year history has been markedby fluctuating insight and periods of noncomplianceduring which she had problems with substance abuseand became dangerous. She has had three hospitaladmissions.

At the hearing in which the patient appealed againsther CTO, the Mental Health Review Board (MHRB)considered one of the required criteria: Has the patientrefused or is she unable to consent to the necessarytreatment for the mental illness? The treating doctorindicated that hospital admissions had been averted bythe application of the CTO, and that when the CTO waslast lifted compliance with medication and appointmentshad ceased. The case manager told the Board thatalthough she might fall back into a cycle of drinking

alcohol after a few days of ceasing medication, Victoriawas generally compliant and manages the illness verywell. He also said that the 16-item version [2] of the LifeSkills Profile [3] had been completed as part of therecent case review and individual service plan. TheseLSP ratings covered the previous 3 months. On the item:Does this person generally look after and take her or hisown prescribed medication (or attend for prescribedinjections on time) without reminding? the rating was1 (slightly unreliable) and on the items: Is this personwilling to take psychiatric medication when prescribedby a doctor? and Does this person cooperate with healthservices (e.g. doctors and/or other health worker)? theratings were 0 (always). Victoria’s legal representativesubmitted that she was consenting to treatment and drewthe Board’s attention to previous MHRB decisions inwhich (a) partial insight did not preclude a sufficientunderstanding of the consequences of not taking medica-tion, and (b) the need to interpret the Act in a way thatleast infringes upon civil rights. The Board dischargedVictoria from her status as an involuntary patient.Despite subsequent deterioration in her substance abuseproblem and an increased frequency of contact with theservice, there has been no contact with the crisis teamnor any hospitalizations.

This case demonstrates that routinely collectedoutcome measures can have a direct impact on patientcare. Did the measures detract from the clinical auton-omy of the health care professionals involved? We thinknot, since the ratings only represent a formal and system-atic record of clinical opinions that could have otherwisebeen expressed verbally; however, these opinions hadnot been documented elsewhere in the file.

References

1. Mental Health Act. Melbourne: Victorian Government Printing Office, 1986.

2. Buckingham W, Burgess P, Solomon S, Pirkis J, Eagar K.

Casemix classification of mental health services

. Canberra: Commonwealth Department of Health and Family Services, 1998.

3. Rosen A, Hadzi-Pavlovic D, Parker G. The Life Skills Profile: a measure assessing function and disability in schizophrenia.

Schizophrenia Bulletin

1989; 15:325–337.