1436
29. Weed L. The computer as a new basis for analytic clinical practice: coupling individual problems with medical knowledge. Mount Sinai J Med 1985; 52: 94-98. 30. Adams ID, Chan M, Clifford PC, et al. Computer aided diagnosis of acute abdominal pain: a multicentre study. Br Med J 1986; 293: 800-04. 31. Pozen MW, d’Agostino RB, Mitchell JB, et al. The usefulness of a predictive instrument to reduce inappropriate admissions to a cardiac care unit. Ann Intern Med 1980; 92: 238-42. 32. Kent D, Shortliffe E, Bischoff M, Scott A, Jacobs C. Improvements in data collection through physician use of a computer-based cancer chemotherapy protocol advisor. J Clin Oncol 1985; 3: 1409-17. 33. Wyatt J. A method for developing medical decision-aids applied to ACORN, a chest pain advisor. DM thesis, Oxford University, 1991. 34. Brahams D, Wyatt J. Decision-aids and the law. Lancet 1989; ii: 632-34. 35. Feinstein AR. The haze of Bayes, the aerial palaces of decision theory, and the computerised Ouija board. Clin Pharmacol Ther 1977; 21: 482-96. 36. Barnett GO, Cimono JJ, Hupp JA, Hoffer EP. DXPlain: an evolving
diagnostic decision-support system. JAMA 1987; 258: 67-74. 37. Bankowitz R, McNeil M, Challinor S, Parker R, Kapoor W, Miller R. A computer-assisted medical diagnostic consultation service. Ann Intern Med 1989; 110: 824-32. 38. Nathwani BN, Heckerman DE, Horwitz EJ, Lincoln TL. Integrated expert systems and videodisk in surgical pathology. Hum Pathol 1990; 21: 11-27. 39. Shiffman S, Wu AW, Poon AD, et al. Building a speech interface to a medical diagnostic system. IEEE Expert 1991 (February): 41-50. 40. Pryor T, Gardner R, Clayton P, Warner H. The HELP system. J Med Systems 1983; 7: 87-102.
Wyatt J, Spiegelhalter D. Evaluating medical expert systems: what to test, and how?. Med Informatics 1990; 15: 205-17. 42. Wyatt J. Lessons learned from the field trial of ACORN, an expert system to advise on chest pain. In: Barber B, Cao D, Qm D, eds. Proceeding of 41.
6th World Conference
on
Medical Informatics. Amsterdam: North
Holland, 1989: 111-15. 43. Stinson ER, Mueller DA. Survey of health professionals’ information habits and needs. JAMA 1980; 243: 140-43. 44. Covell D, Uman G, Manning P. Information needs of office practice: are they being met? Ann Intern Med 1985; 103: 596-99. 45. Williamson J, German P, Weiss R, Skinner E, Bowes F. Health science information management and the continuing education of physicians. Ann Intern Med 1989; 110: 151-60. 46. Carr RM. The point of the pen. Byte Magazine 1991 (February): 211-21. 47. Blois M. The physician’s information environment. In: Cohen GS, ed. Proceedings of 8th Symposium on Computer Applications in Medical Care, Washington, DC: IEEE Press, 1984: 86-88. 48. Huth E. The underused medical literature. Ann Intern Med 1989; 110: 99-100. 49. Greenes RA, Shortliffe EH. Medical informatics: an emerging academic discipline and institutional priority. JAMA 1990; 263: 1114-20. 50. Blois M, Shortliffe E. The computer meets medicine: emergence of a discipline. In: Shortliffe E, Perrault L, Wiederhold G, Fagan L, eds. Medical informatics. Wokingham: Addison Wesley, 1990: 3-18. 51. Wyatt J. Computer phobia. Lancet 1990; 335: 1223. 52. Shortliffe E, Perrault L, Wiederhold G, Fagan L, eds. Medical informatics. Wokingham: Addison Wesley, 1990. 53. Evans D, Patel V, eds. Cognitive science in medicine. London: MIT Press, 1989.
CLINICAL PRACTICE Impact of psychiatric services on prison suicide
Severe restrictions on the transfer of mentally disturbed prisoners to psychiatric hospital were introduced in Auckland in 1983, while policy in other parts of New Zealand was unchanged. Among male prisoners, the suicide rate (per 100 000 man-years) increased from 27·3 in 1973-82 to 178·0 in 198387—an increase in relative risk, compared with unconfined men, from 1·6 to 8·2. Auckland accounted for most of this increase, from 37/100 000 man-years in 1973-82 to 549/100 000 in 1983-87. This striking increase in prison suicide rate in Auckland underlines the importance of ready access to psychiatric care for prisoners. Introduction
Although prison culture may be a major determinant of suicide in prison, another influence might be the availability of transfer of mentally disordered prisoners to psychiatric hospitals. In 1983-87, stringent restrictions on such transfers were abruptly introduced in Auckland, whereas a policy of ready access to psychiatric hospitals was little changed in other parts of New Zealand. We have analysed suicide rates among prisoners and the unconfined population from 1973 to 1988 to identify whether the change in policy in Auckland was associated with an effect on prison suicide rates.
Methods recorded as suicide in New Zealand prisons 1973 to 1988; only 2 were among female prisoners, and subsequent analysis is restricted to male suicides. Crude prison suicide rates were calculated from annual average daily prison populations for the periods 1973-82 and 1983-87. Unfortunately, these data were not available by age group; because almost all prisoners were under the age of 50 years, and no prisoner aged 50 years or older committed suicide, these rates were compared with crude rates of suicide for the same periods among unconfined men aged 15 to 49 years. Indirect standardisation according to the age distribution of a different measure of prison population, the number of prisoners who were sentenced at least once in a given year, barely altered the crude suicide rates obtained for the unconfined population. New Zealand’s highest security prison, Paremoremo, opened in Auckland in 1968. This prison had a close relation with Oakley, a psychiatric hospital with secure facilities. Patients considered mentally disturbed by the prison authorities could readily be admitted to Oakley and many custodial remands were assessed there.2 In 1974, Oakley was split into two hospitals, Oakley and Carrington; the new Oakley continued to provide secure facilities for forensic patients until policy changed in 1983, when a narrow definition of "treatable mental illness" was introduced: it then 39 deaths
were
(including borstals) from
ADDRESSES Departments of Psychological Medicine (K Skegg, MRCPsych) and Preventive and Social Medicine (B Cox, MCCMNZ), University of Otago Medical School, Dunedin, New Zealand. Correspondence to Dr Keren Skegg
1437
TABLE I-CRUDE SUICIDE RATES AMONG UNCONFINED MEN AGED 15-49 AND MALE PRISONERS
*Shown
as
rate/100 000 man-years (number of suicides).
became extremely difficult to transfer mentally disturbed prisoners to a psychiatric hospital in Auckland. To compare suicide rates in Auckland prisons with the rest of the country, the prison population on Dec 31 of each year was used,
instead of the average daily prison population,
as
this denominator
was available
by length of sentence. Suicide rates were calculated for 1973-82 and 1983-87; 1988 was analysed separately because the report of an inquiry into these events was released in that year.2 Because length of sentence, particularly for life,3 and imprisonment on remand4 have been associated with an increased risk of suicide, suicide rates were adjusted for length of sentence (available as less than 3 months, 3 months to 1 year, and 1 or more years), number of remand prisoners, and number of prisoners sentenced to borstal or corrective training. The numbers in these sentence categories in 1980 were chosen to weight the sentence-adjusted suicide rates. The number of male suicides in Auckland psychiatric hospitals changed little over the study period (9 in the 10 years 1973-82 compared with 4 in the 5 years 1983-87).
Results 28 of the 37 male suicides in New Zealand prisons in 1973-88 were serving sentences of between 2 months and life imprisonment (including 1 to borstal training) and 9 were on remand. 33 hanged or strangled themselves and 4 used other methods. Table I shows crude suicide rates for male prisoners and unconfined men aged 15-49 years; a striking increase in the relative risk of suicide in prison was seen in 1983-87. This change was not simply a continuation of a gradual increase over the previous decade because prison suicide rates were lower in 1978-82 than in 1973-77. There were no significant differences in suicide rates between Maori and non-Maori prisoners. Table 11 shows male prison suicide rates in Auckland compared with those for the rest of New Zealand. In 1973-82 there was 1 suicide in Paremoremo, but 13 in 1983-87: thus, for 1983-87 there was a crude annual suicide rate of 1311/100 000 prisoners and a sentenced-adjusted annual rate of 662/100 000 prisoners in Paremoremo. In 1988, there was 1 suicide in Paremoremo and 3 in another Auckland prison (compared with 2 in the rest of New Zealand), and the 1988 rate for Auckland was again high (crude annual rate 551/100 000
prisoners). Discussion Prison suicide increased more than 6-fold in New Zealand after 1982. Compared with unconfined men of similar age, TABLE II-NUMBERS OF SUICIDES AND CRUDE AND SENTENCEADJUSTED SUICIDE RATES AMONG MALE PRISONERS IN AUCKLAND AND REST OF NEW ZEALAND
*Rate/100 000 man-years
male prisoners were less than twice as likely to commit suicide in 1973-82 but more than 8 times as likely to do so in 1983-87. Allowance for different age distributions of the unconfined and prison populations did not alter this result. There has been concern about increased prison suicides in other countries; in England and Wales, for example, prison suicides per 100 000 prisoner years have risen, for both sexes combined, from 31/100 000 per year in 1972-75 to 87/100 000 in 1987.3 But this disturbing increase appears modest when set against the change for New Zealand male prisoners, from 27.3 to 178-0/100 000 man-years in 1973-82 and 1983-87, respectively. Presumably, the key to the abrupt rise in prison suicide rate in New Zealand lies in Auckland, where most of the increase occurred. Auckland prison overcrowding could not be described as worse in 1983-87 compared with 1973-82: the average annual prison muster had increased from 564 to 683, but was more than offset by a new 150-bed prison. Salive et al5 and Dooley3 found that suicide was more likely among prisoners convicted of assault; Auckland, with the only maximum security prison in the country, would have a higher proportion of such prisoners, but adjustment for length of sentence should have reduced this bias. High rates of suicide (per 100 000 prisoner years) have been reported in maximum security prisons in Canada (272),6 Brisbane (266),’ and Maryland (131-5),5but in 1983-87 the crude suicide rate (per 100 000 man-years) at Paremoremo was 1311, compared with 1 suicide and a crude suicide rate of 51 in the 10 years before 1983. These striking changes in suicide rate were associated with the imposition in March, 1983, of stringent restrictions on transfer of mentally disturbed prisoners to psychiatric hospitals. Prisoners become suicidal for various reasons, but psychiatric illness is likely to be a major factor in prison 3 8 as in the community. A causal link cannot be definitively established, but when prisoners’ free access to psychiatric hospital was abolished, their suicide rate soared. In 1988, the Mason inquiry into forensic psychiatry in Auckland2 concluded that "in other circumstances it is likely that eight of the 13 [Paremoremo] prisoners who suicided, being committable, would have been committed and their deaths in all probability prevented". It is possible that the earlier policy of free transfer meant that prison officers were unused to handling suicidal prisoners, and occasional temporal clustering, as noted in Finnish "lock-ups",9 occurred (3 prisoners took their lives within 3 weeks in 1987). Our findings support calls for a coordinated system of psychiatric care for mentally disturbed prisoners which includes access to secure psychiatric hospital facilities. Suicide rates were reduced in New York State jails with the introduction of such a scheme,lO and in the UK the Chief Inspector of Prisons has noted the plight of many disturbed prisoners who were denied psychiatric placements.’ However, comparisons between prison suicide rates in different countries can be complicated by several factors; for example, the suicide rate among all young New Zealand men is roughly double that for England and Wales.11 The Mason report2 recommended many changes to forensic psychiatry in New Zealand, including the establishment of medium secure units in psychiatric hospitals and comprehensive regional forensic psychiatric teams which would provide a service to forensic patients wherever they were-in prison, hospital, or the community. The effects of this return of responsibility for psychiatrically disturbed prisoners to the health service will be watched with interest.
1438
ME, Smith GS,
state
REFERENCES 1. HM Chief Inspector of Prisons for
Brewer TF. Suicide mortality in the Maryland 1979 through 1987. JAMA 1989; 262: 365-69. 6. Burtch BE. Suicide in prison: a commentary. Br J Psychiatry 1979; 135: 90. 7. Hurley W. Suicides by prisoners. Med J Aust 1989; 151: 188-90. 8. Bland RC, Newman SC, Dyck RJ, Orn H. Prevalence of psychiatric disorders and suicide attempts in a prison population. Can J Psychiatry 5. Salive
We thank the New Zealand Departments of Justice, Statistics, and Health (Statistical Services) for data not included in published reports.
England and Wales. Suicide and self harm in prison service establishments m England and Wales. London: HM Stationery Office, 1990. 2. Report of the Committee of Inquiry into procedures used in certain psychiatric hospitals in relation to admission, discharge or release on leave of certain classes of patients. Wellington: Government Printer, 1988. 3. Dooley E. Prison suicide in England and Wales, 1972-87. Br J Psychiatry 1990; 156: 40-45. 4. Backett SA. Suicide in Scottish prisons. Br J Psychiatry 1987; 151: 218-21.
prison system,
1990; 35: 407-13. 9. Niemi T. The time-space distances of suicides committed in the lock-up in Finland in 1963-1967. Psychiatria Fennica 1975: 267-70. 10. Cox JF, McCarty DW, Landsberg G, Paravati MP. A model for crisis intervention services within local jails. Int J Law Psychiatry 1988; 11: 391-407. 11. Skegg K, Cox B. Suicide in New Zealand 1957-1986: the influence of age, period and birth-cohort. Aust NZ J Psychiatry 1991; 25: 181-90.
HYPOTHESIS Uraemia: is
urea more
Urea is accumulated as an osmolyte by some groups of animals even though it impairs protein function. These organisms can withstand high internal urea concentrations because they also accumulate other low-molecular-weight osmolytes, the methylamines, which can offset the effects of urea on proteins. Methylamines have also been found in the medulla of the mammalian kidney (where urea concentrations are high) and in the plasma of human subjects with chronic renal failure. These findings suggest that previous investigations of the potential contribution of urea to the syndrome of uraemia may have been confounded because of the presence of variable concentrations of protective substances. That naturally occurring methylamines or related substances may prove to have a useful therapeutic role in uraemia is also possible. Introduction Loss of functional nephrons in chronic renal failure leads uraemia, which is widely thought to be due to the accumulation of waste products of protein metabolism in the body fluids. These "uraemic toxins" are thought to produce their effects through their diverse actions on protein function, particularly by inhibition of various enzyme activities. Many uraemic toxins have been proposed, including urea, creatinine, guanidines, aliphatic and aromatic amines, phenols, indole, aromatic hydroxyacids, oxalic acid, uric acid, and possibly "middle molecules" ,2.3 all of which accumulate in uraemia and have various toxic effects. However, since no single compound, or family of compounds, correlates well with uraemic symptoms, the development of uraemia is generally attributed to the accumulation of many toxins, acting with electrolyte and other metabolic and hormonal disturbances. Of the potential uraemic toxins, the concentration of urea alone is much higher than that of all the others combined (up to
important than we think?
to tens
of mmol/1 vs a few mmol/1), but urea is conventionally
as one of the least toxic protein metabolites that accumulate in uraemia. This is partly because of the high levels of urea that can be tolerated. Also, plasma urea concentrations are variable (rising with high protein intake and in catabolic states) and hence are difficult to correlate with uraemic symptoms. Clinical studies have generally shown a poor correlation between plasma urea concentration and the clinical state of the patient. In one study, for example, haemodialysis against high concentrations of urea in the dialysate led to a good clinical response by uraemic patients despite negligible change in the blood urea concentration.4 By contrast, in another study when high plasma urea concentrations were produced by the addition of urea to the dialysate, malaise, apathy, drowsiness, and glucose intolerance followed.s The main difficulty with these studies, and similar studies that attempt to assess the role of urea in uraemia, is that they have been unable to control adequately for the simultaneous effects of treatment on electrolytes, hormones, and other variables. In dogs with bilateral nephrectomy, maintained on peritoneal dialysis, an accelerated uraemic syndrome develops if urea is added to the dialysate.6 Such data show that urea can have important toxic effects in uraemia. In fact, it would be surprising if urea were not implicated in the cause of uraemic syndrome, since in addition to its presence in high concentrations, it is also a well-known destabiliser of protein structure. That urea is also able to diffuse across cell membranes and enter cells suggests that it is likely to produce widespread effects on protein function.
regarded
ADDRESSES: University Department of Pathology, Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP (J A. Lee, PhD); Department of Renal Medicine, St Mary’s Hospital, Milton Road, Portsmouth (Prof H A Lee, FRCP); Department of Chemistry, Birkbeck College, University of London, Christopher Ingold Laboratories and Gordon House, Gordon Square, London (P J Sadler, PhD), UK. Correspondence to Dr J.A Lee
29. Weed L. The computer as a new basis for analytic clinical practice: coupling individual problems with medical knowledge. Mount Sinai J Med 1985; 52: 94-98. 30. Adams ID, Chan M, Clifford PC, et al. Computer aided diagnosis of acute abdominal pain: a multicentre study. Br Med J 1986; 293: 800-04. 31. Pozen MW, d’Agostino RB, Mitchell JB, et al. The usefulness of a predictive instrument to reduce inappropriate admissions to a cardiac care unit. Ann Intern Med 1980; 92: 238-42. 32. Kent D, Shortliffe E, Bischoff M, Scott A, Jacobs C. Improvements in data collection through physician use of a computer-based cancer chemotherapy protocol advisor. J Clin Oncol 1985; 3: 1409-17. 33. Wyatt J. A method for developing medical decision-aids applied to ACORN, a chest pain advisor. DM thesis, Oxford University, 1991. 34. Brahams D, Wyatt J. Decision-aids and the law. Lancet 1989; ii: 632-34. 35. Feinstein AR. The haze of Bayes, the aerial palaces of decision theory, and the computerised Ouija board. Clin Pharmacol Ther 1977; 21: 482-96. 36. Barnett GO, Cimono JJ, Hupp JA, Hoffer EP. DXPlain: an evolving
diagnostic decision-support system. JAMA 1987; 258: 67-74. 37. Bankowitz R, McNeil M, Challinor S, Parker R, Kapoor W, Miller R. A computer-assisted medical diagnostic consultation service. Ann Intern Med 1989; 110: 824-32. 38. Nathwani BN, Heckerman DE, Horwitz EJ, Lincoln TL. Integrated expert systems and videodisk in surgical pathology. Hum Pathol 1990; 21: 11-27. 39. Shiffman S, Wu AW, Poon AD, et al. Building a speech interface to a medical diagnostic system. IEEE Expert 1991 (February): 41-50. 40. Pryor T, Gardner R, Clayton P, Warner H. The HELP system. J Med Systems 1983; 7: 87-102.
Wyatt J, Spiegelhalter D. Evaluating medical expert systems: what to test, and how?. Med Informatics 1990; 15: 205-17. 42. Wyatt J. Lessons learned from the field trial of ACORN, an expert system to advise on chest pain. In: Barber B, Cao D, Qm D, eds. Proceeding of 41.
6th World Conference
on
Medical Informatics. Amsterdam: North
Holland, 1989: 111-15. 43. Stinson ER, Mueller DA. Survey of health professionals’ information habits and needs. JAMA 1980; 243: 140-43. 44. Covell D, Uman G, Manning P. Information needs of office practice: are they being met? Ann Intern Med 1985; 103: 596-99. 45. Williamson J, German P, Weiss R, Skinner E, Bowes F. Health science information management and the continuing education of physicians. Ann Intern Med 1989; 110: 151-60. 46. Carr RM. The point of the pen. Byte Magazine 1991 (February): 211-21. 47. Blois M. The physician’s information environment. In: Cohen GS, ed. Proceedings of 8th Symposium on Computer Applications in Medical Care, Washington, DC: IEEE Press, 1984: 86-88. 48. Huth E. The underused medical literature. Ann Intern Med 1989; 110: 99-100. 49. Greenes RA, Shortliffe EH. Medical informatics: an emerging academic discipline and institutional priority. JAMA 1990; 263: 1114-20. 50. Blois M, Shortliffe E. The computer meets medicine: emergence of a discipline. In: Shortliffe E, Perrault L, Wiederhold G, Fagan L, eds. Medical informatics. Wokingham: Addison Wesley, 1990: 3-18. 51. Wyatt J. Computer phobia. Lancet 1990; 335: 1223. 52. Shortliffe E, Perrault L, Wiederhold G, Fagan L, eds. Medical informatics. Wokingham: Addison Wesley, 1990. 53. Evans D, Patel V, eds. Cognitive science in medicine. London: MIT Press, 1989.
CLINICAL PRACTICE Impact of psychiatric services on prison suicide
Severe restrictions on the transfer of mentally disturbed prisoners to psychiatric hospital were introduced in Auckland in 1983, while policy in other parts of New Zealand was unchanged. Among male prisoners, the suicide rate (per 100 000 man-years) increased from 27·3 in 1973-82 to 178·0 in 198387—an increase in relative risk, compared with unconfined men, from 1·6 to 8·2. Auckland accounted for most of this increase, from 37/100 000 man-years in 1973-82 to 549/100 000 in 1983-87. This striking increase in prison suicide rate in Auckland underlines the importance of ready access to psychiatric care for prisoners. Introduction
Although prison culture may be a major determinant of suicide in prison, another influence might be the availability of transfer of mentally disordered prisoners to psychiatric hospitals. In 1983-87, stringent restrictions on such transfers were abruptly introduced in Auckland, whereas a policy of ready access to psychiatric hospitals was little changed in other parts of New Zealand. We have analysed suicide rates among prisoners and the unconfined population from 1973 to 1988 to identify whether the change in policy in Auckland was associated with an effect on prison suicide rates.
Methods recorded as suicide in New Zealand prisons 1973 to 1988; only 2 were among female prisoners, and subsequent analysis is restricted to male suicides. Crude prison suicide rates were calculated from annual average daily prison populations for the periods 1973-82 and 1983-87. Unfortunately, these data were not available by age group; because almost all prisoners were under the age of 50 years, and no prisoner aged 50 years or older committed suicide, these rates were compared with crude rates of suicide for the same periods among unconfined men aged 15 to 49 years. Indirect standardisation according to the age distribution of a different measure of prison population, the number of prisoners who were sentenced at least once in a given year, barely altered the crude suicide rates obtained for the unconfined population. New Zealand’s highest security prison, Paremoremo, opened in Auckland in 1968. This prison had a close relation with Oakley, a psychiatric hospital with secure facilities. Patients considered mentally disturbed by the prison authorities could readily be admitted to Oakley and many custodial remands were assessed there.2 In 1974, Oakley was split into two hospitals, Oakley and Carrington; the new Oakley continued to provide secure facilities for forensic patients until policy changed in 1983, when a narrow definition of "treatable mental illness" was introduced: it then 39 deaths
were
(including borstals) from
ADDRESSES Departments of Psychological Medicine (K Skegg, MRCPsych) and Preventive and Social Medicine (B Cox, MCCMNZ), University of Otago Medical School, Dunedin, New Zealand. Correspondence to Dr Keren Skegg
1437
TABLE I-CRUDE SUICIDE RATES AMONG UNCONFINED MEN AGED 15-49 AND MALE PRISONERS
*Shown
as
rate/100 000 man-years (number of suicides).
became extremely difficult to transfer mentally disturbed prisoners to a psychiatric hospital in Auckland. To compare suicide rates in Auckland prisons with the rest of the country, the prison population on Dec 31 of each year was used,
instead of the average daily prison population,
as
this denominator
was available
by length of sentence. Suicide rates were calculated for 1973-82 and 1983-87; 1988 was analysed separately because the report of an inquiry into these events was released in that year.2 Because length of sentence, particularly for life,3 and imprisonment on remand4 have been associated with an increased risk of suicide, suicide rates were adjusted for length of sentence (available as less than 3 months, 3 months to 1 year, and 1 or more years), number of remand prisoners, and number of prisoners sentenced to borstal or corrective training. The numbers in these sentence categories in 1980 were chosen to weight the sentence-adjusted suicide rates. The number of male suicides in Auckland psychiatric hospitals changed little over the study period (9 in the 10 years 1973-82 compared with 4 in the 5 years 1983-87).
Results 28 of the 37 male suicides in New Zealand prisons in 1973-88 were serving sentences of between 2 months and life imprisonment (including 1 to borstal training) and 9 were on remand. 33 hanged or strangled themselves and 4 used other methods. Table I shows crude suicide rates for male prisoners and unconfined men aged 15-49 years; a striking increase in the relative risk of suicide in prison was seen in 1983-87. This change was not simply a continuation of a gradual increase over the previous decade because prison suicide rates were lower in 1978-82 than in 1973-77. There were no significant differences in suicide rates between Maori and non-Maori prisoners. Table 11 shows male prison suicide rates in Auckland compared with those for the rest of New Zealand. In 1973-82 there was 1 suicide in Paremoremo, but 13 in 1983-87: thus, for 1983-87 there was a crude annual suicide rate of 1311/100 000 prisoners and a sentenced-adjusted annual rate of 662/100 000 prisoners in Paremoremo. In 1988, there was 1 suicide in Paremoremo and 3 in another Auckland prison (compared with 2 in the rest of New Zealand), and the 1988 rate for Auckland was again high (crude annual rate 551/100 000
prisoners). Discussion Prison suicide increased more than 6-fold in New Zealand after 1982. Compared with unconfined men of similar age, TABLE II-NUMBERS OF SUICIDES AND CRUDE AND SENTENCEADJUSTED SUICIDE RATES AMONG MALE PRISONERS IN AUCKLAND AND REST OF NEW ZEALAND
*Rate/100 000 man-years
male prisoners were less than twice as likely to commit suicide in 1973-82 but more than 8 times as likely to do so in 1983-87. Allowance for different age distributions of the unconfined and prison populations did not alter this result. There has been concern about increased prison suicides in other countries; in England and Wales, for example, prison suicides per 100 000 prisoner years have risen, for both sexes combined, from 31/100 000 per year in 1972-75 to 87/100 000 in 1987.3 But this disturbing increase appears modest when set against the change for New Zealand male prisoners, from 27.3 to 178-0/100 000 man-years in 1973-82 and 1983-87, respectively. Presumably, the key to the abrupt rise in prison suicide rate in New Zealand lies in Auckland, where most of the increase occurred. Auckland prison overcrowding could not be described as worse in 1983-87 compared with 1973-82: the average annual prison muster had increased from 564 to 683, but was more than offset by a new 150-bed prison. Salive et al5 and Dooley3 found that suicide was more likely among prisoners convicted of assault; Auckland, with the only maximum security prison in the country, would have a higher proportion of such prisoners, but adjustment for length of sentence should have reduced this bias. High rates of suicide (per 100 000 prisoner years) have been reported in maximum security prisons in Canada (272),6 Brisbane (266),’ and Maryland (131-5),5but in 1983-87 the crude suicide rate (per 100 000 man-years) at Paremoremo was 1311, compared with 1 suicide and a crude suicide rate of 51 in the 10 years before 1983. These striking changes in suicide rate were associated with the imposition in March, 1983, of stringent restrictions on transfer of mentally disturbed prisoners to psychiatric hospitals. Prisoners become suicidal for various reasons, but psychiatric illness is likely to be a major factor in prison 3 8 as in the community. A causal link cannot be definitively established, but when prisoners’ free access to psychiatric hospital was abolished, their suicide rate soared. In 1988, the Mason inquiry into forensic psychiatry in Auckland2 concluded that "in other circumstances it is likely that eight of the 13 [Paremoremo] prisoners who suicided, being committable, would have been committed and their deaths in all probability prevented". It is possible that the earlier policy of free transfer meant that prison officers were unused to handling suicidal prisoners, and occasional temporal clustering, as noted in Finnish "lock-ups",9 occurred (3 prisoners took their lives within 3 weeks in 1987). Our findings support calls for a coordinated system of psychiatric care for mentally disturbed prisoners which includes access to secure psychiatric hospital facilities. Suicide rates were reduced in New York State jails with the introduction of such a scheme,lO and in the UK the Chief Inspector of Prisons has noted the plight of many disturbed prisoners who were denied psychiatric placements.’ However, comparisons between prison suicide rates in different countries can be complicated by several factors; for example, the suicide rate among all young New Zealand men is roughly double that for England and Wales.11 The Mason report2 recommended many changes to forensic psychiatry in New Zealand, including the establishment of medium secure units in psychiatric hospitals and comprehensive regional forensic psychiatric teams which would provide a service to forensic patients wherever they were-in prison, hospital, or the community. The effects of this return of responsibility for psychiatrically disturbed prisoners to the health service will be watched with interest.
1438
ME, Smith GS,
state
REFERENCES 1. HM Chief Inspector of Prisons for
Brewer TF. Suicide mortality in the Maryland 1979 through 1987. JAMA 1989; 262: 365-69. 6. Burtch BE. Suicide in prison: a commentary. Br J Psychiatry 1979; 135: 90. 7. Hurley W. Suicides by prisoners. Med J Aust 1989; 151: 188-90. 8. Bland RC, Newman SC, Dyck RJ, Orn H. Prevalence of psychiatric disorders and suicide attempts in a prison population. Can J Psychiatry 5. Salive
We thank the New Zealand Departments of Justice, Statistics, and Health (Statistical Services) for data not included in published reports.
England and Wales. Suicide and self harm in prison service establishments m England and Wales. London: HM Stationery Office, 1990. 2. Report of the Committee of Inquiry into procedures used in certain psychiatric hospitals in relation to admission, discharge or release on leave of certain classes of patients. Wellington: Government Printer, 1988. 3. Dooley E. Prison suicide in England and Wales, 1972-87. Br J Psychiatry 1990; 156: 40-45. 4. Backett SA. Suicide in Scottish prisons. Br J Psychiatry 1987; 151: 218-21.
prison system,
1990; 35: 407-13. 9. Niemi T. The time-space distances of suicides committed in the lock-up in Finland in 1963-1967. Psychiatria Fennica 1975: 267-70. 10. Cox JF, McCarty DW, Landsberg G, Paravati MP. A model for crisis intervention services within local jails. Int J Law Psychiatry 1988; 11: 391-407. 11. Skegg K, Cox B. Suicide in New Zealand 1957-1986: the influence of age, period and birth-cohort. Aust NZ J Psychiatry 1991; 25: 181-90.
HYPOTHESIS Uraemia: is
urea more
Urea is accumulated as an osmolyte by some groups of animals even though it impairs protein function. These organisms can withstand high internal urea concentrations because they also accumulate other low-molecular-weight osmolytes, the methylamines, which can offset the effects of urea on proteins. Methylamines have also been found in the medulla of the mammalian kidney (where urea concentrations are high) and in the plasma of human subjects with chronic renal failure. These findings suggest that previous investigations of the potential contribution of urea to the syndrome of uraemia may have been confounded because of the presence of variable concentrations of protective substances. That naturally occurring methylamines or related substances may prove to have a useful therapeutic role in uraemia is also possible. Introduction Loss of functional nephrons in chronic renal failure leads uraemia, which is widely thought to be due to the accumulation of waste products of protein metabolism in the body fluids. These "uraemic toxins" are thought to produce their effects through their diverse actions on protein function, particularly by inhibition of various enzyme activities. Many uraemic toxins have been proposed, including urea, creatinine, guanidines, aliphatic and aromatic amines, phenols, indole, aromatic hydroxyacids, oxalic acid, uric acid, and possibly "middle molecules" ,2.3 all of which accumulate in uraemia and have various toxic effects. However, since no single compound, or family of compounds, correlates well with uraemic symptoms, the development of uraemia is generally attributed to the accumulation of many toxins, acting with electrolyte and other metabolic and hormonal disturbances. Of the potential uraemic toxins, the concentration of urea alone is much higher than that of all the others combined (up to
important than we think?
to tens
of mmol/1 vs a few mmol/1), but urea is conventionally
as one of the least toxic protein metabolites that accumulate in uraemia. This is partly because of the high levels of urea that can be tolerated. Also, plasma urea concentrations are variable (rising with high protein intake and in catabolic states) and hence are difficult to correlate with uraemic symptoms. Clinical studies have generally shown a poor correlation between plasma urea concentration and the clinical state of the patient. In one study, for example, haemodialysis against high concentrations of urea in the dialysate led to a good clinical response by uraemic patients despite negligible change in the blood urea concentration.4 By contrast, in another study when high plasma urea concentrations were produced by the addition of urea to the dialysate, malaise, apathy, drowsiness, and glucose intolerance followed.s The main difficulty with these studies, and similar studies that attempt to assess the role of urea in uraemia, is that they have been unable to control adequately for the simultaneous effects of treatment on electrolytes, hormones, and other variables. In dogs with bilateral nephrectomy, maintained on peritoneal dialysis, an accelerated uraemic syndrome develops if urea is added to the dialysate.6 Such data show that urea can have important toxic effects in uraemia. In fact, it would be surprising if urea were not implicated in the cause of uraemic syndrome, since in addition to its presence in high concentrations, it is also a well-known destabiliser of protein structure. That urea is also able to diffuse across cell membranes and enter cells suggests that it is likely to produce widespread effects on protein function.
regarded
ADDRESSES: University Department of Pathology, Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP (J A. Lee, PhD); Department of Renal Medicine, St Mary’s Hospital, Milton Road, Portsmouth (Prof H A Lee, FRCP); Department of Chemistry, Birkbeck College, University of London, Christopher Ingold Laboratories and Gordon House, Gordon Square, London (P J Sadler, PhD), UK. Correspondence to Dr J.A Lee
