Volume 171 Issue 8

Research End-stage renal disease in Aboriginals in New South Wales: a very different picture to the Northern Territory Alan Cass, Adrian G Gillin and John S Horvath MJA 1999; 171: 407-410 Abstract - Introduction - Methods - Results - Discussion - Acknowledgements - References - Authors' details - - More articles on Aboriginal health Abstract Objectives: To compare the incidence of end-stage renal disease (ESRD) among Aboriginals in New South Wales with the incidence among Aboriginals in the Northern Territory, and to compare the patterns of ESRD among Aboriginals and non-Aboriginals in NSW. Design: Secondary data analysis of information from unpublished and published Australia and New Zealand Dialysis and Transplant Registry reports. Main outcome measures: Average annual incidence of ESRD (persons per million); form of renal replacement therapy; mortality at 31 March 1998; patient and graft survival one and five years after transplant. Results: Each year in NSW, 5-17 new Aboriginal patients are treated for ESRD. There was no increase in the average annual incidence of ESRD among NSW Aboriginals (118 per million in 1988-1989 and 111 per million in 1996-1997), whereas incidence in the NT increased from 255 per million to 800 per million. In NSW, ESRD was attributed to diabetes in 32% of Aboriginal patients, compared with 13% of non-Aboriginal patients (P < 0.001). In NSW, Aboriginal patients were younger and more likely to be female, a pattern similar to that in the NT. The outcome of ESRD treatment is not significantly different between Aboriginals and non-Aboriginals in NSW. Conclusion: There is a different pattern of incidence of ESRD and of outcomes with treatment among Aboriginals in NSW compared with those in the NT. A possible explanation is that the lower incidence in NSW reflects less profound socioeconomic disadvantage and better access to primary and specialist care. Introduction Indigenous Australians experience high morbidity and mortality due to end-stage renal disease (ESRD). In the Northern Territory, the average annual incidence of ESRD for Aboriginals in 1988-1993 was 17.4 times that for non-Aboriginals,1 a disparity made more apparent by age adjustment.2 The number of dialysis treatments in the NT is doubling every two years.3The 30 June 1996 estimate of the Indigenous population (386 049) represented 2.1% of the total Australian population,4 but Aboriginals constitute 5% of the Australian members of the Australia and New Zealand Dialysis and Transplant Registry (ANZDATA).5 Whether the increasing incidence and prevalence of renal disease is occurring in NSW as well as nationally and in the NT has not been well documented. The aims of our study were to document the number of new Aboriginal patients with ESRD in NSW during 1987 to 1998 and compare recent trends in incidence with national and NT data, and to compare for Aboriginal and non-Aboriginal patients in NSW: the patterns of aetiology of ESRD; the demographic characteristics at the time of being entered into ANZDATA; the outcomes for individuals who were notified to the Registry during the period 1987 to 1998; and patient and graft survival for those who received transplants during the period 1987 to 1998. Methods Information was obtained from ANZDATA Annual Reports (12 and 18-21)6-10 and unpublished data from ANZDATA. All nephrology units in Australia and New Zealand that provide dialysis or transplant services submit detailed six-monthly reports to ANZDATA. The reports give information regarding new patients accepted onto treatment programs, deaths that have occurred, and any alteration in treatment for current patients, including changing the mode of dialysis or receiving a transplant. For NSW, the NT and across Australia, we analysed: the number of Aboriginal patients entered into ANZDATA from 1987 to 1998 in NSW, the NT and across Australia; and the average annual incidence of ESRD. For NSW only, we analysed: primary renal disease diagnostic category; mean age; outcome data at 31 March 1998 for people who had been entered into ANZDATA since 1 January 1987. Outcomes were categorised as death, functioning transplant, haemodialysis, continuous ambulatory peritoneal dialysis (CAPD), and loss to follow-up or having moved interstate; causes of death, categorised into cardiac, vascular, infection, social, malignancy and other; patient survival and graft survival for transplants performed between 1 January 1987 to 31 March 1998. The average annual incidence of ESRD was calculated using Australian Bureau of Statistics (ABS) estimates and projections of the Aboriginal and Torres Strait Islander population for the years between actual Census counts. These estimates are based upon current trends in fertility and mortality and take into account an increasing propensity for people to identify themselves as being of Indigenous origin. The definition of "Aboriginality" from both data sources (ANZDATA and ABS) relies upon self-identification. Annual incidence was calculated as an average for each two-year period, as there is marked variability in the number of new patients per year, and small absolute numbers. Statistical analysis of demographic and outcome data was performed using STATA 5.0.11 A t test of means and χ2 test or Fisher's exact test of proportions were performed. Survival analysis was performed at the ANZDATA Registry. Data were provided as actuarial life-table estimates and the log rank test was performed. The data were entered into STATA 5.0 and graphed. Results Incidence Each year in NSW, 5-17 new Aboriginal patients are treated for ESRD (Table 1). The average annual incidence of ESRD among Aboriginals in NSW for the two years 1988-1989 was 118 per million. This remained substantially unchanged at 111 per million in 1996-1997. During the same period the average annual incidence of ESRD in Aboriginals across Australia increased significantly (Table 1); in the NT, the rise in incidence was more marked. The crude incidence for non-Aboriginals in NSW was 78 per million for 1993-1997, a slight rise from the 1980s due to increased acceptance for dialysis of patients over the age of 65 years. Diagnostic categories Diabetes, glomerulonephritis and hypertension are the most common primary renal diseases among Aboriginals with ESRD in NSW (Table 2). Diabetes is listed as the primary renal disease in 32% of Aboriginals, compared with 13% of non-Aboriginals (P < 0.001). Analgesic nephropathy affects a significantly greater proportion of the non-Aboriginal population, mainly among females: 28% in non-Aboriginal females, compared with 10% in Aboriginal females. No definite diagnosis was recorded for 11% of Aboriginals, compared with 5% of non-Aboriginals (P = 0.004). Demographics Significantly more Aboriginal females than males entered the ESRD program in NSW (Table 3), the reverse pattern to non-Aboriginals (P = 0.03). The Aboriginal population was younger at entry to the program and there were significantly fewer people over the age of 65 years (P < 0.001). Outcome, or patient status at 31 March 1998, was not significantly different between the groups (P = 0.59). However, no attempt at age or sex standardisation has been made in this analysis. Causes of death The differences between Aboriginals and non-Aboriginals in NSW in causes of death approach statistical significance (P = 0.07). A significantly larger proportion of Aboriginals died from cardiovascular diseases (P = 0.01). A significantly smaller proportion of deaths were due to social reasons (P = 0.02). Patient and graft survival after transplant Aboriginal patients receiving transplants in NSW during the study period were younger (Figure 1), but experienced lower patient survival and graft survival rates (Figures 2a and 2b), although these differences were not significant (Table 4). Discussion Our data show no evidence of an epidemic of renal failure among Aboriginals in NSW, although the incidence remains higher than among the non-Aboriginal population. Aboriginal patients in NSW with ESRD are on average 10 years younger than non-Aboriginal patients, more likely to be female, and more likely to have diabetes and to die of cardiovascular disease. These features are similar to those reported in the NT.2 However, in NSW, there is no significant difference in outcome between Aboriginal and non-Aboriginal patients who have been entered into the Registry since January 1987, whereas, in the NT, survival is significantly worse in Aboriginal than in non-Aboriginal patients.2 The persistently high rate of withdrawal up to 1997 of NT Aboriginal people from ESRD treatment, about 25%,3 is not present in NSW. Our results show that diabetes, glomerulonephritis and hypertension are the prominent primary causes of ESRD among NSW Aboriginals. The rise in renal failure attributed to diabetes follows a similar pattern to that noted in Aboriginals across Australia.10 The pattern of primary causes of renal disease is consistent between Aboriginal populations in different States.10 Impediments to effective and culturally appropriate service delivery to Aboriginal patients have been postulated as reasons for poor survival and high withdrawal rates from treatment.12 Therapeutic programs have typically removed people from their cultural and social support networks by requiring patients to leave their land, families and communities.13 Unlike in the NT, South Australia and Western Australia, there are few remote, non-urbanised communities in NSW; Aboriginals in NSW reside predominantly in cities and rural towns. The higher proportion of Aboriginal patients with uncertain aetiology of their ESRD is consistent with a lower renal biopsy rate, which may relate to late referral and lack of access to renal specialist services. In NSW, specialist renal services are increasingly being provided where Aboriginals live. The Statistical Local Areas with the highest proportion of Indigenous people are Brewarrina (53.1%), Central Darling (25.3%), Bourke (24.5%) and Walgett (20.4%).14 CAPD training is now occurring in some larger rural centres, and haemodialysis facilities are provided in Bourke and Brewarrina. These initiatives, which significantly reduce the dislocation of patients from their community and remove impediments to the delivery of appropriate ESRD services, may facilitate improved survival. There is a tendency towards lower patient survival and graft survival among NSW Aboriginals compared with non-Aboriginals, despite the Aboriginal graft recipients' being younger. In the NT, graft and patient survival among Aboriginals are significantly worse at one and five years than among non-Aboriginals.2 A significant difference in survival is not evident in the NSW data. The larger 95% confidence intervals in the NSW Aboriginal group are a consequence of fewer transplants being performed: 36 among Aboriginal patients, compared with 1755 among non-Aboriginal patients. These numbers do not provide sufficient power to detect a significant difference between the groups. The pattern of rapidly increasing incidence of ESRD among Aboriginals across Australia, especially in the NT, is not seen in NSW. Spencer et al argue that the increase in the NT is real, not due to ageing of the Aboriginal population or improved ascertainment.2 The reason for this difference in incidence is not clear. It may be due to differences between the populations in apparent predisposition to renal disease or to differences in the prevalence of primary causes and promoters of chronic renal disease. The epidemic of disease in the NT is not only due to an increased prevalence of diabetes. Community screening studies show a prevalence of significant proteinuria in marked excess of the prevalence of diabetes or impaired glucose tolerance.2,15 In the NT, from 1988 to 1993, the average annual incidence of ESRD not attributable to diabetes was 350 per million per year among Aboriginals.1 Lower incidence of ESRD in NSW Aboriginals may reflect less profound socioeconomic disadvantage and readier access to effective primary and specialist care. However, there may be poor ascertainment, particularly in rural areas of NSW. Further study is indicated to analyse this question. Acknowledgements The data reported here have been supplied by the Australia and New Zealand Dialysis and Transplant Registry. The interpretation of these data is the responsibility of the authors and in no way should be seen as an official policy or interpretation of the Australia and New Zealand Dialysis and Transplant Registry. Dr Alan Cass is the recipient of a postgraduate research scholarship from the Centre for Kidney Research, New Children's Hospital, Sydney. We thank Dr Wendy Hoy, who critically reviewed the manuscript, and Dr Zhiqiang Wang, who provided statistical advice. References Hoy WE, Mathews JD, Pugsley DJ. Treatment of end-stage renal disease in the Top End of the Northern Territory: 1978-93. Nephrology 1995; 1: 307-313. Hoy WE, McFarlane R, Pugsley DJ, et al. Markers for cardiovascular and renal morbidity: expectations for an intervention programme in an Australian aboriginal community. Clin Exp Pharmacol Physiol 1996; 23: S33-S37. Spencer JL, Silva DT, Snelling P, Hoy WE. An epidemic of renal failure among Australian Aboriginals. Med J Aust 1998; 168: 537-541. Australian Bureau of Statistics. Experimental estimates of the Aboriginal and Torres Strait Islander population. Canberra: ABS, 1998. (Catalogue No. 3230.0.) Disney AP. Demography and survival of patients receiving treatment for chronic renal failure in Australia and New Zealand: report on dialysis and renal transplantation treatment from the Australia and New Zealand Dialysis and Transplant Registry. Am J Kidney Dis 1995; 25: 165-175. Disney APS, Collins J, Russ GR, et al. ANZDATA Registry Report 1989. Adelaide: Australia and New Zealand Dialysis and Transplant Registry, 1989. Disney APS, Collins J, Russ GR, et al. ANZDATA Registry Report 1995. Adelaide: Australia and New Zealand Dialysis and Transplant Registry, 1995. Disney APS, Collins J, Russ GR, et al. ANZDATA Registry Report 1996. Adelaide: Australia and New Zealand Dialysis and Transplant Registry, 1996. Disney APS, Collins J, Russ GR, et al. ANZDATA Registry Report 1997. Adelaide: Australia and New Zealand Dialysis and Transplant Registry, 1997. Disney APS, Collins J, Russ GR, et al. ANZDATA Registry Report 1998. Adelaide: Australia and New Zealand Dialysis and Transplant Registry, 1998. STATA statistical software [computer program]. Version 5.0. College Station, Texas: Stata Corporation, 1997. Bennett E, Manderson L, Kelly B, Hardie I. Cultural factors in dialysis and renal transplantation among aborigines and Torres Strait Islanders in north Queensland. Aust J Public Health 1995; 19: 610-615. Willis J. Fatal attraction: do high technology treatments for end-stage renal disease benefit aboriginal patients in central Australia? Aust J Public Health 1995; 19: 603-609. Australian Bureau of Statistics. Census of population and housing -- selected social and housing characteristics for statistical local areas, New South Wales and Jervis Bay. Canberra: ABS, 1996. (Catalogue no. 2015.1.) Van Buynder PG. The epidemiology of renal disease in Aboriginal Australians [Master of Public Health thesis]. Sydney: University of Sydney, 1991. (Received 12 Feb, accepted 19 Jul, 1999) Authors' details Menzies School of Health Research, Darwin, NT. Alan Cass, MB BS, FRACP, PhD student. Department of Renal Medicine, Royal Prince Alfred Hospital, Sydney, NSW. Adrian G Gillin, FRACP, PhD, Staff Specialist; John S Horvath, MB BS, FRACP, Professor. Reprints will not be available from the authors. Correspondence: Dr A Cass, Menzies School of Health Research, PO Box 41096, Casuarina, NT 0811. alancassATmenzies.edu.au Back to textBack to textBack to textBack to textBack to textBack to text

Alan Cass · Adrian G Gillin · John S Horvath

Research Is sudden infant death syndrome still more common in very low birthweight infants in the 1990s? Beverley Sowter, Lex W Doyle, Colin J Morley, Anne Altmann and Jane Halliday MJA 1999; 171: 411-413 Abstract - Introduction - Methods - Results - Discussion - References - Authors' details - - More articles on Paediatrics Abstract Objective: To determine the rate of sudden infant death syndrome (SIDS) in very low birthweight children (VLBW) relative to children with low (LBW) and normal birthweights. Design, setting and subjects: Cohort study of consecutive live births in Victoria, 1993-1997 inclusive. Main outcome measures: All sudden unexpected deaths in early childhood over this five-year period; all deaths from SIDS (defined as a sudden unexpected death without a definite pathological explanation); and the proportion of SIDS in live births in three birthweight subgroups (VLBW, 500-1499 g; LBW, 1500-2499 g; and normal birthweight, > 2499 g). Results: There were 316 028 live births (with known birthweight) in Victoria over the five-year period; 224 (0.71 per 1000 live births) died unexpectedly. In 10 of these deaths there was a definite pathological explanation, giving a rate of SIDS of 0.68 per 1000 live births. The rate of SIDS in VLBW children was 2.52 per 1000 live births, lower than the rate reported before the 1990s. The rate of SIDS in VLBW children was not significantly different from the rate in LBW children of 1.98 per 1000 live births (difference per 1000 live births, 0.53; 95% CI, 21.45 to 2.52), but was significantly higher than the rate in normal birthweight children of 0.59 per 1000 live births (difference per 1000 live births, 1.93; 95% CI, 0.06-3.79). Conclusions: The rate of SIDS in VLBW children has fallen in the 1990s, along with the overall fall in the rate of SIDS, but remains higher than that in normal birthweight children. Introduction Most parents learn to live with the fear that their baby may die of sudden infant death syndrome (SIDS). However, the fear of SIDS can be even greater for parents of babies with low birthweight, or those with babies who have been in intensive care or who have had apnoea. Before discharge, many parents attend education sessions on reducing the risks of SIDS and on infant resuscitation. At one of these sessions the parents may ask the difficult question: "Is my baby more likely to die of SIDS because he (or she) was so tiny when born?". Before the 1990s, children with very low birthweight (VLBW, 500-1499 g) were known to have a higher rate of SIDS than those with a normal birthweight (> 2499 g).1-3 With the advent of preventive measures, the overall rate of SIDS in Australia has fallen dramatically in the 1990s (from 1.87 per 1000 live births in 1990 to 0.78 per 1000 live births in 1995).4 However, it is unclear whether the rate of SIDS has also fallen in VLBW children. We aimed to determine the rate of SIDS in the 1990s for VLBW children relative to children of other birthweights (low birthweight [LBW], 1500-2499 g; and normal birthweight, > 2499 g). Methods We studied a cohort of all consecutive live births in Victoria during the five-year period from 1993 to 1997, inclusive, and recorded all sudden deaths in early childhood (divided into the first 28 days [the neonatal period], postneonatal infancy [29-365 days], and early childhood [more than 1 year]). SIDS was defined as a sudden unexpected death without definite pathological features to explain the death. In the SIDS group, some children were considered by the pathologist to have pathological features, but these were insufficient to explain the death. Some had only a minor condition, and in the remainder no pathological features were found. All births with unknown birthweight were excluded. Data sources Data on deaths were obtained from the annual reports of the Consultative Council on Obstetric and Paediatric Mortality and Morbidity,5-9 a government-legislated surveillance body. The Council collects data on all perinatal deaths from 20 weeks' gestation, and all infant and child deaths up to 14 years of age. Death registrations are forwarded directly from the Registry of Births, Deaths and Marriages, and information on all sudden unexpected deaths is supplemented by the Victorian State Coroner. These cases are then all reviewed and classified by an expert pathologist working in the field. Data on births in Victoria were supplied by the Perinatal Data Collection Unit of the Public Health and Development Division of the Department of Human Services. The Unit collects data on all births in Victoria from 20 weeks' gestation under a legislated notification system. Statistical analysis The proportions of deaths from SIDS (and 95% confidence intervals) in each of the birthweight subgroups (VLBW, 500-1499 g; LBW, 1500-2499 g; and normal birthweight, > 2499 g) were calculated,10 and comparisons made between the groups.10 Results Over the five-year period 1993-1997, there were 316 028 live births in Victoria for which birthweight was known. (Birthweight was not known for a total of 90 live births.) Over the same period, there were 224 sudden unexpected deaths with known birthweight, of which 10 (4.5%) had a definite pathological explanation, leaving 214 deaths from SIDS (0.68 per 1000 live births). Of these 214 children with SIDS, 23 (10.7%) died in the neonatal period (including one who died during the primary hospitalisation), 171 (79.9%) died in postneonatal infancy, and 20 (9.3%) died after the age of 1 year. VLBW children made up less than 1% of all live births over this period; the rate of SIDS in VLBW children was 2.52 per 1000 live births (Table). This was not significantly higher than the rate in LBW children of 1.98 per 1000 live births (difference per 1000 live births, 0.53; 95% CI, 21.45 to 2.52), but was significantly higher than the rate in normal birthweight children of 0.59 per 1000 live births (difference per 1000 live births, 1.93; 95% CI, 0.06-3.79). LBW children had a significantly higher rate of SIDS than normal birthweight children (difference per 1000 live births, 1.39; 95% CI, 0.69-2.09). Of the seven deaths in VLBW infants, definite pathological features were found in five, but these were insufficient to explain the death; three of these infants had respiratory disease (pneumonia, bronchiolitis, or tracheobronchitis). Discussion Our study showed no significant difference in the rate of SIDS between VLBW and LBW infants; however, the rate in each of these subgroups was significantly higher than in normal birthweight children. Before recommendations for reducing the risk of SIDS were introduced in 1991, the SIDS rate was higher in VLBW infants compared with those with normal birthweight, for both hospital and regional cohorts. In a VLBW hospital cohort, 1977-1978, the rate of SIDS before 2 years of age was 30.3 per 1000 live births (7/231);1 and in a regional cohort in New Zealand (children born in 1986), the incidence of SIDS in the VLBW group was 13 per 1000 live births, more than three times the rate of 4.0 per 1000 live births for all NZ children born in 1986.2 In a Californian study of 2962 children dying of SIDS between 28 days and 1 year of age in 1978-1982, the overall incidence was found to be 1.5 per 1000 live births. The highest incidence was in the VLBW group (7.5 per 1000 live births), decreasing to 1.3 per 1000 live births for the normal birthweight group.3 Studies have not shown evidence of a fall in the rate of SIDS in VLBW infants just before the recommendations were introduced. For example, in 1985-1991, the rate of SIDS in VLBW infants in the first year of life for singleton births in the United States remained relatively constant (average, 3.66 per 1000 live births) compared with rates for normal birthweight singleton infants (average, 1.07 per 1000 livebirths).11 Studies comparing the period before and after the recommendations have shown a change in rate of SIDS in VLBW children around the beginning of the 1990s. One study cited by l'Hoir et al12 estimated the rate of SIDS in VLBW children in the Netherlands to have decreased from 10 per 1000 in 1983 to 1 per 1000 (presumably live births) in 1995-96, a change in the rate of SIDS over time similar to that comparing our results with rates in the late 1980s. A more recent US report described a smaller reduction in the rate of SIDS in VLBW children before and after the recommendations about sleeping position, and the reduction was similar across birthweight subgroups (between 1991 and 1995 reductions of 37%, 36% and 30% were found for birthweight subgroups 500-1499 g, 1500-2499 g, and > 2499 g, respectively).13 Avoidance of risk factors probably explains the fall in the rate of SIDS in VLBW infants in the 1990s, the same reason that it has fallen for infants overall. The reason SIDS remains more prevalent in VLBW infants compared with normal birthweight infants may relate to the underlying pathological features, which were more common in VLBW infants with SIDS. So, what should we be telling parents when they ask if their tiny baby is more likely to die of SIDS? Firstly, VLBW and LBW children are at increased risk of SIDS. However, 399 out of 400 VLBW children, and 499 out of 500 LBW children, do not die of SIDS. Secondly, parents can help to decrease the risk of SIDS by following the recommendations: putting their baby to sleep supine, not smoking, and not allowing the baby to become overheated or covered over by bedding.4 Thirdly, as most VLBW children who died of SIDS had a definite pathological condition at autopsy, parents should seek medical advice early if the baby appears unwell in any way. Parents often recognise that their baby is unwell, but it is not always easy for them to decide what is a minor illness and when they need to seek medical advice. A scoring system such as "Baby Check" 14 can be used both by parents and general practitioners to help them to determine whether or not a baby is seriously ill. In a recent review of 37 sudden unexpected infant deaths, 3 (8%) scored very highly for serious illness on a retrospective score with Baby Check, suggesting that such a scoring system could have identified serious illness before death and led to appropriate treatment.15 The three VLBW children with significant respiratory disease in our study probably would have shown signs of illness before they died. In conclusion, the rate of SIDS in VLBW children has fallen from over 10 per 1000 live births before the 1990s to 2.5 per 1000 live births at the end of the 1990s, but remains higher than the rate in normal birthweight children. LBW children are also at greater risk of SIDS at the end of the 1990s. References Kitchen WH, Yu VYH, Lissenden JV, Bajuk B. Collaborative study of very-low-birthweight infants: techniques of perinatal care and mortality. Lancet 1982; 1: 1454-1457. Darlow BA, Horwood LJ, Mogridge N, Clemett RS. Prospective study of New Zealand very low birthweight infants: outcome at 7-8 years. J Paediatr Child Health 1997; 33: 47-51. Grether JK, Schulman J. Sudden infant death syndrome and birth weight. J Pediatr 1989; 114: 561-567. Henderson-Smart DJ, Ponsonby AL, Murphy E. Reducing the risk of sudden infant death syndrome: a review of the scientific literature. J Paediatr Child Health 1998; 34: 213-219. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Annual Report for the Year 1993, incorporating the 32nd Survey of Perinatal Deaths in Victoria. Melbourne, 1994. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Annual Report for the Year 1994, incorporating the 33rd Survey of Perinatal Deaths in Victoria. Melbourne, 1995. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Annual Report for the Year 1995, incorporating the 34th Survey of Perinatal Deaths in Victoria. Melbourne, 1996. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Annual Report for the Year 1996, incorporating the 35th Survey of Perinatal Deaths in Victoria. Melbourne, 1997. The Consultative Council on Obstetric and Paediatric Mortality and Morbidity. Annual Report for the Year 1997, incorporating the 36th Survey of Perinatal Deaths in Victoria. Melbourne, 1998. Gardner MJ, Altman DG. Statistics with confidence - confidence intervals and statistical guidelines. London: BMJ, 1989. Bigger HR, Silvestri JM, Shott S, Weese-Mayer DE. Influence of increased survival in very low birth weight, low birth weight, and normal birth weight infants on the incidence of sudden infant death syndrome in the United States: 1985-1991. J Pediatr 1998; 133: 73-78. l'Hoir MP, Engelberts AC, van Well GT, et al. Case-control study of current validity of previously described risk factors for SIDS in the Netherlands. Arch Dis Child 1998; 79: 386-393. Malloy MH. Birth weight and gestational age specific sudden infant death syndrome (SIDS) mortality: 1991 vs 1995. Pediatr Res 1999; 45: 249A. Morley CJ, Thornton AJ, Cole TJ, et al. Baby Check: a scoring system to grade the severity of acute systemic illness in babies under 6 months old. Arch Dis Child 1991; 66: 100-105. Cole TJ, Gilbert RE, Fleming PJ, et al. Baby Check and the Avon infant mortality study. Arch Dis Child 1991; 66: 1077-1078. (Received 21 Jun, accepted 6 Sep, 1999) Authors' details Division of Paediatrics, Royal Women's Hospital, Melbourne, VIC. Beverley Sowter, RN, Case Manager. Lex W Doyle, MD, FRACP, Paediatrician; and Associate Professor, Department of Obstetrics and Gynaecology, and Department of Paediatrics, University of Melbourne. Colin J Morley, MD, FRACP, Paediatrician. Consultative Council on Obstetric and Paediatric Mortality and Morbidity, Melbourne, VIC. Anne Altmann, MB BS(Hons), MPH, FAFPHM, Epidemiologist. Victorian Perinatal Data Collection Unit, Melbourne, VIC. Jane Halliday, PhD, Epidemiologist. Reprints will not be available from the authors. Correspondence: Associate Professor L W Doyle, Division of Paediatrics, The Royal Women's Hospital, 132 Grattan Street, Carlton, VIC 3053. l.doyleATobgyn-rwh.unimelb.edu.au Sudden unexpected deaths in early childhood in Victoria, 1993-1997Birthweight subgroup 500-1499 g1500-2499 g> 2499 gTotalLive births278115 630297 617316 028Sudden unexpected deaths (≤ 28 days)07*1623Sudden unexpected deaths (> 28 days)724170201Total sudden unexpected deaths731186224Sudden unexpected deaths explained at autopsy001010Total SIDS731176214Pathological featuresDefinite586174Minor21887107None052833Rate of SIDS (per 1000 livebirths) 2.521.98 0.590.68(95% CI)(1.04-5.19)(1.29-2.68)(0.50-0.68)(0.59-0.77)Data are numbers of infants, unless indicated otherwise. * One infant died while still in hospital after birth. SIDS = Sudden infant death syndrome (sudden unexpected deaths, excluding those explained at autopsy). Back to text

Beverley Sowter · Lex W Doyle · Colin J Morley · Anne Altmann · Jane Halliday

Review Attention deficit hyperactivity disorder in adults: conceptual and clinical issues Julian N Trollor MJA 1999; 171: 421-425 Abstract - Introduction - Conceptual issues - Clinical assessment - Management - Monitoring progress - Conclusion - Acknowledgement - References - Authors' details - - More articles on Psychiatry Abstract Reports published over the past decade indicate that attention deficit hyperactivity disorder (ADHD) is a cause of significant psychological impairment in adults. The adulthood disorder occurs as a continuation of its childhood counterpart, with the full ADHD syndrome persisting into early adulthood in about a third of those with childhood ADHD. Despite advances in the understanding of the neurobiology of adult ADHD, the diagnosis is made clinically by establishing a retrospective childhood diagnosis, evaluating the current symptom profile and excluding alternative medical or psychiatric causes of symptoms. Adults with ADHD have high rates of comorbid psychiatric disorder and suffer significant relationship dysfunction, work and educational failure. There is emerging evidence for the effectiveness of specific treatments for adult ADHD, including stimulant medications and some antidepressants. Clinicians should be aware of this potentially treatable disorder in young adults presenting with psychological difficulties and a history of childhood ADHD symptoms. Introduction Attention deficit hyperactivity disorder (ADHD) is one of the most common disorders of childhood, affecting 3%-5% of school-age children.1 It was previously considered a diagnosis applicable only to children and adolescents, but studies of cohorts of ADHD children followed up prospectively have shown that the condition continues into adulthood in an appreciable proportion of patients.2-6 These studies have highlighted the poor psychosocial outcome of this patient population in adulthood, with high rates of educational failure, substance misuse disorders, personality disorders and other psychopathological disorders. Conceptual issues Definition The diagnosis of adult ADHD, as with most psychiatric disorders, is made on clinical grounds. Case identification is based on systematic assessment of symptom profile and exclusion of alternative psychiatric or medical causes. The Diagnostic and statistical manual of mental disorders, 4th edition1 (DSM-IV), reflects the recent conceptual shift in ADHD diagnosis by using wording applicable to adults as well as children (Box 1). Because some ADHD symptoms (eg, inattention, forgetfulness, motor restlessness) occur commonly in the community to a varying extent, it is difficult to decide where the boundary should be drawn between normal and pathological. This dilemma is partly answered in DSM-IV by allowing only those symptoms that are persistent and maladaptive to be counted toward diagnosis. In addition, impairment in at least two settings (eg, work, university, home or social life) is required before a diagnosis of ADHD can be made. Facility exists in DSM-IV for clinicians to specify "ADHD in partial remission" for patients in whom the full diagnostic criteria, although met in childhood, are no longer fulfilled. The clinical status of this less severely affected group awaits clarification. Relationship to childhood ADHD ADHD symptoms must have been present in childhood (although not necessarily recognised) for an adulthood diagnosis to be sustainable. Follow-up studies of childhood ADHD cohorts show considerable discrepancy in reported rates of retention of ADHD diagnosis by early adulthood. Such discrepancies are multifactorial and relate to different diagnostic and exclusion criteria used for study entry, variation in illness severity in original cohorts and differences in age at follow-up. Although up to two-thirds of patients may continue to have symptoms of ADHD as adults,4 only a third will satisfy full diagnostic criteria at age 18,2,3 with further age-dependent decline continuing into the mid 20s.5,6 Comorbidity in adult ADHD Rates of psychopathology among ADHD children in adulthood are high (2-2.5 times those of controls), with a particularly high risk for antisocial personality disorder (up to 10 times that of controls) and drug or alcohol misuse (4-5 times that of controls).4,7 ADHD adults have elevated rates of mood disorder (2-6 times),7,8 anxiety disorders (2-4 times),7,8 relationship dysfunction (2 times),7 and learning disorder7 compared with control populations. The high rate of comorbid psychopathology seen in adult ADHD may be in part a reflection of the impact of longstanding adaptive impairments on development, as well as shared familial, environmental and possibly genetic vulnerabilities. Theoretical and practical implications of comorbidity in adult ADHD have been reviewed in detail elsewhere.9 Pathophysiology Despite its proposed neurobiological basis and predominantly biological treatment, the precise pathophysiological mechanisms of adult ADHD remain obscure. A complete review of this area is beyond the scope of this article and has been provided elsewhere.10,11 Research has focused on a hypothesised functional deficit of monoamines, especially dopamine and noradrenaline. An understanding of the functional12 and structural13-15 neuroanatomy of ADHD is beginning to emerge, implicating dysfunctional prefrontal-striatal circuits in the pathogenesis of ADHD. Clinical assessment The need for a diagnostic hierarchy The key steps in the diagnostic assessment of adults presenting with possible ADHD are shown in the Figure. Many presenting for assessment readily identify with the symptoms of the disorder. However, up to half of those presenting to specialty clinics for assessment of possible ADHD do not have ADHD as the primary diagnosis.16 Thus, approach to this popular diagnosis demands a standardised and objective assessment. Nature and severity of current symptoms The symptoms of ADHD in adults are an extension of those seen in children. Patients may experience difficulty sustaining attention in a number of settings, particularly when performing demanding cognitive tasks. Hyperactivity manifests physically, but may also have a mental component (having accelerated or multiple simultaneous thoughts); however, hyperactivity is not essential for the diagnosis. Patients may manifest impulsive symptoms verbally (by making tactless comments or interrupting others), or may engage in impulsive high risk activities. Often patients have poor organisational skills and an exaggerated response to minor frustrations. A longitudinal assessment of the impact of symptoms should be consistent with impairment secondary to ADHD symptoms. Common experiences of the ADHD sufferer may include recurrent educational or occupational failure, relationship instability and poor ability to organise personal affairs. Establishing a retrospective childhood diagnosis of ADHD A sound retrospective diagnosis of probable ADHD in childhood should be considered as a central precursor to a diagnosis of ADHD in adulthood. A retrospective assessment of childhood symptoms should be made regardless of whether a past childhood diagnosis of ADHD has been made. A retrospective diagnosis is supported by consistent parental reports of symptoms of ADHD in one or more settings, as well as objective accounts of aberrant behaviour recorded in past school reports. Assessing other psychological and medical problems All patients should be asked about the presence of symptoms of common psychiatric and medical disorders (past and present) that can mimic ADHD (Box 2). This is particularly important when patients present for the first time at a relatively late age (eg, over 35 years). In some cases, diagnostic difficulty arises where superimposed symptoms of a second psychiatric disorder coexist with longstanding symptoms of ADHD. Chronic use of many illicit drugs (eg, cannabis, cocaine, amphetamines) and alcohol should be considered as a possible cause of the presenting cognitive and behavioural symptoms. Adult ADHD patients are at high risk of comorbid drug misuse and are more likely to report failed attempts to curtail their drug use.17,18 In patients in whom possible ADHD symptoms and drug misuse occur together, it is usually prudent to reassess for ADHD symptoms after treatment of the drug misuse. Recent (eg, within the past two or three months) or ongoing misuse of illicit substances is a relative contraindication to prescription of stimulant medication. A non-stimulant treatment may be offered to patients with significant ADHD symptoms who are unable to curtail illicit drug use. Adjunctive diagnostic tests Routine investigations: Routine blood tests (urea, electrolyte, creatinine levels, a full blood count, liver and thyroid function tests) are of use only when the presentation suggests an underlying medical disorder. Random urinary drug screening may be performed to monitor illicit drug use in selected patients. An electrocardiogram (EEG) is performed in older adults or those with a history or signs of cardiac disease, particularly when treatment with tricyclic antidepressants is being considered. Rating scales: Rating scales are a useful adjunct to clinical assessment, but do not provide a diagnostic test for adult ADHD. Scales have been developed for retrospective self-report of childhood symptoms (eg, Wender-Utah Rating Scale19) and retrospective parent report of childhood symptoms (eg, Conners Abbreviated Symptom Questionnaire20). Rating scales can also be used to evaluate the severity of current symptoms and to monitor treatment (eg, Patient's Behavior Checklist for ADHD Adults21). Neuropsychological testing: A range of neuropsychological deficits have been reported in children and adolescents with ADHD. Preliminary neuropsychological studies of adults22-27 have produced some conflicting findings, but, on the whole, are consistent with those in childhood, and provide some support for the validity of adult ADHD. The most commonly administered test in adults is a computerised test of sustained attention (Continuous Performance Task). At present, there is insufficient evidence to recommend detailed neuropsychological evaluation for ADHD adults on a routine basis. However, neuropsychological testing may be useful in patients in whom diagnosis is difficult, or when cognitive impairment secondary to another disorder is suspected (eg, those with previous head injury, alcohol-related cognitive deficits, or early dementias). Neurophysiological testing: Quantitative electroencephalograph (EEG) abnormalities, including decreased power of alpha and beta bandwidths in posterior leads and increased frontal theta, have been demonstrated in ADHD children and adolescents.28-30 Quantitative EEG findings have not yet been systematically studied in adults with ADHD and, at present, cannot be advocated for routine assessment. Studies of event-related potentials (ERPs) in children and adolescents with ADHD have found a number of abnormalities in the late positive potential (P3b) amplitude and latency,30-32 as well as abnormalities of the early negative potentials (N1 and N2).31,33,34 However, these findings are seen in a variety of other disorders (eg, autism, learning disability) and hence lack diagnostic specificity. There are few published studies of ERP findings in adults with ADHD, and thus at present their use is for research rather than diagnostic assessment. Functional neuroimaging: Positron emission tomography (PET) findings, including abnormality of glucose uptake in the premotor and frontal cortices12 and reduced [fluorine-18] fluorodopa ratios in the prefrontal cortex,35 support the hypothesis of prefrontal and dopaminergic deficits as central to the pathophysiology of adult ADHD, but do not have clinical application. Structural and functional neuroimaging studies may be appropriate in selected cases when another cause of cognitive and behavioural symptoms is suspected. Management Education Response to initial diagnosis is highly variable, with reactions ranging from relief at an explanation for the symptoms to grief over the "lost years" of the untreated disorder. Education regarding ADHD and its treatment is essential. Further information can be obtained by patients from popular books, ADHD support groups, and the Internet <http://www.nimh.nih.gov/publicat/adhdmenu.cfm> Pharmacotherapy There are only a few published reports examining the efficacy of pharmacotherapy for adult ADHD.36 Drug treatment is generally reserved for those with moderate or severe symptoms, or when more conservative measures have failed. Current evidence supports stimulant responsiveness across age groups,37 but there have only been six published double-blind placebo-controlled trials of psychostimulant use in adults. A review of these36 noted considerable variability in response rates to stimulants (range, 25%-78%; mean, 52%) and attributed this to multiple factors, including diagnostic and dose variation between studies. No convincing evidence has emerged that long term supervised prescription of stimulants leads to drug tolerance or misuse. Commonly used dose ranges for the two stimulants available in Australia are the same as those for ADHD children (0.3-1.0 mg/kg per day for methylphenidate, and 0.2-0.5 mg/kg per day for dextroamphetamine). The mechanisms of action of stimulant medication have been reviewed.38 Stimulants should not be taken together with other psychotropic drugs, unless recommended by an experienced clinician. Tricyclic antidepressants (TCAs) have been assessed as effective treatments for childhood and adolescent ADHD. Two studies of ADHD in adults39-40 support a role for desipramine, nortriptyline and imipramine at typical antidepressant dosages as second-line treatment for adult ADHD. However, initial treatment with TCAs should be considered in selected patients (those at risk of misuse of prescribed stimulants, and those with comorbid depression and anxiety). The newer antidepressants venlafaxine41-43 and bupropion44 have shown promise in open studies, but further evaluation is required. Serotonin reuptake inhibitors may be appropriate for those with comorbid anxiety, depression, obsessive-compulsive symptoms and severe impulsivity, but as yet there is no evidence of their value for the treatment of ADHD symptoms alone. The monoamine oxidase-B inhibitor L-deprenyl has been shown to reduce ADHD symptoms in a single trial in adults.45 Cognitive behavioural therapy Cognitive and behavioural strategies have yet to be systematically evaluated as independent treatments for adult ADHD. However, to overcome skill deficits commonly seen in ADHD, patients can be taught basic skills such as time management, organisational strategies, problem solving and anger management. Controversial treatments A number of controversial treatments are available for adult ADHD. Dietary supplementation, exclusion diets and herbal supplements have not been shown to be of benefit in adults. EEG biofeedback is an expensive treatment of growing popularity, but has yet to be properly evaluated. A case history of adult ADHD in a 22-year-old man is given in Box 3. Monitoring progress Patient response to treatment can be monitored at various levels: subjective feedback from patient and family; self- and observer-rating scales; educational progress; employer reports; and repeat neuropsychological assessment. No consensus guidelines exist regarding duration of treatment or adequate methods of monitoring progress. If stimulant treatment has been continued through late adolescence into adulthood, it is prudent to review the need for continuing treatment every 6-12 months. A medication-free period (eg, 4-6 weeks) may allow re-evaluation of symptom severity, thus helping to determine the need for ongoing treatment. For patients commencing stimulant medication for the first time as adults, there should be clear evidence of functional improvement over the first 3-6 months of treatment. Clear short-term functional improvement justifies continuing stimulant prescription over the next 12 months. Thereafter, a patient's progress should be reviewed as above. Those with persistence of the full adult ADHD profile may require medication until educational goals have been met, or until stable employment is obtained. This allows the patient to further develop the skills needed to compensate for persisting symptoms. A small group of patients with severe symptoms may require stimulant medication indefinitely. Conclusion There are published reports to support the continuation of ADHD into adulthood in about a third of patients with childhood ADHD. Symptoms of the disorder can be disabling, and considerable comorbid psychopathology may be present. With recognition and appropriate management of the disorder, considerable gains may be anticipated in most patients. As with any emergent condition, our current understanding of adult ADHD is incomplete, and limited published data are available. A systematic and evidence-based approach to diagnosis and management is therefore required, which should be revised as new developments occur. Acknowledgement The assistance of Professor Perminder Sachdev in reviewing a previous draft version of this article is gratefully acknowledged. References American Psychiatric Association. Diagnostic and statistical manual of mental disorders, 4th edition. Washington, DC: American Psychiatric Association, 1994: 83-85. Gittleman R, Mannuzza S, Shenker R, Bonagura N. Hyperactive boys almost grown up: I. Psychiatric status. Arch Gen Psychiatry 1985; 42: 937-947. Mannuzza S, Klein RG, Bonagura N, et al. Hyperactive boys almost grown up: V. Replication of psychiatric status. Arch Gen Psychiatry 1991; 48: 77-83. Weiss G, Hechtman L, Milroy T, Perlman T. Psychiatric status of hyperactives as adults: a controlled prospective 15-year follow-up of 63 hyperactive children. J Am Acad Child Psychiatry 1985; 24: 211-220. Mannuzza S, Klein RG, Bessler A, et al. Adult outcome of hyperactive boys: educational achievement, occupational rank and psychiatric status. Arch Gen Psychiatry 1993; 50: 565-576. Mannuzza S, Klein RG, Bessler A, et al. Adult psychiatric status of hyperactive boys grown up. Am J Psychiatry 1998; 155: 493-498. Biederman J, Faraone SV, Spencer T, et al. Patterns of psychiatric comorbidity, cognition, and psychosocial functioning in adults with attention deficit hyperactivity disorder. Am J Psychiatry 1993; 150: 1792-1798. Biederman J, Newcorn J, Sprich S. Comorbidity of attention deficit hyperactivity disorder with conduct, depressive, anxiety and other disorders. Am J Psychiatry 1991; 148: 564-577. Horning M. Addressing comorbidity in adults with Attention Deficit Hyperactivity Disorder. J Clin Psychiatry 1998; 59 [Suppl 7]: 69-75. Castellanos FX. Toward a pathophysiology of attention deficit hyperactivity disorder. Clin Paediatr 1997; 36: 381-393. Faraone SV, Biederman J. Neurobiology of Attention-Deficit Hyperactivity Disorder. Biol Psychiatry 1998; 44: 951-958. Zametkin AJ, Nordahl TE, Gross M, et al. Cerebral glucose metabolism in adults with hyperactivity of childhood onset. N Engl J Med 1990; 323: 1361-1366. Castellanos FX, Giedd JN, Eckburg P, et al. Quantitative morphology of the caudate nucleus in attention deficit hyperactivity disorder. Am J Psychiatry 1994; 151: 1791-1796. Semrud-Clikeman M, Filipek PA, Biederman J, et al. Attention-deficit hyperactivity disorder: magnetic resonance imaging morphometric analysis of the corpus callosum. J Am Acad Child Adolesc Psychiatry 1994; 33: 875-881. Castellanos FX, Giedd JN, Marsh WL, et al. Quantitative brain magnetic resonance imaging in attention deficit hyperactivity disorder. Arch Gen Psychiatry 1996; 53: 607-616. Roy-Byrne P, Scheele L, Brinkley J, et al. Adult attention deficit hyperactivity disorder: assessment guidelines based on clinical presentation to a specialty clinic. Compr Psychiatry 1997; 38: 133-140. Goodwin DW, Schulsinger F, Hermansen L, et al. Alcoholism and the hyperactive child syndrome. J Nerv Ment Dis 1975; 160: 349-353. Carroll KM, Rounsaville BJ. History and significance of childhood attention deficit hyperactivity disorder in treatment-seeking cocaine abusers. Compr Psychiatry 1993; 34: 75-82. Ward MF, Wender PH, Reimherr FW. The Wender Utah Rating Scale: an aid in the retrospective diagnosis of childhood attention deficit hyperactivity disorder. Am J Psychiatry 1993; 150: 885-890. Goyette CH, Conners CK, Ulrich RF. Normative data on Revised Conners Parent and Teacher Rating Scales. J Abnorm Child Psychol 1978; 6: 221-236. Patient's Behaviour Checklist for ADHD Adults. In: Barkley RA, ed. Attention deficit hyperactivity disorder: a clinical workbook. New York: The Guilford Press, 1991: 43. Seidman LJ, Biederman J, Weber W, et al. Neuropsychological function in adults with attention deficit hyperactivity disorder. Biol Psychiatry 1998; 44: 260-268. Matochik JA, Rumsey JM, Zametkin AJ, et al. Neuropsychological correlates of familial attention deficit hyperactivity disorder in adults. Neuropsychiatry, Neuropsychol Behav Neurol 1996; 9: 186-191. Downey KK, Stelson FW, Pomerleau OF, Giordani B. Adult attention deficit hyperactivity disorder: psychological test profiles in a clinical population. J Nerv Ment Dis 1997; 185: 32-38. Lovejoy DW, Ball JD, Keats M, et al. Neuropsychological performance of adults with attention deficit hyperactivity disorder (ADHD): diagnostic classification estimates for measures of frontal lobe/executive functioning. J Int Neuropsychol Soc 1999; 5: 222-233. Corbett B, Stanczak DE. Neuropsychological performance of adults evidencing attention-deficit hyperactivity disorder. Arch Clin Neuropsychol 1999; 14: 373-387. Jenkins M, Cohen R, Malloy P, et al. Neuropsychological measures which discriminate among adults with residual symptoms of attention deficit disorder and other attentional complaints. Clin Neuropsychol 1998; 12: 74-83. Mann CA, Lubar JF, Zimmerman AW, et al. Quantitative analysis of EEG in boys with attention deficit hyperactivity disorder: a controlled study with clinical implications. Paediatr Neurol 1992; 8: 30-36. Chabot RJ, Merkin H, Wood LM. Sensitivity and specificity of QEEG in children with attentional deficits or specific developmental learning disorders. Clin Electroencephalogr 1996; 27: 26-34. Kuperman S, Johnson B, Arndt S, et al. Quantitative EEG differences in a nonclinical sample of children with ADHD and undifferentiated ADD. J Am Acad Child Adolesc Psychiatry 1996; 35: 1009-1017. Loiselle DL, Stamm JS, Maitinsky S, Whipple SC. Evoked potential and behavioral signs of attentive dysfunctions in hyperactive boys. Psychophysiology 1980; 17: 193-201. Holcomb PH, Ackerman PT, Dykman RA. Cognitive event-related potentials in children with attentional and reading deficits. Psychophysiology 1985; 22: 656-667. Satterfield JH, Schell AM, Nicholas T, Backs RW. Topographic study of auditory event-related potentials in normal boys and boys with attention deficit disorder with hyperactivity. Psychophysiology 1988; 25: 591-606. Klorman R, Brumaghim JT, Salzman LF, et al. Effects of methylphenidate on processing negativities in patients with attention-deficit hyperactivity disorder. Psychophysiology 1990; 27: 328-337. Ernst M, Zametkin AJ, Matochik JA, Cohen RM. Dopa decarboxylase activity in attention deficit hyperactivity disorder adults -- a [fluorine-18] fluorodopa positron emission tomographic study. J Neurosci 1998; 18: 5901-5907. Wilens TE, Biederman J, Spencer TJ, Prince J. Pharmacotherapy of adult attention deficit hyperactivity disorder: a review. J Clin Psychopharmacol 1995; 15: 270-279. Spencer T, Biederman J, Wilens T, et al. Pharmacotherapy of attention-deficit hyperactivity disorder across the life cycle. J Am Acad Child Adolesc Psychiatry 1996; 35: 409-432. Solanto M. Neuropsychopharmacological mechanisms of stimulant drug action in attention-deficit hyperactivity disorder: a review and integration. Behav Brain Res 1998; 94: 127-152. Wilens TE, Biederman J, Mick E, Spencer TJ. A systematic assessment of tricyclic antidepressants in the treatment of adult attention-deficit hyperactivity disorder. J Nerv Ment Dis 1995; 183: 48-50. Wilens TE, Biederman J, Prince J, et al. Six-week, double-blind, placebo-controlled study of desipramine for adult attention deficit hyperactivity disorder. Am J Psychiatry 1996; 153: 1147-1153. Adler LA, Resnick S, Kunz M, Devinsky O. Open-label trial of venlafaxine in adults with attention deficit disorder. Psychopharmacol Bull 1995; 31: 785-788. Hedges D, Reimherr FW, Rodgers A, et al. An open trial of venlafaxine in adult patients with attention deficit hyperactivity disorder. Psychopharmacol Bull 1995; 31: 779-783. Findling RL, Schwartz MA, Flannery DL, Manos MJ. Venlafaxine in adults with attention-deficit hyperactivity disorder: an open clinical trial. J Clin Psychiatry 1996; 57: 184-189. Wender PH, Reimherr FW. Buproprion treatment of attention deficit hyperactivity disorder in adults. Am J Psychiatry 1990; 147: 1018-1020. Wood DR, Reimherr FW, Wender PH. The use of l-deprenyl in the treatment of attention deficit disorder, residual type (ADD, RT). Psychopharmacol Bull 1983; 19: 627-629. (Received 4 Feb, accepted for publication 20 Jul, 1999) Authors' details Neuropsychiatric Institute, Prince of Wales Hospital, Sydney, NSW. Julian N Trollor, MB BS, FRANZCP, Staff Specialist; and Conjoint Lecturer, School of Psychiatry, University of New South Wales. Reprints will not be available from the author. Correspondence: Dr J N Trollor, Neuropsychiatric Institute, McNevin Dickson Building, Prince of Wales Hospital, Randwick, NSW 2031. J. TrollorATunsw.edu.au 1: Summary of DSM-IV criteria for attention deficit hyperactivity disorder1 (all criteria from A to D must be met) A: Six or more symptoms of either Inattention or Hyperactivity-impulsivity present for at least six months to a degree that is maladaptive and inconsistent with developmental level. Inattention Often: fails to give close attention to details or makes careless mistakes in schoolwork, work or other activities has difficulty sustaining attention in tasks or play activities does not seem to listen when spoken to directly does not follow through on instructions and fails to finish schoolwork, chores or duties in the workplace has difficulty organising tasks and activities avoids, dislikes or is reluctant to engage in tasks that require sustained mental effort loses things necessary for tasks or activities easily distracted by extraneous stimuli forgetful in daily activities Hyperactivity-impulsivity Often: fidgets with hands, feet or squirms in seat leaves seat in classroom or other situations in which remaining seated is expected runs about or climbs excessively in situations in which it is inappropriate (in adolescents or adults, may be limited to subjective feelings of restlessness) has difficulty playing or engaging in leisure activities quietly "on the go" or acts as if "driven by a motor" talks excessively blurts out answers before questions completed has difficulty awaiting turn interrupts or intrudes on others B: Some symptoms causing impairment were present before 7 years of age. C: Some impairment is present in two or more settings. D: Evidence of clinically significant impairment in social, academic or occupational functioning. Back to textBack to text 2: Differential diagnoses of adult attention deficit hyperactivity disorder Medical Past head injury or anoxia Sleep disorders (eg, sleep apnoea) Recent viral infection including HIV Long term medical illness (eg, renal or liver failure) Seizure disorder (eg, petit mal) Endocrine disorder (eg, hypothyroidism, hyperthyroidism, hypoglycaemia) Psychiatric Anxiety disorder Major depression Bipolar disorder (eg, chronic hypomania) Cyclothymia Antisocial and borderline personality disorders Effect of prescribed medications (eg, benzodiazepines, anticholinergic drugs, anticonvulsants) Other central nervous system disorder (eg, degenerative disorders) Substance misuse (alcohol, long term cocaine or amphetamine use, cannabis) Back to text Case history -- adult attention deficit hyperactivity disorder (ADHD) Presentation: A 22-year-old unemployed carpenter, referred by his general practitioner, reported difficulty concentrating when reading or listening to verbal instructions, and difficulty following through multistep tasks. He had lost numerous jobs because of poor organisational skills, failure to complete assigned tasks, and a tendency to become easily bored or frustrated in his work. He was disorganised in most aspects of managing his personal affairs. There was a history of experimenting with illicit substances, instability in interpersonal relationships, and low self-esteem. The patient's mother confirmed his account of untreated, moderately severe ADHD symptoms from school entry. Assessment: The patient was physically restless, easily distracted and verbally impulsive. There was no evidence of psychiatric or medical illness. Neuropsychological assessment revealed reduced arithmetic skills, reduced speed of information processing, impulsive responses and failure to maintain attention over time. A diagnosis of ADHD was made. Management: Combined psychological and pharmacological treatment was instituted. Over a series of 12 sessions, the patient was given information about ADHD, and participated in sessions to enhance organisational skills, impulse control and self-esteem. He was prescribed dextroamphetamine, 5 mg twice a day, and later the dose was increased to 5 mg three times a day. Both the patient and his family reported amelioration of his symptoms. He was able to successfully start a part-time job, and later returned to full-time employment as a carpenter. A trial without stimulant medication at 12 months led to appreciable exacerbation of symptoms, and dextroamphetamine was reinstituted. He has remained in stable employment over a follow-up period of 18 months and continues to take dextroamphetamine on work days only. Back to text

Julian N Trollor

Viewpoint Cryptosporidiosis in the immunocompromised: weighing up the risk Current evidence does not support a permanent "boil water" alert for all immunocompromised groups Paul M Byleveld, Amanda Hunt and Jeremy M McAnulty MJA 1999; 171: 426-428 See also Fairley et al Synopsis - Introduction - Transmission risks - Recommendations - Conclusion - References - Authors' details - - More articles on Public and environmental health Synopsis Cryptosporidiosis has been increasingly recognised as a cause of diarrhoeal illness in both immunocompetent and immunocompromised people. Massive outbreaks have been linked to municipal drinking water supplies in North America and Europe, but so far none have been reported in Australia. There is evidence that modes of transmission other than drinking water are more important. There can be no guarantee that infective Cryptosporidium oocysts will not contaminate an Australian water supply. Therefore, a permanent "boil water" warning may be warranted on medical advice in severely immunocompromised people, for whom cryptosporidiosis could be persistent and life threatening. Introduction Between July and September 1998, drinking water in Sydney was contaminated with the protozoan parasites Cryptosporidium and Giardia. Human illness with cryptosporidiosis had been notifiable by laboratories in New South Wales since 1996, but giardiasis was not. In response to the contamination, surveillance for diarrhoeal disease was enhanced and residents in affected areas were advised to boil all drinking water. To determine whether the incidence of diarrhoeal illness had increased, NSW Health's six public health units in Sydney regularly contacted laboratories, general practitioners, emergency departments, pharmacies and nursing homes. In addition, NSW Health conducted telephone surveys of households to determine the residents' disease experience and compliance with warnings. At times during the contamination events, a proportion of the population was exposed to drinking water containing apparently high concentrations of Cryptosporidium and Giardia, because the water reached houses before the contamination was identified and because of poor compliance with the "boil water" alert. Despite this, there was no outbreak of disease attributable to drinking water, as indicated by increases in cases of diarrhoeal disease presenting to emergency departments, sentinel general practices or nursing homes, or laboratory reports of cryptosporidiosis.1The Sydney Water Inquiry was established in August 1998 to investigate the causes of contamination and management of the incidents and to make recommendations about the control and prevention of such events. The Inquiry recommended that a permanent warning be issued to immunocompromised persons to boil all tap water before use, and that advice be provided on the risks of contracting cryptosporidiosis from water and other sources.2 The permanent "boil water" recommendation is a very cautious reaction to a threat that may be small, but is consistent with advice offered in the United Kingdom.3 The implementation of such advice would have a serious effect on the operation and costs for healthcare facilities and the food industry, if required to buy in treated water or provide additional treatments for water used for drinking or as ingredients. In contrast to the recent Sydney experience of high oocyst counts but no detectable disease, large community-wide outbreaks of cryptosporidiosis have occurred in Britain and the United States following contamination of drinking water with concentrations of Cryptosporidium oocysts that were apparently much lower than those in Sydney.4,5 In Britain and the US, several outbreaks of waterborne cryptosporidiosis have resulted in significant morbidity and mortality in people infected with HIV (Box 1).6-8 Other classes of severely immunocompromised persons, including transplant recipients and patients receiving chemotherapy, may also be at greater risk from water contaminated with Cryptosporidium. While the available data are limited, the attack rate in these groups does not appear to be as high as that in those with HIV.6,7 The identification of waterborne disease is more likely in the immunocompromised, as these people may have prolonged illness and receive closer medical surveillance. Compared with Cryptosporidium, the risk posed by Giardia and viral and bacterial pathogens to immunocompromised people from municipal water supplies is thought to be lower, because conventional water treatment processes (including chlorination) more easily control them.14 Transmission risks The public and many clinicians poorly understand the relative importance of transmission of Cryptosporidium by drinking water compared with other modes of transmission (Box 2). Recent evidence shows that contaminated swimming pools are likely to pose a greater risk than a public water supply for the waterborne transmission of human infective forms of C. parvum.18,19There have been no documented outbreaks of cryptosporidiosis or giardiasis associated with municipal water supplies in Australia. For waterborne transmission to occur, viable human-infective forms of C. parvum must be present in sufficient (albeit small) numbers. Available data to date suggest that parasites found in Sydney drinking water and originating from the catchments may not have been infectious to humans.1 However, the potential for transmission of Cryptosporidium and Giardia by drinking water in Australia was demonstrated at a campsite in Victoria, when guests developed cryptosporidiosis and giardiasis after an inground water tank was contaminated by effluent from a septic tank.20 In regional areas, the risk of waterborne cryptosporidiosis and giardiasis may vary from town to town. While the data are scarce, there is currently no evidence to suggest that immunocompromised persons who reside in these areas and receive an appropriately treated drinking water supply are at greater risk. Precautions should be taken with untreated water supplies, particularly those obtained from surface sources (rivers, creeks and dams). In New South Wales, a number of water suppliers have collaborated with health authorities to evaluate the risk of contamination from "catchment to tap". This process -- which involves assessments of (i) the risks to the water catchment area from sources including septic tanks, sewage overflows and agricultural activities, (ii) the integrity of the water treatment processes, and (iii) the distribution system -- better equips water suppliers and health authorities to provide information on local drinking water quality to clinicians and the public. Recommendations Since well before the recent contamination incidents, NSW Health has stated that people living with HIV and AIDS, those receiving treatment for some types of cancer and transplant recipients may (after consulting with their doctor) choose to avoid unboiled drinking water.21 Although evidence to date suggests that appropriately treated drinking water in New South Wales does not place anyone at risk of cryptosporidiosis, this advice is offered as a precautionary measure and is consistent with that offered by the US Centers for Disease Control and Prevention.22Particular care should be taken with drinking water and food at remote accommodation facilities. Boiling is the most effective way to kill Cryptosporidium (and other pathogens) in drinking water, while many, but not all, filters and bottled water meet satisfactory standards. Consumers should carefully examine the labels on filters and bottled water and seek an assurance from manufacturers that their products will protect against waterborne cryptosporidiosis and giardiasis. Water treatment units that incorporate boiling, distillation or reverse osmosis processes are satisfactory. Suitable filters include those labelled "absolute 1 micron" (or smaller) and certified to meet the relevant standard for cyst removal (either ANSI/NSF5323 or AS/NZS434824), but require an additional disinfection unit to inactivate bacterial and viral pathogens. Filters are likely to fail if not maintained in accordance with manufacturer's instructions. Because filters may accumulate pathogens, it is advisable to wear gloves and wash hands after changing filters. It should not be assumed that all bottled water, beverages reconstituted with tap water and ice products are free from contamination. Mineral (or spring) water obtained from well-protected sources should not contain Cryptosporidium and Giardia. Other packaged water and ice products that are treated by distillation, reverse osmosis, or filtering through an absolute 1 micron (or smaller) filter should be free of Cryptosporidium and Giardia. Data available to date have not provided evidence of local drinking water borne cryptosporidiosis and do not support a permanent "boil water" warning for all immunocompromised persons in New South Wales. Although the risk is likely to remain low, there can be no guarantee that infective Cryptosporidium oocysts will not contaminate an Australian water supply. Therefore, a permanent "boil water" warning may be warranted on medical advice in severely immunocompromised people, for whom cryptosporidiosis could be persistent and life threatening. Such people should also be advised to take great care with all other potential risk factors. Given the broad range and dynamic nature of these conditions, it is impossible for health authorities to list all classes of people who should receive this warning. Individual advice can only be provided by a doctor after considering the patient's status and case history. The potential effect of a permanent boil water advice on quality of life for immunocompromised persons should be weighed up against benefits that may be gained. Factors to consider include the need to avoid a range of foods and beverages that may contain tap water, the risk of burns and scalds, and ongoing costs where filters or bottled water are used. Conclusion Health departments rely on the diagnosis and timely notification of diarrhoeal disease and monitoring of water quality to protect the public from waterborne disease outbreaks. Where a reasonable threat to public health is likely to exist, the public is advised to boil drinking water. The recent events suggest that the risk of transmission of cryptosporidiosis by drinking water in Sydney may be very low, and highlight the limitations of water-testing techniques that do not define viability or human infectivity. But more is to be learnt about Cryptosporidium and the risk that it poses to the community. It is essential that health agencies continue to monitor and investigate clusters of cryptosporidiosis cases to learn more about modes of transmission and risk factors. Sound public health decisions can only be made on such evidence. References NSW Department of Health. The Sydney Water Incident: July-September 1998. NSW Public Health Bulletin 1998; 9: 91-94. McClellan P. Sydney Water Inquiry. Final Report. Sydney: NSW Premier's Department, 1998. Bouchier IAD. Cryptosporidium in water supplies. 8. Advice to the immunocompromised individual. <http://www.dwi.detr.gov.uk/crypto/bou008.htm>. UK Drinking Water Inspectorate, Department of the Environment, Transport and Regions, 1998. Accessed 16 September 1999. Atherton F, Newman CPS, Casemore DP. An outbreak of waterborne cryptosporidiosis associated with a public water supply in the UK. Epidemiol Infect 1995; 115: 123-131. MacKenzie WR, Hoxie NJ, Proctor ME, et al. A massive outbreak in Milwaukee of Cryptosporidium infection transmitted through the public water supply. N Engl J Med 1994; 331: 161-167. Clifford CP, Crook DW, Conlon CP, et al. Impact of waterborne outbreak of cryptosporidiosis on AIDS and renal transplant patients. Lancet 1990; 335: 1455-1456. Goldstein ST, Juranek DD, Ravenholt O, et al. Cryptosporidiosis: an outbreak associated with drinking water despite state-of-the-art water treatment. Ann Intern Med 1996; 124: 459-468. Hoxie NJ, Davis JP, Vergeront JM, et al. Cryptosporidiosis-associated mortality following a massive waterborne outbreak in Milwaukee, Wisconsin. Am J Public Health 1997; 87: 2032-2035. 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Paul M Byleveld, PhD, Senior Policy Advisor, Water Unit; Amanda Hunt, BHB, MPhil(Env Sc), Policy Advisor, Water Unit; Jeremy M McAnulty, MB BS, MPH, Medical Epidemiologist, Communicable Diseases Surveillance and Control Unit. Reprints: Dr J M McAnulty, NSW Department of Health, Locked Mail Bag 961, North Sydney, NSW 2059. jmcanATdoh.health.nsw.gov.au 1: Cryptosporidiosis and HIV/AIDS During the 1994 cryptosporidiosis outbreak in Nevada, most of the 78 confirmed cases were in HIV-infected adults (61 people, most of whom had CD4+ lymphocyte counts less than 100 cells/µL).7 The remainder of those infected included 11 immunocompetent children, four adults without HIV infection, two HIV-infected children, a renal transplant recipient receiving corticosteroid therapy, and a patient with testicular cancer receiving chemotherapy. In Australia, there has been a marked decline in the incidence of cryptosporidiosis as the initial AIDS-defining illness since 19949 (Dr G Dore, Lecturer in Epidemiology, National Centre in HIV Epidemiology and Clinical Research, personal communication), and there is little evidence that other classes of immunocompromised persons are currently at greater risk of developing cryptosporidiosis. In Australia and other countries, the prognosis for those with HIV infection has improved dramatically with the introduction of highly active antiretroviral treatments, which extend the time to development of AIDS and survival time, and arrest the decline in CD4+ lymphocyte counts.9-11 The administration of antiretroviral therapy that includes a protease inhibitor in HIV-positive individuals appears to restore immunity to C. parvum, relieves cryptosporidial diarrhoea and, in some cases, helps eradicate the parasite.12,13 It is possible that, if an outbreak of waterborne cryptosporidiosis were to occur tomorrow, it would have a less severe impact on the HIV-positive community than outbreaks that occurred in the first half of this decade.7,8 Back to text 2: Modes of transmission Cryptosporidium is transmitted by: faecal-oral contact with infected persons (particularly in childcare centres, by not washing hands after going to the toilet, after changing nappies, or from sexual activity that involves exposure to faecal matter); bathing in contaminated water or swimming pools; handling young livestock; contact with animals that have diarrhoea; and consumption of contaminated foods and drinking water (including water supplies when camping or travelling). A study conducted in Los Angeles concluded that modes of transmission other than drinking water were more important risk factors for the development of cryptosporidiosis in people with AIDS.15 Similarly, a study in persons with HIV in San Francisco revealed that high-risk sexual behaviours were prevalent even among those who were concerned enough about exposures to consume only boiled or bottled water.16 A recent study conducted in persons with HIV in Melbourne suggested that a number of sexual practices, but not CD4+ cell count or tap water consumption, were significant risk factors for prior Cryptosporidium infection.17 Back to text

Paul M Byleveld · Amanda Hunt · Jeremy M McAnulty