Cause-specific and total mortality in the Canterbury (New Zealand) insulin-treated Diabetic Registry population: a 15-year follow-up study.

AIMS: To establish all-cause and cause-specific death rates, and risk factors for mortality in insulin-treated diabetic individuals living in the province of Canterbury, New Zealand. METHODS: Insulin-treated diabetic subjects (n = 995) on the Canterbury Diabetes Registry were followed up over 15 years and vital status determined. Death rates were standardized and hazard regression was used to model the effects of demographic covariates on relative survival time. RESULTS: There were 419 deaths in 11 226.3 person-years of follow-up with a standardized mortality ratio (SMR) of 2.0 (95% confidence interval (CI) 1.8-2.2). Relative mortality was greatest for the group aged 0-29 years (SMR 3.0 (95% CI 2.4-3.7)). After controlling for diabetes duration and gender, a 10-year increment in age of onset was associated with a 33% decrease in relative hazard (95% CI 29-36%), indicating that excess mortality due to diabetes declines with rising age of onset. After controlling for age of onset and gender, each 10-year increment in duration of diabetes is associated with a 26% decrease in relative hazard (95% CI 24-29%), indicating that with longer survival the mortality hazard approaches the general population hazard. Relative mortalities were increased for cardiovascular, renal and respiratory disease, but not malignancy. Relative mortality from acute metabolic complications was increased in the subgroup with age of onset of diabetes < 30 years and requiring insulin within 1 year of diagnosis. CONCLUSIONS: Mortality rates are high for insulin-treated diabetic individuals relative to the general population.

Predictors of mortality from type 2 diabetes mellitus in Canterbury, New Zealand; a ten-year cohort study.

The aim was to establish mortality rates in a cohort of subjects with type 2 diabetes mellitus over 10 years in Canterbury, New Zealand (NZ) and to determine baseline prognostic factors. Subjects (447) with type 2 diabetes (208 male, 239 female; age range 30-82 years, median 62 years; of predominantly European origin) were characterised in a clinic survey in 1989. Individual status (dead or alive) at June 1 1999 (10 year follow-up) was ascertained. Mortality rates were compared with the general NZ population and the relative risk (RR) of baseline prognostic factors evaluated with Cox's proportional hazards model. At 10 years, 232 subjects were confirmed as alive and 187 as dead - only 28 were untraceable. Ten year survival was 55% (95% CI: 50-60) for the cohort, compared with 70% (95% CI: 65-75) at 6 years. Factors assessed at baseline (1989), that were independently prognostic of total mortality, included age (RR 2.0, 95% CI: 1.6-2.5), pre-existing coronary artery disease (CAD; RR 1.7, 95% CI: 1.2-2.4) and albuminuria (RR 1.58, 95% CI: 1.1-2.3). Glycated haemoglobin was not a significant predictor of total mortality, although was a predictor of CAD mortality in those subjects free of CAD in 1989 (RR 1.6, 95% CI: 1.1-2.3). In the latter subset, independent prognostic factors for CAD mortality also included age (RR 2.5, 95% CI: 1.7-3.8), hypertension (RR 1.9, 95% CI: 1.0-3.7), peripheral vascular disease (RR 2.4, 95% CI: 1.3-4.5) and smoking (RR 2.6, 95% CI: 1.2-5.8). Increased mortality in type 2 diabetic subjects is therefore attributable to multiple risk factors. Improved outcomes will depend on interventions targeted at glycaemic and all other remediable factors.

Age at diagnosis, glycaemic control and the development of retinopathy in a population-based cohort of Type 1 diabetic subjects in Canterbury, New Zealand.

The aim was to determine the relationship between age at diagnosis, glycaemic control and the development of retinopathy in a population-based cohort of Type 1 diabetic subjects. At 1 January 1984, there were 286 individuals with Type 1 diabetes (and age of onset<20 years) on the Canterbury, New Zealand population register who had at least 2 prospective HbA(1c) readings (from 1 January 1984). Of these, 107 already had retinopathy. Of the 179 subjects without retinopathy at baseline 63 developed retinopathy during follow-up. After controlling for duration of diabetes (in the whole group), age at diagnosis was found to be a significant predictor of HbA(1c) level (P=0.001), with higher (mean+/-SD) baseline HbA(1c) in the 10-14 age group (7.95+/-2.14%), compared with (7.62+/-1.77%) in the <10 year group and (7.39+/-2.57%) in the >14 year group. The major predictors of retinopathy (in those without retinopathy at baseline), however were duration of diabetes (mean time to development of retinopathy decreases by 14% (95% CI 10-17%) for each year), baseline HbA(1c) (for each unit increase, mean time to development of retinopathy decreased by 23% (95%CI 13-32%) and HbA(1c) slope (average annual change). Peri-pubertal age at diagnosis (10-14 years) did not influence the time to onset of retinopathy over and above that attributed to duration of diabetes and glycaemic control.

All-cause mortality in the Canterbury (New Zealand) insulin-treated Diabetic Registry population.

OBJECTIVE: To establish all-cause death rates and life expectancies of and risk factors for mortality in insulin-treated diabetic individuals living in Canterbury, New Zealand. RESEARCH DESIGN AND METHODS: Insulin-treated diabetic subjects (n = 1,008) on the Canterbury Diabetes Registry were tracked over 9 years, and their vital status was determined. Death rates were standardized using direct and indirect methods. Cox proportional hazard regression was used to model the effects of demographic and clinical covariates on survival time. RESULTS: At study entry, age ranged from 2.9 to 92.7 years, with mean 48.7 +/- 20.4 years; age at diagnosis was 0.2-88.9 years, mean 34.5 +/- 20.0 years; and duration of diabetes was 0.1-58.5 years, mean 14.0 +/- 10.6 years. There were 303 deaths in 7,372 person-years of follow-up with a standardized mortality ratio (SMR) of 2.6 (95% CI 2.4-3.0). Relative mortality was greatest for those aged 30-39 years (SMR 9.2 [4.8-16.2]). The death rate for the diabetic cohort standardized against the Segi world standard population was 16.2 per 1,000. Attained age, sex, and clinical subtype were significant predictors of mortality The SMR for subjects with type 1 diabetes and age at onset <30 years was 3.7 (CI 2.7-5.0), 2.2 (1.8-2.6) for those with onset > or =30 years, and 3.1 (2.5-3.7) for subjects suspected of having latent autoimmune diabetes in adulthood or insulin-treated type 2 diabetes. Life expectancy was reduced for both sexes at all ages. CONCLUSIONS: Mortality rates for insulin-treated diabetic individuals remain high, resulting in shortened life spans relative to the general population. Marked differences in mortality exist between clinical groups of subjects. Further research is needed to improve diabetes classification and to clarify differences in health outcomes.

Clinical and biochemical outcomes of type 2 diabetes mellitus in Canterbury, New Zealand: a 6-year cohort study.

There is a paucity of data regarding outcomes of Type 2 diabetes mellitus. A cohort of 447 Type 2 diabetic subjects (208 male, 239 female; age range 30-82 years, median 62 years; and of predominantly European origin) was characterised in a clinic survey in 1989. Individual status (dead or alive) at 1 June 1995 was ascertained. At 6 years, 289 subjects were confirmed as alive and 133 as dead--only 25 were untraceable. Of those subjects identified as alive, follow-up clinical and biochemical data were obtained for 253 (87.5%) individuals. In those subjects, glycated haemoglobin deteriorated from 63.1 +/- 18.7 mmol/mol haem in 1989 to 71.7 +/- 24.4 in 1995, P < 0.0001. An increased prevalence of retinopathy was evident at 6-year follow-up, 59.7% cases in 1995 compared with 39.5% in 1989, P < 0.001. Similarly there was an increased prevalence of coronary artery disease (CAD) (33.6 vs 18.2% of cases), albuminuria (26.5 vs 19% of cases; P < 0.001), and hypertension (71.5 vs 54.9% of cases; P < 0.001) in 1995 vs 1989, respectively. Multiple logistic regression analysis showed that glycated haemoglobin (odds ratio (OR) for 18 mmol/mol haem change, 1.78; 95% CI, 1.15-2.85), hypertension (OR, 3.33; 95% CI, 1.40-8.41) and known duration of diabetes (OR for 7 year change, 2.12; 95% CI, 1.24-3.80) were predictors for development of retinopathy. There is therefore a deterioration in glycaemic control in Type 2 diabetes over 6 years and an increased prevalence of complications that present strategies in a multidisciplinary specialist diabetes clinic are unable to prevent on a sustainable basis.

Lipid but not glycaemic parameters predict total mortality from type 2 diabetes mellitus in Canterbury, New Zealand.

A cohort of 447 subjects with Type 2 diabetes mellitus (208 male, 239 female; age range 30-82, median 62 years; and of predominantly European origin) was characterized in a clinic survey in 1989. Individual status (dead or alive) at 1 June 1995 was ascertained. Mortality rates were compared with the general New Zealand population by calculating standardized mortality ratios (SMR) and the hazard ratio (HR) of prognostic factors evaluated with Cox's proportional hazards model. At 6 years, 289 subjects were confirmed as alive and 133 as dead; only 25 were untraceable. Six-year survival for the cohort was 70% (95% CI 66-74). SMR was 2.53 (95% CI 1.99-2.68) for the female cohort and 2.03 (95% CI 1.60-2.59) for the male cohort. Factors assessed at baseline (1989) that were independently prognostic of total mortality included age, male sex, pre-existing coronary artery disease (CAD) (HR 2.2, 95% CI 1.5-3.3) and plasma cholesterol (HR for 1.4 mmol l(-1) change: 1.49, 95% CI 1.2-1.9). HDL-cholesterol was protective in women (HR for 0.4 mmol l(-1) change: 0.72, 95% CI 0.51-1.00) but not men. Glycated haemoglobin was not a significant predictor of total mortality. Predictors of CAD mortality (in those subjects free of CAD in 1989) included plasma cholesterol (HR for 1.4 mmol l(-1) change: 1.86 95% CI 1.20-2.89), glycated haemoglobin (HR for 1.8% change: 1.9 95% CI 1.04-3.47), male sex, peripheral vascular disease, and smoking. There is therefore increased mortality in Type 2 diabetic subjects in Canterbury, New Zealand. HDL-cholesterol is protective against total mortality in females.

Sorbitol 2.5% mannitol 0.54% irrigation solution for hysteroscopic endometrial ablation surgery.

PURPOSE: To determine if systemic absorption of sorbitol 2.5%/mannitol 0.54% irrigation solution (165 mosm.L-1) during hysteroscopic endometrial ablation with diathermy is associated with hyponatraemia and hypoosmolality. METHODS: In 35 day surgery patients in a university hospital we measured baseline preoperative variables: serum sodium and creatinine concentrations and osmolality, haematocrit, haemoglobin, urine osmolality and sodium concentration, and weight. Fractional excretion of sodium (FENa) was calculated. The same observations were obtained postoperatively before discharge (one hour post resection). Volumes of intraoperative fluid irrigation intravasation and perioperative intravenous fluid absorption (lactated Ringer's solution) were estimated clinically (volumetric). RESULTS: The mean (+/-SD) serum sodium concentration preoperatively was 140.3 +/- 2.4 mmol.L-1; and postoperatively, 139.7 +/- 2.2 mmol.L-1 (P = NS). The serum osmolality decreased from 285.4 +/- 4.5 to 282.6 +/- 4.1 mmol.kg-1 (P < 0.001). The mean volume of intravasated irrigation fluid was 26.4 ml (range 0-300). During the same time, the FENa increased from 0.57% to 0.79% (P < 0.001). CONCLUSION: In these patients, closely and continuously observed for imbalance between infused and collected irrigation fluid, these was no clinical evidence for hyponatraemic hypoosmolality. However, there was a small 1% +/- 1.5% (mean +/- SD; range -3.4 to 3.6%) decrease in plasma osmolality despite adequate blood volumes as shown by urinary sodium indices.

Sudden death following cesarean section for placenta previa and accreta.

A case of disseminated intravascular coagulation (DIC) in a young woman after cesarean section for placenta previa and accreta is presented. Evidence of extensive pulmonary embolization by trophoblastic tissue, together with microthrombi in the cerebral and pulmonary blood vessels, is found at autopsy. Awareness of this syndrome and prompt action are necessary to prevent tragic consequences.