The authors assessed the consequences of delayed treatment for ulcer perforation with regard to short-term and long-term survival, complication rates, and length of hospital stay.
Important adverse effects of delayed treatment have not been studied previously. Conflicting results have been given with regard to short-term survival.
One thousand two hundred ninety-two patients operated on for perforated peptic ulcer in the Bergen area between 1935 and 1990 were studied. The effect of delay on postoperative lethality and complications adjusted for age, sex, ulcer site, and year of perforation was analyzed by stepwise logistic regression. The effect of delay on duration of hospital stay adjusted for potential confounding factors was analyzed by Cox proportional hazards regression. Observed survival was estimated by the Kaplan-Meier method, and expected survival was calculated from population mortality data.
Adverse effects increased markedly when delay exceeded 12 hours. Delay of more than 24 hours increased lethality sevenfold to eightfold, complication rate to threefold, and length of hospital stay to twofold, compared with delay of 6 hours or less. The reduced long-term survival for patients treated more than 12 hours after perforation could be attributed entirely to high postoperative mortality.
Delayed treatment after peptic ulcer perforation reduced survival, increased complication rates, and caused prolonged hospital stay. To improve outcome after ulcer perforation, an effort should be made to keep delay at less 12 hours, particularly in elderly patients.
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A twelve-year series of 375 patients with gastric carcinoma has been studied. Primary tumours were classified as intestinal type (58%) or diffuse (26%), whereas 16% were unclassifiable. The relative age and sex incidence rates of intestinal type and diffuse gastric carcinoma were estimated using the age and sex distribution of individuals in Norway as the basis for calculation. There was no difference in the rates of diffuse gastric carcinoma between the sexes. On the other hand, the rate of men with intestinal type carcinoma was more than twice as high as that of women. This difference was consistent within each age group from adolescence to senescence. The findings indicate that Laurén's two types of gastric carcinoma are aetiologically different. The rates of both types increased with age up to the 70-79 age group, whereas the rates in octogenarians tended to be lower than in septuagenarians. A comparison of our data with the data of incidence of gastric cancer in Norway indicates that some of the older patients do not come for surgery.
The occurrence of anencephalus as reported to the Norwegian Medical Birth Registry has fallen from 4.9 per 10,000 births in 1967-71 to 2.7 in 1987-90. The decrease is particularly noticeable for births with a gestational length of 28 weeks or more. On the other hand, there has been a significant increase in the number of cases of anencephalus with a gestational age less than 28 weeks. The occurrence of meningomyelocele has remained relatively stable throughout the same period. Ascertainment error could explain these contrasting trends, since cases of anencephalus detected on ultrasound screening may lead to early termination of pregnancy without notification to the Medical Birth Registry. Better routines for notification of malformations are needed to improve the basis for surveillance in Norway.
BACKGROUND: Studies evaluating safety of different birth settings for low-risk deliveries are often difficult to interpret because of great methodological problems. OBJECTIVE: To assess potential bias in comparisons of mortality between maternity institutions with different size and level of care, particularly when using various definitions of low-risk delivery and when studying stillbirth rates. DESIGN: Population-based study. POPULATION: The population of 1.74 million births in Norway from 1967 to 1996 recorded in The Medical Birth Registry of Norway. METHODS: First we explored the problems of properly identifying low-risk deliveries from population-based data and calculated adjusted perinatal mortality rates in sub-populations by excluding different risk factors. Then we measured the difference in apparent low-risk deliveries between institutions of different size and level of care. Finally we explored bias by using stillbirths and discuss the loss of statistical power by studying only livebirths. RESULTS: The occurrence of a whole spectrum of risk factors differed between small and large institutions, even after adjustment for birthweight. Although the majority of births were from low-risk deliveries, only 1/10th of all perinatal deaths occurred in this group after admission to a maternity unit. There was a systematic difference in the reporting of time of death for stillbirths between types of institutions; the rate of stillbirths occurring during delivery was higher among small institutions, while large institutions were more often uncertain in classifying time of death for stillbirths. CONCLUSIONS: Adjustments for a large number of different risk factors, large sample-sizes and caution in including stillbirth as outcome measure are needed when comparisons of safety between different sizes of delivery units are made for low-risk pregnancies.
Folic acid intake during pregnancy can reduce the risk of neural tube defects (NTDs) and perhaps also oral facial clefts. Maternal autoantibodies to folate receptors can impair folic acid binding. We explored the relationship of these birth defects to inhibition of folic acid binding to folate receptor a (FRa), as well as possible effects of parental demographics or prenatal exposures.
We conducted a nested case-control study within the Norwegian Mother and Child Cohort Study. The study included mothers of children with an NTD (n = 11), cleft lip with or without cleft palate (CL/P, n= 72), or cleft palate only (CPO, n= 27), and randomly selected mothers of controls (n = 221). The inhibition of folic acid binding to FRa was measured in maternal plasma collected around 17 weeks of gestation. On the basis of prior literature, the maternal age, gravidity, education, smoking, periconception folic acid supplement use and milk consumption were considered as potential confounding factors.
There was an increased risk of NTDs with increased binding inhibition [adjusted odds ratio (aOR) = 1.4, 95% confidence interval (CI) 1.0-1.8]. There was no increased risk of oral facial clefts from inhibited folic acid binding to FRa (CL/P aOR = 0.7, 95% CI 0.6-1.0; CPO aOR = 1.1, 95% CI 0.8-1.4). No association was seen between smoking, folate supplementation or other cofactors and inhibition of folic acid binding to FRa.
Inhibition of folic acid binding to FRa in maternal plasma collected during pregnancy was associated with increased risk of NTDs but not oral facial clefts.
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OBJECTIVE: To estimate the risk of adverse outcomes for newborns with a low Apgar score.Study design: Population-based cohort study. All 235,165 children born between 1983 and 1987 in Norway with a birth weight of at least 2500 g and no registered birth defects were followed up from birth to age 8 to 12 years by linkage of 3 national registries. Outcomes were death and cerebral palsy (CP). RESULTS: Five-minute Apgar scores of 0 to 3 were recorded for 0.1%, and scores of 4 to 6 were recorded for 0.6% of the children. Compared with children who had 5-minute Apgar scores of 7 to 10, children who had scores of 0 to 3 had a 386-fold increased risk for neonatal death (95% CI: 270-552) and an 81-fold (48-138) increased risk for CP. If Apgar scores at both 1 and 5 minutes were 0 to 3, the risks for neonatal death and CP were increased 642-fold (442-934) and 145-fold (85-248), respectively, compared with scores of 7 to 10. CONCLUSION: The strong association of low Apgar scores with death and CP in this population with a low occurrence of low scores shows that the Apgar score remains important for the early identification of infants at increased risk for serious and fatal conditions.
The study compares frequencies of birth defects between immigrant groups and the rest of the Norwegian population in Norway and estimates the influence of consanguinity and socioeconomic factors on these frequencies. The authors studied all 1.56 million births in Norway from 1967 to 1993. Of these, 7,494 children had two Pakistani parents, 84,688 had one Norwegian and one immigrant parent, and 25,891 had two immigrant parents from countries other than Pakistan. The risk of birth defects relative to the Norwegian group was 0.98 (95% confidence interval 0.92-1.03) in the group with one foreign and one Norwegian parent, 1.39 (95% confidence interval 1.22-1.60) in the group with two Pakistani parents, and 1.04 (95% confidence interval 0.95-1.14) in the group with two parents from other foreign countries; 0.1% of the Norwegian and 30.1% of the Pakistani children had parents who were first cousins. There was no difference in risk between children of nonconsanguineous Pakistani parents and the other groups. The relative risk of birth defects among children whose parents were first cousins was about 2 in all groups. Among the Pakistani, 28% of all birth defects could be attributed to consanguinity. Low paternal educational level was associated with a slightly increased risk in the Norwegian group, while independent effects of parental educational levels were not found in any other groups.
Erratum In: Am J Epidemiol 1997 May 15;145(10):957
In Norway, external doses of radiation resulting from fallout from the Chernobyl nuclear accident were estimated from detailed measurements, including soil deposition patterns. Internal doses were estimated from measurements of radioactive cesium in meat and milk supplies. The doses were calculated as average monthly doses for each of 454 municipalities during 36 consecutive months after the accident in spring 1986. Prospectively collected data on all newborns listed in the Medical Birth Registry of Norway who were conceived in the period May 1983-April 1989 were used to assess possible dose-response relations between estimated external and food-based exposures and congenital malformations and some other conditions. A positive association was observed between total radiation dose (external plus food-based) and hydrocephaly, while a negative association was observed for Down's syndrome. However, an important conclusion of the study was that no associations were found for conditions previously reported to be associated with radiation, i.e., small head circumference, congenital cataracts, anencephaly, spina bifida, and low birth weight. Potential sources of bias, including exposure misclassification and incomplete ascertainment of cases, are discussed.
OBJECTIVE: To assess the associations between birth weight or gestational age and risk of type 1 diabetes. DESIGN: Population based cohort study by record linkage of the medical birth registry and the National Childhood Diabetes Registry. Setting: Two national registries in Norway. PARTICIPANTS: All live births in Norway between 1974 and 1998 (1 382 602 individuals) contributed a maximum of 15 years of observation, a total of 8 184 994 person years of observation in the period 1989 to 1998. 1824 children with type 1 diabetes were diagnosed between 1989 and 1998. MAIN OUTCOME MEASURES: Estimates of rate ratios with 95% confidence intervals for type 1 diabetes from Poisson regression analyses. RESULTS: The incidence rate of type 1 diabetes increased almost linearly with birth weight. The rate ratio for children with birth weights 4500 g or more compared with those with birth weights less than 2000 g was 2.21 (95% confidence interval 1.24 to 3.94), test for trend P=0.0001. There was no significant association between gestational age and type 1 diabetes. The results persisted after adjustment for maternal diabetes and other potential confounders. CONCLUSION: There is a relatively weak but significant association between birth weight and increased risk of type 1 diabetes consistent over a wide range of birth weights.
BACKGROUND: Survival is lower in ulcer perforation patients than in the general population. This study assesses the causes of death in patients treated for peptic ulcer perforation. METHODS: Cause-specific mortality in a population-based cohort of 817 patients treated for ulcer perforation in western Norway during the period 1962-1990 was compared with cause-specific population death rates. Analyses were based on observed and expected mortality curves for major causes of death and on standardized mortality rates (SMRs). Cox regression models were used to analyse possible differences on the basis of sex, birth cohort, surgical procedure, and ulcer location. RESULTS: Ulcer perforation patients experienced increased mortality from neoplasms (SMR = 1.8; 95% confidence interval (CI) = 1.4-2.1), lung cancer (SMR = 3.6; 95% CI = 2.3-4.9), circulatory diseases (SMR = 1.3; 95% CI = 1.1-1.6), ischaemic heart disease (SMR = 1.3; 95% CI = 1.03-1.6), and respiratory diseases (SMR = 1.9; 95% CI = 1.3-2.6). Postoperative deaths accounted for 38% of all excess deaths. Death from recurrent peptic ulcer was increased also in subjects who survived the 1st year after the perforation (SMR = 5.8; 95% CI = 1.2-10.4) but accounted for only a few deaths. The increase in mortality from lung cancer was higher in subjects born after 1910 than in patients of older generations. Excess mortality from lung cancer and from circulatory diseases was higher in male than in female patients. CONCLUSIONS: Increased mortality in ulcer perforation patients could mainly be attributed to smoking-related diseases. This is indirect evidence that smoking may be an important aetiologic factor for ulcer perforation.