Background and purposeThere is very little information on the cost of different treatments for femoral neck fractures. We assessed whether total hospital and societal costs of treatment of elderly patients with displaced femoral neck fractures differ between patients operated with internal fixation or hemiarthroplasty.Methods222 patients (mean age 83 years, 165 women (74%)) who had been randomized to internal fixation or hemiarthroplasty were followed for 2 years. Resource use in hospital, rehabilitation, community-based care, and nursing home use were identified, quantified, evaluated, and analyzed.ResultsThe average cost per patient for the initial hospital stay was lower for patients in the internal fixation group than in the hemiarthroplasty group (€9,044 vs. €11,887, p < 0.01). When all hospital costs, i.e. rehabilitation, reoperations, and formal and informal contact with the hospital were included, the costs were similar (€21,709 for internal fixation vs. €19,976 for hemiarthroplasty). When all costs were included (hospital admissions, cost of nursing home, and community-based care), internal fixation was the most expensive treatment (€47,186 vs. €38,615 (p = 0.09)).InterpretationThe initial lower average cost per patient for internal fixation as treatment for a femoral neck fracture cannot be used as an argument in favor of this treatment, since the average cost per patient is more than outweighed by subsequent costs, mainly due to a higher reoperation rate after internal fixation.
Forty years ago I studied the heredity of the different subtypes of the red-andgreen blindness (Waaler 1927 a and b). I tested 9049 boys and 9072 girls in the age from 8 to 13 years in the common schools in Oslo, first with Ishihara's pseudoisochromatic tables, and afterwards those who read these tables with uncertainty or as colour-blinds with the anomaloscope. With this apparatus it is possible to divide the colour-blinds into subtypes: The deuteranomals (D1 will here indicate both the gene and the property), the protanomals (PI), the deuteranopes (Dp) and the protanopes (Pp). W e also have two more subtypes, the extreme deuteranomals and the extreme protanomals between the corresponding anomals and anopes. In my old work they were classed with the anomals.It was well known that the gene of colour blindness is located in the Xchromosome, and that the normal gene in females dominates over the gene for colour blindness. Mothers with colour-blind sons, but they themselves with normal colour sense, are therefore heterozygotes (conductors) and have only one gene for colour blindness to give to (half of) their sons. I found in my material 55 groups of two to four colour blind brothers, sons of such conductors, and in all of these groups the brothers belonged to the same subtype. I also had three groups of male cousins, 2 + 1 + 1, 2 +2 and 1 + 1, where the mothers were sisters, and a group of 2+1 second cousins (boys), where the mothers' fathers were brothers, also a boy and his mother's father. In all these cases the subtypes were the same in one family group. From these facts I could draw the conclusion that the four subtypes were inherited as distinct mutants,
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