ABSTRACT
Procedural coding in surgical discharge summaries is extremely important; as well as communicating to healthcare staff which procedures have been performed, it also provides information that is used by the hospital's coding department. The OPCS code (Office of Population, Censuses and Surveys Classification of Surgical Operations and Procedures) is used to generate the tariff that allows the hospital to be reimbursed for the procedure. We felt that the OPCS coding on discharge summaries was often incorrect within our breast and endocrine surgery department. A baseline measurement over two months demonstrated that 32% of operations had been incorrectly coded, resulting in an incorrect tariff being applied and an estimated loss to the Trust of £17,000. We developed a simple but specific OPCS coding table in collaboration with the clinical coding team and breast surgeons that summarised all operations performed within our department. This table was disseminated across the team, specifically to the junior doctors who most frequently complete the discharge summaries. Re-audit showed 100% of operations were accurately coded, demonstrating the effectiveness of the coding table. We suggest that specifically designed coding tables be introduced across each surgical department to ensure accurate OPCS codes are used to produce better quality surgical discharge summaries and to ensure correct reimbursement to the Trust.
ABSTRACT
Cyclo-oxygenase 2 (COX-2) is implicated in the regulation of aromatase transcription in malignant breast tissue and has been considered as a potential target for tissue specific aromatase suppression. We initiated a randomised controlled pre-surgical study of celecoxib versus no treatment in women with primary breast cancer to determine the effects of COX-2 inhibition on markers of biological response. Postmenopausal women (50-80 years of age) with stage I or II, primary breast cancer, were randomised 2:1 to receive 400 mg/day celecoxib or no treatment for 14 days prior to surgery. A core biopsy was obtained pre- and post-treatment. Paired baseline and endpoint biopsies were analysed for Ki67, apoptosis, COX-2, CD31, estrogen receptor (ER) and progesterone receptor (PgR). Comparisons between the treatment groups were conducted using the Mann-Whitney test with a two-sided 5% significance. Of the 25 patients treated, 23 had evaluable data and 19 (83%) were ER positive. Overall the geometric mean change in Ki67, the primary end point, relative to baseline in the celecoxib arm was -16.6% (P = 0.056). The change in the no-treatment group was -8.1% (P = 0.24). There was no statistically significant difference in the change between the two groups. Celecoxib did not significantly affect apoptosis, COX-2, ER or PgR expression. There is only modest evidence for a biological effect of celecoxib in primary breast cancer. However, the trend towards a reduction in Ki67 in ER-positive breast cancer warrants further investigations in a larger cohort of patients.
