A Study of Clinical Coding Accuracy in Surgery: Implications for the Use of Administrative Big Data for Outcomes Management.

BACKGROUND: Clinical coding is the translation of clinical activity into a coded language. Coded data drive hospital reimbursement and are used for audit and research, and benchmarking and outcomes management purposes. METHODS: We undertook a 2-center audit of coding accuracy across surgery. Clinician-auditor multidisciplinary teams reviewed the coding of 30,127 patients and assessed accuracy at primary and secondary diagnosis and procedure levels, morbidity level, complications assignment, and financial variance. Postaudit data of a randomly selected sample of 400 cases were reaudited by an independent team. RESULTS: At least 1 coding change occurred in 15,402 patients (51%). There were 3911 (13%) and 3620 (12%) changes to primary diagnoses and procedures, respectively. In 5183 (17%) patients, the Health Resource Grouping changed, resulting in income variance of £3,974,544 (+6.2%). The morbidity level changed in 2116 (7%) patients (P < 0.001). The number of assigned complications rose from 2597 (8.6%) to 2979 (9.9%) (P < 0.001). Reaudit resulted in further primary diagnosis and procedure changes in 8.7% and 4.8% of patients, respectively. CONCLUSIONS: The coded data are a key engine for knowledge-driven health care provision. They are used, increasingly at individual surgeon level, to benchmark performance. Surgical clinical coding is prone to subjectivity, variability, and error (SVE). Having a specialty-by-specialty understanding of the nature and clinical significance of informatics variability and adopting strategies to reduce it, are necessary to allow accurate assumptions and informed decisions to be made concerning the scope and clinical applicability of administrative data in surgical outcomes improvement.

Influence of in vitro microwave radiation on the fertilizing capacity of turkey sperm.

Turkey sperm were exposed to 2.45-GHz microwave radiation in a temperature-controlled wave-guide apparatus. Temperature was maintained at either 25 or 40.5 degrees C. The sperm were exposed for 30 min at a specific absorption rate (SAR) of 10 or 50 mW/g. Following irradiation, the sperm were used to inseminate virgin turkey hens artificially. During the 9 weeks following the single insemination, the following were assessed: mean number of eggs, percentage of fertile eggs, rate of decrease in egg fertility, percentage of hatched eggs, and percentage of early and late deaths. These data demonstrate that, for the conditions used in these experiments, microwave radiation has no effect on the fertilizing capacity of turkey sperm.

The effect of benzo(a)pyrene on fertility, primordial oocyte number, and ovarian response to pregnant mare's serum gonadotropin.

The polycyclic aromatic hydrocarbon (PAH) benzo(a)pyrene (BP) reduced the fertility of DBA/2N mice in a dose-dependent fashion. Control mice produced offspring at a rate of 0.91 pups/mouse per week. Treatment with BP at doses of 10, 100, 200, and 500 mg/kg decreased offspring production rates to 0.61, 0.20, zero and zero pups/mouse per week, respectively. BP also destroyed primordial oocytes in similarly treated mice. Treatment with BP at doses of 10, 50, 100, and 500 mg/kg destroyed 20%, 58%, 88%, and 100%, respectively, of the primordial oocytes in DBA/2N mouse ovaries. Dose-response curves for fertility reduction and primordial oocyte destruction were identical. The threshold for fertility reduction was 3.4 mg/kg and for primordial oocyte destruction it was 2.7 mg/kg. The 50% effect doses for fertility reduction and primordial oocyte destruction were 25.5 mg/kg and 24.5 mg/kg, respectively. Although BP reduced fertility and destroyed primordial oocytes, it had no effect on the ovarian weight response to pregnant mare's serum gonadotropin (PMSG), consistent with the observations that BP at these doses does not destroy growing or preovulatory oocytes or follicles. The similarity of the dose-response curves for fertility reduction and primordial oocyte destruction suggested that their mechanism of action is similar and resides within the ovary. As BP had no effect on ovarian response to PMSG, the effect was likely to reside outside the regulatory mechanisms controlling ovulation. These data suggest that the site of fertility reduction by BP may reside in the mechanisms of fertilization, implantation, or early conceptus development.