Determining the rate of change in exposure to ionizing radiation from CT Scans: a database analysis from one hospital.

PURPOSE: Cancer risks associated with radiation from CT procedures have recently received increased attention. An important question is whether the combined impact of CT volume and dose reduction strategies has reduced radiation exposure to adult patients undergoing CT examinations. The aim of this study was to determine differences in radiation exposure from 2008 to 2012 to patients receiving CT scans of the abdomen, head, sinus, and lumbar spine at a midwestern academic medical center that implemented dose reduction strategies. METHODS: Data were collected from two internal data sets from 2008 to 2012 for general medicine and intensive care unit patients. These data were used to calculate annual CT volume, rate, average effective dose, radiation exposure, and estimated cancer risk. RESULTS: A 37% reduction in abdominal CT volume was found from 2008 to 2012. However, no volume reductions were found for CT examinations of the head or lumbar spine, and the decrease in sinus imaging was minimal. Dose reduction strategies resulted in 30% to 52% decreases in radiation exposure for the targeted body areas. The combined reduction in volume and dose per procedure reduced estimated induced cancers by 63%. CONCLUSIONS: Exposure to ionizing radiation from these examinations was reduced at one institution because of reduced volumes of procedures and the reduction of each procedure's effective dose through new protocols and technologies. Although both the volume reduction and dose reduction strategies contributed to the reduced exposure, it seems that investments in implementing the protocols and new technology had the greatest effect on future cancer risk.

Handoff practices in undergraduate medical education.

BACKGROUND: Growing data demonstrate that inaccuracies are prevalent in current handoff practices, and that these inaccuracies contribute to medical errors. In response, the Accreditation Council for Graduate Medical Education (ACGME) now requires residency programs to monitor and assess resident competence in handoff communication. Given these changes, undergraduate medical education programs must adapt to these patient safety concerns. OBJECTIVES: To obtain up-to-date information regarding educational practices for medical students, the authors conducted a national survey of Clerkship Directors in Internal Medicine (CDIM) members. DESIGN AND PARTICIPANTS: In June 2012, CDIM surveyed its institutional members, representing 121 of 143 Departments of Medicine in the U.S. and Canada. The section on handoffs included 12 questions designed to define the handoff education and practices of third year clerkship and fourth year sub-internship students. KEY RESULTS: Ninety-nine institutional CDIM members responded (82%). The minority (15%) reported a structured handoff curriculum provided during the internal medicine (IM) core clerkship, and only 37% reported a structured handoff curriculum during the IM sub-internship. Sixty-six percent stated that third year students do not perform handoff activities. However, most respondents (93%) reported that fourth year sub-internship students perform patient handoff activities. Only twenty-six (26%) institutional educators in CDIM believe their current handoff curriculum is adequate. CONCLUSIONS: Despite the growing literature linking poor handoffs to adverse events, few medical students are taught this competency during medical school. The common practice of allowing untrained sub-interns to perform handoffs as part of a required clerkship raises safety concerns. Evidence-based education programs are needed for handoff training.

Perillyl alcohol as a chemopreventive agent in N-nitrosomethylbenzylamine-induced rat esophageal tumorigenesis.

Perillyl alcohol (POH) is a monoterpene found in lavender, spearmint, and cherries. Phase I clinical trials with this agent have shown a favorable toxicity profile and preliminary data indicate some chemotherapeutic efficacy in advanced cancers. Animal studies have demonstrated the ability of POH to inhibit tumorigenesis in the mammary gland, liver, and pancreas. Although the precise mechanism of action is unclear, POH has been shown to inhibit the farnesylation of small G-proteins, including Ras, up-regulate the mannose-6-phosphate receptor, and induce apoptosis. Previous studies in our laboratory using the rat model of squamous cell carcinoma of the esophagus have shown that a specific Ha-ras codon 12 mutation is important for tumor promotion and progression. Given the limited toxicity of POH in humans, its proven efficacy in several animal models and its potential to inhibit Ha-ras farnesylation, we conducted an animal study to evaluate the efficacy of POH as a chemopreventive agent for squamous cell carcinoma of the esophagus. Male Fischer-344 rats were treated s.c. with 0.25 mg/kg b.w. of N-nitrosomethylbenzylamine three times a week for 5 weeks. Three days after the final carcinogen dose, they were started either on control diet or diets containing 0.5 or 1.0% POH. At 25 weeks, the animals were sacrificed, and esophageal tumors were counted. Animals fed either dose of POH showed a significant increase in dysplasia when compared with controls (P < 0.05) and a nonsignificant trend toward increased tumor multiplicity. Additionally, 1.0% POH did not affect Ras membrane localization. These data indicate that POH has a weakly promoting effect early in nitrosamine-induced esophageal tumorigenesis and suggest that POH may not be an effective chemopreventive agent for esophageal cancer in humans.

Piroxicam is an ineffective inhibitor of N-nitrosomethylbenzylamine-induced tumorigenesis in the rat esophagus.

Epidemiological studies indicate an association between the frequent use of nonsteroidal anti-inflammatory drugs and decreased risk for esophageal cancer. These studies suggest that limiting excess prostaglandin production, via inhibition of cyclooxygenase (COX)-mediated arachidonic acid metabolism, may be an important strategy for the prevention of this type of malignancy. N-Nitrosomethylbenzylamine (NMBA)-induced tumorigenesis in the rat esophagus is a model of human esophageal squamous cell carcinoma used for investigations of chemical carcinogenesis and for the evaluation of putative chemopreventive agents. In this study, we characterized COX-mediated arachidonic acid metabolism in NMBA-induced rat esophageal tumorigenesis by measuring COX-1 and COX-2 expression and prostaglandin E(2) production. In addition, we evaluated the ability of piroxicam, a potent COX inhibitor, to prevent postinitiation events of NMBA-induced tumorigenesis in the rat esophagus. After a 2-week acclimatization period, groups of 30 male F344 rats received s.c. injections of NMBA (0.5 mg/kg b.w.) three times/week for 5 weeks. Seventy-two h after the final NMBA treatment and for the remainder of the study, piroxicam was administered in the diet at 200 and 400 ppm. Twenty-five weeks after the initiation of NMBA treatment, we observed an elevation in COX mRNA and protein expression and prostaglandin E(2) production in NMBA-treated esophageal tissues compared with normal epithelium. However, these changes were associated with data indicating that a COX inhibitor is not preventive in NMBA-induced rat esophageal tumorigenesis. Administration of piroxicam in the diet produced no significant reductions in esophageal tumor incidence, multiplicity, or size. The reasons for the lack of effect are largely unknown but may be related to the inability of piroxicam to modulate other biochemical pathways involved in NMBA-induced tumorigenesis.