GP strategies to avoid imaging overuse. A qualitative study in Norwegian general practice

ObjectivesThe aim of the study was to identify general practitioners’ (GPs) strategies to avoid unnecessary diagnostic imaging when encountering patients with such expectations and to explore how patients experience these strategies.Design, setting and subjectsWe conducted a qualitative study that combined observations of consultations and interviews with GPs and patients. A total of 24 patients visiting nine different GPs in two Norwegian urban areas were included in the study. Of these, 12 consultations were considered suitable for studying GP strategies and were therefore selected for a more thorough analysis.Main outcome measuresGPs’ communication strategies to avoid unnecessary medical imaging and patients’ experiences with such strategies.ResultsFive categories of strategies were identified: (1) wait and see – or suggest an alternative; (2) the art of rejection; (3) seek support from a professional authority; (4) partnership and shared decision-making and (5) reassurance, normalisation and recognition. The GPs often used multiple strategies. Factors related to a long-term doctor–patient relationship seemed to influence both communication and how both parties experienced the decision. Three important factors were evident: the patient trusted the doctor, the doctor knew the patient’s medical history and the doctor knew the patient as a person. The patients seemed to be generally satisfied with the outcomes of the consultations.ConclusionGPs largely combine different strategies when meeting patients’ expectations of diagnostic imaging that are not strictly medically indicated. Continuity of the doctor–patient relationship with good personal knowledge and trust between doctor and patient appeared crucial for patients to accept the doctors'' decisions.

Key points

• GPs usually combine a broad range of strategies to avoid unnecessary medical imaging
• The patients appeared generally satisfied regardless of the strategy the strategy used by the GPs and even where their referral request were rejected
• Factors related to a long-term doctor–patient relationship appeared decisive

     

Preoperative Systemic Bone Quality Does Not Affect Tibial Component Migration in Knee Arthroplasty: A 2-Year Radiostereometric Analysis of a Hundred Consecutive Patients

BackgroundBone quality and other preoperative predictive factors may affect implant migration and the survival of knee arthroplasty.MethodsIn a prospective cohort of 100 consecutive patients (65 women) at a mean age of 67.7 years (range 39-87 years), we investigated preoperative predictors of postoperative tibial component migration in cemented and cementless total knee arthroplasties or cemented unicompartmental knee arthroplasty. Predictors consisted of Knee Injury and Osteoarthritis Outcome Score (KOOS) and Oxford Knee Score, questionnaires, bone turnover markers of CTX and P1NP, systemic bone mineral density (BMD), and knee osteoarthritis (OA) grade. Tibial component migration was measured with radiostereometry postoperative, at 1 and 2 years of follow-up.ResultsBetween 1 and 2 years, 19 tibial components migrated continuously (maximum total point motion [MTPM] > 0.2 mm). In general, there was no difference in age, body mass index, BMD, KOOSs, or OA grade between patients with continuous tibial migration compared to patients without continuous migration (P > .11). However, cementless tibial components with continuous migration had a lower KOOS pain score (more pain), lower vitamin D, and a higher bone turnover (CTX) value than patients without continuous migration. There was no association between the BMD and MTPM at 1-year follow-up regardless of prothesis type (P > .17). Patients with osteoporosis and normal BMD had similar mean tibial component MTPM at 2 years (3 prostheses combined; P = .34).ConclusionMigration of tibial components inserted with or without bone cement was not affected by the preoperative bone quality in terms of systemic BMD, bone turnover markers, and OA grade in the knee.     

Microglial cell population dynamics in the injured adult central nervous system

Reactive microgliosis is characteristic of trauma and stroke as well as inflammatory and chronic neurodegenerative disease. A conspicuous feature of the microglial reaction to acute neural injury is a massive expansion of the microglial cell population which peaks a few days following injury. New data based on the use of radiation bone marrow-chimeric mice suggest this expansion also involves recruitment of bone marrow-derived cells, which migrate into the neural parenchyma and differentiate into microglia. Here, we discuss the contribution of bone marrow-derived cells to the injury-induced expansion of the microglial cell population, seen in the dentate gyrus with ongoing anterograde axonal and terminal synaptic degeneration, subsequent to transection of the entorhino-dentate perforant path projection. In this paradigm of minor brain injury, the bone marrow-derived cells are grossly outnumbered by activated resident microglia, which express the stem cell antigen CD34 concurrent to a marked capacity for self-renewal. The observation of a mixed origin of lesion-reactive microglia, consisting of a smaller subpopulation of exogenous bone marrow-derived microglia, and a larger population of activated resident microglia, the majority of which express CD34 and undergo proliferation, suggests that lesion-reactive microglia consist of functionally distinct cell populations. The demonstration of an injury-enhanced recruitment of bone marrow-derived cells into the perforant path-denervated dentate gyrus, raises the possibility of using genetically manipulated cells as vectors for lesion-site-specific gene therapy even in minimally injured areas of the central nervous system.     

Stroke-Related Knowledge and Lifestyle Behavior among Stroke Survivors

Aims: Awareness of stroke symptoms and risk factors, and actions taken in order to reduce the risk of new stroke events, should be of great importance among stroke survivors. The aims of this study were to assess changes in stroke-related knowledge and lifestyle behavior among patients experiencing a cerebrovascular event, and to assess the agreement between the patients’ self-reported diagnosis, and the discharge diagnosis. Methods: All patients discharged with a diagnosis of stroke or transient ischemic attack during a 1-year period, received postal survey questionnaires at 3 and 12 months after discharge. The questionnaires included questions about symptom knowledge, lifestyle behavior, and patients were asked to report on their diagnosis. Results: A total of 282 patients were included (mean age 71.8 years, 57.1% men). Self-reported symptom knowledge was increased at 3 months (P < .001), and this persisted at 12 months. There was a poor correlation (r = .082; P = .171) between increasing symptom knowledge and stated lifestyle behavior changes. In all, 63% of the respondents correctly identified their own cerebrovascular subtype. Thirty-seven percent had quit smoking after 12 months, 30% reported that they used less sugary items, and 26% used less fatty food after the cerebrovascular event. Conclusions: Stroke survivors reported increased stroke symptoms knowledge after 3 and 12 months. A proportion of patients made changes in lifestyle behavior. Only 2 out of 3 patients correctly identified their own cerebrovascular subtype, indicating room for improvement in clinical practice when informing and communicating with stroke and transient ischemic attack patients about their diagnosis.     

Unrecognized viral infections and chromosome abnormalities as a cause of fetal death – examination with fluorescence in situ hybridization,immunohistochemistry and polymerase chain reaction

Fifteen to 50% of fetal deaths remain unexplained after post‐mortem examination depending on inclusion criteria and classification systems. Our aim was to examine a selection of unexplained fetal deaths in order to investigate whether any common chromosome aberrations or viral infections were present. Reports from 351 fetal autopsies performed at the Department of Pathology and Medical Genetics at St. Olavs University Hospital from 2001 through 2010 were reviewed. Of these, 105 fetal deaths were classified as unexplained. Tissue samples from 30 cases were further examined with fluorescence in situ hybridization (FISH) to detect abnormalities in chromosomes 13, 18, and 21. The samples were also examined with immunohistochemistry (IHC) and polymerase chain reaction (PCR) to detect infections with cytomegalovirus, parvovirus B19, herpes simplex virus 1 and 2, enterovirus, and parechovirus. In two cases, a possible trisomy 13 mosaicism was found. No viruses were detected. In our selection of 30 unexplained cases, possible trisomy 13 mosaicism was found in two cases, and no viruses were detected. High degree of maceration and missing placental examination often complicate the investigation of fetal death, and extensive ancillary examinations do not necessarily contribute to a more specific diagnosis.     

Hospitalised patients with suspected 2009 H1N1 Influenza A in a hospital in Norway,July - December 2009

Background  

The main objective of this study was to describe the patients who were hospitalised at Oslo University Hospital Aker during the first wave of pandemic Influenza A (H1N1) in Norway.     

Oral disorders,saliva secretion,and oral health‐related quality of life in patients with primary Sjögren's syndrome

Chemosensory function, burning sensations in the tongue (BST), halitosis, saliva secretion, and oral health‐related quality of life (OHRQoL) were investigated in patients with primary Sjögren's syndrome (pSS). In 31 patients with pSS and 33 controls, olfactory and gustatory functions were evaluated. Self‐reported complaints of dysgeusia, BST, and halitosis were recorded. Saliva secretion rates were measured and OHRQoL was assessed using the short‐form Oral Health Impact Profile (OHIP‐14). Patients had significantly lower olfactory (8.8 ± 3.5 vs. 10.7 ± 1.2) and gustatory (18.9 ± 7.1 vs. 25.4 ± 4.3) scores than controls, and significantly more patients complained of dysgeusia (58.1% vs. 0%), BST (54.8% vs. 6.1%), and halitosis (41.9% vs. 0%). A significantly greater proportion of patients with pSS had ageusia (19% vs. 0%), hypogeusia (32% vs. 12%), anosmia (13% vs. 0%), or hyposmia (29% vs. 9%). Significantly lower saliva secretion rates (ml min^?1) were observed in patients with pSS for stimulated (0.62 ± 0.40 vs. 1.57 ± 0.71) and unstimulated (0.08 ± 0.07 vs. 0.29 ± 0.17) saliva. The mean OHIP‐14 score was significantly higher in patients with pSS (16.2 ± 10.8 vs. 2.7 ± 3.1) and was positively correlated with dysgeusia, BST, and halitosis. In conclusion, patients with pSS reported higher occurrence of dysgeusia, BST, and halitosis, and demonstrated relatively impaired chemosensory and salivary functions. The patients’ poorer OHRQoL was associated with dysgeusia, BST, and halitosis.     

In vivo inhibition of etoposide-mediated apoptosis,toxicity, and antitumor effect by the topoisomerase II-uncoupling anthracycline aclarubicin

A number of clinically important drugs such as the epipodophyllotoxins etoposide (VP-16) and teniposide (VM-26), the anthracyclines daunorubicin and doxorubicin (Adriamycin), and the aminoacridine amsacrine exert their cytotoxic action by stabilizing the cleavable complex formed between DNA and the nuclear enzyme topoisomerase II. We have previously demonstrated in several in vitro assays that the anthracycline aclarubicin (aclacinomycin A) inhibits cleavable-complex formation and thus antagonizes the action of drugs such as VP-16 and daunorubicin. The present study was performed to validate these in vitro data in an in vivo model. At nontoxic doses of 6 and 9 mg/kg, aclarubicin yielded a marked increase in the survival of non-tumor-bearing mice given high doses of VP-16 (80–90 mg/kg) in six separate experiments. In therapy experiments on mice inoculated with Ehrlich ascites tumor cells, aclarubicin given at 6 mg/kg roughly halved the increase in median life span induced by VP-16 at doses ranging from 22 to 33 mg/kg. An attempt to determine a more favorable combination of VP-16 and aclarubicin by increasing VP-16 doses failed, as the two drugs were always less effective than VP-16 alone. The way in which VP-16-induced DNA strand breaks lead to cell death remains unknown. However, VP-16 has been reported to cause apoptosis (programmed cell death) in several cell lines. To ascertain whether the protection given by aclarubicin could have a disruptive effect on the apoptotic process, we used the small intestine as an in vivo model. Whereas VP-16-induced apoptosis in crypt stem cells was detectable at a dose as low as 1.25 mg/kg, aclarubicin given at up to 20 mg/kg did not cause apoptosis. Indeed, aclarubicin caused a statistically significant reduction in the number of cells rendered apoptotic by VP-16. The present study thus confirms the previous in vitro experiments and indicates the value of including an in vivo model in a preclinical evaluation of drug combinations.This work was supported by the Danish Cancer Society