Psychiatry NCHD referrals to the local emergency department in the context of an in-house primary care service.

OBJECTIVES: Patients with psychiatric illness are at increased risk of developing non-psychiatric medical illnesses. There have been positive reports regarding the integration of primary care services into mental health facilities. Here, we evaluate the appropriateness of psychiatry non-consultant hospital doctors (NCHD) transfers to the local emergency department (ED) in the context of an in-house primary care service. METHODS: We reviewed the inpatient transfers from St Patrick's University Hospital (SPUH) to the local ED at St James' Hospital (SJH) from 1 January 2016 to 31 December 2017. We used inpatient admission to SJH as our primary marker of an appropriate transfer. RESULTS: 246 inpatients were transferred from SPUH to the SJH ED for medical review in the years 2016 and 2017. 27 (11%) of these were referred to the ED by the primary care service. 51% of those referred were admitted with similar rates of admission for both general practitioner (n = 27, 54% admitted) and NCHD initiated referrals (n = 219, 51% admitted). Acute neurological illness, concern regarding a cardiac illness, and deliberate self-harm were the most common reasons for referral. CONCLUSION: Our primary finding is that, of those transferred to ED by either primary care or a psychiatry NCHD, a similar proportion was judged to be in need of inpatient admission. This indicates that as a group, psychiatry NCHD assessment of acuity and need for transfer was similar to that of their colleagues in primary care.

ICSH recommendations for modified and alternate methods measuring the erythrocyte sedimentation rate.

INTRODUCTION: The gold standard for the determination of the erythrocyte sedimentation rate (ESR) is the Westergren method. Other methods to measure the ESR have become available. They range from modest modifications of the Westergren method to very different methodologies. The ICSH therefore established a Working Group to investigate these new approaches and compile recommendations for their validation and verification. METHODS: A panel of six experts in laboratory hematology examined the peer-reviewed literature and EQA surveys from over 6000 laboratories on four continents performing ESR testing. This information was used to create lists of ESR instrument manufacturers and their methods. RESULTS: Only 28% of laboratories surveyed used the unmodified Westergren method, while 72% of sites used modified or alternate methods. Results obtained with the new instruments could differ from results obtained with the Westergren method by up to 142%. Different non-Westergren methods showed differences from each other of up to 42%. The new methods were often significantly faster, safer, and less labor-intensive. They reduced costs and often used standard EDTA tubes, eliminating the need for a dedicated ESR tube. CONCLUSION: Based on the consensus of the Working Group, recommendations for manufacturers for the validation of new ESR methods were developed. In addition, a list of recommendations for laboratories that are moving to modified or alternate methods was compiled, addressing instrument performance verification and communications of results to clinical users.

Recommendation for standardization of haematology reporting units used in the extended blood count.

INTRODUCTION: It is desirable in the interest of patient safety that the reporting of laboratory results should be standardized where no valid reason for diversity exists. This study considers the reporting units used for the extended blood cell count and makes a new ICSH recommendation to encourage standardization worldwide. METHODS: This work is based on a literature review that included the original ICSH recommendations and on data gathered from an international survey of current practice completed by 18 countries worldwide. RESULTS: The survey results show that significant diversity in the use of reporting units for the blood count exists worldwide. The use of either non-SI or other units not recommended by the ICSH in the early 1980s has persisted despite the guidance from that time. CONCLUSION: The diversity in use of reporting units occurs in three areas: the persistence in use of non-SI units for RBC, WBC and platelet counts, the use of three different units for haemoglobin concentration and the manual reporting of WBC differential, reticulocytes and nucleated RBCs when the latter are available from automated analysis or can be expressed as absolute numbers by calculation. A new recommendation with a rationale for each parameter is made for standardization of the reporting units used for the extended blood count.

Standardization of haematology critical results management in adults: an International Council for Standardization in Haematology, ICSH, survey and recommendations.

INTRODUCTION: These recommendations are intended to develop a consensus in the previously published papers as to which parameters and what values should be considered critical. A practical guide on the standardization of critical results management in haematology laboratories would be beneficial as part of good laboratory and clinical practice and for use by laboratory-accrediting agencies. METHODS: A working group with members from Europe, America, Australasia and Asia was formed by International Council for Standardization in Haematology. A pattern of practice survey of 21 questions was distributed in 2014, and the data were collected electronically by Survey Monkey. The mode, or most commonly occurring value, was selected as the threshold for the upper and lower alert limits for critical results reporting. RESULTS: A total of 666 laboratories submitted data to this study and, of these, 499 submitted complete responses. Full blood count critical results alert thresholds, morphology findings that trigger critical result notification, critical results alert list, notification process and maintenance of critical results management protocol are described. This international survey provided a snapshot of the current practice worldwide and has identified the existence of considerable heterogeneity of critical results management. CONCLUSION: The recommendations in this study represent a consensus of good laboratory practice. They are intended to encourage the implementation of a standardized critical results management protocol in the laboratory.

Ossification of the anterior longitudinal ligament and Forestier's disease: an analysis of seven cases.

A retrospective review was conducted on the records and radiographs of six symptomatic patients and one asymptomatic patient with Forestier's disease. No other series of patients with this disease is found in the neurosurgical literature. Forestier's disease, also known as diffuse idiopathic skeletal hyperostosis (DISH), is an idiopathic rheumatological abnormality in which exuberant ossification occurs along ligaments throughout the body, but most notably the anterior longitudinal ligament of the spine. It affects older men predominantly; all of our patients were men older than 60 years of age. The disease is usually asymptomatic; however, dyspnea, dysphagia, spinal cord compression, and peripheral nerve entrapment have all been documented in association with the disorder. Five of the six symptomatic patients presented with dysphagia due to esophageal compression by calcified anterior longitudinal ligaments, and one patient developed recurrent spinal stenosis when scar tissue from a previous decompressive laminectomy became calcified. All patients responded well to surgery. Two of the four patients who underwent removal of cervical osteophytes required several months following surgery for the dysphagia to resolve. This would support the hypothesis that not all cases of dysphagia in Forestier's disease are due to mechanical compression. Dysphagia may result from inflammatory changes that accompany fibrosis in the wall of the esophagus or from esophageal denervation. Evaluation of dysphagia even in the presence of Forestier's disease must rule out occult malignancy. The authors' experience suggests that dysphagia in the setting of Forestier's disease is an underrecognized entity amenable to surgical intervention.

In vitro tooth color change with repeated bleaching.

The interest of patients in vital tooth bleaching has created a demand for treatment. However, few objective data are available to help determine the number of bleaching appointments necessary and the lightening that can be expected. The purpose of this study was to measure color changes in bleached extracted teeth and compare these to control groups. Group A was etched and bleached with 35% stabilized hydrogen peroxide. Group B was treated the same as group A, but the bleaching solution was replaced with distilled water. Group C was not treated, but was stored in water. Mean color difference after one treatment was 3.33 for group A, 1.67 for group B, and 0.48 for group C. After six treatments, the overall color difference was 3.82, 2.41, and 1.38 for groups A, B, and C, respectively (P less than .01). Color changes beyond those found after the first treatment were small, suggesting that there was little benefit in repeated bleachings under the conditions of this study.

Hepatic microvascular regulatory mechanisms. X. Effects of alpha-one or -two adrenoceptor blockade on glucoregulation in normotensive endotoxic rats with optimal perfusion and flowrates.

Circulating-blood glucose, hepatic glycogen distribution, and the glycogen contents of liver and skeletal muscle, were determined for 60 min in 31 fed and anesthetized Sprague-Dawley rats. These rats received an endoportal infusion of 15 mg per kg b.w. E. coli endotoxin (026:B6) or of sterile saline solution as a control. Either substance was given intravenously at 9:30 a.m. following an intraperitoneal injection at 9:00 a.m. of 0.1 mg per kg b.w. prazosin or 0.3 mg per kg b.w. yohimbine or of the carrier, distilled water. Infused endotoxin elevated blood glucose without affecting hepatic glycogen distribution and total glycogen contents of liver and skeletal muscle when compared to control. Prazosin inhibited endotoxin-induced hyperglycemia, and prazosin plus endotoxin provoked centrilobular glycogen depletion and decreased total hepatic glycogen content. However, no significant alteration in the glycogen content of skeletal muscle accompanied blockade of glucogenesis. Prazosin administered by itself produced no changes in hepatic and muscle glycogen. Although yohimbine blocked endotoxin-induced hyperglycemia, yohimbine, or yohimbine plus endotoxin, produced no significant change in the glycogen contents of liver and skeletal muscle. Blockade in the latter case was associated with some depletion of glycogen in hepatocytes dispersed randomly throughout the unit lobule and in cells located centrivenously. These results suggested that endotoxin-induced hyperglycemia is evoked by activation of alpha-1 and -2 adrenergic receptors. Since no detectible change in hepatic glycogen distribution and in the contents of liver and muscle glycogen accompanied glucogenesis, glycogen catabolism and deposition are postulated to proceed simultaneously and at equivalent rates by 60 min following the experimental induction of endotoxemia. Blockade of alpha (one or two) adrenoceptors is hypothesized to inhibit endotoxin-induced hyperglycemia by facilitating glucose utilization and not by stimulating glycogenesis or by antagonizing glycogenolysis in the liver or skeletal muscle.

Hepatic microvascular regulatory mechanisms. VIII. Glucogenic responses and morphologic changes following serotonin-induced low flow.

Changes in blood glucose, hepatic glycogen content and distribution, the number of hepatic mast cells, and hepatic morphology were assessed over 30 min in non-fasted and anesthetized Sprague-Dawley rats receiving endoportal or femoral intravenous injections of selected doses of serotonin and/or phentolamine, lodoxamide, or of Ringer's solution (control). Endoportal administration of low-flow producing doses of serotonin (1.0, 10.0, 20.0 micrograms per 100 g b.w.) elevated circulating blood glucose without decreasing hepatic glycogen content when compared to control in unit dry or wet weights. Hyperglycemia was accompanied by centrilobular glycogen depletion and apparent Kupffer cell activation. However, no change in hepatocyte or endothelial cell morphology or in the number of hepatic mast cells was observed following serotonin-induced low flow. The glucotropic response to a nonhypotensive dose of serotonin (1.0 microgram per 100 g b.w.) was modified by phentolamine (100 micrograms per 100 g b.w.) but not lodoxamide (0.1 microgram per 100 g b.w.). These blockers, when given alone, stimulated centrilobular glycogen depletion without producing a net change in blood glucose or hepatic glycogen content. By contrast, injection of serotonin (10.0 micrograms per 100 g b.w.) and/or phentolamine (100 micrograms per 100 g b.w.) into the femoral vein provoked no glucogenesis or systemic hypotension. Given these results, serotonin is suggested to stimulate hyperglycemia by activating alpha-adrenergic receptors. Since centrilobular glycogen depletion proceeds with no detectable change in total hepatic glycogen content, it is postulated that hepatic glycogen catabolism and deposition occur simultaneously and at equivalent rates during conditions of serotonin-induced hyperglycemia and low flow.