Roberts H.,North Manchester General Hospital |
Carroll C.,Salford Royal Hospitals Foundation Trust
Transfusion Alternatives in Transfusion Medicine | Year: 2012
Intraoperative cell salvage (ICS) is widely used in many surgical specialties, but uptake in neurosurgery has been slow. Little direct evidence exists to support the use of ICS in neurosurgical procedures; however, studies suggest that ICS may be safe and cost-effective in intracranial surgery and spinal fusion. Nationwide ICS is used in less than 50% of neurosurgical centers often without clear local guidance. It is most commonly used in major spinal surgery and least often surgery for intracranial glioma or metastatic deposits. The major barriers to more widespread introduction of ICS appear to be concern about tumor dissemination in cases of malignancy, lack of trained staff to use the machinery and perceived lack of necessity. Some evidence suggests that when ICS is used in tumor resection surgery, meningioma (benign) cells are less likely to be detectable in salvaged blood than glioblastoma (malignant) cells but, in contrast to other surgical subspecialties, the use of leukocyte depletion filters to remove tumor cells has not been investigated and the impact of ICS usage on tumor recurrence and long-term survival rates is unknown. The unpredictable nature of blood loss in neurosurgery means that many units do not use ICS routinely even though hemorrhage is often rapid and substantial when it does occur. No nationally recognized guidelines currently exist to support the use of ICS specifically in neurosurgical procedures although the majority of UK neuroanesthetists feel that a standards document would be beneficial. © 2012 Medical Education Global Solutions.
McMahon C.J.,Salford Royal Hospitals Foundation Trust |
Hopkins S.,Salford Royal Hospitals Foundation Trust |
Vail A.,Salford Royal Hospitals Foundation Trust |
King A.T.,Salford Royal Hospitals Foundation Trust |
And 6 more authors.
Journal of NeuroInterventional Surgery | Year: 2013
Background The mechanism of development of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (SAH) is poorly understood. Inflammatory processes are implicated in the development of ischemic stroke and may also predispose to the development of DCI following SAH. The objective of this study was to test whether concentrations of circulating inflammatory markers (C-reactive protein (CRP), interleukin-6 (IL-6) and interleukin 1 receptor antagonist (IL-1Ra)) were predictive for DCI following SAH. Secondary analyses considered white cell count (WCC) and erythrocyte sedimentation rate (ESR). Methods This was a single-center case-control study nested within a prospective cohort. Plasma inflammatory markers were measured in patients up to 15 days after SAH (initial, peak, average, final and rate of change to final). Cases were defined as those developing DCI. Inflammatory markers were compared between cases and randomly selected matched controls. Results Among the 179 participants there were 46 cases of DCI (26%). In primary analyses the rate of change of IL-6 was associated with DCI (OR 2.3 (95% CI 1.1 to 5.0); p=0.03). The final value and rate of change of WCC were associated with DCI (OR 1.2 (95% CI 1.0 to 1.3) and OR 1.3 (95% CI 1.0 to 1.6), respectively). High values of ESR were associated with DCI (OR 2.4 (95% CI 1.3 to 4.6) initial; OR 2.3 (95% CI 1.3 to 4.2) average; OR 2.1 (95% CI 1.1 to 3.9) peak; and OR 2.0 (95% CI 1.2 to 3.3) final value). Conclusions Leucocytosis and change in IL-6 prior to DCI reflect impending cerebral ischemia. The timeindependent association of ESR with DCI after SAH may identify this as a risk factor. These data suggest that systemic inflammatory mechanisms may increase the susceptibility to the development of DCI after SAH.
Livingston M.,Walsall Manor Hospital |
Birch K.,Salford Royal Hospitals Foundation Trust |
Guy M.,Salford Royal Hospitals Foundation Trust |
Kane J.,Salford Royal Hospitals Foundation Trust |
And 2 more authors.
British Journal of Biomedical Science | Year: 2015
Tri-iodothyronine (T3) is a sensitive marker of endogenous hyperthyroidism. In levothyroxine (T4)-induced hyperthyroidism, there is no reason for T3 to be elevated, but this test is often requested in over-treated hypothyroid patients. This study investigated how informative T3 levels are in these patients. Our hypothesis is that T3 measurement would not add anything to the assessment of T4 over-replacement in primary hypothyroidism. Over a 15- week period, consecutive thyroid function test requests in patients on levothyroxine had T3 levels measured if thyroidstimulating hormone (TSH) was below the reference range (RR; <0.27 miu/L) and free T4 was within or above the RR (12-22 pmol/L). Those with fully suppressed TSH (<0.02 mu/L) and high free T4 (>27 pmol/L) were defined as being over-replaced, while those with low, but measurable TSH and a normal free T4 were defined as unlikely to be overreplaced (control group). Receiver operating characteristic (ROC) curve analysis was used to assess the discriminant power of T3 to detect over-replacement. Of the 542 patients examined, 33 were included in the over-replaced group and 236 patients in the control group. A total of 273 patients were excluded for not fulfilling the criteria for either of these groups. In the over-replaced group, none had a raised T3. The most discriminant T3 level, using ROC curve analysis, was 1.6 nmol/L (RR=1.3-2.6 nmol/L), with a corresponding sensitivity and specificity of 58% and 71%, respectively (P=0.16). T3 levels bear little relation to thyroid status in patients on levothyroxine replacement, and normal levels can be seen in over-replaced patients. Measurement of T3 in this situation is of doubtful clinical value. What's already known about this topic?: Thyroid function tests are the way that adequacy of levothyroxine replacement is determined. Where the test is available, T3 is often requested together with T4 and TSH by clinicians. The question is whether T3 measurement adds any further information. What does this article add?: The presented data supports the position that T3 measurement does not add anything to the interpretation of thyroid hormone levels in subjects with hypothyroidism on levothyroxine replacement therapy. Unnecessary testing could be avoided if this were more widely appreciated. In addition, over-replacement, with its attendant risks, would be more readily recognised and not wrongly excluded on the basis of a falsely reassuring normal T3 result.
Heald A.H.,Leighton Hospital |
Blantern E.,Leighton Hospital |
Anderson S.G.,University of Manchester |
Radford D.,Leighton Hospital |
And 6 more authors.
Experimental and Clinical Endocrinology and Diabetes | Year: 2012
Introduction: Prolactin circulates predominantly as a 23-kDa monomer, and a high-molecular-weight form largely consisting of a complex of prolactin and an anti-prolactin IgG autoantibody, called macroprolactin. This cross-reacts with conventional laboratory assays for prolactin. We here describe how quantitative adjustment for this may assist patient management. Methods: In a consecutive series of 218 patients with prolactin elevated to 400 mu/L or more in men (normal range180) (n=79, 36.2% of sample) and 1 000 mu/L or more in women (normal range500) (n=139, 63.8%) a macroprolactin screen was performed using PEG precipitation. Results: Where present, median macroprolactin as a proportion of total prolactin was in women 13% (percentile25-percentile75: 7-25%) and in men 15% (7-30%). The distribution of macroprolactin as a proportion of total prolactin was markedly skewed to the left with 69.7% of women and 62.9% of men having macroprolactin proportion of 20% or less. There was no relation between %macroprolactin and total measured prolactin, age or gender. Of relevance to clinical management, in 24% of men and 20.5% of women, correction for estimated macroprolactin gave an adjusted monomeric prolactin level below the agreed threshold for further investigation, potentially avoiding unnecessarily referral. In our clinical series, quotation of an adjusted monomeric prolactin would have resulted in unnecessary further investigation being avoided in a number of cases. Discussion: Screening for macroprolactin is a key element of laboratory assessment for hyperprolactinaemia. In cases where measured total prolactin is significantly raised, quantitative reporting of estimated monomeric prolactin instead of just macroprolactin positive' can avoid unnecessary investigations. © J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart New York.