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Critical Care (London, England) Apr 2013The duration of red blood cell (RBC) storage before transfusion may alter RBC function and supernatant and, therefore, influence the incidence of complications or even... (Review)
Review
INTRODUCTION
The duration of red blood cell (RBC) storage before transfusion may alter RBC function and supernatant and, therefore, influence the incidence of complications or even mortality.
METHODS
A MEDLINE search from 1983 to December 2012 was performed to identify studies reporting age of transfused RBCs and mortality or morbidity in adult patients.
RESULTS
Fifty-five studies were identified; most were single-center (93%) and retrospective (64%), with only a few, small randomized studies (eight studies, 14.5%). The numbers of subjects included ranged from eight to 364,037. Morbidity outcomes included hospital and intensive care unit (ICU) length of stay (LOS), infections, multiple organ failure, microcirculatory alterations, cancer recurrence, thrombosis, bleeding, vasospasm after subarachnoid hemorrhage, and cognitive dysfunction. Overall, half of the studies showed no deleterious effects of aged compared to fresh blood on any endpoint. Eleven of twenty-two (50%) studies reported no increased mortality, three of nine (33%) showed no increased LOS with older RBCs and eight of twelve (66%) studies showed no increased risks of organ failure. Ten of eighteen (55%) studies showed increased infections with transfusion of older RBCs. The considerable heterogeneity among studies and numerous methodological flaws precluded a formal meta-analysis.
CONCLUSIONS
In this systematic review, we could find no definitive argument to support the superiority of fresh over older RBCs for transfusion.
Topics: Blood Preservation; Erythrocyte Transfusion; Humans; Length of Stay; Microcirculation; Retrospective Studies; Time Factors; Treatment Outcome
PubMed: 23566599
DOI: 10.1186/cc12600 -
Critical Care (London, England) Oct 2012The previous meta-analysis on the use of endothelin-receptor antagonists (ETRAs) to treat aneurysmal subarachnoid hemorrhage (SAH) has become outdated due to recently... (Meta-Analysis)
Meta-Analysis Review
INTRODUCTION
The previous meta-analysis on the use of endothelin-receptor antagonists (ETRAs) to treat aneurysmal subarachnoid hemorrhage (SAH) has become outdated due to recently published phase 3 clinical trials. An up-to-date meta-analysis is needed to provide the best available evidence for the efficacy of ETRAs for aneurysmal SAH.
METHODS
We performed a systematic review and meta-analysis of published randomized controlled trials that investigate efficacy of ETRAs in patients with aneurysmal SAH. Mortality, unfavorable outcome, delayed ischemic neurological deficit (DIND), delayed cerebral infarction (DCI), angiographic vasospasm and adverse events were analyzed. Meta-analysis was performed in terms of the risk ratio (RR) and 95% confidence interval (CI).
RESULTS
Five eligible studies were reviewed and analyzed, involving 2,595 patients. The pooled RRs of mortality and unfavorable outcome after SAH were 1.03 (95% CI = 0.77 to 1.36) and 1.07 (95% CI = 0.93 to 1.22), respectively. The pooled RRs were 0.87 (95% CI = 0.74 to 1.03) for DCI, 0.77 (95% CI = 0.66 to 0.90) for DIND, and 0.66 (95% CI = 0.57 to 0.77) for angiographic vasospasm. There were significant increases in lung complications (RR = 1.80, 95% CI = 1.55 to 2.09), hypotension (RR = 2.42, 95% CI = 1.78 to 3.29) and anemia (RR = 1.47, 95% CI = 1.19 to 1.83) in patients administered ETRAs.
CONCLUSION
There is no evidence that ETRAs could benefit clinical outcome in patients with SAH. Owing to the increased adverse events, further clinical trials of ETRAs in SAH patients should be more carefully formulated and designed. The present results also suggest that DCI may be a better outcome measure than vasospasm and DIND in SAH clinical trials and observational studies.
Topics: Endothelin Receptor Antagonists; Humans; Intracranial Aneurysm; Randomized Controlled Trials as Topic; Subarachnoid Hemorrhage
PubMed: 23078672
DOI: 10.1186/cc11686 -
Journal of Cerebral Blood Flow and... Sep 2012Animal models have been developed to simulate angiographic vasospasm secondary to subarachnoid hemorrhage (SAH) and to test pharmacologic treatments. Our aim was to... (Meta-Analysis)
Meta-Analysis Review
Animal models have been developed to simulate angiographic vasospasm secondary to subarachnoid hemorrhage (SAH) and to test pharmacologic treatments. Our aim was to evaluate the effect of pharmacologic treatments that have been tested in humans and in preclinical studies to determine if animal models inform results reported in humans. A systematic review and meta-analysis of SAH studies was performed. We investigated predictors of translation from animals to humans with multivariate logistic regression. Pharmacologic reduction of vasospasm was effective in mice, rats, rabbits, dogs, nonhuman primates (standard mean difference of -1.74; 95% confidence interval -2.04 to -1.44) and humans. Animal studies were generally of poor methodologic quality and there was evidence of publication bias. Subgroup analysis by drug and species showed that statins, tissue plasminogen activator, erythropoietin, endothelin receptor antagonists, calcium channel antagonists, fasudil, and tirilazad were effective whereas magnesium was not. Only evaluation of vasospasm >3 days after SAH was independently associated with successful translation. We conclude that reduction of vasospasm is effective in animals and humans and that evaluation of vasospasm >3 days after SAH may be preferable for preclinical models.
Topics: Animals; Cerebral Angiography; Data Interpretation, Statistical; Disease Models, Animal; Dogs; Female; Humans; Macaca; Male; Mice; Publication Bias; Rabbits; Randomized Controlled Trials as Topic; Rats; Species Specificity; Subarachnoid Hemorrhage; Treatment Outcome; Vasospasm, Intracranial
PubMed: 22534672
DOI: 10.1038/jcbfm.2012.57 -
Journal of Cerebral Blood Flow and... Jul 2011Despite an undisputed association between vasospasm and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage (SAH), there is debate if this association... (Meta-Analysis)
Meta-Analysis Review
Despite an undisputed association between vasospasm and delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage (SAH), there is debate if this association implies causality. It has been suggested that cerebral infarction is a better outcome measure than vasospasm in clinical trials and observational studies. To further investigate the relationship between infarction and outcome, we performed a systematic review and meta-analysis of all randomized, double-blind, placebo-controlled trials that studied the efficacy of pharmaceutical preventive strategies in SAH patients, and had both cerebral infarction and clinical outcome as outcome events. Effect sizes were expressed in (pooled) risk ratio (RR) estimates with corresponding 95% confidence intervals (CIs). Sensitivity analyses were performed for studies with a low risk of bias and for those who reported outcome at 3 months after SAH. Twenty-four studies including 8,552 patients were included. Pharmaceutical treatments decreased the incidence of both cerebral infarction (RR: 0.83; 95% CI: 0.74 to 0.93) and of poor functional outcome (RR: 0.92; 95% CI: 0.86 to 0.98). The sensitivity analyses did not change the results essentially. These data suggest that the previously observed association between cerebral infarction and functional outcome implies causality, and that cerebral infarction is a better outcome measure than vasospasm in clinical trials and observational studies.
Topics: Cerebral Infarction; Humans; Incidence; Randomized Controlled Trials as Topic; Subarachnoid Hemorrhage
PubMed: 21505477
DOI: 10.1038/jcbfm.2011.56 -
BMJ Clinical Evidence Mar 2011Raynaud's phenomenon is an episodic vasospasm of the peripheral arteries, causing pallor, followed by cyanosis and redness with pain, and sometimes paraesthesia. On rare... (Review)
Review
INTRODUCTION
Raynaud's phenomenon is an episodic vasospasm of the peripheral arteries, causing pallor, followed by cyanosis and redness with pain, and sometimes paraesthesia. On rare occasions it can lead to ulceration of the fingers and toes (and in some cases of the ears or nose). This review focuses on primary (idiopathic) Raynaud's phenomenon, occurring in the absence of an underlying disease. The prevalence of primary Raynaud's phenomenon varies by sex, country, and exposure to workplace vibration.
METHODS AND OUTCOMES
We conducted a systematic review and aimed to answer the following clinical question: What are the effects of treatments for primary Raynaud's phenomenon? We searched: Medline, Embase, The Cochrane Library, and other important databases up to May 2010 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).
RESULTS
We found 16 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.
CONCLUSIONS
In this systematic review we present information relating to the effectiveness and safety of the following interventions: amlodipine, diltiazem, exercise, inositol nicotinate, keeping warm, moxisylyte (thymoxamine), naftidrofuryl oxalate, nicardipine, nifedipine, prazosin, and smoking cessation.
Topics: Administration, Oral; Humans; Nifedipine; Prevalence; Raynaud Disease; Ulcer; Vibration
PubMed: 21401971
DOI: No ID Found -
Journal of Cerebral Blood Flow and... Jun 2011As it is often assumed that delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) is caused by vasospasm, clinical trials often focus on prevention of... (Meta-Analysis)
Meta-Analysis Review
Effect of pharmaceutical treatment on vasospasm, delayed cerebral ischemia, and clinical outcome in patients with aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis.
As it is often assumed that delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) is caused by vasospasm, clinical trials often focus on prevention of vasospasm with the aim to improve clinical outcome. However, the role of vasospasm in the pathogenesis of DCI and clinical outcome is possibly smaller than previously assumed. We performed a systematic review and meta-analysis on all randomized, double-blind, placebo-controlled trials that studied the effect of pharmaceutical preventive strategies on vasospasm, DCI, and clinical outcome in SAH patients to further investigate the relationship between vasospasm and clinical outcome. Effect sizes were expressed in pooled risk ratio (RR) estimates with corresponding 95% confidence intervals (CI). A total of 14 studies randomizing 4,235 patients were included. Despite a reduction of vasospasm (RR 0.80 (95% CI 0.70 to 0.92)), no statistically significant effect on poor outcome was observed (RR 0.93 (95% CI 0.85 to 1.03)). The variety of DCI definitions did not justify pooling the DCI data. We conclude that pharmaceutical treatments have significantly decreased the incidence of vasospasm, but not of poor clinical outcome. This dissociation between vasospasm and clinical outcome could result from methodological problems, sample size, insensitivity of clinical outcome measures, or from mechanisms other than vasospasm that also contribute to poor outcome.
Topics: Brain Ischemia; Humans; Randomized Controlled Trials as Topic; Subarachnoid Hemorrhage; Treatment Outcome; Vasospasm, Intracranial
PubMed: 21285966
DOI: 10.1038/jcbfm.2011.7 -
Expert Review of Cardiovascular Therapy Oct 2010Reversible cerebral vasoconstriction syndrome (RCVS) is a cerebrovascular disorder associated with multifocal arterial constriction and dilation. RCVS is associated with... (Review)
Review
Reversible cerebral vasoconstriction syndrome (RCVS) is a cerebrovascular disorder associated with multifocal arterial constriction and dilation. RCVS is associated with nonaneurysmal subarachnoid hemorrhage, pregnancy and exposure to certain drugs. The primary clinical manifestation is recurrent sudden-onset and severe (‘thunderclap’) headaches over 1–3 weeks, often accompanied by nausea, vomiting, photophobia, confusion and blurred vision. The primary diagnostic dilemma is distinguishing RCVS from primary CNS arteritis. Diagnosis requires demonstration of the characteristic ‘string of beads’ on cerebral angiography with resolution within 1–3 months, although many patients will initially have normal vascular imaging. Many treatments have been reported to ameliorate the headaches of RCVS, but it is unclear whether they prevent hemorrhagic or ischemic complications.
Topics: Arteritis; Cerebral Angiography; Cerebral Arterial Diseases; Diagnosis, Differential; Female; Headache Disorders, Primary; Humans; Pregnancy; Syndrome; Time Factors; Vasoconstriction; Vasospasm, Intracranial
PubMed: 20936928
DOI: 10.1586/erc.10.124 -
Neurology May 2010Treatment of aneurysmal subarachnoid hemorrhage (SAH) has changed substantially over the last 25 years but there is a lack of reliable population-based data on whether... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Treatment of aneurysmal subarachnoid hemorrhage (SAH) has changed substantially over the last 25 years but there is a lack of reliable population-based data on whether case-fatality or functional outcomes have improved.
METHODS
We determined changes in the standardized incidence and outcome of SAH in the same population between 1981 and 1986 (Oxford Community Stroke Project) and 2002 and 2008 (Oxford Vascular Study). In a meta-analysis with other population-based studies, we used linear regression to determine time trends in outcome.
RESULTS
There were no reductions in incidence of SAH (RR = 0.79, 95% confidence interval [CI] 0.48-1.29, p = 0.34) and in 30-day case-fatality (RR = 0.67, 95% CI 0.39-1.13, p = 0.14) in the Oxford Vascular Study vs Oxford Community Stroke Project, but there was a decrease in overall mortality (RR = 0.47, 0.23-0.97, p = 0.04). Following adjustment for age and baseline SAH severity, patients surviving to hospital had reduced risk of death or dependency (modified Rankin score > 3) at 12 months in the Oxford Vascular Study (RR = 0.51, 0.29-0.88, p = 0.01). Among 32 studies covering 39 study periods from 1980 to 2005, 7 studied time trends within single populations. Unadjusted case-fatality fell by 0.9% per annum (0.3-1.5, p = 0.007) in a meta-analysis of data from all studies, and by 0.9% per annum (0.2-1.6%, p = 0.01) within the 7 population studies.
CONCLUSION
Mortality due to subarachnoid hemorrhage fell by about 50% in our study population over the last 2 decades, due mainly to improved outcomes in cases surviving to reach hospital. This improvement is consistent with a significant decrease in case-fatality over the last 25 years in our pooled analysis of other similar population-based studies.
Topics: Cohort Studies; Diagnostic Imaging; Embolization, Therapeutic; Emergency Medical Services; Intraoperative Complications; Outcome Assessment, Health Care; Risk Factors; Subarachnoid Hemorrhage; Survival Rate; Treatment Outcome; United Kingdom; Vascular Surgical Procedures; Vasospasm, Intracranial
PubMed: 20375310
DOI: 10.1212/WNL.0b013e3181dd42b3 -
Journal of Cerebral Blood Flow and... Apr 2010Despite extensive effort to elucidate the cellular and molecular bases for delayed cerebral injury after aneurysmal subarachnoid hemorrhage (aSAH), the pathophysiology... (Review)
Review
Despite extensive effort to elucidate the cellular and molecular bases for delayed cerebral injury after aneurysmal subarachnoid hemorrhage (aSAH), the pathophysiology of these events remains poorly understood. Recently, much work has focused on evaluating the genetic underpinnings of various diseases in an effort to delineate the contribution of specific molecular pathways as well as to uncover novel mechanisms. The majority of subarachnoid hemorrhage genetic research has focused on gene expression and linkage studies of these markers as they relate to the development of intracranial aneurysms and their subsequent rupture. Far less work has centered on the genetic determinants of cerebral vasospasm, the predisposition to delayed cerebral injury, and the determinants of ensuing functional outcome after aSAH. The suspected genes are diverse and encompass multiple functional systems including fibrinolysis, inflammation, vascular reactivity, and neuronal repair. To this end, we present a systematic review of 21 studies suggesting a genetic basis for clinical outcome after aSAH, with a special emphasis on the pathogenesis of cerebral vasospasm and delayed cerebral ischemia. In addition, we highlight potential pitfalls in the interpretation of genetic association studies, and call for uniformity of design of larger multicenter studies in the future.
Topics: Brain; Brain Ischemia; Genetic Association Studies; Humans; Subarachnoid Hemorrhage; Treatment Outcome; Vasospasm, Intracranial
PubMed: 20068580
DOI: 10.1038/jcbfm.2009.278 -
Neuropsychopharmacologia Hungarica : a... Mar 2009Annually about 50,000 patients are hospitalized for acute stroke in Hungary. Of all stroke cases 85% are ischemic, and 15% are hemorrhagic (intracerebral or... (Review)
Review
Annually about 50,000 patients are hospitalized for acute stroke in Hungary. Of all stroke cases 85% are ischemic, and 15% are hemorrhagic (intracerebral or subarachnoid). In acute ischemic stroke the only registered causal treatment with proven efficacy is thrombolysis with intravenous administration of recombinant tissue plasminogen activator with a 3-hour time window. The indication areas of intraarterial thrombolysis are currently being established for selected cases in selected centers. Other studies examine the options to extend the time window and to test new thrombolytic agents. Despite the large number of studies none of the neuroprotectant agents have been found beneficial in randomized controlled clinical trials in acute stroke. According to the results of studies to date anticoagulant therapy (heparin) cannot be recommended for the routine treatment of acute stroke. Aspirin may be safely administered within 48 hours of ischemic stroke and results in a 1% decrease of death or disability at 6 months after stroke. There were no large studies on the use of other antiplatelet agents in acute stroke. If thrombolysis is performed, antiplatelet or anticoagulant agents should not be administered in the first 24 hours. Further studies are needed to test the efficacy and safety of anticoagulants in special cases of stroke (e.g. crescendo TIA-s, progressing stroke), and to test combined antiplatelet treatment in the acute phase of stroke. In acute intracerebral hemorrhage the beneficial effect of recombinant coagulation factor VII found in a small study could not be proved in a large phase III trial. Currently there is no evidence based pharmacotherapy for the specific treatment of intracerebral hemorrhage. In subarachnoid hemorrhage nimodipine was found effective in preventing vasospasm and thus secondary ischemic cerebral damage. Although the results of individual trials are conflicting, a systematic review on the effects of statins suggests a similar effect. Due to the limited options of evidence based treatments of acute stroke primary prevention has utmost importance.
Topics: Acute Disease; Aspirin; Brain Ischemia; Cerebral Hemorrhage; Fibrinolytic Agents; Humans; Hungary; Nimodipine; Primary Prevention; Secondary Prevention; Stroke; Thrombolytic Therapy; Time Factors; Tissue Plasminogen Activator; Vasodilator Agents
PubMed: 19731813
DOI: No ID Found