Surgical Trial in Lobar Intracerebral Haemorrhage (STICH II) Protocol

<p>Abstract</p> <p>Background</p> <p>Within the spectrum of spontaneous intracerebral haemorrhage there are some patients with large or space occupying haemorrhage who require surgery for neurological deterioration and others with small haematomas who should be managed conservatively. There is equipoise about the management of patients between these two extremes. In particular there is some evidence that patients with lobar haematomas and no intraventricular haemorrhage might benefit from haematoma evacuation. The STICH II study will establish whether a policy of earlier surgical evacuation of the haematoma in selected patients will improve outcome compared to a policy of initial conservative treatment.</p> <p>Methods/Design</p> <p>an international multicentre randomised parallel group trial. Only patients for whom the treating neurosurgeon is in equipoise about the benefits of early craniotomy compared to initial conservative treatment are eligible. All patients must have a CT scan confirming spontaneous lobar intracerebral haemorrhage (≤1 cm from the cortex surface of the brain and 10-100 ml in volume). Any clotting or coagulation problems must be corrected and randomisation must take place within 48 hours of ictus. With 600 patients, the study will be able to demonstrate a 12% benefit from surgery (2p < 0.05) with 80% power.</p> <p>Stratified randomisation is undertaken using a central 24 hour randomisation service accessed by telephone or web. Patients randomised to early surgery should have the operation within 12 hours. Information about the status (Glasgow Coma Score and focal signs) of all patients through the first five days of their trial progress is also collected in addition to another CT scan at about five days (+/- 2 days). Outcome is measured at six months via a postal questionnaire to the patient. Primary outcome is death or severe disability defined using a prognosis based 8 point Glasgow Outcome Scale. Secondary outcomes include: Mortality, Rankin, Barthel, EuroQol, and Survival.</p> <p>Trial Registration</p> <p>ISRCTN: <a href="http://www.controlled-trials.com/ISRCTN22153967">ISRCTN22153967</a></p

Early intervention to promote oral feeding in patients with intracerebral hemorrhage: a retrospective cohort study

<p>Abstract</p> <p>Background</p> <p>Stroke is a major cause of dysphagia, but little is known about when and how dysphagic patients should be fed and treated after an acute stroke. The purpose of this study is to establish the feasibility, risks and clinical outcomes of early intensive oral care and a new speech and language therapist/nurse led structured policy for oral feeding in patients with an acute intracerebral hemorrhage (ICH).</p> <p>Methods</p> <p>A total of 219 patients with spontaneous ICH who were admitted to our institution from 2004 to 2007 were retrospectively analyzed. An early intervention program for oral feeding, which consisted of intensive oral care and early behavioral interventions, was introduced from April 2005 and fully operational by January 2006. Outcomes were compared between an early intervention group of 129 patients recruited after January 2006 and a historical control group of 90 patients recruited between January 2004 and March 2005. A logistic regression technique was used to adjust for baseline differences between the groups. To analyze time to attain oral feeding, the Kaplan-Meier method and Cox proportional hazard model were used.</p> <p>Results</p> <p>The proportion of patients who could tolerate oral feeding was significantly higher in the early intervention group compared with the control group (112/129 (86.8%) vs. 61/90 (67.8%); odds ratio 3.13, 95% CI, 1.59-6.15; P < 0.001). After adjusting for baseline imbalances, the odds ratio was 4.42 (95% CI, 1.81-10.8; P = 0.001). The incidence of chest infection was lower in the early intervention group compared with the control group (27/129 (20.9%) vs. 32/90 (35.6%); odds ratio 0.48, 95% CI, 0.26-0.88; P = 0.016). A log-rank test found a significant difference in nutritional supplementation-free survival between the two groups (hazard ratio 1.94, 95% CI, 1.46-2.71; P < 0.001).</p> <p>Conclusions</p> <p>Our data suggest that the techniques can be used safely and possibly with enough benefit to justify a randomized controlled trial. Further investigation is needed to solve the eating problems that are associated with patients recovering from a severe stroke.</p

Comparison of Mortality Following Hospitalisation for Isolated Head Injury in England and Wales, and Victoria, Australia

BACKGROUND: Traumatic brain injury (TBI) remains a leading cause of death and disability. The National Institute for Health and Clinical Excellence (NICE) guidelines recommend transfer of severe TBI cases to neurosurgical centres, irrespective of the need for neurosurgery. This observational study investigated the risk-adjusted mortality of isolated TBI admissions in England/Wales, and Victoria, Australia, and the impact of neurosurgical centre management on outcomes. METHODS: Isolated TBI admissions (>15 years, July 2005-June 2006) were extracted from the hospital discharge datasets for both jurisdictions. Severe isolated TBI (AIS severity >3) admissions were provided by the Trauma Audit and Research Network (TARN) and Victorian State Trauma Registry (VSTR) for England/Wales, and Victoria, respectively. Multivariable logistic regression was used to compare risk-adjusted mortality between jurisdictions. FINDINGS: Mortality was 12% (749/6256) in England/Wales and 9% (91/1048) in Victoria for isolated TBI admissions. Adjusted odds of death in England/Wales were higher compared to Victoria overall (OR 2.0, 95% CI: 1.6, 2.5), and for cases <65 years (OR 2.36, 95% CI: 1.51, 3.69). For severe TBI, mortality was 23% (133/575) for TARN and 20% (68/346) for VSTR, with 72% of TARN and 86% of VSTR cases managed at a neurosurgical centre. The adjusted mortality odds for severe TBI cases in TARN were higher compared to the VSTR (OR 1.45, 95% CI: 0.96, 2.19), but particularly for cases <65 years (OR 2.04, 95% CI: 1.07, 3.90). Neurosurgical centre management modified the effect overall (OR 1.12, 95% CI: 0.73, 1.74) and for cases <65 years (OR 1.53, 95% CI: 0.77, 3.03). CONCLUSION: The risk-adjusted odds of mortality for all isolated TBI admissions, and severe TBI cases, were higher in England/Wales when compared to Victoria. The lower percentage of cases managed at neurosurgical centres in England and Wales was an explanatory factor, supporting the changes made to the NICE guidelines

European research priorities for intracerebral haemorrhage

Over 2 million people are affected by intracerebral haemorrhage (ICH) worldwide every year, one third of them dying within 1 month, and many survivors being left with permanent disability. Unlike most other stroke types, the incidence, morbidity and mortality of ICH have not declined over time. No standardised diagnostic workup for the detection of the various underlying causes of ICH currently exists, and the evidence for medical or surgical therapeutic interventions remains limited. A dedicated European research programme for ICH is needed to identify ways to reduce the burden of ICH-related death and disability. The European Research Network on Intracerebral Haemorrhage EURONICH is a multidisciplinary academic research collaboration that has been established to define current research priorities and to conduct large clinical studies on all aspects of ICH. Copyright (C) 2011 S. Karger AG, Base

Systemic administration of urocortin after intracerebral hemorrhage reduces neurological deficits and neuroinflammation in rats

<p>Abstract</p> <p>Background</p> <p>Intracerebral hemorrhage (ICH) remains a serious clinical problem lacking effective treatment. Urocortin (UCN), a novel anti-inflammatory neuropeptide, protects injured cardiomyocytes and dopaminergic neurons. Our preliminary studies indicate UCN alleviates ICH-induced brain injury when administered intracerebroventricularly (ICV). The present study examines the therapeutic effect of UCN on ICH-induced neurological deficits and neuroinflammation when administered by the more convenient intraperitoneal (i.p.) route.</p> <p>Methods</p> <p>ICH was induced in male Sprague-Dawley rats by intrastriatal infusion of bacterial collagenase VII-S or autologous blood. UCN (2.5 or 25 μg/kg) was administered i.p. at 60 minutes post-ICH. Penetration of i.p. administered fluorescently labeled UCN into the striatum was examined by fluorescence microscopy. Neurological deficits were evaluated by modified neurological severity score (mNSS). Brain edema was assessed using the dry/wet method. Blood-brain barrier (BBB) disruption was assessed using the Evans blue assay. Hemorrhagic volume and lesion volume were assessed by Drabkin's method and morphometric assay, respectively. Pro-inflammatory cytokine (TNF-α, IL-1β, and IL-6) expression was evaluated by enzyme-linked immunosorbent assay (ELISA). Microglial activation and neuronal loss were evaluated by immunohistochemistry.</p> <p>Results</p> <p>Administration of UCN reduced neurological deficits from 1 to 7 days post-ICH. Surprisingly, although a higher dose (25 μg/kg, i.p.) also reduced the functional deficits associated with ICH, it is significantly less effective than the lower dose (2.5 μg/kg, i.p.). Beneficial results with the low dose of UCN included a reduction in neurological deficits from 1 to 7 days post-ICH, as well as a reduction in brain edema, BBB disruption, lesion volume, microglial activation and neuronal loss 3 days post-ICH, and suppression of TNF-α, IL-1β, and IL-6 production 1, 3 and 7 days post-ICH.</p> <p>Conclusion</p> <p>Systemic post-ICH treatment with UCN reduces striatal injury and neurological deficits, likely via suppression of microglial activation and inflammatory cytokine production. The low dose of UCN necessary and the clinically amenable peripheral route make UCN a potential candidate for development into a clinical treatment regimen.</p