View clinical trials related to Hemorrhage.
Filter by:Cardiovascular disease (CVD) is an important public health problem that affects millions of people worldwide. Associations between risk factors, such as smoking, dyslipidaemia or hypertension, and prevalent CVD are well documented. However, few studies have investigated associations with onset of disease. The initial manifestation of CVD, for example an episode of unstable angina, is important because it influences the prognosis, the quality of life and the management of disease. Furthermore, the extent to which social deprivation, alcohol consumption or atrial fibrillation affects presentation of CVD is poorly understood and deserves further consideration. Most previous studies have considered CVD as a single entity. However, differences in aetiology between coronary phenotypes suggest that risk factors may not be shared across specific coronary phenotypes and their relative importance is likely to differ for each phenotype. Gaining knowledge of these differences could provide insights into the pathophysiology of specific forms of CVD and could eventually lead to modification of recommendations for patient management and disease prevention. We propose to use the linkage of the national registry of coronary events to general practice records in the Clinical Practice Research Database (CPRD), to investigate whether demographic, behavioral, and clinico-metabolic risk factors differentially influence the onset of specific types of CVD.
To assess the feasibility of a new neuromonitoring system (NeMoSystem including NeMo Probe and NeMo Patch) and the accuracy of the measurement values (cerebral blood flow (CBF); cerebral blood volume (CBV)) obtained.
Cardiac dysfunction can occur in aneurysmal subarachnoid haemorrhage and might impact patient's neurologic outcome Condition Aneurysmal subarachnoid haemorrhage World Neurosurgeon Federation Score ≥ III
To assess the feasibility of a new brain tissue probe for multi-parameter neuromonitoring (NeMo Probe) and the accuracy of measurement values. To demonstrate the ability of the NeMo probe to detect changes in cerebral hemodynamics and oxygenation during cerebrovascular events monitored with established methods including brain tissue oxygenation tension and microdialysis
Delayed cerebral vasospasm and secondary ischemic infarction are feared complications after aneurysmal subarachnoid hemorrhage (aSAH). To date, there is no effective therapy to prevent these ischemic complications. The arterial partial pressure of carbon dioxide (PaCO2) is one of the main determinants of cerebral blood flow (CBF) in healthy subjects. It is yet largely unknown, if and to what extent modulations of PaCO2 can influence CBF in patients after aSAH. The trial is a phase 1 study in which the feasibility of hypercapnia in SAH patients is tested. PaCO2 is gradually raised to 60 mmHg in 10 mechanically ventilated aSAH patients. Cerebral oxygen saturation measured by NIRS and CBF determined by an intracerebral thermodilution probe are the primary end points. If the feasibility is confirmed, this trial will be followed by a phase 2 dose finding study.
The purpose of this study is to determine the role of Proteomics and Metallomics in Cerebral Vasospasm following Subarachnoid Hemorrhage
The purpose of this study is to compare the profile of microRNA in cerebrospinal fluid from patients suffering subarachnoid hemorrhage with and without delayed cerebral ischemia.
This is a randomized, placebo-controlled, single-center clinical trial investigating the effectiveness of administrating intravenous Cerebrolysin™ (EVER NEURO Pharma, Austria), a preparation of low-molecular weight neurotrophic peptides and free amino acids, in improving the functional outcome of patients suffering from aneurysmal subarachnoid haemorrhage ( SAH). Cerebrolysin™ is a porcine-derived intravenous formulation composed of multiple lipid-soluble active agents that can cross the blood-brain barrier. It is a registered medication in several countries indicated for stroke and Alzheimer's disease. It contains several low molecular weight neuropeptides and free amino acids that possess neuroprotective and neurotrophic properties. It has been proven to arrest or mitigate several crucial steps along the ischemic cascade in preclinical studies. Cerebrolysin™ has been extensively investigated in patients suffering from Alzheimer's disease, brain trauma and ischemic stroke with promising clinical results. It's use in SAH patients has never been investigated and it is believed that it may play a role in improving clinical outcomes. Consecutive patients aged 18 to 70 years-old diagnosed to have spontaneous subarachnoid hemorrhage secondary to a ruptured intracranial aneurysm will be randomly allocated into one of two study arms: (1) to receive intravenous Cerebrolysin™ in additional to standard of care (intervention group) or (2) to receive usual standard of care alone (control group). Permuted-block randomization will be carried out once the eligibility criteria have been fulfilled using a computer system with an allocation list of random order. Instructions on study arm allocation will be contained in sealed envelopes labeled with sequential study numbers. Patients presenting beyond 96 hours after onset of symptoms or if recruitment and randomization cannot be performed within this time period will be excluded. The reason being that post-SAH arterial vasospasm and delayed cerebral ischemia usually occurs four days after aneurysm rupture and lasts for two weeks i.e. 14 days. Should this complication arise before Cerebrolysin™ is administered there would be significant confounding of trial outcome measures . The timing of intervention is in keeping with several landmark clinical studies that have dealt with neuroprotective agents in subarachnoid hemorrhage. Patients in the intervention group will receive in a daily total dose of 30ml of intravenous Cerebrolysin™. The study medication will be administered in three separate 10ml doses (every eight hours) diluted in 0.9% NaCl saline to a total volume of 100 ml as an intravenous infusion over a time period of 15 minutes. An identical amount of 0.9% sodium chloride (NaCl) saline (100 ml) will be used as placebo for patients allocated to the control study group. The total duration of study medication or placebo administration will be 14 days. Cerebrolysin™ is a clear yellow solution. Since it is susceptible to photo-degeneration the preparation after dilution with 0.9% NaCl saline requires masking with a opaque plastic wrap as well as special photo-protective infusion sets. The dilution of the Cerebrolysin™ solution will be performed by ward nursing staff . Subjects in both trial groups will receive identically wrapped preparations so that both the functional outcomes assessor and patient are blind to the study arm allocation. In addition to general demographic data, clinical data including the admission Glasgow Coma Score, severity grading of SAH, hospital stay as well as the extended Glasgow Outcome Score and modified Rankin Score upon discharge, at three months and six months will be prospectively collected. The functional outcomes assessor will be an occupational therapist unaware of the subject's trial group allocation. Hypothesis: compared to patients receiving standard care for the management of aneurysmal subarachnoid hemorrhage alone (control), the additional administration of intravenous Cerebrolysin™ (intervention) within the acute phase of stroke is safe and improves functional outcome at six months after stroke.
Rational: The main danger with intracranial aneurism is its rupture conjugated with subarachnoid hemorrhage (SAH) occurrence. SAH is a severe pathology leading not only to neurological but also extra cerebral disorders. The major cause of morbidity and mortality when developing a SAH is the secondary development of a delayed cerebral ischemia consecutive to a prolonged vasospasm of cerebral arteries. The understanding of the pathophysiological mechanisms of SAH complication, such as vasospasm which is the more frequent, is essential. Vasospasm is defined as a reversible shrinking of an artery lumen diameter in the subarachnoid space, beginning generally between 4 and 12 days after the hemorrhage. Such a vasospasm could have a huge clinical impact leading to delayed neurological ischemic deficiency in 17 to 40 % of cases. Up to day, mechanisms involved in vasospasm occurrence are not well described. Disposing of well-established genetics and transcriptomics databases along with cerebral ischemia and inflammation is essential to unravel the mechanisms leading to vasospasm occurrence on SAH patients. It will enable researchers to better comprehend SAH pathology and elaborate an efficient and individualized therapeutic strategy to SAH acute phase in order to reduce the risk of vasospasm occurrence. Aims: 1) Constitute DNA and RNA Biobank via blood proofing oh SAH patients 2) Constitute a database grouping clinical and biological data 3) Look for genetic and transcriptomic early markers via genomic approaches 4) Correlate these different markers with vasospasm occurrence and clinical evolution of the patients Study: Patients inclusion will be done following their admission (D1) in the " unité de réanimation neurochirurgicale" of Pitié-Salpètrière Hospital. After obtaining of the informed consent, blood proofing will be realized daily during 12 days: one daily 2.5ml tube for the transcriptomic study and a single 10ml EDTA tube for genetic analyses. Clinical and biological follow-up will be performed as usual. 200 patients will be initially included during 2 to 3 years for the transcriptomic study of which 1/3 will develop vasospastic complication. The transcriptomic study will thus be performed by comparing patients developing or not developing this complication Expected Results: Unravel vasospasm early genetic markers.
The investigators hypothesize that the use of heparin-grafted membrane versus conventional membrane in critically-ill patients with bleeding-risk undergoing continuous renal replacement therapy, will effectively prolong the circuit lifespan, without worsening of the systemic APTT or underlying bleeding risk.