13
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      C-reactive protein and vasospasm after aneurysmal subarachnoid hemorrhage1

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          PURPOSE: To evaluate the relationship between C reactive protein levels and clinical and radiological parameters with delayed ischemic neurological deficits and outcome after aneurysmal subarachnoid hemorrhage.METHODS: One hundred adult patients with aneurismal SAH were prospectively evaluated. Besides the baseline characteristics, daily C-reactive protein levels were prospectively measured until day 10 after subarachnoid hemorrhage. The primary end point was outcome assessed by Glasgow Outcome Scale, the secondary was the occurrence of delayed ischemic neurological deficits (DINDs).RESULTS:A progressive increase in the CRP levels from the admission to 3rd postictal day was observed, followed by a slow decrease until the 9th day. Hemodynamic changes in TCD were associated with higher serum CRP levels. Patients with lower GCS scores presented with increased CRP levels. Patients with higher Hunt and Hess grades on admission developed significantly higher CRP serum levels. Patients with higher admission Fisher grades showed increased levels of CRP. A statistically significant inverse correlation was established in our series between CRP serum levels and GOS on discharge and CRP levels.CONCLUSIONS:Higher C-reactive protein serum levels are associated with worse clinical outcome and the occurrence of delayed ischemic neurological deficits. Because C-reactive protein levels were significantly elevated in the early phase, they might be a useful parameter to monitor.

          Related collections

          Most cited references26

          • Record: found
          • Abstract: found
          • Article: not found

          Delayed cerebral vasospasm and nitric oxide: review, new hypothesis, and proposed treatment.

          R Pluta (2004)
          Despite years of research, delayed cerebral vasospasm remains the feared complication of a ruptured intracranial aneurysm. Worldwide effort has led to many promising experimental treatments that reverse or prevent cerebral vasospasm but none were confirmed to be effective in clinical trials. There are several sources for this failure: (1) the pathophysiology of delayed cerebral vasospasm remains poorly understood, (2) many experimental models of subarachnoid hemorrhage (SAH) do not mimic the actual clinical entity, and (3) many researchers erroneously extrapolate the data of peripheral and cerebral vascular physiological responses to the post-SAH situation. Thus, to explain the uniqueness of vasospasm and to address nitric oxide (NO) involvement in delayed vasospasm development, the following issues are addressed in this paper: (1) pathophysiological mechanisms of vasospasm, (2) NO-related contribution to its development. In addition, (3) a two-stage hypothesis of pathogenesis of delayed cerebral vasospasm is presented developed in the Vascular Laboratory of Surgical Neurology Branch of the National Institute of Neurological Disorders and Stroke using a primate model of SAH. According to this hypothesis, initially (Phase I) NO-releasing neurons are destroyed by oxyhemoglobin (oxyHb) leading to diminished availability of NO in the vessel wall and constriction of the vessels (Phase I). Increased shear stress evoked by narrowing of the arterial lumen should stimulate endothelial nitric oxide synthase (eNOS). But further metabolism of hemoglobin to bilirubin oxidized fragments (BOXes) increases asymmetric dimethylarginine (ADMA), an endogenous inhibitor of eNOS, in the vicinity of the artery further decreasing of NO availability and sustaining vasospasm (Phase II). In Phase III, the resolution of vasospasm, elimination of BOXes increases NO production by eNOS resulting in recovery of dilatory activity of endothelium. This hypothesis suggests that the key treatment to prevent delayed cerebral vasospasm should be focused on preventing oxyHb neurotoxicity, inhibiting BOX production, and exogenous NO delivery.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Cerebral vasospasm following aneurysmal subarachnoid hemorrhage.

            Cerebral vasospasm following aneurysmal subarachnoid hemorrhage is one of the most important causes of cerebral ischemia, and is the leading cause of death and disability after aneurysm rupture. There are two definitions of cerebral vasospasm: angiographic and clinical. Care must be exercised to be certain that it is clear which entity is being addressed. The diagnosis of the clinical syndrome is one of exclusion and can rarely be made with absolute certainty. The pathogenesis of cerebral vasospasm is poorly understood. Most current theories focus on the release of factors from the subarachnoid clot. More attention must be given to the role of endothelial damage and alterations in the blood-arterial wall barrier. The application of modern techniques for studying vascular smooth muscle which have been developed as a result of research in the areas of hypertension and atherosclerosis must be applied to the problem of cerebral vasospasm. A stress test to select patients with angiographic arterial narrowing who have adequate cerebral vascular reserve to undergo surgery should be developed. The optimal treatment of vasospasm awaits development of agents for blocking or inactivating spasmogenic substances or blocking arterial smooth muscle contraction. Rheological or hemodynamic manipulations to prevent or reverse ischemic consequences of vasospasm are relatively effective, but complicated and hazardous, and should be viewed principally as interim measures awaiting development of more specific therapies for the arterial narrowing.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Clazosentan (AXV-034343), a selective endothelin A receptor antagonist, in the prevention of cerebral vasospasm following severe aneurysmal subarachnoid hemorrhage: results of a randomized, double-blind, placebo-controlled, multicenter phase IIa study.

              The goal of this study was to investigate the safety and tolerability of the novel endothelin A (ETA) receptor antagonist clazosentan in patients with subarachnoid hemorrhage (SAH) and its potential to reduce the incidence and severity of cerebral vasospasm following surgical clipping of the aneurysm. This Phase IIa multicenter study had two parts: a double-blind, randomized Part A (some patients given clazosentan [0.2 mg/kg/hr] and others given placebo), in which statistical inference was performed, and an open-label Part B (patients with established vasospasm given clazosentan [0.4 mg/kg/hr for 12 hours followed by 0.2 mg/kg/hr]) for exploratory purposes only. Primary end points were the incidence and severity of angiographic vasospasm on Day 8 after SAH and the safety and tolerability of the drug. Thirty-four patients (Hunt and Hess Grades III and IV and Fisher Grade > or = 3) were recruited and 32 (15 in the clazosentan group and 17 in the placebo group) were retained in the intent-to-treat population; 19 patients entered Part B. In Part A, treatment with clazosentan resulted in a reduced incidence of angiographically evident cerebral vasospasm (40% compared with 88% of patients, p = 0.008). In addition, the severity of vasospasm was reduced in the clazosentan group (p = 0.012). In Part B of the study, in 50% of assessable patients who were initially treated with placebo reversal of vasospasm was observed following the initiation of clazosentan therapy. The incidence of new infarctions was 15% in the clazosentan group and 44% in the placebo group (p = 0.130). There was no adverse event pattern indicating a specific organ toxicity of clazosentan. This study indicates that clazosentan reduces the frequency and severity of cerebral vasospasm following severe aneurysmal SAH with the incidence and severity of adverse events comparable to that of placebo.
                Bookmark

                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Journal
                acb
                Acta Cirurgica Brasileira
                Acta Cir. Bras.
                Sociedade Brasileira para o Desenvolvimento da Pesquisa em Cirurgia (São Paulo )
                1678-2674
                May 2014
                : 29
                : 5
                : 340-345
                Affiliations
                [1 ] Universidade Estadual Paulista Brazil
                [2 ] Universidade Estadual Paulista Brazil
                [3 ] Universidade Estadual Paulista Brazil
                Article
                S0102-86502014000500340
                10.1590/S0102-86502014000500009
                24863323
                13989dc5-b64e-47ff-860e-74a88ae2a69f

                http://creativecommons.org/licenses/by/4.0/

                History
                Product

                SciELO Brazil

                Self URI (journal page): http://www.scielo.br/scielo.php?script=sci_serial&pid=0102-8650&lng=en
                Categories
                SURGERY

                Surgery
                C-Reactive Protein,Vasospasm, Intracranial,Subarachnoid Hemorrhage
                Surgery
                C-Reactive Protein, Vasospasm, Intracranial, Subarachnoid Hemorrhage

                Comments

                Comment on this article