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British Journal of Anaesthesia Jul 2007The anaesthetist may be involved at various stages in the management of subarachnoid haemorrhage (SAH). Thus, familiarity with epidemiological, pathophysiological,... (Review)
Review
The anaesthetist may be involved at various stages in the management of subarachnoid haemorrhage (SAH). Thus, familiarity with epidemiological, pathophysiological, diagnostic, and therapeutic issues is as important as detailed knowledge of the optimal intraoperative anaesthetic management. As the prognosis of SAH remains poor, prompt diagnosis and appropriate treatment are essential, because early treatment may improve outcome. It is, therefore, important to rule out SAH as soon as possible in all patients complaining of sudden onset of severe headache lasting for longer than an hour with no alternative explanation. The three main predictors of mortality and dependence are impaired level of consciousness on admission, advanced age, and a large volume of blood on initial cranial computed tomography. The major complications of SAH include re-bleeding, cerebral vasospasm leading to immediate and delayed cerebral ischaemia, hydrocephalus, cardiopulmonary dysfunction, and electrolyte disturbances. Prophylaxis and therapy of cerebral vasospasm include maintenance of cerebral perfusion pressure (CPP) and normovolaemia, administration of nimodipine, triple-H therapy, balloon angioplasty, and intra-arterial papaverine. Occlusion of the aneurysm after SAH is usually attempted surgically ('clipping') or endovascularly by detachable coils ('coiling'). The need for an adequate CPP (for the prevention of cerebral ischaemia and cerebral vasospasm) must be balanced against the need for a low transmural pressure gradient of the aneurysm (for the prevention of rupture of the aneurysm). Effective measures to prevent or attenuate increases in intracranial pressure, brain swelling, and cerebral vasospasm throughout all phases of anaesthesia are prerequisite for optimal outcome.
Topics: Anesthesia; Aneurysm, Ruptured; Humans; Intracranial Aneurysm; Monitoring, Intraoperative; Subarachnoid Hemorrhage; Vasospasm, Intracranial
PubMed: 17525049
DOI: 10.1093/bja/aem119 -
Intensive Care Medicine May 2024Aneurysmal subarachnoid haemorrhage (aSAH) is a rare yet profoundly debilitating condition associated with high global case fatality and morbidity rates. The key... (Review)
Review
Aneurysmal subarachnoid haemorrhage (aSAH) is a rare yet profoundly debilitating condition associated with high global case fatality and morbidity rates. The key determinants of functional outcome include early brain injury, rebleeding of the ruptured aneurysm and delayed cerebral ischaemia. The only effective way to reduce the risk of rebleeding is to secure the ruptured aneurysm quickly. Prompt diagnosis, transfer to specialized centers, and meticulous management in the intensive care unit (ICU) significantly improved the prognosis of aSAH. Recently, multimodality monitoring with specific interventions to correct pathophysiological imbalances has been proposed. Vigilance extends beyond intracranial concerns to encompass systemic respiratory and haemodynamic monitoring, as derangements in these systems can precipitate secondary brain damage. Challenges persist in treating aSAH patients, exacerbated by a paucity of robust clinical evidence, with many interventions showing no benefit when tested in rigorous clinical trials. Given the growing body of literature in this field and the issuance of contemporary guidelines, our objective is to furnish an updated review of essential principles of ICU management for this patient population. Our review will discuss the epidemiology, initial stabilization, treatment strategies, long-term prognostic factors, the identification and management of post-aSAH complications. We aim to offer practical clinical guidance to intensivists, grounded in current evidence and expert clinical experience, while adhering to a concise format.
Topics: Humans; Subarachnoid Hemorrhage; Critical Care; Intensive Care Units; Prognosis; Aneurysm, Ruptured
PubMed: 38598130
DOI: 10.1007/s00134-024-07387-7 -
BMJ Clinical Evidence Nov 2009Subarachnoid haemorrhage (SAH) may arise spontaneously or as a result of trauma. Spontaneous SAH accounts for about 5% of all strokes. Ruptured aneurysms are the cause... (Review)
Review
INTRODUCTION
Subarachnoid haemorrhage (SAH) may arise spontaneously or as a result of trauma. Spontaneous SAH accounts for about 5% of all strokes. Ruptured aneurysms are the cause of 85% of spontaneous SAH. The most characteristic clinical feature is sudden-onset severe headache. Other features include vomiting, photophobia, and focal neurological deficit or seizures, or both. As the headache may have insidious onset in some cases, or may even be absent, a high degree of suspicion is required to diagnose SAH with less typical presentations.
METHODS AND OUTCOMES
We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of surgical treatments for people with confirmed aneurysmal subarachnoid haemorrhage? What are the effects of medical treatments to prevent delayed cerebral ischaemia in people with confirmed aneurysmal subarachnoid haemorrhage? We searched: Medline, Embase, The Cochrane Library, and other important databases up to March 2009 (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 6 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: endovascular coiling; surgical clipping; timing of surgery; and oral and intravenous nimodipine.
Topics: Acute Disease; Administration, Oral; Aneurysm, Ruptured; Humans; Subarachnoid Hemorrhage; Surgical Instruments
PubMed: 21726472
DOI: No ID Found -
Stroke and Vascular Neurology Jun 2023Hyponatraemia often occurs after subarachnoid haemorrhage (SAH). However, its clinical significance and optimal management are uncertain. We audited the screening,... (Review)
Review
BACKGROUND
Hyponatraemia often occurs after subarachnoid haemorrhage (SAH). However, its clinical significance and optimal management are uncertain. We audited the screening, investigation and management of hyponatraemia after SAH.
METHODS
We prospectively identified consecutive patients with spontaneous SAH admitted to neurosurgical units in the United Kingdom or Ireland. We reviewed medical records daily from admission to discharge, 21 days or death and extracted all measurements of serum sodium to identify hyponatraemia (<135 mmol/L). Main outcomes were death/dependency at discharge or 21 days and admission duration >10 days. Associations of hyponatraemia with outcome were assessed using logistic regression with adjustment for predictors of outcome after SAH and admission duration. We assessed hyponatraemia-free survival using multivariable Cox regression.
RESULTS
175/407 (43%) patients admitted to 24 neurosurgical units developed hyponatraemia. 5976 serum sodium measurements were made. Serum osmolality, urine osmolality and urine sodium were measured in 30/166 (18%) hyponatraemic patients with complete data. The most frequently target daily fluid intake was >3 L and this did not differ during hyponatraemic or non-hyponatraemic episodes. 26% (n/N=42/164) patients with hyponatraemia received sodium supplementation. 133 (35%) patients were dead or dependent within the study period and 240 (68%) patients had hospital admission for over 10 days. In the multivariable analyses, hyponatraemia was associated with less dependency (adjusted OR (aOR)=0.35 (95% CI 0.17 to 0.69)) but longer admissions (aOR=3.2 (1.8 to 5.7)). World Federation of Neurosurgical Societies grade I-III, modified Fisher 2-4 and posterior circulation aneurysms were associated with greater hazards of hyponatraemia.
CONCLUSIONS
In this comprehensive multicentre prospective-adjusted analysis of patients with SAH, hyponatraemia was investigated inconsistently and, for most patients, was not associated with changes in management or clinical outcome. This work establishes a basis for the development of evidence-based SAH-specific guidance for targeted screening, investigation and management of high-risk patients to minimise the impact of hyponatraemia on admission duration and to improve consistency of patient care.
Topics: Humans; Ireland; Prospective Studies; Subarachnoid Hemorrhage; Hospitalization; Sodium; Multicenter Studies as Topic
PubMed: 36150732
DOI: 10.1136/svn-2022-001583 -
Journal of Neurology Jan 2011In patients with acute hydrocephalus after aneurysmal subarachnoid haemorrhage (SAH), lumbar drainage is possible if the obstruction is in the subarachnoid space...
In patients with acute hydrocephalus after aneurysmal subarachnoid haemorrhage (SAH), lumbar drainage is possible if the obstruction is in the subarachnoid space (communicating hydrocephalus). In case of intraventricular obstruction (obstructive hydrocephalus), ventricular drainage is the only option. A small fourth ventricle is often considered a sign of obstructive hydrocephalus. We investigated whether the absolute or relative size of the fourth ventricle can indeed distinguish between these two types of hydrocephalus. On CT-scans of 76 consecutive patients with acute headache but normal CT and CSF, we measured the cross-sectional surface of the third and fourth ventricle to obtain normal planimetric values. Subsequently we performed the same measurements on 117 consecutive SAH patients with acute hydrocephalus. These patients were divided according to the distribution of blood on CT-scan into three groups: mainly intraventricular blood (n=15), mainly subarachnoid blood (n=54) and both intraventricular and subarachnoid blood (n=48). The size of the fourth ventricle exceeded the upper limit of normal in 2 of the 6 (33%) patients with intraventricular blood but without haematocephalus, and in 15 of the 54 (28%) patients with mainly subarachnoid blood. The mean ratio between the third and fourth ventricle was 1.45 (SD 0.66) in patients with intraventricular blood and 1.42 (SD 0.91) in those with mainly subarachnoid blood. Neither fourth ventricular size nor the ratio between the third and fourth ventricles discriminates between the two groups. A small fourth ventricle does not necessarily accompany obstructive hydrocephalus and is therefore not a contraindication for lumbar drainage.
Topics: Adult; Data Interpretation, Statistical; Female; Fourth Ventricle; Humans; Hydrocephalus; Male; Middle Aged; Subarachnoid Hemorrhage; Third Ventricle; Tomography, X-Ray Computed
PubMed: 20680324
DOI: 10.1007/s00415-010-5678-1 -
Oxidative Medicine and Cellular... 2019The mechanisms underlying poor outcome following subarachnoid haemorrhage (SAH) are complex and multifactorial. They include early brain injury, spreading... (Review)
Review
The mechanisms underlying poor outcome following subarachnoid haemorrhage (SAH) are complex and multifactorial. They include early brain injury, spreading depolarisation, inflammation, oxidative stress, macroscopic cerebral vasospasm, and microcirculatory disturbances. Nrf2 is a global promoter of the antioxidant and anti-inflammatory response and has potential protective effects against all of these mechanisms. It has been shown to be upregulated after SAH, and Nrf2 knockout animals have poorer functional and behavioural outcomes after SAH. There are many agents known to activate the Nrf2 pathway. Of these, the actions of sulforaphane, curcumin, astaxanthin, lycopene, -butylhydroquinone, dimethyl fumarate, melatonin, and erythropoietin have been studied in SAH models. This review details the different mechanisms of injury after SAH including the contribution of haemoglobin (Hb) and its breakdown products. It then summarises the evidence that the Nrf2 pathway is active and protective after SAH and finally examines the evidence supporting Nrf2 upregulation as a therapy after SAH.
Topics: Animals; Humans; Inflammation; Models, Biological; NF-E2-Related Factor 2; Oxidative Stress; Subarachnoid Hemorrhage
PubMed: 31191800
DOI: 10.1155/2019/6218239 -
Biomolecules Apr 2022The identification of robust circulating biomarkers of stroke may improve outcomes. We conducted a systematic review and meta-analysis of serum concentrations of... (Meta-Analysis)
Meta-Analysis Review
A Systematic Review and Meta-Analysis of Serum Concentrations of Ischaemia-Modified Albumin in Acute Ischaemic Stroke, Intracerebral Haemorrhage, and Subarachnoid Haemorrhage.
The identification of robust circulating biomarkers of stroke may improve outcomes. We conducted a systematic review and meta-analysis of serum concentrations of ischaemia-modified albumin (IMA) in subjects with or without acute ischaemic stroke (AIS), intracerebral haemorrhage (ICH), and subarachnoid haemorrhage (SAH). We searched PubMed, Web of Science, Scopus, and Google Scholar from inception to March 2022. Risk of bias and certainty of evidence were assessed using the Joanna Briggs Institute Critical Appraisal Checklist and GRADE, respectively. In 17 studies, IMA concentrations were significantly higher in patients with AIS (standard mean difference, SMD = 2.52, 95% CI 1.92 to 3.12; p < 0.001), ICH (SMD = 3.13, 95% CI 1.00 to 5.25; p = 0.004), and SAH (SMD = 4.50, 95% CI 0.91 to 7.01; p = 0.014) vs. controls (very low certainty of evidence). In AIS, the effect size was associated with the male gender, and was relatively larger in studies conducted in Egypt and India and those using enzyme-linked immunosorbent assays. IMA concentrations were progressively higher, by direct comparison, in SAH, ICH, and AIS. In sensitivity analysis, the pooled SMDs were not altered when individual studies were sequentially removed. Our meta-analysis suggests that IMA concentrations might be useful to diagnose stroke and discriminate between AIS, ICH, and SAH (PROSPERO registration number: CRD42021320535).
Topics: Biomarkers; Brain Ischemia; Cerebral Hemorrhage; Hemorrhagic Stroke; Humans; Ischemic Stroke; Male; Serum Albumin; Serum Albumin, Human; Stroke; Subarachnoid Hemorrhage
PubMed: 35625582
DOI: 10.3390/biom12050653 -
British Journal of Pharmacology Sep 2021Dioscin has multiple biological activities and is beneficial for cardiovascular and cerebral vascular diseases. Here, we investigated the protective effects of dioscin...
BACKGROUND AND PURPOSE
Dioscin has multiple biological activities and is beneficial for cardiovascular and cerebral vascular diseases. Here, we investigated the protective effects of dioscin against subarachnoid haemorrhage and the molecular mechanisms involved.
EXPERIMENTAL APPROACH
Dioscin was administered after subarachnoid haemorrhage induced in rats. MCC950, a potent selective nod-like receptor pyrin domain-containing 3 (NLRP3) inhibitor, was used to suppress NLRP3 and EX527 (selisistat) was used to inhibit sirtuin 1 (SIRT1).
KEY RESULTS
In vivo, dioscin inhibited acute inflammatory response, oxidative damage, neurological impairment and neural cell degeneration after subarachnoid haemorrhage along with dramatically suppressing NLRP3 inflammasome activation. While pretreatment with MCC950 reduced the inflammatory response and improved neurological outcomes it did not lessen ROS production. However, giving dioscin after MCC950 reduced acute brain damage and ROS production. Dioscin increased SIRT1 expression after subarachnoid haemorrhage, whereas EX527 abolished the up-regulation of SIRT1 induced by dioscin and offset the inhibitory effects of dioscin on NLRP3 inflammasome activation. EX527 pretreatment also reversed the neuroprotective effects of dioscin against subarachnoid haemorrhage. Similarly, in vitro, dioscin dose-dependently suppressed inflammatory response, oxidative damage and neuronal degeneration and improved cell viability in neurons and microglia co-culture system. These effects were associated with inhibition of the NLRP3 inflammasome and stimulation of SIRT1 signalling, which could be inhibited by EX527 pretreatment.
CONCLUSION AND IMPLICATIONS
Dioscin provides protection against subarachnoid haemorrhage via the suppression of NLRP3 inflammasome activation through SIRT1-dependent pathway. Dioscin may be a new candidate to ameliorate early brain injury after subarachnoid haemorrhage.
Topics: Animals; Diosgenin; Inflammasomes; NLR Family, Pyrin Domain-Containing 3 Protein; Rats; Rats, Sprague-Dawley; Sirtuin 1; Subarachnoid Hemorrhage
PubMed: 33904167
DOI: 10.1111/bph.15507 -
Clinical Chemistry and Laboratory... Nov 2013Subarachnoid haemorrhage (SAH) has a high mortality and morbidity rate. Early SAH diagnosis allows the early treatment of a ruptured cerebral aneurysm, which improves... (Review)
Review
Cerebrospinal fluid analyses for the diagnosis of subarachnoid haemorrhage and experience from a Swedish study. What method is preferable when diagnosing a subarachnoid haemorrhage?
Subarachnoid haemorrhage (SAH) has a high mortality and morbidity rate. Early SAH diagnosis allows the early treatment of a ruptured cerebral aneurysm, which improves the prognosis. Diagnostic cerebrospinal fluid (CSF) analyses may be performed after a negative computed tomography scan, but the precise analytical methods to be used have been debated. Here, we summarize the scientific evidence for different CSF methods for SAH diagnosis and describe their implementation in different countries. The principle literature search was conducted using PubMed and Scopus with the search items "cerebrospinal fluid", "subarachnoid haemorrhage", and "diagnosis". CSF analyses for SAH include visual examination, red blood cell counts, spectrophotometry for oxyhaemoglobin or bilirubin determination, CSF cytology, and ferritin measurement. The methods vary in availability and performance. There is a consensus that spectrophotometry has the highest diagnostic performance, but both oxyhaemoglobin and bilirubin determinations are susceptible to important confounding factors. Visual inspection of CSF for xanthochromia is still frequently used for diagnosis of SAH, but it is advised against because spectrophotometry has a superior diagnostic accuracy. A positive finding of CSF bilirubin is a strong indicator of an intracranial bleeding, whereas a positive finding of CSF oxyhaemoglobin may indicate an intracranial bleeding or a traumatic tap. Where spectrophotometry is not available, the combination of CSF cytology for erythrophages or siderophages and ferritin is a promising alternative.
Topics: Clinical Chemistry Tests; Erythrocyte Count; Humans; Spectrophotometry; Subarachnoid Hemorrhage; Sweden
PubMed: 23729569
DOI: 10.1515/cclm-2012-0783 -
International Journal of Molecular... Nov 2023Haptoglobin is the body's first line of defence against the toxicity of extracellular haemoglobin released following a subarachnoid haemorrhage (SAH). We investigated...
Haptoglobin is the body's first line of defence against the toxicity of extracellular haemoglobin released following a subarachnoid haemorrhage (SAH). We investigated the haptoglobin response after SAH in cerebrospinal fluid (CSF) and serum. Paired CSF and serum samples from 19 controls and 92 SAH patients were assayed as follows: ultra-performance liquid chromatography for CSF haemoglobin and haptoglobin, immunoassay for serum haptoglobin and multiplexed CSF cytokines, and colorimetry for albumin. There was marked CSF haptoglobin deficiency: 99% of extracellular haemoglobin was unbound. The quotients for both CSF/serum albumin (qAlb) and haptoglobin (qHp) were used to compute the CSF haptoglobin index (qHp/qAlb). CSF from SAH patients had a significantly lower haptoglobin index compared to controls, especially in Haptoglobin-1 allele carriers. Serum haptoglobin levels increased after SAH and were correlated with CSF cytokine levels. Haptoglobin variables were not associated with long-term clinical outcomes post-SAH. We conclude that: (1) intrathecal haptoglobin consumption occurs after SAH, more so in haptoglobin-1 allele carriers; (2) serum haptoglobin is upregulated after SAH, in keeping with the liver acute phase response to central inflammation; (3) haptoglobin in the CSF is so low that any variation is too small for this to affect long-term outcomes, emphasising the potential for therapeutic haptoglobin supplementation.
Topics: Humans; Subarachnoid Hemorrhage; Haptoglobins; Cytokines; Hemoglobins
PubMed: 38069244
DOI: 10.3390/ijms242316922