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Scandinavian Journal of Trauma,... Nov 2012The prevalence of cardiac arrest among patients with subarachnoid haemorrhage [SAH], and the prevalence of SAH as the cause following out-of-hospital cardiac arrest... (Review)
Review
INTRODUCTION
The prevalence of cardiac arrest among patients with subarachnoid haemorrhage [SAH], and the prevalence of SAH as the cause following out-of-hospital cardiac arrest [OHCA] or in-hospital cardiac arrest [IHCA] is unknown. In addition it is unclear whether cardiopulmonary resuscitation [CPR] and post-resuscitation care management differs, and to what extent this will lead to meaningful survival following cardiac arrest [CA] due to SAH.
AIM
We reviewed the literature in order to describe; 1.The prevalence and predisposing factors of CA among patients with SAH 2.The prevalence of SAH as the cause of OHCA or IHCA and factors characterising CPR 3.The survival and management of SAH patients with CA.
MATERIAL AND METHODS
The following sources, PubMed, CinAHL and The Cochrane DataBase were searched using the following Medical Subheadings [MeSH]; 1. OHCA, IHCA, heart arrest and 2. subarachnoid haemorrhage. Articles containing relevant data based on the abstract were reviewed in order to find results relevant to the proposed research questions. Manuscripts in other languages than English, animal studies, reviews and case reports were excluded.
RESULTS
A total of 119 publications were screened for relevance and 13 papers were included. The prevalence of cardiac or respiratory arrest among all patients with SAH is between 3-11%, these patients commonly have a severe SAH with coma, large bleeds and evidence of raised intracerebral pressure on computed tomography scans compared to those who did not experience a CA. The prevalence of patients with SAH as the cause of the arrest among OHCA cases vary between 4 to 8% among those who die before hospital admission, and between 4 to 18% among those who are admitted. The prevalence of SAH as the cause following IHCA is low, around 0.5% according to one recent study. In patients with OHCA survival to hospital discharge is poor with 0 to 2% surviving. The initial rhythm is commonly asystole or pulseless electrical tachycardia. In IHCA the survival rate is variable with 0-27% surviving. All survivors experience brief cardiac arrests with short latencies to ROSC.
CONCLUSION
Cardiac arrest is a fairly common complication following severe SAH and these patients are encountered both in the pre-hospital and in-hospital setting. Survival is possible if the arrest occurs in the hospital and the latency to ROSC is short. In OHCA the outcome seems to be uniformly poor despite initially successful resuscitation.
Topics: Cardiopulmonary Resuscitation; Databases, Bibliographic; Female; Heart Arrest; Humans; Incidence; Inpatients; Male; Out-of-Hospital Cardiac Arrest; Prevalence; Sex Distribution; Subarachnoid Hemorrhage; Survival Rate
PubMed: 23151345
DOI: 10.1186/1757-7241-20-75 -
BMC Neurology Apr 2020Emotional health disturbances are common after aneurysmal subarachnoid hemorrhage (aSAH) and their causes are largely unexplored. Corticotropin-releasing hormone...
BACKGROUND
Emotional health disturbances are common after aneurysmal subarachnoid hemorrhage (aSAH) and their causes are largely unexplored. Corticotropin-releasing hormone receptor 1 (CRHR1) is a key factor in stress reactivity and development of mental health disturbances after adverse life-events.
METHODS
We explore the effect of CRHR1 genotype on mental health after aSAH in a retrospective cohort study. One hundred twenty-five patients have been assessed using EST-Q mental health questionnaire. Genotyping of CRHR1 single nucleotide polymorphisms (SNP-s) was performed (Rs7209436, Rs110402, Rs242924).
RESULTS
Fatigue was present in almost half of aSAH patients, depression and anxiety in one-third. There was a high prevalence of insomnia and panic complaints. Rs110402 minor allele decreased the risk of depression (OR = 0.25, p = 0.027 for homozygotes). Depression was present in 14% vs 41% in minor and major allele homozygotes, respectively. Rs110402, Rs242924 and Rs7209436 minor alleles and TAT-haplotype, formed by them, were protective against fatigue. After Bonferroni correction only the association of Rs110402 with fatigue remained statistically significant (OR = 0.21, p = 0.006 for minor allele homozygotes). Results remained statistically significant when adjusted for gender, admission state, age and time from aSAH. In multiple regression analysis occurrence of fatigue was dependent on anxiety, modified Rankin score and Rs110402 genotype (R = 0.34, p < 0.001).
CONCLUSIONS
CRHR1 minor genotype was associated with a lower risk of fatigue and depression after aSAH. Genetic predisposition to mental health disturbances associated with negative life-events could be a risk factor for fatigue and depression after aSAH and selected patients might benefit from advanced counselling in the recovery phase.
Topics: Depression; Fatigue; Genetic Predisposition to Disease; Genotype; Humans; Polymorphism, Single Nucleotide; Receptors, Corticotropin-Releasing Hormone; Retrospective Studies; Risk Factors; Subarachnoid Hemorrhage
PubMed: 32305063
DOI: 10.1186/s12883-020-01727-y -
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 -
BMJ Open Apr 2022Cerebral vasospasm (CVS) is the leading cause of mortality and morbidity following aneurysmal subarachnoid haemorrhage (aSAH). One of the recently implicated underlying...
INTRODUCTION
Cerebral vasospasm (CVS) is the leading cause of mortality and morbidity following aneurysmal subarachnoid haemorrhage (aSAH). One of the recently implicated underlying mechanisms of CVS is inflammatory cascades. Specific feasibility objectives include determining the ability to recruit 30 participants over 24 months while at least 75% of them comply with at least 75% of the study protocol and being able to follow 85% of them for 3 months after discharge.
METHODS AND ANALYSIS
This is a feasibility study for a randomised controlled trial. Eligible participants are adult patients who are 18 years of age and older with an aSAH confirmed by a brain CT scan, and CT angiography, or magnetic resonance angiography, or digital subtraction angiography who admitted to the emergency department within 12 hours of the ictus. Eligible subjects will be randomised 1:1 for the administration of either ibuprofen or a placebo, while both groups will concomitantly be treated by the standard of care for 2 weeks. Care givers, patients, outcome assessors and data analysts will be blinded. This will be the first study to investigate the preventive effects of a short-acting non-steroidal anti-inflammatory drug on CVS and the key expected outcome of this pilot study is the feasibility and safety assessment of the administration of ibuprofen in patients with aSAH. The objectives of the definitive trial would be to assess the effect of ibuprofen relative to placebo on mortality, CVS, delayed cerebral ischaemia, and level of disability at 3-month follow-up.
ETHICS AND DISSEMINATION
This study is approved by Mashhad University of Medical Sciences ethical committee (IR.MUMS.MEDICAL.REC.1398.225). Results from the study will be submitted for publication regardless of whether or not there are significant findings.
TRIAL REGISTRATION NUMBER
ISRCTN14611625.
Topics: Adolescent; Adult; Humans; Ibuprofen; Pilot Projects; Randomized Controlled Trials as Topic; Subarachnoid Hemorrhage; Treatment Outcome; Vasospasm, Intracranial
PubMed: 35414560
DOI: 10.1136/bmjopen-2021-058895 -
Anaesthesiology Intensive Therapy 2024
Topics: Humans; Subarachnoid Hemorrhage; Treatment Outcome; Prognosis
PubMed: 38741450
DOI: 10.5114/ait.2024.136026 -
Journal of Rehabilitation Medicine Apr 2019To explore associations between pituitary dysfunction and clinical outcome at 12 months after traumatic brain injury and aneurysmal subarachnoid haemorrhage.
OBJECTIVE
To explore associations between pituitary dysfunction and clinical outcome at 12 months after traumatic brain injury and aneurysmal subarachnoid haemorrhage.
METHODS
Prospective cohort study of 82 patients with traumatic brain injury and 45 with aneurysmal subarachnoid haemorrhage, included at one neurointensive care unit. Baseline data comprised age, sex, Glasgow Coma Scale (GCS) score, S100B and pupil light reactions. Hormone data were collected in the neurointensive care unit and after 3, 6 and 12 months. Outcome was assessed with Barrow Neurological Institute Screen for Higher Cerebral Functions (BNIS), Rancho Los Amigos Cognitive Scale-Revised (RLAS-R) and Glasgow Outcome Scale Extended (GOSE).
RESULTS
The most frequent hormonal deviations were hypogonadotropic hypogonadism (38%) and hypercortisolism (52%). At 12 months, performance on BNIS was impaired in 54% and GOSE in 37%. Controlling for baseline variables, low levels of gonadal hormones were associated with lower GOSE score (b = -0.80, p = 0.033), high levels of prolactin with lower RLAS (b = -1.42, p = 0.034) and high levels of serum insulin-like growth factor I (S-IGF-I) with lower RLAS level (b = -1.78, p = 0.002) and lower GOSE score (b = -1.49, p = 0.006).
CONCLUSION
These data suggest that pituitary dysfunctions during the first year after traumatic brain injury and aneurysmal subarachnoid haemorrhage may have clinically relevant, independent effects on clinical outcome at 12 months.
Topics: Adolescent; Adult; Brain Injuries, Traumatic; Cognition; Cognitive Dysfunction; Female; Glasgow Coma Scale; Glasgow Outcome Scale; Humans; Insulin-Like Growth Factor I; Male; Middle Aged; Pituitary Gland; Prospective Studies; Subarachnoid Hemorrhage; Time Factors; Young Adult
PubMed: 30761404
DOI: 10.2340/16501977-2531 -
Stroke and Vascular Neurology Feb 2022Signal transducer and activator of transcription 3 (STAT3) may contribute to the proinflammation in the central nervous system diseases by modulating the microglial...
BACKGROUND AND PURPOSE
Signal transducer and activator of transcription 3 (STAT3) may contribute to the proinflammation in the central nervous system diseases by modulating the microglial responses. Thus, this study was intended to investigate the effect of STAT3 on microglia-dependent neuroinflammation and functional outcome after experimental subarachnoid haemorrhage (SAH).
METHODS
The SAH model was established by endovascular perforation in the mouse. Real-time PCR (RtPCR) and western blot were used to examine the dynamic STAT3 signalling pathway responses after SAH. To clarify the role of the STAT3 signalling pathway in the microglia-dependent neuroinflammation after SAH, the microglia-specific STAT3 knockout (KO) mice were generated by the Cre-LoxP system. The neurological functions were assessed by Catwalk and Morris water maze tests. Neuronal loss after SAH was determined by immunohistochemistry staining. Microglial polarisation status after STAT3 KO was then examined by RtPCR and immunofluorescence.
RESULTS
The STAT3 and Janus kinase-signal transducer 2 activated immediately with the upregulation and phosphorylation after SAH. Downstream factors and related mediators altered dynamically and accordingly. Microglial STAT3 deletion ameliorated the neurological impairment and alleviated the early neuronal loss after SAH. To investigate the underlying mechanism, we examined the microglial reaction after STAT3 KO. STAT3 deletion reversed the increase of microglia after SAH. Loss of STAT3 triggered the early morphological changes of microglia and primed microglia from M1 to M2 polarisation. Functionally, microglial STAT3 deletion suppressed the SAH-induced proinflammation and promoted the anti-inflammation in the early phase.
CONCLUSIONS
STAT3 is closely related to the microglial polarisation transition and modulation of microglia-dependent neuroinflammation. Microglial STAT3 deletion improved neurological function and neuronal survival probably through promoting M2 polarisation and anti-inflammatory responses after SAH. STAT3 may serve as a promising therapeutic target to alleviate early brain injury after SAH.
Topics: Animals; Disease Models, Animal; Mice; Mice, Inbred C57BL; Microglia; Neuroinflammatory Diseases; STAT3 Transcription Factor; Subarachnoid Hemorrhage
PubMed: 34645687
DOI: 10.1136/svn-2021-001028 -
Lancet (London, England) Jan 2023
Topics: Humans; Subarachnoid Hemorrhage
PubMed: 36681414
DOI: 10.1016/S0140-6736(23)00007-7 -
Scientific Reports Dec 2021The first 72 h following aneurysm rupture play a key role in determining clinical and cognitive outcomes after subarachnoid haemorrhage (SAH). Yet, very little is known...
The first 72 h following aneurysm rupture play a key role in determining clinical and cognitive outcomes after subarachnoid haemorrhage (SAH). Yet, very little is known about the impact of so called "early brain injury" on patents with clinically good grade SAH (as defined as World Federation of Neurosurgeons Grade 1 and 2). 27 patients with good grade SAH underwent MRI scanning were prospectively recruited at three time-points after SAH: within the first 72 h (acute phase), at 5-10 days and at 3 months. Patients underwent additional, comprehensive cognitive assessment 3 months post-SAH. 27 paired healthy controls were also recruited for comparison. In the first 72 h post-SAH, patients had significantly higher global and regional brain volume than controls. This change was accompanied by restricted water diffusion in patients. Persisting abnormalities in the volume of the posterior cerebellum at 3 months post-SAH were present to those patients with worse cognitive outcome. When using this residual abnormal brain area as a region of interest in the acute-phase scans, we could predict with an accuracy of 84% (sensitivity 82%, specificity 86%) which patients would develop cognitive impairment 3 months later, despite initially appearing clinically indistinguishable from those making full recovery. In an exploratory sample of good clinical grade SAH patients compared to healthy controls, we identified a region of the posterior cerebellum for which acute changes on MRI were associated with cognitive impairment. Whilst further investigation will be required to confirm causality, use of this finding as a risk stratification biomarker is promising.
Topics: Adult; Aged; Aneurysm, Ruptured; Brain Injuries; Case-Control Studies; Cerebellum; Cognitive Dysfunction; Female; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Prospective Studies; Subarachnoid Hemorrhage
PubMed: 34853362
DOI: 10.1038/s41598-021-02539-x -
Scientific Reports Jan 2023Timely treatment of aneurysmal subarachnoid haemorrhage (aSAH) is key to prevent further rupture and poor outcome. We evaluated complications and outcome adjusting for...
Timely treatment of aneurysmal subarachnoid haemorrhage (aSAH) is key to prevent further rupture and poor outcome. We evaluated complications and outcome adjusting for time from haemorrhage to treatment. Retrospective analysis of aSAH patients admitted between 2006 and 2020. Data was collected using standardized case report forms. We compared risk factors using multivariable logistic regression. We included 853 patients, 698 (81.8%) were treated within 24 h. Patients with higher Hunt and Hess grades were admitted and treated significantly faster than those with lower grades (overall p-value < 0.001). Fifteen patients (1.8%) rebled before intervention. In the multivariable logistic analysis adjusting for timing, Barrow Neurological Institute score and intracerebral haemorrhage were significantly associated with rebleeding (overall p-value 0.006; OR 3.12, 95%CI 1.09-8.92, p = 0.03, respectively) but timing was not. Treatment > 24 h was associated with higher mortality and cerebral infarction in only the subgroup of lower grades aSAH (OR 3.13, 1.02-9.58 95%CI, p-value = 0.05; OR 7.69, 2.44-25.00, p-value < 0.001, respectively). Therefore treatment > 24 h after rupture is associated with higher mortality and cerebral infarction rates in lower grades aSAH. Delay in treatment primarily affects lower grade aSAH patients. Patients with lower grade aSAH ought to be treated with the same urgency as higher-grade aSAH.
Topics: Humans; Subarachnoid Hemorrhage; Retrospective Studies; Risk Factors; Cerebral Infarction; Aneurysm, Ruptured; Treatment Outcome; Intracranial Aneurysm
PubMed: 36707604
DOI: 10.1038/s41598-022-27177-9