see also Subarachnoid hemorrhage outcome.
In a study by Hammer et al. from the Paracelsus Medical University, complications like pneumonia (β = 5.11; 95% CI = 1.75-8.46; p = 0.0031), sepsis (β = 9.54; 95% CI = 3.27-15.82; p = 0.0031), hydrocephalus (β = 4.63; 95% CI = 1.82-7.45; p = 0.0014), and delayed cerebral ischemia (DCI) (β = 3.38; 95% CI = 0.19-6.56; p = 0.038) were critical factors depending on the LOS in intensive care as well as decompressive craniectomy (β = 5.02; 95% CI = 1.35-8.70; p = 0.0077). All analyzed comorbidities such as hypertension, diabetes, hypothyroidism, cholesterolemia, and smoking history had no significant impact on the LOS in intensive care. LOS in intensive care (OR = 1.09; 95% CI = 1.03-1.15; p = 0.0023), as well as World Federation of Neurosurgical Societies grading for subarachnoid hemorrhage (OR = 3.72; 95% CI = 2.23-6.21; p < 0.0001) and age (OR = 1.06; 95% CI = 1.02-1.10; p = 0.0061), were significant factors that had an impact on the outcome after 1 year. Complications in intensive care but not comorbidities are associated with higher LOS in intensive care. LOS in intensive care is a modest but significant predictor of outcomes after subarachnoid hemorrhage 1).
These two pathological entities seem to have different pathophysiological etiologies and cannot be detected by the same techniques. Vasospasms of the vessels of the circle of Willis can be detected by transcranial Doppler ultrasonography (TCD), whereas microcirculation disturbances can be detected by perfusion imaging techniques. Digital subtraction angiography (DSA) remains until now the gold standard of imaging vasospasms, but it is invasive, and it is proven to be associated with the risk of mild neurological deficit as well as ischemic insults 4).
As angiographic vasospasm is strongly associated with delayed cerebral ischemia (DCI) and clinical outcome, clinical trials in the last few decades focused on prevention of these angiographic spasms. Despite all efforts, no new pharmacological agents have shown to improve patient outcome. As such, it has become clear that our understanding of the pathophysiology of SAH is incomplete and we need to reevaluate our concepts on the complex pathophysiological process following SAH. Angiographic vasospasm is probably important.
Although the pervasiveness of cognitive impairment is widely acknowledged as a long-term sequela of aSAH, the mechanisms underlying its development are poorly understood. The onset of aSAH elicits activation of the inflammatory cascade, and ongoing neuroinflammation is suspected to contribute to secondary complications, such as vasospasm and delayed cerebral ischemia. In this review, we analyze the extant literature regarding the relationship between neuroinflammation and cognitive dysfunction after aSAH. Pro-inflammatory cytokines appear to play a role in maintaining normal cognitive function in adults unaffected by aSAH. However, in the setting of aSAH, elevated cytokine levels may correlate with worse neuropsychological outcomes. This seemingly dichotomous relationship between neuroinflammation and cognition suggests that the action of cytokines varies, depending on their physiologic environment. Experimental therapies which suppress the immune response to aSAH appear to have a beneficial effect on cognitive outcomes. However, further studies are necessary to determine the utility of inflammatory mediators as biomarkers of neurocognitive outcomes, as well as their role in the management of aSAH.
One factor that might influence the initial brain damage or subsequent complications is the use of antiplatelet medication before the initial hemorrhage.
Improvements in multidisciciplinary neurocritical care and advancements in medical and surgical treatment have contributed to a decline in the case fatality rate of aneurysmal subarachnoid hemorrhage 5).
A greater proportion of patients, therefore, are surviving their initial hemorrhagic event but remain at increased risk of a number of complications.
The case fatality after aneurysmal haemorrhage is 50%; one in eight patients with subarachnoid haemorrhage dies outside hospital. Rebleeding is the most imminent danger; a first aim is therefore occlusion of the aneurysm 6).
Prothrombotic states of early brain injury (EBI) and delayed cerebral ischemia (DCI) after aSAH determine morbidity and mortality.
The outcome depends on their condition on arrival at the hospital. However, a small number of patients recover from an initially poor condition.
Generally aSAH has a very high mortality (>25%) and significant morbidity (>50%) among the survivors, and most survivors experience significant cognitive decline across multiple domains, including executive function 7).
Associated with intracerebral hematoma (ICH) typically has a poor outcome. SAH with ICH tends to have a worse prognosis than SAH alone.
It has a high socioeconomic impact as it tends to affect younger patients. The NCEPOD study looking into management of aSAH has recommended that neurovascular units in the United Kingdom should aim to secure cerebral aneurysms within 48 h and that delays because of weekend admissions can increase the mortality and morbidity attributed to aSAH.
A study provides important data showing excess in-hospital mortality of patients with SAH on weekend admissions served by the United Kingdom's National Health Service.; However, there were no effects of weekend admission on long-term outcomes 8).
Clinical prediction models were developed with individual patient data from 10 936 patients and validated with data from 3355 patients after development of the model. In the validation cohort, a core model including patient age, premorbid hypertension, and neurological grade on admission to predict risk of functional outcome had good discrimination, with an area under the receiver operator characteristics curve (AUC) of 0.80 (95% confidence interval 0.78 to 0.82). When the core model was extended to a “neuroimaging model,” with inclusion of clot volume, aneurysm size, and location, the AUC improved to 0.81 (0.79 to 0.84). A full model that extended the neuroimaging model by including treatment modality had AUC of 0.81 (0.79 to 0.83). Discrimination was lower for a similar set of models to predict risk of mortality (AUC for full model 0.76, 0.69 to 0.82). All models showed satisfactory calibration in the validation cohort.
The prediction models reliably estimate the outcome of patients who were managed in various settings for ruptured intracranial aneurysms that caused subarachnoid haemorrhage. The predictor items are readily derived at hospital admission. The web based SAHIT prognostic calculator (http://sahitscore.com) and the related app could be adjunctive tools to support management of patients 9).
Systematic reviews for clinical prognostic factors and clinical prediction tools in aneurysmal subarachnoid hemorrhage (aSAH) face a number of methodological challenges. These include within and between study patient heterogeneity, regional variations in treatment protocols, patient referral biases, and differences in treatment, and prognosis viewpoints across different cultures 10).
It is critical to determine the neural basis for executive deficits in aSAH, in order to better understand and improve patient outcomes.
In a tertiary care center in India, despite recent advances in the treatment of patients with aSAH, the morbidity and mortality rates have failed to improve significantly in unselected patients and natural cohorts. This may be attributed to the natural history of aSAH, and calls for new strategies to diagnose and treat such patients before the catastrophe 11).
In the series of Nieuwkamp et al., despite an increase in the mean age of patients with SAH, case-fatality rates have decreased by 17% between 1973 and 2002 and show potentially important regional differences. This decrease coincides with the introduction of improved management strategies 12).
The case fatality after aneurysmal haemorrhage is 50%; one in eight patients with subarachnoid haemorrhage dies outside hospital.
Mortality is 10% within first few days
30-day mortality rate was 46% in one series, and in others over half the patients died within 2 weeks of their SAH.
overall mortality is 45% (range: 32—67%)
causes of mortality
neurogenic stunned myocardium
about 8% die from progressive deterioration from the initial hemorrhage
of those reaching neurosurgical care, vasospasm kills 7%, and causes severe deﬁcit in another 7%.
about 30% of survivors have moderate to severe disability.
about 66 % of those who hove successful aneurysm clipping never return to the same quality of life as before the SAH.
Individuals who have aneurysmal subarachnoid hemorrhages (SAHs) experience decreased health-related qualities of life (HRQoLs) that persist after the primary insult.
Data collected from the CONSCIOUS-1 trial was used to extract 29 clinical variables including SAH presentation, hospital procedures, and demographic information in addition to 5 HRQoL outcome variables for 256 individuals. A partial least-squares analysis was performed by calculating a heterogeneous correlation matrix and applying singular value decomposition to determine components that best represent the correlations between the 2 sets of variables. Bootstrapping was used to estimate statistical significance.
The first 2 components accounting for 81.6% and 7.8% of the total variance revealed significant associations between clinical predictors and HRQoL outcomes. The first component identified associations between disability in self-care with longer durations of critical care stay, invasive intracranial monitoring, ventricular drain time, poorer clinical grade on presentation, greater amounts of cerebral spinal fluid drainage, and a history of hypertension. The second component identified associations between disability due to pain and discomfort as well as anxiety and depression with greater body mass index, abnormal heart rate, longer durations of deep sedation and critical care, and higher World Federation of Neurosurgical Societies and Hijdra scores.
By applying a data-driven, multivariate approach, we identified robust associations between SAH clinical presentations and HRQoL outcomes 14).
Quantitative estimation of the hemorrhage volume associated with aneurysm rupture is a tool of assessing prognosis.
A prospective cohort of 206 patients consecutively admitted with the diagnosis of aneurysmal subarachnoid hemorrhage to Hospital 12 de Octubre were included in the study. Subarachnoid, intraventricular, intracerebral, and total bleeding volumes were calculated using analytic software. For assessing factors related to prognosis, univariate and multivariate analysis (logistic regression) were performed. The relative importance of factors in determining prognosis was established by calculating their proportion of explained variation. Maximum Youden index was calculated to determine the optimal cut point for subarachnoid and total bleeding volume.
Variables independently related to prognosis were clinical grade at admission, age, and the different bleeding volumes. The proportion of variance explained is higher for subarachnoid bleeding. The optimal cut point related to poor prognosis is a volume of 20 mL both for subarachnoid and total bleeding.
Volumetric measurement of subarachnoid or total bleeding volume are both independent prognostic factors in patients with aneurysmal subarachnoid hemorrhage. A volume of more than 20 mL of blood in the initial noncontrast computed tomography is related to a clear increase in poor outcome risk 15).
Early recording of C reactive protein may prove useful in detecting those good grade patients who are at greater risk of clinical deterioration and poor outcome in aneurysmal subarachnoid hemorrhage 16).
Higher early IL6 serum levels after aSAH are associated with poor outcome at discharge. In addition, involvement of leukemia inhibitory factor (LIF) in the early inflammatory reaction after aSAH has been demonstrated 17).
The APOΕε4 polymorphism was analysed in 147 patients with aSAH. Allele and genotype frequencies were compared to those found in a gender- and area-matched control group of healthy individuals (n = 211). Early cerebral vasospasm (CVS) was identified and treated according to neurointensive care unit (NICU) guidelines. Neurological deficit(s) at admittance and at 1-year follow-up visit was recorded. Neurological outcome was assessed by the National Institute of Health Stroke Scale, Barthel Index and the Extended Glasgow Outcome Scale.
APOEε4 and non-APOEε4 allele frequencies were similar in aSAH patients and healthy individuals. The presence of APOEε4 was not associated with the development of early CVS. We could not find an influence of the APOE polymorphism on 1-year neurological outcome between groups. Subgroup analyses of patients treated with surgical clipping vs endovascular coiling did not reveal any associations.
For Csajbok et al. APOEε4 polymorphism has no major influence on risk of aSAH, the occurrence of CVS or long-term neurological outcome after aSAH 18).
For Cheng et al., Apolipoprotein E (APOEε4) may induce cerebral perfusion impairment in the early phase, contributing to early brain injury (EBI) following aneurysmal subarachnoid hemorrhage (aSAH), and assessment of APOE genotypes could serve as a useful tool in the prognostic evaluation and therapeutic management of aSAH 19).