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Varon, Joseph; Marik, Paul E.

doi:10.1186/cc2351

Cited by 157 publications

(39 citation statements)

References 146 publications

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“…It is not possible to give limits for ‘extreme’ blood pressures, because ‘extreme’ differs in different patients according to their age, previous blood pressure, cardiac history and other factors. If the aneurysm is not yet secured it seems prudent to treat blood pressure if the systolic pressure exceeds 180 mm Hg, for example by means of esmolol or labetolol [74]; it seems reasonable to aim for a modest (e.g. 25%) decrease in mean arterial pressure.…”

Section: Aneurysmal Sah – Ruptured Aneurysm (Ria)mentioning

confidence: 99%

European Stroke Organization Guidelines for the Management of Intracranial Aneurysms and Subarachnoid Haemorrhage

et al. 2013

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Background: Intracranial aneurysm with and without subarachnoid haemorrhage (SAH) is a relevant health problem: The overall incidence is about 9 per 100,000 with a wide range, in some countries up to 20 per 100,000. Mortality rate with conservative treatment within the first months is 50–60%. About one third of patients left with an untreated aneurysm will die from recurrent bleeding within 6 months after recovering from the first bleeding. The prognosis is further influenced by vasospasm, hydrocephalus, delayed ischaemic deficit and other complications. The aim of these guidelines is to provide comprehensive recommendations on the management of SAH with and without aneurysm as well as on unruptured intracranial aneurysm. Methods: We performed an extensive literature search from 1960 to 2011 using Medline and Embase. Members of the writing group met in person and by teleconferences to discuss recommendations. Search results were graded according to the criteria of the European Federation of Neurological Societies. Members of the Guidelines Committee of the European Stroke Organization reviewed the guidelines. Results: These guidelines provide evidence-based information on epidemiology, risk factors and prognosis of SAH and recommendations on diagnostic and therapeutic methods of both ruptured and unruptured intracranial aneurysms. Several risk factors of aneurysm growth and rupture have been identified. We provide recommendations on diagnostic work up, monitoring and general management (blood pressure, blood glucose, temperature, thromboprophylaxis, antiepileptic treatment, use of steroids). Specific therapeutic interventions consider timing of procedures, clipping and coiling. Complications such as hydrocephalus, vasospasm and delayed ischaemic deficit were covered. We also thought to add recommendations on SAH without aneurysm and on unruptured aneurysms. Conclusion: Ruptured intracranial aneurysm with a high rate of subsequent complications is a serious disease needing prompt treatment in centres having high quality of experience of treatment for these patients. These guidelines provide practical, evidence-based advice for the management of patients with intracranial aneurysm with or without rupture. Applying these measures can improve the prognosis of SAH.

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Section: Aneurysmal Sah – Ruptured Aneurysm (Ria)mentioning

confidence: 99%

European Stroke Organization Guidelines for the Management of Intracranial Aneurysms and Subarachnoid Haemorrhage

et al. 2013

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“…Even in normotensive individuals, sudden large rises in arterial pressure can overwhelm autoregula-tory mechanisms, resulting in massive CBF increases, BBB damage, and cerebral edema, as observed in hypertensive encephalopathy and the posterior reversible encephalopathy syndrome. 62–64 In turn, acute hypotension leads to decreases in CBF, causing “watershed” infarcts in border zones between adjacent arterial territories. 27,50 …”

Section: Effects Of Hypertension On Cerebrovascular Structure and Funmentioning

confidence: 99%

Impact of Hypertension on Cognitive Function: A Scientific Statement From the American Heart Association

Iadecola¹,

Yaffe²,

Biller³

et al. 2016

Hypertension

558

474

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Background Age-related dementia, most commonly caused by Alzheimer disease or cerebrovascular factors (vascular dementia), is a major public health threat. Chronic arterial hypertension is a well-established risk factor for both types of dementia, but the link between hypertension and its treatment and cognition remains poorly understood. In this scientific statement, a multidisciplinary team of experts examines the impact of hypertension on cognition to assess the state of the knowledge, to identify gaps, and to provide future directions. Methods Authors with relevant expertise were selected to contribute to this statement in accordance with the American Heart Association conflict-of-interest management policy. Panel members were assigned topics relevant to their areas of expertise, reviewed the literature, and summarized the available data. Results Hypertension disrupts the structure and function of cerebral blood vessels, leads to ischemic damage of white matter regions critical for cognitive function, and may promote Alzheimer pathology. There is strong evidence of a deleterious influence of midlife hypertension on late-life cognitive function, but the cognitive impact of late-life hypertension is less clear. Observational studies demonstrated a cumulative effect of hypertension on cerebrovascular damage, but evidence from clinical trials that antihypertensive treatment improves cognition is not conclusive. Conclusions After carefully reviewing the literature, the group concluded that there were insufficient data to make evidence-based recommendations. However, judicious treatment of hypertension, taking into account goals of care and individual characteristics (eg, age and comorbidities), seems justified to safeguard vascular health and, as a consequence, brain health.

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“…The most prevalent risk factor for ICH is chronic hypertension,24, 25 which also causes a rightward shift in the renal autoregulation curve26 and increases the threshold value of mean arterial pressure needed to maintain renal perfusion 27, 28. Drastic and rapid lowering of blood pressure may also shift the renal autoregulation curve rightward9 and create a new less robust limit, where even nonhypotensive or normotensive blood pressures decrease renal blood flow and exacerbate renal injury.…”

Section: Discussionmentioning

confidence: 99%

“…Intensive blood pressure reduction can induce multiorgan ischemia, particularly in the heart and kidneys 8, 9, 10, 11. The identification and determination of risk factors for acute kidney injury (AKI) is particularly important because of its association with death or major disability after ICH 12.…”

mentioning

confidence: 99%

Evaluation of Acute Kidney Injury and Mortality After Intensive Blood Pressure Control in Patients With Intracerebral Hemorrhage

Burgess

Goyal

Jones

et al. 2018

JAHA

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BackgroundWe sought to assess the risk of acute kidney injury (AKI) and mortality associated with intensive systolic blood pressure reduction in acute intracerebral hemorrhage.Methods and ResultsPatients with acute intracerebral hemorrhage had spontaneous cause and symptom onset within 24 hours. We excluded patients with structural causes, coagulopathy, thrombocytopenia, and preexisting end‐stage renal disease. We defined AKI using the Acute Kidney Injury Network criteria. Chronic kidney disease status was included in risk stratification and was defined by Kidney Disease Outcomes Quality Initiative staging. Maximum systolic blood pressure reduction was defined over a 12‐hour period and dichotomized using receiver operating characteristic curve analysis. Descriptive statistics were done using independent sample t tests, χ2 tests, and Mann‐Whitney U tests, whereas multivariable logistic regression analysis was used to evaluate for predictors for AKI and mortality. A total of 448 patients with intracerebral hemorrhage met inclusion criteria. Maximum systolic blood pressure reduction was dichotomized to 90 mm Hg and found to increase the risk of AKI in patients with normal renal function (odds ratio, 2.1; 95% confidence interval, 1.19–3.62; P=0.010) and chronic kidney disease (odds ratio, 3.91; 95% confidence interval, 1.26–12.15; P=0.019). The risk of AKI was not significantly different in normal renal function versus chronic kidney disease groups when adjusted for demographics, presentation characteristics, and medications associated with AKI. AKI positively predicted mortality for patients with normal renal function (odds ratio, 2.41; 95% confidence interval, 1.11–5.22; P=0.026) but not for patients with chronic kidney disease (odds ratio, 3.13; 95% confidence interval, 0.65–15.01; P=0.154).ConclusionsThese results indicate that intensive systolic blood pressure reduction with a threshold >90 mm Hg in patients with acute intracerebral hemorrhage may be an independent predictor for AKI.

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Untitled

Cited by 157 publications

References 146 publications

European Stroke Organization Guidelines for the Management of Intracranial Aneurysms and Subarachnoid Haemorrhage

European Stroke Organization Guidelines for the Management of Intracranial Aneurysms and Subarachnoid Haemorrhage

Impact of Hypertension on Cognitive Function: A Scientific Statement From the American Heart Association

Evaluation of Acute Kidney Injury and Mortality After Intensive Blood Pressure Control in Patients With Intracerebral Hemorrhage

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