scholarly journals Clinical Treatment and Prognostic Analysis of Patients with Aneurysmal Subarachnoid Hemorrhage

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Xue Yang ◽  
Qiong Cheng ◽  
Yunfei Li ◽  
Zheng Zheng ◽  
Junpeng Liu ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Blood Vessels ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Physiological Mechanism ◽  
Clinical Treatment ◽  
Current Status ◽  
Prognostic Analysis ◽  
Depth Study ◽  
Serious Disease ◽  
All Diseases

Subarachnoid hemorrhage (SAH) is a serious disease caused by blood flow into the subarachnoid space due to rupture of blood vessels. All diseases that cause intracranial hemorrhage are the cause of subarachnoid hemorrhage. Among them, due to the particularity of intracranial blood vessels, intracranial blood vessels are more prone to aneurysms than other parts. Therefore, the incidence of aneurysmal subarachnoid hemorrhage (aSAH) is extremely high. The purpose of this article is to study the clinical treatment and prognosis analysis of aSAH patients. This article first summarizes the current status of SAH research at home and abroad and summarizes its potential value and significance. On this basis, an in-depth study of the clinical treatment of aSAH patients has been carried out. The physiological mechanism and clinical general differences of aSAH were studied and analyzed. This article systematically describes the application of CTP in the treatment and prognosis analysis of aSAH patients. Then, it will use a comparative analysis method, interdisciplinary method, and other research forms to carry out experimental research on the theme of this article. Research shows that rebleeding and blood sodium are the main factors for cerebral ischemia caused by aSAH.

scholarly journals Current Status of Problems with Initial Treatment for Aneurysmal Subarachnoid Hemorrhage

2019 ◽  
Vol 28 (9) ◽  
pp. 542-551
Author(s):  
Hiroharu Kataoka ◽  
Shunsuke Nakagawa ◽  
Jun C Takahashi ◽  
Yasushi Takagi ◽  
Susumu Miyamoto
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Initial Treatment ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Current Status

Controlled transient hypercapnia: a novel approach for the treatment of delayed cerebral ischemia after subarachnoid hemorrhage?

2014 ◽  
Vol 121 (5) ◽  
pp. 1056-1062 ◽  
Author(s):  
Thomas Westermaier ◽  
Christian Stetter ◽  
Ekkehard Kunze ◽  
Nadine Willner ◽  
Judith Holzmeier ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Near Infrared ◽  
Therapeutic Potential ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Rebound Effect ◽  
Delayed Cerebral Ischemia ◽  
Physiological Mechanism ◽  
Tissue Oxygen Saturation ◽  
Poor Grade ◽  
Continuous Drainage

Object The authors undertook this study to investigate whether the physiological mechanism of cerebral blood flow (CBF) regulation by alteration of the arterial partial pressure of carbon dioxide (PaCO2) can be used to increase CBF after aneurysmal subarachnoid hemorrhage (aSAH). Methods In 6 mechanically ventilated patients with poor-grade aSAH, the PaCO2 was first decreased to 30 mm Hg by modification of the respiratory rate, then gradually increased to 40, 50 and 60 mm Hg for 15 minutes each setting. Thereafter, the respirator settings were returned to baseline parameters. Intracerebral CBF measurement and brain tissue oxygen saturation (StiO2), measured by near-infrared spectroscopy (NIRS), were the primary and secondary end points. Intracranial pressure (ICP) was controlled by external ventricular drainage. Results A total of 60 interventions were performed in 6 patients. CBF decreased to 77% of baseline at a PaCO2 of 30 mm Hg and increased to 98%, 124%, and 143% at PaCO2 values of 40, 50, and 60 mm Hg, respectively. Simultaneously, StiO2 decreased to 94%, then increased to 99%, 105%, and 111% of baseline. A slightly elevated delivery rate of cerebrospinal fluid was noticed under continuous drainage. ICP remained constant. After returning to baseline respirator settings, both CBF and StiO2 remained elevated and only gradually returned to pre-hypercapnia values without a rebound effect. None of the patients developed secondary cerebral infarction. Conclusions Gradual hypercapnia was well tolerated by poor-grade SAH patients. Both CBF and StiO2 reacted with a sustained elevation upon hypercapnia; this elevation outlasted the period of hypercapnia and only slowly returned to normal without a rebound effect. Elevations of ICP were well compensated by continuous CSF drainage. Hypercapnia may yield a therapeutic potential in this state of critical brain perfusion. Clinical trial registration no.: NCT01799525 (ClinicalTrials.gov).

Calcium Antagonists in the Management of Patients with Aneurysmal Subarachnoid Hemorrhage: A Review

Angiology ◽  
1990 ◽  
Vol 41 (11) ◽  
pp. 1010-1016 ◽  
Author(s):  
Harold P. Adams
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cause Of Death ◽  
Calcium Antagonists ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Medical Center ◽  
Current Status ◽  
Important Complication ◽  
Arterial Vasospasm ◽  
Major Medical Center

Cerebral arterial vasospasm and infarction is the leading cause of death and disability among patients who reach a major medical center after aneurysmal subarachnoid hemorrhage (SAH). Recent evidence suggests that two calcium antagonists, nimodipine or nicardipine, may be useful in preventing this important complication of SAH. This paper reviews the current status of these two calcium antagonists in the management of SAH.

scholarly journals Experimental and Clinical Treatment of Subarachnoid Hemorrhage after the Rupture of Saccular Intracranial Aneurysms

2020 ◽  
Vol 10 (6) ◽  
pp. 371
Author(s):  
Serge Marbacher ◽  
John H. Zhang
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Intracranial Aneurysms ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Clinical Treatment ◽  
Special Issue ◽  
The Many ◽  
Insight Into

The Special Issue “Experimental and Clinical Treatment of Subarachnoid Hemorrhage after the Rupture of Saccular Intracranial Aneurysms” provides an excellent insight into the many facets of aneurysmal subarachnoid hemorrhage [...]

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