Management of Sodium Balance by Using Fludrocortisone Acetate in Patients with Subarachnoid Hemorrhage in the Acute Stage

✓ A baboon model of subarachnoid hemorrhage (SAH) has been developed to study the changes in cerebral blood flow (CBF), intracranial pressure (ICP), and cerebral edema associated with the acute stage of SAH. In this model, hemorrhage was caused by avulsion of the posterior communicating artery via a periorbital approach, with the orbit sealed and ICP restored to normal before SAH was produced. Local CBF was measured in six sites in the two hemispheres, and ICP monitored by an implanted extradural transducer. Following sacrifice of the animal, the effect of the induced SAH on ICP, CBF, autoregulation, and CO2 reactivity in the two hemispheres was assessed. Brain water measurements were also made in areas of gray and white matter corresponding to areas of blood flow measurements, and also in the deep nuclei. Two principal patterns of ICP change were found following SAH; one group of animals showed a return to baseline ICP quite quickly and the other maintained high ICP for over an hour. The CBF was reduced after SAH to nearly 20% of control values in all areas, and all areas showed impaired autoregulation. Variable changes in CO2 reactivity were evident, but on the side of the hemorrhage CO2 reactivity was predominantly reduced. Differential increase in pressure lasting for over 7 minutes was evident soon after SAH on the side of the ruptured vessel. There was a significant increase of water in all areas, and in cortex and deep nuclei as compared to control animals.

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Comparison of Clinical Results between GDC Treatment and Direct Surgery for Ruptured Cerebral Aneurysms

Interventional Neuroradiology ◽

10.1177/15910199990050s139 ◽

1999 ◽

Vol 5 (1_suppl) ◽

pp. 207-210

Author(s):

K. Fukui ◽

M. Miyazaki ◽

K. Hattori ◽

H. Osawa ◽

S. Miyachi ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Glasgow Outcome Scale ◽

Death Rate ◽

Cerebral Aneurysms ◽

Clinical Results ◽

Acute Stage ◽

Clinical Grade ◽

Systemic Complication ◽

High Death Rate ◽

High Death

We present a comparison of clinical results between GDC treatment and direct surgery for ruptured cerebral aneurysms. From May 97 to April 98, 32 aneurysms were treated by direct surgery (DS) or GDC treatment. Treatments were selected depending on the clinical grade, degree of hematoma and anatomical aspect of the aneurysms. There were 13 GDC treated cases and 19 direct surgery cases. In GDC cases, there were acute stage embolization for ruptured basilar aneurysm, recurrence of case after clipping for BA-SCA aneurysm, advanced age cases, and systemic complication cases. Glasgow outcome scale (GOS) in GDC cases were 8 GR, 2 MD and 3 SD. GOS in direct surgery cases were 7 GR, 4 MD, 4 SD and 4 deaths. Cases of severe subarachnoid hemorrhage with hematoma influenced the high death rate in direct surgery group. There were three complications associated with the procedure in the GDC group, however, the rate improved after advancement of the procedure. In conclusion, GDC treatment for ruptured cerebral aneurysm was satisfactorily acceptable compared to the results of direct surgery, however, more cases will be needed for precise comparison.

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Management of poor-grade patients with aneurysmal subarachnoid hemorrhage in the acute stage: Importance of close monitoring for neurological grade changes

Surgical Neurology ◽

10.1016/j.surneu.2004.01.015 ◽

2004 ◽

Vol 62 (6) ◽

pp. 531-535 ◽

Cited By ~ 38

Author(s):

Tatsuya Sasaki ◽

Mitsuo Sato ◽

Masahiro Oinuma ◽

Jun Sakuma ◽

Kyouichi Suzuki ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Acute Stage ◽

Close Monitoring ◽

Poor Grade

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Cerebral circulation and metabolism in the acute stage of subarachnoid hemorrhage

Journal of Neurosurgery ◽

10.3171/jns.2000.93.6.1014 ◽

2000 ◽

Vol 93 (6) ◽

pp. 1014-1018 ◽

Cited By ~ 47

Author(s):

Toshiaki Hayashi ◽

Akifumi Suzuki ◽

Jun Hatazawa ◽

Iwao Kanno ◽

Reizo Shirane ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Cerebral Circulation ◽

Cerebral Blood Volume ◽

Aneurysmal Subarachnoid Hemorrhage ◽

Cerebral Metabolism ◽

Aneurysm Rupture ◽

Acute Stage ◽

Content Type ◽

Positron Emission ◽

Fine Print

Object. The mechanism of reduction of cerebral circulation and metabolism in patients in the acute stage of aneurysmal subarachnoid hemorrhage (SAH) has not yet been fully clarified. The goal of this study was to elucidate this mechanism further.Methods. The authors estimated cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), O2 extraction fraction (OEF), and cerebral blood volume (CBV) preoperatively in eight patients with aneurysmal SAH (one man and seven women, mean age 63.5 years) within 40 hours of onset by using positron emission tomography (PET). The patients' CBF, CMRO2, and CBF/CBV were significantly lower than those in normal control volunteers. However, OEF and CBV did not differ significantly from those in control volunteers. The significant decrease in CBF/CBV, which indicates reduced cerebral perfusion pressure, was believed to be caused by impaired cerebral circulation due to elevated intracranial pressure (ICP) after rupture of the aneurysm. In two of the eight patients, uncoupling between CBF and CMRO2 was shown, strongly suggesting the presence of cerebral ischemia.Conclusions. The initial reduction in CBF due to elevated ICP, followed by reduction in CMRO2 at the time of aneurysm rupture may play a role in the disturbance of CBF and cerebral metabolism in the acute stage of aneurysmal SAH.

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Pathogenetic role of no-reflow phenomenon in experimental subarachnoid hemorrhage in dogs

Journal of Neurosurgery ◽

10.3171/jns.1977.46.4.0454 ◽

1977 ◽

Vol 46 (4) ◽

pp. 454-466 ◽

Cited By ~ 82

Author(s):

Takao Asano ◽

Keiji Sano

Keyword(s):

Subarachnoid Hemorrhage ◽

Carbon Black ◽

Acute Stage ◽

Cerebrospinal Fluid Leakage ◽

Pathogenetic Role ◽

No Reflow ◽

No Reflow Phenomenon ◽

Sensory Evoked ◽

The Brain

✓ The real pathogenetic role of no-reflow phenomenon in clinical situations such as the acute stage of subarachnoid hemorrhage (SAH) is not yet known. To study this problem, we carried out the following experiment in dogs: SAH was induced by withdrawing a needle previously inserted into the internal carotid artery through a small craniectomy in the lateral base of the skull. Complete dural repair and cranioplasty was done to avoid cerebrospinal fluid leakage. Cortical cerebral blood flow (CBF) changes, measured by a double-needle type thermocouple, intracranial pressure (ICP), electroencephalogram (EEG), and sensory evoked response were monitored under controlled ventilation for 3 hours after SAH. At the end of the experiment, the brain was perfused with carbon black solution at a pressure of 120 mm Hg. The 32 episodes of SAH thus induced yielded two basic patterns of ICP changes which simulated those previously reported with human SAH. In the first pattern, reactive hyperemia was always observed, followed by complete or incomplete recovery of cerebral function. Perfusion defects were frequently seen in the thalamus, basal ganglia, and parietooccipital cortex symmetrically. In the second pattern, prolonged elevation of ICP resulted in failure of recovery of both CBF and EEG. Carbon black filled only the pial arteries and the rest of the brain was totally unperfused. From the results, the pathogenetic role of the no-reflow phenomenon in the acute stage of SAH as influencing the prognosis is strongly suspected.

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