Ultra-early rebleeding in spontaneous subarachnoid hemorrhage

1996 ◽  
Vol 84 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Yukihiko Fujii ◽  
Shigekazu Takeuchi ◽  
Osamu Sasaki ◽  
Takashi Minakawa ◽  
Tetsuo Koike ◽  
...  
Keyword(s):  
Risk Factors ◽  
Blood Pressure ◽  
Multivariate Analysis ◽  
Subarachnoid Hemorrhage ◽  
Early Operation ◽  
Time Interval ◽  
High Systolic Blood Pressure ◽  
Content Type ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Fine Print

✓ To determine the incidence of, and risk factors for, the occurrence of rebleeding between admission and early operation (ultra-early rebleeding) in patients with spontaneous subarachnoid hemorrhage (SAH), the authors reviewed the cases of 179 patients admitted within 24 hours after their last attack of SAH. Thirty-one (17.3%) of these patients had ultra-early rebleeding despite scheduling of early operation (within 24 hours after admission). The incidence of rebleeding significantly decreased as the time interval between the last attack and admission increased. Patients with rebleeding before admission, high systolic blood pressure, intracerebral or intraventricular hematoma, those in poor neurological condition on admission, and those who underwent angiography within 6 hours of the last SAH were significantly more likely to have ultra-early rebleeding than those without these factors. The incidence of rebleeding also significantly increased as levels of enhancement of platelet sensitivity and thrombin—antithrombin complex increased. Multivariate analysis revealed that the following three factors were independently associated with ultra-early rebleeding: the level of enhancement of platelet sensitivity; the time interval between the last attack and admission; and the level of thrombin—antithrombin complex. On the basis of these findings, the authors suggest that many of the risk factors for ultra-early rebleeding are interrelated. A particularly high risk of ultra-early rebleeding was observed in those patients 1) who had platelet hypoaggregability; 2) who were admitted shortly after their last SAH; and 3) whose thrombin—antithrombin complex levels were extremely high and were thus in severe clinical condition.

Surgical experiences with giant intracranial aneurysms

1984 ◽  
Vol 61 (6) ◽  
pp. 1009-1028 ◽  
Author(s):  
Lindsay Symon ◽  
Janos Vajda
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Mortality Rate ◽  
Intracranial Aneurysms ◽  
Visual Loss ◽  
Considerable Improvement ◽  
Brain Circulation ◽  
Content Type ◽  
Space Occupying Lesion ◽  
Fine Print

✓ A series of 35 patients with 36 giant aneurysms is presented. Thirteen patients presented following subarachnoid hemorrhage (SAH) and 22 with evidence of a space-occupying lesion without recent SAH. The preferred technique of temporary trapping of the aneurysm, evacuation of the contained thrombus, and occlusion of the neck by a suitable clip is described. The danger of attempted ligation in atheromatous vessels is stressed. Intraoperatively, blood pressure was adjusted to keep the general brain circulation within autoregulatory limits. Direct occlusion of the aneurysm was possible in over 80% of the cases. The mortality rate was 8% in 36 operations. Six percent of patients had a poor result. Considerable improvement in visual loss was evident in six of seven patients in whom this was a presenting feature, and in four of seven with disturbed eye movements.

Acute cerebral blood flow response to dopamine-induced hypertension after subarachnoid hemorrhage

1994 ◽  
Vol 80 (5) ◽  
pp. 857-864 ◽  
Author(s):  
Joseph M. Darby ◽  
Howard Yonas ◽  
Elizabeth C. Marks ◽  
Susan Durham ◽  
Robert W. Snyder ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Systemic Blood Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Fine Print

✓ The effects of dopamine-induced hypertension on local cerebral blood flow (CBF) were investigated in 13 patients suspected of suffering clinical vasospasm after aneurysmal subarachnoid hemorrhage (SAH). The CBF was measured in multiple vascular territories using xenon-enhanced computerized tomography (CT) with and without dopamine-induced hypertension. A territorial local CBF of 25 ml/100 gm/min or less was used to define ischemia and was identified in nine of the 13 patients. Raising mean arterial blood pressure from 90 ± 11 mm Hg to 111 ± 13 mm Hg (p < 0.05) via dopamine administration increased territorial local CBF above the ischemic range in more than 90% of the uninfarcted territories identified on CT while decreasing local CBF in one-third of the nonischemic territories. Overall, the change in local CBF after dopamine-induced hypertension was correlated with resting local CBF at normotension and was unrelated to the change in blood pressure. Of the 13 patients initially suspected of suffering clinical vasospasm, only 54% had identifiable reversible ischemia. The authors conclude that dopamine-induced hypertension is associated with an increase in flow in patients with ischemia after SAH. However, flow changes associated with dopamine-induced hypertension may not be entirely dependent on changes in systemic blood pressure. The direct cerebrovascular effects of dopamine may have important, yet unpredictable, effects on CBF under clinical pathological conditions. Because there is a potential risk of dopamine-induced ischemia, treatment may be best guided by local CBF measurements.

Chronic subdural hematoma presenting as spontaneous subarachnoid hemorrhage

1985 ◽  
Vol 63 (5) ◽  
pp. 691-692 ◽  
Author(s):  
Zbigniew Kotwica ◽  
Jerzy Brzeziński
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Subdural Hematoma ◽  
Chronic Subdural Hematoma ◽  
Clinical Findings ◽  
Content Type ◽  
Acute Subarachnoid Hemorrhage ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Fine Print

✓ Six cases of chronic subdural hematoma presenting with the clinical findings of acute subarachnoid hemorrhage are reported. No systemic or focal cause for the bleeding was found, and possible mechanisms are discussed.

Effect of early operation for ruptured aneurysms on prevention of delayed ischemic symptoms

1982 ◽  
Vol 57 (5) ◽  
pp. 622-628 ◽  
Author(s):  
Mamoru Taneda
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Reliable Method ◽  
Early Operation ◽  
Permanent Disability ◽  
Content Type ◽  
Giant Aneurysms ◽  
Ruptured Aneurysms ◽  
Blood Clots ◽  
Subarachnoid Blood ◽  
Fine Print

✓ The effect of removal of subarachnoid blood clots on the prevention of delayed ischemic deficit was evaluated in 239 consecutive patients with ruptured supratentorial non-giant aneurysms. All patients were hospitalized within 24 hours after subarachnoid hemorrhage (SAH) and were classified in Grades 1 to 4 according to the system of Hunt and Hess; classification was made immediately preoperatively in patients operated on within 48 hours after SAH, or 48 hours after SAH in patients for whom delayed operation was planned. Delayed ischemic deficit causing permanent disability or death occurred in 11 (25%) of 44 patients in whom surgery was planned to be delayed for 10 days or more, in 26 (27.7%) of 94 patients in whom the aneurysms were obliterated and blood clots adjacent to them were removed within 48 hours of SAH, and in 11 (10.9%) of 101 patients in whom the aneurysms were obliterated and extensive and aggressive removal of thick subarachnoid clots lying along the arteries (identified on computerized tomographic scan) was performed within 48 hours of SAH. Accordingly, early operation is an effective and reliable method to reduce the occurrence of severe delayed ischemic deficit only when subarachnoid blood clots are removed extensively and aggressively along the arteries within 48 hours of SAH.

Reoperative management of intracranial aneurysms

1995 ◽  
Vol 83 (3) ◽  
pp. 387-393 ◽  
Author(s):  
Steven L. Giannotta ◽  
N. Scott Litofsky
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Operative Procedure ◽  
Technical Difficulty ◽  
Mass Effect ◽  
Time Interval ◽  
Anterior Circulation ◽  
Content Type ◽  
Coating Agents ◽  
Intraoperative Rupture ◽  
Fine Print

✓ Nineteen patients underwent 20 operative procedures for the treatment of recurrent or residual aneurysms. There were 13 small, three large, and four giant lesions; with one exception, all were in the anterior circulation. Five individuals presented with recurrent subarachnoid hemorrhage, six were referred for symptoms of mass effect, and nine were known to have had inadequate treatment at the time of the initial operative procedure. The average time interval from initial treatment to either recurrent subarachnoid hemorrhage or compressive effects was 10.5 and 9.75 years, respectively. No deaths resulted from the reoperative procedures. Two patients suffered moderate disability and one had severe disability. Malpositioned or slipped clips, intraoperative rupture, and inadequate exposure were responsible for 75% of the initial operative failures. The technical difficulty of the reoperative procedure correlated with the length of time between initial and reoperative treatment, the presence of clips and coating agents, and the complexity of the lesion. A classification scheme for preoperative planning and case selection is proposed based on the technical adjuncts required for reoperative aneurysm procedures.

Spontaneous subarachnoid hemorrhage associated with spinal cord tumor

1974 ◽  
Vol 40 (2) ◽  
pp. 252-254 ◽  
Author(s):  
John B. Runnels ◽  
John W. Hanbery
Keyword(s):  
Spinal Cord ◽  
Differential Diagnosis ◽  
Subarachnoid Hemorrhage ◽  
Rare Case ◽  
Spinal Cord Tumor ◽  
Content Type ◽  
Upper Thoracic ◽  
Spontaneous Subarachnoid Hemorrhage ◽  
Fine Print

✓ A rare case of spontaneous subarachnoid hemorrhage from an extramedullary upper thoracic astrocytoma is described. The differential diagnosis between cranial and spinal spontaneous subarachnoid hemorrhage is discussed.

The International Cooperative Studyon the Timing of Aneurysm Surgery

1990 ◽  
Vol 73 (1) ◽  
pp. 18-36 ◽  
Author(s):  
Neal F. Kassell ◽  
James C. Torner ◽  
E. Clarke Haley ◽  
John A. Jane ◽  
Harold P. Adams ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Complete Recovery ◽  
Elevated Blood ◽  
Aneurysm Surgery ◽  
Cooperative Study ◽  
Content Type ◽  
Level Of Consciousness ◽  
The Status ◽  
Fine Print

✓ The International Cooperative Study on the Timing of Aneurysm Surgery evaluated the results of surgical and medical management in 3521 patients between December, 1980, and July, 1983. At admission, 75% of patients were in good neurological condition and surgery was performed in 83%. At the 6-month evaluation, 26% of the patients had died and 58% exhibited a complete recovery. Vasospasm and rebleeding were the leading causes of morbidity and mortality in addition to the initial bleed. Predictors for mortality included the patient's decreased level of consciousness and increased age, thickness of the subarachnoid hemorrhage clot on computerized tomography, elevated blood pressure, preexisting medical illnesses, and basilar aneurysms. The results presented here document the status of management in the 1980's.

The effect of nimodipine on cerebral oxygenation in patients with poor-grade subarachnoid hemorrhage

2004 ◽  
Vol 101 (4) ◽  
pp. 594-599 ◽  
Author(s):  
Michael F. Stiefel ◽  
Gregory G. Heuer ◽  
John M. Abrahams ◽  
Stephanie Bloom ◽  
Michelle J. Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Brain Tissue ◽  
Cerebral Oxygenation ◽  
Content Type ◽  
Poor Grade ◽  
Physiological Variables ◽  
Arterial Blood ◽  
End Tidal ◽  
Fine Print

Object. Nimodipine has been shown to improve neurological outcome after subarachnoid hemorrhage (SAH); the mechanism of this improvement, however, is uncertain. In addition, adverse systemic effects such as hypotension have been described. The authors investigated the effect of nimodipine on brain tissue PO2. Methods. Patients in whom Hunt and Hess Grade IV or V SAH had occurred who underwent aneurysm occlusion and had stable blood pressure were prospectively evaluated using continuous brain tissue PO2 monitoring. Nimodipine (60 mg) was delivered through a nasogastric or Dobhoff tube every 4 hours. Data were obtained from 11 patients and measurements of brain tissue PO2, intracranial pressure (ICP), mean arterial blood pressure (MABP), and cerebral perfusion pressure (CPP) were recorded every 15 minutes. Nimodipine resulted in a significant reduction in brain tissue PO2 in seven (64%) of 11 patients. The baseline PO2 before nimodipine administration was 38.4 ± 10.9 mm Hg. The baseline MABP and CPP were 90 ± 20 and 84 ± 19 mm Hg, respectively. The greatest reduction in brain tissue PO2 occurred 15 minutes after administration, when the mean pressure was 26.9 ± 7.7 mm Hg (p < 0.05). The PO2 remained suppressed at 30 minutes (27.5 ± 7.7 mm Hg [p < 0.05]) and at 60 minutes (29.7 ± 11.1 mm Hg [p < 0.05]) after nimodipine administration but returned to baseline levels 2 hours later. In the seven patients in whom brain tissue PO2 decreased, other physiological variables such as arterial saturation, end-tidal CO2, heart rate, MABP, ICP, and CPP did not demonstrate any association with the nimodipine-induced reduction in PO2. In four patients PO2 remained stable and none of these patients had a significant increase in brain tissue PO2. Conclusions. Although nimodipine use is associated with improved outcome following SAH, in some patients it can temporarily reduce brain tissue PO2.

Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a preliminary report

2000 ◽  
Vol 93 (5) ◽  
pp. 743-752 ◽  
Author(s):  
Daniel F. Kelly ◽  
Irene T. Gaw Gonzalo ◽  
Pejman Cohan ◽  
Nancy Berman ◽  
Ronald Swerdloff ◽  
...  
Keyword(s):  
Risk Factors ◽  
Subarachnoid Hemorrhage ◽  
Head Injury ◽  
Severe Head Injury ◽  
Gh Deficiency ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Content Type ◽  
Pituitary Dysfunction ◽  
Function Testing ◽  
Fine Print

Object. Recognition of pituitary hormonal insufficiencies after head injury and aneurysmal subarachnoid hemorrhage (SAH) may be important, especially given that hypopituitarism-related neurobehavioral problems are typically alleviated by hormone replacement. In this prospective study the authors sought to determine the rate and risk factors of pituitary dysfunction after head injury and SAH in patients at least 3 months after insult.Methods. Patients underwent dynamic anterior and posterior pituitary function testing. Results of the tests were compared with those of 18 age-, sex-, and body mass index—matched healthy volunteers. The 22 head-injured patients included 18 men and four women (mean age 28 ± 10 years at the time of injury) with initial Glasgow Coma Scale (GCS) scores of 3 to 15. Eight patients (36.4%) had a subnormal response in at least one hormonal axis. Four were growth hormone (GH) deficient. Five patients (four men, all with normal testosterone levels, and one woman with a low estradiol level) exhibited an inadequate gonadotroph response. One patient had both GH and thyrotroph deficiency and another had both GH deficiency and borderline cortisol deficiency. At the time of injury, all eight patients with pituitary dysfunction had an initial GCS score of 10 or less and, compared with the 14 patients without dysfunction, were more likely to have had diffuse swelling, seen on initial computerized tomography scans (p < 0.05), and to have sustained a hypotensive or hypoxic insult (p = 0.07). Of two patients with SAH who were studied (Hunt and Hess Grade IV) both had GH deficiency.Conclusions. From this preliminary study, some degree of hypopituitarism appears to occur in approximately 40% of patients with moderate or severe head injury, with GH and gonadotroph deficiencies being most common. A high degree of injury severity and secondary cerebral insults are likely risk factors for hypopituitarism. Pituitary dysfunction also occurs in patients with poor-grade aneurysms. Postacute pituitary function testing may be warranted in most patients with moderate or severe head injury, particularly those with diffuse brain swelling and those sustaining hypotensive or hypoxic insults. The neurobehavioral effects of GH replacement in patients suffering from head injury or SAH warrant further study.

The effect of subarachnoid hemorrhage on blood and CSF atrial natriuretic factor

1989 ◽  
Vol 71 (1) ◽  
pp. 32-37 ◽  
Author(s):  
Jeffrey V. Rosenfeld ◽  
Gene H. Barnett ◽  
Cathy A. Sila ◽  
John R. Little ◽  
Emmanuel L. Bravo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Serum Sodium ◽  
Atrial Natriuretic Factor ◽  
Venous Pressure ◽  
Sodium Concentration ◽  
Control Group ◽  
Central Venous ◽  
Content Type ◽  
Fine Print

✓ Atrial natriuretic factor (ANF) is a diuretic natriuretic peptide hormone produced by both the heart and brain which has been postulated to play a role in the hemodynamic and sodium instability that frequently follows subarachnoid hemorrhage (SAH). Levels of ANF were measured in 12 patients with nontraumatic SAH and nine control patients with unruptured cerebral aneurysms. At surgery, the mean plasma ANF level (± standard deviation) of the SAH group was significantly higher than that of the control group (158.1 ± 83.8 vs. 57.8 ± 45.3 pg/ml, respectively; p = 0.01). There was no significant difference in serum sodium concentration, blood pressure, or central venous pressure between these groups. Nine patients with SAH due to aneurysm rupture had plasma ANF levels similar to those in three patients with SAH due to other causes. Four patients with moderate to severe SAH had significantly higher mean cerebrospinal fluid (CSF) ANF values (17.7 ± 12.8 pg/ml) than five patients with minimal SAH (0.6 ± 0.9 pg/ml) or the control group of nine patients (3.7 ± 1.3 pg/ml) (p < 0.05). Five patients with moderate to severe SAH had significantly higher plasma ANF values (202.6 ± 72.2 pg/ml) than five with minimal SAH (86.8 ± 29.2 pg/ml) or the control group (57.8 ± 45.3 pg/ml) (p < 0.05). Plasma ANF values were substantially higher than CSF ANF content in the SAH group (p < 0.01) and in the control group (p = 0.05). From these data it is concluded that: 1) plasma ANF is elevated significantly after SAH; 2) this rise appears unrelated to the cause of hemorrhage, serum sodium concentration, blood pressure, or central venous pressure, but is related to the extent of the hemorrhage; 3) ANF concentrations in the CSF are significantly lower than in plasma, and are elevated after moderate to severe SAH; and 4) the source of CSF ANF is probably the plasma, and the source of plasma ANF is likely the heart.

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