Outcome 1 year after SAH from cerebral aneurysm

Management morbidity, mortality, and functional status in 112 consecutive good-risk patients

Full access

✓ A group of 112 consecutive patients who initially had no neurological deficits after subarachnoid hemorrhage (SAH) was followed intensively for at least 1 year. Ninety-four were in neurological Grade I or II (Hunt and Hess classification) on arrival. A hundred patients underwent late surgery but, despite excellent surgical results, major morbidity and mortality rates were observed related to preoperative complications. In the preoperative period, 14 (13%) rebled, 41 (37%) had symptomatic cerebral vasospasm, and 24 (21%) had hydrocephalus that required treatment. Of the 100 surgical patients, 73 were in Grade I or II, 26 in Grade III, and one in Grade IV. Six patients had intraoperative neurological complications, and two had delayed postoperative cerebral infarction. Six patients died during hospitalization, but only one as a result of operation. Six others died during the year following discharge of causes unrelated to the operation. The ultimate functional outcome at 1 year of these initially good-risk patients was poor. Only 46% were fully recovered, and 25% reported emotional or psychological disturbances that interfered with their daily lives. Forty-four percent could return to their previous jobs or a comparable position, and 20% obtained lesser employment. Management mortality at 1 year was 11%, and morbidity related to persistent neurological deficits (mainly strokes from vasospasm) was 20%. Thus, management mortality and morbidity at 1 year was 31%, and the number of patients returning to useful life was disappointing. The authors support the suggestion by previous workers that an analysis of at least the 6-month and perhaps the 1-year outcome (especially management mortality for all patients) provides the most important parameter for judging outcome and comparing different management protocols for SAH.

Abstract

✓ A group of 112 consecutive patients who initially had no neurological deficits after subarachnoid hemorrhage (SAH) was followed intensively for at least 1 year. Ninety-four were in neurological Grade I or II (Hunt and Hess classification) on arrival. A hundred patients underwent late surgery but, despite excellent surgical results, major morbidity and mortality rates were observed related to preoperative complications. In the preoperative period, 14 (13%) rebled, 41 (37%) had symptomatic cerebral vasospasm, and 24 (21%) had hydrocephalus that required treatment. Of the 100 surgical patients, 73 were in Grade I or II, 26 in Grade III, and one in Grade IV. Six patients had intraoperative neurological complications, and two had delayed postoperative cerebral infarction. Six patients died during hospitalization, but only one as a result of operation. Six others died during the year following discharge of causes unrelated to the operation. The ultimate functional outcome at 1 year of these initially good-risk patients was poor. Only 46% were fully recovered, and 25% reported emotional or psychological disturbances that interfered with their daily lives. Forty-four percent could return to their previous jobs or a comparable position, and 20% obtained lesser employment. Management mortality at 1 year was 11%, and morbidity related to persistent neurological deficits (mainly strokes from vasospasm) was 20%. Thus, management mortality and morbidity at 1 year was 31%, and the number of patients returning to useful life was disappointing. The authors support the suggestion by previous workers that an analysis of at least the 6-month and perhaps the 1-year outcome (especially management mortality for all patients) provides the most important parameter for judging outcome and comparing different management protocols for SAH.

The management of patients with ruptured intracranial aneurysms has passed through a phase of rapid evolution and modification in the past two decades. Despite advanced surgical technique, however, the overall morbidity and mortality rates following aneurysmal rupture remain high. This report presents the long-term results in a group of 112 consecutive patients without initial neurological deficits that may facilitate comparison of management protocols using different pharmacological or surgical strategies. The functional outcome and morbidity at 1 year are emphasized as the central features in comparing results of different studies, and the mortality rate is stressed as the least equivocal indicator of success or failure of care. The patients described here underwent “late” (delayed) operation. Hence, these data may be useful for any future comparisons with the outcome in patients undergoing “early” surgery. The large proportion of patients unable to resume their previous level of performance demonstrates the need for long-term follow-up evaluation in judging study results.

Clinical Material and Methods

We analyzed the outcome of 112 consecutive good-risk patients with a ruptured cerebral aneurysm. The analysis was limited to patients who had normal neurological function following subarachnoid hemorrhage (SAH). The basic therapeutic plan included therapy to minimize rebleeding and vasospasm, and “late” (delayed) surgery. The results of management were judged at 1 year or longer (12 to 24 months) after aneurysm rupture.

This series included 100 consecutive patients who underwent surgery following SAH from a proven aneurysm. The first patient was admitted on March 16, 1977, and the last (the 100th consecutive patient undergoing elective operation) on June 26, 1981. Twelve additional neurologically intact patients were admitted after aneurysmal SAH during this period, but were not operated on because of subsequent deterioration or inoperable aneurysms. Another 61 patients were admitted with neurological deficit (Grade III or higher), but were excluded from this study for that reason. The grading system used is similar to that of Hunt and Miller5,13 and clearly separates patients with severe drowsiness or focal neurological deficits from clinically better patients, as follows:

  1. Normal neurological status

  2. Headache, meningismus, drowsiness without confusion, no neurological deficit except that relating to a cranial nerve

  3. Confusion, obtundation, or focal neurological deficit

  4. Coma

  5. Grade V: Death.

Data were compiled by a full-time research nurse. Each case was reviewed in detail by a neurologist (A.H.R.), who judged the cause of each complicating event and assigned a clinical grade. Judgmental difficulties were resolved by consulting the physician primarily responsible for the particular patient's care.

All 112 patients were categorized as Grade I or II on their initial hospital admission. However, 18 were in Grade III or IV upon ultimate admission to the Massachusetts General Hospital (MGH). Thirty-seven patients were admitted to the MGH within 48 hours of SAH, 74 within 1 week, 27 in the 2nd week, and 11 thereafter. The mean (± standard deviation) time of admission to the MGH was 7 +13 days after SAH. Figure 1 summarizes the distribution of the patients' ages (mean age 48 years). Eighty-one were female, and 31 male. Table 1 describes the location of the aneurysms.

Fig. 1.
Fig. 1.

Ages of 112 consecutive patients in neurological Grade I or II on admission after subarachnoid hemorrhage.

TABLE 1

Location of 122 aneurysms in 112 patients in neurological Grade I or II on admission*

Artery AffectedNo. of Cases
internal carotid (ICA)27
anterior communicating38
posterior communicating (PCoA)11
ICA-PCoA3
middle cerebral11
anterior cerebral3
basilar6
vertebral1
posterior inferior cerebellar3
ophthalmic1
pericallosal1
multiple17

Grading by Hunt and Miller's classification,5 see text.

A fairly conventional and uniform program of management was attempted, as previously described,6 but was altered as dictated by acute problems. A computerized tomographic (CT) scan was obtained within 24 hours of admission in most cases. The patient was then placed on strict bedrest in a dimly lit room, and visitors were restricted. A normal diet was provided but attention was given to hydration and input/output volumes in order to avoid hypovolemia.

Pharmacological management included administration of epsilon aminocaproic acid (EACA), 30 to 36 gm/day intravenously in 107 of the 112 patients, and phenytoin or phenobarbital in conventional oral doses as prophylaxis for seizures. Reserpine, 0.2 mg subcutaneously, and kanamycin, 1 gm orally,14 were given three times daily to assess the impact of these agents on subsequent postoperative vasospasm in 88 of 100 surgical patients. Headache was treated with acetaminophen or codeine, as required. Blood pressure was assiduously kept in the normal range (within 5% of the premorbid range, if known) with hydralazine, or, when required in occasional instances, with nitroprusside, dopamine, or phenylephrine (Neo-Synephrine). Haloperidol and diazepam were used rarely for extreme restlessness, and flurazepam was used liberally to induce sleep. Corticosteroids were administered to patients who had brain edema or parenchymal clots visible on CT scanning.

The diagnosis of SAH was established either by CT demonstration of blood in the cerebral sulci or cisterns or by lumbar puncture if the scan was normal. Operation was planned for Day 9 to 12 and arteriography was delayed until 24 to 48 hours before operation. When the arteriogram demonstrated an aneurysm, operation was carried out even if there was minimal vasospasm (1+ or 2+ on the scale of Fisher, et al.).3 When the arteriogram demonstrated significant vasospasm (3+ or 4+), operation was delayed 5 to 10 days. A second angiogram was usually obtained at this time. If the vasospasm had improved, operation was performed in the next 1 to 2 days in most cases. If the vasospasm was still severe, operation was carried out a week later (approximately 3 weeks after SAH) without benefit of another angiogram. All but three operations were carried out 9 days or more after the last SAH (mean 20 days). Figure 2 shows the timing of operation.

Fig. 2.
Fig. 2.

Timing of operation after subarachnoid hemorrhage (SAH) in 100 patients.

After discharge from the hospital, each patient's functional status was checked as often as possible for at least 1 year. If data from follow-up visits were unobtainable, contact was reestablished by writing or telephoning the patient's relatives, friends, employer, social worker, or insurance company. In collecting follow-up data of missing patients, the State Office of Vital Statistics, the State Income Tax Office, and the local Social Security Office were consulted. Follow-up information for 1 year was eventually obtained for all but one patient.

Summary of Cases
Preoperative Complications
Rebleeding

A presumptive clinical diagnosis of rebleeding was made if a patient experienced a severe headache of sudden onset and neurological deterioration. In all, 14 patients (13%) rebled while hospitalized. The diagnosis was confirmed by lumbar puncture or CT scan in 13 patients. Ten recovered, and four died. Of 107 patients who received EACA, 13 rebled, and, of five patients who did not receive this drug, two rebled.

Symptomatic Cerebral Vasospasm

Symptomatic cerebral vasospasm was defined as deterioration of neurological grade in the presence of focal clinical signs consistent with regional brain ischemia, but without evidence of rebleeding, hydrocephalus, infection, metabolic imbalance, drug intoxication, or other cause.3,6 Forty-one of the 112 patients (37%) developed signs of neurological deterioration judged to be caused by cerebral vasospasm. Symptoms ranged from mild confusion or minimal weakness to severe hemiplegia, hypokinesia, or coma (in two cases of basilar artery vasospasm). The onset of slight pronation of the outstretched arm or flattening of the nasolabial fold was sufficient to include a patient in this category. Verification of vasospasm was obtained by angiography in 37 cases and from CT scan or clinical examination in four cases.

Four patients with symptomatic vasospasm died (4% of the total group). One year later, 15 patients had persistent neurological deficits (see below) but six of these had also undergone shunting for clinically significant hydrocephalus. Twenty-six of the 41 patients with vasospasm recovered without any discernible neurological deficit at 1 year.

Hydrocephalus

The diagnosis of symptomatic hydrocephalus was made in patients who demonstrated neurological deterioration, particularly drowsiness or coma with extensor posturing or increased limb tone, with evidence of enlarged ventricles on CT scanning. Twenty-four patients (21%) had hydrocephalus that was treated by serial lumbar punctures, ventricular drainage, surgical shunting, or a combination of therapies. Fourteen patients received shunts in the preoperative period and seven in the postoperative period.

Preoperative Grades and Management

Of the 112 patients admitted in Grades I and II, 100 underwent operation. The reasons for withholding surgery in the remaining 12 patients and their discharge grades are listed in Table 2. There were three preoperative deaths. Of the 100 patients who underwent surgery, 32 patients were in preoperative Grade I, 41 in Grade II, 26 in Grade III, and one in Grade IV. The number of patients who deteriorated prior to operation and their admission and preoperative grades are shown in Table 3. Thus, two-thirds of patients who were initially in Grade I or II still had normal, or only slightly abnormal, neurological examinations preoperatively.

TABLE 2

Reason for withholding operation and outcome in 12 patients

Case No.Age (yrs)Reason for Not OperatingArtery AffectedDischarge Grade*
141inoperable sitebasilarI
250inoperable sitemultipleI
372poor operative candidatebasilarIII
467poor operative candidateanterior communicatingIII
572rebleedanterior communicatingIV
676spasm & infarctioninternal carotidIV
750spasm & infarctionanterior communicatingIV
846spasm & infarctionposterior communicatingV
953spasm & infarctionposterior communicatingV
1056rebleed, deathinternal carotidV
1143rebleed, deathposterior communicating, middle cerebralV
1285rebleed, deathposterior inferior cerebellarV

Grading by Hunt and Miller's classification,5 see text.

TABLE 3

Results of preoperative management in 112 patients in Grade I or II on initial admission*

Grade on MGH AdmissionNo. of CasesNo OperationPreoperative Grade
IIIIIIIV   
I or II9473240141
III14101120
IV440000
total cases112123241261
percent100113037231

Grading by Hunt and Miller's classification,5 see text. Compare to Table 2 in report of Sundt, et al.11 MGH = Massachusetts General Hospital.

Operations were performed by the attending staff headed by Drs. Robert Ojemann and Robert Crowell and residents.10 The staff surgeon responsible for neurovascular cases supervised all procedures. All operations were carried out with the operating microscope. Balanced anesthesia was used and intraoperative hypotension was achieved by administration of hydralazine or propranolol.

Operative and Postoperative Complications

Intraoperative neurological deterioration occurred in six patients. The causes appeared to involve intraoperative bleeding in two cases, temporary occlusion of a major vessel in one, excessive retraction in one, embolus to the pericallosal artery in one, and in the remaining case the cause was unclear. Only one of these six patients ultimately recovered without neurological deficit.

Eight patients had some evidence of delayed neurological deterioration due to cerebral vasospasm after operation; six recovered without focal deficit. Of 88 patients who had received kanamycin and reserpine in adequate amounts before operation, six exhibited delayed postoperative deterioration because of vasospasm, five of whom recovered. Of 12 patients who had not received kanamycin and reserpine prior to operation, two developed delayed neurological deficits, one of whom recovered (Table 4). Four of our 88 patients treated with these agents died of ischemic stroke and 11 had residual neurological deficit as a result of preoperative ischemia. No death occurred as a result of delayed postoperative vasospasm.

TABLE 4

Outcome related to treatment with kanamycin (K) and reserpine (R)

OutcomeK & R TreatmentNo K & R Treatment
persistent deficit*11
no deficit8711
total cases8812

Persistent neurological deficit from postoperative vasospasm.

Mortality

Six patients died during hospitalization: three deaths resulted from rebleeding, two from infarction, and one from postoperative pulmonary embolus. Six patients died during the year after discharge from the hospital: three patients rebled from an untreated aneurysm and died, one died of unknown causes, and two who were comatose died of late complications of the original hemorrhage. During the ensuing 1 to 3 years, only two additional patients are known to have died: one from complications of cystectomy and one, who was in a vegetative state, of unknown causes.

Outcome at 1 Year

Contact was established with all but one of the 106 patients who were discharged.

Functions of Daily Living

Patients were questioned about their physical capabilities. They were judged to be physically independent if they could perform all tasks related to daily care by themselves without any support from others; partially dependent if they required help in dressing, feeding, ambulation, transportation, or communication; and totally dependent if they were unable to perform any act of daily living without help. Fifty-two patients (46%) were fully independent, 28 (25%) were independent but had emotional or psychological difficulties that interfered with their daily lives, and 19(17%) were totally or partly dependent on others for their care (Fig. 3).

Fig. 3.
Fig. 3.

Overall morbidity and mortality at 1 year after subarachnoid hemorrhage as reflected in ability to carry out daily activities in 112 patients.

No associated neurological cause of emotional impairment was apparent in 14 of the 28 patients who were independent but had emotional or psychological complaints. Their hospital course was unmarked by any specific neurological disturbance or other ictus. Ten patients had sustained a cerebral infarction, one had developed hydrocephalus that required treatment, and three had rebled during hospitalization. None of these 14 patients left the hospital with a focal neurological deficit.

Neurological function

Twenty-two patients (20%) had persistent neurological deficits at 1 year, although four were able to work. These deficits were primarily related to preoperative vasospasm in 15, postoperative vasospasm in one, hydrocephalus in three, and perioperative stroke in three. An additional patient had a seizure disorder that became apparent 1 year after SAH, and another patient had exacerbation of preexisting multiple sclerosis several months after discharge.

Capacity for Work

Patients were asked about their ability to work to determine whether the illness had reduced their premorbid capacity. Seventy-two of the 112 patients were able to return to work: 50 patients (44%) had the same full-time occupation, a comparable position, or were retired but otherwise capable of holding a full-time position. Twenty-two patients (20%) took a less demanding or part-time job, and 27 (24%) were unable to work or were retired and inactive as a direct result of their illness (Fig. 4).

Fig. 4.
Fig. 4.

Ability to work at 1 year after subarachnoid hemorrhage among 112 patients.

In summary, the management mortality rate at 1 year was 11%, and morbidity related to neurological deficits was 20% in these 112 patients. Thus, the combined management mortality and morbidity rate was 31%. Management success related to return to work was 64%, but, when those taking less demanding jobs are excluded, the success rate is 44%. In the majority of patients, deterioration in the capacity for work was not caused by physical deficits, but instead was related to reported psychological or emotional disturbances.

Discussion

Morley9 stressed that the evaluation of treatment of SAH must include the outcome of all patients, regardless of whether they were treated medically or surgically. He observed that “neurosurgeons, with an interest vested in their particular skill, may not be the most detached and objective authorities on the merit of different forms of treatment.”9 Lougheed8 employed the term “management mortality and morbidity” for this purpose and distinguished overall results from surgical mortality and morbidity. This differentiation allowed for a less ambiguous comparison between early and late surgery. Weir and Aronyk13 used this concept to compare the results of management protocols that differed primarily in the timing of surgery. Several authors have made the point that if the stronger patients are selected for surgery, and the sicker ones are managed medically, then surgery, whether early or late, will appear to have a better outcome. Only if overall management outcome is considered can a fair estimate of success be made.

With these concepts in mind, we sought to describe the 1-year outcome of patients with SAH from a ruptured aneurysm who had no initial neurological deficit (Grades I and II). A review of the literature on the management of patients with ruptured aneurysms showed little comparable data. Only a few reports supply mortality and morbidity data at 1 year. The reports of impairment of work capacity are exhaustive in some studies, but neurological and psychological outcomes are difficult to discern.

Mortality seems to be the least equivocal factor that can be used to compare reports from different centers, a point emphasized by Weir and Aronyk13 and Artiola i Fortuny and Prieto-Valiente.1,2 Our data show management mortality for 1 year following admission (11%) to be an important indicator of the overall adequacy of management, since few incidents related to the original ictus occurred after this period. From the surgical point of view, however, it should be noted that only two-thirds of patients who were initially in Grade I or II were still in good neurological condition preoperatively (Table 3). Also, the mortality rate relating to operation in our group was only 1% (due to a postoperative pulmonary embolus), which is comparable to the results at other centers with similar case loads of aneurysm surgery.

Sundt, et al.,12 demonstrated how mortality data can faithfully represent the success or failure of overall management. Their management mortality (calculated from their Table 3) was 7% at 6 months for patients who were in Grade 1 and 2 (Botterell classification) on admission, a result that is similar to our overall rate of 11% at 1 year and 7% for patients who were in Grade I or II on admission (Table 3). Although the admission grades in each series were comparable, their series differs from ours in that a larger proportion of patients were in Grade I preoperatively in their series (43%) than in ours (30%) (Table 3). One major difference between the orientation of the two series is that we used the patients' grade at the time of hemorrhage as the point of departure for analysis, and they considered the grade on admission to their center. They also had no patients who survived without surgery, whereas there were seven survivors in our series who did not have operations.

Artiola i Fortuny and Prieto-Valiente1,2 also stressed mortality as a reflection of overall outcome, but their results are measured from the date of operation. Comparison of our data with theirs is difficult, since no information indicating overall management mortality (including unoperated patients) is given. Five-year mortality for Grade I and II operated patients in the series of Artiola i Fortuny and Prieto-Valiente (calculated from their Table 7) was 15%. This is greater than that in the series of Sundt, et al.,12 at 6 months or in ours at 1 year. Weir and Aronyk13 reported management mortality at 30 days after operation to be 12% for their Grade I and II patients who underwent surgery 9 or more days after hemorrhage.

The rationale for suggesting that outcome at 1 year is representative of the overall result of a management program is supported by several observations. Patients who died in the hospital accounted for only half of the deaths occurring within 1 year that could be attributed to the initial aneurysmal rupture. Two of the patients died as a result of complications suffered during hospitalization, and three others rebled after discharge. The latter three patients died of rebleeding from aneurysms deemed too difficult to treat by operation, or sustained in-hospital complications that precluded elective surgery. In addition, after a 1-year interval, almost every patient had stabilized from the vicissitudes of his/her illness. Few changes in status or deaths occurred in the subsequent 1- to- 3-year period. There may not be a large difference between 1 year and 6 months of follow-up, but we found that some patients who had not returned to work at 6 months did so subsequently.

Our study shows that a large number of patients complain of emotional and psychological incapacities. For example, only 44% of our surviving patients were capable of resuming their premorbid occupation (or a similar position). Another 25% had some vaguely defined (by the patient) psychological problem that was not associated with a focal or obvious global neurological deficit, and this reduced the level of work of which they were capable. Artiola i Fortuny and Prieto-Valiente1,2 found that only 51% of survivors of operation returned to equivalent work, and 27% had emotional disorders, as determined by a standard scoring method and questionnaires. The best study of postoperative capacity to work is that of Sundt, et al.12 They found a better rate of employment and normal mentation than we did, with little or no neurological deficit in 314 (74%) of 422 patients who were in Grades I and II on admission (their Table 3; “excellent” group), but the results are very similar if only those of our patients who were in Grade I or II on admission to the MGH as opposed to another hospital are considered. Comparison of our data to the recent series reported by Shephard11 is difficult, because his report of 80% of patients with normal working capacity represented only 75% of those at risk on admission, and patients of all grades were included.

The date of operation appears to be a less desirable starting point than the date of admission for determining the adequacy of management, because a number of deaths occurred prior to operation. In the future, it may be advisable to restrict comparisons to patients who are admitted on the day of and perhaps the day after hemorrhage to the tertiary center since the variables of management are then reduced. One-third of our patients were admitted to our unit within 48 hours of hemorrhage and two-thirds within 1 week. Differences in the timing of admission may, in part, account for differences in management morbidity, mortality, and functional outcome between our series and those of others.

These reports show a need to evaluate further patients who complain of psychological or emotional impairment. The cause of this difficulty is obscure, but one explanation related specifically to SAH should be considered. Iron deposited in the meninges is toxic to neurons, and an uncommon syndrome of meningeal hemosiderosis, consisting of progressive dementia, mild hydrocephalus, cerebellar ataxia, and impaired audition, occurs after SAH.4 Purkinje cells are particularly susceptible to iron in the adjacent meninges, accounting for the ataxia. It is possible that many patients demonstrate a restricted form of this illness, particularly if most of the blood and meningeal staining is supratentorial. This speculation on our part is the basis of studies we are now conducting in some of these patients. Alternatively, unnoticed hydrocephalus may eventually lead to mild dementia independent of the effects of blood.

As neurosurgeons have come to understand that the poor outcome in many patients with SAH is due to cerebral ischemia and rebleeding, some have argued for early operation. Data collection procedures similar to the one described here allow comparison by a number of criteria of early surgery with other management protocols.

In a randomized study reported by one of us (N.T.Z.),14 reserpine and kanamycin were found to lessen both pre- and postoperative ischemia. Knuckey and Stokes7 recently reported a beneficial effect of reserpine and kanamycin on delayed postoperative ischemia only, in that the incidence was 6% in treated patients and 16% in untreated patients. Their results are comparable with those of the present study, but the number of patients was small in both instances. In the present study, only one of 88 treated patients had a residual neurological deficit due to delayed postoperative ischemia, compared to one of 12 untreated patients (Table 4). Neither our current study nor that of Knuckey and Stokes7 found a clear beneficial effect of these agents on preoperative cerebral ischemia.

In conclusion, this analysis supports the current view that, despite the excellent surgical results that can be obtained by a team dedicated to neurovascular surgery, the problems of preoperative vasospasm and rebleeding remain formidable. The ultimate outcome is unsatisfactory, when reviewed from a wider perspective, in almost half of good-risk patients.

Acknowledgments

Drs. Robert Ojemann and Robert Crowell kindly allowed the inclusion of patients from their services, many of whom are described in their text.10 Dr. J. P. Kistler cared for many of the patients and we acknowledge his help. We thank Dr. Roberto Heros for valuable advice in evaluating the patient data, and Ms. Janet Ploetz and Mrs. Jody Roberts for aiding in data collection and organization.

References

  • 1.

    Artiola i Fortuny LPrieto-Valiente L: Long-term prognosis in surgically treated intracranial aneurysms. Part 1: Mortality. J Neurosurg 54:26341981J Neurosurg 54:

  • 2.

    Artiola i Fortuny LPrieto-Valiente L: Long-term prognosis in surgically treated intracranial aneurysms. Part 2: Morbidity. J Neurosurg 54:35431981J Neurosurg 54:

  • 3.

    Fisher CMRoberson GHOjemann RG: Cerebral vasospasm with ruptured saccular aneurysm — the clinical manifestations. Neurosurgery 1:2452481977Neurosurgery 1:

  • 4.

    Hughes JTOppenheimer DR: Superficial siderosis of the central nervous system. A report on nine cases with autopsy. Acta Neuropathol 13:56741969Acta Neuropathol 13:

  • 5.

    Hunt WEMiller CA: The results of early operation for aneurysm. Clin Neurosurg 24:2082151977Clin Neurosurg 24:

  • 6.

    Kistler JP: Management of subarachnoid hemorrhage from ruptured saccular aneurysmRopper AHKennedy SKZervas NT (eds): Neurological and Neurosurgical Intensive Care. Baltimore: University Park Press1983175188Neurological and Neurosurgical Intensive Care.

  • 7.

    Knuckey NWStokes BAR: Medical management of patients following a ruptured cerebral aneurysm, with ε-aminocaproic acid, kanamycin, and reserpine. Surg Neurol 17:1811851982Surg Neurol 17:

  • 8.

    Lougheed WM: Selection, timing, and technique of aneurysm surgery of the anterior circle of Willis. Clin Neurosurg 16:951131969Clin Neurosurg 16:

  • 9.

    Morley TP: Introduction to intracranial aneurysm: aspects of treatmentMorley TP (ed): Current Controversies in Neurosurgery. Philadelphia: WB Saunders197657Current Controversies in Neurosurgery.

  • 10.

    Ojemann RGCrowell RM: Surgical Management of Cerebrovascular Disease. Baltimore: Williams & Wilkins1983Surgical Management of Cerebrovascular Disease.

  • 11.

    Shephard RH: Ruptured cerebral aneurysms: early and late prognosis with surgical treatment. A personal series, 1958–1980. J Neurosurg 59:6151983J Neurosurg 59:

  • 12.

    Sundt TM JrKobayashi SFode NCet al: Results and complications of surgical management of 809 intracranial aneurysms in 722 cases. Related and unrelated to grade of patient, type of aneurysm, and timing of surgery. J Neurosurg 56:7537651982J Neurosurg 56:

  • 13.

    Weir BAronyk K: Management mortality and the timing of surgery for supratentorial aneurysms. J Neurosurg 54:1461501981J Neurosurg 54:

  • 14.

    Zervas NTCandia MCandia Get al: Reduced incidence of cerebral ischemia following rupture of intracranial aneurysms. Surg Neurol 11:3393441979Surg Neurol 11:

This work was supported in part by Grant HL22573 from the National Heart and Lung Institute.

Article Information

Address reprint requests to: Allan H. Ropper, M.D., Department of Neurology, Massachusetts General Hospital, Boston, Massachusetts 02114.

© AANS, except where prohibited by US copyright law.

Headings

Figures

  • View in gallery

    Ages of 112 consecutive patients in neurological Grade I or II on admission after subarachnoid hemorrhage.

  • View in gallery

    Timing of operation after subarachnoid hemorrhage (SAH) in 100 patients.

  • View in gallery

    Overall morbidity and mortality at 1 year after subarachnoid hemorrhage as reflected in ability to carry out daily activities in 112 patients.

  • View in gallery

    Ability to work at 1 year after subarachnoid hemorrhage among 112 patients.

References

1.

Artiola i Fortuny LPrieto-Valiente L: Long-term prognosis in surgically treated intracranial aneurysms. Part 1: Mortality. J Neurosurg 54:26341981J Neurosurg 54:

2.

Artiola i Fortuny LPrieto-Valiente L: Long-term prognosis in surgically treated intracranial aneurysms. Part 2: Morbidity. J Neurosurg 54:35431981J Neurosurg 54:

3.

Fisher CMRoberson GHOjemann RG: Cerebral vasospasm with ruptured saccular aneurysm — the clinical manifestations. Neurosurgery 1:2452481977Neurosurgery 1:

4.

Hughes JTOppenheimer DR: Superficial siderosis of the central nervous system. A report on nine cases with autopsy. Acta Neuropathol 13:56741969Acta Neuropathol 13:

5.

Hunt WEMiller CA: The results of early operation for aneurysm. Clin Neurosurg 24:2082151977Clin Neurosurg 24:

6.

Kistler JP: Management of subarachnoid hemorrhage from ruptured saccular aneurysmRopper AHKennedy SKZervas NT (eds): Neurological and Neurosurgical Intensive Care. Baltimore: University Park Press1983175188Neurological and Neurosurgical Intensive Care.

7.

Knuckey NWStokes BAR: Medical management of patients following a ruptured cerebral aneurysm, with ε-aminocaproic acid, kanamycin, and reserpine. Surg Neurol 17:1811851982Surg Neurol 17:

8.

Lougheed WM: Selection, timing, and technique of aneurysm surgery of the anterior circle of Willis. Clin Neurosurg 16:951131969Clin Neurosurg 16:

9.

Morley TP: Introduction to intracranial aneurysm: aspects of treatmentMorley TP (ed): Current Controversies in Neurosurgery. Philadelphia: WB Saunders197657Current Controversies in Neurosurgery.

10.

Ojemann RGCrowell RM: Surgical Management of Cerebrovascular Disease. Baltimore: Williams & Wilkins1983Surgical Management of Cerebrovascular Disease.

11.

Shephard RH: Ruptured cerebral aneurysms: early and late prognosis with surgical treatment. A personal series, 1958–1980. J Neurosurg 59:6151983J Neurosurg 59:

12.

Sundt TM JrKobayashi SFode NCet al: Results and complications of surgical management of 809 intracranial aneurysms in 722 cases. Related and unrelated to grade of patient, type of aneurysm, and timing of surgery. J Neurosurg 56:7537651982J Neurosurg 56:

13.

Weir BAronyk K: Management mortality and the timing of surgery for supratentorial aneurysms. J Neurosurg 54:1461501981J Neurosurg 54:

14.

Zervas NTCandia MCandia Get al: Reduced incidence of cerebral ischemia following rupture of intracranial aneurysms. Surg Neurol 11:3393441979Surg Neurol 11:

TrendMD

Cited By

Metrics

Metrics

All Time Past Year Past 30 Days
Abstract Views 1 1 1
Full Text Views 78 78 31
PDF Downloads 47 47 25
EPUB Downloads 0 0 0

PubMed

Google Scholar