Intracranial Aneurysms

Results of Surgical Treatment

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It has often been stated throughout the general literature on intracranial aneurysms and subarachnoid hemorrhage that no large series of cases of verified intracranial aneurysms treated by conservative measures has yet been compiled so that the results of this form of treatment could be evaluated in comparison with the surgical treatment of these lesions. Indeed, it is somewhat doubtful that a large number of patients with arterio-graphically demonstrated aneurysms will ever be observed so that their history can be studied and followed for a number of years. The reason for this, in our opinion, is that improvement in

It has often been stated throughout the general literature on intracranial aneurysms and subarachnoid hemorrhage that no large series of cases of verified intracranial aneurysms treated by conservative measures has yet been compiled so that the results of this form of treatment could be evaluated in comparison with the surgical treatment of these lesions. Indeed, it is somewhat doubtful that a large number of patients with arterio-graphically demonstrated aneurysms will ever be observed so that their history can be studied and followed for a number of years. The reason for this, in our opinion, is that improvement in neurosurgical techniques and increas-ing experience in the surgical treatment of intracranial aneurysms have led to a gradual decrease in the surgical mortality rate and reduced the frequency of recurrent hemorrhage in surgically treated patients.

While it is true that the natural course of the symptomatic aneurysm has not been established with certainty, the literature abounds with overwhelming evidence to indicate that an untreated aneurysm is a potentially explos-sive lesion associated with a high mortality rate and probably accounting for about 80 per cent of the cases of spontaneous subarachnoid hemorrhage at all ages.

Walton,29 in his very detailed monograph on subarachnoid hemorrhage, has made the most thorough review of the literature to date, and has also presented a complete study of 312 patients admitted over a 10-year period to the Royal Victoria Infirmary at Newcastle. The presence of aneurysms was verified in 63 cases and assumed in the majority of those cases of hemorrhage in which the cause was unknown. In a total of 1480 cases collected from 12 reported series, including the Newcastle group, the immediate mortality was approximately 45 per cent. Most of the deaths occurred during the initial hospital stay following subarachnoid hemorrhage. In Walton's series (Table 1), 91 patients died during the first attack and 47 more died of recurrent bleeding within 8 weeks, a total of 138 deaths. It is generally known and agreed that most immediate deaths from subarachnoid hemorrhage caused by a ruptured aneurysm usually occur during the first 24 hours; bleeding is especially likely to recur during the second and third weeks after the initial hemorrhage, with gradually decreasing incidence of further bleeding following this.

Table 1

Newcastle series (Walton29) 312 patients

91 first attack
Immediate deaths 
47 recurrence in 8 weeks
138 
Subsequent deaths 35
 20% of survivors (35 patients) died of recurrent hemorrhage, half of these within 6 months

A later mortality from recurrent hemorrhage has also been reported, and in Walton's particular series, 20 per cent of the survivors (an additional 35 patients) died of recurrent hemorrhage within 6 months of the original hemorrhage. After 6 months, this author concluded that the risk of fatal recurrent bleeding was only 11 per cent; but, in addition, the number of disabling neurological deficits was significant. Thus, of 120 survivors, he found that 39 patients had moderate or severe sequelae and 5 were completely disabled. Magee20 traced 66 survivors from a group of 150 patients and found that 21 (14 per cent) were disabled and were unable to carry on normal lives.

Mount21 compiled a series of 752 conservatively treated cases of subarachnoid hemorrhage from many sources, including 130 of his own. He found that the average mortality rate was around 48 per cent. This should be compared with a 14 per cent mortality in 469 surgically treated cases, including 9 (11.7 per cent) of 77 in his own group. Small et al.27 also have drawn a comparison between the results of conservative and surgical treatment. In their series of 100 consecutive cases, 43 deaths occurred during the initial period of hospitalization, and only one-third of these patients died during the first 24 hours. Of the 57 survivors, 8 died of recurrent hemorrhage and 7 were totally disabled. Neurosurgical treatment is aimed not so much at saving those patients who died within a few hours of an overwhelming intracranial hemorrhage as it is in preventing the disastrous recurrence of bleeding. At the present time such treatment could be applied and would certainly be indicated in those patients who survived the first 24 to 48 hours after the initial hemorrhage. In 50 subsequent consecutive patients treated surgically, 16 had an intracerebral hemorrhage; the immediate surgical mortality was considered to be 12 per cent. Although 52 per cent of the survivors had some neurological disability, only 12 per cent were totally disabled.

McKissock and Walsh,19 in their series of conservatively treated cases of verified aneurysm, found a similar mortality rate of about 50 per cent. They have likewise attempted to assess the results of surgical treatment for purposes of comparison, making a detailed classification of cases according to the severity of hemorrhage and the site of the intracranial aneurysm. They graded the aneurysms in much the same way as malignant lesions would be graded, thereby presenting the most critical comparison yet to appear. In their series of 108 medically treated patients, 57 died (53 per cent). Thirtyeight of the 57 deaths were among patients in so-called category “A” which includes those in danger of immediate death from the hemorrhage for which they were hospitalized, and patients in coma or semicoma with neurological signs. Of 141 patients treated surgically, 47 or 33.3 per cent died, and 34 of the 47 patients who died were in category“A.”

It is generally accepted by neurosurgeons and neurologists that a high operative mortality is associated with the performance of any surgical procedure during the immediate period following a hemorrhage. The experience of Botterell3,4 and others with hypothermia and hypotension may in time reduce this mortality rate; however, present methods of treatment, for the most part, have been directed at the prevention of recurrent bleeding among the 70 per cent of patients who survive the initial hemorrhage and the prevention also of neurological disability caused by repeated bleeding. If these aims are accomplished, then surgical treatment could be judged as effective. With this goal in mind, a study has been made of the results of treatment of patients with intracranial aneurysms; these patients have had follow-up studies on the Lahey Clinic neurosurgical service for periods up to 20 years. A total of 277 patients has been studied, and in each case the presence of aneurysm was verified by arteriogram, at surgery or at postmortem examination. A further group of 36 patients has not been included because the follow-up period had not exceeded 1 year at the time of this writing.

One of us (J.L.P.)25 made a previous report of 101 patients in this group who were subjected to carotid ligation. Three immediate deaths and 8 subsequent deaths occurred, 2 of which were caused by recurrent hemorrhage from the treated aneurysm. At the time of that report, 40 patients had been subjected to craniotomy, resulting in the immediate death of 7 and the subsequent death of 3 patients. The reduction of mortality and morbidity by the use of controlled carotid ligation has subsequently been reported.7,8 The present report deals with the over-all results of the general methods of surgical treatment. It should be emphasized that the selection of the particular operative procedure has been determined chiefly by the location of the aneurysm, its severity and the presence or absence of intracerebral hematoma. Approximately 45 per cent of the patients in this series have had aneurysms arising from the intracranial portion of the internal carotid artery within the cavernous sinus, above the cavernous sinus of the vestigial type or at the bifurcation of the artery itself. In general, these aneurysms have been treated either by carotid ligation in the neck or by the “trapping” procedure with cervical carotid ligation followed by intracranial clipping of the internal carotid artery distal to the aneurysm. Nearly all of the patients discussed below who were subjected to carotid ligation have had internal carotid aneurysms.

In the group of patients subjected to craniotomy (except those in whom craniotomy was utilized to complete a trapping procedure) the intracranial aneurysms arose from the middle cerebral artery, the anterior cerebral-anterior communicating complex, and in a smaller number of cases from the posterior communicating, posterior cerebral and vertebral vessels. While some of these patients have also undergone carotid or vertebral ligation in addition to craniotomy, it has been felt that cervical ligation alone is inadequate in the treatment of these lesions.

When craniotomy has been employed for a direct attack upon an intracranial aneurysm, the general principles of surgery of intracranial aneurysms have been rigidly followed. If the aneurysm proved accessible to clipping or excision without compromising the parent vessel, this was carried out; if not, one of the several alternative procedures was employed. These include muscle wrapping or a combination of clipping and muscle wrapping, proximal clipping of a parent vessel such as the anterior cerebral artery, or intracranial trapping when this appeared feasible without compromising important elements of the cerebral circulation.

Fifty-one patients in this series were not treated surgically (Table 2). Some had refused operation and died of repeated hemorrhages although they had made a good recovery from the first episode of bleeding. Death was the result of the initial or repeated hemorrhage in 21 patients. Twelve of these died shortly after admission to the hospital, that is, within the first 24 to 48 hours, and 9 others died within several weeks of a further rupture. Seven patients died of recurrent hemorrhage between 3 months and 6 years after the initial hemorrhage. It should be noted that of the 19 survivors, only 2 are considered disabled and the others have been well from 1 to 12 years.

TABLE 2

No surgical treatment 51 patients

Death from initial or repeated hemorrhage21 
Death from recurrent hemorrhage (3 mos.–6 yrs.)—includes 4 patients with 2 aneurysms7 
Died of other causes (1 yr.–12 yrs.)4 
Survivors (7 mos.–12 yrs.)—practically all are well; 2 patients are disabled19 

Repeated emphasis on the increased risk of surgery during early periods after rupture of an aneurysm has been documented throughout the surgical literature by reports of very low surgical mortality with delayed operation as compared to early operation, and this tends to lend support to the arguments of those who would advise only conservative treatment. Norlén and Olivecrona24 operated on 15 patients in periods varying from a few hours up to 22 days after rupture of an aneurysm; 8 of these patients died, 6 recovered and 1 was hemiplegic. Of 63 patients who underwent direct intracranial operation 3 to 4 weeks after the hemorrhage, only 2 died and 2 others were left with significant mental disturbances. Graf12 found that among 35 patients subjected to “delayed” operation (after 14 days) 2 died, and of 17 patients who had an “early” operation, 13 died. Three patients in his series operated upon on the 14th day all died, and for this reason he proposed deferring operation for 3 weeks. Hamby's13 comprehensive monograph on intracranial aneurysms includes a series of 32 surgically treated patients of whom 16 died. This author subsequently reported on 51 patients, 38 of whom underwent craniotomy and 13 carotid ligation. Of 17 patients with acute intracerebral hematoma, only 1 survived operation, and of 12 patients who died after a direct attack upon the aneurysm, operation was performed within 11 days after the hemorrhage. Eleven patients who survived were operated on about 2 weeks or more after the hemorrhage.

In this series, no attempt has been made to present specific details concerning the patients operated on within the first few hours or days following hemorrhage. Recognizing that a significant surgical mortality occurs during the first few days, our deliberate aim has been to reduce the subsequent mortality occurring up to 8 weeks, and for this reason the patients have been classified as shown in Tables 3 and 4. It should be noted in Table 3 that carotid ligation was carried out in 58 of 101 cases within 8 weeks from the time of the initial hemorrhage and 41 of these operations were performed within 4 weeks. In those cases in which hemorrhage did not occur, ligation was carried out because of third nerve or other ocular palsies, intractable pain or carotid-cavernous fistula caused by rupture of a carotid aneurysm within the cavernous sinus. Table 4 shows that in 57 of 95 patients who underwent craniotomy, the operation was performed within 4 weeks of hemorrhage. In the 8 cases in which hemorrhage did not occur, operation was performed because of pain or neurological deficit.

TABLE 3

Carotid ligation (all forms) 101 patients

Patients 
Single or multiple hemorrhages 
 1–4 weeks before ligation41 
 4–8 weeks before ligation17 
Interval between hemorrhage and ligation more than 2 months31 
No hemorrhage12 

TABLE 4

Craniotomy 95 patients

Patients 
Single or multiple hemorrhage 
 1–4 weeks before craniotomy57 
 4–8 weeks before craniotomy18 
 Interval greater than 2 months12 
No hemorrhage8 

CAROTID LIGATION ALONE

In the present series, 101 patients were subjected to carotid ligation alone. Practically all had aneurysms arising from the internal carotid artery. The operations include common or internal carotid ligation in the neck performed by earlier methods and those carried out in recent years utilizing the Poppen-Blalock clamp. In the majority of these cases the internal carotid artery was the artery ligated, and this group of patients does not include those upon whom a trapping procedure was performed or craniotomy subsequently carried out for a direct attack on the aneurysm. Table 5 lists the results of carotid ligation alone. Eighty-five of 101 patients recovered fully with no disabling neurological deficits and no subsequent hemorrhage in a follow-up period of 1 to 15 years.

TABLE 5

Results of carotid ligation 101 patients

Recovery 96 
 No disabling deficit (1 to 15 years)85  
 Severe or moderate neurological deficit (hemiplegia before ligation in 4)11  
Death 5 
 Ligation4  
 Rupture of aneurysm1  
Subsequent deaths (1 to 15 years) 17 
 Recurrent hemorrhage (single aneurysm) 2 years and 6 years2  
 Rupture of aneurysm on opposite side 1 month and 2½ years2  
 Expansion of aneurysm on opposite side 5 years1  
 Unknown2  
 Unrelated causes10  

Seventeen patients have subsequently died, 10 of entirely unrelated causes except for one patient in whom it was suspected that death may have been caused by carotid insufficiency several years after ligation. Five patients have died of coronary or other heart disease, 2 of renal disease and 2 committed suicide. In 2 patients the cause of death was unknown, although after studying detailed histories obtained from referring physicians it was felt that they did not die of recurrent hemorrhage. Only 2 patients in this group of 101 who have undergone carotid ligation died of recurrent hemorrhage from the treated aneurysm; these hemorrhages occurred 2 years and 6 years following ligation. Two others died of recurrent hemorrhage from a second aneurysm on the opposite side. Ligation was considered the cause of death in 4 patients; in 2 of these the carotid artery was ligated by earlier techniques and the ligature could not be removed in time to prevent fatal ischemia. In 1 other, death was caused by a fatal hemorrhage in the neck. Eleven patients have had severe or moderate neurological deficit, 7 of these as a result of carotid ligation; 4 patients were hemiplegic before ligation.

If the 12 patients with internal carotid aneurysms who had no hemorrhage are eliminated from this group, it may be seen that only 4 of the 89 patients who had bleeding episodes have died of recurrent hemorrhage after carotid ligation, and 2 of these were patients with bilateral aneurysms.

Reports in the literature on the effectiveness of cervical ligation of the carotid artery have been variable and at times confusing. In a group of 53 patients with internal carotid aneurysms who underwent carotid ligation, McKissock and Walsh19 reported 2 possible fatal recurrent hemorrhages, 1 definite fatal recurrence and 1 nonfatal bleeding episode. Shenkin et al.26 have reported on carotid ligation alone in a series of 19 consecutive patients with internal carotid aneurysms. Follow-up studies of up to 7½ years were made and in this time hemorrhage did not recur. Hemiplegia occurred after operation in 6 cases, 3 patients recovered completely, and 2 are able to work despite some degree of deficit. Bassett et al.1 carried out cervical ligation in 29 cases with a mortality rate of 3.4 per cent. Hemiparesis developed after operation in 12 instances and 8 of these patients recovered completely. Two patients were presumed to have died of recurrent hemorrhage but 1 of these deaths was from an aneurysm on the opposite side. Black and German2 made a follow-up study of 35 patients on whom carotid ligation was performed for aneurysms of the internal carotid artery, with 2 operative deaths. One of these patients had experienced a severe hemorrhage and the other had multiple aneurysms arising from the right internal carotid and middle cerebral arteries. Six other patients in the group subsequently died and it was thought probable that 2 of these deaths were the result of recurrent hemorrhage. The cause of death was unknown in 1 case and unrelated in 3. Calvert*5 reported 26 patients submitted to ligation, with 2 deaths and 4 patients with hemiplegia who, for the most part, recovered. The 20 survivors had no recurrent hemorrhage. In Hamby's13,14 cases the deaths during carotid ligation were believed to have been caused by the hemorrhage itself. In Dandy's6 series, complete ligation of the internal carotid artery was carried out in 36 cases with 2 deaths, and partial ligation in 27 cases with 1 death. Steelman et al.28 ligated the cervical carotid artery in 14 patients with no operative mortality and 1 instance of postoperative hemiplegia. Hardy et al.15 have more recently reported the results of carotid ligation in 54 patients who had follow-up studies for 1 to 13 years, only 36 of whom had internal carotid aneurysms. In the majority of these, the common carotid artery was ligated. Of 3 instances of recurrent hemorrhage, 2 were from aneurysms at the circle of Willis, that is, distal to the internal carotid artery, and 1 patient had multiple lesions. Forty-two of their survivors are working and well.

In contrast with the above findings, Norlén,22 in studying the late results of carotid ligation in 31 of 37 cases, found that as many as 6 patients had died of recurrent hemorrhage. Jefferson17 and Johnson,18 reporting on 142 cases of carotid ligation, noted 12 deaths occurring during the first 6 weeks after ligation. Six of these were the result of a second rupture within 1 month, 4 patients were moribund at the time of operation; 1 death was caused by rupture of a second aneurysm at the time of surgery and 1 by basal compression from a large aneurysm. Ligation was not thought to be a cause of death in any of these 12 cases. Of 8 subsequent deaths, 2 resulted from recurrent rupture of the same aneurysm for which ligation had been carried out. Eleven of the 142 patients were hemiplegic and only 4 showed significant signs of recovery. In neither of these series, however, is it clear whether carotid ligation was carried out primarily for aneurysm of the internal carotid artery and which of the hemorrhages recurred from aneurysms of the anterior communicating or middle cerebral arteries. Mount21 in a recent presentation studied the results of carotid ligation, using the Selverstone clamp in 65 patients, and found a mortality rate of 13.8 per cent. The clamp had to be opened in 27 patients and could be reclosed in only one-third of these. Eleven patients were worse neurologically, 10 because of hemiparesis and 1 because of mental illness. Hemorrhage recurred four times following carotid ligation and in 2 of Mount's21 patients, hemorrhage occurred for the first time after ligation.

Although some conflicting reports have been made as to the effectiveness of carotid ligation alone in preventing further recurrent bleeding from internal carotid aneurysms, it has been the authors' opinion in reviewing the above series that ligation in the neck alone has been of undisputed value. Moreover, in practically every case in which the oculomotor nerve has been involved, either complete or partial remission of visual disturbance has occurred. We have found that with methods of controlled carotid ligation, employing the Selverstone or Poppen-Blalock clamp, the mortality from carotid ligation has been greatly decreased and the morbidity significantly reduced. Thus, in the last 55 consecutive patients at this clinic in whom controlled ligation of the internal carotid artery has been attempted, only 1 death has occurred as a result of ligation. Circulation may be re-established within a few moments if the patient does not tolerate occlusion. Permanent neurological deficits have been few and disabling in only 2 patients.7 In some of these cases total ligation has not been possible, but at least the distressing permanent hemiplegia and speech difficulty which resulted from former methods of ligation have been of low incidence.

TRAPPING PROCEDURE

In addition to the 101 patients listed in Tables 3 and 5 (carotid ligation), 26 patients have been submitted to a trapping procedure for aneurysms of the internal carotid artery. In these cases, the internal carotid artery was ligated successfully and the intracranial portion distal to the aneurysm was clipped within 3 or 4 days. It has been felt in the past and reported in detail by Dandy6 and others that this procedure would certainly prevent further rupture of an internal carotid aneurysm. Twenty-three patients survived the operation and were entirely well without neurological deficit or recurrent hemorrhage (Table 6). One death was directly attributed to the operation and in this case it was felt that the presence of mild cerebral ischemia had not been recognized during the period of clamp ligation or that an arteriosclerotic plaque at the site of intracranial clipping had produced an embolus. The other 2 immediate deaths recorded in Table 6 were patients who were in critical condition at the time of operation. One was actively bleeding during the third hemorrhage and the other had an extremely large aneurysm which was bleeding. Satisfactory clipping of the internal carotid was not accomplished, and the patient died 3 weeks later. The subsequent deaths from unrelated causes resulted from carcinoma of the lung, Addison's disease and an automobile accident.

TABLE 6

Results of trapping procedure 26 patients

Recovery; no deficit (1 yr.–13 yrs.)23 
Immediate deaths 
 Caused by surgery1 
 Caused by rupture of aneurysm2 
Subsequent deaths from unrelated causes (13 mos.–3 yrs.)3 
Death caused by rupture of second aneurysm (7 yrs.)1 
Survivors at present; no recurrent hemorrhage19 

CRANIOTOMY

Ninety-five patients have been operated on by a direct intracranial procedure aimed at some form of definitive treatment of the aneurysm. This group, of course, does not include those in whom a trapping procedure was carried out, although in a number of these cases carotid or vertebral ligation was also accomplished. The great majority of aneurysms treated by direct attack were located in the middle cerebral or anterior cerebral-anterior communicating group. Several patients who did not tolerate ligation had aneurysms arising from the internal carotid artery. Other sites of origin included the posterior cerebral, vertebral, posterior inferior cerebellar, anterior choroidal, ophthalmic and superior cerebellar arteries. Table 7 lists the results in these cases. It should be noted that 60 of 95 patients who underwent craniotomy have recovered completely, with no disabling deficit and no recurrence of hemorrhage; the follow-up periods in these cases varied from 1 to 20 years. Death occurred immediately following craniotomy in 17 patients. Subsequent death was caused by recurrent hemorrhage in 2 patients. Another aneurysm was verified as the cause in 1 of these instances. Another patient had a recurrent hemorrhage 1 year following craniotomy; he recovered and was well 6 years later at the time of the last follow-up. Three patients have subsequently died of unrelated causes—1 from arteriosclerosis 14 years after surgery, 1 from a bleeding ulcer 2 years after and 1 from a glioma 1 year following the craniotomy. Eleven patients recovered but had severe or moderately severe neurological deficit. The deficit was attributed to operation in 6 cases, but 5 patients were hemiplegic preoperatively as a result of intracerebral hemorrhage. Of the latter 5 cases, extensive brain damage had been present in practically every instance before operation was undertaken.

TABLE 7

Craniotomy 95 patients

Recovery; no disabling deficit and no subsequent hemorrhage (1–20 yrs.)60 
Recovery; severe or moderately severe deficit (5 patients hemiplegic before surgery)11 
Death following craniotomy17 
Subsequent deaths (1½–14 yrs.)6 
Unrelated causes 3 
Recurrent hemorrhage 2 
Unknown cause 1 
Recurrent nonfatal hemorrhage (1 yr. postoperative—recovery 6 yrs.)1 

Two of the 17 craniotomy deaths were in patients who were in extremely critical condition at the time of craniotomy as a result of hemorrhage occurring very shortly before the operation. These had been considered more or less hopeless cases but craniotomy was carried out in an attempt to control the hemorrhage. Two others were patients with multiple mycotic aneurysms; both of these had subacute bacterial endocarditis and were seriously ill at the time of operation. In 13 patients, death was considered to result directly from the operation. In reviewing these deaths, it was felt that most of them resulted from attempts at direct clipping or ligation of an aneurysmal neck during which process the aneurysm ruptured, requiring clipping of the important parent vessel to control the hemorrhage. This hazard was not as great in a more conservative type of operation such as muscle wrapping. Death in most instances was caused by postoperative cerebral edema and softening, with the persistence of a comatose state and pulmonary complications in some cases. One patient had a postoperative coronary occlusion. In a few instances thrombosis of the callosal arteries was present, and in 1 case thrombosis of the sagittal sinus was noted. Thus, the mortality in this series which was considered the result of craniotomy per se was 13.7 per cent (13 of 95 patients).

The mortality and morbidity rates for craniotomy vary considerably throughout the literature but this is probably more a reflection of the condition of patients subjected to operation rather than of the actual differences in operative technique. Jaeger16 reported on 31 patients with internal carotid aneurysms, 20 of whom underwent craniotomy; 5 of these died after the operation, a mortality rate of 25 per cent. This report tends to support the view that internal carotid artery ligation is the procedure of first choice for these patients under most circumstances. Falconer9–11 in 1951 and 1952 reported on a total of 70 patients, including those submitted to carotid ligation with craniotomy. Most of his patients had experienced recent bleeding; 47 made a good recovery, 11 had some residual disability and 12 died in the postoperative period, a mortality rate of 17 per cent. Two subsequent deaths were caused by hemorrhage from rupture of a second aneurysm.

Jefferson17 and Johnson18 reported 5 immediate deaths in 35 patients submitted to craniotomy. Norlén's22 initial report in 1951 of patients operated on by Norlén and Olivecrona mentions an immediate mortality of 3 patients among 44 subjected to craniotomy; of 4 other patients with postoperative hemiplegia, 2 recovered partially. The later reports of Norlén and Olivecrona have been referred to above. Norlén and Barnum23 reported on the excellent results of direct surgical procedures in 24 patients with aneurysms of the anterior communicating artery. In 15 of these cases, direct ligation of the aneurysm by a clip or a ligature was possible. Two operative deaths and 2 deaths caused by recurrent hemorrhage occurred. One patient died 1 month after the aneurysm was wrapped by Gelfoam and the other died 1½ years later. In the latter case only exploration of the aneurysm was possible at the time of surgery. In Hamby's14 series reported in 1954, 38 patients were subjected to craniotomy; 15 of these also underwent carotid ligation. Sixteen deaths occurred in this group and, as mentioned previously, acute bleeding was present in most of these patients. In the series reported by Bassett et al.,1 craniotomy alone was carried out in 25 patients with a 40 per cent mortality. The aneurysm ruptured during exposure in 12 of these cases. Of 18 other patients in whom craniotomy was combined with cervical ligation, 9 deaths occurred—a 50 per cent mortality.

Steelman et al.28 carried out craniotomy in 42 cases with an operative mortality of only 4.7 per cent. All patients had a follow-up period of 1 to 6 years. No subsequent death or recurrent hemorrhage was reported. Graf12 carried out a direct intracranial attack in a series of 55 patients; 43 had one or more hemorrhages and 21 of these 43 patients died. Of the 12 patients without hemorrhage, only 4 died. The total number of deaths was 25, a mortality of 45 per cent. In Calvert's5 series reported by Allison and Mullen, 31 patients were submitted to direct craniotomy with 6 immediate deaths. The 25 survivors were alive for periods up to 6 years; 2 were hemiplegic, some had speech disorders and mental and neurological deficits, while 17 patients suffered no disability and were able to do useful work.

The work of Botterell et al.3,4 in the last few years has directed attention to the possibility of reducing the surgical mortality of direct operation by the use of hypothermia and hypotension. His group has now reported 73 cases of ruptured aneurysm and 1 case of unruptured aneurysm. In an attempt to determine the effectiveness of very early operation toward the possible reduction of mortality among very acute cases, Botterell graded cases according to the degree of operative risk and has classified the results of treatment on this basis. Of the 73 patients with ruptured aneurysms, 17 or 23.2 per cent died. Sixteen of these deaths occurred in the group of 44 patients who were operated on within 7 days of the initial hemorrhage. Of the 56 survivors, 50 were considered in excellent or good condition and 6 in bad or fair condition, with neurological deficits. Ten of the 17 patients were classified in grade IV or V (either moribund with failing vital centers or with major neurological deficits and deterioration as a result of large intracerebral hematomas). Four of the patients who died were grade I or II risks and 3 were grade III risks; in these latter cases death resulted from technical difficulties or postoperative complications. One patient died of irreversible ventricular fibrillation. If we exclude the 10 patients who were in grade IV or V, then the oper-tive mortality in Botterell's series would be around 10 per cent.

Table 8 summarizes the surgical mortality in our series. Of 226 patients subjected to some surgical procedure, 18 died as a direct result of surgery, a total operative mortality of 8 per cent. The over-all surgical morbidity, including the patients in whom deficit was considered to result from surgery alone, is an additional 5.7 per cent as recorded in Table 9. From estimates now available, this would appear to be a significant reduction in the over-all mortality and morbidity rates of untreated intracranial aneurysms. The numbers of patients in this group who were not treated by surgical means is much smaller than those who have undergone surgery. Yet, our observations have indicated that 7 of 30 survivors in the untreated group died of recurrent hemorrhage and only 5 of 201 survivors in the treated group have had fatal recurrent bleeding.

TABLE 8

Surgical mortality

OperationPatientsDeaths Caused by Surgery
NumberPer Cent  
Carotid ligation alone101 4 3.9 
Craniotomy95 13 13.7 
Trapping procedure26 1 3.9 
Vertebral ligation4 0 0 
 Total226 18 Av. 8.0 

TABLE 9

Surgical morbidity

OperationPatientsDeficit Caused by Surgery
NumberPer Cent  
Carotid ligation alone101 7 6.9 
Craniotomy95 6 6.3 
Trapping procedure26 0 0 
Vertebral ligation4 0 0 
 Total226 13 Av. 5.7 

SUMMARY

A series of 277 patients with verified intracranial aneurysms has been presented. The follow-up periods ranged from 1 to 20 years. Fifty-one patients were not submitted to any form of surgical treatment and 21 of these died as a result of initial or repeated hemorrhage; 7 further patients died of recurrent hemorrhage from 3 months to 6 years after the initial bleeding episode. These figures compare with most reported series of untreated cases in the literature—approximately 45 per cent early mortality, and 10 to 15 per cent subsequent mortality. At the present time it is questionable whether or not the 30 per cent initial mortality resulting from a devastating first hemorrhage will ever be reduced by surgical means; surgical treatment might be considered effective, however, if early and later recurrent hemorrhage can be prevented among the survivors.

In approximately two-thirds of the 226 patients who were subjected to some surgical procedure, the operation was carried out at varying periods within the first to the eighth week after hemorrhage. The operative mortality and morbidity have been tabulated. In the entire surgically treated group, 18 deaths were a direct result of the operation—a mortality of 8.0 per cent; 13 patients had some neurological deficit as a result of operation—a morbidity of 5.7 per cent. Seven patients have died of recurrent hemorrhage, but at least 3 of these deaths were caused by rupture of a second aneurysm.

These observations lend support to the opinion that surgical treatment may effectively reduce the mortality rate and the risk of recurrent hemorrhage in patients with intracranial aneurysms.

Grateful acknowledgement is made to Dr. David LaFia and Dr. Publio Silva for their review of the mortality.

REFERENCES

  • 1.

    BassettR. C.ListC. F.LemmenL. J. Surgical treatment of intracranial aneurysm. Surg. Gynec. Obstet.195295: 701708.BassettListLemmenSurg. Gynec. Obstet.95: 701–708.

  • 2.

    The treatment of internal carotid artery aneurysms by proximal arterial ligation. A follow-up study. J. Neurosurg.195310: 590601.BlackGermanJ. Neurosurg.10: 590–601.

  • 3.

    BotterellE. H.LougheedW. M.MorleyT. P.VandewaterS. L. Hypothermia in the surgical treatment of ruptured intracranial aneurysms. J. Neu osurg.195815: 418.BotterellLougheedMorleyVandewaterJ. Neu osurg.15: 4–18.

  • 4.

    BotterellE. H.LougheedW. M.ScottJ. W.VandewaterS. L. Hypothermia, and interruption of carotid, or carotid and vertebral circulation, in the surgical management of intracranial aneurysms. J. Neurosurg.195613: 142.BotterellLougheedScottVandewaterJ. Neurosurg.13: 1–42.

  • 5.

    CalvertC. A. Experiences in the treatment of ruptured intracranial aneurysms. J. Neurol. Neurosurg. Psychiat.1957n.s 20: 159164.CalvertJ. Neurol. Neurosurg. Psychiat.20: 159–164.

  • 6.

    DandyW. E. Intracranial arterial aneurysms. Ithaca, N. Y.: Comstock Publishing Co., Inc.1944viii147 pp.Dandy

  • 7.

    FagerC. A. The effectiveness and risk of carotid ligation in the treatment of intracranial aneurysms. Lahey Clin. Bull.195810: 226233.FagerLahey Clin. Bull.10: 226–233.

  • 8.

    FagerC. A.PoppenJ. L. Observations on controlled ligation of the internal carotid artery. Surg. Clin. N. Amer.June 195636: 567582.FagerPoppenSurg. Clin. N. Amer.36: 567–582.

  • 9.

    FalconerM. A. The surgical treatment of bleeding intracranial aneurysms. J. Neurol. Neurosurg. Psychiat.1951n.s. 14: 153186.FalconerJ. Neurol. Neurosurg. Psychiat.14: 153–186.

  • 10.

    FalconerM. A. The future of surgery in the treatment of spontaneous cerebral haemorrhage. Lancet19522: 945950.FalconerLancet2: 945–950.

  • 11.

    FalconerM. [A.] Discussion of Norlen.22 Proc. roy. Soc. Med.195245: 298300.Falconer22Proc. roy. Soc. Med.45: 298–300.

  • 12.

    GrafC. J. Results of direct attack on nonfistulous intracranial aneurysm with remarks on statistics. J. Neurosurg.195512: 146153.GrafJ. Neurosurg.12: 146–153.

  • 13.

    HambyW. B. Intracranial aneurysms. Springfield, Ill.: Charles C Thomas1952xxi564 pp.Hamby

  • 14.

    HambyW. B. The treatment of ruptured intracranial aneurysms. Surg. Clin. N. Amer.Aug. 195434: 10631075.HambySurg. Clin. N. Amer.34: 1063–1075.

  • 15.

    HardyW. G.ThomasL. M.WebsterJ. E.GurdjianE. S. Carotid ligation for intracranial aneurysm. A follow-up study of 54 patients. J. Neurosurg.195815: 281287.HardyThomasWebsterGurdjianJ. Neurosurg.15: 281–287.

  • 16.

    JaegerR. Aneurysm of the intracranial carotid artery. Syndrome of frontal headache with oculomotor nerve paralysis. J. Amer. med. Ass.1950142: 304309.JaegerJ. Amer. med. Ass.142: 304–309.

  • 17.

    JeffersonG. Discussion of Norlén.22 Proc. roy. Soc. Med.195245: 300301.Jefferson22Proc. roy. Soc. Med.45: 300–301.

  • 18.

    Discussion of Norlén.22 Proc. roy. Soc. Med.195245: 301302.Johnson22Proc. roy. Soc. Med.45: 301–302.

  • 19.

    McKissockW.WalshL. Subarachnoid haemorrhage due to intracranial aneurysms. Results of treatment of 249 verified cases. Brit. med. J.19562: 559565.McKissockWalshBrit. med. J.2: 559–565.

  • 20.

    MageeC. G. Spontaneous subarachnoid haemorrhage. A review of 150 cases. Lancet19432: 497500.MageeLancet2: 497–500.

  • 21.

    MountL. A. Treatment of spontaneous subarachnoid hemorrhage. J. Amer. med. Ass.1951146: 693697.MountJ. Amer. med. Ass.146: 693–697.

  • 22.

    NorlenG. The pathology, diagnosis and treatment of intracranial saccular aneurysms. Proc. roy. Soc. Med.195245: 291298.NorlenProc. roy. Soc. Med.45: 291–298.

  • 23.

    NorlenG.BarnumA. S. Surgical treatment of aneurysms of the anterior communicating artery. J. Neurosurg.195310: 634650.NorlenBarnumJ. Neurosurg.10: 634–650.

  • 24.

    NorlenG.OlivecronaH. The treatment of aneurysms of the circle of Willis. J. Neurosurg.195310: 404415.NorlenOlivecronaJ. Neurosurg.10: 404–415.

  • 25.

    PoppenJ. L. Specific treatment of intracranial aneurysms. Experiences with 143 surgically treated patients. J. Neurosurg.19518: 75102.PoppenJ. Neurosurg.8: 75–102.

  • 26.

    ShenkinH. A.PolakoffP.FinnesonB. E. Intracranial internal carotid artery aneurysms. Results of treatment by cervical carotid artery ligation. J. Neurosurg.195815: 183191.ShenkinPolakoffFinnesonJ. Neurosurg.15: 183–191.

  • 27.

    SmallJ. M.HolmesJ. MacD. and ConnollyR. C. The prognosis and role of surgery in spontaneous intracranial haemorrhage. Brit. med. J.19532: 10721075.SmallHolmesMacConnollyBrit. med. J.2: 1072–1075.

  • 28.

    SteelmanH. F.HayesG. J.RizzoliH. V. Surgical treatment of saccular intracranial aneurysms. A report of 56 consecutively treated patients. J. Neurosurg.195310: 564576.SteelmanHayesRizzoliJ. Neurosurg.10: 564–576.

  • 29.

    WaltonJ. N. Subarachnoid haemorrhage. Edinburgh: E. & S. Livingstone Ltd.1956xv350 pp.WaltonEdinburgh: E. & S. Livingstone Ltd.

Prepared by Dr. R. S. Allison (Belfast) and Dr. John F. Mullen (Chicago) from notes used by the late Cecil Calvert for a paper which he delivered to the Society of British Neurological Surgeons in 1954 at Belfast.

Article Information

© AANS, except where prohibited by US copyright law.

Headings

References

1.

BassettR. C.ListC. F.LemmenL. J. Surgical treatment of intracranial aneurysm. Surg. Gynec. Obstet.195295: 701708.BassettListLemmenSurg. Gynec. Obstet.95: 701–708.

2.

The treatment of internal carotid artery aneurysms by proximal arterial ligation. A follow-up study. J. Neurosurg.195310: 590601.BlackGermanJ. Neurosurg.10: 590–601.

3.

BotterellE. H.LougheedW. M.MorleyT. P.VandewaterS. L. Hypothermia in the surgical treatment of ruptured intracranial aneurysms. J. Neu osurg.195815: 418.BotterellLougheedMorleyVandewaterJ. Neu osurg.15: 4–18.

4.

BotterellE. H.LougheedW. M.ScottJ. W.VandewaterS. L. Hypothermia, and interruption of carotid, or carotid and vertebral circulation, in the surgical management of intracranial aneurysms. J. Neurosurg.195613: 142.BotterellLougheedScottVandewaterJ. Neurosurg.13: 1–42.

5.

CalvertC. A. Experiences in the treatment of ruptured intracranial aneurysms. J. Neurol. Neurosurg. Psychiat.1957n.s 20: 159164.CalvertJ. Neurol. Neurosurg. Psychiat.20: 159–164.

6.

DandyW. E. Intracranial arterial aneurysms. Ithaca, N. Y.: Comstock Publishing Co., Inc.1944viii147 pp.Dandy

7.

FagerC. A. The effectiveness and risk of carotid ligation in the treatment of intracranial aneurysms. Lahey Clin. Bull.195810: 226233.FagerLahey Clin. Bull.10: 226–233.

8.

FagerC. A.PoppenJ. L. Observations on controlled ligation of the internal carotid artery. Surg. Clin. N. Amer.June 195636: 567582.FagerPoppenSurg. Clin. N. Amer.36: 567–582.

9.

FalconerM. A. The surgical treatment of bleeding intracranial aneurysms. J. Neurol. Neurosurg. Psychiat.1951n.s. 14: 153186.FalconerJ. Neurol. Neurosurg. Psychiat.14: 153–186.

10.

FalconerM. A. The future of surgery in the treatment of spontaneous cerebral haemorrhage. Lancet19522: 945950.FalconerLancet2: 945–950.

11.

FalconerM. [A.] Discussion of Norlen.22 Proc. roy. Soc. Med.195245: 298300.Falconer22Proc. roy. Soc. Med.45: 298–300.

12.

GrafC. J. Results of direct attack on nonfistulous intracranial aneurysm with remarks on statistics. J. Neurosurg.195512: 146153.GrafJ. Neurosurg.12: 146–153.

13.

HambyW. B. Intracranial aneurysms. Springfield, Ill.: Charles C Thomas1952xxi564 pp.Hamby

14.

HambyW. B. The treatment of ruptured intracranial aneurysms. Surg. Clin. N. Amer.Aug. 195434: 10631075.HambySurg. Clin. N. Amer.34: 1063–1075.

15.

HardyW. G.ThomasL. M.WebsterJ. E.GurdjianE. S. Carotid ligation for intracranial aneurysm. A follow-up study of 54 patients. J. Neurosurg.195815: 281287.HardyThomasWebsterGurdjianJ. Neurosurg.15: 281–287.

16.

JaegerR. Aneurysm of the intracranial carotid artery. Syndrome of frontal headache with oculomotor nerve paralysis. J. Amer. med. Ass.1950142: 304309.JaegerJ. Amer. med. Ass.142: 304–309.

17.

JeffersonG. Discussion of Norlén.22 Proc. roy. Soc. Med.195245: 300301.Jefferson22Proc. roy. Soc. Med.45: 300–301.

18.

Discussion of Norlén.22 Proc. roy. Soc. Med.195245: 301302.Johnson22Proc. roy. Soc. Med.45: 301–302.

19.

McKissockW.WalshL. Subarachnoid haemorrhage due to intracranial aneurysms. Results of treatment of 249 verified cases. Brit. med. J.19562: 559565.McKissockWalshBrit. med. J.2: 559–565.

20.

MageeC. G. Spontaneous subarachnoid haemorrhage. A review of 150 cases. Lancet19432: 497500.MageeLancet2: 497–500.

21.

MountL. A. Treatment of spontaneous subarachnoid hemorrhage. J. Amer. med. Ass.1951146: 693697.MountJ. Amer. med. Ass.146: 693–697.

22.

NorlenG. The pathology, diagnosis and treatment of intracranial saccular aneurysms. Proc. roy. Soc. Med.195245: 291298.NorlenProc. roy. Soc. Med.45: 291–298.

23.

NorlenG.BarnumA. S. Surgical treatment of aneurysms of the anterior communicating artery. J. Neurosurg.195310: 634650.NorlenBarnumJ. Neurosurg.10: 634–650.

24.

NorlenG.OlivecronaH. The treatment of aneurysms of the circle of Willis. J. Neurosurg.195310: 404415.NorlenOlivecronaJ. Neurosurg.10: 404–415.

25.

PoppenJ. L. Specific treatment of intracranial aneurysms. Experiences with 143 surgically treated patients. J. Neurosurg.19518: 75102.PoppenJ. Neurosurg.8: 75–102.

26.

ShenkinH. A.PolakoffP.FinnesonB. E. Intracranial internal carotid artery aneurysms. Results of treatment by cervical carotid artery ligation. J. Neurosurg.195815: 183191.ShenkinPolakoffFinnesonJ. Neurosurg.15: 183–191.

27.

SmallJ. M.HolmesJ. MacD. and ConnollyR. C. The prognosis and role of surgery in spontaneous intracranial haemorrhage. Brit. med. J.19532: 10721075.SmallHolmesMacConnollyBrit. med. J.2: 1072–1075.

28.

SteelmanH. F.HayesG. J.RizzoliH. V. Surgical treatment of saccular intracranial aneurysms. A report of 56 consecutively treated patients. J. Neurosurg.195310: 564576.SteelmanHayesRizzoliJ. Neurosurg.10: 564–576.

29.

WaltonJ. N. Subarachnoid haemorrhage. Edinburgh: E. & S. Livingstone Ltd.1956xv350 pp.WaltonEdinburgh: E. & S. Livingstone Ltd.

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