Postmortem Treated
Examination Non-Surgically Ruptured
of
Patients
with
Aneurysms
Yoji NisxuuIMA, Takashi YosHIMOTO, Shigeaki HORI and Jiro SUZUKI Divisionof Neurosurgery,Institute of Brain Diseases, Tohoku UniversitySchool of Medicine,Sendai, Japan Summary There
is no doubt
that
radical
surgery
has been
successful
in preserving
the
patients with ruptured aneurysms. On the other hand, no matter how successful been we cannot and must not forget the patients who died without undergoing Therefore,
we investigated
from
clinical
course,
laboratory
work,
including
lives of we have surgery.
angiography
and autopsy, 37 cases who died during hospitalization death in the natural course and to find the possibilities
in order to elucidate the causes of of minimizing the number of non
operative
into
atomas, From
fatalities. brain the
appropriate
We classified
ischemia study,
it was
diagnosis
the
causes
due to vasospasm, concluded
and
treatment
natural
course
that
of death
3 groups:
and aggravation most
had been
of the made
intracranial
of the general lives could
as soon
have
as possible
hem
condition. been after
saved,
if
the initial
hemorrhage. Key words: intracranial vasospasm
aneurysm,
postmortem
Introduction The necessity of radical surgery in the treat ment of ruptured intracranial aneurysm is widely recognized today. At the Division of Neurosurgery, Institute of Brain Diseases, Tohoku University, more than 1,000 cases of intracranial aneurysms were experienced by the end of July, 1975. Although successful radical operations were performed in the majority of these cases, some became fatalities without en tering the operation room. Therefore, we exam ined the patients who died during hospitali zation without undergoing surgery, in order to elucidate the causes of death in the natural course and to find the possibilities of minimizing the number of such non-operative deaths. Subjects We experienced 1,083 cases of ruptured in tracranial aneurysm (Table 1) from 1961 to the
examination,
intracranial
hematoma,
cerebral
end of July, 1975. In 1,003 of these cases, the necks of the aneurysm were radically treated. Of the eighty patients without radical operations, 42 died during hospitalization. For the purpose of studying the natural course from the first hemorrhage to death, three patients who died of the complication of hypothermic anesthesia at the time of the radical operation") and two who died due to complication after palliative oper ation for aneurysm (ligation of the carotid ar tery) were excluded from the present study. Therefore we examined the remaining 37 fatal cases which were considered as patients with non-surgically treated ruptured aneurysms since obviously their treatments were conservative. Of these 37 cases, the aneurysms were located in the anterior communicating artery (ACOA) in 17, in the bifurcation of the posterior communicating artery and the internal carotid artery (ICPC) in 13, in the middle cerebral artery (MCA) in four, in the basilar artery (BA) in two, and in the anterior cerebral artery (ACA) in one. The 13 ICPC cases include two cases of multiple aneu
Table
1
Total
aneurysm
cases.
experienced
rysms in which the site of rupture ICPC (Table 2).
was in the
Causes of Death The cases of death were investigated from the clinical course, laboratory work including an giography, and autopsy findings. The possible causes of death were classifiable roughly into three groups : intracranial hematoma in 27, brain ischemia due to cerebral vasospasm in six, and aggravation of the general condition in four (Fig. 1). Autopies were performed on 32 of the 37 cases. 1.
Intracranial
Hematoma
The sites of aneurysm were in the ACOA in 14 cases, ICPC in eight, MCA in three, and BA and ACA in one each. Of the 27 patients, 13 were in their 50s (Table 3). Table
2
Distribution
from
1961 to 1975
7.
Clinical Course: The intervals between initial episode of hemorrhage and death were within one week in two cases, from one to two weeks in four, from two to three weeks in 10, from four weeks to three months in nine, and more than one year in two. The frequency of hemorrhagic episode was one in two patients, two in nine, three in five, and four or more in 11. The intervals between the initial and the second episode of the cases with 2 or more hemorrhagic episodes were within one week in seven cases, one to two weeks in eight, two to three weeks in five, and four weeks or longer in five. Types of' Hematoma: The hematomas were classified into the following three types ac cording to the characteristics of the intracranial hematoma formation. Type I-massive sub arachnoid hematoma formed in the basal and the cerebellomedullary cisterns to directly com press the brain stem (Fig. 2). Type II
of aneurysms
and
age of patients.
Fig. 2 Fig. 1 Causes of ACOA : anterior bifurcation and
the
death in non-operative communicating artery,
of the posterior internal
cerebral
artery,
cerebral
artery
carotid Ba : basilar
communicating artery, artery,
cases. ICPC : artery
MCA
: middle
ACA:
anterior
Type I hematoma
condition gradually hemorrhage.
hematoma having destroyed the brain paren chyma and broken through the cerebral vent ricle forming intraventricular hematoma (Figs. 3 and 4). Type III-hematoma localized in the brain parenchyma (Fig. 5). The relationships among each hematoma type, aneurysmal site, and survival period after last hemorrhage are shoen in Fig. 6. In Type I, all three patients died within two days. In Type II, all 13 patients died within seven days and cases in which the hem atoma from the ACOA aneurysm destroyed the neighborhood of the third ventricle and bled into the lateral ventricle or cases in which mas sive intraventricular hematoma was formed all died within two days. On the other hand, none of the Type III patients died within two days. Their Table
3
Age distribution
case (MCA aneurysm,
57
years old male). Massive subarachnoid hematoma is shown in the basal and the cerebellomedullary cisterns.
2.
aggravated
after
the
final
Cerebral Vasospasm
The site of aneurysm was in the ACOA in one case, ICPC in three, MCA in one, and BA in one. One patient was in his 30s, two in their 40s, and three in their 50s (Table 4). Clinical Course: Symptoms of brain ischemia due to vasospasm manifested on the 8th day after hemorrhagic episode on the average. The course of manifestation of symptoms was classified into two types : In one type, at the time of manifestation of cerebral vasospasm, patients showed mild dyskinesia and consciousness dis turbance which gradually aggravated, leading to death. In the other type, rapid deterioration of
of intracranial
hematoma
patients.
Fig. 3
Type II hematoma case (ACOA aneurysm , 61 years old female). The hemorrhage burst laterally near the 3rd ventricle, forming a massive hem atoma in the lateral ventricle.
Type II hematoma case (ICPC aneurysm , 41 years old male). The hemorrhage destroyed the temporal lobe and bled into the inferior horn forming a massive intraventricular hematoma .
Fig. 5 Type III hematoma case (MCA aneurysm, 53 years old male). Localized intracerebral hematoma in the sylvian fissure destroyed the brain paren chyma inducing severe brain edema.
Fig. 4
Table
4
Deaths
Fig. 6
due to possible
Hematoma
aneurysms
and
types survival
hemorrhage.
cerebral
vasospasm.
in relation period
to distribution following
of
the last
Fig. 8
The brain stem of a cerebral
vasospasm
case
(ICPC aneurysm, 40 years old female). Petechial hemorrhages probably due to tentorial herniation in the pons.
Fig. 7 Cerebral vasospasm case (rt. ICPC aneurysm, 43 years old female). Upper: Severe brain edema chiefly in the right hemisphere and the infarction of the right basal ganglion. Lower: Infarctic foci were disseminated in the bilateral posterior lobe.
consciousness made the differentiation between the aneurysmal rupture and the cerebral vasos pasm difficult from clinical symptoms alone. Autopsy of Brain: No intracranial hematoma that could account for the clinical symptoms was observed in any of the cases including those with sudden deterioration of consciousness. Ex tensive brain swelling and the infarction foci were chiefly found in the same hemisphere as the aneurysm (Fig. 7).In addition prominent hemor rhagic foci secondarily caused by tentorial her niation were observed in the mid-brain and pons (Fig. 8). 3.
Aggravation
of General Condition
Three patients died of pneumonia and one of hypopituitarism. All of the patients complicated by pneumonia, which developed while their con sciousness disturbance persisted after hemor rhagic episodes, were of far advanced age and had past histories of hypertension and myocar dial disturbances. Moreover, all of them were
accompanied by advanced dehydration due to insufficient food intake or dehydration therapy. The interval between the last hemorrhage and death was an average of 25 days (Table 5). In these patients, the autopsy showed only ventricular enlargement or small infarction foci in the brain cortices, but no hematoma, pro minent infarction foci in the hemispheres, nor changes of the brain stem attributable to death. The patient with hypopituitarism was 56 years old and had a giant aneurysm which developed at the ICPC and grew into the sella turcica. She had already shown advanced electrolyte abnor malities at the time of admission and having developed sudden hypotension, she died in spite of various treatments. At autopsy, it became clear that the base of the third ventricle had been raised and compressed by the aneurysm and the hypothalamic region had been destroyed (Fig. 9). Discussion According to the Anglo-American cooper ative study reported in 1966, in the natural history of 830 patients with single aneurysm, about 70 % died in three years after first hemor rhage. About 15 % of the deaths did not recover from the initial hemorrhagic episode, and most of the remainder died of secondary hemor rhages.") Of our 80 non-surgical cases, we in vestigated the causes of death of 37 patients who died in the natural course during hospitalization in this department. The largest number of pa tients, 27 (73 %), died of intracranial hematoma,
Table
*Autopsy
5
showed
Deaths
a giant
attributed
aneurysm
to aggravation
in the sella
of the general
, but no
condition
.
hemorrhage.
and beyond the indication for surgery.' 9,20,20 In the remaining 17 cases (15 with hematoma and 2 with vasospasm), the patients' consciousness de teriorated while waiting for surgery, which made surgery impossible.
Fig. 9
The
case
with
death
attributed
to
hy
popituitarism (ICPC aneurysm, 56 years old female). A giant aneurysm arrow in the sella tur cica, but no sign of aneurysm rupture was found .
and six (16%) died of brain ischemia due to cerebral vasospasm, and four (11 %), of aggra vation of the general condition. Although these 37 patients were referred to this department for surgery, they died without undergoing oper ation. At the time of admission 20 cases (12 with hematoma, 4 with vasospasm and 4 in poor general condition) were evaluated as too serious
Death after the rupture of intracranial aneu rysm seems to be frequently due to intracranial hematoma.2.4,5,6.8,9,13,14,15,16,24,2s~ Therefore, we examined the possibility of surgery, which could have preserved the lives of our patients who died of intracranial hematoma, with special reference to the classification of hematoma that was defined from autopsy findings. In case of Type I, due to the fact that the massive hem atoma directly injured the brain stem, the pa tients fell into a serious state immediately after the episode leading to death shortly afterwards. In Type II cases also, intraventricular hematoma elevated the intracranial pressure rapidly to make most of the patients seriously ill im mediately after the episodes. With the addition of cerebral swelling at the site of rupture, they died within a few days. On the other hand, in Type III cases, although the patients showed a satisfactory state of consciousness at the time the localized intracerebral hematoma developed, the brain parenchyma was destroyed with the lapse of time by the compression of the hematoma and the intracrainial pressure was elevated to grad
ually lead to death. From these results, it seems that hematomas of Type I and Type II were beyond the indication for surgery. Type III hem atoma, however, had indications for surgery to remove the hematoma and prevent secondary hemorrhage to make live-saving possible. How ever, the analysis of the clinical course of pa tients who died of Type I and Type II hem atomas provided more significant facts regard ing the indications for surgery. All three Type I patients had more than two hemorrhagic epi sodes. Consciousness after the initial episode was alert in two and senseless in one ; they developed a fatal episode 14-16 days after the initial episode. All Type II patients also had more than two episodes ; as many as nine of the 13 patients had the initial episode more than one month before the fatal hemorrhagic episode; most of them showing a long period of lucid consciousness. The above facts indicate that although most of the Type I and Type II hem atomas were beyond the indication for surgery at the time, such a fatal hematoma was seldom produced by the initial hemorrhagic episode alone. Therefore, there was opportunity for an early operation even for the Type I and II hematoma cases. Even taking into consideration the fact that different from the emergency hospitals,',") we have experienced selected cases to some extent, on which radical surgery could be performed, it is thought that the life of most of the patients dying of intracranial hematoma after rupture of intracranial aneurysm could be saved by surgery which must be performed as soon as possible after the initial episode. In relation to fatal brain ischemia due to vasospasm, it is well known that cerebral vaso spasm is a detrimental factor influencing the prognosis of the radical operation of ruptured intracranial aneurysm, particularly in the early operation."" However, there seem to be few reports emphasizing vasospasm as the cause of death in the natural course.3) The number of such deaths would probably increase if the true cause of deaths could be determined at in stitutions where close observations of patients' clinical course and appropriate clinical diag nosis could be made. As mentioned previously, deaths due to vasospasm include those cases whose consciousness rapidly falls into a serious state, therefore, the differentiation from the ag
gravation due to hemorrhagic episode is very difficult to make with clinical symptoms alone. It seems possible that in most of these cases the death is erroneously attributed to hemorrhagic episode .22) The autopsies of the patients who died of cerebral vasospasm showed an increase in the brain volume due to prominent cerebral swelling, cerebral herniation and secondary changes of the brain stem. Although absolute treatment for spastic vessels has not been de veloped yet, the autopsy findings indicates that some treatments including cervical sympathec tomy which was reported by Suzuki,23) should be performed early before the onset of irrever sible damages to the brain stem, requiring strict observations of the clinical course. Lastly, some of the deaths due to the aggra vation of general condition are unavoidable es pecially in the aged. However, it is known that even the aged can be the indication for radical operation as long as their consciousness and general condition are satisfactory and that their prognosis is not different from that of the youn ger cases.") All of the fatal patients had already been in a serious state at the time of admission. Therefore, strict management in the early stages is mandatory. In summary, we have described the cases of death in the natural course after the rupture of intracranial aneurysm and the possibility of life saving of these patients by radical surgery. It was thought that the lives of many of our cases could have been saved if the appropriate diagnosis and treatment had been made as soon as possible after the initial hemorrhage. References 1) Allcock, J. M. and Drake, C. G.: Postoperative angiography in cases of ruptured intracranial aneurysm. J. Neurosurg. 20: 752-759, 1963 2) Bebin, J., Currier, R. D. and Mich, A. A.: Cause of death in ruptured intracranial aneurysms. Arch. Intern. Med. 99: 771-790, 1957 3) Buckle, R. M., du Boulay, G. and Smith, B.: Death due to cerebral vasospasm. J. Neurol. Neurosurg. Psychiat. 27: 440-444, 1964 4) Crompton, M. R.: Intracerebral haematoma complicating ruptured cerebral berry aneurysm. J. Neurol. Neurosurg. Psychiat. 25: 378-386, 1962 5) Dial, D. L. and Mauer, G. B.: Intracranial aneurysms. Am. J. Surg. 35: 2-21, 1937
6) Frankel, K. and Alpers, B. J.: The clinical synd rome of aneurysm of middle cerebral artery. A.M.A. Arch. Neurol. & Psychiat. 74: 46-67, 1955 7) Fujinaga, R., Mizukami, M., Araki, G., Mihara, H., and Tomita, T.: The prognosis of ruptured intracranial aneurysm treated by conservative management. Brain Nerve (Tokyo) 23: 1265-1970, 1971 (Japanese) 8) Globus, J. H. and Globus, R. S.: Cerebral aneu rysm and massive non-traumatic cerebral hem morrhage. J. Neuropathol. Exp. Neurol. 2: 365-391,1943 9) Hammers, E. M.: Reaction of the meninges to blood. Arch. Neurol. Psychiat. 52: 505-514, 1944 10) Kwak, R., Okudaira, Y., Suzuki, J., Watabe, Y., Yusa, T. and Shiozawa, S.: Prognosis in hy pothermic anesthesia for direct surgical treat ment of intracranial aneurysms, with special reference to ventricular fibrillation. Brain Nerve (Tokyo) 24: 403-410, 1972 (Japanese) 11) Krayenbuhl, H. A., Yasargil, M. G., Flamm, E. S. and Tew, J. M.: Microsurgical treatment of intracranial saccular aneurysms. J. Neurosurg. 37: 678-686, 1972 12) Locksley, H. B.: Natural history of sub arachnoid hemorrhage, intracranial aneurysms and arteriovenous malformations, Based on 6, 368 Cases in the Cooperative Study. pp. 58-108, In Sahs, A. L., Perret, G. E., Locksley, H. B. and Nishioka, H. (eds.) : Intracranial Aneurysms and Subarachnoic Hemorrhage, A Cooperative Study. Chapter 5, Part II, J. B. Lippincott, Co., Philadelphia and Toronto, 1969 13) Richardson, J. C. and Hyland, H. H.: In tracranial aneurysms, a clinical and pathological study of subarachnoid and intracerebral haemorrhage caused by berry aneurysms. Med icine 20: 1-83, 1941 14) Robertson, E. G.: Cerebral lesions due to in tracranial aneurysms. Brain 72: 150-185, 1949 15) Sakaki, S. and Bito, S.: Clinicopathologicatl
16)
17)
18)
19)
20)
21)
22)
23)
24)
25)
studies on the subarachnoid hemorrhages. Brain Nerve (Tokyo) 23: 143-151, 1971 (Japanese) Schneck, S. A.: On the relationship between ruptured intracranial aneurysm and cerebral infarction. Neurology (Minneap.) 14: 691-702, 1964 Sugai, M. and Kono, R.: Pathological studies on subarachnoid hemorrhage, especially on the origin and localization of aneurysms of the basal arteries of brain. Tr. Soc. Path. Jap. (Tokyo) 44: 330-345, 1956 (Japanese) Suzuki, J., Takaku, A. and Yoshimoto, T.: Early operation of ruptured intracranial aneurysms. Brain Nerve (Tokyo) 23: 1291-1286, 1971 (Jap anese) Suzuki, J., Takaku, A. and Kodama, N.: Prog nostic correlation with the cerebral vasospasm and the direct operation for the intracranial aneurysm. Jap. J. Surg. (Tokyo) 1: 210-215, 1971 Suzuki, J. and Yoshimoto, T.: Early operation for the ruptured intracranial aneurysm. Jap. J. Surg. (Tokyo) 3: 149-156, 1973 Suzuki, J., Yoshimoto, T. and Hori, S.: Con tinuous ventricular drainage to lessen surgical risk in ruptured intracranial aneurysm. Surg. Neurol. 2: 87-90, 1974 Suzuki, J. and Hori, S.: Prediction of reattacks following rupture of intracranial aneurysms. Neurologia inedico-chirurgica (Tokyo) 15: Part 1,35-39,1975 Suzuki, J., Iwabuchi, T. and Hori, S.: Cervical sympathectomy for cerebral vasospasm after aneurysm rupture. Neurologia medico-chirurgica (Tokyo) 15: Part I 41-50, 1975 Tomlinson, B. E.: Brain changes in ruptured intracranial aneurysm. J. Clin. Path. 12: 391-399,1959 Wolfe, H. R. I.: Spontaneous subarachnoid haemorrhage: A surgical challenge. Brit. J. Surg. 40: 319-325, 1953
Examination Non-Surgically Ruptured
of
Patients
with
Aneurysms
Yoji NisxuuIMA, Takashi YosHIMOTO, Shigeaki HORI and Jiro SUZUKI Divisionof Neurosurgery,Institute of Brain Diseases, Tohoku UniversitySchool of Medicine,Sendai, Japan Summary There
is no doubt
that
radical
surgery
has been
successful
in preserving
the
patients with ruptured aneurysms. On the other hand, no matter how successful been we cannot and must not forget the patients who died without undergoing Therefore,
we investigated
from
clinical
course,
laboratory
work,
including
lives of we have surgery.
angiography
and autopsy, 37 cases who died during hospitalization death in the natural course and to find the possibilities
in order to elucidate the causes of of minimizing the number of non
operative
into
atomas, From
fatalities. brain the
appropriate
We classified
ischemia study,
it was
diagnosis
the
causes
due to vasospasm, concluded
and
treatment
natural
course
that
of death
3 groups:
and aggravation most
had been
of the made
intracranial
of the general lives could
as soon
have
as possible
hem
condition. been after
saved,
if
the initial
hemorrhage. Key words: intracranial vasospasm
aneurysm,
postmortem
Introduction The necessity of radical surgery in the treat ment of ruptured intracranial aneurysm is widely recognized today. At the Division of Neurosurgery, Institute of Brain Diseases, Tohoku University, more than 1,000 cases of intracranial aneurysms were experienced by the end of July, 1975. Although successful radical operations were performed in the majority of these cases, some became fatalities without en tering the operation room. Therefore, we exam ined the patients who died during hospitali zation without undergoing surgery, in order to elucidate the causes of death in the natural course and to find the possibilities of minimizing the number of such non-operative deaths. Subjects We experienced 1,083 cases of ruptured in tracranial aneurysm (Table 1) from 1961 to the
examination,
intracranial
hematoma,
cerebral
end of July, 1975. In 1,003 of these cases, the necks of the aneurysm were radically treated. Of the eighty patients without radical operations, 42 died during hospitalization. For the purpose of studying the natural course from the first hemorrhage to death, three patients who died of the complication of hypothermic anesthesia at the time of the radical operation") and two who died due to complication after palliative oper ation for aneurysm (ligation of the carotid ar tery) were excluded from the present study. Therefore we examined the remaining 37 fatal cases which were considered as patients with non-surgically treated ruptured aneurysms since obviously their treatments were conservative. Of these 37 cases, the aneurysms were located in the anterior communicating artery (ACOA) in 17, in the bifurcation of the posterior communicating artery and the internal carotid artery (ICPC) in 13, in the middle cerebral artery (MCA) in four, in the basilar artery (BA) in two, and in the anterior cerebral artery (ACA) in one. The 13 ICPC cases include two cases of multiple aneu
Table
1
Total
aneurysm
cases.
experienced
rysms in which the site of rupture ICPC (Table 2).
was in the
Causes of Death The cases of death were investigated from the clinical course, laboratory work including an giography, and autopsy findings. The possible causes of death were classifiable roughly into three groups : intracranial hematoma in 27, brain ischemia due to cerebral vasospasm in six, and aggravation of the general condition in four (Fig. 1). Autopies were performed on 32 of the 37 cases. 1.
Intracranial
Hematoma
The sites of aneurysm were in the ACOA in 14 cases, ICPC in eight, MCA in three, and BA and ACA in one each. Of the 27 patients, 13 were in their 50s (Table 3). Table
2
Distribution
from
1961 to 1975
7.
Clinical Course: The intervals between initial episode of hemorrhage and death were within one week in two cases, from one to two weeks in four, from two to three weeks in 10, from four weeks to three months in nine, and more than one year in two. The frequency of hemorrhagic episode was one in two patients, two in nine, three in five, and four or more in 11. The intervals between the initial and the second episode of the cases with 2 or more hemorrhagic episodes were within one week in seven cases, one to two weeks in eight, two to three weeks in five, and four weeks or longer in five. Types of' Hematoma: The hematomas were classified into the following three types ac cording to the characteristics of the intracranial hematoma formation. Type I-massive sub arachnoid hematoma formed in the basal and the cerebellomedullary cisterns to directly com press the brain stem (Fig. 2). Type II
of aneurysms
and
age of patients.
Fig. 2 Fig. 1 Causes of ACOA : anterior bifurcation and
the
death in non-operative communicating artery,
of the posterior internal
cerebral
artery,
cerebral
artery
carotid Ba : basilar
communicating artery, artery,
cases. ICPC : artery
MCA
: middle
ACA:
anterior
Type I hematoma
condition gradually hemorrhage.
hematoma having destroyed the brain paren chyma and broken through the cerebral vent ricle forming intraventricular hematoma (Figs. 3 and 4). Type III-hematoma localized in the brain parenchyma (Fig. 5). The relationships among each hematoma type, aneurysmal site, and survival period after last hemorrhage are shoen in Fig. 6. In Type I, all three patients died within two days. In Type II, all 13 patients died within seven days and cases in which the hem atoma from the ACOA aneurysm destroyed the neighborhood of the third ventricle and bled into the lateral ventricle or cases in which mas sive intraventricular hematoma was formed all died within two days. On the other hand, none of the Type III patients died within two days. Their Table
3
Age distribution
case (MCA aneurysm,
57
years old male). Massive subarachnoid hematoma is shown in the basal and the cerebellomedullary cisterns.
2.
aggravated
after
the
final
Cerebral Vasospasm
The site of aneurysm was in the ACOA in one case, ICPC in three, MCA in one, and BA in one. One patient was in his 30s, two in their 40s, and three in their 50s (Table 4). Clinical Course: Symptoms of brain ischemia due to vasospasm manifested on the 8th day after hemorrhagic episode on the average. The course of manifestation of symptoms was classified into two types : In one type, at the time of manifestation of cerebral vasospasm, patients showed mild dyskinesia and consciousness dis turbance which gradually aggravated, leading to death. In the other type, rapid deterioration of
of intracranial
hematoma
patients.
Fig. 3
Type II hematoma case (ACOA aneurysm , 61 years old female). The hemorrhage burst laterally near the 3rd ventricle, forming a massive hem atoma in the lateral ventricle.
Type II hematoma case (ICPC aneurysm , 41 years old male). The hemorrhage destroyed the temporal lobe and bled into the inferior horn forming a massive intraventricular hematoma .
Fig. 5 Type III hematoma case (MCA aneurysm, 53 years old male). Localized intracerebral hematoma in the sylvian fissure destroyed the brain paren chyma inducing severe brain edema.
Fig. 4
Table
4
Deaths
Fig. 6
due to possible
Hematoma
aneurysms
and
types survival
hemorrhage.
cerebral
vasospasm.
in relation period
to distribution following
of
the last
Fig. 8
The brain stem of a cerebral
vasospasm
case
(ICPC aneurysm, 40 years old female). Petechial hemorrhages probably due to tentorial herniation in the pons.
Fig. 7 Cerebral vasospasm case (rt. ICPC aneurysm, 43 years old female). Upper: Severe brain edema chiefly in the right hemisphere and the infarction of the right basal ganglion. Lower: Infarctic foci were disseminated in the bilateral posterior lobe.
consciousness made the differentiation between the aneurysmal rupture and the cerebral vasos pasm difficult from clinical symptoms alone. Autopsy of Brain: No intracranial hematoma that could account for the clinical symptoms was observed in any of the cases including those with sudden deterioration of consciousness. Ex tensive brain swelling and the infarction foci were chiefly found in the same hemisphere as the aneurysm (Fig. 7).In addition prominent hemor rhagic foci secondarily caused by tentorial her niation were observed in the mid-brain and pons (Fig. 8). 3.
Aggravation
of General Condition
Three patients died of pneumonia and one of hypopituitarism. All of the patients complicated by pneumonia, which developed while their con sciousness disturbance persisted after hemor rhagic episodes, were of far advanced age and had past histories of hypertension and myocar dial disturbances. Moreover, all of them were
accompanied by advanced dehydration due to insufficient food intake or dehydration therapy. The interval between the last hemorrhage and death was an average of 25 days (Table 5). In these patients, the autopsy showed only ventricular enlargement or small infarction foci in the brain cortices, but no hematoma, pro minent infarction foci in the hemispheres, nor changes of the brain stem attributable to death. The patient with hypopituitarism was 56 years old and had a giant aneurysm which developed at the ICPC and grew into the sella turcica. She had already shown advanced electrolyte abnor malities at the time of admission and having developed sudden hypotension, she died in spite of various treatments. At autopsy, it became clear that the base of the third ventricle had been raised and compressed by the aneurysm and the hypothalamic region had been destroyed (Fig. 9). Discussion According to the Anglo-American cooper ative study reported in 1966, in the natural history of 830 patients with single aneurysm, about 70 % died in three years after first hemor rhage. About 15 % of the deaths did not recover from the initial hemorrhagic episode, and most of the remainder died of secondary hemor rhages.") Of our 80 non-surgical cases, we in vestigated the causes of death of 37 patients who died in the natural course during hospitalization in this department. The largest number of pa tients, 27 (73 %), died of intracranial hematoma,
Table
*Autopsy
5
showed
Deaths
a giant
attributed
aneurysm
to aggravation
in the sella
of the general
, but no
condition
.
hemorrhage.
and beyond the indication for surgery.' 9,20,20 In the remaining 17 cases (15 with hematoma and 2 with vasospasm), the patients' consciousness de teriorated while waiting for surgery, which made surgery impossible.
Fig. 9
The
case
with
death
attributed
to
hy
popituitarism (ICPC aneurysm, 56 years old female). A giant aneurysm arrow in the sella tur cica, but no sign of aneurysm rupture was found .
and six (16%) died of brain ischemia due to cerebral vasospasm, and four (11 %), of aggra vation of the general condition. Although these 37 patients were referred to this department for surgery, they died without undergoing oper ation. At the time of admission 20 cases (12 with hematoma, 4 with vasospasm and 4 in poor general condition) were evaluated as too serious
Death after the rupture of intracranial aneu rysm seems to be frequently due to intracranial hematoma.2.4,5,6.8,9,13,14,15,16,24,2s~ Therefore, we examined the possibility of surgery, which could have preserved the lives of our patients who died of intracranial hematoma, with special reference to the classification of hematoma that was defined from autopsy findings. In case of Type I, due to the fact that the massive hem atoma directly injured the brain stem, the pa tients fell into a serious state immediately after the episode leading to death shortly afterwards. In Type II cases also, intraventricular hematoma elevated the intracranial pressure rapidly to make most of the patients seriously ill im mediately after the episodes. With the addition of cerebral swelling at the site of rupture, they died within a few days. On the other hand, in Type III cases, although the patients showed a satisfactory state of consciousness at the time the localized intracerebral hematoma developed, the brain parenchyma was destroyed with the lapse of time by the compression of the hematoma and the intracrainial pressure was elevated to grad
ually lead to death. From these results, it seems that hematomas of Type I and Type II were beyond the indication for surgery. Type III hem atoma, however, had indications for surgery to remove the hematoma and prevent secondary hemorrhage to make live-saving possible. How ever, the analysis of the clinical course of pa tients who died of Type I and Type II hem atomas provided more significant facts regard ing the indications for surgery. All three Type I patients had more than two hemorrhagic epi sodes. Consciousness after the initial episode was alert in two and senseless in one ; they developed a fatal episode 14-16 days after the initial episode. All Type II patients also had more than two episodes ; as many as nine of the 13 patients had the initial episode more than one month before the fatal hemorrhagic episode; most of them showing a long period of lucid consciousness. The above facts indicate that although most of the Type I and Type II hem atomas were beyond the indication for surgery at the time, such a fatal hematoma was seldom produced by the initial hemorrhagic episode alone. Therefore, there was opportunity for an early operation even for the Type I and II hematoma cases. Even taking into consideration the fact that different from the emergency hospitals,',") we have experienced selected cases to some extent, on which radical surgery could be performed, it is thought that the life of most of the patients dying of intracranial hematoma after rupture of intracranial aneurysm could be saved by surgery which must be performed as soon as possible after the initial episode. In relation to fatal brain ischemia due to vasospasm, it is well known that cerebral vaso spasm is a detrimental factor influencing the prognosis of the radical operation of ruptured intracranial aneurysm, particularly in the early operation."" However, there seem to be few reports emphasizing vasospasm as the cause of death in the natural course.3) The number of such deaths would probably increase if the true cause of deaths could be determined at in stitutions where close observations of patients' clinical course and appropriate clinical diag nosis could be made. As mentioned previously, deaths due to vasospasm include those cases whose consciousness rapidly falls into a serious state, therefore, the differentiation from the ag
gravation due to hemorrhagic episode is very difficult to make with clinical symptoms alone. It seems possible that in most of these cases the death is erroneously attributed to hemorrhagic episode .22) The autopsies of the patients who died of cerebral vasospasm showed an increase in the brain volume due to prominent cerebral swelling, cerebral herniation and secondary changes of the brain stem. Although absolute treatment for spastic vessels has not been de veloped yet, the autopsy findings indicates that some treatments including cervical sympathec tomy which was reported by Suzuki,23) should be performed early before the onset of irrever sible damages to the brain stem, requiring strict observations of the clinical course. Lastly, some of the deaths due to the aggra vation of general condition are unavoidable es pecially in the aged. However, it is known that even the aged can be the indication for radical operation as long as their consciousness and general condition are satisfactory and that their prognosis is not different from that of the youn ger cases.") All of the fatal patients had already been in a serious state at the time of admission. Therefore, strict management in the early stages is mandatory. In summary, we have described the cases of death in the natural course after the rupture of intracranial aneurysm and the possibility of life saving of these patients by radical surgery. It was thought that the lives of many of our cases could have been saved if the appropriate diagnosis and treatment had been made as soon as possible after the initial hemorrhage. References 1) Allcock, J. M. and Drake, C. G.: Postoperative angiography in cases of ruptured intracranial aneurysm. J. Neurosurg. 20: 752-759, 1963 2) Bebin, J., Currier, R. D. and Mich, A. A.: Cause of death in ruptured intracranial aneurysms. Arch. Intern. Med. 99: 771-790, 1957 3) Buckle, R. M., du Boulay, G. and Smith, B.: Death due to cerebral vasospasm. J. Neurol. Neurosurg. Psychiat. 27: 440-444, 1964 4) Crompton, M. R.: Intracerebral haematoma complicating ruptured cerebral berry aneurysm. J. Neurol. Neurosurg. Psychiat. 25: 378-386, 1962 5) Dial, D. L. and Mauer, G. B.: Intracranial aneurysms. Am. J. Surg. 35: 2-21, 1937
6) Frankel, K. and Alpers, B. J.: The clinical synd rome of aneurysm of middle cerebral artery. A.M.A. Arch. Neurol. & Psychiat. 74: 46-67, 1955 7) Fujinaga, R., Mizukami, M., Araki, G., Mihara, H., and Tomita, T.: The prognosis of ruptured intracranial aneurysm treated by conservative management. Brain Nerve (Tokyo) 23: 1265-1970, 1971 (Japanese) 8) Globus, J. H. and Globus, R. S.: Cerebral aneu rysm and massive non-traumatic cerebral hem morrhage. J. Neuropathol. Exp. Neurol. 2: 365-391,1943 9) Hammers, E. M.: Reaction of the meninges to blood. Arch. Neurol. Psychiat. 52: 505-514, 1944 10) Kwak, R., Okudaira, Y., Suzuki, J., Watabe, Y., Yusa, T. and Shiozawa, S.: Prognosis in hy pothermic anesthesia for direct surgical treat ment of intracranial aneurysms, with special reference to ventricular fibrillation. Brain Nerve (Tokyo) 24: 403-410, 1972 (Japanese) 11) Krayenbuhl, H. A., Yasargil, M. G., Flamm, E. S. and Tew, J. M.: Microsurgical treatment of intracranial saccular aneurysms. J. Neurosurg. 37: 678-686, 1972 12) Locksley, H. B.: Natural history of sub arachnoid hemorrhage, intracranial aneurysms and arteriovenous malformations, Based on 6, 368 Cases in the Cooperative Study. pp. 58-108, In Sahs, A. L., Perret, G. E., Locksley, H. B. and Nishioka, H. (eds.) : Intracranial Aneurysms and Subarachnoic Hemorrhage, A Cooperative Study. Chapter 5, Part II, J. B. Lippincott, Co., Philadelphia and Toronto, 1969 13) Richardson, J. C. and Hyland, H. H.: In tracranial aneurysms, a clinical and pathological study of subarachnoid and intracerebral haemorrhage caused by berry aneurysms. Med icine 20: 1-83, 1941 14) Robertson, E. G.: Cerebral lesions due to in tracranial aneurysms. Brain 72: 150-185, 1949 15) Sakaki, S. and Bito, S.: Clinicopathologicatl
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studies on the subarachnoid hemorrhages. Brain Nerve (Tokyo) 23: 143-151, 1971 (Japanese) Schneck, S. A.: On the relationship between ruptured intracranial aneurysm and cerebral infarction. Neurology (Minneap.) 14: 691-702, 1964 Sugai, M. and Kono, R.: Pathological studies on subarachnoid hemorrhage, especially on the origin and localization of aneurysms of the basal arteries of brain. Tr. Soc. Path. Jap. (Tokyo) 44: 330-345, 1956 (Japanese) Suzuki, J., Takaku, A. and Yoshimoto, T.: Early operation of ruptured intracranial aneurysms. Brain Nerve (Tokyo) 23: 1291-1286, 1971 (Jap anese) Suzuki, J., Takaku, A. and Kodama, N.: Prog nostic correlation with the cerebral vasospasm and the direct operation for the intracranial aneurysm. Jap. J. Surg. (Tokyo) 1: 210-215, 1971 Suzuki, J. and Yoshimoto, T.: Early operation for the ruptured intracranial aneurysm. Jap. J. Surg. (Tokyo) 3: 149-156, 1973 Suzuki, J., Yoshimoto, T. and Hori, S.: Con tinuous ventricular drainage to lessen surgical risk in ruptured intracranial aneurysm. Surg. Neurol. 2: 87-90, 1974 Suzuki, J. and Hori, S.: Prediction of reattacks following rupture of intracranial aneurysms. Neurologia inedico-chirurgica (Tokyo) 15: Part 1,35-39,1975 Suzuki, J., Iwabuchi, T. and Hori, S.: Cervical sympathectomy for cerebral vasospasm after aneurysm rupture. Neurologia medico-chirurgica (Tokyo) 15: Part I 41-50, 1975 Tomlinson, B. E.: Brain changes in ruptured intracranial aneurysm. J. Clin. Path. 12: 391-399,1959 Wolfe, H. R. I.: Spontaneous subarachnoid haemorrhage: A surgical challenge. Brit. J. Surg. 40: 319-325, 1953
