Subarachnoid hemorrhage on computed tomography scanning and the development of cerebral vasospasm:...

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Surgical Neurology 63

Subarachnoid hemorrhage on computed tomography scanning and the

development of cerebral vasospasm: the Fisher grade revisited

Michael L. Smith, MDa,*, John M. Abrahams, MDb, Sid Chandela, MDb

Michelle J. Smith, MDa, Robert W. Hurst, MDa, Peter D. Le Roux, MDa

aDepartment of Neurosurgery, Hospital of the University of Pennsylvania, Philadelphia, PA 19146, USAbDepartment of Neurosurgery, Albert Einstein College of Medicine, New York, NY 10461, USA

Received 2 February 2004; accepted 2 June 2004

Abstract Background: The Fisher grade (FG) is widely used to predict cerebral vasospasm after aneurysmal

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doi:10.1016/j.surneu.2

* Corresponding a

E-mail address: sm

subarachnoid hemorrhage (SAH). We revisited the grading scale to determine its validity in the era of

modern management.

Methods: We retrospectively reviewed the records of 134 patients with SAH. The amount and

distribution of subarachnoid blood on admission computed tomography (CT) scan was quantified

according to the FG and compared with development of symptomatic vasospasm.

Results: We reviewed 134 patients (median age, 54) who presented with aneurysmal SAH. Six (5%)

were FG 1, 34 (25%) were FG 2, 25 (19%) were FG 3, and 69 (51%) were FG 4. Symptomatic

vasospasm developed in no (0%) FG 1, 8 (24%) FG 2, 7 (28 %) FG 3, and 13 (19%) FG 4 patients

(28 of 134 total patients; 21%). Development of symptomatic vasospasm was not associated with

admission FG, Hunt and Hess grade, age, sex, or location of blood on presenting CT scan. Elevated

transcranial Doppler blood flow velocity was associated with blood in the basal cisterns (P = .0047),

lateral ventricles (P = .026), or blood in any ventricle (P = .04). Postoperative angiograms were

obtained in 57 patients; moderate to severe vasospasm was observed in 5 (15%) FG 2, 6 (24%) FG 3,

and 14 (20%) FG 4 patients. Twenty patients (71%) with symptomatic vasospasm had moderate or

severe angiographic vasospasm. Angiographic vasospasm was associated with intraventricular blood

(P = .054) but not with FG.

Conclusions: Symptomatic vasospasm occurred in 21% of cases. The FG correlated with

symptomatic vasospasm in only half the patients. A new predictive CT grading scale for vasospasm

may be necessary.

D 2005 Elsevier Inc. All rights reserved.

Keywords: Aneurysm; Cerebral vasospasm; Fisher grade; Subarachnoid hemorrhage

1. Introduction

Delayed cerebral ischemia from cerebral artery vaso-

spasm after aneurysmal subarachnoid hemorrhage (SAH) is

a known cause of morbidity and mortality. It is important to

predict which patients are at risk for vasospasm, because its

management relies significantly on prevention. The Fisher

computed tomographic grading scale described by Fisher et

al [4] in 1980 is widely used to predict which patients are at

nt matter D 2005 Elsevier Inc. All rights reserved.

004.06.017

uthor. Tel.: +1 215 662 3487; fax: +1 215 349 5534.

[email protected] (M.L. Smith).

risk to develop delayed cerebral ischemia (Table 1). The

grading scale described the amount and distribution of

subarachnoid blood seen on initial head computed tomog-

raphy (CT) as it correlated to the development of cerebral

vasospasm. Fisher et al found that symptomatic vasospasm

only tended to occur in the major subarachnoid blood

vessels that were initially surrounded by a thick subarach-

noid clot. Though the original manuscript described the

findings as preliminary, the scale derived from the 4

groupings of Fisher et al has become a standard tool for

initial patient evaluation and prediction of likelihood of

delayed cerebral ischemia after SAH.

(2005) 229–235

Table 1

The 4 Fisher groups

Fisher group Appearance of SAH on head CT

1 No subarachnoid blood visualized

2 Diffuse or thin sheets (vertical layers b1 mm thick)

3 Localized clot and/or vertical layers (z1 mm thick)

4 Diffuse or no SAH, but with intraventricular or

intraparenchymal clot

M.L. Smith et al. / Surgical Neurology 63 (2005) 229–235230

Evaluation and treatment of patients with ruptured

aneurysms have evolved the description of the Fisher grade

(FG) in 1980. Modern CT scanners have significantly

improved resolution for small volumes of intracranial blood

compared to those available in 1980. In addition, less than

half the patients included in the Fisher et al [4] study had

their CT scan on the day of aneurysm rupture. Today, most

patients are evaluated and imaged on the day of hemor-

rhage. Significant changes in treatment include early

aneurysm occlusion, the use of calcium channel blockers,

which may improve clinical outcome in aneurysmal SAH,

and using hypervolemic, hypertensive, hemodilution (triple

bHQ) therapy at the onset of documented vasospasm in an

attempt to maximize perfusion to areas of brain fed by

spastic vessels. These management strategies were not used

in 1980. Also, supplemental studies such as transcranial

Doppler sonography (TCD) developed during the past

decade now play an important role in assessing patients

for vasospasm. In view of this it is important to determine

whether the FG is a useful tool to predict vasospasm in the

modern era. In this study, we retrospectively reviewed the

medical records, CT scans, angiograms, and TCD findings

of 134 consecutive patients with aneurysmal SAH to

determine whether the FG reliably predicts vasospasm.

Our results suggest that the FG may need to be revised.

2. Patients and methods

2.1. Patient population

We retrospectively reviewed the medical records includ-

ing hospital charts, CT scans, angiograms, and TCD findings

of 134 consecutive patients with a diagnosis of SAH treated

at the Hospital of the University of Pennsylvania. Patients

with SAH due to trauma, arteriovenous malformations, or of

unknown etiology were excluded from the study. Subarach-

noid hemorrhage was diagnosed by either CT scanning or

lumbar puncture. Patient demographics, date of SAH, day of

CT scan, FG, and Hunt and Hess grade were recorded. The

date of the hemorrhage was considered day 1 and day of CT

scan was recorded relative to this.

2.2. Treatment

All patients were treated according to standard protocol,

including preoperative resuscitation, early aneurysm occlu-

sion using coil embolization or surgical clipping, and

aggressive prevention and treatment of vasospasm. All

patients were cared for in the neurosurgical intensive care

unit with invasive hemodynamic monitoring. All patients

received nimodipine and phenytoin. Transcranial Doppler

sonography was obtained every other day for 14 days and

every day for patients suspected of having symptomatic

vasospasm. We define symptomatic vasospasm as a clinical

entity that includes a new, delayed focal neurologic deficit

or mental status decline in the postoperative period without

evidence of hydrocephalus, metabolic abnormality, fever, or

other systemic factors. It was not quantified by an absolute

middle cerebral artery (MCA) blood flow velocity (BFV)

with TCD analysis and was made strictly by clinical criteria.

If patients became symptomatic from clinically suspected

cerebral vasospasm, mean arterial blood pressure was

elevated and intravenous fluid resuscitation was maintained

in keeping with the triple H therapy. If symptoms did not

resolve, patients were taken for angiography.

Transcranial Doppler sonography BFV in the MCA was

evaluated using a scale of 0 for normal (BFV b 90 cm/s), 1

for mild spasm (BFV = 90-120 cm/s), 2 for moderate spasm

(BFV = 120-200 cm/s), and 3 for severe spasm (BFV N 200

cm/s). We tabulated the results from the MCA BVF findings

for the purpose of this study. Transcranial Doppler

sonography analysis was done on each patient assessing

BFV in all vessels but we used MCA BFV for the statistical

analysis. Each patient was administered 0.9% normal saline

and 5% albumin to maintain central venous pressure greater

than 8 mm Hg. CT scanning was used to examine patients

who demonstrated clinical deterioration. When vasospasm

was thought to be the cause of clinical deterioration,

hypertensive and hypervolemic therapy was started to

maintain systolic blood pressure greater than 180 mm Hg.

The diagnosis of symptomatic cerebral vasospasm was

confirmed using angiography. When clinical deterioration

persisted despite medical management, patients underwent

papaverine infusion, balloon angioplasty, or both.

2.3. CT scanning

Computed tomography scans were obtained on a General

Electric Light Speed Scanner according to standard proto-

cols. Each CT scan was examined by 2 independent

observers and in different orders. Cases leading to disagree-

ment between observers were reviewed by both observers

together to reach a consensus. The CT scans were examined

using the FG—grade 1: none or minimal blood detected;

grade 2: diffuse thin layers of subarachnoid blood with

layers less than 1 mm thick; grade 3: localized clot and/or

thick layers of subarachnoid blood greater than 1 mm thick;

grade 4: intracerebral or intraventricular with no or diffuse

subarachnoid blood. Blood was also evaluated based on

location: Sylvian fissure, interhemispheric fissure, basal

cisterns, third ventricle, fourth ventricle, lateral ventricle(s),

and the presence of intraparenchymal clot.

2.4. Angiography

All patients underwent pretreatment digital subtraction

angiography. Aneurysm size and location were recorded.

Table 2

Patient demographics for all patients and those stratified as symptomatic

vasospasm

All patients Symptomatic

vasospasm

Asymptomatic

No. of patients 134 28 (21%)a 106 (79%)b

Male/female 40/94 7/21 33/73

Age (y) 16-82 35-78 16-82

Mean (y) 54.4 51.8 55.0

Hunt and Hess grade

1 57 10 (18%) 47 (82%)

2 16 5 (31%) 11 (69%)

3 29 5 (17%) 24 (83%)

4 25 8 (32%) 17 (68%)

5 7 0 ( 0 %) 7 (100%)

Fisher grade

1 6 0 ( 0%) 6 (100%)

2 34 8 (24%) 26 (76%)

3 25 7 (28%) 18 (22%)

4 69 13 (19%) 56 (81%)

a Percentage of ball patientsQ who develop symptomatic vasospasm.b Percentage of ball patientsQ without signs or symptoms of vasospasm.

able 3

ubarachnoid blood distribution on initial CT scan

All patients Symptomatic

vasospasm

Asymptomatic

nilateral Sylvian

fissure blood

34 6 (18%)a 28

M.L. Smith et al. / Surgical Neurology 63 (2005) 229–235 231

Posttreatment angiograms were obtained when vasospasm

was suspected as the cause for delayed neurologic deteriora-

tion. Angiograms were evaluated by 2 independent observers

unaware of the CT FG and classified according to the

following scale by comparing pre- and posttreatment studies:

0 for no spasm; 1 formild spasm (b25% arterial narrowing); 2

for moderate spasm (25-50% arterial narrowing); and 3 for

severe spasm (N50% arterial narrowing). Vasospasm was

qualified as the most severe narrowing in any one vessel,

independent of the number of other vessels affected.

2.5. Statistical analysis

Data are represented as means F SDs or, where samples

depart from normal distributions, as a median. The Student t

test was used to test differences between groups when the

data were normally distributed. The Mann-Whitney proce-

dure was used to examine data that departed from a normal

distribution. Both univariate and bivariate analyses were

done using analysis of variance, Student t test, and a

Pearson v2 test. The Fischer exact test was substituted when

one or more cells had frequencies less than 5. Statistical

significance was set at a probability value less than .05. All

statistical analyses were performed using commercially

available software (SAS Proprietary Software, Version 8,

1999, SAS Institute, Cary, NC).
ilateral Sylvian
fissure blood

55 13 (24%) 42

terhemispheric

blood

35 8 (23%) 27

asal cisterns 76 18 (24%) 58

hird ventricle 16 2 (13%) 14

ourth ventricle 24 4 (17%) 20

ateral ventricle 49 11 (22%) 38

traparenchymal clot 28 8 (29%) 20

a Percentage of ball patientsQ who develop symptomatic vasospasm.

3. Results

3.1. Patients

There were 134 patients, including 40 males and 94

females (median age, 54 years; range, 16-82 years) (Table 2).

The FGs and Hunt and Hess grades are listed in Table 2. All

patients underwent preoperative digital subtraction angiog-

raphy except one patient who presented with a large

temporal hematoma that required emergent evacuation. In

this patient, the presence of an aneurysm was confirmed

intraoperatively. There were 116 anterior circulation and 18

posterior circulation ruptured aneurysms. Twenty patients

underwent coil embolization (15%) and 114 (85%) under-

went surgical clipping.

3.2. Fisher grade and CT scan

Twenty-eight patients (21%) developed symptomatic

vasospasm. Of these, 8 were FG 2, 7 were FG 3, and 13

were FG 4. The severity of SAH identified on initial CT

scan was not associated with symptomatic vasospasm (P =

.50). In both univariate and bivariate analyses, development

of symptomatic vasospasm was not associated with admis-

sion FG, Hunt and Hess grade, age, sex, or location of blood

on presenting CT scan.

One hundred eleven (83%) patients had their initial CT

scan on the day of SAH (day 1), 6 on day 2, 6 on day 3, 2 on

day 4, 3 on day 5, and 6 between days 6 and 9 after SAH.

Twenty-one of 28 (75%) patients with symptomatic

vasospasm and 90 of 106 (85%) patients without symp-

tomatic vasospasm had their initial CT scan on the day of

SAH with no significant difference between groups (P =

.67). The location of subarachnoid blood was similar in

patients who developed symptomatic vasospasm and those

who were asymptomatic (Table 3) (P values ranged from

.41 to .82 for the different locations analyzed and listed in

Table 3). Symptomatic vasospasm developed in 8 of 28

patients (29%) with a focal homogenous collection of

subarachnoid blood greater than 10 mm in diameter.

Symptomatic vasospasm developed in 15% of patients

who did not have focal clots.

3.3. Fisher grade and TCD

All patients underwent serial TCD examinations. In those

patients with at least 1 episode of TCD BFV greater than 200

cm/s (n = 14), 6 patients (38%) developed symptomatic

vasospasm (Table 4). In both univariate and bivariate

analyses, elevated TCD MCA BFV was not associated with

T

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B

In

B

T

F

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In

Table 4

Assessment of vasospasm using TCD and angiography

All patients Symptomatic vasospasm Asymptomatic

Elevated TCD

None 85 12 (14%)a 73

Mild 24 8 (33%) 16

Moderate 11 2 (18%) 9

Severe 14 6 (43%) 8

Preoperative angiogram

None 120 23 (19%) 97

Mild 11 4 (36%) 7

Moderate 1 1 (100%) 0

Severe 1 0 (0%) 1

Postoperative angiogram (n = 57)

None 20 2 (10%) 18

Mild 12 3 (25%) 9

Moderate 11 8 (73%) 3

Severe 14 12 (86%) 2

a Percentage of ball patientsQ who develop symptomatic vasospasm.


admission FG, Hunt and Hess grade, age, or sex. A

significant association was observed between elevated

TCD MCA BFV and symptomatic (P = .005) or angio-

graphic vasospasm (P = .001). A significant relationship

also was observed between increased TCD MCA BFV and

the location of blood on initial CT; blood in the basal cisterns

(P = .0047), lateral ventricles (P = .026), or in any ventricle

(P = .04) was associated with elevated TCD velocities.

3.4. Fisher grade and angiography

On preoperative angiograms (n = 133), 11 (8%) patients

had mild vasospasm, 1 patient had moderate vasospasm,

and 1 patient had severe vasospasm. Fifty-seven (43%)

patients underwent postoperative angiography between 3

and 18 days (mean = 6 days) after SAH. Angiographic

vasospasm was identified in 37 (65%) patients, including 12

(21%) with mild, 11 (19%) with moderate, and 14 (25%)

with severe angiographic vasospasm. In patients with severe

angiographic MCA vasospasm, all had TCD MCA BFV

greater than 200 cm/s. In contrast, BFV was less than 200

cm/s in all patients with mild or moderate vasospasm.

Among the patients who developed symptomatic vaso-

spasm, moderate to severe angiographic vasospasm was

observed in 5 patients with FG 2, 6 patients with FG 3, and

9 patients with FG 4 SAH. Our results suggest that there is a

statistically significant association between symptomatic

vasospasm and angiographic vasospasm. However, only

43% of our patients had postoperative angiograms depend-

ing on surgeon preference. The results must be interpreted

keeping this in mind.

In univariate and bivariate analysis the severity of

angiographic vasospasm was not predicted by the severity

of SAH classified by the FG on initial head CT scan. In

addition, no significant association was observed between

angiographic vasospasm and admission FG, Hunt and Hess

grade, age, or sex. A significant association was observed

between angiographic vasospasm and symptomatic vaso-

spasm (P b .0001) and elevated TCDMCA BFV (P = .001).

There also was a strong association between angiographic

vasospasm and intraventricular blood (P = .054).

4. Discussion

In this retrospective study, we evaluated the CT,

angiographic, and TCD findings of 134 patients with

aneurysmal SAH to determine whether the initial CT severity

of SAH determined by the FG predicts symptomatic cerebral

vasospasm. The study was undertaken because there have

been significant advances in neurologic imaging and in SAH

management since the FG was devised more than 20 years

ago that may now bias or invalidate the accuracy of the

original grading system. Our results suggest that the FG may

not be valid in the modern era.

4.1. Contemporary management of cerebral vasospasm

There are several important differences between this

study and that which led to the development of the FG.

First, neurologic imaging is now more sophisticated.

Second, among the 47 patients examined by Fisher et al

[4], more than half (26/47) underwent CT scanning in the

days after SAH with delayed diagnosis and treatment. In

contrast, 83% of the patients (111/134) in our study

underwent CT scan on the day of SAH and with the

minority of patients having their initial CT scan days after

hemorrhage. However, this did not influence our results

because 75% of the patients in our study who developed

symptomatic vasospasm had their initial CT scan on the day

of SAH whereas 85% who did not develop vasospasm did

the same. Third, vasospasm prevention and management has

changed significantly in the last 20 years. Nearly half of the

patients (23/47) included in the Fisher et al [4] study

developed symptomatic vasospasm whereas 21% of our

patients developed symptomatic vasospasm. Finally, most

patients in our series underwent treatment within 3 days of

SAH whereas patients examined by Fisher et al [4] had

delayed surgery.

4.2. Transcranial Doppler sonography

The value of TCD is debated by some. However, rapid

and sequential increase in BFV or MCA BFV greater than

200 cm/s is highly correlated with angiographic vasospasm

[7,11]. In our study, elevated TCD BFV in the MCA was

predictive of angiographic and symptomatic vasospasm. In

addition, elevated TCD BFV was significantly correlated

with the presence of blood in the basal cisterns, blood in the

lateral ventricle, and blood in any ventricle. Other inves-

tigators who have recently evaluated predictive factors for

vasospasm have also observed a strong association between

an early increase in TCD BFV greater than 140 cm/s and

vasospasm [3,8]. Seventy-five percent of our patients with

TCD evidence of vasospasm who underwent postoperative

angiography had angiographic vasospasm.

M.L. Smith et al. / Surgical Neurology 63 (2005) 229–235 233

Although the association between large amounts of

subarachnoid blood and vasospasm is well known, our

results, as well as those from other studies, have found

similar limitations to the FG [3,9]. For example, Schaller et al

[9] observed that there was limited association between

severe vasospasm identified by TCD and the FG. In that

study, severe vasospasm documented by TCD (MCA BFV

N160 cm/s on 2 or more consecutive days) was observed in

39% of FG 1 patients, 26% of FG 2 patients, and 34% of FG 3

patients. The authors concluded that the amount of subarach-

noid blood identified on the initial CT scan should no longer

be used as an indicator to predict symptomatic vasospasm.

4.3. Volume of subarachnoid blood

We did not observe a clear association between the FG,

the presence of blood clot, and the subsequent cerebral

vasospasm. In those patients with intraparenchymal or

Sylvian fissure clot, only 8 of 28 patients (29%) developed

symptomatic vasospasm. We did not observe a characteristic

subarachnoid blood pattern that predicted those patients at

high risk for symptomatic vasospasm. We did observe a

relationship between intraventricular blood and vasospasm.

The amount of blood alone is not the only factor that

influences whether someone becomes symptomatic. For

example, advanced age is associated with a reduced

incidence of vasospasm [12], whereas cigarette smoking

may increase the risk of vasospasm [6]. However, this does

not exclude the possibility that the overall blood volume

rather than distribution may be the more important factor.

Friedman et al [5] recently used standard image analysis

software to quantify the volume of blood in FG 3 patients

with SAH; a significantly greater volume of cisternal blood

was observed among patients with symptomatic vasospasm.

Intraparenchymal and intraventricular blood was not asso-

ciated with vasospasm. Our results were consistent with

their findings in that elevated TCD BFV in the MCA was

associated with blood in the basal cisterns and lateral

ventricles. In contrast, others have shown that blood in both

ventricles is associated with later vasospasm [3,10]. Why

intraventricular hemorrhage is associated with vasospasm

however is not certain. This is consistent with a particular

volume of subarachnoid blood rather than distribution alone

being important in the development of vasospasm and

recent studies that demonstrate that thick clot filling any

cistern or fissure is significantly associated with vasospasm

[1-3,8,10]. Blood filling a cistern was not considered as an

independent factor in the FG.

4.4. Study limitations

The purpose of this study was to use a retrospective

cohort to support evidence that the FG may need to be

revisited and developed further to accommodate for con-

temporary management. However, this study presents a

number of limitations. First, although our study is a

retrospective review and this may lessen its credibility when

compared to a prospective cohort, we do not propose a new

grading scale based on these early findings. Second, there

was no correlation in the development of symptomatic

vasospasm to the Hunt and Hess grading scale, another

standard in the evaluation of these patients. One reason for

this discrepancy could be inherent in the difficulty assessing

Hunt and Hess grade 4 and 5 patients for the development of

symptomatic vasospasm. For these patients, assessment

relies heavily on TCD evaluation and we did not select

out this cohort for a separate analysis. Third, based on these

initial findings a prospective study should be developed with

the intent of developing a new grading system. Finally, until

software becomes available such that quantification of blood

volume with admission CT is easy to perform and with high

accuracy, a prospective study may be difficult to perform.

5. Conclusions

The FG did not reliably predict symptomatic vasospasm in

this series of patients. The only admission CT finding that

seemed to predict symptomatic vasospasm was intraventric-

ular blood. There was no correlation between volume of a

subarachnoid blood clot and development of symptomatic

vasospasm. Our results do support the correlation of TCD

findings to the development of both symptomatic and

angiographic vasospasm. For those patients who did develop

symptomatic vasospasm, there were more patients in the

combined group with FGs 2 (n = 8) and 3 (n = 7) when com-

pared to patients with FG 4 (n = 13). Taken together our data

and that ofother recent investigations suggest that although the

FG is useful it may need revision to reflect modern neurologic

imaging and to provide help in vasospasmmanagement.

References

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[9] Schaller C, Rohde V, Meyer B, et al. Amount of subarachnoid blood

and vasospasm: current aspects. A transcranial Doppler study. Acta

Neurochir (Wien) 1995;136:67-71.

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Commentary

Smith et al reviewed 134 patients with SAH and found

no correlation of the admission FG with the development of

symptomatic vasospasm. Table 2 displays these results

nicely. The authors question the validity of the FG in

predicting the risk of vasospasm, given modern CT imaging.

There are significant differences between this study and

that of Fisher et al [1] 24 years ago. Most notably, all the

patients in the first study underwent postoperative angiog-

raphy whereas only 47% of patients in this present study

underwent this test. It can only be assumed that postoper-

ative angiography was selectively used in a manner that

biased the performance of this test toward patients with

clinical (or bsymptomaticQ) vasospasm. Therefore, the

finding of ba significant association . . . between angio-

graphic vasospasm and symptomatic vasospasm . . .Q is

irrelevant. Similarly, the association between angiographic

spasm and elevated TCD MCA BFV is suspect.

The authors propose a prospective study b. . . with the

intent of developing a new grading system.Q It is unclear

what the authors intend to grade because the only predictor

of vasospasm in their study was intraventricular blood.

Has the pathophysiology of SAH changed? Maybe the

mastery of clinical neurology of CM Fisher explains the

higher incidence of symptomatic cerebral ischemia in his

series. Stated another way, it may be that as we rely more on

radiographic imaging, we simultaneously require more

obvious signs of neurologic dysfunction to prod us to order

tests that confirm our crude bedside findings. Whether true

or not, we choose to agree with the authors that it is

improvements in medical management that have reduced the

incidence of vasospasm after SAH.

References




Duke Samson, MD

Christopher L. Taylor, MD

Department of Neurosurgery

UT Southwestern Medical Center

Dallas, TX 75235, USA

Fisher and colleagues were among the first to publish

clinical data relating the volume and location of subarach-

noid blood to the risk of cerebral vasospasm [3,8]. The

technology used by Fisher et al obviously is outdated, but

one cannot argue with several decades of clinical and

experimental data that strongly support, if not prove, that

angiographic arterial narrowing after SAH is related in part

to the volume of clot next to the artery that develops

vasospasm [7]. A review of the 1980 paper shows that the

computed tomograms were obtained within 5 days of SAH

on a scanner with a 160 � 160 matrix and 16-mm-thick

slices. Current imaging has more than 10 times this

resolution. The thickness of the clots refers to measurements

made on the printed images that had been printed at variable

sizes. No magnification standard was included. Therefore,

the 1-mm distinction between groups 2 and 3 is not

equivalent to an actual 1 mm measured on a CT scan today.

With current scanners, a negative head CT scan result within

a day of SAH is uncommon (FG 1) and clots with real

thickness less than 1 mm also are uncommon (FG 2). I

suspect most neurosurgeons distinguish grades 2 and 3 by

relatively thin vs relatively thick clots, which was the

qualitative system used in more recent clinical trials [5].

The paper by Smith and colleagues found it difficult to

correlate FG and vasospasm. This may be because the

method for differentiating the FGs in this study is not

entirely clear, and the distribution of patients is different

from some other series since there is a high percentage of

FG 4 patients in this study. In addition, the study is an

attempt to correlate 2 imprecisely measured phenomena.

The SAH on CT measured by the Fisher scale is only a

rough estimate and would be better measured quantitatively

using a method such as that used by Friedman et al [4]. The

assessment of vasospasm was also imprecise and did not use

the gold standard catheter angiography in all cases. In

addition, other factors influence the risk of vasospasm, such

as the density and duration of persistence of the subarach-

noid clot, the presence of intraventricular hemorrhage, the

clinical grade, and possibly smoking [1,2,6,9]. This paper is

important because it highlights the limitations of the Fisher

scale and hopefully will stimulate, as mentioned by the

authors, the development of software to easily quantify clot

volume and density when the initial CT is acquired, or some

method to better predict vasospasm.

References

[1] Charpentier C, Audibert G, Guillemin F, Civit T, Ducrocq X, Bracard S,

Hepner H, Picard L, Laxenaire MC. Multivariate analysis of predictors

of cerebral vasospasm occurrence after aneurysmal subarachnoid

hemorrhage. Stroke 1999;30:1402-8.

[2] Claassen J, Bernardini GL, Kreiter K, Bates J, Du YE, Copeland D,

Connolly ES, Mayer SA. Effect of cisternal and ventricular blood on

risk of delayed cerebral ischemia after subarachnoid hemorrhage: the

Fisher scale revisited. Stroke 2001;32:2012-20.




Subarachnoid hemorrhage on computed tomography scanning and the development of cerebral vasospasm:...

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