(Stroke. 1995;26:21-24.)
© 1995 American Heart Association, Inc.
Articles |
Relation Between Blood Pressure and Outcome in Intracerebral Hemorrhage
From the Departments of Neurology (B.K.D., S.S., R.E.K., Y.R.-I.) and Oncology, Division of Biostatistics (R.C.D.), University of Miami (Fla) School of Medicine.
Correspondence to Roger E. Kelley, MD, Department of Neurology, 1501 NW 9th Ave, Miami, FL 33136.
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Abstract |
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Background and Purpose Controversy continues to exist regarding optimal blood pressure control in acute hypertensive intracerebral hemorrhage. Persistent marked elevation of the blood pressure can promote further bleeding, increase cerebral blood flow, and raise intracranial pressure. Relative hypotension, on the other hand, may promote hypoperfusion with secondary ischemia. This study was designed to assess outcome in patient groups defined by the degree of elevation in their pretreatment and posttreatment blood pressures.
Methods We retrospectively assessed 87 patients who were
categorized according to an initial mean arterial pressure >145 mm Hg
(n=34) compared with those with a pressure 
145 mm Hg (n=53). We also
studied blood pressure control within the first 2 to 6 hours of
presentation with subjects categorized according to a mean arterial
pressure >125 mm Hg (n=40) or 125 mm Hg (n=47).
Results An improved outcome in both mortality and severe
morbidity was observed in the 145 (
2=7.0,
P<.005) and the 125 mm Hg (2=6.7,
P<.005) groups.
Conclusions Markedly elevated blood pressure on admission and persistent inadequate blood pressure control adversely affect the prognosis in hypertensive intracerebral hemorrhage.
Key Words: hypertension • intracerebral hemorrhage • stroke outcome
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Hypertension is the most common cause of primary intracerebral hemorrhage (ICH).1 Hypertensive ICH is believed to be primarily a monophasic event,2 3 4 but there can be persistent bleeding for up to 6 hours from ictus.5 ICH, acting as a mass-producing lesion, can result in increased intracranial pressure (ICP) and can augment the marked elevation of blood pressure (BP) typically seen on presentation. Persistent marked elevation of BP might not only promote rebleeding but might also increase cerebral blood flow (CBF) and blood volume with resultant elevation of ICP.6 On the other hand, there is often an area of focal ischemia adjacent to the hematoma, and reduction of BP could, theoretically, promote further ischemia.7 8 Meyer and Bauer9 reported that effective hypotensive therapy improved outcome in presumptive hypertensive ICH. This study was performed in the pre–computed tomography (CT) brain scan era, however, and management of the BP appeared to be based, at least in part, on the neurological status at the time of presentation.
The purpose of this study was to assess the relation between acute BP control and outcome. We examined mean arterial blood pressure (MAP) in the initial 0 to 2 hours of admission and control of MAP within the first 2 to 6 hours to determine whether the degree of BP elevation affected neurological status at 30 days. We also examined the mean systolic and diastolic BP during these time frames in reference to outcome.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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We retrospectively assessed 378 consecutive patients with the diagnosis of hypertensive ICH at our medical center from January 1989 through September 1993. Patients who met the following criteria were included in the study: (1) the presence of hypertension based on history, admission medications, hypertensive retinopathy, and/or the presence of left ventricular hypertrophy by electrocardiography or echocardiography; (2) basal ganglionic or thalamic hemorrhage; (3) absence of a bleeding diathesis or anticoagulant therapy; (4) absence of illicit drug use; and (5) no evidence of metastatic disease.
Our selection was based on the basal ganglia and thalamus being the most common sites for hypertensive ICH.10 11 Lobar hemorrhage, on the other hand, is associated with hypertension in roughly 50% of cases.12 13 Hypertension is also commonly associated with ICH in the pons or cerebellum. In pontine ICH, however, the outcome is often catastrophic and is highly dependent on the size of the hematoma within a very confined space. In contrast, cerebellar hematomas are frequently managed surgically. Therefore, patients with hemorrhages in these locations were excluded from our study.
Application of these criteria led to the selection of 87 patients for our study. Serial BP recordings from the time of arrival in the emergency department up to the first 6 hours of admission were assessed. BP readings were recorded at 0 to 2 hours and at 2 to 6 hours, and the values represented the mean of three separate values for each patient at each time interval. MAP was calculated as follows: Diastolic BP+ (Systolic-Diastolic BP)/3.
A CT brain scan was obtained on all patients at the time of presentation. The Glasgow Outcome Scale14 was also derived from the medical records for each subject. The Glasgow Outcome Scale at 30 days from presentation was assessed for those subjects who survived for 30 days or longer. Outcome was divided into two categories: (1) severe disability, persistent vegetative state, and death, which correspond to grades 3 to 1, respectively, on the Glasgow Outcome Scale, and (2) grades 5 and 4, which include good recovery and moderate disability, respectively.
Our 87 subjects were analyzed according to their degree of elevation of
BP at the time of presentation to the emergency department of
Jackson Memorial Hospital, Miami, Fla. Excessive BP was denoted as an
MAP of >145 mm Hg, and patients in this group were compared with
patients who had an admission MAP 145 mm Hg. This cutoff was based
on cumulative averaging of MAP values from four studies that reported
clinical deterioration in association with markedly elevated admission
BP in ICH.5 15 16 17 In addition, as the MAP approaches 150
mm Hg or greater, disruption of cerebral autoregulation occurs, which
is accompanied by global cerebral hyperemia.18
All study subjects were admitted to the emergency department within 8 hours of ictus. No patient was treated for acutely elevated BP until admission. Antihypertensive therapy was not standardized, but the vast majority of subjects received oral nifedipine, which was followed by intravenous sodium nitroprusside if a rapid reduction in BP was not observed within 30 to 60 minutes. Other agents that were used in the acute setting included labetalol, clonidine, and angiotensin-converting enzyme inhibitors, but we were unable to assess the efficacy of specific therapy. In general, sodium nitroprusside was the most effective agent in the acute setting, and no instances of a severe hypotensive response were observed with any of the agents.
After admission, after efforts were made to control the BP in all
subjects, we recorded MAP values (the average of three consecutive
recordings during the 2- to 6-hour interval) to determine how
effectively the BP had been brought under control. Subjects were
divided into a suboptimally treated group with MAP >125 mm Hg and
were compared with a more optimally treated group with MAP 125
mm Hg. Disruption of CBF autoregulation is observed in patients with
severe hypertension when the MAP is reduced to 113 mm Hg, on
average.19 The upper range of autoregulation disruption
with hypotensive therapy is 120 to 130 mm Hg, however.19
In view of the tendency for intracranial mass lesions such as hematomas
to raise the systemic BP in parallel with the increase in
ICP,20 an MAP 125 mm Hg appears to be a reasonable
cutoff for adequate BP control in such patients.
We also assessed the admission systolic and diastolic BP as predictors of outcome. We used the mean values as a cutoff for these measurements. These measurements were also assessed as predictors of outcome after initial BP control within the 2- to 6-hour interval after admission.
The two subsets were compared, in terms of outcome, with a
2 analysis. To correct for the multiple
comparisons with the two subsets, a Bonferroni
correction21 was used with the significance level, 
,
set at P<.025.
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Results |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Of the 87 patients, 54 (62%) were men; the mean age was 59 years. The 30-day case-fatality rate was 31%. The combined mortality and severe morbidity rate was 46%. There was a history of hypertension in 89% (77/87). Cardiac disease, defined by the history or presence of either myocardial infarct, angina, congestive heart failure, and/or cardiac arrhythmia that required active therapy, was present in 25% (22/87). The mean admission systolic BP was 196 mm Hg, and the mean diastolic BP was 115 mm Hg.
Of the 34 subjects who presented with MAP >145 mm Hg, 31 were
admitted within 3 hours of ictus and 3 were admitted beyond 3 hours. Of
the 53 subjects presenting with MAP 145 mm Hg, 40 were admitted
within 3 hours of ictus and 13 were admitted beyond 3 hours. The
presumptive cause of death was herniation in 7 of the 16 who died
(44%) in the MAP >145 mm Hg group and 5 of the 11 who died (45%) in
the MAP 145 mm Hg group. Unfortunately, due to the retrospective
nature of our study, we were unable to directly correlate volumetric
analysis of hematoma size with outcome, and we could not
investigate possible expansion of the hematoma because a number of the
CT scans were unavailable for personal review.
BP Elevation at 0 to 2 Hours
As is evident from Table 1
, the >145 and 145
mm Hg MAP groups had a similar prevalence of previously documented
hypertension and cardiac disease, and the mean age was also fairly
equivalent. The 30-day case-fatality rate was 47% (16/34) in the >145
mm Hg group and 21% (11/53) in the 145 mm Hg group
(2=5.64, P<.01). The combined
mortality and severe morbidity rate was 65% (22/34) in the >145
mm Hg group and 34% (18/53) in the 145 mm Hg group
(2=7.0, P<.005).
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With the use of a systolic BP cutoff of 196 mm Hg, the mortality rate
was 44% in the >196 mm Hg group (n=43) compared with 18% in the
196 mm Hg group (n=44) (2=7.74,
P<.005). The combined mortality and severe morbidity rate
was 58% in the >196 mm Hg group and 34% in the 196 mm Hg group
(2=4.63, P<.05). With a diastolic BP
cutoff of 115 mm Hg, the mortality rate was 41% in the >115 mm Hg
group (n=37) compared with 24% in the 115 mm Hg group (n=50)
(2=3.54, P<.10). The combined
mortality and severe morbidity rate was 62% in the >115 mm Hg group
and 26% in the 115 mm Hg group (2=12.44,
P<.001).
BP Control at 2 to 6 Hours
As mentioned above, all subjects were treated with
antihypertensive medications, and an MAP of 125 mm Hg was designated
as the cutoff for adequate control. The delineation of whether or not
this degree of BP control was attained with respect to the initial MAP
cutoff of 145 mm Hg is as follows: initial MAP 145 mm Hg and 2- to
6-hour MAP 125 mm Hg in 39 patients; initial MAP 145 mm Hg and 2-
to 6-hour MAP >125 mm Hg in 14 patients; initial MAP >145 mm Hg and
2- to 6-hour MAP 125 mm Hg in 11 patients; and initial MAP >145
mm Hg and 2- to 6-hour MAP >125 mm Hg in 23 patients.
We identified 40 patients (46%) with an MAP >125 mm Hg and 47 (54%)
with an MAP 125 mm Hg (Table 2). The groups were
similar in mean age, prevalence of hypertension, and prevalence of
cardiac disease. Patients with an MAP >125 mm Hg had a higher
mortality rate of 43% (17/40) compared with 21% (10/47) in those with
an MAP 125 mm Hg (2=5.4, P<.01).
The group with an MAP >125 mm Hg also had a higher combined mortality
and severe morbidity rate of 60% (24/40) compared with 34% (16/47) in
the MAP 125 mm Hg group (2=6.7,
P<.005).
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The mean systolic BP was 170 mm Hg at 2 to 6 hours. With this value as
a cutoff, the mortality rates were 38% (15/39) in the >170 mm Hg
group and 25% (12/48) in the 170 mm Hg group
(2=1.95, P<.25). For severe morbidity
and mortality, the rates were 62% (24/39) in the >170 mm Hg group
and 33% (16/48) in the 170 mm Hg group
(2=6.73, P<.01).
The mean diastolic BP was 101 mm Hg at 2 to 6 hours. With this value
as a cutoff, the mortality rates were 38% (14/37) in the >101 mm Hg
group and 26% (13/50) in the 101 mm Hg group
(2=0.87, P<.25). For severe morbidity
and mortality, the rates were 65% (24/37) in the >101 mm Hg group
and 60% (30/50) in the 101 mm Hg group
(2=0.21, P<.25).
Of note, the means of the MAP values at 0 to 2 hours (142 mm Hg) and at 2 to 6 hours (124 mm Hg) were very similar to our MAP cutoff values (145 and 125 mm Hg, respectively).
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Cerebral autoregulation protects against a precipitous fall in BP. In chronic hypertension there is a shift in the lower limit of CBF autoregulation toward higher pressure to accommodate increased vascular resistance.19 Disruption of cerebral autoregulation occurs with acute ischemic or hemorrhagic stroke, which renders brain perfusion more susceptible to BP changes.22 In patients with impaired cerebral perfusion, reduction of the BP can further compromise ischemically threatened tissue termed the ischemic penumbra.23 24
In hypertensive ICH the situation is complicated by a mass-producing hematoma, which elevates ICP as a function of the size of the hematoma. A reflex "systemic hypertension" results from the increased ICP, termed the Cushing reflex,20 and this can augment the degree of BP elevation at the time of presentation. In addition, vascular compromise of the tissue surrounding the hematoma secondary to pressure effect may occur. Rapid reduction in BP could, theoretically, promote hypoperfusion and secondary infarction in the surrounding edematous brain tissue. On the other hand, persistent marked elevation of the BP can promote increased CBF with secondary increased ICP, increased vasogenic edema, and persistent bleeding. Clinical studies have provided limited guidance in terms of BP control, but Kaneko et al25 have suggested a BP reduction of no more than 20% in the acute period, based on their studies with CBF.
In the pre–CT scan era, it was a popular belief that hypertensive ICH was a monophasic event and that elevated BP did not promote further bleeding.26 Kelley et al,5 in a study of 4 patients with hypertensive ICH, demonstrated that there was CT evidence of active bleeding up to 6 hours from the ictus. Fehr and Anderson27 reviewed 56 cases of hypertensive ICH in the basal ganglia and thalamus and documented enlargement of the hematoma by CT in 4. Poorly controlled hypertension was a factor in 2 patients who deteriorated within 24 hours.
Chen et al15 noted continued bleeding and clinical
deterioration within the first 12 hours in 8 patients with ICH.
Persistent elevation of BP was noted in 6 of the 8 patients in this
series, and the outcome was poor in all subjects, with 4 patients dying
and 4 left with a severe neurological deficit. They concluded that
persistent severe hypertension may have been a contributing factor in
prolongation of active bleeding or precipitation of rebleeding in their
patients. Broderick et al16 described 8 patients who
underwent CT evaluation of ICH within 2 hours of presentation with
a follow-up scan several hours later. They observed that bleeding could
continue from the initial time of ictus for up to 5 hours.
Deterioration in 5 of the 8 patients was associated with a systolic BP
195 mm Hg.
Our study indicates that patients with hypertensive ICH who present with marked elevation of BP, defined as an MAP >145 mm Hg, have higher mortality and severe morbidity than those patients with lesser degrees of BP elevation, on average. Since the presence of cardiac disease and mean age were similar in the two groups, we can conclude that the outcome was related to BP elevation. The mean admission systolic BP cutoff of 196 mm Hg and mean admission diastolic BP cutoff of 115 mm Hg were also indicators of outcome, but they appear to be less consistent than our MAP value. The elevation at the time of presentation may be reflective of poor compliance with antihypertensive therapy, a reflex elevation secondary to increased ICP, or a combination of both. Of note, we did not observe a relation between BP elevation and predisposition toward death from herniation. This might imply that hematoma size was not a primary factor in the promotion of BP elevation. However, a significant variability in the effect of a mass-producing intracerebral lesion on systemic BP has been reported.28
Effective lowering of the BP in the acute time period appears to have a
favorable effect on prognosis. The patients who had reasonable BP
control, ie, an MAP of 125 mm Hg, had a better outcome in terms of
both morbidity and mortality. The mean treated systolic BP cutoff of
170 mm Hg and the mean treated diastolic BP cutoff of 101 mm Hg
provide support for this finding, but these values were also found to
be less consistent than the MAP value. Several mechanisms might explain
this observation, including prevention of rebleeding or persistent
bleeding, reduction of cerebral edema, or a protective effect against
end-organ damage. Successful lowering of the BP might also have been
reflective of the nature of the intracranial bleed because there is a
clear-cut relation between volume of the hematoma and
prognosis.29 30 Unfortunately, the retrospective nature of
our study did not allow us to do a volumetric analysis on each
patient.
Our overall 30-day case-fatality rate of 31% is similar to the 28% reported by Tuhrim et al31 for the Main Phase Stroke Data Bank and the 30% reported by Fieschi et al,32 although lower than the 40% acute in-hospital mortality rate reported by Douglas and Haerer.33 Our results are also in agreement with those of Carlberg et al.34 They reported that elevated BP was associated with a poorer outcome in both ICH and ischemic stroke, although this was only observed in subjects who had impaired consciousness on admission. It is generally believed that BP elevation is an indicator of adverse prognosis in hypertensive ICH,35 but this was not observed by Hier et al,4 Broderick et al,36 or Mayer et al.37
Once the diagnosis of hypertensive ICH has been made, it would appear that potent antihypertensive therapy to reduce the BP to a more normotensive range as quickly as possible is indicated, with the recognition that the potential deleterious effect of hypoperfusion is outweighed by the effects of an elevated pressure head within the intracranial circulation.
Received July 1, 1994; revision received September 15, 1994; accepted September 27, 1994.
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References |
|---|
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
1. Mohr JP, Caplan LR, Melski JW, Goldstein RJ, Duncan GW, Kistler JP, Pessin MS, Bleich HL. The Harvard Cooperative Stroke Registry: a prospective registry. Neurology. 1978;28:754-762.
2. Fisher CM. Clinical syndromes in cerebral hemorrhage. In: Fields WS, ed. Pathogenesis and Treatment of Cerebrovascular Disease. Springfield, Ill: Charles C Thomas, Publisher; 1961:318-342.
3.
Herbestein DJ, Schaumbaurg HH. Hypertensive intracerebral
hematoma: an investigation of the initial hemorrhage and rebleeding
using chromium Cr 51-labeled erythrocytes. Arch Neurol. 1974;30:412-414.
4. Hier DB, Davis KR, Richardson EP, Mohr JP. Hypertensive putaminal hemorrhage. Ann Neurol. 1977;1:152-159. [Medline] [Order article via Infotrieve]
5.
Kelley RE, Berger JR, Scheinberg P, Stokes N. Active bleeding
in hypertensive intracerebral hemorrhage: computed tomography.
Neurology. 1982;27:217-222.
6. Ropper A. Acute increased intracranial pressure. In: Asbury AK, McKhann GM, McDonald WI, eds. Diseases of the Nervous System. Philadelphia, Pa: W.B. Saunders; 1986:1064-1075.
7.
Powers WJ. Acute hypertension after stroke: the scientific
basis for treatment decisions. Neurology. 1993;43:461-467.
8.
Lavin P. Management of hypertension in patients with acute
stroke. Arch Intern Med. 1986;146:66-68.
9. Meyer JS, Bauer RB. Medical treatment of spontaneous intracranial hemorrhage by use of hypotensive drugs. Neurology. 1962;12:36-47.
10. Furlan AJ, Whisnant JP, Elveback LR. The decreasing incidence of primary intracerebral hemorrhage: a population study. Ann Neurol. 1979;5:367-373. [Medline] [Order article via Infotrieve]
11.
Kunitz SC, Gross CR, Heyman A, Case CS, Mohr JP, Price TR,
Wolf PA. The Pilot Stroke Data Bank: definition, design, and data.
Stroke. 1984;15:740-746.
12. Ropper AH, Davis KR. Lobar cerebral hemorrhages: acute clinical syndromes in 26 cases. Ann Neurol. 1980;8:141-147. [Medline] [Order article via Infotrieve]
13.
Kase CS, Williams JP, Wyatt DA, Mohr JP. Lobar intracerebral
hematomas: clinical and CT analysis of 22 cases.
Neurology. 1982;32:1146-1150.
14. Hall K, Cope DN, Rappaport M. Glasgow Outcome Scale and Disability Rating Scale: comparative usefulness in following traumatic head injury. Arch Phys Med Rehabil. 1985;66:35-37. [Medline] [Order article via Infotrieve]
15.
Chen ST, Chen SD, Hsu CY, Hogan EL. Progression of
hypertensive intracerebral hemorrhage. Neurology. 1989;39:1509-1514.
16. Broderick JP, Brott TG, Tomsick T, Huster G. Ultra early evaluation of intracerebral hemorrhage. J Neurosurg. 1990;72:195-199. [Medline] [Order article via Infotrieve]
17.
Batjer HH, Reisch JS, Allen BC, Plaizier LJ, Su CJ.
Failure of surgery to improve outcome in hypertensive putaminal
hemorrhage: a prospective randomized trial. Arch Neurol. 1990;47:1103-1106.
18.
Burke AM, Greenberg JH, Sladky J, Reivich M. Regional
variation in cerebral perfusion during acute hypertension.
Neurology. 1987;37:94-99.
19.
Strandgaard S. Autoregulation of cerebral blood flow in
hypertensive patients. Circulation. 1976;53:720-727.
20. Cushing H. The blood-pressure reaction of acute cerebral compression, illustrated by cases of intracranial hemorrhage. Am J Med Sci. 1903;125:1017-1045.
21. Kleinbaum DG, Kupper LL, Muller KE. Applied Regression Analysis and Other Multivariate Methods. Boston, Mass: PWS-Kent Publishing Co; 1988:32.
22. Russel RWR. How does blood pressure cause stroke? Lancet. 1975;2:1283-1285. [Medline] [Order article via Infotrieve]
23.
Astrup J, Seisjo B, Symon L. Thresholds in cerebral ischemia:
the ischemic penumbra. Stroke. 1981;12:723-727.
24.
Yatsu FM, Zivin J. Hypertension in acute ischemic strokes: not
to treat. Arch Neurol. 1985;42:999-1000.
25. Kaneko T, Swada T, Niimi T. Lower limit of blood pressure in treatment of acute hypertension in intracranial hemorrhage (AHIH). J Cereb Blood Flow Metab. 1983;29(suppl 1):S51-S52.
26. Ojemann RG, Mohr JP. Hypertensive brain hemorrhage. Clin Neurosurg. 1976;23:220-224. [Medline] [Order article via Infotrieve]
27. Fehr MA, Anderson DC. Incidence of progression or rebleeding in hypertensive intracerebral hemorrhage. J Stroke Cerebrovasc Dis. 1991;1:111-117.
28. Browder J, Meyers R. Observations on behavior of the systemic blood pressure, pulse and spinal fluid pressure following craniocerebral injury. Am J Surg. 1936;31:403-426.
29.
Young WB, Lee KP, Pessin MS, Kwan ES, Rand WM, Caplan LR.
Prognostic significance of ventricular blood in supratentorial
hemorrhage: a volumetric study. Neurology. 1990;40:616-619.
30.
Lisk DR, Pasteur W, Rhoades H, Putnam RD, Grotta JC. Early
presentation of hemispheric intracerebral hemorrhage: prediction of
outcome and guidelines for treatment allocation. Neurology. 1994;44:133-139.
31. Tuhrim S, Dambrosia JM, Price TR, Mohr JP, Wolf PA, Hier DB, Kase CS. Intracerebral hemorrhage: external validation and extension of a model for prediction of 30-day survival. Ann Neurol. 1991;29:658-663. [Medline] [Order article via Infotrieve]
32.
Fieschi C, Carolei A, Fiorelli M, Argentino C, Bozzao L, Fazio
C, Salvetti M, Bastianello S. Changing prognosis of primary
intracerebral hemorrhage: results of a clinical and computed
tomographic follow-up study of 104 patients. Stroke. 1988;19:192-195.
33.
Douglas MA, Haerer AF. Long-term prognosis of hypertensive
intracerebral hemorrhage. Stroke. 1982;13:488-491.
34.
Carlberg B, Asplund K, Hagg E. The prognostic value of
admission blood pressure in patients with acute stroke.
Stroke. 1993;24:1372-1375.
35.
Porteroy RK, Lipton RB, Berger AR, Lesser ML, Lantos G.
Intracerebral hemorrhage: a model for the prediction of
outcome. J Neurol Neurosurg Psychiatry. 1987;50:976-979.
36.
Broderick JP, Brott TG, Duldner JE, Tomsick T, Huster G.
Volume of intracerebral hemorrhage: a powerful and easy-to-use
predictor of 30-day mortality. Stroke. 1993;24:987-993.
37.
Mayer SA, Sacco RL, Shi T, Mohr JP. Neurologic deterioration
in noncomatose patients with supratentorial intracerebral hemorrhage.
Neurology. 1994;44:1379-1384.
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