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Loss of autoregulation in patients with intracerebral hemorrhage
JStroke Cerebrovasc Dis 1995;5:163-165 © 1995 National Stroke Association
Loss of Autoregulation in Patients with Intracerebral Hemorrhage Adnan 1. Qureshi, M.D., Jeffrey R. Ottenlips, V.T., 'Austin R. Calahan, and Michael R. Frankel, M.D.
M.D.,
We evaluated cerebral vasomotor reactivity to acetazolamide in seven consecutive patients with intracerebral hemorrhage (ICH) with transcranial Doppler to evaluate autoregulation of cerebral blood flow in acute ICH. Two patients had prominent loss of vasoreactivity to acetazolamide stimulation. This suggests that autoregulation may be impaired in some patients with acute ICH. Further studies are required to determine the clinical implications of loss of autoregulation in acute phase of ICH. Key Words: Intracerebral hemorrhage-Transcranial Doppler-Autoregulation.
The pathophysiology of intracerebral hemorrhage (ICH) is complex. In addition to the physical disruption produced by the hematoma, local tissue compression produces a zone of ischemia surrounding the clot. Autoregulation to changes in systemic blood pressure may be impaired both due to the effect of ischemia and vasodilation from increased intracranial pressure (ICP) (1). It is important to know the autoregulatory function in patients with ICH in order to define a rational methodology of management of elevated systemic blood pressure in these patients. We prospectively evaluated autoregulation of cerebral blood flow in seven patients with spontaneous intracerebral hemorrhage by means of transcranial Doppler.
. Patients Seven consecutive patients admitted to the Neurology Service at Grady Memorial Hospital in Atlanta, From the Departments of Neurology and 1 Neurosurgery, Emory University School of Medicine, Atlanta, GA, U.S.A. Address correspondence and reprint requests to Dr. A. I. Qureshi at Department of Neurology, Grady Memorial Hospital, BG 007, 80 Butler Street, S.E., Atlanta, GA 30335, U.S.A.
GA, with the diagnosis of ICH were included in the study. All patients had ICH confirmed by admission computed tomography (CT). Care was taken not to include patients with traumatic ICH, hemorrhagic infarct, and ICH secondary to arteriovenous malformation.
Evaluation of Vasomotor Reactivity All patients were evaluated within 12 h of presentation. Mean blood flow velocities of both middle cerebral arteries (MCA) were determined using transcranial Doppler. Measurements were made through the transtemporal windows using a pulsed-wave, 2MHz transducer at a depth of 45-55 mm. Three readings were made on each side and averaged. Attempts were made to insonate MCAs on both sides. After baseline MCA velocities were obtained, 1 g of acetazolamide was administered intravenously. Twenty minutes after the injection, a set of second MCA velocity measurements were made using the same coordinates. During the period of study, all patients (except one who was clinically stable) were on blood pressure monitors and pulse oximeters. Level of consciousness was serially evaluated during the study by a neurologist.
J STROKE CEREBROVASC DIS, VOL. 5, NO.3,
1995
163
A. 1. QURESHI IT AL
Patient characteristics and iranscranial Doppler velocities
Table 1.
Mean MCA velocity (cm/s) Patient/ age/sex
Site a
1/57/M 2/56/M
Hematoma volume
Ipsilateral
Contralateral
VMR
Lobar
36.6ml 25.4 ml
30.0
36.3 25.0
3/52/M
BG
23.2ml
48.3
29.4
4/64/M 5/81/M 6/4o/M
Thai
BG BG
15.oml 88.oml 28.5 ml
36.7
28.3 41.8 55.7
7/86/M
BG
13.6 ml
38.2
14.6% (opp) 45% (same) 32.8% (opp) -9.1% (same) 24.5% (opp) 33.7% (opp) 4.3% (opp) 65.9% (same) 43.6% (opp) 27.0% (same)
BG
aBG = basal ganglia; Thai, thalamus. -, unable to insonate MCA.
Vasomotor reactivity (VMR) was assessed as the percentage change in flow velocity after stimulus application (Va) as compared with flow velocity at rest (V r ) . The VMR was calculated using the folowing equation. VMR = (va -V") X ioo/v. In addition, the volumes of hematoma were calculated from the initial CT scan using a computerized image analysis method that has been described before (2).
Results The mean age of seven male patients was 62.3 years (range, 40-86 years). The mean velocities were evaluated in 10 MCAs (6 contralateral and 4 ipsilateral to the side of ICH). The results of initial and acetazolamide-activated transcranial Doppler studies are summarized in Table 1. Two patients had prominent loss of VMR in this study. In Patient 3, there was a loss of
45
•
40
• •
35 30 25 VMR%
•
20
-
15 10 5
o
o
, 10
20
30
.
40
• 50
60
70
80
90
Hematoma volume (ee)
Figure 1. Relationship of VMR hematoma volume. 164
011
the contralateral side to
J STROKE CEREBROVASC DIS, VOL. 5, NO.3, 1995
VMR on the ipsilateral side of hematoma with relatively adequate VMR on the contralateral side. In Patient 5, there was loss ofVMR on the contralateral side of the hematoma. There was prominent decrease in VMR on the contralateral side in hematomas with volumes greater than 30 ml as compared to those with volumes less than 30 ml (Fig. 1). No patient had elevated MCA velocities on transcranial Doppler evaluation. Adverse reactions were not seen in any patients.
Discussion We assessed cerebral vasomotor reactivity by intravenous acetazolamide in patients with spontaneous ICH. This test is a standard method of assessing the reactivity of cerebral blood vessels (3). The loss of reactivity to vasodilatory stimuli, even though a partially independent mechanism, is always associated with lack of dilatory arterial reaction to diminishing perfusion pressures (4). Our study was limited due to the small number of patients included. In addition, it was technically difficult to insonate the MCA on the affected side in some of the patients. Despite these technical limitations, our study demonstrated that VMR could be completely lost on the affected side or on the contralateral side of the ICH. Diminution of VMR on the contralateral side was more pronounced in the two patients with hematomas greater than 30 rnl, Because MCA velocities were not elevated in any of the patients with impaired VMR, mechanisms other than vasospasm such as increased ICP seem to be responsible for this phenomenon. Our study differs from Kaneko et al, (5), who performed whole-brain measurements of cerebral blood flow in eight patients with ICH and concluded that autoregulation was pre-
AlITOREGULATION LOSS IN PATIENTS WITH fCH
served, although the lower limit was equal to the preICH blood pressure. We found that autoregulation can be impaired in a small subset of patients with ICH either on the ipsilateral or contralateral side of the hematoma. Further studies are required to confirm these findings because of the important clinical implications of loss of cerebral autoregulation on blood pressure management during the acute phase of ICH.
References 1. Powers WJ. Acute hypertension after stroke: the sci-
entific basis for treatment decisions. Neurology 1993; 43:461-7.
2. 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;24:987-93. 3. Ringelstein EB,Eyck SV, Mertens I. Evaluation of cerebral vasomotor reactivity by various vasodilating stimuli: comparison of CO2 to acetazolamide. J Cereb Blood Flow Metab 1992;12:162-8. 4. Symon L Pathological regulation in cerebral ischemia. In: Wood JH, ed . Cerebral bloodflow. Physiologic and clinical aspects. New York: McGraw-Hili, 1987:4234. 5. Kaneko T, Sawada T, Niimi T, et al. Lower limit of blood pressure in treatment of acute hypertensive intracranial hemorrhage. J Neurosurg 1986;65:697-703.
J STROKE CEREBROVASC DIS, VOL 5, NO.3, 1995
165
Loss of Autoregulation in Patients with Intracerebral Hemorrhage Adnan 1. Qureshi, M.D., Jeffrey R. Ottenlips, V.T., 'Austin R. Calahan, and Michael R. Frankel, M.D.
M.D.,
We evaluated cerebral vasomotor reactivity to acetazolamide in seven consecutive patients with intracerebral hemorrhage (ICH) with transcranial Doppler to evaluate autoregulation of cerebral blood flow in acute ICH. Two patients had prominent loss of vasoreactivity to acetazolamide stimulation. This suggests that autoregulation may be impaired in some patients with acute ICH. Further studies are required to determine the clinical implications of loss of autoregulation in acute phase of ICH. Key Words: Intracerebral hemorrhage-Transcranial Doppler-Autoregulation.
The pathophysiology of intracerebral hemorrhage (ICH) is complex. In addition to the physical disruption produced by the hematoma, local tissue compression produces a zone of ischemia surrounding the clot. Autoregulation to changes in systemic blood pressure may be impaired both due to the effect of ischemia and vasodilation from increased intracranial pressure (ICP) (1). It is important to know the autoregulatory function in patients with ICH in order to define a rational methodology of management of elevated systemic blood pressure in these patients. We prospectively evaluated autoregulation of cerebral blood flow in seven patients with spontaneous intracerebral hemorrhage by means of transcranial Doppler.
. Patients Seven consecutive patients admitted to the Neurology Service at Grady Memorial Hospital in Atlanta, From the Departments of Neurology and 1 Neurosurgery, Emory University School of Medicine, Atlanta, GA, U.S.A. Address correspondence and reprint requests to Dr. A. I. Qureshi at Department of Neurology, Grady Memorial Hospital, BG 007, 80 Butler Street, S.E., Atlanta, GA 30335, U.S.A.
GA, with the diagnosis of ICH were included in the study. All patients had ICH confirmed by admission computed tomography (CT). Care was taken not to include patients with traumatic ICH, hemorrhagic infarct, and ICH secondary to arteriovenous malformation.
Evaluation of Vasomotor Reactivity All patients were evaluated within 12 h of presentation. Mean blood flow velocities of both middle cerebral arteries (MCA) were determined using transcranial Doppler. Measurements were made through the transtemporal windows using a pulsed-wave, 2MHz transducer at a depth of 45-55 mm. Three readings were made on each side and averaged. Attempts were made to insonate MCAs on both sides. After baseline MCA velocities were obtained, 1 g of acetazolamide was administered intravenously. Twenty minutes after the injection, a set of second MCA velocity measurements were made using the same coordinates. During the period of study, all patients (except one who was clinically stable) were on blood pressure monitors and pulse oximeters. Level of consciousness was serially evaluated during the study by a neurologist.
J STROKE CEREBROVASC DIS, VOL. 5, NO.3,
1995
163
A. 1. QURESHI IT AL
Patient characteristics and iranscranial Doppler velocities
Table 1.
Mean MCA velocity (cm/s) Patient/ age/sex
Site a
1/57/M 2/56/M
Hematoma volume
Ipsilateral
Contralateral
VMR
Lobar
36.6ml 25.4 ml
30.0
36.3 25.0
3/52/M
BG
23.2ml
48.3
29.4
4/64/M 5/81/M 6/4o/M
Thai
BG BG
15.oml 88.oml 28.5 ml
36.7
28.3 41.8 55.7
7/86/M
BG
13.6 ml
38.2
14.6% (opp) 45% (same) 32.8% (opp) -9.1% (same) 24.5% (opp) 33.7% (opp) 4.3% (opp) 65.9% (same) 43.6% (opp) 27.0% (same)
BG
aBG = basal ganglia; Thai, thalamus. -, unable to insonate MCA.
Vasomotor reactivity (VMR) was assessed as the percentage change in flow velocity after stimulus application (Va) as compared with flow velocity at rest (V r ) . The VMR was calculated using the folowing equation. VMR = (va -V") X ioo/v. In addition, the volumes of hematoma were calculated from the initial CT scan using a computerized image analysis method that has been described before (2).
Results The mean age of seven male patients was 62.3 years (range, 40-86 years). The mean velocities were evaluated in 10 MCAs (6 contralateral and 4 ipsilateral to the side of ICH). The results of initial and acetazolamide-activated transcranial Doppler studies are summarized in Table 1. Two patients had prominent loss of VMR in this study. In Patient 3, there was a loss of
45
•
40
• •
35 30 25 VMR%
•
20
-
15 10 5
o
o
, 10
20
30
.
40
• 50
60
70
80
90
Hematoma volume (ee)
Figure 1. Relationship of VMR hematoma volume. 164
011
the contralateral side to
J STROKE CEREBROVASC DIS, VOL. 5, NO.3, 1995
VMR on the ipsilateral side of hematoma with relatively adequate VMR on the contralateral side. In Patient 5, there was loss ofVMR on the contralateral side of the hematoma. There was prominent decrease in VMR on the contralateral side in hematomas with volumes greater than 30 ml as compared to those with volumes less than 30 ml (Fig. 1). No patient had elevated MCA velocities on transcranial Doppler evaluation. Adverse reactions were not seen in any patients.
Discussion We assessed cerebral vasomotor reactivity by intravenous acetazolamide in patients with spontaneous ICH. This test is a standard method of assessing the reactivity of cerebral blood vessels (3). The loss of reactivity to vasodilatory stimuli, even though a partially independent mechanism, is always associated with lack of dilatory arterial reaction to diminishing perfusion pressures (4). Our study was limited due to the small number of patients included. In addition, it was technically difficult to insonate the MCA on the affected side in some of the patients. Despite these technical limitations, our study demonstrated that VMR could be completely lost on the affected side or on the contralateral side of the ICH. Diminution of VMR on the contralateral side was more pronounced in the two patients with hematomas greater than 30 rnl, Because MCA velocities were not elevated in any of the patients with impaired VMR, mechanisms other than vasospasm such as increased ICP seem to be responsible for this phenomenon. Our study differs from Kaneko et al, (5), who performed whole-brain measurements of cerebral blood flow in eight patients with ICH and concluded that autoregulation was pre-
AlITOREGULATION LOSS IN PATIENTS WITH fCH
served, although the lower limit was equal to the preICH blood pressure. We found that autoregulation can be impaired in a small subset of patients with ICH either on the ipsilateral or contralateral side of the hematoma. Further studies are required to confirm these findings because of the important clinical implications of loss of cerebral autoregulation on blood pressure management during the acute phase of ICH.
References 1. Powers WJ. Acute hypertension after stroke: the sci-
entific basis for treatment decisions. Neurology 1993; 43:461-7.
2. 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;24:987-93. 3. Ringelstein EB,Eyck SV, Mertens I. Evaluation of cerebral vasomotor reactivity by various vasodilating stimuli: comparison of CO2 to acetazolamide. J Cereb Blood Flow Metab 1992;12:162-8. 4. Symon L Pathological regulation in cerebral ischemia. In: Wood JH, ed . Cerebral bloodflow. Physiologic and clinical aspects. New York: McGraw-Hili, 1987:4234. 5. Kaneko T, Sawada T, Niimi T, et al. Lower limit of blood pressure in treatment of acute hypertensive intracranial hemorrhage. J Neurosurg 1986;65:697-703.
J STROKE CEREBROVASC DIS, VOL 5, NO.3, 1995
165