Detection of Vasospasm following Subarachnoid Hemorrhage Using Transcranial Doppler

Transcription

1 The Jornal of Vasclar Technology 14(3): , 199 Detection of Vasospasm following Sbarachnoid Hemorrhage Using Transcranial Doppler Colleen M. Doville, B.A., R.V.T., * David W. Newell, M.D.,* Brian A. Trimble, M.D.,* H. Richard Winn, M.D.* ABSTRACT With the introdction of transcranial Doppler (TCD) ltrasonography, the diagnosis of vasospasm after sbarachnoid hemorrhage from rptred cerebral.a nerys~s can be made noninvasively. By recording daily velocities from the basal intracramal artenes, the time corse and severity of vasospasm can be evalated. This information can be sed to gide therapy for vasospasm..... Recordings have been obtained over a 3-year penod on 67 pahen!s followmg sbara~hn1d hemorrhage. Correlation (R =.82) of middle cerebral artery vessel dtamet~r seen on ang1~ram and TCD velocities was performed on 2 patients. We conclde that TCD 1s a sefl techmqe in the diagnosis of vasospasm following sbarachnoid hemorrhage. Introdction The most common case of spontaneos sbarachnoid hemorrhage (SAH) is rptre of a cerebral berry anerysm. The incidence of anerysmal SAH is approximately 1 per 1, poplation per year in the US. 1 The sal treatment of this condition incldes intracranial srgery to clip the anerysm in order to prevent rebleeding. However, a freqent seqela of SAH is the development of cerebral vasospasm. Spasm of the intracranial vessels following sbarachnoid hemorrhage was first observed sing angiography by Ecker and Riemenschneider in Sbseqently, vasospasm has become recognized as a major case of stroke and death dring the posthemorrhage period. 3-5 Clinical manifestations of vasospasm inclde aphasia, hemiparesis, mtism, and changes in consciosness that can be transient or longlasting, depending on the severity of vasospasm. These deficits most commonly occr after a delay period, sally 5-1 days after the hemorrhage. The pathophysiology of vasospasm is not completely nderstood, bt is probably related to the deposition of blood arond the otside of the basal intracranial arteries, where it cases a delayed narrowing. The condition has been reprodced in experimental animals, and it appears that sbstsances released from the blood as it breaks down injre the arteries and case them to go into spasm. 6 This spasm acts like a Department of Nerological Srgery, University of Washington, School of Medicine, Seattle, W A. Address for reprints: David W. Newell, M.D., Department of Nerological Srgery, Harborview Medical Center, 325 9th Avene, Seattle, WA stenosis hemodynamically and can impair the blood flow to critical parts of the brain. Many treatments for vasospasm have been tried in the past withot significant sccess? Recently, three methods of treatment have shown encoraging reslts. The first is hypervolemic hypertensive therapy.8 This treatment involves giving patients large volmes of intravenos flids as well as increasing their blood pressre with medications to improve the cerebral circlation. The second treatment, which has recently gained favor, is the se of calcim channel blockers. The rationale for their se was that these agents cold block the calcim-dependent smooth mscle contraction in the arterial wall. There have been some encoraging reslts/ bt the mechanism of action is as yet ncertain. The third treatment, perctaneos balloon angioplasty, involves placing a small catheter inside the artery and dilating it in a manner similar to peripheral vessel angioplasty. Preliminary reports indicate that this treatment may be of great benefit in cases that are refractory to other treatments In the past, nerosrgeons and nerologists have sally made the diagnosis of vasospasm in patients with SAH on the basis of clinical findings. A marked deterioration in nerological fnction between 5 and 1 days following hemorrhage that cold not be attribted to other cases was sally ascribed to vasospasm. Angiography can be sed to confirm the diagnosis, bt many physicians in the past were relctant to perform an angiogram in this setting. For the first time, with the introdction of TCD, the diagnosis of vasospasm can be confirmed noninvasively_iz-14 TCD ths offers a techniqe to identify patients who are in danger of developing deficits

2 112 DOUVILLE ET AL. JVT 14(3) 111. : 15 OR : ) ltiz PW POt.ER : 188X AH,tE : 8 FLOt.l > [4) lll : 14 OR : D ltiz PW P O~'ER : 18 Y. AHGt E: 11 FLOt.l < [2) CIYS CHIS... ;... _.,....,,..., DEPTH< 2> 36 CUR SO ~ SY I'EA\1-E 85 P!:AK 2. 3 I S/ RAT IO ~. )::(::;::~~{(i~:.~ :~:;.. t:'. { ~.-:. Figre la Initia l angiogram and TCD tracing on a patient on the day of sbarachnoid hemorrhage, showing normal arterial caliber and normal TCD velocities. from vasospasm as well as the potential to monitor therapy. Materials and Methods Dring a 3-year period, 67 patients sstaining SAH were evalated sing TCD. Eqipment inclded a TC2-64Bt and a Transpect.:j: Both nits tilize a 2-MHz freqency and freqency spectrm analyzer. t Eden Medical Electronics, Uberlingen, West Germany. t Medasonics Corp., Montain View, CA. Patients all had SAH confirmed by either CT scan or lmbar pnctre, and the presence of an anerysm confirmed by angiography. Most patients were operated on within 72 hr of their hemorrhage. Angiograph y was repeated following srgery in all cases to ch eck for clip placement, and in some cases was repeated sbseqently to confirm vasospasm or evalate patients for angioplasty. On admission, TCD recordings of all the basal arteries were obtained rotinely. Readings were then obtained at reglar intervals, sally daily, ntil 2

3 May 199 DETECTION OF VASOSPASM FOLLOWING SUBARACHNOID HEMORRHAGE 113 Ill. 4 11:~ 2 ca I'HZ PU PO'.!:R:18t: jr,icl[: 8 FLOW >I lll Hl:14 DR:t3 2.84) lt!z PW POI. R:t88X AIICLE: 8 FLOJ <I ltl c.vs 81) CI'VS... : ~>$'..~..,. Figre lb 1~. RA:A l PBD 5 PO 4 Sbseqent angiogram on the same patient showing severe spasm of the MCA trnk and ACA with corresponding TCD tracing (open arrow, MCA trnk; closed arrow, ACA). MCA mean velocity= 222 em/sec. ACA shows weak signal; mean velocity= 18 em/sec. weeks after hemorrhage, to assess the state of the vessels. Ten patients had initial and delayed angiograms, where comparative measrements cold be made, as well as TCD recordings within 24 hr of their angiograms. Measrements of the diameter of the MCA's were made from the arteriogram with calipers and compared with TCD readings. Angiograms were obtained sing a standard transfemoral techniqe with injection of Conray 6. Biplane films were obtained and magnified an average of 2 x. Transcranial Doppler examinations were performed on all the basal intracranial arteries, when possible, on all patients via the standard transtemporal, transorbital, and transoccipital rotes. The transtemporal rote was sed to record from the middle cerebral artery (MCA), internal carotid artery (ICA), anterior cerebral artery (ACA), and posterior cerebral artery. The transorbital rote was sed to record from the ophthalmic artery and the internal carotid artery siphon. The transoccipital rote was sed to record from both vertebral arteries and the basilar artery. When high velocities were encon-

4 114 DOUVILLE ET AL. JVT 14(3) - -- E ~ > 1 R = MCA Diameters (mm) Figre 2 Graph illstrating th e relationship between MCA diam eters in millimeters and MCA velocities in centimeters/second. Vales, ncorrected for magnification, were obtained from 1 patients who each had two angiograms: one baseline and one dring vasospasm. tered, indicating vasospasm, the highest velocity in each artery was noted and recorded. Reslts The most common locations for vasospasm as assessed by both angiogram and TCD were the intracranial ICA, proximal MCA, and proximal ACA. Measrements obtained from both sides on 1 patients on the MCA's showed good correlations between the degree of narrowing and increases in mean velocity. When high mean velocities were fond in the ACA, these also correlated with vasospasm, bt on some occasions mean velocities lower than baseline were seen. In certain patients with severe anterior cerebral vasospasm, serial recordings showed initial rises in velocity progressing to very weak high-freqency signals. It is likely that the tre mean velocity of these signals was not registered accrately. Where angiegraphic comparisons were available, this finding correlated with severe vasospasm (see Figre 1). Mean velocities p to 12 em/sec correlated with a mild degree of narrowing by angiography, sally less than 25%. Mean velocities of 12-2 em/sec correlated with moderate narrowing, and mean velocities of greater than 2 em/ sec indicated vessel narrowing of 5% or greater (see Figre 2). Initial baseline recordings in a grop of or patients revealed that velocities in all vessels were less than 1 em/sec within the first 48 hr following SAH. Velocities sally began to rise on the third or forth day following SAH, in most cases reaching a peak within 7-12 days and thereafter declining (see Figre 3). Discssion Transcranial Doppler is becoming an accepted method to assess the degree and extent of vasospasm ~ 175 E 15 ~ 1 > 1: 5 nl :E Time (day) Figre 3 Tim e corse of the MCA velocity changes in the period fo llowing sbarachnoid hemorrhage in a sbgrop of patients. following SAH. The most complete information is obtained by performing daily recordings on all of the basal vessels throghot the first 2 weeks following hemorrhage. This gives information on the severity and distribtion as well as the time corse of vessel narrowing. Previos stdies sggest that the rate of increase in mean velocity is important in identifying patients at high risk of developing ischemic deficits. 14 Mean velocities greater than 2 em/sec by the fifth day following SAH indicate a high risk for developing nerological deficits. It is also very helpfl for the examiner to have obtained baseline vales on patients to become familiar with each patient's particlar anatomy. As vasospasm becomes more severe and the cross-sectional area of the vessels decreases, vessels become more difficlt to locate with TCD. Faint high-freqency signals that are not qantifiable from vessels where good strong signals were fond on previos recordings sally indicate severe vessel narrowing. This is especially tre when recording from the anterior cerebral artery. The signals from the distal branches of the middle cerebral artery shold also be evalated for mean velocity and plsatility. Occasionally with very severe vasospasm, proximal high-freqency MCA signals will diminish in strength as flow decreases, and the distal branches will show lower velocities with low plsatility indicating proximal obstrction to flow. The examiner shold note these indicators of spasm as well as qantifying mean velocity. Transcranial Doppler can be a very valable asset in the management of sbarachnoid hemorrhage. It offers for the first time a way to assess intracranial vessel spasm noninvasively. Good correlations exist between vessel narrowing and mean velocity in the MCA. Acknowledgments. We acknowledge the assistance of Patricia Midtskog in the preparation of this manscript. This work was spported by NIH Grant NS7144.

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