Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5783_Библиотеки_им_академика_М_И_Перельмана.pdf
22 Transcranial Doppler in Subarachnoid Hemorrhage: Usefulness in the Diagnosis…
387
22.5.1.3 Suboccipital/Transforaminal Window
It allows blood ow velocity, ow direction measurement, and visualization (TCCS)
(Fig.22.5): the distal vertebral arteries (VA, V4), basilar artery (BA).
22.5.1.4 Submandibular Window
The submandibular part of the ICA as it enters the skull.
In order to ensure better quality and reproducibility of ultrasound examination by
a certied sonographer, a standardized scanning protocol, including patient and
transducer positioning and orientation, depth selection, vessel and ow direction
identication, blood ow velocity measurement, is mandatory. Transcranial ultrasound monitoring should always include a baseline examination in patients suffering from acute aSAH.Furthermore, in order to detect and to follow CVS, insonation
Fig. 22.5 TCCS through the sub-occipital/transforaminal acoustic bone window showing colorcoded duplex imaging of the “Y-shaped” vertebral (VA) and basilar arteries (BA)
388
of the basal cerebral arteries should be daily performed during a period of time of at
least 15–20days after aSAH.However, the duration of the monitoring period should
be adapted individually, according to the occurrence and to the course and severity of CVS.
As transcranial ultrasound (TCD, TCCS) blood ow velocities are up to a certain
degree of narrowing, inversely related to arterial diameter, cut-off values of the
mean ow have been established to diagnose and to measure the degree of CVS in
the basal cerebral arteries. It should be known that CBFV gained with TCCS may
be lower than those gained with TCD.
Transcranial ultrasound examinations, either TCD or TCCS, should be performed– using a 2MHz pulsed Doppler or a 1–5MHz sectorial transducer– with
the patients in a supine position. In order to allow a comparison with TCD, if both
exams are performed, angle correction should not be performed in TCCS exams.
Spectral or color Doppler is used to locate the basal arteries through the dedicated
acoustic bone windows. Doppler settings and color gain have to be adjusted for each
vessel and CBFV should be measured along the vessel at very close intervals (2mm
to max. 5mm) in both– right and left– sides of the cerebral vasculature. To calculate the Lindegaard and Sloan ratios, mean CBFV of the distal ICAs is measured via
a submandibular approach without angle correction. Regarding the Soustiel index,
mean CBFV of both VA3 segments without angle correction should be used.
F. P err en
22.5.2 Transtemporal Ultrasound Examination (TCD/TCCS):
(Figs.22.3 and22.6)
The patient is lying in a supine position with the head turned laterally
• The MCA, which ow is normally directed toward the transducer, should be per-
formed as much distal/supercial, beyond the bi-/trifurcation (M2 segment), as
possible down to the ACA (A1 segment) bifurcation.
• The ACA, which ow is normally directed away from the transducer, should be
examined from its proximal part (from the bifurcation, A1 segment) to distal, as
far as possible (A2 segment).
• The PCA is found anteriorly to the mesencephalon (Fig.22.2). It has two seg-
ments (P1 and P2) that are dened, by sonographers, according the direction of
the ow: P1 toward the transducer and P2: away from the transducer. Therefore,
one has to be aware that they do not correspond to the anatomical denition (P1:
precommunicating, P2: postcommunicating segments).
40 mm
22 Transcranial Doppler in Subarachnoid Hemorrhage: Usefulness in the Diagnosis…
389
A
2
ACoA
A
65 mm
~60 mm
M
1
M
2
1
tICA
OA
OA
SIP
PCoA
60 mm
P
2
PA
BA
75 mm
VA
40 mm
SIP
PCA
A
tICA
VA
A
2
75 mm
1
70 mm
ACA
M
1
M
2
MCA
PCoA
PA
P
2
100 mm
60 mm
Fig. 22.6 Schematic drawing of the Circle of Willis showing ow directions and insonation
depths of several segments of the basal arteries. SIP carotid siphon, tICA terminal ICA, OA ophthalmic artery, ACA anterior cerebral artery, ACoA anterior communicating artery, MCA middle
cerebral artery, PCA posterior cerebral artery, PcoA posterior communicating artery, BA basilar
artery, VA vertebral pathway
22.5.3 Sub-Occipital/Transforaminal Ultrasound Examination
(TCD/TCCS): (Figs.22.5 and22.6).
The patient is lying in a lateral position, the neck is exed forward in order that the
chin is touching the chest
• The VAs and the BA are easily found as they form a Y-shape on TCCS examina-
tion (Fig.22.5). They should be examined (probe placed over the upper neck at
the skull base and angled toward the nose) at 2–5mm intervals up to the most
distal end of the BA.Their ow is directed away from the probe.
390
F. P err en
22.6 Monitoring ofCerebral Vasospasm
An examination guide of the main cerebral arterial segments showing ow direction and depth of insonation is presented below (Fig.22.6). Regarding cerebral
blood ow velocities, under normal conditions, it is important to remind the “hierarchy” of the MFV: MCA>ACA>Carotid Siphon>PCA>BA>VA.It is also
useful to remember that anatomic variations are common (a fully developed symmetric Circle of Willis is present in only 20% of the patients); therefore, the fact
that an arterial segment is not found does not automatically mean that there is an
occlusion.
A comprehensive examination of all the segments of the major basal arteries
with a report of the MFV, ow direction (including any unusual waveform), pulsatility indices, ratios of CVS (Lindegaard, Soustiel, Sloan) is mandatory. It is important to search in every arterial segment the highest CBFV.In case of missing arterial
segments, a double check should be performed.
Ultrasound monitoring of cerebral vasospasm after SAH should start with a
comprehensive baseline examination, including the extracranial vessels, in order
to follow any sign of increased CBFV. A very simple transcranial ultrasound
protocol that may be used as a guideline in the monitoring of CVS is presented below.
22.7 Conclusion
Cerebral vasospasm may occur after subarachnoidal hemorrhage due to ruptured
intracranial aneurysm. CVS is a feared complication that if not diagnosed and
untreated can lead to delayed neurological decit and sustained disability.
Therefore, beside careful neurological examination, DSA, CT-, and
MR-angiography, a noninvasive repeatable bedside diagnostic tool, such as
Transcranial Ultrasound (TCD,TCCS), is important. Comprehensive ultrasound
examination and monitoring of the blood ow velocities and vasospasm cut-off
indices in the basal cerebral arteries should be performed by experienced sonographers using a strict protocol.
22 Transcranial Doppler in Subarachnoid Hemorrhage: Usefulness in the Diagnosis…
Algorithm
INTENSIVE CARE UNIT (ICU)
EMERGENCY DEPARTMENT (ED)
Clinical Status of the Patient
ABCD
Level of consciousness (GCS)
Headache?
Bilateral Pupillary reactivity?
Hemodynamic stability?
Oxygenation?
Other Symptoms?
Non-contrast Brain CT Scan
Hunt-Hess Grading Scale
Modified Fisher Grading Scale
WFNS Grading Scale
SUBARACHNOID HEMORRHAGE (SAH)
Multimodal Monitoring (MMM)
Transcranial Color-Coded duplex Sonography (TCCS)
YES NO
Transcranial Doppler (TCD)
Baseline TCD/TCCS
(Day 0)
Cerebral Vasospasm
(CVS)
391
RE-ASSESS
Every 24 Hrs. Every 48 Hrs.
Anterior Circulation Anterior Circulation
Lindegaard ratio < 3 Lindegaard ratio< 3
Re-Assess every 48 Hrs. Re-Assess every 48 Hrs.
Lindegaard ratio > 3 Lindegaard ratio > 3
Re-Assess every 24 Hrs.(1) Re-Assess every 24 Hrs.(1)
Sloan ratio < 4 Sloan ratio < 4
Re-Assess every 48 Hrs. Re-Assess every 48 Hrs.
Sloan ratio > 4 Sloan ratio > 4
Re-Assess every 24 Hrs.(1) Re-Assess every 24 Hrs.(1)
Posterior Circulation Posterior Circulation
Soustiel ratio > 2 Soustiel ratio > 2
Re-Assess every 24 Hrs.
Soustiel ratio > 3 Soustiel ratio > 3
Re-Assess every 24 Hrs.(1) Re-Assess every 24 Hrs.(1)
(1) Consider: Comprehensive Neurological
Examination and Neuroimaging (either
BUT IF
Until 48 Hrs CVs Free or
≈ Day 15
CTA / MRA / DSA
RE-ASSESS
Re-Assess every 24 Hrs.
ABCD Airway-breathing-circulation-disability, CTA CT Angiography, MRA MRI Angiography,
DSA digital subtraction angiography
References
1. Moftakhar P, et al. Extent of collateralization predicting symptomatic cerebral vasospasm
among pediatric patients: correlations among angiography, transcranial doppler ultrasonography, and clinical ndings. J Neurosurg Pediatr. 2015;15:282–90.
2. Neulen A, Prokesch E, Stein M, Konig J, Giese A.Image-guided transcranial Doppler sonog-
raphy for monitoring of vasospasm after subarachnoid hemorrhage. Clin Neurol Neurosurg.
2016;145:14–8.
392
3. Kassell NF, Sasaki T, Colohan AR, Nazar G.Cerebral vasospasm following aneurysmal sub-
arachnoid hemorrhage. Stroke. 1985;16:562–72.
4. Macdonald RL, Hunsche E, Schüler R, Wlodarczyk J, Mayer SA.Quality of life and health-
care resource use associated with angiographic vasospasm after aneurysmal subarachnoid
hemorrhage. Stroke. 2012;43:1082–8.
5. Aaslid R.Transcranial Doppler assessment of cerebral vasospasm. Review. Eur J Ultrasound.
2002;16:3–10.
6. Alien GS, etal. Cerebral arterial spasm- a controlled trial of nimodipine in patients with sub-
arachnoid hemorrhage. N Engl J Med. 1983;308:619–24.
7. Harders AG, Gilsbach JM.Time course of blood velocity changes related to vasospasm in the
circle of Willis measured by transcranial Doppler ultrasound. J Neurosurg. 1987;66:718–28.
8. Kumar G, Shahripour RB, Harrigan R.Vasospasm on transcranial Doppler is predictive of
delayed cerebral ischemia in aneurysmal subarachnoid hemorrhage: a systematic review and
meta-analysis. J Neurosurg. 2016;124:1257–64.
9. Li DD, Chang JY, Zhou CX, Cui JB.Clinical diagnosis of cerebral vasospasm after subarach-
noid hemorrhage by using transcranial Doppler sonography. Eur Rev Med Pharmacol Sci.
2018;22:2029–35.
10. Moppett IK, Mahajan RP.Transcranial Doppler ultrasonography in anaesthesia and intensive
care. Br J Anaesth. 2004;93:710–24.
11. Aaslid R, Markwalder T-M, Nornes H.Noninvasive transcranial Doppler ultrasound recording
of ow velocity in basal cerebral arteries. J Neurosurg. 1982;57:769–74.
12. Aaslid R, Nornes H.Musical murmurs in human cerebral arteries after subarachnoid hemor-
rhage. J Neurosurg. 1984;60:32–6.
13. Kantelhardt SR, Greke C, Keric N, Vollmer F, Thiemann I, Giese A.Image guidance for tran-
scranial Doppler ultrasonography. Neurosurgery. 2011;68:257–66.
14. Lysakowski C, Walder B, Costanza MC, Tramèr MR. Transcranial Doppler versus angiog-
raphy in patients with vasospasm due to a ruptured cerebral aneurysm: a systematic review.
Stroke. 2001;32:2292–8.
15. Diringer MN, Bleck TP, Hemphill JC III, Menon D, Shutter L, Vespa P, etal. Critical care
management of patients following aneurysmal subarachnoid hemorrhage: recommendations
from the Neurocritical Care Society’s Multidisciplinary Consensus Conference. Neurocrit
Care. 2011;15:211–40.
16. Perren F, etal. Transcranial ultrasound is useful in guiding treatment of cerebral vasospasm in
aneurysmal subarachnoid haemorrhage. J Neurol. 2010;257:S84.
17. Weber M, Grolimund P, Seiler RW.Evaluation of posttraumatic cerebral blood ow velocities
by transcranial Doppler ultrasonography. Neurosurgery. 1990;27:106–12.
18. Spitzer C, Mull M, Rohde V, Kosinski CM.Non-traumatic cortical subarachnoid haemor-
rhage: diagnostic work-up and aetiological background. Neuroradiology. 2005;47:525.
19. Bramwell B.Spontaneous meningeal haemorrhage. Edinb Med J. 1886;32:101.
20. Symonds CP.Spontaneous subarachnoid hemorrhage. Q J Med. 1924;18(69):93–122.
21. Symonds CP.Spontaneous subarachnoid haemorrhage. Proc R Soc Med. 1924;17:39–52.
22. Todd NV, Howie JE, Miller JD.Norman Dott’s contribution to aneurysm surgery. J Neurol
Neurosurg Psychiatry. 1990;53(6):455–8.
23. Dandy WE.Intracranial aneurysm of the internal carotid artery: cured by operation. Ann Surg.
1938;107(5):654–9.
24. Krayenbühl HA, Yaşargil MG, Flamm ES, Tew JM.Microsurgical treatment of intracranial
saccular aneurysms. J Neurosurg. 1972;37(6):678–86.
25. Kassell NF, Peerless SJ, Durward QJ, Beck DW, Drake CG, Adams HP.Treatment of ischemic
decits from vasospasm with intravascular volume expansion and induced arterial hypertension. Neurosurgery. 1982;11(3):337–43.
26. Zubkov IN, Nikiforov BM, Shustin VA. 1st attempt at dilating spastic cerebral arteries
in the acute stage of rupture of arterial aneurysms. Zh Vopr Neirokhir Im N N Burdenko.
1983;5(5):17–23.
F. P err en
22 Transcranial Doppler in Subarachnoid Hemorrhage: Usefulness in the Diagnosis…
27. Guglielmi G, Viñuela F, Dion J, Duckwiler G.Electrothrombosis of saccular aneurysms via
endovascular approach. Part 2: preliminary clinical experience. J Neurosurg. 1992;75(1):8–14.
28. Ingall T, Aslund K, Mahönen M, Bonita R.A multinational comparison of subarachnoid hem-
orrhage epidemiology in the WHO MONICA stroke study. Stroke. 2000;31:1054.
29. de Rooij NK, Linn FH, van der Plas JA, Algra A, Rinkel GJ.Incidence of subarachnoid haem-
orrhage: a systematic review with emphasis on region, age, gender and time trends. J Neurol
Neurosurg Psychiatry. 2007;78(12):1365.
30. Brown RD Jr, Broderick JP.Unruptured intracranial aneurysms: epidemiology, natural history,
management options, and familial screening. Lancet Neurol. 2014;13:393–404.
31. Kataoka K, Taneda M, Asai T, Kinoshita A, Ito M, Kuroda R.Structural fragility and inam-
matory response of ruptured cerebral aneurysms: a comparative study between ruptured and
unruptured cerebral aneurysms. Stroke. 1999;30:1396–401.
32. Bor AS, Kofjberg H, Wermer MJ, Rinkel GJ.Optimal screening strategy for familial intracra-
nial aneurysms: a costeffectiveness analysis. Neurology. 2010;74:1671–9.
33. Lall RR, Eddleman CS, Bendok BR, Batjer HH. Unruptured intracranial aneurysms and the
assessment of rupture risk based on anatomical and morphological factors: sifting through the
sands of data. Neurosurg Focus. 2009;26(5):E2.
34. Gondar R, etal. Unruptured intracranial aneurysm follow-up and treatment after morphologi-
cal change is safe: observational study and systematic review. J Neurol Neurosurg Psychiatry.
2016;87(12):1277–82.
35. Goljan EF.Rapid review pathology. 2nd ed. St. Louis: Mosby; 2006. p.158.
36. Alway D, Cole WJ, et al. Stroke essentials for primary care: a practical guide, vol. 153.
NewYork: Humana Press; 2009. p.86–8.
37. Caranci F, Briganti F, Cirillo L, Leonardi M, Muto M.Epidemiology and genetics of intracra-
nial aneurysms. Eur J Radiol. 2012;82(10):1598–605.
38. Chalouhi N, Loh BL, Hasan D.Review of cerebral aneurysm formation, growth, and rupture.
Stroke. 2013;44(12):3613–22.
39. Hunt WE, Hess RM.Surgical risk as related to time of intervention in the re-pair of intracranial
aneurysms. J Neurosurg. 1968;28:14–20.
40. Fisher CM, Kistler JP, Davis JM.Relation of cerebral vasospasm to subarachnoid hemorrhage
visualized by computed tomographic scanning. Neurosurgery. 1980;6:1–9.
41. Drake CG, etal. Report of world Federation of Neurological Surgeons committee on a univer-
sal subarachnoid hemorrhage grading scale. J Neurosurg. 1988;68:985–6.
42. Aggarwal A, et al. Comparative evaluation of H&H and WFNS grading scales with modi-
ed H&H (sans systemic disease): a study on 1000 patients with subarachnoid hemorrhage.
Neurosurg Rev. 2018;41(1):241–7.
43. Fisher C, Kistler J, Davis J.Relation of cerebral vasospasm to subarachnoid hemorrhage visu-
alized by computerized tomographic scanning. Neurosurgery. 1980;6(1):1–9.
44. Hunt W, Hess R.Surgical risk as related to time of intervention in the repair of intracranial
aneurysms. J Neurosurg. 1968;28(1):14–20.
45. Dorsch NWC, King MT.A review of cerebral vasospasm in aneurysmal subarachnoid haemor-
rhage: I. incidence and effects. J Clin Neurosci. 1994;1:19–26.
46. Findlay JM, Nisar J, Darsaut T. Cerebral vasospasm: a review. Can J Neurol Sci.
2016;43(1):15–32.
47. Connolly ES Jr, For the American Heart Association Stroke Council, Council on Cardiovascular
Radiology and Intervention, Council on Cardiovascular Nursing, Council on Cardiovascular
Surgery and Anesthesia, Council on Clinical Cardiology, etal. Guidelines for the management
of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the
American Heart Association/American Stroke Association. Stroke. 2012;43(6):1711–37.
48. Westermaier T, etal. Value of transcranial Doppler, perfusion-CT and neurological evaluation
to forecast secondary ischemia after aneurysmal SAH.Neurocrit Care. 2014;20(3):406–12.
49. Frontera JA, etal. Prediction of symptomatic vasospasm after subarachnoid hemorrhage: the
modied sher scale. Neurosurgery. 2006;59(1):21–7.
393
394
50. Nakae R, Yokota H, Yoshida D, Teramoto A.Transcranial Doppler ultrasonography for diag-
nosis of cerebral vasospasm after aneurysmal subarachnoid hemorrhage: mean blood ow
velocity ratio of the ipsilateral and contralateral middle cerebral arteries. Neurosurgery.
2011;69(4):876–83.
51. Lindegaard KF, Nornes H, Bakke SJ, Sorteberg W, Nakstad P.Cerebral vasospasm diagnosis
by means of angiography and blood velocity measurements. Acta Neurochir. 1989;100:12–24.
52. Soustiel JF, Shik V, Shreiber R, Tavor Y, Goldsher D.Basilar vasospasm diagnosis: investiga-
tion of a modied “Lindegaard Index” based on imaging studies and blood velocity measurements of the basilar artery. Stroke. 2002;33:72–7.
53. Kirsch JD, Mathur M, Johnson MH, Gunabushanam G, Scoutt LM.Advances in transcranial
Doppler US: imaging ahead. Radiographics. 2013;33:E1–E14.
54. Budohoski KP, etal. Impairment of cerebral autoregulation predicts delayed cerebral ischemia
after subarachnoid hemorrhage: a prospective observational study. Stroke. 2012;12:3230–7.
55. Pickard JD, Matheson M, Patterson J, Wyper D. Prediction of late ischemic complications
after cerebral aneurysm surgery by the intraoperative measurement of cerebral blood ow. J
Neurosurg. 1980;53:305–8.
56. Lam JM, Smielewski P, Czosnyka M, Pickard JD, Kirkpatrick PJ.Predicting delayed ischemic
decits after aneurysmal subarachnoid hemorrhage using a transient hyperemic response test
of cerebral autoregulation. Neurosurgery. 2000;47:819–25.
57. Rätsep T, Asser T.Cerebral hemodynamic impairment after aneurysmal subarachnoid hemor-
rhage as evaluated using transcranial Doppler ultrasonography: relationship to delayed cerebral ischemia and clinical outcome. J Neurosurg. 2001;95:393–401.
58. Jaeger M, Schuhmann MU, Soehle M, Nagel C, Meixensberger J.Continuous monitoring of
cerebrovascular autoregulation after subarachnoid hemorrhage by brain tissue oxygen pressure
reactivity and its relation to delayed cerebral infarction. Stroke. 2007;38:981–6.
59. Rynkowski C, etal. Early transcranial Doppler evaluation of cerebral autoregulation inde-
pendently predicts functional outcome after aneurysmal subarachnoid hemorrhage. Neurocrit
Care. 2019;31:253–62.
60. Gonzalez NR, Boscardin WJ, Glenn T, Vinuela F, Martin NA.Vasospasm probability index:
a combination of transcranial Doppler velocities, cerebral blood ow, and clinical risk factors to predict cerebral vasospasm after aneurysmal subarachnoid hemorrhage. J Neurosurg.
2007;107:1101–12.
61. Hov MR, Ryen A, Finsnes K, Storor J, Lindner T, Gleditsch J, Lund CG.Pre-hospital ct
diagnosis of subarachnoid hemorrhage. Scand J Trauma Resusc Emerg Med. 2017;25(1):1–4.
F. P err en
Chapter 23
Subarachnoid Hemorrhage (SAH)
intheNeuro-ICU: Usefulness
ofTranscranial Doppler (TCD/TCCS)
forDelayed Cerebral Ischemia (DCI)
Monitoring
FrederickA.Zeiler andJeanneTeitelbaum
Key Points
1. Transcranial Doppler (TCD) employs non-invasive ultrasound technology for
the assessment of cerebral blood ow velocity (CBFV).
2. CBFV measurement via TCD can occur in both the anterior and posterior cere-
bral circulation.
3. TCD can be employed to monitor for the development of cerebral vasospasm
through the measuring middle cerebral artery (MCA) CBFV and assessing the
Lindegaard ratio.
4. Through signal processing techniques, either ofine or in real-time, TCD can
provide continuous measures of cerebral autoregulatory capacity.
5. Non-invasive intra-cranial pressure (ICP) measurement techniques using TCD
are currently being developed.
6. Newer robotic TCD technology will allow for longer duration continuous CBFV
recording.
F. A. Zeiler
Section of Neurosurgery, Department of Surgery, Department of Human Anatomy and Cell
Science, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada
e-mail: frederick.zeiler@umanitoba.ca
J. Teitelbaum (
Section of Neurocritical Care, Department of Neurology, Montreal Neurological Institute,
McGill University, Montreal, QC, Canada
e-mail: Jeanne.teitelbaum@mcgill.ca
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_23
*)
395© Springer Nature Switzerland AG 2022
396
F. A. Zeiler and J. Teitelbaum
23.1 Introduction
Aneurysmal subarachnoid hemorrhage (SAH) carries signicant upfront risk of
mortality, ranging up to 20–30% mortality prior to reaching specialist hospital care
[1]. For those fortunate enough to reach specialized care after onset of SAH, the risk
of complications during the acute and subacute phases of illness remains high [1, 2].
Such complications include, but are not limited to: aneurysm re-rupture prior to
microsurgical or endovascular therapy, seizures, neurogenic pulmonary edema, subendocardial ischemia, electrolyte disturbances, hydrocephalus, and the development of DCI [3]. The mentioned complication prole of SAH argues in favor of
specialized care within experienced dedicated neuro-ICUs (NICUs) [4].
DCI, also referred to as symptomatic cerebral vasospasm, is one of the major
contributors to mortality in the short-term post-SAH and long-term morbidity [3, 4].
The underlying premise behind DCI hinges on the concept of increased cerebrovascular tone, reduction in cerebral blood ow (CBF), and subsequent ischemia and/or
infarction. However, exact pathophysiologic mechanisms leading to the development of increase cerebrovascular tone are unclear [5]. Current theories focus on the
role of hemoglobin and its byproducts within the subarachnoid space leading to an
inammatory cascade that results in increased vascular tone and subsequent reduction in cerebral blood ow [5, 6].
The reduction in CBF post-SAH can occur both regionally and globally [7].
Furthermore, a reduction in cerebral vessel caliber can occur in the absence of clinical symptomatology, referred to as radiographic vasospasm. Our current understanding from epidemiologic studies in SAH patients indicates a risk of
approximately 20% for developing symptomatic DCI secondary to cerebral vasospasm [3, 4, 6]. The risk of developing radiographic cerebral vasospasm (i.e., nonsymptomatic spasm) has been quoted to occur in up to 60% of SAH patients [3, 4,
6]. Increased risk of radiographic vasospasm and DCI appears to be linked to:
females, young age, smokers, hypertensive patients, high modied Fisher computed
tomography (CT) grade, and severe Hunt and Hess (H+H) or World Federation of
Neurological Surgeons (WFNS) clinical grade SAH.Despite these associations, it
still proves difcult to predict those who will develop DCI [8].
The differing rates of DCI and radiographic vasospasm post-SAH highlight the
discrepancy between radiographic abnormalities and the development of symptomatic disease. In an ideal world, we would be able to accurately predict those who
will develop DCI, devoting our attention to the prevention of cerebral vasospasm in
these cases and mitigating the risk of ischemia and its downstream consequences.
However, our current understanding limits us to the early detection of cerebral vasospasm, employing various intermittent and continuous monitoring techniques.
These techniques include: transcranial Doppler (TCD), continuous electroencephalogram (cEEG), transcutaneous near infrared spectroscopy (NIRS), invasive assessment of parenchymal CBF and metabolism, and intermittent neuro-imaging such as
computed tomographic angiography/perfusion and Xenon enhanced CT [4, 5].