Добавил:
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
Скачиваний:
0
Добавлен:
31.08.2026
Размер:
40 Мб
Скачать
ab
25 Carotid Dissection in ICU: Usefulness of Bedside Ultrasound Examination…
427
a
d
Fig. 25.3 Ultrasound assessment of ciliospinal reex (CR). (a) Initial probe positing; (b) elicita­tion of CR; (c) site of stimulation; (d) B-mode visualization of pupil at rest; (e) B-mode visualiza­tion of pupil in mydriasis after stimulus; (f) M-mode measurement of pupillary diameter (in blue) and pupillary dilation time (in yellow)
b
e
c
f
Fig. 25.4 Internal carotid artery dissection: (a) serpiginous stenosis, surrounded by a hypoecho­genic thickening of the vessel wall representing the intramural hematoma. (b) Distal tapering stenosis
25.7 Internal Carotid Artery Dissection (ICAD):
Ultrasound Findings
In patients with ICAD, there are two main types of ultrasound ndings, morphologi­cal and hemodynamic; moreover, they can be direct or indirect (Fig.25.4).
428
C. Baracchini and F. Farina
Direct morphological ndings are represented by hypoechogenic thickening of the vessel wall, lumen narrowing, echolucent intramural hematoma, double lumen, intimal ap, dissecting membrane, and pseudoaneurysm [3133]. Notably, pathog­nomonic signs are found in only one quarter of patients; specically, the detection rates of an intramural hematoma, a double lumen, and an intimal ap are about 15–25%, 2%, and 2%, respectively [19, 23].
Indirect morphological ndings are characterized by a normal carotid bifurcation or only mild atherosclerotic wall changes [4, 32, 34], distal tapering stenosis, increase of outer vessel diameter or circumference, and early thrombus detection [35]. Noteworthy, the most common nding of ICAD, found in 90% of patients, is a hypoechogenic wall thickening determining a stenosis or occlusion at a site not typically involved in atherosclerotic disease [31, 36]. Compared to atherosclerotic luminal narrowing, ICAD stenosis usually begins a few centimeters distal to the bifurcation and extends over a longer distance [23, 32]. Consequently, beware that in a patient with a clinical suspicion of ICAD, an examination of the carotid system must include the distal part of the ICA, especially with a sector probe. In patients with bromuscular dysplasia, a known risk factor for CAD [37], irregular wall thickening, multisegmental stenosis, or an aberrant course of the ICA are frequently found [38, 39]. Morphological criteria alone are diagnostic in only about 50% (20–63%), mainly due to inadequate direct imaging for retromandibular location.
Regarding direct hemodynamic criteria, these are mainly represented by a sig­nicant increase of blood ow velocities due to a distal stenosis, that is, high­cervical, retromastoidal stenosis. Beware when comparing ow velocities with the contralateral vessel, since up to 25% of patients have dissections affecting multiple vessels at the same time [6]. The combination of morphological and hemodynamic criteria is diagnostic in 74–78–95% of ICAD patients and increases with repeated examinations [19, 32, 33, 40].
Indirect hemodynamic criteria are present in patients with intracranial ICAD and they are characterized by pre-stenotic high resistance ow proles, post-stenotic dampened ow proles, and intracranial collateral circulation [19].
Taking into consideration any abnormal nding, sensitivity of combined ultra­sound techniques is high ranging from 80% to 96% [4, 19, 3234, 36, 4143]. Sensitivity, specicity, and positive and negative predictive values for color-coded duplex (CCD) sonography diagnosis of patients with ICAD causing carotid territory ischemia were 96%, 94%, 92%, and 97%, respectively [42]. However, different ultrasound techniques yield different sensitivities: 82% for CCD, 91% for Power Doppler (PD), and 98% for B-ow [44]. Intimal aps, ssures of membranes, and residual ow within the true and false lumen were better detected by B-ow than by CCD and PD [45]. Compared to CCD and PD, B-ow has a better spatial resolution and no angle dependency of the probe during the examination; as B-ow is not based on the Doppler principle, velocity measurements are not possible. Sensitivity is also different according to symptoms: 96% in patients having suffered ischemic events and 71% in patients without ischemic events (painful Horner’s syndrome, cranial nerve palsies: IX–XII or more rarely III, IV, VI) [4, 46]. Accordingly, patients with ischemic events have more often high-grade stenoses or occlusions (83%) than those without ischemic symptoms (40%) [4].
25 Carotid Dissection in ICU: Usefulness of Bedside Ultrasound Examination…
Ultrasound has also limitations, as false-negative ndings are reported in
2.8–16% of cases: subadventitial dissections without lumen compromise, low-grade stenosis with mild mural hematoma, and vessel segment not directly accessible by ultrasound, [19, 47]. These limitations are more often encountered in patients with­out cerebral ischemic signs [4]. Since a normal ultrasound exam does not exclude ICAD, the gold standard for diagnosis is an axial cervical MRI using the T1 fat suppression technique, as it detects the pathognomonic intramural hematoma in more than 90% of cases. Yet, MRI and ultrasound are considered complementary because only ultrasound can show the hemodynamic consequences.
The best method for following patients with CAD is ultrasound as it determines the time of recanalization and therefore the necessary duration of antithrombotic treatment. Recanalization, which results from the resorption of the wall hematoma and from the resolution of the intraluminal thrombus, occurs in about 76% of ICAD; specically, a complete recanalization has been reported in 55% of patients (58.7% in case of initial ICA stenosis, 40% in subjects with initial ICA occlusion). Most lumen changes occur within the rst 6months after dissection and they are only rarely seen (<1%) after 1 year [27]. High-grade (>80%) stenosis and occlusion recanalized less frequently [48]. In very selected cases of ICAD associated with critical hemodynamic insufciency or thromboembolic events that occur despite medical therapy, the patient undergoes endovascular stent placement; in these instances, ultrasound is useful in checking treatment efcacy.
Ultrasound monitoring is also valuable for detecting CAD recurrence: two reports have shown a surprisingly high recurrence rate ranging from 19% to 26% in the acute phase of the disease [27, 39]. Conversely, late recurrence is an uncommon event, occurring only in 2.7% of patients [27].
429
25.8 Common Carotid Artery Dissection (CCAD):
Ultrasound Findings
Common carotid artery dissection (CCAD) is a rare disease representing less than 1% of all CADs. This is possibly due to a different ultrastructure of the vessel wall: the ICA is a muscular artery, whereas the CCA is an elastic artery. The main differ­ence between the two arteries is in the tunica media: in muscular arteries, the tunica media consists mainly of smooth muscle tissue, whereas in elastic arteries, it con­sists of mostly elastic bers. Muscular arteries have two elastic layers in the tunica media (the external elastic lamina and internal elastic lamina), which might make them more susceptible to dissection [49].
CCAD can be traumatic, iatrogenic, spontaneous, or associated with aortic dis­section. Specically, CCAD is the most common mechanism of ischemic stroke of type A thoracic aortic dissection (AAD), seen in 85% of cases in one series, more commonly on the right side [50].
The most frequently reported ultrasound ndings (Fig.25.5) include a double lumen, mural thrombus, intraluminal hyperechoic/isoechoic lesion, and intimal ap; more rare ndings are carotid occlusion and pseudoaneurysm [3]. When urgent
430
C. Baracchini and F. Farina
a
c
Fig. 25.5 Common carotid artery dissection. (a, c) Longitudinal view showing a double lumen and a dissecting membrane. (b, d) Axial view showing a dissecting membrane and intramural hematoma
b
d
ultrasound is performed for suspected CCAD, axial views of the vessel should be acquired. In cases of CCA occlusion, blood will usually ow from the ECA to the ICA, even though occasionally ow reversal may be seen with the ICA owing retrograde and into the ECA.This dynamic information regarding ow within the ICA and ECA distal to the CCA occlusion provides complementary information for cerebral angiography and revascularization planning. Given its possible association with aortic dissection, early recognition of CCAD might affect the decision regard­ing thrombolysis in acute ischemic stroke patients. Since thrombolysis is potentially harmful in patients with CCAD secondary to AAD, a chest CT scan is mandatory to exclude an aortic dissection extending to the cerebroafferent vessels [51].
25.9 Ultrasound ofIntracranial Arterial Dissection
Intracranial ICADs seem to occur most frequently in the supraclinoid segment [52]. Overall they are rare and affect younger patients with a mean age less than 30years. Clinically, they present with severe headache, ischemic symptoms, or subarachnoid hemorrhage. An extensive diagnostic workup which includes conventional angiog­raphy is usually necessary not to miss a correct diagnosis. The visualization of the
ce
25 Carotid Dissection in ICU: Usefulness of Bedside Ultrasound Examination…
431
mural hematoma in intracranial arteries is very difcult with any non-invasive method. Ultrasound examination usually shows stenosis or occlusion of the involved vessel, but there are no data regarding sensitivity or specicity of ultrasound ndings.
25.10 Pupillary Ultrasound: Findings inCarotid Dissection
In patients with CAD, pupillary response to light is comparable on both sides, while mydriatic dilation after CR elicitation is completely absent ipsilaterally in the acute phase (Fig.25.6). This nding is especially important when CAD involves the distal segments and/or is subadventitial, and the pupillary dysfunction is not easily appar­ent to the clinician’s eye.

25.11 Conclusion

In summary, ultrasound is a fundamental diagnostic tool for patients with a clinical suspicion of CAD since it is widely available, non-invasive and it has a high sensitiv­ity, especially in patients with signs of cerebral ischemia. Moreover, bedside ultra­sound examination of the pupil might reveal a subtle pupillary dysfunction determined by a hidden distal/subadventitial CAD, especially in the acute phase. This might be extremely useful when assessing a polytraumatic patient admitted to the ICU.
a
b
Fig. 25.6 Right internal carotid artery dissection. (a, b) Pupillary diameter at rest in both eyes; (c, d) normal pupillary reex to light in right and left eye; (e) no pupillary reaction to ciliospinal
stimulus (pinching of the trapezius muscle) on the right side; (f) normal mydriatic reaction on the nonaffected side
d
f
432
C. Baracchini and F. Farina
CAD diagnosis should be conrmed by MRI because of its exquisite sensitivity in detecting intramural hematoma also in patients with local symptoms only. Complementarily to MRI, ultrasound discloses hemodynamic consequences in the intracranial circulation which might indicate the need for an endovascular treatment.
Ultrasound is the method of choice for monitoring recanalization once treatment is started, detecting CAD recurrence and establishing the duration of antithrombotic therapy.

Algorithm

Clinical Status of the Patient
ABCD Level of Consciousness (GCS) Pupillary Reactivity? Hemodinamic Stability? Oxygenation?
DIAGNOSIS
Trauma: PolytraumaticPatient ?
Ischemic Stroke ?
1. Extracranial Color-Coded Sonography (ECCS)
2. Pupillar Ultrasound (PuUS)
3. Transcranial Color-Coded duplex Sonography (TCCS)
ECCS
Pathognomonic
Signs of CAD
NO
Indicative signs
Of CAD
NO
Indirect
Hemodynamic signs
NO Clinical Suspicion and/or
TCCS
Hemodynamic signs
NO
END
YES
YES
YES
YES
PuUS
PuUS
Start Treatment
Indicative Signs of CAD
Indicative Signs of CAD
Dubious Findings
Axial Fat
Suppression MRI
Mural Hematoma
Start Treatment
YES
NO
YES
ABCD Airway-Breathing-Circulation-Disability, GCS Glasgow coma scale, CAD Carotid Dissection, MRI Magnetic resonance image
25 Carotid Dissection in ICU: Usefulness of Bedside Ultrasound Examination…
433

References

1. Schievink WI.Spontaneous dissection of the carotid and vertebral arteries. N Engl J Med.
2001;344:898–906.
2. Debette S.Pathophysiology and risk factors of cervical artery dissection: what have we learnt
from large hospital-based cohorts? Curr Opin Neurol. 2014;27:20–8.
3. Zach V, Zhovtis S, Kirchoff-Torres KF, Weinberger JM.Common carotid artery dissection: a
case report and review of the literature. J Stroke Cerebrovasc Dis. 2012;21(1):52–60.
4. Baumgartner RW, Arnold M, Baumgartner I, etal. Carotid dissection with and without isch-
emic events: local symptoms and cerebral artery ndings. Neurology. 2001;57:827–32.
5. Hassan AE, Zacharatos H, Mohammad YM, etal. Comparison of single versus multiple spon-
taneous extra-and/or intracranial arterial dissection. J Stroke Cerebrovasc Dis. 2013;22:42–8.
6. Baracchini C, Tonello S, Vitaliani R, Giometto B, Meneghetti G, Ballotta E. Vasomotion in
multiple spontaneous cervical artery dissections. Stroke. 2008;39:1148–51.
7. Béjot Y, Aboa-Eboulé C, Debette S, CADISP Group, etal. Characteristics and outcomes of
patients with multiple cervical artery dissection. Stroke. 2014;45(1):37–41.
8. Barbour PJ, Castaldo JE, Rae-Grant AD, etal. Internal carotid artery redundancy is signi-
cantly associated with dissection. Stroke. 1994;25:1201–6.
9. Baracchini C, Farina F, Tonello S, et al. Endothelial dysfunction in carotid elongation. J
Neuroimaging. 2013;23(1):18–20.
10. Dittrich R, Nassenstein I, Harms S, etal. Arterial elongation (“redundancy”) is not a feature of
spontaneous cervical artery dissection. J Neurol. 2011;258:250–4.
11. Menon RK, Norris JW.Cervical arterial dissection– current concept. Ann N Y Acad Sci.
2008;1142:200–17.
12. Vučurević G, Marinković S, Puškaš L, Kovačević I, Tanasković S, et al. Anatomy and radi-
ology of the variations of aortic arch branches in 1,266 patients. Folia Morphol (Warsz). 2013;72(2):113–22.
13. Natsis K, Tsitouridis I, Didagelos M, Fillipidis A, Vlasis K, etal. Anatomical variations in the
branches of the human aortic arch in 633 angiographies: clinical signicance and literature review. Surg Radiol Anat. 2009;31:319–23.
14. Sacco S, Totaro R, Baldassarre M, Carolei A.Morphological variations of the internal carotid
artery: prevalence, characteristics and association with cerebrovascular disease. Int J Angiol. 2007;16(2):59–61.
15. Osborn AG. Diagnostic cerebral angiography. 2nd ed. Philadelphia: Lippincott Williams &
Wilkins; 1999.
16. McDougal DH, Gamlin PD.Autonomic control of the eye. Compr Physiol. 2015;5:439–73.
17. Mullaguri N, Katyal N, Sarwal A, Beary JM, George P, Karthikeyan N, etal. Pitfall in pupil-
lometry: exaggerated ciliospinal reex in a patient in barbiturate coma mimicking a nonreac­tive pupil. Cureus. 2017;9(12):e2004.
18. Tripathy K, Simakurthy S, Jan A.Ciliospinal reex. StatPearls Publishing; 2020.
19. Nebelsieck J, Sengelhoff C, Nassenstein I, etal. Sensitivity of neurovascular ultrasound for the
detection of spontaneous cervical artery dissection. J Clin Neurosci. 2009;16:79–82.
20. Völker W, Dittrich R, Grewe S, etal. The outer arterial wall layers are primarily affected in
spontaneous cervical artery dissection. Neurology. 2011;76:1463–71.
21. Baumgartner RW, Lienhardt B, Mosso M, Gandjour J, Michael N, Georgiadis D.Spontaneous
and endothelial-independent vasodilation are impaired in patients with spontaneous carotid dissection: a case-control study. Stroke. 2007;38:405–6.
22. Benninger DH, Georgiadis D, Kremer C, Studer A, Nedeltchev K, Baumgartner RW.Mechanism
of ischemic infarct in spontaneous carotid dissection. Stroke. 2004;35:482–5.
23. Benninger D, Caso V, Baumgartner RW.Ultrasound assessment of cervical artery dissection.
In: Baumgartner RW, Bogousslavsky J, Caso V, Paciaroni M, editors. Handbook of cerebral artery dissection. Frontiers of neurology and neuroscience, vol. 20. Basel: Karger; 2005. p.87–101.
434
24. Ozdoba C, Sturzenegger M, Schroth G.Internal carotid artery dissection: MR imaging features
and clinical-radiologic correlation. Radiology. 1996;199:191–8.
25. Guillon B, Levy C, Bousser MG.Internal carotid artery dissection: an update. J Neurol Sci.
1998;153:146–58.
26. Kirsch E, Kaim A, Engelter S, et al. MR angiography in internal carotid artery dissec-
tion: improvement of diagnosis by selective demonstration of the intramural hematoma. Neuroradiology. 1998;40:704–9.
27. Baracchini C, Tonello S, Meneghetti G, Ballotta E.Neurosonographic monitoring of 105 spon-
taneous cervical artery dissections: a prospective study. Neurology. 2010;75:1864–70.
28. Barnett SB.World Federation for Ultrasound in Medicine and Biology (WFUMB) Symposium
on safety of ultrasound in medicine: conclusions and recommendations on thermal and non­thermal mechanisms for biological effects of ultrasound. Ultrasound Med Biol. 1998;24:1–55.
29. Sargsyan AE, Hamilton DR, Melton SL, Amponsah D, Marshall NE, Dulchavsky
SA.Ultrasonic evaluation of pupillary light reex. Crit Ultrasound J. 2009;1:53–7.
30. Farina F, Brunner C, Schreiber SJ, Palmieri A, Struhal W, Baracchini C, Vosko MR.Ultrasound
examination of the pupil suggestive for carotid dissection. Neurology. 2017;89:973–4.
31. de Bray JM, Lhoste P, Dubas F, Emile J, Saumet JL.Ultrasonic features of extracranial carotid
dissections: 47 cases studied by angiography. J Ultrasound Med. 1994;13:659–64.
32. Sturzenegger M, Mattle HP, Rivoir A, Baumgartner RW.Ultrasound ndings in carotid artery
dissection: analysis of 43 patients. Neurology. 1995;45:691–8.
33. Arning C.Ultrasonographic criteria for diagnosing a dissection of the internal carotid artery.
Ultraschall Med. 2005;26:24–8.
34. Steinke W, Rautenberg W, Schwartz A, Hennerici M. Non-invasive monitoring of internal
carotid artery dissection. Stroke. 1994;25:998–1005.
35. Pannone A, Bertoletti GB, Nesi F, Varakin I, Maritati G, Rabitti G.Carotid artery dissection.
Correlation of different diagnostic techniques. Minerva Cardioangiol. 2000;48:19–27.
36. Benninger DH, Baumgartner RW.Ultrasound diagnosis of cervical artery dissection. Front
Neurol Neurosci. 2006;21:70–84.
37. de Bray JM, Marc G, Pautot V, etal. Fibromuscular dysplasia may herald symptomatic recur-
rence of cervical artery dissection. Cerebrovasc Dis. 2007;23:448–52.
38. Dittrich R, Nassenstein I, Ringelstein EB, Kuhlenbaumer G, Nabavi DG.A distinctive case of
bromuscular dysplasia. Neurol Res. 2007;29:551–2.
39. Dittrich R, Nassenstein I, Bachmann R, et al. Polyarterial clustered recurrence of cervical
artery dissection seems to be the rule. Neurology. 2007;69:180–6.
40. Gobin-Metteil MP, Oppenheim C, Domigo V, et al. Critères diagnostiques en échographie-
Doppler des dissections artérielles cervicales à la phase aigue. J Radiol. 2006;87:367–73.
41. Treiman GS, Treiman RL, Foran RF, et al. Spontaneous dissection of the internal carotid
artery: a nineteen-year clinical experience. J Vasc Surg. 1996;24:597–607.
42. Benninger DH, Georgiadis D, Gandjour J, Baumgartner RW.Accuracy of color duplex ultra-
sound diagnosis of spontaneous carotid dissection causing ischemia. Stroke. 2006;37:377–81.
43. Alecu C, Fortrat JO, Ducrocq X, Vespignani H, de Bray JM.Duplex scanning diagnosis of
internal carotid artery dissections. A case control study. Cerebrovasc Dis. 2007;23:441–7.
44. Clevert DA, Rupp N, Reiser M, Jung EM.Improved diagnosis of vascular dissection by ultra-
sound B-ow: a comparison with color-coded Doppler and power Doppler sonography. Eur Radiol. 2005;15:342–7.
45. Clevert DA, Jung EM, Johnson T.Cervical artery dissection: improved diagnosis with B-ow
ultrasound. Clin Hemorheol Microcirc. 2007;36:141–53.
46. Arnold M, Baumgartner RW, Stapf C, etal. Ultrasound diagnosis of spontaneous carotid dis-
section with isolated Horner syndrome. Stroke. 2008;39:82–6.
47. Dittrich R, Dziewas R, Ritter MA, etal. Negative ultrasound ndings in patients with cervical
artery dissection. J Neurol. 2006;253:424–33.
48. Nedeltchev K, Bickel S, Arnold M, etal. R2-recanalization of spontaneous carotid artery dis-
section. Stroke. 2009;40:499–504.
C. Baracchini and F. Farina
25 Carotid Dissection in ICU: Usefulness of Bedside Ultrasound Examination…
49. Dittrich R, Draeger B, Nassenstein I, etal. Dissection of the common and external carotid
artery. Cerebrovasc Dis. 2006;21:208–10.
50. Cambria RP, Brewster DC, Gertler J, etal. Vascular complications associated with spontane-
ous aortic dissection. J Vasc Surg. 1988;7:199–209.
51. Uchino K, Estrera A, Calleja S, Alexandrov AV, Garami Z.Aortic dissection presenting as an
acute ischemic stroke for thrombolysis. J Neuroimaging. 2005;15(3):281–3.
52. Chaves C, Estol C, Esnaola MM, etal. Spontaneous intracranial internal carotid artery dissec-
tion: report of 10 patients. Arch Neurol. 2002;59:977–81.
435
Chapter 26
Carotid Disease: Usefulness oftheUltrasound
GyulaPánczél, VendelKemény, LászlóOláh, andLászlóCsiba
Key Points
1. Carotid ultrasound is the rst noninvasive imaging modality for diagnosis and
follow-up of different carotid diseases.
2. Duplex ultrasound (DUS) is the optimal method for investigation.
3. The DUS should assess the degree of stenosis, plaque characteristics, intima-
media- thickness and hemodynamic parameters.
4. Peak systolic velocities of 125–230 cm/s are typical for 50–69% stenosis
(NASCET) and 230cm/s for 70% internal carotid artery stenosis. But in some cases, peak systolic velocity ratio, end-diastolic velocity and velocity ratios may depict better the degree of stenosis.
5. Using spectral Doppler criteria can be also useful for increasing the sensitivity
or specicity.
G. Pánczél Department of Neurology, Ferenc Flór County Hospital, Kistarcsa, Hungary e-mail: panczel.gyula@orhosp.hu
V. Kemény Director of Early Phase Clinical Services at ICON plc, Budapest, Hungary
Szentendre Medical Center, Szentendre, Hungary
L. Oláh Neurologist, Department of Neurology, Debrecen University, Committee Member - ESNCH, Debrecen, Hungary e-mail: olah@med.unideb.hu
L. Csiba ( Neurologist, Department of Neurology, Clinical Center Debrecen University, Debrecen, Hungary. Advisory Board - ESNCH, Hungarian Neurological Society, Debrecen, Hungary e-mail: csiba@med.unideb.hu
C. N. Rodríguez et al. (eds.), Neurosonology in Critical Care,
https://doi.org/10.1007/978-3-030-81419-9_26
*)
437© Springer Nature Switzerland AG 2022