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_3591_Библиотеки_им_академика_М_И_Перельмана.pdf
170
ICA
)
N. Kumar et al.
16.2.1 Imaging
Duplex ultrasound (DUS) is the rst-line imaging modality
and is reliable with the added advantage of low cost and easy
accessibility. Percent stenosis can also be estimated as per
NASCET criteria by measuring peak systolic velocity (PSV)
of common carotid artery (CCA) and ICA and end diastolic
velocity (EDV) of CCA using Doppler study [4] (Table16.1).
For all patients undergoing carotid artery intervention,
duplex ultrasound study should be followed by computed
tomography angiography (CTA) or MR angiography (MRA)
(Class I B). CTA and MRA have added advantage of
B
% stenosis (ECST method
= (1 – A/C) × 100
% stenosis (NASCET
method)
C
A
Fig. 16.1 North American Symptomatic Carotid Endarterectomy Trial
(NASCET) and European Carotid Surgery Trial (ECST) methods for
measuring carotid stenosis severity
CCA
= (1 – A/B) × 100
simultaneous assessment of the aortic arch, arch vessels, distal ICA, vertebral arteries, and circle of Willis.
16.2.2 Management ofCarotid Artery Stenosis
Carotid artery stenosis has been classied into symptomatic
and asymptomatic patients.
16.2.2.1 Symptomatic Carotid Artery Stenosis
Symptomatic carotid artery stenosis refers to patients having
stenosis of extracranial carotid arteries who had prior history
of stroke or transient ischaemic attack (TIA) including amaurosis fugax and chronic ocular ischaemia syndrome involving ipsilateral brain territory in last 6 months.
Revascularization is indicated in symptomatic carotid artery
stenosis if stenosis is ≥50%, but the class of recommendation varies with the degree of stenosis as shown in Fig.16.2.
As per current guidelines, revascularization should ideally
be performed within two weeks of the index event.
Two most recent randomized controlled trials (RCTs),
CREST (Carotid Revascularization and Medical Management
for Asymptomatic Carotid Artery Stenosis) trial and ICSS
(International Carotid Stenting Study) trial, have included
symptomatic carotid artery stenosis patients having average
surgical risk (ASR). These RCTs published their initial results
in 2010 and their 5-year and 10-year follow-up subsequently.
In CREST Trial, 668 symptomatic patients underwent
carotid artery stenting (CAS) and 653 underwent carotid
endarterectomy (CEA). There was more periprocedural
stroke in CAS group (CAS: 5.5±0.9 vs CEA: 3.2±0.7; HR:
1.74; 95% CI: 1.02–2.98; P: 0.04) and more myocardial
infarction (MI) in CEA group (CAS: 1.0 ± 0.4 vs CEA:
2.3±0.6; HR: 0.45; 95% CI: 0.18–1.11; P: 0.08). Increased
periprocedural stroke in CAS group was attributed to minor
non-disabling strokes. There was no signicant difference
between these groups for 30-day stroke/MI/death (CAS:
6.7%; CEA: 5.4%; P: NS) or any ipsilateral stroke/ death at
4-year and 10-year follow-up [5].
Table 16.1 Doppler velocity criteria for NASCET-based carotid stenosis measurement
% stenosis (NASCET) PSV ICA (cm/s) PSVICA/ PSVCCA ratio
<50% <125 <2 <8
50–69%
60–69% 11–13
70–79% >230
80–89% 22–29
>90%
Near occlusion High, low string ow Variable Variable
Occlusion No ow Not applicable Not applicable
≥125
≥400 ≥5 ≥30
2.0–4 8–10
≥4
St Mary’s ratio
PSV ICA/ EDV CCA
14–21
16 Carotid Artery Interventions
171
S
Y
M
P
T
O
M
A
T
I
C
A
S
Y
M
P
T
O
M
A
T
I
C
Fig. 16.2 Management of average-risk patients with carotid artery stenosis. BMT Best medical therapy, CEA Carotid endarterectomy, CAS
Carotid artery stenting [11]
Carotid stenosis
70–99%
Carotid stenosis
50–69%
Carotid stenosis
<50%
Carotid occlusion/
Near total occlusion +
distal vessel collapse
Carotid stenosis
<60%
Carotid stenosis
60–99%
CEA + BMT Class I A
CAS + BMT Class II B
CEA + BMT Class IIa A
CAS + BMT Class IIa B
If recurrent symptoms on
BMT
BMT Class I A
No
• Life expectancy >5 years
• Favourable anatomy
• ≥1 features suggesting higher
stroke risk on BMT
CEA + BMT Class IIb A
CAS + BMT Class IIb B
CEA + BMT Class IIa A
CAS + BMT Class IIa B
Similarly, ICSS Trial recruited 855 symptomatic patients
in CAS group and 858in CEA group, and no signicant difference was observed for cumulative 5-year risk of fatal or
disabling stroke between CAS and CEA cohorts (6.4% vs
6.5%; HR: 1.06; 95% CI: 0.72–1.57; P: 0.77) [6].
SAPHHIRE (Stenting and Angioplasty with Protection in
patients at High Risk for Endarterectomy) trial is the only
RCT that has compared CEA in high surgical risk (HSR)
patients with CAS.The primary endpoint in this study was
30days stroke/MI/death plus death from neurological cause
or ipsilateral stroke between 31 days and 1 year which
occurred in 12.2% of CAS group patients and 20.1% of CEA
group patients (P: 0.004 for non-inferiority) [7]. As per current guidelines, CAS is preferred over CEA in symptomatic
HSR patients.
16.2.2.2 Asymptomatic Carotid Artery Stenosis
Asymptomatic Carotid Artery Stenosis are those patients
having stenosis of carotids without previous history of stroke
or TIA or stroke history is older than six months.
Carotid revascularization is recommended when carotid
artery stenosis is 60–90% along with a life expectancy of
>5 years and favourable anatomy. In these cases, CEA is
class IIa B recommendation and CAS is class IIb B
recommendation.
Only BMT is recommended if carotid stenosis is <60% or
there is complete occlusion or life expectancy is <5years or
anatomy is not favourable for revascularization.
Four recent RCTs, CREST trial, ACT-1 (Asymptomatic
Carotid Trial) trial, SPACE-2 (Stent Protected Angioplasty
versus Carotid Endarterectomy-2) trial and ACST-2
(Asymptomatic Carotid Surgery Trial-2) trial, have compared CAS with CEA in asymptomatic carotid artery stenosis patients.
Most recently published trial among these is ACST-2 [8]
in which 1811 asymptomatic patients were enrolled in CAS
group and 1814in CEA group and has reported no signicant difference in periprocedural strokes in these groups.
Follow-up results are awaited.
SPACE-2 trial [9] recruited 513 patients in three groups:
Best medical therapy (BMT), CAS + BMT, and CEA+
BMT.No stroke occurred in BMT group in 30-day period.
Thirty-day stroke/death was similar in both CAS and CEA
groups (2.5%). Cumulative stroke or death rate at 1year was
2.5% for CAS, 3.0% for CEA, and 0.9% for BMT (P:NS).
However, in all CAS patients with major secondary outcome,
embolic protection device (EPD) was not used. One-year
TIA incidence was 5.3% in BMT group which was almost
double of intervention groups (2% for CAS and 2.5% for
CEA).
172
N. Kumar et al.
Similarly, no signicant difference was noted in 30-day
stroke/death rate among CAS and CEA groups in CREST [5]
and ACT-1 trials [10]. CREST trial also showed no signicant difference even at 10-year follow-up.
Regarding high surgical risk (HSR) patients of asymptomatic carotid artery stenosis, SAPHHIRE trial [7] showed
1-year cumulative rate of primary endpoint of 9.9% in CAS
group and 21.5% in CEA group (P: 0.02). CAS is preferred
over CEA for HSR patients requiring intervention for carotid
artery stenosis (asymptomatic or asymptomatic stenosis).
16.2.3 Best Medical Therapy
Medical therapy includes antiplatelets and statins with management of associated hypertension and diabetes mellitus.
Low-dose aspirin (75–325 mg) is recommended in all
patients with carotid artery stenosis whether symptomatic or
asymptomatic. Aspirin can be replaced with clopidogrel in
persons who are intolerant to aspirin.
Cochrane review which included 56,934 patients observed
signicant reductions in all-cause mortality, fatal/non-fatal
stroke, and revascularization procedures in patients randomized to statins [12]. Various studies involving patients with
cardiovascular disease advise high-intensity statin treatment
goals, including a low-density lipoprotein (LDL) level of
<70mg/dL) or 50% reduction of LDL by using atorvastatin
or rosuvastatin. Low-dose aspirin and statins are class I recommendations (Level A) for asymptomatic carotid artery
stenosis patients for the prevention of stroke, myocardial
infarction, and other cardiovascular events.
Hypertension is a risk factor for the development and progression of carotid artery stenosis. Hypertension management in patients with carotid artery stenosis is associated with
reduced stenosis progression and even regression of intimamedia thickness (IMT) [13]. The goal of antihypertensive
therapy in carotid artery stenosis is to maintain blood pressure
<140/90mm of Hg (Class I recommendation, Level A).
Diabetes doubles the risk of stroke and is also associated
with increased risk of hypertension and dyslipidaemia [14].
Tight glycaemic control does not reduce stroke risk, but it
reduces other diabetes-related complications like microangiopathy [15]. Diabetes warrants stricter control of hypertension with target blood pressure of 140/85mmHg.
Smoking cessation and maintaining a healthy lifestyle are
also critical components for all revascularization strategies
to prevent stroke.
16.3 Carotid Artery Stenting
As per 2023 Clinical Practice Guidelines of the European
Society for Vascular Surgery (ESVS), carotid artery stenting
has been an alternative to CEA (Fig.16.2) [16].
Indications of carotid artery stenting (CAS) include
patients at high surgical risk (like severe pulmonary disease,
unstable angina, recent myocardial infarction, or severe congestive heart failure); prior neck radiation that can cause difcult open surgical dissection; history of damage to
contralateral vocal cords; tracheostomy in situ, contralateral
carotid occlusion; and previous CEA with recurrent
stenosis.
Main contraindications for CAS include heavily calcied
aortic arch or type III arch (arch having a distance greater
than twice the diameter of the left common carotid artery
(LCCA) between the highest point of the arch and the origin
of the brachiocephalic artery.
16.3.1 Preprocedure
Dual antiplatelet therapy with aspirin (75–300mg) and clopidogrel (75mg) is to be started three days prior to the procedure and continued for at least 4weeks after the procedure
and then platelet monotherapy is to be continued indenitely
[11].
For patients undergoing carotid artery stenting, Doppler
examination should be followed by axial imaging (CT or
MRI) for better evaluation of access vessels, arch morphology, plaque morphology, and intracranial vessel involvement. Brain imaging is also done to rule out infarcts,
haemorrhages, watershed infarcts, and white matter lesions.
Presence of ≥7 white matter lesions indicates worse
prognosis.
Ensure adequate hydration and uids are started prior to
procedure.
16.3.2 Hardware
Access sheath, carotid shuttle, catheters, guidewires, stent
(oversized by 1mm), predilation balloon (≤5 mm) if indicated, and embolic protection device.
16.3.2.1 Procedure
All patients should be closely monitored during the procedure since pronounced haemodynamic changes are anticipated during this procedure in the form of bradycardia and
hypotension.
Femoral artery access is taken using a modied Seldinger
technique and 6 Fr sheath is introduced. Then 0.035 guidewire is advanced into the aortic arch. Stenotic common
carotid artery (CCA) is selectively cannulated using an
angled catheter. 0.035 guidewire is carefully introduced into
the external carotid artery (ECA) followed by catheter
advancement. After this, the shuttle sheath is advanced into
CCA over stiffer guidewire. The stenotic lesion is identied
using carotid arteriograms taken in multiple projections.
16 Carotid Artery Interventions
abc
173
Fig. 16.3 CT angiography and DSA ndings of a 58-year-old woman
with amourosis fugax. (a) Oblique sagittal CTA and (b) lateral DSA
showed 80–90% stenosis of ostio-proximal left ICA (arrow). (c) DSA
0.014 guidewire is used to traverse the stenotic lesion followed by placement of embolic protection device in the
internal carotid artery if indicated. If required, predilation of
lesion is done using a small prole balloon. Haemodynamic
changes may occur at this stage and require careful monitoring. An appropriately sized stent is deployed across the
lesion. If signicant (>30%) residual stenosis is noted after
stent deployment, then post-dilation using appropriate sized
balloon is done. Finally check angiograms of carotid and
cerebral circulation are performed followed by the removal
of catheters and sheaths. Haemostasis is achieved at the femoral insertion site (Fig. 16.3).
16.4 Types ofCarotid Stents
Self-expandable stents have high radial force and are
therefore commonly used in carotid stenting. Balloon
expandable stents are susceptible to compression by
external force. Currently most used carotid stents are nitinol stents (made of nickel-titanium alloy) and may be
divided into open cell type, closed cell type, and hybrid
cell type. Closed cell type stents have small cell area with
higher radial strength due to which it has better plaque
coverage and reduced plaque embolization. Open cell
type stents are more exible and are preferred in tortuous
carotid arteries. Hybrid cell type stents have open cell
design in the periphery and closed cell design in the middle part thereby having both features of exibility and
plaque coverage. Tapered stents are also available these
days having smaller diameter in ICA thereby not producing excessive stretching of ICA as compared to nontapered stents [17].
after carotid artery stenting with tapered stent showing no signicant
residual stenosis
16.5 Complications
16.5.1 Early Complications
Stroke
The risk of stroke after carotid artery stenting is 4.7% on the
day of stenting and an additional 2.7% in the rst month.
Causes of stroke include embolization, carotid dissection,
hyperperfusion syndrome, and intracranial haemorrhage.
Most of these strokes are ischaemic (94%) and ipsilateral to
stented ICA (91%) [18].
Hypotension
Post-stenting hypotension and bradycardia are reported in
12% of patients, while both are reported in 13% patients
[19]. Hypotension is due to carotid sinus manipulation and
baroreceptor dysfunction [20]. Atropine is usually used to
treat hypotension. However, it is to be cautiously used in
benign prostate hypertrophy (BPH), glaucoma, and urinary
retention patients. Recent studies have shown glycopyrrolate
to be more effective than atropine in preventing postoperative hypotension and bradycardia [21].
16.5.2 Late Complications
Stent Infection
Only nine cases of carotid stent infection have been reported,
and the organisms involved were Staph. aureus, Streptococcus,
and Candida. Clinical presentation of the patient may be typical of neck abscess, swelling, septic embolization, and stroke.
Treatment advisable is complete excision of infected material
and reconstruction of the artery [22].
174
N. Kumar et al.
In-Stent Restenosis (ISR)
In-stent restenosis occurs in 3.5–14% patients of carotid
artery stenting and is associated with stroke in up to 2%
patients [23]. Multiple randomized control trials and metaanalysis have shown signicantly higher restenosis rates
after CAS as compared to CEA.Various risk factors associated with restenosis after CAS include diabetes mellitus,
chronic kidney disease, dyslipidaemia, stenosis >70%, and
smoking. Duplex ultrasound diagnostic criteria are different
for restenosis as compared to primary atherosclerotic disease
because CAS causes increased in-stent velocities even when
fully deployed. Higher PSV thresholds have been proposed
including >220cm/sec (ICA/CCA ratio≥2.5) for diagnosing >50% re-stenosis and≥300cm/sec (end diastolic velocity≥90cm/sec; ICA/CCA ratio≥3.8) for diagnosing >70%
re-stenosis [24].
Revascularization is indicated in cases of symptomatic
patients (late ipsilateral stroke or transient ischaemic attack)
having 50–99% in-stent restenosis (Class I recommendation,
Level B) which may be in the form of CEA, angioplasty, and
CAS. Medical therapy is recommended in other in-stent
restenosis scenarios which include all asymptomatic patients
and symptomatic patients having restenosis <50%.
at 3years. In agreement with SAMMPRIS trial, this trail also
did not show any incremental benet of angioplasty and
stenting over medical therapy alone in the management of
ICAD.
Intracranial stenting is used in patients with intracranial
acute large vessel occlusion stroke, failed medical therapy,
and large vessel embolic stroke [27]. The incidence of instent restenosis can be reduced with the use of drug-coated
balloons and drug-eluting stents [28].
16.7 Conclusion
At present routine screening for all is not recommended to
see if they have carotid artery disease because the chances of
identifying an asymptomatic person with signicant stenosis
(>70%) are very less. Screening may be considered for subgroups of patients having heart disease, hypertension, vascular disease of limbs, dyslipidaemia, and smokers. Patients
having carotid artery stenosis should be referred to a vascular
surgeon or interventional radiologist. Patients who are not
candidates for revascularization should be counselled for
lifestyle modication and control of vascular risk factors.
16.6 Internal Carotid Artery Stenting
Intracranial atherosclerotic disease (ICAD) is a common
cause of intracranial internal carotid artery stenosis, and it
accounts for 10–15% of strokes. Currently aggressive medical management with dual antiplatelet therapy is the mainstay of the treatment.
SAMMPRIS (Stenting and Aggressive Medical
Management for Preventing Recurrent stroke in Intracranial
Stenosis) trial [25] randomly enrolled patients with symptomatic ICAD on medical therapy (dual antiplatelet therapy
(DAPT), management of vascular risk factors, and lifestyle
modication) with and without angioplasty and stenting.
Thirty-day stroke rate was 14.7% in stenting group and 5.8%
in medical therapy group (P: 0.02). These early benets of
the medical therapy group persisted over the stenting group
even on a follow-up of 3years. Results of this trial favoured
aggressive medical management rather than stenting for the
management of symptomatic ICAD.
Another recent RCT, CASSISS (China Angioplasty and
Stenting for Symptomatic Intracranial Severe Stenosis) trial
[26], enrolled 380 patients with symptomatic severe intracranial stenosis (70–90%) and divided them into medical therapy (DAPT for 90days followed by monotherapy) group and
medical therapy with stenting group. No signicant difference was noted in the primary outcome of stroke or death.
Similarly, no signicant difference was observed for stroke
in qualifying artery territory at 2years and 3years and death
References
1. Abdu H, Tadese F, Seyoum G.Comparison of ischemic and hemorrhagic stroke in the medical Ward of Dessie Referral Hospital,
Northeast Ethiopia: a retrospective study. Milligan C, editor. Neurol
Res Int. 2021;2021:1–9.
2. Van Velzen TJ, Kuhrij LS, Westendorp WF, Van De Beek D,
Nederkoorn PJ. Prevalence, predictors and outcome of carotid
stenosis: a sub study in the Preventive Antibiotics in Stroke Study
(PASS). BMC Neurol. 2021;21(1):20.
3. Rothwell PM, Gibson RJ, Slattery J, Sellar RJ, Warlow
CP.Equivalence of measurements of carotid stenosis. A comparison
of three methods on 1001 angiograms. European Carotid Surgery
Trialists’ Collaborative Group. Stroke. 1994;25(12):2435–9.
4. Oates CP, Naylor AR, Hartshorne T, Charles SM, Fail T, Humphries
K, et al. Joint recommendations for reporting carotid ultrasound
investigations in the United Kingdom. Eur J Vasc Endovasc Surg.
2009 Mar;37(3):251–61.
5. Brott TG, Hobson RW, Howard G, Roubin GS, Clark WM, Brooks
W, etal. Stenting versus endarterectomy for treatment of carotidartery stenosis. N Engl J Med. 2010;363(1):11–23.
6. International Carotid Stenting Study investigators, Ederle J,
Dobson J, Featherstone RL, Bonati LH, van der Worp HB, et al.
Carotid artery stenting compared with endarterectomy in patients
with symptomatic carotid stenosis (International Carotid Stenting
Study): an interim analysis of a randomised controlled trial. Lancet.
2010;375(9719):985–97.
7. Yadav JS, Wholey MH, Kuntz RE, Fayad P, Katzen BT, Mishkel
GJ, etal. Protected carotid-artery stenting versus endarterectomy in
high-risk patients. N Engl J Med. 2004;351(15):1493–501.
8. Halliday A, Bulbulia R, Bonati LH, Chester J, Cradduck-Bamford
A, Peto R, etal. Second asymptomatic carotid surgery trial (ACST-
2): a randomised comparison of carotid artery stenting versus
carotid endarterectomy. Lancet. 2021;398(10305):1065–73.
16 Carotid Artery Interventions
175
9. Reiff T, Eckstein HH, Mansmann U, Jansen O, Fraedrich G, Mudra
H, etal. Angioplasty in asymptomatic carotid artery stenosis vs. endarterectomy compared to best medical treatment: one-year interim
results of SPACE-2. Int J Stroke. 2019;15(6):1747493019833017.
10. Roseneld K, Matsumura JS, Chaturvedi S, Riles T, Ansel
GM, Metzger DC, et al. Randomized trial of stent versus
surgery for asymptomatic carotid stenosis. N Engl J Med.
2016;374(11):1011–20.
11. Naylor R, Rantner B, Ancetti S, De Borst GJ, De Carlo M, Halliday
A, etal. Editor’s Choice—European Society for Vascular Surgery
(ESVS) 2023 Clinical Practice Guidelines on the Management of
Atherosclerotic Carotid and Vertebral Artery Disease. Eur J Vasc
Endovasc Surg. 2023;65(1):7–111.
12. Taylor F, Huffman MD, Macedo AF, Moore TH, Burke M, Davey
Smith G, etal. Statins for the primary prevention of cardiovascular disease. Cochrane Heart Group, editor. Cochrane Database Syst
Rev. [Internet]. 2013 Jan 31 [cited 2023 May 3];2021(9). Available
from: https://doi.org/10.1002/14651858.CD004816.pub5
13. Boutouyrie P, Bussy C, Hayoz D, Hengstler J, Dartois N, Laloux
B, etal. Local pulse pressure and regression of arterial wall hypertrophy during long-term antihypertensive treatment. Circulation.
2000;101(22):2601–6.
14. Banerjee C, Moon YP, Paik MC, Rundek T, Mora-McLaughlin C,
Vieira JR, etal. Duration of diabetes and risk of ischemic stroke:
the Northern Manhattan Study. Stroke. 2012;43(5):1212–7.
15. Zhang C, Zhou YH, Xu CL, Chi FL, Ju HN.Efcacy of intensive
control of glucose in stroke prevention: a meta-analysis of data
from 59197 participants in 9 randomized controlled trials. Malaga
G, editor. PLoS ONE. 2013;8(1):e54465.
16. Naylor AR, Ricco JB, De Borst GJ, Debus S, De Haro J, Halliday
A, etal. Editor’s Choice—Management of Atherosclerotic Carotid
and Vertebral Artery Disease: 2017 Clinical Practice Guidelines
of the European Society for Vascular Surgery (ESVS). Eur J Vasc
Endovasc Surg. 2018;55(1):3–81.
17. Castriota F, De Campos Martins EC, Liso A, etal. Technical evolution of carotid stents. Intervent Cardiol Rev. 2008;3(1):74.
18. Batchelder AJ, Saratzis A, Ross NA.Editor’s choice—overview of
primary and secondary analyses from 20 randomised controlled trials comparing carotid artery stenting with carotid endarterectomy.
Eur J Vasc Endovasc Surg. 2019;58(4):479–93.
19. Mylonas SN, Moulakakis KG, Antonopoulos CN, Kakisis JD,
Liapis CD.Carotid artery stenting–induced hemodynamic instability. J Endovasc Ther. 2013;20(1):48–60.
20. Altinbas A, Algra A, Brown MM, Featherstone RL, Kappelle LJ,
De Borst GJ, etal. Effects of carotid endarterectomy or stenting on
blood pressure in the International Carotid Stenting Study (ICSS).
Stroke. 2011;42(12):3491–6.
21. Chung C, Cayne NS, Adelman MA, Riles TS, Lamparello P, Han
D, et al. Improved hemodynamic outcomes with glycopyrrolate
over atropine in carotid angioplasty and stenting. Perspect Vasc
Surg Endovasc Ther. 2010;22(3):164–70.
22. Lejay A, Koncar I, Diener H, Vega De Ceniga M, Chakfé N.Postoperative infection of prosthetic materials or stents involving the
supra-aortic trunks: a comprehensive review. Eur J Vasc Endovasc
Surg. 2018;56(6):885–900.
23. Hrbáč T, Fiedler J, Procházka V, Jonszta T, Roubec M, Pakizer D,
etal. Comparison of carotid endarterectomy and repeated carotid
angioplasty and stenting for in-stent restenosis (CERCAS trial): a
randomised study. Stroke Vasc Neurol. 2023;8:399.
24. Lal BK, Hobson RW, Toghi B, Kapadia I, Cuadra S, Jamil
Z.Duplex ultrasound velocity criteria for the stented carotid artery.
J Vasc Surg. 2008;47(1):63–73.
25. Derdeyn CP, Chimowitz MI, Lynn MJ, Fiorella D, Turan TN,
Janis LS, et al. Aggressive medical treatment with or without
stenting in high-risk patients with intracranial artery stenosis
(SAMMPRIS): the nal results of a randomised trial. Lancet.
2014;383(9914):333–41.
26. Gao P, Wang T, Wang D, Liebeskind DS, Shi H, Li T, et al.
Effect of stenting plus medical therapy vs medical therapy alone
on risk of stroke and death in patients with symptomatic intracranial stenosis: the CASSISS randomized clinical trial. JAMA.
2022;328(6):534–42.
27. Lee JS, Lee SJ, Hong JM, Alverne FJAM, Lima FO, Nogueira
RG.Endovascular treatment of large vessel occlusion strokes due
to intracranial atherosclerotic disease. J Stroke. 2022;24(1):3–20.
28. Alexander MJ, Yu W.Intracranial atherosclerosis update for neurointerventionalists. J NeuroIntervent Surg [Internet] 2023 Jun 9
[cited 2024 Apr 2]; Available from: https://jnis.bmj.com/content/
early/2023/06/09/jnis- 2022- 019628
JunaidKazimi andPriyankaNaranje
Key Messages
1. Central venous accesses (CVA) are particularly valuable
in critical care settings, oncology treatments and for
patients requiring long-term intravenous therapies such
as haemodialysis.
2. Main types of CVA devices include peripherally inserted
central catheter (PICC), non-tunnelled central venous
catheters, tunnelled catheters and totally implantable
catheters.
3. Fluoroscopic and ultrasound guidance during the procedure signicantly reduces the complications.
4. Internal jugular vein is the most chosen access site for
central venous catheter placement.
5. Use of PICC has increased recently due to easier and
safer insertion with reduced morbidity and reduced rates
of complications.
6. Tunnelled central venous catheters are long-term lines,
intended to be used for >6weeks up to a year, reducing
the risk of infection and mechanical complications.
7. Implantable ports consist of a small reservoir or port
secured subcutaneously and connected to a catheter that
is inserted in the subclavian or IJV and used for
chemotherapy.
8. The complications of CVC could be mechanical, infectious or thrombotic complications, and the most reported
mechanical complications of CVC are haematoma, inadvertent arterial puncture and pneumothorax.
9. Most of the mechanical and thrombotic complications
can be managed effectively by IR intervention.
10. The Michigan Appropriateness Guide for Intravenous
Catheters (MAGIC) proposed an evidence-based algo-
J. Kazimi
Fellow Thoracic and GI Radiology, Department of Radiodiagnosis
and Interventional Radiology, All India Institute of Medical
Sciences, Delhi, India
P. Naranje (
Department of Radiodiagnosis and Interventional Radiology,
All India Institute of Medical Sciences, Delhi, India
*)
rithmic approach to central venous access device selection in patients based on clinical indication.
Central venous access (CVA) (i.e. placement of the catheter in inferior vena cava (IVC) or superior vena cava
(SVC)) is particularly valuable in critical care settings,
oncology treatments and for patients requiring long-term
intravenous therapies. In emergency settings, central
venous access devices may be inserted bedside with or
without the guidance of ultrasonography. However, the
long-term lines and complex access require the transfer of
the patient to the interventional radiology suite for proper
guidance of ultrasound and uoroscopy for the insertion
of these lines.
The objective of CVA is to ensure safe and reliable venous
access for prolonged infusion of various infusates with minimal patient discomfort. Some of the major indications are
enlisted in Box 17.1.
Box 17.1 Indications for Central Venous Access
• Chemotherapy infusion
• Blood product infusions
• Total parenteral nutrition
• Haemodialysis
• Plasmapheresis
• Emergency access and for rapid infusion of uids
• Administration of drugs likely to induce phlebitis
• To monitor central venous pressure
• For repeated blood sampling
• Temporary cardiac pacemaker
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2024
S. H. Chandrashekhara (ed.), Textbook of Interventional Radiology, https://doi.org/10.1007/978-981-97-9601-4_17
177
178
ab
Central venous access devices (CVADs) can be of several
types, and the choice of catheter depends on the purpose and
likely required time for use.
• Non-tunnelled catheters
• Peripherally inserted central catheter (PICC)
• Tunnelled catheters
• Totally implantable catheters
• Impregnated and coated catheters: heparin bonding and
antimicrobial impregnated catheters
Non-tunnelled central venous catheters are introduced through
direct percutaneous puncture of the internal jugular (IJV), subclavian (SCV), femoral (FV) or upper arm veins. These are relatively temporary short-term lines (dwell time from 7days to
2weeks), maybe double/triple lumen (usually >4Fr) (Fig.17.1a),
and are usually of low cost and require a relatively simple procedure for insertion. The technique of access is discussed in
subsequent sections. These lines are useful in emergency access
for uid administration, CVP monitoring, inotropes, and emergency dialysis. These lines require minimal nursing care and are
easy to remove once the purpose is achieved.
J. Kazimi and P. Naranje
straight course of the right IJV into SVC. Table17.1 lists
various advantages and disadvantages of access sites [1, 2].
Contraindication for access sites is noted in Table17.2 [3].
Access can be secured under ultrasound guidance (standard
of care), landmark guided/blind, and a combination of ultrasound and uoroscopic guidance.
Landmark Technique
Central:
The landmark for IJV is Sedillot’s triangle, formed by
lateral and medial insertion heads of sternocleidomastoid
muscle and clavicle. The needle is inserted at the apex of
this triangle, lateral to carotid pulsation, at a 30-degree
angle from the skin and directed towards the ipsilateral
nipple [4, 5].
Posterior:
The needle is inserted along the posterior edge of SCM at
the junction of the middle and lower third of the muscle,
approximately 5cm above the clavicle [5].
Supraclavicular Approach
The needle is introduced at a point 1cm superior to the clavicle
Vascular catheters can be placed in SVC via the IJV or SCV
and in IVC via the FV.Site and laterality of access depends
on the availability of site, and the preferred site of access
includes IJV followed by SCV and FV; as far as laterality is
considered right side is preferred over the left due to the
and 1cm posterior to the SCM.The needle is directed upwards
by depressing it 10 to 15 degrees below the coronal plane and
oriented to bisect the angle between the clavicle and SCM.The
needle is advanced behind the medial clavicle along a trajectory directed just below the contralateral nipple [6].
17 Central Venous Access
179
IJV SCV FV
Most common site
used for access
Easiest
Least thrombosis
Less complications
Prone for infection
Absolute Relative
Overlying skin infection
Anatomical distortion
Presence of implantable devices
Vascular injury distal or proximal
to insertion site
Most difcult
Less thrombosis
Least infection
Most complications
Coagulopathy
INR>3
Thrombocytopenia <20,000
Uncooperative patient
Morbid obesity
Easier
Most thrombosis
Most infections
Least complications
Infraclavicular Approach
The needle is inserted at 2–3cm inferior to the midpoint of
the clavicle and is further advanced while aiming for suprasternal notch [6].
Several safety advocacy organizations and professional societies recommend real-time ultrasound guidance during needle
placement for CVA [7]. Longitudinal views and short-axis
transverse views are used to visualize the selected vein [8, 9].
Vessel entry should be done at 12 o’clock position on vein
wall. Avoid access through lateral aspect of the vessel, as that
is associated with inability to cannulate, perivascular haematoma or more difcult haemostasis after catheter removal. The
longitudinal view (parallel to the course of vein) is ideal for
access in subclavian, external jugular, brachiocephalic and
axillary veins. This view permits direct observation of needle
penetration into the vein and passage of the guidewire [10].
• Identify the selected vessel (IJV, SCV, FV) by ultrasound
at the specic anatomic site.
• Insertion site is prepared using betadine and chlorhexidine and draped using sterile sheets.
• Local anaesthesia is inltrated using 1 or 2% lignocaine.
• Puncture the vein using the introducer needle.
• Conrm the needle position by aspiration of venous
blood.
• Pass a J-tip guidewire and gently advance through the
needle; never force the wire.
• Remove the needle while holding the guidewire.
• Make a small skin nick using a scalpel blade contiguous
with the wire entry point.
Immediate Delayed
Bleeding
Inadvertent arterial puncture
Pneumothorax
Hemothorax
Arrhythmia
Catheter malposition
Air embolism
Thoracic duct injury
Venous thrombosis
Infection
Pulmonary emboli
Catheter malfunction
Catheter embolization
Venous stenosis
Myocardial perforation
Nerve injury
• Advance the dilator while holding guidewire followed by
withdrawal of dilator.
• Flush the catheter lumens.
• Advance the catheter over the guidewire.
• Remove the guidewire over catheter.
• Evaluate ease of aspiration and ushing from each port of
the catheter.
• Suture the catheter securely, and dress the site.
The complications of CVC could be mechanical, infectious
or thrombotic complications [11]. These can be immediate
or delayed (Table17.3). The most common mechanical complications of CVC are haematoma, arterial puncture and
pneumothorax. These are more common with the landmark
approach than the guided approach. In addition, these are
more frequent with the femoral vein route than IJV or
SCV.Inadvertent arterial puncture is identied by rapid, pulsatile ow in the needle hub with bright red blood; though
these features are doubtful to achieve in cases with profound
hypotension.
The catheter-related bloodstream infections (CRBSI)
are less likely to occur with subclavian vein access as compared to femoral venous catheterization. The pathogenesis
includes the presence of exit site skin infection, catheter
hub contamination or haematogenous seeding of the catheter [12].
The risk of venous thrombosis secondary to catheters has
been reported in up to 15% of the cases and is more commonly seen in femoral vein access as compared to the subclavian vein route [12].
Complications Avoided by Dynamic USG Guidance [13]
Some of the complications listed in Table 17.3 may be
avoided by the use of USG.These include
• Inadvertent arterial puncture
• Failure to place the catheter
• Initial guidewire/catheter malposition
• Pneumothorax
• Hemothorax
180
J. Kazimi and P. Naranje
Tips to Identify Catheter Malpositions
Left internal jugular and subclavian vein–approach catheters
that do not cross the midline at the approximate location of
the manubrium or just below the sternoclavicular joint should
raise suspicion for malpositioning [14]. It may terminate in
other venous branches such as the internal mammary vein, or
outside the vessel lumen of the brachiocephalic vein or arterial or nonvascular locations. Right IJV or SCV catheters that
cross to the left of the mediastinum should raise doubt of
intra-arterial placement. SCV approach catheters that take a
high course much superior to the rst rib may be in the subclavian artery.
The use of PICC has increased recently due to easier and
safer insertion with reduced morbidity and reduced rates of
complications. The catheter is inserted through the upper
arm peripheral vein, and the tip is localized in the superior
vena cava. PICCs are usually recommended for short- and
medium-term use (4weeks to 6months) (Fig.17.1b). These
are usually available in sizes ranging from 3Fr to 5Fr, are
made up of polyurethane or silicone and mainly have an end
hole (power PICC) or a side hole conguration with a valve
(Groshong type). The open-end conguration requires a heparinized ush to maintain patency as blood may back up in
the tubing. Whereas the valved lines prevent the thrombosis
of the line by pressure-directed opening of the valve which
opens only with a positive forward ow of uid administration or negative suction for blood aspiration, at other times,
the valve remains closed. These are especially valuable in
paediatric access since it is associated with fewer needle
punctures and can be inserted with mild or no sedation.
These are suitable for both inpatient and outpatient settings.
There are no absolute contraindications for its use. However,
some relative contraindications include expected puncture
site burns, trauma, skin infections, radiation, active bacteraemia, prior mastectomy and lymph node dissection, and
patients requiring crutches. PICC insertion is a low bleeding
risk procedure and can be performed with INR in the range
of 2–3 and platelet >50,000u/L.Few papers also suggest that
PICC placement does not require discontinuation of antiplatelet therapy or correction of coagulation parameters [15].
The upper arm veins, i.e. basilic, cephalic or brachial
veins, are preferred for the insertion of PICC, and the basilic
vein is usually the choice given that this vein has a more
straight route towards the subclavian vein and is larger in
calibre than the cephalic vein. The cephalic vein is more
prone to spasms and may have an angled entry into the axillary vein. Sometimes, saphenous or femoral veins may be
used for access in children.
The PICC line kit usually contains the puncture needle,
guidewire, peel-away sheath with the dilator, syringes, blade
and sterile dressing kit.
The technique of insertion is summarized in Fig.17.2.
A few tips for puncturing the vein are to apply the arm
cuff to distend the vein adequately. Use USG guidance to
puncture under aseptic precaution and look for good backow of blood. It is advisable not to puncture the opposite
wall of the vein so as to prevent haematoma formation which
may decrease the lumen calibre and cause difculty in
manipulating the guidewire.
After line placement, the patients should be instructed to
avoid lifting heavy weights and swimming and to be watchful for any signs of infection or swelling at the site of entry
and may use PICC line covers for protection.
Few newer PICC lines are also available with the pres-
ence of a cuff, and these are tunnelled in the subcutaneous
plane for a longer and durable access.
Some complications associated with the PICC lines are
summarized in Table17.4. Accidental withdrawal and catheter occlusion are the most common complications, both
potentially preventable with appropriate measures. Catheter
malpositions are also seen at times (Fig.17.3).