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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3591_Библиотеки_им_академика_М_И_Перельмана.pdf
17 Central Venous Access
a bc
181
d
ef g
hi j
ow in the needle. (e) Placement of sheath-dilator assembly over the
set—1 Puncture needle, 2 straight tip 0.021″ guidewire, 3 surgical blade
number11, 4 dilator with peel-away sheath, 5 4Fr Groshong PICC, 6
connector assembly. (b) Basilic vein on USG (arrow). (c) USG depicting the intraluminal guidewire placement. (d) Instillation of local
anaesthesia along the needle tract after puncture. Note the blood back-
guidewire. (f) Removal of guidewire with insertion of PICC line into
the sheath. (g) Peeling the sheath. (h) Connecting the PICC line end
with connector. (i) Securing the line with statlock and checking for
backow. (j). Fluoroscopy spot image showing the tip position of the
line in SVC-RA junction
Infections:
Insertion site infections such as cellulitis or abscess formation
Catheter-related bloodstream infection (CRBSI)
Infection chances are lower in the upper arm access site as
compared to the antecubital fossa
Cardiac arrhythmias:
Caused by the catheter tip in the right ventricle or very low in the
right atrium
Catheter malposition/migration:
Brachiocephalic vein or azygos vein
Phlebitis:
Mechanical damage from catheter or chemical irritation may lead
to phlebitis
Usually occurs within the rst week of catheter insertion
Managed with non-steroidal anti-inammatory drugs and warm
compresses
Catheter occlusion:
Can occur as a result of thrombosis or non-thrombotic causes
Unable to withdraw or infuse
182
a b
(arrow)
J. Kazimi and P. Naranje
Tunnelled central venous catheters (TCVC) are long-term
lines, intended to use for >6weeks up to a year. Unlike nontunnelled catheters that are directly inserted into a vein, tunnelled catheters are inserted into a large vein and are tunnelled
under the skin before exiting the body. This design reduces
the risk of infection and mechanical complications, as the
tunnel acts as a barrier between the external environment and
the bloodstream. These catheters are usually made of silicone and consist of a Dacron cuff near the distal end of the
catheter which has to be placed inside the subcutaneous tunnel, and it prevents the migration of skin bacteria.
Tunnelled central venous catheters are frequently used
in patients undergoing chemotherapy, bone marrow transplantation, haemodialysis or long-term antibiotic therapy.
Standard TCVCs include Hickman lines, Broviac catheter
and haemodialysis permacaths (Fig. 17.4). Commonly
selected veins for TCVC insertion include the internal jugular, subclavian and femoral veins. The internal jugular
vein is often preferred due to its straighter course, ease of
access and lower risk of pneumothorax compared to the
subclavian vein. However, in certain cases where the internal jugular vein is inaccessible, such as in patients with
thrombosis or previous surgeries, the subclavian or femoral
veins may be chosen as alternative sites. The decision is
made based on careful assessment and consideration of the
patient’s individual circumstances to ensure the safest and
most effective placement of the TCVC.Usual catheter sizes
range from 4F to 9Fr for Hickman lines and 8Fr to 16Fr for
haemodialysis permacaths.
The typical procedure for TCVC consists of access into
the lowermost part of IJV using standard USG guidance
followed by placement of guidewire into IVC.An oblique
subcutaneous tunnel is created extending from the site of
entry into IJV up to 2–3cm below the clavicle under adequate local anaesthesia. This is followed by the placement
of peel- away sheath-dilator assembly over the guidewire,
removal of dilator and guidewire with insertion of the catheter into the sheath. The outer sheath is then peeled which
leads to stabilization of catheter from subcutaneous tunnel
into the IJV and with a tip in SVC-RA junction or upper
right atrium (Fig.17.5).
Totally implantable catheters, also known as implantable
ports or port-a-caths, are CVCs used to provide long-term
access, especially for chemotherapy. Unlike external catheters, which are visible outside the body, totally implantable
catheters are surgically placed under the skin, typically in
the chest or upper arm region. They consist of a small reservoir or port connected to a catheter that is inserted into a
large vein, such as the subclavian or jugular vein (Fig.17.6)
The port is accessed using a special needle for the administration of the drugs. Totally implantable catheters offer several advantages, including reduced risk of infection,
improved patient comfort and increased mobility compared
to external catheters.
Procedure-related complications are similar to those
described under non-tunnelled CVCs. In addition to these,
17 Central Venous Access
ab c
183
d
of the tunnelled catheters (arrows)
a
bcdef
gh ij k
Contents of the Hickman line kit consisting of double lumen silicon catheter, plastic fascial dilator, puncture needle, peel-away sheath with dilator
assembly. It also contains a 0.035″ non-hydrophilic curved tip guidewire
(not shown). (b) USG-guided access of the distal IJV through the sternomastoid triangle fat (arrow). (c) Fluoroscopic conrmation of guidewire
in SVC. (d) Subcutaneous tunnel creation from 2 to 3cm below clavicle
margin up to the skin entry point of the guidewire. (e) Catheter placement
along the tunnel with cuff seen just at entry (arrow). Cuff is further pulled
into the tunnel and kept just within 1cm of skin entry and below clavicle
level. (f) Subsequently the sheath-dilator assembly is passed over guidewire and (g) position checked on uoroscopy. (h) Required catheter
length is cut and the tip of the catheter (arrow) is inserted into the peelaway sheath. (i) Sheath is broken and peeled apart (arrow). (j) The nal
position of the catheter exiting from the tunnel over the chest wall. (k)
Fluoroscopic spot depicting the tip in SVC/RA junction
184
J. Kazimi and P. Naranje
a
b
tissue (arrows) encircling the catheter along the tip and proximal part
s/o brin sheath formation
catheter is implanted in subcutaneous plane
the brin sheath formation is a unique complication of such
long-term lines.
Fibrin Sheath and Its Management
Fibrin sheath formation is a phenomenon that involves the
development of a brous structure around the catheter,
primarily composed of brin, platelets and other blood
components. This sheath can hinder catheter function and
may lead to various complications if left untreated.
Fibrin sheath formation typically begins when a catheter
is inserted, extends from the insertion site and continues distally along the catheter. The trauma caused by catheter insertion triggers a cascade of events involving the coagulation
system and the host’s response to injury. The coagulation
cascade is activated in response to vascular injury. This cascade involves a series of enzymatic reactions that ultimately
lead to the formation of brin, which is a key component of
blood clots. Fibrinogen, a soluble plasma protein, is converted into insoluble brin strands through the action of
thrombin, a key enzyme in the coagulation cascade. As the
coagulation cascade progresses, brinogen is converted to
brin at the site of catheter insertion. Fibrin strands begin to
accumulate around the catheter, forming a mesh-like structure. Platelets adhere to the brin strands and become activated. Activated platelets release various factors that promote
1. Catheter dysfunction: The presence of a brin sheath can impede
catheter function by obstructing the lumen or interfering with
uid ow.
2. Thrombus formation: Fibrin sheaths provide a surface for further
thrombus formation, which can increase the risk of catheterrelated thrombosis.
3. Infection risk: Fibrin sheaths may serve as a nidus for bacterial
colonization, increasing the risk of catheter-related bloodstream
infections.
4. Difculty removal: In severe cases, brin sheaths may adhere tightly
to the catheter, making catheter removal challenging and increasing
the risk of complications such as vascular injury or embolization.
further coagulation at the site of injury. Over time, the accumulation of brin and platelets results in the formation of a
dense brous sheath around the catheter (Fig. 17.7) This
sheath may extend along the length of the catheter, particularly in areas where blood ow is relatively stagnant.
Eventually, there is migration of smooth muscle cells towards
the intimal layer of the vein with resultant deposition of collagen [16]. Clinical implications of the brin sheath formation are shown in Table17.5.
Prevention of brin sheath formation is predominantly
based on proper catheter maintenance which includes regular ushing of catheters with saline or heparin solution.
However, the use of systemic anticoagulation or antiplatelet
therapy has not shown a signicant effect on delaying the
brin sheath formation in some studies [17].
In cases where brin sheaths have already formed, bri-
nolytic agents such as urokinase may be instilled into the
catheter to dissolve the sheath and restore catheter function
temporarily. IR management techniques include catheter
exchange over the wire, mechanical stripping and balloon
17 Central Venous Access
Type of catheter Vein site Points to note
Temporary non-tunnelled catheters IJV, SCV, FV Account for the majority of catheter-related bloodstream
Tunnelled central venous catheters IJV, SCV or femoral veins A cuff in the subcutaneous tunnel inhibits the migration of
Totally implantable catheters Tunnelled beneath skin and have a
subcutaneous port/reservoir which is
accessed with a Huber needle;
implanted in IJV or SCV
Heparin bonding catheters Prevents catheter-related thrombosis
Impregnated catheters Silver-impregnated collagen cuff: Less likely to be colonized
CRBSI Catheter-related bloodstream infection
infections
organisms into the catheter tract, lowers rate of infection than
non-tunnelled catheters, as well as helps in the xation of the
catheter
Lowest risk for CRBSI
Surgery required for catheter insertion and removal
Antimicrobial-impregnated catheters: Chlorhexidine- silversulfadiazine and minocycline-rifampin; risk of allergy and
antibiotic resistance
dilation of brin sheath with catheter replacement.
Mechanical stripping may be done using a loop snare around
the catheter (via femoral vein approach). This procedure has
been safe and effective in restoring catheter functionality in
several studies [18, 19].
A summary of major types of CVCs is shown in
Table17.6.
The Michigan Appropriateness Guide for Intravenous
Catheters (MAGIC) introduced an evidence-based, algorithmic approach to select central venous access devices [20]. It
is depicted as a owchart in Fig.17.8.
185
186
No
Central venous access indicated
-Complex, multiple infusions
-Total parenteral nutrition
-Plasmapheresis
-Hemodialysis
CKD stage IIIB
Expected duration of access
>14 days
mid to long term
14 days
short term
>3 months
long term
1-3 months
mid term
Non tunneled CVC Tunneled CVC
TPN
PICC
Tunneled CVC
J. Kazimi and P. Naranje
Tunneled CVC
CVC with
subcutaneous port
Emergent Venous access requirement
No CKD
Expected duration of access
>14 days to 1 month
mid term
14 days
short term
Non tunneled CVC PICC
Yes
> 14 days
Long term
Two large bore peripheral lines
Non-tunneled central venous catheter
No
5-14 days
Mid term
CKD
PICC
USG PIV
Midline catheter
Small bore CVC
Avoid subclavian vein
Avoid arm veins
5 days
short term
USG guided PIV
eter, TPN total parenteral nutrition. Adapted from Chopra V, Flanders SA, Saint S, etal. [20]
17 Central Venous Access
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S, Scoppettuolo G, Feller-Kopman D, Schummer W, Bif R,
Desruennes E, Melniker LA, Verghese ST.International evidencebased recommendations on ultrasound-guided vascular access.
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10. Resnick JR, Cydulka R, Jones RA.Comparison of two transducers
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Interventions oftheAorta
SanjeevKumar andAprateemMukherjee
18
Key Messages
1. Aortic dissection is characterized by a rupture of the media
layer resulting in a bleed in the aortic wall with resulting
separation of the adventitia and intimal layers: DeBakey
and Standford classications are used to classify.
2. Aortic aneurysms are dened as having a diameter of at
least 1.5 times the normal expected diameter. A true aneurysm involves all the layers of the arterial wall whereas
pseudoaneurysm is a contained rupture dened by
adventitia.
3. Intramural hematoma (IMH)—non-enhancing crescentic
or circular thickening of the aortic wall, without the typical intimal ap seen in aortic dissection due to rupture of
vasa-vasorum in the medial layer. Penetrating atherosclerotic ulcer (PAU)—ulcerated atherosclerotic plaque
which penetrates the intima of the vessel into the media.
4. Endovascular management options for thoracic aorta
include thoracic endovascular repair of aorta (TEVAR),
fenestrated endovascular repair of aorta (FEVAR), and
TEVAR chimney technique.
5. EVAR is the endovascular management option in abdominal aortic aneurysm treatment and can reduce operative
mortality by 66% in patients with appropriate anatomy;
however, this comes with an increased need for
re-intervention.
6. A common complication of endovascular stent-graft in
aorta is endoleak which is dened as leakage of blood
into an excluded aneurysm sac after placement of
stent-graft.
7. Five types of endoleaks have been described with standardized management strategies for each subtype.
18.1 Introduction
The biggest conduit in the body, the aorta transports blood
from the heart to all of the organs and is divided into 11
landing zones for endovascular intervention planning
(Figs. 18.1 and 18.2). Acute aortic syndrome is a lifethreatening condition presenting with tearing chest pain
and includes aortic dissection, aortic intramural hematoma
(IMH), and penetrating atherosclerotic ulcer (PAE) warranting urgent management. CT angiography and MR angiography are preferred non-invasive diagnostic modalities to
evaluate aorta. The early detection and management of
these conditions decide the prognosis and survival of the
patients.
From a histological standpoint, the aortic wall is comprised of three distinct layers. The inner layer, known as
intima, is thin and is composed of endothelial cells embedded in a connective tissue matrix. The medial layer is
thick and is primarily made of smooth muscle cells and
elastin, collagen, and polysaccharides. This layer is
responsible for providing the aorta with its strength and
distensibility. The outermost layer, known as the adventitia, consists of vasa vasorum (the blood supplier to the
aortic wall and a portion of the media), nerves, and connective tissues.
S. Kumar (*) · A. Mukherjee
Department of Cardiovascular Radiology and Endovascular
Interventions, All India Institute of Medical Sciences, Delhi, India
© 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_18
189
190
Ascending
aorta
Sinutubular junction
Innominate trunk
LCCA
S. Kumar and A. Mukherjee
LSCA
Arch of aorta
Sinus of valsalva
Annulus
Fig. 18.1 Anatomical segments of aorta. Of greater relevance to interventionalists is the technical categorization of aortic anatomy, particularly when planning aortic interventions such as aortic stent-grafts. This
classication system divides the aorta into 11 landing zones, each with
its own distinct boundaries. Zone 0 extends from the ascending aorta to
the distal aspect of brachiocephalic artery origin, while Zone 1 spans
from distal end of the brachiocephalic artery to the left common carotid
artery. Zone 2 ranges from the end of Zone 1 to the distal end of the left
subclavian artery ostium, and Zone 3 covers the proximal DTA from the
end of Zone 2 to the T4 vertebral body. Zone 4 spans from the end of
Zone 3 to the mid-descending aorta at T6, while Zone 5 stretches from
the mid-descending aorta up to the celiac. Zones 6 through 11 pertain to
the abdominal aorta
DTA
Abdominal
aorta
18.2 Anatomical Considerations
The biggest conduit in the body, the aorta transports blood
from the heart to all of the organs. It is organized anatomically into ve sections:
Fig. 18.2 Graphic depicting the zonal anatomy of aorta
18.3 Aortic Dissection
18.3.1 Introduction
Aortic dissection is characterized by a rupture of the media
layer resulting in a bleed in the aortic wall with the resulting
separation of the adventitia and intimal layers. The acute aortic syndrome triad includes aortic dissection and other entities such as intramural hematoma and penetrating aortic
ulcer. Although relatively uncommon, the incidence of aortic
dissection is 14 per 100,000 [1] with Type B dissections
accounting for 30% of these cases [2].
Risk Factors:
1. The aortic root extends from the annulus of the aortic
valve to the sinotubular junction.
2. Ascending aorta: Sinotubular junction to the innominate
artery.
3. Aortic arch: From innominate artery to the left subclavian
artery.
4. Descending thoracic aorta: From the left subclavian
artery to the diaphragm.
5. Abdominal aorta: Starting at the diaphragm and ending at
the aortic bifurcation.
1. Hypertension is a major risk factor for dissections.
2. Connective tissue abnormalities, Turner syndrome,
Marfan syndrome, and bicuspid aortic valve.
3. Infectious or inammatory causes, such as syphilis or
cocaine usage.
4. Iatrogenic causes, such as the use of aortic instruments
during surgery or percutaneous interventions.
5. A familial history of aortic dissection also predisposes to
risk, with mutations in genes such as α-actin 2 (ACTA 2),
brillin-1 (FBN1), transforming growth factor-β2
18 Interventions oftheAorta
(TGFRB2), transforming growth factor-β1 (TGFBR1),
and myosin heavy chain 11 (MYH11) being implicated in
the pathogenesis of aortic dissection [3].
191
TBAD
18.3.2 Classication
18.3.2.1 Morphological/Anatomical
Classication
Aortic dissection is classied depending on the segment of
the aorta involved. The management plan changes as per the
anatomical involvement of dissection.
There are many anatomical classications described in
the literature. However, Stanford and DeBakey classication
are generally followed.
1. DeBakey Classication was originally described in 1964
and 1965 and further modied in 1975 by Reul.
• Type I: Involvement of both ascending aorta and DTA
• Type II: The dissection is limited to ascending aorta
• Type IIIA: The dissection is limited to DTA
• Type IIIB: Involvement of DTA and abdominal aorta
• Type IIID: Retrograde involvement of ascending
aorta secondary to dissection originating in descending thoracic aorta
2. Stanford classication was originally described in 1970
and commonly followed classication for the management of patients.
• Type A: Dissection involving of ascending aorta
(proximal to brachiocephalic artery).
• Type B: Dissection involving aorta distal to brachio-
cephalic artery.
• Stanford Type A aortic dissection is conventionally
treated with open surgery as a rst choice. Further discussion will be on Type B aortic dissection.
3. Based on temporal sequence of events: Type B aortic
dissection (TBAD) can be classied depending on the
duration of symptoms into the following:
1. Acute: Symptoms for <15days
2. Sub-acute: Symptoms for 15–90days
3. Chronic: Symptoms for >90days (Fig.18.3)
18.3.2.2 Clinical Classication forTBAD
Each type of TBAD can be further sub-classied into complicated and uncomplicated.
A. Complicated TBAD includes patients with the
following:
• Refractory chest pain or back pain
• Impending rupture of the aneurysmally dilated false
lumen
• Branch vessel occlusion causing visceral malperfusion or claudication
Acute
(<15 days)
Complicated Uncomplicated
Fig. 18.3 Classication of Type B aortic dissection (TBAD) depending on the duration of symptoms
Sub-acute
(15-90 days)
Chronic
(> 90 days)
B. Patients with uncomplicated TBAD include patients
in whom symptoms are well controlled on medical
therapy.
C. It can also be an incidental nding detected during the
scan done for some other indications.
18.3.2.3 Natural History
• The false lumen can progress antegrade resulting in aortic
regurgitation or rupture of the aorta. It can progress retrograde to cause visceral artery occlusion with resultant
ischemic changes in viscera or kidneys.
• Patient generally presents with abrupt onset severe back
pain mainly in the interscapular region after an inciting
event (sudden rise in blood pressure). The pain may
extend in the lumbar spinal region presenting as vague
abdominal pain.
• The patient may also present with the complication of aortic dissection such as stroke, abdominal pain (due to visceral ischemia), limb claudication, or myocardial ischemia.
In these cases, aortic dissection is difcult to suspect.
1. TBAD is relatively benign in comparison to Type A
dissection (TAAD) and mortality rate ranges from
10% to 70% in high-risk groups [2].
2. Aortic rupture, although rare in TBAD, remains the
most common cause of death followed by malperfusion secondary to branch vessel occlusion [4].
3. Uncomplicated TBAD has a benign course and can
be managed successfully on medical therapy.
Elefteriades et al. [5] found that early survival in
uncomplicated TBAD was 91%, and 66% of these
patients were treated with medical therapy alone.
4. A select group of acute and sub-acute uncomplicated
TBAD is prone for aorta-related complications.
Tadros etal. [6] have identied a few risk factors such
as primary entry tear >10 mm, initial total aortic
diameter 40mm, false lumen diameter 22 mm, and