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22 Pulmonary Angiography: Arteriovenous Malformation andPseudoaneurysm
to decompressive air bubble formation, and embolization of
larger lesions. Given their signicant risk of bacteremia,
dental procedures including cleaning are of high concern.
With advances in technology and interventional management,
surgical resection is rarely indicated for PAVM anymore.
Key Point
While PAVMs with feeding arteries greater than
2–3mm should be embolized, even smaller ones create
the risk of bacterial paradoxical embolization, indicat-
ing the need for prophylactic antibiotics before proce-
dures, including dental hygiene.
Pulmonary Artery Pseudoaneurysm
Pseudoaneurysms require denitive therapy given their propensity to bleed. Antibiotics for mycotic pseudoaneurysms
Fig. 22.5 Left upper lobe pseudoaneurysm (white arrow) on coronal
CT image in a patient with interstitial brosis and repeated infections
who has had episodes of hemoptysis up to as much as 100ml/episode
it is also a reasonable technical lower threshold.
Morphological risk factors for PAVM hemorrhage are not
clear, but larger lesions are of greater concern. Pregnant
women can be treated during the second trimester.
Pulmonary Artery Pseudoaneurysm
Contrast-enhanced chest CT (or CTA) is the best imaging
modality, with most pseudoaneurysms found in segmental or
subsegmental arteries (Fig.22.5) [36]. While the vast majority of patients presenting with massive hemoptysis bleed
from bronchial or other systemic arterial supply into the
lungs, a pulmonary artery source may be found either alone
or in combination with the systemic source in 5–11%.
Key Point
Pulmonary artery pseudoaneurysms have a high propensity to hemorrhage, indicating a need for embolization.
Conventional Therapy
Pulmonary Arteriovenous Malformation
The treatment of PAVM consists of antibiotic prophylaxis
before procedures prone to produce bacteremia that would
place the patient at risk for abscess formation, avoidance of air
or clots in intravenous lines, avoidance of SCUBA diving due
may result in resolution; however more direct therapy is
typically needed, especially if the patient has had bleeding
[36]. Peripheral lesions are amenable to endovascular techniques, most commonly embolization but occasionally a
stent graft. More central ones can be more challenging for
endovascular therapy; parent artery embolization here
would entail the loss of a large amount of normal lung perfusion, and the rapid caliber changes and branching can be
prohibitive for a stent graft. Aneurysm resection, patch
repair, vessel ligation, graft placement, and pulmonary
resection may be considered; however, many such patients
have comorbidities placing them at higher risk for these surgical approaches.
Interventional Therapy
Pulmonary Arteriovenous Malformation
When present, hypoxemia, dyspnea, and impaired exercise
tolerance from right-to-left shunting will improve after
occlusion of PAVM, resulting in improved quality of life [41,
42]. The risks of stroke and brain abscess associated with
PAVM are decreased and migraines often improve [6, 43].
Patients with diffuse PAVM can have larger components
embolized to prevent larger paradoxical emboli, but eradication of the disease is not feasible unless conned to a local
region, and hypoxemia generally persists [30–32].
Pulmonary arteriovenous malformation embolization is
typically done as an outpatient with moderate sedation.
General anesthesia is only needed for children and adults
with special indications. Routine preparatory laboratory values are a CBC, BMP, and coagulation parameters. Patients
with signicant polycythemia may benet from phlebotomy
to reduce the risk of pericatheter thrombosis.
251
252
J. S. Pollak
The How To: PAVM
1. Antibiotic prophylaxis is administered, typically
cefazolin 1–2 grams based on weight.
2. The femoral vein is accessed using the Seldinger
heparin are administered to prevent pericatheter
thrombus formation. Scrupulous care is needed to
avoid introducing air or clots through the
catheters.
3. A 7 or 8 French sheath is advanced over the wire
into the femoral vein.
4. A pigtail catheter is advanced through the sheath
and then across the right side of the heart into the
right or left pulmonary artery, obtaining pressures. The risk of therapeutic embolization in the
setting of severe pulmonary hypertension is not
clear [44].
5. Selective right and/or left lung angiography is per-
scan, with oblique imaging as needed to outline
22.2).
6. The pigtail catheter is exchanged for a coaxial
catheter system consisting of an outer 7 or 8
French guiding catheter, which may be straight or
angled, and an inner short angled 5 French catheter. This system is used to select lobar and segmental arteries leading to PAVM(s) followed by
22.6a). The inner
catheter can be changed to different shaped ones if
needed. A microcatheter is not typically needed.
7. Once the catheter is located distally within the
feeding artery, preferably starting adjacent to the
arteriovenous connecting sac, a mechanical embolization agent is introduced to occlude the vessel
22.6). Embolization of the sac itself is
not felt to be necessary, but there is some controversy about this [45].
8. When coils are used, it is important to create a
dense cross-sectional framework of metal to
achieve a more durable occlusion rather than
22.7) [45]. Pushable
lowed by smaller ones to pack them in tightly.
when there is concern over distal migration with
paradoxical embolization and for the last one
when there is concern over prolapsing into nontarget vessels. Soft platinum Nester and Tornado
coils (Cook, Bloomington, IN) work well for
small- and medium-sized PAVMs, while higher
9. Amplatzer Vascular Plugs (AVP) (St. Jude
Medical, Abbott, St. Paul, MN) are highly effective in occluding PAVMs. They additionally have
the advantage of being detachable and so can be
repositioned, often very distally even in large ves-
22.6b). While more expensive than
coils, usually only one AV P is needed, although
occasionally in conjunction with a coil(s).
10. The Micro Vascular Plug (Covidien, Medtronic,
Minneapolis, MN) consists of a nitinol frame with
thrombus. Four devices are available to treat ves-
has been favorable but no mid- or long-term data
is available [46].
11. After a PAVM is embolized, angiography is per-
22.7b).
Due to the femoral vein access, light activity is recomended for 2–3 days. A nonsteroial anti-inammatory agent
such as ibuprofen is useful for the 5–15% of patient who may
develop pleurisy afterward, assuming this does not exacerbate HHT-related bleeding [5]. Complications of PAVM are
rare in experienced centers. Paradoxical embolization of air,
clot, or a device may result in a neurological event, angina,
or other organ ischemia in less than 1–2%. Hemorrhage with
hemoptysis is unusual and treated with completing the
embolization.
A follow-up chest CT is done in 6–12 months to assess
for adequate occlusion (Fig.22.8) The aneurysmal sac and/
or draining vein should be reduced by 30–70%, although it is
not certain how accurate this is [47]. The lesion should no
longer enhance if contrast is used, but care to avoid introduction of intravenous air bubbles needs to be remembered
given the risk of reperfusion or other PAVMs. Magnetic reso-
-
nance angiography of embolized PAVMs has been successfully used by some [48]. If the lesion remains occluded,
further imaging follow-up should be done at 5-year intervals
to assess for continued occlusion and enlargement of tiny
PAVMs. This has typically been done with CT, but concerns
over cumulative radiation have prompted investigations into
alternatives.
22.6c and
22 Pulmonary Angiography: Arteriovenous Malformation andPseudoaneurysm
253
Fig. 22.6 Embolization of the left upper lobe PAVM depicted in
Figs.22.2a and 22.4. (a) Outer guiding catheter (black arrow) distally
in the feeding artery and inner 5 French catheter (white arrow) within
the arteriovenous sac. (b) Occlusion of this PAVM after placement of an
8mm Amplatzer Vascular Plug II in its distal segment of the feeding
artery (arrows), with stasis of previously administered contrast in the
sac beyond the plug. (c) Completion angiogram demonstrating no lling
of the AVM (arrow)
Fig. 22.7 Embolization of the right lower lobe complex PAVM shown
in Fig.22.2b. (a) Better visualization of two accessory feeding arteries
(black arrows) from the posterior segmental artery after embolization
of the main feeding artery from the medial segmental artery with an
Key Point
Long-term follow-up is necessary for PAVM even after
embolization due to the risks of reperfusion and
enlargement of initially tiny lesions.
Amplatzer Vascular Plug II (white arrow). (b) The two accessory feeing
arteries and their common trunk were embolized with densely packed
platinum coils, with no remaining ow to the PAVM
Reperfusion after coil embolization may occur in
3–25%, although occasionally higher rates are reported
[5, 49–52]. Predisposing factors are inadequate coil packing,
coil placement more than 1 cm proximal to the sac, and
larger feeding arteries. This is usually amenable to repeat
254
Fig. 22.8 Follow-up CT scan shows involution of the embolized left
upper lobe PAVM depicted in Figs.22.2a, 22.4, and 22.6. Only a thin
scar (arrow) remains of the connecting sac and immediate draining vein
beyond the embolization device in the distal segment of the feeding
artery, with no enhancement
J. S. Pollak
Fig. 22.10 A previously coil-embolized right middle lobe PAVM had
reperfusion through pulmonary artery collateral ow from two adjacent
subsegmental branches, one of which is shown here (arrow)
Fig. 22.9 A 51-year-old woman with a sporadic isolated right lower
lobe PAVM had a transient ischemic attack 16years following her rst
embolization session in which the coils were relatively loosely placed
and are now recanalized (arrow). Further embolization was performed
(not shown)
embolization (Fig.22.9). Reported recanalization rates for
AVPs are lower than for coils, ranging from 0% to 7%; one
retrospective comparison showed no recanalizations in
Key Point
Four mechanisms for reperfusion after embolization:
1. Recanalization
2. Pulmonary artery collateral formation to the feeding
artery or aneurysm sac
3. Missed or enlarged accessory feeding artery
4. Systemic collateral reperfusion, typically bronchial
arteries
PAVMs treated solely with AVPs compared to 19% with
coils [41, 53–59]. Pulmonary-to-pulmonary arterial collaterals arising from adjacent subsegmental branches and reconstituting the feeding artery beyond the site of occlusion or the
sac itself may occur in up to 24% and can be more difcult
to retreat (Fig.22.10). A missed or enlarged accessory feeding artery (up to 15%) is usually readily treated. These three
aforementioned mechanisms maintain right-to-left shunting
and can place the patient at risk for adverse effects of this.
The fourth mechanism is systemic collateral reperfusion
(reported in 0–32%) primarily from bronchial arteries, which
leads to a left-to-left shunt that may uncommonly place the
patient at higher risk for hemoptysis given the PAVM exposure
to systemic pressure.
22 Pulmonary Angiography: Arteriovenous Malformation andPseudoaneurysm
The How To: Pseudoaneurysm
1. The same basic steps 1–6 are followed as for embolization a PAVM.
2. For peripheral pseudoaneurysms where the subseg-
lization of the artery across the entire origin of the
lesion is most reliable for a durable occlusion
22.11). If just the supplying pulmonary artery
embolization is being considered, the presence of
to be excluded as these could then supply the lesion
temic-to-pulmonary collaterals, particularly in the
setting of an infectious etiology, and can even result
in nonvisualization of the pseudoaneurysm on pulmonary angiography [61]. If the catheter cannot be
advanced beyond the pseudoaneurysm, occlusion
Fig. 22.11 The left upper lobe pseudoaneurysm depicted in Fig.22.5
was occluded using a microcatheter to enter its sac and deliver polyvinyl alcohol particles to treat its outow followed by detachable coils in
the sac and feeding artery
using an embolization agent that is carried by blood
255
a mechanical agent in the feeding artery, starting in
the aneurysm. Additionally, systemic angiography
and embolization of the culprit systemic supplying
vessel can be done.
3. Isolated endoaneurysmal embolization with coils
has been described where coils are only placed
within the aneurysmal sac [36, 60]. This may be a
higher consideration for more central pseudoaneurysms where preservation of the parent artery is
more important.
4. Placement of a stent graft across the origin of the
pseudoaneurysm has also been described [36, 60],
again more valuable when the parent artery needs to
be preserved.
Complications related to the embolization procedure for
pseudoaneurysm appear quite rare [36, 60]. Hemoptysis
afterward may occur from incomplete occlusion, including
possibly systemic collateral supply, additional pseudoaneurysms, or other pathology. Contrast-enhanced CT or CTA is
valuable for reassessing patients.
Pulmonary Artery Pseudoaneurysm
All pseudoaneurysms should be considered for interventional
therapy, especially those who have already had hemoptysis.
The limited data on this condition demonstrates a high degree
of success in the immediate control of bleeding, with recurrences generally related to development of other lesions or
bronchial artery sources [36, 60]. Pre-procedural preparation
of pulmonary pseudoaneurysm is the same as for PAVM.
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Lymphatic Interventions
GregoryJ.Nadolski II andMaximItkin
Pathophysiology
Thoracic lymphatic interventions are performed to treat the
accumulation of lymphatic or chylous uid in the pleural or
pericardial space. The source of these leaks can generally be
categorized as traumatic or non-traumatic in etiology.
Iatrogenic injury of the thoracic duct (TD) or its branches
during thoracic, cardiac, or cervical neck surgery is the main
cause of traumatic chylothorax, while the remainder are
caused by blunt or penetrating trauma to the chest (Fig.23.1).
Traumatic chylothoraces account for 80% of all lymphatic
leaks in the chest, and the incidence of these injuries has
been reported to occur in up to 4% of all thoracic surgeries
[1]. The etiologies of the non-traumatic chylothorax include
idiopathic, malignancy, congenital lymphatic anomalies
(e.g., Gorham’s disease), systemic diseases (e.g., SLE,
Behçet’s disease), and infection (e.g., tuberculosis) [2].
Idiopathic effusions and lymphoma are responsible for the
majority of cases of non-traumatic chylothorax [2, 3]. In
malignant effusions, the tumorous compression of posterior
mediastinal or retroperitoneal lymph nodes can either (1)
cause obstruction of lymphatic ow resulting in high pressure of the small lymphatic channels causing spontaneous
rupture or (2) directly erode into these small lymphatic channels
leading to leakage.
23
Fig. 23.1 Traumatic chylothorax.Traumatic chylothorax following left
upper lobectomy for non-small cell lung cancer with contrast leaking
from injury to the main thoracic duct (black arrowhead). This was successfully treated with platinum-based coils (white arrow) and n-butyl
cyanoacrylate glue (white arrowhead) below the level of the leak
Key Point
Causes of chylothorax:
• Iatrogenic
• Chest trauma
• Malignancy (lymphoma most common)
G. J. Nadolski II · M. Itkin (*)
Perelman School of Medicine of the University of Pennsylvania,
Diagnostic Imaging, Philadelphia, PA, USA
e-mail: Gregory.nadolski@uphs.upenn.edu;
maxim.itkin@uphs.upenn.edu
© Springer International Publishing AG, part of Springer Nature 2018
N. A. Keefe et al. (eds.), IR Playbook, https://doi.org/10.1007/978-3-319-71300-7_23
• Congenital lymphatic anomalies
• Systemic disease
• Infection
• Idiopathic
259
260
G. J. Nadolski II and M. Itkin
Fig. 23.2 Non-traumatic chylothorax in a patient with lymphoma.
Non-traumatic chylothorax in a patient with lymphoma involving the
mediastinum with leak from small lymphatic branches adjacent to
the thoracic duct (white arrow) and from lymphatic branches along the
distal thoracic duct surrounding the aortic arch (black arrow)
Lymphatic anomalies, primarily resulting in abnormal
lymphatic channels or masses, such as Gorham’s disease
(GSD), generalized lymphatic anomaly (GLA), kaposiform
lymphangiomatosis (KLA), and lymphangiomatosis (LM),
may present with chylothorax [2]. The mechanism of leak in
this population can be variable. Leaks may originate from
retroperitoneal lymphatic masses or malformations that
extend into the mediastinum. These masses or malformations appear to generate a large amount of lymphatic uid,
which can cause seeping from or rupture of lymphatic ducts.
Similar to malignancy, these masses may obstruct the normal
pattern of lymphatic ow resulting in the spontaneous leak
of chyle from small lymphatic channels (Fig.23.2).
Lastly, lymphatic conduction disorders are a group of
poorly understood conditions in which the normal unidirectional pattern of lymphatic ow toward the central venous
system is disrupted or reversed, resulting in abnormal pulmonary lymphatic ow from the thoracic duct toward lung
parenchyma, a phenomenon that has been termed pulmonary
lymphatic perfusion syndrome (PLPS) [4]. PLPS can present
as neonatal chylothorax, idiopathic chylothorax, or plastic
bronchitis (Fig.23.3) [5]. The etiology of PLPS is not well
understood but is thought to be the result of congenital
abnormal formation of thoracic lymphatic ducts or their
valves. PLPS may not present clinically until a secondary
Fig. 23.3 Plastic bronchitis. Lymphangiogram of a patient with plastic
bronchitis demonstrating multiple lymphatic branches surrounding and
leaking into the bilateral main and lobar bronchi (black arrowheads)
arising from the main thoracic duct (white arrow)
insult results in increased lymphatic volume or ow such as
heart failure, cirrhosis, or other conditions that may damage
the malformed ducts such as mild accidental blunt trauma or
severe upper respiratory infection [6].
Clinical Indication
In general, the diagnosis of a chylothorax is made by the
presence of milky-colored uid after thoracentesis or surgery
with laboratory analysis of the uid revealing a triglyceride
count above 200 mg/dL in patients on regular diet.
Additionally, the presence of chylomicrons is traditionally
considered to be the gold standard for diagnosis of chylous
effusion [7] Lastly, a cell count and differential demonstrating uid rich in lymphocytes (>70%) support the diagnosis
of chylous leak although no agreed upon threshold exists in
the literature [8].
Key Point
Chylothorax, milky-colored uid with a triglyceride
count >200mg/dL, high lymphocyte count and presence
of chylomicrons.
23 Lymphatic Interventions
261
Indications for intervention to treat a thoracic chylous
effusion typically are persistent symptoms (cough, shortness
of breath, hypoxia) or high drainage output despite conservative management. Most patients with >500 mL/day will
require treatment although no absolute output volume has
been established for when to intervene on a chylothorax [9].
Conventional Therapy
Conservative management of chylous leaks consists of chest
tube drainage, diet modication (low-fat diet, NPO, and/or
total parenteral nutrition), and intravenous infusion of
octreotide [3]. Conservative management can fail in up to
70% of cases [10].
Key Point
First-line treatment for chyle leak is conservative
management. This is followed by thoracic duct embo-
lization and/or surgery if unsuccessful.
Historically prior to the development of percutaneous
thoracic duct embolization, surgical management of chylous
effusions with thoracic duct (TD) ligation and pleurodesis
was performed for cases failing conservative management.
The reported success rates of surgical thoracic duct ligation
vary depending on inclusion criteria and surgical technique
but can be as low as 67% [11].
Given the invasive nature of open TD ligation and the fact
it often would be performed in patients who have had recent
or prior thoracotomy, percutaneous thoracic duct embolization (TDE) has become the primary treatment of traumatic
chylothorax as opposed to open or thoracoscopic thoracic duct
ligation. Additionally, with its capability to identify the location of the chyle leak and variation in thoracic duct anatomy,
TDE is a more appropriate intervention for non- traumatic
chylothoraces and plastic bronchitis [12].
Interventional Therapy
Pedal Lymphangiography (PL)
Traditional pedal lymphangiography (PL) is both timeconsuming and technically challenging and requires specialized equipment, which may not be readily or commercially
available. Briey, to opacify the pedal lymphatic vessels and
facilitate lymphatic vessel dissection, isosulfan blue 1%
(Lymphazurin, US Surgical, Norwalk, CT) mixed with
lidocaine 1% is injected into the dermis in the web spaces
between the toes. The blue color delineates the lymphatic
vessels of the foot. After several minutes, through a small
horizontal incision on the dorsum of the foot, a lymphatic
duct is dissected and cannulated using a 30-gauge needle.
The procedure is repeated on the other foot, and then
ethiodized oil is injected through the needles using a dedicated lymphangiogram pump (Cordis, Johnson and Johnson,
Miami Lakes, FL). Typically, up to a total of 20 mL of
ethiodized oil is used (i.e., 10mL per leg). At the completion
of the contrast injection, 20mL of normal saline is injected
using the lymphatic pump to propel the contrast into the pelvic
and abdominal lymphatics ultimately opacifying the cisterna
chyli and thoracic duct [2, 13].
Intranodal Lymphangiography (IL)
Intranodal lymphangiography (IL) has been described for
the use in TDE and is a less technically challenging alternative to the conventional pedal lymphangiography [14].
Key Point
• Pedal lymphangiography– access a lymphatic duct
on the dorsum of the foot.
• Intranodal lymphangiography – access a lymph
node, typically in the medial thigh.
• IL is faster and less invasive than PL.
Using real-time ultrasound guidance, bilateral inguinal
lymph nodes are accessed with a 25-gauge spinal needle. To
minimize needle movement, the needle is preassembled
prior to nodal access as follows: the stylet is removed, and
the needle is attached to a 3-mL syringe using the short
extension tubing used for an IV angiocatheter and ushed
with oil-based contrast. The needle tip is positioned in the
transitional zone between the cortex and hilum of the lymph
node using a shallow angle to create a relatively long subcutaneous tract to assist in stabilizing the needle.
Under uoroscopic guidance, contrast is injected by hand
at a rate of about 0.1mL per minute (Fig.23.4). If an efferent
lymphatic and/or lymph node is identied under uoroscopy
to conrm proper positioning of the needle, the syringe can
be removed, and further injection of contrast can be performed using an angioplasty balloon ination device preloaded with 10mL of ethiodol. The ination handle can be
tightened to administer a pressure of around 3 mmHg to
propagate the contrast into the lymphatic system. A total volume of approximately 6–12mL of Lipiodol can be injected
into each lymph node. Infusion of contrast is terminated
once the contrast opacies the lymphatics at approximately
the L3 level as the typical location of the largest abdominal