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262
G. J. Nadolski II and M. Itkin
Fig. 23.4 Intranodal lymphangiogram. (a) Schematic of intranodal
access depicting needle puncture of a supercial inguinal lymph node
in the upper medial thigh which then communicates to the lymph nodes
along the femoral artery. (b) Fluoroscopic image of bilateral inguinal
lymphatics leading into the cisterna chyli is between L1 and
L3. If at the end of the contrast injection the cisterna chyli or
upper abdominal lymphatic for access is not visualized, the
initial bolus of contrast can be followed by injection of normal saline at 1mL per 1min to facilitate propagation of the
contrast [8, 14]. Injection of Lipiodol should be limited to
20mL to minimize the risk of Lipiodol-induced pneumonitis. The injection of saline into the lymph nodes can be preceded by injection of 1mL of 1% lidocaine to anesthetize
the node.
Key Point
The largest abdominal lymphatics leading into the
cisterna chyli occur at the L3 level.
Dynamic Contrast Enhanced MR Lymphangiography (DCMRL)
lymphangiograms demonstrating needle placement within supercial
inguinal lymph nodes in the bilateral upper medial thigh (black arrows)
with contrast lling the lymphatic channels and lymph nodes along the
femoral and iliac chains (black arrowheads)
this chapter but involve the injection of gadolinium-based
contrast into the inguinal lymph nodes followed by imaging
with using a 4D MRA protocol in the coronal plane (Fig.23.5).
The acquisition and interpretation of DCMRL can be found in
greater detail elsewhere [5, 15, 16].
Thoracic Duct Embolization
The technique of TDE has been previously described in
detail [17].
Key Point
The most common symptoms following TDE:
• Diarrhea
• Lower extremity swelling
Given the high degree of variability in mechanisms and etiology of non-traumatic leaks, the treatment of these disorders is
more challenging than traumatic leaks. Consequently, a thorough understanding of the underlying lymphatic anatomy,
ow patterns, and possible leak source with imaging is often
essential for planning an intervention [8]. Pre- intervention
assessment of the lymphatic system can be performed with
DCMRL.The details of this technique are beyond the scope of
The How To
1. Intranodal lymphangiography is performed to identify upper abdominal lymphatics or cisterna chyli
23.6, 23.7, and 23.8).
2. The lymphatic system is accessed transabdominally
with a 21 or 22G needle. To prevent the possible
leakage of the chyle from cisterna chyli, access to
(continued)
23 Lymphatic Interventions
263
Fig. 23.5 Dynamic contrast MR lymphangiography. (a) Normal
DCMRL appearance of the thoracic duct (white arrow). (b) Abnormal
perfusion of the left lung (black arrow) in patient with plastic bronchitis.
Fig. 23.6 A 25G spinal needle (white arrow) is inserted under ultra-
sound guidance until needle tip is in the hilum of the lymph node (white
asterisk)
the lymphatic system should be attempted into the
cysterna’s contributing lymphatic vessels just below
23.9).
3. A stiff 0.018″
MA) is advanced through the needle into the TD
23.10).
4. The needle is removed and exchanged for a 3F
microcatheter. Most typically a short microcatheter
(c) Bilateral lung perfusion (white arrowheads) on DCMRL in the setting of plastic bronchitis
5. Nonionic iodinated contrast is then injected
through the catheter to demonstrate the cause of
the chylous effusion. In traumatic chylothoraces,
the cause of the leak is most often a tear of the
thoracic duct or leakage from a TD branch/collateral which courses through the recent operative
races, frequently the cause of the chylothorax is the
occlusion of the upper part of the thoracic duct
23.11).
6. If the TD appears to be normal and there is unob-
the TD should not be embolized. In these cases,
alternative sites/causes of chylothorax, such as chylous ascites or pleural-based lymphatic malformations, must be considered [2].
7.
embolization of the thoracic duct is performed
below the leak point or abnormality. If the leak is
eterization of the branch can be attempted although
this is not necessary.
8. Embolization is performed using a combination of
coils and n-butyl cyanoacrylate (N-BCA) glue
contain platelets, concentrated glue (1:1 dilution with
Lipiodol) is typically used, and the coils are used to
provide scaffolding to aid in glue polymerization. If
the leak is suspected to be from multiple small col-
used so a standard length 0.018″ wire can be used.
may be attempted (Figs. 23.12 and 23.13).
264
Fig. 23.7 Lipiodol is injected under uoroscopy to conrm proper
positioning of the needle as indicated by rapid lling of the efferent
lymphatics (white arrow) arising from the accessed lymph node
G. J. Nadolski II and M. Itkin
Fig. 23.8 Once proper needle position is conrmed, diagnostic
lymphangiogram is performed by continuing Lipiodol injection
Fig. 23.9 (a) An upper abdominal lymphatic (white arrow) below the cisterna chyli is selected for transabdominal access. (b) The target lymphatic
is marked with a clamp prior to access. (c) Relative relationship between target lymphatic (white arrow) and cisterna chyli (black arrow)
23 Lymphatic Interventions
Fig. 23.10 A guide wire is advanced through the target lymphatic and
cisterna chyli (black arrow) and into the lower segment of the thoracic
duct (white arrow)
265
Fig. 23.12 Coil deployed (white arrow) immediately inferior to the
site of leak
Fig. 23.11 Contrast injection from a catheter positioned in the cisterna
chyli (black arrow) demonstrates a partially duplicated lower segment
of the thoracic duct (white arrow) and disruption of the mid-thoracic
duct with extravasation of contrast (white asterisk)
Fig. 23.13 Fluoroscopic demonstrating glue cast within the thoracic
duct extending from the level of the leak (white arrow) to superior to the
cisterna chyli (black arrow)
266
Key Point
Traumatic/iatrogenic chylothorax – leak is due to a
tear of thoracic duct or leakage from TD branch or
collateral
Non-traumatic chylothorax – occlusion of upper
TD causes retrograde ow into the pleural space
After thoracic duct embolization, the patient should remain
NPO overnight and receive a daily chest x-ray. Once the
chest tube output decreases below 200mL/day and the chest
x-ray shows resolving effusion, the diet should be advanced
to include fat. If chest tube output remains unchanged in volume and consistency after the introduction of fat, the chest
tube can be removed. If the chest tube output increases or
consistency changes, the uid should be sent for triglycerides and cell count to conrm persistence of the chylothorax
before repeating the TDE.
In cases where TD catheterization is technically unsuccessful, TD needle disruption can be performed as previously
described [18, 19]. Using this technique, the retroperitoneal
lymphatics are disrupted using a “twiddling motion with the
needle” [18]. The theory of how needle disruption works is
traumatic disruption of the lymphatic vessels results in controlled venous bleeding into the lymphatic vessels with subsequent formation of blood clots and/or local inammation,
which close the leak [18].
Key Point
If TD catheterization is unsuccessful, TD needle disruption has been proven to be benecial to disrupt the
retroperitoneal lymphatics.
Embolization ofLymphatic Masses
In cases of leakage of chyle from a retroperitoneal or mediastinal mass, which consists of multiple small intervening
vessels, catheterization of the TD may not be possible or is
not necessary as the source of leak does not arise from the
TD. In these cases the embolization material (N-BCA glue)
can be injected into the mass through the needle positioned
under uoroscopic guidance [20].
In the initial series of TDE using PL for treating traumatic
chylous effusions, 73 of 109 thoracic ducts were successfully catheterized (67%) [19]. Of those, 71 patients underwent TDE with endovascular coils and/or glue; the leak
resolved in 90% of these patients (N=64). Needle interruption
of the thoracic duct below the diaphragm was successful in
G. J. Nadolski II and M. Itkin
72% of attempted cases where TD catheterization was
unsuccessful. Overall success on an intent-to-treat basis of
the entire series of patients was 71% (N = 77). In the 20
patients in the study who had failed previous surgical ligation, embolization or interruption was attempted in 17 and
successful in 15 (88%) demonstrating the utility of TDE
after failed surgical intervention.
More recently, studies have compared IL to PL for TDE
to treat traumatic chylothorax [21]. Thoracic duct cannulation on rst attempt was successful in 82% (n=73/89) of PL
and 84% (n = 71/89) of IL patients (p= 0.65). The mean
procedure time was signicantly shorter for IL than for PL,
128.5min and 198.2min, respectively (p<0.0001). Clinical
success on an intention to treat basis was achieved in 82% of
PL and 88% of IL patients (p=0.18).
In general, the clinical success of treating non-traumatic
chylothorax is not as high as traumatic leaks largely due to
difculty in identifying the site of leak. The largest published series on treating adults with non-traumatic chylothorax was published prior to the advent of intranodal
lymphangiography and DCMRL and only included 34
patients [2]. In this series, TD catheterization via PL was
performed in only 70% of cases with the location of leak
identied in only 65% of patients. Overall, the intention to
treat cure rate was 53% (N=18 of 34). In the group in which
the TDE was technically successful (N=24), the cure rate
was 68% (N=16).
As the main challenge in treating non-traumatic chylothorax is identifying the cause and site of the chyle leak, the
poorer results in this series likely reect early experience
with TDE for non-traumatic chylothorax and inadequate
imaging from that time period. Although the intention to
treat success rate was only 52% in this study, the result compared favorably with a previous study by Maldonado et al.,
who reported an overall success rate of 27% using a combined approach of conservative and surgical management for
non-traumatic chylothorax [22]. Lastly, when the site of leak
could be identied, the technical success rate increased to
67%. Future studies using the current algorithm for managing non-traumatic chylothorax with current imaging
techniques will likely demonstrate an improved success rate
similar that see [23].
Plastic Bronchitis
The literature investigating embolization of the thoracic duct
for plastic bronchitis is less robust but none the less very
promising. In the initial case series, seven adults who presented with expectoration of branching bronchial casts were
evaluated by lymphatic imaging with DCMRL [6].
Subsequently, all patients underwent bilateral intranodal
lymphangiography and thoracic duct cannulation. In six of
23 Lymphatic Interventions
267
the seven patients, DCMRL demonstrated the presence of
abnormal pulmonary lymphatic ow which was conrmed
on TD cannulation to represent lymphatic reux or communication with abnormal lymphatic channels with airways.
In cases where abnormal pulmonary lymphatic ow was
demonstrated, embolization of pulmonary lymphatics was
performed. After lymphatic embolization using a combination of endovascular glue and coils, ve patients reported
immediate and complete resolution of the symptoms, and
one patient reported partial, but signicant, improvement.
Key Point
Plastic bronchitis– lymphatic ow disorder leading to
lymph accumulation in the airways resulting in cast
formation within the bronchi and respiratory issues
References
1. McGrath EE, Blades Z, Anderson PB. Chylothorax: aetiology,
diagnosis and therapeutic options. Respir Med. 2010;104(1):1–8.
2. Nadolski GJ, Itkin M. Thoracic duct embolization (TDE) for
nontraumatic chylous effusion: experience in 34 patients. Chest.
2013;143(1):158–63.
3. Valentine VG, Rafn TA.The management of chylothorax. Chest.
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4. Itkin M.Interventional treatment of pulmonary lymphatic anomalies. Tech Vasc Interv Radiol. 2016;19(4):299–304.
5. Dori Y, Dori Y, Keller MS, Keller MS, Rychik J, Rychik J, Itkin
M, Itkin M. Successful treatment of plastic bronchitis by selective lymphatic embolization in a Fontan patient. Pediatrics.
2014;134(2):e590–5.
6. Itkin MG, McCormack FX, Dori Y. Diagnosis and treatment of
lymphatic plastic bronchitis in adults using advanced lymphatic
imaging and percutaneous embolization. Ann AmThorac Soc.
2016;13(10):1689–96.
7. Seriff NS, Cohen ML, Samuel P, Schulster PL.Chylothorax: diagnosis by lipoprotein electrophoresis of serum and pleural uid.
Thorax. 1977;32(1):98–100.
8. Nadolski G, Itkin M.Thoracic duct embolization for the management of chylothoraces. Curr Opin Pulm Med. 2013;19(4):1–386.
9. Stecker MS, Fan C-M.Lymphangiography for thoracic duct interventions. Tech Vasc Interv Radiol. 2016;19(4):277–85.
10. Cerfolio RJ, Allen MS, Deschamps C, Trastek VF, Pairolero
PC. Postoperative chylothorax. J Thorac Cardiovasc Surg.
1996;112(5):1361–5. discussion 1365–6.
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2016;49(1):18–24.
12. Kerlan RK, LaBerge JM. Intranodal lymphangiography: coming
soon to a hospital near you. JVasc Interv Radiol. 2012;23(5):617.
13. Cope C, Salem R, Kaiser LR.Management of chylothorax by percutaneous catheterization and embolization of the thoracic duct:
prospective trial. JVasc Interv Radiol. 1999;10(9):1248–54.
14. Nadolski GJ, Itkin M. Feasibility of ultrasound-guided intranodal lymphangiogram for thoracic duct embolization. JVasc Interv
Radiol. 2012;23(5):613–6.
15. Dori Y, Zviman MM, Itkin M, Dynamic Contrast-enhanced
MR. Lymphangiography: feasibility study in swine. Radiology.
2014;273(2):410–6.
16. Krishnamurthy R, Hernandez A, Kavuk S, Annam A, Pimpalwar
S. Imaging the central conducting lymphatics: initial experience with dynamic MR lymphangiography. Radiology.
2015;274(3):871–8.
17. Chen E, Itkin M. Thoracic duct embolization for chylous leaks.
Semin Interv Radiol. 2011;28(1):63–74.
18. Cope C, Kaiser LR. Management of unremitting chylothorax by percutaneous embolization and blockage of retroperitoneal lymphatic vessels in 42 patients. J Vasc Interv Radiol.
2002;13(11):1139–48.
19. Itkin M, Kucharczuk JC, Kwak A, Trerotola SO, Kaiser
LR.Nonoperative thoracic duct embolization for traumatic thoracic
duct leak: experience in 109 patients. JThorac Cardiovasc Surg.
2010;139(3):584–90.
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2016;27:1177–86.
21. Kozlov A, Itkin M, Dori Y, Nadolski G. Comparison of pedal
and intranodal lymphangiography for thoracic duct embolization (TDE) of traumatic chylous leaks. J Vasc Interv Radiol.
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Part VI
Abdominal/Pelvic Arterial Interventions
Mesenteric Ischemia
AndrewChi andJamesR.Stone
Pathophysiology
Acute Mesenteric Ischemia
Acute mesenteric ischemia (AMI) is a serious and lifethreatening condition. Common etiologies include mesenteric arterial embolus (embolic AMI), mesenteric arterial
thrombosis (thrombotic AMI), mesenteric and/or portal
venous thrombosis, and nonocclusive mesenteric ischemia
(NOMI). Less common etiologies include vasculitides,
trauma, aortic dissection, volvulus, intussusception, hernia,
adhesions, drugs (cocaine), cholesterol emboli, and intestinal obstruction [1, 2]. Risk factors are multifactorial and
include prothrombotic and embolic states (Table 24.1).
When bowel infarction is present, mortality rates increase
signicantly and can approach 90% [4]. Thus, early diagnosis and aggressive treatment are important goals in order to
prevent bowel infarction and death.
24
The classic clinical presentation of acute mesenteric ischemia is abrupt onset of severe abdominal pain that is out of
proportion to the physical exam (Table 24.2). Patients may
have diarrhea, hematochezia, vomiting, bloating, hypotension, shock, and/or sepsis. Laboratory ndings may include
leukocytosis, elevated liver enzymes, and lactic acidosis (a
late nding). Physical examination ndings of an acute
abdomen accompanied by metabolic acidosis should raise
clinical suspicion for bowel ischemia until proven otherwise
[5]. An acute abdomen should prompt urgent or emergent
management to elucidate the etiology of these ndings and
provide denitive management.
Key Point
Classic physical exam nding of mesenteric ischemia:
abdominal pain out of proportion to physical exam.
Chronic Mesenteric Ischemia
Chronic mesenteric ischemia (CMI) is relatively rare due to
Key Point
Four main causes of acute mesenteric ischemia:
• Embolic
• Thrombotic
• Venous
• Nonocclusive (NOMI)
A. Chi
University of Colorado, Department of Radiology,
Denver, CO, USA
J. R. Stone (
University of Virginia Health System, Department of Radiology
and Medical Imaging, Charlottesville, VA, USA
e-mail: jrs7r@virginia.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_24
*)
the inherently rich collateral intestinal circulation.
Historically, it was believed that at least two of the three primary mesenteric arteries are needed to be compromised for
symptoms to occur. However, there is increased recognition
that symptoms may result if any of the main mesenteric
arteries are compromised [6], particularly in the setting of
prior abdominal surgery and/or inadequate collateral ow
between mesenteric arterial segments.
The most common cause of CMI is atherosclerotic disease resulting in ostial narrowing of mesenteric arterial vessels, often accompanied by post-stenotic dilation. In contrast
to most other atherosclerotic diseases, CMI is seen more
often in females [7]. Although the cause of this gender difference remains unclear, mesenteric vessels in females are
known to arise at a more acute angle with respect to the aorta
than males [8]. Whether this anatomic difference results in
271
272
A. Chi and J. R. Stone
Table 24.1 Risk factors for acute mesenteric ischemia [3, 6]
Risk factors for acute mesenteric ischemia
Atrial brillation Prior myocardial infarction
Atherosclerosis Prior embolic event
Chronic mesenteric
ischemia
Connective tissue disorder Abdominal inammatory disease
Portal hypertension Prior portal venous system intervention
Oral contraceptives Meds (vasopressors, dopamine,
Table 24.2 Symptoms of acute and chronic mesenteric ischemia
Symptoms of acute mesenteric ischemia
Acute, severe abdominal pain out of proportion to physical exam
Hematochezia, diarrhea Postprandial pain
Nausea, vomiting, bloating Hypotension,
Symptoms of chronic mesenteric ischemia
Postprandial pain (intestinal angina) out of proportion to physical
exam shortly after eating, lasting for 1–2h
Food fear or aversion Weight loss
Nausea, vomiting Diarrhea
Hypercoagulable state
digoxin)
(intestinal angina)
shock, sepsis
increased susceptibility in females to ostial mesenteric
vascular disease remains unknown. Other causes of chronic
mesenteric ischemia include bromuscular dysplasia, vasculitides, and intimal hyperplasia [6]. Risk factors for CMI
include smoking, peripheral vascular disease, and coronary
artery disease [9].
The typical presentation of CMI is postprandial pain out
of proportion to physical exam for 1–2 h duration (see
Table 24.2). This “intestinal angina” is due to insufcient
mesenteric blood ow during periods of heightened demand
after food intake [6]. The association of food with pain may
lead to a fear of food and weight loss leading to a chronic
malnourished state [5]. Differential considerations of postprandial pain and weight loss should also include functional
bowel disorders, atrophic gastritis, gallbladder disease,
chronic pancreatitis, hernias, abdominal adhesions, median
arcuate ligament compression syndrome, and malignancy [7,
11]. Patients may exhibit nonspecic gastrointestinal symp-
toms such as nausea, diarrhea, and vomiting.
and can reveal critical stenoses or occlusions of the mesenteric arteries or thrombosis of the mesenteric veins while
also providing information concerning the presence of bowel
ischemia or infarction. Furthermore, CTA can identify mucosal edema, ileus, abdominal aortic aneurysm, aortic dissection, or internal hernias. However, CTA is of limited utility in
detecting small emboli or subtle vasculitides. It may be contraindicated in patients with acute kidney injury or chronic
renal insufciency, particularly when estimated glomerular
ltration rate (eGFR) is <30.
Magnetic resonance angiography (MRA) can provide
insight into the etiology of AMI, though it is considered less
useful than CTA due to its limited ability to evaluate bowel
integrity, inferior spatial resolution, required length of MRI
exam, and greater demands for monitoring an ill patient deep
within the magnet bore. Similar to CTA, MR gadolinium
contrast may be contraindicated in the setting of severe renal
insufciency (eGFR <30) due to concern for developing
nephrogenic systemic brosis (NSF) [14, 15].
Plain radiographs of the abdomen may demonstrate
bowel wall thickening (thumbprinting), bowel dilation,
intramural gas (pneumatosis), portal venous gas, or pneumoperitoneum, all of which are secondary signs of endorgan damage from ischemia. When obtained early in the
course of the disease, radiographs may appear normal before
bowel ischemia occurs.
The gold standard for diagnosis is catheter-based digital
subtraction angiography (DSA). It offers superior resolution,
high diagnostic accuracy for both large and small vessel disease, and the ability to dynamically follow a contrast bolus
from arterial through venous phases, obtain intravascular
pressure measurements to determine functional signicance
of a given vascular lesion, and use alternative contrast agents
such as CO2 for patients with poor renal function or severe
contrast dye allergies. This approach may be used for clarication of equivocal noninvasive imaging ndings and the
possibility of immediate endovascular therapy or presurgical
planning. Today, the signicant advances in CT technology
have moved DSA to the setting of endovascular intervention
or assessment of equivocal CT ndings.
Clinical Indication
Acute Mesenteric Ischemia
Physical examination ndings may range from benign to
abdominal guarding, rigidity, and rebound tenderness if
bowel infarction is present. CT angiography (CTA) is the
most commonly performed imaging study for evaluation of
mesenteric ischemia [12, 13]. CTA may be obtained quickly
Key Point
Digital subtraction angiography is the gold standard
for diagnosis of mesenteric ischemia although CTA is
performed frequently as the rst step.
Arterial Occlusive Disease
Acute arterial occlusion of the mesenteric vessels due to
embolization of remote thrombus or plaque is seen in
40–50% of AMI cases. Approximately 33% of individuals
24 Mesenteric Ischemia
273
Fig. 24.1 An 87-year-old male with paroxysmal atrial brillation with
sudden onset acute abdominal pain and elevated lactate concerning for
acute mesenteric ischemia. CTA demonstrates lling defect (arrowheads) consistent with thrombus located several cm distal to the SMA
ostium without signicant proximal atherosclerotic disease, consistent
with embolic AMI have had a history of prior arterial
embolization. Emboli most commonly originate from the
heart and are associated with cardiac arrhythmias such as
atrial brillation or prior myocardial infarction. Imaging
typically demonstrates an intravascular lling defect 3cm
distal to the SMA origin (Fig. 24.1), minimal collateral
vessels, and poor distal perfusion. In the setting of embolic
AMI, imaging of the heart with echocardiogram and/or
CTA should be obtained and reviewed to ensure that the
heart is free of thrombus. In about 20% of cases, mesenteric arterial embolization from a cardiac source will be
accompanied by peripheral arterial embolus; identifying
another affected vessel can provide conrmation of the
embolic etiology.
with embolic mesenteric occlusion (a). Selective angiography demonstrates occlusion of the SMA (arrow) without appreciable reconstitution of the vessel (b). Pharmacomechanical thrombectomy was
performed (c) with subsequent clearance of thrombus within the main
trunk of the SMA (d)
Key Point
An SMA embolism distal to the middle colic artery
carries the highest risk of intestinal ischemia, as there
are few native distal collaterals. The middle colic
artery connects with the IMA via the marginal artery
of Drummond and the arc of Riolan.
In situ thrombosis occurs in roughly 25% of cases of acute
mesenteric ischemia. Patients typically have underlying atherosclerotic disease. Up to half may report postprandial pain
or other symptoms of intestinal angina. In contrast to acute
thrombotic mesenteric ischemia, patients with chronic throm-