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17 May-Thurner Syndrome
https://t.me/med1917
Fig. 17.2 Digital subtraction angiographic image showing non opacication of left common iliac vein subsequent to the level of common iliac arterial crossing due to
venous thrombosis
Venography also helps in assessment of hemodynamic status of MTS through pressure gradient
measurements. Iliofemoral stenosis is considered
signicant with a measurement of >2mm Hg at rest
and more than 3mm Hg during strenuous work.
The main drawbacks of ascending venography
are that it is time-consuming and invasive and
cannot be performed in patients with widespread
iliofemoral DVT, and post-procedural complications such as phlebitis may occur [
17].
Venography also provides information toward
chronicity of lesion as well as variable congenital
features that may be associated, e.g., duplicated
or rudimentary venous system [21].
The accuracy of this technique can be further
improved by taking two or three projections during injection phase since in pancaked vein (i.e.,
externally compressed in anteroposterior plane),
it will not exhibit diameter narrowing in the AP
view [22]. It is equally effective to perform hand
injection venography through the access sheath
rather than using a power injector.
187
17.12 Intravascular Ultrasound
This modality can be used for diagnosis as well
as a valuable adjunct for treatment of MTS.It has
high sensitivity and specicity (>98%) [23]. It
helps in detecting the precise morphology of the
spur and thus can determine the severity and distribution of pathology. It is useful for determining vessel diameter, aiding stent placement, and
ensuring full stent expansion.
17.13 Treatment
The treatment of MTS depends on whether deep
vein thrombosis is present or not. If DVT is not present and patient is having mild symptoms, the treatment is conservative, and compression stockings are
sufcient enough in relieving the symptoms.
For advanced non-thrombotic MTS with
severe symptoms of chronic venous insufciency,
e.g., limb swelling, pain, and skin discoloration,
treatment is focused toward reducing the severity
of the stenotic venous lesion using angioplasty
and stenting the affected segment. Angioplasty if
done alone is associated with high recurrence
rates [24]. Recurrence rates in case of stenting
depends upon type of stent used [25].
If MTS is associated with venous thromboembolism, treatment is initiated with full therapeutic
anticoagulation unless contraindicated. Further
treatment requires decreasing the volume of
thrombus using catheter-directed thrombolysis or
pharmacomechanical thrombolysis. The underlying venous stenosis is evaluated, and if present,
angioplasty and stenting of the given iliocaval
segment are done.
With successful treatment, chances of postthrombotic syndrome get reduced to <10%, but if
no treatment is provided, the chances of occurrence
of postthrombotic syndrome go as high as 80–90%.
After successful intervention for symptomatic
MTS, the patient is prescribed to use knee or thigh
high compression stockings (30–40mm Hg).
Patients having DVT, after intervention, are
kept on therapeutic anticoagulation. The dosing,
monitoring, and duration of anticoagulation are
188
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S. Khanna and A. K. Khanna
as per VTE guidelines [26]. If stenting has been
performed and bleeding risk is low, then antiplatelet therapy is given [27]. If thrombolysis is
contraindicated, a common femoral venotomy is
performed to remove the thrombus [21]. If endovascular therapy fails, then open surgery is indicated [28].
The open surgery is done by dissection of the
iliac vein from the overlying iliac artery, open
thrombectomy, and possible patch angioplasty of
the left iliac vein and may need adjunctive procedures, such as an arteriovenous stula to enhance
ow in the diseased vein [24].
If iliac vein is occluded, then surgical options
include cross-femoral venous bypass (PalmaDale procedure) [29] and femorofemoral or
ileoileal prosthetic bypass, and femorocaval and
aortic elevation may be done [30].
To assist long-term patency of the bypass
grafts or reconstructed veins, an arteriovenous
stula is often created which is ligated after
6weeks.
Complications of endovascular therapy may
lead to jailing the contralateral common iliac vein
which can cause thrombosis, rupture of iliac vein,
migration or displacement of stent, and erosion
of stent into overlying artery.
17.14 Ecacy ofEndovenous
Therapy
With the development of minimally invasive
techniques and devices, the endovenous techniques have become treatment of choice in treating iliofemoral stenotic lesions and for decreasing
the long-term consequences of venous outow
obstructions [31]. Even in cases with challenging
anatomy, endovascular treatment has proved to
be safer and has higher patency rates in cases of
iliac vein stenosis [32].
It has been noted by reviewing of various studies that catheter-directed thrombolysis has shown
to have more thrombus resolution and reduced
risk for postthrombotic syndrome as compared to
the anticoagulation treatment alone.
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16. Labropoulos N, Borge M, Pierce K, Pappas
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25. Gloviczki P, Lawrence PF.Iliac vein stenting and contralateral deep vein thrombosis. J Vasc Surg Venous
Lymphat Disord. 2017;5:5.
26. Jaff MR, McMurtry MS, Archer SL, et al.
Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis,
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29. Palma EC, Esperon R.Vein transplants and grafts in
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30. Dale WA, Harris J. Cross-over vein grafts for iliac
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31. Binkert CA, Schoch E, Stuckmann G, etal. Treatment
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2000;11:823.
Nutcracker Syndrome
https://t.me/med1917
AjaySavlania andShivanesanPitchai
18
18.1 Introduction
Left renal vein (LRV) compression between the
superior mesenteric artery (SMA) and abdominal
aorta is referred to as the nutcracker phenomenon
(NCP) or LRV entrapment and was rst described
by anatomist Grant in 1937 [1]. Abdominal aorta
and superior mesenteric artery (SMA) act as two
arms of a ‘nutcracker’ that can potentially compress the left renal vein [2]. The term nutcracker
syndrome (NCS) is the clinical presentation of
this phenomenon which is assigned to those
patients who present with signs or symptoms of
left renal venous congestion and have the anatomical LRV compression [3]. De Schepper, a Belgian
physician named this phenomenon as ‘nutcracker
syndrome’ [4]. Anatomically classical anterior
nutcracker syndrome, in which there is compression of distal LRV between aorta and proximal
SMA, is analogous to superior mesenteric artery
syndrome (Wilkie’s syndrome) wherein the third
part of duodenum gets compressed anteriorly by
SMA and posteriorly by aorta [5–10]. The retroaortic or circumaortic renal vein may get compressed between the aorta and the vertebral body
causing symptom which is called posterior nut-
A. Savlania (*)
Postgraduate Institute of Medical Education and
Research, Trivandrum, India
S. Pitchai
Sree Chitra Tirunal Institute for Medical Sciences and
Technology, Trivandrum, India
cracker syndrome [11]. NCP on the right side, due
to compression of large veins by the gravid uterus,
has been also reported [12].
A case of concurrent anterior and posterior
NCS affecting circumaortic left renal vein (collar) where the anterior tributary of LRV compressed between the aorta and the SMA, while
the posterior tributary of LRV compressed
between the aorta and the vertebral column has
been described [13].
18.2 Anatomy inRelation
toNutcracker Compression
ofRenal Vein
The left-sided renal vein is 5–9 cm long and
2.5–3 times the length of the right renal vein. It
starts from the left renal hilum and receives tributaries of the left adrenal gland and left gonadal,
ureteral and sometimes lumbar veins before
draining into the inferior vena cava between T12
and L2 [14–16].
The angle of origin normally between the
superior mesenteric artery and the abdominal
aorta is approximately 90°. The left renal vein
(LRV) usually passes in front of the aorta through
the crotch formed by superior mesenteric artery
and the abdominal aorta. Superior mesenteric
artery origin from the aorta makes a unique conguration, so that SMA has a 4–5mm course in
the anterior direction before taking downward
© Springer Nature Singapore Pte Ltd. 2018
A. K. Khanna, R. Jindal (eds.), Venous Disorders, https://doi.org/10.1007/978-981-13-1108-6_18
191
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A. Savlania and S. Pitchai
direction thus forming conguration of an
inverted J. This distinctive anatomy prevents
compression of the left renal vein in the aortomesenteric window. In contrast, patients with
nutcracker syndrome have superior mesenteric
artery origin from aorta at angle less than 90°,
which makes aortomesenteric window narrow
due to steep descent of SMA from aorta leading
to compression of the LRV distally and left renal
vein hypertension proximally. This is termed as
anterior nutcracker syndrome [17]. The retroaortic left renal vein is an anatomical variant which
makes LRV susceptible to compression between
the aorta and the vertebral column leading to left
renal venous hypertension. This is termed as posterior nutcracker syndrome [18].
18.3 Pathophysiology
The anomalies of both superior mesenteric artery
and left renal vein have been implicated in causation of NCS.Anatomically critical factors in relation to the superior mesenteric artery include
acute angle associated with abnormally low or
anterolateral origin from the abdominal aorta.
Venous anatomical variants noted in cases of
NCS include retroaortic course of the left renal
vein or circumaortic left renal vein. Abnormal
dorsal ptosis of the left kidney with secondary
stretching of the left renal vein over the aorta and
high course of the left renal vein has also been
cited as possible factors which can contribute to
compression of LRV [19]. Excessive brotic tissue around the origin of the SMA can also contribute to the compression of the left renal vein
[20]. LRV compression is aggravated by the
standing position because of the weight of the
bowel and may be underestimated in imaging
carried out in the supine position (CT, MR angiography). Lower body mass index has been
shown to correlate with increased incidence of
NCP probably due to reduced retroperitoneal fat
which in turn reduces the angle between SMA
takeoff and aorta [13].
Venous compression induces LRV hypertension
and development of collateral pathways with variceal dilatation of tributaries, which causes the
symptoms. Beinart etal. described normal gradient
of pressure between LRV and inferior vena cava is
less than 1mmHg [21]. The gradient of pressure
between the LRV and inferior vena cava may
increase up to 3mmHg due to compression by the
SMA leading to rupture of thin-walled septum
between the small veins and the collecting system
in the renal fornix leading to haematuria [22]. It has
also been postulated that haematuria may be the
result of communication between dilated venous
sinuses and adjacent renal calices [23].
18.4 Clinical Features
Nutcracker syndrome occurs more commonly in
females, and age group affected ranges from
childhood to seventh decade, but most cases are
reported in second to fourth decades of their lives.
The most commonly reported symptom is haematuria and is due to elevated venous pressure
which leads to rupture of thin-walled varices into
the collecting system. It varies from micro- to
macro-haematuria, occasionally resulting in anaemia that may require blood transfusions [24, 25].
Abdominal or ank pain is the second most
common symptom, which may radiate to the posteromedial region of the thigh or gluteal region.
The pain can be exacerbated by sitting position,
standing position, walking or riding on a bicycle
[26, 27]. Flank pain due to left ureteric colic can
occur because of the passage of clots in the
ureter.
Left renal vein hypertension is the usual cause
of varicoceles [28]. The compression of LRV is
noticed in 50–100% of patients with varicocele,
although not every patient with varicocele will
have distended LRV [29, 30] . Varicosities in relation with distended LRV can be noticed around the
renal calyces, renal pelvis and ureter and sometimes at the gluteal or vulvar region [31, 32]. Large
variceal veins can be picked up on pelvic and
abdominal duplex or venography [33]. Symptoms
that changes with position change are hallmark of
NCS and should be correlated with duplex sonography [34–37]. Nutcracker phenomenon usually
becomes more prominent in standing than supine
positions because of visceral proptosis and acute
angulation of aortomesenteric angle (the angle
between the aorta and the SMA) [38].
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Orthostatic proteinuria is seen in some 14% of
patients where albumin in urine appears in standing position and minimal to no protein excretion
seen in supine position [39]. Nutcracker syndrome
has also been reported to be associated with
chronic fatigue syndrome in few patients [40].
Nutcracker syndrome with venous reux in
pelvic collaterals may lead to pelvic congestion.
This group of patients may have dysuria, dyspareunia, dysmenorrhoea, increased polycystic
changes in the ovaries and variations in venous
duplex waveform while performing Valsalva
manoeuver. Most patients have associated pelvic
varicoceles. Patients of pelvic congestion syndrome up to 10% were found to have nutcracker
syndrome. In some patients, gonadal vein ow
interruption improves symptoms, but gonadal
veins may act as main outow vessels, and so
their ow interruption may increase NCS symptoms [26, 30, 31].
It is not clear why some patients with NCP
which are incidentally detected on imaging, and
in cases with even ligated LRV [15], remain
asymptomatic, whereas others have symptoms.
18.5 Diagnosis
18.5.1 Duplex Scanning
193
Fig. 18.1 Ultrasonography of the upper abdomen in
transverse section showing the classical compression of
LRV in aortomesenteric window (white arrows), and size
of proximal LRV is almost ve times that of narrowed
portion
ciated pelvic congestion syndrome. Duplex scan
has sensitivity and specicity of 78% and 100%,
respectively, when ow reversal in the collateral
veins is included in the diagnostic criteria. In NCS
both distended and non-distended left renal vein
can exist, and even normal ow can also exist in
distended LRV.The ability to assess colour ow in
collateral veins also aids in diagnosis of the nutcracker syndrome [33].
Duplex assessment should be the rst choice for
evaluation, as it is a noninvasive modality. A
duplex scan (Fig.18.1) should be performed after
overnight fasting and bre-free diet on the previous day of imaging. The viscerorenal arteries bearing segment of abdominal aorta must be examined
via horizontal, sagittal sections, and most importantly LRV diameter and peak systolic velocity in
LRV should be measured in transverse section. In
nutcracker syndrome, left renal vein stenosis at the
aortomesenteric window is considered signicant
only if the diameter specically anteroposterior of
the LRV on the left side of the aorta is ve times
than that of stenotic region and if the peak systolic
velocity (PSV) at the stenotic segment is ve time
higher than the PSV measured at the hilum of the
left kidney [41] (Fig.18.1). The examiner should
also look for collateral pathways, particularly for
reux in the left gonadic vein in the cases of asso-
18.5.2 Computerised Tomographic
andMagnetic Resonance
Angiography
Computerised tomography angiogram is a noninvasive imaging modality, which offers multiplanar imaging for assessment. Portal venous phase
of CT angiography should be used, which clearly
shows the status of left renal vein and delineates
its relationship with the surrounding structures.
Magnetic resonance angiography (MRA) can
provide the same information and has the advantage of avoiding exposure to radiation.
CT angiogram (CTA) ndings can include
LRV compression between the SMA and the
abdominal aorta (aortomesenteric window) with
proximal dilatation of the vein (Fig.18.2) and the
presence of left kidney hilar region varicose veins
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Fig. 18.2 CT angiogram abdomen, transverse section,
reveals the compression of LRV between SMA anteriorly
and aorta posteriorly. Red arrows marking the compressed
area
and collateral pathways. In posterior nutcracker
syndrome, the vein follows a posterior course to
aorta (retroaortic), and CTA may show compression of LRV between aorta and lumbar vertebra.
CTA can show acute angle takeoff by SMA from
the aorta and can have a relatively low or anterolateral origin, and the space between the SMA
and the aorta at the level of the left renal vein
crossing is reduced [42]. A classical triangular
narrowing of the LRV at the aortomesenteric portion, named beak sign of the LRV, can be useful
in diagnosis of the noncompensated nutcracker
syndrome [43].
18.5.3 Phlebography
andRenocaval Gradient
A. Savlania and S. Pitchai
gradient by pullback technique between the left
renal vein and vena cava should be >3mmHg to
clinch the diagnosis of NCS which is otherwise in
normal situation is <1mmHg [21].
18.6 Urology Evaluation
forHaematuria
Haematuria in NCS, which is often microscopic
in presentation, mandates urological evaluation.
Urine microscopy and urine culture should be
performed to rule out glomerular cause and infectious aetiology of haematuria. Urologic assessment can include cystoscopy to locate haematuria
to left ureter and exible ureterorenoscopy or
even renal biopsy. Andrianne et al. described a
preoperative technique, in which clamping of the
renal vein is followed by appearance of immediate reversible gross haematuria. Haematuria
provocation test by percutaneous technique has
also been proposed, which can be performed during conventional phlebography by temporarily
occluding LRV in preoperative evaluation for
formal diagnosis of this syndrome in suspected
patients [44].
18.7 Other Investigations
The platelet counts and coagulation prole
should be checked. Other causes of haematuria as
urinary tract, tuberculosis and bilharziasis should
be ruled out.
Left renal vein phlebography can be performed by
percutaneous technique using femoral vein or brachial vein access under local anaesthesia.
Phlebography with renocaval pressure gradient
assessment is considered as propitious in establishing the nal diagnosis of NCS. Left renal
venous phlebography allows visualisation of the
point of LRV compression at the mesoaortic window with stasis of dye or delayed clearance of dye
and also shows venous collaterals in perirenal and
periureteral region with reux into the gonadal
and adrenal tributaries. The renocaval pressure
18.8 Dierential Diagnosis
It is often challenging to diagnose NCS; all other
causes of haematuria and ank pain should be
ruled out before diagnosing NCS.Differential
diagnosis includes glomerulonephritis, urinary
tract infection, renal calculi, primary varicocele, pelvic congestion syndrome due to other
causes, vascular malformation, endometriosis
and musculoskeletal problems causing ank
pain.
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195
18.9 Indications forIntervention
The proper correlation between the degree of the
LRV compression and severity of the symptoms
is lacking. Hence for optimal results of endovascular or surgical management of NCS, selection
of the patient for intervention is of prime importance. The interventions are considered only if
there is severe and intractable symptoms or failure to respond after conservative management,
which some authors recommend a period of
2 years of conservative approach for patients
aged <18years and for a duration of 6months in
case of adults [17, 45, 46] .
18.10 Treatment
Management of the nutcracker syndrome has
evolved over the last ve decades. The available
options can be categorised as:
1. Surveillance
2. Endovascular management:
(a) Stenting
(b) Embolisation of gonadal veins
3. Surgical management:
(a) Renal vein transpositioning/reimplantation
(b) Other procedures—renal autotransplanta-
tion, renal vein bypass, etc.
18.10.1 Surveillance
Conservative management is generally advocated
in young patients (<18 years) especially when
patients present with microscopic haematuria,
short-lived intermittent episode of painless gross
haematuria, insignicant pain or atypical symptoms. General advice is to encourage weight gain
so that the retroperitoneal fat increases which
may decrease the posterior renal ptosis thereby
reducing the tension over the renal vein. With
physical growth, an increase in brofatty tissue
around the takeoff of the SMA may also relieve
the LRV compression. The conservative approach
should be favoured up to a period of 2years fol-
lowing detection of problem in young patients
below 18years. Nearly 75% of patients respond
to conservative approach probably due to physical development [
Mayo Clinic, Reed etal. reported a 30% success
in decreasing LRV compression by nonintervention approach with stress given on weight
gain to increase the fat in retroperitoneum [48].
Angiotensin-converting enzyme (ACE) inhibitors have been shown to be benecial in patients
with NCS having orthostatic proteinuria [49].
47]. In another series from
18.10.2 Endovascular Treatment
Endovascular management of NCS is gaining
acceptance recently mainly due to advantage of
being minimally invasive and associated with
least morbidity and mortality. With experience
gained in treating various venous occlusive conditions such as May-Thurner syndrome, BuddChiari syndrome and superior vena caval
obstruction, the same principle is applied in treating NCS.First described by Neste etal. in 1996,
it has become more appealing than the traditional
open surgical treatment [50]. The procedure is
done via femoral access. A wide and long selfexpanding stent (10–20 mm in diameter and
40–70mm in length) is preferable. The stent is
deployed from the rst division of the renal vein
and extended into IVC, to reduce the chance of
stent migration. Post-procedural gradient is
measured. Around 3–6-month period of dual
antiplatelet followed by single-antiplatelet therapy is usually advised although few authors prefer initial treatment with anticoagulation.
Other endovascular options include embolisation of the left gonadal vein or other tributaries of
the LRV especially in patients presenting with
isolated varicocele or pelvic congestion syndrome. In patients with pelvic congestion syndrome and demonstrable pelvic varicoceles,
embolisation of ovarian veins may provide signicant symptomatic improvement in 56–98% of
patients [27]. Although good results have been
reported in the literature [51], this technique
occludes the main (and symptomatic) collateral
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A. Savlania and S. Pitchai
outow pathways and thus could lead to worsening of the obstruction with resultant aggravation
of renal symptoms.
18.10.3 Surgical Management
Surgical treatment should be guided by symptomatic nature of disease entity rather than mere
presence of nutcracker phenomenon, because of
the poor correlation between imaging evidence of
NCP and symptoms [17, 46]. Since the basic
pathology is compression of the LRV, any direct
procedures on the LRV are likely to be most efcacious with least risk to other structures.
Ever since the rst procedure reported by
Pastershank [9], multiple techniques of surgical
management have been reported of varying surgical complexity to resolve the problem, but the most
commonly used procedure is left renal vein direct
reimplantation into the inferior vena cava below the
normal anatomical opening to prevent direct compression in acute angle of aortomesenteric window.
To date, LRV reimplantation is the surgical method
of choice as reported by Mayo Clinic group [52].
Procedure ofLRV Transposition
The surgical procedure of choice has been transposition of the LRV caudally into the inferior
vena cava. The procedure is performed through a
midline laparotomy, transperitoneal approach.
The small and large bowels are packed away, and
retroperitoneum is opened in midline, inferior to
the transverse mesocolon between duodenum on
right side and inferior mesenteric vein on left
side. The LRV is completely mobilised after dissecting from brofatty tissue all around. The left
adrenal vein is routinely ligated and divided to
facilitate LRV mobilisation. The gonadal vein
can be ligated in patients with varicocele, and
descending lumbar vein can be ligated selectively, if necessary. The patient is systemically
heparinised by unfractionated heparin 1 mg/kg
dose with target activated clotting time of 250s,
a side-biting clamp applied on the IVC across the
LRV conuence and the LRV transected with a
mini-cuff of IVC and re-anastomosed to the left
lateral aspect of the caudal portion of IVC in an
end-to-side tension-free manner with continuous
or interrupted sutures of 4.0 or 5.0 polypropylene
(Fig.18.3). The proximal opening in the IVC is
SMA
LRA
LRA
LRV
SMA
LRV
Fig. 18.3 Image showing the most commonly done surgery in NCS, the reimplantation of left renal vein in caudal
segment of inferior vena cava in end-to-side fashion
18 Nutcracker Syndrome
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oversewn with continuous sutures of 4.0 or 5.0
polypropylene. Other adjuncts used in this procedure include saphenous vein patch, vein cuff or
combination of patch and cuff. These adjuncts
either enlarge the renal vein (e.g. vein patch)
thereby reducing anastomotic narrowing or
lengthen the vein (e.g. vein cuff) thereby facilitating tension-free anastomosis [52]. LRV transposition can also be done via laparoscopy as
reported by Hartung etal. [53]. But being a technically difcult procedure and requiring a signicant learning curve, laparoscopic repair did not
gain widespread acceptance and is limited to centres of excellency. Early complications of the
LRV transposition are thrombosis of the LRV,
bleeding, chylous ascites and postoperative ileus.
Delayed complications of anastomotic stenosis
and recurrence of symptoms have been reported.
Other Surgical Procedures
Various other surgical procedure have been
described for treating NCS, which includes renal
autotransplantation, SMA transposition, gonadocaval bypass, spleno-renal bypass, aortic transposition, renopexy, external stenting, nephrectomy,
etc. Renal autotransplantation involves nephrectomy and transplantation of the kidney into either
ipsilateral or contralateral iliac fossa as in live
donors. It offers maximum efcacy in terms of
normalisation of renal venous congestion, but it
is a more invasive and complex surgery (requiring three anastomosis) when compared with the
other procedures [54, 55].
In gonadal vein transposition technique, the
left gonadal vein is transected and reimplanted
into IVC. It drains not only the left kidney but
also decompresses the pelvic congestion, so
especially indicated when associated with pelvic
varices with high-pressure gradient. But this procedure did not receive much appreciation, and
only a limited literature is available [26]. Superior
mesenteric artery transposition entails transection of the SMA at its junction with the abdominal aorta and re-anastomosis to the abdominal
aorta at a lower level away from the left renal
vein. But since this procedure entails high risk for
mesenteric ischemia, it is generally not preferred
[56]. Laparoscopic spleno-renal bypass was
reported by Chung and Gill in a symptomatic
young female with NCS with complete resolution of the symptoms [57]. Barnes etal. described
an external stenting procedure wherein an externally supported PTFE graft was wrapped around
the LRV [58]. But due to lesser invasive endovascular stenting, this procedure is no longer performed now.
18.10.4 Long-Term Results
Gloviczki etal. from Mayo Clinic in their experience with LRV transposition (with or without
adjuncts) in 36 patients showed complete resolution of symptoms in 87% of them. Primary, primary assisted, and secondary patencies at 2years
were 74%, 97% and 100%, respectively. Freedom
from reintervention at 1 and 2years were 76%
and 68%, respectively [52]. Hohenfellner etal.
reported 88% success after the open surgical
treatment, but the reintervention was required in
24% patients because of stenosis/occlusion.
However secondary patency was 100% in this
series [59].
Chen et al. published the largest series of
endovascular treatment of NCS which included
61 patients with midterm and long-term outcomes. In their series almost majority of the
patients showed resolution of symptoms with
follow-up ranging from 6months to 72months
[60]. Similarly Wang et al. reported nearcomplete resolution of symptoms in 30 patients
with NCS managed with endovascular stenting
with mean follow-up of 3years [61].
Even though the results are attractive, the
main complications associated with LRV stenting are stent migration, in-stent stenosis, erosion
and vein occlusion resulting from bromuscular
hyperplasia, thrombosis or fracture. The reported
incidence of these complications is very rare
[19]. Stent migration into right atrium requiring
open surgical management has been reported
[60]. Cohen etal. reported one case of stent compression by the SMA at 18-month follow-up
which needed an open surgical reconstruction
[62]. Despite the fact that this technique is minimally invasive, further studies will be required to
establish its role in the management of nutcracker
syndrome.
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