Fennis, Theodorus F. M.

Koehler, Peter J.

Schreuder, Antonia H. C. M. L.

Teijink, Joep A. W.

English

PubMed

Antonia H. C. M. L. Schreuder

Theodorus F. M. Fennis

Joep A. W. Teijink

Peter J. Koehler

Springer - Publisher Connector

Lumbosacral plexopathy associated with aortoiliac occlusive disease

Antonia H.C.M.L. Schreuder
Theodorus F.M. Fennis
Joep A.W. Teijink
Peter J. Koehler
Lumbosacral plexopathy
associated with aortoiliac
occlusive disease
Received: 15 May 2006
Received in revised form: 6 August 2006
Accepted: 22 August 2006
Published online: 22 March 2007
Sirs: Acute cauda equina syndrome
is usually caused by an interverte-
bral disc herniation. Other causes
are epidural compression from
traumatic injury, primary and
metastatic neoplasms, and epidu-
ral haematoma. Non-compressive
etiologies include inflammatory
and infectious disorders [1]. We
describe a rare vascular cause of a
cauda equina-like syndrome.
A 49-year-old man underwent
vertical banded gastroplasty for
morbid obesity (BMI 44 kg/m2).
His history mentioned myocardial
infarction, but no neurological
illness or coagulation disorders.
He was taking diuretics and beta-
blockers for hypertension, and a
statine for dyslipidemia. He didn’t
smoke or use any alcoholic bev-
erages.
The postoperative period was
complicated by deep vein throm-
bosis (DVT) in the right leg, for
which he received fenprocoumon
and low-molecular heparin. In this
period diabetes mellitus type II
was diagnosed, for which he was
treated with metformin. During
his stay in the hospital, blood
glucose levels were measured two
or three times daily and were
never above 8,7 mmol/L. Five
weeks after surgery the patient
complained of a sudden inability
to rise from his chair and acute
stabbing pain in his lower back,
irradiating to the left leg, and
shortly thereafter to the right. He
had a numb feeling in both legs
and buttocks and could not lift his
right leg. He also suffered from
urinary incontinence and sponta-
neous micturition was not possi-
ble. Defecation was normal.
Examination revealed severe
paresis of the right leg and absent
tendon reflexes of both legs with
normal plantar responses. He had
sensory loss for touch and pain
below the level of Th12 on the right
side and below the knee on the left.
On the right side, he had saddle
anesthesia. Anal sphincter function
was normal. Vibration and propri-
oception were absent in both legs.
Straight-leg raising aggravated the
pain in the right leg. Peripheral
arterial pulsations were present.
MRI of the thoracic and lumbar
spine was done immediately as a
cauda equina syndrome was sus-
pected, but this did not disclose any
abnormalities. Laboratory investi-
gations showed an ESR of 81 mm/h
with a normal peripheral blood
count. Blood glucose level was
7,5 mmol/L. The INR was 2.3, all
other blood tests, including vitamin
status, were normal. The next day,
the paresis of the right leg was less
pronounced, but now the left leg
was found to have a slight paresis.
He still had sensory loss in the right
leg, but no saddle anesthesia. Re-
peated MRI of the spine for sus-
pected spinal cord ischemia was
normal. A few days later peripheral
arterial pulsations of both legs were
absent. Immediate CT-angiogra-
phy showed a subtotal occlusion of
the abdominal aorta at the bifur-
cation, continuing in the left iliac
artery and a total occlusion in the
right iliac artery (Fig. 1). The pa-
tient underwent successful throm-
bolysis with urokinasis followed by
PTA of both common iliac arteries.
At the time of thrombolysis he was
already recovering and after PTA
further improvement was ob-
served. A month later he was able to
walk.
Electrophysiological investiga-
tions two months later showed
extensive abnormalities consistent
with bilateral lumbosacral
plexopathy. Sensory nerve action
potentials were absent in both
sural nerves. The H-reflex in the
left tibial nerve was absent; in the
right tibial nerve there was
prolonged latency of the H-reflex
with reduction of the compound
motor action potential. Electro-
myography revealed denervation
and reduced recruitment of all
proximal and distal lower
extremity musculature. No abnor-
malities were seen in paraspinal
muscles, as we would expect to see
in a cauda equina syndrome.
Lumbosacral plexopathy may
be caused by structural or non-
structural lesions. Well-known
structural causes include
(ilio)psoas or retroperitoneal
haematoma, psoas abscess, aneu-
rysm of the abdominal aorta or
traumatic injury. It may also result
from complicated abdominal
A.H.C.M.L. Schreuder, MD
P.J. Koehler, MD, PhD, FAAN (&)
Dept. of Neurology
Atrium Medical Centre
P.O. Box 4446
6401 CX Heerlen
The Netherlands
Tel.: 31-45/5766700
Fax: 31-45/5767416
E-Mail: pkoehler@knmg.nl
Th.F.M. Fennis, MD, PhD
Dept. of Clinical Neurophysiology
Atrium Medical Centre
P.O. Box 4446,
6401 CX Heerlen
The Netherlands
J.A.W. Teijink, MD, PhD
Dept. of Surgery
Atrium Medical Centre
P.O. Box 4446
6401 CX Heerlen
The Netherlands
LETTER TO THE EDITORS
J Neurol (2007) 254:803–805
DOI 10.1007/s00415-006-0421-7
surgery, pelvic radiation therapy,
neoplasms or diabetes mellitus,
and is rarely seen in pregnancy
and delivery [2].
The events described in our
patient occurred five weeks after
gastroplasty. The most frequent
neurological complications after
bariatric surgery are peripheral
neuropathy and encephalopathy,
followed by cranial nerve deficits,
myopathy, myotonia and myelop-
athy. Plexopathy has been
described sporadically [3–6]. The
etiology of these complications is
believed to be multifactorial, and
is mostly subscribed to a state of
nutritional deficiency. However,
vitamin suppletion was started the
day of surgery and a clinical pre-
sentation of acute cauda equina
syndrome has, to our best knowl-
edge, never been described after
bariatric surgery.
Gastric bypass surgery induces
a postoperative hypercoagulable
state and obese patients undergo-
ing bariatric surgery are at high
risk of developing embolism or
post-thrombotic syndrome. These
patients have increased plasma
levels of thrombin-antithrombin
complex, D-dimer, fibrinogen and
prothrombin after surgery,
suggesting a marked increase in
the generation of thrombin and
the presence of intravascular clot-
ting that has undergone lysis,
while they also have decreased
levels of antithrombin III, protein
C, and plasminogen, again
increasing thrombin and fibrin
formation.
Moreover, obese people, like
our patient, have higher plasmin-
ogen activator inhibitor type 1
plasma levels than normal con-
trols, resulting in a hypofibrino-
lytic state, and elevated plasma
levels of coagulation factor VII,
fibrinogen and tissue factor, lead-
ing to a hypercoagulability state
[7–9]. Myocardial infarction is
also a risk factor for perioperative
thrombo-embolic syndrome [10].
Coagulation tests had not been
ordered in our patient, but the
DVT was suggestive of such a
condition.
Occlusive vascular disease, dis-
section, and aneurysms of the
aorta are associated with spinal
cord ischemia, as is aortic surgery.
Lumbosacral plexopathy, mainly
unilateral, has also been described
as a complication of aortoiliac
surgery and endovascular proce-
dures [11–13]. The blood supply
of the lumbosacral plexus usually
derives from the iliolumbar artery,
superior and inferior gluteal ar-
tery, and the lateral sacral artery,
which are all branches of the
internal iliac artery, and the deep
iliac circumflex artery [14]. The
abdominal aorta bifurcates ante-
rolaterally to the fourth lumbar
vertebral body into the right and
left common iliac arteries. These
divide at the level of the lumbo-
sacral intervertebral disc into
external and internal iliac arteries.
The lumbar arteries, usually four
on each side, arise posterolaterally
from the aorta, opposite the
lumbar vertebrae. The spinal
branch of the first lumbar supplies
the terminal cord and the
remainder supply the cauda equ-
ina [15–16]. The subtotal occlu-
sion of the abdominal aorta in our
patient occurred at the level of the
bifurcation, at the fourth lumbar
vertebra. MRI disclosed that the
conus ends at the level of the dis-
cus intervertebralis between the
twelfth thoracal vertebra and the
first lumbar vertebra. The second
and third pair of lumbar arteries,
that also supply the cauda equina,
are not affected by this near-
occlusion. However, due to indi-
vidual anatomic variability, we
cannot be completely certain of
the arterial supply of cauda and
plexus in this particular patient.
Although ischemia of the spinal
roots can not entirely be excluded,
the most plausible explanation for
the neurological symptoms and
signs, presenting as a cauda equ-
ina syndrome in this patient, is a
disruption of blood flow to the
lumbosacral plexus resulting from
the aortoiliac occlusion. The
assumption is supported by the
intact spinal muscles at EMG
Fig. 1 A. CT angiography shows subtotal occlusion
of the aorta continuing in the left iliac artery, total
occlusion in the right iliac artery. B. CT angiography
reveals subtotal occlusion of the abdominal aorta at
the level of the bifurcation
804
examination of the patient and the
different vascularisation pattern of
the lumbosacral plexus and caudal
roots in relation to the site of the
vascular occlusion, since the latter
receive their vascularisation
mainly from more proximal aortic
branches. We also considered
diabetic plexus neuropathy, but
diabetic plexopathy presents with
pain and weakness followed by
wasting of the pelvifemoral
muscles, characteristically without
sensory impairment. It is associ-
ated with weight loss in more than
half of the patients. The weakness
and atrophy are progressive in the
course of months, the pain usually
persists for months, and recovery
is slow. Urinary retention or
incontinence is not a presenting
feature of diabetic plexopathy
[17–18]. Moreover, the diabetes in
our patient was reasonably well
under control and his neurological
deficits improved drastically after
thrombolytic therapy and stenting
of both iliac arteries. The pain
resolved in a few days and he
never developed atrophy. How-
ever, diabetes mellitus may have
influenced the susceptibility of the
plexus lumbosacralis to ischemic
injury.
Aortoiliac occlusive disease has
to be taken into account as a
possible cause of acute cauda
equina syndrome in particular
when a structural lesion cannot be
demonstrated by MR of the cauda.
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805


A controlled study of peripheral neuropathy after bariatric surgery.

Arterial vascularization of the cauda equina.

Cauda equina syndrome.

Comerota AJ (2004) Unilateral lower extremity paralysis after coil embolization of an internal iliac artery aneurysm.

Diabetic amyotrophy: current concepts.

Diabetic neuropathy: an update.

Gastric partitioning complicated by peripheral neuropathy with lumbosacral plexopathy.

Ischemic injury to the spinal cord or lumbosacral plexus after aorto-iliac reconstruction.

Lumbosacral plexopathy.

Maniati A

Neurologic complications after surgery for obesity.

Preexisting morbidity as an independent risk factor for perioperative acute thromboembolism syndrome.

Rabbat A

Systemic coagulation and ﬁbrinolysis after laparoscopic and open gastric bypass.

The arteries of the trunk. In:

The blood supply of the lumbar and sacral plexuses in the human foetus.

The neurological complications of bariatric surgery.

Weight loss reduces tissue factor in morbidly obese patients.

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Lumbosacral plexopathy associated with aortoiliac occlusive disease

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