Keywords
bronchial artery embolization - anterior spinal artery infarct - monoparesis
Introduction
Bronchial artery embolization (BAE) is an established minimally invasive treatment
for massive or recurrent hemoptysis. Anterior spinal artery (ASA) infarct is an uncommon
but serious complication of the procedure. The interventional radiologist doing these
procedures must be well versed with the bronchial artery anatomy, its variations,
and its relation with ASA to avoid this dreaded complication. We report a case in
which the patient developed monoparesis and mild transient autonomic dysfunction post
BAE but magnetic resonance imaging (MRI) of spine showed diffuse symmetric cord involvement
in ASA territory from D1–D4 level.
Case Report
A 62-year-old diabetic hypertensive male patient with history of treated pulmonary
Koch's infection presented with cough and recurrent mild hemoptysis. Patient was admitted
and was managed conservatively. Chest X-ray revealed patchy areas of fibrobronchiectasis
in both lobes ([Fig. 1]). An evening before planned discharge, the patient had an episode of massive hemoptysis
following which he was taken up for BAE after informed consent. Preprocedure computed
tomography (CT) angiography was not done in view of X-ray changes and due to financial
constraints of the family.
Fig. 1 X-ray chest posteroanterior view showing patchy fibrobronchiectatic changes in both
upper and middle zones, predominant on right side.
Through femoral vascular access the right intercostobronchial trunk (ICBT) was catheterized
with a 5F RC-1 (Cook Medical Inc.) catheter and angiography was performed which revealed
abnormal parenchymal blush with bronchopulmonary shunting in right upper lobe ([Fig. 2a, b]). Similar abnormal vascularity was seen in left upper lobe through left ICBT ([Fig. 2c]) and mild abnormal parenchymal blush through both bronchial arteries having a common
origin ([Fig. 2d]). After thorough evaluation of the angiograms to rule out opacification of ASA,
embolization was performed using 500–700 µm and 350–500 µm polyvinyl alcohol (PVA)
particles (Boston Scientific) till the parenchymal blush was gone. No ASA feeder opacified
in intermittent check angiograms. Sheath was removed and right leg was immobilized
with a compression dressing over the puncture site. Post procedure, the patient complained
of dull aching pain in the left lower limb. However, sensory and motor functions in
left limb were normal.
Fig. 2 (a) Right upper lobe fibrobronchiectatic changes with angiographic catheter at ostium
of right ICBT. (b) Angiogram from right ICBT showing abnormal parenchymal blush with bronchopulmonary
shunting. (c) Angiogram from left ICBT showing mild parenchymal blush with bronchopulmonary shunting.
(d) Angiogram from common origin of both bronchial arteries showing abnormal parenchymal
blush, mainly on right side.
The following day the patient complained of weakness in the right lower limb and was
immediately referred back to rule out any local neural injury. Sonographic examination
of the puncture and right lower limb Doppler were unremarkable. Nerve conduction study
was normal. Patient also developed bladder dysfunction and neurological examination
revealed upgoing plantar, loss of deep tendon reflexes, power 2/5 on right side, and
relatively cold right foot. MRI spine revealed T2 hyper intensity suggesting infarct
in the ASA territory, extending from D1–D4 level ([Fig. 3]).
Fig. 3 (a) Short Tau Inversion Recovery (STIR) sagittal magnetic resonance imaging (MRI) section
of cervicodorsal spine showing hyperintensity in anterior two-thirds of the dorsal
cord extending from D1–D4 level. (b–d) T2 axial MRI sections at various levels from D1–D4 showing bilaterally symmetric
hyperintensity in anterior two-thirds, consistent with anterior spinal artery territory
infarct.
Patient was started on steroids; bladder function improved and right lower limb power
improved to Grade 3/5. He was discharged on tapering dose of oral steroids and was
advised follow-up after a week. No recurrent episode of hemoptysis was noted till
discharge. It was also decided to repeat MRI dorsal spine after review; however, the
patient never reported back.
Discussion
Bronchial artery embolization is widely accepted minimally invasive procedure for
patients expectorating massive amounts of blood.
Relevant Vascular Anatomy
Bronchial arteries that arise between superior endplate of D5 vertebral body and inferior
endplate of D6 vertebral body are termed as orthotopic, and angiographically they
are within 1 cm above or below the left main bronchus where it crosses descending
aorta. Arteries arising from other locations are termed as ectopic (8.3–56%), the
usual sites being the inferior aortic arch proximal to ligamentum arteriosum, distal
descending thoracic aorta, inferior phrenic artery, subclavian artery, brachiocephalic
trunk, thyrocervical trunk, internal mammary artery, and coronary artery.[1]
Anterior spinal artery courses longitudinally along the anterior sulcus of the spinal
cord from foramen magnum to conus medularis and supplies anterior two-thirds of cord.
It is formed by confluence of descending branches of the intracranial segments of
the vertebral arteries and is joined by multiple feeders from the radiculomedullary
branches of the spinal trunks of segmental arteries in cervicothoracic, midthoracic
and thoracolumbar regions. Midthoracic and thoracolumbar feeders to the ASA are variable
and unpredictable. Angiographically small radicular arteries in upper and midthoracic
region are difficult to visualize.[2]
[3] The artery of Adamkiewicz (AKA) is the most important anterior radiculomedullary
feeder to the ASA and angiographically has a classic “hairpin” loop when it reaches
the ASA. AKA is about 0.5 to 1.0 mm in diameter and almost always arises on the left
side between T8–L2 (75%).
Angiographic demonstration of nonopacification of the radiculomedullary feeders to
ASA from common ICBT is very important during BAE as thoracic and upper lumbar portions
of spinal cord have minimal collateral circulation, thus vulnerable to any ischemic
compromise.[2]
[3]
Bronchial Artery Embolization
Bronchial artery embolization is performed through bronchial artery or ICBT demonstrating
angiographic abnormal parenchymal blush and various projections are taken to rule
out opacification of ASA or AKA. Agents used for embolization are gelfoam, PVA, and
n-butyl-2-cyanoacrylate (NBCA) to achieve good distal embolization. Theoretically,
using larger PVA particles (> 350 μm) is a safeguard for avoiding nontargeted spinal
artery embolization.[4] Coils are not preferred mode of embolization as putting coil would “close the door”
for any future intervention.[5] Some authors have also shown better 1-year, 3-year, and 5-year hemoptysis-free periods
with NBCA.[6] Use of microcatheter is recommended to avoid central reflux and nontargeted embolization
especially if injecting embolizing agent from common ICBT; however, a study has shown
that small invisible radiculomedullay feeders to the ASA may still get embolized even
with use of microcatheter.[7]
Anterior Spinal Artery Infarct
Anterior spinal artery infarct is a rare but dreaded complication associated with
BAE. Incidence is reported between 1.0 and 6.5% and patients usually present with
ASA syndrome.[8] Patients have bilateral lower limb motor loss, loss of pain, and temperature sensations
below the level of the lesion with relative sparing of proprioception and vibratory
sensations. Autonomic dysfunctions like hypotension, sexual dysfunction, and bladder–bowel
dysfunction may also be present. Deep tendon reflexes are absent in acute phase; however
in few days/weeks spasticity and hyper-reflexia ensue.
Spinal artery infraction post BAE has also been reported even in patients in whom
spinal artery feeders were not identified on angiography and this has been implicated
to redirection of the blood to invisible connections once hypertrophied vessels start
getting embolized.[9]
Monoparesis with mild autonomic dysfunction with symmetric ASA territory cord changes
in MRI has not been described in English literature. Few authors have described transient
lower limb monoparesis but they implicated it to particle reflux in main aorta.[10] Few sporadic reports on monoparesis due to spinal infarct post abdominal surgical
procedures have been described; however, the cord involvement in them had been focal
and unilateral.[11]
[12] Some authors have also attributed unilateral symptoms in ASA infarcts in their studies
to duplication of anterior spinal artery and in those patients MRI T2 hyperintensity
was localized to one side.[13]
[14] This is possibly the first case report with diffuse symmetric spinal cord changes
in territory of anterior spinal artery and patient presenting with unilateral weakness.
Explanation to the presentation could be acute edematous T2 hyperintensity in the
region surrounding the ischemic insult and sparing of the motor tracts, probably due
to duplication of the ASA in our patient which was not evaluated by us on imaging;
however, it is reported in literature.[2]
[13]
