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Cerebral infarction complicating subclavian vein catheterization.

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Cerebral Infarction Complicating
Subclavian Vein Catheterization
B a r r i e J. H u r w i t z , MRCP, a n d Jerome
B.
P o s n e r , MD
Cerebral infarction has not previously been r e p o r t e d as a complication of a t t e m p t e d subclavian vein catheterization
f o r p a r e n t e r a l nutrition. T w o patients developed clinical a n d pathological evidence of embolic infarction i n t h e left
carotid a n d left v e r t e b r a l distributions, respectively, w h e n a n a r t e r y was inadvertently p u n c t u r e d d u r i n g a t t e m p t s t o
catheterize the left subclavian vein. T h e s e tw-o complications o c c u r r e d i n more t h a n 1,000successful subclavian vein
catheterizations.
Hurwitz BJ, Posner JB: Cerebral infxction complicating subclavian vein catheterization.
Ann Neurol 1:253-254, 1977
Since 1952, p e r c u t a n e o u s infraclavicular subclavian
v e i n catheterization has become a widely u s e d a n d
a c c e p t e d p r o c e d u r e in clinical m e d i c i n e [ 11. The app a r e n t e a s e and usefulness of t h e t e c h n i q u e is, however, offset by numerous complications [2]. The 2
p a t i e n t s d e s c r i b e d illustrate a h e r e t o f o r e u n d o c u m e n t e d complication: c e r e b r a l infarction, probably from arterial p u n c t u r e a n d emboiization.
Patient 1
A 56-year-old woman with metastatic breast carcinoma and
bowel obstruction was receiving parenteral nutrition
through a left subclavian venous catheter. The catheter was
removed when its tip was noted to be in the left jugular vein.
An attempt at replacement was made the following day into
the same (left) side. During the procedure the patient
reported a peculiar "taste" in her mouth and then became
unresponsive. T h e needle, which was believed t c be i n the
subclavian artery, was immediately removed. Physical examination revealed global aphasia, eye deviation to the left, a
right homonymous hemianopia, and decreased sensation in
the right side of the face. There was right central facial
paresis, a right flaccid hemiplegia, and hyperactive deep
tendon reflexes with bilateral extensor planrar responses.
T h e pulse was 100 and regular with a blood pressure of
lOO/SO mm Hg. T h e heart was enlarged, and a soft systolic
murmur was audible at the left sternal border. T h e hematocrit was 26?, and other routine laboratory investigations
revealed nixma1 findings. T h e EKG demonstrated a normal
sinus rhythm with mild S-T and T-wave changes but was n o
different from that done the previous day. H e r neurological
deficit did not improve, and she died three weeks later.
Autopsy revealed multiple, extensive areas of nonhernorrhagic infarction in the left cerebral hemisphere. Macrophage proliferation suggested that the infarcts were at least
10 days old. T h e r e were organized rhrombi occluding small
From the Departments of Neurology, Memorial Sloan-Kertering
Cancer Center and Corriell University Medical College, New York,
NY.
vessels in the distribution of the left internal carotid artery.
The great vessels were unremarkable except for a moderate
plaque of atherosclerosis in the intracavernous portion of
the left carotid artery. The heart was enlarged, with 1-111613static tumor in the atrial myocardium and septum. T h e endocardium and heart valves were normal.
Patient 2
A cachectic 28-year-old man with metastatic adenocarcinoma ofrhe colon arid bowel obstruction was scheduled to
receive parenteral nutrition. During percutaneous right
subclavian vein catheterization the subclavian artery %'as
accidentally punctured. The catheter was withdrawn and
local pressure was applied for five minutes. A further attempt to catheterize the right subclavian vein was successful.
Immediately after the procedure the patient was noteJ to
be confused. Physical examination revealed skew deviation
of the eyes, right central facial weakness, and right tongue
weakness. His speech was dysarthric. There was mild weakness and poor coordination o f his right limbs and a flaccid
left hemiparesis. H e was totally areflexic (due to prior
vincristine chemotherapy) and had bilateral extensor plantar
responses. T h e pulse was 80 and rebalar, and the blood
pressure was 110180 mm Hg. The heart was normal. T h e
hematocrit was 33";; the findings of other routine laboratory investigations were within normal limits. The EKG was
normal. Examination 12 hours later revealed mild right
facial paresis, left hemiparesis, and left extensor plantar
response. Except for diffuse weakness, the neurological
deficit slowly improved until his death from the systemic
disease three weeks later.
Autopsy revealed a 0.4 cm infarct in the left thalamus and
a 1.5 cm infarct in the right cerebellar hemisphere. They
were nonhemorrhagic and becoming organized, with macrophage infiltration. T h e remainder of the brain was normal macroscopically. Apart from mild aortic atherosclerosis,
the heart and great vessels were normal.
Accepted for puhlication Ocr 5 , 1976.
Address reprint requests to Dr Posner, 1275 York Av, New York,
NY 10021.
253
Discussion
Cerebral infarction has not previously been reported
as a complication of attempted subclavian vein
catheterization [2, 31, although air embolism [4]and
carotid artery laceration [3] have been. In our 2
patients the onset of signs and symptoms of cerebral
infarction immediately following inadvertent arterial
puncture and the pathological changes of embolic
infarction with no cardiac or other arterial source for
emboli strongly implicate the procedure. These represent the only 2 such complications in more than
1,000 subclavian vein catheter placements for total
parenteral nutrition at Memorial Sloan-Kettering
Cancer Center. W e suspect that in both cases thrombi
farmed on the needle tip, broke loose, and entered
cerebral vessels.
In Patient 1 t h e needle was probably misplaced into
the left common carotid artery, because the patient
complained of a peculiar sensation (“taste”) o n her
tongue, possibly a result of embolism to the tongue via
the external carotid artery; the pathological changes
were compatible with embolization in the left carotid
distribution. In Patient 2 the embolus was in the distribution of the vertebrobasilar arterial system. It
seems likely that the event occurred after the inadvertent arterial puncture but was not noticed until successful venipuncture was completed. Even if the needle had not entered the vertebral and carotid arteries,
embolitation to those vessels from the subclavian artery is possible; vertebrobasilar embolization from a
right subclavian arterial thrombus has been described
previously, usually in association with a cervical rib
[53. A left middle cerebral artery embolus arisingfrom
254
Annals of Neurology
Vol 1 No 3 March 1977
a thrombus of the left subclavian artery extending into
the common carotid has also been reported [GI. Forcible unblocking of arteriovenous shunts in patients
having hemodialysis has also resulted in retrograde
cerebral embolization [ 7 ] but cannot play a role here
since no injection was made.
Because of its intimate location posterior to the
subclavian vein, the subclavian artery can be entered
inadvertently in attempted subclavian venipunctures
[21. Care must be taken t o recognize this complication
and to withdraw the needle immediately without
either flushing or manipulation. Fluoroscopic observation of needle placement is not usually helpful,
since the vein and artery are close together and cannot
be distinguished.
References
I . Aubaniac R: Linjection inrraveii~eusesous-claviculaire: avanrages e t technique. Presse Med 60:1456, 1952
2. Borja A R Currenc sratus of infraclavicular subclavian vein
catheterization. Ann Thorac Surg 13:615-621, 1972
3. Ryan J A J r , Abel RM, Ahbott WM, et al: Catheter complications
in rota1 parenteral nutrition: a prospective study of 200 consecutive patients. N Engl J Mcd L9U:757-7hl, 197.4
4. Flanagan JP, Gradisar IA, Gross RJ, e t al: Air embolus-alerhal
complication of subclavian venipuncture. N Engl J Med
281:488-489, 1969
5 . Shucksmith HS: Cerebral and peripheral emboli caused by cervical ribs. Br Med J 2:835-837, 1963
6. Hutchinson EC, Acheson EJ: Strokes: Nacural Hisrory, Parhologp and Surgical Trea:menr. Philadelphia, X’B Saunders Company, 1975, pp 58-5:)
7. Gaan D, Mallick N P , Urewis RAL, et al: Cerebral damage from
declotring Scribner shunts. Lancer 2:77-79,1969
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