Brachial Plexus Injury Following Axillary Artery Puncture
Further Comments on ManagemenF
S. DUDRICK, M.D., W. MASLAND, M.D.,2 and M. MISHKIN, M.D.
puncture of the axillary
P E R CUTANE OUS
artery has proved a useful approach for
angiographic examination of both proximal
and distal portions of the aorta and its
branches (1-3). Significant injury to the
brachial plexus was not encountered until
recently when Staal and his co-workers (4)
reported two cases following axillary angi-
ography. Two additional cases of similar
plexus deficits following axillary angiog-
raphy are presented below to suggest
strongly immediate surgical exploration of
the axilla should evidence of significant
brachial plexus injury appear after axillary
artery puncture. The necessity for prompt
surgical intervention derives from the
inverse correlation between duration of
nervous deficit and probability of return of
function.
CASE I: A 78-year-old white woman was ad-
mitted on Jan. 25, 1966, with a one-year history of
episodic burning pain in all of the left toes. The pain
was accompanied by their reddening, and it was
worse at night or following exercise. A sensation
of coldness and numbness in the left foot was con-
stant, but there had been no foot or leg ulcerations.
Past medical history included a myocardial in-
farction in 1956 and mild diabetes mellitus, cur-
rently controlled by diet and 500 mg of tolbutamide
per day. The blood pressure, which had been ele-
vated for the preceding twenty-five years, was being
regulated by 10 mg of guanethidine sulfate per day.
On physical examination the patient was noted to
be of slight build and oriented. Blood pressure while
sitting was 210/80 mm of mercury in both arms;
the pulse was 88 and irregular. There was a systolic
high-pitched bruit over the right carotid artery.
Examination of the heart revealed cardiomegaly and
a soft basal systolic murmur. Bilateral femoral
arterial systolic bruits were heard. The skin over
both legs was atrophic, and there was marked rubor
in the left foot. The temperature of the left foot
was less than that of the right foot. No ulcers were
noted on either leg. Both radial pulses were present
and equal. The popliteal, dorsalis pedis, and
posterior tibial pulses were absent bilaterally.
1 From the Departments of Surgery, Neurology, and Radiology, Hospital of the University of Pennsylvania,
Philadelphia, Penna. Accepted for publication in September 1966.
2 Recipient of Research Career Development Award, National Institute of Neurological Diseases and Blindness.
RADIOLOGY 88: 271-273, February 1967.
271
Pertinent laboratory data included a fasting blood
sugar of 107 mg per 100 ml, blood urea nitrogen of
20 mg per 100 ml, and creatinine of 1.1 mg per 100
ml. Prothrombin time was 72 per cent. An electro-
cardiogram showed atrial fibrillation with a rapid
ventricular rate and occasional ventricular extra-
systoles, with patterns suggestive of left ventricular
hypertrophy and ischemia. Chest roentgenograms
disclosed the heart to be top normal size with promi-
nent pulmonary vasculature. Roentgenographic
examination of the abdomen demonstrated extensive
calcification of the abdominal aorta and pelvic ves-
sels without evidence of aneurysm formation.
On Jan. 26, left axillary arteriography was at-
tempted through two separate skin punctures. This
was unsuccessful and no contrast agent was in-
jected because of excessive bleeding from the punc-
ture sites and evidence of hematoma formation. It
was estimated that 250 to 500 cc of blood were lost.
At this time the left radial pulse was full and strong,
although there was prominent venous distention in
the left upper extremity. There was also weakness
of the left arm, the extent of which was not entirely
clear. During the following day, the axillary hema-
toma spread to the medial side of the arm and lateral
chest wall. Motor deficit in the left upper extremity
also progressed.
On Jan. 28, to control continued bleeding, the left
axilla was explored, revealing about 900 cc of clot
and liquefied blood. As the brachial plexus was ex-
posed, a pulsatile jet of blood was seen coming from
a hole in the axillary artery. This was controlled by
three sutures placed over the arterial wall defect.
The patient's clinical condition stabilized and
complete neurological examination two days after
surgery revealed no movement of the left wrist or
left fingers. The strength in the left biceps and tri-
ceps was grade 2 and the left deltoid, supra- and
infraspinatus was grade 3. The serratus anterior
was normal. There was decreased sensation to
pinprick in the left hand and in the ulnar aspect of
the forearm and arm, and a decrease in light touch
sensation over the entire arm. Both right and left
biceps tendon reflexes were hypoactive but equal
and both triceps tendon reflexes were absent.
Electromyography performed Feb. 5 showed mark-
edly increased chronaxie in all muscles of the left
upper extremities except the deltoid and the biceps.
Nerve stimulation gave no response in either the
left median or left ulnar nerve. No voluntary motor
unit potentials or fibrillation potentials were seen.
272 S. DUDRICK, W. MASLAND,
There was no change in the deficit in the left upper
extremity at the time of discharge two weeks later.
CASE II: A 63-year-old white male, who had
sustained a traumatic amputation above the right
knee thirty-five years before, was admitted Feb. 7,
1966. Intermittent, aching abdominal pain with
radiation to the lumbar area posteriorly had de-
veloped one to two years before this admission.
Laparotomy at another hospital in October 1965 re-
vealed an abdominal aortic aneurysm which in-
volved both renal arteries. He was transferred to
the University Hospital for further management.
On admission vital signs were normal. There was
an above-the-knee stump on the right and a well
healed midline abdominal incision. The anterior-to-
posterior chest diameter was increased with hyper-
resonance on percussion and distant breath sounds.
A 15 X 10 ern pulsatile abdominal mass was felt
in the left upper quadrant. The liver was 1 to 2
fingerbreadths below the right costal margin in the
midc1avicular line. Pedal pulses on the left were
present.
Routine laborat.ory studies were unremarkable.
On Feb. ] 2 surgery was undertaken for resection of
the aneurysm and insert.ion of a prosthet.ic replace-
ment including both renal arteries. The post.opera-
tive course was complicated by gast.rointestinal
bleeding which necessitated a second abdominal
operation to over-sew the gast.ric bleeding point.
Pneumonia later developed and was successfully
t.reated.
The patient improved steadily, and on April 12
follow-up axillary arteriography was performed.
Several attempts were necessary to puncture the left
axillary artery. After one of these endeavors, the
patient experienced a tingling, burning pain over t.he
medial aspect of the left forearm radiating into the
little and ring fingers. Injection of the contrast
medium outlined a fully patent graft.
The evening after arteriography, the patient com-
plained of sharp, burning pain over the medial aspect
of the forearm and in the fingers. Examination the
following day revealed a strength of grade 2 in the
muscles innervat.ed by the left median and ulnar
nerves and the presence of occasional fasciculations.
There was hypesthesia to pin and light touch over
the left medial brachial and antebrachial cutaneous
nerves and the left ulnar and median nerves. A
1 X 2 em firm mass was felt in the axilla, which on
palpation was tender locally and produced typical
radiating pain int.o t.he left upper extremity.
The neurological deficit remained stable until the
night of April 21 when function in the muscles sup-
plied by the left radial nerve distal to the circumflex
nerve was lost as well as sensation in the radial dis-
tribution. The axillary mass had increased appre-
ciably in size at this time.
Exploration of the axillary artery undertaken
on the afternoon of April 22 revealed a hematoma in
the neurovascular sheath. Following evacuation
of the clot, active bleeding from a small laceration in
M. MISHKIN February 1967
the axillary artery was encountered and controlled
by suture.
The pain diminished promptly postoperatively.
At the time of discharge three and a half weeks later
some sensory function in the distribution of the
radial nerve had returned, as well as extensor func-
tion of the left thumb.
Electromyography undertaken on the morning of
April 22 prior to surgery had disclosed the left
musculocutaneous nerve and the left axillary nerve
to be minimally involved; the left radial nerve had
complete functional denervation, but direct elec-
trical stimulation produced a good response in the
muscles supplied by this nerve. The left ulnar and
median nerves showed complete denervation without
response to direct electrical stimulation in the
muscles supplied by these nerves. Electromyog-
raphy repeated prior to discharge on May 1(j
showed evidence of reinnervation of the muscles
supplied by the left radial nerve. There was no
change in the motor function of the left ulnar or
median nerves, but slight sensory return in the left
median nerve.
Percutaneous puncture of the axillary
artery has proved a useful approach to the
aorta, using the Seldinger technic. Staal
et al. recently reported two cases of distal
brachial plexus injury following axillary ar-
teriography. The first was that of a 59-year-
old woman who exhibited a median and ul-
nar palsy, and a swollen, painful area in the
axilla which was surgically explored slightly
less than three months after arteriography.
The distal part of the brachial plexus was
found to be adherent to the artery by
fibrous tissue and was freed only with diffi-
culty. The second patient was a 27-year-
old woman who presented with a causalgic
syndrome following axillary angiography;
on examination there was evidence of
partial median and ulnar palsy. The axilla
in the second patient was also swollen and
very painful on palpation. About one
month after arteriography the axilla was
explored and a false aneurysm was found
closely connected to the plexus. A hema-
toma was evacuated, and two small gaps
in the arterial wall were closed by suture.
The two cases presented in our comrnun-
ication are representative of experience in
305 axillary arteriographic examinations.
The ulnar and median nerves likewise
were conspicuously involved in both
patients. In our second case, prior to
Vol. 88 BRACHIAL PLEXUS INJURY FOLLOWING AXILLARY ARTERY PUNCTURE
signs of radial nerve palsy, a tender, firm
mass in the axilla produced, upon palpa-
tion, typical pain radiating into the arm.
In our series there were two forms of
neurological complications associated with
axillary angiography, which is in accord
with the observations of Staal et al. The
first type most likely represents direct
mechanical trauma to the nerves either
from positioning of the arm or from the
needle. It is characterized by a tingling,
numb sensation, usually in the distribution
of the ulnar nerve. In our experience, this
has cleared, usually within a few days.
The second, more serious type of com-
plication is illustrated in our two cases. It
appears to be associated with continued
bleeding from the axillary artery into the
neurovascular sheath, an inelastic continua-
tion of cervical fascia surrounding the large
vessels and the nerves as they pass through
the axilla into the proximal arm. It would
appear that hematoma formation in the
neurovascular sheath leads to compression
of the distal brachial plexus, particularly
the ulnar and median nerves as they arise
from the medial and lateral cords of the
plexus.
Our second case is of particular interest
in that electromyography was performed
shortly after onset of the radial palsy.
Concomitant with that was the observa-
tion that the axillary mass had increased
in size. The important point at this time
was the fact that the median and ulnar
nerves gave no response whatever to direct
electrical stimulation, indicating a break in
anatomic continuity. This, however, was
not the case with the radial nerve which
still gave normal response to direct elec-
trical stimulation, indicating a functional
block of this nerve, presumably at the level
of the hematoma. That this was so was
clearly demonstrated by repeat electro-
myography following evacuation of the
hematoma, wherein there was evidence of
return of function in the radial distribution
and minimal, if any, evidence of return of
function in the ulnar or median nerves.
(Pro le summario in interlingua, vider le pagina 292)
273
Ten days had elapsed between onset of the
median and ulnar palsies and decompres-
sion, but only about twelve hours between
onset of radial nerve deficit and surgery.
It should be borne in mind that if evi-
dence of neurological deficit, either sensory
or motor, appears after axillary angiog-
raphy, immediate exploration of the
axilla should be undertaken. The validity
of this proposition is certainly indicated by
the electrical studies and clinical responses
in our second case. Certainly early relief
of pressure on the plexus is more likely to
produce a favorable recovery from the
neurological deficit. There should be no
difficulty in distinguishing between the mi-
nor paresthesias of the first type of com-
plication and the major deficits of the
second. If there is, electrical studies will be
useful in assessing the degree of impair-
ment.
SUMMARY
Two additional cases of brachial plexus
deficit following axillary angiography are
presented. They sustained, as did the two
previously reported cases, mainly ulnar
and median nerve palsies and were asso-
ciated with continued bleeding into the
neurovascular sheath from puncture sites
in the axillary artery. These cases are
presented to further emphasize that, should
evidence of brachial plexus deficit become
apparent after axillary angiography, im-
mediate exploration of the axilla is in-
dicated to attempt to obviate or minimize
permanent neurological deficit.
w. S. Masland, M.D., Department of Neurology
Hospital of the University of Pennsylvania
Philadelphia, Penna. 19104
REFERENCES
1. HANAFEE, W.: Axillary Artery Approach to
Carotid, Vertebral, Abdominal Aorta, and Coronary
Angiography. Radiology 81: 559-567, October 1963.
2. NEWTON, T. H.: The Axillary Artery Approach
to Arteriography of the Aorta and Its Branches. Am.
J. Roentgenol. 89: 275~283, February 1963.
3. WEIDNER, W., ET AL.: Percutaneous Transaxil-
lary Selective Coronary Angiography. Radiology 84:
652-657, October 1965.
4. STAAL, A., ET AL.: Neurological Complications
Following Arterial Cathetcrisation by the Axillary
Approach. Brit. J. Radial. 39: 115-116, February
1966.