(Chest. 2001;120:309-311.)
© 2001
American College of Chest Physicians
Compressive Neuropathy of the Brachial Plexus and Long Thoracic Nerve*
A Rare Complication of Heparin Anticoagulation
Ahmad A. Elesber, MD;
Peter D. Kent, MD and
Constance A. Jennings, MD, FCCP
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Abstract
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We present a case of a 69-year-old woman who developed brachial
plexopathy and long thoracic nerve palsy secondary to compression from
a hematoma while receiving heparin therapy for the treatment of a
stroke. The patient was treated conservatively with discontinuation of
heparin and had complete resolution of her compressive neuropathy. This
is the first report of a patient with long thoracic nerve palsy with a
brachial plexopathy complicating anticoagulation. We review the
literature on hematoma-induced compressive neuropathies and treatment
options. Our review concludes by emphasizing the importance of clinical
judgment in determining the best therapeutic
modality.
Key Words: anticoagulation • brachial plexus • compression • hematoma • long thoracic nerve
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Introduction
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Anticoagulant therapy is frequently used in both the
inpatient and outpatient settings. As a consequence, clinicians
frequently have to deal with the side effects of anticoagulation. In an
attempt to increase general awareness, we report an unusual
complication of heparin treatment and explore treatment options after a
brief review of the literature.
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Case Report
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A 69-year-old woman with a history of hemicolectomy for Dukes
class D colon cancer was admitted to the hospital for evaluation and
treatment of the ileus in association with findings of multiple
mesenteric and omental soft tissue masses that were consistent with
metastases on CT scans of the abdomen and pelvis. A chest radiograph
was normal, and the results of a total body bone scan were negative.
Two days later, she developed acute binocular vision loss and was
started on IV heparin therapy. A CT scan of the head revealed ischemic
changes in both occipital lobes, an ultrasound of the neck showed
normal flow in the vertebral arteries, and transesophageal
echocardiography showed a small patent foramen ovale with trivial
right-to-left shunting. No evidence of deep venous thrombosis was found
on duplex ultrasonography of the lower extremities. The patient’s
vision returned to normal over the next few days.
On day 5 of heparin therapy, the patient was grasping the bed-rail with
her left hand in an attempt to roll over and developed a sudden onset
of moderate left shoulder pain. Initially, there were no positive
findings on physical examination, and she was treated with morphine.
The results of laboratory tests at that time showed the following:
activated partial thromboplastin time (APTT), 101 s (range, 21 to
33 s); hemoglobin level, 11.5 g/dL (range, 12 to 15.5 g/dL);
platelet count, 233,000/µL (range, 150,000 to 450,000/µL). The rate
of heparin infusion was decreased to achieve a target APTT of 60 to
90 s.
By the following day, the patient’s left shoulder pain had increased.
Inspection revealed a large ecchymosis over the left axilla and flank,
as well as mild left scapular winging, but no raised
subcutaneous hematoma could be felt. The patient was not able to abduct
her left arm beyond 50°, and the scapular winging was accentuated by
having her push against the examiner’s hands. She was able to
reasonably adduct, internally and externally rotate, and flex and
extend the humerus, but a full assessment of left shoulder motor
strength was limited by pain. Motor strength was normal in the
remainder of the arm. Sensory examination, deep tendon reflexes, and
upper extremity arterial pulses were normal. At that time, her APTT was
78 s, hemoglobin level was 10.4 g/dL, and platelet count was
224,000/µL. Heparin therapy was discontinued, and an MRI of the left
brachial plexus was obtained, revealing a 7 x 4-cm mass subjacent to
the left scapula in the region of the left axilla, which was consistent
with a large hematoma (Fig 1
). The hematoma involved the subscapularis muscle on the left and
compressed the brachial plexus anteriorly (Fig 2
). The hematoma also compressed the posterolateral left thorax in the
region of the long thoracic nerve (Fig 3
). An underlying metastasis was not seen.
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Figure 2.. T1-weighted sagittal view through the hematoma
shows it within the subscapularis muscle (black arrow) and compressing
the brachial plexus in the region of the axillary artery and vein
(white arrow).
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Since the patient had only mild deficits, she was treated
conservatively with analgesics and by withholding further
administration of anticoagulant drugs. She had complete resolution of
pain and a return of normal motor strength over the next 5 days, and
winging of the scapula was no longer evident after 1 week.
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Discussion
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The brachial plexus is formed by the union of the ventral
rami of C5–T1. The plexus runs in the posterior triangle of the neck
then emerges between the scalene muscles, passes posterior to the
clavicle, and lies on the first digitation of the serratus anterior and
the subscapularis muscles. The long thoracic nerve is a supraclavicular
branch of the brachial plexus and is formed by the roots from the fifth
to the seventh cervical rami. It descends dorsal to the brachial plexus
as well as the first part of the axillary artery and crosses the
superior border of the serratus anterior to reach its lateral surface.
It then continues downward to the lower border of the serratus
anterior, supplying branches to each of its digitations.1
Compressive neuropathies from hematomas were first described in the
mid-1960s as treatment with anticoagulant drugs became more widely
utilized. Of the reports in the literature, this complication
seems to be more common with heparin therapy (45%) than
with warfarin therapy (18%) and more frequently involves the lower
extremity nerves (87%).2
Hematomas causing compressive
neuropathies may occur within the intended therapeutic range of
anticoagulation (40%).2
A conservative approach to
management seems to yield good results in 85% of cases.2
In one review, early surgical evacuation of the hematoma within 48 h,
when necessary for severe symptoms, resulted in improvements in all
patients, while late operations after 48 h resulted in
improvements in about half of all patients.2
Merrick et
al, 3
in 1991, were the first to report good results after
percutaneous decompression of a retroperitoneal hematoma secondary to
heparin treatment in a patient who was not an immediate candidate for
surgery.
Neuropathy in association with a hematoma likely results from local
injury to nerves by compression. In minor cases, this may result in
temporary demyelination of the nerve locally, but in more severe cases
axonal injury may occur with wallerian degeneration distal to the site
of compression.4
Our patient had progressive signs and symptoms of brachial plexopathy.
This was evident by her inability to fully abduct her left arm, even
with control of her pain by analgesics. Abduction of the arm is a
coordinate function of several muscles. The deltoid and supraspinatus
muscles, aided by the stabilizing early contraction of the
subscapularis, teres minor, and infraspinatus muscles, result in early
abduction to 90°; this is followed by the action of the serratus
anterior muscle, which is indispensable for full abduction (90° to
180°).
The scapular winging and difficulty with abduction implicates
compression of the long thoracic nerve in our patient. The impairment
of other nerves or nerve roots supplying the subscapularis, teres
minor, supraspinatus, and deltoid muscles also may have contributed to
her difficulty with abduction. Her mild scapular winging at rest could
have been a manifestation of the subscapular hematoma itself, but it is
very unlikely for static winging (ie, that due to an
anatomic defect) to be accentuated by pushing against a
wall.5
The hematoma in this patient may have resulted from trauma or from
bleeding into a metastasis, or it may have occurred spontaneously. It
is very rare for colon cancer to metastasize to muscles,
although a few cases have been described.6
Rather, the
more likely explanation is a minor muscle or soft tissue injury that
occurred while she was pulling herself over in bed and resulted in a
capillary bleed.
On review of the literature, no previous report of long thoracic nerve
palsy and very few reports of brachial plexopathy as a complication of
anticoagulation came to our attention. Salam7
reported a
case of a 68-year-old woman receiving warfarin therapy and using
crutches who developed total paralysis and a complete loss of sensation
in the left arm. That patient underwent evacuation of a large tense
hematoma from her left axilla, with satisfactory return of both motor
and sensory function. Another report8
included two cases
of brachial plexus compression by a hematoma following jugular
puncture. The two patients, one of whom was receiving warfarin therapy,
developed partial deficits of upper limb motor and sensory function and
were managed successfully with conservative treatment.8
In
a third report,9
a 68-year-old woman receiving warfarin
therapy experienced a fall and had progressive motor loss below the
shoulder. A large hematoma compressing the brachial plexus was drained.
The patient had progressive return of function over 2
years.9
Finally, Hoyt et al2
reported on a
61-year-old man receiving warfarin therapy who fell and developed
progressive right extremity weakness culminating in a right wrist drop
after 7 days. This patient underwent surgical evacuation of a large
hematoma within the coracobrachialis muscle, which was displacing the
brachial plexus. Unfortunately, a follow-up examination did not
demonstrate significant improvement in his motor or sensory functions.
While the literature contains only a few reports of brachial plexopathy
as a complication in patients receiving anticoagulant therapy, there
are frequent case reports of brachial plexopathy secondary to a
compressive hematoma as a complication of axillary arteriography or
arteriotomy.10
11
12
In these cases, the mechanism of
plexopathy is thought to be an expanding hematoma within the axillary
sheath with secondary compression of the nerves and cords within this
sheath.11
Satisfactory results in affected patients are
usually obtained from early surgical intervention, and delaying surgery
may result in permanent neurologic damage.10
11
12
Whether a hematoma compressing the brachial plexus should be treated
conservatively or surgically depends on anatomic and clinical features.
Surgical intervention should be considered for the treatment of
hematomas in the axillary sheath and in patients with severe motor or
sensory impairment. On the other hand, when the hematoma is small to
moderate in size, free to expand into the surrounding soft tissues of
the axilla, and the neuropathy is not progressive or severe,
conservative treatment is likely warranted with discontinuation or
reversal of anticoagulation therapy using vitamin K, protamine sulfate,
or fresh frozen plasma to help halt the expansion of the hematoma.
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Footnotes
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Abbreviation: APTT = activated partial
thromboplastin time
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References
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Williams P, Bannister LH, Berry MM, et al, eds. Gray’s anatomy. 38th ed. New York, NY: Churchill Livingstone, 1995; 840–842, 1266–1268
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Hoyt, TE, Tiwari, R, Kusske, JA (1983) Compressive neuropathy as a complication of anticoagulant therapy. Neurosurgery 12,268-271[ISI][Medline]
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Merrick, HW, Zeiss, J, Woldenberg, LS (1991) Percutaneous decompression for femoral neuropathy secondary to heparin-induced retroperitoneal hematoma. Am Surg 57,706-711[ISI][Medline]
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Sunderland, S (1978) Nerves and nerve injuries 2nd ed. ,147 Churchill Livingston London, UK.
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Fiddian, NJ, King, RJ (1984) The winged scapula. Clin Orthop 185,228-236
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Yoshikawa, H, Kameyama, M, Ueda, T, et al (1999) Ossifying intramuscular metastasis from colon cancer: report of a case. Dis Colon Rectum 42,1225-1227[CrossRef][ISI][Medline]
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Salam, AA (1972) Brachial plexus paralysis: an unusual complication of anticoagulant therapy. Am Surg 38,454-455[Medline]
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Fuller, GN, Dick, JPR, Colquhoun, IR (1994) Brachial plexus compression by hematoma following jugular puncture. Neurology 44,775-776[Free Full Text]
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Desai, DC, Uribe, A, Lachman, T (1997) Brachial plexus injury due to compression: an alternate mechanism of injury: case report and review of the literature. Am Surg 63,487-489[ISI][Medline]
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Molnar, W, Paul, DJ (1972) Complication of axillary arteriotomies: an analysis of 1,762 consecutive studies. Radiology 104,269-276[ISI][Medline]
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O’Keefe, DM (1980) Brachial plexus injury following axillary arteriography. J Neurosurg 53,853-857[ISI][Medline]
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Gierson, ED, Kilpatrick, W (1974) Brachial plexus compression following preaxillary artery angiography. Angiology 25,777-779
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Abstract
Introduction
