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Prolonged Horners Syndrome After Interscalene Block:
A
Management Dilemma
Radha Sukhani,
MD,
Joanna Barclay,
MD,
and Mark Aasen,
MD
Department of Anesthesiology, Loyola University Medical Center, Maywood, Illinois
he interscalene approach to brachial plexus
block as described by Winnie (1) is a valuable
T nesthetic technique for shoulder surgery, since
it can provide intraoperative anesthesia as well
as
pro-
longed postoperative analgesia. Reversible neural
complications, such as phrenic nerve block, recurrent
laryngeal nerve block, and cervical sympathetic block
presenting as Horner
s
syndrome, are not unusual
with interscalene block, especially when larger vol-
umes of local anesthetics are employed.
Horners syndrome occurs with a frequency of
60 -75 with supraclavicular techniques of brachial
plexus block
2,3).
The clinical manifestations of Hor-
ners syndrome are usually temporary and not
of
much concern to the patient or to the anesthesiologist,
since they do not cause significant patient discomfort.
We recently encountered a patient who developed
prolonged Horners syndrome after interscalene
block. The case presented a diagnostic as well as a
therapeutic dilemma.
A
pharmacologic intervention
described in the anesthesia literature failed to resolve
the patients ptosis
4).
Case Report
A 45-yr-old female with left shoulder instability and radio-
logic findings consistent with subdeltoid bursitis presented
for left acromioplasty and rotator cuff repair. The past history
was significant for two general anesthetics, one for a hyster-
ectomy and the other for a left breast lumpectomy; both of
these were complicated by prolonged postoperative emesis
and excessive sedation. The patient readily accepted the op-
tion of regional anesthesia for her shoulder surgery. She was
138 cm tall and weighed 52 kg. There were no abnormal
physical findings, and routine laboratory investigationswere
normal.
The patient received midazolam 4 mg administered in
small increments immediately preoperatively. After applica-
tions of routine monitors, a left brachial plexus block was
performed via the interscalene approach using a 22-gauge,
3.8-cm, B-beveled needle and extension tube assembly, i.e.,
Accepted for publication May 19,1994.
Address correspondence and reprint requests to Radha Sukhani,
MD, Assistant Professor, Department of Anesthesiology, Loyola Uni-
versity Medical Center, 2160South First Avenue, Maywood, IL 60153.
immobile needle as described by Winnie
(1).
Prior to injection
of the local anesthetic, appropriate needle position was con-
firmed by eliciting a motor response at the shoulder and up-
per arm using a nerve stimulator. Four attempts at needle
insertion were required to achieve an appropriate motor re-
sponse at 0.5 ma. A local anesthetic solution, consisting of 40
mL of mepivacaine 1.5%, tetracaine 0.1 , and epinephrine
1 200,000, was injected in small increments. No paresthesias
were reported during the entire procedure.
A
satisfactory sen-
sory and motor block was obtained which permitted un-
eventful completion of the surgery with minimal additional
sedation.
In the recovery room the patient did not report any dis-
comfort or concern as she lay recumbent. The following
morning, however, as she became ambulatory, she was con-
cerned by a droopy left upper eyelid. Two days postopera-
tively the ptosis improved slightly and the patient was dis-
charged home. A month later, the patient continued to
experience a left ptosis. On examination at this time, the
patient was found to have partial ptosis with normal, vol-
untary, and conjugate lid elevation and an intact tarsal fold,
indicating that the ptosis was secondary to Mullers muscle
dysfunction. The patient denied having nasal stuffiness or
dryness of the skin of the face. There was no conjunctival
hyperemia or facial discoloration. The patient indicated
that the condition was impinging on her social life, but that
she would prefer a pharmacologic, rather than a surgical,
intervention.
In accordance with the recommendations proposed in the
anesthesia literature (4,5), a diluted solution of the ophthal-
mic preparation of
10%
phenylephrine was administered
topically in the affected eye. We noted that, when we ad-
ministered phenylephrine in concentrations lower than
0.25%, the ptosis resolved for less than
1
h. However, asso-
ciated with this relief was mild blurriness of vision from pu-
pillary dilation. To prolong the duration of ptosis relief, we
increased the concentration of phenylephrine to over 0.5%,
but found that the duration of relief increased only margin-
ally. The associated pupillary dilation, however, became in-
capacitating and lasted for almost a day. At this time the pa-
tient was referred to ophthalmology for both the specific
diagnosis of the site of the lesion and further management of
the ptosis. Neuroophthalmologic evaluation revealed mild
ptosis with an intrapalpebral fissure measuring
11
mm on the
right side and
8
mm on the left side. Anisocoria was present,
with the right pupil larger than the left. Instillation of 10%
cocaine ophthalmic drops caused dilation of the right pupil
and minimal dilation of the left pupil. Subsequent pharma-
cologic testing with hydroxyamphetamine (Paredrinem)oph-
thalmic drops resulted in dilation of both pupils, confirming
01994 by the International Anesthesia Research Society
0003-2999/94/$5.00
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the diagnosisof a preganglionic Horners syndrome. The pa-
tient decided to defer the surgery to correct the ptosis. On
subsequent follow-up visits
her
ptosis continued to resolve
steadily.
Discussion
Two unusual clinical features of this case are
1)
pro-
longed Horners syndrome and
2)
supersensitivity to
topical phenylephrine. Temporary Horner ssyndrome
is a common accompaniment of stellate ganglionic
block and various supraclavicular techniques of bra-
chial plexus block 2,3). Permanent Horners syn-
drome, on the other hand, is rare and is a matter of
significant concern, since it may represent traumatic or
pathologic interruption of the oculosympathetic path-
way anywhere from the brainstem to the eye.
The location of the lesion along the oculosympathetic
pathway determines whether the Horner
s
syndrome
is
1)
central, 2) preganglionic, or
3
postganglionic
6 ) .
The central Horners syndrome is produced by damage
to the first-order neuron within the central nervous sys-
tem and is usually associated with other neurologic
signs and symptoms. This lesion is unlikely in our pa-
tient since she had isolated Horner
s
syndrome.
Preganglionic Horner
s
syndrome results from a lesion
of
the second-order neuron which emerges from the
spinal cord and ascends in the cervical sympathetic
chain to synapse in the superior cervical ganglion. Fi-
nally, postganglionic Horners syndrome results from
damage to the third-order neuron which emerges from
the superior cervical ganglion, follows the carotid
plexus into the skull, and is carried into the orbit with
the ophthalmic division of the trigeminal nerve. The
distinction between pre- and postganglionic lesions
can be made by clinical signs and pharmacologic test-
ing. The postganglionic cholinergic sympathetic fibers
to the sweat glands on the lower face follow the ex-
ternal carotid artery. Loss of sweating and vasocon-
striction on the whole ipsilateral side of the face are,
therefore, characteristic of preganglionic Horners syn-
drome, while the loss of sweating limited only to the
forehead region is characteristic of postganglionic Hor-
ner s syndrome. This clinical sign, however, is unreli-
able in differentiating between pre- and postganglionic
Hornerssyndrome because the sweating abnormality
is noticeable only after significant exertion and patients
may not become aware of it
(6).
Pharmacologic testing with topically applied oph-
thalmic preparations of cocaine and hydroxyamphet-
amine (Paredrinem) s helpful in defining the site of the
lesion in the oculosympathetic chain as well as in dif-
ferentiating patients who have pseudo-Horners syn-
drome, i.e., ipsilateral ptosis unrelated to lesions of the
oculosympathetic chain (67). Cocaine is useful only in
confirming the presence of Horners syndrome; it does
not dilate the Horners syndrome pupil as completely
as it dilates a normal or pseudo-Horners syndrome
pupil
7).
Hydroxyamphetamine (ParedrineT, an in-
directly acting adrenergic mydriatic, helps in differen-
tiating pre- and postganglionic Horners syndrome pu-
pils. When a
1
opical preparation of Paredrinem is
instilled in the eye that has a normal pupil or a pupil
rendered miotic as a result of a central or preganglionic
lesion, the pupil will dilate. This occurs because the cell
bodies of the third-order neuron in the superior cervical
ganglion and their nerve terminals in the iris are intact
with their norepinephrine stores. The postganglionic
Horners pupil, however, will not dilate with
Paredrinem since the third-order neuron and its nerve
terminals are damaged and have depleted their nor-
epinephrine stores (6,8).
Clinical symptonnatology and pharmacologic testing
in our patient revealed that the site of the lesion was
preganglionic. Since the injury occurred periopera-
tively, the likely etiology
of
this lesion could be trau-
matic or chemical injury to the sympathetic fibers. Lo-
cal anesthetic neurotoxicity is an unlikely possibility,
since recommended concentrations of local anesthetics
were used. Compounding of mepivacaine and tetra-
caine has been used widely with no reports
of
neuro-
toxicity (5,9). Traumatic neuropraxia from needle
trauma, surgical clamps, retractors, or positional
stretching may cause persistent neurologic deficit. The
surgical site in this case was a significant distance away
from the cervical sympathetic chain, making surgical
trauma an unlikely etiology. Clausen (10) reported an
association between Horner
s
syndrome and neuro-
logic deficit involviing the lower cords of the brachial
plexus. Mechanical stretching from malposition was
cited as the underlying etiology of traumatic neuro-
praxia by the author. We believe that this type of injury
would also be unliikely since, besides Horners syn-
drome, the patient had no other neurologic deficits. Al-
though we used a Ei-beveled needle, neuropraxia from
the needle trauma cannot be ruled out completely, since
multiple attempts were required to locate the plexus.
There is at least one case report in the literature where
needle injury was incriminated in the etiology of per-
sistent phrenic nerve paresis after interscalene brachial
plexus block
(11).
Winnie et al. (4) in 1974 proposed that topical ap-
plication of directly acting sympathomimetics such as
phenylephrine could effectively reverse unpleasant
ocular manifestations, i.e., ptosis and miosis associated
with Horners syndrome. Thompson and Mensher (81,
on the other hand, demonstrated that a Horners syn-
drome pupil, irrespective of the site of the lesion in the
sympathetic chain, is supersensitive to directly acting
sympathomimetics owing to upregulation of sympa-
thetic receptors in the iris (denervation supersensitiv-
ity). Phenylephrine,, therefore, may not be a suitable
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ANESTH
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CASE
REPORTS
6 3
therapeutic option, as it would produce significant pu-
pillary dilation. We did observe this phenomenon in
our case. Reversal
of
ptosis was short-lived, while the
glare and blurry vision from pupillary dilation per-
sisted for many hours after the topical application of
pheny ephrine
In summary, we report an unusual case of pro-
longed Horner s syndrome after an interscalene bra-
chial plexus block. On pharmacologic testing the le-
sion was identified as being at the preganglionic site in
the oculosympathetic chain. Contrary
to
the previous
recommendations in the anesthesia literature, we
found that phenylephrine is not a suitable therapeutic
option to manage ptosis associated with Horner's syn-
drome. We believe that surgical correction of ptosis,
i.e., a sling procedure or levator resection, may be a
safer option when the patient is compromised by the
persistent ptosis associated with Horner's syndrome.
~ ~
The authors wish to thank Dr. Walter Jay, Professor and Chairman,
Department of Ophthalmology, for his helpful suggestions and com-
ments in the preparation of this manuscript.
References
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3. Hickey R, Garland TA, Ramaurthy
S.
Subclavian perivascular
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S,
Durrani 2 et al. Pharmacological
reversal
of
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JJ,
Kline LB, et al. Pseudo Horner's syn-
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