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
anesthetic technique for shoulder surgery, since
it can provide intraoperative anesthesia as well as prolonged 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 volumes 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 Horners 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 Horner s 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 radiologic 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 hysterectomy 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 option 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 applications 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 University Medical Center, 2160 South First Avenue, Maywood, IL 60153.
01994 by the International Anesthesia Research Society
0003-2999/94/$5.00

immobile needle as described by Winnie (1).Prior to injection

of the local anesthetic, appropriate needle position was confirmed by eliciting a motor response at the shoulder and upper arm using a nerve stimulator. Four attempts at needle
insertion were required to achieve an appropriate motor response 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 sensory and motor block was obtained which permitted uneventful completion of the surgery with minimal additional
sedation.
In the recovery room the patient did not report any discomfort or concern as she lay recumbent. The following
morning, however, as she became ambulatory, she was concerned by a droopy left upper eyelid. Two days postoperatively the ptosis improved slightly and the patient was discharged 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, voluntary, 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 ophthalmic preparation of 10% phenylephrine was administered
topically in the affected eye. We noted that, when we administered phenylephrine in concentrations lower than
0.25%, the ptosis resolved for less than 1 h. However, associated with this relief was mild blurriness of vision from pupillary 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 marginally. The associated pupillary dilation, however, became incapacitating and lasted for almost a day. At this time the patient 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 11mm 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 pharmacologic testing with hydroxyamphetamine (Paredrinem)ophthalmic drops resulted in dilation of both pupils, confirming

Anesth Analg 1994;79:601-3

601

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CASE REPORTS

the diagnosis of a preganglionic Horners syndrome. The patient 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) prolonged Horner s syndrome and 2) supersensitivity to
topical phenylephrine. Temporary Horner s syndrome
is a common accompaniment of stellate ganglionic
block and various supraclavicular techniques of brachial plexus block (2,3). Permanent Horners syndrome, on the other hand, is rare and is a matter of
significant concern, since it may represent traumatic or
pathologic interruption of the oculosympathetic pathway 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 system and is usually associated with other neurologic
signs and symptoms. This lesion is unlikely in our patient 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. Finally, 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 testing. The postganglionic cholinergic sympathetic fibers
to the sweat glands on the lower face follow the external carotid artery. Loss of sweating and vasoconstriction on the whole ipsilateral side of the face are,
therefore, characteristic of preganglionic Horners syndrome, while the loss of sweating limited only to the
forehead region is characteristic of postganglionic Horner s syndrome. This clinical sign, however, is unreliable in differentiatingbetween pre- and postganglionic
Horner s syndrome because the sweating abnormality
is noticeable only after significant exertion and patients
may not become aware of it (6).
Pharmacologic testing with topically applied ophthalmic preparations of cocaine and hydroxyamphetamine (Paredrinem)is helpful in defining the site of the
lesion in the oculosympathetic chain as well as in differentiating patients who have pseudo-Horners syndrome, 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

ANESTH ANALG
1994;79601-3

not dilate the Horners syndrome pupil as completely

as it dilates a normal or pseudo-Horners syndrome
pupil (7). Hydroxyamphetamine (ParedrineT, an indirectly acting adrenergic mydriatic, helps in differentiating pre- and postganglionic Horners syndrome pupils. When a 1%topical 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 norepinephrine stores (6,8).
Clinical symptonnatologyand pharmacologic testing
in our patient revealed that the site of the lesion was
preganglionic. Since the injury occurred perioperatively, the likely etiology of this lesion could be traumatic or chemical injury to the sympathetic fibers. Local anesthetic neurotoxicity is an unlikely possibility,
since recommended concentrations of local anesthetics
were used. Compounding of mepivacaine and tetracaine has been used widely with no reports of neurotoxicity (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 neurologic deficit involviing the lower cords of the brachial
plexus. Mechanical stretching from malposition was
cited as the underlying etiology of traumatic neuropraxia by the author. We believe that this type of injury
would also be unliikely since, besides Horners syndrome, the patient had no other neurologic deficits. Although 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 persistent phrenic nerve paresis after interscalene brachial
plexus block (11).
Winnie et al. (4) in 1974 proposed that topical application 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 syndrome pupil, irrespective of the site of the lesion in the
sympathetic chain, is supersensitive to directly acting
sympathomimetics owing to upregulation of sympathetic receptors in the iris (denervation supersensitivity). Phenylephrine,, therefore, may not be a suitable

ANESTH ANALG

CASE REPORTS

1994;79:601-3

therapeutic option, as it would produce significant pupillary dilation. We did observe this phenomenon in
our case. Reversal of ptosis was short-lived, while the
glare and blurry vision from pupillary dilation persisted for many hours after the topical application of
phenylephrine .
In summary, we report an unusual case of prolonged Horner 's syndrome after an interscalene brachial plexus block. On pharmacologic testing the lesion 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 syndrome. 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 comments in the preparation of this manuscript.

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