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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

Anesth Analg 1994;79:601-3

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ANESTH ANALG

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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

ANALG

1994;79:601-3

CASE

REPORTS

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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

1. Winnie AI? InterscaIene brachial plexus block. Anesth Analg

1970;49:455-66.

2. Vester-Andersen T, Christiansen C, Hansen A, et al . Interscalene

brachial plexus block: area of analgesia, complications and blood

concentrations of local anesthetics. Acta Anaesthesiol Scand

1981;25:814.

3. Hickey R, Garland TA, Ramaurthy

S.

Subclavian perivascular

block influence of location of paresthesia. Anesth Analg 1989;

4. Winnie AP, Ramamurthy

S,

Durrani 2 et al. Pharmacological

reversal

of

Horner's syndrome following stellate ganglion block.

Anesthesiology 1974;41:615-7.

5. Winnie AP. Considerations concerning complications, side ef-

fects and untoward sequelae. In: Plexus anesthesia, vol. I:

perivascular techniques

of

brachial plexus block. Philadelphia:

WB Saunders, 1993:221-6.

6. Miller NR. Disorders of pupil lary function, accommodation and

lacrimation. In: Walsh, Hoyt, eds. Clinical neuro-ophthalmology

4th ed. Baltimore: Williams Wilkins, 1985:469-556.

7. Thompson BM, Corbett

JJ,

Kline LB, et al. Pseudo Horner's syn-

drome. Arch Neurol 1982;39:108-11.

8. Thompson HS, Mensher JH. Adrenergic mydriasis in Horner's

syndrome: hydroxyamphetamine test for diagnosis of post-

ganglionic defects. Am Ophthalmol 1971;72:472-80.

9. Moore DC, Bridenbaugh LD, Thompson GE, et al. Does com-

pounding of local anesthetic agents increase their toxicity in hu-

mans? Anesth Analg 1972;51:579-85.

10. Clausen EG. Postoperative anesthetic paralysis of the brachial

plexus. Surgery 1942;12:933-42.

11. Bashein G, Robertson HT, Kennedy WE Persistent phrenic nerve

paresis following interscalene brachial plexus block. Anesthesi-

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68~767-71.