catheters or other permanent medical devices. It can
cause peritonitis, osteomyelitis, and meningitis.3'5 On
the basis of in vitro testing, ciprofloxacin, trimethoprim-sulfamethoxazole, aminoglycosides, and imipenem are reasonable therapeutic choices, although no
drug is uniformly effective against all reported isolates.
Ochrobactrum anthropi should be considered as a
cause of endogenous endophthalmitis in debilitated
patients with indwelling medical devices.
REFERENCES
1. Ezzedine H, Mourad M, Van Ossel C, et al. An outbreak of
Ochrobactrum anthropi bacteremia in five organ transplant
patients. J Hosp Infect 1994;27:35-42.
2. Braun M, Jonas JB, Schonherr U, Naumann GOH. Ochrobac'
trum anthropi endophthalmitis after uncomplicated cataract
surgery. Am J Ophthalmol 1996;122:272-273.
3. Chang HJ, Christenson JC, Pavia AT, et al. Ochrobactrum
anthropi meningitis in pediatric pericardial allograft transplant
recipients. J Infect Dis 1996;173:656-660.
4. Kern WV, Oethinger M, Kaufhold A, Rozdzinski E, Marre R.
Ochrobactrum anthropi bacteremia: report of four cases and
short review. Infection 1993;5:306-310.
5. Cieslak TJ, Robb ML, Drabick CJ, Fischer GW. Catheterassociated sepsis caused by Ochrobactrum anthropi: report of a
case and review of related nonfermentative bacteria. Clin
Infect Dis 1992;14:902-907.

Horner Syndrome as an Isolated
Manifestation of an Intrapetrous
Internal Carotid Artery Dissection
Rafael Bilbao, MD, Sonia Amoros, MD,
and Juan Murube, MD
PURPOSE: To describe the atypical localization
and unusual clinical manifestation of an internal
carotid artery dissection.
METHODS: We examined a 43-year-old woman
who had sudden onset of left ptosis and miosis
with vague dysesthesia around her eye.
RESULTS: Her examination showed an intrape­
trous carotid artery dissection.
CONCLUSIONS: The intrapetrous segment is an
extremely rare localization for an internal carotid
artery dissection. The differential diagnosis of
acute Horner syndrome should include carotid
dissection, which is usually accompanied by other
neurologic manifestations.

562

E EXAMINED A 43-YEAR-OLD WOMAN WITH SUD-

den left-sided ptosis and mild discomfort and
tenderness around her eye that had lasted 3 days.
There were no other ocular or systemic symptoms.
She reported no previous episodes of head or neck
trauma. Corrected visual acuity, extraocular motility,
and slit-lamp and fundus examination were all unre­
markable. External examination disclosed a 2-mm
left ptosis. Pupils measured RE, 5 mm and LE, 3 mm
in room lighting; anisocoria was more perceptible in
dim illumination, with pupils measuring RE, 8 mm
and LE, 4 mm. Pupillary reaction to light and near
stimulus was normal. Hemifacial anhidrosis was ab­
sent, and left trigeminal sensitivity was normal.
Neurologic examination, chest x-ray, contrast brain
and neck computed tomographic scan, magnetic
resonance imaging, and supra-aortic Doppler ultra­
sound were all unremarkable.
To localize the site of the sympathetic deficit, we
performed a phenylephrine 1% test (hydroxyamphetamine drops were not available). Fifteen minutes after
phenylephrine 1% instillation in each eye, there was
greater mydriasis in the left eye (Figure 1), providing
evidence of a postganglionic lesion (presumably left
denervation hypersensitivity). Finally, carotid angiography showed a narrowing area at the intrapetrous
segment of the carotid siphon, with a mild poststenotic dilation because of a subintimal dissection in the
resolution phase (Figure 2). The patient began anticoagulation with heparin and then warfarin sodium
for a suggested duration of 6 months. Five months
after its onset, Horner syndrome had not recovered,
but the patient was otherwise asymptomatic.
Horner syndrome is present in up to 58% of
internal carotid artery dissections1 but usually mani­
fests with other focal neurologic deficits because of
local compression in the area of the dissection or,
more commonly, thrombotic embolization from the
dissected wall. Most patients experience neck, facial,
or head pain ipsilateral to the lesion because of
ischemia or stretching of the trigeminal pain fibers
surrounding the carotid artery. Other associated
manifestations may include transient monocular
Accepted for publication Nov 11, 1996.
Ophthalmology Department, Hospital Ram6n y Cajal.
Inquiries to Rafael Bilbao, Mauricio Legendre, 13, Madrid 28046,
Spain; fax: 1-5622974.

AMERICAN JOURNAL OF OPHTHALMOLOGY

APRIL 1997

4
■»

Figure 1. (Top) The patient before the phenylephrine
1% test, with ptosis and miosis of the left eye. (Bottom)
Fifteen minutes after the instillation, the patient experi­
enced greater mydriasis and palpebral retraction in the
left eye because of a denervation hypersensitivity in a
postganglionic lesion.

blindness, central retinal artery occlusion, cranial
nerve palsies, syncope, and neck swelling, as well as
contralateral focal sensory and motor deficits.2 In the
literature, we found only two cases with intrapetrous
dissection; one manifested with intolerable pulsatile
tinnitus and the other with cerebral infarction. Nei­
ther showed evidence of Horner syndrome.3
Carotid dissections are either spontaneous or trau­
matic. Some authors have emphasized that anteced­
ent trauma may be minimal. Fibromuscular dysplasia,
cystic medial necrosis, Marfan and Ehlers-Danlos
syndromes, and large-vessel vasculitides have been
reported to cause internal carotid artery dissection.
However, in the majority of patients, as in our patient,

VOL.123,

No. 4

Figure 2. Cerebral angiography showing stenosis of the
intrapetrous segment into the temporal bone (arrow) and
poststenotic dilation.

the cause is unknown. The origin of the dissection is
usually 2 to 3 cm distal to the carotid bulb and seldom
extends beyond the base of the skull; the dissection is
rarely located in the intrapetrous segment.4
Carotid dissection must be ruled out as the cause of
acute Horner syndrome, especially when painful, after
a postganglionic location has been determined. 5 Be­
cause the extracranial Doppler examination can be
normal if the localization is above the angle of the
jaw, magnetic resonance angiography or traditional
cerebral angiography should be performed when pre­
vious examinations are negative.

REFERENCES
1. Bogousslavsky J, Despland PA, Regli F. Spontaneous carotid
dissection with acute stroke. Arch Neurol 1987;44:479-482.

BRIEF REPORTS

563

2. Cullom RD, Cullom ME. Two neurophthalmic episodes
separated in time and space. Surv Ophthalmol 1995;40:
217-2243. Saeed SR, Hinton AE, Ramsden RT, Lye RH. Spontaneous
dissection of the intrapetrous internal carotid artery. ] Laryngol Otol 1990;4:491-493.
4. Van Damme H, Martin D, Stassen MP, et al. Dissections
spontan6es de la carotide interne. J Mai Vase 1990;15:14-22.
5. Kline LB, Vitek JJ, Raymon BC. Painful Homer's syndrome
due to spontaneous carotid artery dissection. Ophthalmology
1987;94:226-230.

Mucoepidermoid Carcinoma
of the Caruncle
Richard C. Rodman, MD, Bartley R. Frueh, MD,
and Victor M. Elner, MD, PhD
PURPOSE: To report a case of mucoepidermoid
carcinoma, a highly aggressive variant of conjunctival squamous cell carcinoma.
METHODS: We examined and treated a 57-yearold man with mucoepidermoid carcinoma of the
caruncle, a highly unusual site for this tumor.
RESULTS: In the past, simple excision of this
tumor has been followed by rapid recurrence. Our
patient underwent wide surgical excision of the
tumor and has shown no evidence of recurrence
after 16 months of follow-up.
CONCLUSION: Mucoepidermoid carcinoma may
first manifest in the caruncle. Histologically veri­
fied, tumor-free surgical margins are necessary for
complete excision.

M

UCOEPIDERMOID CARCINOMA IS A RARE CONjunctival tumor that tends to occur near the
corneoscleral limbus of elderly patients. This tumor is
considered a highly invasive variant of squamous cell
carcinoma, in which rapid recurrence is the rule after
simple excision.1 Therefore, early detection and wide
local excision yield optimal results. We report a
5 7-year-old man with mucoepidermoid carcinoma of
the caruncle.
A 57-year-old man was referred to the W. K.

Acceptedforpublication Nov 18, 1996.
W. K. Kellogg Eye Center, Department of Ophthalmology, University
of Michigan.
Inquiries to Richard Rodman, MD, Wills Eye Hospital Cornea Service,
900 Walnut St, Philadelphia, PA 19107-5598; fax: (215) 928-3854.

564

Figure 1. Biomicroscopic appearance of mucoepidermoid
carcinoma of the caruncle.

Kellogg Eye Center, University of Michigan, for
evaluation of epiphora secondary to cicatricial ectropion. He had undergone excision of a recurrent basal
cell carcinoma of the left lower eyelid 13 years
previously. Complete ophthalmic examination dis­
closed a cicatricial ectropion of the left lower eyelid
and a fleshy, 2.5 X 3.5 X 2.0-mm vascular mass
replacing the left caruncle (Figure 1). This mass was
adherent to underlying medial canthal tissues. The
upper and lower canalicular systems were patent. A
biopsy was performed on the caruncular tumor, and
histopathologic examination showed the lesion to be
mucoepidermoid carcinoma.
The patient returned 3 weeks later for complete
excision of the tumor of the left caruncle. After initial
excision of remaining tumor, including surrounding
areas of normal-appearing tissue, frozen sections dis­
closed margins positive for tumor (Figure 2). Addi­
tional excision of deeper tissue was also positive for
mucoepidermoid carcinoma. Ultimately, deep resec­
tion of medial canthal tissue, as well as of the superior
and inferior canaliculi, was required to achieve
tumor-free margins. Sixteen months after wide exci­
sion of the mucoepidermoid carcinoma, our patient
has shown no evidence of tumor recurrence.

AMERICAN JOURNAL OF OPHTHALMOLOGY

APRIL 1997