the experience with our patients suggests that the abducensnerve is more vulnerable to the anti-GQ1b IgG antibodythan are other cranial nerves and that bilateral abducens palsyis a characteristic sign of the pathologic state.

An immunohistochemical study showed that the GQ1bepitope was expressed mainly in the paranodal regions ofthe oculomotor, trochlear, and abducens nerves, and thatthe oculomotor nerve had the highest content.2,4 Thevulnerability of the abducens nerve cannot be explainedsimply by the difference in ganglioside content. Althoughno studies have been published about age-related distribu-tion of GQ1b, one possibility is that the abducens nerve ofyoung persons such as our patients may be more susceptibleto the anti-GQ1b IgG antibody.

Recently, Kusunoki and associates5 reported five pa-tients with increased anti-GQ1b IgG antibody titer whopresented with ataxia without ophthalmoplegia, thus, in-dicating that the anti-GQ1b IgG antibody does not disruptonly the three cranial nerves involved in ocular move-ment. In our patients, the anti-GQ1b IgG antibody wasclosely related with acute ophthalmoparesis. Anti-GQ1bIgG antibody is not a natural antibody, and a highone-point increase of the antibody titer is pathologicallymeaningful, so that the antibody assay should be useful fordiagnostic purposes.

Plasmapheresis or intravenous immunoglobulin therapyis selected for the treatment for Guillain–Barre syndromeand Miller Fisher syndrome. Because some patients ofatypical Miller Fisher syndrome spontaneously improved,the cost–benefit advantage of those therapies for theatypical Miller Fisher syndrome has yet to be confirmed.Studies with controls are needed to clarify the problem.

ACKNOWLEDGMENTS

The authors wish to thank Drs. Michiaki Koga andNobuhiro Yuki of the Dokkyo University School of Med-icine, Japan, for their antiganglioside antibody assay, andDrs. Masaki Takahashi and Kahiko Saito of the TokyoMetropolitan Research Laboratories of Public Health,Japan, for the culture and serological assay of Campy-lobacter jejuni.

REFERENCES

1. Yuki N. Acute paresis of extraocular muscles associated withIgG anti-GQ1b antibody. Ann Neurol 1996;39:668–672.

2. Chiba A, Kusunoki S, Obata H, Machinami R, Kanazawa I.Serum anti-GQ1b IgG antibody is associated with ophthal-moplegia in Miller Fisher syndrome and Guillain-Barre syn-drome: clinical and immunohistochemical studies. Neurology1993;43:1911–1917.

3. Sakurai Y, Mannen T, Kusunoki S. Acute isolated ophthal-moplegia as a variant of Miller-Fisher syndrome. MuscleNerve 1998;21:1107.

4. Chiba A, Kusunoki S, Obata H, Machinami R, Kanazawa I.Ganglioside composition of the human cranial nerves, withspecial reference to pathophysiology of Miller Fisher syn-drome. Brain Res 1997;745:32–36.

5. Kusunoki S, Chiba A, Kanazawa I. Anti-GQ1b IgG antibodyis associated with ataxia as well as ophthalmoplegia. MuscleNerve 1999;22:1071–1074.

Delayed Orbital Hemorrhage afterRoutine Strabismus SurgeryBrian Todd, MBBS,Timothy J. Sullivan, FRACO, FRACS, FRCOphth,and Glen A. Gole, MD, FRACO, FRACS

PURPOSE: To report a case of delayed rectus musclehemorrhage after strabismus surgery.METHODS: Case report.RESULTS: Rectus muscle hemorrhage occurred 36 hoursafter strabismus surgery in a 26-year-old man, causingtemporary loss of vision and reduced ocular motility.Urgent lateral cantholysis and orbital exploration torestore hemostasis were undertaken. Full recovery ofvision occurred and a small residual motility disturbancewas present 3 months postoperatively.CONCLUSION: Delayed rectus muscle hemorrhage post-strabismus surgery is rare but can have sight-threateningeffects. When vision is threatened because of optic nervecompromise, urgent orbital exploration may allow fullrecovery of function. (Am J Ophthalmol 2001;131:818–819. © 2001 by Elsevier Science Inc. All rightsreserved.)

A26-YEAR-OLD MAN UNDERWENT STRABISMUS SUR-

gery for a 45 prism diopter infantile esotropia forwhich he had no prior surgery. Preoperatively, he had20/20 corrected visual acuity bilaterally and otherwisenormal extraocular movements. His ocular examinationwas normal. He was otherwise well but with a history of amid-third facial fracture at 18 months of age and maxillarysurgery at the time. There was no history of abnormalbleeding or bruising.

Surgery involved an uneventful 5.5-mm left medialrectus recession [using one double-armed 6/0 Vicryl (poly-glactin 910 suture)] Ethicon Inc., Somerville, New Jerseyand 8.0-mm left lateral rectus resection (using two double-armed 6/0 Vicryl sutures), through limbal conjunctivalincisions. The medial rectus bled before disinsertion andvisible vessels were cauterized, achieving complete hemo-stasis. The clamped lateral rectus distal end was diather-mied postdisinsertion. Muscle reattachment was achievedusing a crossed swords technique, and conjunctival closurewas interrupted via 6/0 catgut.

Accepted for publication Nov 14, 2000.From the Royal Children’s Hospital (B.T., T.J.S., G.A.G.) and the

Royal Brisbane Hospital (T.J.S.), Brisbane, Australia.Inquiries to Glen A. Gole, MD, FRACO, FRACS, Department of

Ophthalmology, Royal Children’s Hospital, Herston, Queensland, 4029Australia; e-mail g.gole@mailbox.uq.edu.au

AMERICAN JOURNAL OF OPHTHALMOLOGY818 JUNE 2001

Postoperative review at 24 hours revealed a residual 6prism diopter esotropia with normal movements. Severalhours postreview he developed left orbital pain necessitatingoral analgesia. However, 36 hours postsurgery he experiencedsevere left orbital pain with fresh hemorrhage from the orbit.He returned for examination 48 hours after surgery.

On examination, the left eye visual acuity was countingfingers. A relative afferent pupil defect, gross proptosis,chemosis, fresh hemorrhage from the medial conjunctivalincision, and an exotropia with total external ophthalmo-plegia existed. Computed tomography (CT) scanningshowed an enlarged medial rectus, consistent with amuscle hematoma causing globe compression1 (Figure 1,left and right). His hematological investigations (plateletcount/bleeding time/Lupus anticoagulant/Von Willebrandand hemophilia A screens) were normal.

After urgent referral, lateral canthotomy was performedto decompress the orbit, and the nasal aspect of the globewas explored. The massively enlarged medial rectus wasfound to be still secured to the sclera and with pulsatilebleeding from the proximal stump. The muscle was de-tached, diathermied to achieve haemostasis, and resuturedto the original insertion site.

Postoperatively, he was given 5 days oral dexametha-sone (5 mg daily) and then commenced on topical pred-nisolone acetate 1%, six times per day for 2 weeks. By 3months postoperatively, he had normal visual acuity(20/20 corrected), no proptosis, mild adduction deficit, anda persisting 8-prism-diopter exotropia.

Although not stated on initial review, the patient hadrecalled some coughing on the first postoperative day.Spontaneous orbital hemorrhage, although rare, has beennoted after childbirth and straining,2 where it is thought tobe caused by the absence of venous valves allowingtransmission of raised venous pressure. We are unaware ofpreviously reported cases of delayed arterial hemorrhagewithin the rectus muscle subsequent to strabismus surgery,and we could find no reference to it in a computer searchusing MEDLINE.

This case highlights several points: that the eye istolerant of moderately prolonged periods of raised intraor-bital pressure, that a good result is still possible withprompt orbital decompression and hemostasis, and thathemorrhage should always be mentioned as a possiblecomplication of strabismus surgery.

ACKNOWLEDGMENT

We would like to thank Dr. Robert J. Bird, ClinicalHematology Unit, Royal Brisbane Hospital, Brisbane,Australia, for coagulation studies.

REFERENCES

1. Polito E, Leccisotti A. Diagnosis and treatment of orbitalhemorrhagic lesions. Ann Ophthalmol 1994;26:85–93.

2. Sullivan TJ, Wright JE. Non-traumatic orbital haemorrhage.Clin Exper Ophthalmol 2000;28:26–31.

FIGURE 1. Computed tomography scans axial (left) and coronal (right) show left medial rectus hematoma (arrow) causing globedistortion. No evidence of a vascular anomaly existed.

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