Exp. Clin. Endocrinol. Vol. 97, No. 2/3, 1991, pp. 338-343
J. A. Barth, Leipzig
Mayo Clinic, Department of Ophthalmology (Head: R. F. Brubaker, M.D.), and Division of Endocrinology, Department of Internal Medicine (Head: C. A. Gorman, M.B., B.CH.),
Rochester, Minnesota/U.S.A.
Pitfalls Associated with Orbital Decompression for Thyroid-Related Orbitopathy
With 3 Figures
Introduction
Many of the clinical manifestations of thyroid-related orbitopathy can be treated directly to a discrepancy between the volume of the retro-ocular tissues and the space available to accommodate them. This has led to the concept that primary therapy for thyroid-related orbitopathy can be thought of as being directed either toward shrinkage of the expanded retro-ocular tissues or to expansion of the space available to accom-
modate them. The process of tissue shrinkage is attempted by therapy with corticosteroids, cyclosporin or radiation therapy. Expansion of the retrobulbar space has been approached by multiple routes, and operative techniques which involve removal of 1, 2, 3 or 4 orbital walls have been described. In general, their efficacy, as measured in terms of recessioh of proptosis, is related to the extent of bone removal. We have reviewed the effectiveness of various types of orbital decompression both in relation to reduction of retro-ocular tissue resistance and in terms of recession of proptosis (Garrity et al., 1989). In other studies we have examined the comparative effectiveness of transantral versus transfrontal orbital decompression for relief of optic neuropathy (Gorman et al., 1974). From these studies and analysis of our experience with large numbers of patients who have had transantral orbital decompression, we have concluded that transantral orbital decompression represents an effective and generally well tolerated approach to the management of patients with severe orbitopathy. Transantral decompression is used to relieve optic neuropathy, as a preliminary to extraocular muscle surgery in patients with excessive proptosis, and sometimes simply to diminish severe proptosis which on average is reduced between 4 and 5 5 millimeters (Baylis et al., 1980; De Santo, 1984; Hurwitz and Birt, 1985; Lamberg et al., 1985; McCord, 1985; Warren et al., 1989). In patients with reduced visual acuity either from optic neuropathy or a corneal ulcer, visual acuity improved in 101 of 143 (71 Wo) eyes. The operation is associated with rather consistent postoperative numbness of the upper lid, occasional episodes of cerebrospinal fluid leakage, nasolacrimal duct obstruction, oro-antral fistulae and medial entropion (De Santo, 1984). In general, however, it has
Downloaded by: Universite Laval. Copyrighted material.
J. GARRITY and C. Goiu&&r
339
J. GARRITY and C. GORMAN, Pitfalls of Orbital Decompression
proved to be a highly satisfactory procedure for most patients with severe Graves' ophthalmopathy (Garrity et al., 1989). In this presentation we wish to focus mainly on the potential pitfalls surrounding transantral orbital decompression. We will use illustrative examples of the specific problems we have encountered. These problems in general are related to difficulty in making the correct diagnosis or errors in choice, timing or circumstances of therapy. Some of the postoperative problems related to transantral orbital decompression will also be reviewed. Diagnostic Problems
(Fig. 1).
The following case (Fig. 2) illustrates this point. The profound unilateral chemosis and the lack of typical eye lid findings raise questions regarding the diagnosis of thyroidrelated orbitopathy. Computerized tomography (CT) is a powerful tool in the differential
DIAGNOSIS OF GRAVES' OPHTHALMOPATHY Examination of extraocular muscle movement
CT scan Ultrasound Visual acuity
Clinical evaluation
and color perception
Serum T4 - T3
TSI
Ophthalmoscopy
TRH
+ perimetry
T3
Ultrasound
suppression sTSH
Visual evoked
responses Unilateral
Bilateral
Exophthalmometry
Clinical and laboratory findings associated with thyroid-related orbitopathy. When all features are present, the diagnosis is ensured. The diagnosis is likely when all features in a single quadrant are presented. Isolated eyelid, muscle or optic nerve involvement is uncommon in thyroid-related orbitopathy. (from Gorman, C. A.: Extrathyroidal manifestations of Graves' disease. In: The Thyroid. Eds. Ingbar, S. H.; Braverman, L. E., Philadelphia: JB Lippincott 1984, with permission). Fig. 1
Downloaded by: Universite Laval. Copyrighted material.
Bilateral proptosis with upper lid retraction, clinical and biochemical evidence of hyperthyroidism and the presence of pretibial myxedema characterize the full clinical expression of Graves' disease. An accurate diagnosis is assured in this situation. Diagnostic difficulties can arise when the orbitopathy is asymmetric ("unilateral"), the findings are subtle and the patient is found to be euthyroid or even hypothyroid on examination. For example, in a recent review of 200 patients undergoing orbital decompression for severe thyroid-related orbitopathy, 16% had never been hyperthyroid prior to decompression (De Santo, 1984). In such circumstances, with an atypical presentation, one must carefully search for ancillary diagnostic features as there is no single pathognomonic finding
Fig. 2 A 57-year-old female experienced "recurrent right eye infections'' over the previous year which had become worse 2 weeks prior to evaluation. The vision was normal and there was no proptosis. Continuous diplopia began 1 week prior to evaluation. Note the profound unilateral chemosis. The CT scan however shows typical thyroid-related bilateral extraocular muscle enlargement. She was clinically euthyroid although minimal hyperthyroidism was detected biochemically.
diagnosis of thyroid-related orbitopathy. Characteristic bilateral extraocular muscle changes were demonstrated. Subtle hyperthyroidism was found on thyroid fqnction tests. The combination of thyroid hyperfunction and thyroid stimulating immunoglobulins in
serum with abnormal CT scan findings was sufficient to establish the diagnosis of thyroid-related orbitopathy. A transantral orbital decompression produced prompt resolution.
A different diagnostic hazard was encountered in a 64-year-old female with Hashimoto's thyroiditis. She had never been thyrotoxic. Microsomal and thyroglobulin
antibody titers were elevated. Horizontal diplopia began which progressed over 2 months. Over the same period the right eye became increasingly injected and chemotic. In the few days prior to admission the vision declined to 20/200 in the right eye. She was
referred for an urgent brbital decompression. Visual acuity was 20/200 right eye and 20/20 left eye. A right afferent pupillary defect was present. The right globe was 5 mm proptotic, diffusely injected and chemotic. Abduction was moderately impaired in the right eye and mildly impaired in the left eye. Visual field examination showed a cecocentral scotoma centered slightly above fixation. A CT scan of the orbits showed an asymmetric dilation of the right superior ophthalmic vein. The findings of the atypical visual
field defect which extended above the fixation point and the asymmetrically dilated superior ophthalmic vein led us to suspect a dural-cavernous sinus fistula. This was confirmed by angiography and spontaneously closed shortly thereafter. Other potential sources of diagnostic confusion include sphenoid wing meningioma,
optic nerve sheath meningioma, Wegener's granulomatosis, orbital lymphoma, mucocele, and orbital myositis. Ocular myasthenia gravis with diplopia, unilateral ptosis and "retraction" of the contralateral lid is rarely difficult to distinguish from thyroidrelated orbitopathy. Errors in diagnosis represent the first set of opportunities for errors in sequencing,
choice of surgical approach, and technical errors. A second set is associated with preoperative medical problems. Clinicians should be alert for inadequately treated hyperthyroidism or adrenal insuffiency in the patient abruptly withdrawn from corticosteroids.
Downloaded by: Universite Laval. Copyrighted material.
Exp. Clin. Endocrinol. 97 (1991) 2/3
340
J. GARRITY and C. GORMAN, Pitfalls of Orbital Decompression
341
Stress associated with general anesthesia can precipitate acute adrenal insufficiency which can be avoided by administering corticosteroids parenterally with the premedication for anesthesia. Technical Problems
muscles mandates inclusion of the superior or medial wall. Apical decompression can only be accomplished effectively when these walls are removed. The transantral route allows for adequate decompression of the posterior ethmoids which makes this procedure particularly effective for treating patients in whom a lateral or inferior decompression has failed. For this and other reasons the transantral route has become our preferred technique for the majority of the orbital decompressions. Technical aspects of the transantral decompression have been described elsewhere (De Santo, 1984). The maximum potential for life threatening complications however arises during the ethmoidectomy. The roof of the ethmoid sinus is also the floor of the anterior cranial fossa. Cerebrospinal fluid leaks arise from breaks in the dura in this region. It is
important to preoperatively obtain an orbital CT sca with direct coronal views (preferable to reformatted coronal views) to examine for an anomalous roof. The CT scan will also disclose potential operative difficulty from small sinuses or thick bone. If an anomalous roof is present, knowledge of this will call for extra caution to avoid a CSF leak when working near these areas. The threat of a CSF leak persists even after successful decompression surgery. A patient with an anomalous roof underwent an uneventful transantral decompression. Three months postoperatively a paraoxysmal coughing episode
was followed by clear rhinorrhea. An intrathecal metrizamide study confirmed cerebrospinal fluid leakage (Fig. 3). The leak was successfully repaired via an external ethmoidectomy approach. Anbther female with severe steroid dependent congestive orbitopathy had been taking high dose corticosteroids for a year. In addition to exhibiting clinical signs of exogenous cortisone excess, the orbital bones seemed brittle. When removal of the medial orbital wall was attempted at surgery, it fractured into the roof of the ethmoid sinus producing a CSF leak. This eventually required surgical repair also by an external ethmoidectomy approach. Postoperative Problems Decompressions of the orbital floor are associated with downward displacement of the globe. The transantral route is particularly effective at decompression of the floor and the effect is especially apparent after a unilateral transantral decompression. This vertical separation of the visual axes can induce vertical diplopia. For this reason, in the rare circumstance when unilateral decompression is advised, we prefer anterior or transorbital approaches. Diplopia is a well recognized postoperative consequence of transantral orbital decompression (De Santo, 1984; Shorr et al., 1982). Sometimes it is clear that actual prolapse of the extraocular muscle(s) into the opened sinus(es) has occurred. More often prolapse of
Downloaded by: Universite Laval. Copyrighted material.
Surgeons should tailor the decompression procedure to the problem at hand. The presence of an optic neuropathy from apical compression by enlarged extraocular
Exp. Clin. Endocrinol. 97 (1991) 2/3
Fig. 3 Direct coronal CT scans of orbit. Preoperative (left) and postoperative metrizamide study (right). Note the absence of bone in the ethmoid sinus roof (white arrow). The metrizamide is seen in the
left ethmoid sinus confirming CSF leakage (black arrow).
retrobulbar fat exerts traction on the velamentous fibrous intermuscular septae so elegantly described by Koornneef (1984, 1989). Further restriction and diplopia follow. Postoperative exposure keratitis can be seen in conjunction with globe depression following decompression of the orbital floor. One of our patients who had prominent upper lid retraction and lid lag had extremely large superior rectus/levator muscles noted on the CT scan. The apparent lid retraction increased postoperatively because the globes
"dropped" and the lids remained in the sanie relative position producing severe lagophthalmos. An urgent recession of Muellers muscle and the levator was required. The presence of these preoperative findings should alert one to the possibility of postoperative exposure keratitis. A medial entropion of the lower lid may also be seen in association with a decompression of the floor. As the inferior rectus muscle, with the associated lower lid retractors, prolapses into the opened maxillary sinus, traction is transmitted to the tarsus which can cause an entropion. Excessive traction on the orbital connective tissue at surgery potentiates this problem. Recession of the lower lid retractors is curative (Wailer, 1982). Sinus opacification is a normal postoperative x-ray finding. Postoperative swelling and discomfort may be incorrectly classified as infective sinusitis especially in light of sinus X-rays which show opacification. An adequate naso-antral window promotes maxillary sinus drainage and should obviate any infection. Postoperative tearing may be related to placement of the nasoantral windows. The nasolacrimal duct exits below the inferior turbinate and can be compromised while the nasoantral windows are being made (Colvard et al., 1979; Seiff and Shorr, 1980). Either
Downloaded by: Universite Laval. Copyrighted material.
342
J. GARRITY and C. Goiu&.&, Pitfalls of Orbital Decompression
343
intubatial of the lacrimal system with silastic tubing or a lacryocystorhinostomy may be required. Despite these caveats, we believe that bilateral transantral orbital decompression is an
effective and safe procedure. Proper patient selection with a thorough preoperative general medical evaluation correction of thyroid dysfunction, an eye examination to
care.
References BAYLIS, H. I.; CALL, N. B.; SHIBATA, C. S.: The transantral orbital decompression (Ogura techni-
que) as performed by the ophthalmologist. Ophthalmology. 87 (1980) 1005-1012. CoLvuw, D. M.; WALLER, R. R.; NEALT, R. W.; DE SANTO, L. W.: Nasolacrimal duct obstruction
following transantral-ethmoidal orbital decompression. Ophthaln'iic Surg. 10 (1979) 25-28. DE SAro, L. W.: Transantral orbital decompression. In: The Eye and Orbit in Thyroid Disease. Eds. Goiu&, C. A.; WALLER, R. R.; DYER, J. A.; New York: Raven Press 1984, pp. 231-251. GARRITY, J. A.; MCCAFFREY, T. V.; GORMAN, C. A.: Compression and decompression of orbital
contents in Graves' ophthalmopathy. Acta Endocrinol. (Copenh.) 121 (Suppi. 2) (1989) 160-168. Go1kN, C. A.; DESANio, L. W.; MACCARTY, C. S.; RILEY, E C.: Optic neuropathy of Graves' disease. 'fleatment by transantral or transfrontal orbital decompression. N. Engl. J. Med. 290 (1974) 70-75. HURWITZ, J. J.; BWT, D.: An individualized approach to orbital decompression in Graves' ophthalmopathy. Arch. Ophthalmol. 103 (1985) 660-665. KOORNNEEF, L.: Orbital bony and soft tissue anatomy. In: The Eye and Orbit in Thyroid Disease. Eds. G0LtMAN, C. A.; WALLER, R. R.; DYER, J. A.; New York: Raven Press 1984, pp. 5-23.
KOORNNEEF, L.: Orbital connective tissue. In: Biomedial Foundations of Ophthalmology. Eds. TASMAN, W.; JAEGER, E. A.; Vol. 1, Chap 32, Philadelphia: Lippincott 1989, pp. 1-23. LAMBERG, B. A.; GRAHNE, B.; 1bMM1LA, V.; PELKONEN, R.; RINNE, J.; LIESMAA, M.; VALIMAIU, M.:
Orbital decompression in endocrine exophthalmos of Graves' disease. Acta Endocrinol. (Copenh.) 109 (1985) 335-340. McCoiu, C. D.: Current trends in orbital decompression. Ophthalmology 92 (1985) 21-33. [111 SEHu, S. R.; SHORR, N.: Nasolacrimal drainage system obstruction after orbital decompression. Am. J. Ophthalmol. 106 (1988) 204-209. SHORR, N.; NEUHAUS, R. W.; BAYLIS, H. I.: Ocular motility problems after orbital decompression for dysthyroid ophthalmopathy. Ophthalmology 89 (1982) 323-328. WALLER, R. R.: Eyelid malpositions in Graves' ophthalmopathy. Trans. Am. Ophthalmol. Soc. 80 (1982) 855-930. WA1N, J. D.; SPECTOR, J. G.; BURDE, R.: Long term follow-up and recent observations on 305 cases of orbital decompression for dysthyroid orbitopathy. Laryngoscope 99 (1989) 35-40.
Author's address: Dr. C. A. GoIAN, M.B., B.Ch., Division of Endocrinology, Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota 55905, U.S.A.
Downloaded by: Universite Laval. Copyrighted material.
determine visual acuity, amount of proptosis and lid retraction, status of the cornea, optic nerve function, and ocular motility are required. Preoperative CT scanning provides confirmatory diagnostic information in addition to a survery of the relevant sinus anatomy. Orbital decompression for the appropriate indications followed in sequence by extraocular muscle surgery and eyelid surgery if required, complete the surgical rehabilitation of the Graves' patient. An integrated coordinated team approach is most efficient in terms of optimal patient
J. A. Barth, Leipzig
Mayo Clinic, Department of Ophthalmology (Head: R. F. Brubaker, M.D.), and Division of Endocrinology, Department of Internal Medicine (Head: C. A. Gorman, M.B., B.CH.),
Rochester, Minnesota/U.S.A.
Pitfalls Associated with Orbital Decompression for Thyroid-Related Orbitopathy
With 3 Figures
Introduction
Many of the clinical manifestations of thyroid-related orbitopathy can be treated directly to a discrepancy between the volume of the retro-ocular tissues and the space available to accommodate them. This has led to the concept that primary therapy for thyroid-related orbitopathy can be thought of as being directed either toward shrinkage of the expanded retro-ocular tissues or to expansion of the space available to accom-
modate them. The process of tissue shrinkage is attempted by therapy with corticosteroids, cyclosporin or radiation therapy. Expansion of the retrobulbar space has been approached by multiple routes, and operative techniques which involve removal of 1, 2, 3 or 4 orbital walls have been described. In general, their efficacy, as measured in terms of recessioh of proptosis, is related to the extent of bone removal. We have reviewed the effectiveness of various types of orbital decompression both in relation to reduction of retro-ocular tissue resistance and in terms of recession of proptosis (Garrity et al., 1989). In other studies we have examined the comparative effectiveness of transantral versus transfrontal orbital decompression for relief of optic neuropathy (Gorman et al., 1974). From these studies and analysis of our experience with large numbers of patients who have had transantral orbital decompression, we have concluded that transantral orbital decompression represents an effective and generally well tolerated approach to the management of patients with severe orbitopathy. Transantral decompression is used to relieve optic neuropathy, as a preliminary to extraocular muscle surgery in patients with excessive proptosis, and sometimes simply to diminish severe proptosis which on average is reduced between 4 and 5 5 millimeters (Baylis et al., 1980; De Santo, 1984; Hurwitz and Birt, 1985; Lamberg et al., 1985; McCord, 1985; Warren et al., 1989). In patients with reduced visual acuity either from optic neuropathy or a corneal ulcer, visual acuity improved in 101 of 143 (71 Wo) eyes. The operation is associated with rather consistent postoperative numbness of the upper lid, occasional episodes of cerebrospinal fluid leakage, nasolacrimal duct obstruction, oro-antral fistulae and medial entropion (De Santo, 1984). In general, however, it has
Downloaded by: Universite Laval. Copyrighted material.
J. GARRITY and C. Goiu&&r
339
J. GARRITY and C. GORMAN, Pitfalls of Orbital Decompression
proved to be a highly satisfactory procedure for most patients with severe Graves' ophthalmopathy (Garrity et al., 1989). In this presentation we wish to focus mainly on the potential pitfalls surrounding transantral orbital decompression. We will use illustrative examples of the specific problems we have encountered. These problems in general are related to difficulty in making the correct diagnosis or errors in choice, timing or circumstances of therapy. Some of the postoperative problems related to transantral orbital decompression will also be reviewed. Diagnostic Problems
(Fig. 1).
The following case (Fig. 2) illustrates this point. The profound unilateral chemosis and the lack of typical eye lid findings raise questions regarding the diagnosis of thyroidrelated orbitopathy. Computerized tomography (CT) is a powerful tool in the differential
DIAGNOSIS OF GRAVES' OPHTHALMOPATHY Examination of extraocular muscle movement
CT scan Ultrasound Visual acuity
Clinical evaluation
and color perception
Serum T4 - T3
TSI
Ophthalmoscopy
TRH
+ perimetry
T3
Ultrasound
suppression sTSH
Visual evoked
responses Unilateral
Bilateral
Exophthalmometry
Clinical and laboratory findings associated with thyroid-related orbitopathy. When all features are present, the diagnosis is ensured. The diagnosis is likely when all features in a single quadrant are presented. Isolated eyelid, muscle or optic nerve involvement is uncommon in thyroid-related orbitopathy. (from Gorman, C. A.: Extrathyroidal manifestations of Graves' disease. In: The Thyroid. Eds. Ingbar, S. H.; Braverman, L. E., Philadelphia: JB Lippincott 1984, with permission). Fig. 1
Downloaded by: Universite Laval. Copyrighted material.
Bilateral proptosis with upper lid retraction, clinical and biochemical evidence of hyperthyroidism and the presence of pretibial myxedema characterize the full clinical expression of Graves' disease. An accurate diagnosis is assured in this situation. Diagnostic difficulties can arise when the orbitopathy is asymmetric ("unilateral"), the findings are subtle and the patient is found to be euthyroid or even hypothyroid on examination. For example, in a recent review of 200 patients undergoing orbital decompression for severe thyroid-related orbitopathy, 16% had never been hyperthyroid prior to decompression (De Santo, 1984). In such circumstances, with an atypical presentation, one must carefully search for ancillary diagnostic features as there is no single pathognomonic finding
Fig. 2 A 57-year-old female experienced "recurrent right eye infections'' over the previous year which had become worse 2 weeks prior to evaluation. The vision was normal and there was no proptosis. Continuous diplopia began 1 week prior to evaluation. Note the profound unilateral chemosis. The CT scan however shows typical thyroid-related bilateral extraocular muscle enlargement. She was clinically euthyroid although minimal hyperthyroidism was detected biochemically.
diagnosis of thyroid-related orbitopathy. Characteristic bilateral extraocular muscle changes were demonstrated. Subtle hyperthyroidism was found on thyroid fqnction tests. The combination of thyroid hyperfunction and thyroid stimulating immunoglobulins in
serum with abnormal CT scan findings was sufficient to establish the diagnosis of thyroid-related orbitopathy. A transantral orbital decompression produced prompt resolution.
A different diagnostic hazard was encountered in a 64-year-old female with Hashimoto's thyroiditis. She had never been thyrotoxic. Microsomal and thyroglobulin
antibody titers were elevated. Horizontal diplopia began which progressed over 2 months. Over the same period the right eye became increasingly injected and chemotic. In the few days prior to admission the vision declined to 20/200 in the right eye. She was
referred for an urgent brbital decompression. Visual acuity was 20/200 right eye and 20/20 left eye. A right afferent pupillary defect was present. The right globe was 5 mm proptotic, diffusely injected and chemotic. Abduction was moderately impaired in the right eye and mildly impaired in the left eye. Visual field examination showed a cecocentral scotoma centered slightly above fixation. A CT scan of the orbits showed an asymmetric dilation of the right superior ophthalmic vein. The findings of the atypical visual
field defect which extended above the fixation point and the asymmetrically dilated superior ophthalmic vein led us to suspect a dural-cavernous sinus fistula. This was confirmed by angiography and spontaneously closed shortly thereafter. Other potential sources of diagnostic confusion include sphenoid wing meningioma,
optic nerve sheath meningioma, Wegener's granulomatosis, orbital lymphoma, mucocele, and orbital myositis. Ocular myasthenia gravis with diplopia, unilateral ptosis and "retraction" of the contralateral lid is rarely difficult to distinguish from thyroidrelated orbitopathy. Errors in diagnosis represent the first set of opportunities for errors in sequencing,
choice of surgical approach, and technical errors. A second set is associated with preoperative medical problems. Clinicians should be alert for inadequately treated hyperthyroidism or adrenal insuffiency in the patient abruptly withdrawn from corticosteroids.
Downloaded by: Universite Laval. Copyrighted material.
Exp. Clin. Endocrinol. 97 (1991) 2/3
340
J. GARRITY and C. GORMAN, Pitfalls of Orbital Decompression
341
Stress associated with general anesthesia can precipitate acute adrenal insufficiency which can be avoided by administering corticosteroids parenterally with the premedication for anesthesia. Technical Problems
muscles mandates inclusion of the superior or medial wall. Apical decompression can only be accomplished effectively when these walls are removed. The transantral route allows for adequate decompression of the posterior ethmoids which makes this procedure particularly effective for treating patients in whom a lateral or inferior decompression has failed. For this and other reasons the transantral route has become our preferred technique for the majority of the orbital decompressions. Technical aspects of the transantral decompression have been described elsewhere (De Santo, 1984). The maximum potential for life threatening complications however arises during the ethmoidectomy. The roof of the ethmoid sinus is also the floor of the anterior cranial fossa. Cerebrospinal fluid leaks arise from breaks in the dura in this region. It is
important to preoperatively obtain an orbital CT sca with direct coronal views (preferable to reformatted coronal views) to examine for an anomalous roof. The CT scan will also disclose potential operative difficulty from small sinuses or thick bone. If an anomalous roof is present, knowledge of this will call for extra caution to avoid a CSF leak when working near these areas. The threat of a CSF leak persists even after successful decompression surgery. A patient with an anomalous roof underwent an uneventful transantral decompression. Three months postoperatively a paraoxysmal coughing episode
was followed by clear rhinorrhea. An intrathecal metrizamide study confirmed cerebrospinal fluid leakage (Fig. 3). The leak was successfully repaired via an external ethmoidectomy approach. Anbther female with severe steroid dependent congestive orbitopathy had been taking high dose corticosteroids for a year. In addition to exhibiting clinical signs of exogenous cortisone excess, the orbital bones seemed brittle. When removal of the medial orbital wall was attempted at surgery, it fractured into the roof of the ethmoid sinus producing a CSF leak. This eventually required surgical repair also by an external ethmoidectomy approach. Postoperative Problems Decompressions of the orbital floor are associated with downward displacement of the globe. The transantral route is particularly effective at decompression of the floor and the effect is especially apparent after a unilateral transantral decompression. This vertical separation of the visual axes can induce vertical diplopia. For this reason, in the rare circumstance when unilateral decompression is advised, we prefer anterior or transorbital approaches. Diplopia is a well recognized postoperative consequence of transantral orbital decompression (De Santo, 1984; Shorr et al., 1982). Sometimes it is clear that actual prolapse of the extraocular muscle(s) into the opened sinus(es) has occurred. More often prolapse of
Downloaded by: Universite Laval. Copyrighted material.
Surgeons should tailor the decompression procedure to the problem at hand. The presence of an optic neuropathy from apical compression by enlarged extraocular
Exp. Clin. Endocrinol. 97 (1991) 2/3
Fig. 3 Direct coronal CT scans of orbit. Preoperative (left) and postoperative metrizamide study (right). Note the absence of bone in the ethmoid sinus roof (white arrow). The metrizamide is seen in the
left ethmoid sinus confirming CSF leakage (black arrow).
retrobulbar fat exerts traction on the velamentous fibrous intermuscular septae so elegantly described by Koornneef (1984, 1989). Further restriction and diplopia follow. Postoperative exposure keratitis can be seen in conjunction with globe depression following decompression of the orbital floor. One of our patients who had prominent upper lid retraction and lid lag had extremely large superior rectus/levator muscles noted on the CT scan. The apparent lid retraction increased postoperatively because the globes
"dropped" and the lids remained in the sanie relative position producing severe lagophthalmos. An urgent recession of Muellers muscle and the levator was required. The presence of these preoperative findings should alert one to the possibility of postoperative exposure keratitis. A medial entropion of the lower lid may also be seen in association with a decompression of the floor. As the inferior rectus muscle, with the associated lower lid retractors, prolapses into the opened maxillary sinus, traction is transmitted to the tarsus which can cause an entropion. Excessive traction on the orbital connective tissue at surgery potentiates this problem. Recession of the lower lid retractors is curative (Wailer, 1982). Sinus opacification is a normal postoperative x-ray finding. Postoperative swelling and discomfort may be incorrectly classified as infective sinusitis especially in light of sinus X-rays which show opacification. An adequate naso-antral window promotes maxillary sinus drainage and should obviate any infection. Postoperative tearing may be related to placement of the nasoantral windows. The nasolacrimal duct exits below the inferior turbinate and can be compromised while the nasoantral windows are being made (Colvard et al., 1979; Seiff and Shorr, 1980). Either
Downloaded by: Universite Laval. Copyrighted material.
342
J. GARRITY and C. Goiu&.&, Pitfalls of Orbital Decompression
343
intubatial of the lacrimal system with silastic tubing or a lacryocystorhinostomy may be required. Despite these caveats, we believe that bilateral transantral orbital decompression is an
effective and safe procedure. Proper patient selection with a thorough preoperative general medical evaluation correction of thyroid dysfunction, an eye examination to
care.
References BAYLIS, H. I.; CALL, N. B.; SHIBATA, C. S.: The transantral orbital decompression (Ogura techni-
que) as performed by the ophthalmologist. Ophthalmology. 87 (1980) 1005-1012. CoLvuw, D. M.; WALLER, R. R.; NEALT, R. W.; DE SANTO, L. W.: Nasolacrimal duct obstruction
following transantral-ethmoidal orbital decompression. Ophthaln'iic Surg. 10 (1979) 25-28. DE SAro, L. W.: Transantral orbital decompression. In: The Eye and Orbit in Thyroid Disease. Eds. Goiu&, C. A.; WALLER, R. R.; DYER, J. A.; New York: Raven Press 1984, pp. 231-251. GARRITY, J. A.; MCCAFFREY, T. V.; GORMAN, C. A.: Compression and decompression of orbital
contents in Graves' ophthalmopathy. Acta Endocrinol. (Copenh.) 121 (Suppi. 2) (1989) 160-168. Go1kN, C. A.; DESANio, L. W.; MACCARTY, C. S.; RILEY, E C.: Optic neuropathy of Graves' disease. 'fleatment by transantral or transfrontal orbital decompression. N. Engl. J. Med. 290 (1974) 70-75. HURWITZ, J. J.; BWT, D.: An individualized approach to orbital decompression in Graves' ophthalmopathy. Arch. Ophthalmol. 103 (1985) 660-665. KOORNNEEF, L.: Orbital bony and soft tissue anatomy. In: The Eye and Orbit in Thyroid Disease. Eds. G0LtMAN, C. A.; WALLER, R. R.; DYER, J. A.; New York: Raven Press 1984, pp. 5-23.
KOORNNEEF, L.: Orbital connective tissue. In: Biomedial Foundations of Ophthalmology. Eds. TASMAN, W.; JAEGER, E. A.; Vol. 1, Chap 32, Philadelphia: Lippincott 1989, pp. 1-23. LAMBERG, B. A.; GRAHNE, B.; 1bMM1LA, V.; PELKONEN, R.; RINNE, J.; LIESMAA, M.; VALIMAIU, M.:
Orbital decompression in endocrine exophthalmos of Graves' disease. Acta Endocrinol. (Copenh.) 109 (1985) 335-340. McCoiu, C. D.: Current trends in orbital decompression. Ophthalmology 92 (1985) 21-33. [111 SEHu, S. R.; SHORR, N.: Nasolacrimal drainage system obstruction after orbital decompression. Am. J. Ophthalmol. 106 (1988) 204-209. SHORR, N.; NEUHAUS, R. W.; BAYLIS, H. I.: Ocular motility problems after orbital decompression for dysthyroid ophthalmopathy. Ophthalmology 89 (1982) 323-328. WALLER, R. R.: Eyelid malpositions in Graves' ophthalmopathy. Trans. Am. Ophthalmol. Soc. 80 (1982) 855-930. WA1N, J. D.; SPECTOR, J. G.; BURDE, R.: Long term follow-up and recent observations on 305 cases of orbital decompression for dysthyroid orbitopathy. Laryngoscope 99 (1989) 35-40.
Author's address: Dr. C. A. GoIAN, M.B., B.Ch., Division of Endocrinology, Department of Internal Medicine, Mayo Clinic, Rochester, Minnesota 55905, U.S.A.
Downloaded by: Universite Laval. Copyrighted material.
determine visual acuity, amount of proptosis and lid retraction, status of the cornea, optic nerve function, and ocular motility are required. Preoperative CT scanning provides confirmatory diagnostic information in addition to a survery of the relevant sinus anatomy. Orbital decompression for the appropriate indications followed in sequence by extraocular muscle surgery and eyelid surgery if required, complete the surgical rehabilitation of the Graves' patient. An integrated coordinated team approach is most efficient in terms of optimal patient
