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Graves’ disease, an autoimmune disorder that consists of hyperthyroidism, goiter, and exophthalmos, is the most common cause of hyperthyroidism (incidence 5 in 10,000). More women are afflicted, but men show more severe orbit-opathy. Immunoglobins activate thyrotropin receptors causing thyromegaly and thyroxin release. Antibody-mediated infiltrates thicken the orbital tissues, but uniquely spare the lateral rectus muscle (Figure 1A). Only 6% of Graves’ patients have clinical thyroid eye disease (TED). As orbital volumes expand, globes become proptotic and eyelids cannot fully close (Figure 1B). The resultant exposure keratitis causes painful irritation and redness. Optic nerve compression and diplopia from muscle fibrosis may further deteriorate vision, culminating in blindness. Although the mechanism is unclear, radioactive iodine ablation therapy and smoking significantly accelerate the development and progression of TED. Medical therapy aims to control orbital inflammation. Oral steroids benefit acutely, but fail to halt overall progression. External-beam radiation (XRT) may improve the acute inflammation but potentiates long-term fibrosis. The modest benefit of XRT has the high cost of long-term dry eye keratitis and premature cataracts. Orbital decompression, the surgical removal of the orbital walls, displaces the orbital girth and relieves the pressure on the globe, thus resolving the proptosis. By performing equal
Orbital Decompression for Thyroid Eye Disease
(A) Coronal CT of a patient s/p left orbital decompression. Inferior and medial rectus hypertrophy (*) is present as is com-‐pression of the right optic nerve (arrow). The left apex is more relaxed as the orbital contents displace into the temporal fossa and sinuses (arrowheads). (B) Axial CT shows severe TED. The entire globe is anterior to a dashed line drawn from the lateral canthus to the lacrimal crest. This extreme proptosis causes
decompression of the medial and lateral orbital walls, the globe remains centered and does not list (e.g. eso- or exo-tropia). Therefore, balanced orbital decompression maximally relieves proptosis while minimizing diplopia. CASE REPORT A 24 year-old transmission mechanic found it impossible to work because of a new tremor, blurry vision, and heat intolerance. He was diagnosed with Graves’ disease and his hyperthyroidism was effectively controlled with methimazole. His vision, however, continued to deteriorate and his eyes were red and painful. Exam revealed severe scleral injection and proptosis (Hertel = 28 mm). CT confirmed no orbital masses (Figure 2A). He underwent bilateral balanced orbital decompression. The lateral and inferior walls were removed via concealed transconjunctival and lateral canthotomy incisons. Concur-rently, an endoscopic endonasal approach allowed the medial wall and strut to be removed. The lateral orbital rims were advanced anteriorly and secured with bone grafts, thus moving the lateral canthus forward and optimizing lid closure. Stereotactic image-guidance surgical navigation safely allowed for maximum decompression of the orbital walls to the skull base and orbital apex. He had a succesful resultant decompression (Figure 2B). His eye pain and irritation resolved, and his vision and proptosis improved dramatically (Hertel = 17 mm) with an 11
(A) Coronal CT after left orbital decompression. Inferior and medial rectus hypertrophy (*) and right optic nerve (arrow) com-pression are present. Removed orbital walls allow displacement into the temporal fossa and sinuses (arrowheads) resulting in a less crowded orbit. (B) Axial CT shows severe TED. The entire globe is anterior to the orbital plane: a line from the lateral canthus to the lacrimal crest. This extreme proptosis causes stretching of the optic nerve (arrow) and exposure keratitis.
Amol Bhatki, MD, Grant Gilliland, MD and Manu Gupta, MD
(A) Preop axial CT shows significant proptosis with hypertrophy of both the orbital fat and extraocular muscles. The majority of the globe is anterior to the orbital plane (dashed line). (B) After bilateral balanced orbital decompression, the orbital tissues have been displaced successfully into the temporal fossa (arrowheads) and ethmoid sinuses (*). Because of this, the proptosis has resolved and the equator of the globe is now posterior to the orbital plane.
Figure 1 Figure 2
Graves’ disease, an autoimmune disorder that consists of hyperthyroidism, goiter, and exophthalmos, is the most common cause of hyperthyroidism (incidence 5 in 10,000). More women are afflicted, but men show more severe orbit-opathy. Immunoglobins activate thyrotropin receptors causing thyromegaly and thyroxin release. Antibody-mediated infiltrates thicken the orbital tissues, but uniquely spare the lateral rectus muscle (Figure 1A). Only 6% of Graves’ patients have clinical thyroid eye disease (TED). As orbital volumes expand, globes become proptotic and eyelids cannot fully close (Figure 1B). The resultant exposure keratitis causes painful irritation and redness. Optic nerve compression and diplopia from muscle fibrosis may further deteriorate vision, culminating in blindness. Although the mechanism is unclear, radioactive iodine ablation therapy and smoking significantly accelerate the development and progression of TED. Medical therapy aims to control orbital inflammation. Oral steroids benefit acutely, but fail to halt overall progression. External-beam radiation (XRT) may improve the acute inflammation but potentiates long-term fibrosis. The modest benefit of XRT has the high cost of long-term dry eye keratitis and premature cataracts. Orbital decompression, the surgical removal of the orbital walls, displaces the orbital girth and relieves the pressure on the globe, thus resolving the proptosis. By performing equal
Orbital Decompression for Thyroid Eye Disease
(A) Coronal CT of a patient s/p left orbital decompression. Inferior and medial rectus hypertrophy (*) is present as is com-‐pression of the right optic nerve (arrow). The left apex is more relaxed as the orbital contents displace into the temporal fossa and sinuses (arrowheads). (B) Axial CT shows severe TED. The entire globe is anterior to a dashed line drawn from the lateral canthus to the lacrimal crest. This extreme proptosis causes
decompression of the medial and lateral orbital walls, the globe remains centered and does not list (e.g. eso- or exo-tropia). Therefore, balanced orbital decompression maximally relieves proptosis while minimizing diplopia. CASE REPORT A 24 year-old transmission mechanic found it impossible to work because of a new tremor, blurry vision, and heat intolerance. He was diagnosed with Graves’ disease and his hyperthyroidism was effectively controlled with methimazole. His vision, however, continued to deteriorate and his eyes were red and painful. Exam revealed severe scleral injection and proptosis (Hertel = 28 mm). CT confirmed no orbital masses (Figure 2A). He underwent bilateral balanced orbital decompression. The lateral and inferior walls were removed via concealed transconjunctival and lateral canthotomy incisons. Concur-rently, an endoscopic endonasal approach allowed the medial wall and strut to be removed. The lateral orbital rims were advanced anteriorly and secured with bone grafts, thus moving the lateral canthus forward and optimizing lid closure. Stereotactic image-guidance surgical navigation safely allowed for maximum decompression of the orbital walls to the skull base and orbital apex. He had a succesful resultant decompression (Figure 2B). His eye pain and irritation resolved, and his vision and proptosis improved dramatically (Hertel = 17 mm) with an 11
(A) Coronal CT after left orbital decompression. Inferior and medial rectus hypertrophy (*) and right optic nerve (arrow) com-pression are present. Removed orbital walls allow displacement into the temporal fossa and sinuses (arrowheads) resulting in a less crowded orbit. (B) Axial CT shows severe TED. The entire globe is anterior to the orbital plane: a line from the lateral canthus to the lacrimal crest. This extreme proptosis causes stretching of the optic nerve (arrow) and exposure keratitis.
Amol Bhatki, MD, Grant Gilliland, MD and Manu Gupta, MD
(A) Preop axial CT shows significant proptosis with hypertrophy of both the orbital fat and extraocular muscles. The majority of the globe is anterior to the orbital plane (dashed line). (B) After bilateral balanced orbital decompression, the orbital tissues have been displaced successfully into the temporal fossa (arrowheads) and ethmoid sinuses (*). Because of this, the proptosis has resolved and the equator of the globe is now posterior to the orbital plane.
Figure 1 Figure 2
Graves’ disease, an autoimmune disorder that consists of hyperthyroidism, goiter, and exophthalmos, is the most common cause of hyperthyroidism (incidence 5 in 10,000). More women are afflicted, but men show more severe orbit-opathy. Immunoglobins activate thyrotropin receptors causing thyromegaly and thyroxin release. Antibody-mediated infiltrates thicken the orbital tissues, but uniquely spare the lateral rectus muscle (Figure 1A). Only 6% of Graves’ patients have clinical thyroid eye disease (TED). As orbital volumes expand, globes become proptotic and eyelids cannot fully close (Figure 1B). The resultant exposure keratitis causes painful irritation and redness. Optic nerve compression and diplopia from muscle fibrosis may further deteriorate vision, culminating in blindness. Although the mechanism is unclear, radioactive iodine ablation therapy and smoking significantly accelerate the development and progression of TED. Medical therapy aims to control orbital inflammation. Oral steroids benefit acutely, but fail to halt overall progression. External-beam radiation (XRT) may improve the acute inflammation but potentiates long-term fibrosis. The modest benefit of XRT has the high cost of long-term dry eye keratitis and premature cataracts. Orbital decompression, the surgical removal of the orbital walls, displaces the orbital girth and relieves the pressure on the globe, thus resolving the proptosis. By performing equal
Orbital Decompression for Thyroid Eye Disease
(A) Coronal CT of a patient s/p left orbital decompression. Inferior and medial rectus hypertrophy (*) is present as is com-‐pression of the right optic nerve (arrow). The left apex is more relaxed as the orbital contents displace into the temporal fossa and sinuses (arrowheads). (B) Axial CT shows severe TED. The entire globe is anterior to a dashed line drawn from the lateral canthus to the lacrimal crest. This extreme proptosis causes
decompression of the medial and lateral orbital walls, the globe remains centered and does not list (e.g. eso- or exo-tropia). Therefore, balanced orbital decompression maximally relieves proptosis while minimizing diplopia. CASE REPORT A 24 year-old transmission mechanic found it impossible to work because of a new tremor, blurry vision, and heat intolerance. He was diagnosed with Graves’ disease and his hyperthyroidism was effectively controlled with methimazole. His vision, however, continued to deteriorate and his eyes were red and painful. Exam revealed severe scleral injection and proptosis (Hertel = 28 mm). CT confirmed no orbital masses (Figure 2A). He underwent bilateral balanced orbital decompression. The lateral and inferior walls were removed via concealed transconjunctival and lateral canthotomy incisons. Concur-rently, an endoscopic endonasal approach allowed the medial wall and strut to be removed. The lateral orbital rims were advanced anteriorly and secured with bone grafts, thus moving the lateral canthus forward and optimizing lid closure. Stereotactic image-guidance surgical navigation safely allowed for maximum decompression of the orbital walls to the skull base and orbital apex. He had a succesful resultant decompression (Figure 2B). His eye pain and irritation resolved, and his vision and proptosis improved dramatically (Hertel = 17 mm) with an 11
(A) Coronal CT after left orbital decompression. Inferior and medial rectus hypertrophy (*) and right optic nerve (arrow) com-pression are present. Removed orbital walls allow displacement into the temporal fossa and sinuses (arrowheads) resulting in a less crowded orbit. (B) Axial CT shows severe TED. The entire globe is anterior to the orbital plane: a line from the lateral canthus to the lacrimal crest. This extreme proptosis causes stretching of the optic nerve (arrow) and exposure keratitis.
Amol Bhatki, MD, Grant Gilliland, MD and Manu Gupta, MD
(A) Preop axial CT shows significant proptosis with hypertrophy of both the orbital fat and extraocular muscles. The majority of the globe is anterior to the orbital plane (dashed line). (B) After bilateral balanced orbital decompression, the orbital tissues have been displaced successfully into the temporal fossa (arrowheads) and ethmoid sinuses (*). Because of this, the proptosis has resolved and the equator of the globe is now posterior to the orbital plane.
Figure 1 Figure 2
Graves’ disease, an autoimmune disorder that consists of hyperthyroidism, goiter, and exophthalmos, is the most common cause of hyperthyroidism (incidence 5 in 10,000). More women are afflicted, but men show more severe orbit-opathy. Immunoglobins activate thyrotropin receptors causing thyromegaly and thyroxin release. Antibody-mediated infiltrates thicken the orbital tissues, but uniquely spare the lateral rectus muscle (Figure 1A). Only 6% of Graves’ patients have clinical thyroid eye disease (TED). As orbital volumes expand, globes become proptotic and eyelids cannot fully close (Figure 1B). The resultant exposure keratitis causes painful irritation and redness. Optic nerve compression and diplopia from muscle fibrosis may further deteriorate vision, culminating in blindness. Although the mechanism is unclear, radioactive iodine ablation therapy and smoking significantly accelerate the development and progression of TED. Medical therapy aims to control orbital inflammation. Oral steroids benefit acutely, but fail to halt overall progression. External-beam radiation (XRT) may improve the acute inflammation but potentiates long-term fibrosis. The modest benefit of XRT has the high cost of long-term dry eye keratitis and premature cataracts. Orbital decompression, the surgical removal of the orbital walls, displaces the orbital girth and relieves the pressure on the globe, thus resolving the proptosis. By performing equal
Orbital Decompression for Thyroid Eye Disease
(A) Coronal CT of a patient s/p left orbital decompression. Inferior and medial rectus hypertrophy (*) is present as is com-‐pression of the right optic nerve (arrow). The left apex is more relaxed as the orbital contents displace into the temporal fossa and sinuses (arrowheads). (B) Axial CT shows severe TED. The entire globe is anterior to a dashed line drawn from the lateral canthus to the lacrimal crest. This extreme proptosis causes
decompression of the medial and lateral orbital walls, the globe remains centered and does not list (e.g. eso- or exo-tropia). Therefore, balanced orbital decompression maximally relieves proptosis while minimizing diplopia. CASE REPORT A 24 year-old transmission mechanic found it impossible to work because of a new tremor, blurry vision, and heat intolerance. He was diagnosed with Graves’ disease and his hyperthyroidism was effectively controlled with methimazole. His vision, however, continued to deteriorate and his eyes were red and painful. Exam revealed severe scleral injection and proptosis (Hertel = 28 mm). CT confirmed no orbital masses (Figure 2A). He underwent bilateral balanced orbital decompression. The lateral and inferior walls were removed via concealed transconjunctival and lateral canthotomy incisons. Concur-rently, an endoscopic endonasal approach allowed the medial wall and strut to be removed. The lateral orbital rims were advanced anteriorly and secured with bone grafts, thus moving the lateral canthus forward and optimizing lid closure. Stereotactic image-guidance surgical navigation safely allowed for maximum decompression of the orbital walls to the skull base and orbital apex. He had a succesful resultant decompression (Figure 2B). His eye pain and irritation resolved, and his vision and proptosis improved dramatically (Hertel = 17 mm) with an 11
(A) Coronal CT after left orbital decompression. Inferior and medial rectus hypertrophy (*) and right optic nerve (arrow) com-pression are present. Removed orbital walls allow displacement into the temporal fossa and sinuses (arrowheads) resulting in a less crowded orbit. (B) Axial CT shows severe TED. The entire globe is anterior to the orbital plane: a line from the lateral canthus to the lacrimal crest. This extreme proptosis causes stretching of the optic nerve (arrow) and exposure keratitis.
Amol Bhatki, MD, Grant Gilliland, MD and Manu Gupta, MD
(A) Preop axial CT shows significant proptosis with hypertrophy of both the orbital fat and extraocular muscles. The majority of the globe is anterior to the orbital plane (dashed line). (B) After bilateral balanced orbital decompression, the orbital tissues have been displaced successfully into the temporal fossa (arrowheads) and ethmoid sinuses (*). Because of this, the proptosis has resolved and the equator of the globe is now posterior to the orbital plane.
Figure 1 Figure 2
Graves’ disease, an autoimmune disorder that consists of hyperthyroidism, goiter, and exophthalmos, is the most common cause of hyperthyroidism (incidence 5 in 10,000). More women are afflicted, but men show more severe orbitopathy. Immunoglobins activate thyrotropin receptors causing thyromegaly and thyroxin release. Antibody-mediated infiltrates thicken the orbital tissues, but uniquely spare the lateral rectus muscle (Figure 1A).
Only 6% of Graves’ patients have clinical thyroid eye disease (TED). As orbital volumes expand, globes become proptotic and eyelids cannot fully close (Figure 1B). The resultant exposure keratitis causes painful irritation and redness. Optic nerve compression and diplopia from muscle fibrosis may further deteriorate vision, culminating in blindness. Although the mechanism is unclear, radioactive iodine ablation therapy and smoking significantly accelerate the development and progression of TED.
Medical therapy aims to control orbital inflammation. Oral steroids benefit acutely, but fail to halt overall progression. External-beam radiation (XRT) may improve the acute inflammation but potentiates long-term fibrosis. The modest benefit of XRT has the high cost of long-term dry eye keratitis and premature cataracts.
Orbital decompression, the surgical removal of the orbital walls, displaces the orbital girth and relieves the pressure on
the globe, thus resolving the proptosis. By performing equal decompression of the medial and lateral orbital walls, the globe remains centered and does not tilt (e.g. eso- or exotropia). Therefore, balanced orbital decompression maximally relieves proptosis while minimizing diplopia.
CASE STUDYA 24 year-old transmission mechanic found it impossible to work because of a new tremor, blurry vision, and heat intolerance. He was diagnosed with Graves’ disease and his hyperthyroidism was effectively controlled with methimazole.His vision, however, continued to deteriorate and his eyes were red and painful. Exam revealed severe scleral injection and proptosis (Hertel = 28 mm). CT confirmed no orbital masses (Figure 2A).
He underwent bilateral balanced orbital decompression. The lateral and inferior walls were removed via concealed transconjunctival and lateral canthotomy incisons. Concurrently, an endoscopic endonasal approach allowed the medial wall and strut to be removed. The lateral orbital rims were advanced anteriorly and secured with bone grafts, thus moving the lateral canthus forward and optimizing lid closure. Stereotactic image-guidance surgical navigation safely allowed for maximum decompression of the orbital walls to the skull base and orbital apex.
He had a succesful resultant decompression (Figure 2B).
Continued
Amol Bhatki, MD, Grant Gilliland, MD and Manu Gupta, MD
(A) Coronal CT after left orbital decompression. Inferior and medial rectus hypertrophy (*) and right optic nerve (arrow) compression. Displacement into the temporal fossa and sinuses (arrowheads) results in less orbital crowding. (B) Axial CT of another patient. The entire globe is anterior to the orbital plane. Extreme proptosis causes optic nerve stretching (arrow) and exposure keratitis.
(A) Preop CT shows proptosis with both muscle and fat hypertrophy. Most of the globe is anterior to the orbital plane (dashed line). (B) After bilateral balanced orbital decompression, the orbital tissues have displaced successfully into the temporal fossa (arrowheads) and ethmoid sinuses (*). The proptosis has resolved and the equator of the globe is now posterior to the orbital plane.
Orbital Decompression for Thyroid Eye Disease
FIGURE 1 FIGURE 2
Volume 1 • Number 6 • Winter 2017
A B A B
Modern Surgical Approaches to Tuberculum Sellae Meningiomas
Coronal
Figure 1
Skull Base Center Clinical Case Report
Coronal contrast-enhanced MRI anterior (A) and more pos-terior (B). The optic nerves (white arrow) are seen lateral to the tumor (T) throughout their course. Note the dural tail (blue arrow), optic canal extension (white arrowhead), and intimate relationship to cavernous carotid (black arrowhead) typical of TSM.
(A) Preoperative MRI shows expansile, homogenously enhancing tumor with dural tail (blue arrow) that displac-es the infundibulum dorsally (white arrowhead). (B) One year after EEA, MRI shows a normal infundibulum (white arrowhead) and the outline of a well-healed vascularized flap (white arrows).
Figure 2
Amol Bhatki, M.D. (Otolaryngology); Caetano Coimbra, M.D. (Neurosurgery)
Patients with tuberculum sellae meningiomas (TSM) often present with subtle, progressive visual deterioration. These tumors expand the suprasellar space displacing the optic nerves and chiasm; optic canal extension is frequent. TSM typically demonstrate homogenous contrast enhancement, normal sellar dimensions, and dural tails on MRI differentiating them from pituitary adenomas.
Conventional pterional, bifrontal, or orbito-zygomatic crani-otomy requires frontal and temporal lobe retraction, extensive subarachnoid dissection, and facial disassembly. Modern techniques can resolve these shortcomings. The endoscopic endonasal approach (EEA) provides a transnasal corridor obviating brain retraction, neural manipulation, and facial osteotomies. Alternatively, the focused orbito-zygomatic keyhole craniotomy (FOZA) with extradural dissection, a technique developed at the Skull Base Center, provides direct extradural access to the tumor minimizing brain and optic nerve manipulation. The position of the optic nerve defines the appropriate approach.
This report describes two cases that illustrate our modern approach to the treatment of TSM at the Skull Base Center at Baylor University Medical Center at Dallas.
Patient 1: A 41 year-old woman presented with a 1-year history of visual deterioration and a bitemporal visual field deficit. MRI (Figure 1) revealed a sellar and suprasellar mass that enhanced homogenously. The 2.6 cm tumor displaced the infundibulum dorsally and the optic nerve laterally, and extended along a hyperostotic planum sphenoidale.
Because the TSM was medial to the optic nerves, the patient underwent an EEA. Complete tumor excision (Simpson Grade I) was achieved without optic nerve or brain traction. A vas-cularized nasoseptal flap reconstructed the skull base. The patient was discharged on POD#6 and pathology revealed a WHO Grade I meningioma. The patient had total visual recov-ery and normal hormonal function. At 1-year follow-up, there was no evidence of recurrent disease (Figure 2).
Patient 2: A 53 year-old woman presented with similar visual field deficits and headache. MRI again revealed a 2.5 cm enhancing sellar/suprasellar mass. However, this tumor extended lateral to the right optic canal (Figure 3), and would be difficult to remove endonasally without undue nerve traction.
Modern Surgical Approaches to Tuberculum Sellae Meningiomas
Coronal
Figure 1
Skull Base Center Clinical Case Report
Coronal contrast-enhanced MRI anterior (A) and more pos-terior (B). The optic nerves (white arrow) are seen lateral to the tumor (T) throughout their course. Note the dural tail (blue arrow), optic canal extension (white arrowhead), and intimate relationship to cavernous carotid (black arrowhead) typical of TSM.
(A) Preoperative MRI shows expansile, homogenously enhancing tumor with dural tail (blue arrow) that displac-es the infundibulum dorsally (white arrowhead). (B) One year after EEA, MRI shows a normal infundibulum (white arrowhead) and the outline of a well-healed vascularized flap (white arrows).
Figure 2
Amol Bhatki, M.D. (Otolaryngology); Caetano Coimbra, M.D. (Neurosurgery)
Patients with tuberculum sellae meningiomas (TSM) often present with subtle, progressive visual deterioration. These tumors expand the suprasellar space displacing the optic nerves and chiasm; optic canal extension is frequent. TSM typically demonstrate homogenous contrast enhancement, normal sellar dimensions, and dural tails on MRI differentiating them from pituitary adenomas.
Conventional pterional, bifrontal, or orbito-zygomatic crani-otomy requires frontal and temporal lobe retraction, extensive subarachnoid dissection, and facial disassembly. Modern techniques can resolve these shortcomings. The endoscopic endonasal approach (EEA) provides a transnasal corridor obviating brain retraction, neural manipulation, and facial osteotomies. Alternatively, the focused orbito-zygomatic keyhole craniotomy (FOZA) with extradural dissection, a technique developed at the Skull Base Center, provides direct extradural access to the tumor minimizing brain and optic nerve manipulation. The position of the optic nerve defines the appropriate approach.
This report describes two cases that illustrate our modern approach to the treatment of TSM at the Skull Base Center at Baylor University Medical Center at Dallas.
Patient 1: A 41 year-old woman presented with a 1-year history of visual deterioration and a bitemporal visual field deficit. MRI (Figure 1) revealed a sellar and suprasellar mass that enhanced homogenously. The 2.6 cm tumor displaced the infundibulum dorsally and the optic nerve laterally, and extended along a hyperostotic planum sphenoidale.
Because the TSM was medial to the optic nerves, the patient underwent an EEA. Complete tumor excision (Simpson Grade I) was achieved without optic nerve or brain traction. A vas-cularized nasoseptal flap reconstructed the skull base. The patient was discharged on POD#6 and pathology revealed a WHO Grade I meningioma. The patient had total visual recov-ery and normal hormonal function. At 1-year follow-up, there was no evidence of recurrent disease (Figure 2).
Patient 2: A 53 year-old woman presented with similar visual field deficits and headache. MRI again revealed a 2.5 cm enhancing sellar/suprasellar mass. However, this tumor extended lateral to the right optic canal (Figure 3), and would be difficult to remove endonasally without undue nerve traction.
mm improvement in proptosis (Figure 3). He returned to his previous employment in full capacity and his vision no longer limited in his fine motor tasks. DISCUSSION At the Baylor University Medical Center at Dallas, a team of oculoplastic and ENT surgeons utilize minimally-invasive surgical techniques to perform more than 50 balanced orbital decompressions annually for patients with clinically significant TED. A unique collaboration of specialists com-bined with endoscopic and image-guidance technology resolves troublesome eye symptoms and restores vision without disfiguring scars, a prolonged recovery, or significant risk of new-onset diplopia.
Figure 3
(A) Pre-operative photograph of patient with clinically signi-ficant thyroid eye disease. Note the bilateral proptosis. Closer inspection reveals scleral injection and stretched eyelids. (B) Post-operative photograph showing resolution of proptosis and scleral injection. Lid closure and corneal dryness are also significantly improved. Lateral eye crease scars are well camouflaged.
mm improvement in proptosis (Figure 3). He returned to his previous employment in full capacity and his vision no longer limited in his fine motor tasks. DISCUSSION At the Baylor University Medical Center at Dallas, a team of oculoplastic and ENT surgeons utilize minimally-invasive surgical techniques to perform more than 50 balanced orbital decompressions annually for patients with clinically significant TED. A unique collaboration of specialists com-bined with endoscopic and image-guidance technology resolves troublesome eye symptoms and restores vision without disfiguring scars, a prolonged recovery, or significant risk of new-onset diplopia.
Figure 3
(A) Pre-operative photograph of patient with clinically signi-ficant thyroid eye disease. Note the bilateral proptosis. Closer inspection reveals scleral injection and stretched eyelids. (B) Post-operative photograph showing resolution of proptosis and scleral injection. Lid closure and corneal dryness are also significantly improved. Lateral eye crease scars are well camouflaged. His eye pain and irritation resolved, and his vision and
proptosis improved dramatically (Hertel = 17 mm) with an 11 mm improvement in proptosis (Figure 3). He returned to his previous employment in full capacity and his vision no longer limited in his fine motor tasks.
At Baylor University Medical Center at Dallas, a team of oculoplastic and ENT surgeons on the medical staff utilize minimally-invasive surgical techniques to perform more than 50 balanced orbital decompressions annually for patients with clinically significant TED. A unique collaboration of specialists combined with endoscopic and image-guidance technology resolves troublesome eye symptoms and restores vision usually without disfiguring scars, a prolonged recovery, or significant risk of new-onset diplopia.
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FIGURE 3
(A) Pre-operative patient with thyroid eye disease. Note the bilateral proptosis, scleral injection, and stretched eyelids. (B) Post-operative photo shows resolution of proptosis and scleral injection. Lid closure and corneal dryness are also significantly improved.
A BEditors
Amol Bhatki, MD, Co-Medical Director and NeurotologistCaetano Coimbra, MD, Co-Medical Director and Neurotologist
Baylor Neuroscience Center Skull Base Center Medical Staff Members
David Barnett, MD, Neurosurgery
Amol Bhatki, MD, Otolaryngology, Skull Base Surgery
Caetano Coimbra, MD, MSc, FACS, Neurosurgery
Yoav Hahn, MD, Neurotologist
Grant Gilliland, MD, Oculoplastic Surgery
Joe Hise, MD, Interventional Neuroradiology
Kennith Layton, MD, Interventional Neuroradiology
Lance Oxford, MD, Otolaryngology, Head and Neck Surgery
Ike Thacker, MD, Interventional Neuroradiology
Skull Base Center Clinical Case Report
For New Patient Referrals:Kim Wiser – Referral Coordinator
Phone: 214.820.3900
Fax: 214.820.3884
Email: [email protected]
Treating Tumors of the Brain, Sinus, and Orbit
• Case Review
• Physician Consultation
• Continuing EducationPhysicians provide clinical services as members of the medical staff at one of Baylor Scott & White Health’s subsidiary, community or affiliated medical centers and do not provide clinical services as employees or agents of those medical centers, Baylor Health Care System, Scott & White Healthcare or Baylor Scott & White Health. © 2017 Baylor Scott & White Health. BSWNEURO_21_2016 SD
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