- •Preface
- •Contents
- •Contributors
- •1 Primary Orbital Cancers in Adults
- •1.1 Lymphoproliferative Disorders
- •1.1.1 Presenting Signs and Symptoms, Histopathologic and Molecular Genetic Characteristics, and Diagnosis
- •1.1.2 Treatment
- •1.1.3 Follow-up
- •1.2 Mesenchymal Tumors
- •1.2.1 Fibrous Histiocytoma
- •1.2.2 Solitary Fibrous Tumor
- •1.2.3 Hemangiopericytoma
- •1.2.4 Other Mesenchymal Tumors
- •1.3 Lacrimal Gland Tumors
- •References
- •2 Nonmalignant Tumors of the Orbit
- •2.1 Presentation
- •2.2 Cystic Lesions
- •2.3 Vascular Tumors
- •2.4 Lymphoproliferative Masses
- •2.6 Mesenchymal Tumors
- •2.7 Neurogenic Tumors
- •2.8 Lacrimal Gland Tumors
- •References
- •3 Pediatric Orbital Tumors
- •3.1 Introduction
- •3.2 Cystic Lesions
- •3.2.1 Dermoid Cyst
- •3.2.1.1 Clinical Presentation
- •3.2.1.2 Imaging
- •3.2.1.3 Histopathology
- •3.2.1.4 Treatment
- •3.2.1.5 Prognosis
- •3.2.2 Teratoma
- •3.2.2.1 Clinical Presentation
- •3.2.2.2 Imaging
- •3.2.2.3 Histopathology
- •3.2.2.4 Treatment
- •3.2.2.5 Prognosis
- •3.3 Vascular Tumors
- •3.3.1 Capillary Hemangioma
- •3.3.1.1 Clinical Presentation
- •3.3.1.2 Imaging
- •3.3.1.3 Histopathology
- •3.3.1.4 Treatment
- •3.3.1.5 Prognosis
- •3.3.2 Lymphangioma
- •3.3.2.1 Clinical Presentation
- •3.3.2.2 Imaging
- •3.3.2.3 Histopathology
- •3.3.2.4 Treatment
- •3.3.2.5 Prognosis
- •3.4 Histiocytic Lesions
- •3.4.1 Eosinophilic Granuloma
- •3.4.1.1 Clinical Presentation
- •3.4.1.2 Imaging
- •3.4.1.3 Histopathology
- •3.4.1.4 Treatment
- •3.4.1.5 Prognosis
- •3.5 Neural Tumors
- •3.5.1 Optic Nerve Glioma
- •3.5.1.1 Clinical Presentation
- •3.5.1.2 Imaging
- •3.5.1.3 Histopathology
- •3.5.1.4 Treatment
- •3.5.1.5 Prognosis
- •3.5.2.1 Clinical Presentation
- •3.5.2.2 Imaging
- •3.5.2.3 Histopathology
- •3.5.2.4 Treatment
- •3.5.2.5 Prognosis
- •3.6 Malignant Lesions
- •3.6.1 Ewing Sarcoma
- •3.6.1.1 Clinical Presentation
- •3.6.1.2 Imaging
- •3.6.1.3 Histopathology
- •3.6.1.4 Treatment
- •3.6.1.5 Prognosis
- •3.6.2 Neuroblastoma
- •3.6.2.1 Clinical Presentation
- •3.6.2.2 Imaging
- •3.6.2.3 Histopathology
- •3.6.2.4 Treatment
- •3.6.2.5 Prognosis
- •3.6.3 Retinoblastoma
- •3.6.3.1 Clinical Presentation
- •3.6.3.2 Imaging
- •3.6.3.3 Histopathology
- •3.6.3.4 Treatment
- •3.6.3.5 Prognosis
- •3.6.4 Granulocytic Sarcoma
- •3.6.4.1 Clinical Presentation
- •3.6.4.2 Imaging
- •3.6.4.3 Histopathology
- •3.6.4.4 Treatment
- •3.6.4.5 Prognosis
- •3.6.5 Rhabdomyosarcoma
- •References
- •4.1 Introduction
- •4.2 Clinical and Radiological Presentation
- •4.3 Staging
- •4.4 Surgery
- •4.5 Chemotherapy
- •4.6 Radiation Therapy
- •4.7 Conclusions and Future Directions
- •References
- •5 Metastatic Orbital Tumors
- •5.1 Introduction
- •5.2 Incidence
- •5.3 Anatomical Considerations
- •5.4 Presentation and Clinical Features
- •5.5 Diagnosis
- •5.6 Treatment
- •5.7 Types of Cancer Metastatic to the Orbit
- •5.7.1 Breast Carcinoma
- •5.7.2 Lung Carcinoma
- •5.7.3 Prostate Carcinoma
- •5.7.4 Melanoma
- •5.7.5 Carcinoid Tumors
- •5.7.6 Other Cancers
- •5.8 Conclusion
- •References
- •6.1 Tumors of Intraocular and Ocular Adnexal Origin
- •6.1.1 Eyelid Tumors
- •6.1.2 Intraocular Tumors
- •6.2 Tumors of Sinus and Nasopharyngeal Origin
- •6.2.1 Squamous Cell Carcinoma
- •6.2.2 Other Tumors of Sinus and Nasopharyngeal Origin
- •6.3 Tumors of Brain Origin
- •6.3.1 Meningioma
- •6.3.2 Other Intracranial Tumors
- •References
- •7 Lacrimal Gland Tumors
- •7.1 Introduction
- •7.2 Lymphoproliferative Lesions of the Lacrimal Gland
- •7.3 Benign Epithelial Tumors of the Lacrimal Gland
- •7.3.1 Pleomorphic Adenoma
- •7.3.2 Other Benign Epithelial Tumors
- •7.4 Malignant Epithelial Tumors of the Lacrimal Gland
- •7.4.1 Adenoid Cystic Carcinoma
- •7.4.2 Other Malignant Epithelial Tumors
- •7.5 AJCC Staging for Lacrimal Gland Tumors
- •References
- •8.1 Introduction
- •8.2 Indications
- •8.3 Surgical Techniques
- •8.3.1 Medial Orbitotomy Approach
- •8.3.2 Medial Eyelid Crease Approach
- •8.3.3 Lateral Orbitotomy Approach
- •8.3.4 Lateral Canthotomy Approach
- •8.4 Possible Indications for ONSF in Cancer Patients
- •8.4.1 Metastatic Breast Cancer
- •8.4.2 Lymphomatous Optic Neuropathy Diagnosed by Optic Nerve Biopsy
- •8.4.3 Adjuvant Therapy in Optic Nerve Sheath Meningioma
- •8.4.4 Papilledema Associated with Brain Tumors
- •8.4.5 Radiation-Induced Optic Neuropathy
- •8.5 Complications of ONSF
- •8.6 Future Research
- •References
- •9 Management of Primary Eyelid Cancers
- •9.1 Introduction
- •9.2 Types of Eyelid Malignancies
- •9.2.1 Basal Cell Carcinoma
- •9.2.2 Squamous Cell Carcinoma
- •9.2.3 Melanoma
- •9.2.4 Sebaceous Gland Carcinoma
- •9.2.5 Other Primary Eyelid Malignancies
- •9.3 Management
- •9.3.1 Evaluation
- •9.3.2 Tumor Excision and Eyelid Reconstruction
- •9.3.3 Sentinel Lymph Node Biopsy
- •9.3.4 Nonsurgical Treatment
- •9.3.5 Follow-up
- •References
- •10 Management of Conjunctival Neoplasms
- •10.1 Introduction
- •10.2 Squamous Cell Neoplasms of the Conjunctiva
- •10.2.1 Conjunctival Intraepithelial Neoplasia
- •10.2.2 Invasive Squamous Cell Carcinoma
- •10.2.3 Management
- •10.2.3.1 Local Excision and Cryotherapy
- •10.2.3.2 Treatment of More Advanced Disease
- •10.2.4 Surveillance
- •10.3 Melanocytic Neoplasms
- •10.3.1 Nevus
- •10.3.2 Primary Acquired Melanosis
- •10.3.3 Conjunctival Melanoma
- •References
- •11 Surgical Specimen Handling for Conjunctival and Eyelid Tumors
- •11.1 Introduction
- •11.2 Communication with the Pathologist
- •11.3 Conjunctival Specimens
- •11.4 Eyelid Specimens
- •11.5 Mohs Micrographic Surgery
- •11.6 Summary
- •References
- •12 Neuroradiology of Ocular and Orbital Tumors
- •12.1 Introduction: Imaging and Protocol
- •12.2 Anatomy
- •12.3 Intraocular Lesions
- •12.3.1 Retinoblastoma
- •12.3.2 Uveal Melanoma
- •12.3.3 Uveal Metastases
- •12.4 Orbital Lesions
- •12.4.1 Lymphoma
- •12.4.2 Orbital Rhabdomyosarcoma
- •12.4.3 Orbital Nerve Sheath Tumors
- •12.4.4 Mesenchymal Tumors of the Orbit
- •12.4.5 Orbital Pseudotumor
- •12.4.6 Orbital Metastases
- •12.5 Optic Nerve Tumors
- •12.5.1 Optic Nerve Glioma
- •12.5.2 Optic Nerve Sheath Meningiomas
- •12.6 Lacrimal Gland Tumors
- •12.7 Secondary Tumor Spread to the Orbit
- •12.8 Periorbital Skin Cancer and Perineural Spread
- •12.9 Conclusion
- •References
- •13 Radiation Therapy for Orbital and Adnexal Tumors
- •13.1 Indications
- •13.2 Radiation Therapy Terminology
- •13.3 Radiation Therapy Techniques
- •13.4 Radiation Therapy for Squamous Cell Carcinoma of the Eyelid
- •13.5 Adjuvant Radiation Therapy for Ocular Adnexal Tumors
- •13.6 Radiation Therapy for Optic Nerve Meningiomas and Orbital Rhabdomyosarcomas
- •13.7 Toxic Effects of Radiation Therapy
- •13.8 Summary
- •References
- •14.1 Historical Perspective
- •14.2 Presentation and Workup
- •14.4 Genetics
- •14.5 Pathologic Features
- •14.6 Treatment Options
- •14.6.1 General Considerations
- •14.6.2 Enucleation
- •14.6.3 Chemoreduction
- •14.6.4 Subtenon (Subconjunctival) Chemotherapy
- •14.6.5 Unilateral Disease
- •14.6.6 Bilateral Disease
- •14.7 Focal Therapies
- •14.7.1 Cryotherapy
- •14.7.2 Laser Photocoagulation
- •14.7.3 Brachytherapy
- •14.7.4 Thermotherapy
- •14.7.5 Radiation Therapy
- •14.8 Multi-institutional Clinical Trials
- •14.9 Animal Models of Retinoblastoma
- •14.10 Gene Transfer Technology for Treatment of Retinoblastoma
- •14.11 Future Development
- •References
- •15 Management of Uveal Melanoma
- •15.1 Epidemiology
- •15.2 Clinical Features
- •15.3 Diagnosis
- •15.4 Staging and Prognostic Factors
- •15.5 Background Studies
- •15.6 Overview of Management
- •15.7 Brachytherapy
- •15.8 Charged-Particle Radiotherapy
- •15.9 Surgical Techniques
- •15.9.1 Uveal Resection
- •15.9.2 Enucleation
- •15.9.3 Transpupillary Thermotherapy
- •15.9.4 Pathologic Assessment
- •15.9.5 Histologic Examination
- •15.10 Conclusion
- •References
- •16 Uveal Metastases from Solid Tumors
- •16.1 Introduction
- •16.2 Patient Characteristics
- •16.3 Symptoms
- •16.4 Clinical Features
- •16.5 Diagnosis
- •16.6 Treatment
- •16.6.1 Observation
- •16.6.2 External-Beam Radiation Therapy
- •16.6.3 Chemotherapy
- •16.6.4 Plaque Brachytherapy
- •16.6.5 Transpupillary Thermotherapy
- •16.6.6 Enucleation
- •16.7 Prognosis
- •16.8 Conclusions
- •References
- •17 Vascular Tumors of the Posterior Pole
- •17.1 Introduction
- •17.3 Circumscribed Choroidal Hemangioma
- •17.4 Management of Posterior Choroidal Hemangiomas
- •17.5 Acquired Vasoproliferative Tumors of the Retina
- •17.6 Conclusions
- •References
- •18 Reconstructive Surgery for Eyelid Defects
- •18.1 Introduction
- •18.2 General Principles
- •18.3 Eyelid Defects Not Involving the Eyelid Margin
- •18.4 Small Defects Involving the Lower Eyelid Margin
- •18.5 Moderate Defects Involving the Lower Eyelid Margin
- •18.6 Large Defects Involving the Lower Eyelid Margin
- •18.7 Small Defects Involving the Upper Eyelid Margin
- •18.8 Moderate Defects Involving the Upper Eyelid Margin
- •18.9 Large Defects Involving the Upper Eyelid Margin
- •18.10 Lateral Canthal Defects
- •18.11 Medial Canthal Defects
- •References
- •19.1 Introduction
- •19.2 Anatomy
- •19.3 Causes of Obstruction
- •19.4 Evaluation
- •19.5 Treatment
- •References
- •20.1 Introduction
- •20.2 Ectropion
- •20.2.1 Ectropion Due to Facial Nerve Paralysis
- •20.2.2 Cicatricial Ectropion
- •20.3 Entropion
- •20.4 Ptosis
- •20.5 Eyelid Retraction
- •20.6 Periorbital Edema Secondary to Imatinib Mesylate
- •References
- •21.1 Introduction
- •21.2 Anatomic Considerations
- •21.2.1 Orbital Margin
- •21.2.2 Nasal and Paranasal Sinuses
- •21.2.3 The Lacrimal System
- •21.2.4 Maxilla
- •21.3 Repair of Orbital Defects
- •21.3.1 Overview of Approaches
- •21.3.1.1 Maxillectomy with Orbital Exenteration
- •21.3.1.2 Maxillectomy Without Orbital Exenteration
- •21.3.2 Types of Maxillary Defects and Strategies for Their Repair
- •21.3.2.1 Type I Defect
- •21.3.2.2 Type II Defects
- •21.3.2.3 Type III Defects
- •21.3.2.4 Type IV Defects
- •21.3.3 Reconstruction After Orbital Exenteration
- •21.4 Conclusion
- •References
- •22.1 Introduction
- •22.2 Surgical Technique
- •22.2.2 Resection of Optic Nerve in Patients with Retinoblastoma
- •22.2.3 Maintenance of Globe Integrity
- •22.3 Choice of Implant
- •22.4 Management of the Anophthalmic Socket After Enucleation and Radiation Therapy
- •22.4.1 Patients with Retinoblastoma
- •22.4.2 Patients with Uveal Melanoma with Microscopic Extrascleral Extension
- •22.4.3 Patients with Head and Neck Cancer
- •22.5 Evisceration
- •References
- •23.2 Indications
- •23.3 Preoperative Evaluation
- •23.4 Surgical Techniques of Orbital Exenteration
- •23.5 Reconstructive Options
- •23.6 Surgical Complications
- •23.7 Rehabilitation After Orbital Exenteration
- •Suggested Readings
- •24.1 Introduction
- •24.2 Relevant Anatomy
- •24.3 Clinical Evaluation
- •24.3.1 Evaluation of Muscle Function
- •24.3.2 Evaluation of Lacrimal Gland and Lacrimal Drainage System Function
- •24.4 Medical Management
- •24.5 Surgical Management
- •24.5.1 Treatment of Lagophthalmos and Exposure Keratopathy
- •24.5.2 Treatment of Lower Eyelid Laxity and Ectropion
- •24.5.3 Reanimation of the Midface
- •24.5.3.1 Static Reanimation
- •24.5.3.2 Dynamic Reanimation
- •24.5.4 Options for Correction of Brow Ptosis
- •24.5.5 Additional Procedures for Management of Facial Droop
- •24.6 Special Circumstances in Cancer Patients with Facial Nerve Paralysis
- •24.7 Conclusion
- •References
- •25.1 Introduction
- •25.4 Conclusions and Recommendations
- •References
- •26 Lacrimal and Canalicular Toxicity
- •26.1 Introduction
- •26.2 5-Fluorouracil
- •26.4 Docetaxel
- •26.5 Epiphora Associated with Other Chemotherapeutic Drugs
- •26.6 Conclusions
- •References
- •27.1 Introduction
- •27.2 Orbital, Periorbital, and Orbital Teratogenic Side Effects by Individual Drug
- •27.2.1 Busulfan
- •27.2.2 Capecitabine
- •27.2.3 Carmustine
- •27.2.4 Cetuximab
- •27.2.5 Cisplatin
- •27.2.6 Cyclophosphamide
- •27.2.7 Cytarabine
- •27.2.8 Docetaxel
- •27.2.9 Doxorubicin
- •27.2.10 Erlotinib
- •27.2.11 Etoposide
- •27.2.12 Fluorouracil
- •27.2.13 Imatinib Mesylate
- •27.2.14 Interferons
- •27.2.15 Interleukin-2, Interleukin-3, and Interleukin-6
- •27.2.16 6-Mercaptopurine
- •27.2.17 Methotrexate
- •27.2.18 Mitomycin C
- •27.2.19 Mitoxantrone Dihydrochloride
- •27.2.20 Plicamycin
- •27.2.21 Thiotepa
- •27.2.22 Vincristine
- •27.3 Summary
- •References
- •28.1 Introduction
- •28.2 Epidemiology
- •28.2.1 Bacterial
- •28.2.2 Viral
- •28.2.3 Fungal
- •28.3 Pathogenesis and Host Defense
- •28.4 Ocular and Orbital Manifestations of Infection
- •28.4.1 Bacterial
- •28.4.2 Viral
- •28.4.3 Fungal
- •28.4.3.1 Candida Species
- •28.4.3.2 Aspergillus Species
- •28.4.3.3 Other Fungal Species
- •28.5 Conclusion
- •References
- •29.1 Introduction
- •29.2 Ophthalmologic Findings with CN III, IV, and VI Palsies
- •29.3 CN III, IV, and VI Palsies due to Primary Cranial Nerve Neoplasms and Direct Extension from Primary Brain, Brain Stem, or Skull base Tumors
- •29.4 CN III, IV, and VI Palsies due to Metastasis to the Brain, Brain, Stem and Skull Base from Distant Sites
- •29.5 Cranial Nerve III, IV, and VI Palsies due to Head and Neck Cancers
- •29.6 Cranial Nerve III, IV, and VI Palsies due to Leptomeningeal Disease
- •29.7 Other Causes of CN III, IV, and VI Palsies in Cancer Patients
- •29.8 Conclusion
- •References
- •30 Skull Base Tumors
- •30.1 Introduction
- •30.2 Anatomy of the Skull Base
- •30.3 Imaging and Diagnosis of Skull Base Tumors
- •30.4 Skull Base Tumors and Neuro-ophthalmic Correlations
- •30.4.1 Esthesioneuroblastoma
- •30.4.2 Chordoma
- •30.4.3 Craniopharyngioma
- •30.4.4 Meningioma
- •30.4.5 Sinonasal and Nasopharyngeal Tumors
- •30.4.6 Schwannoma
- •30.4.7 Pituitary Tumors
- •30.4.8 Myeloma
- •30.4.9 Paraganglioma
- •30.4.10 Metastases
- •References
- •31.1 Optic Pathway Gliomas
- •31.1.1 Demographics and Presentation
- •31.1.2 Histopathology
- •31.1.3 Imaging and Lesion Location
- •31.1.4 Differential Diagnosis
- •31.1.5 Management
- •31.1.6 Prognosis
- •31.2 Optic Nerve Sheath Meningiomas
- •31.2.1 Incidence
- •31.2.2 Histology and Pathophysiology
- •31.2.3 Clinical Presentation
- •31.2.4 Imaging
- •31.2.5 Treatment
- •References
- •32 Leptomeningeal Disease
- •32.1 Introduction
- •32.2 Epidemiology
- •32.3 Clinical Presentation
- •32.3.1 LMD due to Solid Tumors
- •32.3.2 LMD due to Hematogenous Tumors
- •32.3.3 LMD due to Primary Brain Tumors
- •32.4 Diagnosis
- •32.4.1 Radiographic Imaging
- •32.4.2 Optic Neuropathies in LMD
- •32.5 Treatment
- •32.6 Prognosis
- •32.7 Conclusion
- •References
- •33 Paraneoplastic Visual Syndromes
- •33.1 Introduction
- •33.2 Pathogenesis
- •33.3 Carcinoma-Associated Retinopathy
- •33.4 Carcinoma-Associated Cone Dysfunction Syndrome
- •33.5 Melanoma-Associated Retinopathy
- •33.6 Autoimmune Retinopathy
- •33.7 Paraneoplastic Optic Neuropathy
- •33.8 Diagnostic Testing
- •33.9 Differential Diagnosis
- •33.10 Treatment and Prognosis
- •33.11 Conclusion
- •References
- •34.1 Introduction
- •34.2 NF1 and the Optic Pathway
- •34.3.1 Description and Clinical Issues
- •34.3.2 Evaluation and Management
- •34.4 Intraorbital Optic Nerve Glioma
- •34.4.1 Description and Clinical Issues
- •34.4.2 Evaluation and Management
- •34.5 Chiasmal and Hypothalamic Glioma
- •34.5.1 Description and Clinical Issues
- •34.5.2 Evaluation and Management
- •34.6 Intraparenchymal Astrocytoma
- •34.6.1 Description and Clinical Issues
- •34.6.2 Evaluation and Management
- •34.7 Conclusion
- •References
- •35 Other Optic Nerve Maladies in Cancer Patients
- •35.1 Introduction
- •35.2 Optic Neuropathies Related to Elevated ICP
- •35.2.1 Causes of Elevated ICP
- •35.2.2 Treatment of Elevated ICP
- •35.4 Optic Neuropathies Caused by Drugs
- •35.4.1 Optic Disc Edema Secondary to Drug-Induced Elevated ICP
- •35.4.1.1 Retinoids
- •35.4.1.2 Imatinib Mesylate
- •35.4.1.3 Cyclosporine A
- •35.4.1.4 Cytarabine
- •35.4.2 Elevated ICP Secondary to Cerebral Venous Thrombosis
- •35.4.2.1 Cisplatin
- •35.4.2.2 L-Asparaginase
- •35.4.3 Optic Disc Edema Usually Without Elevated ICP
- •35.4.3.1 Cisplatin
- •35.4.3.2 Carboplatin
- •35.4.3.3 Carmustine
- •35.4.3.4 Vincristine
- •35.4.3.5 5-Fluorouracil
- •35.4.3.6 Cyclosporine A
- •35.4.3.7 Tacrolimus
- •35.4.4 Optic Neuropathy Without Disc Edema
- •35.4.4.1 Fludarabine
- •35.4.4.2 Tacrolimus
- •35.4.4.3 Paclitaxel
- •35.4.4.4 Methotrexate
- •35.4.4.5 Cytarabine
- •35.5 Optic Neuropathies Caused by Radiation
- •References
- •36 Management of Endogenous Endophthalmitis
- •36.1 Introduction
- •36.2 Epidemiology
- •36.3 Microbiology
- •36.4 Clinical Manifestations and Diagnosis
- •36.5 Treatment
- •36.5.1 Bacterial Endophthalmitis
- •36.5.2 Fungal Endophthalmitis
- •36.5.2.1 Yeast Endophthalmitis
- •36.5.2.2 Mold Endophthalmitis
- •36.6 Prognosis
- •36.7 Summary
- •References
- •37 Viral Retinitis in the Cancer Patient
- •37.1 Introduction
- •37.2 Epidemiology
- •37.3 Clinical Features
- •37.3.1 CMV Retinitis
- •37.3.2 Acute Retinal Necrosis
- •37.3.3 Progressive Outer Retinal Necrosis
- •37.4 Treatment
- •37.4.1 CMV Retinitis
- •37.4.1.1 Intravitreal Injections
- •37.4.1.2 Ganciclovir Implant
- •37.4.2 Acute Retinal Necrosis
- •37.4.3 Progressive Outer Retinal Necrosis
- •37.5 Role of Vitreoretinal Surgery in Viral Retinitis
- •37.5.1 Argon Laser Photocoagulation
- •37.5.2 Retinal Detachment Repair
- •37.6 Prognosis
- •37.6.1 CMV Retinitis
- •37.6.2 Acute Retinal Necrosis
- •37.6.3 Progressive Outer Retinal Necrosis
- •37.7 Conclusion
- •References
- •38.1 Introduction
- •38.2 Indications for Diagnostic Vitrectomy
- •38.2.1 Vitreous Biopsy
- •38.2.2 Uveal Biopsy
- •38.3 Preoperative Considerations
- •38.3.1 Thrombocytopenia
- •38.3.2 Anesthesia
- •38.4 Vitreous Biopsy
- •38.4.1 Technique
- •38.4.2 Effect of Vitrector Gauge on Vitreous Sample
- •38.5 Uveal Biopsy
- •38.5.1 Technique
- •38.5.2 Complications
- •38.5.3 Collaboration with Pathology
- •38.6 Pathologic Processing
- •38.6.1 Cytology
- •38.6.2 Interleukin Measurement
- •38.6.3 Polymerase Chain Reaction
- •38.6.4 Genetic Analysis
- •38.6.5 Cytogenetic Uveal Melanoma Studies
- •38.7 Results of Diagnostic Vitrectomy
- •38.7.1 Common Diagnoses
- •38.7.2 Diagnostic Utility
- •38.8 Postoperative Considerations
- •38.9 Conclusion
- •References
- •39.1 Introduction and Epidemiology
- •39.2 Presentation and Diagnosis
- •39.3 Management
- •39.4 Future Considerations
- •39.5 Conclusions
- •References
- •Index
Chapter 18
Reconstructive Surgery for Eyelid Defects
Roman Shinder and Bita Esmaeli
Abstract With a depleting ozone layer and increasing ultraviolet radiation exposure, the incidence of eyelid cancers is on the rise, and we can expect a growing need for eyelid reconstruction. Several reconstructive techniques may be appropriate for a particular eyelid defect. The choice of procedure by the surgeon depends on the patient’s age, the degree of eyelid laxity and quality of eyelid skin, the location and size of the defect, and the surgeon’s preference. Regardless of the surgical procedure chosen, the goals of the procedure should be restoration of both the anatomy and the dynamic function of the eyelid, creation of a stable eyelid margin, acceptable vertical eyelid height, adequate eyelid closure, smooth posterior epithelial surface, and maximum cosmesis and symmetry.
18.1 Introduction
With a depleting ozone layer and increasing ultraviolet radiation exposure, the incidence of eyelid cancers is on the rise, and we can expect a growing need for eyelid reconstruction. The following chapter details eyelid reconstruction following tumor resection.
18.2 General Principles
Regardless of the surgical procedure chosen, the goals of the procedure should be restoration of both the anatomy and the dynamic function of the eyelid, creation of a stable eyelid margin, acceptable vertical eyelid height, adequate eyelid closure, smooth posterior epithelial surface, and maximum cosmesis and symmetry. The
R. Shinder (B)
Section of Ophthalmology, Department of Head and Neck Surgery, The University of Texas M.D. Anderson Cancer Center, Houston, TX, USA
e-mail: romanshinder@hotmail.com
B. Esmaeli (ed.), Ophthalmic Oncology, M.D. Anderson Solid Tumor |
231 |
Oncology Series 6, DOI 10.1007/978-1-4419-0374-7_18,
C Springer Science+Business Media, LLC 2011
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reconstructive technique chosen for eyelid defects largely depends on the extent of full-thickness horizontal lid resection. The surgeon may be surprised at the final size of a lid defect following tumor excision if frozen-section histopathologic examination proves the tumor to be more extensive than clinically estimated. Therefore, the patient should be counseled about the potential extent of the eyelid defect based on the anatomic location and type of cancer.
For the purposes of repair, the eyelids can be thought of as being made of an anterior and a posterior lamella. The anterior lamella consists of the skin and orbicularis muscle, while the posterior lamella is made up of the tarsus and conjunctiva. It is important to reconstruct both the anterior and posterior lamellae. Reconstruction of either the anterior or the posterior lamella may be accomplished with a graft, but grafts should not be used to reconstruct both lamellae since one of the layers must act as a pedicle flap and provide the blood supply. A graft placed upon another graft has a high probability of failure. Horizontal tension should be maximized at the expense of vertical tension to avoid postoperative eyelid malposition. In so doing, the surgeon must evaluate for horizontal lid laxity.
Medial and lateral canthal fixation should always be optimized, and an attempt should be made to match like tissue to like tissue in each lamella. Before any graft is sized, the anatomical defect should be narrowed as much as possible. The surgeon should avoid, whenever feasible, creating a defect that cannot be closed. When presented with alternatives, choosing the simplest technique is often wise. Finally, for complex and large defects encompassing more than the immediate periorbital soft tissues, it may be necessary to engage specialists from other disciplines, such as facial plastic surgery, to collaborate with the oculoplastic surgeon in surgical planning and reconstruction.
18.3 Eyelid Defects Not Involving the Eyelid Margin
Partial-thickness eyelid defects not involving the eyelid margin frequently result from Mohs surgery for skin cancers. Defects that do not involve the eyelid margin can be repaired by direct closure as long as the procedure does not distort the eyelid margin. Undermining of superficial tissues may sometimes be necessary to avoid undue wound tension. Tension of wound closure should be directed horizontally to avoid lower eyelid ectropion, eyelid retraction, and lagophthalmos. Avoiding vertical tension requires the placement of vertically oriented incision lines.
When undermining does not allow direct approximation, advancement or transposition procedures utilizing local skin flaps may be undertaken. The most commonly used flaps are advancement flaps, including sliding and rotation flaps, and transposition flaps, including z-plasty and rhomboid flaps [1]. The simplest skin- and-muscle flap is a sliding flap. It requires wide undermining to allow it to “slide” into the defect. The second simplest flap is the advancement flap, which requires wide undermining followed by relaxing incisions to allow the flap to “advance” into the defect. The resultant excess tissue adjacent to the flap can be trimmed by
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removing Burrow’s triangles of skin on either side of the flap [2]. Semicircular and rotation flaps are types of advancement flaps that are rotated into the defect. Z-plasty and rhomboid flaps are transposition flaps, entailing transfer of the flap from a nonadjacent area into the defect by lifting the flap over normal tissue [3]. Transposition flaps are often helpful in the repair of larger defects. These different flaps are often used in combination to work around facial contours. Flaps typically provide the best tissue match and cosmetic result but necessitate planning to limit secondary deformities. Although skin graft procedures are usually less challenging to perform, a skin graft may not be an appropriate choice for a deep defect or if postoperative adjuvant radiation therapy is planned.
Upper eyelid defects involving the anterior lamella are best repaired with fullthickness skin grafts from the contralateral upper lid. Preauricular or retroauricular grafts may also be utilized, but their greater thickness may hinder upper lid mobility and cosmesis. Lower eyelid defects not involving the margin and without significant soft tissue depth can be repaired using a skin graft from the upper eyelid or the preauricular or retroauricular skin. When tissue is not available from the upper lid or periauricular locations, full-thickness grafts may be harvested from the supraclavicular fossa or the inner upper arm. It should be remembered that skin grafts will shrink, somewhat, and produce some traction on the eyelid in the direction of the graft [2]. Surgeons must be vigilant not to place hair-bearing skin grafts near the eyelid margin as this may lead to future corneal irritation.
Split-thickness grafts should be avoided in periocular reconstructions as the cosmetic result is inferior to full-thickness grafts. They are only recommended in the surgical care of severe facial burns when adequate full-thickness skin is unavailable.
18.4 Small Defects Involving the Lower Eyelid Margin
Small defects that involve the lower eyelid margin can be repaired by direct closure assuming that the surrounding tissue is sufficiently lax so that undue tension is not placed on the wound. Primary closure is typically carried out when less than 33% of the lid margin is involved (Fig. 18.1). If a larger defect is present, adjacent tissue advancement or grafting of distant tissue may be needed. During primary closure, an additional 3–5 mm of medial mobilization may be obtained from the remaining lateral lid margin by severing the inferior limb of the lateral canthal tendon via a canthotomy and a cantholysis. During closure, the lid margin should be repaired with interrupted 6-0 silk sutures, which are left long and incorporated into subsequent skin sutures to ensure that they do not rub against the cornea. Three margin sutures should be placed—through the tarsus, the lash line, and the gray line. The tarsus should be repaired with 5-0 absorbable polyglactin suture.
Possible complications resulting from direct closure include a notch at the eyelid margin and wound dehiscence. A notch at the eyelid margin can be prevented by ensuring precise approximation of the tarsal margin and placing additional silk sutures at the eyelid margin [2]. Occasionally, wound dehiscence may occur. This
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Fig. 18.1 Small right lower eyelid margin defect closed directly (pentagonal wedge). (a) Defect. (b) Intraoperative appearance after closure
tends to happen when there is excess tension on the wound or when the tissues are chronically inflamed. If the wound is too tight, thought should be given to performing a cantholysis to relieve the tension. Additionally, well-placed tarsal sutures at the lid margin and tarsal base help prevent dehiscence.
18.5 Moderate Defects Involving the Lower Eyelid Margin
Moderate defects are defined as those involving 33–50% of the margin. They are repaired by advancement of the lateral portion of the eyelid using semicircular advancement or rotation flaps. The most common repair technique utilizes a modified superior Tenzel semicircular rotation flap in conjunction with an inferior cantholysis. The flap should not extend as far as the brow superiorly, nor should it extend beyond the lateral orbital rim laterally [2]. Complications resulting from the use of the semicircular flap are usually caused by poor placement of the flap at the lateral canthus. The deep tissue of the flap must be securely fixed to the periorbita on the inner aspect of the lateral orbital rim [2], since ectropion is likely to result from poor fixation. Also, the semicircular rotation flap may result in a rounded lateral canthus, making secondary revisions necessary.
Tarsoconjunctival flaps are very useful for larger lower eyelid defects. These flaps are taken from the undersurface of the upper eyelid and may be transplanted into the lower lid defect to reconstruct the posterior lamella. Please see the next section for more details.
18.6 Large Defects Involving the Lower Eyelid Margin
Lower eyelid defects that involve greater than 50% of the lid margin—require adjacent tissue advancement for repair (Fig. 18.2a). One such approach involves the use of a modified tarsoconjunctival flap (Hughes flap) taken from the undersurface of
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Fig. 18.2 Large left lower eyelid defect closed with a Hughes flap. (a) Defect. (b) Intraoperative appearance after tarsoconjunctival flap harvested from upper eyelid has been sutured to lower eyelid. (c) Intraoperative appearance after full-thickness skin graft harvested from upper eyelid has been sutured over tarsoconjunctival flap of lower eyelid. (d) Postoperative appearance 6 months after repair and administration of postoperative adjuvant radiation therapy
the upper eyelid. The flap is advanced from the upper lid into the posterior lamellar defect of the lower lid (Fig. 18.2b) [4]. Care should be taken when tarsal grafts are harvested to preserve the marginal 3–4 mm tarsal height in the upper eyelid to prevent donor-lid margin distortion. The tarsoconjunctival flap can be covered with various types of skin flaps or a full-thickness skin graft; the latter is our preferred choice for anterior lamella reconstruction over the tarsoconjunctival flap [5, 6]. The skin graft can be harvested from the upper eyelid using a blepharoplasty-type incision, usually from the same side, or it can be harvested from the retroauricular area (Fig. 18.2c). The modified Hughes procedure thus results in a bridge of conjunctiva from the upper lid across the visual axis for approximately 6 weeks. The vascularized pedicle of conjunctiva is subsequently released in a staged, second procedure once vascularization of the lower lid flap is achieved (Fig. 18.2d). The timing of the second stage of the modified Hughes procedure (when the pedicle of the flap is severed) depends on many factors. From the standpoint of vascular supply, studies have shown that a Hughes flap with good blood supply can be separated as early as 2 weeks after the first stage. However, there is a higher likelihood of lower eyelid ectropion after early separation of the flap. When postoperative adjuvant radiation
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therapy is planned for cutaneous cancers of the lower eyelid, it is necessary to separate the Hughes flap within 4–6 weeks after the first stage to allow for shielding of the globe and to allow radiation therapy to begin in a timely fashion (within 4–6 weeks after ablative surgery).
Because it is an eyelid-sharing technique and may result in complications, the modified Hughes procedure should be avoided in certain patient groups whenever possible. Children under age 7 should not undergo this procedure as it may precipitate occlusion amblyopia. This procedure should also be avoided in the seeing eye of a monocular patient. Several complications may result following a modified Hughes procedure. For instance, the patient may develop an eyelid malposition. If the lower eyelid margin skin rotates inward, the patient is likely to develop keratitis, either from the keratinized skin surface or from the fine lanugo hairs arising from the skin [2]. The risk of this complication can be reduced during the second stage of the procedure when the surgeon transects the advancement flap. Specifically, care should be taken to angle the incision to create a longer posterior lamella with more conjunctiva than skin [2]. The conjunctiva can then be advanced over the lid margin, leaving it nonkeratinized. Another complication that may occur following the modified Hughes procedure is upper lid retraction. To reduce this risk, the Müller muscle should be dissected away from conjunctiva and not be advanced with the tarsoconjunctival flap during the first stage of the procedure [2]. During the second stage of the procedure, the conjunctiva of the upper lid is left unsutured; it may even be recessed if retraction is a concern [2]. Sloughing of the skin graft may also occur following the Hughes procedure, but this is an uncommon occurrence. If blood or fluid collect beneath the donor graft, poor donor–host apposition will occur, resulting in graft failure. Drainage holes in the skin graft will prevent any fluid accumulation under the graft [2]. A bolster suture that is placed over the graft will keep it firmly apposed to the underlying vascular bed [2]. Necrosis of the tarsoconjunctival flap is another rare complication and results from a poorly vascularized flap.
Alternative procedures include full-thickness pedicled flaps [7, 8] and a free tarsoconjunctival graft from the contralateral upper lid with an overlying vascularized bipedicled skin-and-muscle flap [9]. Another useful technique is the tarsal transposition flap, as described by Hewes et al. [10]. The advantage of these procedures is that only one surgical stage is needed and visual axis occlusion is avoided, but in our experience the outcomes are not as predictable as those of a modified Hughes procedure for large defects of the lower eyelid.
A large rotating cheek flap (Mustardé flap) works well for repair of a large anterior lamellar defect, but for posterior lamellar replacement, it must be coupled with a tarsal substitute, such as a free tarsoconjunctival autograft, hard palate mucosa, nasal septum cartilage and mucosa, full-thickness buccal mucous membrane, Hughes flap, free periosteal graft, or homologous tarsus [11–17]. The Mustardé cheek rotation flap often results in a rounded lateral canthus and is associated with a high risk of lower eyelid ectropion; thus, secondary revisions are often needed.
