- •Chapter 1
- •Ocular Adnexal Lymphoproliferative
- •1.1 Pathogenesis
- •1.2 Chronic Antigen Stimulation
- •1.3 Immunosuppression
- •1.4 Pathology
- •1.5 Cytogenetics
- •1.6 Clinical Features
- •1.7 Imaging Findings
- •1.8 Staging
- •1.9 Positron Emission Tomography
- •1.10 Treatment
- •1.11 Follicular Lymphoma
- •1.12 Mantle Cell Lymphoma
- •1.13 Radiotherapy
- •1.14 Chemotherapy
- •1.15 Immunotherapy
- •1.16 Radioimmunotherapy
- •1.17 Outcome
- •1.18 The Future
- •References
- •Chapter 2
- •2.1 General Introduction
- •2.2 The Aging Process and Facial Analysis
- •2.3 Endoscopic Brow Lift
- •2.3.1 Introduction
- •2.3.2 Endoscopic Browlift Anesthesia Pearls
- •2.3.4 Endoscopic Browlift Postoperative Care Pearls
- •2.4 Upper Blepharoplasty
- •2.4.1 Introduction
- •2.4.2 Patient Evaluation
- •2.4.3 Upper Blepharoplasty Anesthesia Pearls
- •2.4.4 Upper Blepharoplasty Surgical Procedure Pearls
- •2.5 Lower Blepharoplasty, Fillers, and Midface Augmentation
- •2.5.1 Introduction
- •2.5.2 Patient Evaluation
- •2.5.3 Lower Blepharoplasty Anesthesia Pearls
- •2.5.4 Lower Blepharoplasty Surgical Procedure Pearls
- •References
- •Chapter 3
- •3.1 Introduction
- •3.2 What Is the Diagnosis?
- •3.2.1 Pitfalls of Diagnosis
- •3.2.2 A Diagnostic Corticosteroid Trial?
- •3.2.3 The Question of Biopsy
- •3.3 Treatment
- •3.3.1 Corticosteroids
- •3.3.2 Radiation
- •3.3.3 Other Agents
- •3.4 Special Circumstances
- •3.4.1 Pediatric IOIS
- •3.4.2 Sclerosing Pseudotumor
- •3.4.3 Tolosa–Hunt Syndrome
- •References
- •Chapter 4
- •4.1 Introduction
- •4.2 Embryology, Anatomy, Physiology, and Pathophysiology of the Canalicular System
- •4.3 Infective Causes
- •4.3.1 Periocular Herpes Simplex Infection
- •4.3.2 Bacterial Canaliculitis
- •4.4.1 Lichen Planus
- •4.4.2 Ocular Cicatricial Pemphigoid
- •4.5 Iatrogenic Causes
- •4.5.1 Systemic Drugs
- •4.5.1.2 Docetaxel (Taxotere)
- •4.5.2 Radiotherapy
- •4.5.3 Topical Ophthalmic Treatments
- •4.5.3.2 Mitomycin C (MMC) Therapy
- •4.5.4 Lacrimal Stents and Plugs
- •4.6 The Surgical Approach to Managing Canalicular Disease
- •4.6.1 Surgical Technique for Dacryocystorhinostomy with Retrograde Canaliculostomy
- •References
- •Chapter 5
- •5.1 Introduction
- •5.2 Nomenclature
- •5.3 Clinical Manifestations of NF1
- •5.4 Orbitofacial Tumors in NF1
- •5.4.2 Malignant Peripheral Nerve Sheath Tumors
- •5.4.3 Optic Pathway Gliomas
- •5.5 Genetics
- •5.5.1 The NF1 Gene
- •5.5.2 Overlapping NF1-Like Phenotype (SPRED1)
- •5.6.1 Introduction
- •5.7 Surgical Management of Orbitofacial Tumors in NF1
- •5.7.1 Introduction
- •5.7.2 Timing of Surgery
- •5.7.3 Periorbital Involvement
- •5.7.3.1 The Upper Eyelid
- •5.7.3.2 The Lower Eyelid and Midface
- •5.7.4 Orbital Involvement
- •5.7.4.1 Proptosis
- •5.7.4.3 Proptosis Due to Optic Nerve Glioma
- •5.7.4.4 Orbital Enlargement with Dystopia and Hypoglobus
- •5.8 The Natural History of NF1 Tumor Growth from Birth to Senescence
- •References
- •Chapter 6
- •6.1 Introduction
- •6.2 Surgical Anatomy of the Lacrimal Drainage System
- •6.3 Basic Diagnostics for Disorders of the Lacrimal Drainage System
- •6.4 Selective Lacrimal Sac Biopsy in External Dacryocystorhinostomy
- •6.5.1 Case A
- •6.5.2 Case B
- •6.5.3 Case C
- •6.5.4 Case D
- •6.5.5 Case E
- •6.5.6 Case F
- •6.5.7 Case G
- •References
- •Chapter 7
- •7.1 Introduction
- •7.2 Patients and Methods
- •7.2.1 Patients
- •7.2.2 Examination
- •7.3 Results
- •7.3.1 Patient Data
- •7.3.3 Family History
- •7.3.4 Pregnancy History
- •7.3.5 Birth
- •7.3.6 Associated Systemic and Ocular Diseases
- •7.3.8 Neuroradiological Findings (Brain MRI)
- •7.3.9 Nasolacrimal System Findings
- •7.4 Discussion
- •7.4.1 Patients
- •7.4.2 Obstetric and Family History
- •7.4.3 Associated Pathologies
- •7.4.3.1 Ophthalmological Findings in Unilateral Disease
- •7.4.3.2 Neuroradiological Findings
- •7.4.3.3 Systemic Diseases
- •7.4.3.4 Nasolacrimal Duct Findings
- •7.5 Conclusions
- •References
- •Chapter 8
- •8.1 Introduction
- •8.2 Evaluation of Complicated Ptosis
- •8.2.1 Compensatory Eyebrow Elevation
- •8.2.3 Innervation Patterns of the Frontalis Muscle
- •8.2.4 Checklist of Preoperative Evaluation of Complicated Ptosis
- •8.3 Surgical Technique of Levator Muscle Recession
- •8.3.1 Principle
- •8.3.2 Approach to the Levator
- •8.3.3 Partial Levator Recession
- •8.3.4 Total Levator Recession
- •8.3.6 Undercorrection and Overcorrection
- •8.4 Surgical Technique of Brow Suspension
- •8.4.1 Materials for Brow Suspension
- •8.4.1.1 Nonautogenous Materials
- •8.4.1.2 Autogenous Fascia Lata
- •8.4.2 Our Technique of Harvesting Autogenous Fascia Lata
- •8.4.3 Mechanical Principals of Brow Suspension
- •8.4.4 Upper Lid Approach
- •8.4.5 Fascia Implantation
- •References
- •Chapter 9
- •Modern Concepts in Orbital Imaging
- •9.1 Computerized Tomography
- •9.2 Three-Dimensional Imaging
- •9.3 Magnetic Resonance Imaging
- •9.3.1 The T1 Constant
- •9.3.2 The T2 Constant
- •9.3.3 Creating the MR Image
- •9.4 Imaging of Common Orbital Lesions
- •9.4.1 Adenoid Cystic Carcinoma
- •9.4.2 Cavernous Hemangioma
- •9.4.3 Dermoid Cyst
- •9.4.4 Fibrous Dysplasia
- •9.4.5 Lymphangioma
- •9.4.6 Lymphoma
- •9.4.7 Myositis
- •9.4.8 Optic Nerve Glioma
- •9.4.9 Pseudotumor
- •9.4.10 Rhabdomyosarcoma
- •9.6 Positron Emission Tomography
- •9.7 Orbital Ultrasound
- •9.7.1 Physics and Instrumentation
- •9.7.1.1 Topographic Echography
- •9.7.1.2 Quantitative Echography
- •9.7.1.3 Kinetic Echography
- •9.7.2 Extraocular Muscles
- •9.7.3 Optic Nerves
- •References
- •Chapter 10
- •10.1 Introduction
- •10.3 Etiology
- •10.4 Microbiology
- •10.5 Changing Pathogens and Resistance
- •10.5.2 Orbital MRSA
- •10.6 Evaluation of Orbital Cellulitis
- •10.7 Medical Treatment of Orbital Cellulitis
- •10.8 Surgical Treatment of Orbital Cellulitis
- •10.9 Prevention of Orbital Cellulitis After Orbital Fracture
- •References
- •Chapter 11
- •11.1 Clinical Picture
- •11.1.1 Clinical Phases
- •11.2 Ocular Complications
- •11.3 Investigation
- •11.3.1 Angiography
- •11.4 Management
- •11.4.1 Active Nonintervention
- •11.4.2 Indications for Treatment
- •11.5 Modalities of Treatment
- •11.5.1 Steroids
- •11.5.1.1 Topical Steroids
- •11.5.1.2 Intralesional Corticosteroid Injection
- •11.5.1.3 Oral Corticosteroids
- •11.5.2 Interferon-Alfa
- •11.5.3 Vincristine
- •11.5.4 Laser
- •11.5.5 Embolization
- •11.5.6 Surgery
- •References
- •Chapter 12
- •12.1 Introduction
- •12.2 Epidemiology
- •12.3 Biological Behavior and Timing of Metastasis
- •12.4 Lateralization
- •12.5 Localization
- •12.6 Clinical Features
- •12.7 Imaging and Patterns of Orbital Metastatic Disease
- •12.8 Biopsy
- •12.9 Common Types of Orbital Metastases
- •12.9.1 Breast Carcinoma
- •12.9.2 Lung Carcinoma
- •12.9.3 Prostatic Cancer
- •12.9.4 Melanoma
- •12.9.5 Carcinoid Tumor
- •12.11 Treatment
- •12.11.1 Radiotherapy
- •12.11.2 Chemotherapy
- •12.11.3 Hormonal Therapy
- •12.11.4 Surgery
- •12.12 Prognosis and Survival
- •References
- •Chapter 13
- •13.1 Introduction
- •13.2 Rituximab
- •13.3 Yttrium-90-Labeled Ibritumomab Tiuxetan
- •13.4 Imatinib Mesylate
- •13.5 Cetuximab
- •References
- •Chapter 14
- •14.1 Introduction
- •14.2 Porous Orbital Implants
- •14.3 Orbital Implant Selection in Adults
- •14.4 Orbital Implant Selection in Children
- •14.5 Volume Considerations in Orbital Implant Selection
- •14.7 Which Wrap to Use
- •14.8 To Peg or Not to Peg Porous Implants
- •14.9 Summary
- •References
- •Chapter 15
- •15.1 Introduction
- •15.2 Etiology and Presentation
- •15.2.1 Etiology of Orbital Volume Loss
- •15.2.2 Etiology of Periorbital Volume Loss
- •15.2.3 Features of Orbital Volume Loss
- •15.2.4 Features of Periorbital Volume Loss
- •15.3 Background to Injectable Soft-Tissue Fillers
- •15.3.1 Historical Perspective on Volume Replacement
- •15.4 Types of Injectable Soft-Tissue Filler
- •15.4.1 Collagen Fillers
- •15.4.2 Hyaluronic acid Fillers
- •15.5 Treatment Areas
- •15.5.1 Orbit
- •15.5.2 Upper Eyelid and Brow
- •15.5.3 Tear Trough
- •15.5.4 Temple and Brow
- •15.6 Other Periorbital Uses of Injectable Soft-Tissue Fillers
- •15.6.1 Upper Eyelid Loading
- •15.6.2 Lower Eyelid Elevation
- •15.6.3 Treatment of Cicatricial Ectropion
- •15.7 Future Developments
- •References
72 |
4 Lacrimal Canalicular Inflammation and Occlusion: Diagnosis and Management |
There are two putative mechanisms for canalicular damage: First, bathing of the puncta and canaliculi in 5-FU secreted into the tears may lead to chronic mucosal inflammation per se. Second, 5-FU may damage rapidly
4proliferating canalicular epithelium, causing chronic inflammation and fibrosis within the underlying substantia propria. These theories are similar to those proposed for the canalicular stenosis associated with docetaxel (Taxotere , v.i.), discussed below.
and syringing (followed by a short course of topical steroids) appear adequate to prevent problems in most patients on a ie every 3 weeks dosing schedule. Docetaxel is, however, an increasingly used chemotherapy, and with a trend toward weekly dosing to reduce systemic complications, lacrimal complications are set to increase. Treating physicians should counsel patients about the risk of lacrimal problems and seek appropriate early referral if symptoms arise.
4.5.1.2 Docetaxel (Taxotere) |
4.5.2 Radiotherapy |
Docetaxel is a semisynthetic taxane used in the treatment of advanced solid malignancies, especially those of breast, prostate, and non-small cell lung cancers. It is secreted into the tears [13] and may lead to canalicular stenosis or occlusion, with this troublesome side effect related to both the dosing frequency and total cumulative dose. Histological studies have shown fibrosis within the mucosal lining of the lacrimal drainage apparatus [11].
Clinical features of docetaxel toxicity include symptomatic punctal and canalicular stenosis or occlusion in up to a half of patients while on a weekly dosing schedule [12, 32]. Temporary canalicular intubation has been recommended for patients on weekly therapy, but probing
Due to their propensity to invade the medial orbit, tumors at the medial canthus carry a relatively worse prognosis, and Mohs surgery is now the preferred approach in managing such basal or squamous cell carcinomas. Historically, radiotherapy has often been used in this location, with almost universal canalicular occlusion (Fig. 4.4a). In 1981, Call and Welham described 13 patients with severe epiphora following radiotherapy for medial basal cell carcinomas, all of whom had complete obstruction of both upper and lower canaliculi; 12 were successfully managed by DCR and insertion of a Jones tube, and 1 settled with canaliculo-DCR for a common canalicular block [6].
a |
b |
c |
d |
e |
Fig. 4.4 (a) Radiation treatment for medial canthal BCC causing canalicular occlusion and requiring subsequent DCR and secondary bypass tube (note lash loss and depigmentation); (b) drop sensitivity to unpreserved chloramphenicol with secondary canaliculitis and epiphora; (c) silicone stent-induced canalicular inflammation with developing granuloma (arrow) and medial canthal staphylococcal infection; (d) medial canthal granuloma secondary to monocanalicular stent; (e) impacted intracanalicular plug at the entrance of the common canaliculus to the sac. Note the inflamed sac mucosa due to recurrent episodes of dacrocystitis
