- •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
Summary for the Clinician
■Twenty-five percent of patients with unilateral microphthalmos and 50% of patients with unilateral anophthalmos had anomalies in the fellow eye, chiefly in the form of coloboma, dermoid, sclerocornea, and glaucoma.
7.3 Results |
111 |
Summary for the Clinician
■Nineteen percent of the children were found to have pathological findings on MRI. Most frequently encountered and in clinical terms, the most serious were developmental anomalies of the corpus callosum; these were about four times more common in bilateral than in unilateral anophthalmos (21.4% vs 4.5%) but were not observed at all in microphthalmos.
7.3.8Neuroradiological Findings (Brain MRI)
Table 7.1. History taking and previous findings in patients treated
|
Unilateral |
Bilateral |
||
|
(n = 54) |
(n = 21) |
||
Normal for age |
44 |
|
14 |
|
Pathological |
5 |
|
6 |
|
(Fig. 7.4) |
Anophthalmos |
■ |
One agenesis |
|
|
■ |
One almost |
|
of corpus |
|
|
total hypoplasia |
|
callosum |
|
|
of the corpus |
■ |
One agenesis |
|
|
callosum, |
|
of corpus |
|
|
extreme |
|
callosum, |
|
|
enlargement of |
|
moderate |
|
|
the lateral |
|
ventricular |
|
|
ventricles |
|
enlargement |
|
■ |
One hypoplasia |
■ |
One agenesis |
|
|
of the corpus |
|
of corpus |
|
|
callosum |
|
callosum, |
|
■ |
One suprasellar |
|
small sella/ |
|
|
hamartoma |
|
pituitary |
|
Microphthalmos |
■ |
One minimally |
|
|
■ |
One minimally |
|
enlarged CSF |
|
|
enlarged CSF |
|
spaces |
|
|
spaces |
■ |
One small |
|
■ |
One general |
|
subarachnoid |
|
|
reduction in |
|
cyst |
|
|
cerebral |
Microphthalmos |
|
|
|
volume |
■ |
One |
|
|
|
|
myelinization |
|
|
|
|
disorder |
Findings still |
2 |
|
0 |
|
awaited |
|
|
|
|
Findings not |
3 (all |
1 (anophthalmos) |
||
available |
|
anophthalmos) |
|
|
(abroad) |
|
|
|
|
CSF cerebrospinal fluid
7.3.9Nasolacrimal System Findings
Patients who had undergone extensive previous surgical procedures involving the nasolacrimal system—or with a history of manipulation performed elsewhere—were excluded from this assessment because otherwise it would not have been possible to differentiate between primary and secondary nasolacrimal system pathology (Table 7.1).
Evaluable findings obtained during probing and irrigation of the nasolacrimal system were available for 61 of the 75 children (30 of 38 with unilateral anophthalmos, 18 of 20 with bilateral anophthalmos, and 13 of 17 with microphthalmos) (Fig. 7.5). Consequently, 80 a total of 96 affected orbits (83.3%) were considered here.
Inpatientswithunilateralanophthalmos/microphthalmos the contralateral healthy side was normally developed and freely irrigable, except for two cases with classic congenital stenosis of the lacrimal fold.
Normal anatomy and irrigation outcome were noted in barely one quarter of cases with anophthalmos. Well over half of the patients showed an association with stenosis of both canaliculi, which could be probed for a distance of between 1 and 8 mm (mean 4 ± 1.9 mm). Eight children showed typical stenosis at the level of the valve of Hasner. Stenoses of one canaliculus (5%) and of the common canaliculus (6%) were comparatively rare. Other pathologies, such as aplasia of the lacrimal puncta or fistulas, were not observed.
Summary for the Clinician
■Nasolacrimal duct pathology was present in about 75% of the children in the study sample. This primarily took the form of canalicular stenosis. Typical congenital stenosis of the lacrimal fold was not encountered more frequently than normal.
