- •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
Table 4.2. Causes of nontraumatic canalicular obstruction and their approximate incidence
Cause of canalicular obstruction |
Average annual |
|
caseload (%) |
Postherpetic |
8/23 (35%) |
Iatrogenic |
6/23 (26%) |
Cicatricial conjunctival diseasea |
6/23 (26%) |
5-Fluorouracil chemotherapy |
2/23 (9%) |
Lichen planus |
1/23 (5%) |
Based on cases presenting to Moorfields Eye Hospital over an 8-year period
aIncluding risk factors such as topical glaucoma therapy, severe blepharitis
There are many causes for canalicular dysfunction (Table 4.2), and symptoms vary according to the extent, severity, and duration of the underlying disease. Unfortunately, irreversible canalicular fibrosis is often present at presentation due to delayed diagnosis (e.g., retained punctal plugs or stents), misdiagnosis (as with chronic canaliculitis [34]), or the rapid onset of disease (herpes simplex canaliculo-conjunctivitis). Restoration of canalicular function is hampered by the challenge of providing effective immunosuppression for local disease,
a
c
4.3 Infective Causes |
69 |
such as ocular cicatricial pemphigoid, and the very small caliber of the canaliculi, with surgery failing due to both annular fibrosis and disruption of the dynamic (lacrimal “pump”) function of the orbicularis oculi muscle.
4.3Infective Causes
Severe ocular surface infections can cause canaliculitis either by a direct infection or by spillover of the toxic tear film from an “upstream” hyperacute conjunctivitis.
4.3.1Periocular Herpes Simplex Infection
Apart from trauma, primary periocular infections with herpes simplex virus (Fig. 4.2a) are probably the most common cause of canalicular obstruction (Fig. 4.2b). In 160 patients presenting with lacrimal symptoms after primary herpetic blepharo-conjunctivitis, canalicular block was typically unilateral and significantly more common in women [10, 20]. Primary open lacrimal surgery-DCR with anterograde or retrograde intubation—was undertaken in 94 eyes, of which fewer than a quarter required subsequent bypass tube insertion, emphasizing the role for primary canalicular surgery before resorting to placement of a glass bypass tube.
b
d
Fig. 4.2 Microbial canaliculitis. (a) Primary periocular herpes simplex infection: blepharoconjunctivitis with vesicles; (b) probe identifying proximal lower canalicular block; (c) Actinomyces canaliculitis with large granuloma bulging out of punctum; (d) expression of stones and debris after canaliculotomy
70 |
4 Lacrimal Canalicular Inflammation and Occlusion: Diagnosis and Management |
4.3.2Bacterial Canaliculitis
Numerous microbes may infect the canalicular epithelial surface (Table 4.3), but the most characteristic is due to
4Actinomyces species. Such patients usually present after many months of a painless chronic discharge at the medial canthus, this typically being misdiagnosed as conjunctivitis, chalazion, or nasolacrimal duct obstruction [1, 3]. Although rare, microbial canaliculitis may also lead to chronic or recurrent nasolacrimal obstruction in children [26], and may also be a cause of blood-stained tears. Typically, there is swelling with mild inflammation, centered on the midcanaliculus, and the characteristically stringy yellow discharge at a pouting punctum (Fig. 4.2c). Pressure over the canaliculus may lead to discharge of pus or gritlike “granules,” but in most cases the debris is typically not expressible (unlike that of a lacrimal sac mucocele). Actinomyces, especially A. israelii, is a cast-forming gram-positive filamentous anaerobe that can be difficult to isolate, and the organism has a propensity for colonizing hollow spaces and forming “stones,” such as canaliculiths (Fig. 4.2d).
In all but the mildest cases, Actinomyces canaliculitis is resistant to topical antibiotics alone. Antibiotic syringing of the affected canaliculus is well described [23], but this tends to be ineffective [35] and, more importantly, carries the risk of microbial dissemination into the lacrimal sac and nasolacrimal duct. Definitive treatment entails canaliculostomy with expression of all inflammatory and infective debris; a 6-mm incision is made along the conjunctival border of the affected canaliculus, and the canalicular contents are expressed with firm pressure on either side of its walls. Although a large chalazion spoon may be used to curette stones, this instrument is best avoided as it is liable to damage the severely inflamed canalicular mucosa and result in canalicular occlusion. Chronic infection may lead
Table 4.3. Microbial isolates in canaliculitis
Actinomycetes spp.
Arcanobacterium haemolyticum
Eikenella corrodens
Haemophilus aphrophilus
Lactococcus lactis cremoris
Molluscum contagiousuma
Mycobacterium chelonae
Nocardia asteroides
Propionobacterium propionicum
Staphylocococcus spp.
aPrimary involvement of the conjunctiva or cornea by molluscum is rare and is often associated with HIV infection
to gross distension of the canaliculus by the large number of stones, all of which require removal. The canaliculotomy incision heals spontaneously, and the patient should be placed on a week’s course of a topical antibiotic, such as ofloxacin; because the incision lies along, rather than across, the canaliculus, ring contracture is rare and postoperative epiphora most unusual [1]. Recurrence of symptoms is a likely indication of persistent canalicular stones, and a further canaliculotomy should be performed if necessary; occasionally, such recurrent infection is centered on the lacrimal sac rather than the canaliculi.
4.4Systemic Inflammatory Disease
4.4.1Lichen Planus
Lichen planus (LP), an idiopathic autoimmune disease of the skin and oral or genital mucosa, may rarely affect conjunctiva [15, 28] and lead to severe canalicular obstruction [10, 22]. Etiological mechanisms include autoreactive T cells to keratinocytes and activated tissue matrix metalloproteinases and mast cells. Systemic lesions show suband intraepithelial lymphocytic infiltration with degeneration of basal keratinocytes, and although conjunctival disease is less well characterized, case reports describe reticular subconjunctival scarring, forniceal shortening, and symblepharon formation. These features resemble those seen in ocular cicatricial pemphigoid [21, 25], but immune complex deposition within the conjunctival basement membrane—pathognomonic for ocular cicatricial pemphigoid—is absent in LP.
Canalicular LP leads to extensive bilateral, bicanalicular occlusion in three quarters of patients with symptomatic disease [10]; these changes probably reflect inflammation within the subepithelial substantia propria of the canaliculus, with consequent deep fibrosis “throttling” the canaliculus (Fig. 4.3a). LP patients with proximal or midcanalicular block are offered DCR with retrograde canaliculostomy [36] but are warned of the high likelihood of requiring secondary placement of a Jones bypass tube.
4.4.2Ocular Cicatricial Pemphigoid
Distal spillover of the severe conjunctival inflammation of ocular cicatricial pemphigoid will often cause proximal canalicular blockage (Figs. 4.3c, d). Retention of inflammatory debris will, in some cases, be associated with an exacerbation of ocular surface disease, and consideration will be given to the reestablishment of tear drainage; in
