- •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
Chapter 4 |
|
Lacrimal Canalicular Inflammation and |
4 |
Occlusion: Diagnosis and Management |
David H. Verity and Geoffrey E. Rose
Core Messages
■Canalicular inflammation may lead to loss of compliance and stenosis, with lacrimal symptoms occurring despite anatomical patency.
■Microbial canaliculitis is frequently overlooked, leading to a delay in diagnosis and management.
■Failure adequately to remove canalicular stones and debris is a common cause for persistent canaliculitis.
■Canalicular epithelial inflammation due to primary herpes simplex infection is a common cause of canalicular, or common canalicular, occlusion.
■Subepithelial canalicular inflammation—as seen with lichen planus (LP)—may lead to a more severe and extensive annular fibrosis and carries a poor prognosis.
■Systemic chemotherapeutic agents, including radioiodine, 5-fluorouracil (5-FU), mitomycin C (MMC), and docetaxel, may injure the canalicular epithelium, the evidence suggesting active concentration of these agents by the lacrimal outflow structures.
■The surgical approach to canalicular occlusion depends on the extent of disease.
■Dacryocystorhinostomy (DCR) with retrograde canaliculostomy is the preferred surgery for proximal and midcanalicular occlusion.
■The indication for primary placement of a Jones canalicular bypass tube is the total absence of all distal canalicular and common canalicular structures, with this ascertained during open lacrimal surgery.
■The indication for secondary Jones tube placement is a functional failure after primary DCR with retrograde canaliculostomy.
■A canalicular bypass tube should be sutured such that the tube flange is held clear of the healing carunculectomy site; the function is not to prevent prolapse of the tube. As such, an encirclage suture is required only during primary placement of a bypass tube, when carunculectomy has just been performed.
4.1Introduction
Canaliculitis, either epithelial or pericanalicular inflammation, has many underlying causes with rather characteristic clinical patterns. Although certain etiologies, such as herpetic canaliculitis, are rapidly progressive, others are insidious and frequently pass unrecognized until the onset of lacrimal symptoms. Inflammation, either within the epithelium or deep to its basement membrane, leads to scarring with a reduction of both longitudinal compliance and cross-sectional area of the affected canaliculus; these changes result in impaired function of both the active pumping mechanism and the static drainage (Table 4.1).
This review considers idiopathic, infective, and iatrogenic causes of canalicular inflammation and obstruction, but canalicular trauma—comprehensively reviewed elsewhere—is excluded [24, 27].
4.2Embryology, Anatomy, Physiology, and Pathophysiology of the Canalicular System
The lacrimal drainage pathway arises, at day 32, from a thickening of the ectoderm in the naso-optic fissure. This ectoderm descends into the surrounding mesoderm and forms a cord that extends from the developing eyelids to the nasal space, the cord subsequently forming a lumen by disintegration of the central ectoderm.
The lacrimal puncta, ampullae, and canaliculi form the proximal, high-resistance, elements of the lacrimal drainage system: Measuring 0.3 mm in diameter, the puncta lie within the lacrimal papillae and drain into the
vertical |
ampullae, |
each |
being 1–2 mm in length and |
2.5 mm |
in width. |
The |
horizontal canaliculi are about |
6 mm long in the upper lid and 8 mm in the lower, have an internal diameter of about 0.4 mm, and are surrounded
68 |
4 Lacrimal Canalicular Inflammation and Occlusion: Diagnosis and Management |
Table 4.1. Canalicular inflammation: etiology
Infection
1. Chronic staphylococcal lid disease
42. Periocular herpes simplex infection
3. Bacterial and fungal canaliculitis
Systemic inflammatory diseases
1.Lichen planus
2.Ocular cicatricial pemphigoid
3.Drug eruptions (Stevens–Johnson syndrome)
Iatrogenic causes
1.Chemotherapeutic agents
■5-Fluorouracil
■Taxanes: docetaxel (taxotere) and paclitaxel
2.Local radiotherapy
3.Topical treatment
■Preservative related
■Mitomycin C
4.Lacrimal stents and plugs
by the muscle of Duverney–Horner, which is one element of the physiological lacrimal pump. In about 80% of individuals, the upper and lower canaliculi unite to form the common canaliculus, which—with a diameter of about 0.6 mm—runs medially for 2–3 mm before angulating anteriorly to enter the sac. The internal opening of the common canaliculus lies near the midpoint of the sac, at the level of the lower border of the medial canthal tendon, and the anterior angulation of the common canaliculus (about 60°) as it passes through the lateral wall of the sac forms, in part, the physiological “valve” of Rosenmüller; in addition to punctal apposition on lid closure, the valve helps to prevent the retrograde flow of tears [33].
These structures are lined by a stratified squamous epithelium, with a change to pseudostratified, nonciliated columnar epithelium—similar to that found in the upper respiratory system—occurring near the common canaliculus (Fig. 4.1a). The canaliculi form a low-con- ductance conduit, with tear delivery to the lacrimal sac being dependent on the active “compression pump” mechanism of the pretarsal orbicularis oculi. Thus, physiological pump failure, anatomical misalignment, and canalicular stenosis or obstruction may all lead to lacrimal symptoms, examples being facial palsy, ectropion, and herpetic canalicular block, respectively. Depending on the rate of tear clearance, symptoms include a troublesome awareness of wet or moist eyelids, impaired vision due to a raised tear meniscus (Fig. 4.1b), a “wicking” of the tear meniscus onto the skin at the lateral canthus (Fig. 4.1c), and frank epiphora, with this frequently associated with a secondary eczema of the eyelids.
The relative contribution of the upper and lower canaliculi to tear drainage varies between individuals, and most reports suggest that a single canaliculus is adequate for basal tear drainage [18] but will not cope with drainage during reflex lacrimation.
Summary for the Clinician
■In about 80% of individuals, the upper and lower canaliculi unite to form the common canaliculus.
■Physiologic pump failure, anatomic misalignment, and canalicular stenosis or obstruction may all lead to lacrimal symptoms.
■Most reports suggest that a single canaliculus is adequate for basal tear drainage.
a |
b |
c |
Fig. 4.1 (a) Histology of cross section of healthy canaliculus showing stratified squamous epithelium (hematoxylin and eosin, ×20); (b) delayed spontaneous clearance of 2% fluorescein from the conjunctival sac of left eye due to upper and lower herpetic canalicular block with medial overflow; (c) lateral “wicking” of the tear meniscus
