Ординатура / Офтальмология / Английские материалы / Applied Pathology for Ophthalmic Microsurgeons_Naumann, Holbach, Kruse_2008

er such as mucous membrane graft (e.g., hard palate) and everting sutures.

Upper Lid Entropion

1.Upper lid entropion (mild): anterior lamella repositioning with everting sutures

2.Upper lid entropion (moderate): anterior lamella repositioning with everting sutures and lid split in the gray line

3.Upper lid entropion with thickened tarsus: anterior lamella repositioning with tarsal wedge resection and everting sutures (Fig. 3.1.16)

4.Upper lid entropion with thinned tarsus and mild retraction: lamellar division and posterior lamella advance

5.Upper lid entropion with marked retraction and insufficient lid closure prior to keratoplasty: mucous membrane graft (e.g., hard palate or thinned nasal septal cartilage) to lengthen the posterior lamella

Distichiasis

Lamellar division and cryotherapy to the posterior lamella.

3.1.2.1.3

Surgical Pathology and Anatomic Principles of Blepharoptosis Repair

Clinically relevant blepharoptosis with a distance from the upper lid margin to the central corneal light reflex not exceeding 2.5 mm may result in defect of peripheral visual field and in severe cases in loss of central vision. Aponeurotic, mechanical, myogenic, neurogenic and dysgenetic etiologies are responsible for acquired ptosis (Table 3.1.1). Aponeurotic ptosis as the most common type of acquired ptosis in the elderly is due to agerelated disinsertion or dehiscence of the aponeurosis. In mechanical ptosis the eyelid tissues will be stretched by the increased weight due to dermatochalasis, orbital fat prolapse, eyelid tumors or scar formations. Myogenic ptosis is attributed to abnormalities of the levator muscle reducing the potential of eyelid elevation into proper position, such as chronic progressive external ophthalmoplegia (CPEO), myasthenia gravis or ocular

myopathies. Neurogenic causes of blepharoptosis include dysfunction of the oculomotor nerve (third nerve palsy, Marcus Gunn jaw-winking), of the sympathetic nerves (Horner’s syndrome) or of the central nervous system. Dysgenesis, such as congenital levator dystrophy with/without superior rectus weakness or blepharophimosis syndrome, may also result in blepharoptosis.

In addition to taking the history with a special look at family history, diurnal changes, diplopia and dysphagia, the levator function defined as the excursion of the upper lid from extreme downgaze to extreme upgaze is the most important factor in determining the cause of blepharoptosis and in the choice of therapy.

1.Aponeurotic blepharoptosis with good levator function (8 mm): levator aponeurosis advancement (Fig. 3.1.17)

2.Mechanical blepharoptosis with moderate

(5 – 7 mm)/good (8 mm) levator function: removal of excess eyelid skin (blepharoplasty, Fig. 3.1.18), orbital fat prolapse, tumor or scar formation with/ without adjunctive levator resection

3.Myogenic blepharoptosis with poor levator function (4 mm): frontalis sling procedure, levator resection, brow suspension (Fig. 3.1.19)

4.Neurogenic blepharoptosis with poor, moderate or good levator function: observing, causal therapy, frontalis suspension, shortening of Müller’s muscle

3.1.2.2

Eyelid Tumors

History and clinical examination using inspection, palpation and slit lamp biomicroscopy are important in the assessment of eyelid tumors. Ultrasonography, CT and MRI are rarely necessary to determine the borders of a lesion. Experienced clinicians are often correct (up to 90 %) in the clinical diagnosis of basal cell carcinomas. Clinical diagnosis, however, requires histopathologic confirmation (Figs. 3.1.20 – 3.1.24). Knowledge about the frequency of individual benign and malig-

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Fig. 3.1.21. Sebaceous gland carcinoma of the eyelids: a, b Ulcerated sebaceous gland carcinoma involving the left upper eyelid in a 60-year-old woman (a). Histopathologic section (he- matoxylin-eosin, original magnification × 50) of sebaceous gland carcinoma showing lobules of pleomorphic atypical tumor cells (inset right) with foamy cytoplasm strongly positive for fat using Oil Red O (inset left) (b). c, d Diffuse sebaceous gland carcinoma presenting as unilateral blepharitis of the left upper eyelid in a 55-year-old woman (c). Histopathologic section (hematoxylin-eosin, original magnification × 150) showing diffuse tumor invasion of the epidermis (pagetoid spread of sebaceous gland carcinoma cells contributing to the clinical appearance of diffuse blepharitis) (d). (From Conway et al. 2004)

nant lesions is helpful in their clinical differential diagnosis (Table 3.1.2). Histopathologic findings may be helpful to explain clinical findings. Moreover, they are essential in providing a microscopically controlled excision. Methods include conventional frozen section control, Mohs’ surgery (frozen sections) and/or a twostep procedure using paraffin sections. The classification of the World Health Organization (WHO) provides guidelines for the diagnosis of eyelid tumors. The TNM classification (WHO and American Joint Committee of Cancer – AJCC) is helpful in determining the clinical and histopathologic stage of malignant eyelid tumors.

Depending on the extent of microscopically controlled tumor excision, the reconstruction of the eyelid must be performed with different techniques:

1.Partial defects only of the anterior eyelid lamella: direct closure (Fig. 3.1.25), flap, free graft

2.Partial defects only of the posterior eyelid lamella: tarsoconjunctival flap, periosteal flap, free grafts (tarsal graft, tarsomarginal graft, oral mucosa graft, nasal mucosa graft, auricular cartilage graft)

3.Full-thickness defects of both the anterior and posterior eyelid lamellae: flap combined with flap, flap combined with graft or vice versa (Figs. 3.1.26 – 3.1.28). (Do not combine two grafts!)

Table 3.1.2. Frequency of eyelid tumors (from Holbach et al. 2002a, b)

II. Malignant eyelid lesions (n = 907)

References (see also page 379)

Adenis JP, Morax S: Pathologie orbito-palp´ebrale. Paris: Masson; 1998

American Joint Committee on Cancer: Carcinoma of the eyelid. In: AJCC: Cancer staging manual – sixth edition. New York: Springer; 2002: 349 – 354

Collin JRO: A manual of systematic eyelid surgery. London: Butterworth Heinemann; 2006

Colombo F et al: Merkel cell carcinoma: Clinicopathologic correlation, management, and follow-up in five patients. Ophthal Plast Reconstr Surg 2000;16:453 – 8

Conway RM et al: Frequency and clinical features of visceral malignancy in a consecutive case series of patients with periocular sebaceous gland carcinoma. Graefes Arch Clin Exp Ophthalmol 2004;242:674 – 8

Conway RM, Themel S, Holbach LM: Surgery for primary basal cell carcinoma including the eyelid margins with intraoperative frozen section control: comparative interventional study with a minimum clinical follow-up of 5 years. Br J Ophthalmol 2004; 88: 236 – 238

Font RL: Eyelids and lacrimal drainage system. In: Spencer

WH (ed): Ophthalmic pathology. Vol. 4. Philadelphia, London, Tokyo: WB Saunders; 1996

Holbach LM et al: Differential diagnosis of lid tumors – Part 1 [in German]. Ophthalmologe 2002;99:394 – 413

Holbach LM et al: Differential diagnosis of lid tumors – Part 2 [in German]. Ophthalmologe 2002;99:490 – 509)

Hübner H: Chirurgische Therapie der Lidtumoren. I. In: Lommatzsch PK (ed): Ophthalmologische Onkologie. Stuttgart: Enke; 1999:48 – 61

Kröner B. Multiple ischemic infarction in the retina and uvea due to crystalline corticosteroid embolism following subcutaneous facial infections (in German). Klin Monatsbl Augenheilkd 1981; 178: 121 – 3

Kruse FE et al.: Konjunktiva. In: Naumann GOH et al.: Pathologie des Auges. Vol. 1. Berlin, Heidelberg: Springer;1997:398 Schlötzer-Schrehardt U et al: The pathogenesis of floppy eyelid syndrome – involvement of matrix metalloproteinases in elastic fiber degradation. Ophthalmology 2005;112:694 – 704 Shields JA, Shields CL: Atlas of eyelid and conjunctival tumors.

Philadelphia: Lippincott Williams & Wilkins; 1999

Tyers AG, Collin JRO: Colour atlas of ophthalmic plastic surgery. London: Butterworth Heinemann; 2001:10 – 1;12

3.2.1

Surgical Anatomy

On lid closure tears are wiped to the nasal bulbar conjunctiva and tear meniscus and are then drained through the superior and inferior lacrimal puncta – which are open only with open eyes – and canaliculi into the lacrimal sac and by a sort of “lacrimal peristalsis” into the nose (Fig. 3.2.1). The canaliculi start with a 2-mm vertical component and continue with a horizontal portion 8 – 10 mm long. The common canaliculus, 1 – 2 mm long, leads into the lacrimal sac. Its entry into the sac at the internal ostium is often partially covered by a mucosal flap which is based anteriorly and also called “the valve of Rosenmüller.” The lacrimal sac lies in the fossa between the anterior (frontal process of

maxilla) and posterior (lacrimal bone) lacrimal crest and is surrounded by the anterior and posterior limbs of the medial canthal tendon. The body of the sac measures 10 – 12 mm in vertical height, and 3 – 5 mm of the sac (fundus) lie above the internal ostium. The suture line in the lacrimal fossa runs vertically between the thin lacrimal bone and the thicker frontal process of the maxilla. It is mostly located one-half of the way from the anterior to the posterior lacrimal crest. The sac leads into the bony nasolacrimal duct, which measures 12 – 15 mm in length and travels within the wall of the maxillary sinus and the lateral nasal wall. The duct extends for about 5 mm below the bony portion and opens beneath the inferior turbinate in the lateral wall of the nose. A mucosal valve (Hasner) usually prevents retrograde passage of mucus or air upwards. The nasal

entry site of a dacryocystorhinostomy lies at the anterior tip of the middle turbinate. The ethmoid sinus may extend to the lacrimal sac fossa. Bony removal of the lacrimal sac fossa may result in these situations in entry into the ethmoid sinus rather than into the nasal vault.

3.2.2

Surgical Pathology

The most common symptoms and signs indicating dysfunction of the lacrimal drainage system include epiphora, punctal discharge and medial canthal swelling.

Epiphora occurring in punctal, canalicular, lacrimal sac, nasolacrimal duct and nasal disorders (Table 3.2.1) is typically worse in the winter months and windy weather. The eye can be sticky due to an expressible

Table 3.2.1. Differential diagnosis of lacrimal drainage system disorders causing epiphora

Punctal causes of epiphora

Congenital punctal atresia

Punctal ectropion in eyelid malposition

Acquired punctal stenosis due to age-related atrophic processes, chronic inflammation, cicatricial conjunctival disease, systemic chemotherapeutic agents

Canalicular causes of epiphora

Congenital absence or fistula

Acquired intrinsic disorders: postherpetic infection (herpes simplex, varicella zoster), bacterial infection (e.g., actinomyces, chlamydia), trauma, postirradiation, pharmacological, intrinsic tumor (e.g., squamous papilloma, squamous cell carcinoma)

Acquired extrinsic disorders: compression and/or invasion and occlusion by adjacent tumor (e.g., basal cell carcinoma, squamous cell carcinoma, non-Hodgkin B-cell lymphoma)

Lacrimal sac causes of epiphora

Congenital diverticulum or fistula (from sac to nose or cheek) Acquired intrinsic disorders: inflammation (extension of primary acquired nasolacrimal duct obstruction including dacryoliths, Wegener’s granulomatosis, sarcoidosis, allergy, hay fever, atopy), trauma, intrinsic tumor arising within the sac and/or the sac walls (Table 3.2.2)

Acquired extrinsic disorders: adjacent tumor compressing and/or invading the sac from the outside (e.g., basal cell carcinoma, squamous cell carcinoma, non-Hodgkin B-cell lymphoma, neurofibroma)

Nasolacrimal duct causes of epiphora

Congenital nasolacrimal duct obstruction (delayed opening of valve of Hasner with/without dacryocele, craniofacial abnormality, rare nasolacrimal duct agenesis)

Primary acquired nasolacrimal duct obstruction (most common cause in adults)

Secondary acquired lacrimal obstruction, including trauma and tumors (as for sac and those extending from the maxillary sinus)

Nasal causes of epiphora

Allergic rhinitis, severe rhinosinus disease (e.g., polyps), previous nasal surgery

Tumors spreading from nasal space and/or adjacent sinuses

mucocele or collected dried tears. The vision can be blurred secondary to an elevated tear meniscus (prismatic effect – especially on downgaze, for example when reading) or tear-splattered glasses. Chronic epiphora can induce red, sore lower-lid skin, with secondary anterior lamella (vertical) shortening (mild cicatricial ectropion). Excessive wiping away of tears can cause or exacerbate a medial ectropion.

Mucopurulent punctal discharge suggests stasis in the lacrimal sac or canaliculi, mostly secondary to nasolacrimal duct obstruction. Accumulation of inflammatory debris can result in dacryolithiasis seen in up to 15 % of dacryocystorhinostomy surgeries. Lacrimal sac stones consist of dried mucus, lipid and inflammatory cells and are more likely to be found in chronically inflamed sacs.

Medial canthal swelling may be caused by an abscess, a dacryolith or a tumor in the lacrimal sac. But not all masses in the medial canthal area arise from the lacrimal sac (acute skin infection, acute ethmoiditis, ruptured dermoid cyst).

Actinomyces canaliculitis presents a characteristic clinical picture: epiphora and intense itching! This cannot be cured by local or systemic antibiotics: This is a “surgical entity” requiring internal slitting of the canaliculus – discharging a cotton-cheese like granula material. The sphincter muscle of Riolani controlling the punctum should be saved.

Swellings below the medial canthal tendon are typical of dacryocystitis. Differential diagnostic signs in favor of a tumor of the lacrimal sac (Fig. 3.2.2, Table 3.2.2) include a mass above the medial canthal ligament (absent in dacryocystitis), the presence of telangiectases in the skin overlying the mass (instead of the diffuse erythema of dacryocystitis) and the presence of serosanguineous discharge or a bloody reflux with atraumatic irrigation (both of which are not usually observed in dacryocystitis).

Table 3.2.2. Lacrimal sac tumors (from Font 1996)

I.Epithelial tumors

1.Squamous cell papilloma

2.Transitional cell papilloma

3.Mixed cell papilloma (exophytic or endophytic)

4.Oncocytic adenoma (oncocytoma)

5.Squamous cell carcinoma

6.Transitional cell carcinoma

7.Adenocarcinoma

8.Mucepidermoid carcinoma

9.Oncocytic adenocarcinoma

II.Non-epithelial tumors

1.Fibrous histiocytoma

2.Pyogenic granuloma

3.Neurilemmoma

4.Lymphoid tumors

5.Malignant melanoma

6.Angiosarcoma

3.2.3

Principles of Lacrimal Surgery

In lacrimal surgery the level of the obstruction revealed clinically by irrigation and probing of the nasolacrimal system is critical to the choice of operation:

1.Obstruction at or distal to the entry of the common canaliculus into the lacrimal sac: external dacryocystorhinostomy (with or without silicone tube intubation)

2.Obstruction at or beyond 8 mm from the punctum of one or both canaliculi, but proximal to the entry of the common canaliculus into the lacrimal sac: external canaliculo-dacryocystorhinostomy

3.Obstruction less than 8 mm from the punctum in both canaliculi: external dacryocystorhinostomy with bypass tube insertion.

3.2.3.1

External Dacryocystorhinostomy

(with or without Silicone Tube Intubation)

The principle is a side-to-side anastomosis between the lacrimal sac and nasal mucosa, effectively incorporating the lacrimal sac into the lateral wall of the nose. In order to prevent closure and scarring of the osteotomy or restenosis of the lacrimal outflow system, lacrimal canaliculi, common canaliculus, sac and anastomosis can be stented with fine silicone tubing.

Indications for external dacryocystorhinostomy include lacrimal mucocele (obstruction at the sac and nasolacrimal duct junction), dacryolithiasis, nasolacrimal duct obstruction in children not responding to probing and intubation, nasolacrimal duct obstruction in adults and functional lacrimal obstruction not responding to simpler methods of treatment such as horizontal lid tightening. Especially in the case of a common canalicular obstruction, a small scarred lacrimal sac or a repeat dacryocystorhinostomy, silicone tube intubation is indicated. The silicone tubing should be removed 2 – 4 months postoperatively, but earlier if the canaliculi are cheesewired by too tightly tied tubing.

3.2.3.2

External Canaliculo-Dacryocystorhinostomy

The principle is an anastomosis between the end of one or both canaliculi and the nose, using the lacrimal sac if present as a bridging flap.

Indications include canalicular obstructions with eight or more millimeters of remaining patent canaliculus, particularly in patients without any residual lacrimal sac following previous dacryocystorhinostomy.