Ординатура / Офтальмология / Английские материалы / Surgical Atlas of Orbital Diseases_Mallajosyula_2009

76.Converse JM and Smith B. Blowout fracture of the floor of the orbit. Trans Am Acad Ophthalmol Otolaryngol 1960;

64:676-88.

77.Tenzel RR and Miller GR. Orbital blow-out fracture repair, conjunctival approach. Am J Ophthalmol 1971; 71: 1141-2.

78.Tessier P The conjunctival approach to the orbital floor and maxilla in congenital malformation and trauma. J Maxillofac Surg 1973; 1: 3-8.

79.Kushner GM Surgical approaches to the infraorbital rim and orbital floor: the case for the transconjunctival approach. J Oral Maxillofac Surg 2006; 64: 108-10.

80.Goldberg RA, Lessner AM, Shorr N, and Baylis HI. The transconjunctival approach to the orbital floor and orbital fat. A prospective study. Ophthal Plast Reconstr Surg 1990;

6:241-6.

81.Westfall CT, Shore JW, Nunery WR, et al. Operative complications of the transconjunctival inferior fornix approach. Ophthalmology 1991; 98: 1525-8.

82.Grove AS, Jr., Tadmor R, New PF, and momose KJ. Orbital fracture evaluation by coronal computed tomography. Am J Ophthalmol 1978; 85: 679-85.

83.Jordan DR, White GL, Jr., Anderson RL, and Thiese SM. Orbital emphysema: a potentially blinding complication following orbital fractures. Ann Emerg Med 1988;17:853-5.

84.Gruss JS, Hurwitz JJ, Nik NA, and Kassel EE. The pattern and incidence of nasolacrimal injury in naso-orbital- ethmoid fractures: the role of delayed assessment and dacryocystorhinostomy. Br J Plast Surg 1985; 38:116-21.

85.Becelli R, Renzi G, Mannino G, et al. Posttraumatic obstruction of lacrimal pathways: a retrospective analysis of 58 consecutive naso-orbitoethmoid fractures. J Craniofac Surg 2004; 15: 29-33.

86.Garcia GH, Goldberg RA, and Shorr N. The transcaruncular approach in repair of orbital fractures: a retrospective study. J Craniomaxillofac Trauma 1998; 4: 7-12.

87.Shorr N, Baylis HI, Goldberg RA, and Perry JD. Transcaruncular approach to the medial orbit and orbital apex. Ophthalmology 2000; 107: 1459-63.

88.Kim S, Helen Lew M, Chung SH, et al. Repair of medial orbital wall fracture: transcaruncular approach. Orbit 2005;

24:1-9.

89.Kim KS, Kim ES, and Hwang JH. Combined transcutaneous transethmoidal/transorbital approach for the treatment of medial orbital blowout fractures. Plast Reconstr Surg 2006; 117: 1947-55.

90.Rees JE. Where have all the bubbles gone? An ode to Hydrogen peroxide, the champagne of all wound cleaners. Accid Emerg Nurs 2003; 11: 82-4.

Orbital Fractures 243

91.Miranda P, Cabrera A, Esparza J, and Jerez A. An oxygen embolism after hydrogen peroxide scalp infiltration. Case illustration. J Neurosurg 2006; 104: 152.

92.Detorakis ET, Drositis I, Drakonaki EE, et al. Pneumocephalus and presumed meningitis following inconspicuous penetrating periocular trauma. Acta Ophthalmol Scand 2004; 82: 603-5.

93.Sargent LA and Rogers GF. Nasoethmoid orbital fractures: diagnosis and management. J Craniomaxillofac Trauma 1999; 5: 19-27.

94.Shaw RC and Parsons RW. Exposure through a coronal incision for initial treatment of facial fractures. Plast Reconstr Surg 1975; 56: 254-9.

95.Leipziger LS and Manson PN. Nasoethmoid orbital fractures. Current concepts and management principles. Clin Plast Surg 1992; 19: 167-93.

96.Shore JW, Rubin PA, and Bilyk JR. Repair of telecanthus by anterior fixation of cantilevered miniplates. Ophthalmology 1992; 99: 1133-8.

97.Converse JM, Firmin F, Wood-Smith D, and Friedland JA. The conjunctival approach in orbital fractures. Plast Reconstr Surg 1973; 52: 656-7.

98.Nunery WR. Lateral canthal approach to repair of trimalar fractures of the zygoma. Ophthal Plast Reconstr Surg 1985; 1: 175-83.

99.Chang EL, Hatton MP, Bernardino CR, and Rubin PA. Simplified repair of zygomatic fractures through a transconjunctival approach. Ophthalmology 2005; 112: 1302-9.

100.Courtney DJ. Upper buccal sulcus approach to management of fractures of the zygomatic complex: a retrospective study of 50 cases. Br J Oral Maxillofac Surg 1999; 37: 464-6.

101.Zingg M, Laedrach K, Chen J, et al. Classification and treatment of zygomatic fractures: a review of 1,025 cases. J Oral Maxillofac Surg 1992; 50: 778-90.

102.Honig JF and Merten HA. Classification system and treatment of zygomatic arch fractures in the clinical setting. J Craniofac Surg 2004; 15: 986-9.

103.Kreutziger KL. Zygomatic fractures: reduction with the T-bar screw. South Med J 1992; 85: 1193-202.

104.Emery JM, Noorden GK, and Sclernitzauer DA. Orbital floor fractures: long-term follow-up of cases with and without surgical repair. Trans Am Acad Ophthalmol Otolaryngol 1971; 75: 802-12.

105.Putterman AM, Stevens T, and Urist MJ. Nonsurgical management of blow-out fractures of the orbital floor. Am J Ophthalmol 1974; 77: 232-9.

Secondary orbital tumors are due to the extension of a primary tumor into the orbit. The orbit may be affected secondarily by tumors arising in the adjacent structures. Such tumors commonly arise from the globe, lids, conjunctiva, nasopharynx, paranasal sinus, and lacrimal sac. Intracranial tumors can also have intraorbital extension. Several factors contribute to the extension of tumors into the orbit. These include the site of the primary tumor, aggressiveness of the tumor and adequacy of initial treatment.

Orbital Extension of Intraocular Tumors

This is more commonly seen in less developed countries due to a delay in presentation for treatment of a primary tumor. In more advanced countries systems of ocular screening have reduced both the morbidity and mortality from these neoplasms. Though most intraocular tumors can invade the orbit if not managed aggressively and adequately, however higher frequency is encountered amongst retinoblastoma, medulloepithelioma and uveal melanoma.1 Retinoblastoma and medulloepithelioma are usually found in pediatric population whilst melanomas are more common amongst adults.

Orbital Extension of Retinoblastoma

Retinoblastoma (RB) is the most common childhood intraocular tumor. The incidence is approximately 1 in 15,000 to 1 in 20,000 live births. Diagnosis and treatment can salvage life. However, early diagnosis can salvage not only the eye, but also sight. In developed countries the mortality rate from extraocular retinoblastoma is as low as 5 %, but this increases to over 90% in underdeveloped countries.2

Retinoblastomas generally remain within the globe for a considerable duration of time. However, once they penetrate Bruch's membrane they become highly aggressive. With time this leads onto extraocular spread. This may remain localized to the soft tissues surrounding the eye or the orbit (Figure 18.1) or may extend via the optic nerve into the brain (Figure 18.2) and meninges with subsequent seeding of the spinal fluid. Distant metastasis may occur through hematogenous spread involving the bones, bone marrow, liver, pancreas, kidney, spleen, lungs and gonads.

Extraocular extension of retinoblastoma into the orbit most commonly occurs through the periemissarial blood vessels. Extension also occurs directly into the choroid and through erosion of the globe. Once the tumor enters the orbit, it enters a state of neoplastic proliferation and rapidly develops into an orbital mass. Spread of retinoblastoma into

Figure 18.1: Bilateral retinoblastoma with orbital extension

the central nervous system usually occurs by direct invasion of the optic nerve and the subarachnoid space by the tumor cells. Very rarely retinoblastoma of peripapillary choroid can egress into the central nervous system via the posterior ciliary vessels.

Orbital invasion of retinoblastoma carries a poor prognosis and is a predictive factor of metastasis (Figures 18.3 and 18.4). Kapelman JE et al3 produced a multivariate analysis suggesting that orbital invasion and optic nerve invasion were the most highly predictive risk factors of death from retinoblastoma.

Secondary and Metastatic Orbital Tumors 245

The main goal of treatment for extraocular retinoblastoma is to extend survival and the disease free interval. Rootman J et al4 reported that only 9.4 % of patients with orbital extension lived more than 2 years after diagnosis. It was noted that orbital extension of retinoblastoma was frequently associated with distant metastasis. Zyguiska Manchowa H et al5 had reported 14 cases of extraocular retinoblastoma or with recurrence of which 78.6% had died.

Though there is no proven effective therapy for extraocular retinoblastoma, it should be managed with aggressive chemotherapy and radiotherapy to the orbit. When there is meningeal involvement craniospinal irradiation and/or intrathecal chemotherapy is indicated. However, often palliative treatment is required if therapy is ineffective. Highly individualized aggressive therapy enhances longer survival in patients with overt extraocular retinoblastoma (Figure 18.5). Chantada G had reported use of neoadjuvant combination chemotherapy followed by surgery in the form of enucleation and/or resection of residual orbital tumor mass and adjuvant chemotherapy and radiotherapy.6 Chemotherapy includes Vincristine, Etoposide, Carboplatin, Cyclophosphamide, Doxorubicin, Idorubicin, and Cisplatin.7 They reported that this treatment regimen was highly efficacious for patients with orbital extension of retinoblastoma.

Figure 18.3: Bilateral advanced retinoblastoma with extraocular extension involving the orbit and adnexae on the left side

Figure 18.4: Bilateral retinoblastoma. The child had undergone six cycles of chemotherapy. The left eye was salvaged , however the right eye had undergone enucleation

246 Surgical Atlas of Orbital Diseases

Figure 18.5: Fundus photograph illustrating regression of retinoblastoma following SALT

Keralli H et al8 reported that exenteration followed by chemotherapy and radiotherapy does not prolong the survival of patients with massive orbital involvement of intraocular retinoblastoma.

Orbital Extension of Medulloepithelioma

Intraocular medulloepithelioma of the ciliary body is a rare tumor occurring during the first decade of life. This embryonal tumor usually arises from the neuroepithelium of the ciliary body.9 Rarely, it may arise from iris, retina and optic nerve.10-12

Though the tumor tends to locally invade the surrounding ocular structures, it can also extend into the orbit and rarely metastasize. It can be classified as teratoid or nonteratoid medulloepithelioma. Medulloepithelioma that contains heterogenous tissues like skeletal muscle, cartilage and hair are classified as teratoid.13,14

Histologically, medulloepithelioma consists of two cellular components: epithelial cords and a fibrillar matrix. Epithelial cells are arranged in convoluted patterns or in a circular pattern around a lumen or more commonly as elongated, interlacing cords. Both pigmented and non-pigmented cells may be present. More malignant tumors contain some very poorly differentiated cells which may resemble

retinoblastoma cells. Medulloepithelioma forms a stroma composed of loose, delicate fibrils with abundant ground substance resembling embryonic mesenchyme or myxoid tissue.

Clinically it presents with loss of vision, pain, photophobia, ciliary body or anterior chamber mass,leucocoria and as proptosis in advanced cases (Figures 18.6 to18.9). Presence of a fleshy grey, pink, yellow or brown color mass with cystic areas in the ciliary body region is very characteristic. Very often lens coloboma may be the only presenting sign occurring due to absent zonules.The tumor may present either as a solid or polycystic mass or as sheet behind the lens, resembling a cyclitic membrane.The cysts of the tumor may be free floating cysts or may settle in anterior chamber or vitreous.The tumor may contain heterogenous tisues like cartilage which presents like chalk particles as grey-white opacities. Complications are rubeosis, glaucoma (Buphthalmos), cataract and retinal detachment. Malignant changes of medulloepithelioma are rare. These changes are characterized by increased pleomorphic and mitotic activity with areas of poorly differentiated neuroblastic cells or sarcomatous changes with invasion of surrounding ocular structures.15 Charif CM et al. reported a case of a 4 years old child with malignant medulloepithelioma involving the sclera with extension into the orbital fat.16 Though tumors predominantly occur in children, they can rarely present in adults. J Michael Jumper had reported a case of a 45 years old man with invasive medulloepithelioma.17

Diagnosis is usually established by slit lamp examination along with radiological investigations like ultrasound biomicroscopy, CT scan and MRI. Julian G Feijoo had reported characteristic ultrasonographic features of medulloepithelioma which included echogenic heterogenicity of the tumor with presence of multiple cysts with stalk-like prolongation of the surface.18 However diagnosis is confirmed by histopathological examination and by immunohistochemistry.

Treatment of choice is wide local excision. In malignant tumors enucleation is preferred. However, with extensive extraocular spread exenteration is performed followed by chemotherapy.Role of radiotherapy is palliative only.

Orbital Extension of Uveal Melanoma

Orbital involvement of uveal melanomas occur after extrascleral extension of massive intraocular lesions. Although extraocular spread may present with its own set of clinical problems, ultimately it is the distant metastases which ultimately decide the long-term prognosis of the patient.

Uveal melanomas are a diverse group of pigmented tumors originating in the iris, ciliary body

and most commonly the choroid. They are the most common primary intraocular tumors with an annual incidence that varies worldwide. Melanomas tend to be more common in those of caucasian descent and tend to have increased incidence with decreasing latitude suggesting that increased sun exposure may be a factor in development. They predominate in the older age group peaking in the sixth decade.19 Predisposing factors include ocular melanosis and melanocytoma.

248 Surgical Atlas of Orbital Diseases

The tumors can be subclassified by histological cell type using the modified version of the prognostic cell type introduced by Callendar. Spindle A, spindle B, epithelioid and mixed types can be seen (Figures 18.10A to G) with epithelioid cells having the worst

prognosis.20 Other prognostic factors include size of the primary and age of the patient at presentation.21 Recently, genetic mutations have also been noted including monosomy 3 and duplication of chromosome 8q confer worse prognosis.

Extrascleral extension has also been found to portend a worse prognosis.21 This is linked to the fact that there is increased risk of distant metastasis.22 Orbital extension of an intraocular primary occurs via scleral emissary channels, vortex vein and posterior ciliary artery (Figures 18.11A to C) . Rare cases of extension through the optic nerve have also been reported.23 Shammas et al found that upto 0.4% of uveal melanomas showed orbital extension however, it is thought that microscopic extension has already occurred in between 10-40% of cases.24,25

Clinically, uveal melanomas may be difficult to diagnose. Patients will rarely complain of any visual disturbance unless central vision is affected. Occasionally, pain may be noted due to impingement on the posterior ciliary nerves. Nevertheless, the vast majority remain asymptomatic. The advent of indirect ophthalmoscopy has greatly assisted in peripheral viewing and perception of depth. However, simple examination may still provide some difficulty in differentiating these lesions from eccentric disciform lesions, naevi or other choroidal lesions such as hemangiomas. This is where ultrasound B-scan may be of some assistance in determining the size and depth of the lesion. Although CT may have little place in investigation, contrast enhanced MRI can assist.26 It is especially useful in determining early extra scleral spread as well as assisting in finding the extent of the tumor to assist management.

It is thought that by the time of presentation 40-45% of tumors will have metastasized.27 Epithelioid and mixed cell types and larger tumors are more likely to involve the orbit.24 It is this distant spread which will ultimately decide the long-term survival of the patient. Consequently, signs and symptoms of spread should be sought and liver function tests and chest-radiograph can be performed at diagnosis to assist early screening. There is still little effective treatment for metastatic disease. As a result, it has been shown that aggressive surgical treatment of these tumors has had little effect on

A

survival and consequently management has tended to be more conservative. Treatment is partly tailored to the size and type of extrascleral extension. Plaque radiotherapy has been shown to be effective against flat or small nodular extensions, whereas with larger nodular extension and recurrence external beam radiotherapy followed by exenteration can be used. Vortex vein involvement requires resection of the vortex vein followed by further enucleating or radiotherapy. Recently, brachytherapy has also been proposed for as a substitute for radiotherapy. Early findings suggest that the technique requires less time for completion of treatment whilst delivering a higher dose of radiation to the tumor.

Despite improving diagnosis and management of melanoma, survival has improved little. Thus the aim is still to be able to diagnose these tumors prior to extrascleral extension.28

Orbital Extension of Lacrimal Sac Tumors

Occurance of lacrimal sac tumor is very rare. In majority of patients they are epithelial in origin These epithelial tumors include squamous and transitional cell papillomas, oncocytic adenomas and carcinomas like transitional cell carcinoma, squamous cell carcinoma, adenocarcinoma, adenoid cystic carcinoma, mucoepidermoid carcinoma and poorly differentiated carcinoma.29,30 Amongst the nonepithelial tumor the most common is fibrous

histiocytoma followed by a variety of other tumors including lymphoid tumor, malignant melanoma, hemangiopericytoma, neurofibroma, granulocytic sarcoma and lipoma.30 It has been found that approximately 55% of lacrimal sac tumors undergo malignant transformation.30 Though these tumors are locally invasive, however at times it can invade the orbit and can also metastasize becoming life threatening.

The age of presentation of lacrimal sac tumors depend on the histologic pattern of the neoplasm. Benign tumors like papillomas are found in younger age group. However, the malignant tumors are seen within 41-75 years of age.31 Ni C and co-worker had reported that genetic and environmental factors may play a role in clinical presentation of lacrimal sac tumor.32

The signs and symptoms are usually insidious with epiphora being the most common symptom and lacrimal sac mass as the most common presenting sign.

Histopathologically, lacrimal sac tumors are classified as epithelial tumors and non-epithelial tumors. These tumors are either benign or malignant. The malignant tumors are found to arise either from pre-existing tumors or arise de novo.

The papillomas are the most common lacrimal sac tumors .According to their growth the papillomas

are subdivided as exophytic, inverted and mixed. However according to the histologic patterns, papillomas are classified as squamous cell papillomas characterized by acanthotic, stratified squamous epithelium transitional cell papilloma with stratified columnar epithelium and mixed papilloma with a mixture of squamous cell and transitional cell. Malignant transformation in the form of carcinomas like squamous cell, transitional cell or adeno carcinoma seem to originate from the epithelial lining of the lacrimal sac. Other epithelial tumors are oncocytic adenomas and mucoepidermoid carcinoma. Oncocytic tumors are composed of special types of epithelial cell called oncocytes due to their abundant eosinophilic cytoplasm. These tumors rarely undergo metastasis. Mucoepidermoid carcinoma is a rare epithelial tumor of the lacrimal sac. These tumors are composed of a mixture of different cells like mucus secreting cells, epidermoid cells and basal cells. Seven types of non-epithelial tumors of lacrimal sac are reported. The common amongst them are fibrous histiocytoma, lymphoma, melanoma and hemangioopericytoma.30 In general, lacrimal sac tumors are rarely life threatening. Distant metastasis can be fatal.

A thorough history directed to pertinent clinical features is very important. A comprehensive ocular and systemic examination is necessary to assess the firmness and location of the mass in relation to the medial canthal tendon. Careful examination to rule out any punctal discharge and regional lymphadenopathy and a complete nasal and sinus evaluation should be done.

Lacrimal function tests the rapidity of flow from the lacrimal sac. Benign tumors demonstrate outflow stenosis and carcinomas show complete obstruction. Dacryocystogram of a lacrimal sac tumor shows a discrete mass with a filling defect or a distended sac shadow with uneven or mottled density of the contrast media and some patency.

Computed tomography of orbit and sinuses is essential to outline the tumor and assess erosion or invasion into nearby structures. Located within the lacrimal sac fossa, anterior to the posterior lacrimal

Secondary and Metastatic Orbital Tumors 251

crest along the medial orbital wall, the nasolacrimal sac is usually not prominently identified on radiographic imaging (CT/MRI). Expansion of lacrimal sac fossa, destruction of bone, a mass extending beyond the lacrimal sac suggest a lacrimal sac tumor. A chest X-ray, hematologic tests including full blood count with differential, ESR, renal and hepatic function tests, antineutrophil cytoplasmic antibody and leutic serology may be considered. Swabbing for microbiologic culture is essential in an ulcerated lesion. Biopsy for histopathological diagnosis is mandatory for treatment.

Traditionally, suspected lacrimal sac tumor is managed by dacryocystectomy with tissue biopsy and frozen section analysis (Figures 18.12A and B). This was followed by further treatment as required including radical resection, radiotherapy, or chemotherapy.

Nowadays, incisional biopsy is done in large ulcerative tumors to plan subsequent therapy. Following definitive histological examination, if no evidence of tumor is found, a DCR is performed. If the only suggestion of a lacrimal sac tumor is a filling defect on DCG, a DCR and biopsy should be performed. If the biopsy reveals a locally invasive tumor, nasal endoscopic monitoring is advised. Aggressive tumors are treated with radical surgery or radiotherapy.

Figures 18.12: A case of lacrimal sac tumor which was later diagnosed as squamous cell carcinoma of lacrimal sac

252 Surgical Atlas of Orbital Diseases

Management varies as to the tumor origin. For lacrimal sac neoplasms, surgery with adjuvant radiotherapy is advised. In lymphomas, chemotherapy is the definitive treatment. For localized epithelial and mesenchymal tumors, wide surgical excision is performed. Postoperative radiotherapy is recommended for malignant epithelial tumors. Further surgery and adjuvant radiotherapy is performed for recurrent lesions.

For malignant melanomas extensive surgical resection, radiotherapy or chemotherapy may delay recurrence but survival remains poor.

A partially or totally irreducible lacrimal sac mucocele indicates an underlying neoplasm. This is managed by DCR followed by definitive therapy determined by histology with biopsy if bone erosion is absent on CT. If radiology suggests malignancy, treatment is as outlined above.

Orbital Extension of Eyelid Tumors

Malignant eyelid tumors have the propensity of aggressive growth and for metastasis necessitating aggressive management.Though there are different types of eyelid tumors, however epithelial tumors are most common malignant eyelid tumors. These are usually slowly enlarging and destructive tumors which can invade the adnexal tissues and the orbit.

The clinical features of malignant eyelid tumors are variable.Very often they present as chronic blepheritis or meibomianitis or as a lid mass.There may be associated loss of eyelashes or pitting or notching of lid lamella.Presence of superficial telengiectatic blood vessels on the surface of the mass is characteristic of malignant eyelid tumors.The important and common epithelial malignancies of the eyelid are basal cell carcinoma, squamous cell carcinoma and sebaceous gland carcinoma.

Basal Cell Carcinoma (BCC)

Basal cell carcinoma is the most common malignant eye lid tumor in Caucasians (80 to 90%), while it shares equal incidence with sebaceous gland and squamous cell carcinoma in Japan and Asia (20 to 40%).33,34 Its incidence is increasing worldwide.35 Incidence of BCC in caucasians is generally higher in males than females. It occurs rarely before 20 years of age, but age specific incidence increases thereafter peaking between 40 to 80 years with an average age of onset of 48 years.

Independent risk factors for BCC include red hair and light skin color.36 Dynamic tanning and burning reaction to the skin is also a clear predisposing factor.37 Other risk factors include ionizing radiation, arsenic exposure, smoking history and patients with AIDS.38,39 Rare syndromes associated with BCC include albinism, xeroderma pigmentosum, Gorlin's syndrome, milia, spina bifida and syndactyly.

The most frequent site of involvement is the lower lid (50 to 60%) and medial canthus (25 to 30%). Upper lid (15%) and lateral canthus (5%) are less frequently involved.39 In the early stages BCC appears as a pearly, raised area, through which dilated vessels are seen. They ultimately undergo ulceration and present as destructive lesions which distort the eyelid anatomy. It has an indolent and painless course. Histologically, BCC can be classified as nodulo-ulcerative (rodent ulcer), pigmented, morphea or sclerosing, superficial, keloidal and fibroepithelial variety (pinkuus tumor). It may cause loss of eyelash and mimic chronic infection of eyelid margin. The nodular variety is the most common and it appears as a raised pearly nodule with telangectasia and central ulceration. Histology shows nests of basal cells that originate from the basal cell layer of the epithelium with peripheral palisading. Morpheoform lesions are firm and slightly elevated with ill-defined margins. Histology shows thin cords which radiate peripherally. Morpheoform is more aggressive than nodular tumor. BCC is a slow growing tumor and it is locally invasive. It rarely spreads to distal parts of the body.40 Reported incidence of metastasis is 0.0028 to 0.55%.3 Choroidal invasion occurs at advanced stages with median survival of 3 years at presentation. Orbital extension is usually found with inner canthal lesions (Figure 18.13). This is due to delayed presentation or treatment and multiple recurrence following incomplete excision.

Surgical excision is the most common mode of treatment, followed by curettage and cautery, cryosurgery and radiotherapy.41 Mohs micrographic surgery as practised in many centers allow 100% freeing of excision margin. Micrographic surgery allows 99% success rate with tumor removal by smaller margin.42

Cryosurgery is suitable for superficial lid tumors and gives 92% five years cure rate.43 Curettage is usually combined with cautery and usually requires