Ординатура / Офтальмология / Английские материалы / Comprehensive Ophthalmology_Khurana_2007

Diagnosis. Clinically pseudotumour is suspected only by exclusion of the known conditions.

Ultrasonic and CT-scanning show a diffuse infiltrative lesion with irregular ill-defined margins and variable density.

Fine-needle aspiration biopsy may give histological clue.

Incisional biopsy may be needed to confirm the diagnosis.

Treatment. It consists of a course of systemic corticosteroids (60-80 mg of prednisolone per day for 2 weeks, initially and then gradually tapered). Usually, more than half of the patients show a positive response. In non-responsive patients, radiotherapy is usually effective. A few recalcitrant cases may require treatment with cytotoxic agents.

GRAVES’ OPHTHALMOPATHY

This term is coined to denote typical ocular changes which include lid retraction, lid lag, and proptosis. These changes have also been labelled as : endocrine exophthalmos, malignant exophthalmos, dysthyroid ophthalmopathy, ocular Graves’ disease (OGD), and thyroid eye disease (TED).

Etiology

It may be a part of Graves’ disease (the syndrome consisting of hyperthyroidism, goitre and eye signs) or may be associated with hypothyroidism or even euthyroidism. Thus, a direct causative connection between the thyroid dysfunction and the ocular changes remains elusive. There is an increasing evidence to suggest that Graves’ ophthalmopathy has an autoimmune etiology.

Pathogenesis

The histopathologic reaction of various tissues is dominated by a mononuclear cell inflammatory reaction, which is characteristic of, but by no means limited to, an immunologically-mediated disease mechanism. Deposition of glycosaminoglycans (GAGs) such as hyaluronic acid together with interstitial oedema and inflammatory cells are considered to be the causes of swelling of various tissues in the orbit and dysfunction of extraocular muscles in thyroid ophthalmopathy. Swelling of the

various tissues of the orbit results in eyelid oedema, chemosis, proptosis, thickening of extraocular muscles and other signs of thyroid ophthalmopathy. Most data presently support the postulate that the orbital fibroblast is the primary target of inflammatory attack, with extraocular muscles being secondarily involved. The following scheme for the pathogenesis of Graves’ ophthalmopathy has been recently proposed:

Circulating T cells in patients with Graves’ disease directed against an antigen on thyroid follicular cells, recognize this antigen on orbital and pretibial fibroblasts (and perhaps extraocular myocytes). How these lymphocytes came to be directed against a self-antigen, escaping deletion by the immune system, is unknown.

The T cells then infiltrate the orbit and pretibial skin. An interaction between the activated CD4 T cells and local fibroblasts results in the release of cytokines into the surrounding tissue – in particular, interferon-interleukin-1, and tumor necrosis factor.

These or other cytokines then stimulate the expression of immunomodulatory proteins (the 72-kd heat-shock protein, intercellular adhesion molecules, and HLA-DR) in orbital fibroblasts, thus perpetuating the autoimmune response in the orbital connective tissue.

Furthermore, particular cytokines (interferon-, interleukin-1, transforming growth factor, and insulin-like growth factor 1) stimulate glycosaminoglycan production in fibroblasts, proliferation of fibroblasts, or both, leading to the accumulation of glycosaminoglycans and oedema in the orbital connective tissue. In addition, thyrotropin-receptor or other antibodies may have direct biological effects on orbital fibroblasts or myocytes; alternatively, these antibodies may reflect the on going autoimmune process.

The increase in connective-tissue volume and the fibrotic restriction of extraocular-muscle movement resulting from fibroblast stimulation lead to the clinical manifestations of ophthalmopathy. A similar process occurring in the pretibial skin results in the expansion of dermal connective tissue, which in turn leads to the nodular or diffuse skin thickening characteristic of pretibial dermopathy.

Clinical features (Fig. 16.11)

1. Lid signs. These are:

Retraction of the upper lids producing the characteristic staring and frightened appearance (Dalrymple’s sign);

Lid lag (von Graefe’s sign) i.e., when globe is moved downward, the upper lid lags behind;

Fullness of eyelids due to puffy oedematous swelling (Enroth’s sign);

Difficulty in eversion of upper lid (Gifford’s sign);

Infrequent blinking (Stellwag’s sign).

Fig. 16.11. A patient with Graves’ ophthalmopathy having bilateral exophthalmos and lid retraction.

2.Conjunctival signs. These include ‘deep injection’ and ‘chemosis’.

3.Pupillary signs. These are of less importance and may be evident as inequality of dilatation of pupils.

4.Ocular motility defects. These range from convergence weakness (Mobius’s sign) to partial or complete immobility of one or all of the extrinsic ocular muscles. The most common ocular motility defect is a unilateral elevator palsy caused by an involvement of the inferior rectus muscle followed by failure of abduction due to involvement of medial rectus muscle.

5.Exophthalmos. It is a common and classical sign of the disease. As a rule both eyes are symmetrically affected; but it is frequent to find one eye being more porminent than the other. Even unilateral proptosis is not uncommon. In majority of cases it is self-limiting.

6.Exposure keratitis and symptoms of ocular surface discomfort. These include sandy or gritty

sensation, lacrimation and photophobia. Corneal exposure has been attributed to upper lid retraction, exophthalmos, lagophthalmos, inability to elevate the eyes and a decreased blink rate.

7.Optic neuropathy. It occurs due to direct compression of the nerve or its blood supply by the enlarged rectus muscles at the orbital apex. It may manifest as papilloedema or optic atrophy with associated slowly progressive impairment of vision.

Classification

American Thyroid Association (ATA) has classified Graves’ophthalmopathy, irrespective of the hormonal status into following classes, characterised by the acronym ‘NOSPECS’.

Class 0 : No signs and symptoms.

Class 1 : Only signs, no symptoms (signs are limited to lid retraction, with or without lid lag and mild proptosis).

Class 2 : Soft tissue involvement with signs (as described in Class-1) and symptoms including lacrimation, photophobia, lid or conjunctival swelling.

Class 3 : Proptosis is well established.

Class 4 : Extraocular muscle involvement (limitation of movement and diplopia).

Class 5 : Corneal involvement (exposure keratitis).

Class 6 : Sight loss due to optic nerve involvement with disc pallor or papilloedema and visual field defects.

For practical purposes it has been described as ‘early’ (which include ATA Class 1 & 2) and ‘Late Graves’ ophthalmopathy’ (Class 3 to 6).

Clinical types

1.Thyrotoxic exophthalmos (Exophthalmic goitre): In this form a mild exophthalmos is associated with lid signs and all signs of thyrotoxicosis which include tachycardia, muscular tremors, and raised basal metabolism. Graves’ disease is the commonest variety of hyperthyroid state. It typically affects the women between 20 and 45 years of age.

2.Thyrotropic exophthalmos (exophthalmic ophthalmoplegia). In this clinical variety, an extreme exophthalmos and external ophthalmoplegia (due to infiltrative thyroid ophthalmopathy) are associated

with euthyroidism or hypothyroidism. The condition usually affect middle-aged persons, and runs a selflimiting course characterised by remissions and relapses. Some prefer to use the term ocular Graves’ disease (OGD) for this entity.

Differential diagnosis

Clinical diagnosis is not difficult in advanced cases of Graves’ ophthalmopathy with bilateral proptosis. However, early cases having unilateral proptosis need to be differentiated from other causes of unilateral proptosis of adulthood onset.

Investigations

1.Thyroid function tests. These should include: serum T3, T4, TSH and estimation of radioactive iodine uptake.

2.Positional tonometry. An increase in intra-ocular pressure in upgaze helps in diagnosis of subclinical cases.

3.Ultrasonography. It can detect changes in extraocular muscles even in class 0 and class 1 cases and thus helps in early diagnosis. In addition to the increase in muscle thickness, erosion of temporal wall of orbit, accentuation of retrobulbar fat and perineural inflammation of optic nerve can also be demonstrated in some early cases.

4.Computerised tomographic scanning. It may show proptosis, muscle thickness, thickening of optic nerve and anterior prolapse of the orbital septum (due to excessive orbital fat and/or muscle swelling).

Management of Graves’ ophthalmopathy

It is in addition to and independent of the therapy for the associated thyroid dysfunction; as the latter usually does not alter the course of ophthalmic features. The treatment modalities employed are as follows:

1.Topical artificial tear drops in the day time and ointment at bed time are useful for relief of foreign body sensation and other symptoms of ocular surface drying.

2.Guanethidine 5% eyedrops may decrease the lid retraction caused by overaction of Muller’s muscle.

3.Systemic steroids may be indicated in acutely inflamed orbit with rapidly progressive chemosis and proptosis with or without optic neuropathy.

4.Radiotherapy (2000 rads given over 10 days period). It may help in reducing orbital oedema in patients where steroids are contraindicated.

5.Lateral tarsorrhaphy should be performed in patients with exposure keratopathy (with mild to moderate proptosis) not responding to topical artificial tears.

6.Extraocular muscle surgery. It should be carried out for left-out diplopia in primary gaze, after the congestive phase of disease is over and the angle of deviation is constant for the last 6 months.

7.Surgical orbital decompression. It should be performed only when systemic steroids and radiotherapy have proved ineffective in patients with marked proptosis associated with severe exposure keratopathy and/or optic neuropathy with imminent danger of permanent visual loss.

The most commonly employed technique is ‘two wall decompression’ in which part of the orbital floor and medial wall are removed.

8.Cosmetic surgery for persistent lid retraction. It consists of levator and Muller’s muscle recession. Recently, implantation of scleral grafts has become a popular technique.

9.Blepharoplasty. It may be performed by removal of excess fatty tissue and redundant skin from around the eyelids.

ORBITAL TUMOURS

Orbital tumours are not very common. These include primary, secondary and metastatic tumours.

(A) Primary tumours. Those arising from the various orbital structures are as follows:

1.Developmental tumours: Dermoid, epidermoid, lipodermoid and teratoma.

2.Vascular tumours: Haemangioma and lymphangioma.

3.Adipose tissue tumours: Liposarcoma

4.Fibrous tissue tumours: Fibroma, fibrosarcoma and fibromatosis.

5.Osseous and cartilaginous tumours: Osteoma, chondroma, osteoblastoma, osteogenic sarcoma after irradiation, fibrous dysplasia of bone, and Ewing’s sarcoma.

6.Myomatous tumours: Rhabdomyoma, leomyoma and rhabdomyosarcoma.

7.Tumours of optic nerve and its sheaths: Glioma and meningioma.

8.Tumours of lacrimal gland: Benign mixed tumour, malignant mixed tumours and lymphoid tumours.

9.Tumours of lymphocytic tissue: Benign and malignant lymphomas.

10.Histiocytosis-X.

(B)Secondary tumours, spreading from surrounding structures.

(C)Metastatic tumours, from distant primary tumours.

(A) PRIMARY ORBITAL TUMOURS

I. Developmental tumours

1. Dermoids. These are common developmental tumours which arise from an embryonic displacement of the epidermis to a subcutaneous location. The cystic component is lined with keratinizing epithelium and may contain one or more dermal adnexal structures such as hair follicles and sebaceous glands. Dermoids are of two types:

(a)Simple dermoid. It is seen in infancy. Appears as a firm, round, localised lesion in the upper temporal or upper nasal aspect of the orbit. These do not extend deep into the orbit and are not associated with bony defects. Displacement of globe is also not seen as these are located anterior to the orbital septum (Fig. 16.12).

(b)Complicated dermoids. These are present in adolescence with proptosis or a mass lesion having indistinct posterior margins (as they arise from deeper sites). They may be associated with bony defects.

Fig. 16.12. Dermoid right orbit.

Treatment is surgical excision. Care should be taken not to leave behind the contents of cyst which are potentially irritating.

2.Epidermoid. It is composed of epidermis without any epidermal appendages in the wall of the cyst. These are almost always cystic. The cyst wall contains keratin debris. Treatment is surgical excision.

3.Lipodermoids. These are solid tumours usually seen beneath the conjunctiva. These are mostly located adjacent to the superior temporal quadrant of the globe (Fig. 16.13). These do not require any surgical intervention unless they enlarge significantly. Also see page 86.

Fig. 16.13. Lipodermoid.

4. Teratomas (Fig. 16.14). These are composed of ectoderm, mesoderm and endoderm. These may be solid, cystic or a mixture of both. The cystic form is more prevalent. Most of these are benign but some solid tumours in newborns are malignant. Exenteration is usually performed for solid tumours to effect a permanent cure. Cystic tumours may be excised without removing the eyeball.

II. Vascular tumours

These are the most common primary benign tumours of the orbit. These can be either haemangiomas or lymphangiomas. Haemangiomas are further divided into two types — capillary and cavernous.

1. Capillary haemangioma. It is commonly seen at birth or during the first month. It appears as periocular swelling in the anterior part of the orbit. It tends to increase in size on straining or crying. This tumour may initially grow in size followed by stabilization and then regression and disappearance.

Fig. 16.14. Congenital teratoma.

Treatment. These tumours usually do not require any treatment. Indications for treatment are: optic nerve compression, exposure keratitis, ocular dysfunction or cosmetic blemish. Mode of therapy are: systemic and/or intralesional steroids, low-dose superificial radiations, surgery and cryotherapy.

2.Cavernous haemangioma. It is the commonest benign orbital tumour among adults. The tumour is usually located in the retrobulbar muscle cone. So, it presents as a slowly progressing unilateral axial proptosis in the second to fourth decade. It may occasionally compress the optic nerve without causing proptosis.

Treatment. Surgical excision of the tumour is undertaken via lateral orbitotomy approach. Since the tumour is well encapsulated, complete removal is generally possible.

3.Lymphangioma. It is an uncommon tumour presenting with slowly progressive proptosis in a young person. It often enlarges because of spontaneous bleed within the vascular spaces, leading to formation of ‘chocolate cysts’ which may regress spontaneously.

III. Myomatous tumours

Rhabdomyosarcoma. It is a highly malignant tumour of the orbit arising from the extraocular muscles. It is the most common primary orbital tumour among children, usually occurring below the age of 15 years (90%).

Clinical features. It classically presents as rapidly progressive proptosis of sudden onset in a child of 7-8 years (Fig. 16.15). Massive proptosis due to rhabdomyosarcoma located in the superonasal quadrant (mimmicking acute inflammatory process).

Fig. 16.15. Massive proptosis due to rhabdomyosarcoma located in the superonasal quadrant (mimmicking acute inflammatory process).

The clinical presentation mimics an inflammatory process. The tumour commonly involves the superionasal quadrant; but may invade any part of the orbit.

Diagnosis. The clinical suspicion is supported by X- rays showing bone destruction and CT scan demonstrating tumour in relation to an extraocular muscle. Diagnosis is confirmed by biopsy.

Treatment. High dose radiation therapy (5000 rads in 5 weeks) combined with systemic chemotherapy is very effective. Chemotherapy regime consists of Vincristine 2 mg/m2 on day 1 and 5, actinomycin-D 0.015 mg/kg IV once a day for 5 days and cyclophosphamide 10 mg/kg once a day for 3 days; to be repeated every 4 weeks for a period of 2 years. Exenteration is required in a few unresponsive patients.

IV. Tumours of the optic nerve and its meninges

1. Optic nerve glioma. It is a benign tumour arising from the astrocytes. It usually occurs in first decade of life. It may present either as a solitary tumour or as a part of von Recklinghausen’s neurofibromatosis (55%).

Clinical features. It is characterised by early visual loss associated with a gradual, painless, unilateral axial proptosis occurring in a child usually between 4 and 8 years of age (Fig. 16.16A). Fundus examination may show optic atrophy (more common) or papilloedema and venous engorgement. Intracranial extension of the glioma through optic canal is not uncommon.

Diagnosis. Clinical diagnosis well supported by X- rays showing uniform regular rounded enlargement of optic foramen in 90 percent of cases (Fig. 16.16B) and CT scan and ultrasonography depicting a fusiform growth in relation to optic nerve (Fig. 16.16 C & D).

Treatment. It consists of excision of the tumour mass with preservation of the eyeball, by lateral orbitotomy when the cosmetically unacceptable proptosis is present in a blind eye (due to optic atrophy). Tumours with intracranial extensions are dealt with the neurosurgeons. In unoperable cases, radiotherapy should be given.

2. Meningiomas. These are invasive tumours arising from the arachnoidal villi. Meningiomas invading the

orbit are of two types: primary and secondary.

(a)Primary intraorbital meningiomas. These are also known as ‘optic nerve sheath meningiomas’. These produce early visual loss associated with limitation of ocular movements, optic disc oedema or atrophy, and a slowly progressive unilateral proptosis. During the intradural stage, it is clinically indistinguishable from optic nerve glioma. However, the presence of opticociliary shunt is pathognomonic of an optic nerve sheath meningioma.

(b)Secondary orbital meningiomas. Those intracranial meningiomas which secondarily invade the orbit either arise from the sphenoid bone or involve it en route to the orbit. Orbital invasion may occur through : floor of anterior cranial fossa, superior

orbital fissure and optic canal. Meningioma enplaque, affecting the greater and lesser wings of sphenoid and taking origin in the region of pterion, is the most common variety affecting the orbit secondarily. These tumours typically occur in middleaged women.

Clinical features. These are characterised by greater proptosis and lesser visual impairment than the primary intraorbital meningiomas. Other characteristic features of these tumours are boggy eyelid swelling and an ipsilateral swelling in the temporal region of the face, especially when the intracranial tumour arises from the lateral part of sphenoid ridge (Fig. 16.17A). In such cases proptosis is due to hyperostosis on the lateral wall and roof of the orbit. CT scan is very useful in assessing the extent of tumour (Figs. 16.17 B & C).

Management of secondary orbital meningiomas is the domain of neurosurgeons.

V. Lymphomas

These are malignant tumours of lymphoreticular origin. Clinically and pathologically, these are quite heterogeneous. Broadly, these can be classified in two distinct clinico-pathologic groups: Hodgkin’s lymphomas (HL) and non-Hodgkin’s lymphomas (NHL). Both groups include many histopathologic subtypes. Orbits are involved more commonly by non-Hodgkin’s lymphomas.

Clinical features. These may involve orbit, lacrimal glands, lids and subconjunctival tissue and produce varied clinical features.

Diagnosis. In case of suspected orbital lymphoma, an incisional needle aspiration biopsy should be carried out. On getting histopathologic evidence of lymphoma, a thorough systemic evaluation including search for lymph nodes, peripheral blood picture, bone marrow examination, chest X-rays, serum immunoprotein electrophoresis, lymphangiography and even a whole body CT scan should be carried out to establish systemic involvement.

Treatment. Most of the lymphocytic tumours are radiosensitive and thus in cases without dissemination radiotherapy (4000 rads in 4 weeks) is the best treatment. Chemotherapy is recommended in cases with dissemination.

A

B

C

Fig. 16.17. Secondary orbital involvement in a patient with sphenoidal ridge meningioma, clinical photograph:

(A) CT scan, coronal (B) and axial (C) sections.

VI. Histiocytosis-X

This is a group of diseases characterised by an idiopathic abnormal proliferation of histiocytes with granuloma formation. These diseases primarily affect children with an orbital involvement in 20 per cent of cases. This group includes following three diseases:

1.Hand-Schuller-Christian disease. It is a chronic disseminated form of histiocytosis involving both soft tissues and bones in older children of either sex. It is characterised by a triad of proptosis, diabetes insipidus and bony defects in the skull.

2.Letterer-Siwe disease. It is systemic form of histiocytosis-X characterised by widespread soft tissue and visceral involvement with or without bony changes. The disease has a slight male preponderance and often occurs in the first three years of life. Orbital involvement is comparatively rare.

3.Eosinophilic granuloma. It is characterised by a solitary or multiple granulomas involving the bones. The disease occurs in elder children and frequently involves the orbital bones.

(B) SECONDARY ORBITAL TUMOURS

These may arise from the following structures:

1.Tumours of eyeball: retinoblastoma (Fig. 11.36) and malignant melanoma (Fig. 7.24).

2.Tumours of the eyelids: squamous cell carcinoma and basal cell carcinoma.

3.Tumours of nose and paranasal sinuses: These tumours very commonly involve the orbit (50%). These include:carcinomas, sarcomas and osteomas.

4.Tumours of nasopharynx. Carcinoma of nasopharynx is the commonest tumour involving the orbit. Thirty-eight percent cases with this tumour show ophthalmoneurological symptoms which include proptosis and involvement of fifth and sixth cranial nerves. Rarely, third, fourth and second cranial nerves are also involved.

5.Tumours of cranial cavity invading orbit are glioma and meningioma.

(C) METASTATIC ORBITAL TUMOURS

These involve the orbit by haematogenous spread from a distant primary focus and include the following:

1.Neuroblastoma — from adrenals and sympathetic chain.

2.Nephroblastoma —from kidneys.

3.Carcinoma — from lungs, breast, prostate, thyroid and rectum.

4.Malignant melanoma — from skin.

5.Ewing’s sarcoma —from the bones.

6.Leukaemic infiltration.

ORBITAL BLOW-OUT FRACTURES

These are isolated comminuted fractures which occur when the orbital walls are pressed indirectly, ‘Blowout fractures’ mainly involve orbital floor and medial wall.

Etiology

Blow-out orbital fractures generally result from trauma to the orbit by a relatively large, often rounded object, such as tennis ball, cricket ball, human fist (Fig. 16.18) or part of an automobile. The force of the blow causes a backward displacement of the eye and an increase in intraorbital pressure; with a resultant fracture of the weakest point of the orbital wall. Usually this point is the orbital floor, but this may be the medial wall also.

Fig. 16.18. Mechanism of blow-out-fracture of the orbital floor.

Classification

1.Pure blow-out fractures: These are not associated with involvement of the orbital rim.

2.Impure blow-out fractures: These are associated with other fractures about the middle third of the facial skeleton.

Clinical features

1.Periorbital oedema and blood extravasation in and around the orbit (such as subconjunctival ecchymosis) occur immediately. This may mask certain signs and symptoms seen later.

2.Emphysema of the eyelids occurs more frequently with medial wall than floor fractures. It may be made worse by blowing of nose.

3.Paraesthesia and anaesthesia in the distribution of infraorbital nerve (lower lid, cheek, side of nose, upper lip and upper teeth) are very common.

4.Ipsilateral epistaxis as a result of bleeding from maxillary sinus into the nose is frequently noted in early stages.

5.Proptosis of variable degree may also be present initially because of the associated orbital oedema and haemorrhage.

6.Enophthalmos and mechanical ptosis. After about 10 days, as the oedema decreases, the eyeball sinks backward and somewhat inferiorly resulting in enophthalmos and mechanical ptosis (Fig. 16.19). Three factors responsible for producing enophthalmos are:

escape of orbital fat into the maxillary sinus;

backward traction on the globe by entrapped in-ferior rectus muscle; and

enlargement of the orbital cavity from displacement of fragments.

7.Diplopia also becomes evident after the decrease in oedema. It typically occurs in both up and down gaze (double diplopia) due to entrapment of soft tissue structures in the area of the blowout fracture. The presence of muscle restriction can be confirmed by a positive ‘forced duction test’.

8.Severe ocular damage associated with blowout fracture is rare. This is because a ‘blow-out fracture’ is nature’s way of protecting the globe from injury. Nevertheless, the eye should be carefully examined to exclude the possibility of intraocular damage.

Fig. 16.19. Enophthalmos and mechanical ptosis in a patient with blow-out-fracture of orbit.

Roentgen examination

1.Plain X-rays. The most useful projection for detecting an orbital floor fracture is a nose-chin (Water’s) view. The common roentgen findings are : fragmentation and irregularity of the orbital floor; depression of bony fragments and ‘hanging drop’ opacity of the superior maxillary antrum from orbital contents herniating through the floor (Fig. 16.20).

2.Computerised tomography scanning and magnetic resonance imaging (MRI). These are of greater value for detailed visualisation of soft tissues. Coronal sections are particularly useful in evaluating the extent of the fracture.

Fig. 16.20. Plain X-ray orbit (AP view) showing herniated orbital contents (arrow) with blow-out fracture of the orbital floor.

Management

Surgical repair to restore continuity of the orbital floor may be made with or without implants. It may not be required in many cases. The optimal time for surgery, when indicated, is after 10-14 days of injury.

Indications of surgical intervention include:

1.Diplopia not resolving significantly in the early days after trauma.

2.A fracture with a large herniation of tissues into the antrum.

3.Incarceration of tissues in the fracture with resulting globe retraction and increased applanation tension on attempted upward gaze.

4.Enophthalmos greater than 3 mm.

Any of these factors, alone or combinedly could

indicate that early orbital repair is necessary.

ORBITAL SURGERY

ORBITOTOMY

Orbitotomy operation refers to surgical approach for an orbital mass lesion. There are four surgical approaches to the orbit:

1.Anterior orbitotomy. It can be performed through the skin (transcutaneous approach) or conjunctiva (transconjunctival approach) at a selected site near the orbital margin and more or less directly anterior to the lesion which is to be explored or removed. Therefore, anterior orbitotomy is indicated only when the lesion is readily palpable through the eyelids and is judged to be mainly in front of the equator of eyeball.

2.Lateral orbitotomy. In this approach lateral half of the supraorbital margin with the quadrilateral piece of bone forming the lateral orbital wall is temporarily removed. This approach provides an adequate exposure to the orbital contents and is particularly valuable for the retrobulbar lesions. The classical technique of lateral orbitotomy using S-shaped brow skin incision is called Kronlein’s operation.

3.Transfrontal orbitotomy. In this technique orbit is opened through its roof and thus mainly the domain of neurosurgeons. Transfrontal orbitotomy is used to decompress the roof of the optic canal and to explore and to remove when possible tumours of the sphenoidal ridge involving the superior orbital fissure.

4.Temporofrontal orbitotomy. This approach provides an access to the orbit (through its roof) and anterior and middle cranial fossa simultaneously.

Fig. 16.21. Exenteration of the orbit : A, skin incision;

B, periosteal reflection and C, amputation of the orbital contents.

EXENTERATION

It is a mutilating surgery in which all the contents of the orbits along with the periorbita are removed through an incision made along the orbital margins (Fig. 16.21). Exenteration is indicated for malignant tumours arising from the orbital structures or spreading from the eyeball. Now-a-days, debulking of the orbit is preferred over exenteration.