The Orbit and Lacrimal System

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20 The Orbit and Lacrimal System


The orbit is conical with a volume of approximately 27 ml. It contains the globe and the optic nerve, external ocular muscles, ophthalmic artery and its branches, orbital veins and nerves and the lacrimal gland. Orbital fat fills the remaining space and acts as a supportive cushion and fibrous septa run in planes between the ocular muscles and periosteum to support the orbital contents (see Ch. 18).


Fig. 20.2 The superior orbital fissure lies between the greater wing of the sphenoid inferiorly and the lesser wing superiorly (see Fig. 20.1). The lacrimal and frontal branches of the fifth nerve, the trochlear nerve and the superior ophthalmic vein are found superiorly and external to the annulus of Zinn; the superior and inferior divisions of the third nerve, the sixth nerve and nasociliary nerve lie within the annulus. The optic canal lies in the body of the sphenoid, medial and superior to the superior orbital fissure. It is lined with dura and transmits only the optic nerve and ophthalmic artery which lies inferior to the nerve. Space-occupying lesions at the orbital apex may compress the optic nerve and ocular motor nerves. Infiltrating lesions can spread through the superior orbital fissure into the cavernous sinus and middle cranial fossa to cause pain and loss of sensation in the distribution of the ophthalmic division of the trigeminal nerve. The sphenoidal sinus lies medial to the optic canal and the two are separated by extremely thin bone, which may even be absent, so that the optic nerve is easily damaged by surgery or disease within the sphenoidal sinus.


Table 20.1 Causes of orbital disease

Children Adults
Orbital cellulitis Trauma
Dermoid and epidermoid cysts Thyroid eye disease
Capillary haemangioma and lymphangioma Idiopathic orbital inflammatory disease (formerly known as ’pseudotumour’)
Neurofibroma* Lacrimal gland inflammation and tumours
Rhabdomyosarcoma* Cavernous haemangioma
Optic nerve glioma* Varices and lymphangioma
Leukaemia* Lymphoma and lymphoproliferative disease
  Meningioma (optic nerve or sphenoid wing)




A diverse range of pathology is found in the orbit and a careful history is essential in all patients. The onset, duration and variability of symptoms and the presence of pain, diplopia or visual failure must be ascertained. The importance of progressive symptoms indicating deterioration or an expanding lesion cannot be overemphasized. Old photographs of the patient are useful in dating the onset of long standing proptosis. Many orbital diseases are related to systemic conditions (e.g. neurofibromatosis, thyroid dysfunction, metastases) and a history and examination for systemic disease that includes a neuro-ophthalmic examination for associated intracranial disease is obligatory.

Proptosis must be distinguished from pseudo-proptosis due to enlargement of the globe, congenital bony deformity or facial asymmetry, enophthalmos of the fellow eye and lid disease such as retraction. Ptosis will occasionally present as ‘proptosis’ of the contralateral eye (see Ch. 2).

Initial examination of a patient with orbital disease should include optic nerve function (corrected visual acuities, colour vision, visual fields, pupillary reflexes), ocular muscle balance and movements, fundoscopy and retinoscopy. It is essential to document proptosis, displacement of the globe and upper and lower lid positions. Any mass should be assessed carefully for location, colour, consistency, mobility and dynamic alteration. Clinical evidence of spread of disease from the orbit into neighbouring areas (or vice versa) should be sought, particularly from the nose, sinuses, nasopharynx and cavernous sinus and middle or frontal cranial fossa. Periorbital and corneal sensation should be tested.

CT is the initial investigation of choice for most orbital diseases. Ultrasonography is useful to distinguish cystic (echolucent) from solid lesions (echogenic) quickly and to demonstrate blood flow. MRI is the investigation of choice for optic nerve disease.


Rapid onset of proptosis accompanied by pain and chemosis of the conjunctiva is usually caused by infective orbital cellulitis or idiopathic orbital inflammatory disease (formerly termed ‘pseudo-tumour’). Less common causes are retrobulbar haemorrhage, caroticocavernous fistula of acute inset or a rapidly infiltrating carcinoma. In children, rapidly growing tumours such as rhabdomyosarcoma and neuroblastoma may mimic orbital cellulitis.

Orbital cellulitis is usually associated with an infected adjacent sinus and requires careful management to prevent permanent visual impairment, ocular motility problems or the disaster of cavernous sinus thrombosis. It is important to differentiate preseptal cellulitis, usually associated with lid infection, from the potentially much more serious postseptal orbital involvement. Restricted ocular movement and proptosis are features of the latter. Chronically obstructed drainage of a paranasal sinus can cause sterile accumulation of mucus, chronic sinus enlargement and formation of a ‘mucocele’ which may encroach into the orbit displacing the globe.


Axial proptosis results from a lesion within the external ocular muscle cone and is caused by a benign or malignant expansion of one of its normal constituents or a metastasis from elsewhere.


The commonest cause of axial proptosis is thyroid eye disease which can affect the orbits symmetrically or asymmetrically, with the latter producing apparently uniocular proptosis. Patients may be hypothyroid, euthyroid or hyperthyroid. T3, T4 and thyroid autoantibodies should be measured in all patients but about 15 per cent of patients have completely normal findings; in these patients the diagnosis is made clinically and by CT. Patients should be assessed for cosmesis, corneal exposure, diplopia and optic nerve involvement, all of which may occur independently of each other. Patients may have sore, irritable or watery eyes from exposure keratopathy, superior limbic keratitis (see Ch. 5) or disturbance of tear film metabolism. Smoking has been shown to be a significant risk factor for the development of dysthyroid eye disease which may also deteriorate at the time of treatment of hyperthyroidism with I131.

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