21 Ophthalmic surgery

The conjunctiva of the eye is a thin, but important layer (see Fig. 21.1). It helps lubricate the eye, protects the eye from infection, and provides mucus for the corneal tear film.

Laceration size can affect whether surgical repair may be required or not. The larger the gap, the less chance that the conjunctiva will heal, or it will just take longer to heal. There is also a chance of scarring.

The cornea is the clear window of the eye. It has an approximate thickness of 0.5mm and a diameter of 12mm. It is separated from the iris by the aqueous filled anterior chamber. It has five layers from superficial to deep: epithelium, Bowman's membrane, stroma, Descemet's membrane, and endothelium (see Fig. 21.4). Any or all of these layers can become affected by pathology, perforation, or damage to the cells from inflammation or injury. Any distortion or opacity will result in blurring of vision. A corneal graft will replace the damaged layers and restore clearer vision, particularly when there is no damage within the eye itself.

There are 2 main types of corneal grafts:

Posterior lamellar grafts have the advantage of being smaller operations through a small incision requiring a few stitches. The integrity of the eyeball is much stronger compared with a full-thickness graft.

Generally performed when the cornea has a normal endothelium and pathology is limited to the stroma. Compared to full thickness grafts, in the presence of ocular surface disease it is safer, but more difficult to perform and may take longer. The recipient cornea is prepared first in case the surgeon has to convert to a full-thickness graft.

This is commonly performed in patients with endothelial disease only.

The ciliary body contains the ciliary processes that are responsible for aqueous humour production (see Fig. 21.3). Destroying the ciliary processes will ultimately reduce aqueous production and lower intraocular pressure. These procedures are associated with unwanted complications and are unpredictable in their pressure lowering effects. They are usually indicated as a last resort particularly in eyes with very limited visual potential.

Sympathetic ophthalmitis (also known as sympathetic ophthalmia/uveitis) is a rare, autoimmune (delayed-type hypersensitivity reaction) granulomatous uveitis (towards melanin-containing structures in the eye) that occurs following penetrating trauma (from surgery or injury) to an eye. This can result in inflammation appearing in the contralateral eye, and can lead to loss of vision in both eyes.

Tears are produced by the lacrimal glands and drain continuously through the nasolacrimal ducts. The nasolacrimal ducts are situated in the medial corners of the eye (see Fig. 21.8). They connect the small lower eyelid puncta to the middle meatus of the nose. The drainage channel becomes narrower with age and can become blocked. This can cause troublesome watery eyes (epiphora) which may require surgery to re-create a new drainage channel.

Silicone tubes may be inserted via the eyelid puncta into the nose for 2–3 months. They are removed in clinic although in children short general anaesthesia may be required. Permanent bypass tubes (e.g. Lester–Jones tube) are sometimes needed if there is significant canalicular damage.

The eyelids (see Figs. 21.6 and 21.7) play an important role in protecting the eye, and in keeping it lubricated through blinking. Lacerations away from the margin and not involving deep structures can be repaired simply in the emergency department if needed. Deeper lacerations may require exploration in theatre if contaminated, or if there is a concern that damage to deeper structures (such as the LPS, which raises the upper lid) has occurred.

Lacerations involving the lid margins should ideally be taken to theatre to ensure proper repair, as incorrect healing can cause subsequent complications (e.g. irregular lid margins, lid notching, and exposure keratopathy if lids do not close properly). The margin must be aligned antero-posteriorly (using a suture through the grey line to help ensure this), in order to ensure that tissue structures are in the correct place. Until this is satisfactory, the repair should not progress any further. The tarsal plate is next repaired, with muscles and subcutaneous tissue following. The skin is repaired last.

Lacerations of the medial canthus are important as the canalicular apparati can be torn, affecting tear drainage. These must always be taken to theatre for repair, as the nasolacrimal system will likely need to be probed from both the punctual (canalicular punctum) and nasal (nasolacrimal duct) ends, in order to identify if the nasolacrimal system has been affected, and if it has, an attempt can be made to repair the damage. This is usually performed by stenting the nasolacrimal system and repairing the lid laceration, in the hope that healing will allow the nasolacrimal system to heal around the stent, so that when it is removed in the future, the system will work once more.

Sometimes it is not possible to repair the damage to the canalicular system, or the canaliculus scars up after the stent is removed. In these cases, additional surgery may be required to provide an alternative route for tear drainage. It is also important to repair the medial or lateral canthal tendons that provide support to the eyelids.

The eyelid skin with its appendages can develop various benign and malignant lesions. Many eyelid lesions can be identified by their appearance and location and do not require histological confirmation.

However, some with suspicious features will require excision and histological confirmation with the possibility of wider excisions suggested. These larger defects usually require grafts or flaps to repair.

Fluorescence is the emission of light of one wavelength by a substance after it has been stimulated by light of a different wavelength. The stimulating wavelength is normally shorter (closer to the ultraviolet end of the electromagnetic spectrum) than the wavelength emitted (which would be closer to the infrared end of the electromagnetic spectrum). Fluorescein is a water-soluble dye that absorbs light at a wavelength of 465–490nm (blue), and emits light at a wavelength of 520–530nm (yellow-green). Indocyanine green is a water soluble dye (that binds tightly to plasma proteins) that absorbs light at a wavelength of 805nm (infrared) and emits light at a wavelength of 835nm (infrared).

When the retinal or choroidal circulation in the eye has been damaged/affected (or if there is suspicion of damage) following an event in the eye, it needs to be assessed to determine the extent of the injury, and the subsequent potential effect on retinal function. This is done by injecting a water-soluble dye (such as fluorescein or indocyanine green) through a peripheral vein. As the dye passes through the retinal and choroidal circulation, it is exposed to light filtered (excitation filter) to only allow wavelengths designed to cause fluorescence through. A camera takes pictures using a lens filter (barrier filter) that is designed to block out all light entering except light at the wavelengths the dye fluoresces at. Areas with high/low circulation, leakage, or obstruction can then be seen.

Fluorescein angiography is used to assess the retinal circulation, whereas indocyanine green is used to assess the choroidal circulation. This is because indocyanine green binds tightly to plasma proteins and therefore remains in the choroidal circulation, and because the retinal pigment epithelium does not absorb infrared wavelengths, allowing stimulating light and fluoresced light to pass unimpeded.

The quoted rates are for fluorescein angiography specifically. However, indocyanine green has been shown to have a similar level of complications and the same rates could be quoted.²

The macula is the area of the retina responsible for best vision (see Fig. 21.5). Disturbance of the normal anatomy of the macula will generally result in functional visual symptoms, such as blurred vision, or metamorphopsia (distortion of vision, such as straight lines looking wavy). One of the most common problems to affect the macula is the development of oedema (fluid swelling) within the retina (macula oedema—not to be confused with subretinal fluid). This commonly occurs as a result of a breakdown in the blood–retinal barrier in this area through microvascular damage, allowing plasma constituents to cross into the retina (which is normally not allowed to occur). The commonest conditions that can cause macular oedema are venous occlusions, and diabetes mellitus.

Argon laser photocoagulation can be used in some of these cases to try to treat such oedema. Depending on the type of oedema, different methods of laser exist. For areas of oedema that appear to be caused by a few points of leakage (such as a microaneurysm), focal laser can be used. For diffuse (spread out) oedema, grid laser is used.

In focal laser, using a relatively weak powered beam (compared with argon laser pan-retinal photocoagulation), a mild thermal coagulative effect is placed on the macula vessels caught in the beam, which is believed to help seal microvascular leaks that may exist. For this to work, the wavelength used for the laser beam should be absorbed by the blood cells inside the blood vessels. Green and yellow wavelengths work well, red works poorly. Blue is avoided as it is taken up very easily by the xanthophyll pigment present in the macula, and raises the chance that macular function could be damaged in treatment.

In grid laser, a beam (similar in strength to that used for focal laser) is fired at the macula in an ordered set of rows with regular gaps in between. There are a number of theories as to how grid laser works. One theory suggests that the underlying vascular endothelium or retinal pigment epithelial cells are stimulated to improve integrity or absorb more fluid, respectively. Another suggests that the laser removes unhealthy/poorly functioning retinal pigment epithelial cells, allowing new healthy cells to take their place. A third theory suggests retinal photoreceptors are destroyed by the laser, reducing oxygen demand locally, causing reduced blood flow in leaking vessels (and theoretically, thus reducing leakage). In reality, it may be a combination of some or all of these theories that occur (or even possibly something completely different!).

Also known as:

They are used to drain aqueous from within the eye into a small bleb created beneath the upper eyelid. By draining the aqueous they reduce intraocular pressure and control glaucoma (see Figs. 21.9 and 21.10).

There are many types of devices including (but not limited to):

Both valved and non-valved devices have their advantages and disadvantages. Valved devices must be blocked with a stitch at the time of surgery to prevent excessive drainage of aqueous in the first few weeks postsurgery. Draining fluid is slowly reabsorbed into the blood vessels on the conjunctival surface.

A globe rupture is one of the greatest significant injuries an eye can receive (see Fig. 21.3). Damage can vary, depending on the size and location of the rupture, as well as the mechanism of injury. It is important that all trauma injuries to the eye are described appropriately, so appropriate planning of management can occur.

The most common terms you should therefore be aware of are:¹

Globe rupture injuries are therefore caused by blunt trauma, penetrating, or perforating injuries. The most common causes of these are assault, domestic, and sporting injuries.

The aim of primary repair is to close up the eye and try to replace displaced tissues back to their appropriate plan (i.e. retinal/choroidal prolapse should be replaced, and vitreous should be cleared from the wound). The injured area should be exposed clearly enough to see adequately, and the repair should be methodical, working either anterior to posterior, or vice versa. Antibiotics should be used to prevent infection, as open globe injuries have a high chance of developing endophthalmitis (severe infection in the eye) or panophthalmitis.

Once primary repair is complete, secondary repair will be required to assess and repair damaged retina, or other intraocular structures. Eyes which have no visual potential or which are damaged too severely to repair adequately should be considered for enucleation within 10 days of injury in order to prevent/reduce the chance of sympathetic ophthalmitis.

Sympathetic ophthalmitis (also known as sympathetic ophthalmia/uveitis) is a rare, autoimmune (delayed-type hypersensitivity reaction) granulomatous uveitis (towards melanin-containing structures in the eye) that occurs when penetrating trauma (from surgery or injury) occurs to an eye. This can result in inflammation appearing in the contralateral eye, and can lead to loss of vision in both eyes.

The meibomian glands in the eyelids (see Figs. 21.6 and 21.7) can become blocked. The blockage may be due to blepharitis, which is inflammation along the lid margin associated with irritation, crusting, and build-up of secretions/meibom, which is normally produced by the meibomian glands. There is development of chronic inflammation with associated formation of a lump within the tarsal plate. This lump is called a chalazion.

It can occur in both upper and lower eyelids. Some do resolve spontaneously after a few months but if they are symptomatic then they require incision and curettage.

Chalazia can sometimes become infected and lead to preseptal cellulitis. Oral/topical antibiotics can treat this overlying infection, but will do nothing to treat the underlying chalazion.

Incision and curettage should only be carried out once acute inflammation has settled. Non-surgical options are usually recommended in most cases as first-line treatment, with evidence suggesting around 50% of cases might settle with regular conservative management within 3 weeks.¹ However, there is no strong evidence for or against the effectiveness of conservative management strategies.²

Beware the recurrent chalazion, as the diagnosis may need to be re-considered. Eyelid malignancy needs to be considered in these situations.

Due to the presence of the blood–ocular and blood–retinal barriers, it can be difficult to develop significant concentrations of a drug inside the eye in order to treat certain conditions, as most drugs have poor ocular penetration. In situations where it is imperative to get the requisite treatment to sites inside the eye, intravitreal injection of the drug in question is the solution. This allows the drug to sit in the vitreous cavity (see Fig. 21.3), where it can get to work directly.

Obstruction or delayed canalization of the nasolacrimal duct occurs in about 5% of newborns. A remnant of a small valve at the lower end of the nasolacrimal duct is the usual cause. This can cause persistent watering (epiphora) and sticky eyes in infants, and can sometimes lead to recurrent infections. Probing is required in a minority of children. This involves dilating the canalicular punctum and then attempting to irrigate the nasolacrimal duct. A probe is usually inserted and as it slides through the duct, distal obstruction is overcome.

A dacryocystogram (X-ray of the nasolacrimal system following injection of radiopaque dye through the canalicular punctum) or a scintillogram (using radiosensitive material to demonstrate nasolacrimal duct anatomy) can be a helpful investigation to determine the cause of epiphora. These are also helpful before DCR ( see‘Dacryocystorhinostomy ± bypass tube insertion’, p.617).

The eyelid is the thinnest external structure of the body. It is divided into skin, subcutaneous tissue, orbicularis muscle, tarsal plate, and conjunctiva (see Figs. 21.1, 21.6, and 21.7).

In the lower eyelid, there are retractors which help to maintain normal lower lid position. The retractors are the capsulopalpebral fascia and the inferior tarsal muscle.

Ectropion is an outward turning (eversion) of the eyelid away from the globe primarily due to horizontal lid laxity.

The main types of ectropion are:

Most cases are due to involutional ectropion, which occurs with age. This can cause corneal exposure and recurrent infections.

The eyelid is the thinnest skin of the body. It is divided into skin, subcutaneous tissue, orbicularis muscle, tarsal plate and conjunctiva. In the lower eyelid, there are retractors which help to maintain normal lower lid position (see Fig. 21.6). The retractors are the capsulopalpebral fascia and the inferior tarsal muscle.

Entropion is an inward turning (inversion) of the eyelid towards the globe, due to horizontal lid laxity and disinsertion of the lower eyelid retractors.

In cicatricial cases, scarring of the conjunctiva and tarsal plate has to be corrected with a mucous membrane graft (e.g. from the inner lip).

The main types of entropion are:

Most cases are due to involutional entropion, which occurs with age. This can cause corneal irritation, infection, and scarring due to inwardly turning eyelashes rubbing on the cornea.

Eyelash irritation from entropion should be differentiated from:

An epiretinal membrane is a proliferation of glial cells at the vitreo-retinal interface. The glial cells are from the retina, and normally arrive at the retinal surface through breaks in the internal limiting membrane. While epiretinal membranes can occur idiopathically, other causes include previous retinal surgery/procedures, trauma, intraocular inflammation, and retinal vascular conditions.

If left unchecked, epiretinal membranes can cause traction on the macula (where it commonly forms). This is commonly noted symptomatically through metamorphopsia and reduced vision. On examination, an irregular light reflex can be seen at the macula, with obvious surface distortion visible at more advanced stages.

Macular holes can occur when there has been an abnormal vitreo-macular (or more specifically a vitreo-foveolar) attachment, resulting in combined anteroposterior and horizontal traction. This results in displacement of photoreceptors at the fovea. Unless the tractional forces are relieved, displacement can continue to occur, and the hole can continue to develop into a full thickness macular hole. Holes can be differentiated from pseudoholes (other conditions which have the gross appearance of a macular hole) using the Watzke-Allen test. (Shine a thin bright beam of light that passes through the hole. Patients with a macular hole will see a break in the light where it passes through the hole, whereas those with a pseudohole will see an unbroken line.)

In both of the conditions mentioned, treatment consists of relieving the traction being applied to the macula by detaching remaining vitreous attachments that might still be having an effect, and ‘peeling’ away any membrane that has formed. These steps give the macula a chance to settle back anatomically within days/weeks. However, it takes longer (months) to determine final functional outcome.

Failure, narrowed, or delayed canalization of the nasolacrimal duct can occur in babies/children (see Fig. 21.8). Adults can develop nasolacrimal duct stenosis (or have had it all their life and have just never been treated for it). Silicone tube intubation is usually recommended after multiple probing and syringing have failed. Ideally the tubes are left in place for 3–6 months before being removed. If they have not been successful in canalizing the nasolacrimal duct then a DCR will be required.

There are a number of conditions (such as venous occlusion or diabetes mellitus) that can cause retinal damage through bleeding. Significant damage causes ischaemia (lack of oxygen), and results in the promotion and release of growth factors (including vascular endothelial growth factor, or VEGF) that cause new blood vessel growth to occur (neovascularization), in an attempt to fix the oxygen deficit. However, these new vessels have a tendency to break and bleed, resulting in further damage to the retina, and additional neovascularization.

In order to preserve the remaining vision in the eye (and in particular the macula, as it is responsible for best vision), this ischaemic ‘demand’ for oxygen needs to be dealt with, as the vascular ‘supply’ can no longer cope. This is achieved by applying an argon laser beam to the peripheral retina at strength sufficient to destroy the retina permanently. Such destroyed areas no longer require oxygen, and as a result, the ischaemic drive is reduced. This results in reduced VEGF release and reversal of neovascularization as the vascular ‘supply’ can now keep up with the oxygen ‘demand’ of the remaining ‘live’ retina.

In order for any surgical procedure to be performed effectively in the posterior segment of the eye, there needs to be a clear space to work in. For this reason, and to reduce the potential future risk of retinal breaks/detachments through remaining tractional attachments of vitreous, vitrectomy is performed prior to any other work being carried out.

This is a full thickness corneal graft that replaces all the layers of the cornea. It is performed when corneal pathology involves both the stroma and endothelium. Damaged cornea is replaced by donor tissue.

They are the most widely used type of corneal graft. One major disadvantage compared with partial thickness grafts is rejection. This is the commonest complication of full thickness grafts.

There is also a long period of aftercare with frequent clinic visits. The corneal sutures usually remain in situ for about 12 months during which time the vision may not be optimal. There may be suture-related problems, which will require removal and/or replacement during the long period of wound healing and stability. However, final visual outcome is usually better with a partial thickness graft.

Choroidal expulsive haemorrhage usually results in severe loss of vision or loss of the eye. The risk is higher than for cataract surgery. Risk factors are old age, coughing, hypertension, glaucoma, or straining during surgery if carried out under local anaesthesia.

Sympathetic ophthalmitis (also known as sympathetic ophthalmia/uveitis) is a rare, autoimmune (delayed-type hypersensitivity reaction) granulomatous uveitis (towards melanin-containing structures in the eye), which occurs following penetrating trauma (from surgery or injury) to an eye. This can result in inflammation appearing in the contralateral eye, and can lead to loss of vision in both eyes.

The natural lens of the eye sits behind the iris (see Fig. 21.3), and provides approximately a third of the refractive (focusing) power of the eye. The lens is encased in a transparent capsule (capsular bag), and is normally suspended along the visual axis of the eye by zonules (fibrous strings), which come from the ciliary body. Contraction/relaxation of the ciliary body muscles causes changes in the tension of these zonular attachments, which is transmitted to the lens capsule and causes the lens to change shape and thus alter its refractive power (accommodation).

The width of the lens increases with age, as new lens fibres are laid down on top of existing fibres. Eventually, the lens may become large enough to touch the posterior aspect of the iris at the pupillary border (Fig. 21.2), and potentially block transmission of aqueous fluid from the posterior chamber (where it is produced by the ciliary body) to the anterior chamber (where it drains out of the trabecular meshwork at the ‘angle’) via the pupil. This may result in acute angle closure glaucoma developing where intraocular pressure rises extremely quickly (minutes to hours), resulting in damage to the optic nerve, and thus to the vision in the eye (see Figs. 21.9 and 21.10). If the lens only occasionally blocks passage of aqueous fluid via the pupil, the patient can develop chronic angle closure glaucoma instead (weeks to years). When the lens is responsible for causing glaucoma through its size obstructing aqueous fluid drainage, it is called phacomorphic glaucoma.

The natural lens of the eye can develop opacities and become cloudy. This is an acquired cataract. If this occurs, the only way to improve the vision is to remove the cataract and replace the natural lens with an artificial one.

Common causes for acquired cataract include (but are not limited to):

While advanced classification systems exist, cataracts are routinely described in clinical practice by location: