LITMIR.BIZ

      Equation 1. Intraocular pressure (IOP) calculation

      A ‘normal’ intraocular pressure is between 10 and 21 mmHg, which encompasses 95% of the normal population.

      A gross simplification of the flow of aqueous within the eye is shown in Fig. 2.1. The aqueous is produced by the ciliary body (shown in pink) at a rate of approximately 2.5 μl per minute (normal AC volume is approximately 170 μl). The aqueous passes between the posterior surface of the iris and the anterior lens, then on through the pupil into the anterior chamber of the eye. The aqueous is primarily returned to the episcleral veins by filtration through the trabecular meshwork, which is located at the interface of the anterior iris and the cornea, known as ‘the angle’. The ‘uveo-scleral’ outflow pathway, which does not rely on the trabecular meshwork, plays a smaller role in the recycling of aqueous. The aqueous is absorbed by the iris and the sclera directly and is returned passively to the blood.

      The classification and correct identification of the specific type of glaucoma the patient has is important because it will alter how the patient’s condition is managed and the likely clinical course. The specific diagnosis can be made clinically with examination and testing as discussed in the following chapters.

      Fig. 2.1. Normal movement of aqueous within the eye.

      Currently; medical, LASER, and surgical therapies available to us rely on manipulation of the secretion, reabsorption and movement of the aqueous humour within, and out of the eye. Therefore, the classification of glaucomatous disease will focus on this anatomical and etiological mechanism. Two large sub-classifications of glaucoma are therefore possible; if the flow of aqueous present within the eye under study is unimpeded from ciliary body to the iridocorneal angle, the glaucoma is said to be ‘open angle’; if this passage of aqueous is structurally impeded, the glaucoma is defined as ‘closed angle’.

       OCULAR HYPERTENSION

      Ocular hypertension is a condition where the measured intraocular pressure is higher than 24 mmHg, but no glaucomatous visual field loss or optic nerve damage has occurred. In the landmark Ocular Hypertension Study (OHTS) there was shown to be a 5-year risk of conversion to glaucoma in approximately 9.5% of patients. Factors which increase the risk of conversion to glaucoma (and therefore increase probability of starting treatment) include:

      •Higher pressure at presentation.

      •Older age at presentation.

      •Thinner corneas.

      •Increased cup/disc ratio.

      •Afro-Caribbean heritage.

      •Males are more likely to convert to glaucoma than females.

       CLOSED ANGLE GLAUCOMA

      If the flow of aqueous is impeded, the resulting glaucoma is said to be ‘closed angle’ as the trabecular meshwork is obstructed (Fig. 2.2). This is the underlying pathological mechanism in primary angle closure, phacomorphic glaucoma and inflammatory processes which result in 360° posterior synechiae (adhesions of the iris at the pupillary margin and the anterior lens).

      Fig. 2.2. Restriction of aqueous flow.

       Primary Angle Closure

      Primary angle closure glaucoma is due to the iridocorneal angle (and therefore trabecular meshwork) being occluded by the iris. Primary angle closure is more common in hyperopic persons, because the iridocorneal angle is more acute at baseline.

      The clinical presentation of the patient with primary angle closure glaucoma is either acute with severe symptoms or chronic, which may be asymptomatic.

      The chief symptom of acute primary angle closure is an extremely painful red eye, which is due to raised pressure within the eye (usually in the range of 50–100 mmHg). Due to the severity of the symptoms, patients often present to the A&E Department and initially diagnoses of subarachnoid haemorrhage or cluster headache are often considered.

      Characteristic clinical signs are a deeply injected eye and opaque cornea. The cornea is often oedematous due to the corneal endothelial pumps being overwhelmed by the significant hydrostatic pressure from the anterior chamber. The iris is fixed and usually mid-dilated due to a combination of ischemia and inflammatory reaction. There is an inflammatory component due to the ischaemic damage to the iris causing breakdown of the blood-aqueous barrier. This inflammation can cause adhesions between the iris and lens (posterior synechiae) or between the iris and cornea (peripheral anterior synechiae).

      Breaking this attack medically is the first stage in management, which should be followed by laser iridotomy and/or surgical lens extraction and intraocular lens insertion, which will be covered in more detail in later chapters.

      There may be chronic angle closure where the pressure within the eye has been raised for many months or years due to partial occlusion of the trabeculum. This is usually asymptomatic. Definitive management is lens extraction to make more space within the anterior chamber.

      It is possible to have narrow iridocorneal angles without raised pressure and without signs of glaucoma. The risk of developing high pressure with this anatomical configuration is significant, and prophylactic laser peripheral iridotomies are often performed if there is greater than 180° of Shaeffer Grade 1 or 0 on the gonioscopy.

      In plateau iris syndrome, anteriorly rotated ciliary body processes can push the peripheral iris forward thereby causing narrowing of the iridocorneal angle.

       Phacomorphic Angle Closure Glaucoma

      This situation can present acutely with an ‘angle closure’ type event (described above) or more insidiously. As one ages, the lens of

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