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Glaucoma: an overview
Glaucoma is no longer a single, non-significant disease. It is a serious condition that stipulates as the number one cause of preventable, irreversible blindness. Glaucoma is described as a group diseases that result in damage of the optic nerve head (ONH). This damage results in progressive peripheral visual field loss. The damage may or may not be related to raised intraocular pressure (IOP). Glaucoma can be challenging to diagnose. It sits on a continuum where the early stages of the disease are undetectable, so it is important to identify the risk factors and patients who are susceptible to development of glaucoma. Later, the disease becomes detectable but there are no symptoms and thus clinical techniques are used to look for any signs (Weinreb and Khaw, 2004). Once glaucoma is determined in a patient, it is important to identify the type of glaucoma to offer appropriate treatment.
Mechanism of Glaucoma
Intraocular pressure (IOP) has an important role in glaucoma. To understand its mechanism of action, it is very important to look at aqueous humor production and drainage (Kass, 2005). Aqueous humour is primarily produced by active secretion at the ciliary processes of the ciliary body, mediated by aquaporins and carbonic anhydrase; the prior requiring energy and the latter requiring enzymatic action. Fifteen percent of aqueous humour production is from ultrafiltration of blood from capillaries of the ciliary processes (Levin, 2011). Aqueous humour drains through two pathways: the majority through the conventional, and the rest through the unconventional pathway. The conventional pathway involves the iridocorneal angle, where the aqueous humour will drain through the trabecular meshwork (TM) and subsequent meshworks (uveal, corneoscleral, and juxtacanalicular). The effectiveness of drainage improves with reduced episcleral venous pressure and contraction of the ciliary muscle opening the TM. The unconventional pathway involves the uveoscleral route through the insertions of the ciliary muscles which then drain through to the lymphatic system. This route is independent to episcleral venous pressure. IOP is predicted to increase with age and to be higher during the morning. The reasoning behind this is with age results in reduced aqueous humour outflow. Being in a supine position all night also results in reduced aqueous humour outflow, giving higher IOP which would be observed in the morning (Jorge, 2010). This is important to know when monitoring IOP as factors like time of day come into play when observing an individual’s IOP over time and treatment.
Now that the genesis and exodus of aqueous humour is understood, it is important to recognise the debated mechanism of damage by glaucoma. The first mechanism concerns itself with mechanical damage caused by increased IOP. Increased IOP is thought to damage the lamina cribrosa, deforming the axons’ cytoskeleton compromising flow of neurotrophin resulting in the death of retinal ganglion cells (RGC). Death of enough RGC can result in loss of visual field and if advanced, blindness (Gupta, 2009). The second mechanism involves the perfusion around the ONH whether by systemic conditions or high IOP. Poor blood regulation around the nerve can result in cell death and then similar features to mechanical damage (Drance, 1996). However, IOP is not the sole reason behind glaucomatous visual field loss, hence no single mechanism can be determined (Gupta, 2009).
The aforementioned cell death can be seen clinically as loss of neural retinal rim at the optic nerve and associated visual field loss on perimetry (Gupta, 2009). Glaucoma acts as a continuum: the early stages of the disease are undetectable, where there is death of RGC but no detectable loss of neural retinal rim or visual field loss; later the disease becomes detectable but there are no symptoms; finally, at the later stage of the disease – a point considered too late to treat – the disease manifests as vision loss for the patient (Weinreb and Khaw, 2004). With this type of disease pathway, it becomes very important to develop a screening programme or eye examination routine to detect the disease at the earliest and provide an appropriate treatment plan. However, the disease can even start without any detectable method in the clinical exam, and thus it is important to identify high risk groups to provide appropriate care.
Risk factors and Clinical Detection of Glaucoma
It is paramount to be able to identify individuals that have high risk of developing glaucoma especially when there are no signs at the early stage of the disease and no symptoms at the intermediary of the disease. The NHMRC guidelines from 2010 developed for screening, diagnosing, managing and preventing glaucoma include a number of risk factors, listing them in categories based on their strength of association. Age of the individual stands out as one of the most influential risks of developing glaucoma with prevalence being a staggering 11.8% in over 90 year olds compared to 0.6% in the 50-59 years of age group (Wensor, 2001). Family history is also an important risk factor to consider. The inheritance patterns are multifactorial and complex for the various types of glaucoma. An example of mutations in the genes for MYOC (associated with myocilin production responsible for development of the extracellular matrix, which is important for the drainage properties of the TM) and OPTN (associated with the production of optineurin, which is important in the pathway of RGC programmed death) can increase one’s susceptibility to developing glaucoma (Wiggs, 2007). This is obviously not the entire list of mutable genes, showing the complexity of genetic inheritance, but it proves that family history acts as a risk factor. The strongest association lies between siblings (Sung, 2006). IOP stands out as one of the great risk factors, being the only modifiable one. IOP above 21 mmHg indicates greater risk of developing glaucoma, and the higher the IOP, the greater the risk (Bonomi, 2000). Reducing IOP has shown to reduce the risk of progression in glaucoma (Heijl, 2002). Moreover, evidence is available to establish individuals who are at risk of developing glaucoma without clinical assessment. A recommendation can be made for individuals above the age of 40 to get their eyes tested for glaucoma (NHMRC, 2010).
Clinical assessment needs to be performed to ensure if the patient has glaucoma or has risk of developing glaucoma. A number of factors need to be assessed, and there are a number of techniques at the disposal of the optometrist. First is the assessment of IOP, as high IOP increases risk of glaucoma as well as progression. The “optimum modality” of measuring IOP involves using Goldmann Applanation Tonometry (GAT) with Perkins also becoming accepted due to it high comparability (Arora, 2014). Treatments for glaucoma centre around reducing IOP, so being able to measure it is important; however, IOP alone cannot determine whether an individual has glaucoma or is at risk of developing glaucoma. As mentioned above, it is important to classify the type of glaucoma, which will later guide the treatment process. Assessment of the anterior chamber angle is important to determine if the patient has closed angle or open angle glaucoma and whether the profile of the angle can put the individual at risk of developing glaucoma. Van Herrick provides a good estimate of angle width to determine if an angle is narrow and at risk of closed angle glaucoma, but it cannot replace gonioscopy (Gonioscopy Video Atlas, 2017). Gonioscopy is vital to assess the iridocorneal angle as the rays of light totally internally reflect of the posterior cornea and are not viewed without special equipment like a Goniolens. Assessment of the angle allows the clinician to determine if the angle is closed or opened and to see the characteristics of the angle, for example neovascularisation and pigment (Alward, 2011). Due to Imbert-Fick law, if corneal thickness is not accounted, an inaccurate IOP reading can be given; for example, thin corneas will give misleadingly lower IOP readings. However, even when this systematic error is accounted, central corneal thickness shows an association with development of glaucoma. Individuals with thinner corneas (less than 550 micrometers) have greater risk of developing glaucoma (Kass, 2005). Therefore, it is important to include measurement of corneal thickness as an independent risk factor for glaucoma. Central corneal thickness can be measured using ultrasound pachymetry (Sadoughi, 2015).
Following external examination, it is important to assess the optic nerve as this is the structure damaged in glaucoma. First, the vertical cup-to-disc (CD) ratio – the ratio of neuroretinal rim to empty space – is examined. A large CD ratio may represent less nerves and damage due to glaucoma loss, although the size of the nerve must be considered. A large nerve may give an appearance of a larger CD ratio. Smaller optic nerves provide more accurate CD ratios (Garway-Heath, 1998). Thus, it is important to also consider the size of the optic nerve when assessing the CD ratio (Hoffmann, 2007). Next is to assess the neural retinal rim looking for any notches, focal thinning or non-conformity of the ISNT rule (Bourne, 2006). The presence of haemorrhages around the discs raise high suspicion for glaucoma (Healey, 1998). Observing any retinal nerve fibre layer (RNFL) drop out can represent dying axons and RGC atrophy, which can be a sign of damage due to glaucoma; using red-free filters aids in determining this (Hoyt, 1973) or even the use of Optical Coherence Tomography or OCT (Greaney, 2002). Parapapillary atrophy (PPA), especially beta-zone which represents hypopigmentation as a result of chorioretinal thinning and is detectable using computer imaging, can be a sign of glaucomatous damage (Miki, 2017). It is important to assess these using fundoscopy, but it is also important to assess change in these features. This is where photography taken over time offers excellent reference to observe any changes (e.g. increase in beta-zone PPA, increase in C:D ratio, etc.), and this aids forming a diagnosis: if this patient has glaucoma, or is at risk of developing glaucoma, or if they have glaucoma, provides a means of monitoring progress of treatment.
Visual field assessment is very important in diagnosing glaucoma. After all, glaucoma causes visual field loss and thus it is important to assess visual field changes. Visual field testing is commonly performed using the Humphrey perimeter for performing standard automated perimetry. There are other methods such as using frequency doubling technology to increase the speed of the testing and increase reliability (NHRMC, 2010). There are a variety of types of visual loss (e.g. paracentral, arcuate, nasal step) that can be characteristic of glaucoma, and these must be repeatable at least 3 times. However, it is important to realise that some visual field loss may be caused by other conditions (e.g. hemianopia resulting from brain tumours), hence it is important to look at the visual field result in conjunction with the previously mentioned signs (e.g. optic nerve appearance, where cupping corresponds to the loss in visual field) (Keltner, 2003). Due to the arrangement of the retinal raphe, visual fields for glaucoma are characteristic in that visual field loss does not cross the horizontal midlines (Drance, 1972); this is not the case with neurological visual field loss which obeys the vertical midline, due to decussation of the optic nerve chiasm (Hershenfeld, 1993). As well as being able to see present signs of glaucoma, changes in visual field can be monitored in patients over time. If there is a change that is deemed to be glaucomatous, then a diagnosis of glaucoma can be made and the decision to treat or not can be made as well. While under treatment, the progression of change in visual field can give perspective on the progression of the disease. This is the reason for why visual field testing is important.
Forms of Glaucoma
One of the most prevalent forms of glaucoma is Primary Open Angle Glaucoma (POAG) (Kyari, 2015). In POAG, the angle is noted to be open using gonioscopy, and no cause is found for the increase in IOP or glaucomatous damage to the nerve, having adult onset, and usually asymmetrical in nature (Weinreb, 2004). POAG can be further classified based on age of onset, pressure, and level of suspicion. In POAG, no symptoms are present until very late stage; the IOP is above 21 mmHg; the optic nerve shows glaucomatous damage and corresponding glaucomatous visual field defects; and gonioscopy reveals an open and unobstructed iridocorneal angle. High pressure alone (ocular hypertension) is not a definitive sign of glaucoma. Other factors need to be considered such as age, family history, the difference in IOP between eyes, central corneal thickness to calculate or categorise the level of risk, where appropriate management and follow-up appointments can be set (RANZCO, 2016). Treatment would obviously involve lowering the IOP in order to halt progression of glaucoma (Kass, 2005) and this will be discussed.
If a cause is found as to why there is glaucomatous damage or increased IOP and the angle is open, then this is under the classification of Secondary Open Angle Glaucoma (Secondary OAG). There are various causes and it is important to realise some of these causes may be life threatening, some causes are more aggressive compared to simple POAG. These causes may require differing management strategies. A predominate example is pseudoexfoliative (PEX) glaucoma, where a white-grey insoluble protein is found in the aqueous humour and deposits on the anterior structures of the eye. This material also deposits in the TM eventually reducing aqueous humour outflow resulting in a rise in IOP. However, the angle remains open but there is a cause as to why the IOP is rising, hence secondary OAG. Signs for this syndrome include a white ring forming on the anterior lens surface as these are the protein deposits. PEX is regarded as highly aggressive. Treatment is similar to POAG, but laser treatment is considered very effective (Diagnosis and Management of Pseudoexfoliation Glaucoma, 2016). This is an example where knowing the cause of the IOP increase can guide the treatment plan, offering laser treatment sooner. Another common example of secondary OAG is Pigmentary Dispersion Syndrome (PDS). This is where the posterior surface of the iris is disrupted by the zonules of the lens releasing iris pigment into the anterior chamber. This pigment accumulates at the TM resulting in the reduction in outflow, similar to PEX. Clinical features involve spoke-like, radial transillumination of the iris and pigment on the corneal endothelium (Michelessi, 2016). Treatment includes medication, laser iridotomy, surgery (Farrar, 1993); though laser iridotomy may not be highly effective (Michelessi, 2016). One more example involves neovascular glaucoma. This involves an event where there is retinal hypoxia resulting in release in VEGF such as in central retinal vein occlusion or proliferative diabetic retinopathy. VEGF enters the anterior chamber and can result in growth of new blood vessels at the TM, causing blockage and subsequent IOP increase. This is another example where the underlying cause needs to be controlled. Anti-VEGF and panretinal photocoagulation are needed to reduce the growth of new vessels in the angle, treating the rise in IOP and prevent damage (Horsley, 2010). As with these examples, it is important to classify glaucoma if there is a secondary cause in order for treatment to be effective.
Usually, POAG involves the IOP being above 21 mmHg. However, it has been established that IOP is not necessary for glaucoma to be present. The IOP can still be at a normal range and glaucoma can still develop. This type of glaucoma is classed as Normal Tension Glaucoma (NTG), where the features are similar to POAG with the angle being open but the difference is that the IOP is not above 21 mmHg. Firstly, it is important to consider the differentials to NTG. For example, previous optic neuritis and ischemic optic neuropathy can give appearance of optic nerve damage similar to glaucoma; as these conditions do not involve increased IOP. Therefore, MRI, good history and colour vision testing can determine these differentials. Systemic issues such as migraines, Raynaud’s phenomenon, systemic hypotension, being on hypotensive medication, and sleep apnea can all be risk factors for NTG (Mallick, 2016). From this, the vascular mechanism of action gives an outcome akin to NTG. Despite IOP being at a ‘normal’ level, the treatment of NTG still involves lowering IOP by 30% and fluctuation of IOP in order to reduce progression (CNTGSG, 1998).
On the converse, angle closure glaucoma (ACG) is another paradigm that involves the angle being closed on gonioscopy. Similar to open angle, the classification of primary and secondary is similar. Primary ACG is without secondary cause; it is where signs of glaucoma are present (visual field loss and optic nerve head damage) due to a rise in IOP. The rise in IOP is caused by a decrease in outflow of aqueous humour. This is because there is iridotrabecular contact – the apposition of iris to the TM resulting in the angle closing as observed in gonioscopy (Salmon, 1999). PACG is multi-mechanistic. Relative pupillary block results from resistance of flow between pupil and anterior lens surface. This causes iris bowing and the closure of the TM angle. Individuals who are at risk are hyperopes due to their small anterior chamber depths. Age can be a factor as the lens increases with number of years resulting in minimising anterior chamber depth. The best way to assess for risk of PACG is through use of gonioscopy: it is important to observe the pigmentary TM and to see if it is blocked by the iris. Synechial closure occurs with permanent iridotrabecular contact as opposed to appositional closure which is temporary and may only be present in a dark room. It is important to identify those at risk of PACG as the IOP must be stabilised to reduce risk vision loss due to glaucomatous damage (Tham, 2016). The IOP can be treated medically but the underlying cause of the angle closure needs to be treated as well. This is done by surgeries which will be discussed.
Like with POAG, in ACG, if there is a cause to the blockage of the angle, the disease is deemed to be secondary. An example is inflammatory glaucoma. In uveitis, there is inflammation of the anterior chamber. This can lead to scar tissue forming in the angle – synechial closure, resulting in an increase in IOP and potential for glaucomatous damage. In some cases, there is a reduction of aqueous humour production caused by inflammation at the ciliary body. Therefore, an increase in IOP is not so dramatic. However, once again, this is a situation where it is important to know the underlying cause in order to treat. The first line of inflammation is to treat the uveitis and then the IOP, medically and/or surgically. Another example is neovascularisation. This is also present with secondary OAG if the angle remains open. However, there are situations where the new fibrovascular membrane can cause the angle to close. Treatment will involve treating the underlying cause which is the neovascularisation with anti-VEGF and PRP and then to control the IOP (Annadurai & Vijaya, 2014).
Treatment of Glaucoma
Now that the variety of glaucomas are discussed and their mechanisms, it is important to discuss treatment. It has been shown that medical treatment of reducing IOP has shown to reduce the progression of glaucoma (Kass, 2003; Heijl, 2002; and AGIS, 1994), hence the importance of treatment. Firstly, it is important to establish a target IOP: a reduction of 30% is evidenced to reduce progression (CNTGSG, 1998), but this will depend on age, severity of vision loss and disease-type. Shorter life expectancy and less damage will contribute to a higher target IOP; the opposite will deem lower IOP and more aggressive treatment. The first line of medical treatment is prostaglandins analogues (e.g. XALATAN®, Latanoprost). A strongly supported mechanism is the reduction of IOP is achieved by increasing the uveoscleral outflow pathway, increasing aqueous humour outflow, by remodelling extracellular matrix through regulation of metalloproteinases (Toris, 2008). Side effects include burning, irritation and changing iris colour (Uusitalo, 2009). Next are beta-blockers (e.g. Arrow-Timolol, Timolol), which block the adrenergic receptors and thus reduce ciliary secretion of aqueous humour. Beta-blockers like timolol can lower blood pressure, cause shortness in breath, and reduced pulse rate. Drug interactions exist as well. For example, Proventil is used for asthma; it is a an adrenergic agonist, where a beta-blocker can act as a direct competitor. Therefore, great care must be taken when prescribing Timolol by examining patient history (Hoscheit, 2003). Following is alpha-agonist (e.g. IOPIDINE, Apraclonidine) which too reduces aqueous humour secretion. Iopidine is problematic in that extended use can lead to severe allergic conjunctivitis, reducing it success in use. Carbonic anhydrase inhibitors (e.g. DIAMOX, Acetazolamide) acts on its namesake also reducing secretion at the ciliary body, decreasing aqueous humour production. However, it can also lead to severe burning on eye drop instillation, metallic taste if taken orally (Glaucoma Medications and their Side Effects, 2016). Obviously, the patient will be reviewed in hope for a decrease in IOP. If target pressure is not maintained, it may be due to adverse side-effects or efficacy of the medication. This is where switching to another class of medication will need to be considered or using another class in addition. Understanding the side effects and communicating this to patients is paramount. The side effects are undesirable, which can stop patients taking antiglaucoma medication all together. Patients have to be educated about these side effects and that the medication, though will not improve any symptoms, it is there to prevent blindness. 6-monthly reviews ensure patients adhere to compliance and if there are any problems with certain medications, changes to management can be made swifty. If medical treatment fails, then other forms of treatment have to be considered such as laser or surgery.
Laser treatment aims to increase aqueous humour outflow or decrease aqueous humour production. Selective Laser Trabeculoplasty (SLT) is a prime example of laser treatment. The process uses a Nd:YAG laser and works by initiating migration of macrophages and phagocytosis of TM debris, or stimulates growth of healthy TM tissue, resulting in increased outflow. The main advantage is that SLT can be repeated and provide the same IOP lowering effect. SLT is used when the angle is open, such as in POAG and PEX. There are situations that exist where SLT would be first line of treatment. An example can be when a patient has severe allergies to drops or if there are issues with compliance. SLT has shown to be effective for a number of years and repeat procedures may be required in order to keep IOP low. (Latina, 2003). An example of laser treatment that acts to reduce aqueous humour production is Endoscopic Cyclophotocoagulation (ECP) as an example. A diode laser is used to destroy the ciliary epithelium, which produces aqueous humour, which will decrease aqueous humour output and thus reduce IOP. This is an invasive procedure and will involve an operating room. It is often combined with cataract surgery (Lindfield, 2012). A final example is Peripheral Iridotomy (PI). It is used as a prophylactic treatment for angle-closure glaucoma. It involves a Nd:YAG laser targeted at the peripheral iris, creating a hole to allow aqueous humour to bypass the pupil. The change in aqueous humour dynamics reduces relatively pupillary block, decreasing the chance of iris bombe and appositional closure of the angle. Hence, this reduces the chance of a PACG event; however, when PACG is present further medical and surgical treatment may be needed on top of the PI (Nolan, 2000).
When maximal medical therapy is provided with no success, surgical methods such as a Trabeculectomy, have to be performed in order to lower IOP and reduce progression of glaucoma (DeBry, 2002). Trabeculectomy is proven to reduce IOP and is considered gold standard (Philadelphia, 2013). The surgery involves creating a bypass for aqueous humour to flow from the anterior chamber to subconjunctival space. The bypass created increases aqueous humour outflow, hence controlling IOP. The fluid build-up in the subconjunctival space creates a bleb. Trabeculectomy can often be combined with cataract surgery, as performing cataract surgery after can worsen the trabeculectomy (Nishizawa, 2016). Trabeculectomies, despite offering very good reduction in IOP, have a plethora of risks. After the surgery is performed, it is normal to have poor VA, change in refraction, hypotony, hyphema and foreign body sensation (Guzman, 2016). Urgent problems that can result are the bleb leaking, which can increase chance of infection leading to blebitis and endophthalmitis (DeBry, 2002). Here, it is important to weigh the risk and benefit of surgery. Trabeculectomy can offer a drop in IOP better than medication and laser treatment, but being an invasive surgery there are many complications and there is intensive postoperative care required. Conversely, there will be situations where trabeculectomy will not be suitable (e.g. a previously failed trabeculectomy). Glaucoma drainage devices are a form of minimally invasive glaucoma surgery (MIGS). An example is the iStent, which is a stent that bypasses the TM and allows aqueous humour to flow into suprachoroidal space. MIGS provide less risk than the trabeculectomy as they are less invasive and the drop in IOP is sufficient in most cases but not as good as a trabeculectomy (Gazzard, 2016).
Glaucoma is regarded as a challenging disease to diagnose and manage. First, it is important to consider risk factors in a patient such as family history. Clinical assessment of the optic nerve, the iridocorneal angle, and visual field testing become important in determining the presence of glaucomatous optic neuropathy and the type. Treatment options can be divided into three categories: medical, laser, and surgical. The order of combination of treatment depends on the type of glaucoma, patient lifestyle and response to treatment. Medical treatment such as prostaglandin analogues, beta-blockers, alpha agonists, and carbonic anhydrase inhibitors is used as first line treatment; these each drugs have side effects and drug interactions that have to be considered in order to prescribe the appropriate medication for the patient. Following involves laser treatment such as SLT or photocoagulation can be employed to lower IOP and are favoured in cases like pseudoexfoliative glaucoma. Invasive surgery like trabeculectomies can provide excellent reduction of IOP but is associated with significant ocular side effects that can result in permanent loss of vision. Minimally invasive glaucoma surgeries (e.g. iStent) provide less side effects than invasive surgeries with comparable IOP reduction. With all this carefully studied, the best can be offered to patients in preventing the disease of glaucoma.
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