PRIMARY OPEN ANGLE GLAUCOMA

INTRODUCTION:

Glaucoma is characterized by the common characteristic feature of retinal ganglion cell loss and optic nerve degeneration. There are different methods to classify glaucomas. It can be categorized on the basis of etiology (Primary vs. secondary), duration (Acute vs. chronic), and anatomy of the anterior chamber angle (open vs. closed).

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Primary Open Angle Glaucoma (POAG) is defined as a chronic, slowly progressive, optic neuropathy with characteristic patterns of optic nerve damage and visual field loss. It is a subset of the glaucomas characterized by an open, normal appearing anterior chamber angle and raised intraocular pressure (IOP), with no other underlying disease.

World-wide this type of glaucoma is the most prevalent. The global prevalence of glaucoma among individuals in the 40-80 years age group is around 3.54%. POAG accounts for 3.05% and primary angle closure glaucoma (PACG) 0.5% of the total prevalence. According to the WHO, nearly 5.2 million people are blind world-wide due to glaucoma. Of these, congenital glaucoma accounts for 200,000; POAG 3 million and 2 million from PACG.

There are many theories to explain the development of POAG. These include the mechanical, vascular, biochemical, genetic and intraluminal pressure theories. However, it is not known which etiology might be active in any particular patient. It is often assumed that multiple mechanisms could be responsible for glaucomatous damage in an individual. 

CLINICAL FEATURES:

POAG is usually insidious in onset, slowly progressive, and painless. It is often a bilateral, asymmetric disorder. The condition is called the “silent thief of sight” as central visual acuity is relatively unaffected until late in the disease. A number of risk factors for the development of POAG are known. These include intra-ocular pressure, increasing age, race, decreased central corneal thickness (CCT) and positive family history.

Intra-ocular pressure:

Based on population studies the normal mean IOP is 15.5 mmHg with a standard deviation of 2.6 mmHg. This makes the range of mean normal IOP between 10-21 mmHg. However, it is known that IOP in the general population is skewed to the right. A number of abnormalities in IOP measurement have been presented over the last few years. The role of normal diurnal fluctuation of IOP has shown that IOP measurements can be biased depending upon the time of measurement. This is more obvious in glaucoma patients where IOP may fluctuate by more than 8-10 mmHg (compared to 5 mmHg in normal eyes). 

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Central corneal thickness:

CCT was found to be a powerful predictor for the development of POAG in OHTS. The relative risk of POAG increased 81% for every 40 μ thinning of cornea. Both OHTS and the European Glaucoma Prevention Study found that the risk of developing POAG was greater in eyes with CCT <555 μ compared with eyes having CCT of 588 μ or greater. Another study has reported that patients with thinner corneas tend to have more severe glaucoma even on initial examination and have a higher risk of progression. The actual IOP can be overestimated on Goldman applanation tonometry in eyes with thicker corneas, whereas an underestimation may happen in eyes with less than average CCT. Refractive surgery can alter the corneal biomechanics and corneal thickness, thus resulting in falsely low IOP readings. However, in the presence of corneal edema IOP tends to be underestimated and is overestimated when measured over corneal scars due to the increased rigidity of fibrous tissue.

Thicker corneas resist indentation during tonometry leading to erroneously high IOP readings. Conversely, in thin corneas the measured IOP can be falsely low. This can affect the diagnosis of POAG. Corneal thickness may be measured (pachymetry) by optical and ultrasonic methods.

Average corneal thickness, determined by optical and ultrasonic pachymetry, is approximately 530-545 µ in eyes without glaucoma. Central corneal thickness (CCT) is increased in patients with ocular hypertension (OHT). 

Other confounding factors in IOP measurement are corneal steepness (Steeper corneas resist indentation) and a mechanical factor called corneal hysteresis. Certain new instruments such as dynamic contour tonometry and Ocular Response Analyzer are able to overcome some of these factors.

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Optic disc assessment and visual field loss:

Abnormal cupping or an increase in the cup‑to‑disc ratio (CDR) is frequently associated with glaucoma suspects. Stereoscopic evaluation of the optic discs has shown a Gaussian distribution of the mean CDR at 0.4 with only an approximately 5% normal population having CDRs of 0.7 or more. A difference of 0.2 between the two eyes should be viewed with suspicion. Such a finding is present in only 1% of the normal population.

It is still not very clear whether structural changes (obvious on optic disc assessment and other tests) develop earlier than functional changes (seen on perimetric tests). However, careful periodic evaluation of the optic disc and visual field is vital in the follow-up of glaucoma patients. Stereophotographs of the optic discs are ideal to preserve the records of the patient for future reference. However, computerized digital images or even hand drawings may suffice, with the relevant details marked in the drawing. Stereophotographic documentation or computerized imaging of the disc are useful as they enhance the clinician's ability to detect subtle changes over time. 

A number of mechanical and vascular signs are found in glaucoma patients. These include:

Mechanical signs	Vascular signs
Large optic cup	Disc hemorrhage
Asymmetrical cups	Nasal displacement of vessels
Progressive enlargement of cup	Baring of circumlinear vessels
Narrowing/notching of rim	Tortuosity of retinal vessels on the disc
Vertical elongation of cup
RNFL loss
Exposed lamina cribrosa (laminar dot sign)
Peripapillary atrophy

RNFL= Retinal nerve fiber layer

Particular attention should be paid to the neuroretinal rim (NRR). The rim is broadest inferiorly among all quadrants, followed by the superior, nasal, and temporal rims (ISNT‑rule). The loss of inferior or superior NRR leads to a vertical elongation of the cup and loss of the ISNT‑rule leading to a suspicion of glaucoma. It needs to be highlighted that ISNT rule is only applicable to normal sized discs.

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Visual field loss should correlate with the appearance of the optic disc. Significant discrepancies in the pattern of field loss and optic nerve damage warrant additional investigation. As perimetry remains a highly subjective test, on an average, 3 VF assessments should be done in the 1st year to detect an overall change in mean deviation of 4 dB over 2 years in a patient with average VF variability. Progressive VF loss is the hallmark sign which separates a true pathology from a glaucoma suspect.

Gonioscopy:

Assessment of anterior chamber angles is imperative for the diagnosis of POAG. The clinician should be well versed with the procedure of gonioscopy. Angles which are more than Grade 2 are regarded as open. If peripheral anterior synechiae are present, the extent of PAS should be recorded. 

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Increasing age:

In a number of landmark studies increasing age was noted as a significant risk factor. In the Baltimore Eye Study the risk of glaucoma increased significantly in patients above 80 years of age. In the Collaborative Initial Glaucoma Treatment Study (CIGTS) visual field defects were more common in patients above 60 years of age compared to those below 40 years.

Family history:

The lifetime risk for first-degree relatives of affected individuals to develop open angle glaucoma is 22% when compared with a 2% risk in controls. it is likely both monogenic and polygenic. Instances where a single gene causes glaucoma (monogenic) have emerged (e.g., the myocilin and optineurin genes), but in other instances glaucoma is much more likely the result of multiple genes (polygenic).

Unique susceptibility genes and genetic variants also likely play a significant role in glaucoma.

TREATMENT:

Management of open angle glaucoma has to be tailored for every patient. Initial treatment usually consists of pharmacological therapy. Prostaglandin analogues and beta blockers are the preferred agents to initiate treatment. Depending upon various factors drugs can be changed or added. Compliance is an essential factor to be considered when target IOP is not achieved. Some clinicians prefer to perform laser procedures (Argon Laser Trabeculoplasty) or even implantation of glaucoma drainage devices (GDDs) as initial procedures. However, usually GDDs are used in advanced cases. Trabeculectomy or Minimally Invasive Glaucoma Surgery (MIGS) can also be utilized in certain patients. Glaucoma filtering surgery is usually performed in the situation of uncontrolled IOP despite maximally tolerable medical therapy. MIGS is usually combined with cataract surgery. In case there is poor visual potential and ocular discomfort (painful, blind eye) the eye may be treated with cyclodestructive procedures. A number of laser and surgical methods are available. These include diode laser cyclophotocoagulation, micropulse-trans-scleral cyclophotocoagulation and endocyclophotocoagulation. Surgical techniques such as cyclodialysis are not commonly in vogue now.

 

Progressive glaucomatous optic atrophy