Glaucoma

Patients suffering from glaucoma may present with a wide range of symptoms. Most commonly, they present with periorbital pain and visual deficit [7]. Other symptoms include headache, redness of the eye and swelling, sighting of multicoloured halos and uveitis. Patients may sometimes complain solely of a severe headache, often accompanied with vomiting, which may be confused with intracranial hemorrhage. Primary infantile glaucoma may present as mostly bilateral but sometimes asymmetric involvement of eyes that are red, itchy and tearing. The infant is often unable to focus his or her eyes at one particular object clearly.

Laboratory tests

• Complete blood count
• Erythrocyte sedimentation rate
• Micro-hemagglutination-Troponema pallidum (serology for syphilis)
• Tonometry

Imaging 

No specific imaging studies are available for the diagnosis of glaucoma. A CT scan may be conducted to exclude CNS involvement.

Test results

On the basis of history and physical examination, along with supportive evidence from laboratory tests results, a diagnosis can be made and treatment should be immediately begun.

Medication

Medications are used to primarily reduce the IOP with causing minimal adverse effects. Drugs that are commonly used include non selective beta adrenergic blockers like levobunolol, timolol and carteolol, selective beta 1 antagonists like betaxolol and metipranolol, and Alpha-2 adrenergic agonists like brimonidine. Carbonic anhydrase inhibitors like dorzolamide and acetozolamide as well as prostaglandin analogs like latanoprost and tafluprost are also used. Diuretics, such as mannitol and isosorbide dinitrate may also be necessary in cases with very high IOP.

Surgery

• Open-angle glaucoma

When a patient is on maximum tolerated medical therapy (MTMT) but still in worsening condition, surgery is indicated. Commonly used procedures include Argon laser trabeculoplasty (ALT) and selective laser trabeculoplasty (SLT). ALT has a higher rate of reoccurrence of symptoms than SLT.

If ALT or SLT has failed, trabeculectomy may be performed. The worst complication of this procedure includes loss of vision. Attendant risk factors such as split fixation on visual fields prior to surgery, preoperative number of quadrants with split fixation, and postoperative choroidal effusions with eventual resolution are possible [8]. If repeated trabeculectomy fails, a drainage shunt may be placed to help relieve pressure. If all else fails, the patient may have to undergo ciliary body ablation to treat the disease. The ciliary body epithelium can be destroyed by cyclocryotherapy, diathermy, ultrasound, transscleral Nd:YAG or diode laser (known as cyclophotocoagulation), or a newer endoscopic laser [9].

• Closed-angle glaucoma

If conservative therapy fails, a corneal indentation (CI) may be performed. It provides a temporary relief from raised IOP. The definitive treatment of closed-angle glaucoma is Argon laser peripheral iridoplasty (ALPI) along with anterior chamber paracentesis (ACP). An alternative procedure is lens replacement. The exact role of this procedure is unclear but it offers a therapeutic advantage for individuals with coexisting cataracts [10].

Glaucoma is a progressive, chronic condition. It may begin with mild, reversible symptoms like headache and redness of the eyes but may progress to lasting, irreversible ocular damage. Peripheral vision loss occurs first, but if glaucoma is untreated, central vision loss and complete blindness can occur [6].

Glaucoma is a collective term used for conditions that lead to an increased intraocular pressure (IOP) resulting in visual deficits. Open-angle glaucoma is primarily due to conditions and diseases that result in a high IOP. These include hypertension, vascular defects, renal disease and diabetes. Immune mediated nerve damage, excessive production of retinal glutamate and oxidative stress may also contribute. Some people are genetically predisposed to this condition.
Acute closed-angle glaucoma can be due to narrow anterior chamber, thin ciliary body, thin iiris, short axial length of the eyeball, lens swelling and narrow anterior chamber angle.
Other factors such as blood supply, nerve metabolism, and extracellular matrix likely play a role in the progressive optic neuropathy of glaucoma [2].

Incidence

Glaucoma is a common condition and it is the 2nd most common cause of blindness worldwide (the 1st is cataracts). Exact incidence varies in accordance with the type of glaucoma.

Age

Peaks according to age depend upon the type of glaucoma. The onset of signs and symptoms of infantile glaucoma occurs at birth in 40 percent of affected patients and before one year of age in 86 percent [3]. Peak incidence of closed-angle glaucoma is in the 6th and 7th decade of life. In primary open-angle glaucoma, incidence is highest in the 4th decade and above, but it may also occur in younger patients.

Sex

Acute close-angle glaucoma is more common in females while primary open-angle glaucoma has an unclear sex predilection.

Discussed below is the pathogenesis of 3 common types of glaucoma:

Open-angle glaucoma

In open-angle glaucoma, optic nerve damage results in a progressive loss of retinal ganglion cell axons, which is manifested initially as visual field loss and, ultimately, irreversible blindness if left untreated [4]. Increased intraocular pressure causes the axons of the optic nerve, where they exit the eyeball at the optic disc, to become compressed. Studies reveal that it is this compression that blocks axonal flow of cytoplasm from the neuronal somas (cell bodies) of the retina into the optic nerve fibres that lead to the brain. As a result, optic fibres start to gradually die out due to lack of nutrients. Another pathway which may add to this neuronal damage or may occur alone is compression of the retinal artery which enters the eyeball at the optic disc. In this case too, the nutrient supply to the neurons is decreased and eventually completely cut off which leads to blindness.

Closed-angle glaucoma

The anterior chamber angle provides a pathway for the aqueous humor to drain. If this angle is narrowed or closed off, the humor is unable to drain out and IOP starts to rise. In acute episodes of closed-angle glaucoma, pressures are often 30 mm Hg or higher [5].

Infantile glaucoma

It may be present at birth, called congenital glaucoma, or it may develop in the first few years of life, called infantile glaucoma. It is a rare autosomal-recessive condition but in some patients, there are multifactorial causes of disease development.

Controlling predisposing factors such as hypertension, diabetes mellitus and taking particular care in case of renal disease may somewhat help in preventing occurrence of glaucoma.

Glaucoma is defined as an optic neuropathy involving a characteristic atrophy of the optic nerve head, often accompanied by typical visual field defects [1]. Glaucoma is a disease of the eye in which the intraocular pressure becomes very high, sometimes as much as 60-70mm Hg during acute attacks. Intraocular pressure greater than 25-30mm Hg, if maintained for a long period is enough to cause blindness, whereas extremely high pressures may cause blindness within a few hours or days. Indeed, glaucoma is one of the most common causes of blindness worldwide.

Definition

Glaucoma is a term used to define conditions and diseases that result in increased fluid (aqueous humor) in the eye which leads to raised intraocular pressure.

Cause

It may be present from birth due to family inheritance or it may develop later on in life due to old age, vascular compromise, hypertension, small eyeball size, trauma, etc. 

Signs and symptoms

Common symptoms include pain around the eyeballs and headache, redness and swelling of eyes and disturbed vision. There may also be nausea, vomiting, double vision and dizziness. 

Treatment

Initial treatment is conservative, with oral medications and eye drops. If after optimum medical treatment symptoms are not alleviated, surgery is indicated. 

1. American Academy of Ophthalmology. Primary angle closure, preferred practice pattern. American Academy of Ophthalmology, San Francisco 2005. 
2. Kwon YH, Fingert JH, Kuehn MH, Alward WL. Primary open-angle glaucoma. N Engl J Med 2009; 360:1113. 
3. Yanoff M, Fine BS. Glaucoma. In: Ocular Pathology, 2nd ed, JB Lippincott, Philadelphia 1982. p.74.
4. Weinreb RN, Khaw PT. Primary open-angle glaucoma. Lancet 2004; 363:1711. 
5. Pokhrel PK, Loftus SA. Ocular emergencies. Am Fam Physician 2007; 76:829.
6. Kipp MA. Childhood glaucoma. Pediatr Clin North Am 2003; 50:89.
7. Rahim SA, Sahlas DJ, Shadowitz S. Blinded by pressure and pain. Lancet. Jun 25-Jul 1 2005;365(9478):2244. 
8. Francis BA, Hong B, Winarko J, et al. Vision loss and recovery after trabeculectomy: risk and associated risk factors. Arch Ophthalmol. Aug 2011;129(8):1011-7 
9. Allen RC, Netland PA, eds. Glaucoma Medical Therapy: Principles and Management. American Academy of Ophthalmology; 1999.
10. Foster PJ, Buhrmann R, Quigley HA, Johnson GJ. The definition and classification of glaucoma in prevalence surveys. Br J Ophthalmol. Feb 2002;86(2):238-42.

• Microdontia
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