The Pathophysiology and Treatment of Glaucoma. As a result of the associated systemic symptoms, acute angle closure glaucoma carries a significant risk of being incorrectly diagnosed. A thorough history and physical examination with documented raised intraocular pressure is imperative for diagnosis.
Patients with acute angle closure glaucoma present with abrupt onset of pain in the affected eye. In addition patients may present with blurred vision, frontal headache, nausea and vomiting, photophobia, and colored halos around lights. When the pupil is mid-dilated, the contact between the iris and the lens is maximal and the iris thickens, which worsens pupillary block. Medications that dilate the pupil have the potential to precipitate an attack; these include adrenergic agents, drugs with anticholingeric effects, sulfa-based drugs, tricyclic antidepressants, anticonvulsants, and antiparkinsonian drugs.
Patients with acute angle closure glaucoma present with conjunctival injection and a fixed, mid-dilated pupil measuring mm in diameter. The visual acuity is often reduced.
Raised intraocular pressure is necessary for the diagnosis of this condition, and is measured using a Tonopen. A pressure that exceeds 21 mmHg characterizes elevated intraocular pressure, however the pressure may exceed mmHg.
Cupping occurs due to atrophy of the optic nerve fibers that results in the central cup of the optic nerve appearing enlarged. The normal cup-to-disc ratio is 0. Slit lamp examination will reveal a shallow anterior chamber and a cloudy cornea due to edema. The attack of acute glaucoma can last for a few hours and then symptoms can improve again.
However, attacks will usually happen again and, with each attack, your vision may be damaged further. If you have these symptoms you should see a doctor urgently, in case you need treatment to prevent a more severe attack. The diagnosis is made from the symptoms and the appearance of your eye.
A likely diagnosis may be made by your GP, by an emergency doctor or by an optician. The diagnosis is confirmed by an examination done by an eye specialist an ophthalmologist. This usually involves examining your eye using a special light and magnifier called a slit lamp and measuring the pressure in your eye.
A specialist can also use a gonioscope to directly examine the outflow channels around the trabecular meshwork area of your eye. Quick treatment is needed for acute glaucoma. You should be seen by an eye specialist as soon as possible. If it will take time getting to the ophthalmologist, some treatment can be started. You should not try to cover the affected eye with a patch or a blindfold.
If you do this, your pupil will dilate further and this can worsen the situation. Don't lie down in a darkened room - lying down can tend to raise the pressure in your eye still further. A darkened room will further dilate the pupil, making things worse. The first treatment is medication to lower the pressure within your eye. There are various types of medicine and eye drops that may be used in different combinations. Treatments may include:. You may also be given painkillers and antisickness medication if needed.
When the pressure in your eye has gone down, further treatment is needed to prevent acute glaucoma from coming back. This involves using laser treatment or surgery to make a small hole in your iris. The hole allows fluid to flow freely around your iris and can stop the iris bulging forwards and blocking the trabecular meshwork in the future.
Usually, laser or surgical treatment will be advised for the other eye, often at the same time. This is to prevent acute glaucoma in the other eye, which is otherwise quite likely. Sometimes eye drops are needed longer-term to help keep your eye pressure under control. The outlook prognosis is good if treatment is started quickly.
Your eye can recover and laser treatment or surgery can prevent the problem coming back. If the attack is severe, or if treatment is delayed, the high pressure in your eye can damage the optic nerve and blood vessels. If this is the case, there is a risk that your vision will be permanently reduced in the affected eye. Many people will be allowed to drive after recovering from acute angle-closure glaucoma.
Make an appointment with an ophthalmologist. Simple tests performed during these routine eye checks may be able to detect damage from glaucoma before it advances and begins causing vision loss.
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Eye irrigation with normal saline or lactated Ringer's solution should be initiated as soon as injury from a chemical is suspected. Non-sterile water can be used if no other options are available. In an office setting, the eye can be irrigated using an intravenous tube, nasal cannula, or Morgan Medi-flow lens. After about 30 minutes of irrigation, the eye should be closed for approximately five minutes. Then the pH of the injured eye should be tested with litmus paper that is touched to the conjunctival fornix the area between the eyelid and globe inside the lower eyelid.
Irrigation should be continued until a neutral pH level 7. Once pH is stabilized, a cycloplegic agent 0. Duration of irrigation has been shown to have a direct positive impact on the outcome of treatment and hospital stay. Up to 10 liters of an irrigant may be necessary to achieve neutral pH.
In a retrospective study, 36 patients irrigated 49 injured eyes with tap water before seeking medical help, whereas 17 patients with 29 injured eyes did not irrigate after the injury. Of the patients who irrigated their eyes, 76 percent had a minimal grade 1 injury, whereas 86 percent of patients who did not irrigate their eyes had a more severe grade 2 injury.
Mean healing time was eight days for the patients who irrigated and 29 days for those who did not. Acid should not be used to neutralize a base, and vice versa. Once the pH is within normal range 7. The central retinal artery is a branch of the ophthalmic artery, which supplies blood mainly to the retina via retinal branches. Occlusion of the central retinal artery quickly leads to ocular stroke, which can cause severe vision loss. Partial loss of the visual field may occur if only distal branches of the retinal arteries are occluded.
Patients with CRAO describe painless and sudden loss of vision in one eye. The patient may report a history of amaurosis fugax transient, painless unilateral vision loss before presentation. The pupil may be dilated with sluggish reaction to light Table 2. If vision loss is acute, transient, and bilateral, other causes such as migraine auras, heart failure, and hypertensive emergencies should be suspected. Acute vision loss secondary to retinal ischemia can also be caused by severe unilateral or bilateral carotid artery stenosis.
An embolus in a retinal vessel may be seen Figure 2 A Normal right fundus and B a left fundus with retinal edema secondary to central retinal artery occlusion. The central macula is still being perfused because of the presence of a cilioretinal artery, which is found in 15 percent of the U.
Risk factors for CRAO include age older than 70, atherosclerosis, diabetes, endarteritis, glaucoma, high cholesterol levels, hypertension, hypercoagulable states, and migraine. Although rare, CRAO also can occur in association with syphilis or sickle cell disease. CRAO is associated with giant cell arteritis in 5 to 10 percent of cases; an appropriate review of systems and measurement of erythrocyte sedimentation rate or C-reactive protein should be performed to rule it out.
Patients with symptoms and signs of CRAO must be referred immediately to an ophthalmologist because irreversible damage occurs in as little as minutes of occlusion. Several can be initiated in a primary care setting before the patient is seen by an ophthalmologist.
These include ocular-digital massage or lowering of intraocular pressure with intravenous mannitol Osmitrol 0. The theory behind ocular-digital massage is that the steep increase in pressure followed by a sudden return to normal pressure may plunge an embolus farther along the vasculature into a distal branch, minimizing the area of ischemia and vision loss. A systematic review of several randomized controlled trials concluded that there is currently not enough evidence to recommend one treatment over another for acute CRAO.
In patients with negative results on carotid ultrasonography, transesophageal echocardiography should be considered to exclude a cardiac origin of the embolus. If acute angle-closure glaucoma is not treated immediately, damage to the optic nerve and significant and permanent vision loss can occur within hours. Patients with acute angle-closure glaucoma often present with blurred vision, eye redness, frontal headache, colored halos around lights, severe eye pain, discomfort, nausea, and vomiting Table 2.
Physical findings include increased intraocular pressure greater than 30 mm Hg normal range: 10 to 23 mm Hg , a mid-dilated pupil 4 to 6 mm , sluggish reaction of the pupil to direct illumination, a shallow anterior chamber, a hazy cornea, and hyperemic conjunctiva. Risk factors for acute angle-closure glaucoma include anterior placement of the lens, hyperopia, myopia, narrow angle, and shallow anterior chamber.
An attack of acute angle-closure glaucoma in predisposed persons can occur as a result of dim lighting or use of certain medications e. Medications such as sulfa derivatives and topiramate Topamax can cause swelling of the ciliary body and secondary angle closure.
During an acute attack, medical therapy is initiated to lower the increased intra-ocular pressure. If there is high suspicion of acute angle-closure glaucoma, one drop each of 0. The eyedrops should be repeated three times at five-minute intervals.
Therapy is initiated to lower the intraocular pressure, reduce pain, and clear corneal edema in preparation for iridotomy. Definitive treatment for primary acute angle-closure glaucoma is laser iridotomy.
Surgical iridectomy can be performed if a laser iridotomy is not successfully performed. Retinal detachment is the separation of the neurosensory layer of the retina from the choroid and retinal pigment epithelium underneath. Although retinal detachment is uncommon affecting one in 10, persons per year , it leads quickly to degeneration of photoreceptors because of ischemia.
Permanent vision loss can be prevented by early diagnosis and treatment. Patients with retinal detachment often complain of unilateral photopsia i. Floaters may move in and out of central vision. Vision loss may be curtain-like, filmy, or cloudy. If the macula or the central vision is involved, the patient may lose the ability to read, have loss of light perception, or may not be able to see a hand waved in front of his or her face Table 2.
Direct ophthalmoscopic examination aids in the diagnosis of retinal detachment Figure 3. Asymptomatic retinal breaks and lattice degeneration i. If funduscopic examination reveals either of these risk factors, laser demarcation of these areas may be considered to prevent future retinal detachment and vision loss. Of note, ophthalmologic consultation is necessary with this procedure, and there is insufficient evidence to prove its effectiveness.
Extensive superior retinal detachment that extends to just below the fovea. Retinal tear is visible superiorly. Already a member or subscriber? Log in.
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