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dog eye problem /acute glaucoma and its solutions?

Glaucoma is an elevation of the intraocular pressure (IOP) with associated optic nerve and retinal damage. Glaucoma in dogs is always due to a decreased drainage of aqueous humor (AH)—increased production does not occur.
Glaucoma in dogs is an eye disease characterized by damage to the optic nerve and peripheral vision loss which is caused by the increased pressure (intraocular pressure or IOP) within the animal’s eye. The cause is usually inadequate drainage of aqueous fluid in the eye and not overproduction of it.

dog eye problem /acute glaucoma and its solutions
dog eye problem /acute glaucoma and its solutions

What is Glaucoma?

Glaucoma is the condition of increased pressure in the eye. Eye pressure is normally regulated by fluid flowing into and out of the eye at a balanced rate. If too much fluid is made or too little fluid is drained, the pressure in the eye increases, causing damage to the retina and optic nerve. Glaucoma can be painful and approximately 40 percent of cases lead to blindness within one year. If treatment is not started within hours of pressure increase, vision will likely be lost. Glaucoma is the elevation of pressure inside the eye, known as intraocular pressure (IOP) beyond a specific point at which vision is compromised or is no longer possible. Glaucoma is a frequent cause of blindness in both humans and animals.

Symptoms of Glaucoma in Dogs

Symptoms of glaucoma should be treated as an emergency as vision can be lost within hours of disease signs. Glaucoma usually begins in one eye. 50 percent of cases spread to the other eye if left untreated.

Symptoms may include one or more of the following:

  • Pupils of eyes different sizes
  • Mild to severe eye pain (rubbing eye on the floor or with paw)
  • Appearance of vessels in the white of the eye
  • Redness of the eye
  • Cloudy cornea
  • Fluttering eye lid
  • Squinting
  • Tearing
  • Appetite loss and anti-social behavior (due to pain)
  • Light avoidance
  • Weak blink response
  • No response of pupil to light
  • Vision problems (bumping into objects, difficulty finding toys, walking gingerly)
  • Bulging swollen eye
Types

There are two forms of glaucoma in dogs:

  • Primary Glaucoma

    – The fluid flow rate into or out of the eye is abnormal resulting in an increase in eye pressure.

  • Secondary Glaucoma

    – A separate condition causes intraocular fluid drainage to be slowed or blocked, resulting in increased pressure. Twice as common as primary glaucoma.

Intraocular pressure is measured using a tonometer:

  • Normal Intraocular Pressure – 15-25mmHg
  • Primary Glaucoma – 25-30mmHg
  • Secondary Glaucoma – 10-30mmHg

Causes of Glaucoma in Dogs

  • Primary Glaucoma

    – Caused by genetic predisposition. Usually appears at or after 2 years of age. Genetically predisposed breeds include (but are not limited to) the basset hound, beagle, chihuahua, chow, cocker spaniel, dachshund, maltese, miniature poodle, samoyed and siberian husky.

  • Secondary Glaucoma

    – Caused by infection, inflammation, injury, lens luxation, or tumor.

Diagnosis of Glaucoma in Dogs

As irreversible eye damage and vision loss can occur within hours of symptoms, if any one of the symptoms are noted, visit your veterinarian immediately. Your vet will want to know onset of symptoms and any history of trauma or behavioral patterns associated with pain or vision loss. He will perform an ophthalmologic exam and may choose to treat your pet in the clinic or may refer you to veterinary ophthalmologist.

Tonometry

Intraocular pressure is measured with a tonometer. A drop of anesthetic may be put on the eye first. One type of tonometer blows a puff of air on the eye and measures the indentation. Another type presses a small plastic disk against the eyeball to measure pressure. The Mueller method uses an electronic tonometer.

In sudden glaucoma, the pupil has a sluggish response to light, the blink response is weak or absent, the cornea is swollen or cloudy, the eye is red, inflamed and tearing, and the pet may be squinting.

In chronic glaucoma, the pupil has no response to light and the blink response is absent. The cornea is cloudy and the eye is red and inflamed. Tearing is possible and vessels are seen on the cornea. The eye is often enlarged.

X-ray

Your veterinarian may want to rule out the presence of an eye abscess, injury or tumor. An x-ray or ultrasound will allow the space around the eye to be visualized.

Treatment of Glaucoma in Dogs

Treatment depends on cause and severity of the glaucoma. The goal of treatment is to restore normal eye pressure (by decreasing fluid production and/or increasing fluid drainage) and provide pain relief. In the case of secondary glaucoma, the cause of the condition must be treated as well. This may include repair of trauma, surgical removal of any tumors, or antibiotics for infection. If only one eye is affected, steps will be taken to prevent glaucoma’s development in the other eye.

Medications

Most medications are topical drops or ointments that will lower the pressure of the eye and/or treat inflammation or infection. Topicals are often administered 3 times daily for a defined period of time. Some medications are oral.

Beta-blockers reduce fluid production. Carbonic anhydrase inhibitor diuretics reduce fluid production. Cholinesterase inhibitors help delay the onset of glaucoma in the unaffected eye. Corticosteroids can help control inflammation. Mitotic medications shrink the pupil to allow fluid release. Osmotic diuretics dehydrate the eye (used with caution in diabetics or cardiac patients). Prostaglandin analogs can improve fluid flow from the eye.

Surgery

Surgery may be required in cases of primary or secondary glaucoma. There are a variety of surgical approaches used for the varying degrees of severity and vision damage:

  • Cyclophotocoagulation

    – A laser instrument destroys the secretory epithelium of the eye’s ciliary body (responsible for fluid production within the eye).

  • Gonioimplantation

    – A shunt (small tube) is implanted to provide a fluid drainage outlet.

  • Enucleation

    – Complete removal of the globe of the eye (eyeball). Used in severe cases or when other therapies aren’t effective.

Repeat surgeries may be required depending on the underlying cause and the eye’s response to surgery.

Recovery of Glaucoma in Dogs

Glaucoma medications can help delay progression and provide comfort, but most pets lose vision in one or both eyes within two years without surgery.

If the condition is caught early, follow-up appointments will be scheduled to determine if treatment is helping or if the condition is worsening. The unaffected eye will continue to be examined for signs of glaucoma. When treating with drops, keep the tip of the dropper sterile. Never touch it to the surface of the eye or with hands. Surgery patients will need to wear an Elizabethan collar (e-collar or cone) to prevent rubbing the eye.

Breeds predisposed to developing glaucoma should have the eyes checked every 6 months so that cases can be detected and treated as early as possible. Always watch for any abnormalities with the eyes and report them to your vet as soon as possible.

In cases of enucleation surgery, loss of an eye is usually not difficult to adapt to and pets only suffer a mild loss of depth perception. You can speak with your veterinarian on how to make the house safe for transitioning to seeing with one eye. Watch off-leash pets outdoors as it will take a while to adapt fully.

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Glaucoma Questions

  • AH is drained through 2 different pathways:
    • Most AH exits the eye via the iridocorneal angle (ICA), or conventional pathway, which is a complex sieve-like structure formed by the junction of the peripheral iris and cornea.
    • Approximately 15% of AH drains through the nonconventional, or uveoscleral outflow, pathway.
  • This drainage pathway is the target of the most effective glaucoma drugs, the prostaglandin analogs.
    The balance between AH formation and drainage determines the IOP.

CLASSIFICATION OF GLAUCOMA

Classification of glaucoma is important to enable proper diagnosis and therapy. Glaucoma should be classified according to the underlying cause of the decreased AH drainage and the duration of the glaucoma (TABLE 1).1–3

Cause of Glaucoma

Primary Glaucoma

FIGURE 1. Primary glaucoma. The right eye of an 8-year-old female spayed basset hound with primary, chronic glaucoma. Note the episcleral injection, corneal edema, buphthalmos, and lens subluxation (secondary to buphthalmos). The retina appears hyperreflective, with a significant lack of retinal blood vessels (retinal degeneration).

Primary glaucoma in dogs (FIGURE 1) is associated with an inherited malformation and malfunction in the ICA. Over time, the capacity for AH outflow is reduced and IOP increases. Primary glaucoma is strongly breed related, and some of the most commonly affected dog breeds are the beagle, basset hound, Boston terrier, cocker spaniel, and shar-pei. Other breeds that are commonly affected include the Siberian husky, Samoyed, Labrador retriever, and toy poodle. Mixed-breed dogs are also affected by primary glaucoma.

Secondary Glaucoma

Secondary glaucoma (FIGURE 2) results from a physical obstruction to AH drainage, usually occurring at the ICA or pupil. The ICA can become obstructed with cellular debris (red blood cells, white blood cells, tumor cells) or inflammatory proteinaceous debris. The pupillary flow of AH may be obstructed by iris adhesions to the lens (posterior synechia) or an anteriorly luxated lens. Certain breeds, such as terriers, Chinese crested dogs, and the shar-pei, are predisposed to anterior lens luxation because of an inherited abnormality in the lens zonule suspension system. Acute glaucoma in these breeds should prompt the clinician to look closely for an anterior lens luxation.

Duration of Glaucoma

Acute Glaucoma:

FIGURE 2. Secondary glaucoma. The left eye of an 11-year-old male castrated husky with secondary glaucoma. Note the diffuse iris discoloration and focal region of hyphema.

This type of glaucoma (FIGURE 3) is defined as an elevation in IOP of less than 12 to 24 hours’ duration. If patients are treated during this phase, vision may be salvageable. Unfortunately, there are often subclinical spikes in IOP before the sustained elevation, which are quite detrimental. Thus, only about 50% of patients regain sight even when treated in the acute phase.1

Chronic Glaucoma:

This type (FIGURE 4) occurs when the IOP elevation is sustained for days or longer. Medical therapy may reduce the IOP, but vision cannot be regained. With time, many of the ocular structures undergo both physiologic and morphologic changes in response to the persistently high IOP (see Clinical Signs). Many dogs present with chronic glaucoma because the acute phase is misdiagnosed or is overlooked completely by the owners.

Secondary glaucoma results from a physical obstruction to AH drainage, usually occurring at the ICA or pupil.

CLINICAL SIGNS OF GLAUCOMA

FIGURE 3. Acute glaucoma. The right eye of a 5-year-old female spayed cocker spaniel with acute glaucoma. Note the normal globe size, elevated third eyelid, diffuse corneal edema, and ocular inflammation.

  • Signs of ocular pain
    • Blepharospasm
    • Epiphora
    • Head shyness
    • Elevated third eyelid
    • Lethargy, decreased appetite, and sleeping more are subtle signs of pain that may be overlooked
  • Ophthalmic examination findings consistent with acute glaucoma:
    • Episcleral congestion and conjunctival hyperemia
    • Corneal edema, present in dogs with IOPs >40 mm Hg
    • A dilated, nonresponsive pupil and negative menace response
      • The pupil size may be normal in cases of mild IOP elevation, or even constricted in cases of glaucoma secondary to anterior uveitis
    • The presence of a consensual pupillary light reflex (PLR; constriction of the contralateral pupil when light is shone into the affected eye) and dazzle reflex
      • These are important keys to diagnosing acute glaucoma because they indicate existing retinal function and the possibility of regaining vision with IOP control
      • Significant and abrupt IOP elevations may lack a consensual PLR, even if vision is salvageable
  • Ophthalmic examination findings consistent with chronic glaucoma:
    • Buphthalmos
    • Chronic corneal disease (Haab’s stria, neovascularization, exposure keratitis)
    • Lens subluxation or luxation
    • Retinal degeneration
    • Optic nerve degeneration and cupping

DIAGNOSIS OF GLAUCOMA

FIGURE 4. Chronic glaucoma. The left eye of a 10-year-old male castrated cocker spaniel with chronic glaucoma. Note the buphthalmos, corneal neovascularization, and central corneal scarring secondary to exposure keratitis.

Measurement of IOP is indicated in any patient with a red, painful eye. Normal IOP in dogs is 15 to 25 mm Hg1–3 and decreases normally with age. A dilated pupil and decreased vision are further suggestions that glaucoma may be present. Importantly, a dog with significant anterior uveitis and an IOP in the normal range should raise great concern for impending glaucoma. This is an indication of AH outflow obstruction because the IOP should be low in cases of uveitis.

Tonometry determines IOP and is truly just an estimation using various measuring devices. It is crucial that tonometry be performed with proper restraint and correct use of equipment to obtain accurate measurements. Studies have demonstrated large variations in IOP with jugular pressure, excessive eyelid manipulation, and even changes in body position.4

The 2 commonly used and accurate methods to measure IOP are applanation and rebound tonometry.

Applanation tonometers, such as the Tono-Pen VET (reichert.com), measure IOP by flattening the corneal surface and are commonly used in general practice. This method is highly accurate when performed correctly, is portable, and can be used with light restraint and variable head positions. A series of readings is obtained, and a digital display shows the average IOP of the readings and a percentage error indicating the consistency of the measurements. This method requires the use of a topical anesthetic.

Rebound tonometers, such as the TonoVet (tonovet.com), measure IOP by projecting a small probe at the corneal surface and analyzing the characteristics of its rebound. Rebound tonometers are as accurate and easy to use as applanation tonometers. The probe must be held horizontally; thus, proper head positioning is necessary. These tonometers are slightly more expensive and do not require topical anesthetic before use.

TREATMENT OF ACUTE GLAUCOMA

Acute glaucoma is considered an emergency, and the IOP should be reduced as quickly as possible to attempt to salvage vision. It is also important to address the specific underlying cause that led to the decreased AH outflow. In cases of acute glaucoma secondary to anterior lens luxation, referral to an ophthalmologist for emergency surgical removal of the lens is advised.

Osmotic Diuretics

Hyperosmotic agents reduce the formation of AH by reducing plasma flow through the ciliary body and cause dehydration of the vitreous. For maximum efficacy, water should be withheld for 4 hours after hyperosmotic treatment.5

  • Mannitol significantly reduces IOP within 15 minutes of administration and can remain effective for 6 to 10 hours.
  • Mannitol can be used safely in most dogs but should be used with caution in dogs with cardiac or renal disease, or in dehydrated patients.
  • I usually begin with 1 g/kg IV over 30 to 45 minutes. IOP should be measured at the end of the infusion to assess for efficacy.
  • If the IOP remains elevated at >25 mm Hg, an additional 1 g/kg IV dose may be given.
    Monitoring of electrolytes should be considered.

Prostaglandin Analogs

Prostaglandin analogs lower IOP primarily by increasing AH outflow via their action on iris and ciliary body musculature. They induce a profound miosis and may physically open the ICA and improve flow. Prostaglandin analogs should be avoided in cases of glaucoma secondary to anterior lens luxation or severe uveitis.6–8

  • Latanoprost (Xalatan [xalatan.com]) results in a dramatic decrease (about 45%) in IOP within
    20 minutes.

    • The duration of effect is 8 to 12 hours, although this can vary between dogs.
    • Additional doses may be given every 15 to 20 minutes if the initial response is insufficient.
    • If the IOP remains >25 mm Hg after 3 doses/1 hour of treatment, alternate methods of IOP reduction should be attempted.

Anterior Chamber Paracentesis

FIGURE 5. Anterior chamber paracentesis. The left eye of a 6-year-old male castrated cocker spaniel with acute glaucoma is undergoing anterior chamber paracentesis. A 30-gauge needle has been inserted at the dorsolateral limbus and directed in a plane parallel to the iris. No syringe is attached, and aqueous humor is allowed to passively fill the needle hub. In this procedure, care should be taken not to touch the corneal endothelium, the iris, or the lens with the needle tip.

Removing AH from the anterior chamber is a reliable method to quickly reduce IOP (FIGURE 5). Depending on the clinician’s skill level and the temperament of the patient, this procedure can be performed awake or with mild to moderate levels of sedation. The duration of effect of paracentesis varies widely, and additional hypotensive methods should be instituted.

  • Rinse the ocular surface with a dilute solution of povidone–iodine (1:20 diluted in saline).
  • Instill topical anesthetic.
  • If the patient is sedated, place a lid speculum and stabilize the globe with small, toothed forceps. In my opinion, when used without sedation these instruments cause undesired patient distress.
  • Use a small-gauge needle (30-, 27-, or 25-gauge) without a syringe attached.
  • Insert the needle at the dorsolateral limbus and direct it in a plane parallel to the iris; take caution not to touch the corneal endothelium, iris, or lens.
  • Allow the hub of the needle to passively fill; 1 to 3 drops of AH can spill over. Do not use suction.
  • Slowly remove the needle and measure the IOP immediately.
  • Note that the desired IOP is <15 mm Hg; repeat the process if necessary.
Topical anti-inflammatories are beneficial for ocular surface inflammation and also treat any anterior segment inflammation.

Maintenance Therapy to Control IOP

All of the emergency methods to reduce IOP have limited durations of efficacy. Thus, once IOP has been reduced, additional therapy to maintain control of the IOP should be instituted.

Carbonic Anhydrase Inhibitors

Both systemic and topical carbonic anhydrase inhibitors (CAIs) are available. Inhibition of carbonic anhydrase decreases AH production by reducing synthesis of bicarbonate in the ciliary body.9–11

  • Methazolamide is an oral CAI that can be used in dogs for control of IOP.
  • Commonly used dosages include 2.5 to 5 mg/kg PO q8–12h.
  • Methazolamide has potential adverse systemic effects, including gastrointestinal upset, metabolic acidosis, and hypokalemia.
  • I use this medication to treat glaucoma in dogs only if it cannot be treated topically.
  • Topical CAIs have the advantage of providing adequate ocular concentrations of the drug and reducing the risk for systemic adverse effects.
  • Brinzolamide (Azopt; novartis.com) and dorzolamide (Trusopt; merck.com) are commercially available and reduce IOP effectively in dogs and cats.
    • Dorzolamide 2% is available in a generic form, which makes it more cost-effective.
  • The degree of IOP reduction observed with topical CAIs is similar to that of oral CAIs, and combination of the drugs does not further decrease IOP.
  • The most common adverse effect of topical dorzolamide is transient blepharospasm after instillation; this is less common with brinzolamide.
  • Topical CAIs are most often used q8–12h.

β-Blockers

β-Blockers reduce the formation of AH via their effects on β receptors present in the ciliary body. Undesirable cardiac and respiratory effects can be seen with topical β-blockers, including bradycardia and bronchoconstriction. Thus, these medications should be avoided in patients with cardiovascular disease and asthma.11,12

  • The degree of IOP reduction with β-blockers is mild; thus, these medications are often combined with other antiglaucoma therapy.
  • A solution of 2% dorzolamide and 0.5% timolol (Cosopt; merck.com) is available in generic form.
    • This combination therapy is as efficacious in reducing IOP as concurrent use of each drug, but the combination improves client compliance because it requires only 1 drop to be instilled 2 to 3 times daily.
  • Betaxolol and timolol are also commonly used as prophylactic treatment for prolonging the onset of glaucoma in the fellow eye of dogs with primary glaucoma.13,14
  • β-Blockers are most often used q12h.

Miscellaneous Therapy for Acute Glaucoma

Pain Control

Pain control is advocated for most patients during an acute glaucoma spike. Systemic pain control will improve patient comfort and also likely improve compliance for repeated IOP measurements. Numerous analgesic medications are available; however, I generally use one of the following options:

  • Methadone, 0.2 to 0.3 mg/kg IV q4–6h
  • Tramadol, 4 to 6 mg/kg PO q8–12h

Anti-inflammatories

Anti-inflammatory therapy is indicated in most cases of acute glaucoma. Topical anti-inflammatories are beneficial for ocular surface inflammation and also treat any anterior segment inflammation. The frequency of use and drug chosen depends on the degree of inflammation, the presence of concurrent uveitis, and the health of the cornea. Most patients are treated q8–12h. Topical nonsteroidal anti-inflammatories should be avoided because they can reduce the efficacy of latanoprost therapy and exacerbate IOP elevation.15 Oral anti-inflammatories are considered important to treat the posterior segment (retina and optic nerve) inflammation that develops during an acute IOP spike.1–3

  • Topical anti-inflammatories:
    • Prednisolone acetate 1%
    • Dexamethasone 0.1%
  • Oral anti-inflammatories:
    • Carprofen, 2.2 mg/kg PO q12h
    • Meloxicam, 0.1 mg/kg PO q24h
    • Prednisone, 0.5 mg/kg PO q12h

Prophylactic Therapy

Primary glaucoma is a bilateral disease, and prophylactic therapy of the contralateral eye should be recommended. Therapy with 0.5% betaxolol q24h delays the onset of glaucoma from an average of 8 months to 31 months in dogs.13

MONITORING OF IOP

Once the IOP has been reduced, the patient should be monitored for 8 to 12 hours on maintenance therapy to ensure continued control of the pressure. A recheck examination is recommended within 2 to 5 days of discharge, and all medications must be given as directed on the day of the recheck exam. It is always important to note the time that medications were given in relation to the IOP measurement and to keep tonometer types consistent.

In cases of primary glaucoma, medications become less effective over time, and the IOP will again rise. It is important to educate owners that combination therapy and increasing medication frequencies are often necessary, and eventually all medical therapies fail. Referral to an ophthalmologist for advanced surgical procedures (ciliary body laser ablation, anterior chamber shunts) should be considered in visual patients, while chronically blind patients eventually require a salvage procedure (enucleation, evisceration, chemical ciliary body ablation).

Types of Glaucoma in Dogs

The Different Types of Glaucoma in Dogs

Primary Open Angle Glaucoma (POAG)

Primary open angle glaucoma in dogs is a rare type of glaucoma that is related to a mutation in the ADAMTS10 gene. This mutation and consequent POAG is seen most often in Beagles.

POAG in dogs is similar to the type of glaucoma found in humans and it progresses over time. Clinical signs of POAG in dogs include progressive narrowing of the iridocorneal angle (the angle created by the cornea and iris that lets the clear fluid between the lens and cornea drain from the eye).

The narrowing is caused by the accumulation of debris, decrease in pore size, and changes to the structure of the “drainage system” within the dog’s eye. As it gets harder for fluid to drain from the eye, pressure will build up and damage the structure of the eye itself.

Symptoms

Symptoms of primary open angle glaucoma in dogs include:

  • Luxation (dislocation) of the eye lens
  • Pupil dilation
  • Atrophy of the optic nerve
  • Eye discomfort
  • Increased intraocular pressure
  • Peripheral vision loss
  • Complete loss of vision

Dogs are generally not diagnosed with primary open angle glaucoma until they reach middle-age, which is when the progression of POAG usually begins to be more noticeable. However, POAG can be detected as early as 8 months old in puppies. At this time, a veterinary ophthalmologist should look at your dog’s eyes

The only way to diagnose primary open angle glaucoma in dogs is to run DNA testing to verify the presence of the affected gene type. Once the eye is damaged from POAG and the retinal ganglia cells of the eye die, that damage is permanent.

Treatment

Treating this type of dog glaucoma is costly and difficult. Most often, the treatment is focused on using medications to limit the dog’s eye’s fluid production rather than draining fluid from the eye because this is a difficult process in animals.

There is no cure for genetic glaucoma, but management can help to delay serious damage to the eye and offer some symptom relief for your pet.

Common dog treatments for primary open angle glaucoma include medication, alternative medicine, and surgery to relieve pressure within the eye or to attempt to improve drainage.

In some cases, a shunt or drainage tube may be surgically implanted to promote better drainage of fluid from the eye. This type of surgery can be troublesome because scar tissue can impede the function of the tube or shunt, and tubes may need to be ligated post-surgery to cause fibrosis.

Lifetime treatment of POAG does have a high failure rate, and your dog will most likely wind up with some degree of vision loss if that happens.

Primary Closed Angle Glaucoma (PCAG)

Primary Closed Angle Glaucoma (PCAG)

Primary closed-angle glaucoma in dogs is the most common type of primary canine glaucoma. With this glaucoma type, the angle created by the iris and the cornea within the eye is severely restricted most often due to structural abnormality rather than an eventual buildup of debris.

This type of abnormality can be present in the puppy at birth or it can also develop with age as the iridocorneal angle narrows and ligaments within the dog’s eye that may already be dysplastic might become more dysplastic with age.

Dog breeds that are most prone to developing PCAG include the Chow Chow, Bassett Hound, Siberian Husky English Cocker Spaniel, and American Cocker Spaniel. Female dogs are also more likely to develop PCAG than males.

Symptoms

Symptoms associated with primary closed angle glaucoma in dogs include:

  • Multiple attacks of congestion within the eye
  • Swelling of the cornea
  • Atrophy of the optic nerve
  • Eye discomfort
  • Increased intraocular pressure
  • Complete loss of vision

PCAG can be characterized by numerous attacks of congestion or one long, ongoing attack. These attacks are regularly caused by dim light exposure or any situation that triggers a stress reaction (stress causes a “midrange pupil” size and this increases the severity of blockage of the eye’s already compromised drainage system).

PCAG almost always results in the complete loss of vision in dogs because of how quickly it progresses in comparison to primary open-angle glaucoma.

Treatment

Treatment for primary closed-angle glaucoma is similar to the above mentioned POAG.

Surgery for PCAG may be used to open drainage within the eye if the iris and cornea are adhered, but if the lens covers the majority of the cornea, this surgery cannot be performed successfully.

PCAG is most often diagnosed in dogs at around age 5 due to the ability of the eye to compensate in the younger dog. As ocular components grow, the eye is less capable of compensating for limited fluid drainage and symptoms appear quickly.

Once symptoms are noticed in PCAG, it’s crucial to seek out a veterinary ophthalmologist immediately to manage symptoms and avoid retinal damage of your dog’s eyes.

Secondary Glaucoma in Dogs

Secondary Glaucoma in Dogs

The above mentioned primary open angle glaucoma and primary closed angle glaucoma in dogs are the result of natural defects within the eye or defects that develop as your pet gets older. These types of dog glaucoma are not the result of another illness or event.

In the case of secondary glaucoma, however, the development of glaucoma symptoms (which are similar to the above signs) is the result of something else happening.

Most often, secondary glaucoma in dogs results from trauma, injury, or cataracts in the eye. As the dog’s eye is damaged or injured, the fluid drainage system within the eye is slowed or completely blocked.

Treatment

Depending on the specific cause, treatments vary but they should always be administered as soon as possible. If an injury contributing to glaucoma is not treated immediately and pressure within the eye is allowed to build up, the optical nerve can become permanently damaged and result in your dog’s blindness.

Secondary glaucoma may be classified as open or closed angle glaucoma depending on the ability of the dog’s eye to drain and the eye structure post-injury.

Treatment for secondary glaucoma in dogs requires treating the underlying condition that prompted the development of glaucoma. For example, in dogs with cataracts that can be removed surgically, it may be effective to put a halt to any progression of glaucoma symptoms and pressure within the eye can be relieved with medication or laser treatment.

In other instances, such as after an accident that causes significant damage to the dog eye structure, the best solution may simply be to remove the eye to reduce pain and stop glaucoma from becoming an ongoing problem.

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