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Cluj Vet J 2021, 26, 3 http://clujveterinaryjournal.ro 

 

Communication 

The glaucomas in dogs 
Andreea Alina Zăvoi 1*, Andra Elena Enache 2 

1 University of Agricultural Sciences and Veterinary Medicine Cluj Napoca, Faculty of Veterinary Medicine; 
andreea-alina.zavoi@usamvcluj.ro 

2 North Downs Specialist Referrals, Bletchingley, UK; Andra.Enache@ndsr.co.uk 
* Correspondence: andreea-alina.zavoi@usamvcluj.ro 

Abstract: The glaucomas (the plural term is used intentionally) represent a group of diseases commonly defined by an increased 
intraocular pressure which interferes with normal function of the optic nerve and retina. Characteristic changes of glaucomas include 
reduced axoplasmic flow in the optic nerve head, retinal ganglion cells death, cupping of the optic disc and visual damage or blind-
ness due to retinal and optic nerve atrophy. This communication describes the clinical signs, diagnosis and medical treatment of 
glaucomas in dogs. 

Keywords: glaucoma, blindness, ocular hypertension, gonioscopy, dogs 
 

 

1. Introduction 

   According to the European College of Veterinary Ophthalmologists (www.ecvo.org)       
Manual ‘Glaucoma is characterized by an elevation of intraocular pressure (IOP) which, 
when sustained, results in destruction of the intraocular structures and function, resulting 
in blindness. The elevated IOP occurs mainly with developmental abnormalities or 
disease processes affecting the intraocular circulation and especially the drainage of 
aqueous humour from the eye through the irido-corneal angle (ICA). DNA-tests for Open 
Angle Glaucoma (POAG) in specific breeds are available.’ 

Glaucoma typically occurs as a result of impaired aqueous humor drainage 
whereby the obstruction of the drainage pathway may lie at the level of either the pupil 
(pupil block glaucoma), the ICA (trabecular meshwork, the conventional pathway), the 
uveo-scleral outflow (unconventional pathway), the lens, the ciliary body or the vitreous 
[1, 2]. 
 The main function of the aqueous humor is to provide nutrients to the cornea and 
lens. The aqueous humor is constantly produced at the level of the non-pigmented 
epithelium of the ciliary processes (Fig. 1). It flows through the posterior chamber, the 
pupil and into the anterior chamber (in a dorsal to ventral direction due to thermal 
convection currents) to be drained into the ICA (the filtration angle, the anterior most 
portion of the ciliary body, Fig 2.). The ICA is formed by the junction of the inner cornea 
(the corneoscleral tunic), base of the iris and cilioscleral cleft (which contains the pectinate 
ligaments). The aqueous humor is then drained through the trabecular meshwork and 
associated aqueous collecting channels (the conventional and main pathway) and less 
through the ciliary body and anterior uvea (the uveoscleral pathway, also called the 
unconventional/alternative pathway).  

Received: 14.12.2021 

Accepted: 30.12.2021 

Published: 31.12.2021 

DOI: 10.52331/cvj.v26i3.34 

 

 

Copyright: © 2021 by the authors. 

Submitted for possible open access 

publication under the terms and 

conditions of the Creative Commons 

Attribution (CC BY) license 

(http://creativecommons.org/licenses

/by/4.0/). 



Cluj Vet J 2021, 26, 3  
 

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The entire anterior chamber volume (0.4 ml in the dog) is replaced within an hour in most species (46-80 
minutes in the dog) [1,2]. Therefore, the IOP is the result of the balance between production and outflow of 
aqueous humor. The production of aqueous humor is a dynamic process, the inflow of aqueous humor equals the 
outflow [1,2].  

In glaucoma, both the aqueous humor production and outflow are altered. In understanding the pathogen-
esis of glaucoma it is important to understand the anatomy and physiology of the aqueous humor outflow path-
ways in normal and glaucomatous eyes. 

 
Figure 1. Aqueous humor drainage routes in canine eye. After being produced at the level of the ciliary processes, the aqueous 

humor flows through the posterior chamber into the anterior chamber (dorso-ventral direction, via convection currents). Here, it is 

drained via the trabecular meshwork of the ciliary cleft and into the angular aqueous plexus then directed anteriorly into the 

episcleral venules (1) or posteriorly into the scleral venous plexus and the vortex venous system (2). An alternative aqueous humor 

drainage pathway (3) is the diffusion through the ciliary muscle interstitium to the suprachoroidal space and through the sclera (ie, 

uveoscleral outflow). 

Source: Original AZ adapted after [3] 

 

 
Figure 2. The pectinate ligament visualized by gonioscopy (accolade ‘{‘) (AE Enache) 

 
         2. Causes and clinical signs of glaucoma 

Glaucomas have been classified according to their cause into congenital, primary or breed-related (open 
angle and closed angle glaucoma) and secondary to other intra-ocular diseases (eg. chronic uveitis, primary lens 

3 2 

1 



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luxation and intraocular neoplasia, Table 1). The canine glaucomas can also be classified according to the stage 
of progression into acute or chronic.  

 
Table 1. Causes of glaucoma adapted after [3] 

Congenital glaucoma Goniodysgenesis associated with multiple ocular defects 

 

Primary glaucoma 

Goniodysgenesis/narrow/closed irido-corneal angle:  

Breeds affected www.ecvo.org: 

• Japanese Shiba Inu 

• Dandie Dinmont terrier 

• Leonberger 

• Retriever (Flat Coated) 

• Siberian Husky 

• Spaniel (American Cocker) 

• Spaniel (Cocker) 

• Spaniel (English Springer) 

• Spaniel (Welsh Springer) 

• Spanish Water Dog and others 

Primary open angle glaucoma - Beagle, Norwegian Elkhound, Petit Basset Griffon 

Vendéen, Basset Hound, Shar Pei 

 

 

 

 

 

 

 

 

 

Secondary glaucoma 

Formation of pre-iridal fibrovascular membranes (PIFM) over the ciliary cleft 

opening - secondary to retinal detachment, neoplasia or uveitis  

Intraocular haemorrhage (due to systemic hypertension, coagulopathies, 

thrombocytopaenia) 

Intumescence of a cataractous lens (phacomorphic glaucoma in diabetic cataracts) 

Golden Retrievers pigmentary uveitis 

Intraocular neoplasia  

Postoperative following cataract surgery  

Ocular melanosis and pigmentary glaucoma in Cairn Terriers 

Primary lens luxation - terrier breeds, Border collie and other breeds 

Uveitis, including lens - induced uveitis (phacolytic, phacoclastic uveitis) 

Vitreous prolapse after surgical lens extraction (obstruction of the drainage angle by 

the vitreous) 

 
Clinical signs of glaucoma vary with the duration, intensity and cause of the IOP elevation from simple 

ocular surface redness (conjunctival hyperaemia and episcleral congestion that can be misdiagnosed as 



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conjunctivitis or retrobulbar disease), third eyelid protrusion and ocular discharge (commonly mistaken for 
conjunctivitis) to diffuse corneal oedema (cloudiness) that comes and goes (due to intermittent pressure spikes) 
and enlarged globe. Visual impairment may not be obvious to the owner as the dog will likely rely on vision from 
the contralateral eye, however the owner may report that the dog had been bumping into things on a particular 
side, missing things or being startled when approached from a particular side.  

As the dog is presented with a red eye, other ocular diseases should be included on the differential list such 
as uveitis (Fig. 3), episcleritis, conjunctivitis, retrobulbar disease. It is not uncommon to misdiagnose glaucoma as 
conjunctivitis which leads to irreversible blindness due to the delay in the appropriate treatment. Distinguishing 
between various diseases that can cause ocular redness should be based on the result of the clinical examination 
(the presence of menace response, pupillary light and dazzle reflexes) and tonometry (when available).  

 

Figure 3. Uveitis, Border terrier, 7yo, MN- note the diffuse conjunctival hyperaemia, mid-dilated pupil, hyphaema, 

hypermature cataract (North Downs Specialist Referrals) 

Primary sudden onset congestive glaucoma is easier to recognize as the dog will be typically middle age, 
female and will have absent menace response, fixed dilated pupil +/- absent dazzle reflexes, diffuse corneal 
oedema, episcleral congestion and conjunctival hyperaemia (Fig. 4). Cases of secondary glaucoma are more 
difficult to recognize solely based on the clinical signs but one should carefully look for signs of uveitis, retinal 
detachment or intraocular neoplasia, mid-dilated pupil with absent PLR and reduced or absent menace response. 

 

 
Figure 4. English Cocker Spaniel, 8yo FN- Primary closed angle acute congestive glaucoma left eye, note the anisocoria with dilated 

left pupil, diffuse corneal oedema, third eyelid protrusion (North Downs Specialist Referrals) 

Clinical signs of acute onset glaucoma (more common in primary glaucoma cases)  



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- Severe ocular and head pain; 

- Lethargy, reduced appetite; 

- Diffuse corneal oedema (Fig. 5); 

- Blepharospasm; 

- Epiphora; 

- Marked conjunctival hyperaemia which can be misdiagnosed as conjunctivitis; 

- Third eyelid protrusion; 

- Marked episcleral vascular congestion; 

- Mid to large dilated and unresponsive pupil; 

- Deep perilimbal corneal vascularisation; 

- Mild aqueous flare or pigment dispersion in the anterior chamber 

- Changes in the appearance of the optic nerve appearance: pale or dark optic nerve head (atrophy), attenuation 

of the retinal vasculature, cupped optic nerve head (retinal vessels stop at the rim of the optic nerve, no vessels 

are seen crossing the optic nerve), hyperreflectivity of the tapetal fundus. 

 

Figure 5. 8y6mo Cocker spaniel, FN with primary angle closed glaucoma – note the mucoid discharge at the medial 

canthus, third eyelid protrusion, moderate conjunctival hyperaemia, episcleral congestion, diffuse corneal oedema and 

dilated pupil (North Downs Specialist Referrals) 

Clinical signs of chronic glaucoma (more common in secondary glaucoma): 

- Development of Haab’ striae (Fig. 6): these are breaks in the Descemet membranes (allowing aqueous humor 

to enter the posterior stroma) secondary to stretching of the eye globe. 

- Buphthalmos: physical enlargement of the globe, resulting from severe and chronic elevations in IOP. It may 

be especially pronounced in young animals and Shar Pei dogs (with POAG), who have a more easily distended 

cornea and sclera than most adult dogs; buphthalmic eyes are almost always blind [1,2]. 

- Scleral thinning and visualization of the underlying choroid owing to globe enlargement. 



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- Phthisis bulbi: this develops with advanced cases of glaucoma when the ciliary body stops producing aqueous 

humor. 

 

Figure 6. 6yo FN Whippet- Anterior uveitis and secondary chronic glaucoma- note the Haab’s striae (curvilinear grey/white lines 

across the cornea), the pupil was miotic owing to the recent application of latanoprost (North Downs Specialist Referrals) 

 

Congenital glaucoma 
Congenital glaucoma is a rare condition which develops owing to the presence of severe ocular 

malformation and extensive goniodysgenesis associated with multiple ocular defects. Affected animals display 
severe, bilateral, ocular pathology, very early in life (generally within weeks to months) [1].  

 
Primary glaucoma 

Primary glaucoma is a bilateral disease which is not associated with any pre-existing intraocular disease, 
but has been associated with dysgenesis of the mesenchymal structures of the ICA (pectinate ligament 
dysplasia/goniodysgenesis) and/or narrowing or closure of the iridocorneal angle and/or the ciliary cleft (CC) in 
some breeds [1]. 

Clinical signs usually do not become evident until relatively late in life and this could be the consequence 
of age-related changes in the ICA. Primary glaucoma is a bilateral disease, however the onset of disease varies 
between the eyes [4].  

Based on the appearance of the drainage angle at gonioscopy, primary glaucoma may be classified as open-
angle glaucoma (Beagle, Petit Basset Griffon Vendeen, Basset Hound, Shar Pei, Norwegian Elkhound) and closed 
angle glaucoma more common in the majority of breeds (Cocker spaniel, Welsh springer spaniel etc). When the 
ICA appears abnormal on gonioscopy then goniodysgenesis has been diagnosed. A defect in the development of 
the ICA leads to a decreased width or malformation of the pectinate ligament. It is advised against breeding of 
dogs diagnosed with PCAG. 

Typical presentation of a dog with PCAG is a sudden onset of unilateral acute congestive glaucoma (sudden 
blindness, dilated pupil, third eyelid protrusion, diffuse corneal oedema, marked episcleral congestion) in a 
middle aged dog (6-8 years of age) more common in female dogs belonging to one of the following breeds: 
American/English Cocker spaniel, Springer spaniel, Beagle, Boston Terrier, Norwegian elkhound (full list of 
affected breeds available at https://www.bva.co.uk/canine-health-schemes/eye-scheme/ or 



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https://www.ecvo.org/hereditary-eye-diseases/ecvo-manual.html to check if a specific breed can be affected by 
primary glaucoma). The second eye typically follows the same outcome within 6-12 months after diagnosis.  

Bilateral presentation of PCAG is rare and other intraocular conditions should be considered particularly 
uveitis/panuveitis, uveo-dermatologic syndrome, chorioretinitis and retinal detachment when a dog is presented 
with bilateral high IOPs. 

 
Secondary glaucoma (post-inflammatory) 

Describes elevated IOP that occurs secondary to underlying ocular disease. Common causes of secondary 
glaucoma include cataract (Fig. 7), post-cataract surgery, lens (sub)luxation, intraocular neoplasia, severe or 
chronic uveitis, retinal detachment, lens-induced uveitis, uveo-dermatologic syndrome.  

Secondary glaucoma can develop acutely, subacutely, or chronically and may affect one or both eyes. 
Clinical signs include ocular discomfort, blepharospasm, corneal oedema, episcleral congestion (Fig 8), third 
eyelid protrusion, miosis or mydriasis, uveitis, buphthalmos and/or blindness [1-3]. Cases of glaucoma may be 
mistaken for conjunctivitis or retrobulbar disease due to the conjunctival hyperaemia, third eyelid protrusion and 
ocular discharge. 

        

Figure 7. 13yo FN Miniature Schnauzer- chronic lens-induced uveitis and secondary pupil block glaucoma, under treatment- 

pigment dispersion on the surface of the iris and anterior lens capsule, posterior synechiae, fixed pupil (North Downs Specialist 

Referrals) 



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Figure 8. 8yo FN Miniature Poodle - posterior lens luxation and secondary glaucoma. Note the conjunctival hyperaemia, 

engorged episcleral vessels and the aphakic crescent dorsally indicating a posteriorly luxated lens. (North Downs 

Specialist Referrals) 

Pigmentary glaucoma 
 

Pigmentary glaucoma (ocular melanosis) is a form of glaucoma which occurs as a result of the proliferation 
and accumulation of cells containing melanin in the aqueous outflow [1]. Studies support a hereditary aetiology. 
Ocular signs are generally bilateral, although not always symmetrical. Commonly affected breeds include the 
Cairn Terrier, Boxer and Labrador Retriever.  

 
3. Diagnosis of glaucoma in the dog 

Vision loss can happen gradually over a few weeks or months or acutely in dogs with glaucoma. Ophthalmic 
examination, including funduscopy, should be performed to rule out other ocular causes such as retinal disease 
or uveitis. The history, clinical presentation and full ophthalmic examination findings support the diagnosis of 
glaucoma. IOP values greater than 25 mmHg are consistent with ocular hypertension and should raise the 
suspicion of glaucoma. 

For the evaluation of visual function, the most important part is the assessment of the PLRs (pupillary 
light reflexes). It is important to evaluate the size of both pupils, and note any difference in pupil size (anisocoria). 
With raised intraocular pressure the PLR function is affected, the pupil will be fixed and dilated. 

Evaluating the menace response (Fig. 9) is another important step of the ophthalmic examination. This 
response is elicited by a threatening hand gesture heading towards the eye. A blinking response and globe 
retraction are expected to occur. This response involves cerebral cortical integration and interpretation, therefore 
it is not a reflex. It requires the entire peripheral (retina, optic nerve) and central visual pathways, as well as the 
visual cortex and the facial nucleus of cranial nerve VII, to be intact [1,4]. 



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Figure 9. Evaluation of the menace response- note the contralateral eye should be covered during the assessment (North 

Downs Specialist Referrals) 

 
To avoid false positive response from the visual, contralateral eye, the menace response should be evaluated 

in one eye, while the other eye is covered. It is important to avoid touching the eyelashes/hairs of the patient, or 
causing air movement, as this may also elicit false positive response. A facial nerve paralysis may cause a false 
negative response. Therefore, in the absence of a menace response the blinking reflex should be assessed by tap-
ping the skin at the canthus. The menace response is absent in very young (<10–12 weeks) animals, and may also 
be affected by the patient’s mental status [1, 5]. 

In glaucoma, the menace response will be either reduced/inconsistent or absent, due to the retinal ganglion 
cells damage and reduced axoplasmic flow. If the high IOP persists, the damage can be irreversible leading to 
blindness.  

The dazzle reflex (Fig. 10) is a subcortical reflex (mediated by reflex centers in the midbrain with fibers to the 
facial nucleus) whereby a strong light shone into the eye leads to blinking, globe retraction, third eyelid protru-
sion, and/or head movement [1]. This is helpful when the ocular media are opaque (hyphaema, cataract) and when 
the menace response and/or PLRs can’t be evaluated. However, it doesn’t indicate that the eye is visual, as this 
reflex can still be present even after retinal detachment due to the presence of a subspecialized population of 
retinal ganglion cells that are involved in the control of the PLR. Though, when the dazzle reflex is absent in a dog 
with high IOP it most likely indicates retinal damage and unless immediate action is taken (medical treat-
ment/aqueous centesis), blindness is likely to be permanent. 

 
Figure 10. Assessment of dazzle and pupillary light reflexes (North Downs Specialist Referrals) 

1. Tonometry: there are three methods of estimating the intraocular pressure in animals: the indentation 
tonometer (Schiøtz) which is not routinely available in clinical practice, applanation tonometer (TonoPen) 



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and the rebound tonometer (TonoVet, Fig. 11). Tonometry is also useful for identifying low IOP, which is 
common with anterior uveitis; normal values vary between individuals and time of the day (diurnal 
variation). Normal reported range for the IOP in dogs is 10-20 mmHg. Diurnal variation has been reported 
in the dog with higher IOPs in the early morning, therefore IOP curves (IOP checks every 3 hours over 24 
hours in hospital regime) may be recommended in order to detect IOP spikes in dogs predisposed to or 
diagnosed with glaucoma [6]. 

 
Figure 11. Estimation of the intraocular pressure using the TonoVet (rebound tonometer) in a dog (North Downs Specialist 

Referrals) 

 

2. Ophthalmoscopy: direct and indirect ophthalmoscopy (Fig. 12) may be used to examine the retina (look 
for hyperreflective striations or generalized hyperreflectivity) and the health of the optic nerve (Fig. 13, 
normally the optic nerve head should be well vascularised, the blood vessels should be seen crossing its 
border). Optic disc cupping (the blood vessels stop at the rim of the optic disc due to increased pressure) 
is the hallmark of glaucoma [1]; however, this may be difficult to notice in cases of acute congestive 
glaucoma due to the marked corneal oedema. 

 

Figure 12. Indirect ophthalmoscopy using a 30 D Volk lens- note the optic disc at the top with the retinal vessels, tapetal fundus at 

the bottom (the image is inverted in indirect ophthalmoscopy) North Downs Specialist Referrals 



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Figure 13. Normal appearance of the optic disc - pink with a physiologic pit centrally, retinal vessels are seen crossing the border of 

the optic disc (North Downs Specialist Referrals) 

3. Gonioscopy: facilitates visualization of the pectinate ligament using a goniolens (eg. Koeppe lens) which 
refracts the incoming light in such a way that the posterior cornea, ICA and anterior iris can be assessed 
[1,2]. This test is performed on the conscious dog under local anaesthetic and is used to diagnose 
goniodysgenesis (predisposition factor for primary glaucoma in a few breeds of dogs); it also provides 
information regarding the anatomy of the pectinate ligament which makes up the ICA.  

There are three categories of ICA appearance (ECVO scheme): open, narrow or closed angle; with this test 
you can also visualise the base of the iris, pectinate ligaments and the base of the cornea. Abnormalities of the 
pectinate ligament may be classified into: fibre latae and laminae. Depending on the % of the affected area within 
the pectinate ligament, the dog may be classed as unaffected or affected (mild, moderate or severe).  

4. Ocular ultrasonography: can be used to rule out intraocular neoplasia, haemorrhage, vitriitis/vitreous 
membranes and retinal detachement. 

5. Ultrasound biomicroscopy: high frequency (50-100 MHz) ultrasound, useful to assess the width of the 
ciliary cleft/ the opening of the iridocorneal angle [1]. 

Other tests are available and are not discussed here: chromatic PLR testing, electroretinography (pattern 
ERG to assess the retinal ganglion cell function), optical coherence tomography (OCT, used to measure the retinal 
layer and optic nerve head thickness [7]), scanning laser polarimetry (evaluates the retinal nerve fibre layer, may 
be of use for early detection of glaucoma patients). 

4. Discussion 

There are two options of dealing with glaucoma in dogs: medical and surgical treatment either alone or in 
combination. Very early diagnosis and aggressive therapy are generally required to preserve vision and delay the 
onset of blindness due to retinal and optic nerve degeneration.  

In primary glaucoma, despite normalization of the IOP following medical management, the glaucoma 
continues to progress, thereby supporting the evidence that changes occur at a molecular level and the condition 
can only be delayed but not cured. Despite aggressive medical or surgical treatment, the outcome is always the 
same which is blindness and loss of the eye and this needs to be explained to the owner. 

Sadly, by the time the owner notices changes in the eye, often the IOP exceeds 40 mmHg therefore glaucoma 
is a leading cause of irreversible vision loss in dogs. The patient is lethargic and reluctant to exercise and the 
affected eye becomes blind and appears red, painful and sore with a bluish tinge (corneal oedema) over the cornea. 
Often the eyes are enucleated because of the painfully high and uncontrolled IOP. Glaucomas can easily mask 



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underlying systemic diseases, such as infectious uveitis and neoplasia (lymphoma). Submission of the enucleated 
eyes for histopathological examination is always recommended [1,2]. 

Treatment of primary glaucoma (table 2): acute glaucoma should be considered an emergency and the IOP 
must be reduced to the normal range in order to save the patient’s vision; hospitalization is required and treatment 
is generally commenced with topical prostaglandin analogues. If the IOP doesn’t returns to normal within the 
first 30–60 min then the use of osmotic diuretics or aqueous centesis should be considered.  

In current clinical practice, ophthalmologists rarely use osmotic diuretics due to the availability of 
prostaglandin analogues which are as or even more efficient without the risk of inducing side effects. 
Furthermore, osmotic diuretics should be cautiously used as they are contraindicated in patients with kidney 
disease, owing to the risk of causing dehydration and electrolytes imbalance. The use of osmotic diuretics has 
been generally replaced by prostaglandin analogues (eg latanoprost) combined with topical carbonic anhydrase 
inhibitors (brinzolamide, dorzolamide) and beta-blockers (eg timolol).  

Treatment of glaucoma should be aimed at two directions: 
- Decreasing the aqueous humor production: carbonic anhydrase inhibitors, beta-blockers. Alternatively, surgery 

aimed at destroying the ciliary processes thereby reducing the aqueous humor production may be considered: 
endocyclophotocoagulation, transscleral laser with its potential risks and complications [7,8]. Because newly 
developed glaucoma medications are emerging at a very slow rate and may not be effective, working toward 
improving surgical options may be the most rewarding approach in the near term [8]. 

- Increasing the aqueous humor outflow: eg. prostaglandin analogues (eg. latanoprost). One effect of this class of 
hypotensive drugs is the secondary miosis as well as conjunctival hyperaemia, due to the increased vasodilation 
(Fig. 14). Surgery to create alternate pathways of drainage within or outside of the eye (anterior chamber bypass 
surgery) may be considered with its potential risks and complications [8, 9]. 

Others less commonly used hypotensive drugs include osmotics, adrenergics (non-selective alfa, beta-agonists 
epinephrine, dipivalyl epinephrine, alfa-2 agonists such as apraclonidine, brimonidine) and adrenergic blockers, 
parasympathomimetics (pilocarpine, carbachol, demecarium bromide, ectothiopate iodide) and are not discussed here 
[1,2]. 

Typically, a primary glaucoma patient will receive combinations of carbonic anhydrase inhibitors, beta-blockers 
and prostaglandin analogues (eg. dorzolamide, timolol and latanoprost) as ongoing medical treatment with frequency 
which depends on the IOP readings. 

 

Figure 14. The effect of latanoprost application, leading to extreme pupil (North Downs Specialist Referrals) 



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Although there is no clear-cut evidence, long-term anti-glaucoma medication (e.g. with topical carbonic 
anhydrase inhibitors and beta-blockers such as dorzolamide and timolol q8 hours) for the second, predisposed, 
but normotensive eye should be considered [2]. 

Analgesia should be considered in dogs with glaucoma. An IOP over 35 mmHg causes migraines in people. 
Dogs with glaucoma are typically less active, lethargic, they sleep more, eat less and are less willing to go for 
walks. Analgesia should be provided in the form of systemic non-steroidal medication, paracetamol and/or 
opioids if there are no contraindications. 

Treatment of secondary glaucoma depends on the etiology; therapy may consist in the removal of the lens 
in cases of primary lens luxation to enucleation for those secondary to an intraocular tumor, but in all cases referral 
to a veterinary ophthalmologist should always be considered and discussed with the owner. 

In blind eyes, the treatment options include: transscleral laser, intravitreal injection of gentamicin [10, 11] 
with a reported IOP control of 65%- 85%, intravitreal injection of cidofovir [12] with a reported IOP control of 97% 
and enucleation. 

Table 2. Most commonly used hypotensive drugs for glaucoma in dogs and cats 

Source: Adapted after [8] 

 

Drug Available Preparations Dose or Timing Contraindications 

Osmotic diuretics 

Mannitol 20% solution 

Only in acute congestive 

glaucoma 

1-1.5 g/kg i.v. 

slowly over 20 min 

cardiac or renal disease, 

dehydration, chronic 

glaucoma 

Prostaglandin analogues 

Latanoprost 0.005% solution q12-24 h, can be increased 

to q6-8 hours until a 

response is seen 

severe uveitis, anterior lens 

luxation 
Travoprost 0.004% solution 

Bimatoprost 0.03% solution 

Carbonic anhydrase inhibitors 

Brinzolamide 1% solution  

q8-12h 

none in dogs, but may 

cause local irritation 

shortly after instillation; 

keratitis, corneal oedema, 

blepharitis (especially 

dorzolamide) 

systemic absorption can 

lead to acute kidney injury 

in cats (check electrolytes 

before starting treatment) 

[13, 14] 

Dorzolamide 2% solution 



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β -adrenergic blockers 

Timolol maleate  

0.25% and 0.5% solution 

 

Q8-12h 

 

cardiac or respiratory 

disease 

use cautiously in cats and 

small dogs due to systemic 

absorption, cautious in 

dogs with asthma and 

chronic bronchitis 

 

5. Conclusions 

Despite medical therapy, a significant proportion of cases may require surgery in an attempt to keep the IOP 
within the normal range and delay the progression of glaucoma and blindness or to reduce the ocular discomfort. The 
prognosis depends on the underlying cause of glaucoma. Long-term therapy is necessary and regular intraocular 
pressure checks are required in order to ensure a normotensive and comfortable eye. Eyes that have lost vision but still 
have an increased pressure are a source of chronic pain. In such cases, enucleation must be considered to guarantee the 
well-being and comfort of the patient. Due to the aggressive and progressive nature of the disease, most animals lose 
their vision despite treatment, therefore their owners should be carefully advised regarding the prognosis of this 
disease. 

 
Author Contributions: All authors have read and agreed to the published version of the manuscript. 

Funding: This research received no external funding. 

Conflicts of Interest: The authors declare no conflict of interest. 

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