Congenital Glaucoma

Congenital glaucoma is a serious ocular condition present at birth in which developmental abnormalities of the eye's drainage structures lead to elevated intraocular pressure during the critical early weeks and months of a puppy's life. This condition differs fundamentally from glaucoma that develops later in life because the affected structures never formed properly during embryonic development, meaning the drainage dysfunction is present from the moment the puppy is born. The immature and highly elastic tissues of a young puppy's eye are particularly vulnerable to pressure-induced damage, and without early intervention, congenital glaucoma rapidly causes globe enlargement, optic nerve destruction, and permanent blindness.

The underlying developmental defect in congenital glaucoma involves malformation of the iridocorneal angle, the region where aqueous humor normally drains from the eye. During fetal development, this drainage system should differentiate from mesenchymal tissue to create a porous trabecular meshwork and open drainage channels. When this developmental process fails or remains incomplete, the resulting goniodysgenesis blocks aqueous outflow from birth. The severity can range from partial developmental arrest, which may not cause problems until later triggered by other factors, to complete absence of functional drainage structures that cause immediate and severe pressure elevation.

The impact of congenital glaucoma on affected puppies is profound, affecting not only vision but overall development and quality of life. Puppies with severe congenital glaucoma may be identified within the first weeks of life due to obvious eye enlargement, cloudiness, or apparent visual impairment. The rapidly growing puppy eye enlarges dramatically under sustained pressure, a phenomenon called buphthalmos or hydrophthalmos, creating a visibly distorted appearance. Beyond cosmetic concerns, this enlargement stretches and damages all internal eye structures, including the cornea, lens, retina, and optic nerve. Affected puppies may fail to develop normal visual behavior and may show delayed social development due to their inability to see and interact normally with littermates and humans.

Treatment of congenital glaucoma typically requires aggressive surgical intervention because the structural abnormalities causing the condition cannot be corrected by medications alone. While topical pressure-lowering drugs may help stabilize the eye before surgery and supplement surgical treatment afterward, achieving adequate pressure control in eyes with severely malformed drainage systems usually necessitates procedures that either create alternative drainage pathways or reduce aqueous production at its source. Early diagnosis and prompt treatment offer the best chance of preserving vision, though the prognosis remains guarded because significant damage often occurs before the condition is recognized. Genetic counseling is essential for breeders whose lines produce affected puppies.

The primary cause of congenital glaucoma is abnormal embryonic development of the eye's aqueous humor drainage system, specifically the iridocorneal angle and trabecular meshwork. During normal fetal development, these structures differentiate from mesenchymal tissue through a complex process of cell migration, tissue remodeling, and programmed cell death that creates open channels for fluid drainage. When genetic mutations or developmental insults disrupt this process, the drainage angle fails to form properly, leaving either dysfunctional tissue obstructing outflow or complete absence of the normal drainage apparatus. This developmental failure is established before birth, meaning affected puppies enter the world with a fundamental structural defect that predetermines their susceptibility to elevated pressure.

Genetic and hereditary factors represent the most significant cause of congenital glaucoma in dogs, with the condition following recognizable inheritance patterns in multiple breeds. The mode of inheritance varies by breed and may include autosomal recessive, autosomal dominant with variable penetrance, or polygenic inheritance involving multiple genes. Specific genetic mutations causing goniodysgenesis have been identified in some breeds, enabling DNA testing to identify carriers and affected individuals. The strong hereditary component means that congenital glaucoma tends to cluster in certain bloodlines, and breeding affected dogs or known carriers perpetuates the defect in future generations.

Environmental factors during pregnancy may contribute to congenital ocular malformations in some cases, though this is less common than genetic causes. Maternal infections during critical periods of fetal eye development can disrupt normal tissue formation. Exposure to certain toxins or medications during pregnancy may be teratogenic, causing developmental defects in the eyes and other organs. Nutritional deficiencies, while rare in dogs fed commercial diets, could theoretically impact normal fetal development. However, for most cases of congenital glaucoma in dogs, no specific environmental trigger can be identified, and the condition is attributed to inherited genetic defects.

Risk factors for congenital glaucoma center primarily on breed and family history rather than individual characteristics. Puppies born to parents with goniodysgenesis or clinical glaucoma carry dramatically elevated risk regardless of their own appearance at birth. Certain breeds have such high prevalence of drainage angle abnormalities that all breeding stock should undergo screening before mating. The absence of clinical glaucoma in parents does not guarantee puppies will be unaffected, as many dogs carry the genetic predisposition without developing clinical disease during their lifetimes. First-generation offspring of affected dogs in breeds with recessive inheritance may appear normal but carry the mutation that will affect future generations.

The mechanism by which congenital drainage defects lead to elevated pressure and eye damage involves the fundamental physiology of aqueous humor dynamics. The ciliary body continuously produces aqueous fluid regardless of whether drainage pathways are functional, creating relentless pressure buildup when outflow is obstructed. In congenital glaucoma, this buildup begins immediately after birth when the fetal circulatory patterns that bypassed the trabecular meshwork cease to function. The immature puppy eye, with its elastic sclera and developing structures, deforms under pressure rather than resisting it, leading to the characteristic globe enlargement. This stretching damages the optic nerve, corneal endothelium, lens zonules, and retina, often causing irreversible harm before the puppy reaches an age when behavioral signs of vision loss become apparent.

Early warning signs of congenital glaucoma may be apparent within the first few weeks of life, though recognition requires awareness and careful observation. Affected puppies may show asymmetry between their eyes, with one appearing larger or more prominent than the other. The corneas may appear hazy or cloudy rather than crystal clear, giving the eyes a dull or gray appearance. Excessive tearing or discharge may occur as irritated eyes produce more tears. Some puppies show photophobia, squinting or avoiding bright light. Attentive breeders or owners may notice that an affected puppy seems less responsive to visual stimuli than littermates, failing to track moving objects or make appropriate eye contact.

Common symptoms that become increasingly obvious as congenital glaucoma progresses include dramatic enlargement of the affected eye or eyes. This buphthalmos can cause the eye to protrude noticeably and may make it difficult for the eyelids to close completely. The cornea typically becomes increasingly cloudy due to fluid absorption into the corneal stroma under pressure, progressing from subtle haziness to dense opacity that obscures view of internal eye structures. Blood vessels on the surface of the eye may become prominent and engorged. The pupil often appears dilated and may respond sluggishly or not at all to light stimulation.

Behavioral changes in puppies with congenital glaucoma reflect their developing visual impairment and potential discomfort. Affected puppies may be less playful and interactive than their littermates, hanging back during group activities that require visual coordination. They may startle easily when touched unexpectedly, not having seen the approaching hand. Navigation difficulties may manifest as bumping into objects, hesitance in unfamiliar areas, or falling when attempting stairs or uneven surfaces. Some puppies become more vocal or clingy, seeking contact and reassurance that does not require vision. Feeding behavior may differ, with affected puppies having difficulty locating nipples or food bowls without guidance.

Physical signs visible during examination of puppies with congenital glaucoma include the characteristic globe enlargement that gives the condition its alternative name of buphthalmos, meaning ox eye. The stretched cornea may develop breaks in Descemet's membrane, creating linear opacities called Haab's striae that are pathognomonic for congenital glaucoma. Lens subluxation or luxation may occur as stretching weakens the zonular fibers holding the lens in place. Examination of the fundus, when visible through a cloudy cornea, may reveal optic nerve cupping and retinal changes indicative of pressure damage. The drainage angle, when examined by gonioscopy, shows characteristic abnormalities ranging from narrowing to complete absence of identifiable drainage structures.

Symptom progression in congenital glaucoma can be rapid due to the high pressures often present and the vulnerability of developing tissues. Without treatment, eyes typically enlarge progressively over weeks, with increasing corneal cloudiness and deteriorating visual function. The rate of progression varies among individuals but tends to be faster in younger puppies with higher pressures. Some puppies show apparent stabilization followed by sudden worsening, possibly related to acute pressure spikes superimposed on chronic elevation. Bilateral cases often progress at different rates in each eye, with one becoming more severely affected while the other maintains partial function.

Emergency symptoms requiring immediate veterinary attention include signs of acute severe pressure elevation or complications of the enlarged globe. Sudden severe cloudiness of the cornea, intense redness, or apparent severe pain indicated by crying, head pressing, or complete inability to open the eye constitute emergencies. Corneal ulceration may develop in enlarged eyes where lid coverage is inadequate, appearing as a white spot or area on the corneal surface that may progress rapidly to perforation. Any injury to an enlarged, fragile eye warrants urgent evaluation. Puppies showing systemic signs such as lethargy, reduced nursing, or failure to thrive along with eye abnormalities need comprehensive veterinary assessment to address all aspects of their condition.

Initial examination of puppies suspected of having congenital glaucoma begins with careful visual assessment and comparison of both eyes if available. The veterinarian will note any asymmetry in eye size, corneal clarity, or external appearance. Observation of the puppy's visual behavior, including response to moving objects and navigation ability, provides functional information. The examination continues with assessment of pupil size and light response, evaluation of corneal health, and estimation of eye size relative to age-appropriate normal values. History from the breeder or owner regarding when abnormalities were first noted, the presence of affected littermates, and any known family history of eye disease provides essential context.

Tonometry to measure intraocular pressure is the definitive test for confirming glaucoma, though interpretation requires consideration of age-appropriate normal values. Puppies normally have slightly lower intraocular pressure than adults, so pressures that might be borderline in an adult are clearly abnormal in a young puppy. Applanation tonometry using instruments designed for veterinary use provides reliable measurements even in small puppy eyes. Serial measurements may be needed to document consistent elevation versus transient increases. In some cases, pressure may be so high that standard tonometry is unreliable, and diagnosis must be based on clinical findings and response to treatment.

Gonioscopy examination of the drainage angle provides crucial information about the structural basis for congenital glaucoma. Using specialized lenses, the examiner can directly visualize the iridocorneal angle to assess whether functional drainage structures are present. Typical findings in congenital glaucoma include sheets of tissue covering the drainage angle, pectinate ligament abnormalities, or complete absence of identifiable trabecular meshwork. Comparison between eyes in bilateral cases may reveal differing degrees of abnormality that explain asymmetric clinical presentations. Gonioscopy findings help predict prognosis and guide treatment planning by characterizing the severity and type of drainage defect present.

Additional diagnostic testing helps characterize the full extent of damage and identify any concurrent abnormalities. Ocular ultrasound can measure globe dimensions objectively, assess lens position, and evaluate posterior segment structures when corneal opacity prevents direct visualization. Electroretinography assesses retinal function and helps determine whether visual potential remains despite visible structural damage. If systemic abnormalities are present, additional testing may be warranted to identify underlying syndromes that include ocular malformations as one component. Documentation through photography establishes baselines for monitoring progression or treatment response. Referral to a veterinary ophthalmologist provides access to specialized expertise and equipment essential for optimal diagnosis and treatment planning in these complex cases.

Emergency treatment for puppies presenting with severe congenital glaucoma and very high pressures focuses on rapid pressure reduction to prevent or minimize ongoing damage. Intravenous mannitol draws fluid osmotically from the eye and can lower pressure substantially within hours. Topical and systemic carbonic anhydrase inhibitors reduce aqueous production while preparations are made for definitive treatment. Pain management is essential because high pressures cause significant discomfort. These stabilization measures buy time for proper diagnostic evaluation and treatment planning but do not address the underlying structural defect that caused the pressure elevation.

Medical management alone is rarely sufficient for controlling congenital glaucoma because the structural defect preventing normal drainage cannot be corrected by medications. However, pressure-lowering drugs play important supportive roles before and after surgical intervention. Prostaglandin analogs may have limited effectiveness in eyes lacking normal drainage pathways but are sometimes tried. Carbonic anhydrase inhibitors and beta-blockers can reduce aqueous production and contribute to overall pressure control. Medical therapy may help maintain stability while awaiting surgery or supplement surgical treatment to optimize pressure levels post-operatively. Long-term medical management may be necessary even after successful surgical intervention.

Surgical treatment represents the primary therapeutic approach for congenital glaucoma and may involve procedures to create alternative drainage pathways or reduce aqueous production. Goniotomy attempts to open the malformed drainage angle by incising the abnormal tissue covering the trabecular meshwork, potentially restoring some drainage function. This procedure has best results in eyes where some trabecular meshwork development has occurred but remains covered by dysplastic tissue. Multiple goniotomy procedures may be needed to achieve adequate effect. When the trabecular meshwork is severely malformed or absent, creating entirely new drainage pathways through trabeculectomy or gonioimplant placement may be necessary.

Cyclodestructive procedures reduce aqueous humor production by destroying portions of the ciliary body and may be appropriate when other surgical approaches fail or are not feasible. Transscleral cyclophotocoagulation uses laser energy applied through the sclera to target ciliary body tissue. Endoscopic cyclophotocoagulation allows more precise targeting under direct visualization. These procedures can effectively lower pressure but carry risks of inflammation, hypotony (pressure becoming too low), and phthisis bulbi (globe shrinkage). Multiple treatment sessions may be needed, and careful monitoring for complications is essential during the post-operative period.

Alternative approaches and combination therapies may be employed based on individual patient needs and response to initial treatment. Some cases benefit from combining drainage procedures with cyclodestructive procedures to address both outflow enhancement and production reduction simultaneously. When eyes have become blind and painful despite treatment attempts, enucleation provides definitive relief from discomfort and eliminates the need for ongoing intensive management. Evisceration with intraocular prosthesis may be considered for cosmetic purposes in blind but non-painful eyes. The choice among these options involves careful consideration of visual potential, comfort, cosmesis, and owner preferences.

Treatment decisions in congenital glaucoma must account for the young age of patients, the severity of structural defects, and realistic prognosis for visual outcomes. Puppies with early diagnosis and less severe defects may achieve meaningful vision preservation with aggressive surgical management. Those presenting late with severe damage may benefit most from interventions focused on comfort rather than vision. Honest discussion with owners about expected outcomes helps establish appropriate goals and avoid futile interventions. The expertise of a veterinary ophthalmologist is essential for navigating these complex decisions and performing the specialized procedures required for optimal management.

Recovery timeline following surgical treatment for congenital glaucoma varies by procedure type and individual response. After goniotomy or trabeculectomy procedures, initial healing typically spans two to three weeks during which inflammation subsides and the created drainage pathways establish function. Pressure may fluctuate during this period before stabilizing at new levels. After cyclodestructive procedures, inflammation may be more pronounced and prolonged, with final pressure levels not apparent for several weeks. Puppies generally heal faster than adult dogs but require especially careful monitoring because their rapidly growing eyes continue changing even as surgical sites heal.

Post-treatment care requirements for puppies recovering from glaucoma surgery include close monitoring, medication compliance, and activity restriction. Frequent pressure checks, often daily or every few days initially, allow early detection of pressure rises or complications. Anti-inflammatory medications help control post-operative inflammation that could compromise surgical results. Antibiotic drops prevent infection during the vulnerable healing period. Elizabethan collars prevent rubbing that could disrupt healing. Activity restriction, challenging in energetic puppies, helps prevent trauma and reduces inflammation. Owners must balance the need for restriction against the puppy's developmental need for normal activity and socialization.

Prognosis factors in congenital glaucoma include the severity of structural defects, the extent of damage present at diagnosis, surgical success in achieving pressure control, and the development of complications. Puppies diagnosed and treated early, before significant optic nerve damage and globe enlargement, have better prognosis than those presenting late with advanced disease. Eyes with moderate goniodysgenesis that respond well to goniotomy may achieve long-term pressure control and vision preservation. Severely malformed eyes requiring cyclodestructive procedures have more guarded prognosis because these approaches sacrifice some aqueous production capacity and carry higher complication rates.

Long-term outlook for dogs with congenital glaucoma requires ongoing vigilance because the structural predisposition to pressure problems remains throughout life. Eyes that achieve initial surgical success may still require ongoing medical therapy and face risk of late treatment failure. The fellow eye in unilateral cases warrants close monitoring and possibly prophylactic treatment given the high likelihood of eventual involvement. Growth and development continue to affect eye structure during the first year of life, potentially altering pressure dynamics. Dogs with controlled congenital glaucoma can live happy lives, but they require lifelong monitoring and may need additional interventions over time. Owners who commit to this ongoing care partnership provide affected dogs their best opportunity for maximizing quality of life.

Primary prevention of congenital glaucoma depends entirely on responsible breeding practices that avoid producing affected puppies. Dogs diagnosed with congenital glaucoma should never be bred under any circumstances, as they definitively carry genetic mutations for the condition. Parents of affected puppies should be removed from breeding programs, as they are obligate carriers of causative mutations. Siblings of affected dogs should be considered high-risk carriers and either excluded from breeding or bred only after careful genetic counseling and appropriate screening. These strict measures are essential because congenital glaucoma causes significant suffering and often results in blindness despite treatment efforts.

Breeding and genetic prevention strategies extend beyond individual affected animals to systematic screening of breeding populations. Gonioscopy examination of breeding dogs in predisposed breeds allows identification of goniodysgenesis before clinical disease develops. Breed clubs maintaining eye examination registries help breeders identify bloodlines with higher or lower risk. Where DNA tests for causative mutations are available, testing all breeding stock before mating enables completely informed decisions. Selecting mates to minimize the concentration of risk alleles in offspring reduces population-level disease incidence. Collaboration between breeders, veterinary ophthalmologists, and geneticists advances these prevention efforts.

Nutritional considerations for pregnant dogs are unlikely to prevent truly genetic congenital glaucoma but may support overall healthy fetal development. Feeding high-quality commercial diets formulated for reproduction ensures adequate nutrient supply during the demanding period of pregnancy. Supplementation is generally unnecessary and potentially harmful unless specifically recommended by a veterinarian for documented deficiencies. Avoiding exposure to potential teratogens during pregnancy is prudent even though most congenital glaucoma in dogs is genetic rather than environmental. Proper prenatal care through regular veterinary checkups supports the best possible outcomes for all puppies.

Health maintenance for dogs in breeds at risk for producing congenital glaucoma includes screening examinations that inform breeding decisions. Baseline gonioscopy before breeding age, typically by one to two years, documents the individual dog's drainage angle morphology. Annual comprehensive eye examinations detect any changes over time. Recording and sharing results through breed registries contributes to population-level understanding of disease prevalence and inheritance patterns. Prospective puppy buyers should request documentation of parental eye examinations and inquire about any family history of eye disease before purchasing puppies from breeds at risk for congenital glaucoma.

Early intervention when congenital glaucoma is suspected requires immediate action to maximize chances of preserving vision. Breeders who notice eye abnormalities in young puppies should seek veterinary ophthalmology consultation without delay. Veterinarians examining litters of predisposed breeds should be alert to early signs of congenital glaucoma during routine puppy examinations. Prompt referral for specialized evaluation and treatment gives affected puppies their best chance. Education of breeders about signs of congenital glaucoma empowers them to recognize problems early. The window for meaningful intervention may be narrow, making awareness and rapid response essential for affected individuals.

Daily management of puppies and dogs with congenital glaucoma requires dedicated commitment to medication schedules and ongoing monitoring. Young puppies may need medications administered four to six times daily in the early treatment period, requiring significant time and consistency from owners. Proper technique for administering eye drops to small, squirming puppies takes practice to master. Tracking medication times and observing for any changes in eye appearance or behavior helps detect problems early. As dogs mature and stabilize, management typically becomes less intensive, though lifelong treatment is usually necessary. Establishing reliable routines from the beginning supports long-term compliance.

Home environment modifications help puppies with visual impairment from congenital glaucoma develop and thrive despite their disability. Keeping the environment consistent with stable furniture arrangements allows visually impaired puppies to develop spatial maps for confident navigation. Baby gates block dangerous areas like stairs until the puppy demonstrates safe navigation ability. Soft surfaces cushion inevitable bumps and falls during the learning period. Using scent markers and textured surfaces to identify important locations like food bowls and bed areas provides non-visual navigation cues. Introducing changes gradually with guidance helps visually impaired dogs adapt without anxiety.

Quality of life for dogs with congenital glaucoma can be excellent despite visual limitations when owners provide appropriate support. Puppies are remarkably adaptable and develop compensatory skills using their superior senses of smell and hearing. Training using voice commands and scent cues rather than visual signals allows effective communication. Interactive play with noisy or scented toys maintains mental stimulation and physical activity. Socialization with other dogs and people should continue, with supervision to ensure safety and prevent overwhelm. The bond between owner and visually impaired dog often becomes especially close as they develop unique ways of communicating and connecting.

Monitoring and ongoing care requirements continue throughout the affected dog's life. Regular pressure checks, typically monthly once stable, detect treatment failure before severe damage occurs. Eye examinations assess for complications such as lens luxation, retinal detachment, or corneal problems. Owners must learn to recognize signs of pressure spikes, including increased cloudiness, redness, squinting, or behavior changes suggesting discomfort. Any sudden changes warrant immediate veterinary evaluation. Communication with the veterinary team about observations and any difficulties with the treatment regimen allows timely adjustments that optimize outcomes.

Caregiver support is important because raising a puppy with congenital glaucoma demands significant emotional, physical, and financial resources. Connecting with communities of owners whose dogs have visual impairments provides practical advice and emotional support. Understanding that treatment goals may shift from vision preservation to comfort maintenance helps owners adapt expectations appropriately. Planning financially for long-term care needs, including emergency funds for complications, reduces stress when decisions must be made quickly. Celebrating successes and milestones in the dog's adaptation and development maintains positive perspective. When end-of-life decisions become necessary, support from the veterinary team and other understanding pet owners helps owners navigate this difficult process.

High-risk breeds for congenital glaucoma include those with well-documented hereditary predisposition to goniodysgenesis and early-onset glaucoma. Basset Hounds have among the highest documented prevalence rates, with goniodysgenesis identified in a large majority of individuals examined in some studies. Great Danes show significant risk for congenital glaucoma, often presenting with bilateral disease at young ages. Samoyeds demonstrate inherited predisposition with characteristic early onset. Bouvier des Flandres carry genes for severe goniodysgenesis that can cause clinical glaucoma in puppies. Flat-Coated Retrievers have emerging recognition as an at-risk breed. These breeds warrant systematic screening of breeding stock and careful monitoring of puppies for early signs of glaucoma.

Moderate-risk breeds and categories include numerous purebreds with elevated incidence compared to mixed-breed populations, though with less dramatically high rates than the highest-risk breeds. Cocker Spaniels, while more typically developing glaucoma in adulthood, may occasionally show early-onset disease. Various spaniel breeds share genetic predisposition to some degree. Siberian Huskies and other Nordic breeds show increased susceptibility. Terrier breeds as a group have elevated glaucoma rates. Mixed-breed dogs with ancestry from high-risk breeds may inherit the condition, making family history relevant even when exact breeding is unknown. The expanding recognition of breed predispositions continues as more screening studies are completed.

Screening recommendations for breeds at risk emphasize examination by veterinary ophthalmologists with expertise in gonioscopy interpretation. All dogs of high-risk breeds intended for breeding should undergo gonioscopy examination before mating, with repeat examinations if findings are equivocal. Results should be submitted to breed registries to contribute to population-level data. Puppies from affected lines warrant early examination to detect congenital glaucoma promptly if present. DNA testing for known mutations, where available, enables identification of carriers who may appear normal on examination. Working with breed clubs actively engaged in reducing glaucoma incidence helps breeders access current protocols and contribute to ongoing prevention efforts.

Commonly co-occurring conditions with congenital glaucoma include other developmental ocular abnormalities that may share genetic or developmental origins. Congenital cataracts may be present in the same individuals or bloodlines, sometimes as part of recognized syndromes involving multiple eye malformations. Persistent pupillary membranes, remnants of fetal vascular structures that normally regress before birth, occur more frequently in dogs with goniodysgenesis. Lens colobomas and other lens abnormalities may accompany angle malformations. Retinal dysplasia, abnormal development of the retina, may be seen in conjunction with glaucoma. Dogs with multiple congenital eye defects face compounded challenges for vision and require comprehensive ophthalmologic evaluation.

Conditions with similar symptoms to congenital glaucoma require differentiation during diagnostic evaluation of puppies with eye abnormalities. Congenital anterior segment dysgenesis can cause corneal clouding and eye abnormalities that overlap with glaucoma presentation. Infectious causes of ocular inflammation in puppies, including those transmitted from the mother, may cause cloudy corneas and tearing. Traumatic eye injuries from rough littermate play can cause swelling and cloudiness. Corneal dermoids, abnormal skin-like tissue on the cornea, may be confused with corneal pathology from glaucoma. Thorough examination including tonometry differentiates glaucoma from these other conditions requiring different management approaches.

Potential complications of congenital glaucoma relate to the structural damage caused by pressure elevation in the developing eye. Lens luxation occurs when stretched zonular fibers fail, allowing the lens to displace and potentially causing secondary acute glaucoma if the lens blocks the pupil. Retinal detachment may occur in severely enlarged eyes where the retina separates from underlying structures. Corneal ulceration develops when enlarged eyes cannot be adequately protected and lubricated by the eyelids. Globe rupture, while rare, can occur in severely enlarged eyes subjected to trauma. Phthisis bulbi, shrinkage of the globe, represents end-stage failure of the eye's structural integrity. Preventing or managing these complications is an important component of comprehensive care for dogs with congenital glaucoma.