Dermatochalasis commonly affects the elderly, although sometimes it is congenitally acquired. The elderly version may begin to develop as early as 40 years of age, and it continues to progress with age. The congenital version may begin around 20 years of age. There is no racial predisposition towards developing dermatochalasis, and men and women are equally affected.

Ectropion in dogs usually involves the lower eyelid. Often the condition has no symptoms, but tearing and conjunctivitis may be seen. Breeds associated with ectropion include the Cocker Spaniel, the Saint Bernard, the Bloodhound, the Clumber Spaniel, and the Basset Hound. It can also result from trauma or nerve damage. Treatment (surgery) is recommended only if there is chronic conjunctivitis or if there is corneal damage. A small part of the affected lid is removed and then the lid is sewn back together.

People with dermatochalasis often also have blepharitis, a condition caused by the plugging of glands in the eye that produce lubricating fluid (meibomian glands). Dermatochalasis can be severe enough that it pushes the eyelashes into the eye, causing entropion.

Weakness in the orbital septum may cause the herniation of the orbital fat pads. This is observed as the presence of bulges (fat pads) in the soft tissue of the baggy eyes.

Ectropion is a medical condition in which the lower eyelid turns outwards. It is one of the notable aspects of newborns exhibiting congenital Harlequin-type ichthyosis, but ectropion can occur due to any weakening of tissue of the lower eyelid. The condition can be repaired surgically. Ectropion is also found in dogs as a genetic disorder in certain breeds.

The number of cases is around 0.5 to 0.7 per 10,000 births, making it a relatively rare condition.

Colobomas can be associated with a mutation in the "PAX2" gene.

Eye abnormalities have been shown to occur in over 90% of children with fetal alcohol syndrome.

Cryptophthalmos is a rare congenital anomaly in which the skin is continuous over the eyeball with absence of eyelids. It is classified into three types: complete, incomplete and abortive. Failure of eyelid separation can be associated with maldevelopment of the underlying cornea and microphthalmia. Cryptophthalmos usually occurs on both sides and occurs in association with other multiple malformations collectively referred to as Fraser syndrome.

BPES is very rare: only 50-100 cases have been described. It affects slightly more males than females.

Very few risk factors for choanal atresia have been identified. While causes are unknown, both genetic and environmental triggers are suspected. One study suggests that chemicals that act as endocrine disrupters may put an unborn infant at risk. A 2012 epidemiological study looked at atrazine, a commonly used herbicide in the U.S., and found that women who lived in counties in Texas with the highest levels of this chemical being used to treat agricultural crops were 80 times more likely to give birth to infants with choanal atresia or stenosis compared to women who lived in the counties with the lowest levels. Another epidemiological report in 2010 found even higher associations between increased incidents of choanal atresia and exposure to second-hand-smoke, coffee consumption, high maternal zinc and B-12 intake and exposure to anti-infective urinary tract medications.

An ectopic cilia is a special type of distichia. It is usually found in younger dogs. Commonly affected breeds include Poodles, Golden Retrievers, and Shih Tzus. The eyelash exits through the conjunctiva of the eyelid facing toward the eye, usually at the middle of the upper eyelid. It can cause intense pain and corneal ulcers. Treatment is surgery or cryotherapy.

Inverse Marcus Gunn phenomenon is a rare condition that causes the eyelid to fall upon opening of the mouth. In this case, trigeminal innervation to the pterygoid muscles of the jaw is associated with an inhibition of the branch of the oculomotor nerve to the levator palpebrae superioris, as opposed to stimulation in Marcus Gunn jaw-winking.

Blepharophimosis is a congenital condition characterized by a horizontally narrow palpebral fissure. It is also part of a syndrome blepharophimosis, ptosis, and epicanthus inversus syndrome, also called blepharophimosis syndrome, which is a condition where the patient has bilateral ptosis with reduced lid size, vertically and horizontally. The nasal bridge is flat and there is hypoplastic orbital rim. Both the vertical and horizontal palpebral fissures (eyelid opening) are shortened; the eyes are also spaced more widely apart than usual, also known as telecanthus.

Vignes (1889) probably first described this entity, a dysplasia of the eyelids.

Use of high doses of opioid drugs such as morphine, oxycodone, heroin, or hydrocodone can cause ptosis. Pregabalin (Lyrica), an anticonvulsant drug, has also been known to cause mild ptosis.

It is encountered more commonly in younger rather than older individuals.

Entropion is a medical condition in which the eyelid (usually the lower lid) folds inward. It is very uncomfortable, as the eyelashes continuously rub against the cornea causing irritation. Entropion is usually caused by genetic factors. This is different from when an extra fold of skin on the lower eyelid causes lashes to turn in towards the eye (epiblepharon). In epiblepharons, the eyelid margin itself is in the correct position, but the extra fold of skin causes the lashes to be misdirected. Entropion can also create secondary pain of the eye (leading to self trauma, scarring of the eyelid, or nerve damage). The upper or lower eyelid can be involved, and one or both eyes may be affected. When entropion occurs in both eyes, this is known as "bilateral entropion." Repeated cases of trachoma infection may cause scarring of the inner eyelid, which may cause entropion. In human cases, this condition is most common to people over 60 years of age.

Ptosis occurs due to dysfunction of the muscles that raise the eyelid or their nerve supply (oculomotor nerve for levator palpebrae superioris and sympathetic nerves for superior tarsal muscle). It can affect one eye or both eyes and is more common in the elderly, as muscles in the eyelids may begin to deteriorate. One can, however, be born with ptosis. Congenital ptosis is hereditary in three main forms. Causes of congenital ptosis remain unknown. Ptosis may be caused by damage/trauma to the muscle which raises the eyelid, damage to the superior cervical sympathetic ganglion or damage to the nerve (3rd cranial nerve (oculomotor nerve)) which controls this muscle. Such damage could be a sign or symptom of an underlying disease such as diabetes mellitus, a brain tumor, a pancoast tumor (apex of lung) and diseases which may cause weakness in muscles or nerve damage, such as myasthenia gravis or Oculopharyngeal muscular dystrophy. Exposure to the toxins in some snake venoms, such as that of the black mamba, may also cause this effect.

Ptosis can be caused by the aponeurosis of the levator muscle, nerve abnormalities, trauma, inflammation or lesions of the lid or orbit. Dysfunctions of the levators may occur as a result of autoimmune antibodies attacking and eliminating the neurotransmitter.

Ptosis may be due to a myogenic, neurogenic, aponeurotic, mechanical or traumatic cause and it usually occurs isolated, but may be associated with various other conditions, like immunological, degenerative, or hereditary disorders, tumors, or infections

Acquired ptosis is most commonly caused by aponeurotic ptosis. This can occur as a result of senescence, dehiscence or disinsertion of the levator aponeurosis. Moreover, chronic inflammation or intraocular surgery can lead to the same effect. Also, wearing contact lenses for long periods of time is thought to have a certain impact on the development of this condition.

Congenital neurogenic ptosis is believed to be caused by the Horner syndrome. In this case, a mild ptosis may be associated with ipsilateral ptosis, iris and areola hypopigmentation and anhidrosis due to the paresis of the Mueller muscle. Acquired Horner syndrome may result after trauma, neoplastic insult, or even vascular disease.

Ptosis due to trauma can ensue after an eyelid laceration with transection of the upper eyelid elevators or disruption of the neural input.

Other causes of ptosis include eyelid neoplasms, neurofibromas or the cicatrization after inflammation or surgery. Mild ptosis may occur with aging.

A drooping eyelid can be one of the first signals of a third nerve palsy due to a cerebral aneurysm, that otherwise is asymptomatic and referred to as an oculomotor nerve palsy.

Nocturnal lagophthalmos is the inability to close the eyelids during sleep. It may reduce the quality of sleep, cause exposure-related symptoms or, if severe, cause corneal damage (exposure keratopathy). The degree of lagophthalmos can be minor (obscure lagophthalmos), or quite obvious.

It is often caused by an anomaly of the eyelid that prevents full closure. Treatment may involve surgery to correct the malposition of the eyelid(s). Punctal plugs may be used to increase the amount of lubrication on the surface of the eyeball by blocking some of the tear drainage ducts. Eye drops may also be used to provide additional lubrication or encourage the eyes to increase tear production.

The condition is not widely understood; in at least one instance a passenger was removed from a US Airways flight because of it.

Marcus Gunn phenomenon, also known as Marcus Gunn jaw-winking or trigemino-oculomotor synkinesis, is an autosomal dominant condition with incomplete penetrance, in which nursing infants will have rhythmic upward jerking of their upper eyelid. This condition is characterized as a synkinesis: when two or more muscles that are independently innervated have either simultaneous or coordinated movements.

Common physiologic examples of synkineses occur during sucking, chewing, or conjugate eye movements. There are also several abnormal cranial nerve synkineses, both acquired and congenital. Marcus Gunn jaw-winking is an example of a pathologic congenital synkinesis.

First described by the ophthalmologist Marcus Gunn in 1883, this condition presents in approximately 5% of neonates with congenital ptosis. This condition has been associated with amblyopia (in 54% of cases), anisometropia (26%), and strabismus (56%).

Entropion has been documented in most dog breeds, although there are some breeds (particularly purebreds) that are more commonly affected than others. These include the Akita, Pug, Chow Chow, Shar Pei, St. Bernard, Cocker Spaniel, Boxer, English Springer Spaniel, Welsh Springer Spaniel, Labrador Retriever, Cavalier King Charles Spaniel, Neapolitan Mastiff, Bull Mastiff, Great Dane, Irish Setter, Shiba Inu, Rottweiler, Poodle and particularly Bloodhound. The condition is usually present by six months of age. If left untreated, the condition can cause such trauma to the eye that it will require removal.

Entropion has also been seen in cat breeds. Typically it is secondary to trauma, or infection leading to chronic eyelid changes. It is also seen secondary to enophthalmos. Congenital cases are also seen with the brachicephalic breeds being over represented.

Upper lid entropion involves the eyelashes rubbing on the eye, but the lower lid usually has no eyelashes, so little or no hair rubs on the eye. Surgical correction is used in more severe cases. A number of techniques for surgical correction exist. The Hotz-Celsus technique involves the removal of strip of skin and orbicularis oculi muscle parallel to the affected portion of the lid and then the skin is sutured.

Alternative techniques such as the Wyman technique focus on tightening the lower eyelid, this technique is not as effective in cases of enophthalmos.

Shar Peis, who often are affected as young as two or three weeks old, respond well to temporary eyelid tacking. The entropion is often corrected after three to four weeks, and the sutures are removed.

Blepharophimosis syndrome is an autosomal dominant characterized by blepharophimosis (horizontal shortening of the palpebral fissures), ptosis (upper eyelid drooping, usually with the characteristics of congenital ptosis), epicanthus inversus (skin folds by the nasal bridge, more prominent lower than upper lid), and telecanthus (widening of the distance between the medial orbital walls). This syndrome is caused by mutations in the FOXL2 gene, either with premature ovarian failure (BPES type I) or without (BPES type II). It may also be associated with lop ears, ectropion, hypoplasia of superior orbital rims, and hypertelorism.

Controversies exist around eliminating this disorder from breeding Collies. Some veterinarians advocate only breeding dogs with no evidence of disease, but this would eliminate a large portion of potential breeding stock. Because of this, others recommend only breeding mildly affected dogs, but this would never completely eradicate the condition. Also, mild cases of choroidal hypoplasia may become pigmented and therefore undiagnosable by the age of three to seven months. If puppies are not checked for CEA before this happens, they may be mistaken for normal and bred as such. Checking for CEA by seven weeks of age can eliminate this possibility. Diagnosis is also difficult in dogs with coats of dilute color because lack of pigment in the choroid of these animals can be confused with choroidal hypoplasia. Also, because of the lack of choroidal pigment, mild choroidal hypoplasia is difficult to see, and therefore cases of CEA may be missed.

Until recently, the only way to know if a dog was a carrier was for it to produce an affected puppy. However, a genetic test for CEA became available at the beginning of 2005, developed by the Baker Institute for Animal Health, Cornell University, and administered through OptiGen. The test can determine whether a dog is affected, a carrier, or clear, and is therefore a useful tool in determining a particular dog's suitability for breeding.

It is known to occur in Scotch Collies (smooth and rough collies), Shetland Sheepdogs, Australian Shepherds, Border Collies, Lancashire Heelers, and Nova Scotia Duck Tolling Retrievers. Frequency is high in Collies and Shetland Sheepdogs, and low in Border Collies and NSDTRs. In the United States, incidence in the genotype of collies has been estimated to be as high as 95 percent, with a phenotypic incidence of 80 to 85 percent.

Cherry eye is a disorder of the nictitating membrane (NM), also called the third eyelid, present in the eyes of dogs and cats. Cherry eye is most often seen in young dogs under the age of two. Common misnomers include adenitis, hyperplasia, adenoma of the gland of the third eyelid; however, cherry eye is not caused by hyperplasia, neoplasia, or primary inflammation. In many species, the third eyelid plays an essential role in vision by supplying oxygen and nutrients to the eye via tear production. Normally, the gland can evert without detachment. Cherry eye results from a defect in the retinaculum which is responsible for anchoring the gland to the periorbita. This defect causes the gland to prolapse and protrude from the eye as a red fleshy mass. Problems arise as sensitive tissue dries out and is subjected to external trauma Exposure of the tissue often results in secondary inflammation, swelling, or infection. If left untreated, this condition can lead to Keratoconjunctivitis sicca (KCS) and other complications.

Lagophthalmos is the inability to close the eyelids completely.

Blinking covers the eye with a thin layer of tear fluid, thereby promoting a moist environment necessary for the cells of the exterior part of the eye. The tears also flush out foreign bodies and wash them away. This is crucial to maintain lubrication and proper eye health. If this process is impaired, as in lagophthalmos, the eye can suffer abrasions and infections. Lagopthalmos leads to corneal drying and ulceration.

Congenital cystic eye (also known as "CCE" or "cystic eyeball") is an extremely rare ocular malformation where the eye fails to develop correctly "in utero" and is replaced by benign, fluid-filled tissue. Its incidence is unknown, due to the very small number of cases reported. An audit by Duke-Elder of the medical literature from 1880 to 1963 discovered only 28 cases. The term was coined in 1937 by the renowned ophthalmologist Ida Mann.

Embryologically, the defect is thought to occur around day 35 of gestation, when the vesicle fails to invaginate. Dysgenesis of the vesicle later in development may result in coloboma, a separate and less severe malformation of the ocular structures.

CCE is almost always unilateral, but at least 2 cases of bilateral involvement have been described. Patients may also present with skin appendages attached to the skin surrounding the eyes. Association with intracranial anomalies has been reported.

Treatment of CCE is usually by enucleation, followed by insertion of an ocular implant and prosthesis.