Symptoms of entropion include:

- Redness and pain around the eye

- Sensitivity to light and wind

- Sagging skin around the eye

- Epiphora

- Decreased vision, especially if the cornea is damaged

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.

Epiphora is an overflow of tears onto the face. A clinical sign or condition that constitutes insufficient tear film drainage from the eyes in that tears will drain down the face rather than through the nasolacrimal system.

Diagnosis of epiphora is clinical by history presentation and observation of the lids. Fluorescein dye can be used to examine for punctal reflux by pressing on the canaliculi in which the clinician should note resistance of reflux as it irrigates through the punctum into the nose.

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.

Dermatochalasis is caused by a loss of elasticity in the connective tissue supporting the structure of the front portion of the eyelid. Normally, in Caucasians, the orbicularis muscle and overlying skin form a crease near the tarsal border. In dermatochalasis, the excess tissues hangs down, over the front edge of the eyelid. The excess tissue can sometimes obstruct the visual field, especially the superior visual field. In severe cases, it may obstruct as much as 50 percent of the superior visual field.

With anterior lens luxation, the lens pushes into the iris or actually enters the anterior chamber of the eye. This can cause glaucoma, uveitis, or damage to the cornea. Uveitis (inflammation of the eye) causes the pupil to constrict (miosis) and trap the lens in the anterior chamber, leading to an obstruction of outflow of aqueous humour and subsequent increase in ocular pressure (glaucoma). Better prognosis is valued in lens replacement surgery (retained vision and normal intraocular pressure) when it is performed before the onset of secondary glaucoma. Glaucoma secondary to anterior lens luxation is less common in cats than dogs due to their naturally deeper anterior chamber and the liquification of the vitreous humour secondary to chronic inflammation. Anterior lens luxation is considered to be an ophthalmological emergency.

Lens subluxation is also seen in dogs and is characterized by a partial displacement of the lens. It can be recognized by trembling of the iris (iridodonesis) or lens (phacodonesis) and the presence of an aphakic crescent (an area of the pupil where the lens is absent). Other signs of lens subluxation include mild conjunctival redness, vitreous humour degeneration, prolapse of the vitreous into the anterior chamber, and an increase or decrease of anterior chamber depth. Removal of the lens before it completely luxates into the anterior chamber may prevent secondary glaucoma. A nonsurgical alternative involves the use of a miotic to constrict the pupil and prevent the lens from luxating into the anterior chamber.

Corneal ulcers are extremely painful due to nerve exposure, and can cause tearing, squinting, and vision loss of the eye. There may also be signs of anterior uveitis, such as miosis (small pupil), aqueous flare (protein in the aqueous humour), and redness of the eye. An axon reflex may be responsible for uveitis formation—stimulation of pain receptors in the cornea results in release inflammatory mediators such as prostaglandins, histamine, and acetylcholine.

Sensitivity to light (photophobia) is also a common symptom of corneal ulcer.

Blepharochalasis results from recurrent bouts of painless eyelid swelling, each lasting for several days. This is thought to be a form of localized angioedema, or rapid accumulation of fluid in the tissues. Recurrent episodes lead to thin and atrophic skin. Damage to the levator palpebrae superioris muscle causes ptosis, or drooping of the eyelid, when the muscle can no longer hold the eyelid up.

Dermatochalasis is sometimes confused with blepharochalasis, but these are two different conditions.

It is a characterized by a breakdown or damage of the epithelium of the cornea in a pinpoint pattern, which can be seen with examination with a slit-lamp. Patients may present with non-specific symptoms such as red eye, tearing, foreign body sensation, photophobia and burning.

Corneal ulcers are a common human eye disease. They are caused by trauma, particularly with vegetable matter, as well as chemical injury, contact lenses and infections. Other eye conditions can cause corneal ulcers, such as entropion, distichiasis, corneal dystrophy, and keratoconjunctivitis sicca (dry eye).

Many micro-organisms cause infective corneal ulcer. Among them are bacteria, fungi, viruses, protozoa, and chlamydia:

- Bacterial keratitis is caused by "Staphylococcus aureus", "Streptococcus viridans", "Escherichia coli", "Enterococci", "Pseudomonas", "Nocardia", "N. Gonorrhoea" and many other bacteria.

- Fungal keratitis causes deep and severe corneal ulcer. It is caused by "Aspergillus" sp., "Fusarium" sp., "Candida" sp., as also "Rhizopus", "Mucor", and other fungi. The typical feature of fungal keratitis is slow onset and gradual progression, where signs are much more than the symptoms. Small satellite lesions around the ulcer are a common feature of fungal keratitis and hypopyon is usually seen.

- Viral keratitis causes corneal ulceration. It is caused most commonly by Herpes simplex, Herpes zoster and Adenoviruses. Also it can be caused by coronaviruses & many other viruses. Herpes virus cause a dendritic ulcer, which can recur and relapse over the lifetime of an individual.

- Protozoa infection like "Acanthamoeba keratitis" is characterized by severe pain and is associated with contact lens users swimming in pools.

- "Chlamydia trachomatis" can also contribute to development of corneal ulcer.

Superficial ulcers involve a loss of part of the epithelium. Deep ulcers extend into or through the stroma and can result in severe scarring and corneal perforation. Descemetoceles occur when the ulcer extends through the stroma. This type of ulcer is especially dangerous and can rapidly result in corneal perforation, if not treated in time.

The location of the ulcer depends somewhat on the cause. Central ulcers are typically caused by trauma, dry eye, or exposure from facial nerve paralysis or exophthalmos. Entropion, severe dry eye and trichiasis (inturning of eyelashes) may cause ulceration of the peripheral cornea. Immune-mediated eye disease can cause ulcers at the border of the cornea and sclera. These include Rheumatoid arthritis, rosacea, systemic sclerosis which lead to a special type of corneal ulcer called Mooren's ulcer. It has a circumferential crater like depression of the cornea, just inside the limbus, usually with an overhanging edge.

Punctate epithelial erosions may be seen with different disorders:

- Rosacea

- Dry-eye syndrome

- Blepharitis

- Acute bacterial conjunctivitis

- Trauma

- Exposure keratopathy from poor eyelide closure

- Ultraviolet or chemical burn

- Contact lens-related disorder such as toxicity or tight lens syndrome

- Trichiasis

- Entropion or ectropion

- Floppy eyelid syndrome

- Chemotherapy i.e. cytosine arabinoside

- Thygeson's Superficial Punctate Keratopathy

The bacterium has an incubation period of 5 to 12 days, after which the affected individual experiences symptoms of conjunctivitis, or irritation similar to "pink eye." Blinding endemic trachoma results from multiple episodes of reinfection that maintains the intense inflammation in the conjunctiva. Without reinfection, the inflammation will gradually subside.

The conjunctival inflammation is called “active trachoma” and usually is seen in children, especially pre-school children. It is characterized by white lumps in the undersurface of the upper eyelid (conjunctival follicles or lymphoid germinal centres) and by non-specific inflammation and thickening often associated with papillae. Follicles may also appear at the junction of the cornea and the sclera (limbal follicles). Active trachoma will often be irritating and have a watery discharge. Bacterial secondary infection may occur and cause a purulent discharge.

The later structural changes of trachoma are referred to as “cicatricial trachoma”. These include scarring in the eyelid (tarsal conjunctiva) that leads to distortion of the eyelid with buckling of the lid (tarsus) so the lashes rub on the eye (trichiasis). These lashes will lead to corneal opacities and scarring and then to blindness. Linear scar present in the Sulcus subtarsalis is called Arlt's line (named after Carl Ferdinand von Arlt). In addition, blood vessels and scar tissue can invade the upper cornea (pannus). Resolved limbal follicles may leave small gaps in pannus (Herbert’s Pits).

Most commonly children with active trachoma will not present with any symptoms as the low-grade irritation and ocular discharge is just accepted as normal. However, further symptoms may include:

- Eye discharge

- Swollen eyelids

- Trichiasis (turned-in eyelashes)

- Swelling of lymph nodes in front of the ears

- Sensitivity to bright lights

- Increased heart rate

- Further ear, nose and throat complications.

The major complication or the most important one is corneal ulcer occurring due to rubbing by concentrations, or trichiasis with superimposed bacterial infection.

About 60 percent of initial attacks of dacryocystitis will recur. Individuals with a poorly functioning immune system (immunocompromised) may develop orbital cellulitis, which may lead to optic neuritis, proptosis, motility abnormalities, or blindness.

Dacryocystitis is an infection of the lacrimal sac, secondary to obstruction of the nasolacrimal duct at the junction of lacrimal sac. The term derives from the Greek "dákryon" (tear), "cysta" (sac), and "-itis" (inflammation). It causes pain, redness, and swelling over the inner aspect of the lower eyelid and epiphora. When nasolacrimal duct obstruction is secondary to a congenital barrier it is referred to as dacrocystocele. It is most commonly caused by "Staphylococcus aureus" and "Streptococcus pneumoniae". The most common complication is corneal ulceration, frequently in association with "S. pneumoniae". The mainstays of treatment are oral antibiotics, warm compresses, and relief of nasolacrimal duct obstruction by dacryocystorhinostomy.

The World Health Organization recommends a simplified grading system for trachoma. The Simplified WHO Grading System is summarized below:

Trachomatous inflammation, follicular (TF)—Five or more follicles of >0.5 mm on the upper tarsal conjunctiva

Trachomatous inflammation, intense (TI)—Papillary hypertrophy and inflammatory thickening of the upper tarsal conjunctiva obscuring more than half the deep tarsal vessels

Trachomatous scarring (TS)—Presence of scarring in tarsal conjunctiva.

Trachomatous trichiasis (TT)—At least one ingrown eyelash touching the globe, or evidence of epilation (eyelash removal)

Corneal opacity (CO)—Corneal opacity blurring part of the pupil margin

CVG is classified according to the presence, or lack of underlying cause. Studies suggest that CVG often occurs in individuals in a secondary form to other ailments. However, the condition can also be present on its own. CVG can be classified into two forms: ‘primary’ (essential and non-essential) and ‘secondary’.

The classifications are:

Primary essential CVG is where the cause of the condition in unknown. It has no other associated abnormalities. This occurs mainly in men, with a male:female ratio of 5 or 6:1, and develops during or soon after puberty. Because of the slow progression of the condition, which usually occurs without symptom, it often passes unnoticed in the early stage

Primary non essential CVG can be associated with neuropsychiatric disorders including cerebral palsy, epilepsy, seizures and ophthalmologic abnormalities, most commonly cataracts.

Secondary CVG occurs as a consequence of a number of diseases or drugs that produce changes in scalp structure. These include: acromegaly (excessive growth hormone levels due to pituitary gland tumours), excessive drug use that mimics acromegaly (including the injection of growth hormone itself and drugs that stimulate growth hormone output, such as GHRP-6 and CJC-1295), melanocytic naevi (moles), birthmarks (including connective tissue naevi, fibromas and naevus lipomatosus), and inflammatory processes (e.g., eczema, psoriasis, Darier disease, folliculitis, impetigo, atopic dermatitis, acne).

Cutis verticis gyrata (CVG) is a medical condition usually associated with thickening of the scalp. People show visible folds, ridges or creases on the surface of the top of the scalp. The number of folds can vary from 2 to roughly 10 and are typically soft and spongy. These folds cannot be corrected with pressure. The condition typically affects the central and rear regions of the scalp, but sometimes can involve the entire scalp.

Hair loss can occur over time where the scalp thickens, though hair within any furrows remains normal. Thus far, due to the (apparent) rarity of the condition, limited research exists and causes are as yet undetermined. What is known, is that the condition is not exclusively congenital.

The condition was first reported by Alibert in 1837, who called it "cutis sulcata". A clinical description of the condition was provided by Robert in 1843 and was named by Unna in 1907. It has also been called "Robert-Unna syndrome", "bulldog scalp", "corrugated skin", "cutis verticis plicata", and "pachydermia verticis gyrata".

There are no objective physical examination findings that definitely diagnose ENS. Generally, one or more turbinates may be reduced or absent when viewed in medical imaging or via endoscope with no sign of physical obstruction, the mucosa will be dry and pale, and there may be signs of secondary infection.

Symptoms of ENS include a sensation of being unable to breathe, a feeling of nasal obstruction and dryness, and crusting, oozing, and foul smells inside the nose from infections. A person with ENS may complain of pain in their nose or face, an inability to sleep and fatigue, and of feeling irritated, depressed, or anxious; they may be constantly distracted by the sense that they are not getting enough air.

Empty nose syndrome (ENS), one form of secondary atrophic rhinitis, is a rare clinical syndrome in which people who have clear nasal passages experience a range of symptoms, most commonly feelings of nasal obstruction, nasal dryness and crusting, and a sensation of being unable to breathe. People who experience ENS have usually undergone a turbinectomy (removal or reduction of turbinates, structures inside the nose) or other surgical procedures that interfere with turbinates; the overall incidence is unknown but it appears to occur in a small percentage of those who undergo nasosinal procedures. It appears to be a health care caused condition but its existence as a medical condition, cause, diagnosis and management are controversial.

All aspects have been subject to debate, including whether it should be considered solely rhinologic, or may have neurological or psychosomatic aspects. As of 2015 many ear, nose, and throat doctors do not recognize the condition.

If there are symptoms, people with empty sella syndrome can have headaches, as symptoms, which subsides when lying down. Additional symptoms are as follows:

- Abnormality (middle ear ossicles)

- Cryptorchidism

- Dolichocephaly

- Arnold-Chiari type I malformation

- Meningocele

- Patent ductus arteriosus

- Muscular hypotonia

- Platybasia

There are two types of ESS: "primary" and "secondary".

- Primary ESS happens when a small anatomical defect above the pituitary gland increases pressure in the sella turcica and causes the gland to flatten out along the interior walls of the sella turcica cavity. Primary ESS is associated with obesity and increase in intracranial pressure in women.

- Secondary ESS is the result of the pituitary gland regressing within the cavity after an injury, surgery, or radiation therapy. Individuals with secondary ESS due to destruction of the pituitary gland have symptoms that reflect the loss of pituitary functions, such as intolerance to stress and infection.

Feline acne is a problem seen in cats primarily involving the formation of blackheads accompanied by inflammation on the cat's chin and surrounding areas that can cause lesions, alopecia, and crusty sores. In many cases symptoms are mild and the disease does not require treatment. Mild cases will look like the cat has dirt on its chin, but the dirt will not brush off. More severe cases, however, may respond slowly to treatment and seriously detract from the health and appearance of the cat. Feline acne can affect cats of any age, sex or breed, although Persian cats are also likely to develop acne on the face and in the skin folds. This problem can happen once, be reoccurring, or even persistent throughout the cat's life.

Sebaceous glands are skin glands that produce oil and are mostly found in the skin of the chin, at the base of the tail, and in the eyelids, lips, prepuce, and scrotum. They are connected to hair follicles. In acne, the follicles become clogged with black sebaceous material, forming comedones (also known as blackheads). Comedones can become irritated, swollen, infected, and ultimately pustules. These may elicit itching and discomfort due to swelling and bacterial growth inside infected glands. Cats may continue to scratch and reopen wounds, allowing bacterial infections to grow worse. Bacterial folliculitis occurs when follicules become infected with "Staphylococcus aureus", and commonly associated with moderate-to-severe feline acne. Secondary fungal infections (species "malassezia") may also occur.

Other conditions that can cause similar-appearing conditions include skin mites, ringworm, yeast infection, or autoimmune diseases such as eosinophilic granuloma complex ("rodent ulcers"). These can be ruled out by a simple biopsy of affected cells.

Feline acne is one of the top five most common skin conditions that veterinarians treat.