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Keratic Precipitates (KP)

What is Keratic precipitates?

Keratic precipitates, abbreviated as KP, are tiny deposits of inflammatory cells, protein, and pigment that settle on the inner surface of the cornea (the posterior corneal epithelium). They appear as small, white‑to‑brown specks that can be seen during a slit‑lamp examination. KP are not a disease themselves; rather, they are a sign that the eye’s anterior chamber (the fluid‑filled space between the cornea and iris) is inflamed, a condition known as anterior uveitis or iridocyclitis.

Because the cornea is transparent, the presence of KP can be one of the earliest clues that an ocular inflammatory process is occurring, even before a patient notices visual changes. The type, size, and distribution of KP give clinicians valuable information about the underlying cause and the duration of the inflammation.

Common Causes

KP may be seen in a wide range of eye disorders, systemic diseases, and infections. The most frequent culprits include:

• Anterior uveitis (idiopathic or autoimmune) – the leading cause of KP.
• Herpes simplex virus (HSV) keratouveitis – viral infection of the cornea and iris.
• Herpes zoster (shingles) ophthalmicus – reactivation of VZV in the ophthalmic branch.
• Sarcoidosis – granulomatous disease that can involve the eye.
• Behçet’s disease – systemic vasculitis with recurrent oral/genital ulcers and ocular inflammation.
• Syphilis (secondary or tertiary) – spirochetal infection presenting with uveitis.
• Toxoplasmosis – parasitic infection often causing posterior segment disease, but anterior involvement can produce KP.
• Traumatic or post‑surgical inflammation – e.g., after cataract extraction or penetrating trauma.
• Intra‑ocular lens (IOL) implantation complications – especially if the lens material triggers inflammation.
• Systemic autoimmune conditions – such as rheumatoid arthritis, systemic lupus erythematosus, and ankylosing spondylitis.

Associated Symptoms

Keratic precipitates rarely appear in isolation. They are usually accompanied by other signs of ocular inflammation, including:

• Redness of the eye (conjunctival injection)
• Pain or a deep, aching sensation
• Photophobia (sensitivity to light)
• Blurred or decreased vision
• Tearing or watery discharge
• Pupil irregularities – typically a smaller, sluggish pupil (miotic pupil)
• Floaters – small moving specks in the visual field, indicating vitreous inflammation
• Eye pressure changes – either elevated (secondary glaucoma) or low (due to ciliary body shutdown)

When to See a Doctor

Any new eye redness, pain, or visual disturbance warrants prompt evaluation. Seek medical care especially if you notice:

• Sudden worsening of vision or a “black spot” in the visual field.
• Severe eye pain that does not improve with over‑the‑counter lubricants.
• Photophobia that interferes with daily activities.
• Persistent redness lasting more than 24–48 hours.
• History of systemic autoimmune disease or recent infection.
• Recent eye surgery or trauma.

Early assessment can prevent complications such as synechiae (iris‑cornea adhesions), cataract formation, or secondary glaucoma.

Diagnosis

Diagnosing the underlying cause of KP involves a step‑wise approach:

1. Comprehensive eye exam – slit‑lamp biomicroscopy is the gold standard for visualizing KP, grading their size (small, medium, large) and distribution (diffuse, mutton‑fat, granulomatous).
2. Pupil examination – checking for irregularities, relative afferent pupillary defect, or posterior synechiae.
3. Intra‑ocular pressure (IOP) measurement – using tonometry to rule out pressure spikes.
4. Fundus examination – indirect ophthalmoscopy to assess posterior segment involvement (e.g., vitritis, retinal lesions).
5. Laboratory work‑up (guided by history):
   • Serologic tests for syphilis (RPR/VDRL, FTA‑ABS).
   • HLA‑B27 typing if ankylosing spondylitis or related spondyloarthropathies are suspected.
   • ACE level and chest imaging for sarcoidosis.
   • Lyme serology, TB Quantiferon, or PCR of aqueous humor when specific infections are in the differential.
6. Imaging – ultrasound B‑scan or anterior segment OCT may be used if media opacity precludes direct view.
7. Anterior chamber tap (rare) – acquiring fluid for PCR or culture when infectious uveitis is strongly suspected and the patient is not responding to empiric therapy.

References: American Academy of Ophthalmology (AAO) Preferred Practice Pattern for uveitis; Mayo Clinic, “Uveitis.”

Treatment Options

Treatment is directed at two goals: (1) suppressing inflammation and (2) addressing the underlying cause.

Medical Therapy

• Topical corticosteroids – prednisolone acetate 1% (Pred Forte) or difluprednate 0.05% are first‑line for acute anterior uveitis. Tapered over weeks based on response.
• Cycloplegic agents – homatropine or cyclopentolate to relieve ciliary spasm, prevent synechiae, and improve comfort.
• Non‑steroidal anti‑inflammatory drugs (NSAIDs) – topical NSAIDs (e.g., ketorolac) can adjunctively reduce inflammation.
• Systemic steroids – oral prednisone (0.5–1 mg/kg) for severe or bilateral disease, or when posterior segment involvement is present.
• Immunomodulatory therapy (IMT) – agents such as methotrexate, mycophenolate mofetil, or biologics (adalimumab) for chronic or recurrent uveitis, especially when associated with systemic autoimmune disease.
• Antiviral therapy – oral acyclovir or valacyclovir for HSV/VZV keratouveitis; topical antivirals may be added.
• Antibiotics/antiparasitics – doxycycline for suspected toxoplasmosis, or intravitreal clindamycin in severe cases.
• Antitubercular therapy – when ocular TB is confirmed, a standard 6‑month regimen (isoniazid, rifampin, ethambutol, pyrazinamide) is required.

Procedural / Surgical Management

• Peripheral iridectomy – performed when secondary glaucoma is due to angle closure from synechiae.
• Trabeculectomy or glaucoma drainage devices – for uncontrolled IOP despite medical therapy.
• Laser photocoagulation – used for retinal neovascularization that can accompany chronic inflammation.

Home / Supportive Care

• Artificial tears (preservative‑free) to alleviate dryness and discomfort.
• Cold compresses for pain relief (no ice directly on the eye).
• Shield the eye at night to prevent accidental rubbing.
• Strict adherence to medication schedule – missing doses can cause flare‑ups.

Prevention Tips

While not all cases of KP are preventable, several strategies can reduce risk:

• Control systemic autoimmune conditions with regular rheumatology follow‑up.
• Promptly treat ocular infections (herpes, bacterial, fungal) before they become chronic.
• Follow postoperative eye‑care instructions after surgery; use prescribed drops as directed.
• Avoid eye rubbing, especially if you have allergic conjunctivitis or contact lens wear.
• Maintain good hygiene with contact lenses – daily cleaning, proper storage, and discarding as recommended.
• Stay up to date on vaccinations (e.g., shingles vaccine) to lower the chance of viral reactivation.
• Regular eye examinations (at least once every 1–2 years) for people with known risk factors.

Emergency Warning Signs

If you experience any of the following, seek emergency ophthalmic care immediately (e.g., go to an eye‑care emergency department or call 911):

• Sudden, severe eye pain unrelieved by medication.
• Rapid loss of vision or a large “shadow”/blackout in part of the visual field.
• Marked swelling of the eyelids or surrounding face.
• Onset of double vision (diplopia) with eye pain.
• Signs of high intra‑ocular pressure: halos around lights, headache, nausea/vomiting.
• History of recent eye trauma with persistent redness or discharge.

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© 2026 HealthCheck.org – All content reviewed by board‑certified ophthalmologists and based on current guidelines from the American Academy of Ophthalmology, Mayo Clinic, and the National Institutes of Health.

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