Wednesday, November 5, 2014

Opthalmologist sees cells 11/3

Follow up 1 week RE; iritis/uevitis.

Interesting video on DNA Pinterest board...

 The uveal tract is the highly vascular and densely pigmented layer of the eyeball, lying between the sclera (superficial to it) and the retina (deep to it).

The anterior, visible portion is the iris. This extends back into the ciliary body (at the level of the lens) and then extends round to the posterior pole, where it is known as the choroid.

Uveitis means inflammation at any point of the uveal tract, with or without inflammation of neighbouring structures (eg, the retina or vitreous).[1]


About 50% of patients with acute anterior uveitis are HLA-B27 positive. Nongranulomatous disease can be associated with:

The only group of patients currently screened for uveitis is children with juvenile idiopathic arthritis.

Management[2][7] 

If uveitis is suspected, immediate specialist referral is appropriate to confirm diagnosis and facilitate treatment. Delay in appropriate management can lead to the development of significant complications and irreversible loss of vision. Exact treatment is determined by the type of uveitis (anterior versus posterior), whether the uveitis is secondary to an infection or not and whether it is likely to threaten sight. All patients with anterior disease and most with intermediate or posterior disease require treatment. For patients with systemic disease, a collaborative approach between ophthalmologists and other specialities is important.

Refer people with suspected uveitis for an assessment by an ophthalmologist within 24 hours. Also refer people who have had uveitis before and feel the symptoms coming on before the signs are present. Do not initiate treatment for recurrent uveitis in primary care, unless asked to do so by an ophthalmologist.

  • Corticosteroids are used to reduce inflammation and prevent adhesions in the eye. They may be given topically, orally, intravenously, intramuscularly, or by peri-ocular or intra-ocular injection, depending on the severity of the uveitis. Corticosteroids are reduced slowly, as withdrawing them too quickly may lead to rebound inflammation.
  • A cycloplegic-mydriatic drug (for example, cyclopentolate 1% or atropine 1%) is also given to paralyse the ciliary body. This relieves pain and prevents adhesions between the iris and lens.
  • Infectious uveitis (bacterial, viral, fungal, or parasitic) is treated with an appropriate antimicrobial drug as well as corticosteroids and cycloplegics.
  • People with severe or chronic uveitis may also be given systemic (non-corticosteroid) immunosuppressive drugs, laser phototherapy, or cryotherapy, or have the vitreous removed surgically (vitrectomy).

Adjunctive therapy

  • Secondary causes should be treated as appropriate. Where there is an infection, this needs to be treated as a priority.[2] (See the separate article on Chorioretinal Inflammation for more details about treatment of ocular toxoplasmosis.)
  • Ongoing research is looking at the use of immune modulators such as tumour necrosis factor alpha-blockers (eg, etanercept, infliximab) and the interleukin-2 receptor blockers. A number of studies on less invasive sustained ocular drug delivery systems, including episcleral implants, nanospheres, and cyclodextrin particles are being conducted.[9] Interferon alfa may also have potential in treating refractory sight-threatening uveitis from a variety of causes.[10]
  • Azathioprine has been found to be useful in steroid-resistant autoimmune uveitis.[11] Ciclosporin and tacrolimus have also been investigated and have been shown to be associated with control of ocular inflammation and preservation or restoration of sight. However, currently immunosuppressive treatment has not been licensed for uveitis.
  • There may be a role for the family of anti-vascular endothelial growth factor drugs (eg, ranibizumab, Lucentis®, which is currently used for 'wet' age-related macular degeneration) in managing chronic, non-infective uveitis but these drugs are not yet licensed for this use.[2]Furthermore, any intravitreal injection carries a small inherent risk of complications (including sight loss) in itself.

Surgery

Surgery is only considered in a small proportion of patients with severe or intractable disease or where a diagnostic vitreous sample is required (eg, to diagnose infection or malignancy). Other reasons for surgery include removal of a secondary cataract or for preservation of vision in uveitic glaucoma.[2]

Monitoring the disease[3]

  • This is almost entirely by clinical examination but some investigations provide a useful adjunct.
  • Optical coherence tomography (OCT) is very helpful in looking for macular causes of worsening vision, particularly where slit-lamp view is not good.
  • Fluorescein angiography is helpful where retinal vascular involvement needs to be assessed. Visual fields are also helpful for monitoring optic nerve damage.

Visual loss as a result of:[2]

  • Cystoid macular oedema (swelling of the macula) - this is the leading cause of visual loss in the UK along with secondary cataract formation.
  • Secondary cataract.
  • Acute rise in intraocular pressure, with or without glaucoma:
    • This may occur either as a direct consequence of the inflammatory process or secondary to steroid treatment.
    • Some patients, especially those with a history of glaucoma, are prone to developing high intraocular pressure as a result of steroid treatment and require treatment to reduce the intraocular pressure. Treatment to reduce intraocular pressure can be stopped when the steroid treatment is stopped if the patient doesn't have pre-existing glaucoma.
  • Vitreous opacities (inflammatory debris or haemorrhage).
  • Retinal detachment.
  • Neovascularisation of the retina, optic nerve, or iris.
  • Macular ischaemia, vascular occlusions and optic neuropathy - can be complications of posterior uveitis.

Posterior synechiae are a common complication of anterior uveitis; if numerous they can cause blockage of the aqueous flow, leading to a rise in intra-ocular pressure, and can complicate cataract operations

  • Anterior uveitis is sometimes a self-limiting condition.
  • With prompt and effective treatment, there is usually a good visual outcome (a study found that 91% of these patients retain normal vision).[2]
  • The factors which cause spontaneous resolution in some patients and complications in others are unclear.[12]
  • Relapse after a first episode of acute anterior uveitis is probably more common than previously thought - a recent study suggested an incidence of about 24% per person-year, this occurring more commonly in the younger patient age group (18-35 year-olds).[13]
  • The prognosis of chronic granulomatous uveitis depends on the cause and whether the underlying condition is recognised and treated early enough.
  • Outcomes have been improved by the use of immune modulators in previously refractory cases.[14]

http://www.patient.co.uk/doctor/uveitis#nav-6

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