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Fundamentals Of Glaucoma: A Guide For Ophthalmic Nurse Practitioners, Optometrists And Orthoptists. Группа авторов
Читать онлайн.Название Fundamentals Of Glaucoma: A Guide For Ophthalmic Nurse Practitioners, Optometrists And Orthoptists
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isbn 9789811216466
Автор произведения Группа авторов
Жанр Медицина
Издательство Ingram
Secondary Angle Closure
Secondary angle closure may be generated by any swelling of the posterior chamber of the eye, for example; iris/ciliary body/choroidal tumours, choroidal effusions secondary to chorio-retinal inflammation/scleritis or choroidal haemorrhage. Treatment is directed towards removing the provoking stimulus if possible.
It can also be caused by intraocular inflammation, whereby adhesions between the peripheral iris and the cornea (known as peripheral anterior synechiae) can contract and close the iridocorneal angle. This mechanism is also seen with fibrovascular sheets that can develop within the iridocorneal angle in neovascular glaucoma and close the angle.
The use of the anti-epileptic medication, Topiramate, can cause bilateral ciliary body oedema, thereby causing angle closure. Treatment is directed towards cessation of Topiramate and medical control of the intraocular pressure until the oedema resolves.
OPEN ANGLE GLAUCOMA
Primary Open Angle Glaucoma (POAG)
Primary open angle glaucoma is the most frequently diagnosed of the glaucoma syndromes. Patients are usually asymptomatic until the later stages of their disease, unless a paracentral scotoma is present. In the absence of other neurological reasons for the visual impairment, the diagnosis is made by a triad of clinical signs:
•Open angles gonioscopically.
•Glaucomatous damage to the optic nerve with corresponding field defect.
•Raised intraocular pressure (>21 mmHg).
The clinical signs and resulting visual field defects are discussed in more detail in later chapters.
Treatment is aimed at reducing the intraocular pressure either medically (drops), by laser (SLT/ALT), or surgically (e.g. trabeculectomy or aqueous shunt device). Reducing the IOP has been shown to reduce progression of glaucomatous field defects.
Prognosis is important to discuss with the patient when first diagnosing the condition and may be the source of concerns at future visits. Most POAG patients will not go blind within their lifetime due to glaucoma if the condition is optimally managed.
Normal Tension Glaucoma (NTG)
Normal tension glaucoma is a variant of POAG where glaucomatous damage to the optic nerve occurs at ‘normal’ pressures. The central corneal thickness must be accounted for, which, if significantly below 520 μm, can mean that the Goldmann pressure measurement is significantly underestimated. Also consider that if the patient is on a systemic beta blocker there will be some IOP lowering effect of this medication, thereby taking a previously diagnosed NTG patient into a pressure range in keeping with POAG. Visual field defects close to fixation are more common in this cohort of patients.
The differential diagnosis of glaucoma must be considered before a final diagnosis of NTG is made, and the practitioner must be confident that the probability of alternative etiologies is as low as possible, by careful history taking and thorough clinical examination.
Differential diagnosis:
•Progressive structural neurological disease — can be effectively ruled out with MRI brain.
•Previous anterior ischaemic optic neuropathy.
•Previous neurological insult, such as severe head trauma or septicemic shock, which results in either compressive or ischaemic optic nerve damage.
•Previously raised IOP e.g. due to acute anterior uveitis, or steroid use (peri-ocularly or systemically at high dose).
Pressure lowering is of benefit for some patients, but significant progression of visual field loss can still occur with pressures in the mid-teens. If a 30% reduction in IOP from the baseline is achieved, 80% of patients achieve stability and no progression of their visual field defects.
Secondary Open Angle Glaucoma
This may be classified based on the site of the anatomical abnormality causing raised intraocular pressure as follows:
•Trabecular Secondary Open Angle Glaucoma
This is caused by dysfunction of the trabeculum. The trabecular meshwork may be obstructed by deposited material such as pseudoexfoliation, pigment from pigment dispersion or lens protein from phacolytic glaucoma.
Pseudoexfoliation glaucoma is an important diagnosis to make for both prognostic reasons and for surgical planning. The signs and symptoms are discussed in the clinical examination chapter. A fine filamentous deposit is lain down on the internal structures of the eye. This clogs the trabecular meshwork and weakens the zonular fibres.
The trabeculum can become inflamed especially in herpetic disease (Herpes zoster) or in Posner-Schlossman syndrome. These conditions usually respond well to administration of topical steroids.
The trabeculum can become dysfunctional due to the administration of steroids, either topically or systemically. This causes a secondary pressure increase and may result in glaucomatous nerve damage if left untreated. Patients with POAG appear to be more sensitive to developing steroid-response pressure rises.
•Post-trabecular Secondary Open Angle Glaucoma
Increased episcleral venous pressure causes increased intraocular pressure. If the pressure is too high for too long, ganglion cell damage can occur. Examples of diseases causing raised episcleral venous pressure are: carotid-cavernous fistula, dysthyroid orbitopathy and Sturge-Weber Syndrome. If the underlying causative pathology can be treated, the IOP can normalize, and glaucomatous field damage progression can be halted.
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