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Dit zijn bijvoorbeeld bestanden om de structuur van de website te verbeteren en persoonlijk advies te geven op basis van eerder gekochte artikelen. Skip to the end of the images gallery. Skip to the beginning of the images gallery. Bekijk online exemplaar. Inhoudsopgave Detailed table of contents. Tumours of the epithelium and adnexa. Benign tumours. Precancerous epithelial tumours. Malignant epithelial tumours. Pigmented tumours of the lids and the conjunctiva.
Benign pigmented tumours. Malignant melanomas of the eyelids and the conjunctiva. Xanthomatous tumours. Tuberous xanthoma of the lid. Juvenile xanthogranuloma of the eyelid and conjunctiva.
Vascular benign tumours. Palpebro-conjunctival lymphangiomas. Vascular malignant tumours. Kaposi's sarcoma. Tumours of adipose tissue. Lipoma of the conjunctiva. Palpebro-conjunctival tumours of nerve tissue.
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Merkel cell tumour. Dysgenetic tumours of the conjunctiva, lids and orbit. Dermoid cyst. Dermoid of the limbus and dermis-like choristoma. Complex choristoma.
Epibulbar osteoma. Inflammatory and degenerative pseudo-tumoral lesions. Pyogenic granuloma. Palpebro-conjunctival amyloidosis. Fibrohistiocytic tumours. Benign fibrohistiocytoma. Malignant fibrohistiocytoma. Corneal abrasions are usually the result of either trauma or an anatomic corneal defect that causes recurrent erosions. The overwhelming majority of patients will describe trauma with a foreign object immediately before the onset of symptoms. Patient with recurrent erosion from inadequate adhesion of the corneal epithelium to the basement membrane typically describe onset of tearing, pain and foreign body sensation upon awakening.
Conjunctival injection and a swollen eyelid may also be present. It is important to evert the upper lid to ensure there is no retained subtarsal foreign body. Topical antibiotic should be given four times per day for one week. Patching is generally not recommended and is contraindicated in contact lens wearers. Rapidity of healing depends on the size of the abrasion, but generally most abrasions heal in two to three days.
Fungal ulcers should be suspected in cases of corneal injury with plant material. Pain, redness, photophobia, and foreign body sensation are the usual symptoms. The physician should ask about contact lens use, swimming with contact lenses, trauma, and a foreign body to the eye. A white or yellowish-white infiltration of the cornea with fluorescein staining of the overlying epithelial defect is the key finding. Herpes viruses often have a dendrite like appearance to their epithelial defects.
An ophthalmologist should be consulted to obtain corneal cultures. If the patient is a contact lens wearer, their contact lens case and contact lens solution bottles should also be sent to the microbiology lab. An ophthalmologist should make this determination. Patients initially need daily follow-up to ensure the ulcer is improving and to rapidly implement the results of the cultures and sensitivities. If the ulcer is outside of the visual axis, recovery of vision is the norm.
If the ulcer is in the visual axis, scarring may limit vision and corneal transplantation may be necessary for visual rehabilitation. More than half of the cases of anterior uveitis are idiopathic. Blunt trauma can cause a self-limited form of the disease. Being HLA-B27 positive is most common systemic association among adults while juvenile idiopathic arthritis is more prevalent in children.
Sarcoidosis and other systemic inflammatory conditions can be causative even when the systemic signs of the illness have not yet appeared. Patients present with a painful red eye and photophobia. A review of systems to elicit history of associated systemic symptoms is crucial. Slit lamp examination needs to be performed to look for cell and flare in the anterior chamber.
Ocular Symptoms and Signs
Keratic precipitates, white cell deposits on the corneal endothelium, are a suggestive finding. If the patient has a unilateral uveitis without any history of systemic symptoms, no work-up is needed. If the uveitis is bilateral or recurrent, a systemic work-up is indicated and should be directed by findings from the review of systems.
Topical steroid is the usual treatment with the frequency of application dependent on the severity of disease. Cycloplegic drops such as scopolamine 0. Periocular steroid injections are needed in cases refractory to drop therapy. Oral steroid therapy is rarely needed; it is reserved for cases that are unresponsive to periocular steroid therapy. Of course, infectious causes should be treated with drops and the appropriate systemic antimicrobials.
Most initial episodes of unilateral anterior uveitis resolve within one or two weeks. If uveitis is recurrent, it may necessitate chronic immunomodulatory therapy and underlying systemic disease processes must be addressed. About half of the cases of scleritis are idiopathic. Infections are a much less common cause: corneal ulcer pathogens can extend onto the sclera.
Alternatively, some infections such as tuberculosis and Lyme disease can affect the sclera directly. Patients with scleritis describe severe, boring eye pain which often radiates to the forehead and head. This pain may keep them awake at night. Examination with natural light can reveal a bluish hue to the sclera along with dilation of blood vessels and redness.
These dilated vessels do not blanch with 2. Testing for the systemic disorders, directed by findings on history and exam, should be done in all cases of scleritis. Oral NSAIDs may be sufficient in milder cases, but oral steroids are often needed in moderate to severe cases. Recurrent scleritis may need systemic immunomodulatory therapy. Infectious causes are treated with systemic antibiotics. Scleritis can be a chronic disease requiring long term therapy. Patients need to be monitored for scleral thinning in areas of previous inflammation.
Patients with acute angle-closure glaucoma have a sudden onset of pain, blurred vision and halos around lights. They often have associated nausea, vomiting and headache. Increased intraocular pressure, a closed angle with a shallow anterior chamber, and corneal edema are the usual findings. These patients should be referred to an ophthalmologist for gonioscopy to confirm diagnosis. Treatment consists of intraocular pressure control with drops and laser peripheral iridectomy. Pterygia are caused by elastotic degeneration of the conjunctiva from exposure to sunlight and dry, windy conditions.
They are most commonly located on the inner corner of the eye. When they become inflamed, they cause burning, irritation and redness. On examination, an inflamed pterygium is a red, wing-shaped fibrovascular tissue that extends onto the cornea. Aggressive lubrication with artificial tears can often relieve symptoms. Pterygia that are in the visual axis and impairing vision can be removed surgically.
Inflammation can recur, and patients are advised to avoid dry, windy conditions that can exacerbate this. Amaurosis fugax is caused by an embolus, usually from the carotid artery. It can also result from atherosclerotic disease causing vascular insufficiency and ocular hypoperfusion with postural changes. Profound vision loss occurs in one eye and lasts seconds to minutes with vision returning to normal after episode. The ocular examination is usually normal. One may see an embolus in a retinal arteriole. The work-up should include a Doppler ultrasound of the carotid arteries and cardiac echocardiogram to look for an embolic source.
The patient should also have an assessment for atherosclerosis risk factors including lipid levels, fasting blood glucose, and a HBA1C.
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If carotid narrowing is present, the physician should consider referral for evaluation of endarterectomy. A daily aspirin, control of atherosclerotic risk factors and smoking cessation are also important. If a patient has recurrence despite a negative work-up, a more thorough evaluation is necessary immediately. This disease can be a precursor to a central artery occlusion which almost always causes permanent, profound vision loss.
Ocular migraine can cause a transient loss of vision and is not necessarily accompanied by headache and eye pain. The visual disturbance may be in the form of a visual field defect or flashes of light typical of a migraine aura. Brain imaging is indicated if migraines are atypical in any way, e.
Treatment is with anti-migraine medications such as sumatriptan. Identification and avoidance of precipitating factors such as certain foods may help the patient substantially. Most patients can achieve good control of their disease by anticipating migraine episodes by early symptoms and treating themselves before symptoms progress. Giant cell arteritis is an inflammation of medium sized arteries that affects primarily elderly, Caucasian patients.
Patients can present early with headaches and vague visual complaints or later with sudden painless vision loss. They may have concurrent systemic symptoms including jaw claudication, weight loss, and temporal headaches. Palpation of temporal arteries for tenderness and enlargement is important. The patient may not have any exam findings if symptoms are transient. An immediate sedimentation rate and C-reactive protein are required.
Temporal artery biopsy is needed in most cases to confirm the diagnosis. Immediate treatment with intravenous steroids followed by a slow taper of oral steroids over several months is usually necessary. Patients should have serial exams and ESRs during steroid taper to ensure no recurrence of inflammation.
Clinicians need to maintain a high level of suspicion for this disease in elderly patients with headaches and vague eye complaints because when the disease progresses it can cause rapid, profound, and irreversible vision loss. Dilated examination is most helpful but the view to the fundus may be limited to varying degrees by the hemorrhage.
If there is no view to fundus, an ultrasound is needed to rule out a retinal detachment. A fasting blood glucose and HBA1C should be done to rule out diabetes. If retinal detachment is not present, no intervention is done initially; vitreous hemorrhage most often clears within months. If vitreous hemorrhage persists or if there is an associated retinal detachment, vitrectomy is recommended. Tractional retinal detachments can occur in diabetes.
Serous retinal detachments can occur with hypertension, pregnancy and certain autoimmune vasculopathies such as lupus. Typical symptoms are loss of vision, flashes of light, floaters, a dark curtain covering part of visual field. Diagnosis requires referral to a retinal specialist for a dilated exam. For the typical rhegmatogenous retinal detachment a retinal detachment caused by a tear in the retina , no work up is necessary. Most diabetics that develop a tractional detachment have had a known history of diabetes and diabetic retinopathy before they progress to this late stage.
Serous detachments require a blood pressure check and screening for autoimmune vasculopathies. Surgical repair is necessary for rhegmatogenous and tractional detachments, while treatment of underlying conditions usually sufficient for serous detachments. Central retinal artery occlusion is caused by an embolus, usually from the carotid artery or heart. It can also be a complication of giant cell arteritis see above or collagen vascular diseases such as systemic lupus erythematosus.
Patients describe painless, sudden, profound vision loss in one eye that is often noticed on waking up in the morning. Fundus examination reveals a cherry red spot in center of macula with surrounding whitening ischemia of the retina. An afferent papillary defect is often present. The embolus itself is often not visible.
The Cornea in Measles
As for amaurosis fugax patient, central artery occlusion patients require a Doppler ultrasound of the carotid arteries and cardiac echocardiogram to look for an embolic source. Blood tests looking for atherosclerosis risk factors lipid levels, fasting blood glucose, HBA1C may also be useful. No treatment has proven effective for central retinal artery occlusions. Only treatments instituted within 1. These include ocular massage to dislodge the embolus , anterior chamber paracentesis, and intraocular pressure lowering medications.
A daily aspirin, control of atherosclerotic risk factors and smoking cessation are important for preventing an occlusion from occurring in the contralateral eye. Vision usually does not recover, but patients need to be monitored closely initially for development of neovascularization. Central retinal vein occlusion is most associated with atherosclerosis or hypercoagulable states can lead to thrombosis. Less commonly, it can be a consequence of a vasculitis from infectious causes e.
Patients describe unilateral painless loss of vision. The patient should be investigated for atherosclerotic risk factors. In younger patients without atherosclerotic risk factors, a hypercoagulability panel should be done. A daily aspirin as well as control of atherosclerotic risk factors or hypercoagulable states is crucial to prevent involvement of the contralateral eye. There are also new anti-vascular endothelial growth factor compounds that may help patients recover vision from macular edema, a common complication of vein occlusions. Patients need to be examined every month for the first three months after diagnosis - when they are at highest risk for neovascularization, a complication which requires prompt laser treatment.
The visual prognosis is variable and depends most on the extent of ischemia and macular edema. Diabetes, hypertension, and elevated lipids are risk factors for ischemic anterior optic neuropathy. See photograph under Giant Cell Arteritis. Relative nocturnal hypotension may also play a role, particularly in patients on antihypertensive medications. Recht Steuern Wirtschaft. Erschienen: Auf die Merkliste Drucken Weiterempfehlung. Dekkers The Cornea in Measles lieferbar ca.
Softcover Springer. Produktbeschreibung The need to study the corneal complications of measles was not very obvious. Everyone knew of the kerato conjunctivitis of measles and considered it to be an innocuous feature of the disease.