STUDY - Technical - New Dacian's Medicine
Eye and
Vision Disorders (4)
Translation Draft
We continue with the many diseases/signs of the eye...
Episcleritis is inflammation of the episcleris, a thin layer of connective tissue located between the conjunctiva and the sclera. Episcleritis resembles conjunctivitis, but it is a much more localized process, and secretion is absent. Most cases of episcleritis are idiopathic, but some cases occur in autoimmune diseases.
Scleritis signifies a deep, more severe inflammatory process, commonly associated with a connective tissue disease such as rheumatoid arthritis, lupus erythematosus, node polyarteritis, Wegener granulomatosis or recurrent polychondritis. Inflammation and fog of the sclera may be diffuse or nodular. In previous sclerosis forms, the eyeball acquires a purple tinge and the patient blames severe ocular sensitivity and pain.
In posterior scleritis, pain and hyperemia may be less important, but exophthalmia, choroid albeit effusions, reduced motility and visual disturbances frequently occur. Episcleritis and scleritis should be treated with nonsteroidal anti-inflammatory agents. if treatment with these agents does not work, tonic or even systemic therapy with glucocorticoids may be necessary, especially when a pre-existing autoimmune process is active.
Uveitis affecting the anterior structures of the eye is called irritate or iridocyclitis. Diagnosis requires examination with slit lamp to identify inflammatory cells that float in aqueous humor or are stored on the corneal endothelium (keratin precipitate).
Previous uveitis develops in sarcoidosis, ankylosing spondylitis, juvenile rheumatoid arthritis, inflammatory bowel disorders, psoriasis, Reiter syndrome and Behcet's disease. It is also associated with herpes infection, syphilis, Lyme disease, oncocercosis, tuberculosis and leprosy.
Although previous uveitis may occur in association with a multitude of conditions, in most cases the cause has not been identified. For this reason, laboratory testing is usually reserved for patients with recurrent or severe previous uveitis.
Treatment is directed towards reducing inflammation and scarring through judicious use of topical steroids. Pupil dilation reduces pain and prevents the formation of sinechi. The posterior one is diagnosed by observing inflammation of the vitreous body, retina or choroid when examining the bottom of the eye.
The possibility of posterior uveitis being associated with an identifiable systemic disease is greater than in the case of a previous one. Some patients experience panicuveitis or inflammation of both segments of the eye, both anterior and posterior. Posterior unitis is a manifestation of autoimmune diseases such as sarcoidosis, Behcet disease, Vogt-Koyanagi-Harada syndrome and inflammatory bowel disorders.
It also accompanies diseases such as toxoplasmosis, oncocercosis, cysticrcosis, cocciodioidomycosis, toxocariosis and histoplasmosis (infections caused by microorganisms such as Candida, Pneumocystis carinii, Cryptococcus, Aspergillus, herpes and cytomegal virus, as well as other diseases such as syphilis, Lyme disease, tuberculosis, cat scratch disease, Whipple disease and brucellosis). In multiple sclerosis, changes in chronic inflation can occur in the extreme periphery of the retina (pars planitis or intermediate uveitis).
Acute closed-angle glaucoma is a rare, commonly misdiagnosed cause of the hyperemic, painful eye. Eyes that may be affected by acute closed-angle glaucoma have a narrow anterior chamber, either due to a short antero-posterior diameter (presbitism) or due to an enlarged lens following the gradual evolution of cataracts. At an average pupil dilation, the peripheral iris blocks the drainage of the aqueous humor to the angle of the anterior chamber and the intraocular pressure increases sharply, producing pain, congestion, corneal edema, blurred vision and shadows.
In some patients, eye symptoms are overshadowed by nausea, vomiting or headache, requiring unnecessary abdominal or neurological examination. The diagnosis is made by measuring intraocular tension during an acute attack or by gonioscopy to highlight the narrowing of the angle of the anterior chamber, using a contact lens.
Treatment of acute closed-angle glaucoma is done with oral or intravenous acetazolamide, topical beta-blockers and pilocarpine for the induction of myosis. if these measures do not work, the laser may be used to create a hole on the periphery of the iris for the purpose of puillary unlocking.
Many doctors oppose the routine use of induced midriasis to examine the bottom of the eye because they fear that it could precipitate closed-angle glaucoma. The risk is actually small and far outweighed by the potential benefits to the patient, in the sense of detecting a hidden lesion of the bottom of the eye, visible only through a fully dilated pupil.
Moreover, a single closed-angle glaucoma attack after pharmacological dilation rarely causes permanent damage to the eye and serves as an accidental challenge test to identify patients with narrow angles who may benefit from laser prophylactic iridectomy.
Endophthalmitis occurs through bacterial, viral, fungal or parasitic infections of the internal structures of the eye. It usually occurs as a result of hematogenous dissemination from a distant outbreak. Patients with chronic diseases, diabetes, immunodepression, especially those with a history of prolonged intravenous catheterization or positive hemocultures, are at the highest risk of endogenous endofthalmitis.
Although most patients experience eye pain and congestion, sometimes the only symptom is vision loss. Septic embolisms in an affected heart valve or dental abscess, which stop in the retinal circulation, can give rise to endophthalmitis. Retinal haemorrhages (Roth spots) are considered pathognomonic for subacute bacterial endocarditis, but are also found in leukemia, diabetes and many other diseases.
Endophthalmitis also occurs as a complication of ophthalmological surgery, sometimes months or even years after surgery. In any patient with an intraocular infection or inflammation, occult penetration of a foreign body or an unnoticed trauma of the eyeball should be considered.
Let's move now on to transient or sudden loss of vision. The retinal transient ischemic attack is called fleeting amaurosis. Because nervous tissue shows a high rate of metabolism, disruption of blood flow to the retina for more than a few seconds produces transient monocular cetate, a term alternately used for fleeting amaurosis.
Patients describe a rapid decrease in vision, similar to a descending curtain, which sometimes affects only a portion of the field of vision. Fugitive amaurosis can usually occur following the blockage of an embolus in a retinal arteriol. If the embolus breaks or moves on, the blood flow resumes and vision quickly returns to normal, without causing permanent damage. In case of prolonged interruption of blood flow, the internal retina is infarcted.
Ophthalmoscopy highlights areas of whitish retina, edematized following the distribution of retinal arterioles branches. Complete occlusion of the central artery of the retina causes the blood flow to stop and the appearance of the milky retina with bright red fovea. Embols are made up of cholesterol (Hollenhorst plate), calcium or residues of platelets and fibrin. The most common source is an atherosclerotic plaque in the carotid or aorta, although embolisms may come from the heart, especially in patients with valvular diseases, atrial fibrillation or cardiac wall motility abnormalities.
In rare cases, fleeting amaurosis occurs due to low infusion pressure in the central artery of the retina in patients with critical ipsilateral carotid artery stenosis and poor collateral circulation through Willis' polygon. In this situation, fleeting amaurosis occurs during a decrease in systolic tension or a slight aggravation of carotid stenosis. Sometimes a contralateral motor or sensory deficit occurs, indicating concomitant hemispheric cerebral ischemia.
Fugitive amaurosis warns the doctor of a patient at increased risk of stroke. Carotid arteries should be examined ultrasound. Endarterectomy for a stenosis of 60% or more, even in asymptomatic patients, has been shown to reduce the subsequent incidence of ipsilateral stroke. Treatment with aspirin, warfarin or other anticoagulants is appropriate for some patients. if no carotid lesionisis is identified, echocardiography and ambulatory EKG monitoring will be performed.
Pronounced systemic hypertension causes sclerosis of retinal arterioles, cliferanhemorrhage, focal infarctions of the nerve fiber layer (skins with a padded appearance) and overflowing lipids and fluids (hard exudate) in the macula. In hypertensive crisis, sudden loss of vision may occur due to vasospasm of retinal arterioles and consecutive retinal ischemia.
In addition, acute hypertension can cause loss of vision following ischemic swelling of the optic disc. Patients with acute hypertensive retinopathy should be treated by reducing blood pressure levels. However, blood pressure should not be reduced sharply, as there is a risk of an optical disc infarction following sudden hypoperfusion.
Imminent occlusion of the central vein of the retina or its branches may produce prolonged visual shadows similar to those described by patients with fleeting amaurosis. The veins are congested and phlebitis, with numerous retinal hemorrhages. In some patients, venous flow resumes spontaneously, while other patients develop obvious obstructions with extensive retinal hemorrhages ("violent" appearance), infarction and vision loss.
Retinal venous occlusion is commonly idiopathic, but hypertension, diabetes and glaucoma are major risk factors. The benefits of anticoagulants have not been demonstrated, this treatment also favours the risk of bleeding in the vitreous body. Polycytemia, thrombocytemia or other factors that cause a state of hypercoagulability should be corrected.
I will continue in the next post (even though I have announced the relative stop of posts - at least to finish with the group of posts related to eye disorders - so there will be at least 4 more posts, if I manage to go through everything I set out to do) with optical neuropathies, starting with the anterior (NOIA) and posterior (NOIP) ischemic optic neuropathies ( NOIA).
We continue with the many diseases/signs of the eye...
Episcleritis is inflammation of the episcleris, a thin layer of connective tissue located between the conjunctiva and the sclera. Episcleritis resembles conjunctivitis, but it is a much more localized process, and secretion is absent. Most cases of episcleritis are idiopathic, but some cases occur in autoimmune diseases.
Scleritis signifies a deep, more severe inflammatory process, commonly associated with a connective tissue disease such as rheumatoid arthritis, lupus erythematosus, node polyarteritis, Wegener granulomatosis or recurrent polychondritis. Inflammation and fog of the sclera may be diffuse or nodular. In previous sclerosis forms, the eyeball acquires a purple tinge and the patient blames severe ocular sensitivity and pain.
In posterior scleritis, pain and hyperemia may be less important, but exophthalmia, choroid albeit effusions, reduced motility and visual disturbances frequently occur. Episcleritis and scleritis should be treated with nonsteroidal anti-inflammatory agents. if treatment with these agents does not work, tonic or even systemic therapy with glucocorticoids may be necessary, especially when a pre-existing autoimmune process is active.
Uveitis affecting the anterior structures of the eye is called irritate or iridocyclitis. Diagnosis requires examination with slit lamp to identify inflammatory cells that float in aqueous humor or are stored on the corneal endothelium (keratin precipitate).
Previous uveitis develops in sarcoidosis, ankylosing spondylitis, juvenile rheumatoid arthritis, inflammatory bowel disorders, psoriasis, Reiter syndrome and Behcet's disease. It is also associated with herpes infection, syphilis, Lyme disease, oncocercosis, tuberculosis and leprosy.
Although previous uveitis may occur in association with a multitude of conditions, in most cases the cause has not been identified. For this reason, laboratory testing is usually reserved for patients with recurrent or severe previous uveitis.
Treatment is directed towards reducing inflammation and scarring through judicious use of topical steroids. Pupil dilation reduces pain and prevents the formation of sinechi. The posterior one is diagnosed by observing inflammation of the vitreous body, retina or choroid when examining the bottom of the eye.
The possibility of posterior uveitis being associated with an identifiable systemic disease is greater than in the case of a previous one. Some patients experience panicuveitis or inflammation of both segments of the eye, both anterior and posterior. Posterior unitis is a manifestation of autoimmune diseases such as sarcoidosis, Behcet disease, Vogt-Koyanagi-Harada syndrome and inflammatory bowel disorders.
It also accompanies diseases such as toxoplasmosis, oncocercosis, cysticrcosis, cocciodioidomycosis, toxocariosis and histoplasmosis (infections caused by microorganisms such as Candida, Pneumocystis carinii, Cryptococcus, Aspergillus, herpes and cytomegal virus, as well as other diseases such as syphilis, Lyme disease, tuberculosis, cat scratch disease, Whipple disease and brucellosis). In multiple sclerosis, changes in chronic inflation can occur in the extreme periphery of the retina (pars planitis or intermediate uveitis).
Acute closed-angle glaucoma is a rare, commonly misdiagnosed cause of the hyperemic, painful eye. Eyes that may be affected by acute closed-angle glaucoma have a narrow anterior chamber, either due to a short antero-posterior diameter (presbitism) or due to an enlarged lens following the gradual evolution of cataracts. At an average pupil dilation, the peripheral iris blocks the drainage of the aqueous humor to the angle of the anterior chamber and the intraocular pressure increases sharply, producing pain, congestion, corneal edema, blurred vision and shadows.
In some patients, eye symptoms are overshadowed by nausea, vomiting or headache, requiring unnecessary abdominal or neurological examination. The diagnosis is made by measuring intraocular tension during an acute attack or by gonioscopy to highlight the narrowing of the angle of the anterior chamber, using a contact lens.
Treatment of acute closed-angle glaucoma is done with oral or intravenous acetazolamide, topical beta-blockers and pilocarpine for the induction of myosis. if these measures do not work, the laser may be used to create a hole on the periphery of the iris for the purpose of puillary unlocking.
Many doctors oppose the routine use of induced midriasis to examine the bottom of the eye because they fear that it could precipitate closed-angle glaucoma. The risk is actually small and far outweighed by the potential benefits to the patient, in the sense of detecting a hidden lesion of the bottom of the eye, visible only through a fully dilated pupil.
Moreover, a single closed-angle glaucoma attack after pharmacological dilation rarely causes permanent damage to the eye and serves as an accidental challenge test to identify patients with narrow angles who may benefit from laser prophylactic iridectomy.
Endophthalmitis occurs through bacterial, viral, fungal or parasitic infections of the internal structures of the eye. It usually occurs as a result of hematogenous dissemination from a distant outbreak. Patients with chronic diseases, diabetes, immunodepression, especially those with a history of prolonged intravenous catheterization or positive hemocultures, are at the highest risk of endogenous endofthalmitis.
Although most patients experience eye pain and congestion, sometimes the only symptom is vision loss. Septic embolisms in an affected heart valve or dental abscess, which stop in the retinal circulation, can give rise to endophthalmitis. Retinal haemorrhages (Roth spots) are considered pathognomonic for subacute bacterial endocarditis, but are also found in leukemia, diabetes and many other diseases.
Endophthalmitis also occurs as a complication of ophthalmological surgery, sometimes months or even years after surgery. In any patient with an intraocular infection or inflammation, occult penetration of a foreign body or an unnoticed trauma of the eyeball should be considered.
Let's move now on to transient or sudden loss of vision. The retinal transient ischemic attack is called fleeting amaurosis. Because nervous tissue shows a high rate of metabolism, disruption of blood flow to the retina for more than a few seconds produces transient monocular cetate, a term alternately used for fleeting amaurosis.
Patients describe a rapid decrease in vision, similar to a descending curtain, which sometimes affects only a portion of the field of vision. Fugitive amaurosis can usually occur following the blockage of an embolus in a retinal arteriol. If the embolus breaks or moves on, the blood flow resumes and vision quickly returns to normal, without causing permanent damage. In case of prolonged interruption of blood flow, the internal retina is infarcted.
Ophthalmoscopy highlights areas of whitish retina, edematized following the distribution of retinal arterioles branches. Complete occlusion of the central artery of the retina causes the blood flow to stop and the appearance of the milky retina with bright red fovea. Embols are made up of cholesterol (Hollenhorst plate), calcium or residues of platelets and fibrin. The most common source is an atherosclerotic plaque in the carotid or aorta, although embolisms may come from the heart, especially in patients with valvular diseases, atrial fibrillation or cardiac wall motility abnormalities.
In rare cases, fleeting amaurosis occurs due to low infusion pressure in the central artery of the retina in patients with critical ipsilateral carotid artery stenosis and poor collateral circulation through Willis' polygon. In this situation, fleeting amaurosis occurs during a decrease in systolic tension or a slight aggravation of carotid stenosis. Sometimes a contralateral motor or sensory deficit occurs, indicating concomitant hemispheric cerebral ischemia.
Fugitive amaurosis warns the doctor of a patient at increased risk of stroke. Carotid arteries should be examined ultrasound. Endarterectomy for a stenosis of 60% or more, even in asymptomatic patients, has been shown to reduce the subsequent incidence of ipsilateral stroke. Treatment with aspirin, warfarin or other anticoagulants is appropriate for some patients. if no carotid lesionisis is identified, echocardiography and ambulatory EKG monitoring will be performed.
Pronounced systemic hypertension causes sclerosis of retinal arterioles, cliferanhemorrhage, focal infarctions of the nerve fiber layer (skins with a padded appearance) and overflowing lipids and fluids (hard exudate) in the macula. In hypertensive crisis, sudden loss of vision may occur due to vasospasm of retinal arterioles and consecutive retinal ischemia.
In addition, acute hypertension can cause loss of vision following ischemic swelling of the optic disc. Patients with acute hypertensive retinopathy should be treated by reducing blood pressure levels. However, blood pressure should not be reduced sharply, as there is a risk of an optical disc infarction following sudden hypoperfusion.
Imminent occlusion of the central vein of the retina or its branches may produce prolonged visual shadows similar to those described by patients with fleeting amaurosis. The veins are congested and phlebitis, with numerous retinal hemorrhages. In some patients, venous flow resumes spontaneously, while other patients develop obvious obstructions with extensive retinal hemorrhages ("violent" appearance), infarction and vision loss.
Retinal venous occlusion is commonly idiopathic, but hypertension, diabetes and glaucoma are major risk factors. The benefits of anticoagulants have not been demonstrated, this treatment also favours the risk of bleeding in the vitreous body. Polycytemia, thrombocytemia or other factors that cause a state of hypercoagulability should be corrected.
I will continue in the next post (even though I have announced the relative stop of posts - at least to finish with the group of posts related to eye disorders - so there will be at least 4 more posts, if I manage to go through everything I set out to do) with optical neuropathies, starting with the anterior (NOIA) and posterior (NOIP) ischemic optic neuropathies ( NOIA).
Christ has risen! I'm up
to all the people who've finished the Easter holiday!
Dorin, Merticaru