STUDY - Technical - New Dacian's Medicine
Eye and
Vision Disorders (3)
Translation Draft
As for the patient's approach I will start with the hyperemic or painful eye. Corneal abrasions are best visualized by placing a drop of fluoroscein in the eye and examining it with the slit lamp using blue-cobalt light.
A blue filter pen flashlight is sufficient for cases where the slot lamp is not available. The lesions of the corneal epithelium are highlighted by the yellow fluorescence of the membrane exposed bases. Examination for the detection of foreign bodies is important.
For the examination of the conjunctival sacs, the lower eyelid must be towed downwards and the upper eyelid must be twisted upwards. Foreign bodies can be removed with a cotton wool applicator, moistened, after applying a drop of local anesthetic, such as proparacain, into the eye. Alternatively, it is possible to remove the foreign body from the eye by abundant irrigation with physiological serum or artificial tears.
If the corneal epithelium shows abrasions, antibiotic ointment and a bandage will be applied to the eyes. A drop of an intermediate-acting cycloplegic agent, e.g. 1% cyclopentolat hydrochloride, helps reduce pain by relaxing the ciliary body. The eye must be examined again the next day. Minor abrasions may not require dressing and cycloplegia.
Subconjunctival haemorrhage results from the rupture of small vessels passing through the virtual space between the episcler and the conjunctiva. Blood entering this space can produce an extremely red eye, but vision is not affected and bleeding resolves without treatment. Subconjunctival bleeding is usually spontaneous, but can occur as a result of closed trauma, eye rub or strong cough. Occasionally it is a clue to a pre-existing hemorrhagic disorder.
Pinguecula is a small nodule that occurs in the temporal or nasal conjunctival limb. In adults, such lesions are extremely common and of little importance, except in cases where they become inflamed (pingueculitis). Pterigioma resembles pinguecula, but crossed the conjunctival limb affecting the surface of the cornea. Its removal is justified by the appearance of symptoms of irritation or blurred vision, but relapse is a common problem.
Blepharitis is inflammation of the eyelids. Its most common form occurs in association with rosacea or seborrheic dermatitis. The edges of the eyelids are usually massively colonized with staphylococcus. on careful inspection, they appear greasy, ulcerated, with crusts from detritus that stick to the eyelashes.
Treatment consists in the application of warm compresses, rigorous hygiene of the eyelids and local antibiotics, such as erythromycin. The external orjelet (climb) is produced by staphylococcal infection of the superficial accessory glands Ziess or Moll, located at the edge of the eyelids. The internal orjelet occurs following the dissemination of infection of the Meibomius sebaceous glands in the posterior face of the eyelid.
Systemic antibiotics, usually tetracyclines, are sometimes necessary for the treatment of inflammation of the Meibomius glands (meibomitis) or severe chronic blepharitis. Chalazion is a granulomatous, painless inflammation of a Meibomius gland, which produces a lump the size of a pea inside the eyelid. It can be incised and drained or injected with glucocorticoids. Basal cell carcinoma, squamous cell carcinoma or Meibomius gland carcinoma should be suspected whenever there is an ulcerated lesion of the eyelid that does not heal.
Dacriocystitis or inflammation of the lacrimal drainage system, can produce epipora (tear) and appearance of injected eyes. The gentle pressure exerted on the tear sac causes pain and reflux of mucus or pus from the openings of the tear glands. Dacriocystitis usually occurs following obstruction of the tear system. Treatment consists of topical and systemic antibiotherapy, followed by permeability testing or surgery to restore permeability. Entropion (inversion of the eyelid) or ectropion (eversion or depression of the eyelid) may also cause tear and eye irritation.
Conjunctivitis is the most common cause of hyperemia and eye pain. The pain is minimal, and the visual acuity is reduced only to a small extent. The most common viral etiological agent is adenovirus. It can produce a watery secretion, moderate foreign body sensation and photophobia.
Bacterial infections tend to produce a mucopurulent exudate. Mild forms of infectious conjunctivitis are usually treated empirically with topical broad-spectrum eye antibiotics such as sulfacetamide 10%, polymixin-bacitracin-neomycin or trimetoprim-polymixin association. Smears and cultures are usually reserved for severe, resistant or recurrent cases of conjunctivitis.
To prevent contamination, patients should be advised to wash their hands often, not to touch their eyes and to avoid direct contact with others. Allergic conjunctivitis is extremely common and is often mistaken for infectious conjunctivitis. Three forms are known with closely overlapping manifestations.
Hay fever conjunctivitis has a seasonal incidence of the release of airborne antigens by plants into the atmosphere. IgE-mediated activation of mastocytes in conjunctivitis produces pruritus, hyperemia and edema. Spring conjunctivitis is also seasonal, getting worse during the warm months. It affects children or adolescents exclusively and is more common in boys. The cause is unknown, but the symptoms are assumed to be triggered by airborne antigens.
Pruritus, photophobia, epiphorea and mucous secretion are typical. Palpebral conjunctivitis can become hypertrophic, with giant growths called cubic papillae. Irritation caused by contact lenses or any chronic foreign body can also induce the formation of cubic papillae. Atopic conjunctivitis occurs in subjects with atopic dermatitis or asthma. Symptoms of allergic conjunctivitis can be improved with cold compresses, topical vasoconstrictors, antihistamines and mastocytic stabilizers such as sodium chromolin.
Topical glucocorticoid solutions achieve a substantial improvement in immunologically mediated forms of conjunctivitis, but their long-term use is contraindicated due to complications such as glaucoma, cataracts and secondary infection. Topical nonsteroidal anti-inflammatory agents (NSAIDs) such as ketorolac tromethamine are a better alternative.
Keratoconjunctivitis sicca or dry eye produces burning sensation, foreign body sensation, injected appearance and photophobia. In light forms, the eye seems surprisingly normal, but the production of tears measured by watering a filter paper (Schirmer tape) is deficient.
A number of systemic drugs, including antihistamines, anticholinergics and psychotropic medication produce dry eyes by reducing tear secretion. Diseases that directly concern the lacrimal gland, such as sarcoidosis or Sjogren's syndrome, also produce dry eyes. Patients may experience dry eyes after radiotherapy, if the treatment field includes orbits.
Symptoms of dry eye are also common after lesions affecting cranial nerves V or VII. Corneal anesthesia is particularly dangerous, as the absence of the normal blinking reflex exposes the cornea to the lesions, without the pain being able to warn the patient. Treatment of the dry eye consists in the frequent application and abundance of artificial tears and eye lubricants. In severe forms, the tear carncula can be clogged or cauterized to reduce the leakage of tear fluid.
Keratitis is a threat to vision due to the risk of opacification, scarring and perforation of the cornea. Around the globe, the two major causes of keratitis blindness are the trahima following Chlamydia infection and vitamin A deficiency correlated with malnutrition.
An important role in corneal infection and ulceration is also held by contact lenses (no person with active eye infection should wear such lenses). In examining the cornea, it is important to distinguish between a superficial infection (keratoconjunctivitis) and a more serious, deep ulcerative process. The latter is accompanied by a more marked deterioration of vision, pain, photophobia, hyperemia and secretion.
Examination with slit lamp reveals the destruction of the corneal epithelium, cloudy infiltration or abscess into the stroma and inflammatory cellular reaction in the anterior chamber. In severe forms, the pus attaches to the base of the anterior chamber, giving rise to a hypopion. Immediately after corneal sampling for Gram, Giemsa and culture dyes, empirical antibiotic therapy should be initiated.
Topical forte antibiotics are particularly effective, supplemented with antibiotics applied subconjunctivally as needed. The most common bacterial pathogens are Staphylococcus, Streptococcus (especially S. pneumoniae), Pseudomonas, Enterobacteriaceae, Haemophilus and Neisseria. For Neisseria, topical antibiotics should be associated with systemic antibiotics in order to eliminate systemic infection. In a patient with keratitis, a fungal etiology should also be considered. Fungal infections are common in areas with wet and warm climates, especially after penetration of the cornea by plants or plant material.
Herpetic viruses are a major cause of keratitis blindness. most adults have antiherpes simplex serum antibodies, indicating a history of viral infection. Primary eye infection is generally caused by herpes simplex type 1, more than type 2. Unilateral follicular blepharoconjunctivitis is manifested, which is easily confused with adenoviral conjunctivitis, except in cases where the periocular or conjunctiva skin appears signaling vesicles.
A dendritic aspect of corneal epithelium ulceration, evidenced by fluoroscein staining, is pathognomonic for herpetic infection, but is found only in a few primary infections. Recurrent eye infection occurs by reactivation of the latent herpes virus. Viral rash in the corneal epithelium may lead to the development of characteristic herpetic dendrites.
Damage to the stroma of the cornea produces edema, vascularization and iridocyclitis. Herpetic keratitis is treated with topical antiviral agents, cycloplegic and oral acyclovir. Topical glucocorticoids are effective in reducing corneal scarring, but should be used with particular caution due to the risk of corneal melting and perforation. Topical steroids also have the risk of prolonging infection and inducing glaucoma.
Herpes zoster produced by reactivation of latent varicella-zoster virus (varicella) causes painful vesicular dermatitis in the area of a dermatoma. Eye symptoms may occur after the zosterian rash in any of the branches of the trigeminal nerve, but are extremely common when blisters appear in the nose, reflecting damage to the nasociliar nerve (V1) (Hutchinson sign).
Ophthalmic zoster herpes produces corneal dendrites, which can be difficult to differentiate from those seen in herpes simplex. Stromal keratitis, anterior uveitis, increased intraocular pressure, paralysis of motor ocular nerves, acute retinal necrosis, postherpetic scarring and neuralgia are other common complications. Treatment of ophthalmic zoster herpes is done with antiviral and cycloplegic agents. In severe forms, steroids can be added to prevent permanent visual disturbances due to corneal scarring.
As for the patient's approach I will start with the hyperemic or painful eye. Corneal abrasions are best visualized by placing a drop of fluoroscein in the eye and examining it with the slit lamp using blue-cobalt light.
A blue filter pen flashlight is sufficient for cases where the slot lamp is not available. The lesions of the corneal epithelium are highlighted by the yellow fluorescence of the membrane exposed bases. Examination for the detection of foreign bodies is important.
For the examination of the conjunctival sacs, the lower eyelid must be towed downwards and the upper eyelid must be twisted upwards. Foreign bodies can be removed with a cotton wool applicator, moistened, after applying a drop of local anesthetic, such as proparacain, into the eye. Alternatively, it is possible to remove the foreign body from the eye by abundant irrigation with physiological serum or artificial tears.
If the corneal epithelium shows abrasions, antibiotic ointment and a bandage will be applied to the eyes. A drop of an intermediate-acting cycloplegic agent, e.g. 1% cyclopentolat hydrochloride, helps reduce pain by relaxing the ciliary body. The eye must be examined again the next day. Minor abrasions may not require dressing and cycloplegia.
Subconjunctival haemorrhage results from the rupture of small vessels passing through the virtual space between the episcler and the conjunctiva. Blood entering this space can produce an extremely red eye, but vision is not affected and bleeding resolves without treatment. Subconjunctival bleeding is usually spontaneous, but can occur as a result of closed trauma, eye rub or strong cough. Occasionally it is a clue to a pre-existing hemorrhagic disorder.
Pinguecula is a small nodule that occurs in the temporal or nasal conjunctival limb. In adults, such lesions are extremely common and of little importance, except in cases where they become inflamed (pingueculitis). Pterigioma resembles pinguecula, but crossed the conjunctival limb affecting the surface of the cornea. Its removal is justified by the appearance of symptoms of irritation or blurred vision, but relapse is a common problem.
Blepharitis is inflammation of the eyelids. Its most common form occurs in association with rosacea or seborrheic dermatitis. The edges of the eyelids are usually massively colonized with staphylococcus. on careful inspection, they appear greasy, ulcerated, with crusts from detritus that stick to the eyelashes.
Treatment consists in the application of warm compresses, rigorous hygiene of the eyelids and local antibiotics, such as erythromycin. The external orjelet (climb) is produced by staphylococcal infection of the superficial accessory glands Ziess or Moll, located at the edge of the eyelids. The internal orjelet occurs following the dissemination of infection of the Meibomius sebaceous glands in the posterior face of the eyelid.
Systemic antibiotics, usually tetracyclines, are sometimes necessary for the treatment of inflammation of the Meibomius glands (meibomitis) or severe chronic blepharitis. Chalazion is a granulomatous, painless inflammation of a Meibomius gland, which produces a lump the size of a pea inside the eyelid. It can be incised and drained or injected with glucocorticoids. Basal cell carcinoma, squamous cell carcinoma or Meibomius gland carcinoma should be suspected whenever there is an ulcerated lesion of the eyelid that does not heal.
Dacriocystitis or inflammation of the lacrimal drainage system, can produce epipora (tear) and appearance of injected eyes. The gentle pressure exerted on the tear sac causes pain and reflux of mucus or pus from the openings of the tear glands. Dacriocystitis usually occurs following obstruction of the tear system. Treatment consists of topical and systemic antibiotherapy, followed by permeability testing or surgery to restore permeability. Entropion (inversion of the eyelid) or ectropion (eversion or depression of the eyelid) may also cause tear and eye irritation.
Conjunctivitis is the most common cause of hyperemia and eye pain. The pain is minimal, and the visual acuity is reduced only to a small extent. The most common viral etiological agent is adenovirus. It can produce a watery secretion, moderate foreign body sensation and photophobia.
Bacterial infections tend to produce a mucopurulent exudate. Mild forms of infectious conjunctivitis are usually treated empirically with topical broad-spectrum eye antibiotics such as sulfacetamide 10%, polymixin-bacitracin-neomycin or trimetoprim-polymixin association. Smears and cultures are usually reserved for severe, resistant or recurrent cases of conjunctivitis.
To prevent contamination, patients should be advised to wash their hands often, not to touch their eyes and to avoid direct contact with others. Allergic conjunctivitis is extremely common and is often mistaken for infectious conjunctivitis. Three forms are known with closely overlapping manifestations.
Hay fever conjunctivitis has a seasonal incidence of the release of airborne antigens by plants into the atmosphere. IgE-mediated activation of mastocytes in conjunctivitis produces pruritus, hyperemia and edema. Spring conjunctivitis is also seasonal, getting worse during the warm months. It affects children or adolescents exclusively and is more common in boys. The cause is unknown, but the symptoms are assumed to be triggered by airborne antigens.
Pruritus, photophobia, epiphorea and mucous secretion are typical. Palpebral conjunctivitis can become hypertrophic, with giant growths called cubic papillae. Irritation caused by contact lenses or any chronic foreign body can also induce the formation of cubic papillae. Atopic conjunctivitis occurs in subjects with atopic dermatitis or asthma. Symptoms of allergic conjunctivitis can be improved with cold compresses, topical vasoconstrictors, antihistamines and mastocytic stabilizers such as sodium chromolin.
Topical glucocorticoid solutions achieve a substantial improvement in immunologically mediated forms of conjunctivitis, but their long-term use is contraindicated due to complications such as glaucoma, cataracts and secondary infection. Topical nonsteroidal anti-inflammatory agents (NSAIDs) such as ketorolac tromethamine are a better alternative.
Keratoconjunctivitis sicca or dry eye produces burning sensation, foreign body sensation, injected appearance and photophobia. In light forms, the eye seems surprisingly normal, but the production of tears measured by watering a filter paper (Schirmer tape) is deficient.
A number of systemic drugs, including antihistamines, anticholinergics and psychotropic medication produce dry eyes by reducing tear secretion. Diseases that directly concern the lacrimal gland, such as sarcoidosis or Sjogren's syndrome, also produce dry eyes. Patients may experience dry eyes after radiotherapy, if the treatment field includes orbits.
Symptoms of dry eye are also common after lesions affecting cranial nerves V or VII. Corneal anesthesia is particularly dangerous, as the absence of the normal blinking reflex exposes the cornea to the lesions, without the pain being able to warn the patient. Treatment of the dry eye consists in the frequent application and abundance of artificial tears and eye lubricants. In severe forms, the tear carncula can be clogged or cauterized to reduce the leakage of tear fluid.
Keratitis is a threat to vision due to the risk of opacification, scarring and perforation of the cornea. Around the globe, the two major causes of keratitis blindness are the trahima following Chlamydia infection and vitamin A deficiency correlated with malnutrition.
An important role in corneal infection and ulceration is also held by contact lenses (no person with active eye infection should wear such lenses). In examining the cornea, it is important to distinguish between a superficial infection (keratoconjunctivitis) and a more serious, deep ulcerative process. The latter is accompanied by a more marked deterioration of vision, pain, photophobia, hyperemia and secretion.
Examination with slit lamp reveals the destruction of the corneal epithelium, cloudy infiltration or abscess into the stroma and inflammatory cellular reaction in the anterior chamber. In severe forms, the pus attaches to the base of the anterior chamber, giving rise to a hypopion. Immediately after corneal sampling for Gram, Giemsa and culture dyes, empirical antibiotic therapy should be initiated.
Topical forte antibiotics are particularly effective, supplemented with antibiotics applied subconjunctivally as needed. The most common bacterial pathogens are Staphylococcus, Streptococcus (especially S. pneumoniae), Pseudomonas, Enterobacteriaceae, Haemophilus and Neisseria. For Neisseria, topical antibiotics should be associated with systemic antibiotics in order to eliminate systemic infection. In a patient with keratitis, a fungal etiology should also be considered. Fungal infections are common in areas with wet and warm climates, especially after penetration of the cornea by plants or plant material.
Herpetic viruses are a major cause of keratitis blindness. most adults have antiherpes simplex serum antibodies, indicating a history of viral infection. Primary eye infection is generally caused by herpes simplex type 1, more than type 2. Unilateral follicular blepharoconjunctivitis is manifested, which is easily confused with adenoviral conjunctivitis, except in cases where the periocular or conjunctiva skin appears signaling vesicles.
A dendritic aspect of corneal epithelium ulceration, evidenced by fluoroscein staining, is pathognomonic for herpetic infection, but is found only in a few primary infections. Recurrent eye infection occurs by reactivation of the latent herpes virus. Viral rash in the corneal epithelium may lead to the development of characteristic herpetic dendrites.
Damage to the stroma of the cornea produces edema, vascularization and iridocyclitis. Herpetic keratitis is treated with topical antiviral agents, cycloplegic and oral acyclovir. Topical glucocorticoids are effective in reducing corneal scarring, but should be used with particular caution due to the risk of corneal melting and perforation. Topical steroids also have the risk of prolonging infection and inducing glaucoma.
Herpes zoster produced by reactivation of latent varicella-zoster virus (varicella) causes painful vesicular dermatitis in the area of a dermatoma. Eye symptoms may occur after the zosterian rash in any of the branches of the trigeminal nerve, but are extremely common when blisters appear in the nose, reflecting damage to the nasociliar nerve (V1) (Hutchinson sign).
Ophthalmic zoster herpes produces corneal dendrites, which can be difficult to differentiate from those seen in herpes simplex. Stromal keratitis, anterior uveitis, increased intraocular pressure, paralysis of motor ocular nerves, acute retinal necrosis, postherpetic scarring and neuralgia are other common complications. Treatment of ophthalmic zoster herpes is done with antiviral and cycloplegic agents. In severe forms, steroids can be added to prevent permanent visual disturbances due to corneal scarring.
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