1) Chemical burns to the eye are ophthalmic emergencies that require immediate irrigation to remove the chemical. The severity depends on factors like the substance, concentration, and contact time.
2) Management involves continued irrigation, controlling inflammation with steroids and other medications, preventing infection with antibiotics, and controlling intraocular pressure. For more severe burns, additional treatments like amniotic membrane transplantation may be needed.
3) Outcomes depend on the extent of limbal stem cell damage. Mild burns may fully heal while more extensive damage can lead to permanent scarring and visual impairment due to conjunctivalization of the cornea.
Fungal infections of eye cause one of the most dangerious infections. Accurate diagnosis and proper institution of anti-fungal therapy is essential. Here we discuss the various anti-fungal agents available to be used in ophthalmology.
This document summarizes recent advances in treating age-related macular degeneration (AMD). It discusses new drugs that aim to prevent retinal damage or slow AMD progression by inhibiting angiogenesis, inflammation, the complement pathway, oxidative stress, and retinal toxin accumulation. It also describes surgeries like maculoplasty and bionic eye implants, as well as rehabilitation techniques and low vision aids. Promising new drug classes discussed include anti-angiogenics, complement inhibitors, neurotrophic factors, and antioxidants.
This document discusses dry eyes, also known as aqueous tear deficiency. It defines dry eyes as a non-infectious ocular surface disorder caused by a lack of tear fluid. The three layers of the normal tear film are described: the lipid layer from meibomian glands, the aqueous layer from lacrimal glands, and the mucin layer from goblet cells. Various causes of dry eyes are classified, including deficiencies in the aqueous, lipid, or mucin layers. Signs, symptoms, and diagnostic tests are outlined. Management involves tear supplementation, preservation, treatment of underlying conditions, punctal plugs, anti-inflammatories, and surgery in severe cases.
Interpretation of visual fields with special reference to octopusHaitham Al Mahrouqi
The document provides an overview of visual field interpretation using the Octopus perimeter. It discusses what a visual field is, why they are important, and types of perimetry including static and kinetic. It describes advantages of different test strategies like TOP and SITA fast that can reduce test time. Key aspects of the Octopus 7-in-1 printout are outlined including demographic data, reliability indices, threshold values compared to norms, and mean deviation and pattern deviation plots.
WHAT IS NEW IN GLAUCOMA MANAGEMENT? FROM DRUGS TO STEM THERAPY TO YOGA AND MEDITATION, IT'S ALL THERE. GOOD FOR EVERY OPHTHALMOLOGIST AND POST - GRADUATES. INNOVATION IS THE NEW NORMAL.
Performing Trabeculectomy is one thing...managing a failed bleb is all together another ball game. Describes the various precautions to be taken in preventing bleb failure and how to revive a failing bleb
Chemical (alkali and acid) injury of the conjunctiva and cornea is a true ocular emergency and requires immediate intervention.
Epidemiology:>-Chemical injuries to the eye represent between 11.5%-22.1% of ocular traumas.
etiology:-Chemical injuries occur as a result of acid, alkali, or neutral agents.Alkalis being responsible for 60%.
pathophysiology:-Alkali agents are lipophilic and therefore penetrate tissues more rapidly than acids.the damaged tissues then secrete proteolytic enzymes, which lead to further damage.Acids are generally less harmful than alkali .
coagulated proteins act as a barrier to prevent further penetration .
Symptoms & signs:-Pain,Lacrimation,Photophobia,Blepharospasm
Grading of severity:=1) Roper-Hall (modified Hughes) classification
2) Dua classification
MANAGEMENT:-Emergency treatment
Medical treatment
Surgical treatment
This document discusses chemical injuries to the eye. It begins with an introduction and overview of the epidemiology, etiology, pathogenesis, classification, clinical course, features, and management of such injuries. It notes that alkali injuries are more common and can be more deleterious. The pathogenesis and healing process differs for acid versus alkali injuries. Classification systems include Hughes, Roper-Hall, and Dua's, which predicts outcomes. Management involves immediate irrigation, acute medical treatment with steroids and antibiotics, and potential surgical interventions like debridement or amniotic membrane transplantation. Long-term goals are promoting healing, controlling inflammation and preventing complications.
Fungal infections of eye cause one of the most dangerious infections. Accurate diagnosis and proper institution of anti-fungal therapy is essential. Here we discuss the various anti-fungal agents available to be used in ophthalmology.
This document summarizes recent advances in treating age-related macular degeneration (AMD). It discusses new drugs that aim to prevent retinal damage or slow AMD progression by inhibiting angiogenesis, inflammation, the complement pathway, oxidative stress, and retinal toxin accumulation. It also describes surgeries like maculoplasty and bionic eye implants, as well as rehabilitation techniques and low vision aids. Promising new drug classes discussed include anti-angiogenics, complement inhibitors, neurotrophic factors, and antioxidants.
This document discusses dry eyes, also known as aqueous tear deficiency. It defines dry eyes as a non-infectious ocular surface disorder caused by a lack of tear fluid. The three layers of the normal tear film are described: the lipid layer from meibomian glands, the aqueous layer from lacrimal glands, and the mucin layer from goblet cells. Various causes of dry eyes are classified, including deficiencies in the aqueous, lipid, or mucin layers. Signs, symptoms, and diagnostic tests are outlined. Management involves tear supplementation, preservation, treatment of underlying conditions, punctal plugs, anti-inflammatories, and surgery in severe cases.
Interpretation of visual fields with special reference to octopusHaitham Al Mahrouqi
The document provides an overview of visual field interpretation using the Octopus perimeter. It discusses what a visual field is, why they are important, and types of perimetry including static and kinetic. It describes advantages of different test strategies like TOP and SITA fast that can reduce test time. Key aspects of the Octopus 7-in-1 printout are outlined including demographic data, reliability indices, threshold values compared to norms, and mean deviation and pattern deviation plots.
WHAT IS NEW IN GLAUCOMA MANAGEMENT? FROM DRUGS TO STEM THERAPY TO YOGA AND MEDITATION, IT'S ALL THERE. GOOD FOR EVERY OPHTHALMOLOGIST AND POST - GRADUATES. INNOVATION IS THE NEW NORMAL.
Performing Trabeculectomy is one thing...managing a failed bleb is all together another ball game. Describes the various precautions to be taken in preventing bleb failure and how to revive a failing bleb
Chemical (alkali and acid) injury of the conjunctiva and cornea is a true ocular emergency and requires immediate intervention.
Epidemiology:>-Chemical injuries to the eye represent between 11.5%-22.1% of ocular traumas.
etiology:-Chemical injuries occur as a result of acid, alkali, or neutral agents.Alkalis being responsible for 60%.
pathophysiology:-Alkali agents are lipophilic and therefore penetrate tissues more rapidly than acids.the damaged tissues then secrete proteolytic enzymes, which lead to further damage.Acids are generally less harmful than alkali .
coagulated proteins act as a barrier to prevent further penetration .
Symptoms & signs:-Pain,Lacrimation,Photophobia,Blepharospasm
Grading of severity:=1) Roper-Hall (modified Hughes) classification
2) Dua classification
MANAGEMENT:-Emergency treatment
Medical treatment
Surgical treatment
This document discusses chemical injuries to the eye. It begins with an introduction and overview of the epidemiology, etiology, pathogenesis, classification, clinical course, features, and management of such injuries. It notes that alkali injuries are more common and can be more deleterious. The pathogenesis and healing process differs for acid versus alkali injuries. Classification systems include Hughes, Roper-Hall, and Dua's, which predicts outcomes. Management involves immediate irrigation, acute medical treatment with steroids and antibiotics, and potential surgical interventions like debridement or amniotic membrane transplantation. Long-term goals are promoting healing, controlling inflammation and preventing complications.
Dr. Nitish Narang's document discusses ocular injuries, including mechanical injuries from foreign bodies or trauma, and non-mechanical injuries from thermal, electrical, or radiation sources. It also covers chemical injuries to the eyes from acids, alkalis, and toxins. The document provides classifications for different types and severities of chemical injuries and outlines immediate emergency treatments, as well as longer-term management approaches including topical medications, surgical procedures like amniotic membrane transplantation, and potential outcomes depending on the grade of injury.
Limbal Stem Cell Deficiency & its managementKaran Bhatia
1) Limbal stem cells are located in the palisades of Vogt region of the limbus and are responsible for maintaining the normal corneal epithelium. Limbal stem cell deficiency occurs when the source of these cells is damaged, causing severe problems to the ocular surface.
2) Limbal stem cell deficiency can be partial or total, and is classified based on extent and etiology. Common causes include chemical/thermal burns, Stevens-Johnson syndrome, and multiple ocular surgeries.
3) Management is based on the extent and severity of deficiency, and involves steps from conservative treatment to more invasive procedures like limbal stem cell transplantation or keratoprosthesis. The goal is to replace
This document provides information on Vernal Keratoconjunctivitis (VKC), including:
- VKC is a chronic, seasonal inflammatory eye disease that primarily involves the conjunctiva and can affect the cornea. It usually affects young males.
- Treatment involves mast cell stabilizers, antihistamines, dual-acting agents, and NSAIDs to control inflammation and symptoms. Chronic or severe cases can lead to complications like shield ulcers, keratoconus, dry eyes, lid abnormalities, and limbal stem cell deficiency.
- The cause involves a combination of environmental allergens, immune system factors, and genetics. Management focuses on controlling inflammation and preventing long-term complications through medication and occasionally
This document discusses choroidal neovascularization (CNV), which is the abnormal growth of blood vessels from the choroid into the retina or subretinal space. It is a cause of vision loss and the main feature of exudative age-related macular degeneration. The document defines CNV and lists various conditions that can cause it. It then focuses on CNV caused by age-related macular degeneration, covering risk factors, pathogenesis, symptoms, diagnostic findings on fluorescein angiography and OCT, and various treatment options including anti-VEGF drugs, photodynamic therapy, and laser photocoagulation.
This presentation describes the nature of amniotic membrane grafts, Indications, and limitations with presentation of two cases of corneal perforations treated with it as a self experience
This document discusses macular edema in diabetic retinopathy and its treatment. It explains that macular edema is caused by chronic hyperactivity of the polyol pathway and increased vascular endothelial growth factor, which leads to increased vascular permeability. Laser photocoagulation and intravitreal anti-VEGF injections are effective treatments that work by reducing hypoxia and VEGF levels in the retina. Several studies found that treatments with drugs like ranibizumab and aflibercept were more effective at improving vision outcomes than laser alone in patients with diabetic macular edema.
Neovascular glaucoma is a severe form of secondary glaucoma characterized by fibrovascular proliferation in the anterior chamber angle caused by chronic retinal ischemia. The most common causes are diabetic retinopathy, central retinal vein occlusion, and ocular ischemic disease. The proliferation of new blood vessels leads to the formation of a membrane that can cause open or closed angle glaucoma with very high intraocular pressure. Treatment involves controlling the underlying cause, lowering intraocular pressure through medications, laser treatment or surgery like trabeculectomy with anti-metabolites or tube shunts, and preventing further neovascularization through panretinal photocoagulation. Early diagnosis and aggressive treatment is important but successful management is challenging and
Meibomian gland dysfunction (MGD) is a chronic abnormality of the meibomian glands that results in an altered tear film and ocular surface disease. The meibomian glands secrete an oily substance called meibum that prevents tear film evaporation. MGD can be obstructive or non-obstructive and is commonly caused by ductal blockage that impairs meibum secretion. Symptoms include eye irritation, redness, burning and watering. Treatment involves warm compresses, lid scrubs, and topical agents like antibiotics, anti-inflammatories, and tear supplements.
Angle recession glaucoma is a type of secondary glaucoma that can develop years after blunt ocular trauma causes tearing of the ciliary body and recession of the iris root. It is often underdiagnosed due to delayed onset and forgotten injury history. Management involves topical glaucoma medications, with filtering surgeries used if medication fails to control pressure. Early diagnosis and aggressive treatment are important to prevent glaucoma-related vision loss from this condition.
This document provides information on anti-VEGF drugs used in ophthalmology. It discusses the role of VEGF in various eye diseases and conditions. It summarizes the properties, mechanisms of action, administration, and safety profiles of major anti-VEGF drugs including bevacizumab, pegaptanib, and ranibizumab which are used to treat wet age-related macular degeneration, diabetic retinopathy, and other retinal diseases by inhibiting abnormal blood vessel growth and leakage caused by VEGF.
VKC is a chronic allergic inflammation of the ocular surface that is more common in children under 10 years of age. It involves the conjunctiva and cornea and causes symptoms like itching, redness, watering and sensitivity to light. Signs include thick mucus, transient yellow-white deposits called Horner-Tranta's dots, and large papillae on the conjunctiva that are graded based on their size. Corneal involvement can lead to punctate keratitis, erosions, ulcers and scarring if left untreated. The disease is seasonal in onset but may become perennial over time.
This document summarizes various classes of anti-glaucoma medications, including their mechanisms of action and examples of drugs. It focuses on prostaglandins, describing how latanoprost, bimatoprost, and travoprost work. It also discusses adrenergic medications, carbonic anhydrase inhibitors, cholinergic drugs, and hyperosmotic agents for treating glaucoma. Side effects are provided for each class.
This presentation emphasizes the importance of screening for chloroquine retinopathy according to new AAO guidelines. While bull's eye maculopathy is a classic late-stage sign, initial photoreceptor damage typically occurs parafoveally in Europeans and peripherally near the arcades in Asians. Screening tests like automated visual fields and SD-OCT can detect toxicity before visible RPE damage, as irreversible progression often occurs by the time bull's eye maculopathy appears. Risk of toxicity depends on daily dose, with very thin patients at increased risk when dose is based on ideal rather than actual weight.
Dry eye is a disease of the tear film and ocular surface caused by reduced tear production or increased tear evaporation. It results in eye discomfort, visual disturbance, and potential ocular surface damage. Dry eye can be caused by problems with the lacrimal functional unit such as aging, autoimmune disease like Sjogren's syndrome, or environmental factors. Diagnosis involves evaluating tear production via tests like Schirmer's test and tear breakup time, and assessing ocular surface staining. Treatment depends on dry eye severity and may include artificial tears, anti-inflammatories, punctal plugs, and management of underlying conditions. The goal is to supplement tears, reduce evaporation, stimulate natural tear production, and minimize
This document provides information on secondary angle closure glaucoma. It defines secondary angle closure glaucoma as glaucoma caused by impairment of aqueous outflow due to apposition of the peripheral iris and trabeculum, where an identifiable ophthalmic condition is present. It discusses two mechanisms - the anterior pulling mechanism where the iris is pulled forward, and the posterior pushing mechanism where the iris is displaced forward. Specific conditions that can cause a secondary angle closure glaucoma include neovascular glaucoma, iridocorneal endothelial syndromes, posterior polymorphous dystrophy, epithelial downgrowth, and inflammation. The document provides details on diagnosis and treatment of secondary angle closure glaucoma.
Allergic conjunctivitis is inflammation of the conjunctiva (the membrane covering the white part of the eye) due to allergy.Although allergens differ among patients, the most common cause is hay fever. Symptoms consist of redness (mainly due to vasodilation of the peripheral small blood vessels), edema (swelling) of the conjunctiva, itching, and increased lacrimation (production of tears). If this is combined with rhinitis, the condition is termed allergic rhinoconjunctivitis.
The symptoms are due to release of histamine and other active substances by mast cells, which stimulate dilation of blood vessels, irritate nerve endings, and increase secretion of tears.
Treatment of allergic conjunctivitis is by avoiding the allergen (e.g., avoiding grass in bloom during "hay fever season") and treatment with antihistamines, either topical (in the form of eye drops), or systemic (in the form of tablets). Antihistamines, medications that stabilize mast cells, and nonsteroidal anti-inflammatory drugs (NSAIDs) are generally safe and usually effective.
This document discusses various tear substitutes and artificial tears. It begins by covering the history of eye baths and artificial tears dating back to the 16th century. It then discusses different types of artificial tears including autologous serum, various polymers like cellulose derivatives, polyols, dextran 70, and hyaluronic acid. It also discusses newer technologies like punctal plugs, collagen implants, soft contact lenses, and electrical stimulation to increase tear production. The document concludes by discussing various preservatives used in artificial tears and newer disappearing preservatives.
Dry eye occurs when there is inadequate tear production or function, resulting in an unstable tear film and ocular surface disorder. It can be caused by conditions that reduce tear production such as Sjogren's syndrome, vitamin A deficiency, Stevens-Johnson syndrome, or medications. Other causes affect the tear film layers, like meibomian gland dysfunction reducing the outer lipid layer. Symptoms include dryness, burning, and blurred vision. Treatment focuses on replacing tears, improving ocular surface health, addressing underlying causes, and escalating care based on severity through the DEWS treatment guidelines.
Dry eye management involves evaluating a patient's history, symptoms, and signs of dry eye through examination and tests. Treatment aims to relieve discomfort, maintain a smooth optical surface, and prevent damage. It includes lifestyle modifications, medical treatments like tear substitutes, anti-inflammatory agents, and procedures like punctal occlusion. Regular follow up and counseling are important for monitoring response and providing support.
Lacrimal system ii,03.08.2016, a.r.rajalakshmiSrikanth K
The document discusses the lacrimal system and dry eye disease. It describes the structure and functions of the normal tear film and its three layers: lipid, aqueous, and mucin. Signs and symptoms of dry eye include dryness, irritation, blurry vision, redness, and corneal staining. Investigations include tear breakup time, Schirmer test, and ocular surface staining. Treatment is based on disease severity and may include artificial tears, anti-inflammatories, punctal plugs, and surgery for advanced cases.
Dr. Nitish Narang's document discusses ocular injuries, including mechanical injuries from foreign bodies or trauma, and non-mechanical injuries from thermal, electrical, or radiation sources. It also covers chemical injuries to the eyes from acids, alkalis, and toxins. The document provides classifications for different types and severities of chemical injuries and outlines immediate emergency treatments, as well as longer-term management approaches including topical medications, surgical procedures like amniotic membrane transplantation, and potential outcomes depending on the grade of injury.
Limbal Stem Cell Deficiency & its managementKaran Bhatia
1) Limbal stem cells are located in the palisades of Vogt region of the limbus and are responsible for maintaining the normal corneal epithelium. Limbal stem cell deficiency occurs when the source of these cells is damaged, causing severe problems to the ocular surface.
2) Limbal stem cell deficiency can be partial or total, and is classified based on extent and etiology. Common causes include chemical/thermal burns, Stevens-Johnson syndrome, and multiple ocular surgeries.
3) Management is based on the extent and severity of deficiency, and involves steps from conservative treatment to more invasive procedures like limbal stem cell transplantation or keratoprosthesis. The goal is to replace
This document provides information on Vernal Keratoconjunctivitis (VKC), including:
- VKC is a chronic, seasonal inflammatory eye disease that primarily involves the conjunctiva and can affect the cornea. It usually affects young males.
- Treatment involves mast cell stabilizers, antihistamines, dual-acting agents, and NSAIDs to control inflammation and symptoms. Chronic or severe cases can lead to complications like shield ulcers, keratoconus, dry eyes, lid abnormalities, and limbal stem cell deficiency.
- The cause involves a combination of environmental allergens, immune system factors, and genetics. Management focuses on controlling inflammation and preventing long-term complications through medication and occasionally
This document discusses choroidal neovascularization (CNV), which is the abnormal growth of blood vessels from the choroid into the retina or subretinal space. It is a cause of vision loss and the main feature of exudative age-related macular degeneration. The document defines CNV and lists various conditions that can cause it. It then focuses on CNV caused by age-related macular degeneration, covering risk factors, pathogenesis, symptoms, diagnostic findings on fluorescein angiography and OCT, and various treatment options including anti-VEGF drugs, photodynamic therapy, and laser photocoagulation.
This presentation describes the nature of amniotic membrane grafts, Indications, and limitations with presentation of two cases of corneal perforations treated with it as a self experience
This document discusses macular edema in diabetic retinopathy and its treatment. It explains that macular edema is caused by chronic hyperactivity of the polyol pathway and increased vascular endothelial growth factor, which leads to increased vascular permeability. Laser photocoagulation and intravitreal anti-VEGF injections are effective treatments that work by reducing hypoxia and VEGF levels in the retina. Several studies found that treatments with drugs like ranibizumab and aflibercept were more effective at improving vision outcomes than laser alone in patients with diabetic macular edema.
Neovascular glaucoma is a severe form of secondary glaucoma characterized by fibrovascular proliferation in the anterior chamber angle caused by chronic retinal ischemia. The most common causes are diabetic retinopathy, central retinal vein occlusion, and ocular ischemic disease. The proliferation of new blood vessels leads to the formation of a membrane that can cause open or closed angle glaucoma with very high intraocular pressure. Treatment involves controlling the underlying cause, lowering intraocular pressure through medications, laser treatment or surgery like trabeculectomy with anti-metabolites or tube shunts, and preventing further neovascularization through panretinal photocoagulation. Early diagnosis and aggressive treatment is important but successful management is challenging and
Meibomian gland dysfunction (MGD) is a chronic abnormality of the meibomian glands that results in an altered tear film and ocular surface disease. The meibomian glands secrete an oily substance called meibum that prevents tear film evaporation. MGD can be obstructive or non-obstructive and is commonly caused by ductal blockage that impairs meibum secretion. Symptoms include eye irritation, redness, burning and watering. Treatment involves warm compresses, lid scrubs, and topical agents like antibiotics, anti-inflammatories, and tear supplements.
Angle recession glaucoma is a type of secondary glaucoma that can develop years after blunt ocular trauma causes tearing of the ciliary body and recession of the iris root. It is often underdiagnosed due to delayed onset and forgotten injury history. Management involves topical glaucoma medications, with filtering surgeries used if medication fails to control pressure. Early diagnosis and aggressive treatment are important to prevent glaucoma-related vision loss from this condition.
This document provides information on anti-VEGF drugs used in ophthalmology. It discusses the role of VEGF in various eye diseases and conditions. It summarizes the properties, mechanisms of action, administration, and safety profiles of major anti-VEGF drugs including bevacizumab, pegaptanib, and ranibizumab which are used to treat wet age-related macular degeneration, diabetic retinopathy, and other retinal diseases by inhibiting abnormal blood vessel growth and leakage caused by VEGF.
VKC is a chronic allergic inflammation of the ocular surface that is more common in children under 10 years of age. It involves the conjunctiva and cornea and causes symptoms like itching, redness, watering and sensitivity to light. Signs include thick mucus, transient yellow-white deposits called Horner-Tranta's dots, and large papillae on the conjunctiva that are graded based on their size. Corneal involvement can lead to punctate keratitis, erosions, ulcers and scarring if left untreated. The disease is seasonal in onset but may become perennial over time.
This document summarizes various classes of anti-glaucoma medications, including their mechanisms of action and examples of drugs. It focuses on prostaglandins, describing how latanoprost, bimatoprost, and travoprost work. It also discusses adrenergic medications, carbonic anhydrase inhibitors, cholinergic drugs, and hyperosmotic agents for treating glaucoma. Side effects are provided for each class.
This presentation emphasizes the importance of screening for chloroquine retinopathy according to new AAO guidelines. While bull's eye maculopathy is a classic late-stage sign, initial photoreceptor damage typically occurs parafoveally in Europeans and peripherally near the arcades in Asians. Screening tests like automated visual fields and SD-OCT can detect toxicity before visible RPE damage, as irreversible progression often occurs by the time bull's eye maculopathy appears. Risk of toxicity depends on daily dose, with very thin patients at increased risk when dose is based on ideal rather than actual weight.
Dry eye is a disease of the tear film and ocular surface caused by reduced tear production or increased tear evaporation. It results in eye discomfort, visual disturbance, and potential ocular surface damage. Dry eye can be caused by problems with the lacrimal functional unit such as aging, autoimmune disease like Sjogren's syndrome, or environmental factors. Diagnosis involves evaluating tear production via tests like Schirmer's test and tear breakup time, and assessing ocular surface staining. Treatment depends on dry eye severity and may include artificial tears, anti-inflammatories, punctal plugs, and management of underlying conditions. The goal is to supplement tears, reduce evaporation, stimulate natural tear production, and minimize
This document provides information on secondary angle closure glaucoma. It defines secondary angle closure glaucoma as glaucoma caused by impairment of aqueous outflow due to apposition of the peripheral iris and trabeculum, where an identifiable ophthalmic condition is present. It discusses two mechanisms - the anterior pulling mechanism where the iris is pulled forward, and the posterior pushing mechanism where the iris is displaced forward. Specific conditions that can cause a secondary angle closure glaucoma include neovascular glaucoma, iridocorneal endothelial syndromes, posterior polymorphous dystrophy, epithelial downgrowth, and inflammation. The document provides details on diagnosis and treatment of secondary angle closure glaucoma.
Allergic conjunctivitis is inflammation of the conjunctiva (the membrane covering the white part of the eye) due to allergy.Although allergens differ among patients, the most common cause is hay fever. Symptoms consist of redness (mainly due to vasodilation of the peripheral small blood vessels), edema (swelling) of the conjunctiva, itching, and increased lacrimation (production of tears). If this is combined with rhinitis, the condition is termed allergic rhinoconjunctivitis.
The symptoms are due to release of histamine and other active substances by mast cells, which stimulate dilation of blood vessels, irritate nerve endings, and increase secretion of tears.
Treatment of allergic conjunctivitis is by avoiding the allergen (e.g., avoiding grass in bloom during "hay fever season") and treatment with antihistamines, either topical (in the form of eye drops), or systemic (in the form of tablets). Antihistamines, medications that stabilize mast cells, and nonsteroidal anti-inflammatory drugs (NSAIDs) are generally safe and usually effective.
This document discusses various tear substitutes and artificial tears. It begins by covering the history of eye baths and artificial tears dating back to the 16th century. It then discusses different types of artificial tears including autologous serum, various polymers like cellulose derivatives, polyols, dextran 70, and hyaluronic acid. It also discusses newer technologies like punctal plugs, collagen implants, soft contact lenses, and electrical stimulation to increase tear production. The document concludes by discussing various preservatives used in artificial tears and newer disappearing preservatives.
Dry eye occurs when there is inadequate tear production or function, resulting in an unstable tear film and ocular surface disorder. It can be caused by conditions that reduce tear production such as Sjogren's syndrome, vitamin A deficiency, Stevens-Johnson syndrome, or medications. Other causes affect the tear film layers, like meibomian gland dysfunction reducing the outer lipid layer. Symptoms include dryness, burning, and blurred vision. Treatment focuses on replacing tears, improving ocular surface health, addressing underlying causes, and escalating care based on severity through the DEWS treatment guidelines.
Dry eye management involves evaluating a patient's history, symptoms, and signs of dry eye through examination and tests. Treatment aims to relieve discomfort, maintain a smooth optical surface, and prevent damage. It includes lifestyle modifications, medical treatments like tear substitutes, anti-inflammatory agents, and procedures like punctal occlusion. Regular follow up and counseling are important for monitoring response and providing support.
Lacrimal system ii,03.08.2016, a.r.rajalakshmiSrikanth K
The document discusses the lacrimal system and dry eye disease. It describes the structure and functions of the normal tear film and its three layers: lipid, aqueous, and mucin. Signs and symptoms of dry eye include dryness, irritation, blurry vision, redness, and corneal staining. Investigations include tear breakup time, Schirmer test, and ocular surface staining. Treatment is based on disease severity and may include artificial tears, anti-inflammatories, punctal plugs, and surgery for advanced cases.
Dry eye, also known as keratoconjunctivitis sicca, is a condition caused by inadequate tear production or unstable tear film. It results in ocular irritation, redness, and visual disturbance. The tear film consists of an outer lipid layer, middle aqueous layer, and inner mucin layer. In chronic dry eye, tears have increased salts and decreased proteins and lipocalins. Treatment focuses on lubricating the eyes, managing underlying conditions like blepharitis, and occasionally punctal plugs or anti-inflammatory drugs. Diagnosis involves tests of tear production, stability, and ocular surface staining to determine the best lubricating and anti-inflammatory treatments.
1. Chemical injuries to the eye can result from exposure to acids or alkalis and are a true ophthalmic emergency. 2. The severity depends on factors like type, concentration, and duration of exposure and can lead to significant vision loss. 3. Management involves immediate irrigation, controlling inflammation, promoting healing, and preventing complications. Treatment may include debridement, amniotic membrane transplantation, and long-term use of medications.
chemical injury to eye by alkali, acids and irritants.
pathophysiology and management.
recent advances in management.
ITS A TRUE EMERGENCY IN OPHTHALMOLOGY
Alkali burns are severe chemical injuries caused by strong bases like lime and caustic soda. They damage tissues through saponification of lipids and extraction of water from cells. Clinically, they cause necrosis, edema, and inflammation of the conjunctiva, cornea, and iris. Treatment involves immediate and prolonged irrigation, debridement of dead tissue, topical antibiotics, steroids, and anti-collagenase agents to promote healing and prevent complications like symblepharon and corneal ulceration. More severe cases may require surgical procedures like conjunctival advancement or limbal stem cell transplantation. Despite treatment, prognosis remains guarded due to the extensive tissue damage caused by alkalis.
This document discusses the diagnosis and management of dry eye disease. It outlines tests to evaluate tear secretion, volume, clearance, and ocular surface damage. Diagnostic tests include Schirmer's test, phenol red thread test, tear meniscus height, fluorescein clearance, and impression cytology. Management involves identifying and eliminating exacerbating factors, supplementing tears, retaining tears, anti-inflammatory therapies like cyclosporine, and new drugs that stimulate tear secretion or have mucolytic properties. The goals are to eliminate causes, replace tears, maintain moisture, increase tear secretion, inhibit inflammation, and reestablish the tear film.
This document discusses chemical injuries to the eyes and their management. It begins by describing chemical burns as ocular emergencies that can cause blindness. Alkaline and acidic burns are discussed in terms of their pathophysiology and common home substances that cause them. Diagnosis is based on history and clinical picture. Goals of treatment include removing the chemical, promoting healing, controlling inflammation and infection, and managing intraocular pressure. Immediate management focuses on copious irrigation until the pH is neutralized. Later management includes medications to promote healing, control inflammation, infection, and IOP. Surgical interventions like grafting and keratoplasty may be needed for late complications. Prevention emphasizes safety equipment and education.
The document provides an overview of common eye presentations to the emergency department, outlining 10 case studies that demonstrate a range of conditions including infected corneal ulcers, corneal abrasions, uveitis, glaucoma, hyphema, retinal detachments, and orbital cellulitis, and provides guidance on examination findings, differential diagnoses, and management for each case.
1) Chemical injury to the eye is a true ocular emergency that requires immediate irrigation to remove the chemical. Common chemicals involved are acids and alkalis.
2) Examination involves assessing the extent of injury to the cornea, conjunctiva and limbus. Classification systems help determine prognosis.
3) Management of acute injury focuses on copious irrigation, topical steroids, antibiotics and cycloplegics. Surgery may include debridement, amniotic membrane grafting or tenonplasty.
4) Chronic management addresses complications like symblepharon, persistent epithelial defects and limbal stem cell deficiency. Transplants and keratoprostheses can help stabilize the ocular surface long
CHEMICAL INJURIES OF EYEnew.p dr manuptxManuBansal32
This document discusses chemical eye injuries, including common causes, pathophysiology, clinical presentation, grading, complications, and management. Some key points:
- Chemical exposures can cause ocular trauma ranging from mild irritation to severe damage and vision loss. Common causes include household cleaners, industrial chemicals, and agricultural chemicals.
- Injuries are classified based on extent of corneal and limbal damage. Grade 1-2 injuries often recover with medical treatment while grade 3-4 generally require surgery in addition to medical management.
- Immediate irrigation is critical. Examination evaluates clarity, ischemia, IOP, and debridement may be needed. Treatment goals are removing the chemical, promoting healing, controlling inflammation,
Ophthalmologic approach to chemical burns Chimozi Tembo
Chemical burns are one of the true ophthalmologic emergencies. The ophthalmologist and general practitioner thus needs to be aware of the management of this type of eye injury.
The document summarizes the effects of chemical burns on the ocular surface and the different treatment phases. Basic substances penetrate the eye more rapidly than acids, lysing cell membranes and triggering inflammation. Acids cause protein coagulation in the epithelium. Factors like pH, temperature, and concentration determine damage. The reparative phases are immediate, acute, early, and late. Early signs include epithelial defects and conjunctival inflammation. The acute phase involves reestablishing the corneal epithelium and potential glaucoma. Later phases involve chronic inflammation, scarring, and secondary complications like glaucoma. Emergency therapy focuses on irrigation, lubricants, and antibiotics. Surgical management includes debridement, amniotic membrane transplantation
This document summarizes different types of chemical injuries to the eye including alkalis and acids. It describes the mechanisms of injury from various sources like domestic, agricultural, or deliberate chemical attacks. It provides details on the clinical features and stages of alkali and acid burns. Treatment involves irrigation, removal of contaminants, antibiotics, steroids, cycloplegics, and addressing complications. Other non-chemical eye injuries from thermal, electrical, ultraviolet, infrared, and ionizing radiation are also summarized.
chemical eye injuries, approach and managementDana Sultan
This document discusses chemical injuries of the eye, specifically alkali and acid burns. It describes the epidemiology, physical exam findings, classification systems, management, and treatment approaches for different grades of injuries. For mild injuries (Grade I), topical steroids, antibiotics and artificial tears are used. More severe injuries (Grade II-III) involving the cornea and conjunctiva may also require oral vitamins, debridement, amniotic membrane grafts, and surgery. The most severe injuries (Grade IV) often necessitate early surgical intervention like Tenonplasty to reestablish limbal vascularity and prevent further necrosis. Proper irrigation, classification, and multimodal medical and surgical management can help improve outcomes for
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This document discusses chemical burns to the eye. It notes that both thermal and chemical burns can cause blindness. Common causes of chemical burns are cleaning products, fertilizers, cement, fireworks, battery acid, and bleach. Alkaline agents like these cause more damage than acids as they penetrate cell membranes and disrupt collagen. A classification system grades injuries based on extent of limbal ischemia and corneal haze. Treatment involves immediate and copious irrigation, controlling inflammation with steroids, promoting healing with artificial tears and ascorbate, and managing intraocular pressure. The goal is to remove the chemical, promote healing, prevent infection, and control inflammation.
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2. Introduction
• True ophthalmic emergency
• Only ocular condition where history
taking and examination should be
delayed
B/L Chemical
Exposure
Devastating
effect
Complete
visual disability
2
3. Types of chemicals
Alkalies
Most dangerous
Rapid Penetration
Acid
Less severe than alkali
Do not penetrate into eye as
readily as alkaline substances
Exception HFL acid burn
‘As dangerous as an alkali
burn’
Irritants
Neutral pH
More discomfort to eye rather
than actual damage
Most household detergents,
pepper spray
Can cause significant pain, but
usually does not affect vision
3
4. Alkalies
Penetrate rapidly
(often in less than one minute)
Disruption of cells & Necrosis of tissue
Combine with cell membrane lipids,
mucopolysaccharides and to collagen
On Ocular Surface
Facilitates rapid penetration Deeper layers,
aqueous, vitreous
Saponify cell membranes & intercellular
bridges
Necrosis of conjunctival blood vessels “Cooked fish eye” (Cornea – as white as chalk & opaque
5. Acids
Quickly denature proteins
in the corneal stroma
Form precipitates
Retard additional
penetration
• Coagulation effect
• Protein
precipitations at
epithelium level
Localized
damage
Physical
barrier
5
6. Chemical Example
Sulfuric Acid Battery Acid, Industrial Cleaner
Acetic Acid Vinegar, Glacial Acetic Acid
Hydrochloric Acid Chemical Laboratories
Sulfurous Acid Bleach, Refrigerant, fruit and vegetable preservative
Hydrofluoric Acid Glass polishing, gasoline alkylation, silicone production
Ammonia Fertilizers, refrigerants
Lye Drain cleaner
Lime Plastic, mortar, cement, white wash
Potassium hydroxide Caustic potash
Magnesium hydroxide Sparklers, incendiary devices
6
7. Severity of burn
Surface area
of contact
Depth of
penetration
Concentration
of substance
Time of
contact
Time of
interference
Degree of
limbal stem
cell injury
7
8. Phase Day Recovery
Initial 0 • Clinical findings relate to severity of injury
• Graded according to degree of limbal, corneal and conjunctival involvement
Acute 0-7 • Epithelial regrowth begins to occur (if there is sufficient amount of undamaged limbal
stem cells)
• Rx – directed at encouraging growth while quelling inflammation
Early Repair 7-21 • Corneal/ conjunctival epithelium & keratocytes proliferate
• Mild injuries complete re-epithelialization
• Severe injuries persistent epithelial defects
• Activity of collagenase peaks by day 14-21, while collagen synthesis continues
• Rx – should attempt to maximize collagen synthesis while minimizing collagenase
activity
Late Repair >21 • Mild injuries (limbal stem population intact) Repair is completed
• Grade II injuries (focal stem cell loss) Focal conjunctivalization of cornea
• More Severe injuries Delayed re-epithelization of cornea Repopulation by
conjunctival epithelium/ stromal ulceration Permanent scarring
• Severe limbal damage (despite optimal management) – Eye cannot be salvaged
8
9. Pathophysiology – Damage
Necrosis of the conjunctival & corneal epithelium
Disruption & occlusion of the limbal vasculature
Loss of limbal stem cells
Conjunctivalisation & vascularization of the corneal surface
Persistent corneal epithelial defects with sterile corneal
ulceration
9
10. Other long term effects
• Ocular surface wetting disorders
• Symblepharon formation
• Cicatricial entropion
Anterior chamber penetration
• Iris damage
• Lens damage
Ciliary epithelial damage
• Impairs secretion of ascorbate
Required for collagen production &
corneal repair
Hypotony & phthisis bulbi
10
11. Pathophysiology
Centripetal movement of cells from the peripheral cornea, limbus, or conjunctiva Responsible
for normal & posttraumatic replacement of corneal epithelium
Only partial trans-differentiation of conjunctival epithelium to corneal epithelium – possible
• But conjunctiva-derived epithelium never fully expresses corneal epithelial phenotypic features
Associated with delayed re-epithelialization, superficial & deep stromal vascularization, persistence
of goblet cells in the corneal epithelium & poor epithelium-basement membrane adhesion
Limbal stem cells cells most qualified to restore the functional competence of the corneal
epithelial surface after injury
11
Healing of corneal epithelium and stroma
12. Healing of damaged stromal collagen
Keratocytes
• Pluripotent cells
• Responsible for maintenance & regeneration of corneal stroma
• Phagocytosis of collagen fibrils
• Synthesis & secretion of collagen GAG ground substance, collagenase & collagenase inhibitors
• Modulated by cytokines from epithelium, inflammatory cells, & other keratocytes
12
13. Degradation of the basement membrane
collagen
(initiated by MMP–9 )
Degradation of the corneal stromal matrix
(by MMP–1 and MMP–8(collagenase types)
Detected earliest at 9 hrs
Collagen type 1 synthesis peak point
(at 14-21 days)
Coincide with maximum MMP activity
Intervening period may show sterile corneal
ulceration
13
17. Roper Hall Classification
Grade Prognosis Limbal Ischaemia Corneal Involvement
I Good None Epithelial Damage
II Good <1/3 Haze
But Iris details visible
III Gaurded 1/3-1/2 Total Epithelial Loss
With haze that obscures Iris details
IV Poor >1/2 Cornea opaque
With Iris and pupil obscured
17
18. Dua’s Classification
18
Grade Prognosis Limbal involvement Conjunctival involvement Analogue scale
I Very good 0 CH 0% 0/0%
II Good ⩽3 CH ⩽30% 0.1–3/1–29.9%
III Good >3–6 CH >30–50% 3.1–6/31–50%
IV Good to guarded >6–9 CH >50–75% 6.1–9/51–75%
V Guarded to poor >9–<12 CH >75–<100% 9.1–11.9/75.1–99.9%
VI Very poor Total limbus (12 CH) involved Total conjunctiva (100%)
involved
12/100%
22. Immediate Management
Immediate copious irrigation of eye (every second counts) with
• Normal saline solution
• Ringer's lactate solution
• Normal saline with bicarbonate
• Balanced salt solution(BSS)
• Ideal solution not available Plain Tap Water
Evert UL, LL Irrigate
• Remove all solid particles from under lids
• After 5 to 10 minutes of irrigation , If litmus paper available Test pH of lower inside of
lid Continue irrigation until pH is below or above a pH of 7.0.
• Litmus paper unavailable irrigate for 20 min
22
24. History
Time of injury
Eyes rinsed or not, if yes- duration, solution, speed
Mechanism of injury
Type of chemical
Packaging of chemical available?
Eye protection used?
24
26. 1) Steroids
Reduce inflammation
Neutrophil infiltration
Impair stromal healing by reducing collagen synthesis & inhibiting fibroblast
migration
Must be tailed off after 7-10 days when sterile corneal ulceration is most likely to
occur
May be replaced by topical NSAIDS, which do not affect keratocyte function
26
27. 2) Ascorbic Acid
Reverses a localized tissue scorbutic state
Promote synthesis of mature collagen by corneal
fibroblasts
Topical sodium ascorbate 10% is given 2 -hourly in
addition to a systemic dose of 2g QID
27
28. 3) Citric Acid
Powerful inhibitor of neutrophil activity
Reduces the intensity of the inflammatory response
Chelation of extracellular calcium by citrate also appears to inhibit collagenase.
Topical sodium citrate 10% given 2 hourly for about 10 days.
Aim is to eliminate the second wave of phagocytes, which normally occurs 7 days after
the injury
28
30. Tear Substitutes
Topical antibiotics
Bandage Soft Contact Lens
Autologous Serum
• Fibronectin and epidermal growth factors
Retinoic Acid
• May promote goblet cell recovery and improve ocular surface function
• Transdifferentiation of the conjunctival epithelium to a corneal epithelial
phenotype.
30
31. Grade I
Topical antibiotic ointment QID
Prednisolone acetate 1% QID
Preservative free artificial tears as needed
Cycloplegics
31
32. Grade II
As for grade I
Prednisolone acetate 1%
• 1 hourly while awake for the first 7-10 days
• Tapering if the epithelium has not healed by day 10-14
• Epithelial defect persists after day 10 consider progestational steroids (1% medroxyprogesterone QID)
Long acting cycloplegics
• Atropine
Oral Vitamin C
• 2 grams four times a day
Doxycycline
• 100 mg BD (avoid in children)
Sodium ascorbate drops (10%) hourly while awake
Preservative free artificial tears as needed
Debridement of necrotic epithelium & application of tissue adhesive as needed
32
33. Grade III
As for Grade II
Consider AMT
•Ideally be performed in the first week of injury
33
Grade IV
As for Grade II/III
Early surgery usually necessary
For significant necrosis Tenonplasty can help reestablish limbal vascularity
AMT – often necessary
42. Prevention
• Education & training regarding prevention of chemical exposures
workplace
• Persons who may be exposed to chemicals in workplace advised to
wear safety goggles
42