Hypertensive retinopathy is caused by chronically elevated blood pressure and progresses through vasoconstrictive, sclerotic, and exudative phases. It is diagnosed through fundus examination showing arteriolar narrowing, arteriovenous nicking, hemorrhages, exudates and other changes. The severity is classified using systems like Keith-Wagener-Barker or Wong-Mitchell, with more severe grades indicating complications like papilledema. Differentiating it from similar conditions like diabetic retinopathy requires considering the medical history of hypertension versus other risk factors.
This document provides an overview of polypoidal choroidal vasculopathy (PCV), including its history, definitions, pathogenesis, histopathology, demographics, clinical features, investigations, differential diagnosis, classification, treatment and guidelines. PCV is characterized by polyp-like subretinal vascular lesions associated with hemorrhagic detachments of the retinal pigment epithelium. Indocyanine green angiography is the gold standard for diagnosis, showing focal hyperfluorescence arising from the choroidal circulation within minutes. Treatment options include observation, thermal laser photocoagulation, photodynamic therapy, anti-VEGF therapy and combination therapies.
Hypertensive Retinopathy (HTN-R) for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, Classification and management of HTN-R.
Also encompasses salient points for PGMEE
Hypertensive retinopathy is caused by high blood pressure and damages the small blood vessels in the retina. It is diagnosed through an eye exam where signs include narrowed retinal arteries, arteriovenous nicking, and cotton wool spots. Left untreated, it can progress to vision loss from hemorrhages, fluid buildup, or optic nerve damage. Treatment involves controlling the underlying hypertension through medication to prevent further eye and health issues.
Iridodialysis repair with modified double armed closed chamber techniqueRidho Ranovian
To elaborate the modified closed-chamber technique with ICCE in managing subtotal iridodialysis with traumatic cataract due to contusion ocular trauma.
Diabetic retinopathy is caused by pathological changes to the retina due to hyperglycemia. The breakdown of the blood-retinal barrier leads to vascular permeability and leakage. This results in retinal edema, hemorrhages, and exudates. Over time, there is loss of pericytes and endothelial cells, capillary nonperfusion, and upregulation of growth factors like VEGF. Eventually, this causes the development of proliferative retinopathy characterized by neovascularization and fibrovascular proliferation. The pathological effects of hyperglycemia are mediated through increased polyol pathway flux, formation of advanced glycation end products, activation of protein kinase C, and increased oxidative stress - all of which disrupt the normal vascular physiology in
1) A macular star is formed when lipid-rich exudate accumulates in the outer plexiform layer of the retina, precipitating in a star-shaped pattern following the layer's anatomy.
2) Macular stars are commonly seen in hypertensive retinopathy as a result of increased vascular permeability and leakage from small retinal vessels.
3) Other findings associated with hypertensive eye disease include arteriolar narrowing, hemorrhages, exudates, optic disc swelling, and vision loss. Grading of hypertensive retinopathy depends on the severity of retinal changes seen on examination.
Sickling hemoglobinopathies are genetic blood disorders caused by abnormal hemoglobins that cause red blood cells to take on an anomalous sickle shape and become rigid under conditions of low oxygen and acidity. These misshapen red blood cells can get stuck in and block small blood vessels. Specific disorders include sickle cell anemia, sickle cell trait, sickle cell C disease, and sickle cell thalassemia. Ocular complications range from mild and asymptomatic to proliferative retinopathy, which involves the growth of abnormal new blood vessels on the retina and can lead to vision loss from bleeding or retinal detachment. Non-proliferative retinopathy presents as venous tortuosity, silver wiring of
This document provides an overview of polypoidal choroidal vasculopathy (PCV), including its history, definitions, pathogenesis, histopathology, demographics, clinical features, investigations, differential diagnosis, classification, treatment and guidelines. PCV is characterized by polyp-like subretinal vascular lesions associated with hemorrhagic detachments of the retinal pigment epithelium. Indocyanine green angiography is the gold standard for diagnosis, showing focal hyperfluorescence arising from the choroidal circulation within minutes. Treatment options include observation, thermal laser photocoagulation, photodynamic therapy, anti-VEGF therapy and combination therapies.
Hypertensive Retinopathy (HTN-R) for undergraduate MBBS Students.
Covers the basics of Aetiology, pathophysiology, clinical features, Classification and management of HTN-R.
Also encompasses salient points for PGMEE
Hypertensive retinopathy is caused by high blood pressure and damages the small blood vessels in the retina. It is diagnosed through an eye exam where signs include narrowed retinal arteries, arteriovenous nicking, and cotton wool spots. Left untreated, it can progress to vision loss from hemorrhages, fluid buildup, or optic nerve damage. Treatment involves controlling the underlying hypertension through medication to prevent further eye and health issues.
Iridodialysis repair with modified double armed closed chamber techniqueRidho Ranovian
To elaborate the modified closed-chamber technique with ICCE in managing subtotal iridodialysis with traumatic cataract due to contusion ocular trauma.
Diabetic retinopathy is caused by pathological changes to the retina due to hyperglycemia. The breakdown of the blood-retinal barrier leads to vascular permeability and leakage. This results in retinal edema, hemorrhages, and exudates. Over time, there is loss of pericytes and endothelial cells, capillary nonperfusion, and upregulation of growth factors like VEGF. Eventually, this causes the development of proliferative retinopathy characterized by neovascularization and fibrovascular proliferation. The pathological effects of hyperglycemia are mediated through increased polyol pathway flux, formation of advanced glycation end products, activation of protein kinase C, and increased oxidative stress - all of which disrupt the normal vascular physiology in
1) A macular star is formed when lipid-rich exudate accumulates in the outer plexiform layer of the retina, precipitating in a star-shaped pattern following the layer's anatomy.
2) Macular stars are commonly seen in hypertensive retinopathy as a result of increased vascular permeability and leakage from small retinal vessels.
3) Other findings associated with hypertensive eye disease include arteriolar narrowing, hemorrhages, exudates, optic disc swelling, and vision loss. Grading of hypertensive retinopathy depends on the severity of retinal changes seen on examination.
Sickling hemoglobinopathies are genetic blood disorders caused by abnormal hemoglobins that cause red blood cells to take on an anomalous sickle shape and become rigid under conditions of low oxygen and acidity. These misshapen red blood cells can get stuck in and block small blood vessels. Specific disorders include sickle cell anemia, sickle cell trait, sickle cell C disease, and sickle cell thalassemia. Ocular complications range from mild and asymptomatic to proliferative retinopathy, which involves the growth of abnormal new blood vessels on the retina and can lead to vision loss from bleeding or retinal detachment. Non-proliferative retinopathy presents as venous tortuosity, silver wiring of
OCT-Angiography is a non-invasive imaging method that uses light to visualize the retinal and choroidal vasculature in 3D without dye injection. It works by detecting the movement of red blood cells on sequential OCT scans to identify blood vessels. The document describes the technical aspects and clinical applications of several commercial OCT-Angiography systems.
Optical coherence tomography angiography optovue a very basic lecture detailing the new advancement of dyeless angiography by spectral domain OCT system and SSADA and Motion correction algorithm
1. The document discusses various causes and types of diplopia including monocular diplopia caused by refractive errors or macular disorders and binocular diplopia caused by cranial nerve palsies or muscle restrictions.
2. Evaluation of diplopia involves assessing head posture, eye movements, refractive error and neurological function through tests like the three-step test for fourth nerve palsy. Special tests like diplopia testing and cyclodeviation measurements localize the site of muscle weakness.
3. Causes of transient or intermittent diplopia include decompensated phoria, convergence insufficiency, myasthenia gravis or TIAs, while surgical procedures can also cause diplopia through restrictions
Optic neuritis is an inflammatory condition of the optic nerve that commonly affects people ages 20-50. It is more common in females. The document defines optic neuritis and discusses its various classifications, clinical features, diagnosis, relationship to multiple sclerosis, treatment, and prognosis. Treatment typically involves intravenous steroids like methylprednisolone to hasten recovery of vision, though long-term outcomes are generally good with many patients regaining near-normal vision. The presence of lesions on MRI increases the risk of developing multiple sclerosis within 10 years.
Indocyanine green (ICG) videoangiography provides high-resolution imaging of the choroidal vasculature. It has several advantages over fluorescein angiography, including better visualization through pigmented tissues. ICG is protein-bound, allowing enhanced imaging of the choroidal vasculature. Clinical applications include imaging choroidal neovascularization, polypoidal choroidal vasculopathy, central serous chorioretinopathy, and inflammatory choroidal diseases. ICG angiography aids diagnosis and management for these conditions by delineating vascular patterns and lesion activity not visible on fluorescein angiography.
Vitreous hemorrhage occurs when blood leaks into the vitreous cavity in the eye. It can be caused by abnormal blood vessels like those seen in proliferative diabetic retinopathy, tears or detachment of the retina, trauma, or tumors. Patients experience symptoms like decreased vision and floaters. Examination may reveal an absent red reflex or old yellow vitreal hemorrhage. Management depends on the underlying cause and includes observation, laser treatment if the retina can be visualized, vitrectomy if the view is obscured or treatment can't be delivered, and anti-VEGF drugs to reduce neovascularization until laser can be performed.
This document outlines principles of retinal detachment surgery, including scleral buckling procedures, pneumatic retinopexy, and vitrectomy. Scleral buckling involves configuring scleral buckles, localizing retinal breaks, applying cryotherapy, and inserting an explant. Pneumatic retinopexy uses gas injection and postoperative positioning. Vitrectomy is used for giant retinal tears, proliferative vitreoretinopathy, and diabetic tractional retinal detachments to release traction and unfold retinal flaps. The causes and techniques addressed aim to reattach the retina and prevent early failure.
This document summarizes a presentation on normal tension glaucoma (NTG). It begins with an introduction defining NTG as open-angle glaucoma with characteristic optic nerve damage and visual field defects in patients with consistently low intraocular pressure (IOP) below 21 mmHg. It then describes a case presentation of a 47-year-old female patient. The remainder of the document discusses the history, examination, investigations, differential diagnosis, management, pathogenesis involving both IOP-dependent and independent factors, and epidemiology of NTG. Key points are that lowering IOP through medication or surgery can help prevent progression even in NTG, and that NTG may have an underlying vascular component involving low ocular perfusion pressure
This document summarizes various types of gaze palsies, including their causes and clinical presentations. Supranuclear gaze palsies can result from lesions in areas that control eye movements, like the brainstem or cerebral cortex. Clinical exams help localize lesions and differentiate organic from functional disorders. Specific syndromes discussed include Parinaud's syndrome, progressive supranuclear palsy, internuclear ophthalmoplegia, and one-and-a-half syndrome. The document provides details on symptoms, locations of lesions, and distinguishing features of different supranuclear gaze palsy conditions.
This document provides an overview of sixth nerve palsy, including:
- The sixth cranial nerve innervates the lateral rectus muscle to enable eye abduction. Sixth nerve palsy results in limited ability to turn the eye outward.
- Causes of sixth nerve palsy include idiopathic, vascular issues like hypertension and diabetes, trauma, and tumors. Symptoms include esotropia and diplopia.
- Diagnosis involves assessing eye movement limitations and diplopia. Treatment options include occlusion to control diplopia, botulinum toxin injection, or strabismus surgery if no spontaneous recovery occurs. Prognosis is generally good, with many cases recovering spontaneously in
The document describes the anatomy and histology of the upper eyelid as well as common eyelid disorders. It discusses the layers of the eyelid skin and the various glands located within the eyelid, including meibomian glands and sebaceous glands. It then covers inflammatory conditions of the eyelid such as blepharitis, hordeolum, and chalazion. It also describes cysts that can form on the eyelid from blocked glands or ducts. The terminology used for clinical descriptions and histological findings of eyelid lesions is defined.
This document discusses various causes of optic disc edema. It begins by defining disc edema as swelling of the optic disc that can be caused by active or passive factors other than papilledema. Several pseudoedemas are described including drusen, myelinated fibers, tilted discs, and hypoplastic discs. True disc edemas can result from inflammation, vascular issues like CRVO, infiltrative diseases, or papilledema from increased intracranial pressure. Papilledema is usually bilateral non-inflammatory swelling caused by conditions that raise ICP like brain tumors, infections, pseudotumor cerebri, or venous sinus thrombosis. The pathogenesis and features of optic neuritis, multiple sclerosis, and papille
Looking deep into retina : indirect ophthalmoscopy and fundus drawingPrachir Agarwal
Indirect ophthalmoscopy provides a panoramic view of the fundus and is essential for a complete examination. It works by forming an aerial image of the retina between the condensing lens and observer. The power of the condensing lens determines the working distance, magnification, and field of view. Indirect ophthalmoscopy has advantages over direct including an unaffected view by refractive error and better illumination, resolution, and peripheral visualization. Proper technique involves adjusting the device, positioning the patient, and using scleral depression for stereoscopic viewing. Fundus drawings document examination findings and utilize various colors and line styles to depict different retinal structures and pathologies.
Branch retinal vein occlusions (BRVOs) are caused by compression of the retinal vein by an adjacent artery, causing turbulent blood flow and thrombus formation. This leads to retinal ischemia, macular edema, and neovascularization. While BRVOs are typically idiopathic, risk factors include hypertension, atherosclerosis, and thrombophilic conditions. Treatment involves monitoring for complications like macular edema and neovascularization, and using corticosteroids, anti-VEGF agents, laser photocoagulation, or vitrectomy depending on the case. Prognosis depends on how distal the occlusion is from the optic disc, with more distal occlusions having a better visual outcome.
This document discusses imaging techniques used to identify and characterize the pachychoroid phenotype. Key features of the pachychoroid phenotype include choroidal vascular hyperpermeability on ICGA, increased choroidal thickness on OCT imaging, and pathologically dilated choroidal vessels. Advanced imaging such as EDI-OCT, SS-OCT, and ultrawide field imaging have provided more detailed analysis of choroidal abnormalities associated with diseases like central serous chorioretinopathy and polypoidal choroidal vasculopathy. Identification of the pachychoroid phenotype helps explain the spectrum of clinical manifestations in these diseases.
1. Differential diagnosis of disc edema includes conditions like papilledema, optic neuritis, ischemic optic neuropathy, diabetic papillopathy, and hypertensive retinopathy.
2. Papilledema is caused by increased intracranial pressure and presents with bilateral disc swelling and normal vision, while optic neuritis typically causes unilateral vision loss and eye pain.
3. Diabetic papillopathy presents as transient unilateral or bilateral disc edema that resolves within months without vision loss, while malignant hypertension can lead to bilateral disc edema and vision changes as part of hypertensive retinopathy.
Central retinal vein occlusions are caused by blockages in the central retinal vein that drains the retina. This leads to defective vision in the morning. The blockages can be caused by vascular diseases like diabetes and hypertension in the vein wall, increased coagulability of the blood in the vein itself, or external pressure on the vein from issues like orbital cellulitis. Symptoms include defective vision in the morning. Signs include dilated and sluggish pupils, engorged and tortuous veins, extensive retinal hemorrhages, and macular edema. Complications can include neovascularization and glaucoma. Treatment options include anticoagulants, cyclodiathermy, cyclocryotherapy,
The document discusses retinal arterial occlusion, including the central retinal artery and its branches. It describes the anatomy and blood supply of the retina. There are several potential mechanisms of retinal arterial occlusion, most commonly atherosclerosis-related thrombosis. Clinical presentations vary depending on the site of occlusion, such as central retinal artery occlusion presenting with a cherry red spot and cilioretinal artery occlusion causing pericentral scotomas. Management includes treating the acute event to restore vision as well as workup and management of any underlying systemic conditions. However, visual recovery is often poor due to retinal infarction.
Disc anomalies, pits and treatment of associatedabhishek ghelani
This document discusses various optic disc anomalies including megalopapilla, aplasia, hypoplasia, and optic disc pits. Optic disc pits can cause serous retinal detachments, with fluid passing through the pit and accumulating subretinally. Visual defects may include scotomas or visual field changes. Treatments discussed include observation, steroids, decompression, scleral buckling, photocoagulation, vitrectomy with gas or creating retinotomies to drain subretinal fluid. More effective treatments appear to be vitrectomy with gas and photocoagulation or vitrectomy combined with retinotomies and gas tamponade.
Jessica Alper Chief complaintThe chief complaint stated in t.docxLaticiaGrissomzz
The document describes a case of a patient presenting with increasing shortness of breath and cough over the last month. Upon examination, the patient is found to have distant breath sounds, crackles in both lower lobes, and an S3 gallop. The presumptive diagnosis is congestive heart failure, supported by the patient's symptoms and physical exam findings. Differential diagnoses include cardiogenic pulmonary edema and acute kidney injury. The treatment plan for congestive heart failure involves both pharmacological and non-pharmacological approaches, as well as some invasive strategies when medications have failed or the condition has progressed to end-stage.
1. Patients with chronic kidney disease (CKD) have a high prevalence of arterial and valvular disorders such as endothelial dysfunction, vascular calcification, arterial stiffness, annular and valvular calcification, and valvular stenosis and regurgitation.
2. The pathophysiology of these disorders in CKD involves impaired endothelial function, altered collagen turnover, and vascular smooth muscle cell dysfunction leading to calcification.
3. Arterial and valvular disorders in CKD result in increased cardiovascular disease and mortality. Progression of calcification is associated with higher mortality in dialysis patients.
OCT-Angiography is a non-invasive imaging method that uses light to visualize the retinal and choroidal vasculature in 3D without dye injection. It works by detecting the movement of red blood cells on sequential OCT scans to identify blood vessels. The document describes the technical aspects and clinical applications of several commercial OCT-Angiography systems.
Optical coherence tomography angiography optovue a very basic lecture detailing the new advancement of dyeless angiography by spectral domain OCT system and SSADA and Motion correction algorithm
1. The document discusses various causes and types of diplopia including monocular diplopia caused by refractive errors or macular disorders and binocular diplopia caused by cranial nerve palsies or muscle restrictions.
2. Evaluation of diplopia involves assessing head posture, eye movements, refractive error and neurological function through tests like the three-step test for fourth nerve palsy. Special tests like diplopia testing and cyclodeviation measurements localize the site of muscle weakness.
3. Causes of transient or intermittent diplopia include decompensated phoria, convergence insufficiency, myasthenia gravis or TIAs, while surgical procedures can also cause diplopia through restrictions
Optic neuritis is an inflammatory condition of the optic nerve that commonly affects people ages 20-50. It is more common in females. The document defines optic neuritis and discusses its various classifications, clinical features, diagnosis, relationship to multiple sclerosis, treatment, and prognosis. Treatment typically involves intravenous steroids like methylprednisolone to hasten recovery of vision, though long-term outcomes are generally good with many patients regaining near-normal vision. The presence of lesions on MRI increases the risk of developing multiple sclerosis within 10 years.
Indocyanine green (ICG) videoangiography provides high-resolution imaging of the choroidal vasculature. It has several advantages over fluorescein angiography, including better visualization through pigmented tissues. ICG is protein-bound, allowing enhanced imaging of the choroidal vasculature. Clinical applications include imaging choroidal neovascularization, polypoidal choroidal vasculopathy, central serous chorioretinopathy, and inflammatory choroidal diseases. ICG angiography aids diagnosis and management for these conditions by delineating vascular patterns and lesion activity not visible on fluorescein angiography.
Vitreous hemorrhage occurs when blood leaks into the vitreous cavity in the eye. It can be caused by abnormal blood vessels like those seen in proliferative diabetic retinopathy, tears or detachment of the retina, trauma, or tumors. Patients experience symptoms like decreased vision and floaters. Examination may reveal an absent red reflex or old yellow vitreal hemorrhage. Management depends on the underlying cause and includes observation, laser treatment if the retina can be visualized, vitrectomy if the view is obscured or treatment can't be delivered, and anti-VEGF drugs to reduce neovascularization until laser can be performed.
This document outlines principles of retinal detachment surgery, including scleral buckling procedures, pneumatic retinopexy, and vitrectomy. Scleral buckling involves configuring scleral buckles, localizing retinal breaks, applying cryotherapy, and inserting an explant. Pneumatic retinopexy uses gas injection and postoperative positioning. Vitrectomy is used for giant retinal tears, proliferative vitreoretinopathy, and diabetic tractional retinal detachments to release traction and unfold retinal flaps. The causes and techniques addressed aim to reattach the retina and prevent early failure.
This document summarizes a presentation on normal tension glaucoma (NTG). It begins with an introduction defining NTG as open-angle glaucoma with characteristic optic nerve damage and visual field defects in patients with consistently low intraocular pressure (IOP) below 21 mmHg. It then describes a case presentation of a 47-year-old female patient. The remainder of the document discusses the history, examination, investigations, differential diagnosis, management, pathogenesis involving both IOP-dependent and independent factors, and epidemiology of NTG. Key points are that lowering IOP through medication or surgery can help prevent progression even in NTG, and that NTG may have an underlying vascular component involving low ocular perfusion pressure
This document summarizes various types of gaze palsies, including their causes and clinical presentations. Supranuclear gaze palsies can result from lesions in areas that control eye movements, like the brainstem or cerebral cortex. Clinical exams help localize lesions and differentiate organic from functional disorders. Specific syndromes discussed include Parinaud's syndrome, progressive supranuclear palsy, internuclear ophthalmoplegia, and one-and-a-half syndrome. The document provides details on symptoms, locations of lesions, and distinguishing features of different supranuclear gaze palsy conditions.
This document provides an overview of sixth nerve palsy, including:
- The sixth cranial nerve innervates the lateral rectus muscle to enable eye abduction. Sixth nerve palsy results in limited ability to turn the eye outward.
- Causes of sixth nerve palsy include idiopathic, vascular issues like hypertension and diabetes, trauma, and tumors. Symptoms include esotropia and diplopia.
- Diagnosis involves assessing eye movement limitations and diplopia. Treatment options include occlusion to control diplopia, botulinum toxin injection, or strabismus surgery if no spontaneous recovery occurs. Prognosis is generally good, with many cases recovering spontaneously in
The document describes the anatomy and histology of the upper eyelid as well as common eyelid disorders. It discusses the layers of the eyelid skin and the various glands located within the eyelid, including meibomian glands and sebaceous glands. It then covers inflammatory conditions of the eyelid such as blepharitis, hordeolum, and chalazion. It also describes cysts that can form on the eyelid from blocked glands or ducts. The terminology used for clinical descriptions and histological findings of eyelid lesions is defined.
This document discusses various causes of optic disc edema. It begins by defining disc edema as swelling of the optic disc that can be caused by active or passive factors other than papilledema. Several pseudoedemas are described including drusen, myelinated fibers, tilted discs, and hypoplastic discs. True disc edemas can result from inflammation, vascular issues like CRVO, infiltrative diseases, or papilledema from increased intracranial pressure. Papilledema is usually bilateral non-inflammatory swelling caused by conditions that raise ICP like brain tumors, infections, pseudotumor cerebri, or venous sinus thrombosis. The pathogenesis and features of optic neuritis, multiple sclerosis, and papille
Looking deep into retina : indirect ophthalmoscopy and fundus drawingPrachir Agarwal
Indirect ophthalmoscopy provides a panoramic view of the fundus and is essential for a complete examination. It works by forming an aerial image of the retina between the condensing lens and observer. The power of the condensing lens determines the working distance, magnification, and field of view. Indirect ophthalmoscopy has advantages over direct including an unaffected view by refractive error and better illumination, resolution, and peripheral visualization. Proper technique involves adjusting the device, positioning the patient, and using scleral depression for stereoscopic viewing. Fundus drawings document examination findings and utilize various colors and line styles to depict different retinal structures and pathologies.
Branch retinal vein occlusions (BRVOs) are caused by compression of the retinal vein by an adjacent artery, causing turbulent blood flow and thrombus formation. This leads to retinal ischemia, macular edema, and neovascularization. While BRVOs are typically idiopathic, risk factors include hypertension, atherosclerosis, and thrombophilic conditions. Treatment involves monitoring for complications like macular edema and neovascularization, and using corticosteroids, anti-VEGF agents, laser photocoagulation, or vitrectomy depending on the case. Prognosis depends on how distal the occlusion is from the optic disc, with more distal occlusions having a better visual outcome.
This document discusses imaging techniques used to identify and characterize the pachychoroid phenotype. Key features of the pachychoroid phenotype include choroidal vascular hyperpermeability on ICGA, increased choroidal thickness on OCT imaging, and pathologically dilated choroidal vessels. Advanced imaging such as EDI-OCT, SS-OCT, and ultrawide field imaging have provided more detailed analysis of choroidal abnormalities associated with diseases like central serous chorioretinopathy and polypoidal choroidal vasculopathy. Identification of the pachychoroid phenotype helps explain the spectrum of clinical manifestations in these diseases.
1. Differential diagnosis of disc edema includes conditions like papilledema, optic neuritis, ischemic optic neuropathy, diabetic papillopathy, and hypertensive retinopathy.
2. Papilledema is caused by increased intracranial pressure and presents with bilateral disc swelling and normal vision, while optic neuritis typically causes unilateral vision loss and eye pain.
3. Diabetic papillopathy presents as transient unilateral or bilateral disc edema that resolves within months without vision loss, while malignant hypertension can lead to bilateral disc edema and vision changes as part of hypertensive retinopathy.
Central retinal vein occlusions are caused by blockages in the central retinal vein that drains the retina. This leads to defective vision in the morning. The blockages can be caused by vascular diseases like diabetes and hypertension in the vein wall, increased coagulability of the blood in the vein itself, or external pressure on the vein from issues like orbital cellulitis. Symptoms include defective vision in the morning. Signs include dilated and sluggish pupils, engorged and tortuous veins, extensive retinal hemorrhages, and macular edema. Complications can include neovascularization and glaucoma. Treatment options include anticoagulants, cyclodiathermy, cyclocryotherapy,
The document discusses retinal arterial occlusion, including the central retinal artery and its branches. It describes the anatomy and blood supply of the retina. There are several potential mechanisms of retinal arterial occlusion, most commonly atherosclerosis-related thrombosis. Clinical presentations vary depending on the site of occlusion, such as central retinal artery occlusion presenting with a cherry red spot and cilioretinal artery occlusion causing pericentral scotomas. Management includes treating the acute event to restore vision as well as workup and management of any underlying systemic conditions. However, visual recovery is often poor due to retinal infarction.
Disc anomalies, pits and treatment of associatedabhishek ghelani
This document discusses various optic disc anomalies including megalopapilla, aplasia, hypoplasia, and optic disc pits. Optic disc pits can cause serous retinal detachments, with fluid passing through the pit and accumulating subretinally. Visual defects may include scotomas or visual field changes. Treatments discussed include observation, steroids, decompression, scleral buckling, photocoagulation, vitrectomy with gas or creating retinotomies to drain subretinal fluid. More effective treatments appear to be vitrectomy with gas and photocoagulation or vitrectomy combined with retinotomies and gas tamponade.
Jessica Alper Chief complaintThe chief complaint stated in t.docxLaticiaGrissomzz
The document describes a case of a patient presenting with increasing shortness of breath and cough over the last month. Upon examination, the patient is found to have distant breath sounds, crackles in both lower lobes, and an S3 gallop. The presumptive diagnosis is congestive heart failure, supported by the patient's symptoms and physical exam findings. Differential diagnoses include cardiogenic pulmonary edema and acute kidney injury. The treatment plan for congestive heart failure involves both pharmacological and non-pharmacological approaches, as well as some invasive strategies when medications have failed or the condition has progressed to end-stage.
1. Patients with chronic kidney disease (CKD) have a high prevalence of arterial and valvular disorders such as endothelial dysfunction, vascular calcification, arterial stiffness, annular and valvular calcification, and valvular stenosis and regurgitation.
2. The pathophysiology of these disorders in CKD involves impaired endothelial function, altered collagen turnover, and vascular smooth muscle cell dysfunction leading to calcification.
3. Arterial and valvular disorders in CKD result in increased cardiovascular disease and mortality. Progression of calcification is associated with higher mortality in dialysis patients.
Cardio renal care-An integated best Practice Approchdrucsamal
This document provides information about a continuing medical education (CME) activity on cardio-renal syndromes (CRS). It begins with a declaration of disclosure stating the National Kidney Foundation's policy to ensure independence and manage any conflicts of interest among activity planners and faculty. The document then outlines the learning objectives, agenda, and pre-program questions. It also includes an overview of CRS, defining the different subtypes and discussing the bidirectional relationship between cardiac and renal dysfunction. Two case studies are presented to illustrate examples of acute cardiorenal syndrome type 1 and acute renocardiac syndrome type 3.
Thermal Imaging for the Diagnosis of Early Vascular Dysfunctions: A Case Reportasclepiuspdfs
Diseases of blood vessels (referred in this article as vascular dysfunction) cause more morbidity and mortality, than combined impact of any other major non-communicable disease including cancer. We strongly feel that the development of a therapy system based on the management of disease of the vessel than management of the risk factors will yield better results and provide greater opportunity for individualized therapy. Detection of early vascular changes before clinical manifestations of endothelial dysfunction, hardening of the arteries, increased intima-media thickness, is of great importance for early identification of individuals with increased risk of accelerated atherosclerosis.
Hypertensive retinopathy consists of retinal vascular changes caused by elevated blood pressure. It progresses through vasoconstrictive, exudative, and sclerotic phases. Key features include arteriolar narrowing, AV nicking, hemorrhages, and cotton wool spots. Left untreated, malignant hypertension can lead to hypertensive choroidopathy characterized by Elsching spots and Siegrist streaks, as well as hypertensive optic neuropathy. Strict blood pressure control and regular screening can help prevent progression of hypertensive eye disease.
Diabetic neuropathy is a major cause of neuropathy worldwide and may lead to amputations and incapacity. This study aimed at a detailed and updated review on diabetic neuropathy, focusing on its epidemiology, classification, clinical features, risk factor, diagnostic investigation and treatment. Dr. Siva Rami Reddy E "A Basic Review on Diabetic Neuropathy" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-3 | Issue-2 , February 2019, URL: https://www.ijtsrd.com/papers/ijtsrd21391.pdf
Paper URL: https://www.ijtsrd.com/other-scientific-research-area/other/21391/a--basic-review-on-diabetic-neuropathy/dr-siva-rami-reddy-e
Diabetic ketoacidosis induced cerebral infarct - A missing link in pathogenes...Apollo Hospitals
Diabetic ketoacidosis (DKA) is a known complication of acute pancreatitis (AP). We report a case of DKA precipitated by AP. This patient developed watershed infarct in brain during her course of disease which was possibly attributed to hypercoagulability, stasis and endothelial injury triggered by ketosis.
An elderly diabetic and hypertensive male presented with acute renal failure and rhabdomyolysis. He experienced cardiac arrest with moderate hyperkalemia despite medical treatment and hemodialysis. Telemetry changes were retrospectively studied and found to have significant rhythm changes that occurred just less than 10 minutes prior to the cardiac arrest.
Giant cell arteritis is a disease that affects medium and large arteries, often causing ischemia. It typically affects older adults and presents with symptoms of temporal headache, jaw claudication, and scalp tenderness. Laboratory tests often show elevated ESR and CRP levels. Diagnosis is made through temporal artery biopsy or response to treatment with corticosteroids like prednisone. Treatment involves high doses of prednisone tapered over two years to prevent vision loss and other complications.
Nitrous oxide is a colourless gas that is commonly used for sedation and pain relief, but is also used by people to feel intoxicated or high. It is commonly used by dentists and medical professionals to sedate patients undergoing minor medical procedures
Hypertension can damage the eye and lead to hypertensive retinopathy. Chronic high blood pressure causes gradual changes to the retinal blood vessels including arteriolar narrowing, nicking at arteriovenous crossings, and changes to the light reflex seen in the vessels. Malignant or acute hypertension can additionally cause retinal hemorrhages, cotton wool spots, and exudates due to damage to the small blood vessels in the retina. Strict control of blood pressure is important to prevent further eye damage and risk of other end-organ complications.
Diabetic retinopathy is a complication of diabetes causing progressive damage to the retina, located at the back of the
eye, potentially leading to clouded vision or blindness. Disease signs may be visualized by Optical Coherence Tomography
(OCT) and include formation of new and weaker blood vessels, fluid accumulation, exudates and changes to Retinal Vascular
Geometry (RVG). Presence of these indicators can provide information as to the stage of the disease. Image-processing
strategies are applied for the automated detection, segmentation, extraction, classification toward likelihood estimation of
progression of diabetic retinopathy to visual biomarkers present in OCT, using time-sequenced data in the early stages of the
disease. Gabor and Savitsky-Golay filtering enables extraction of the vessel map and fuzzy control for segmentation of hard
exudates. Feature data are extracted using bounding boxes, vector map and connected component methodology for binary
decision tree classifier construction, training and testing. Feature values comprising classifier nodes include: exudate features
of compactness, area, convexity and form factor, in addition to vessel features: width, elongation, bifurcation angles, form
factor and solidity. Classifier accuracy is 93.3%, with 6.7% misclassification and 0% false-negative classification. Automated
image processing of diabetic retinopathy is achieved with high classification accuracy for the extraction of vessel map and
hard exudate biomarkers from OCT. Application of smoothing algorithms and removal of vessel map shadows may further
improve classification accuracy.
This document discusses disseminated intravascular coagulation (DIC), including its classification, risk factors, pathophysiology, clinical manifestations, diagnostic tests, nursing management, and recent advances. DIC can be acute, subacute, or chronic. Acute DIC occurs rapidly and is dominated by bleeding and shock, often seen with severe infections. Chronic DIC progresses slowly over weeks and thrombosis may predominate, as seen in cancer. Risk factors include shock, transfusions, obstetric conditions, malignancies, and tissue damage. Circulating histones and neutrophil extracellular traps are implicated in DIC pathogenesis and may be novel biomarkers or therapeutic targets. Nursing management focuses on hemodynamic stability, skin integrity, fluid balance
Early Detection of High Blood Pressure and Diabetic Retinopathy on Retinal Fu...IJAAS Team
In this paper we present a lifting wavelet based CBRIR image retrieval system that uses color and texture as visual features to describe the content of a retinal fundus images. Our contribution is of three directions. First, we use lifting wavelets 9/7 for lossy and SPL5/3 for lossless to extract texture features from arbitrary shaped retinal fundus regions separated from an image to increase the system effectiveness. This process is performed offline before query processing, therefore to answer a query our system does not need to search the entire database images; instead just a number of similar class type patient images are required to be searched for image similarity. Third, to further increase the retrieval accuracy of our system, we combine the region based features extracted from image regions, with global features extracted from the whole image, which are texture using lifting wavelet and HSV color histograms. Our proposed system has the advantage of increasing the retrieval accuracy and decreasing the retrieval time. The experimental evaluation of the system is based on a db1 online retinal fundus color image database. From the experimental results, it is evident that our system performs significantly better accuracy as compared with traditional wavelet based systems. In our simulation analysis, we provide a comparison between retrieval results based on features extracted from the whole image using lossless 5/3 lifting wavelet and features extracted using lossless 9/7 lifting wavelet and using traditional wavelet. The results demonstrate that each type of feature is effective for a particular type of disease of retinal fundus images according to its semantic contents, and using lossless 5/3 lifting wavelet of them gives better retrieval results for almost all semantic classes and outperform 4-10% more accuracy than traditional wavelet.
Hypertension can cause hypertensive retinopathy by damaging blood vessels in the retina. It progresses through vasoconstrictive, sclerotic, and exudative phases causing signs like hemorrhages, exudates, and cotton wool spots. Retinal imaging can diagnose and monitor the condition. Treatment focuses on controlling blood pressure through medication and lifestyle changes to prevent further vision loss and systemic complications. Patients with severe retinopathy have increased risk of other vascular issues and require close monitoring.
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Osvaldo Bernardo Muchanga-GASTROINTESTINAL INFECTIONS AND GASTRITIS-2024.pdfOsvaldo Bernardo Muchanga
GASTROINTESTINAL INFECTIONS AND GASTRITIS
Osvaldo Bernardo Muchanga
Gastrointestinal Infections
GASTROINTESTINAL INFECTIONS result from the ingestion of pathogens that cause infections at the level of this tract, generally being transmitted by food, water and hands contaminated by microorganisms such as E. coli, Salmonella, Shigella, Vibrio cholerae, Campylobacter, Staphylococcus, Rotavirus among others that are generally contained in feces, thus configuring a FECAL-ORAL type of transmission.
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These are generally consequences (signs and symptoms) resulting from gastrointestinal infections: diarrhea, vomiting, fever and malaise, among others.
The treatment consists of replacing lost liquids and electrolytes (drinking drinking water and other recommended liquids, including consumption of juicy fruits such as papayas, apples, pears, among others that contain water in their composition).
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Gastritis and Gastric Health
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Computer in pharmaceutical research and development-Mpharm(Pharmaceutics)MuskanShingari
Statistics- Statistics is the science of collecting, organizing, presenting, analyzing and interpreting numerical data to assist in making more effective decisions.
A statistics is a measure which is used to estimate the population parameter
Parameters-It is used to describe the properties of an entire population.
Examples-Measures of central tendency Dispersion, Variance, Standard Deviation (SD), Absolute Error, Mean Absolute Error (MAE), Eigen Value
2. The arteriosclerotic changes in hypertensive retinopathy are caused by chronically
elevated blood pressure (BP)
Elevated blood pressure defined as SBP >140 mmHg and DBP >90 mmHg.[1]
Can be caused by either chronic primary or secondary hypertension (e.g.
pheochromocytoma, primary hyperaldosteronism, Cushing’s syndrome, renal parenchymal
disease, renal vascular disease, coarctation of the aorta, obstructive sleep apnea,
hyperparathyroidism, and hyperthyroidism).[2]
ETIOLOGY
1. American Academy of Ophthalmology. Basic and Clinical Sciences Course (Lifelong Education for the Ophthalmologist). San Fransisco. 2006.
2. Katakam, R., Brukamp, K., and Townsend, R.R. What is the proper workup of a patient with hypertension? Cleve Clin J Med. 2008;75:663-72.
3. EPIDEMIOLOGY
Erden et al. showed that the incidence of hypertensive retinopathy directly proportional to
the severity and duration of hypertension[1]
A study in German population, the incidence of hypertensive retinopathy was 10.7% (from
12,751 persons) with a median follow-up time of 8.6 years[2]
A study in DR. M. Djamil Hospital, Padang, Indonesia, found that hypertensive retinopathy
was present in 66.67% hypertensive patients[3]
Chronic kidney disease (CKD) was found to be the most significant factor to predict severe
hypertensive retinopathy[4]
1. Erden S, Bicakci E. Hypertensive retinopathy: incidence, risk factors, and comorbidities. Clin Exp Hypertens. 2012;34(6):397-401
2. Alexander Karl-Georg Schuster, Stella Hoh, Karl Neubert, Ahmad Haj Ibrahim, Stefan Nickels, Christina A. Korb, Andreas Schulz, Thomas Muenzel, Matthias Michal, Irene Schmidtmann, Karl Lackner, Philipp Wild,
Norbert Pfeiffer; Prevalence of hypertensive retinopathy and its risk for mortality – results from the Gutenberg Health Study. Invest. Ophthalmol. Vis. Sci. 2020;61(7):1308.
3. Rahman K, Yusticia RY. Profil Retinopathy Hipertensi di Rumah Sakit Dr. M Djamil Padang. J Kesehat Andalas. 2018;7(Supplement 1):19. .
4. Kabedi NN, Mwanza JC, Lepira FB, Kayembe TK, Kayembe DL. Hypertensive retinopathy and its association with cardiovascular, renal and cerebrovascular morbidity in Congolese patients. Cardiovasc J Afr. 2014
Sep-Oct;25(5):228-32.
4. PATOPHYSIOLOGY
Retinal blood vessels have distinct features that differentiate them from other blood vessels, including:[1]
1. The absence of sympathetic nerve supply
2. Local autoregulation of blood flow
3. Presence of blood-retinal barrier
An increase in systemic BP is transferred directly to the to the vessels which initially constrict.
A further increase in BP overcomes this compensatory tone and damage to the muscle layer and endothelium
ensues.
Blood pressure elevation continues
Hypertensive retinopathy goes through 3 phases: vasoconstrictive, sclerotic, and exudative phases[2]
1. Chaine G, Kohner EM. [Hypertensive retinopathy]. J Fr Ophtalmol. 1983;6(12):995-1005.
2. Modi, P., Arsiwalla, T. Hypertensive retinopathy [Internet]. StatPearls Publishing. 2021 [Accessed on 22 February 2022]. Available on: https://www.ncbi.nlm.nih.gov/books/NBK525980/
5. 3 PHASES OF HYPERTENSIVE RETINOPATHY
Vasoconstrictive Phase
The local autoregulatory mechanisms
come into play
This autoregulatory mechanisms cause
vasospasm and retinal arteriole
narrowing, which is evident by the
decrease in the arteriole to venule ratio
(Normal = 2:3).
Sclerotic Phase
Persistent elevated BP cause
changes in vessel wall
These changes include:
Thickening of the intimal layer
Hyperplasia of the media layer
Hyaline degeneration of the
arteriolar wall
Exudative Phase
Disruption of the blood-brain barrier
and leakage of plasma and blood
into the vessel wall
Typically seen in severely increased
BP patients
Leakage of plasma and blood into
the vessel wall cause disruption in
the local autoregulatory mechanism
Causing retinal hemorrhages (flame-shaped and
dot blot), hard exudates, retinal ischemia (cotton-
wool spots), and necrosis of smooth muscle.
Leads to a severe form of arteriolar narrowing,
arteriovenous (AV) crossing changes, and
widening and accentuation of light reflex
(silver and copper wiring)
Modi, P., Arsiwalla, T. Hypertensive retinopathy [Internet]. StatPearls Publishing. 2021 [Accessed on 22 February 2022]. Available on: https://www.ncbi.nlm.nih.gov/books/NBK525980/
6. DIAGNOSIS
Diagnosis based upon its clinical appearance on dilated fundoscopic exam and coexistent hypertension[1,2]
HISTORY OF
HYPERTENSION
Focus on disease history, symptoms of hypertension, and its complications
Most patients are asymptomatic
Symptoms: headaches*, eye pain*, reduced visual acuity*, focal neurological deficits, chest pain,
shortness of breath, dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, and
palpitation
Complications: history of stroke/transient ischemic attack, coronary or peripheral vascular disease,
and heart failure
PHYSICAL
EXAMINATION
Focus on vital signs (especially blood pressure) and dilated fundoscopy
Fundus exam is necessary for staging of hypertensive retinopathy
1. Modi, P., Arsiwalla, T. Hypertensive retinopathy [Internet]. StatPearls Publishing. 2021 [Accessed on 22 February 2022]. Available on: https://www.ncbi.nlm.nih.gov/books/NBK525980/
2. American Academy of Ophthalmology. Hypertensive retinopathy [Internet]. 2021 [Accessed on 22 February 2022]. Available on: https://eyewiki.aao.org/Hypertensive_Retinopathy#Diagnosis
*Symptoms of acute malignant hypertension
7. FUNDOSCOPIC FEATURES
AV crossing changes[1]
Salus’s sign: retinal vein deflection as it crosses the arteriole
Gunn’s sign: retinal vein tapering on either side of the AV crossing
Bonnet’s sign: banking of retinal vein distal to the AV crossing
1. Modi, P., Arsiwalla, T. Hypertensive retinopathy [Internet]. StatPearls Publishing. 2021 [Accessed on 22 February 2022]. Available on: https://www.ncbi.nlm.nih.gov/books/NBK525980/
2. Epomedicine. Hypertensive Retinopathy Grading – Simplified [Internet]. Epomedicine; 2019 Jun 1 [cited 2022 Feb 19]. Available from: https://epomedicine.com/medical-students/hypertensive-retinopathy-grading-simplified/.
Figure 1. AV crossing changes[2]
8. Arterial Changes[1]
Decrease in AV ratio to 1:3 (normal ratio 2:3)
Change in the arteriolar light reflex (copper
and/or silver wiring)
Figure 2. Copper-wiring, arteriovenous nicking and silver-wiring
seen in a patient with hypertensive retinopathy[2]
1. Modi, P., Arsiwalla, T. Hypertensive retinopathy [Internet]. StatPearls Publishing. 2021 [Accessed on 22 February 2022]. Available on: https://www.ncbi.nlm.nih.gov/books/NBK525980/
2. American Academy of Ophthalmology. Hypertensive retinopathy [Internet]. 2021 [Accessed on 22 February 2022]. Available on: https://eyewiki.aao.org/Hypertensive_Retinopathy#Diagnosis
9. NORMAL A/V RATIO (2:3)
Point of measurement for the A/V ratio:
One disc diameter away from the optic nerve, around the second bifurcation
Schramm Od Cns Fsls, Nathan. (2019). Re: How to find the avr ratio?. Retrieved from: https://www.researchgate.net/post/How-to-find-the-avr-ratio/5d8d4a0bd7141b9cc85eff2a/citation/download.
Figure 3. Normal A/V ratio
10. ARTERIOLE
DECREASED A/V RATIO (1:3)
VENULE
Modi, P., Arsiwalla, T. Hypertensive retinopathy [Internet]. StatPearls Publishing. 2021 [Accessed on 24 February 2022]. Available on: https://www.statpearls.com/ArticleLibrary/viewarticle/35600
Figure 4. Decreased A/V ratio
11. Retinal Changes[1]
Retinal hemorrhages
Dot-blot hemorrhages
Bleeding in the inner retinal layer
Flame shaped hemorrhage
Bleeding in the superficial retinal layer
Retinal exudates
Hard exudate
Lipid deposits in the retina
Soft exudate
Ischemia of the nerve fibers (cotton wool
spots)
Figure 5. AV crossing changes, macular star, and cotton wool
spots[2]
1. Modi, P., Arsiwalla, T. Hypertensive retinopathy [Internet]. StatPearls Publishing. 2021 [Accessed on 22 February 2022]. Available on: https://www.ncbi.nlm.nih.gov/books/NBK525980/
2. American Academy of Ophthalmology. Hypertensive retinopathy [Internet]. 2021 [Accessed on 22 February 2022]. Available on: https://eyewiki.aao.org/Hypertensive_Retinopathy#Diagnosis
Macular Changes[1]
Formation of macular star due to deposition of hard
exudates around the macula.
12. Figure 6. Features of hypertensive retinopathy[2]
1. American Academy of Ophthalmology. Hypertensive retinopathy [Internet]. 2021 [Accessed on 22 February 2022]. Available on: https://eyewiki.aao.org/Hypertensive_Retinopathy#Diagnosis
2. Kulenkamp, E. Hypertensive retinopathy [Internet]. Available on: http://morancore.utah.edu/basic-ophthalmology-review/hypertensive-retinopathy/
Optic Nerve Changes[1]
Hypertension may lead to optic
neuropathy (specifically presents as optic
disk swelling)
Signs of optic neuropathy are:
1. Flame shaped hemorrhage at the disc
margin
2. Blurred disc margin
3. Congested retinal vein
4. Papilledema
5. Secondary macular exudates
13. MODIFIED SCHEIE CLASSIFICATION OF HYPERTENSIVE RETINOPATHY[1]
1. American Academy of Ophthalmology. Hypertensive retinopathy [Internet]. 2021 [Accessed on 22 February 2022]. Available on: https://eyewiki.aao.org/Hypertensive_Retinopathy#Diagnosis
2. Epomedicine. Hypertensive Retinopathy Grading – Simplified [Internet]. Epomedicine; 2019 Jun 1 [cited 2022 Feb 19]. Available from: https://epomedicine.com/medical-students/hypertensive-retinopathy-grading-simplified/.
Grade 0: No changes
Grade 1: Barely detectable arterial narrowing
Grade 2: Obvious arterial narrowing with focal irregularities
Grade 3: Grade 2 + retinal hemorrhages, exudates, cotton wool spots, or retinal edema
Grade 4: Grade 3 + papilledema
Figure 7. Grade 3-4 of hypertensive retinopathy[2]
14. MODIFIED SCHEIE CLASSIFICATION
OF HYPERTENSIVE RETINOPATHY
Walsh JB et al. Chapter 13: Systemic Hypertension and the Eye. [Internet]. 2022. Available from:
http://www.oculist.net/downaton502/prof/ebook/duanes/pages/v3/v3c013.html
A. Grade I narrowing of the arterioles
B. Grade II: generalized narrowing,
focal constriction, arteriolar sclerosis
with widening of the reflex stripe.
C. Grade III: generalized narrowing,
focal constriction, hemorrhages, and
exudate, arteriolar sclerosis with
widening of the light reflex.
D. Grade IV: generalized narrowing,
focal constriction, hemorrhages, and
exudates and edema of the disc with
arteriolar sclerosis.
Figure 8. Funduscopic findings based on Modified Scheie Classification[2]
15. KEITH-WAGENER-BARKER CLASSIFICATION[1]
A. Grade 1:
Mild, generalized constriction of retinal arterioles
B. Grade 2:
Definite focal narrowing of retinal arterioles + AV
nicking (arrows)
C. Grade 3:
Grade 2 + flame-shaped hemorrhages + cotton-
wool spots + hard exudates
D. Grade 4:
Severe Grade 3 retinopathy + papilledema or
retinal edema
Figure 9. Funduscopic findings based on Keith-Wagener-Barker Classification[2]
1. American Academy of Ophthalmology. Hypertensive retinopathy [Internet]. 2021 [Accessed on 22 February 2022].
Available on: https://eyewiki.aao.org/Hypertensive_Retinopathy#Diagnosis
2. Anonymous. Hypertensive retinopathy [Internet]. [Accessed on 24 February 2022]. Available on:
https://basicmedicalkey.com/hypertensive-retinopathy-2/
16. WONG AND MITCHELL CLASSIFICATION OF HYPERTENSIVE RETINOPATHY
1. Wong TY, Mitchell P. Hypertensive retinopathy. N Engl J Med. 2004;351:2310–2317. doi:10.1056/NEJMra032865
2. Aissopou EK, Papathanassiou M, Nasothimiou EG, Konstantonis GD, Tentolouris N, Theodossiadis PG, Papaioannou TG, Sfikakis PP, Protogerou AD. The Keith-Wagener-Barker and Mitchell-Wong grading systems for hypertensive
retinopathy: association with target organ damage in individuals below 55 years. J Hypertens. 2015 Nov;33(11):2303-9. doi: 10.1097/HJH.0000000000000702. PMID: 26335430.
Mitchell-Wong seems preferable to the Keith-Wagener-Barker classification system, for reasons of simplifying
clinical practice and the grades of retinopathy were more strongly associated with systemic issues[1,2]
17. DIFFERENTIAL DIAGNOSIS
Conditions that have similar features with hypertensive retinopathy includes most notably diabetic
retinopathy, radiation retinopathy, and retinal vein occlusion[1]
CLINICAL FINDINGS HYPERTENSIVE RETINOPATHY DIABETIC RETINOPATHY RADIATION RETINOPATHY
History History of hypertension History of diabetes
History of radiation
(e.g. nasopharyngeal carcinoma
treatment)[2,3]
Funduscopic Findings
AV changes
Arterial changes
Retinal changes
Macular changes
Optic nerve changes
Similar findings with
hypertensive retinopathy
Similar findings with
hypertensive retinopathy
Optic disc edema can also be found in diabetic papillopathy, anterior ischemic optic neuropathy, and
neuroretinitis[1]
1. American Academy of Ophthalmology. Hypertensive retinopathy [Internet]. 2021 [Accessed on 22 February 2022]. Available on: https://eyewiki.aao.org/Hypertensive_Retinopathy#Diagnosis
2. Ho, IV. Radiation retinopathy [Internet]. 2012 [Accessed on 24 February 2022]. Available on: http://www.retina.com.au/case-of-the-monthdec-2012/
3. Raja V, Rajagopalan S, Kashab T, Moriarty B. Radiation retinopathy: a mistaken diagnosis of hypertensive retinopathy. Clinical and Experimental Optometry. 2007;90(6):468-470.