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article-22264_27 | Open Angle Glaucoma -- Epidemiology -- Risk Factors: | High blood pressure (systemic arterial hypertension has been associated with but is not a confirmed risk factor for OAG) [35] | Open Angle Glaucoma -- Epidemiology -- Risk Factors:. High blood pressure (systemic arterial hypertension has been associated with but is not a confirmed risk factor for OAG) [35] |
article-22264_28 | Open Angle Glaucoma -- Epidemiology -- Risk Factors: | Type 2 diabetes mellitus [36] | Open Angle Glaucoma -- Epidemiology -- Risk Factors:. Type 2 diabetes mellitus [36] |
article-22264_29 | Open Angle Glaucoma -- Epidemiology -- Risk Factors: | High pattern standard deviation on visual fields [37] | Open Angle Glaucoma -- Epidemiology -- Risk Factors:. High pattern standard deviation on visual fields [37] |
article-22264_30 | Open Angle Glaucoma -- Epidemiology -- Risk Factors: | Migraine or vasospasm [38] | Open Angle Glaucoma -- Epidemiology -- Risk Factors:. Migraine or vasospasm [38] |
article-22264_31 | Open Angle Glaucoma -- Epidemiology -- Risk Factors: | Low intracranial (cerebral spinal fluid) pressure [39] | Open Angle Glaucoma -- Epidemiology -- Risk Factors:. Low intracranial (cerebral spinal fluid) pressure [39] |
article-22264_32 | Open Angle Glaucoma -- Epidemiology -- Risk Factors: | Oral contraceptive pill [40] | Open Angle Glaucoma -- Epidemiology -- Risk Factors:. Oral contraceptive pill [40] |
article-22264_33 | Open Angle Glaucoma -- Epidemiology -- Risk Factors: | Lifestyle risk factors include smoking, obesity, alcohol, anxiety, stress, and sleep apnea [41] | Open Angle Glaucoma -- Epidemiology -- Risk Factors:. Lifestyle risk factors include smoking, obesity, alcohol, anxiety, stress, and sleep apnea [41] |
article-22264_34 | Open Angle Glaucoma -- Pathophysiology -- Retinal Ganglion Cells | The exact cause of glaucoma is not fully known, but the underlying pathology lies in the apoptosis of retinal ganglion cells. [7] Retinal ganglion cells (RGC) are the third class of photoreceptors recently noted in scientific literature for their intrinsic photosensitivity. RGCs form functional microcircuits with rods, cones, amacrine cells, and bipolar cells that help transmit image-forming and non-image-forming information to the brain. RGC axons target the suprachiasmatic nucleus, intergeniculate leaflet, olivary pretectal nucleus, ventral division of the lateral geniculate nucleus, and the preoptic area. | Open Angle Glaucoma -- Pathophysiology -- Retinal Ganglion Cells. The exact cause of glaucoma is not fully known, but the underlying pathology lies in the apoptosis of retinal ganglion cells. [7] Retinal ganglion cells (RGC) are the third class of photoreceptors recently noted in scientific literature for their intrinsic photosensitivity. RGCs form functional microcircuits with rods, cones, amacrine cells, and bipolar cells that help transmit image-forming and non-image-forming information to the brain. RGC axons target the suprachiasmatic nucleus, intergeniculate leaflet, olivary pretectal nucleus, ventral division of the lateral geniculate nucleus, and the preoptic area. |
article-22264_35 | Open Angle Glaucoma -- Pathophysiology -- Retinal Ganglion Cells | RGCs play a role in modulating circadian rhythm, releasing melatonin, regulating pupil size, and forming relays in on-off retina centers. [42] RGC axons remain unmyelinated until they have passed through the lamina cribrosa and converged to form the optic nerve. | Open Angle Glaucoma -- Pathophysiology -- Retinal Ganglion Cells. RGCs play a role in modulating circadian rhythm, releasing melatonin, regulating pupil size, and forming relays in on-off retina centers. [42] RGC axons remain unmyelinated until they have passed through the lamina cribrosa and converged to form the optic nerve. |
article-22264_36 | Open Angle Glaucoma -- Pathophysiology -- Retinal Ganglion Cells | After passing through the lamina cribrosa, oligodendrocytes myelinate the axons of the RGCs. Iatrogenically induced ocular hypertension in mice, cats, and monkeys has shown blockade of orthograde and retrograde axonal transport, integral in transporting growth factors such as brain-derived neurotrophic factors. Regardless of whether IOP is elevated, normal, or decreased, the death of RGCs underlies glaucoma pathology. [43] [44] | Open Angle Glaucoma -- Pathophysiology -- Retinal Ganglion Cells. After passing through the lamina cribrosa, oligodendrocytes myelinate the axons of the RGCs. Iatrogenically induced ocular hypertension in mice, cats, and monkeys has shown blockade of orthograde and retrograde axonal transport, integral in transporting growth factors such as brain-derived neurotrophic factors. Regardless of whether IOP is elevated, normal, or decreased, the death of RGCs underlies glaucoma pathology. [43] [44] |
article-22264_37 | Open Angle Glaucoma -- Pathophysiology -- Lamina Cribrosa | The lamina cribrosa is a sieve-like fenestration at the back of the sclera that allows for a conglomeration of retinal axons and blood vessels to exit the posterior of the eye. Changes in the three-dimensional structure of the lamina cribrosa have been implicated in the pathogenesis of glaucomatous optic atrophy. [45] The superior and inferior channels of the lamina cribrosa contain larger pores and thinner connective tissue support for the passage of nerve-fiber bundles than the nasal and temporal parts of the lamina. The most common pattern of glaucomatous optic nerve thinning occurs at the inferior and superior portions of the optic nerve. Also, the superior and inferior laminar zones of the lamina cribrosa are where the arcuate area ganglion cell axons travel, and these axons are the most susceptible to glaucomatous damage. | Open Angle Glaucoma -- Pathophysiology -- Lamina Cribrosa. The lamina cribrosa is a sieve-like fenestration at the back of the sclera that allows for a conglomeration of retinal axons and blood vessels to exit the posterior of the eye. Changes in the three-dimensional structure of the lamina cribrosa have been implicated in the pathogenesis of glaucomatous optic atrophy. [45] The superior and inferior channels of the lamina cribrosa contain larger pores and thinner connective tissue support for the passage of nerve-fiber bundles than the nasal and temporal parts of the lamina. The most common pattern of glaucomatous optic nerve thinning occurs at the inferior and superior portions of the optic nerve. Also, the superior and inferior laminar zones of the lamina cribrosa are where the arcuate area ganglion cell axons travel, and these axons are the most susceptible to glaucomatous damage. |
article-22264_38 | Open Angle Glaucoma -- Pathophysiology -- Lamina Cribrosa | Mechanical damage to axons and the prevention of essential trophic factors, such as the brain-derived neurotrophic factor, being appropriately delivered is conducive to the disease process. Results from studies show that statistically significant depth variability exists among the superior and inferior lamina cribrosa of healthy patients and those with OAG. Patients with OAG have greater depth at the optic cup floor, possibly due to increased IOP pressure. One study examined the lamina cribrosa using Heidelberg retina tomograph and found greater topographic variability and "spikiness" when looking at the lamina cribrosa of patients with OAG; this is most likely a sign of fragility in the lamina, as increased spikiness is inversely related to Humphrey mean deviation ( P < 0.05), and cup-disc ratio ( P < 0.004) and was directly related to nerve fiber layer thickness ( P < 0.005). [46] [47] | Open Angle Glaucoma -- Pathophysiology -- Lamina Cribrosa. Mechanical damage to axons and the prevention of essential trophic factors, such as the brain-derived neurotrophic factor, being appropriately delivered is conducive to the disease process. Results from studies show that statistically significant depth variability exists among the superior and inferior lamina cribrosa of healthy patients and those with OAG. Patients with OAG have greater depth at the optic cup floor, possibly due to increased IOP pressure. One study examined the lamina cribrosa using Heidelberg retina tomograph and found greater topographic variability and "spikiness" when looking at the lamina cribrosa of patients with OAG; this is most likely a sign of fragility in the lamina, as increased spikiness is inversely related to Humphrey mean deviation ( P < 0.05), and cup-disc ratio ( P < 0.004) and was directly related to nerve fiber layer thickness ( P < 0.005). [46] [47] |
article-22264_39 | Open Angle Glaucoma -- Pathophysiology -- Elevated Intraocular Pressure | High IOP is an important risk factor for glaucoma progression. Elevated IOP is the most studied and modifiable risk factor that causes OAG. When IOP rises above 21 mm Hg, a significant risk of developing visual field loss exists (with only small increases in IOP), especially if IOP rises above 26 mm Hg to 30 mm Hg. The high fluctuation of IOP may also lead to glaucoma progression. Reduction of IOP leads to less progression or stabilization of the glaucomatous optic nerve and visual field changes. About 40% to 50% of all OAG cases have IOP below 22 mm Hg in a single screening. [35] [48] | Open Angle Glaucoma -- Pathophysiology -- Elevated Intraocular Pressure. High IOP is an important risk factor for glaucoma progression. Elevated IOP is the most studied and modifiable risk factor that causes OAG. When IOP rises above 21 mm Hg, a significant risk of developing visual field loss exists (with only small increases in IOP), especially if IOP rises above 26 mm Hg to 30 mm Hg. The high fluctuation of IOP may also lead to glaucoma progression. Reduction of IOP leads to less progression or stabilization of the glaucomatous optic nerve and visual field changes. About 40% to 50% of all OAG cases have IOP below 22 mm Hg in a single screening. [35] [48] |
article-22264_40 | Open Angle Glaucoma -- Pathophysiology -- Aqueous Outflow | The 2 main proposed mechanisms by which an elevated IOP is thought to contribute to glaucomatous damage include vascular dysfunction resulting in ischemia to the optic nerve [49] and mechanical dysfunction due to compression of the axons. [50] When OAG in a patient is attributed to elevated IOP, the cause of this increase in IOP is commonly thought to occur due to dysfunction in aqueous outflow through the trabecular meshwork of the eye. [51] This may occur as a result of partial obstruction due to foreign material (eg, accumulated mucopolysaccharides in the trabecular meshwork), a reduction in the number of trabecular endothelial cells, a decreased density of trabecular pores, number of vacuoles, or size of the inner wall endothelium of the canal of Schlemm, loss of phagocytic activity, or dysfunction in the neurological feedback loop involved in drainage of aqueous humor. | Open Angle Glaucoma -- Pathophysiology -- Aqueous Outflow. The 2 main proposed mechanisms by which an elevated IOP is thought to contribute to glaucomatous damage include vascular dysfunction resulting in ischemia to the optic nerve [49] and mechanical dysfunction due to compression of the axons. [50] When OAG in a patient is attributed to elevated IOP, the cause of this increase in IOP is commonly thought to occur due to dysfunction in aqueous outflow through the trabecular meshwork of the eye. [51] This may occur as a result of partial obstruction due to foreign material (eg, accumulated mucopolysaccharides in the trabecular meshwork), a reduction in the number of trabecular endothelial cells, a decreased density of trabecular pores, number of vacuoles, or size of the inner wall endothelium of the canal of Schlemm, loss of phagocytic activity, or dysfunction in the neurological feedback loop involved in drainage of aqueous humor. |
article-22264_41 | Open Angle Glaucoma -- Pathophysiology -- Aqueous Outflow | Other proposed mechanisms for obstruction of aqueous humor outflow include oxidative damage to the meshwork, abnormal corticosteroid metabolism, adrenergic dysfunction, or an immunological process. Unlike angle-closure glaucoma, the drainage angle between the iris and cornea remains open in OAG. Specific individuals may have a genetic predisposition [52] to cell death of individual axons in the eye, resulting in the release of potentially cytotoxic substances such as glutamate, calcium, nitric oxide, and free radicals, as well as the apoptosis of neighboring cells. | Open Angle Glaucoma -- Pathophysiology -- Aqueous Outflow. Other proposed mechanisms for obstruction of aqueous humor outflow include oxidative damage to the meshwork, abnormal corticosteroid metabolism, adrenergic dysfunction, or an immunological process. Unlike angle-closure glaucoma, the drainage angle between the iris and cornea remains open in OAG. Specific individuals may have a genetic predisposition [52] to cell death of individual axons in the eye, resulting in the release of potentially cytotoxic substances such as glutamate, calcium, nitric oxide, and free radicals, as well as the apoptosis of neighboring cells. |
article-22264_42 | Open Angle Glaucoma -- Histopathology | Early in the disease process, glaucomatous optic nerve atrophy can present with thinning and atrophy of the retinal ganglion cell layer and, thus, thinning of the nerve fiber layer above the ganglion cells. [53] The nerve fiber layer consists of the unmyelinated ganglion cell axons, which shrink concomitantly. [54] In more advanced glaucomatous optic nerve atrophy, cupping of the optic nerve and atrophy of the ganglion cell and nerve fiber layers is prevalent. As the ganglion cells deteriorate, the structural integrity of the nerve is compromised. Increased IOP can push into the optic nerve and cause the visible phenomenon of cupping. Retinal ganglion cell loss also leads to increased space and widening of the subdural optic nerve space (see Image. Glaucomatous Optic Nerve Head With Inferotemporal Retinal Nerve Fiber Layer Defect). [55] | Open Angle Glaucoma -- Histopathology. Early in the disease process, glaucomatous optic nerve atrophy can present with thinning and atrophy of the retinal ganglion cell layer and, thus, thinning of the nerve fiber layer above the ganglion cells. [53] The nerve fiber layer consists of the unmyelinated ganglion cell axons, which shrink concomitantly. [54] In more advanced glaucomatous optic nerve atrophy, cupping of the optic nerve and atrophy of the ganglion cell and nerve fiber layers is prevalent. As the ganglion cells deteriorate, the structural integrity of the nerve is compromised. Increased IOP can push into the optic nerve and cause the visible phenomenon of cupping. Retinal ganglion cell loss also leads to increased space and widening of the subdural optic nerve space (see Image. Glaucomatous Optic Nerve Head With Inferotemporal Retinal Nerve Fiber Layer Defect). [55] |
article-22264_43 | Open Angle Glaucoma -- Toxicokinetics | In OAG, particulate matter can lodge into the fine openings in the trabecular meshwork (TM) and increase the passive resistance to aqueous humor drainage. Different substances can disrupt the flow of aqueous across the TM, which include: | Open Angle Glaucoma -- Toxicokinetics. In OAG, particulate matter can lodge into the fine openings in the trabecular meshwork (TM) and increase the passive resistance to aqueous humor drainage. Different substances can disrupt the flow of aqueous across the TM, which include: |
article-22264_44 | Open Angle Glaucoma -- Toxicokinetics | Lens proteins: During cataract surgery, high-molecular-weight lens proteins produced by phacolysis can lodge into the trabecular meshwork and increase drainage resistance. [56] [57] | Open Angle Glaucoma -- Toxicokinetics. Lens proteins: During cataract surgery, high-molecular-weight lens proteins produced by phacolysis can lodge into the trabecular meshwork and increase drainage resistance. [56] [57] |
article-22264_45 | Open Angle Glaucoma -- Toxicokinetics | Red blood cells: In the event of a traumatic injury to the eye, senescent red blood cells are lodged in the trabecular meshwork, a variant of OAG known as "Ghost cell glaucoma." [58] | Open Angle Glaucoma -- Toxicokinetics. Red blood cells: In the event of a traumatic injury to the eye, senescent red blood cells are lodged in the trabecular meshwork, a variant of OAG known as "Ghost cell glaucoma." [58] |
article-22264_46 | Open Angle Glaucoma -- Toxicokinetics | Pigment granules: Pigment from the epithelium of the iris can detach and become lodged in the fine trabecular meshwork, as seen in pigmentary glaucoma [59] and pigment dispersion syndrome. [56] [60] | Open Angle Glaucoma -- Toxicokinetics. Pigment granules: Pigment from the epithelium of the iris can detach and become lodged in the fine trabecular meshwork, as seen in pigmentary glaucoma [59] and pigment dispersion syndrome. [56] [60] |
article-22264_47 | Open Angle Glaucoma -- Toxicokinetics | Pseudoexfoliation syndrome: Deposits of white dandruff-like material on the anterior lens surface, iris, and anterior chamber structures. [61] | Open Angle Glaucoma -- Toxicokinetics. Pseudoexfoliation syndrome: Deposits of white dandruff-like material on the anterior lens surface, iris, and anterior chamber structures. [61] |
article-22264_48 | Open Angle Glaucoma -- Toxicokinetics | Tumor debris: Necrotic tumor debris from necrotic tumors can also clog the trabecular meshwork in a variant known as melanomalytic glaucoma. [62] | Open Angle Glaucoma -- Toxicokinetics. Tumor debris: Necrotic tumor debris from necrotic tumors can also clog the trabecular meshwork in a variant known as melanomalytic glaucoma. [62] |
article-22264_49 | Open Angle Glaucoma -- Toxicokinetics | Corticosteroids: Steroid therapy of any kind can contribute to elevated IOP; however, topical eye and periocular steroids are most likely to increase IOP. [26] [63] | Open Angle Glaucoma -- Toxicokinetics. Corticosteroids: Steroid therapy of any kind can contribute to elevated IOP; however, topical eye and periocular steroids are most likely to increase IOP. [26] [63] |
article-22264_50 | Open Angle Glaucoma -- History and Physical | OAG is often asymptomatic in its early stages; a thorough history and eye exam are instrumental in detecting the disease early (see Image. Glaucoma Field Changes in Left Eye). [64] Early changes in OAG involve a loss of peripheral vision that the patient is usually unaware of until 40% of their nerve fibers are compromised; only then do they start to notice having “tunnel vision.” Visual field defects typically occur after asymptomatic retinal nerve fiber layer thinning and optic nerve cupping (see Image. A Cup-to-Disk Ratio of .75 of the Optic Nerve). Patients do not avert glaucomatous signs and symptoms, unlike maculopathies and cataracts that lead to decreased visual acuity. | Open Angle Glaucoma -- History and Physical. OAG is often asymptomatic in its early stages; a thorough history and eye exam are instrumental in detecting the disease early (see Image. Glaucoma Field Changes in Left Eye). [64] Early changes in OAG involve a loss of peripheral vision that the patient is usually unaware of until 40% of their nerve fibers are compromised; only then do they start to notice having “tunnel vision.” Visual field defects typically occur after asymptomatic retinal nerve fiber layer thinning and optic nerve cupping (see Image. A Cup-to-Disk Ratio of .75 of the Optic Nerve). Patients do not avert glaucomatous signs and symptoms, unlike maculopathies and cataracts that lead to decreased visual acuity. |
article-22264_51 | Open Angle Glaucoma -- History and Physical | Older patients might give clues about their history of losing peripheral vision by admitting to difficulties driving or running into objects around the home more frequently. Primary care patients with the above risk factors should undergo direct ophthalmoscopy to visualize the optic disc. [65] Visualization of the optic disc can provide reliable diagnostic information as it shows changes before the visual field deficits are symptomatic. OAG is often bilateral, and the 2 optic discs can be compared to one another as a useful metric, but the damage can also be asymmetric. Primary care clinicians should refer patients to an ophthalmologist in the presence of the following risk factors, clinical findings, or symptoms that are suggestive of glaucoma: | Open Angle Glaucoma -- History and Physical. Older patients might give clues about their history of losing peripheral vision by admitting to difficulties driving or running into objects around the home more frequently. Primary care patients with the above risk factors should undergo direct ophthalmoscopy to visualize the optic disc. [65] Visualization of the optic disc can provide reliable diagnostic information as it shows changes before the visual field deficits are symptomatic. OAG is often bilateral, and the 2 optic discs can be compared to one another as a useful metric, but the damage can also be asymmetric. Primary care clinicians should refer patients to an ophthalmologist in the presence of the following risk factors, clinical findings, or symptoms that are suggestive of glaucoma: |
article-22264_52 | Open Angle Glaucoma -- History and Physical | A previous ocular history, such as the history of eye pain or redness, headaches, uveitis, diabetic retinopathy, cataracts, vascular occlusions, or multicolored halos African-American race Refractive error Chronic use of topical or systemic corticosteroids Ocular surgery like photocoagulation or refractive procedures, cataract surgery, glaucoma surgery, and systemic surgery/ medications Head or ocular trauma Certain medications, such as hypertensive medications that may influence IOP or systemic/topical steroids Medical history of diabetes mellitus, migraine headaches, hypertension, vasospasm, cardiovascular disease, breathlessness, cardiac arrhythmia Family history (eg, first-degree relative with glaucoma, especially significant if this is a sibling) that would place them at a greater risk of developing OAG Old medical documentation of IOP, optic disc, visual field, and others | Open Angle Glaucoma -- History and Physical. A previous ocular history, such as the history of eye pain or redness, headaches, uveitis, diabetic retinopathy, cataracts, vascular occlusions, or multicolored halos African-American race Refractive error Chronic use of topical or systemic corticosteroids Ocular surgery like photocoagulation or refractive procedures, cataract surgery, glaucoma surgery, and systemic surgery/ medications Head or ocular trauma Certain medications, such as hypertensive medications that may influence IOP or systemic/topical steroids Medical history of diabetes mellitus, migraine headaches, hypertension, vasospasm, cardiovascular disease, breathlessness, cardiac arrhythmia Family history (eg, first-degree relative with glaucoma, especially significant if this is a sibling) that would place them at a greater risk of developing OAG Old medical documentation of IOP, optic disc, visual field, and others |
article-22264_53 | Open Angle Glaucoma -- Evaluation | OAG can be clinically evaluated using a variety of diagnostic tools, but the following triad is the cornerstone of diagnosis: Optic disc or retinal nerve fiber layer changes Visual field changes Elevated IOP [66] | Open Angle Glaucoma -- Evaluation. OAG can be clinically evaluated using a variety of diagnostic tools, but the following triad is the cornerstone of diagnosis: Optic disc or retinal nerve fiber layer changes Visual field changes Elevated IOP [66] |
article-22264_54 | Open Angle Glaucoma -- Evaluation -- Optic Nerve | The optic nerve should be evaluated using a slit lamp and 90D or 78D lens so that the three-dimensional features of the optic nerve are appreciated. The inferior neuroretinal rim (NRR) is the thickest, followed by superior, nasal, and temporal NRR; this is called the ISNT rule. [67] In OAG, the superior and inferior NRR are thinned, breaking the ISNT rule. The optic cup should be determined by its contour and not color. A recent Journal of the Americal Medical Association Rational Clinical Examination systematic review of primary OAG diagnosis found that the risk of glaucoma was highest when an examination revealed an increased cup-disk ratio (CDR), CDR asymmetry, disc hemorrhage, or elevated IOP. [68] Typical optic nerve head changes in OAG include: | Open Angle Glaucoma -- Evaluation -- Optic Nerve. The optic nerve should be evaluated using a slit lamp and 90D or 78D lens so that the three-dimensional features of the optic nerve are appreciated. The inferior neuroretinal rim (NRR) is the thickest, followed by superior, nasal, and temporal NRR; this is called the ISNT rule. [67] In OAG, the superior and inferior NRR are thinned, breaking the ISNT rule. The optic cup should be determined by its contour and not color. A recent Journal of the Americal Medical Association Rational Clinical Examination systematic review of primary OAG diagnosis found that the risk of glaucoma was highest when an examination revealed an increased cup-disk ratio (CDR), CDR asymmetry, disc hemorrhage, or elevated IOP. [68] Typical optic nerve head changes in OAG include: |
article-22264_55 | Open Angle Glaucoma -- Evaluation -- Optic Nerve | Diffuse or focal narrowing (notching/shelving) of the NRR precisely at the superior or inferior part of the optic disc Symmetrically enlarged cup-to-disc ratios greater than 0.5 Increased vertical cup-to-disc ratio and thinning of NRR Asymmetry of CDR of 0.2 or more Hemorrhage at or around the optic disc Peripapillary atrophy Baring of circumlinear vessels (the gap between the superficial vessels and disc margin) Bayonetting of vessels (the vessel first goes back and then climbs along the wall of the deep cup and then angles again on the disc margin) Very deep (excavated) cup with bean-pot cupping and laminar dot sign Nasalization of optic disc vessels Diffuse or focal (arcuate) thinning/defect of the retinal nerve fiber layer contiguous with an area of NRR-notch The NRR is typically pink and not pale in OAG. The pallor of the NRR usually denotes an atrophic optic nerve, as seen in primary angle closure glaucoma. | Open Angle Glaucoma -- Evaluation -- Optic Nerve. Diffuse or focal narrowing (notching/shelving) of the NRR precisely at the superior or inferior part of the optic disc Symmetrically enlarged cup-to-disc ratios greater than 0.5 Increased vertical cup-to-disc ratio and thinning of NRR Asymmetry of CDR of 0.2 or more Hemorrhage at or around the optic disc Peripapillary atrophy Baring of circumlinear vessels (the gap between the superficial vessels and disc margin) Bayonetting of vessels (the vessel first goes back and then climbs along the wall of the deep cup and then angles again on the disc margin) Very deep (excavated) cup with bean-pot cupping and laminar dot sign Nasalization of optic disc vessels Diffuse or focal (arcuate) thinning/defect of the retinal nerve fiber layer contiguous with an area of NRR-notch The NRR is typically pink and not pale in OAG. The pallor of the NRR usually denotes an atrophic optic nerve, as seen in primary angle closure glaucoma. |
article-22264_56 | Open Angle Glaucoma -- Evaluation -- Visual Field | Perimetry, also known as visual field testing, is an important diagnostic tool that maps out the patient’s visual field on a printout, making it helpful and necessary in diagnosing and managing OAG. The testing provides a baseline visual field for glaucoma suspects and confirmed OAG cases so clinicians can track disease progression. To make a diagnosis of acquired glaucomatous visual field defect, Hoddap–Parrish–Anderson criteria are used: Glaucoma hemifield test outside normal limits on at least 2 fields. A cluster of 3 or more non-edge points in a location typical for glaucoma, all of which are depressed on the pattern deviation plot at a P <5% and one of which is depressed at a P <1% on 2 consecutive fields. A corrected pattern standard deviation that occurs in less than 5% of normal fields on 2 consecutive fields. [69] | Open Angle Glaucoma -- Evaluation -- Visual Field. Perimetry, also known as visual field testing, is an important diagnostic tool that maps out the patient’s visual field on a printout, making it helpful and necessary in diagnosing and managing OAG. The testing provides a baseline visual field for glaucoma suspects and confirmed OAG cases so clinicians can track disease progression. To make a diagnosis of acquired glaucomatous visual field defect, Hoddap–Parrish–Anderson criteria are used: Glaucoma hemifield test outside normal limits on at least 2 fields. A cluster of 3 or more non-edge points in a location typical for glaucoma, all of which are depressed on the pattern deviation plot at a P <5% and one of which is depressed at a P <1% on 2 consecutive fields. A corrected pattern standard deviation that occurs in less than 5% of normal fields on 2 consecutive fields. [69] |
article-22264_57 | Open Angle Glaucoma -- Evaluation | Static automated threshold perimetry is used with white stimulus on a white background. Most studies used the Humphrey Field Analyzer, but other perimeters like Octopus have also been used successfully. Non-conventional perimetry like SWAP (short-wavelength automated perimetry using blue stimulus on yellow background), [70] pulsar perimetry, [71] [72] rarebit, [73] [74] Matrix, [75] and frequency-doubling technology [76] have been proposed in earlier studies for the detection of early glaucoma visual field loss, however, tend not to be used in routine clinical practice. | Open Angle Glaucoma -- Evaluation. Static automated threshold perimetry is used with white stimulus on a white background. Most studies used the Humphrey Field Analyzer, but other perimeters like Octopus have also been used successfully. Non-conventional perimetry like SWAP (short-wavelength automated perimetry using blue stimulus on yellow background), [70] pulsar perimetry, [71] [72] rarebit, [73] [74] Matrix, [75] and frequency-doubling technology [76] have been proposed in earlier studies for the detection of early glaucoma visual field loss, however, tend not to be used in routine clinical practice. |
article-22264_58 | Open Angle Glaucoma -- Evaluation | The visual field must be reliable, and defects should be repeatable on at least 2 fields. When treating patients long-term, it is preferable to use the same machine, the same degree of field, and protocol (eg, 24-2, 30-3, or 10-2) to compare the fields to note for progression or stability. At least 40% to 50% ganglion cell loss is needed to reliably show visual field defects in threshold perimetry. [77] [78] Structural changes of the optic nerve and retinal nerve fiber layer (RNFL) tend to occur earlier than functional change (visual field loss) in most patients with OAG; | Open Angle Glaucoma -- Evaluation. The visual field must be reliable, and defects should be repeatable on at least 2 fields. When treating patients long-term, it is preferable to use the same machine, the same degree of field, and protocol (eg, 24-2, 30-3, or 10-2) to compare the fields to note for progression or stability. At least 40% to 50% ganglion cell loss is needed to reliably show visual field defects in threshold perimetry. [77] [78] Structural changes of the optic nerve and retinal nerve fiber layer (RNFL) tend to occur earlier than functional change (visual field loss) in most patients with OAG; |
article-22264_59 | Open Angle Glaucoma -- Evaluation | this is relevant to the concept of preperimetric glaucoma, which is defined as ‘the presence of characteristic glaucomatous changes in the optic disc and increased vulnerability to damage in the RNFL, without the presence of visual field defects detectable with standard automated perimetry. [79] For patients with risk factors, suspect optic discs, and/or ocular hypertension (OHT), periodic visual field and OCT testing are recommended to detect early visual field defects and changes to determine whether therapy is needed. Typical visual field changes in OAG include: | Open Angle Glaucoma -- Evaluation. this is relevant to the concept of preperimetric glaucoma, which is defined as ‘the presence of characteristic glaucomatous changes in the optic disc and increased vulnerability to damage in the RNFL, without the presence of visual field defects detectable with standard automated perimetry. [79] For patients with risk factors, suspect optic discs, and/or ocular hypertension (OHT), periodic visual field and OCT testing are recommended to detect early visual field defects and changes to determine whether therapy is needed. Typical visual field changes in OAG include: |
article-22264_60 | Open Angle Glaucoma -- Evaluation | Increased variability of responses in an area that later developed field defects Asymmetry of the visual field between the eyes Paracentral scotoma- commonly superonasal Roenne’s nasal step- an area of depression above or below the horizontal meridian on the nasal side Temporal wedge Sickle-shaped (Seidel) scotoma Bjerrum scotoma or arcuate scotoma Annular or ring scotoma when arcuate scotoma is present on both above and below the horizontal meridian General constriction of peripheral field A temporal island of the visual field | Open Angle Glaucoma -- Evaluation. Increased variability of responses in an area that later developed field defects Asymmetry of the visual field between the eyes Paracentral scotoma- commonly superonasal Roenne’s nasal step- an area of depression above or below the horizontal meridian on the nasal side Temporal wedge Sickle-shaped (Seidel) scotoma Bjerrum scotoma or arcuate scotoma Annular or ring scotoma when arcuate scotoma is present on both above and below the horizontal meridian General constriction of peripheral field A temporal island of the visual field |
article-22264_61 | Open Angle Glaucoma -- Evaluation -- Intraocular Pressure | IOP is measured with tonometry; [80] several different tonometers are used. [81] The gold standard remains to be Goldmann applanation tonometry. [82] When determining the IOP of a patient using tonometry, certain variables must be considered. Tonometry measurements can, for example, vary between examiners by approximately 10% per individual, translating to a difference in IOP measurement of 1 mm Hg to 2 mm Hg (see Image. Goldmann Applanation Tonometer [GAT] Procedure). [83] | Open Angle Glaucoma -- Evaluation -- Intraocular Pressure. IOP is measured with tonometry; [80] several different tonometers are used. [81] The gold standard remains to be Goldmann applanation tonometry. [82] When determining the IOP of a patient using tonometry, certain variables must be considered. Tonometry measurements can, for example, vary between examiners by approximately 10% per individual, translating to a difference in IOP measurement of 1 mm Hg to 2 mm Hg (see Image. Goldmann Applanation Tonometer [GAT] Procedure). [83] |
article-22264_62 | Open Angle Glaucoma -- Evaluation -- Intraocular Pressure | An individual’s corneal thickness measured with pachymetry or diurnal variations of IOP (eg, higher IOP in early morning hours or other times of the day or variability in the time of day of maximal IOP between patients) [84] can also have a tremendous effect on the accuracy of IOP measurements. Study results have shown that IOP is overestimated in individuals with thick corneas while underestimated in those with thinner corneas. [85] Multiple measurements should be taken and correlated with optic nerve and visual field examinations when a patient is suspected of elevated IOP. | Open Angle Glaucoma -- Evaluation -- Intraocular Pressure. An individual’s corneal thickness measured with pachymetry or diurnal variations of IOP (eg, higher IOP in early morning hours or other times of the day or variability in the time of day of maximal IOP between patients) [84] can also have a tremendous effect on the accuracy of IOP measurements. Study results have shown that IOP is overestimated in individuals with thick corneas while underestimated in those with thinner corneas. [85] Multiple measurements should be taken and correlated with optic nerve and visual field examinations when a patient is suspected of elevated IOP. |
article-22264_63 | Open Angle Glaucoma -- Evaluation -- Intraocular Pressure | If previous tonometry measurements are available, they should be reviewed and compared to the most recent ones. Also, the IOP may be different on different days, and different instruments may capture different values of IOP. If a difference of 3 mm Hg or more is noted between the 2 eyes, there is an increased suspicion of glaucoma. Clinicians should expect approximately 10% variation between individual and repeat measurements over 2 to 3 occasions before deciding on the treatment. | Open Angle Glaucoma -- Evaluation -- Intraocular Pressure. If previous tonometry measurements are available, they should be reviewed and compared to the most recent ones. Also, the IOP may be different on different days, and different instruments may capture different values of IOP. If a difference of 3 mm Hg or more is noted between the 2 eyes, there is an increased suspicion of glaucoma. Clinicians should expect approximately 10% variation between individual and repeat measurements over 2 to 3 occasions before deciding on the treatment. |
article-22264_64 | Open Angle Glaucoma -- Evaluation -- Intraocular Pressure | Elevated IOP is an important and modifiable risk factor; however, it is not a diagnostic factor for OAG. An ophthalmologist should check the patient’s IOP using applanation tonometry, remaining aware that the applanation tonometry test causes patients to squeeze their eyes and elevate their pressure readings. Normal IOP should range between 12 mm Hg and 21 mm Hg. Approximately 75% of patients with elevated IOP never develop glaucomatous optic nerve atrophy or visual field deficits. When a patient has recorded a reliably high IOP reading above 21 mm Hg, they are deemed patients with glaucoma or patients with ocular hypertension. [35] [86] | Open Angle Glaucoma -- Evaluation -- Intraocular Pressure. Elevated IOP is an important and modifiable risk factor; however, it is not a diagnostic factor for OAG. An ophthalmologist should check the patient’s IOP using applanation tonometry, remaining aware that the applanation tonometry test causes patients to squeeze their eyes and elevate their pressure readings. Normal IOP should range between 12 mm Hg and 21 mm Hg. Approximately 75% of patients with elevated IOP never develop glaucomatous optic nerve atrophy or visual field deficits. When a patient has recorded a reliably high IOP reading above 21 mm Hg, they are deemed patients with glaucoma or patients with ocular hypertension. [35] [86] |
article-22264_65 | Open Angle Glaucoma -- Evaluation -- Gonioscopy | OAG is a diagnosis of exclusion, and other ocular emergencies, such as closed-angle glaucoma, must be ruled out. [87] Gonioscopy determines whether the diagnosis is considered “open” or “closed” angle glaucoma. Gonioscopy is an acquired skill that allows the ophthalmologist to visualize the angle between the cornea and iris and determine if it is open. The angle between the iris and cornea should be 20° to 45° to be considered “open” so that aqueous humor can circumvent the posterior chamber to the anterior chamber. [35] | Open Angle Glaucoma -- Evaluation -- Gonioscopy. OAG is a diagnosis of exclusion, and other ocular emergencies, such as closed-angle glaucoma, must be ruled out. [87] Gonioscopy determines whether the diagnosis is considered “open” or “closed” angle glaucoma. Gonioscopy is an acquired skill that allows the ophthalmologist to visualize the angle between the cornea and iris and determine if it is open. The angle between the iris and cornea should be 20° to 45° to be considered “open” so that aqueous humor can circumvent the posterior chamber to the anterior chamber. [35] |
article-22264_66 | Open Angle Glaucoma -- Evaluation -- Optical Coherence Tomography | Optical coherence tomography (OCT) is a diagnostic imaging modality that provides high-resolution cross-sectional imaging of the retina, optic nerve, and anterior segment. Low-coherence infrared light is directed toward the back of the eye, and the path of scattered photons helps recreate an image of the retina. OCT is highly reproducible and is widely used as an adjunct in routine glaucoma patient management. Peripapillary RNFL analysis (see Image. Normal Visual Field and Optical Coherence Tomography [OCT] Results) can show thinning in this layer. As the most commonly used scanning protocol for glaucoma diagnosis, it samples RGCs from the entire retina. [88] Some of the drawbacks included variability in ONH morphology from patient to patient. The macular thickness is proposed as a means of glaucoma detection, given that 50% of RGCs are found in the macula, and RGC bodies are thicker than their axons and potentially easier to detect. [89] RNFL, macular thickness measurements, and visual field results are key in managing cases. | Open Angle Glaucoma -- Evaluation -- Optical Coherence Tomography. Optical coherence tomography (OCT) is a diagnostic imaging modality that provides high-resolution cross-sectional imaging of the retina, optic nerve, and anterior segment. Low-coherence infrared light is directed toward the back of the eye, and the path of scattered photons helps recreate an image of the retina. OCT is highly reproducible and is widely used as an adjunct in routine glaucoma patient management. Peripapillary RNFL analysis (see Image. Normal Visual Field and Optical Coherence Tomography [OCT] Results) can show thinning in this layer. As the most commonly used scanning protocol for glaucoma diagnosis, it samples RGCs from the entire retina. [88] Some of the drawbacks included variability in ONH morphology from patient to patient. The macular thickness is proposed as a means of glaucoma detection, given that 50% of RGCs are found in the macula, and RGC bodies are thicker than their axons and potentially easier to detect. [89] RNFL, macular thickness measurements, and visual field results are key in managing cases. |
article-22264_67 | Open Angle Glaucoma -- Evaluation -- Corneal Photokeratoscopy | Corneal photokeratoscopy, or corneal topography, is a potential biological marker to monitor patients with primary OAG. Preliminary results have shown a forward shift of the posterior and anterior corneal surfaces; this is correlated with more advanced stages of functional damage, indicating a link between corneal structural changes and the duration and intensity of elevated IOP. Further studies are needed to validate this marker in patients with POAG. [57] | Open Angle Glaucoma -- Evaluation -- Corneal Photokeratoscopy. Corneal photokeratoscopy, or corneal topography, is a potential biological marker to monitor patients with primary OAG. Preliminary results have shown a forward shift of the posterior and anterior corneal surfaces; this is correlated with more advanced stages of functional damage, indicating a link between corneal structural changes and the duration and intensity of elevated IOP. Further studies are needed to validate this marker in patients with POAG. [57] |
article-22264_68 | Open Angle Glaucoma -- Treatment / Management | The goal of OAG treatment is: Preventing the progression of optic nerve head changes Preventing deterioration of the visual field | Open Angle Glaucoma -- Treatment / Management. The goal of OAG treatment is: Preventing the progression of optic nerve head changes Preventing deterioration of the visual field |
article-22264_69 | Open Angle Glaucoma -- Treatment / Management | The concept of target IOP was introduced to achieve this goal. [90] Below a certain upper limit of IOP, it is estimated that the visual field, the optic nerve head, and RNFL parameters will not deteriorate. This helps to maintain a patient’s quality of life. | Open Angle Glaucoma -- Treatment / Management. The concept of target IOP was introduced to achieve this goal. [90] Below a certain upper limit of IOP, it is estimated that the visual field, the optic nerve head, and RNFL parameters will not deteriorate. This helps to maintain a patient’s quality of life. |
article-22264_70 | Open Angle Glaucoma -- Treatment / Management -- Glaucoma Medications | Debate exists over the optimal time to initiate treatment of OAG, with some clinicians initiating treatment of IOP when it reaches above only 21 mm Hg and others reserving treatment either until evidence of optic nerve or RNFL damage or if the patient is at high risk of damage or progression of OAG. | Open Angle Glaucoma -- Treatment / Management -- Glaucoma Medications. Debate exists over the optimal time to initiate treatment of OAG, with some clinicians initiating treatment of IOP when it reaches above only 21 mm Hg and others reserving treatment either until evidence of optic nerve or RNFL damage or if the patient is at high risk of damage or progression of OAG. |
article-22264_71 | Open Angle Glaucoma -- Treatment / Management -- Glaucoma Medications | Treatment should be initiated if signs of damage as a result of OAG are evident (eg, disc hemorrhage, nerve fiber layer defects, asymmetric cupping, vertical vocalization, or notching of the cup) or if symptoms of elevated IOP are present (eg, halos, blurred vision, pain, IOP consistently above 28 mm Hg to 30 mm Hg) due to the high risk of optic nerve damage in the setting of elevated IOP. Some clinicians begin a monocular trial with medications only in 1 eye to assess the chosen medications’ effectiveness and side effects before treating both eyes. However, different eyes might respond differently to the same drug, asymmetric IOP fluctuation may occur, and the drug may have a contralateral effect. | Open Angle Glaucoma -- Treatment / Management -- Glaucoma Medications. Treatment should be initiated if signs of damage as a result of OAG are evident (eg, disc hemorrhage, nerve fiber layer defects, asymmetric cupping, vertical vocalization, or notching of the cup) or if symptoms of elevated IOP are present (eg, halos, blurred vision, pain, IOP consistently above 28 mm Hg to 30 mm Hg) due to the high risk of optic nerve damage in the setting of elevated IOP. Some clinicians begin a monocular trial with medications only in 1 eye to assess the chosen medications’ effectiveness and side effects before treating both eyes. However, different eyes might respond differently to the same drug, asymmetric IOP fluctuation may occur, and the drug may have a contralateral effect. |
article-22264_72 | Open Angle Glaucoma -- Treatment / Management -- Glaucoma Medications | A target IOP should be set depending on the severity of structural and functional damage, baseline IOP, age, race, family history, corneal thickness, hysteresis, and other risk factors. [91] Follow-up should also be scheduled based on the level of success in IOP reduction between visits (eg, more frequent follow-up with slower progression in treatment response) and the severity of optic nerve damage or visual field loss. Treatment should be individualized, considering the risk factors, systemic complications of medication use, the patient’s life expectancy, medical history, concomitant conditions, and desire to comply with treatment. The target IOP should be revised based on the behavior of optic nerve head damage and visual function. | Open Angle Glaucoma -- Treatment / Management -- Glaucoma Medications. A target IOP should be set depending on the severity of structural and functional damage, baseline IOP, age, race, family history, corneal thickness, hysteresis, and other risk factors. [91] Follow-up should also be scheduled based on the level of success in IOP reduction between visits (eg, more frequent follow-up with slower progression in treatment response) and the severity of optic nerve damage or visual field loss. Treatment should be individualized, considering the risk factors, systemic complications of medication use, the patient’s life expectancy, medical history, concomitant conditions, and desire to comply with treatment. The target IOP should be revised based on the behavior of optic nerve head damage and visual function. |
article-22264_73 | Open Angle Glaucoma -- Treatment / Management -- Glaucoma Medications | If IOP, visual field, or optic nerve inflammation worsens while the patient is on medical therapy, compliance to treatment must be checked. [92] Systemic factors, including diabetes, smoking, and nocturnal hypotension, should be controlled. The managing clinician should confirm with the patient which drops are used and how many times the drops are applied daily. Closing eyelids after administration of drops with nasolacrimal duct occlusion may prevent systemic absorption of the topical medication. | Open Angle Glaucoma -- Treatment / Management -- Glaucoma Medications. If IOP, visual field, or optic nerve inflammation worsens while the patient is on medical therapy, compliance to treatment must be checked. [92] Systemic factors, including diabetes, smoking, and nocturnal hypotension, should be controlled. The managing clinician should confirm with the patient which drops are used and how many times the drops are applied daily. Closing eyelids after administration of drops with nasolacrimal duct occlusion may prevent systemic absorption of the topical medication. |
article-22264_74 | Open Angle Glaucoma -- Treatment / Management -- Topical medications | Prostaglandin analogs: Reduces IOP 25% to 33% by increasing the uveoscleral outflow of the aqueous humor (AH). [93] The usual dose is daily. Side effects include lengthening of eyelashes, pigmentation of lids or iris, exacerbation of uveitis or herpetic infection, and cystoid macular edema; it is preferred as initial therapy. The types of prostaglandin analogs used in routine clinics include: Latanoprost Travoprost Bimatoprost Tafluprost Latanoprostene Bunod: This has nitric oxide-donating properties. | Open Angle Glaucoma -- Treatment / Management -- Topical medications. Prostaglandin analogs: Reduces IOP 25% to 33% by increasing the uveoscleral outflow of the aqueous humor (AH). [93] The usual dose is daily. Side effects include lengthening of eyelashes, pigmentation of lids or iris, exacerbation of uveitis or herpetic infection, and cystoid macular edema; it is preferred as initial therapy. The types of prostaglandin analogs used in routine clinics include: Latanoprost Travoprost Bimatoprost Tafluprost Latanoprostene Bunod: This has nitric oxide-donating properties. |
article-22264_75 | Open Angle Glaucoma -- Treatment / Management -- Topical medications | Adrenergic agents: Reduces IOP 20% to 25% by decreasing AH production and increasing uveoscleral outflow. [94] Brimonidine may cause allergic blepharoconjunctivitis and apnea, lethargy, or bradycardia in children. These agents include: Brimonidine Apraclonidine | Open Angle Glaucoma -- Treatment / Management -- Topical medications. Adrenergic agents: Reduces IOP 20% to 25% by decreasing AH production and increasing uveoscleral outflow. [94] Brimonidine may cause allergic blepharoconjunctivitis and apnea, lethargy, or bradycardia in children. These agents include: Brimonidine Apraclonidine |
article-22264_76 | Open Angle Glaucoma -- Treatment / Management -- Topical medications | Beta-blockers: Reduces IOP 20% to 25% by decreasing the production of AH. [95] Non-selective beta-blockers should be avoided in chronic obstructive pulmonary disease and asthma. Other contraindications include heart block, hypotension, and bradycardia. These drops include: Non-selective (may have effects on other receptors in the body and thus may have more side effects in some patients) Timolol Carteolol Levobunolol Metipranolol Selective (show better safety profile about respiratory symptoms) Betaxolol Carbonic anhydrase inhibitor: Reduces IOP by 15% to 20%, decreasing the production of AH. [96] Dorzolamide Brinzolamide Cholinergic or parasympathomimetic agents reduce IOP by 20% to 25% by increasing the outflow of AH. [97] These agents are poorly tolerated and normally not considered first-line treatment. Pilocarpine | Open Angle Glaucoma -- Treatment / Management -- Topical medications. Beta-blockers: Reduces IOP 20% to 25% by decreasing the production of AH. [95] Non-selective beta-blockers should be avoided in chronic obstructive pulmonary disease and asthma. Other contraindications include heart block, hypotension, and bradycardia. These drops include: Non-selective (may have effects on other receptors in the body and thus may have more side effects in some patients) Timolol Carteolol Levobunolol Metipranolol Selective (show better safety profile about respiratory symptoms) Betaxolol Carbonic anhydrase inhibitor: Reduces IOP by 15% to 20%, decreasing the production of AH. [96] Dorzolamide Brinzolamide Cholinergic or parasympathomimetic agents reduce IOP by 20% to 25% by increasing the outflow of AH. [97] These agents are poorly tolerated and normally not considered first-line treatment. Pilocarpine |
article-22264_77 | Open Angle Glaucoma -- Treatment / Management -- Systemic agents | These are used in the acute rise of IOP and angle-closure glaucoma or when topical medications are not tolerated. Carbonic anhydrase inhibitor: Acetazolamide Osmotic agents: Mannitol Glycerol | Open Angle Glaucoma -- Treatment / Management -- Systemic agents. These are used in the acute rise of IOP and angle-closure glaucoma or when topical medications are not tolerated. Carbonic anhydrase inhibitor: Acetazolamide Osmotic agents: Mannitol Glycerol |
article-22264_78 | Open Angle Glaucoma -- Treatment / Management -- Laser trabeculoplasty | The indications of laser trabeculoplasty include The primary therapy for OAG Reduce the number of glaucoma drops Non-compliance or intolerance to medical therapy Failure of medical therapy as a less invasive alternative therapy compared to surgery The available methods of laser trabeculoplasty are: | Open Angle Glaucoma -- Treatment / Management -- Laser trabeculoplasty. The indications of laser trabeculoplasty include The primary therapy for OAG Reduce the number of glaucoma drops Non-compliance or intolerance to medical therapy Failure of medical therapy as a less invasive alternative therapy compared to surgery The available methods of laser trabeculoplasty are: |
article-22264_79 | Open Angle Glaucoma -- Treatment / Management -- Laser trabeculoplasty | Argon laser trabeculoplasty: More than 75% of unoperated eyes initially have a good IOP reduction. Within 5 years, 30% to >50% of eyes need additional surgical management. [98] Selective laser trabeculoplasty: This uses Q-switched frequency-doubled Nd-YAG and is preferred to argon laser trabeculoplasty (ALT) because it utilizes less laser energy, reducing inflammation and less mechanical injury to the TM. The efficacy of selective laser trabeculoplasty is similar to ALT and possible to repeat over time. [99] Micropulse Diode Laser Trabeculoplasty: This laser is based on subthreshold micropulse laser techniques that aim to cause less damage and side effects to angle structures without compromising efficacy. [100] | Open Angle Glaucoma -- Treatment / Management -- Laser trabeculoplasty. Argon laser trabeculoplasty: More than 75% of unoperated eyes initially have a good IOP reduction. Within 5 years, 30% to >50% of eyes need additional surgical management. [98] Selective laser trabeculoplasty: This uses Q-switched frequency-doubled Nd-YAG and is preferred to argon laser trabeculoplasty (ALT) because it utilizes less laser energy, reducing inflammation and less mechanical injury to the TM. The efficacy of selective laser trabeculoplasty is similar to ALT and possible to repeat over time. [99] Micropulse Diode Laser Trabeculoplasty: This laser is based on subthreshold micropulse laser techniques that aim to cause less damage and side effects to angle structures without compromising efficacy. [100] |
article-22264_80 | Open Angle Glaucoma -- Treatment / Management -- Diode laser cyclophotocoagulation | This is a method for ablation of the ciliary processes that secrete aqueous. [101] Indications include: Uncontrolled IOP in eyes with ambulatory vision if chances of surgical success are poor Management of refractory glaucoma Uncontrolled IOP in painful blind eyes or eyes with minimal visual potential Uncontrolled IOP with maximal medication after failed glaucoma surgery(ies) | Open Angle Glaucoma -- Treatment / Management -- Diode laser cyclophotocoagulation. This is a method for ablation of the ciliary processes that secrete aqueous. [101] Indications include: Uncontrolled IOP in eyes with ambulatory vision if chances of surgical success are poor Management of refractory glaucoma Uncontrolled IOP in painful blind eyes or eyes with minimal visual potential Uncontrolled IOP with maximal medication after failed glaucoma surgery(ies) |
article-22264_81 | Open Angle Glaucoma -- Treatment / Management -- Surgical Management of OAG | Indications for surgical management of glaucoma are: IOP above target pressure or progression of visual fields and optic disc changes after compliance and maximally tolerable glaucoma medication To avoid excessive glaucoma drops Significant barriers to effective and regular medication: cost, compliance, physical disability, inconvenience, side effects, and psychosocial Primary therapy for advanced glaucoma requires low target IOP Patient preference over other options [102] Surgical options include: | Open Angle Glaucoma -- Treatment / Management -- Surgical Management of OAG. Indications for surgical management of glaucoma are: IOP above target pressure or progression of visual fields and optic disc changes after compliance and maximally tolerable glaucoma medication To avoid excessive glaucoma drops Significant barriers to effective and regular medication: cost, compliance, physical disability, inconvenience, side effects, and psychosocial Primary therapy for advanced glaucoma requires low target IOP Patient preference over other options [102] Surgical options include: |
article-22264_82 | Open Angle Glaucoma -- Treatment / Management -- Surgical Management of OAG | Trabeculectomy: The success rate may vary from 31% to 88%, increasing with using mitomycin C or 5-fluorouracil (These agents, however, increase the risk of late-onset bleb leak, hypotony, and bleb-related infection.) [103] Glaucoma drainage device and valve: Molteno, Baerveldt, Ahmed [104] Non-penetrating glaucoma surgery: Deep sclerectomy Viscocanalostomy Canaloplasty [105] Minimally invasive or micro-invasive glaucoma surgery [106] provides a conjunctiva-sparing surgery with an ab-interno approach to reduce IOP in mild to moderate glaucoma. The different approaches include: Increasing trabecular outflow (Trabectome, iStent, Hydrus stent, gonioscopy-assisted transluminal trabeculotomy, excimer laser trabeculotomy) Suprachoroidal shunts (Cypass micro-stent) Reducing aqueous production (endocyclophotocoagulation) Subconjunctival filtration (XEN gel stent) [107] | Open Angle Glaucoma -- Treatment / Management -- Surgical Management of OAG. Trabeculectomy: The success rate may vary from 31% to 88%, increasing with using mitomycin C or 5-fluorouracil (These agents, however, increase the risk of late-onset bleb leak, hypotony, and bleb-related infection.) [103] Glaucoma drainage device and valve: Molteno, Baerveldt, Ahmed [104] Non-penetrating glaucoma surgery: Deep sclerectomy Viscocanalostomy Canaloplasty [105] Minimally invasive or micro-invasive glaucoma surgery [106] provides a conjunctiva-sparing surgery with an ab-interno approach to reduce IOP in mild to moderate glaucoma. The different approaches include: Increasing trabecular outflow (Trabectome, iStent, Hydrus stent, gonioscopy-assisted transluminal trabeculotomy, excimer laser trabeculotomy) Suprachoroidal shunts (Cypass micro-stent) Reducing aqueous production (endocyclophotocoagulation) Subconjunctival filtration (XEN gel stent) [107] |
article-22264_83 | Open Angle Glaucoma -- Treatment / Management -- Cyclocryotherapy | This is another method of cycloablation using cryotherapy, reserved for painful vision loss. [108] | Open Angle Glaucoma -- Treatment / Management -- Cyclocryotherapy. This is another method of cycloablation using cryotherapy, reserved for painful vision loss. [108] |
article-22264_84 | Open Angle Glaucoma -- Treatment / Management -- Other options for painful blind eyes from glaucoma | Enucleation or evisceration [109] Retrobulbar injection of absolute alcohol [110] | Open Angle Glaucoma -- Treatment / Management -- Other options for painful blind eyes from glaucoma. Enucleation or evisceration [109] Retrobulbar injection of absolute alcohol [110] |
article-22264_85 | Open Angle Glaucoma -- Differential Diagnosis | The differential diagnoses should include: Optic nerve head diseases Physiological cup: Deep cup with healthy neuroretinal rim is seen with normal retinal nerve fiber layer thickness and no visual field defect; disc size may be large Optic disc drusen Optic disc coloboma Anomalous optic disc Tilted disc Ischemic optic neuropathy Retinal diseases causing similar visual field defects Branch retinal vein occlusion Branch retinal artery occlusion Retinitis pigmentosa Panretinal photocoagulation Central nervous system diseases Pituitary tumor: NRR is typically pale, pallor more than cupping, and bitemporal hemianopia exists, which respects the vertical line passing through the fixation (contrary to glaucoma, whose visual field respects the horizontal meridian) Intracranial hypotension due to cerebrospinal fluid shunts or other neurologic pathologies Foster Kennedy Syndrome Cerebrovascular pathologies or traumas Multiple sclerosis | Open Angle Glaucoma -- Differential Diagnosis. The differential diagnoses should include: Optic nerve head diseases Physiological cup: Deep cup with healthy neuroretinal rim is seen with normal retinal nerve fiber layer thickness and no visual field defect; disc size may be large Optic disc drusen Optic disc coloboma Anomalous optic disc Tilted disc Ischemic optic neuropathy Retinal diseases causing similar visual field defects Branch retinal vein occlusion Branch retinal artery occlusion Retinitis pigmentosa Panretinal photocoagulation Central nervous system diseases Pituitary tumor: NRR is typically pale, pallor more than cupping, and bitemporal hemianopia exists, which respects the vertical line passing through the fixation (contrary to glaucoma, whose visual field respects the horizontal meridian) Intracranial hypotension due to cerebrospinal fluid shunts or other neurologic pathologies Foster Kennedy Syndrome Cerebrovascular pathologies or traumas Multiple sclerosis |
article-22264_86 | Open Angle Glaucoma -- Staging | The Americal Academy of Ophthalmology's preferred practice pattern [35] classifies the severity of glaucomatous damage into different categories: | Open Angle Glaucoma -- Staging. The Americal Academy of Ophthalmology's preferred practice pattern [35] classifies the severity of glaucomatous damage into different categories: |
article-22264_87 | Open Angle Glaucoma -- Staging | Mild: Definite optic disc or RNFL abnormalities consistent with glaucoma as detailed above and a normal visual field tested with standard automated perimetry (SAP) are seen. Moderate: Definite optic disc or RNFL abnormalities consistent with glaucoma, as detailed above, are seen, and visual field abnormalities in one hemifield are not within 5° of fixation as tested with SAP. Severe: Definite optic disc or RNFL abnormalities consistent with glaucoma as detailed above are seen, and visual field abnormalities in both hemifields or loss within 5° of fixation in at least one hemifield as tested with SAP. Indeterminate: Definite optic disc or RNFL abnormalities consistent with glaucoma, as detailed above, are seen, and the patient cannot perform visual field testing, has unreliable or uninterpretable visual field test results, or has not performed visual fields yet. | Open Angle Glaucoma -- Staging. Mild: Definite optic disc or RNFL abnormalities consistent with glaucoma as detailed above and a normal visual field tested with standard automated perimetry (SAP) are seen. Moderate: Definite optic disc or RNFL abnormalities consistent with glaucoma, as detailed above, are seen, and visual field abnormalities in one hemifield are not within 5° of fixation as tested with SAP. Severe: Definite optic disc or RNFL abnormalities consistent with glaucoma as detailed above are seen, and visual field abnormalities in both hemifields or loss within 5° of fixation in at least one hemifield as tested with SAP. Indeterminate: Definite optic disc or RNFL abnormalities consistent with glaucoma, as detailed above, are seen, and the patient cannot perform visual field testing, has unreliable or uninterpretable visual field test results, or has not performed visual fields yet. |
article-22264_88 | Open Angle Glaucoma -- Staging | Several different staging systems are recognized based on visual field damage, [111] [112] optic disc cupping, [65] [113] and RNFL defects with OCT, [114] some of which are applicable in a routine clinical setting or clinical trials. [115] | Open Angle Glaucoma -- Staging. Several different staging systems are recognized based on visual field damage, [111] [112] optic disc cupping, [65] [113] and RNFL defects with OCT, [114] some of which are applicable in a routine clinical setting or clinical trials. [115] |
article-22264_89 | Open Angle Glaucoma -- Prognosis | Advanced POAG may cause optic atrophy and no perception of light, though most OAG patients will not lose vision in their lifetime. Risk factors for progression of OAG include: Old age Elevated IOP Increased cup-to-disc ratio or small optic rim area Beta peripapillary atrophy Disc hemorrhage Thin central corneal thickness Reduced corneal hysteresis Low ocular perfusion pressure Poor compliance with therapy Pseudoexfoliation [35] In 10 years, the cumulative probability of end-stage glaucoma in at least one eye in untreated cases was shown to be 35% in study results. [116] | Open Angle Glaucoma -- Prognosis. Advanced POAG may cause optic atrophy and no perception of light, though most OAG patients will not lose vision in their lifetime. Risk factors for progression of OAG include: Old age Elevated IOP Increased cup-to-disc ratio or small optic rim area Beta peripapillary atrophy Disc hemorrhage Thin central corneal thickness Reduced corneal hysteresis Low ocular perfusion pressure Poor compliance with therapy Pseudoexfoliation [35] In 10 years, the cumulative probability of end-stage glaucoma in at least one eye in untreated cases was shown to be 35% in study results. [116] |
article-22264_90 | Open Angle Glaucoma -- Complications | Complications of glaucoma include: Blindness: usually painless Painful blind eye or absolute glaucoma: OAG predisposes to central retinal venous occlusion, leading to neovascular glaucoma and painful blind eye [117] | Open Angle Glaucoma -- Complications. Complications of glaucoma include: Blindness: usually painless Painful blind eye or absolute glaucoma: OAG predisposes to central retinal venous occlusion, leading to neovascular glaucoma and painful blind eye [117] |
article-22264_91 | Open Angle Glaucoma -- Consultations | Screening and management of OAG are typically performed by the following healthcare professionals that deal with: Ophthalmology, comprehensive general Ophthalmology, glaucoma specialist Optometry with special training in ocular hypertension and glaucoma | Open Angle Glaucoma -- Consultations. Screening and management of OAG are typically performed by the following healthcare professionals that deal with: Ophthalmology, comprehensive general Ophthalmology, glaucoma specialist Optometry with special training in ocular hypertension and glaucoma |
article-22264_92 | Open Angle Glaucoma -- Deterrence and Patient Education | Glaucoma is a preventable cause of blindness, making patient education crucial in managing and preventing the progression of OAG. Effective and successful treatment of OAG can prevent the evolution of optic nerve atrophy and preserve patient vision. [118] However, patient adherence and compliance with medical therapy are notoriously difficult. [119] Treatment regimens require daily treatment to control IOP, and this can be a challenging task for patients for the rest of their lives. [120] | Open Angle Glaucoma -- Deterrence and Patient Education. Glaucoma is a preventable cause of blindness, making patient education crucial in managing and preventing the progression of OAG. Effective and successful treatment of OAG can prevent the evolution of optic nerve atrophy and preserve patient vision. [118] However, patient adherence and compliance with medical therapy are notoriously difficult. [119] Treatment regimens require daily treatment to control IOP, and this can be a challenging task for patients for the rest of their lives. [120] |
article-22264_93 | Open Angle Glaucoma -- Deterrence and Patient Education | The nature of medication regimens requiring daily dosage is challenging for many patients, and inconsistent medication administration does not adequately control IOP. Some patients will attempt to use their drops daily but fail to deliver the medications to their eyes. Thus, the medication will not be absorbed, specifically in at-risk older populations. Over a prolonged time frame, failure to adhere to daily drops or oral medication will increase the likelihood of progression to blindness. [121] | Open Angle Glaucoma -- Deterrence and Patient Education. The nature of medication regimens requiring daily dosage is challenging for many patients, and inconsistent medication administration does not adequately control IOP. Some patients will attempt to use their drops daily but fail to deliver the medications to their eyes. Thus, the medication will not be absorbed, specifically in at-risk older populations. Over a prolonged time frame, failure to adhere to daily drops or oral medication will increase the likelihood of progression to blindness. [121] |
article-22264_94 | Open Angle Glaucoma -- Deterrence and Patient Education | Studies have confirmed an inverse relationship between the number and frequency of dosage and patient adherence concerning glaucoma treatment. One study looked into the reasons why patients struggled to adhere to their regimens, and the most commonly cited reasons were forgetfulness (30%), other priorities (11%), lack of information (9%), emotional factors (7%) with 27% of individuals surveyed not providing a reason. | Open Angle Glaucoma -- Deterrence and Patient Education. Studies have confirmed an inverse relationship between the number and frequency of dosage and patient adherence concerning glaucoma treatment. One study looked into the reasons why patients struggled to adhere to their regimens, and the most commonly cited reasons were forgetfulness (30%), other priorities (11%), lack of information (9%), emotional factors (7%) with 27% of individuals surveyed not providing a reason. |
article-22264_95 | Open Angle Glaucoma -- Deterrence and Patient Education | Previous studies have shown that improved patient education regarding disease processes and the rationale behind treatment regimens makes patients consistently more likely to adhere to their prescribed medication regimens. A 2018 study found that physician-centric multifaceted informational and educational mailings were ineffective in improving adherence to IOP-lowering treatment in older patients with glaucoma. [122] [123] | Open Angle Glaucoma -- Deterrence and Patient Education. Previous studies have shown that improved patient education regarding disease processes and the rationale behind treatment regimens makes patients consistently more likely to adhere to their prescribed medication regimens. A 2018 study found that physician-centric multifaceted informational and educational mailings were ineffective in improving adherence to IOP-lowering treatment in older patients with glaucoma. [122] [123] |
article-22264_96 | Open Angle Glaucoma -- Deterrence and Patient Education | Educating patients is crucial for effective glaucoma management, but the best way to provide such education is still unknown. Interestingly, other studies have found no link between medication adherence and side effects and that side effects are unlikely to discourage patients. One of the tricky aspects of glaucoma is that patients often do not experience any symptoms until it is too late. An interprofessional approach is required to tackle this issue, as not all patients visit their ophthalmologist regularly. Therefore, nurses, therapists, social care workers, and primary care clinicians should be the first line of defense. | Open Angle Glaucoma -- Deterrence and Patient Education. Educating patients is crucial for effective glaucoma management, but the best way to provide such education is still unknown. Interestingly, other studies have found no link between medication adherence and side effects and that side effects are unlikely to discourage patients. One of the tricky aspects of glaucoma is that patients often do not experience any symptoms until it is too late. An interprofessional approach is required to tackle this issue, as not all patients visit their ophthalmologist regularly. Therefore, nurses, therapists, social care workers, and primary care clinicians should be the first line of defense. |
article-22264_97 | Open Angle Glaucoma -- Enhancing Healthcare Team Outcomes | Open-angle glaucoma is a chronic eye condition characterized by increased intraocular pressure, potentially leading to optic nerve damage and vision loss. As the most common type of glaucoma, it often develops gradually without noticeable symptoms until advanced stages. Regular eye exams, including measuring intraocular pressure and assessing optic nerve health, are crucial for early detection. Treatment aims to lower intraocular pressure through medications, laser therapy, or surgery. Clinicians should emphasize the importance of adherence to prescribed treatments and routine follow-up appointments. Given its asymptomatic nature, raising awareness among at-risk populations, such as individuals older than 40 or those with a family history, is essential for early intervention and optimal management of open-angle glaucoma. | Open Angle Glaucoma -- Enhancing Healthcare Team Outcomes. Open-angle glaucoma is a chronic eye condition characterized by increased intraocular pressure, potentially leading to optic nerve damage and vision loss. As the most common type of glaucoma, it often develops gradually without noticeable symptoms until advanced stages. Regular eye exams, including measuring intraocular pressure and assessing optic nerve health, are crucial for early detection. Treatment aims to lower intraocular pressure through medications, laser therapy, or surgery. Clinicians should emphasize the importance of adherence to prescribed treatments and routine follow-up appointments. Given its asymptomatic nature, raising awareness among at-risk populations, such as individuals older than 40 or those with a family history, is essential for early intervention and optimal management of open-angle glaucoma. |
article-22264_98 | Open Angle Glaucoma -- Enhancing Healthcare Team Outcomes | If untreated, OAG leads to progressive loss of peripheral vision followed by central visual field loss. Due to its chronicity, the condition is best managed by an interprofessional team that provides patient education and ensures that daily dosing is maintained. The best outcomes occur when the clinician, ophthalmic specialty-trained nurse, and pharmacist work together to educate and support the patient. | Open Angle Glaucoma -- Enhancing Healthcare Team Outcomes. If untreated, OAG leads to progressive loss of peripheral vision followed by central visual field loss. Due to its chronicity, the condition is best managed by an interprofessional team that provides patient education and ensures that daily dosing is maintained. The best outcomes occur when the clinician, ophthalmic specialty-trained nurse, and pharmacist work together to educate and support the patient. |
article-22264_99 | Open Angle Glaucoma -- Review Questions | Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. | Open Angle Glaucoma -- Review Questions. Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. |
article-29047_0 | Sinus Bradycardia -- Continuing Education Activity | Sinus bradycardia is a cardiac rhythm with appropriate cardiac muscular depolarization initiating from the sinus node and a rate of fewer than 60 beats per minute (bpm). The diagnosis of this condition requires an ECG showing a normal sinus rhythm at a rate lower than 60 bpm. The majority of patients are asymptomatic, while others may present with fatigue, lightheadedness, dizziness, exercise intolerance, syncope or presyncope, worsening of anginal symptoms, worsening of heart failure, or cognitive slowing. This activity outlines the evaluation and management of sinus bradycardia and highlights the role of the interprofessional team in improving care for patients with this condition. | Sinus Bradycardia -- Continuing Education Activity. Sinus bradycardia is a cardiac rhythm with appropriate cardiac muscular depolarization initiating from the sinus node and a rate of fewer than 60 beats per minute (bpm). The diagnosis of this condition requires an ECG showing a normal sinus rhythm at a rate lower than 60 bpm. The majority of patients are asymptomatic, while others may present with fatigue, lightheadedness, dizziness, exercise intolerance, syncope or presyncope, worsening of anginal symptoms, worsening of heart failure, or cognitive slowing. This activity outlines the evaluation and management of sinus bradycardia and highlights the role of the interprofessional team in improving care for patients with this condition. |
article-29047_1 | Sinus Bradycardia -- Continuing Education Activity | Objectives: Describe the key features of sinus bradycardia. Outline how the diagnosis of sinus bradycardia is made on ECG. Review how a patient with sinus bradycardia will most likely present. Describe the importance of improving care coordination among the interprofessional team in educating patients at risk for sinus bradycardia and making a closed-loop communication between them and their providers to further help improve the management of sinus bradycardia. Access free multiple choice questions on this topic. | Sinus Bradycardia -- Continuing Education Activity. Objectives: Describe the key features of sinus bradycardia. Outline how the diagnosis of sinus bradycardia is made on ECG. Review how a patient with sinus bradycardia will most likely present. Describe the importance of improving care coordination among the interprofessional team in educating patients at risk for sinus bradycardia and making a closed-loop communication between them and their providers to further help improve the management of sinus bradycardia. Access free multiple choice questions on this topic. |
article-29047_2 | Sinus Bradycardia -- Introduction | The sinoatrial node (SA) is the default pacemaker and, therefore, a crucial component of the heart's conduction system. It is located subepicardial and is crescent in shape. In an average adult, a sinoatrial node is 13.5 millimeters in length and is innervated by the vagus and sympathetic nerves. The sinoatrial nodal artery supplies blood to the sinoatrial node, it branches off the right coronary artery in 60% of cases, whereas in 40% of cases, it comes off the left circumflex coronary artery. [1] [2] Sinus bradycardia is a cardiac rhythm with appropriate cardiac muscular depolarization initiating from the sinus node generating less than 60 beats per minute (bpm). The diagnosis of sinus bradycardia requires visualization of an electrocardiogram showing a normal sinus rhythm at a rate lower than 60 bpm. Where a normal sinus rhythm has the following criteria [3] [4] : | Sinus Bradycardia -- Introduction. The sinoatrial node (SA) is the default pacemaker and, therefore, a crucial component of the heart's conduction system. It is located subepicardial and is crescent in shape. In an average adult, a sinoatrial node is 13.5 millimeters in length and is innervated by the vagus and sympathetic nerves. The sinoatrial nodal artery supplies blood to the sinoatrial node, it branches off the right coronary artery in 60% of cases, whereas in 40% of cases, it comes off the left circumflex coronary artery. [1] [2] Sinus bradycardia is a cardiac rhythm with appropriate cardiac muscular depolarization initiating from the sinus node generating less than 60 beats per minute (bpm). The diagnosis of sinus bradycardia requires visualization of an electrocardiogram showing a normal sinus rhythm at a rate lower than 60 bpm. Where a normal sinus rhythm has the following criteria [3] [4] : |
article-29047_3 | Sinus Bradycardia -- Introduction | Regular rhythm, with a P wave before every QRS. The p wave is upright in leads 1 and 2; the P wave is biphasic in V1. The maximum height of a P wave is less than or equal to 2.5 mm in leads 2 and 3. The rate of the rhythm is between 60 bpm and 100 bpm. | Sinus Bradycardia -- Introduction. Regular rhythm, with a P wave before every QRS. The p wave is upright in leads 1 and 2; the P wave is biphasic in V1. The maximum height of a P wave is less than or equal to 2.5 mm in leads 2 and 3. The rate of the rhythm is between 60 bpm and 100 bpm. |
article-29047_4 | Sinus Bradycardia -- Etiology | Sinus bradycardia has many intrinsic and extrinsic etiologies. [5] ] [6] [7] [8] [9] [10] | Sinus Bradycardia -- Etiology. Sinus bradycardia has many intrinsic and extrinsic etiologies. [5] ] [6] [7] [8] [9] [10] |
article-29047_5 | Sinus Bradycardia -- Etiology -- Inherent Etiologies | Chest trauma Ischemic heart disease Acute myocardial infarction Acute and chronic coronary artery disease Repair of congenital heart disease Sick sinus syndrome Radiation therapy Amyloidosis Pericarditis Lyme disease Rheumatic fever Collagen vascular disease Myocarditis Neuromuscular disorder X-linked muscular dystrophy Familial disorder Inherited channelopathy | Sinus Bradycardia -- Etiology -- Inherent Etiologies. Chest trauma Ischemic heart disease Acute myocardial infarction Acute and chronic coronary artery disease Repair of congenital heart disease Sick sinus syndrome Radiation therapy Amyloidosis Pericarditis Lyme disease Rheumatic fever Collagen vascular disease Myocarditis Neuromuscular disorder X-linked muscular dystrophy Familial disorder Inherited channelopathy |
article-29047_6 | Sinus Bradycardia -- Etiology -- Extrinsic Etiologies | Vasovagal simulation (endotracheal suctioning) Carotid sinus hypersensitivity Beta-blockers Calcium channel blockers Digoxin Ivabradine Clonidine Reserpine Adenosine Cimetidine Antiarrhythmic class I to IV Lithium Amitriptyline Narcotics Cannabinoids Hypothyroidism Sleep apnea Hypoxia Intracranial hypertension Hyperkalemia Anorexia nervosa | Sinus Bradycardia -- Etiology -- Extrinsic Etiologies. Vasovagal simulation (endotracheal suctioning) Carotid sinus hypersensitivity Beta-blockers Calcium channel blockers Digoxin Ivabradine Clonidine Reserpine Adenosine Cimetidine Antiarrhythmic class I to IV Lithium Amitriptyline Narcotics Cannabinoids Hypothyroidism Sleep apnea Hypoxia Intracranial hypertension Hyperkalemia Anorexia nervosa |
article-29047_7 | Sinus Bradycardia -- Epidemiology | In clinical practice, adults over the age of 65 and young athletes of both sexes are commonly known to present with sinus bradycardia. One in 600 adults over 65 has sinus node dysfunction, but more research needs to be done to collect epidemiologic data within the United States and globally for patients with sinus bradycardia. [11] | Sinus Bradycardia -- Epidemiology. In clinical practice, adults over the age of 65 and young athletes of both sexes are commonly known to present with sinus bradycardia. One in 600 adults over 65 has sinus node dysfunction, but more research needs to be done to collect epidemiologic data within the United States and globally for patients with sinus bradycardia. [11] |
article-29047_8 | Sinus Bradycardia -- Pathophysiology | Sinus bradycardia, as any of the other bradyarrhythmias, is caused by a multitude of intrinsic and extrinsic factors which may compromise the integrity of the sinus node. These factors can cause failure of the impulse formation at the sinus node, impulse conduction at the atrioventricular node, or bundle of His-Purkinje fibers. [9] Sinus bradycardia is an incidental finding in many healthy adults. This is common in athletes and during sleep. Physiological causes that increase vagal tone are more common in athletes. Pathological causes are stated in the etiology. | Sinus Bradycardia -- Pathophysiology. Sinus bradycardia, as any of the other bradyarrhythmias, is caused by a multitude of intrinsic and extrinsic factors which may compromise the integrity of the sinus node. These factors can cause failure of the impulse formation at the sinus node, impulse conduction at the atrioventricular node, or bundle of His-Purkinje fibers. [9] Sinus bradycardia is an incidental finding in many healthy adults. This is common in athletes and during sleep. Physiological causes that increase vagal tone are more common in athletes. Pathological causes are stated in the etiology. |
article-29047_9 | Sinus Bradycardia -- Pathophysiology | Sinus bradycardia is a common occurrence in sick sinus syndrome. In this disorder, there is dysfunction of the SA node. The condition is most common in elderly patients with concomitant heart disease. | Sinus Bradycardia -- Pathophysiology. Sinus bradycardia is a common occurrence in sick sinus syndrome. In this disorder, there is dysfunction of the SA node. The condition is most common in elderly patients with concomitant heart disease. |
article-29047_10 | Sinus Bradycardia -- Histopathology | A specific group of patients with sinus bradycardia may show no nodal histopathology, yet associated findings are as follows [9] [12] : Nodal cell reduction and fibrosis Nodal region amyloidosis Sinus node hypoplasia or atrophy | Sinus Bradycardia -- Histopathology. A specific group of patients with sinus bradycardia may show no nodal histopathology, yet associated findings are as follows [9] [12] : Nodal cell reduction and fibrosis Nodal region amyloidosis Sinus node hypoplasia or atrophy |
article-29047_11 | Sinus Bradycardia -- History and Physical | The majority of patients with sinus bradycardia do not have symptoms. Healthy young adults and athletes tend to have an increased vagal tone which keeps them in sinus bradycardia at rest. Also, patients above the age of 65 tend to have sinus bradycardia during sleep secondary to the aging of the sino-atrial node. Using history to relate to the symptoms of a patient with sinus bradycardia on an electrocardiogram is essential to come to the correct diagnosis. Those who present with symptoms may present with fatigue, exercise intolerance, lightheadedness, dizziness, syncope or presyncope, worsening of anginal symptoms, worsening of heart failure, or cognitive slowing. When taking a history, a health care provider must include relevant questions that help narrow down the differential, such as any recent medication changes, medication overdoses, chest pain, shortness of breath, history of prior myocardial infarction, symptoms of intermittent palpitations, history of chest trauma, rash or recent tick bite, current or past diagnosis of streptococcus pharyngitis, family history of sinus bradycardia, family history of muscular dystrophy. Moreover, physical exam findings should be correlated with the history given by the patient to help narrow the differential diagnosis, such as any murmur heard during the physical exam or any skin exam findings of a developing rash. [13] [14] | Sinus Bradycardia -- History and Physical. The majority of patients with sinus bradycardia do not have symptoms. Healthy young adults and athletes tend to have an increased vagal tone which keeps them in sinus bradycardia at rest. Also, patients above the age of 65 tend to have sinus bradycardia during sleep secondary to the aging of the sino-atrial node. Using history to relate to the symptoms of a patient with sinus bradycardia on an electrocardiogram is essential to come to the correct diagnosis. Those who present with symptoms may present with fatigue, exercise intolerance, lightheadedness, dizziness, syncope or presyncope, worsening of anginal symptoms, worsening of heart failure, or cognitive slowing. When taking a history, a health care provider must include relevant questions that help narrow down the differential, such as any recent medication changes, medication overdoses, chest pain, shortness of breath, history of prior myocardial infarction, symptoms of intermittent palpitations, history of chest trauma, rash or recent tick bite, current or past diagnosis of streptococcus pharyngitis, family history of sinus bradycardia, family history of muscular dystrophy. Moreover, physical exam findings should be correlated with the history given by the patient to help narrow the differential diagnosis, such as any murmur heard during the physical exam or any skin exam findings of a developing rash. [13] [14] |
article-29047_12 | Sinus Bradycardia -- History and Physical | The physical exam may reveal the following: Cyanosis Peripheral edema An altered state of consciousness Dyspnea Rales and crackles | Sinus Bradycardia -- History and Physical. The physical exam may reveal the following: Cyanosis Peripheral edema An altered state of consciousness Dyspnea Rales and crackles |
article-29047_13 | Sinus Bradycardia -- Evaluation | The most significant component of evaluation for a patient who presents with signs and symptoms of sinus bradycardia is history and physical exam. These should include vital signs (respiratory rate, blood pressure, temperature, and heart rate) and an electrocardiogram. During the evaluation, it should be established whether the patient is hemodynamically unstable; evaluation for this includes high blood pressure, altered mental status, or difficulty breathing. If the patient is healthy, athletic, and has no symptoms, then no further medical intervention is required. On the contrary, in older individuals, sinus bradycardia may point towards an unhealthy sinus node. Patients with congestive heart failure often have sinus bradycardia. These patients may have compromised blood supply from the right coronary artery or left circumflex artery to the sinus node secondary to some underlying ischemic heart disease. [15] Laboratory studies that should be ordered include: | Sinus Bradycardia -- Evaluation. The most significant component of evaluation for a patient who presents with signs and symptoms of sinus bradycardia is history and physical exam. These should include vital signs (respiratory rate, blood pressure, temperature, and heart rate) and an electrocardiogram. During the evaluation, it should be established whether the patient is hemodynamically unstable; evaluation for this includes high blood pressure, altered mental status, or difficulty breathing. If the patient is healthy, athletic, and has no symptoms, then no further medical intervention is required. On the contrary, in older individuals, sinus bradycardia may point towards an unhealthy sinus node. Patients with congestive heart failure often have sinus bradycardia. These patients may have compromised blood supply from the right coronary artery or left circumflex artery to the sinus node secondary to some underlying ischemic heart disease. [15] Laboratory studies that should be ordered include: |
article-29047_14 | Sinus Bradycardia -- Evaluation | Glucose level Electrolytes Calcium, magnesium Thyroid function Troponin Toxicological drug screen A 12-lead ECG is necessary to make the diagnosis. | Sinus Bradycardia -- Evaluation. Glucose level Electrolytes Calcium, magnesium Thyroid function Troponin Toxicological drug screen A 12-lead ECG is necessary to make the diagnosis. |
article-29047_15 | Sinus Bradycardia -- Evaluation | If there are no signs or symptoms of acute myocardial infarction in a hemodynamically stable patient, then workup should be initiated for an infectious etiology (including chest x-ray, blood cultures, urinary analysis, viral panel) together with thyroid function tests. If a patient is found to have an infectious etiology or a thyroid abnormality, the patient should be appropriately treated for these underlying etiologies and re-evaluated. Upon re-evaluation, if this patient is no longer symptomatic and his heart rate returns to within normal limits patient could be evaluated for a possible sick sinus syndrome or a long-term implantable loop recorder. | Sinus Bradycardia -- Evaluation. If there are no signs or symptoms of acute myocardial infarction in a hemodynamically stable patient, then workup should be initiated for an infectious etiology (including chest x-ray, blood cultures, urinary analysis, viral panel) together with thyroid function tests. If a patient is found to have an infectious etiology or a thyroid abnormality, the patient should be appropriately treated for these underlying etiologies and re-evaluated. Upon re-evaluation, if this patient is no longer symptomatic and his heart rate returns to within normal limits patient could be evaluated for a possible sick sinus syndrome or a long-term implantable loop recorder. |
article-29047_16 | Sinus Bradycardia -- Treatment / Management | A patient with sinus bradycardia should be evaluated for hemodynamic instability. If found to be hemodynamically unstable, the patient can be treated with intravenous (IV) atropine 0.5 mg push every 3 to 5 minutes up to 3 mg total. If the patient's symptoms and heart rate do not improve, the patient is a candidate for a temporary pacemaker. If the patient on arrival is hemodynamically stable but has signs and symptoms of acute myocardial infarction, they should be treated for an acute myocardial infarction appropriately. Hypothermic patients should be warmed to normothermia before making definitive decisions on treatment. | Sinus Bradycardia -- Treatment / Management. A patient with sinus bradycardia should be evaluated for hemodynamic instability. If found to be hemodynamically unstable, the patient can be treated with intravenous (IV) atropine 0.5 mg push every 3 to 5 minutes up to 3 mg total. If the patient's symptoms and heart rate do not improve, the patient is a candidate for a temporary pacemaker. If the patient on arrival is hemodynamically stable but has signs and symptoms of acute myocardial infarction, they should be treated for an acute myocardial infarction appropriately. Hypothermic patients should be warmed to normothermia before making definitive decisions on treatment. |
article-29047_17 | Sinus Bradycardia -- Treatment / Management | While management decisions are being made for a patient with sinus bradycardia, the patient's medication list should also be reviewed for possible causes of bradycardia, and those medications should be withdrawn if possible. If a patient has comorbid conditions that require him to be on certain medications, which may be causing the sinus bradycardia, then in that case-patient may be a candidate for a permanent pacemaker. In cases where medication can be withdrawn, withdrawal is made, and if symptoms and heart rate still do not improve, then the patient may be evaluated for a permanent pacemaker. [16] | Sinus Bradycardia -- Treatment / Management. While management decisions are being made for a patient with sinus bradycardia, the patient's medication list should also be reviewed for possible causes of bradycardia, and those medications should be withdrawn if possible. If a patient has comorbid conditions that require him to be on certain medications, which may be causing the sinus bradycardia, then in that case-patient may be a candidate for a permanent pacemaker. In cases where medication can be withdrawn, withdrawal is made, and if symptoms and heart rate still do not improve, then the patient may be evaluated for a permanent pacemaker. [16] |
article-29047_18 | Sinus Bradycardia -- Differential Diagnosis | Differentiation of sinus bradycardia from other bradyarrhythmias is done by establishing a relationship between P waves and QRS complexes on an electrocardiogram. Nondiscernible P waves are associated with junctional or ventricular escape rhythms. Whereas second or third-degree AV blocks will have more than a 1-to-1 relationship between P waves and QRS complexes [11] [12] . Rhythms on the differentials are: Sick sinus rhythm Wandering atrial pacemaker Junctional escape rhythm Ventricular escape rhythm | Sinus Bradycardia -- Differential Diagnosis. Differentiation of sinus bradycardia from other bradyarrhythmias is done by establishing a relationship between P waves and QRS complexes on an electrocardiogram. Nondiscernible P waves are associated with junctional or ventricular escape rhythms. Whereas second or third-degree AV blocks will have more than a 1-to-1 relationship between P waves and QRS complexes [11] [12] . Rhythms on the differentials are: Sick sinus rhythm Wandering atrial pacemaker Junctional escape rhythm Ventricular escape rhythm |
article-29047_19 | Sinus Bradycardia -- Prognosis | Prognosis is good when the rhythm is promptly identified by a healthcare provider. However, patients with sick sinus syndrome who have bradycardia tend to have a poor prognosis with 5-year survival rates between 45 to 70%. | Sinus Bradycardia -- Prognosis. Prognosis is good when the rhythm is promptly identified by a healthcare provider. However, patients with sick sinus syndrome who have bradycardia tend to have a poor prognosis with 5-year survival rates between 45 to 70%. |
article-29047_20 | Sinus Bradycardia -- Prognosis | With the number of bariatric procedures increasing each year, it has been observed that many of these patients also develop sinus bradycardia. Whether this is linked to the sudden loss of weight is not yet known. | Sinus Bradycardia -- Prognosis. With the number of bariatric procedures increasing each year, it has been observed that many of these patients also develop sinus bradycardia. Whether this is linked to the sudden loss of weight is not yet known. |
article-29047_21 | Sinus Bradycardia -- Complications | If not identified promptly symptomatic complications such as syncope, fatigue or dizziness can occur. | Sinus Bradycardia -- Complications. If not identified promptly symptomatic complications such as syncope, fatigue or dizziness can occur. |
article-29047_22 | Sinus Bradycardia -- Deterrence and Patient Education | Multiple resources are available for providers to help educate patients about this rhythm and its potential symptomatic complications. A patient who comes to the hospital or a clinic and has this rhythm identified should be provided with educational pamphlets if they are available at the facility. | Sinus Bradycardia -- Deterrence and Patient Education. Multiple resources are available for providers to help educate patients about this rhythm and its potential symptomatic complications. A patient who comes to the hospital or a clinic and has this rhythm identified should be provided with educational pamphlets if they are available at the facility. |
article-29047_23 | Sinus Bradycardia -- Pearls and Other Issues | There is a growing clinical consensus to lower the diagnosis threshold of sinus bradycardia to less than 50 bpm as there is a significant population size with a resting heart rate between 50 to 60 bpm. At present, the diagnostic consensus remains at a rate lower than 60 bpm with only the American College of Cardiology/American Heart Association/American College of Physicians–American Society of Internal Medicine (ACC/AHA/ACP–ASIM) Task Force recommending that it be diagnosed at 50 bpm. [4] | Sinus Bradycardia -- Pearls and Other Issues. There is a growing clinical consensus to lower the diagnosis threshold of sinus bradycardia to less than 50 bpm as there is a significant population size with a resting heart rate between 50 to 60 bpm. At present, the diagnostic consensus remains at a rate lower than 60 bpm with only the American College of Cardiology/American Heart Association/American College of Physicians–American Society of Internal Medicine (ACC/AHA/ACP–ASIM) Task Force recommending that it be diagnosed at 50 bpm. [4] |
article-29047_24 | Sinus Bradycardia -- Enhancing Healthcare Team Outcomes | Because there are many causes of sinus bradycardia, an interprofessional team approach is necessary for making an early diagnosis. Nurses on the floor and in the emergency department should understand bradycardia and its treatment. The pharmacist should ensure that the cause is not potentially related to any patient medications; if there is a risk, the clinical team should be contacted. The primary care provider should refer all symptomatic patients to the cardiologist for further workup. If a pacemaker is inserted, then the patient should be closely followed by a pacemaker nurse. Educating patients at risk for this rhythm and making a closed-loop communication between them and their providers can help further improve the management of these rhythms. | Sinus Bradycardia -- Enhancing Healthcare Team Outcomes. Because there are many causes of sinus bradycardia, an interprofessional team approach is necessary for making an early diagnosis. Nurses on the floor and in the emergency department should understand bradycardia and its treatment. The pharmacist should ensure that the cause is not potentially related to any patient medications; if there is a risk, the clinical team should be contacted. The primary care provider should refer all symptomatic patients to the cardiologist for further workup. If a pacemaker is inserted, then the patient should be closely followed by a pacemaker nurse. Educating patients at risk for this rhythm and making a closed-loop communication between them and their providers can help further improve the management of these rhythms. |
article-29047_25 | Sinus Bradycardia -- Review Questions | Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. | Sinus Bradycardia -- Review Questions. Access free multiple choice questions on this topic. Click here for a simplified version. Comment on this article. |
article-27818_0 | Propranolol -- Continuing Education Activity | Propranolol can be used to ameliorate the sympathetic response in angina, tachyarrhythmias, prevention of acute ischemic attacks, migraine prophylaxis, and restless leg syndrome. Propranolol can be used in almost all cases if the desired result is to slow contractility and decrease a patient’s heart rate. Propranolol is also used off-label in a variety of other cases, for instance, in performance anxiety, which is a subset of social phobia, a psychiatric condition whose symptoms also include tachycardia, sweating, and flushing secondary to the activation of the sympathetic nervous system. This activity examines the indications, dosing, contraindications, mechanism, and management of propranolol therapy by the interprofessional healthcare team. | Propranolol -- Continuing Education Activity. Propranolol can be used to ameliorate the sympathetic response in angina, tachyarrhythmias, prevention of acute ischemic attacks, migraine prophylaxis, and restless leg syndrome. Propranolol can be used in almost all cases if the desired result is to slow contractility and decrease a patient’s heart rate. Propranolol is also used off-label in a variety of other cases, for instance, in performance anxiety, which is a subset of social phobia, a psychiatric condition whose symptoms also include tachycardia, sweating, and flushing secondary to the activation of the sympathetic nervous system. This activity examines the indications, dosing, contraindications, mechanism, and management of propranolol therapy by the interprofessional healthcare team. |
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