Glaucoma classification: Difference between revisions

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== Overview ==
The glaucoma is typically classified is as open angle or closed angle and as primary or secondary. There have been multiple schemes proposed for the classification for glaucoma. However the classification of the
The glaucoma is typically classified is as open angle or closed angle and as primary or secondary. There have been multiple schemes proposed for the classification for glaucoma. However the classification of the
glaucomas based on initial events and classification based on mechanisms of outflow obstruction are commonly used.
glaucomas based on initial events and classification based on mechanisms of outflow obstruction are commonly used.


==Classification on basis of angle==
==Classification Based Upon Angle==
===Open-angle Glaucoma===
{| class="wikitable"
#Primary open-angle glaucoma (POAG)  
! colspan="2" |Open-angle Glaucoma
#::* not associated  with  known  ocular  or  systemic  disorders  that  cause increased resistance to aqueous outflow or damage to optic nerve
|-
#::*  usually associated with elevated IOP
|Primary open-angle glaucoma (POAG) (H40.11)
#Normal-tension glaucoma  
|
#::*    considered in continuum of POAG; often used when IOP is not elevated
:* Not associated  with  known  ocular  or  systemic  disorders  that  cause increased resistance to aqueous outflow or damage to optic nerve
#Juvenile open-angle glaucoma
:*  Elevated IOP
#::* used when open-angle glaucoma diagnosed at young age (typically 10-30 years of age)
|-
#Glaucoma suspect
|Normal-tension glaucoma (H40.12)
#::*  normal optic disc and visual field associated with elevated IOP
|
#::*    suspicious optic disc and/or visual field with normal IOP
:*    Continuum of POAG
#Secondary open-angle glaucoma
:*    IOP is not elevated
#::* increased resistance  to  trabecular  meshwork  outflow  associated  with other conditions (e.g. pigmentary-, phacolytic-, steroid-induced-)
|-
#::* increased posttrabecular resistance  to  outflow  secondary  to  elevated episcleral venous pressure (e.g. carotid cavernous sinus fistula)
|Juvenile open-angle glaucoma  
===Angle-Closure Glaucoma===
|
#:* Primary ACG with relative pupillary block
:* Open-angle glaucoma diagnosed at young age (typically 10-30 years of age)
#::* movement of aqueous humor from posterior chamber to anterior chamber restricted
|-
#::*   peripheral iris in contact with trabecular meshwork
|Glaucoma suspect (H40.0)
#:* Acute angle closure
|
#::* occurs when IOP rises rapidly as a result of relatively sudden blockage of the trabecular meshwork
:*  Normal optic disc and visual field associated with elevated IOP
#:* Subacute angle closure (intermittent angle closure)
:*    Suspicious optic disc and/or visual field with normal IOP
#::* repeated, brief episodes of angle closure with mild symptoms and elevated IOP, often a prelude to acute angle closure
|-
#:* Chronic angle closure
|Secondary open-angle glaucoma
#::* IOP elevation caused by variable portions of anterior chamber angle being permanently closed by PAS
:
#:* Secondary ACG with pupillary block
|
#::*   e.g. swollen lens, secluded pupil
:* Increased resistance  to  trabecular  meshwork  outflow  associated  with other conditions (e.g. pigmentary-, phacolytic-, steroid-induced-)
#:* Secondary ACG without pupillary block
:* Increased post-trabecular resistance  to  outflow  secondary  to  elevated episcleral venous pressure (e.g. carotid cavernous sinus fistula)
#::* posterior pushing mechanism: lens-iris diaphragm pushed forward (e.g. posterior segment tumor, scleral buckling procedure, uveal effusion)
|}
#::* anterior pulling mechanism: anterior segment process pulling iris forward to form PAS (e.g. iridocorneal endothelial syndrome, neovascular glaucoma, inflammation)
{| class="wikitable"
#:* Plateau iris syndrome
! colspan="2" |Angle-Closure Glaucoma
#::* primary angle closure with or without component of pupillary block, but pupillary block is not predominant mechanism of angle closure
|-
===Childhood Glaucoma===
|Primary ACG with relative  
:* Primary congenital/infantile glaucoma
pupillary block
::*    primary glaucoma present from birth to first few years of life
|
:* Glaucoma associated with congenital anomalies
:*Movement of aqueous humor from posterior chamber to anterior chamber restricted
::* associated  with  ocular  disorders  (e.g.  anterior  segment  dysgenesis, aniridia)
:*Peripheral iris in contact with trabecular meshwork
::*    associated with systemic disorders (e.g. rubella, Lowe syndrome)
|-
:* Secondary glaucoma in infants and children
|Acute angle closure
::*    e.g. glaucoma secondary to retinoblastoma or trauma
:
|
:*Occurs when IOP rises rapidly as a result of relatively sudden blockage of the trabecular meshwork
|-
|Subacute angle closure (intermittent angle closure)
:
|
:*Repeated, brief episodes of angle closure with mild symptoms and elevated IOP, often a prelude to acute angle closure
|-
|Chronic angle closure
|
:*IOP elevation caused by variable portions of anterior chamber angle being permanently closed by PAS
|-
|Secondary ACG with pupillary block
|
:*Swollen lens, secluded pupil
|-
|Secondary ACG without pupillary block
:
|
:* Posterior pushing mechanism: lens-iris diaphragm pushed forward (e.g. posterior segment tumor, scleral buckling procedure, uveal effusion)
:* Anterior pulling mechanism: anterior segment process pulling iris forward to form PAS (e.g. iridocorneal endothelial syndrome, neovascular glaucoma, inflammation)
|-
|Plateau iris syndrome
|
:*Primary angle closure with or without component of pupillary block, but pupillary block is not predominant mechanism of angle closure
|}


==Classification on basis of etiology==
{| class="wikitable"
|+
!Childhood Glaucoma
!
|-
|Primary congenital/infantile glaucoma
:
|
:*Primary glaucoma present from birth to first few years of life
|-
|Glaucoma associated with congenital anomalies
:
|
:*Associated  with  ocular  disorders  (e.g.  anterior  segment  dysgenesis, aniridia)
:* Associated with systemic disorders (e.g. rubella, Lowe syndrome)
|-
|Secondary glaucoma in infants and children
:
|
:*Glaucoma secondary to retinoblastoma or trauma                                                                     
|}
 
==Classification based upon initial event==


=== Congenital and Developmental Glaucoma (Q15.0)===
=== Congenital and Developmental Glaucoma (Q15.0)===
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===Absolute Glaucoma (H44.5)===
===Absolute Glaucoma (H44.5)===
*Absolute glaucoma
*Absolute glaucoma
==Classification based upon mechanism of outflow obstruction==
===Open Angle Glaucoma Mechanisms===
#Pre-trabecular (membrane overgrowth)
#:*Fibrovascular membrane (neovascular glaucoma)
#:*Endothelial  layer,  often  with  Descemet-like  membrane  (iridocorneal endothelial  syndrome,  posterior  polymorphous dystrophy,  penetrating and non-penetrating trauma)
#:*Epithelial downgrowth
#:*Fibrous ingrowth
#:*Inflammatory  membrane  (Fuchs  heterochromic  iridocyclitis,luetic interstitial keratitis)
#Trabecular
#:*Idiopathic (chronic open-angle glaucoma, juvenile open-angle glaucoma)
#:*"Clogging” of trabecular meshwork
#::*Red blood cells (hemorrhagic-, ghost cell-, sickled red blood cells)
#::*Macrophages (hemolytic-, phacolytic-, melanomalytic-)
#::*Neoplastic cells (primary ocular tumors, neoplastic tumors, juvenile xanthogranuloma)
#::*Pigment particles (pigmentary-, exfoliation syndrome /  glaucoma capsulare, malignant melanoma)
#::*Protein (uveitis, lens-induced glaucoma)
#::*Viscoelastic agents
#::*α-chymotrypsin-induced glaucoma
#::*Vitreous
#:*Alterations of the trabecular meshwork
#::*Steroid-induced glaucoma
#::*Edema (uveitis, scleritis, episcleritis, alkali burns)
#::*Trauma (angle recession)
#::*Intraocular foreign bodies (hemosiderin, chalcosis)
#Post-trabecular
#:*Obstruction of Schlemm’s canal (e.g. collapse at canal)
#:*Elevated episcleral venous pressure
#:*Carotid cavernous fistula
#:*Cavernous sinus thrombosis
#:*Retrobulbar tumors
#:*Thyroid ophthalmopathy
#:*Superior vena cava obstruction
#:*Mediastinal tumors
#:*Sturge-Weber syndrome
#:*Familial episcleral venous pressure elevation
===Angle Closure Glaucoma Mechanisms===
#Anterior (“pulling”)
#:*Contracture of membranes
#::*Neovascular glaucoma
#::*Iridocorneal endothelial syndrome
#::*Posterior polymorphous dystrophy
#::*Penetrating and non-penetrating trauma
#:*Consolidation of inflammatory products
#Posterior (“pushing”)
#:*With pupillary block
#::*Pupillary block glaucoma
#::*Lens-induced mechanisms (phacomorphic lens, ectopia lentis)
#::*Posterior synechiae (iris-vitreous block, pseudophakia, uveitis)
#:*Without pupillary block
#::*Ciliary block (malignant) glaucoma
#::*Lens-induced mechanisms (phacomorphic lens, ectopia lentis)
#::*Following lens extraction (forward vitreous shift)
#::*Anterior rotation of ciliary body (following scleral buckling or panretinal photocoagulation, central retinal vein occlusion)
#::*Intraocular tumors (retinoblastoma, malignant melanoma)
#::*Cysts of the iris and ciliary body
#::*Retrolenticular  tissue  contracture  (retinopathy  of  prematurity, persistent hyperplastic primary vitreous)
===Developmental Anomalies of Angle===
#Incomplete development of trabecular meshwork / Schlemm’s canal
#:*Congenital (infantile) glaucoma
#:*Axenfeld-Rieger syndrome
#:*Peter’s anomaly
#:*Glaucomas associated with other developmental anomalies
#Iridocorneal adhesions
#:*Broad strands (Axenfeld-Rieger syndrome)
#:*Fine strands that contract to close angle (aniridia)
===Combined Mechanism Glaucoma===
#Combination of two or more forms of glaucoma present either sequentially or simultaneously
#IOP elevation can occur as a result of either or both of the following:
#:*The intrinsic resistance of the trabecular meshwork to aqueous outflow in open-angle glaucoma
#:*The direct anatomic obstruction of the filtering meshwork by synechiae in ACG


==References==
==References==
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[[Category:Emergency medicine]]
[[Category:Emergency medicine]]
[[Category:Mature chapter]]
[[Category:Mature chapter]]
[[Category:Primary care]]
[[Category:Needs overview]]
[[Category:Needs overview]]

Latest revision as of 21:52, 29 July 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Rohan Bir Singh, M.B.B.S.[2]

Overview

The glaucoma is typically classified is as open angle or closed angle and as primary or secondary. There have been multiple schemes proposed for the classification for glaucoma. However the classification of the glaucomas based on initial events and classification based on mechanisms of outflow obstruction are commonly used.

Classification Based Upon Angle

Open-angle Glaucoma
Primary open-angle glaucoma (POAG) (H40.11)
  • Not associated with known ocular or systemic disorders that cause increased resistance to aqueous outflow or damage to optic nerve
  • Elevated IOP
Normal-tension glaucoma (H40.12)
  • Continuum of POAG
  • IOP is not elevated
Juvenile open-angle glaucoma
  • Open-angle glaucoma diagnosed at young age (typically 10-30 years of age)
Glaucoma suspect (H40.0)
  • Normal optic disc and visual field associated with elevated IOP
  • Suspicious optic disc and/or visual field with normal IOP
Secondary open-angle glaucoma
  • Increased resistance to trabecular meshwork outflow associated with other conditions (e.g. pigmentary-, phacolytic-, steroid-induced-)
  • Increased post-trabecular resistance to outflow secondary to elevated episcleral venous pressure (e.g. carotid cavernous sinus fistula)
Angle-Closure Glaucoma
Primary ACG with relative

pupillary block

  • Movement of aqueous humor from posterior chamber to anterior chamber restricted
  • Peripheral iris in contact with trabecular meshwork
Acute angle closure
  • Occurs when IOP rises rapidly as a result of relatively sudden blockage of the trabecular meshwork
Subacute angle closure (intermittent angle closure)
  • Repeated, brief episodes of angle closure with mild symptoms and elevated IOP, often a prelude to acute angle closure
Chronic angle closure
  • IOP elevation caused by variable portions of anterior chamber angle being permanently closed by PAS
Secondary ACG with pupillary block
  • Swollen lens, secluded pupil
Secondary ACG without pupillary block
  • Posterior pushing mechanism: lens-iris diaphragm pushed forward (e.g. posterior segment tumor, scleral buckling procedure, uveal effusion)
  • Anterior pulling mechanism: anterior segment process pulling iris forward to form PAS (e.g. iridocorneal endothelial syndrome, neovascular glaucoma, inflammation)
Plateau iris syndrome
  • Primary angle closure with or without component of pupillary block, but pupillary block is not predominant mechanism of angle closure
Childhood Glaucoma
Primary congenital/infantile glaucoma
  • Primary glaucoma present from birth to first few years of life
Glaucoma associated with congenital anomalies
  • Associated with ocular disorders (e.g. anterior segment dysgenesis, aniridia)
  • Associated with systemic disorders (e.g. rubella, Lowe syndrome)
Secondary glaucoma in infants and children
  • Glaucoma secondary to retinoblastoma or trauma

Classification based upon initial event

Congenital and Developmental Glaucoma (Q15.0)

  • Developmental glaucoma

Primary Glaucoma and its Variants (H40.1-H40.2)

  • Primary glaucoma
  • Primary open-angle glaucoma, also known as chronic open-angle glaucoma, chronic simple glaucoma, glaucoma simplex
  • Low-tension glaucoma
  • Primary angle-closure glaucoma, also known as primary closed-angle glaucoma, narrow-angle glaucoma, iris- block glaucoma, acute congestive glaucoma
  • Variants of primary glaucoma

Secondary Glaucoma (H40.3-H40.6)

  • Secondary glaucoma
  • Phacogenic glaucoma
  • Angle-closure glaucoma with mature cataract
  • Phacoanaphylactic glaucoma secondary to rupture of lens capsule
  • Phacolytic glaucoma due to phacotoxic meshwork blockage
  • Subluxation of lens
  • Traumatic glaucoma
  • Angle recession glaucoma: Traumatic recession on anterior chamber angle
  • Postsurgical glaucoma
  • Glaucoma of miscellaneous origin

Absolute Glaucoma (H44.5)

  • Absolute glaucoma

Classification based upon mechanism of outflow obstruction

Open Angle Glaucoma Mechanisms

  1. Pre-trabecular (membrane overgrowth)
    • Fibrovascular membrane (neovascular glaucoma)
    • Endothelial layer, often with Descemet-like membrane (iridocorneal endothelial syndrome, posterior polymorphous dystrophy, penetrating and non-penetrating trauma)
    • Epithelial downgrowth
    • Fibrous ingrowth
    • Inflammatory membrane (Fuchs heterochromic iridocyclitis,luetic interstitial keratitis)
  2. Trabecular
    • Idiopathic (chronic open-angle glaucoma, juvenile open-angle glaucoma)
    • "Clogging” of trabecular meshwork
    • Red blood cells (hemorrhagic-, ghost cell-, sickled red blood cells)
    • Macrophages (hemolytic-, phacolytic-, melanomalytic-)
    • Neoplastic cells (primary ocular tumors, neoplastic tumors, juvenile xanthogranuloma)
    • Pigment particles (pigmentary-, exfoliation syndrome / glaucoma capsulare, malignant melanoma)
    • Protein (uveitis, lens-induced glaucoma)
    • Viscoelastic agents
    • α-chymotrypsin-induced glaucoma
    • Vitreous
    • Alterations of the trabecular meshwork
    • Steroid-induced glaucoma
    • Edema (uveitis, scleritis, episcleritis, alkali burns)
    • Trauma (angle recession)
    • Intraocular foreign bodies (hemosiderin, chalcosis)
  3. Post-trabecular
    • Obstruction of Schlemm’s canal (e.g. collapse at canal)
    • Elevated episcleral venous pressure
    • Carotid cavernous fistula
    • Cavernous sinus thrombosis
    • Retrobulbar tumors
    • Thyroid ophthalmopathy
    • Superior vena cava obstruction
    • Mediastinal tumors
    • Sturge-Weber syndrome
    • Familial episcleral venous pressure elevation

Angle Closure Glaucoma Mechanisms

  1. Anterior (“pulling”)
    • Contracture of membranes
    • Neovascular glaucoma
    • Iridocorneal endothelial syndrome
    • Posterior polymorphous dystrophy
    • Penetrating and non-penetrating trauma
    • Consolidation of inflammatory products
  2. Posterior (“pushing”)
    • With pupillary block
    • Pupillary block glaucoma
    • Lens-induced mechanisms (phacomorphic lens, ectopia lentis)
    • Posterior synechiae (iris-vitreous block, pseudophakia, uveitis)
    • Without pupillary block
    • Ciliary block (malignant) glaucoma
    • Lens-induced mechanisms (phacomorphic lens, ectopia lentis)
    • Following lens extraction (forward vitreous shift)
    • Anterior rotation of ciliary body (following scleral buckling or panretinal photocoagulation, central retinal vein occlusion)
    • Intraocular tumors (retinoblastoma, malignant melanoma)
    • Cysts of the iris and ciliary body
    • Retrolenticular tissue contracture (retinopathy of prematurity, persistent hyperplastic primary vitreous)

Developmental Anomalies of Angle

  1. Incomplete development of trabecular meshwork / Schlemm’s canal
    • Congenital (infantile) glaucoma
    • Axenfeld-Rieger syndrome
    • Peter’s anomaly
    • Glaucomas associated with other developmental anomalies
  2. Iridocorneal adhesions
    • Broad strands (Axenfeld-Rieger syndrome)
    • Fine strands that contract to close angle (aniridia)

Combined Mechanism Glaucoma

  1. Combination of two or more forms of glaucoma present either sequentially or simultaneously
  2. IOP elevation can occur as a result of either or both of the following:
    • The intrinsic resistance of the trabecular meshwork to aqueous outflow in open-angle glaucoma
    • The direct anatomic obstruction of the filtering meshwork by synechiae in ACG

References

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