Uveitis is an interesting disease of the with such a varied and diverse pathogenesis, various systemic causes and Dangerous complications in relation to the eye which makes it difficult and challenging to treat in a proper way. I hope this share will help.
Uveitis is an interesting disease of the with such a varied and diverse pathogenesis, various systemic causes and Dangerous complications in relation to the eye which makes it difficult and challenging to treat in a proper way. I hope this share will help.
A surgical procedure featuring a partial thickness scleral flap that creates a fistula between AC and subconjunctival space for filtration of aqueous and creation of conjunctival bleb in an effort to lower IOP
A surgical procedure featuring a partial thickness scleral flap that creates a fistula between AC and subconjunctival space for filtration of aqueous and creation of conjunctival bleb in an effort to lower IOP
Retinal Arterial Obstructions is a common eye disease that causes loss of vision due to the blockage of the blood flow, runs into the retina which is to be found in the back of your eye.
Leukocoria ( or white pupillary reflex) is an abnormal white reflection from the eye.
Leukocoria is a medical sign for a number of several conditions.
- this presentation at annual conference of the Ophthalmic department, faculty of medicine - Al-Azhar University in association with DOS & EOS Cairo, Egypt January 2017
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
3. SECONDARY ANGLE CLOSURE GLAUCOMA
Caused by impairment of aqueous outflow secondary to
apposition between the peripheral iris and the trabeculum.
Related or identifiable ophthalmic condition is known to be
present with the onset of angle closure : “secondary” ACG
3
4. Two fundamental mechanisms:
Anterior pulling mechanism:
peripheral iris pulled forward onto
TM by contraction of a membrane,
inflammatory exudate, or fibrous
band
Posterior pushing mechanism:
peripheral iris is displaced forward by
lens, vitreous, or ciliary body
4
5. CLASSIFICATION
1. Anterior ‘pulling mechanism:
Contraction of an inflammatory, hemorrhagic, or vascular
membrane, band, or exudate in the angle
PAS
Forward displacement of lens-iris interface
Often accompanied by swelling and anterior rotation of ciliary body
5
6. ANTERIOR ‘PULLING MECHANISM
a. Neovascular glaucoma
b. Iridocorneal endothelial
syndromes (e.g. Chandler’s
syndrome)
c. Posterior polymorphous
dystrophy
d. Epithelial down growth
e. Fibrous ingrowth
f. Flat anterior chamber
g. Inflammation
6
7. NEOVASCULAR GLAUCOMA
Secondary glaucoma resulting from
neovascularization of anterior segment,
including iris and angle often
associated with retinal hypoxia.
SYNONYMS
1. Hemorrhagic glaucoma
2. Thrombotic glaucoma
3. Rubeotic glaucoma
4. Congestive glaucoma
5. Diabetic hemorrhagic glaucoma
9
8. NEOVASCULAR GLAUCOMA (NVG)
Primary initiating events : hypoxia
and poor retinal capillary
circulation
Begins as formation of new vessels
Ends with fibrovascular membranes
migrating over drainage angle,
potentially leading to end-stage
glaucoma 10
9. HISTORY
1906 Coates , NVI in CRVO termed as RUBEOSIS IRIDIS
1937 Kurtz , NVA leading to PAS formation
1963 Weiss et al, coined the term NEOVASCULAR GLAUCOMA
11
12. PATHOGENESIS
Theory of angiogenesis factor:
Michaelson 1948
Postulated existence of “X factor”, a vasoformative factor
which controlled development of new vessels
Folkman et al
Isolated a soluble substance from a solid neoplasm capable
of producing neovascularisaton and popularised the term
“tumor angiogenesis factor”
16
13. VEGF (Vascular endothelial growth factor)
Potent angiogenic stimulator
Has role in both normal and pathologic angiogenesis
Also known as “vascular permeability factor” as induces
vascular hyperpermeability and endothelial cell
proliferation
Four isoforms:
1. VEGF121
2. VEGF165 - most abundant form in most tissues
3. VEGF189
4. VEGF206
17
14. Lens and vitreous acts as mechanical barriers and also releases
vaso inhibitory factors
So any complicated cataract sx PCR, APHAKIA more
predisposition
VEGF synthesised by all tissues in retina, mainly
MULLERS CELL.
VEGF conc 50-100 times more in aqueous humour
in NVG
18
16. Muller cells –primary source in conditions of retinal
ischemia
Retinal capillary or venous obstruction
Hypoxia of retinal cells
Production of vasoformative factor
Diffuses anteriorly
Stimulates iris angiogenesis
20
17. Theory of vasoinhibitory factors (VIF):
Source of VIF : Vitreous, lens and retinal pigment
epithelial cells
Risk increased by vitrectomy and lensectomy
22
19. Features Normal vessels New vessels
Location Iris stroma Pupillary margins
Angles
Arrangement Regular Irregular
Appearance Tortuous Thin
Course Radial Arbourising
Character Not fenestrated Fenestrated
Scleral spur Not cross Crosses
Flouroscein No leakage leakage
24
20. (A)Pre-glaucoma stage with new vessels appearing at pupillary margin
and in angle.
(B)Open-angle glaucoma stage with new vessels spreading and
fibrovascular tissue covering angle.
(C)Heavy neovascularization and extensive peripheral anterior
synechiae.
(D) Regression stage with angle sealed and vessels less visible
25
Stages of neovascular glaucoma.
21. DIAGNOSIS:
Gonioscopy: vitally important to detect in early stage as NVA
can occur without NVI
Strong association with CRVO
Treatment of choice
Clear media : Panretinal photocoagulation
Cloudy media
Prevent laser therapy
Panretinal cryotherapy - alternative to Vitrectomy to clear
the media with endophotocoagulation
Or subsequent panretinal photocoagulation
Anti -VEGF
33
22. IRIDOCORNEAL ENDOTHELIAL (ICE)
SYNDROME
Group of disorders
characterized by abnormal
corneal endothelium
Usually includes-
iris atrophy
corneal edema
secondary angle-closure
glaucoma without pupillary
block
35
23. Cause:
Abnormal corneal endothelium forming a membrane over
anterior surface of iris and angle structures
Contraction of this membrane
Distorts iris and closes angle
36
24. In Variants:
In early to mid adult life
whites > blacks
women > men
U/L > B/L (fellow eye may have subclinical
abnormalities)
37
25. PATHOGENESIS
Defect site: corneal endothelium – dysfunction corneal
edema
Corneal endothelium elaborates a membrane contracts
forms PAS glaucoma
Ischemia may be a secondary phenomenon ‘melt holes.’
Few postulations:
Abnormal proliferation of neural crest cells or a fetal crest of
epithelial cells
Inflammatory endothelial proliferation
Electron micrographic, immunohistochemical, and serologic
studies - herpes simplex virus and EBV as cause 38
27. CLINICAL PRESENTATION
PAS: extensive in quadrant toward which
pupil is displaced
Thinner iris stroma in opposite quadrant to
PAS
Full-thickness iris holes
Anteriorly projected pigmented lesions
from iris surface with multilayered
membrane
40
28. THREE WELL CHARACTERIZED CLINICAL
ENTITIES
Progressive iris atrophy
Chandler’s syndrome
Cogan-reese syndrome
41
29. Slit-lamp: ‘beaten silver’
endothelium
Specular reflection: loss of
the normal, regular
endothelial mosaic
Specular microscopy:
alterations in size and shape
of endothelial
42
30. PROGRESSIVE (ESSENTIAL) IRIS ATROPHY
Corectopia and ectopion uvea
(synechiae lift the iris off the surface
of the lens)
Iris dissolution - patchy
disappearance of the stroma
progresses to full-thickness holes
‘stretch holes’
‘melt holes’
Broad patchy PAS – extend ant to
schwalbe line
43
31. SYNDROM
E
- Most common variant
- Marked corneal changes
- Corectopia is minimal or absent
- Endothelium - hammered silver
appearance.
44
32. Iris involvement - mild and limited to superficial stromal
dissolution.
Peripheral anterior synechiae
- not diffuse
- do not extend as far anteriorly as in progressive iris atrophy
46
33. THE IRIS NAEVUS (COGAN–REESE)
SYNDROME
diffuse naevus which covers the anterior iris or iris nodules .
Iris atrophy - absent - 50% of cases
- remainder - mild to moderate although
corectopia may be severe.
47
34. TREATMENT
• Hypertonic solutions or soft contact lenses
• If corneal edema produces pain or reduced vision if IOP
is reduced - penetrating keratoplasty
Goniotomy- short term sucess
Filtering surgery or glaucoma drainage devices
49
35. POSTERIOR POLYMORPHOUS DYSTROPHY
Disease of corneal endothelium sometimes associated
with glaucoma
B/L
Inheritence: autosomal dominant trait (AR also reported)
Defect on: long arm of chromosome 20, three different
forms PPCD 1-3
50
36. HISTOPATHOLOGY
Thin descemet’s membrane covered by multiple layers of
collagen
Cell layers resembles endothelium, epithelium or
fibroblasts
Some cases: membrane in angle and on anterior surface
of iris
51
37. PATHOGENESIS
Cause -controversial
Analogous to ICE syndrome
Some postulates:
Dysplastic corneal endothelium produces BM-like material
Extends into angle Onto iris Contraction of
membrane Iris atrophy, corectopia, and iridocorneal
adhesions
developmental disorder
Viral infection (herpes simplex)metaplasia of the
corneal endothelium
52
38. CLINICAL PRESENTATION
Variable
Most typical physical finding: cluster
or linear arrangement of vesicles in
posterior cornea surrounded by a gray
haze
Deep corneal stroma and DM :
Band-like thickenings
White patches
Peau d’orange appearance
excrescences projecting on AC
53
40. Mostly non-progressive, asymptomatic
Good vision throughout life
Few cases: progressive corneal changes: corneal edema
Glaucoma seen in 10–15%
Differential diagnosis:
Fuchs’ corneal dystrophy
Congenital hereditary corneal dystrophy
Axenfeld’s syndrome
Congenital glaucoma:
55
41. TREATMENT
Most : need no treatment
For edematous cornea
Hypertonic solutions
Soft contact lenses
Penetrating keratoplasty (as needed)
glaucoma - medication
- filtering surgery
56
42. EPITHELIAL DOWNGROWTH
Pathophysiology
Due to entry of epithelial membrane via wound
Proliferation over corneal endothelium, TM, anterior iris
surface, and vitreous face
Membrane in angle contracts
PAS
Severe angle-closure glaucoma without pupillary block
57
44. Most common cause - Cataract surgery (ICCE)
- penetrating keratoplasty
- glaucoma surgery
- penetrating trauma,
- unsuccessful removal of epithelial
cysts of anterior segment
59
45. CLINICAL PRESENTATION
low-grade persistent
postoperative inflammation:
conjunctival injection
photophobia
Cells in AC
discomfort
Evidence of current or past
wound leak
61
46. Diagnostic finding: Hypotonic if
fistula is still functional
Grayish white membrane with a
scalloped, thickened leading edge
on the posterosuperior corneal
surface.
Cornea : edematous
Iris: drawn up to old wound or
incision.
Advanced cases:
Painful eye with bullous
keratopathy and intractable
glaucoma 62
47. TREATMENT
Difficult and unrewarding
Techniques used are to close fistula and then to excise or
destroy epithelium
For corneal portion of membrane: destroyed with cryotherapy
or chemical cauterization.
Iris membrane: excised
Cryotherapy applied to any remaining membrane on ciliary
body and retina
En-bloc excision of all involved tissues 63
48. FIBROVASCULAR INGROWTH
Occurs in an eye with open wound after penetrating
trauma or surgery
Specially if associated with
Hemorrhage
Inflammation
Incarcerated tissue
Membrane is seen as interlacing pattern of gray
fibers(woven cloth)
64
49. Attributing factor:
Invading fibroblasts to subconjunctival connective tissue,
corneal stroma, limbal tissue, metaplastic endothelium
Invading tissue grows over corneal endothelium, anterior
iris surface, vitreous face, and angle
Contraction of membrane
Formation of PAS
65
50. Other factors contributing to glaucoma:
Uveitis
Pupillary block
Underlying trauma
Less virulent in course than epithelial ingrowth
66
51. FLAT ANTERIOR CHAMBER
After penetrating trauma or surgery
Formation of PAS
SACG without pupillary block
Development of synechiae
Duration of flat AC
Degree of inflammation
SACG common - AC remain flat for 5 days or more after
cataract extraction 67
52. IRIDOSCHISIS
Patchy dissolution of iris in
which the ant stroma
separates from post stroma
and muscle layer
rare condition
elderly
bilateral.
69
53. Slit lamp biomicroscopy
Shallow anterior chamber
usually involves the inferior iris
severity ranges from intrastromal
atrophy to disintegrated iris
fibrils
Anterior stroma splits into
strands
Project into AC
Touch cornea
70
54. Gonioscopy - narrow occludable angle – may be
associated with PAS.
Treatment
peripheral laser iridotomy.
Subsequent treatment is aimed at limiting
glaucomatous damage.
71
55. 2. POSTERIOR ‘PUSHING MECHANISM
a. Ciliary block glaucoma (malignant glaucoma)
b. Intraocular tumors
c. Nanophthalmos
d. Suprachoroidal hemorrhage
e. Intravitreal air injection (e.g., retinal pneumopexy)
f. Ciliochoroidal effusions (e.g., panretinal
photocoagulation)
a. Inflammation (e.g., posterior scleritis)
b. Central retinal vein occlusion
g. Scleral buckling procedure
h. Retrolental fibroplasias 72
56. POSTERIOR PUSHING (OR ROTATIONAL)
MECHANISM
Peripheral iris is displaced by lens, vitreous, or ciliary body often
accompanied by swelling and anterior rotation of the ciliary body
1. Swelling of ciliary body
Rotates forward about its attachment at scleral spur
Loosens the zonules
Diminishes diameter of ciliary ring
Displaces the root of iris
Which further acts to close angle.
73
57. MECHANISMS:
2. swelling of anterior uveal tract (inflammation or vascular
congestion)
Narrowing of ciliary ring
Reduced tension on lens zonules
Allows lens to come forward
Displaces peripheral iris
74
58. 3. Swelling of ciliary body is often accompanied by
accumulation of suprachoroidal and supraciliary fluid
further rotates ciliary body and iris root into angle
75
59. CILIARY BLOCK GLAUCOMA
Syn:
Aqueous misdirection
Malignant glaucoma
Hyaloid block glaucoma
Posterior aqueous entrapment
Described by von graefe 1869
Definition: A shallow or flat AC with an inappropriately high IOP
despite a patent iridectomy
Affects primarily patients who have narrow anterior chamber
angles 76
60. Precipitating factors:
As a complication of a filtering procedure in eyes
with pre-existing ACG or shallow AC
Laser iridotomy
Miotic usage
Infectious endophthalmitis
77
61. PATHOGENESIS…
Posterior misdirection of aqueous flow by a relatively
impermeable hyaloid membrane into or behind vitreous
body Increase in vitreous volume Shallower
AC Increase in IOP
Provocating factors:
Small, crowded anterior segment
Angle closure
Swelling and inflammation of ciliary processes
Anterior rotation of ciliary body
Movement of lens-iris diaphragm forward 79
62. OCULAR MANIFESTATIONS
red, painful eye: commonly after surgery for AACG
Timing:
Immediate- during surgery
Months to years later
Often corresponds to cessation by cycloplegic therapy or
initiation due to miotic drops
Slit-lamp examination
Shallow or flat anterior chamber(central and peripheral)
Asymmetry of AC with respect to fellow eye
No iris bombé 80
64. DIAGNOSIS
Clinical suspicion after ruling out
Pupillary block
Suprachoroidal hemorrhage
Serous choroidal effusions
Or other causes of a flat anterior chamber
High-resolution ultrasound biomicroscopy:
Anterior rotation of ciliary body against peripheral iris
Forward displacement of posterior chamber intraocular
lens
Shallow central AC 83
65. TREATMENT
1st line: medical (cycloplegics and mydriatics)
Atropine 1% and phenylephrine 2.5% QID : move lens-iris
diaphragm back and relax ciliary muscle
Decrease aqueous production by:
Topical β-blockers
Oral or topical CAI
α-agonists
Shrink the vitreous volume. :
Isosorbide 1.5 mg/kg orally
Mannitol 2 g/kg intravenously over a 45-minute period
85
66. No oral foods or liquids given 2 hours before and after
administration of a hyperosmotic agent
Thus, avoid reduction in osmotic effect
Atropine for prolonged period
Very slow taper to avoid high risk of recurrence
Miotic agents (contraindicated - may cause or contribute
to aqueous misdirection)
86
67. 2nd line of treatment: laser therapy:
Neodymium:yttrium-aluminum-garnet (Nd:YAG)
To create a large PI and anterior hyaloid rupture
To release trapped aqueous from vitreous
Re-establish normal aqueous flow
Peripheral placement :
Enable anterior migration aqueous
Maximize likelihood of resolution of malignant
glaucoma.
87
68. Pars plana vitrectomy
Failed medical or laser therapy
Phakic eyes for which laser treatment is not a good
option:
Narrow angle in fellow eye - laser peripheral
iridectomy performed before any other surgical
procedures.
88
69. INTRAOCULAR TUMORS
Ocular malignant melanoma
Mechanisms:
Direct extension of tumor into TM
Seeding of tumor cells into outflow channels
Obstruction of meshwork by pigment or pigment-
laden macrophages
Neovascularization
PAS
Iridocyclitis
Hyphema
89
71. Leiomyoma pushing the peripheral iris
forward and closing off chamber angle.
Adenomas and leiomyomas:
Pushes iris forward and cause
angle-closure glaucoma.
91
72. Retinoblastoma: frequently associated with glaucoma
Mechanisms
Neovascularization
Angle seeding
Iridocyclitis
Hyphema
By rapidly developing as posterior mass thus
displacing lens–iris diaphragm
the mechanism in 27% of cases with elevated IOP.
92
73. NANOPHTHALMOS
Normal shaped but small sized eye
sporadic or inherited in an AD/AR pattern
B/L
M =F
Prevalence: 0.06% and 0.1%
93
74. Features:
Short AP length (20 mm)
Small corneal diameter
Lens: normal (even somewhat large, in size)
Volume of lens: volume of eye =10–25% (normal=3–
4%)
AC (central / peripheral): shallow
Iris: anteriorly displaced
Sclera: thick
High hyperopia
94
76. Develop ACG :4th – 6th decades of life
Can progress to total synechial closure
Angle closure precipitated by:
Development of a choroidal effusion
Rotates ciliary body anteriorly
Displaces peripheral iris
Loosens zonules
Allows lens to move forward 96
77. SUPRACHOROIDAL HEMORRHAGE
non-expulsive suprachoroidal hemorrhage
rapidly developing posterior mass
produce angle-closure glaucoma without pupillary block.
most often seen after filtering operations in aphakic eyes
97
78. POSTERIOR SEGMENT INFLAMMATORY
DISEASE
Posterior scleritis - increased IOP in 12–46%
Mechanisms
increased viscosity of the aqueous humor
inflammation of the outflow channels
obstruction of the trabecular meshwork by inflammatory cells
and debris
PAS
Neovascularization
Elevated episcleral venous pressure
also be associated with choroidal effusion
secondary angle-closure glaucoma without pupillary block
swelling and anterior rotation of the ciliary body 98
79. CLINICAL FEATURES
shallow anterior chamber both centrally and peripherally,
partial to total angle closure
sectorial or circumferential choroidal effusion
IOP - normal, high, or even low depending on the rate of
aqueous hum
Treatment
Medical management
- systemic non-steroidal anti-inflammatory agents
- topical cycloplegic agents
- topical and systemic corticosteroids
- control IOP
99
80. CENTRAL RETINAL VEIN OCCLUSION
Vein occlusion interferes with the venous
drainage of the uveal tract
swelling and anterior rotation of the ciliary
body.
transudation of fluid into the choroid, retina,
and vitreous.
Medical treatment
Laser gonioplasty
Pupillary block - laser iridectomy
If ischemia - retinal ablation after the anterior
chamber deepens
100
81. SCLERAL BUCKLING PROCEDURE
ocular pain, nausea, vomiting, and
chemosis.
Examination
shallow anterior chamber both
centrally and peripherally
corneal edema
total angle closure
Intraocular pressure - 25–50 mmHg
serous or bloody choroidal detachment
101
82. MECHANISM
displaces the lens, iris and ciliary body
encircling band - temporary interference with the venous
drainage of the uveal tract
swelling and anterior rotation of the ciliary body and
accumulation of supraciliary and suprachoroidal fluid.
buckle may directly compress one or more vortex veins,
leading to vascular congestion and angle-closure
glaucoma..
102
83. PANRETINAL PHOTOCOAGULATION
often followed by a shallow anterior
chamber and angle
Asymptomatic
Examination
corneal epithelial edema
shallow anterior chamber both
centrally and peripherally
myopic shift in refraction
choroidal detachment
IOP in the range of 20–50 mmHg
partial to total angle closure.
103
84. Anterior chamber- deepens spontaneously over a few
days to a few weeks
Mechanism
interference with the venous drainage of the uveal tract
leading to choroidal detachment
swelling and anterior rotation of the ciliary body.
Medical therapy
104
86. PHACOMORPHIC GLAUCOMA
abnormal lens either
compromises the lens–iris
channel (pupillary block) or
mechanically pushes the
peripheral iris forward into the
angle structures.
intumescent cataracts - crowd
the anterior chamber
swelling, dislocation or
subluxation –laser iridotomy
106
87. Intumescent and swollen lens
Increased pupillary block - develop slowly with an age-
related cataract or rapidly with a traumatic, swollen
cataract.
Unilateral and resembles PACG
Definitive treatment - cataract extraction.
Iridotomy
107
88. ECTOPIA LENTIS :
Displacement of lens from its normal anatomical position
Forward displacement
Iris bombe
Shallowing of the anterior chamber angle
Pupillary block
Secondary angle closure. 109
89. CLINICAL PRESENTATION:
Acute:
Pain
Conjunctival hyperemia
Loss of vision
Chronic ACG:
PAS formation secondary to repeated attacks
110
90. TREATMENT
Long term treatment with miotic agents to prevent
forward movement of lens.
Treatment of choice to relieve pupillary block :
Two laser iridotomies (180° apart) pupillary block
Definitive t/m: lensectomy
Lens extraction- Indication:
to restore vision
to reduce risk of recurrence of pupillary block 111
91. APHAKIC OR PSEUDOPHAKIC ANGLE-
CLOSURE GLAUCOMA
Extensive adhesions of the
iris to the vitreous face -
produce pupillary block and
secondary angle-closure
glaucoma
Iridectomy is not patent,
occluded, or omitted
Adherence of the iris to an
intraocular lens (IOL)
112
92. With anterior chamber lenses the
optic may form a ball valve type seal
over the pupil while the haptic covers
the iridectomy.
Iridectomies spaced far enough apart
to prevent the haptics from occluding
the openings
113
93. MICROSPHEROPHAKIA
Congenital
Spherical or globular lens
Often familial
May occur as an isolated condition
Or as part of either Weill-Marchesani or Marfan syndrome.
Can cause ectopia lentis and subsequent pupillary block and
ACG
lens (arrow) is trapped anteriorly by pupil,
resulting in iris bombe and dramatic shallowing of AC
114
94. TREATMENT
Cycloplegia
tighten zonule, flatten lens, and pull it posteriorly,
breaking pupillary block
Miotics may worses the condition by
Rotating ciliary body forward
loosening the zonule
Allowing lens to become more globular
115
95. BIBLIOGRAPHY
# Becker-Shaffer's Diagnosis and Therapy of the Glaucomas;
8th Ed.
# American Academy of Ophthalmology BCSC. Section 10;
2015-2016
# Shields Textbook of Glaucoma; 6th Ed.
# Yanoff and Duker Ophthalmology 5th Ed
116
When discrete causative factors are known – such as PAS following laser trabeculoplasty for primary open-angle glaucoma (POAG)1,2 – such cases can be conceptualized as ‘secondary angle-closure glaucomas’, and etiologic mechanisms identified according to the explanatory model elaborated below.
Post pushing-gas is injected into the vitreous cavity to repair a retinal detachment, displacing the lens–iris diaphragm sufficiently forward to close the angle. This can happen despite the presence of a patent iridotomy.
Shaffers .. Rubeosis iridis refers to new vessels on the surface of the iris regardless of the state of the angle or the presence of glaucoma.
In npdr if there are large areas of capillary non perfusion.. Neovascular glaucoma may present anywhere from 2 weeks to 2 years following a central retinal vein occlusion.82 However, the condition often presents about 3 months after central retinal vein occlusion: hence its reputation as the ‘100-day glaucoma’. Younger patients with central retinal vein occlusions often have associated vascular diseases, such as hypertension or one of the collagen vascular disorders.
Baker shaffer
Vascular endothelial growth factor (VEGF), a dimeric glycoprotein of approximately 40 kDa, is a potent, endothelial cell mitogen that stimulates proliferation, migration and tube formation leading to angiogenic growth of new blood vessels. It is essential for angiogenesis during development; the deletion of a single allele arrests angiogenesis and causes embryonic lethality.. VEGF206 and VEGF189 bind very tightly to heparin and, thus, remain sequestered in the extracellular matrix. VEGF165 binds heparin with less affinity, but also can be associated with the matrix, and VEGF121 lacks heparin-binding capacity, rendering it highly soluble. VEGF receptor activation requires dimerization
retinal pigmented epithelium (RPE) (Miller et al., 1997), astrocytes (Stone et al., 1995), Müller cells (Robbins et al., 1997), vascular endothelium (Aiello et al., 1995) and ganglion cells.. Müller cells and astrocytes generally produce the greatest amounts of VEGF under hypoxic condition
Ectropion uvea: traction from the fibrovascular membrane lifts the iris anteriorly gives the stroma a compacted appearance and produces ectropion uvea.
radial traction of fibrovascular membrane in angle and iris, pulls the post layer of iris around pupillary margin onto ant iris surface
Histology..endothelial tube in new vwssels..normal-all 3 coats
Blood aquous barriei-intact in normal..poor in new..
Lucentis® (ranibizumab.. monoclonal antibodies that bind to all three forms of VEGF.
Avastin-bevacizumab…bevacizumab, ranibizumab, aflibercept, and pegaptanib
Collectively, ICE syndrome describes a group of disorders characterized by abnormal corneal endothelium that is responsible for variable degrees of iris atrophy, secondary angle-closure glaucoma in association with characteristic peripheral anterior synechiae (PAS), and corneal edema.
Viral theory is attractive and might explain the unilaterality of this syndrome in the vast majority of patients
(A) Membrane forms in one area of angle. (B) Additional areas of angle are involved, and contraction of membrane displaces pupil. (C) As membrane contracts, iris thins and peripheral anterior synechiae form. (D) Almost total closure of angle with thinning of iris, pupillary displacement, and hole formation
in quadrants away from pupillary displacement due to traction…. ’- without correctopia and ischaemic in nature-melt holrs
displacement of the eye's pupil from its normal, central position
In contrast to the marked corneal changes. For this reason glaucoma is often mild
Characterized by
Vsx1 col8a2 zeb1.. bilateral autosomal dominant disorder characterized by polymorphic posterior corneal surface irregularities with variable degrees of corneal decompensation.
Vesicular, curvilinear, and placoid irregularities found on slit-lamp examination • Rounded dark areas with central cell detail that produce a doughnut-like pattern on specular microscopy • Epithelial-like transformation of endothelium on histological examination • Reduced vision from the corneal edema
haab’s striae of congenital glaucoma are thin areas surrounded by a thickened, retracted DM
PPD: thickened areas without breaks in Descemet’s membrane.
Ched- focal orr diffuse thickening of descemet membrane and endothelial degeneration
Fuch- bl asscelerated endothelial cell loss
Rare but potentially blinding complication f ant segment surgery or trauma ocuruing when conjunctival or corneal epithelium cells migrate through wound and proliferate ove….
Advanced cases- eye painful due to bullous keartopathy and intractatble glaucoma
Translucnet membrane with scalloped border involving post conreal surface
Fibrovascular ingrowth can occur from pars plana incisions, as well as from more anterior ones.259 In some cases the ingrowth resembles a vascu-lar stalk that enters the eye through an old wound and then fans out over the anterior segment. In other cases the ingrowth forms a gray-white membrane posterior to the corneal endothelium, with-out an obvious entry site or a vascular stalk.
better to prevent fibrovascular ingrowth than to treat the condition once established. In the past this condition was a com-mon finding in eyes enucleated after cataract surgery or trauma.. With current microsurgical techniques, fibrovascular ingrowth is encountered far less often. The glaucoma associated with fibrovascular ingrowth is usually managed by medical therapy. In some cases posterior glaucoma drainage device implantation or cyclophotocoagulation is required to control IOP.
trabecular meshwork is functional behind the apparent PAS; that is, the synechiae are bridging rather than closing the angle if the duration of tissue approximation is short enough. If medical treatment is inadequate, a laser trabeculoplasty can be considered if at least one-third to one-half of the angle is open. However, the clinician must be aware that a sustained post-laser IOP rise may necessitate filtering surgery. Other alternatives include filtering operations, cyclodestructive procedures, and surgi-cal goniosyneechialysis of the PAS
term ‘malignant glaucoma’ is not related to the pathophysiology of the condition and is often frightening to patients who believe they have a malignancy of the eye. The term ciliary block or malignant glaucoma refers to a spectrum of atypical angle-closure glaucomas that share several essential fea-tures. 266,305,306
Angle closure glaucoma..anterior cha,ber
If the angle is open or has been opened prophylactically via a laser iridectomy before the development of an angle-closure attack, aqueous misdirection seems less likely to occur after subsequent surgery.[2
. A high index of suspicion is necessary to make the appropriate diagnosis, since initially the IOP may not be elevated much. The key is that the IOP is elevated and the anterior chamber is axially shallow. Furthermore, if an attempt is made to reform the anterior chamber postoperatively through the paracentesis site using a viscoelastic substance, a great deal of posterior resistance may be noted, the anterior chamber may not deepen as much as in a hypotonic eye that does not have aqueous misdirection, and the IOP may rise substantially.
relaxing and widening blood vessels so blood can flow more easily to the heart…isosorbide
Neodymium:yttrium-aluminum-garnet (Nd:YAG) laser may be used in aphakic and pseudophakic patients to create a large peripheral iridectomy and anterior hyaloid rupture to release the trapped aqueous from the vitreous and re-establish normal aqueous flow.
If there is corneal-lenticular contact there is the risk of corneal decompensation; therefore, the chamber should be reformed by the injection of a viscoelastic substance via a 30-gauge cannula through the original paracentesis at the slit lamp following Nd:YAG laser hyaloidectomy.[1]
The risk of aqueous misdirection may be reduced in the fellow eye after iridectomy if the angle remains open and the IOP is normal; failure to provide prompt therapy to the fellow eye has been reported to result in bilateral blindness
In most cases, glaucoma occurs when the melanoma is already large, and enucleation is the appropriate therapy. There have been a few reports of surgery for angle-closure glaucoma in eyes that were determined later to harbor undetected melanomas.363–365 At times, iris melanomas invade the angle and cause secondary angle closure without pupillary block (Fig. 16–12).
If the diagnosis of metastatic disease is uncertain, a paracentesis can be performed, and the cells can be examined histologically. In most cases enucleation is not warranted for metastatic disease, and medical treatment is instituted to control IOP and relieve the patient’s symptoms. Some metastatic tumors are responsive to radiation therapy.
Nanophthalmic eyes with normal IOPs and open angles should be followed carefully for signs of progressive angle narrowing. If narrowing occurs, a laser iridectomy should be performed. Topical -adrenergic antagonists, 2-adrenergic ago-nists, prostaglandins and topical carbonic anhydrase inhibitors are prescribed for elevated IOP. Because these patients often tend to be young, oral carbonic anhydrase inhibitors are often not toler-ated well. Miotic agents lower IOP in some nanophthalmic eyes but raise pressure in others, presumably by allowing the lens to move forward; it is best to avoid them here. Systemic corticoster-oids have little effect on the uveal effusions 384 If laser and medical treatments are inadequate to control angle-closure glaucoma, some authorities recommend surgically unroofing at least two vortex veins to relieve venous obstruction. Other authorities recommend creating permanent drainage sites for suprachoroidal fluid in two to four quadrants
Histopathologic examination of these globes reveals a thickened sclera with abnormal sclerocytes, an abnormal arrange-ment of collagen, an abnormal glycosaminoglycan metabolism, and an accumulation of proteoglycans.379–382
The effusion acts as an acutely developing posterior mass that displaces the lens–iris diaphragm, possibly by trans-vitreal pressure
Topical b-adrenergic antagonists, a2-adrenergic agonists, and topical carbonic anhydrase inhibitors are administered to control IOP.
The fluid acts like an acutely developing posterior mass that displaces the lens–iris diaphragm… cycloplegic agents,
topical corticosteroids, b-adrenergic antagonists, topical a2-adrenergic agonists, topical carbonic anhydrase inhibitors, and hyperosmotic agents
Occasionally - ocular discomfort or headache
This theory is supported by ultrasound studies demonstrating ciliary body thickening after PRP. Photocoagulation may break the blood–ocular barriers and cause a transudation of fluid into the retina, choroid, and vitreous. This fluid may act as an acutely developing mass and displace the lens–iris diaphragm forward. Pupillary block may contribute to the development of glaucoma in some cases…- cycloplegic agents, topical corticosteroids, prostaglandins, topical b-adrenergic antagonists, topical alpha2-adrenergic agonists, and topical carbonic anhydrase inhibitors
the Greek etymology refers to ‘lens-shape’ or ‘lens-form’.. , except for the presence of an intumescent lens and a normal anterior chamber depth in the fellow eye.
Pupillary block may not be the sole mechanism of angle closure because the enlarging lens may also push the peripheral iris forward into the angle…. If cataract extraction is not possible because of extenuating circumstances (e.g., gravely ill patient) or must be delayed,.. Iridotomy may not be curative in all cases, especially those in which direct pressure from the lens is playing a greater role than is pupillary block.
). This occurs most often with anterior chamber lenses, but can be seen with posterior chamber and iris-supported lenses as well, especially in eyes in which the iridectomy was omitted or occluded
pseudophakic pupillary block - vigorous pupillary dilation to break the posterior synechiae. If this is inadequate, pupillary dilation can be augmented by laser photomydriasis (pupilloplasty),433 where multiple intense, focused argon laser applications are applied to the 12 o’clock margin of the pupil radially for 2–3 mm, thereby stretching the pupil into a ‘tear-drop’ shape and often breaking the block.
Pseudoexfoliation-acquired zonual insuffiency and crystalline lens subluxation