Transcript 02- glaucoma overview.ppt

GLAUCOMA OVERVIEW
Essam Osman
Associate Professor
Chief Glaucoma Unit
Department of Ophthalmology
College of Medicine
King Saud University
GLAUCOMA
*A major cause of blindness.
*Often A symptomatic; in early stage.
*Damage is irreversible.
*Effective treatment is available.
HEADACHE
IMPORTANT POINTS
Diagnosis of glaucoma.
What Subtype of glaucoma.
The exact
Treatment.
First post mortem glaucoma case
reported
Gupta N et al. Br J Ophthalmol 2006.
79 Y Old Man
Visual acuity:
20/20
in each eye
Pupils:
equally reactive to light
IOP :
16 mm Hg OU
Angle:
wide open
Cup/disc ratio:
0.9 OU
Humphrey visual fields show (A) right eye superior visual field defect with the glaucoma
hemifield test (GHT) outside normal limits, mean deviation (MD) −7.38 dB and pattern
standard deviation (PSD) 10.78 dB; and (B) left eye superior visual field defect with GHT
outside normal limits, MD −14.91 dB and PSD 12.01 dB.
DIAGNOSIS
Primary open angle glaucoma
COSOPT eye drops
Prechiasmal intracranial right (A) and left (B) glaucoma optic nerves (arrows) are
surrounded by four corresponding control optic nerves (immunostained for phosphorylated
heavy neurofilament subunit).
Magnocellular LGN neurons appeared smaller in glaucoma (A) than in controls (B).
A
B
Parvocellular LGN neurons appeared smaller in glaucoma (A) than in controls (B).
A
B
A
B
The inferior bank of the visual cortex (Nissl stained) showed marked thinning of the cortical
ribbon in glaucoma (A) compared to control (B).
A
B
Many Factors Influence
RGC Health
Microcirculation
IOP
Ischemia - hypoxia
Lateral geniculate
nucleus and other targets
Retinal
Ganglion
Cell
Aberrant
immunity
Lamina cribrosa
T
Inflammatory
cytokines
Blockade of
neurotrophins and other
target derived factors
Glial cells
Microglia
Excessive
glutamate
stimulation
Nitric oxide, TNF, ROS
ROS, PGE2, nitric oxide
Courtesy of Robert N. Weinreb, MD
Apoptosis in the trabecular
meshwork of glaucomatous
patients
Jimena Baleriola,1 Julián GarcíaFeijoo,2 José M. Martínez-de-laCasa,2 Arturo Fernández-Cruz,3
Enrique J. de la Rosa,1 Raquel
Fernández-Durango3
Molecular Vision 2008; 14:1513-1516
GLAUCOMA
A group of diseases with:
*characteristic optic nerve damage.
*visual field loss.
*elevated IOP; variable
ANATOMY AND PHYSIOLOGY
NORMAL IOP
10-21
Mean= 15.9mmHg ± 2 SD
IOP > 21.7 is abnormal.
Factor affect IOP
*Age *Sex *Race *Heredity
*Diurnal & Seasonal variation
*Blood pressure *Obesity *Drugs
*Posture *Exercise *Neural *Hormone
*Refractive error *Eye movement *Eyelid closure
*Inflammation *Surgery
PASCAL
GONIOSCOPY
OPEN ANGLE VESUS CLOSED ANGLE
OPEN ANGLE
Trabecular meshwork not occluded by
peripheral iris
CLOSED ANGLE
Trabecular meshwork occluded by
peripheral iris
IMPORTANCE OF GONIOSCOPY
CLASSIFICATION
ACORDING TO AETIOLOGY
*Primary.
*Secondary.
*Congenital.
CLASSIFICATION
ACCODING TO APPERANCE OF THE ANGLE
*Open angle glaucoma.
*Closed angle glaucoma.
*Combined mechanism glaucoma.
CLASIFICATION
PRIMARY VERSUS SECONDRY
*primary
@No detectable ocular or systemic
abnormality.
@Often bilateral.
@Often familial.
CLASIFICATION
*SECONDRY
Predisposing ocular or systemic
abnormality.
Often unilateral.
Often sporadic.
POAG
*Intrinsic defect in outflow tract.
*Angle open in gonioscopy.
*Risk factor
~Family history
~Black
~Age
~Myopia
~Diabetes
~Hypertension
Diagnosis by exclusion
INCREASED EVP
*SUPERIOR VENA CAVA OBSTRUCTION
*THYROID EYE DISEASE
*A/V FISTULA
*STURGE WEBER SYNDROME
PIGMENTARY GLAUCOMA
*Pigment dislodged from iris in myopic white patient.
*After dilation or exercise release of pigment to AC and
increase IOP
*Open angle, homogenous dense pigmentation.
*krukenbug,s spindle(intr and extra pigment granule)
*Peripheral iridectomy prevent reverse papillary block
*UBM for diagnosis and indication of PI
*LTP.
NB:NTG can be remission of pigmentary glaucoma
PIGMENTARY GLAUCOMA
LENS INDUCED GLAUCOMA
1-Phacomorphic
2-Dislocated lens
3-Lens protein (phacolytic)
4-Lens particle
5-Phacoanaphylaxis
PSUDOEXFOLIATION
GLAUCOMA
*Open angle with heavy patchy distributed pigment
with sampaolesi,s line
*Dandruff like flakes on corneal endothelium ,T.M,
pupillary margin, anterior &posterior iris, zonule,
ciliary processes and anterior hyaloid face in
aphakic patient.
*Iris atrophy.
*Week zonules. capsular tension ring.
Corticosteroid glaucoma
STERIOD RESPONDER
*POAG *DIABETICS *HIGH MYOPIA
MECHANISM
MANAGMENT
GLAUCOMATOCYCLITIC CRISIS
*Young middle adults.
*Recurrent anterior uveitis with marked high IOP.
*Unilateral.
*Frequency of recurrence diminish with age.
*Topical steriods ,antiglaucoma med.
*Change to OAG.
Angle Closure Glaucomas
Primary Angle Closure
Glaucomas
• Angle is inherently
narrow
“small eye,
hyperopia”
• Relative pupillary
block
Primary Angle Closure
Glaucomas
PRIMARY ANGLE-CLOSURE
GLAUCOMA
ANATOMIC FEATURES:
•
•
•
•
SMALL CORNEAL DIAMETER
SHALLOW ANTERIOR CHAMBER
THICKER LENS
SMALL RADIUS OF THE ANTERIOR LENS
CURVATURE
• ANTERIOR LENS POSITION
• SHORT AXIAL LENGTH
• HYPEROPIC EYES
PRIMARY ANGLE-CLOSURE
GLAUCOMA
A.
B.
C.
D.
E.
PRPDROMAL STAGE
INTERMITENT ANGLE-CLOSURE GLAUCOMA
SUBACUTE ANGLE-CLOSURE GLAUCOMA
ACUTE ANGLE-CLOSURE GLAUCOMA
CHRONIC ANGLE-CLOSURE GLAUCOMA
PLATEAU IRIS SYNDROME
Pushing Mechanism
Pushing Mechanism
Pushing Mechanism
Pulling Mechanism
NVG
Neovascular membrane developed in the surface
of the iris and angle
causes:
Diabetic retinopathy
Central retinal vein occlusion
Carotid occlusive disease
Atropine
Ocular ischemic syndrome
Central retinal artery occlusion
Radiotherapy, RD surgery, uveal melanoma
TRAUMATIC HYPHEMA
sickling
ANGLE RECESSION GLAUCOMA
Unilateral.
Many patients have no memory of ocular trauma.
Wide ciliary body band on gonioscopy.
50% POAG other eye.why?
F/U long life of angle recession.
GHOST CELL GLAUCOMA
*Vitreous hge. degenerated RBC migrate to AC
through a disturbed anterior hyaloid face.
*Ghost cells are rigird RBC unable to go through
T.M.
*Vitrectomy with AC washout with or without
trab.
Childhood glaucoma
*Congenital, present at birth.
*Infantile, present in first year of life.
*Juvenile, present in late childhood.
Clinical feature of primary
congenital glaucoma
*depend on age of onset
*bilateral in75% but frequent
asymmetrical.
MANAGEMENT OF PCG
Surgical
Rule of medication
Glaucoma Management
MEDICAL THERAPY
LASER
SURGERY
GLAUCOMA THERAPY
GOAL OF GLAUCOMA TREATMENT
Preservation of visual function adequate to
the individual needs with minimal or no
side effects.
Minimal disruption to normal activities, at a
sustainable cost.
Clinical care must be individualized to each
patient.
GLAUCOMA THERAPY
Target pressure
is set at which it is believed that further
progression of optic nerve damage can be
prevented
MONOTHERAPY
ADJUNCTIVE OR COMBINATION
THERAPY
ADDITIONAL THERAPY
GLAUCOMA THERAPY
Medical therapy consideration
Efficacy
Safety & side effect
Compliance & adherance
Drug cost
QUALITY OF LIFE
.
First line of medication
Prostaglandins take the lead as firstline glaucoma therapy
Monotherapy with lipid structural
derivatives in glaucoma
Oftalmologia. 2010
Preservative free prostaglandin
TAFLUPROST 0.0015% eye drops
CONCLUSION
Diagnosis of •
glaucoma on hard
base
Every type of •
glaucoma has its ttt
Medical ttt is not •
the same for all
type
Surgical indication •
should be in mind
PETERS ANOMALY
Usually sporadic
Bilateral in 80%of cases
Glaucoma in 50%
GLAUCOMA SURGERY
TRABECULECTOMY
NPDS-CANALOPLASTY
TUBE SURGERY
CYCLODESTRUCTIVE PROCEDURES
GONIOTOMY
TRABECULOTOMY
Laser treatment
PI
LTP
LASER SUTURE LYSIS
AXENFELD ANOMALY
bilateral but a symmetrical
glaucoma is uncommon
ANIRIDIA
*AN-1 85%
AD
Isolated
*AN-2 13%
Deletion of short arm chromosome 11
Wilms tumor,mentally handicaped
*AN-3 2%
AR
Mentally handicapped ,cerebellar ataxia
NEUROFIBROMATOSIS-1
STURGE WEBER SYNDROME
ANIRIDIA
RIEGER SYNDROME
RIEGER ANOMALY
Autosomal dominant
Bilateral but a symmetrical
Glaucoma in 50%
Direct damage by pressure
Capillary occlusion
Interference with
axoplasmic flow
HIGH IOP
TYPE OF GLAUCOMA
INDICATION OF SURGERY
TTT AVOIDED