Download Glaucoma Management – Co-regulation of Intraocular Pressure and

Glaucoma Management – Co-regulation of Intraocular
Pressure and Ocular Blood Flow
I.
Multi-factorial pathogenesis of glaucoma
A. Intraocular pressure
1. Direct physical insult from intolerable IOP levels
B. Ischemia
1. NFL stress and demise from anoxia, neuronal starvation and
toxicity from reduced nutrient delivery and reduced waste removal
C. Genetic predisposition
D. Combined
II.
Optic nerve axonal blood supply
A. Internal carotid artery
B. Ophthalmic artery
C. Central retinal artery
1. Pial plexus and centrifugal arteries
D. Short posterior ciliary arteries (PCA’s)
1. Circle of Zinn-Haller
2. Choroid
III.
Relative contribution of optic nerve vascular resources
A. 95% of orbital portion of supply to nerve is derived from the PCA’s
B. 85% of total ocular perfusion is choroidal perfusion
C. 70% of choroidal perfusion is the pulsatile component
IV.
History and definition of Pulsatile Blood Flow Analysis; ocular
pneumoplethysmography
A. Perkins –1070’s - observed applanation mire pulsation and
speculated that a blood flow value could be calculated by interpreting
the dynamics of that pulsation
B. Maurice Langham (OBF Labs, U.K.) - mid 1980’s – first BFA
C. Malcolm Redman, David Silver (OBF Labs, U.K.) – mid 1990’s
D. David Silver (Maurice Langham, David Massey
Paradigm-Dicon Medical, Salt Lake City) - 2000 – present
E. Ocular pneumoplethysmography The measurement of the relative quality of the ocular pulse
(pulsatile ocular blood flow – POBF) by calculating the change in
size of the globe which occurs in synchrony with the systemic
pulse, rise and fall of intraocular pressure
F. 1997 normative database established – Moorfields Eye Hospital London
G. Video – demonstration ocular blood flow analysis
V.
Vascular risk factors in glaucoma
A. Cardiovascular deficiencies
1. Reduced cardiac output
2. Large vessel disease
3. Asymmetries
a. Carotid occlusion
B. Physical limitations of micro vascular architecture
1. Individual variation
a. Eye size – refractive status
b. Limited vascular architecture of individual physiologic
2. Factors influencing vessel drop out
a. Diabetes
b. Age
c. Arterial sclerosis
d. Lifestyle
C. Limitations of autoregulation
D. IOP induced hypoperfusion
1. Acute perfusion pressure effect
E. Vasospasm
a. Renaulds
b. Migraine
F. Nocturnal hypotensive episodes
a. Essential
b. Pharmacologically induced
G. Blood coagulation abnormalities
VI.
Watershed zones
A. Hypoperfused areas of retinal neurons or marginally hypoperfused
peripapillary zones, which are most prone to impose ischemic insult
1. Often at inferior margin of nerve
2. More frequent in large, myopic, eyes
3. Augmented by any diseases process which causes
reduction in perfusion to ocular tissues
4. S. S Hayreh
B. Supportive to the concept of the ischemic component in glaucoma
pathogenesis
VII.
Autoregulation
A. The system which attempts to mitigate variations in intraocular
pressure and systemic blood pressure so that the metabolic
requirements of the axons are met
B. Defects in auto-regulation
1. A defect in the system which otherwise seeks to normalize
pulsatile ocular blood flow in the presence of hemodynamic
extremes and variable tissue demands
2. Possible over action of Endothelin-1
3. Defects in endothelium-derived contracting or relaxing
factors
4. Vasospasm or migraine

VIII. Research and techniques which demonstrate the influence of
ischemia in the pathogenesis of glaucoma
A. Perfusion pressure videoangiography
1. Observation of fluorescein inflow dynamics, while
artificially changing I.O.P.
B. Pulsatile ocular blood flow normative database – comparison to
NTG patients – Moorfields Eye Hospital
C. Studies associating NTG with vasospastic diseases
D. Studies demonstrating decreased POBF in patients with Dranse
hemorrhage
E. Color Doppler imaging
F. Laser Doppler flowimetry
1. Heidelberg HRT-F
G. Metabolic mapping
2. Determination of relative metabolic demands of neural
tissue
H. Watershed zones
1. Hypoperfused areas or marginally hypoperfused areas,
which are most likely to impose ischemic insult to optic
nerve tissue
2. Often at inferior margin of nerve
3. More frequent in large, myopic, eyes
4. S. S Hayreh
5. Supportive to the concept of the ischemic
component in glaucoma pathogenesis
IX.
Acute perfusion pressure effect
A. The effect on pulsatile ocular blood flow, which precipitates as the
result
of change in intraocular pressure.
B. Pulsatile blood flow increases when IOP decreases
C. Pulsatile blood flow decreases when IOP increases
X.
Cornerstones of traditional management
A.
B.
C.
D.
E.
XI.
I.O.P. measurement
Threshold field analysis
NFL analysis and photography
Gonioscopy and biomicroscopy
History
Effect and goals of treatment on pulsatile ocular blood flow”
A. Beta Blockers
1. Nocturnal hypotension
B. CAI inhibitors
C. Alpha 2 Agonists
D. Prostaglandin analogs
E. Docosinoids
F. Surgery
G. Increasing perfusion in hypoperfused eyes
1. Attempt to use available IOP lowering medications to
enhance POBF
XII.
Case presentations
A.
B.
C.
D.
E.
F.
POAG with reduced pulsatile ocular blood flow
Optic nerve disparity with no glaucoma
Suspect nerve with no glaucoma
Unreliable fields – ocular hypertensive
Normotensive glaucoma
Change in POBF with systemic Ca channel blocker
References and suggested research
current concepts on ocular blood flow in glaucoma – Pillunat, Harris,
Anderson, Greve
Ocular Blood Flow – Kaiser, Flammer, Hendrickson
www.onjoph.com lectures: J. W. Keil, S. S. Hayreh
www.google.com Search “ocular blood flow”
www.obflabs.com “research”