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Dr. Stefano Pizzirani has assembled an expert panel of authors on the topic of small animal Glaucoma. Articles include: Functional anatomy of the outflow facilities,Epidemiology of idiopathic canine glaucoma,Pathophysiology and classification of idiopathic canine glaucoma,Genetics of idiopathic canine glaucoma,Clinical signs,Medical treatment of idiopathic canine glaucoma,Ocular pathology in canine glaucoma,Feline Glaucoma, and more!

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G l a u c o m a
Veterinary Clinics of North America: Small
Animal Practice
EDITOR
Stefano Pizzirani, DVM, PhD
Comparative Ophthalmology, Cummings School of Veterinary Medicine, Tufts University,
Grafton, MA, USA

Clinics Review Articles

www.vetsmall.theclinics.com

November 2015 • Volume 45 • Number 6Table of Contents
Cover image
Title page
Copyright
Contributors
Editor
Authors
Forthcoming Issues
Forthcoming Issues
Recent Issues
Preface. Glaucoma
Functional Anatomy of the Outflow Facilities
Key points
Aqueous production
Pathways of aqueous outflow
Trabecular outflow
Angular aqueous plexus
Posterior, uveoscleral, or unconventional outflow
Summary
References
Definition, Classification, and Pathophysiology of Canine Glaucoma
Key pointsDefinition
Classification of glaucomas
Pathogenesis and pathophysiology of primary glaucoma
Theories and mechanisms
Summary
Acknowledgments
References
Genetics of Canine Primary Glaucomas
Key points
Introduction
Techniques used to study genetic disorders
Genetics of human glaucoma and its relevance to canine glaucoma studies
Genetics of extracellular matrix abnormalities associated with primary glaucoma
Genetics of canine primary angle-closure glaucoma
Genetics of pectinate ligament dysplasia and ciliary cleft opening
Genetics of primary open-angle glaucoma
Genetics of primary lens luxation
Strategies to target primary glaucoma in canine populations
Summary
Acknowledgments
References
Clinical Signs and Diagnosis of the Canine Primary Glaucomas
Key points
Definition of primary glaucoma
Primary open angle glaucoma
Primary angle closure glaucoma
Clinical forms of primary angle closure glaucoma
Clinical signs of primary angle closure glaucomaEarly to midstage clinical signs
Chronic clinical signs
Diagnosis of primary angle closure glaucoma
Techniques that evaluate intraocular pressure
Techniques that evaluate the iridocorneal angle
Techniques that evaluate the visual capabilities of the eye
Techniques that evaluate the optic disc
Techniques that evaluate the retinal nerve fiber layer
References
Microscopic Lesions in Canine Eyes with Primary Glaucoma
Key points
Introduction
Glaucoma-induced changes in the canine anterior segment
Glaucoma-induced changes in the canine posterior segment
Summary
References
Medical Treatment of Primary Canine Glaucoma
Key points
Introduction
Topical ocular hypotensive drugs
Cholinergic agonists (miotics)
Drugs acting on adrenoceptors
Carbonic anhydrase inhibitors
Prostaglandin analogues
Osmotic agents
Prophylactic treatment of primary canine glaucoma
Neuroprotective therapy in primary canine glaucoma
Emerging treatments for glaucomaSummary
References
Surgical Treatment of Canine Glaucoma: Filtering and End-Stage Glaucoma
Procedures
Key points
Introduction
Filtering procedures
General considerations in current gonioimplant design
Subconjunctival implants
Frontal sinus shunts
Suprachoroidal shunts
Intrascleral shunts
Complications
End-stage glaucoma procedures
Summary
Acknowledgments
References
Surgical Treatment of Canine Glaucoma: Cyclodestructive Techniques
Key points
Introduction
Cyclophotocoagulation
Diode transscleral cyclophotocoagulation
Surgical procedure
Postoperative management
Success rate
Complications
Endoscopic cyclophotocoagulation
Surgical procedure
Surgical approach to the ciliary processesEndoscopic cyclophotocoagulation treatment and techniques
Postoperative management
Success rate
Complications
Summary
References
Feline Glaucoma
Key points
Aqueous humor dynamics in cats
Epidemiology and causes of glaucoma in cats
Primary glaucoma in cats
Secondary glaucoma in cats
Clinical signs and diagnosis of feline glaucoma
Clinical management of glaucoma in cats
Medical therapy for feline glaucoma
Intraocular pressure–lowering drugs
Drugs with variable response
Surgical management of glaucoma in cats
Enucleation and evisceration for feline glaucoma
References
Canine Secondary Glaucomas
Key points
Uveitis
Cataracts and cataract surgery
Lens instability and lens luxation
Neoplasia
Hyphema
Retinal detachmentsPenetrating and blunt trauma
Specific immune-mediated and/or pigment-mediated diseases
References
IndexC o p y r i g h t
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Printed in the United States of America.Contributors
Editor
STEFANO PIZZIRANI, DVM, PhD, Diplomate, American College of Veterinary
Ophthalmologists; Diplomate, European College of Veterinary Surgeons (inactive);
Associate Professor, Comparative Ophthalmology, Department of Clinical Sciences,
Cummings School of Veterinary Medicine, Tufts University, North Grafton,
Massachusetts
Authors
ANTHONY F. ALARIO, DVM, Diplomate, American College of Veterinary
Ophthalmologists; Head Ophthalmologist, VCA Capital Area Veterinary Emergency and
Specialty, Concord, New Hampshire
GILLIAN BEAMER, VMD, PhD, Diplomate, American College of Veterinary
Pathologists; Assistant Professor, Department of Infectious Disease and Global Health,
Tufts University, North Grafton, Massachusetts
ELLISON BENTLEY, DVM, Diplomate, American College of Veterinary
Ophthalmologists; Clinical Professor of Comparative Ophthalmology, Department of
Surgical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison,
Madison, Wisconsin
DINELI BRAS, DVM, MS, Diplomate, American College of Veterinary
Ophthalmologists; Ophthalmology Department, Centro de Especialistas Veterinarios de
Puerto Rico (CEVET), Guaynabo, Puerto Rico; Veterinary Specialists Center of Puerto
Rico, San Juan, Puerto Rico
HAIYAN GONG, MD, PhD, Professor, Ophthalmology and Anatomy and
Neurobiology, Boston University School of Medicine, Boston, Massachusetts
ANDRÁS M. KOMÁROMY, DrMedVet, PhD, Diplomate, American College of
Veterinary Ophthalmologists; Diplomate, European College of Veterinary
Ophthalmologists; Associate Professor, Department of Small Animal Clinical Sciences,
Veterinary Medical Center, College of Veterinary Medicine, Michigan State University,
East Lansing, Michigan
FEDERICA MAGGIO, DVM, Diplomate, American College of Veterinary
Ophthalmologists; Ophthalmology Department, Tufts Veterinary Emergency Treatment
and Specialties (Tufts VETS), Walpole, Massachusetts
GILLIAN J. McLELLAN, BVMS, PhD, MRCVS, Diplomate, European College of
Veterinary Ophthalmologists; Diplomate, American College of Veterinary
Ophthalmologists; Diploma in Veterinary Ophthalmology; Assistant Professor,
Departments of Ophthalmology and Visual Sciences and Surgical Sciences;
McPherson Eye Research Institute, University of Wisconsin-Madison, Madison,
WisconsinPAUL E. MILLER, DVM, Diplomate, American College of Veterinary
Ophthalmologists; Clinical Professor of Comparative Ophthalmology, Department of
Surgical Sciences, School of Veterinary Medicine, University of Wisconsin-Madison,
Madison, Wisconsin
SIMON M. PETERSEN-JONES, DVetMed, PhD, DVOphthal, Diplomate, European
College of Veterinary Ophthalmologists; Professor, Department of Small Animal Clinical
Sciences, Veterinary Medical Center, College of Veterinary Medicine, Michigan State
University, East Lansing, Michigan
STEFANO PIZZIRANI, DVM, PhD, Diplomate, American College of Veterinary
Ophthalmologists; Diplomate, European College of Veterinary Surgeons (inactive);
Associate Professor, Comparative Ophthalmology, Department of Clinical Sciences,
Cummings School of Veterinary Medicine, Tufts University, North Grafton,
Massachusetts
STEPHANIE PUMPHREY, DVM, Diplomate, American College of Veterinary
Ophthalmologists; Staff Ophthalmologist, VCA South Shore, South Weymouth,
Massachusetts
CHRISTOPHER M. REILLY, DVM, MAS, Diplomate, American College of Veterinary
Pathologists; Assistant Professor of Clinical Pathology, Microbiology and Immunology,
School of Veterinary Medicine, University of California, Davis, California,
TRAVIS D. STRONG, DVM, MS, Ophthalmology Resident and Adjunct Instructor,
Lloyd Veterinary Medical Center, Iowa State University College of Veterinary Medicine,
Ames, Iowa
LEANDRO B.C. TEIXEIRA, DVM, MS, Diplomate, American College of Veterinary
Pathologists; McPherson Eye Research Institute; Assistant Professor, Department of
Pathobiological Sciences, University of Wisconsin-Madison, Madison, WisconsinForthcoming Issues
Forthcoming Issues
January 2016
Endoscopy
MaryAnn Radlinsky, Editor
March 2016
Congenital Malformations of the Brain and Spine
Curtis Dewey, Editor
May 2016
Diagnostic Radiology
Angela Marolf, Editor
Recent Issues
September 2015
Perioperative Care
Lori S. Waddell, Editor
July 2015
Urology
Joseph W. Bartges, Editor
May 2015
Soft Tissue Surgery
Lisa Howe and Harry Boothe, Editors
Related Interest
Veterinary Clinics of North America: Exotic Animal Practice September 2015, Volume
18, Issue 3
Endoscopy
Stephen J. Divers and Laila M. Proença, Editors
P R E F A C E
G l a u c o m a
Stefano Pizzirani, DVM, PhD
Comparative Ophthalmology, Cummings School of Veterinary Medicine, Tufts University,
200 Westboro Road, Grafton, MA 01536, USA, E-mail: stefano.pizzirani@tufts.edu
Stefano Pizzirani, DVM, PhD, Editor
I know that I know nothing.
—Socrates
With time, I have learned to be humbled by my ignorance and by the in nite,
additional speculative thoughts that arise every time I presume I understand
something, and I have the illusion that I have reached an endpoint. Opening a single
door in the building of knowledge brings the investigator into a room with a
multitude of new, mysterious doors. What appeared to be an answer turns out to be
only fertile ground for new questions, and new horizons keep expanding
exponentially and confusingly.




The same feeling of vast ignorance strikes me when I attempt to de ne and
understand glaucoma. The word “glaucoma” comes from the Greek word “glaucos,”
which means gray or bluish. The semantics of the word itself seems to pre gure the
foggy state of our current knowledge surrounding this group of diseases.
As human beings, we like to classify things in boxes. That’s how our minds work
best. However, when we try to delve into the ner aspects of the mechanisms and
molecular cascades involved in glaucoma, simple categories fail us as we face the
confusing, often overlapping but sometimes contradictory nature of a disease that
bears a common name but may take very di( erent forms across di( erent species,
breeds, and individuals. Things are blurry; multiple shades of gray make the
transition between di( erent phenotypes hazy, and we, or at least I, seem to be lost
in a state of “quantum confusion.”
When asked to coordinate this issue of Veterinary Clinics of North America: Small
Animal Practice, I was excited and concerned at the same time. My goal in this issue
has been to try to illuminate that which is currently known and that which is
currently unknown about this group of diseases that we classify under the single
term “glaucoma.” My challenge has been to provide both practical, useful
information and stimulus for further speculation. As veterinarians, we need clear
clinical guidance to help our current patients and clients, but we also need to
honestly acknowledge the lack of speci c, in-depth information regarding di( erent
forms of glaucoma, particularly in veterinary patients.
It’s an ongoing journey. We have made some inroads and changed directions a few
times over the years. Our working assumptions about glaucoma are sometimes
preliminary and often based on anecdotal evidence. Our numbers are small, and our
results are based mostly on retrospective studies, which are truly useful but also
constrained by obvious limitations. Each species (and, within each species, each
breed and each di( erent stage of disease) likely warrants its own classi cation
scheme and set of treatment recommendations, but the paucity of currently available
data makes our job difficult.
I hope this issue will provide rational, useful information to general clinicians
while stimulating more questioning and increased collaboration among specialists to
further the collection of useful data.
Several people and resources have helped me in the preparation of this issue. I am
thankful to the publisher for o( ering me this opportunity, and I can’t value enough
the great contributions provided by the authors of this issue.
To all of them goes my sincere gratitude.









=










Functional Anatomy of the Outflow Facilities
a, b aStefano Pizzirani, DVM, PhD * and Haiyan Gong, MD, PhD , Ophthalmology, Department of Clinical Sciences, Cummings School of
bVeterinary Medicine, Tufts University, 200 Westboro Road, North Grafton, MA 01536, USA, Ophthalmology and Anatomy and Neurobiology,
Boston University School of Medicine, 72 East Concord Street, L905, Boston, MA 02118, USA, *Corresponding author. Department of Clinical
Science, Cummings School of Veterinary Medicine, Tufts University, 200 Westboro Road, North Grafton, MA 01536. E-mail:
stefano.pizzirani@tufts.edu
In order to understand the pathophysiology, select optimal therapeutic options for patients and provide clients with honest expectations
for cases of canine glaucoma, clinicians should be familiar with a rational understanding of the functional anatomy of the ocular
structures involved in this group of diseases. The topographical extension and the structural and humoral complexity of the regions
involved with the production and the out ow of aqueous humor undergo numerous changes with aging and disease. Therefore, the
anatomy relative to the uid dynamics of aqueous has become a pivotal yet exible concept to interpret the di erent phenotypes of
glaucoma.
Keywords
Aqueous; Formation; Outflow; Trabecular meshwork; Anatomy; Canine
Key points
• Understanding the composition and function of the outflow system helps to interpret clinical signs, choose therapies, and formulate the
prognosis for patients affected with glaucoma.
• Normal intraocular pressure is maintained because there is a balance between aqueous formation and outflow.
• The outflow pathways in dogs have clear morphologic and topographic differences from the corresponding structures in primates.
• The functional anatomy is a dynamic concept and there are physiologic changes that occur with age and tissue remodeling.
• More advanced and extensive changes that are similar to those occurring with aging may occur in glaucoma.
The aqueous humor (AH) is the uid that ' lls the anterior and posterior chambers of the eye. Its main roles are to provide nourishment and
metabolic waste removal to active metabolic ocular structures that are avascular and to contribute maintaining a normal intraocular pressure
(IOP) without altering the refractive status of the eye. Its composition and the fluid dynamics associated with its flow are voluble and undergo
changes associated with age and disease. Of particular importance is that the resistance to the out ow of AH from the anterior chamber is
1in uenced by morphologic, physiologic, and biochemical dynamic factors. Beside aqueous nutritional importance, its solutes also participate
in establishing the anterior chamber associate immune deviation, and carry and distribute the di erent proteins and molecules that promote
and direct tissue remodeling and changes in the anterior segment that are associated with both age and disease.
Three major distinct aspects of the aqueous need to be considered:
1. Aqueous production
2. Aqueous composition
3. Aqueous outflow
In this review, the authors focus on aqueous out ow and introduce concepts of aqueous production, mentioning some of the dynamic
variations in aqueous composition that may influence the physiologic and pathologic changes seen with aging and glaucoma.
The physiologic range of IOP is maintained through the constant balance between aqueous production and aqueous out ow. The pressure
gradient within the eye is comprised within speci' c values that may vary individually in di erent daily patterns and with aging. A rule of the
2–6thumb indicates normal IOP in dogs to be between 12 and 25 mm Hg; however, most dogs tend to have a normal pressure below the 20s.
IOP values may also vary depending on the time and technique of measurement. The IOP uctuates during the day with circadian phases that
peak and drop at different times of the day, depending on the species. In dogs, like in humans, the highest normal IOP values are measured in
3,5 2the morning, and IOPs are lower in the evening. In dogs, a decrease in baseline IOP is associated with increased age ; a range of diverse
7' ndings has been reported in di erent human studies. There are di erences in ethnic groups, and both positive and negative relationships
8,9between increased age and IOP have been described. Although the out ow seems to decrease with age, the production of AH may also
10decrease.
Aqueous production
11Two mechanisms—passive and active—are responsible for aqueous production and contribute to its composition. Passive di usion and
ultra' ltration of plasma occur in the vascularized ciliary body stroma. The passive mechanisms do not contribute signi' cantly to the
formation of AH. Because the ciliary blood vessel endothelia are fenestrated, di usion of solutes travels according to a concentration
gradient, trying to maintain a balance between di erent tissues/compartments. Substances with high lipid solubility coe cients can easily
move across cellular membranes.
Ultra' ltration allows molecules to cross a cell membrane following a hydrostatic force or an osmotic gradient, and it results from
di erences between the pressure of the ciliary body capillaries and the IOP and solute di erences. The hydrostatic pressure of ciliary body





12,13 14capillaries has been estimated to be between 25 and 33 mm Hg, whereas the oncotic pressure of vascular proteins is about 14 mm Hg.
15Hydrostatic and oncotic forces would both actually favor resorption of AH. If we consider the IOP around the value of 15 mm Hg, we can
understand how a much higher hydrostatic pressure would be needed to achieve relevant amount of aqueous formation through this passive
mechanism.
16Passive mechanisms are, however, able to generate a reservoir uid within the ciliary body. Furthermore, because of the lack of a true
epithelium on the anterior surface of the iris, leakage and di usion of diluted plasma occurs from the ciliary vessels into the anterior
17chamber.
Basically, AH is secreted across the ciliary epithelium by transferring solutes, mainly NaCl, from the stroma to the posterior chamber of the
18eye, with a subsequent passive movement of water in the same direction. At least 80% to 90% of AH formation occurs with active
19mechanisms. Active secretion requires energy that is provided by the hydrolysis of adenine triphosphate and relies mainly on 2 enzymes: an
adenosine triphosphatase Na/K pump and carbonic anhydrase. The structural site for active secretion resides in the inner (facing the posterior
chamber), nonpigmented ciliary epithelium of the ciliary processes where these 2 enzymes are highly concentrated. Active formation through
13,20an adenosine triphosphatase Na/K pump is responsible for more than 70% of the aqueous production. Besides the increased
+concentration of NA ions in the posterior chamber, secondary active transport mechanisms increase the concentration of other solutes,
−including Cl . Active formation is also catalyzed by the enzyme carbonic anhydrase that is particularly present in the nonpigmented
21 22epithelium of the ciliary body. The latter accounts for about 40% to 50% of the aqueous production. Carbonic anhydrase catalyzes the
− + +reaction H O + CO ↔ HCO + H . Bicarbonate moves then in the posterior chamber in uencing uid transport by also a ecting Na ,2 2 3
15possibly by regulating the pH for optimal active ion transport. The 2 active mechanisms share some of the pathways, explaining the
+ −mathematics of the rate of production. When active release of sodium (Na ) or bicarbonate (HCO3 ) ions into the posterior chamber is
mediated by these enzymes, an osmotic gradient is created and the plasma ultra' ltrate can move from the stroma of the ciliary body into the
posterior chamber (Fig. 1). This mechanism is sensitive to the level of IOP and decreases with increased IOP. However, this e ect is
insufficient to serve as a protective mechanism against the development of glaucoma.











+ −FIG. 1 Mechanism for aqueous secretion. An active movement of Na and HCO increases the solute concentrations in3
the posterior chamber in proximity of the ciliary processes and creates a positive osmotic gradient that recalls fluids
collected in the ciliary tissues because of diffusion and ultrafiltration. ATPase, adenosine triphosphatase; NPE,
nonpigmented epithelium; PE, pigmented epithelium.
23The amount of AH production is indirectly calculated by measuring the amount of out ow. Out ow facility (c) indirectly indicates the
amount of aqueous production and it can be expressed as μL/min or μL/min/mm Hg. In normal humans, c is about 2.75 ± 0.63 μL/min
24(range, 1.8–4.3) or about 0.3 μL/min/mm Hg. In dogs, the total value has been manually calculated with a mean ± SD equal to 5.22 ±
251.87 μL/min, whereas when calculated by an automatic software the ow rate was 4.54 ± 2.57 μL/min. These values grossly mirror the
26values of 0.24 to 0.30 μL/m/mm Hg reported by Gum and colleagues.
24,27Individual variations are following circadian rhythms and are also in uenced by age. In humans, AH formation and out ow both
10,28decrease with aging.
Although the site and the mechanisms of aqueous formation seem to be well-established and described, the mechanisms for out ow are still
a large field for research, especially when related to the pathophysiology of the different phenotypes of glaucoma.
Pathways of aqueous outflow
The out ow facilities are a complex hydraulic system that allows the AH to exit the eye consistently, yet maintaining a physiologic IOP
balanced with aqueous secretion. When the regulation of the out ow is impaired, an increase in IOP occurs. No active transport mechanisms
is involved in the out ow. AH passes through the trabecular meshwork (TM) as bulk ow driven by the pressure gradient, which is higher in
29,30the eye when compared with the distal out ow vessels. The posterior, uveoscleral out ow (USO) is passive and largely independent





31from the IOP; it is mostly regulated by osmotic gradients.
The pathways of canine aqueous out ow include several di erent anatomic structures whose nomenclature has been variously and
32–38di erently described, used, and classi' ed. The understanding of the normal morphology and composition of these structures, and the
array of dynamic physiologic changes that occur in di erent breeds and aging are important considerations when pathologic changes are
then analyzed and therapeutic agents selected.
Besides an irrelevant corneal and uveal permeability, 2 main, di erent out ow pathways are usually considered the most essential to IOP
balance:
• The anterior/trabecular or conventional outflow
• The posterior or unconventional, or the USO
Trabecular outflow
The anatomic terminology related to the trabecular outflow system (Figs. 2–4) includes the following:
• Iridocorneal angle (ICA)
• Ciliary cleft (CC)
• Pectinate ligament (PL)
• The TM system, which includes
Uveal TM (UTM)
Corneoscleral TM (CSTM) and uveoscleral TM (USTM)
Juxtacanalicular tissue (JCT)
• Angular aqueous plexus (AAP)
Inner wall (IW)
Inner collector channels
• Radial collector channels
• Episcleral veins and intrascleral venous plexus (ISVP) or circle of Hovius