hi i'm dr dj hoisler and welcome to the module on anterior uveitis in small
animals
all right so where we headed in this module we're going to look at anatomy of the eye
pathophysiology of uveitis diagnosis canine anterior uveitis feline anterior uveitis
how to work these cases up and therapy the structure of the uvea is variably pigmented
fiber vascular layer it's highly vascular which contributes to the nourishment and cooling of the
eye it's composed of fibrocytes and melanocytes there's an anterior and a posterior portion of
the uvea the anterior portion is the iris and the ciliary body the posterior portion is the choroid
the anterior and the posterior portion are both continuous with each other there's a muscular
layer to the uvea which is the iris sphincter and the dilator there's also a ciliary body muscle
which is an additional muscular layer of the uvia the function of the uvea is that it provides
nourishment to the eye is the main intraocular vascular supply it brings oxygen to a highly
metabolic retina it produces aqueous humor which is a clear ultrafiltrate
it regulates light via the pupillary aperture and it assists in accommodation being able to see
depth within objects anterior uveitis is inflammation of the iris
and the ciliary body but this doesn't tell us a whole lot so let's look at this deeper
common clinical signs that we see with uveitis include blepharospasm and photophobia conjunctival
hyperemia an episcleral injection epiphyra meiosis because there's a prostaglandin release
we see aqueous flare we see iritis or rubiosis iridus we can see hyphema within the eye corneal
edema corneal neovascularization and when we see corneal neovascularization in cases of uveitis
these blood vessels will be deep stromal vessels deep stromal vessels indicate that something is
going on inside the eye whereas superficial corneal vessels indicates surface disease
we'll also see keratic precipitates and we can see intraocular pigment dispersion pathophysiology of
uveitis includes that there is a tissue injury to the uvl tract there becomes increased blood flow
to the uvea inflammatory cell infiltrate increases to the uvs such as lymphoplasmacytic separative
and granulomatous reactions there's vascular permeability a breakdown of blood aqueous barrier
cytokine and prostaglandin release and activation and then plasmoid and fibrinoid aqueous there is
cytokine and prostaglandin release and activation there becomes plasmoid and fibrinoid aqueous
and lastly a pre-irrital fibrovascular membrane or pipham forms across the surface of the iris
here are two pictures histologic pictures of a pre-irrital fiber vascular membrane that's forming
across the surface of the iris this membrane then will grow over the ear to corneal angle
and leads to increased intraocular pressures or glaucoma ocular sequela of uveitis includes sinica
anterior and posterior sinekia an iris bombay which is where the iris adheres to the lens
and then aqueous pushes that iris forward that's what this picture is here that's provided
glaucoma can occur secondary to uveitis which is secondary to a pre-irrital fiber vascular membrane
and peripheral anterior synechia occur cataract formation is common in cases of severe uveitis
and retinal detachments can occur as a consequence of uveitis the number of causes of
uveitis is intense which can lead to a frustrating attempt to try to diagnose the cause of uveitis
there are non-infectious causes as well as infectious causes non-infectious causes include
autoimmune cataracts or lens induced ulcerative keratitis scleritis neoplasia and trauma
infectious causes include fungal causes protozoal viral parasitic algae and bacterial here are two
pictures which show uveitis in small animals this first picture shows a lens induced uveitis
this cataract came on very quickly and created in increased inflammation on the inside of the
eye which is represented by rubiosis iridus or the engorged blood vessels of the iris
the second picture was caused by blastomycosis which created intense inflammation on the inside
of the eye resulting in hyphena corneal edema and fibrin within the anterior chamber this next
picture shows intense inflammation secondary to cataract formation and lens capsule rupture
there are large amounts of caratic precipitates and fibrin within the anterior chamber as well as
posterior sinekia and the second picture shows a nice description of rubiosis iridus or an
iritis this first picture shows another eye with intense uveitis with deep corneal blood vessels
conjunctival hyperemia and the second picture shows intraocular cancer most likely associated
with lymphoma causing inflammation within the eye diagnosing anterior uveitis is important the
classic eye with uveitis shows blepharospasm and photophobia conjunctival hyperemia with episcleral
injection aqueous flare meiosis mild corneal edema rubiosis iridus and hypotony compared
to the contralateral eye but not every uveitis patient presents classically so what do i need
to get a proper diagnosis don't skip the basics complete ophthalmic examination obtain a thorough
history examine at an arm's length assess menace dazzle responses and pupillary light reflexes
retro illumination of the eye utilizing a strong pen light or trans illuminator obtain intraocular
pressures perform fluorescein staining and perform a shermer tear test this is a photo
of an eye with intense aqueous flare that can be seen in between the iris and the cornea aqueous
flare is essentially pathognomonic for uveitis so if you see this the patient does have uveitis
so with aqueous flare how do i detect it well with a slit lamp biomicroscopy there's a slit
or focal beam setting which gives you a very fine beam to detect aqueous flare and this is
the gold standard for diagnosing anterior uveitis however with a direct ophthalmoscope it's a small
light most of them do have a slit beam and you can take this at a tangential view and
diagnose anterior uveitis or aqueous flare that way however with this case of anterior uveitis
this aqueous flare is very obvious the most common over interpretation is with intraocular pressures
if you take a pressure a patient's pressures and they're low with no other signs of uveitis that
does not necessarily mean that they have uveitis they can also be high with the secondary glaucoma
with meiosis that's not always present sometimes there's a madriotic pupil due to synechia
sometimes there's a pharmacologic madriasis meaning that someone gave this patient atropine
or tropicamide before you saw them and cause them a mydriatic pupil there could be a secondary
glaucoma so the glaucoma is causing the pupil to be madriatic or you could have horner's syndrome
where they do have meiosis but it is due to horner syndrome and not due to uveitis so don't
forget a thorough physical examination and this is important for testing other non-infectious
causes include autoimmune which is very common pigmentary uveitis is very common which is this
picture here that's provided pigmentary uveitis is very common in golden retrievers and results in
deposition of pigment on the anterior lens capsule which also results in cataract loss of vision and
secondary glaucoma uvo dermatologic syndrome is another non-infectious cause of uveitis
cataracts which were caused by diabetes can cause lens induced uveitis
all sort of keratitis can cause a secondary uveitis trauma to the eye neoplasia to the eye
such as lymphoma melanoma or multiple myeloma and then infectious causes such as fungal
which in this area would be blastomycosis neoplasia within the eye can also cause a
secondary uveitis neoplasia including lymphoma melanoma multiple myelomyeloma and other
tumors that can occur within the eye infectious causes such as fungal blastomycosis aspergillosis
histoplasmosis or carcinoid mycosis rickettsial causes and parasitic causes
pigmentary uveitis or what's also known as golden retriever uveitis is highly under diagnosed in
this breed you must dilate the pupil in order to see most of the lens capsule which is how you make
your diagnosis of the radial pigment on the lens capsule if the patient has radial streaking on
the lens capsule this is typically indicative of this disease patients will have a very low-grade
non-painful uveitis which can lead to cataracts cataracts will cause additional uveitis and then
this can lead to a secondary glaucoma at minimum these patients should be managed
on topical flurboprofin or diclofenac once to twice daily and rechecked every four months
cataracts are one of the leading causes of uveitis in dogs diabetic cataracts progress
very quickly and this leads to not only uveitis but also leads to lens capsule ruptures
lens capsule ruptures result in intense uveitis which can lead to retinal detachments and glaucoma
one should not wait on performing surgery on diabetic cataracts topical anti-inflammatory
treatment with diclofenac or flurboprofen should be utilized once to twice daily all sorts of
keratitis can also lead to secondary uveitis corneal ulceration can lead to a reflex uveitis
it's important to not only manage the ulcer but also the uveitis atropine helps these patients
quite a bit and can be dosed at once or twice daily in this patient consider topical antibiotics
such as o-floxacin and terramycin topical anti-inflammatories such as diclofenac
oral anti-inflammatories such as carprophen and topical atropine not use topical steroids with
corneal ulceration under any circumstances neoplasia within the eye is a common cause
of secondary uveitis in patients tumors can be primary intraocular tumors or secondary as distant
metastasis primary intraocular tumors generate very low-grade uveitis that is not typically
witnessed by the client or the veterinarian secondary tumors typically create intense
inflammation and secondary glaucoma that is able to be seen by the client and the veterinarian
so if you look at these two photos the first one shows a secondary tumor that has metastasized to
the eye creating intense damage whereas the second photo shows a primary intraocular tumor which
creates low-grade uveitis fungal causes are common with secondary uveitis blastomycosis aspergillosis
histoplasmosis and coccidiomycosis in many cases the eye is the only clinical abnormality
the patient may not be sick just yet it's important to obtain an ideologic diagnosis
in order to not only treat the eye appropriately but also to potentially save the patient's life
in cats non-infectious causes include autoimmune which is the most common or neoplasia with the
most common being lymphoma ulcerative keratitis can also cause uveitis as well as trauma
infectious causes include viral such as feline leukemia virus feline immunodeficiency virus and
feline infectious peritonitis fungal causes such as cryptococcus histoplasmosis and aspergillosis
and toxoplasmosis primary feline neoplasia causing uveitis includes uveal melanomas
uveal adenoma or adenocarcinoma post-traumatic sarcomas or solitary ocular lymphomas secondary
tumors or metastatic tumors include lymphoma adenocarcinoma and fibrosarcoma amongst others
there's questions to ask yourself following your diagnosis is this a primary or secondary uveitis
is there a corneal ulcer a cataract is there a mass in the eye is my patient systemically ill
is there vomiting diarrhea coughing etc are lymph nodes enlarged lymphoma is a very common cause of
uveitis make sure to check your lymph nodes check mucous membranes petechia jaundice depigmentation
etc assuming that you've ruled out trauma and ulcerative care titus in your canine patient
how are we going to work these cases up first and foremost let's do a physical examination this will
help direct and prioritize your testing next would be routine lab work complete blood count serum
biochemistry and urinalysis next we're looking at we're going to look at disease specific testing
such as a snap 40x which which includes tick titers fungal urine and serology and
lymph node aspirates next would be imaging such as x-rays and ultrasound of the abdomen
next would be biopsy of any lesions that you may find on the body
further down the list would be aqueocentesis or vitriocentesis which are rarely performed
and lassie lastly would be a nucleation removal of the eye with biopsy with cats it's very similar
we're going to start with a physical examination to help direct and prioritize testing we're
going to run routine labs such as complete blood count serum biochemistry and urinalysis disease
specific testing including feline leukemia virus feline immunodeficiency virus coronavirus tighter
toxoplasmosis titer and fungal serology imaging can include chest x-rays and abdominal ultrasound
biopsy of any lesions that you may find aqueocentesis vitriocentesis
and finally a nucleation with biopsy so where do we start therapy therapy we start topically
as it's the first line for the anterior segment corticosteroids only if corneal fluorescein stain
is negative we're going to dose that every six to eight hours and then taper it over time based on
response non-steroidal is generally safe with corneal ulceration and that's also every six
to eight hours and then we taper it over time based on response you can use mydry addicts
such as atropine every eight to twelve hours but taper this one quickly do not use atropine if the
intraocular pressure is high or high normal do not use atropine if there is concurrent
keratoconjunctivity zika and use atropine ointment in cats so that the atropine liquid does not go
down their nasal lacrimal duct because it's bitter and it will really aggravate the cat for systemic
treatments use if posterior segment involvement or if topical alone is ineffective corticosteroids
it's important to rule out systemic microsis first before prescribing corticosteroids
dose and taper is cause and disease dependent non-steroidal anti-inflammatories can be used such
as carpal fin and maloxicam analgesia includes nsaids and tramadol which are quite effective
anti-microbials are disease dependent and immunosuppressants may be required
in autoimmune cases it's important to manage the underlying concurrent disease ulcerative keratitis
or a cataract and glaucoma etc etc make sure you're keeping the entire picture in front of you
continued management we're going to recheck early in the beginning we're going to recheck them in
about one week after their initial consult then two weeks after that maximum for initial recheck
irreversible intraocular changes can happen very quickly there's a high likelihood of
glaucoma if the inflammation persists initially this is a guarded prognosis
there's no underlying cause that's been determined yet
state of the eye at presentation response to treatment often this is a chronic disease
we need to educate clients that it's a chronic disease there are going to be periodic rechecks
and medication adjustments are likely some take-home points include uveitis is a non-specific
diagnosis what's driving the inflammation we need to do a complete ophthalmic examination
find the aqueous flare be careful of diagnostic pitfalls perform thorough physical examinations
as these are essential testing should always be offered to the client and encouraged
in order to find a definitive cause don't go light on topical anti-inflammatories as we want to get
the inflammation under control quickly we're going to recheck these cases early and referral
in severe cases can be beneficial if you feel like you are overwhelmed with these cases you shouldn't
be embarrassed or ashamed of referring a case that is what's in the best interest of the patient
if you feel like you do not know how to approach a case then those should be referred as well