Most causes for the breakdown of blood ocular barriers are a result of either 1) acute-onset of traumatic causes -either obvious
sharp trauma often involving laceration of the globe, or blunt-compressive trauma or choking) or 2) is the result of a chronic
ocular condition that has led to the formation of "pre-iridal fibrovascular membranes (PIFM)" as a response to chronic intraocular
hypoxia. PIFM formation is usually the result of glaucoma, retinal detachment, neoplasia, or after intraocular surgery, and
is associated with uveitis) or 3) is related to uveitis and blood ocular barrier disruption which is either caused by systemic
illness or remains idiopathic, or 4) by other inherited or congenital ocular abnormalities, but these are rare. Examples might
include hemorrhage in the posterior segment of the eye as the result of a retinal detachment (Collie Eye Anomaly), or persistent
vasculature (persistent hyperplastic primary vitreous in Doberman Pinschers or Staffordshire Terriers).
Sharp and blunt traumatic ocular hemorrhage
The goals of therapy when approaching a bleeding eye always include identifying the cause of bleeding if possible (in this
case we know it was trauma); preventing bleeding from recurring; controlling the resultant uveitis and limiting the sequelae
of uveitis (glaucoma, cataracts, senechiae, etc). In general, surgically lavaging hyphema or pulling clots out from the anterior
chamber often results in recurrence of bleeding as the anterior chamber must be decompressed and the iris is traumatized during
this procedure. Lacerations to the cornea or globe should be sutured primarily (referral situation). Lacerations to the lens
capsule also occur, especially when the sharp trauma includes a history of a cat scratch. If a lens capsular tear can be seen
or is suspected, this requires immediate referral as other more aggressive surgical interventions including phacoemulsification
of the lens may be necessary to avoid blinding phacoclastic uveitis. If medical therapy alone is indicated, strict rest and
removing the potential source of trauma is the first important step. Administration of topical steroids such as 1% prednisolone
acetate, or dexamethasone is recommended when bleeding is subconjunctival or intraocular and infected corneal wounds are not
present. Topical hydrocortisone will not penetrate well into the anterior chamber so should not be used for the treatment
of uveitis and bleeding, but can be used to limit inflammation associated with mild conjunctival hemorrhage. Initial therapy
may be 3-8x/day depending on the severity of hemorrhage and inflammation. Subconjunctival injections of triamcinolone may
be useful, especially in patients that cannot be medicated frequently at home. Injectable, subconjunctival steroids should
be avoided when there is concurrent ulcerative/infectious keratitis, as they can have devastating effects on the eye; however
oral anti-inflammatory doses of glucocorticoids can be used in these situations. Generally oral and topical NSAIDS should
not be used because of their effects on platelets and clotting, which may lead to re-bleeding. Intracameral or intravitreal
injections of 25ug of tissue plasminogen activator (TPA) in small animals may be of some use in breaking up clots or treatment
of hemorrhage/uveitis induced secondary glaucoma. Bleeding in the posterior segment of the eye (often from blunt trauma may
lead to the development of intravitreal traction bands, whereby fibrin condenses in the vitreous placing traction on the retina,
ultimately leading to a detachment. TPA injections should only be attempted when the cause of hyphema is known, and has not
occurred within the last 72 hours, as re-bleeding may occur. If glaucoma is beginning or anticipated, topical and/or systemic
carbonic anhydrase inhibitors and timolol are indicated. Topical prostaglandin analogues such as xalatan, or drugs that worsen/cause
uveitis such as pilocarpine should not be used in these cases as worsening uveitis and bleeding is expected. Intraocular pressure
should be monitored regularly, especially if dilating drops are part of the treatment protocol.
Pre-iridal fibrovascular membranes (what they didn't teach us in veterinary school): Fibrovascular membranes form on the surface
of the iris, retina and optic disc as a result of VEGF that is released in response to chronic intraocular ischemia (Gelatt).
The most common causes for this are retinal detachments, glaucoma, and chronic uveitis (for a variety of causes) as well as
intraocular tumors. The sources of VEGF are many. Domestic animals form PIFMs on the iris more than in the posterior segment
in contrast to humans. Clinical manifestations of PIFM formation are difficult to detect in most animals, especially since
the disease process may be insidious and the other eye often remains visual, so owners do not present these dogs until the
second eye has had an issue.
If the cause of bleeding is unclear (no known history of trauma and no obvious wounds/bruising) my general diagnostic profile
includes a CBC, manual platelet count (especially in cats given their platelet clumping issues), blood chemistry and blood
pressure assessment. Clotting profiles are submitted if toxicities are possible.
However, when there is recurrent bleeding in the eye without a known history of trauma, with a normal physical exam, blood
pressure, and hematologic findings, this should alert you to the possibility of recurrent uveitis (for a variety of causes)
or intraocular neoplasia and therefore more specific blood testing for infectious diseases and recommended. An ocular ultrasound
may also be helpful in establishing a diagnosis since often the posterior segment is not visible through the hemorrhage.