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Departmental Papers (Vet) School of Veterinary Medicine

11-1-1999

Hyphema. Part I. Pathophysiologic Considerations

András M. Komáromy

David T. Ramsey

Dennis E. Brooks

Cynthia C. Ramsey

Maria E. Kallberg

See next page for additional authors

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Recommended Citation Komáromy, A. M., Ramsey, D. T., Brooks, D. E., Ramsey, C. C., Kallberg, M. E., & Andrew, S. E. (1999). . Part I. Pathophysiologic Considerations. Compendium on Continuing Education for the Practicing Veterinarian, 21 (11), 1064-1069. Retrieved from https://repository.upenn.edu/vet_papers/51

Dr. Komáromy was affiliated with the University of Pennsylvania from 2003-2012. Part II can be found at http://repository.upenn.edu/vet_papers/52/

This paper is posted at ScholarlyCommons. https://repository.upenn.edu/vet_papers/51 For more information, please contact [email protected]. Hyphema. Part I. Pathophysiologic Considerations

Abstract Hemorrhage in the anterior chamber of the eye, or hyphema, results from a breakdown of the blood-ocular barrier (BOB) and is frequently associated with inflammation of the , , or . Hyphema can also occur by retrograde blood flow into the anterior chamber via the aqueous humor drainage pathways without BOB breakdown. Hyphema attributable to blunt or perforating ocular trauma is more common than that resulting from endogenous causes. When trauma has been eliminated as a possible cause, it is prudent to assume that every animal with hyphema has a serious systemic disease until proven otherwise.

Disciplines Medicine and Health Sciences | Ophthalmology | Veterinary Medicine

Comments Dr. Komáromy was affiliated with the University of Pennsylvania from 2003-2012.

Part II can be found at http://repository.upenn.edu/vet_papers/52/

Author(s) András M. Komáromy, David T. Ramsey, Dennis E. Brooks, Cynthia C. Ramsey, Maria E. Kallberg, and Stacy E. Andrew

This journal article is available at ScholarlyCommons: https://repository.upenn.edu/vet_papers/51 1064 20TH ANN IVERSARY Vol. 21, No . 11 November 1999

and e with, CE Article #5 (1.5 contact hours) of pel Helereed Peer Review of the frequ rna; blood Iy cal Hyphema. Part 1. and ( but i Pathophysiologic Considerations hyph( FOCAL POINT capsu do nl Hyphema is frequently associated University of florida Michigan State University move: with iridocyclitis and generally Andras M. Komaromy, DLmed.vet. David T. Ramsey, DVM anteri indicates severe intraocular or ous a\ systemic disease. Dennis E. Brooks, DVM, PhD Cynthia C. Ramsey, DVM, MS Be( Maria E. Kallberg, DVM highe age F KEY FACTS Stacy E. Andrew, DVM blooe lower Athorough diagnostic evaluation ABSTRACT: Hemorrhage in the anterior chamber of the eye, or hyphema, results from a break· predi. should be initiated when down of the blood-ocular barrier (BOB) and is frequently associated with inflammation of the the al hyphema is present, p. 1064. iris, ciliary body, or retina. Hyphema can also occur by retrograde blood flow into the anterior chamber via the aqueous humor drainage pathways without BOB breakdown. Hyphema at· PAn tributable to blunt or perforating ocular trauma is more common than that resulting from en· Hyphema generally results from Wi dogenous causes. When trauma has been eliminated as a possible cause, it is prudent to as­ a breakdown of the blood-ocular sume that every animal with hyphema has aserious systemic disease until proven otherwise. agnos barrier, p. 1064. tially body The diagnostic differentials )'Phema is defined as hemorrhage within the anterior chamber of the eye diagn for hyphema do not differ (Figure 1). In contrast, the accumulation of leukocytes in the ;:nterior hyphl substantially from those for H chamber is termed h)'P0pyon. The etiopathogenesis of hyphema is mul­ dison hemorrhage into other areas tifactorial, but ultimately the final common pathway is breakdown of the soum of the body, p. 1065. blood-ocular barrier (BOB) and subsequent inrraocular hemorrhage that is of­ so thl ten associated with inflammation. Many of the mechanisms that cause intraocu­ ation:

When trauma has been lar hemorrhage may also result in hemorrhage in other parts of the body. This I1Ism~ eliminated as source of hyphema, article foclIses on hyphema as a "red flag" for sight-threatening ocular or life­ the diagnostic and therapeutic threatening systemic hemorrhagic disease. Irido approach is directed by results When hyphema is present, a thorough diagrwstic evaluation similar ro that in­ lri( of the physical and ophthalmic dicated for any third-compartment hemorrhage (e.g., hemoabdomen, hemotho­ ocula examinations, p. 1065. rax) should be initiated. Attentive clinicians will recognize the importance of a aque( thorough diagnostic workup before or during the initial treatment of hyphema. ner. ,I Death attributable to systemic or vital organ hemorrhage may occur if the diag­ terns) nostic workup is incomplete. Part I of this two-parr presentation focuses on the rncltJ many pathophysiologic mechanisms that most frequenrly result in hyphema, the f each of which is considered as a separate entity in this article. However, concur­ discu rent involvement of more than one mechanism is common. Part II will cover di­ ble c agnosis and treatment of hyphema. left L cyclil BLOOD-OCULAR BARRIER cei'ls The BOB, which consists of the blood-aqueous and blood-retinal barriers, pre­ vents erythrocytes and leukocytes and inhibits tissue fluids and proteins from enter­ Trau ing nonvascular ocular tissues and compartments. The BOB consists of endothelial H~ Compendium November 1999 20TH ANNIVERSARY Small Animal/Exotics 1065

and epithelial tight junctions perforating trauma) is prob­ with variations in their degree ably more common than that of permeability. l Dysfunction resulting from endogenous of the blood-aqueous barrier causes (see Causes of Hyphe­ frequently results in hyphe­ rna) . Blunt trauma to the rna; breakdown of the head seldom resuhs in hyphe­ blood-r.-:tinal barrier general­ rna because the eyebal'l is pro­ ly causes retinal, subretinal, tected by anterior portions and choroidal hemorrhage of the bony and orbital but infrequently results in soft tissues. However, severe hyphema. The posterior blunt trauma to the anterior capsule and zonules limit but orbital rim or periorbital soft do not com pletely preven t tissues and eyeball may re­ movement of blood from the Figure 1-Hyphema in a dog. suit in hyphema. In this case, anterior chamber to the vitre­ ------examination and palpation ous and vice versa. of the periorbital area usual­ Because the (lOP) is normally I,y reveals clinical signs of trauma, such as swelling and higher than the pressure in the aqueous humor drain­ bruising of the and , fracture of the age pathways (the scleral venous plexus), retrograde bony orbit, or orbital hemorrhage and resultant orbital blood flow into the anterior chamber is prevented. lOP mass effect. Bilateral hyphema is seldom caused by lower than the pressure in the scleral venous plexus may mild trauma. When blunt ocular trauma occurs, the predispose to hyphema via retrograde blood flow into sudden rise in lOP associated with ocular indentation the anterior chamber. causes anterior chamber angle distortion and may result in rupture of iris stromal or ciliary body vessels and PATHOPHYSIOLOGIC APPROACH subsequent hyphema.4 With the exception ofsevere intraocular disease, the di­ Perforating trauma (e.g., cat scratch, BB pellets) to agnostic differentials for hyphema do not differ substan­ the eye baH (, ) with direct damage to in­ tially from those for hemorrhage in other areas of the traocular vasculature is more likely to result in trau­ body (e.g., . hemoabdomen); therefore, the matic hyphema than is blunt trauma. Traumatic hy­ diagnostic approach to determine the underlying cause of phema can also be associated with proptosis of the hyphema is similar. In addition to systemic causes, ocular and may be accompanied by structural damage disorders should be considered. Clinicians must develop a to the eye, including lens subluxation and dislocation, sound understanding of the potential causes of hyphema , or .' Head ra­ so they are able to construct a list of differential consider­ diographs help to reveal fractures of the orbit or skull ations for each mechanism. The most common mecha­ in trauma cases. When exogenous sources of hyphema nisms ofhemorrhage that may result in hyphema follow. have been eliminated, the diagnostic approach is fur­ ther directed by results of physical and ophthalmic ex­ Ir.idocyclitis amll1atIons. Iridocyclitis (anterior ) is the most common ocular disease associated with a breakdown of the blood­ aqueous barrier. Disruption of the blood-aqueous bar­ Lack of an adequate number of circulating rier may lead to aqueous flare (predominantly pro­ can result in hyphema and hemorrhage secondary to teins), , and/or hyphema, depending on the ongoing capi,uary microtrauma induced by normal ac­ inciting stimulus and duration of the disease. Most of tiviry or exogenous insult.6 Thrombocytopenia is typi­ the pathophysiologic mechanisms of BOB breakdown fied clinically by petechial hemorrhage of mucosal and discussed in the remainder of this article are also possi­ cutaneous surfaces. Hyphema and concurrent petechial ble causes for iridocyclitis. Regardless of the caLIse, ,if hemorrhages should prompt clinicians to consider left untreated, hyphema will eventually result in irido­ thrombocytopenia as a likely mechanism of disease. cyclitis when chemotactic triggers recruit inflammatory Thrombocywpenia may be induced by immune-medi­ cells for cleanup. ated destruction of platelets, infectious agents (e.g., Ehrlichia canis, platys, or risticii; Leptojpira species; Trauma Rickettsia rickettsil) , sepsis, splenomegaly, neoplasia, or Hyphema attributable to exogenous causes (blunt or disseminated intravascular .

ANTERIOR UVEITIS • PERFORATING TRAUMA PETECHIAL HEMORRHAGE 1066 Small An imal/Exotics 20TH ANNIVERSARY Compendium November 1999

Causes of Hyphema

Trauma2-5 hereditary thrombopathias, including breed-specific Hypel thrombopathias • Blunt • M( • Penetrating (with or without foreign body) • SystemiC illness: Uremia, collagen deficiency disease, hepatic disease, pancreatitis, ehrlichiosis (E. canis, an Thrombocytopenia6-10 £. platys) , FeLV, dysproteinemia, gammopathies, eh • Decreased production in the bone marrow myeloproliferative/myelodysplastic disorders, DIG , • Se -Drug or chemical toxicity-induced bone marrow Iymphoproliferative disorders, multiple myeloma po hypoplasia (e .g., estrogens, antiinflammatory • Drug-induced: NSAIDs, corticosteroids, diuretic agents, antibiotics, tranquilizing agents, diuretic agents, tranquilizers, synthetic colloid solutions Syste agents, dapsone, myelosuppressive chemotherapy) (e .g., dextran), 0:- and ~-blockers and stimulators, -Toxic doses of irradiation hormonal agents (e.g., prostacyclin , estrogen), vinca Neov; -Chronic infections (e .g., feline virus alkaloids, antibiotics and antiparasitic agents, heparin • Re [FeLV], Ehrlichia canis, Ehrlichia platys, canine • Antibody-mediated platelet dysfunction : Immune­ distemper, parvovirus, heartworm disease) mediated thrombocytopathy, systemic lupus -Myeloproliferative disorders (e.g., FeLV, feline erythematosus immunodeficiency virus [FIV]), lymphoma, tumor metastasis 8.10.12-14 -Estrogen-secreting tumors (e.g ., Sertoli cell tumor) • Inherited -Myelofibrosis • Acquired -Immune-mediated megakaryocytic hypoplasia or aplasia Vasculitis and uveitis l 5-21 -Chronic renal disease • Infectious: Rocky Mountain spotted fever, Throm • Reduced circulating platelet life span ehrlichiosis, leptospirosis, brucellosis, piroplasmosis, Defe ca n res -Sequestration (e.g., splenomegaly) leishmaniasis, ophthalmomyiasis interna, ocular fen s m -Immune-mediated platelet destruction filariasis (Dirofilaria immitis) , tuberculosis, be ind -Nonimmunologic platelet destruction geotrichosis, protothecosis, toxoplasmosis quired • Microangiopathic thrombocytopenia (e.g., (Toxoplasma gondii), FIV, FeLV, feline infectious rain dr disseminated intravascular coagulation [DIG], peritonitis (FIP), canine adenovirus 1, cryptococcosis, rhy she re nden · tumor microvasculature [hemangiosarcoma, blastomycosis, coccidioidomycosis, candidiasis counr, hepatic tumors]) • Immune-mediated (e.g ., uveodermatologic syndrome) • Microangiopathic hemolytic anemia • Neoplasia (e .g., lymphosarcoma, ocular sarcoma, Coagu • Severe vascular injury and vasculitis (see metastatic tumors) Abnc Vasculitis and uveitis) • Lens-induced uveitis parhwa abnorrr • Drug-induced (e.g., heparin) • rna. C. • Platelet loss via hemorrhage (usually mild • SystemiC inflammatory response syndrome: SepSiS, rhird-cc thrombocytopenia) endotoxemia (e.g., pyometra) body c • Infectious agents (e.g ., E. canis, Rickettsia • Secondary to or trauma be inhe rickettsii, Dirofilaria) • Idiopathic rhages neous I coagulc Thrombocytopathy (defects in platelet adhesion, Noninflammatory vascular disorders22 bocYlOl aggregation, or release reactions)'o", • Hyperadrenocorticism able de • Inherited: von Willebrand's disease and other • Ehlers-Danlos syndrome signs 0 1 owners Compendium November 1999 20TH ANNIVERSARY Small Animal/Exotics 1067

Causes of Hyphema (continued)

Hyperviscosity syndrome9.23-27 Systemic Hypertension section in text), congenital • Mono- or polyclonal gammopathies: Multiple abnormalities (e.g., retinal dysplasia), senile myeloma, lymphoma, leukemia, chronic inflammation, degenerative changes antigenic stimulation (e.g., dirofilariasis), FIV, FIP, • Chronic '6 ehrlichiosis (E. canis, E. platys) • Intraocular neoplasia34 • Severe erythrocytosis: Hemorrhagic gastroenteritis, -Primary: Lymphosarcoma, adenoma and polycythemia vera, erythropoietin-secreting neoplasms adenocarcinoma, , posttraumatic ocular sarcoma in cats Systemic hypertension 28-30 -Secondary: Adenocarcinoma, transitional cell carcinoma, lymphoma, multiple myeloma of uveal and retinal tissues • Retinal detachment'61831-JJ Congenital anomalies 31.35 -Primary • Collie eye anomaly -Secondary: Lenticular disease, infectious diseases • Vitreoretinal dysplasia (e.g., in Bedlington terriers, (see Vasculitis and uveitis), nonseptic inflammation Sealyham terriers, Labrador retrievers) (see Vasculitis and uveitis), trauma (see Trauma), • Persistent hyaloid artery (e.g., with persistent intraocular neoplasia (see Neoplasia), systemic hyperplastic primary vitreous in Doberman pinschers) neoplasia (e.g., multiple myeloma), systemic hypertension (i.e., hypertensive ; see Anemia

Thrombocytopathy Vasculitis Defects in platelet adhesion, aggregation, or release Vascular endothelial cell abnormalities may result in can result in ineffectual platelet function. II These de­ transmural extravasation of blood from vascular chan­ fects may be inherited (e.g., von Willebrand's disease); nels in the iris and ciliary body, resulting in breakdown be induced by systemic disorders; or, as in most ac­ of the blood-aqueous barrier and hyphema. Vasculitis quired cases, occur as an idiosyncratic reaction to cer­ may result from primary or secondary immune-mediat­ tain drugs (see Causes of Hyphema). Thrombocytopa­ ed destruction of endothelial cells (e.g., immune-medi­ thy should be suspected in patients with hemorrhagic ated vasculitis, toxoplasmosis), infectious diseases (e.g., tendency, prolonged time, appropriate platelet leptospirosis, Rocky Mountain spotted fever, feline in­ count, and normal tests of secondary hemorrhage. fectious peritonitis), neoplasia, or systemic inflammato­ ry response syndrome (e.g., sepsis). Noninflammatory Coagulopathy vascular disorders, including hyperadrenocorticism and Abnormalities of the intrinsic, extrinsic, or common Ehler-Danlos syndrome, can also result in hemorrhage. pathways of the clotting cascade may result in clotting abnormalities and subsequent hemorrhage and hyphe­ Hyperviscosity Syndrome mao are typified clinically by large Diseases that produce excessive globulins or other plas­ third-compartment or major organ hemorrhages (e.g., ma proteins may result in hyphema because of (1) vascu­ body cavity, pulmonary, musde/deep tissue) and may lar endothelial cell compromise caused by intravascular be inherited or acquired. Although ecchymotic hemor­ sludging of blood with vessel wall necrosis, (2) infiltra­ rhages are classically described in coagulopathies, cuta­ tion of proteins into the vessel wall, (3) inhibition of neous hemorrhages are less common in animals with hemostasis secondary to reduction in clotting factors, coagulopathies than are thrombocyropenias and throm­ and/or (4) coating of platelets by abnormal paraproteins bocytopathies. Clinical presentation is extremely vari­ resulring in abnormal platelet aggregation. 23 Funduscopic able depending on the site of hemorrhage. Secondary examination of the contralateral eye may reveal engorged signs of anemia (weakness, pallor) are often noted by retinal vasculature and retinal hemorrhages. Common owners of animals with a coagulopathy. causes of hyperviscosity include plasma cell myeloma,

ECCHYMOTIC HEMORRHAGE • NONINFLAMMATORY VASCULAR DISORDERS • PLASMA PROTEINS 1068 Small Animal/Exotics 20TH ANNIVERSARY Compendium November 1999 , ,.

lymphoma, ehrlichiosis, and chronic inflammatory dis­ cell and fibroblast proliferation and subsequent ftbrovas­ often I 6 ease. Serum total solids will generally be excessively ele­ cular membrane formation..l The most frequent site of intrao, vated because of hyperglobulinemia. Hyperviscosity syn­ fibrovascular membrane formation in eyes with chronic older; drome can also be induced by severe erythrocytosis, such retinal detachment is overlying the anterior iris surface glOsar, as hemorrhagic gastroenteritis, po'lycythemia vera, and (pre-iridal ftbrovascular membrane). 16 Acute hyp hema montl­ erythropoietin~secreting neoplasms. may occur if the retinal vasculature tears when the neu­ unilatc rosensory retina detaches from the underlying retinal traoCI SystemiC Hypertension pigment epithelial cells. Clinicians must derermine the intrao Hyphema arrributable to systemic hyperrension is cause of the retinal detach­ ondaI"' most common in old cats and dogs and is often caused ment because life-threaren­ oma) by chronic renal insufftciency. Systemic hypertension ing systemic disease may be suit in affects only the arterial vascular system. Chronic high the underlying abnormality arterial pressure may result in arteriosclerosis and au­ (see Causes of Hyphema). in Cong toregulatory arteriolar vasospasm. Arteriolar disease our experience, sponrane­ H)'! causes and capillary permeability changes ous (idiopathic) retinal de­ to cor (with leakage of plasma proteins) and eventually hem­ tachment is rare in dogs and cawse. orrhage. In our experience, most cases of hyphema cats and an underlying cause The more commoll causes of is cha from vasoular hypertension are attribu table to retinal is usually present. illtraocular hemorrhage were tribU[; detachment (see Neovascularization of Uveal and Reti­ kllown 20 years ago. Since then, severe nal Tissues section) and most likely occur in response Chronic Glaucoma new infictiom causes of rerrler to choroidal vascular hypertension. Hyphema may be Pre-iridal fibrovascular hyp"ema, such as felille er spa less commonly caused by tearing of retinal vasculature membranes are also frequent­ immunodeficiency virus, have plere that occurs during retinal detachment. Otber common ly detected in eyes with been detected. Research Oller the subse< causes of vascular hypertension include hyperthyroidism , chronic (end-stage) glauco­ past 20 years has demollstrated and v hyperadrenocorticism , hyperaldosteronism, and pheo­ ma. ,G It is likely that hyphe­ marty mediators of curs s chromocytoma. ma attributable to chronic neollasclilarizatiort and fetal r glaucoma occurs secondary tent h intraocular inflammation. The Neovascularization of Uveal and Retinal Tissues to tearing and leakage of the body, methodologies for diAgnostic Although the presence of blood vessels is necessary in fragile pre-iridal mlcrovascu­ most tissues, neovascularization or of tissues lature.' f, workup hmle improved with the Anen can cause severe disease. The surfaces of the retina and advent ofB-mode Acc 6 iris are vulnerable to symptomatic neovasCldarization..l Intraocular Neoplasia ultrasonography, computed severe Possible causes for neovascularization are ischemia (in­ Growth ofa neoplasm larg­ l tomography, and magnetic can cc cluding long-standing retinal detachment), intraocular er than 2 to 3 mm-l requires resonallce imaging. Howeller, low 5 neoplasia, and inflammation. \6 Vascular proliferation on development of a microvas­ the primar), management issues dothe the anterior iris surhce () leads to the for­ cular network to facilitate ofhyphema halle remained vessel: mation of a pre-iridal ftbrovascular membrane, which delivery of nutrients and unchartged. A few new can involve the peripheral iris and iridocorneal drainage oxygen and removal of treatment OptiOIlS have been angle and result in obstruction of aqueous humor out­ catabolites. 38 Primary and added, such as tissue flow. Angiogenesis, a complex process that incllldes metastatic intraocular neo­ I. B( plasminogm actillator and degradation of extracellular matrix and endothelial cell plasms of the anterior uveal m topical carbonic anhydrllSe proliferation, is stringently regulated by numerous tissues are highly vascular. th 2. \l(­ proangiogenic and antiangiogenic factors. Examples of These neoplasms secrete inhibitors. UnfortulUltely, the m growth factors that stimulate endothelial cell prolifera­ prognosis for main fair-ling lIisioll vascular growth factors (e.g., 3. \l(­ in an eye with hyphema has tion include fibroblast growth factors, insulinlike growth VEGF, TGF-~) that stimu­ Ai factors, transforming growth factor-~ (TGF-~), and vas­ late formation and rapid generally remained the Sf/me 4. G cular endothelial growth factor (VEGF).lG The newly growth of vessels to support oller the past 20 years. H grown vessels are exceedingly fragile, leal( readily, and can and sustain rumor growthY 5. G potentially result in hemorrhage and hyphema;17 Newly developed capillaries pI 2( of neoplasms are prone to 6. M Retinal Detachment hemorrhage because they p, Long-standing retinal detachment stimulates produc­ have incomplete basement 15 tion of growth factors that induce vascular endothelial membranes, are leaky, and 7. Jo

ARTERIOLAR DISEASE . PRE-IRIDAL FIBROVASCULAR MEMBRANE . GROWTH FACTORS Compendium November 1999 20TH ANNIVERSARY '''''' S~nia'' Animal/Exotics 1069

often fracture. J6 ..lS Animals with hyphema attributable to topenia in cats: A retrospective study of 41 cases. j Vet Intern intraocular neoplasia are usually in late middle age or Med7(5):261-265, 1993. 8. Peterso n JL, Couto CG, Wellman ML: H emostatic disor­ older; however, we have diagnosed ciliary body heman­ der. in cats: A retrospective study and review of the litera­ giosarcoma and iris melanoma in dogs as young as 7 ture. j Vet Illtem Med ') (5 ):298-302, 1995. months of age. Most primary inrraocu'lar neoplasms are 9. Shelton G H, Linenberger ML: Hematologic abnormalities unilateral, and thus hyphema attributable to primary in­ associated with retroviral in fectio ns in the car. Semi" Vet traocular neoplasia is unilateral. Bilateral primary Med Surg Small Anim 10(4):220-233, 1')95 . 10. Boudreaux MK: Platelets and coagulation. Vet Clin North intraocular neoplasms are reponed infrequenrly.j~ Sec­ Am Small Anim hart 26(5): I 065-1087, 1996. ondary or metastatic intraocular neoplasia (e.g., lymph­ I\, Ruiz de Gopegui R, Feldman BF: Acquired and inherited oma) may affect one or both eyes and may -therefore re­ platelet dysfunction in small animals. Compelle! C.'onlill Edltc sult in unilateral or bilateral hyphema. Pract Vet 20(9): 1039- 1052, 1998. 12. Fogh JM, f ogh IT: Inherited coagulation disorders. Vet Clin NorthAm Small Anim Pmct 18(1 ):231-243, 1988. Congenital Ocular Anomalies 13. Hart SW, Noire I: Hemostatic disorders in feline immuno­ Hyphema in young animals should prompt clinicians deficiency virus-seropositive cats. j Vet [ntem Med 8(5):355­ to consider congenital ocular malformation as a ilikely 362, 1994. cause. Collie eye anomaly, which is recessively inherited, 14. Lisciandro Sc, H ohenhaus A, Brooks M: Coagulation ab­ is characterized by defects of the and sclera at­ normalities in 22 cats with naturally occurring liver disease. 5J j Vet [ntem Med 12(2) :71-75, 1998. tributable to abnormal mesodermal differentiation. In 15. Davidson MG, Breitschwerdt EB, Nasisse MP, Roberts SM: severe cases of vitreoretinal dysplasia (e.g., in Bedlington Ocular manifestations of Rocky Mountain sported fever in terriers, Sealyham terriers, Labrador retrievers, or spring­ dogs.jAVMA 194(6):777-78 1, 1989. er spaniels), retinal folding is sufficient to permit com­ 16. Peiffer J I' RL, Wilcock BP, Yin H : The padlOgenc.:s is and sig­ 3 nificance of pre-iridal fibrovasc ular membrane in domes ti c plete retinal detachmenr. 1.35 Retinal detachment and animals. Vet PathoI 27(I):4 1-45, 1990. subsequent hyphema may occur w~h collie eye anomaly 17. Collins BK, Moore CPo Diseases and surgery of the canine and vitreoretinal dysplasia. Persistent hyaloid artery oc­ anterior , in Gdatt KN (ed): Veteril1/UJ Ophthalmology, curs sporadically in dogs and is caused by failure of the ed 3. Baltimore, Lippincott Williams & Wilkins, 1999, pp l5 I fetal hyaloid vasculature to regress. Rupture of a persis­ 755-795. 18 . Glaze MB, Gelatt KN: Feline ophthalmology, in Gelart KN tent hyaloid artery leads to hemorrhage into the vitreolls l5 (ed): VeterinalJ' Ophthalmology, ed 3. Baltimore, Lippincott body, with blood passing into the anterior chamber. Williams & Wilkins, 1999, pp 997-1052. 19. Peiffer J r RL, Wilcock BP: Histopathologic study of uveitis Anemia in cats: 139 caSes (1978- 1988). jAVMA 198(1):135-138 , According to our experience and a previous report, 40 1991. severe acute anemia (e.g., severe tick or flea infestation) 20. Chavkin MJ, Lappin MR, Powell Cc, et al: Seroepidemio­ logic and clinical observations of 93 cases of uveitis in (:1[.1. can cause hyphema when hemoglobin rapidly drops be­ Prog Vet Comp OphthalmoI2(1):29-36, 1992. low 5 mg/dl. Insufficient oxygen supply may cause en­ 2 \. Bisrner S: Allergic- and immunologic-mediared diseases of dothelial cells to die, which leads to leaking of blood the eye and adncxae. Vet Clin North Am Small Anim Prtlct vessels. 24 (4):7 11-734,1994. 22. Freeman LJ, Hegreberg GA, Robinette JD: Ehlers-Danlos syndrome in dogs and cats. Semin Vet /IIled Surg Sma!! Al1im 2(3):221 - 227, 1987. REFERENCES 23. Lane IF, RobertS SM, Lappin MR: Ocular manifestations of I . Bel/horn R\'\!: An overview of the blood-ocular barriers: Sey­ vascular disease: Hypertension, hyperviscos ity, and hyper­ mour R. Roberts Memorial Lecture. Prog Vet Comp Oph­ lipidemia. jAAHA 29( 1):28-36, 1993. thalmoll(3):205- 217,1991. 24. Hendrix DVH, Celatt KN, Smith PJ, et al: Ophthalmic dis­ 2. Wilson FM: Traumatic hyphema. Pathogenesis and manage­ ease as the presenting complaim in five dogs with multiple ment. Ophthalmology 87(9):910- 919, 1980. myeloma.jAAHA34(2):121 - 128,1998. 3. Winston SM: Ocular emergencies. Vet Clin North Am Small 25. Foster ES, Lothrop Jr CD: Pol),c),themia vera in a cat wirh ca rdiac hypertrophy. jAVMA 192( (2): 1736-1738, 1988. Anim Pract II (1 ):59-76, 1981. 26. Hammer AS, Couto CG: Complications of multiple myelo­ 4. Gottsch JD: Hyphema: Diagnosis and mallJgemenr. Retina ma. jAAHA 30(1):9-14, 1994. 10(Suppll):S65-S71 ,1990. 27. Forresror SD, G reco DS, Relford RL: Serum hyperviscos it)' 5. Gilger Be, Hamilton HL, Wilkie DA, et a1: Traumatic oculat syndrome associated with multiple myeloma in rwo cats. proptosis in dogs and cats: 84 cases (1980-199.3). jAVMA jAVMA 200(1):79-82, 1992. 206(8):1186-1190,1995. 28. Dimski DS, Hawkins EC: Canine sys temic hypertension. 6. Mackin A: Canine immune-mediated thrombocytopcnia­ Compend Con tin Educ Pract Vet 10(10): 1152- 1158, 1988. Parr I. Compend Contin Educ l'ract Vet 17(3) :353-.364, 29. Stiles J, Polzin DJ, Bisrner SI: The prevalence of retinoparhy 1995. in cats with systemic hypertension and chronic renal failure 7. Jordan HL, Grindem CB, Breitschwerdt EB: Thrombocy­ Ot hyperthyroidism. jAAHA 30(6):564-572, 1994.

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COLLIE EYE ANOMALY . VITREORETINAL OYSPLASIA • PERSISTENT HYALOIO ARTERY