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Hyphema. Part I. Pathophysiologic Considerations

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Hyphema. Part I. Pathophysiologic Considerations University of Pennsylvania ScholarlyCommons 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 Follow this and additional works at: https://repository.upenn.edu/vet_papers Part of the Ophthalmology Commons, and the Veterinary Medicine Commons Recommended Citation Komáromy, A. M., Ramsey, D. T., Brooks, D. E., Ramsey, C. C., Kallberg, M. E., & Andrew, S. E. (1999). Hyphema. 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 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 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 orbit and orbital but infrequently results in soft tissues. However, severe hyphema. The posterior lens 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 intraocular pressure (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 eyelids and conjunctiva, 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 (cornea, sclera) 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., hemothorax. 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 globe 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 vitreous hemorrhage, or retinal detachment.' 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 uveitis) is the most common ocular disease associated with a breakdown of the blood­ Thrombocytopenia aqueous barrier. Disruption of the blood-aqueous bar­ Lack of an adequate number of circulating platelets rier may lead to aqueous flare (predominantly pro­ can result in hyphema and hemorrhage secondary to teins), hypopyon, 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
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