Traumatic Hyphema.pdf

Traumatic Hyphema Pathogenesis and Management FRED M. WILSON II, MD

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Abstract: Traumatic hyphema is a potentially serious problem, but the overall prognosis is good unless associated injuries are severe. Medical treatment is of little value for hyphema itself but is useful for complications. Surgical treatment is hazardous and should be resorted to only in select circumstances. Severity of injury is more important than is treatment in determining the outcome . Practitioners should not feel obliged to use ritualistic therapy that they consider to be of uncertain value. [Key words: angle recession, corneal blood staining, hemorrhage, hyphema, trauma, traumatic cyclodialysis, traumatic glaucoma.] Ophthalmology 87:910-919, 1980

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Hyphema is the presence of blood in the anterior chamber. Tiny hemorrhages may be visible only with the slit lamp, in the form of erythrocytes floating and circulating in the aqueous humor. Slightly larger amounts of blood settle as variously shaped masses on the surface of the iris, lens, or vitreous. Still larger hemorrhages gravitate to the inferior aspect of the anterior chamber, producing a grossly visible, "layered" hyphema. The most severe hemorrhages can fill the anterior chamber; these tend to clot, probably because of impaired circulation of aqueous, and nearly always produce glaucoma. Total, clotted hyphemas are dark brown, purple, or black and are referred to as "black-ball" or "eight-ball" hemorrhages (Fig 1). Causes of hyphema include trauma, surgery, neoplasms, vascular anomalies, neovascularization, blood dyscrasias, and sudden lowering

of intraocular pressure in an inflammed eye.! This paper deals with traumatic hyphema and my approach to its management based on personal experience, available evidence, and what I consider to be currently valid opinion.

CLASSIFICA TION Classification of hyphemas in terms of several variables is useful for evaluating severity of injury, prognosis, and management. The most important variable is the amount of blood, which is best classified according to the scheme of Edwards and Layden. 2 My classification (Table 1) is otherwise a modification and expansion of one proposed by Lebekhov and Iandiev. 3

PATHOPHYSIOLOGY SOURCE OF HEMORRHAGE

From the Corneal and External Ocular Disease Service , Department of Ophthalmology, Indiana University School of Medicine, Indianapolis. Presented at the Eighty-Fourth Annual Meeting , American Academy of Ophthalmology, San Francisco, November 5 - 9, 1979. Supported in part by a grant from Research to Prevent Blindness, Inc., New York. Reprint requests to Dr. Wilson, Department of Ophthalmology, Indiana University School of Medicine, 1100 West Michigan Street, Indianapolis, IN 47223.

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Intraocular bleeding can be caused by lacerations or ruptures of the ocular coats, but most traumatic hyphemas occur after blunt, contusive injuries to the eye. Indentation of the anterior surface of the eye causes a sudden rise in pressure in the anterior chamber, stretching of the limbal tissues, posterior and peripheral movement of aqueous, and retrodisplacement of the iris and lens. The result can be a tear in the ciliary body or iris, usually in the area of the angle4 (Fig 2).

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Fig 1. "Black-ball" hyphema. Dark, clotted blood fills the anterior chamber and obscures the iris.

« Table 1. Classification of Nonsurgical Traumatic Hyphema * Etiology Contusion Laceration or rupture Origin Iris sphincter or stroma Iris root (iridodialysis) Ciliary body face (angle recession) Ciliary body disinsertion (cyclodialysis) Vascular anomalies or neovascularization Vitreous hemorrhage (with spillover to anterior chamber) Type Primary Secondary (rebleed) Continual Volumet Grade I (less than one-third of anterior chamber) Grade II (one-third to one-half of anterior chamber) Grade III (greater than one-half of anterior chamber) Duration Acute (1-7 days) Subacute (7-14 days) Chronic (over 14 days) Character Liquid (red) Clotted (brown or black) Mixed Organized (tan, gray, or white) Patient Normal Clotting disorder Sickling hemoglobinopathy * Modified and expanded from Lebekhov and landiev. 3

t From Edwards and Layden!

A tear in the anterior face of the ciliary body (also known as traumatic recession ofthe angle; Figs 2, 3) is the most common source of bleed-

ing, occurring in perhaps 71 to 94% of all cases. 5- 7 The circular and oblique muscle fibers of the ciliary body are torn from the longitudinal (meridional) fibers, which remain attached to the scleral spur (Fig 3).8 The injury disrupts the major arterial circle of the iris, arterial branches to the ciliary body, recurrent choroidal arteries, or veins coursing between the ciliary body and episcleral venous plexus.9 Healing of this kind of injury results in postcontusion deformity of the angle, which is characterized by localized deepening of the anterior chamber and by equatorial and posterior retraction of the angle recess, the iris root, the anterior ciliary processes, and the circular and oblique fibers ofthe ciliary muscle. 8 •10 The ciliary body loses its normal wedge shape and becomes fusiform. 8 Traumatic cyclodialysis (Figs 2, 4) is occasionally responsible for hyphema. 9 The longitudinal fibers of the ciliary muscle are separated completely from the scleral spur, producing a cleft in the supraciliary space (Fig 4).8 Iridodialysis (disinsertion of the root of the iris) and tears of the iris stroma or sphincter are uncommon as causes of hyphema, as these injuries generally cause little or no bleeding. 9 Abnormal blood vessels of the iris or cornea are another possible source of traumatic hyphema. Blood in the vitreous can find its way into the anterior chamber if the eye is aphakic or has a subluxated lens.

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ABSORPTION OF HEMORRHAGE

Blood leaves the anterior chamber by way of the trabecular meshwork, and the juxtacanalicular tissue, or Schlemm's canal. Jl - 16 The iris is probably insignificant as a source of absorption of blood,12 although it can be a source of fibrinolysin. 15 ,17 Fibrinolysin is important in

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Fig 2. Usual pathogenesis of traumatic hyphema. Ocular contusion indents cornea, raises intracameral pressure, and produces tear in anterior face of ciliary body (left arrow) or cyclodialysis (right arrow). Modified from a concept of R. N. Shaffer, MD, San Francisco, as cited by H. D. Hoskins, MD.4

freeing erythrocytes from fibrin clots, so that the red blood cells can escape by way of the meshwork. SECONDARY HEMORRHAGE

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Secondary hemorrhages (" rebleeds") occur in 0 to 65% of patients with traumatic hyphema, depending on the extent of the initial hemorrhage, the treatment, and the series of patients being reported. 2,18-22 My review of the literature

and that of others,23,24 indicate that the overall incidence of rebleeding is probably about 20 to 25%. Most secondary hemorrhages occur from two to five days after the initial injury, and nearly all occur before the seventh day.7· 19 ,2o,24 The pathogenesis of rebleeding is not known. It may be related to fibrinolysis and retraction of clots 15 .20 ,21 or to bleeding of fragile new capillaries. 25 Rebleeds are sometimes multiple or continual.

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Fig 3. Tear in anterior face of ciliary body (traumatic recession of the angle; arrow). Longitudinal ciliary muscle fibers (L) remain attached to scleral spur. Note blood (B) in anterior chamber (hematoxylin and eosin x 30).

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Fig 4. Traumatic cyclodialysis. The ciliary body (C) is separated completely from the scleral spur, producing a cleft in the supraciliary space (S) (hematoxylin and eosin x 30).

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COMPLICATIONS Aside from associated mJuries, the major complications of traumatic hyphema are glaucoma and blood staining of the cornea (Table 2). A recently emphasized cause of glaucoma with hyphema is obstruction of aqueous outflow by sickled erythrocytes. Goldberg29 has shown that patients with hyphema and sickling hemoglobinopathies (AS, SC, and perhaps others) can have a higher percentage of sickled erythrocytes in the anterior chamber than in the peripheral blood and that such patients are apt to develop glaucoma with relatively small hyphemas. These patients seem also to be highly susceptible to optic-nerve damage, and even to occlusion of the central retinal artery, after only mild or moderate elevations of intraocular pressures. Blood staining of the cornea is the result of impregnation of the corneal stroma by .hemoglobin and small amounts of hemosiderin (Fig 5).8 The stroma shows rust-brown discoloration and loss of normal relucency (Fig 6), seen first only in the deep stroma and only with the aid of the slit lamp. Later, blood staining can affect

the full thickness of the stroma and can cause substantial loss of vision (Fig 7). Factors that predispose to the development of blood staining are: (1) a large amount of blood in the anterior chamber;23.3o (2) prolonged duration of hyphema;30,31 (3) increased intraocular pressure,23,30 and (4) dysfunction of the corneal endothelium. 23 ,3o

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PROGNOSIS The larger the hyphema, the worse the prognosis. Small hyphemas usually disappear within four or five days.24 Those that occupy half or more of the anterior chamber (grade II or III) are more likely to be associated with delayed clearing, glaucoma, blood staining, rebleeding, and poor visual resuits. 2,22 The chance of recovering visual acuity of 20150 or better is 75-90% with grade I hyphemas ;2,24 65 - 70% with grade II ;2,24 and 25-50% with grade III.2,23,24 About 25% of patients with grade I hyphemas experience secondary hemorrhages, as compared with 65% of those with grade III.2 Rebleeding worsens the prognosis,4,19,32 but only because secondary hemorrhages are likely

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Table 2. Complications of Traumatic Hyphema

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Early glaucoma Trauma to meshwork Obstruction of meshwork by blood or inflammatory debris Erythrocytes Normal: free or clotted Sickled Leukocytes and fibrin Hemolytic glaucoma 26 (lysed and degenerated red blood cells, hemoglobin, bilirubin, iron, macrophages) Ghost-cell glaucoma 27 (rigid, degenerated red blood cells from vitreous hemorrhage of 7 -30 days) Phacolytic glaucoma Pupillary block "Collar-button" clot 42 Swelling or rupture of lens Late glaucoma Traumatic fibrosis and atrophy of meshwork (with or without postcontusion angle deformity) Hemosiderotic glaucoma 28 (fibrosis from iron in meshwork) Ghost-cell glaucoma 27 Peripheral anterior synechiae Pupillary block Posterior synechiae Swelling or rupture of lens Obstruction of angle by proliferation of corneal endothelium and Descemet's membrane Corticosteroid-induced glaucoma Blood stai ni ng of cornea Prolonged hypotony

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to be larger than primary ones ;2,24,32 about one-third of rebleeds are of grade III severity.30 The visual prognosis for a hyphema of a given grade of severity is unchanged whether the hemorrhage is primary or secondary. The incidence of glaucoma with rebleeds is at least 50%.32-34 There is danger of damage to the optic nerve if the intraocular pressure remains above 50 mm Hg for more than five days;30,35 above 45 mm Hg for more than one week,4 or above 35 mm Hg for more than two weeks. 30 ,35 These guidelines apply only to relatively young and healthy optic nerves. The risks are greater for patients who are of advanced age or who have vascular disease. The patient with a sickling hemoglobinopathy is predisposed to develop stagnation of blood flow to the optic nerve and so may be unable to tolerate pressures above 25 mm Hg for more than a day or twO. 29 About 6 to 10% of patients with traumatic hyphema develop late glaucoma in association with postcontusion deformity of the angle. 4 ,8.23 The glaucoma can appear many years after the injury and is usually associated with recession of at least half of the angle. Blood staining of the cornea is apt to develop

when the intraocular pressure stays above 25 - 30 mm Hg for more than six days in an eye with grade III hyphema. 23 ,24,30 Blood staining clears, first peripherally (Fig 7), but may require several months to two or three years to do SO.9,23

MANAGEMENT The management of hyphema begins with examination of the patient. Examination of the traumatized eye in general, and of the eye with hyphema in particular, has been detailed elsewhere,35.36 but a few points are Worthy of emphasis. Diseases or drugs that might contribute to abnormal bleeding or clotting, such as aspirin or anticoagulants, should be asked about when taking the patient's history. If the patient is black, a screening test for sickle hemoglobin or a hemoglobin electrophoresis should be performed as soon as possible. 29 A site of bleeding should be looked for, especially in the presence of persistent or black-ball hyphema; an area of red blood in the periphery of an anterior chamber that is otherwise filled with dark blood sometimes indicates a site of active or continual bleeding. Gonioscopy should be avoided until the danger of rebleeding has passed. It can be too traumatic for an eye with hyphema, and its findings would have no bearing on initial therapy. In most _cases I prefer to avoid dilating the pupil for the purpose of examining the fundus because it is possible, although uncertain, that the use of cycloplegic agents delays the absorption of blood15 or increases the incidence of secondary hemorrhage. 33 .37 As is true of the findings of gonioscopy, it is unlikely that the discovery of abnormalities of the posterior segment would influence early treatment. Even with pupillary dilation, it is often impossible in the presence of hyphema to perform more than a cursory examination of the posterior segment; as much information might be obtained by measurement of visual acuity, biomicroscopic examination of the media, plotting of visual fields, ultrasonography, or radiography to detect foreign bodies. Admittedly, there is some evidence that cycloplegic agents are not harmful,18 and even that they may be beneficial,t9 so pupillary dilation is justifiable in any case in which early examination of the fundus is thought to be important. SITUATIONAL TREATMENT

Practitioners should no longer feel compelled to treat hyphema patients ritualistically with

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Fig 5. Histopathology of blood staining of the cornea. Dots in corneal stroma consist offree hemoglobin and small amounts of hemosiderin (hematoxylin and eosin x 2(0) .

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Fig 6. Mild blood staining of the cornea, seen as a r ust-brown haze in the deep stroma (arrow).

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Fig 7. Severe blood staining of the cornea. Note tendency for spontaneous clearing, beginning in the periphery. Reprinted with permission from Grayson M, Wilson FM II. Traumatic hyphema. In: Freeman HM, ed. Ocular Trauma. New York: Appleton-Century-Crofts, 1979; 145-9.

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strict bed rest, binocular patching, and sedation. Controlled and prospective studies indicate that it makes little difference whether hospitalized patients are confined to bed or are allowed to ambulate, and that it is unimportant whether they are given one, two, or no patches. 7,18,22 It has been said that patients who are hospitalized within 24 hours after injury have a better prognosis than do those who enter the hospital later. 24 I know of no studies that have compared hospitalization with home-care, but the opinion has been expressed that home-care, with avoidance of strenuous activity, is acceptable. 15 The need to examine the patient at least daily is probably the strongest argument in favor of hospitalization. 35 I hospitalize nearly all patients with traumatic hyphema. I patch (only) the injured eye but consider the application of a protective metal shield to be more important. I allow free ambulation within the hospital room but instruct the patient to avoid bending far forward with the head low, lying on the side of the injury, and lying in the prone position. I elevate the head of the bed 30 to 45 degrees so as to lower the pressure in the ocular vasculature and to allow for

gravitation of blood and fibrin away from the pupi1. 30,35 I advise against reading but allow the watching of television. MEDICAL TREATMENT

Many drugs have been used in attempts to treat traumatic hyphemas: miotics, cycloplegics, adrenergics, vitamins, calcium, rutin, estrogens, anticoagulants, proteolytic enzymes, corticosteroids, carbonic anhydrase inhibitors, osmotic agents, and others. 15 For nearly every study that has purported to show benefits derived from any of these agents, there has been at least one contradictory study that showed no effect or even a deleterious effect,18 Havener reviewed the subject in detail and concluded that: " ... the spontaneous course of hyphema is totally unchanged by any form of medical management. "15 I agree. The outcome depends far more on the nature and severity of the injury than on any medical treatment that the physician might prescribe. There is no harm in using a nontoxic, topical antibiotic, eg, sulfacetamide, for prophylaxis of infection of corneal abrasion or even for placebo effect. Otherwise, I use no medications

in the routine treatment of hyphema itself, but I do not hesitate to use any medications that might be indicated for the symptoms or complications of hyphema. When necessary, I use cycloplegic agents for ciliary pain or for prevention of posterior synechiae; miotics and other antiglaucoma drugs for increased intraocular pressure; and corticosteroids for severe iridocyclitis, fibrin, threatened synechiae, or inflammatory glaucoma. There is an unconfirmed report that the use of oral corticosteroids reduce the incidence of secondary hemorrhage. 38 Yet the use of topical corticosteroids, which is known to produce higher levels of drug in the anterior chamber, has been found not to be beneficial in a controlled, prospective study.18 Aminocaproic acid20 and tranexamic acid39 are antifibrinolytic agents. Administered orally, each has been reported to be efficacious in preventing secondary hemorrhage, presumably by inhibiting lysis of clots in damaged vessels. The inhibition of fibrinolysis probably also delays absorption of hyphema. 20 These studies are as yet unconfirmed, and the dangers of these drugs are not well understood. Antifibrinolytic therapy must be considered still to be experimental, but it could be resorted to in difficult cases. Sedation to prevent rebleeding has been largely abandoned. Light sedation itself does not bring about restriction of activity, and heavy sedation can cause confusion, apprehension, depression, and fatigue. Barbiturates suppress the rapid eye movements (REMs) of sleep,40 but there is no evidence that this effect prevents rebleeds. Moreover, REMs can be inhibited for only very limited periods of time; their suppression can interfere with the recuperative powers of sleep and can produce the same symptoms as does loss of sleep. Benzodiazepines do not affect REMs, but interfere with stages three and four of sleep.40 Aspirin and alcohol inhibit platelet aggregation and should be avoided. 15.21 SURG leAL TREATMENT

Surgery for hyphema is not innocuous41 and should be avoided whenever possible. Risks include damage to the cornea, iris, or lens; inadvertent extraction of the iris; prolapse of intraocular contents; renewed bleeding; increased inflammation and formation of synechiae; and postoperative glaucoma. Some studies have suggested that surgical intervention may actually worsen the overall prognosis.18.37.41 The indications for surgery are said to be: (1) uncontrolled glaucoma; (2) early blood staining of the cornea; (3) large or total hyphemas of

more than nine days' duration; and (4) detection of a site of active bleeding. Elevated intraocular pressures that cannot be controlled medically and that have reached dangerous levels are an obvious and undisputed indication for surgery. These levels are lower for patients who have sickling hemoglobinopathy, and they should be treated with paracentesis of the anterior chamber if the pressure remains above 25 mm Hg for more than one day.29 There is no reason to operate for blood staining unless it is mild. Evacuation of hyphema cannot bring about restoration of vision once the cornea has become opaque. It can be argued that even early blood staining is not an indication for surgery ,9 and I do not consider the risks of surgery to be justified for this generally self-limited problem. The dangers of mild blood staining may have been overrated,23 as not all cases progress. Even advanced blood staining usually clears; if it does not do so within a reasonable length of time, keratoplasty can be performed and probably poses fewer risks than does operating for hyphema. A large or total hyphema is not itself an indication for surgery unless there is no sign of clearing after nine days-the time after which peripheral anterior synechiae are likely to develop.7 Total hyphema virtually always causes increased intraocular pressure. If the pressure is normal or low, especially if extensive subconjunctival hemorrhage is present, surgical exploration for rupture of the globe is indicated.35 Surgery for hyphema should be preceded by the administration of intravenous mannitol if the intraocular pressure is elevated. Ocular compression should be avoided. The simplest procedures are paracentesis29 or the release of blood through a smalllimbal inc ision. 25 If these approaches are not successful, an attempt can be made to irrigate blood from the anterior chamber; this requires enlarging the first incision or making a second one so as to allow for the release of fluid and blood. Aspiration can be combined with irrigation by means of a simple two-needle technique or with the aid of an irrigation-aspiration instrument inserted through a single limbal incision. Ultrasonic vibration of the tip is unnecessary,23 and cutting instruments should not be used unless visualization is good. Fibrinolytic agents such as fibrinolysin34 or urokinase18 can be used for irrigation if the blood is partially clotted. A large limbal incision is preferable for dealing with black-ball hyphema. 23 ,35 Four or five days after hemorrhage may be the ideal time for intervention, as that is when the clot begins to retract from surrounding tissues but is not yet

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organized and attached to themY Earlier surgery may hold more risk for renewed bleeding. Upon opening the eye, the clot may prolapse spontaneously; if not, it can be rolled or scooped gently from the eye with a cotton swab, cellulose sponge, or lens loop. Mild pressure over the inferior limbus can help to express the clot. The clot can be extracted with a cryoprobe,42 but great care must be taken to avoid incorporating the iris within the ice ball. Some practitioners,23 including myself, believe that extraction with a cryoprobe (or with forceps) is too dangerous to be attempted unless the position of the iris can be visualized clearly. Occasionally, a site of active bleeding can be treated.23 If it is encountered after opening the anterior chamber, it may be possible to cauterize it. More often, the bleeding is from the ciliary body and cannot be reached. This kind of bleeding might be stopped by applying diathermy to the overlying sclera. 23 ,43 A large air bubble can be put into the anterior chamber to tamponade the source of bleeding; but the air pressure must be considerable to stop bleeding, and such pressure cannot be maintained for long because the air tends to absorb quickly. Techniques have been described for the surgical treatment of prolonged hypotony following traumatic cyclodialysis. 44

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SUMMARY The most common cause of bleeding in traumatic hyphema is a tear in the anterior face of the ciliary body, with traumatic cyclodialysis being next in frequency. The prognosis depends on the size of the hyphema and that of any secondary hemorrhage and, ultimately, on the severity of the injury. The major complications are glaucoma (early or late) and blood staining of the cornea. Binocular patching, strict bed rest, and sedation are no longer advised. No medical therapy has been shown to be reliably beneficial for hyphema itself, although drugs may be used as indicated for complications . Surgical intervention is hazardous and should be used only when absolutely necessary, usually for intractable glaucoma.

REFERENCES 1. Roy FH. Ocular Differential Diagnosis. 2nd ed. Philadelphia: Lea and Febiger, 1975; 283-5. 2. Edwards WC , Layden WE . Traumatic hyphema : a report of 184 consecutive cases . Am J Ophthalmol 1973; 75:110 - 6

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3. Lebekhov PI, landiev 1M. Statistika i klassifikatsiiagifemy. Oftalmol Zh 1972 ; 27:327-30. 4. Hoskins HD : Secondary glaucomas. In : Heilmann K, Richardson KT, eds. Glaucoma Conceptions of a Disease. Pathogenesis , Diagnosis, Therapy. Philadelphia: WB Saunders, 1978; 376 - 89. 5. Blanton FM. Anterior chamber angle recession and secondary glaucoma: a study of the aftereffects of traumatic hyphemas. Arch Ophthalmol 1964; 72:39-43. 6 . Howard GM , Hutchinson BT , Frederick AR Jr . Hyphema resulting from blunt trauma: gonioscopic, tonographic, and ophthalmoscopic observations following resolution of the hemorrhage. Trans Am Acad Ophthalmol Otolaryngol 1965; 69:294-306. 7. Read J, Goldberg MF. Comparison of medical treatment for traumatic hyphema. Trans Am Acad Ophthalmol Otolaryngol 1974; 78799-815. 8. Yanoff M, Fine BS. Ocular Pathology. A Text and Atlas. Hagerstown : Harper & Row, 1975; 143-8. 9. Keeney AH. Trauma of the globe, adnexa, and orbital walls: prophylaxis and immediate therapy. In: Harley RD, ed . Pediatric Ophthalmology. Philadelphia: WB Saunders, 1975; 413- 28. 10. Wolff SM, Zimmerman LE. Chronic secondary glaucoma associated with retrodisplacement of iris root and deepening of the anterior chamber angle secondary to contusion . Am J Ophthalmol 1962; 54:547-63. 11. Sinskey RM, Krichesky A, Henrickson R. (Abstract) Experimental hyphema in rabbits. Am J Ophthalmol 1957; 43:292. 12 Sinskey RM, Krichesky AR. Experimental hyphema in rabbits . III. Effect of iridectomy, iridencleisis, and temporary elevation in intraocular pressure on the rate of absorption. Am J Ophthalmol 1961; 52 :58-61. 13. Cahn PH, Havener WHo Factors of importance in traumatic hyphema. With particular reference to and study of routes of absorption. Am J Ophthalmol 1963 ; 55 :591-7 . 14. HqJrven I. Erythrocyte passage into Schlemm's canal. Am J Ophthalmol 1972; 74:168-9. 15. Havener WHo Ocular Pharmacology. 4th ed. St. Louis: CV Mosby, 1978 ; 330-341; 703-19. 16. Shabo AL, Maxwell DS. Observations on the fate of blood in the anterior chamber: a light and electron microscopic study of the monkey trabecular meshwork. Am J Ophthalmol 1972; 73:25 - 36. .17 . . Pandolfi M, Kwaan HC. Fibrinolysis in the anterior segment of the eye. Arch Ophthalmol 1967; 77:99-104. 18. Rakusin W. Traumatic hyphema. Am J Ophthalmol 1972; 74:284-92. 19. Gilbert HD, Jensen AD. Atropine in the treatment of traumatic hyphema. Ann Ophthalmol 1973; 5: 1297-1300. 20. Crouch ER Jr, Frenkel M. Aminocaproic acid in the treatment of traumatic hyphema. Am J Ophthalmol 1976; 81 :355-60. 21 . Crawford JS, Lewandowski RL, Chan W. The effect of aspirin on rebleeding in traumatic hyphema. Am J Ophthalmol 1975; 80:543-5. 22. Edwards WC, Layden WE. Monocular versus binocular patching in traumatic hyphema. Am J Ophthalmol 1973; 76:359-62 . 23. Paton D, Goldberg MF. Management of Ocular Injuries. Philadelphia: WB Saunders, 1976; 288-303.

24, Sham mas HF, Matta CS, Outcome of traumatic hyphema, Ann Ophthalmol 1975; 7:701-6, 25, Callahan WP, Injuries of the eye, In: Toronto Hospital for Sick Children, Dept of Ophthalmology, The Eye ih Childhood, Chicago: Year Book Medical Publishers, 1967; 310-2, 26, Fenton RH, Zimmerman LE, Hemolytic glaucoma: an unusual cause of acute open-angle secondary glaucoma, Arch Ophthalmol 1963; 70:236-9, 27, Campbell DG, Simmons RJ, Grant WM, Ghost cells as a cause of glaucoma, Am J Ophthalmol 1976; 81 :441-50, 28, Winter FC, Ocular hemosiderosis, Trans Am Acad Ophthalmol Otolaryngol 1967; 71 :813-9, 29, Goldberg MF, Sickled erythrocytes, hyphema, and secondary glaucoma, I. The diagnosis and treatment of sickled erythrocytes in human hyphemas, Ophthalmic Surg 1979; 10(4):17-31, 30, Gorin G, Clinical Glaucoma, New York: Marcel Dekker Inc, 1977; 337-51, 31, Brodrick JD, Comeal blood staining after hyphaema, Br J Ophthalmol 1972; 56:589-93 32, Thygeson P, Beard C, Observations on traumatic hyphema, Am J Ophthalmol 1952; 35:977-85 33, Darr JL, Passmore JW, Management of traumatic hyphema, A review of 109 cases, Am J Ophthalmol 1967; 63:134-6, 34, Kwitko ML, Hyphema, In: Kwitko ML, ed, Surgery of the

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36,

37, 38, 39,

40,

41, 42,

43,

44,

Infant Eye, New York: Appleton-Century-Crofts, 1979; 291-5, Grayson M, Wilson FM II. Traumatic hyphema, In: Freeman HM, ed, Ocular Trauma, New York: Appleton-Century-Crofts, 1979; 145-9, Freeman HM, McDonald PR, Scheie HG, Examination of the traumatized eye and adnexa, In: Freeman HM, ed, Ocular Trauma, New York: Appleton-CenturyCrofts, 1979; 1-13, Pilger IS, Medical treatment of traumatic hyphema, Surv Ophthalmol 1975; 20:28-34, Yasuna E. Management of traumatic hyphema, Arch Ophthalmol1974; 91:190-1, Bramsen T, Traumatic hyphema treated with the antifibrinolytic drug tranexamic acid, Acta Ophthalmol 1976; 54:250-6, Update on sedative hypnotics, Institute of Medicine report on use of sleeping pills, FDA Drug Bull 1979; 9:16-18, Read J, Traumatic hyphema: surgical medical management. Ann Ophthalmol 1975; 7:659 -70, Sears ML, Surgical management of black ball hyphema, Trans Am Acad Ophthalmol Otolaryngol 1970; 74820-6, Gilbert HD, Smith RE, Traumatic hyphema: treatment of secondary hemorrhage with cyclodiathermy, Ophthalmic Surg 1976; 7(3):31-5, Paton D, Goldberg MF, Management of Ocular Injuries, Philadelphia: WB Saunders, 1976; 239-40,

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