sign in sign up
<<
Home , Ghost cell glaucoma, Hyphema, Intraocular pressure

Introduction he following case report is to be used as a teaching guide appropriate for third- and T fourth-year optometry stu- dents as well as optometry residents. The case report describes a patient with as a result of closed- in- jury who develops a number of associ- ated sequelae of blunt force trauma to include increased , vitreous hemorrhage and angle reces- sion with . The paper dis- cusses appropriate management and treatment options as well as short- and Traumatic Hyphema: long-term complications of traumatic hyphema. This case demonstrates the A Teaching Case Report importance of identifying clinical find- ings related to poor visual outcome and Priscilla Lenihan, OD how to manage them appropriately. Dorothy Hitchmoth, OD, FAAO Learning Objectives At the conclusion of this case discus- sion, participants should be able to: 1. Discuss of ini- tial presentation of traumatic hy- phema Abstract 2. Discuss appropriate treatment for Hyphema is the presence of blood in the anterior chamber of the eye and is most often the initial presentation of traumat- caused by blunt ocular injury. Hyphema, its complications and associated ocular ic hyphema injuries can pose a serious threat to vision and therefore require appropriate medi- 3. Recognize short- and long-term cal management and careful examination and follow-up. This teaching case report complications associated with trau- reviews the management of traumatic hyphema and discusses treatment options, po- matic hyphema tential complications and visual prognosis. 4. Recognize initial and long-term Key Words: traumatic hyphema, closed-globe injury, medications, trau- clinical findings related to poor matic glaucoma visual outcome as a result of trau- matic hyphema 5. Discuss appropriate treatment op- tions for management of increased intraocular pressure (IOP) or glau- coma that results from hyphema or associated complications 6. Provide proper patient education on self-care needed to avoid com- plications. Key Concepts 1. Pathophysiology and natural his- tory of traumatic hyphema and its complications 2. Risk factors associated with poor visual prognosis Dr. Lenihan is a Staff Optometrist for the VA Maine Healthcare System at the Bangor Community Based Outpatient Clinic in Bangor, Maine. 3. The role of medication in reducing Dr. Hitchmoth is Chief of Optometry at the White River Junction Veterans Affairs Medical the risk of developing complica- Center in White River Junction, Vt. tions

Optometric Education 110 Volume 39, Number 3 / Summer 2014 4. Medications, activities and diag- significant for mellitus type 2, were clear of defect with nostic testing to avoid in the pa- hypertension, mixed hyperlipidemia, fluorescein staining and there was tient with traumatic hyphema. obstructive sleep apnea, insomnia, negative Seidel sign. Anterior chamber , post-traumatic stress angles were open to grade III Van Discussion Points disorder and adjustment disorder with Herick OU. The anterior chamber of 1. Anatomical considerations of mixed anxiety. His list of medications the right eye was well-formed, clear closed-globe injury included , , and quiet. The left anterior chamber a. bupropion, tramadol, sertraline, was well-formed but 2+ red blood glyburide, metformin, lisinopril, cells and a hyphema that measured b. Anterior chamber and angle metoprolol, simvastatin, nifedipine a vertical height of 2.2 mm were c. and and prazosin. noted (Figure 1). The right iris was d. Vitreous and posterior pole normal and without rubeosis; the left Entering visual acuities without iris was dyscoric (irregularly shaped) 2. Treatment considerations (initial correction were 20/20 OD and 20/150 and free of rubeosis. Goldmann and subsequent) OS. The right was round and tonometry revealed pressures of 14 a. Worsening of the condition responsive to light and measured mmHg OD and 18 mmHg OS. b. Development of complications 2.5 mm. The left pupil was fixed, The patient was dilated with two mid-dilated, and measured 4.0 mm. drops of 1.0% and two c. Improvement of the condition (EOMS) were drops of 2.5% phenylephrine OS. d. Contraindications and side ef- smooth, accurate, full and extensive No clear view of the left fundus was fects of medication (SAFE) OU. There was no irregularity observed with either binocular indirect of the left orbital bone or sinus 3. Clinical examination ophthalmoscopy (BIO) or 90D crepitus on palpation of the and due to the debris in the anterior a. Slit lamp and fundus examina- adnexal structures. Slit lamp exam tion chamber. A B-scan ultrasonography revealed clear lids and lashes OD was performed OS, which revealed b. Ocular ultrasound and mild edema and of no , vitreous c. the upper and lower left lids without hemorrhage or subluxated lens. lacerations. The and d. Imaging of the globe, orbit were clear of defect or hemorrhage The patient was diagnosed with and adnexal structures OD. The left eye showed a traumatic hyphema OS and was 4. Visual prognosis subconjunctival hemorrhage involving prescribed prednisolone acetate 1% a. Complications and associated the entire bulbar conjunctiva. The ophthalmic solution QID OS and injuries b. Risk factors Figure 1 Patient RM seen with a hematoma of the upper and lower lids, c. Medical and surgical interven- dense subconjunctival hemorrhage and grade 1 hyphema of the tion. left eye. Case Description

Patient RM, a 60-year-old Caucasian male, presented to the eye clinic at the White River Junction Veterans Affairs Medical Center on Aug. 21, 2012, complaining of severe pain, and sensitivity to light in the left eye. The patient reported someone threw a rock at him that hit his left eye the previous evening around 7 p.m. The patient had glasses, but was not wearing them at the time of the injury. RM denied flashes and . RM was an established patient at the eye clinic. His ocular history included a branch retinal vein occlusion in the right eye diagnosed in 2010, early bilateral and mild non- proliferative diabetic without clinically significant OU. His medical history was

Optometric Education 111 Volume 39, Number 3 / Summer 2014 atropine sulphate 1% ophthalmic stable. An orbital X-ray was ordered TID. Acetazolamide 500 mg PO BID solution BID OS. RM was released and was negative for orbital or other was added to the patient’s medication from the clinic and given instructions facial bone fractures. Medication regimen, which otherwise remained for self-care at home. He was educated and instructions remained the same the same. Patient medical history, in- to shake the bottle of topical steroid with the exception that timolol 0.5% cluding allergies and kidney function, before instillation. He was also given ophthalmic solution was replaced was carefully reviewed prior to initiat- a non-pressure eye patch to reduce with dorzolamide 2%/timolol 0.5% ing oral acetazolamide. The patient when outdoors or in (Cosopt) BID OS. The patient was was also educated on the side effects bright light only. In addition, the instructed to return to clinic in two of acetazolamide to include increased patient was given a pair of clear days and to continue all other self-care urination, metallic taste and tingling in protective goggles to be worn during instructions. the extremities. IOP remained elevated sleep. He was instructed to sleep at an at 36 mmHg OS the following day. angle of approximately 45 degrees, to Summary of Visits and Pachymetry revealed thick and asym- rest as much as possible, and to avoid Clinical Outcomes metric corneas (607 um OD, 662 um any strenuous activity. A follow-up OS); thickness was significantly greater The traumatic hyphema slowly resolved appointment was scheduled for 24 in the left eye due to corneal edema that after nine days. The anterior segment, hours, and the patient was instructed to had developed. The patient’s medica- level of hyphema and IOP were moni- return to clinic sooner if he developed tion was kept the same, and the follow- tored at each visit. Retinal examina- visual changes or increased pain. ing day his IOP dropped to 21 mmHg tions through direct fundoscopy and OS. Over the next several visits, vision B-scan (Figure 2) continued through- The following day, RM reported the continued to improve, anterior seg- out the course of follow-up as well to pain in the left eye had improved. He ment and corneal edema monitor for cystoid macular edema was using his drops as instructed and slowly resolved, and intraocular pres- and to ensure the vitreous hemorrhage had worn the protective goggles at sure dropped and stabilized. Predniso- was resolving without additional com- night. RM denied flashes but noted lone acetate 1%, Cosopt and acetazol- plications such as retinal tear, retinal that vision in the left eye fluctuated. amide were correspondingly tapered detachment or vitreoretinal traction. Visual acuity was measured at 20/80-2 and discontinued. See Appendix A A encountered during OS; EOMS were SAFE OU. There was for a detailed account of the patient’s resolution of the hyphema was a rise in no pain or crepitus on palpation of the pertinent exam findings. Final best cor- IOP. One week after the initial trauma, left orbit and adnexa. Anterior segment rected visual acuity was 20/20- in the intraocular pressure increased to 34 exam was the same with the exception left eye. of the hyphema which was measured mmHg OS despite the use of Cosopt at 2.1 mm. IOPs were measured to be Gonioscopy was performed 12 weeks 14 mmHg OD and 26 mmHg OS. The lens was well-positioned with mild nuclear sclerotic cataracts in both Figure 2 eyes. BIO of the posterior segment OS B-scan of the left eye taken nine days after the initial trauma revealed diffuse vitreous hemorrhage showing a mild, diffuse vitreous hemorrhage seen as short lines with noted to be greatest in and faint dots within the vitreous cavity. the inferior view. The had a cup/disc ratio of 0.20 with healthy and distinct rims. The macula was clear and the periphery was flat and intact 360 degrees. RM was instructed to continue with atropine sulphate 1% ophthalmic solution BID OS and prednisolone acetate 1% ophthalmic solution QID OS. Timolol 0.5% ophthalmic solution BID OS was added to treat the . The patient was instructed to discontinue oral aspirin after consultation with his primary care physician. The patient was instructed to return to clinic again the following day. The next day, in the left eye, vision measured 20/50-, the hyphema was measured to be 2.0 mm, and intraocular pressure was measured at 25 mmHg. All other findings were

Optometric Education 112 Volume 39, Number 3 / Summer 2014 after the initial trauma with a three- mirror lens. The right eye was open to Figure 3 ciliary body in all quadrants with 2+ Gonioscopic view of the inferior angle of the left eye showing pigmentation of the trabeculum. The heavy pigmentation and clumps of pigment on the iris and angle left eye was open to ciliary body tempo- structures. rally and nasally. The inferior angle was open to scleral spur with 4+ pigmenta- tion and pigment clumping on the iris (Figure 3). The superior angle revealed four clock hours of angle recession with iridodialysis (Figure 4). Literature Review Hyphema is defined as a collection of blood in the anterior chamber. The se- verity of hyphema can vary from dif- fuse red blood cells circulating in the aqueous humor to a hemorrhage that fills the entire anterior chamber. Most often hyphema is caused by trauma or intraocular surgery, but may also occur spontaneously in patients with rubeo- sis iridis, vascular tufts at the pupillary margin, , iris , , Figure 4 keratouveitis, , hemophilia, Gonioscopic view of the superior angle of the left eye showing or Von Willebrand iridodialysis. Ciliary processes (black arrows) are visible in the cleft disease. Hyphema may also be associ- between the iris and cornea. ated with drugs that alter or thrombin function, such as aspirin or .1 Hyphemas are graded according to ex- amination features as noted in Table 1. The grading system is helpful for pre- dicting clinical outcomes, which assists in educating the patient about short- and long-term prognosis. Epidemiology The mean annual incidence of hyphe- ma from all causes is approximately 17 per 100,000.1 The majority of hyphe- mas occur in males (75%-78%) with a median age of 15.5 to 18.2 years.2 A study of 238 patients with traumatic hyphema showed that the leading cause of trauma was projectile stones, and the majority of the trauma occurred as a result of street violence (43%) Table 1 and accidents in the home (33%). In Hyphema Grading children, siblings and friends were re- sponsible for most of the trauma, and Microhyphema Red blood cells suspended in the AC without the formation of a layered clot in adults the main cause of trauma was Grade 1 Layered blood occupying less than one-third of the AC 3 accidents. Another significant source Grade 2 Layered blood filling one-third to one-half of the AC

of injury is sports, which accounted for Grade 3 Layered blood filling one-half to less than the total volume of theAC 60% of traumatic hyphemas in a dif- Blood filling the entire volume of the AC ferent study.4 High-risk sports in which Grade 4 the ball hits the eye include baseball, “Eight-ball” Total hyphema of blackish-purplish color softball, basketball, soccer and paint- AC = anterior chamber.

Optometric Education 113 Volume 39, Number 3 / Summer 2014 ball. The stick or racquet is more likely creasingly hypoperfused and hypoxic, activities should remain restricted until to be the source of injury in other high- thereby perpetuating a cycle in which blood resorption occurs.10 risk sports such as hockey, racquetball further sickling and sludging of eryth- 5 9 Iritis is common in patients presenting and squash. rocytes occurs. Therefore, the inci- with traumatic hyphema. Corticoste- Pathophysiology dence of elevated IOP in the presence roids are prescribed to reduce the in- of hyphema is higher in patients with Hyphema that occurs as a result of flammation and cycloplegic drugs are these disorders, and may occur even in used to improve patient comfort and trauma is typically caused by dam- 6 cases of small hyphemas. prevent the formation of posterior syn- age to the major arterial circle and its 1 branches as a result of a tear in the iris Associated Trauma echia. Cycloplegics are or ciliary body.6 Blunt trauma causes The pattern of injury from blunt trau- drugs. They temporarily inhibit acetyl- antero-posterior compression of the ma is due to the equatorial expansion choline receptors in the iris sphincter globe and simultaneous equatorial ex- of the globe. These injuries have been muscle and ciliary body. This results pansion. This expansion creates stress described as seven rings and include: in pupillary , which helps re- on the structures of the anterior cham- radial tears of the pupillary sphincter, duce the risk of posterior by ber angle, causing a tear of the ciliary iridodialysis, angle recession, cyclodi- minimizing contact between the poste- body or iris stromal vessels.1 alysis, tear, zonu- rior iris and the anterior lens capsule. Inhibition of acetylcholine receptors in Patients with hyphema may initially lar dehiscence and retinal dialysis. The presence of these clinical findings, even the ciliary body paralyzes the muscle, present with low or high IOP. A low which relaxes ciliary spasm and reduces years after the event, provides evidence 11 IOP may be the result of an accom- 8 pain. In addition, both cycloplegics panying iritis causing reduction in of previous blunt trauma. Blunt ocular trauma may also cause iridoschisis (sep- and corticosteroids may reduce the risk aqueous production or due to tempo- of secondary hemorrhage. Steroids sta- rary increase in outflow from the dis- aration of the layers of the iris stroma) iritis, cataracts or chorioretinal injury.6 bilize the blood-ocular barrier and di- ruption of structures in the anterior rectly inhibit fibrinolysis.1 Cycloplegics 6 chamber angle. More commonly, IOP Treatment and Management minimize iris movement and stress on rises acutely because red blood cells and Management of hyphema from all the original ruptured vessels.12 immune-inflammatory cells block the causes is aimed at preventing secondary trabecular meshwork.7 Fresh red blood In patients with elevated IOP higher hemorrhage, preventing further trauma than 25 mmHg, beta blockers and car- cells are able to pass through the tra- to the eye, promoting the settling of becular meshwork without much diffi- bonic anhydrase inhibitors (CAIs) are blood to the bottom of the anterior 8 culty; however, the presence of an over- usually first-line treatment. Topical chamber and controlling traumatic CAIs must be used cautiously in pa- whelming number of cells in addition .4 Close monitoring is essential to plasma, fibrin and other cellular de- tients with sickle cell hemoglobinopa- so that treatment for associated com- thies because these medications may bris can lead to a transient obstruction plications is initiated promptly if they of outflow.6 Swelling of the trabecular lower the aqueous pH and promote occur. 10 meshwork (trabeculitis) may also be further sickling of the blood cells. If a contributing factor in limiting out- Hospitalization or outpatient care topical medication is not adequate in flow.8 In severe cases, acute elevation of with daily follow-up is recommended. managing IOP, an oral CAI, such as IOP may occur secondary to pupillary Hospitalization should be consid- acetazolamide and methazolamide, can block, due to a collar button-shaped ered for patients with severe injuries be prescribed. The ocular hypotensive clot involving both the anterior and or blood disorders and those who are effect of acetazolamide in tablet form posterior chambers.1 The clot prevents not capable of self-care or may be non- peaks in two hours and lasts for six the normal flow of aqueous from the compliant with the treatment regimen. hours, whereas in capsule form it peaks posterior chamber, through the space Additionally, hospitalization should be in eight hours and persists beyond 12 between the iris and lens, and into the considered for children at risk for am- hours. Acetazolamide is generally dosed anterior chamber. As a result, pressure blyopia or if child abuse is suspected. as 500 mg PO twice a day for adults. builds in the posterior chamber, push- Management consists of eye protec- For children, the recommended dose is ing the peripheral iris anteriorly which tion with plastic or metal shields, lim- 5-10 mg/kg of body weight every four then closes part or all of the trabecular ited physical activity, elevation of head to six hours. Methazolamide dosing can meshwork via apposition. posture, and avoidance of aspirin and begin with 25 mg twice a day and be other non-steroidal anti-inflammatory increased to 50 mg twice a day or up Aqueous outflow may be further ob- agents.10 Having patients sleep at a 30- to 100 mg three times a day if need- structed in patients with sickle cell 45-degree angle promotes more rapid ed. Oral CAIs are effective in lowering hemoglobinopathies. Erythrocytes in blood resorption and lowers venous IOP; however, they have many side these patients become elongated and pressure to the globe, helping to reduce effects. Common systemic side effects rigid (sickled) in the aqueous humor, IOP and to allow for clot formation include increased urinary frequency making passage through the trabecular 7 and paresthesia of the fingers, toes and 6 and resolution. Normal activities may meshwork difficult. As a result of an resume one week after the initial injury around the mouth. Other side effects increase in IOP, the anterior and pos- or rebleed. However, if blood remains include abdominal discomfort, metal- terior segments of the eye become in- in the anterior chamber after one week, lic taste, nausea and diarrhea. Higher

Optometric Education 114 Volume 39, Number 3 / Summer 2014 doses of oral CAIs may cause metabolic for aqueous outflow. Verma14 reported acid also has similar side effects, but less acidosis and should be avoided in pa- that the combination of trabeculecto- gastric side effects. Although data sug- tients with hepatic insufficiency, renal my, peripheral and manual gest that antifibrinolytic agents reduce failure, adrenocortical insufficiency, extraction of blood clots was satisfac- the risk of secondary hemorrhage, they hyperchloremic acidosis, depressed tory in lowering IOP. All patients in do not have a significant effect on visual sodium or potassium levels or severe the study had light projection acuity, acuity, and their use is controversial.4 pulmonary obstruction. Oral CAIs are corneal blood staining and an average Therefore, several authors recommend contraindicated in patients with sulfa IOP of 45 mmHg before surgery. Aver- reserving antifibrinolytics only for allergies, as CAIs belong to the sulfon- age IOP at the last follow-up visit after those patients at higher risk for second- amide class of drugs.6 If a systemic CAI surgery was 18.4 mmHg, but visual ary hemorrhage based on individual is necessary in patients with sickle cell, prognosis was still poor. Laser trabecu- patient characteristics, including race methazolamide is used because it cre- loplasty is usually ineffective in cases of and the presence of sickle cell hemoglo- ates less systemic acidosis, and therefore ocular trauma, due to the damage to binopathy.9,4 8 promotes less erythrocyte sickling, than the trabecular meshwork. Complications acetazolamide.1 Intravenous , Additional medications may be used Elevated IOP a diuretic, may also be given in cases in the treatment of hyphema as blood of uncontrolled IOP; however, extreme in the anterior chamber begins to form Elevated IOP is the most serious com- caution must be used in patients with a clot. Blood clots are cleared from plication of traumatic hyphema as it sickle cell, as diuretics induce acidosis the body through a process known as may result in optic and corneal 5 17 and volume contraction. fibrinolysis. It is during this process blood staining. Elevated IOP occurs Prostaglandins and are that the risk of rebleed is the high- in approximately one-third of all hy- generally avoided in the treatment of est.12 Antifibrinolytic agents, includ- phema patients. In general, the larger elevated IOP because of inflammation ing ϵ- (ACA) and the hyphema, the higher the risk of 1 associated with the traumatic hyphema. , are used to reduce developing increased IOP. In a study Some early studies showed that large the risk of secondary hemorrhage by of 162 patients with microhyphema, doses of topical prostaglandins resulted slowing or inhibiting the resorption of IOP was elevated (above 22 mmHg) in in inflammation and breakdown of the the blood clot within the traumatized only 8.6%, and in those patients with blood-aqueous barrier. In more recent blood vessel. ACA acts as a competitive elevated IOP there was a significantly 18 reports, a few patients developed ante- inhibitor to lysine for binding sites on higher incidence of angle recession. rior uveitis while on . Other tissue plasminogen activator, thereby Patients with sickle cell hemoglobinop- studies, however, have not shown in- inhibiting the conversion of plasmino- athies require aggressive IOP lowering traocular inflammatory effects from gen to plasmin. Plasmin is the enzyme measures, as these patients are at higher prostaglandins.6 An increase in blood- involved in the breakdown of the fibrin risk for central retinal artery occlusion aqueous barrier permeability to plasma clot. In addition to preventing the for- and optic nerve damage, even with only 9 proteins has been shown clinically after mation of plasmin, ACA also competi- marginal increases in IOP. instillation of pilocarpine.13 Addition- tively inhibits the binding of plasmin to Recurrent hemorrhage ally, induced by pilocarpine in- the fibrin clot itself.4 These actions sta- Recurrent, or secondary, hemorrhage creases the zone of contact between the bilize the fibrin clot, thereby prevent- occurs if the size of the hyphema in- iris and lens, and therefore increases the ing rebleeding while permanent vessel creases, if fresh blood is seen over the risk of posterior synechia. repair occurs.1 Side effects of systemic older and darker clot, or if dispersed ACA occur in up to 50% of patients Surgical intervention is required in red blood cells appear over the clot after and include nausea, , sys- up to 5% of hyphemas in cases of in- the initial blood has settled.1 Lysis and temic hypotension, tinnitus (less com- creased IOP, corneal blood staining, or contraction of the fibrin plug in the monly), numbness, skin rash, myalgia total hyphemas lasting more than 10 injured vessels is responsible for the re- and hematuria.15 It is contraindicated days. If the IOP remains greater than bleed, which usually occurs two to five in patients with , renal 50 mmHg for five days, or greater days after the initial injury.16 Recurrent disease, and in patients who are preg- than 35 mmHg for seven days, despite hemorrhage is associated with compli- nant, and should be used cautiously in medical management, surgery is indi- cations including elevated IOP, corneal 12 patients with hepatic, cardiovascular or cated. Anterior chamber paracentesis blood staining, optic atrophy and pe- cerebrovascular diseases. ACA in a topi- is effective for lowering IOP; however ripheral anterior synechia.1 While these cal gel form has comparable effective- it is often only a temporary measure complications can result in permanent ness as the oral form, but with few side and additional surgical intervention is 4 16 loss of vision, some studies have shown 10 effects. Karkhaneh et al found topical anticipated. Irrigation of the anterior that secondary hemorrhage is associ- ACA did not affect the rate of rebleed- chamber can be performed to remove ated with a worsening of visual progno- ing, but was associated with a longer dispersed red blood cells, and a formed sis,3,17 while others have not.19,20 blood clot can be manually extracted time for clot absorption in the anterior The highest prevalence of hyphema re- through clear corneal incisions.1 If nec- chamber. Tranexamic acid, another an- bleed in the United States is in the non- essary, is performed to tifibrinolytic agent, has a similar mech- white population. Patients with an ini- manage IOP by creating a new opening anism of action as ACA. Tranexamic tial higher grade hyphema (grade 3-4) Optometric Education 115 Volume 39, Number 3 / Summer 2014 are also at higher risk.15 In a study of 40 ghost cells are less pliable than fresh of the hyphema itself. Vision may be children with traumatic hyphema, the erythrocytes and cause approximately entirely normal to no light perception overall rate of secondary hemorrhage three times the obstruction to trabecu- with hyphema ranging from microhy- was 10.3% and was significantly higher lar outflow than an equal number of phema to “eight ball” hyphema. The in African American patients.9 Rah- fresh erythrocytes. degree of pain and photophobia is re- mani et al3 found a greater chance of can also occur with large traumatic hy- lated to the severity of associated uveitis rebleeding in patients with poor vision phemas that extend into the vitreous and the level of IOP.7 or elevated IOP at the time of presen- cavity. The ghost cells that form in the A ruptured globe must be ruled out tation. Aspirin has been shown to in- vitreous cavity migrate back into the at the initial examination. The cornea crease the risk of rebleeding. Therefore, anterior chamber weeks to months af- should be carefully evaluated for posi- it, along with other non-steroidal anti- ter the initial injury, creating another 22 tive Seidel sign to rule out full-thick- inflammatory drugs, should be avoided spike in IOP. Slit lamp examination ness laceration. Other signs of ruptured for two weeks after traumatic hyphema will reveal khaki-colored cells freely 18 globe include a deep or shallow anterior due to their antithrombotic effect. floating in the anterior chamber, or a chamber compared to the fellow eye, Acetaminophen or codeine, however, tan stripe in a background of red cells, 8 peaked or irregular pupil, iris transillu- are safe to use as an analgesic if not oth- creating the candy-stripe sign. Medical mination defects, and low IOP. Addi- erwise contraindicated for other medi- therapy is frequently sufficient to man- 10 tionally, orbital fracture must be ruled cal reasons. age IOP until the supply of ghost cells out. Signs and symptoms of orbital is exhausted, but surgery may be neces- The incidence of rebleed in patients 22 fracture include pain and restriction with microhyphema is lower. Rec- sary. on eye movement, local tenderness, chia et al18 found that only three out Traumatic glaucoma binocular , crepitus after nose- of 162 patients (1.9%) with microhy- The most common site of damage in blowing or on palpation, and hypoes- phema developed rebleed, and all three blunt ocular trauma is the anterior seg- thesia along the ipsilateral upper lip, occurred on post trauma day three. ment. The most common of these in- cheek and forehead. Orbital imaging ϵ-aminocaproic acid is not used in pa- (X-ray or CT scan) should be ordered if juries is angle recession, which is a tear 10 tients with traumatic microhyphema between the longitudinal and circular an orbital fracture is suspected. because the risk of significant rebleed- muscles of the ciliary body.6 More than Patients must be seen daily during the ing is much lower in these patients, and 50% of patients with traumatic hy- first five to seven days post-hyphema. the benefits ofϵ -aminocaproic acid do phema will have some degree of angle This exam frequency is critical because not outweigh the risks of the medica- 18 recession. Greater amounts of angle re- recurrent hemorrhage almost always tion. cession, typically 180 degrees or more, occurs before the seventh day. Visual Corneal blood staining are associated with higher risk for devel- acuity, slit lamp exam with careful 8 Corneal blood staining occurs when oping glaucoma. Angle recession itself monitoring of corneal clarity and size hemoglobin and hemosiderin enter is not the cause of chronically elevated of hyphema, tonometry, and assess- 7 IOP, but rather it provides evidence of ment of patient compliance with medi- the corneal stroma. Corneal blood 7 staining is more common with larger previous trauma and represents perma- cation and self-care are required. The hyphemas, rebleeding, prolonged clot nent damage to the trabecular mesh- vertical height of the hyphema should duration, sustained elevated IOP and work. Another mechanism of chroni- be measured at the initial examination corneal endothelial cell dysfunction. cally elevated IOP is the extension of an because an increase in size at a subse- Slit lamp examination reveals straw yel- endothelial layer from the cornea over quent visit is an indication that a re- the structures in the anterior chamber current hemorrhage has occurred. A low discoloration of the deep stroma 6 greater centrally than peripherally in angle. The presence of heavy trabecu- careful evaluation of the anterior cham- the early stages.1 Corneal blood staining lar pigmentation, elevated baseline ber is needed to identify the presence remains for years and does not respond IOP, hyphema, angle recession and lens of, and to distinguish between, white to medical treatment. In young chil- displacement with a are sig- blood cells, red blood cells and ghost nificant predictors of chronic traumatic cells. The clarity of the cornea must be dren, staining may cause . 23 For these reasons, surgical intervention glaucoma. In patients with angle re- closely monitored to assess for corneal is required when the presence of micro- cession, 5-20% will develop glaucoma blood staining. scopic blood staining is noted.21 in the injured eye, and of those who do Dilated fundus exam, without scleral develop glaucoma, up to 50% will de- Ghost cell glaucoma indentation, is necessary to assess the velop glaucoma in the fellow uninjured posterior segment for complications Ghost cells are degenerated erythro- eye, which suggests these patients may 8 secondary to the initial trauma. Poste- cytes that form within the vitreous have a predisposition to this condition. rior segment injuries are significant pre- cavity over the course of several weeks Discussion dictors of poor visual outcome; howev- after a vitreous hemorrhage. If the ante- er, the detection of these findings can be rior hyaloid face is ruptured by trauma, A patient with traumatic hyphema challenging during initial examination surgery or spontaneously, the ghost may present with variable symptoms due to poor visualization through the cells can freely move into the anterior of blurred vision, pain and photopho- hyphema and/or vitreous hemorrhage. chamber. These rigid, khaki-colored bia. Vision typically follows the severity Ultrasound can be helpful in evaluating

Optometric Education 116 Volume 39, Number 3 / Summer 2014 the posterior segment if it cannot be ex- mm or more and dark red or black in References amined initially. Care must be taken to color have a more guarded prognosis. 1. Walter W, Von Hagen S, Grigorian avoid too much pressure on the globe The dark color of the blood indicates R, et al. Management of traumatic due to the risk for rebleed. Virtually poor circulation of the aqueous humor hyphema. Survey of Ophthalmol- no pressure needs to be applied over and lack of oxygen supply in the ante- ogy. 2002;47(4):297-334. closed lids to obtain useful echograms. rior chamber.17 2. Brandt TM, Haug RH. Trau- On B-scan, a fresh, mild hemorrhage The major determining factor in the matic hyphema: A comprehensive shows dots and short lines in the vitre- final visual outcome in traumatic hy- review. J Oral Maxillofac Surg. ous cavity. Denser hemorrhages show phema is usually an associated ocular 2001;59:1462-1470. higher reflectivity and a greater number 1 injury, not the hyphema itself. Fac- 3. Rahmani B, Jahadi H, Rajaeef- of opacities. The vitreous hemorrhage tors associated with a poor final visual ard A. An analysis of risk for may also organize into layers in the outcome include the presence of pos- secondary hemorrhage in trau- lower periphery of the globe, forming terior segment injuries such as macular matic hyphema. . highly reflective pseudomembranes. B- edema, retinal hemorrhage, epiretinal 1999;106(2):380-385. scan of a retinal tear will show a small, membrane or choroidal rupture. Ante- 4. Gharaibeh A, Savage H, Scherer R, focal, echo-dense membrane of the pos- rior segment findings including corneal et al. Medical interventions for trau- terior surface attaching to the posterior blood staining, traumatic mydriasis, matic hyphema. Cochrane Data- hyaloid. A retinal detachment appears iridodialysis, cataract and lens sub- base Syst Rev. 2012;1:CD005431. as a bright, continuous, somewhat luxation are also significant predictive 5. Andreoli C, Gardiner M. Trau- folded membrane that may insert at factors of a poor final visual outcome. matic hyphema: epidemiology, the ora serrata, or elsewhere While the presence of traumatic my- anatomy, and pathophysiology. in the fundus. Ultrasound may also be driasis and iridodialysis may not sig- UpToDate. 2012. used to assess the anterior segment in nificantly compromise the visual func- 6. Allingham R. Shields textbook cases of corneal opacification or large 24 tion, they likely reflect the severity of of glaucoma. 6th ed. Philadel- hyphema. High frequency ultrasound 19 the initial trauma. In a study of 425 phia, PA: Lippincott Williams biomicroscopy provides high resolution individuals with traumatic hyphema, a &Wilkins; 2011. images and can be useful in detecting higher grade of hyphema on presenta- 7. Catania L. Primary care of the an- areas of angle recession, cyclodialysis or tion and the presence of retinal damage terior segment. 2nd ed. Norwalk, weak zonules.6 were each associated with a poorer final CT: Appleton & Lange; 1995. Gonioscopy is performed three to six visual outcome.20 8. Milder E, Davis K. Ocular weeks after the injury to assess for angle trauma and glaucoma. Interna- recession. Gonioscopy should not be per- Conclusion tional Ophthalmology Clinics. formed before this time because the pro- 2008;48(4):47-64. 8 The most common mode of clinical cedure may increase the risk of rebleed. presentation in blunt ocular trauma is 9. Lai J, Fekrat S, Barron Y, et al. Signs of angle recession include a poste- hyphema.6 Hyphema does not typically Traumatic hyphema in children. riorly recessed iris revealing an irregular cause permanent loss of vision; however, Arch Ophthalmol. 2001;119:64- widening of the ciliary body band, an its presence signifies considerable insult 70. uneven iris insertion, and an area of torn 10. Elhers JP, Shah CP. The Wills eye 10 to the globe and therefore requires care- or absent iris processes. In addition, the ful follow-up and management. Patient manual. 5th ed. Philadelphia, PA: presence of pigment balls or clumps on education is essential to minimize com- Wolters Kluwer/Lippincott Wil- the trabecular meshwork may be seen, plications in the first several days after liams & Wilkins; 2008. which is highly associated with previous 11. Sowka JW, Kabat AG. Open your 6 the injury as well as for the long-term traumatic hyphema. ocular health of the patient. The risk of eyes to . Review of Op- Traumatic hyphema is usually a self- glaucoma remains years after injury and tometry. 2007;144(3). limiting condition that typically has should always be considered in cases of 12. Macsai M. Surgical management good visual prognosis. Approximately unilateral glaucoma at any time in life.7 and rehabilitation of anterior seg- 75% of patients with traumatic hyphe- The patient in our case description had ment trauma. In: Krachmer J, ma have a final visual acuity of 20/50 a good visual outcome. However, due Mannis M, Holland E, ed. Cornea. or better.2 Vision gradually improves to the area of angle recession and iri- 2nd ed. Volume 2. Philadelphia, as blood settles to the bottom of the dodialysis, he is now at higher risk for PA: Elsevier Mosby; 2005. anterior chamber and is eventually re- developing glaucoma and will therefore 13. Mori M, Araie M, Sakurai M, et sorbed. Most uncomplicated hyphemas continue to require careful monitoring al. Effects of pilocarpine and tropi- will resolve within approximately one throughout his life. camide on blood-aqueous barrier week.1 Certain characteristics of hy- permeability in man. Invest Oph- phemas such as height and blood color Disclosures thalmol Vis Sci. 1992;33(2):416- relate to the prognosis. Hyphemas mea- 423. Dr. Dorothy Hitchmoth is a consultant 14. Verma N. Trabeculectomy and suring 3-4 mm or less typically have a for Annidis Health Systems Corpora- favorable course, as do hyphemas with manual clot evacuation in trau- tion and is on the speakers bureau for matic hyphema with corneal blood light red color. Hyphemas that are 5 Zeavision.

Optometric Education 117 Volume 39, Number 3 / Summer 2014 staining. Australian and New Zea- hyphemas. Clinical Ophthalmol- of trabeculectomy in the manage- land Journal of Ophthalmology. ogy. 2009;3:287-290. ment of hypertensive traumatic 1996;24(1):33-38. 18. Recchia F, Saluja R, Hammel K, total hyphema. Journal of the Col- 15. Beiran I, Talmon T, Miller B. Jeffers J. Outpatient management lege of Physicians and Surgeons Characteristics and functional of traumatic microhyphema. Oph- Pakistan. 2009;19(8):496-499. outcome of traumatic hyphema thalmology. 2002;109(8):1465- 22. Ritch R. Ghost cell glaucoma. without routine administration 1470. Journal of Glaucoma. 1994;3:333- of ȝ-aminocaproic acid. IMAJ. 19. Cho J, Jun B, Lee Y, et al. Factors 338. 2002;4:1009-1010. associated with the poor final vi- 23. Sihota R, Kumar S, Gupta V, et 16. Karkhaneh R, Naeeni M, Chams sual outcome after traumatic hy- al. Early predictors of traumatic H, et al. Topical aminocaproic phema. Korean J. Ophthalmol. glaucoma after closed globe in- acid to prevent rebleeding in cases 1998;12:122-129. jury. Arch Ophthalmol. 2008;126 of traumatic hyphema. European 20. Ng C, Sparrow J, Strong N, et al. (7):921-926. Journal of Ophthalmology. 2003; Factors related to the final visual 24. Byrne SF, Green RL. Ultrasound of 13(1):57-61. outcome of 425 patients with trau- the eye and orbit. 2nd ed. Philadel- 17. Papaconstantinou D, Georgalas I, matic hyphema. Eye. 1992;6:305- phia, PA: Mosby;2002. Kourtis N, et al. Contemporary as- 307. pects in the prognosis of traumatic 21. Baig MSA, Ahmed J, Ali MA. Role

Appendix A: Summary of Examination Findings for the Left Eye

Visual Hyphema Anterior Chamber IOP mmHg Diagnostic Medications Acuity Vertical Height Testing (mm) 8/21/12 20/150 2.2 2+RBC 18 B-scan Pred QID, Atropine BID 8/22/12 20/80- 2.1 2+RBC 26 Pred QID, Atropine BID, Timolol BID

8/23/12 20/50- 2.0 2+RBC 25 Orbital X-ray Pred QID, Atropine BID, Cosopt BID, D/C aspirin 8/24/12 20/50+ 2.0 3++RBC 25 Anterior segment Pred 6x/day, Atropine BID, Cosopt TID photos 8/27/12 20/80+ <1.0 2-3+RBC, Flare 34 Pred 6x/day, Atropine BID, Cosopt TID, Acetazolamide 8/28/12 20/100 Trace 3+RBC, Flare 36 Pachymetry: 607 Pred 6x/day, Atropine BID, Cosopt TID, um OD, 662 um Acetazolamide OS 8/29/12 20/80- Trace 3+RBC, Flare 21 B-scan Pred 6x/day, Atropine BID, Cosopt TID, Acetazolamide 8/30/12 20/80 Resolved 2+RBC, Flare 20 Pred 8x/day, Atropine BID, Cosopt TID, Acetazolamide 9/4/12 20/50 Resolved 2+ RBC, Flare 16 Pred 8x/day, Atropine BID, Cosopt TID, Acetazolamide 9/6/12 20/50 Resolved 2-RBC, Flare 18 Pred 6x/day, Atropine QD, Cosopt TID, Acetazolamide 9/13/12 20/40- Resolved Trace RBC 17 Pred QID, Atropine QD, Cosopt TID, D/C Acetazolamide 9/20/12 20/30- Resolved Trace RBC and flare 17 Pred TID, Cosopt BID, D/C Atropine 9/28/12 20/40- Resolved Trace RBC and flare 16 Pred BID, Cosopt BID 10/4/12 20/20- Resolved Trace RBC and flare 14 Pred QD, D/C Cosopt, Re-start Aspirin 10/11/12 20/25- Resolved Trace RBC and flare 20 Pred QD 10/25/12 20/25+ Resolved Clear 19 Pred QOD 11/14/12 20/30+ Resolved Clear 15 Gonioscopy None

Pred = prednisolone acetate 1% ophthalmic solution; Atropine = atropine sulfate 1% ophthalmic solution; Timolol = timolol ophthalmic solution 0.5%; Cosopt = dorzolamide 2%/timolol 0.5%; Acetazolamide = acetazolamide 500 mg PO BID.

Optometric Education 118 Volume 39, Number 3 / Summer 2014