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Traumatic hyphema: Clinical features and diagnosis

Traumatic hyphema: Clinical features and diagnosis
Literature review current through: Jan 2024.
This topic last updated: Jan 30, 2024.

INTRODUCTION — Traumatic hyphema, or blood in the anterior chamber, is a common complication of blunt or penetrating injury to the eye and can result in permanent vision loss. The goals of initial assessment include recognition and characterization of the hyphema and identification of associated orbital and ocular injuries. If ruptured globe is suspected, then emergent consultation with an ophthalmologist is critical. In addition, optimal outcome following a hyphema depends on early ophthalmologic intervention focused on prevention of rebleeding and avoidance of intraocular hypertension. In most instances, patients recover with normal vision. Vision loss is more likely in patients with large hyphemas, sickle hemoglobinopathy/trait, or bleeding disorders.

This review covers the clinical features and diagnosis of traumatic hyphema. The management of traumatic hyphemas is discussed separately. (See "Traumatic hyphema: Management".)

DEFINITION

Hyphema refers to grossly visible blood in the anterior chamber of the eye (picture 1).

Microhyphema describes dispersed red blood cells in the anterior chamber that do not layer out to form a gross fluid level (figure 1).

EPIDEMIOLOGY

Incidence — The annual incidence of traumatic hyphema has been estimated at 12 injuries per 100,000 population, with males being affected three to five times more frequently than females [1-4]. Up to 70 percent of traumatic hyphemas occur in children, with a peak incidence between 10 and 20 years of age [1,3,4].

Required use of appropriate ocular protection can significantly decrease the incidence of traumatic eye injury during recreational sports in children [5-7].

Mechanism of injury — The mechanism of injury varies by age. In younger children, traumatic hyphema typically results from blunt trauma to the eye [4-6,8,9]. Younger children often report being hit in the eye by a ball in the course of playing baseball, softball, basketball, or soccer [9]. Other high risk sports include hockey, racquetball, and squash. The hockey stick or racquet is more likely to be the source of the eye injury than the puck or ball in these instances [4,6].

Teenagers and adults are more likely to develop a traumatic hyphema after a high energy blow to the eye [4,10-15]. Assault is the most common mechanism, occurring in over 40 percent of patients in one study [10]. Other sources of injury include elastic cords (bungee cords), paintballs, airsoft guns, airbag deployment during automobile crashes, and other projectiles [12-16].

Paintball injuries to the eye result in hyphema in over 80 percent of cases and are more likely to cause serious damage to posterior structures (lens, vitreous, retina, and optic nerve) than lower-velocity projectiles [17,18]. Most eye injuries from paintball occur when the participant is not wearing ocular protection [17,19].

Airsoft guns (guns that mechanically propel BB-sized round plastic bullets at high speeds) have been reported to cause novel "donut" erosions in the cornea on fluorescein staining with significant deformation of the anterior segment and hyphema [16].

Traumatic hyphema frequently accompanies penetrating eye injuries as well [10,11]. Common etiologies include BB, pellet, or shot gun blast injury; explosions with shrapnel; and foreign bodies produced by high speed power tools, such as drills or saws [5,10,11]. Thus, a high incidence of suspicion for globe rupture and intraocular foreign body should be maintained when evaluating a patient with a traumatic hyphema. (See 'Open globe' below.)

ANATOMY — The anterior chamber is anatomically defined as the space bordered by the cornea, iris, angle, and the lens. Clear aqueous humor normally fills this space (figure 2).

The angle of the eye is the recess formed by the irido-corneal junction. The scleral spur, trabecular meshwork, and Schwalbe's line lie within this angle. The trabecular meshwork is a fenestrated structure that transmits aqueous fluid to Schlemm's canal, from which it drains into the venous system (figure 3). When aqueous flow out of the eye is impaired, intraocular pressure increases (figure 4).

PATHOPHYSIOLOGY — Hyphemas may arise following trauma or, in patients with certain underlying conditions, may occur spontaneously.

Traumatic hyphema — Traumatic hyphema may result from blunt or penetrating injuries:

Blunt trauma – Blunt force to the eyeball results in an instantaneous increase in intraocular pressure, equatorial stretching of the globe, and posterior pressure being transferred to the iris and its root. The transient rise in pressure results in shear forces acting on the angle structures and can mechanically disrupt the angle (figure 3).

Bleeding results from tears in the vessels of the ciliary body or iris. A grading system has been established based on the degree of anterior chamber hemorrhage (figure 1) [3,20]. More commonly, hyphemas are described according to millimeters in height from the inferior limbus to the top of the blood layer in a patient sitting upright at the slit lamp.

Following blunt eye injury, the bleeding usually stops quickly due to increased intraocular pressure, vessel spasm, and formation of clot. Maximal clot integrity does not occur until four to seven days after the initial injury. Blood in the anterior chamber is cleared by filtration through the trabecular meshwork (figure 3) [21].

The risk of vision loss from an isolated hyphema following blunt trauma depends upon the degree and duration of elevated intraocular pressure which may worsen following episodes of rebleeding.

Penetrating/perforating trauma – Hyphema occurs frequently in patients with penetrating or perforating trauma and is caused by direct damage to the iris. History and physical examination usually identify those patients who require immediate application of an eye shield and consultation by an ophthalmologist. In these patients, risk to vision is most dependent upon the location of the wound, degree of injury to the eye, whether an intraocular foreign body is present and timely surgical repair by an ophthalmologist to prevent endophthalmitis. (See "Open globe injuries: Emergency evaluation and initial management", section on 'Outcomes'.)

Spontaneous hyphema — Hyphemas can occur spontaneously or after relatively minor trauma in patients with bleeding diatheses. It can also occur in conditions that cause chronic ocular ischemia and subsequent neovascularization or can be seen in the presence of other vascular anomalies of the anterior chamber structures. This includes [4,22-27]:

Diabetes mellitus [26]

Iris melanoma, retinoblastoma, and other eye tumors [25,28]

Juvenile xanthogranuloma [27]

Clotting disorders (eg, thrombocytopenia, hemophilia, Von Willebrand disease) [22,23]

Medications that inhibit platelet function, such as warfarin or aspirin [24,29]

Congenital vascular tufts of the iris

In children with no predisposing condition or witnessed trauma, ocular tumors and abuse should be entertained [28,30]. (See "Physical child abuse: Recognition" and "Retinoblastoma: Clinical presentation, evaluation, and diagnosis", section on 'Clinical features'.)

Predisposing conditions — Patients with sickle cell disease or sickle cell trait are at increased risk for complications of hyphema such as increased intraocular pressure (IOP), optic atrophy, and secondary hemorrhage. These factors put them at a higher risk of permanent vision loss when compared to individuals without sickle cell mutations [4,5,8]. Sickling of red blood cells is more likely in the low oxygen environment of the aqueous humor and these sickled cells clog the trabecular meshwork which leads to increased IOP [4]. Furthermore, based upon small observational studies, increased IOP may cause central retinal artery occlusion and optic atrophy at lower absolute pressures and after a shorter duration of elevated IOP in patients with sickle cell disease or trait when compared to normal patients. Thus, patients with sickle cell disease or trait warrant very close observation of IOP and surgical intervention at lower IOP and after a shorter duration of elevated IOP than other patients. (See "Traumatic hyphema: Management", section on 'Monitoring of intraocular pressure' and "Traumatic hyphema: Management", section on 'Surgical clot evacuation'.)

Patients with clotting disorders or on anticoagulants are also at increased risk of vision loss because of the greater frequency of rebleeding. Patients with primary disorders (eg, hemophilia) require rapid correction of the clotting disorder. For patients on anticoagulant treatment, rapid reversal or cessation of anticoagulants in conjunction with management of the hyphema may be warranted in some patients, but others (eg, patients with prosthetic heart valves or vascular stents) may have unacceptable risk from stopping anticoagulation. Prior to cessation, the clinician should discuss the therapeutic need for anticoagulation with the prescribing physician to determine the best plan of action. (See "Traumatic hyphema: Management", section on 'Initial management' and "Traumatic hyphema: Management", section on 'Ophthalmologic management'.)

EVALUATION — A rapid overview summarizes the important clinical features and initial management of traumatic hyphema (table 1).

History — Vision loss and eye pain are common presenting complaints in patients with a traumatic hyphema. In addition, nausea and vomiting may accompany high eye pressures [8]. History reveals blunt injury to the eye in most cases of traumatic hyphema [4-6,8,9,11]. (See 'Mechanism of injury' above.)

Patient or family history of sickle cell hemoglobinopathy, including sickle cell trait, identifies a greater risk of glaucoma, optic atrophy, and vision loss complicating traumatic hyphema [4,5,8,31,32].

Physical examination — The performance of an eye examination is discussed separately. (See "The pediatric physical examination: HEENT", section on 'Eyes' and "The red eye: Evaluation and management" and "Slit lamp examination".)

Precautions and approach — An open globe must be excluded prior to any examination procedure that might apply pressure to the eyeball, such as eyelid retraction or intraocular pressure measurement by tonometry (table 1). (See 'Open globe' below.)

Patients with signs of an orbital compartment syndrome (eg, proptosis, decreased visual acuity, diffuse subconjunctival hemorrhage, tight eyelids) require emergent lateral canthotomy and inferior cantholysis to decompress the orbit. (See "Overview of eye injuries in the emergency department", section on 'Orbital compartment syndrome' and "Approach to diagnosis and initial treatment of eye injuries in the emergency department", section on 'Orbital compartment syndrome'.)

Topical analgesia, reduced ambient light, and parental presence facilitate cooperation in children. A rapid overview summarizes the important clinical features and initial management of traumatic hyphema (table 1).

The clinician should grossly inspect the lids, lashes, lacrimal ducts, and cornea as well as assess direct and consensual pupillary response for the presence of a relative afferent pupillary defect (figure 5), check visual acuity (table 2), extraocular movement, and visual fields by confrontation. Direct ophthalmoscopy or slit lamp exam is useful for closer visualization of anterior structures and the lens. Funduscopic examination may be difficult to perform due to miosis (pupillary constriction), and photophobia may make it initially impossible to perform an exam in a patient with a large hyphema.

Corneal abrasion often accompanies these injuries. Thus, fluorescein staining of the cornea should be performed once an open globe is excluded. (See "Corneal abrasions and corneal foreign bodies: Clinical manifestations and diagnosis", section on 'Fluorescein examination'.)

Findings of hyphema — A hyphema appears as a layering of red blood cells in the anterior chamber that may be grossly apparent on visual inspection with a penlight, especially with the patient in a sitting position (picture 2A-C). Slit lamp examination provides the ability to detect microhyphema and to measure directly the height of the hyphema (in millimeters). Alternatively, a grading system based on the estimated amount of anterior chamber hemorrhage can be used to describe the severity of the hyphema (figure 1) [3,20]. (See "Slit lamp examination".)

All patients with a traumatic hyphema warrant prompt evaluation by an ophthalmologist. (See "Traumatic hyphema: Management", section on 'Indications for ophthalmology consultation or referral'.)

Physical findings often associated with traumatic hyphema include:

Photophobia – Direct illumination of the affected eye to bright light leads to pupillary constriction and contraction of the iris musculature causing pain. In the patient who is unable to open the affected eye, exposure of the unaffected eye to bright light will frequently cause pain in the affected eye due to consensual pupillary constriction and associated traumatic iritis.

Decreased visual acuity – Emergent examination by an ophthalmologist is necessary in patients with significant vision loss after an eye injury (table 1). Vision reduction can range from "slightly blurry" in a patient with microhyphema to "light perception only" with a Grade III to IV hyphema (>50 to 100 percent hemorrhagic filling of the anterior chamber) (figure 1 and picture 1). Decreased vision may improve markedly over a matter of hours if the head is elevated, thus allowing anterior chamber blood to layer below the visual axis. If a patient lies flat for a period of time, they may complain of worsening vision as the blood settles onto the lens or cornea. (See "Traumatic hyphema: Management", section on 'Ophthalmologic management'.)

Other injuries, including corneal abrasion or edema, vitreous hemorrhage, commotio retinae (disruption of the photoreceptors with vision loss), retinal detachment, or cataract, may contribute to vision loss. (See 'Injury to adjacent structures' below and "Approach to diagnosis and initial treatment of eye injuries in the emergency department".)

Anisocoria – Torn iris sphincter muscles can result in miosis or mydriasis (pupillary dilation). The combination of physical damage to the iris and scarring in response to inflammation over the first 24 to 48 hours can result in poor pupil reactivity and anisocoria relative to the unaffected eye. The iris can also tear away from its insertion, referred to as iridodialysis (picture 3 and picture 4).

Elevated intraocular pressure – Intraocular hypertension (greater than 21 mmHg) occurs in over 30 percent of patients at some point following a hyphema [5]. Acutely, intraocular pressure (IOP) may be low, representing ciliary body shutdown. However, if the eye's ability to drain fluid has been compromised by the injury and outflow channels clogged by blood, the pressure can increase quickly. This pressure elevation may not occur for several days after the injury, necessitating close monitoring during the first week.

Patients with sickle cell disease or trait are at higher risk for elevation of intraocular pressure within the first 24 hours [5,31,32].

Corneal blood staining – Corneal blood staining describes diffusion of red blood cell breakdown products into the corneal stroma resulting in golden discoloration of the cornea [5,8]. This condition may limit vision and can obscure visualization of the lens and posterior portion of the eye, thereby complicating the diagnosis of associated injuries. The risk of this complication is increased in patients with a large amount of blood in the anterior chamber (especially “eight ball” or Grade IV (100 percent) hyphema) and elevated intraocular pressure. Peak occurrence is at four days after Grade IV hyphema or six days after Grade III or less hyphema with IOP >25 mmHg [4].

Injury to adjacent structures — A traumatic hyphema is associated with injury to other ocular structures in the majority of cases [5]. The presence of hyphema should alert the examiner to look for other injuries such as an open globe, corneal abrasion, iritis, cataract, lens subluxation or dislocation, retinal tear, retinal hemorrhage, vitreous hemorrhage, choroidal rupture, scleral rupture, optic neuropathy and commotio retinae (whitening of the retina from disruption of the photoreceptor cells with vision loss). Thus, all patients with a traumatic hyphema warrant prompt evaluation by an ophthalmologist to identify associated eye injuries. (See "Open globe injuries: Emergency evaluation and initial management" and "Corneal abrasions and corneal foreign bodies: Clinical manifestations and diagnosis" and "Retinal detachment" and "Approach to diagnosis and initial treatment of eye injuries in the emergency department" and "Optic neuropathies", section on 'Trauma'.)

Open globe — An open globe must be excluded prior to any examination procedure that might apply pressure to the eyeball, such as eyelid retraction or intraocular pressure measurement by tonometry. In most instances, intraocular pressure measurement should be deferred until after complete evaluation by an ophthalmologist, unless the examiner has the proper experience to effectively exclude an open globe and reliably measure intraocular pressure.

The clinical features and initial management of an open globe are provided in a rapid overview (table 3).

Physical findings of an open globe include:

Markedly decreased visual acuity

Eccentric pupil (picture 5)

Increased or decreased anterior chamber depth (picture 6)

Low intraocular pressure

Extrusion of vitreous (picture 7)

External prolapse of the uvea or other internal ocular structures (picture 8 and picture 9 and picture 10)

Tenting of the cornea or sclera at the site of globe injury

Seidel's sign – fluorescein stain clearing in a streaming, tear drop pattern away from a puncture site (picture 11)

A high index of suspicion for posterior rupture should be maintained in the setting of high-risk mechanisms coupled with hyphema obscuring posterior visualization. The presence of hyphema may also mask a posterior rupture of the sclera (by obscuring assessment of anterior chamber depth), particularly in conjunction with a circumferential subconjunctival hemorrhage which can obscure direct inspection of the sclera.

Patients with a possible open globe should have an eye shield placed immediately for protection and should undergo prompt evaluation by an ophthalmologist. These patients require aggressive pain control and treatment of nausea and/or vomiting to avoid extrusion of ocular contents caused by crying or emesis. In addition, further diagnostic imaging of the eye is necessary. (See "Open globe injuries: Emergency evaluation and initial management", section on 'Primary evaluation and management'.)

Corneal abrasion — Corneal abrasions cause severe pain, photophobia with reluctance to open the eye and a foreign body sensation. They frequently accompany traumatic hyphemas, especially when blunt trauma is the mechanism of injury. A working diagnosis of corneal abrasion should be made based upon the history, physical findings, and lack of signs of other disorders. Fluorescein examination should be performed to confirm the diagnosis only after completion of visual acuity measurement and the penlight and fundus examination. Earlier instillation of dye may interfere with visual acuity measurement and visualization of the anterior segment and fundus. Fluorescein should not be placed in the eye until an open globe is excluded. The staining defect can appear linear or geographic depending upon the epithelial defect (picture 12).

The clinical findings and management of corneal abrasions are discussed in greater detail separately. (See "Corneal abrasions and corneal foreign bodies: Clinical manifestations and diagnosis" and "Corneal abrasions and corneal foreign bodies: Management".)

Iris — Traumatic iritis may accompany a traumatic hyphema. Inflammation of the iris causes pain, photophobia, alteration in pupillary sphincter response to light, and perilimbal conjunctival injection [33]. White blood cells and flare may be seen on slit lamp examination of the anterior chamber. Treatment consists of cycloplegia and, in more severe cases topical steroids.

Iridodialysis refers to tearing of the outer circumference of a portion of the iris from its attachment at the iris root/scleral spur (picture 3 and picture 4) [33]. Patients may have glare and photophobia. These patients warrant ophthalmology referral and follow-up to monitor for increased ocular pressure and to determine medical versus surgical treatment.

Lens — Damage to the lens zonules can result in abnormal lens mobility (phacodonesis) or lens subluxation. The lens can dislocate forward into the anterior chamber, fall backward into the vitreous cavity (complete luxation), or merely subluxate in its normal plane (picture 13). (See "Ectopia lentis (dislocated lens) in children".)

Traumatic cataracts may develop immediately or over many years (picture 14). (See "Cataract in children", section on 'Ocular trauma' and "Cataract in adults".)

Angle recession — Separation of the longitudinal fibers from the circular fibers of the ciliary body results in angle recession. Separation of the ciliary body from the scleral spur represents a cyclodialysis cleft. These injuries are not apparent on gross examination but are seen with gonioscopy done many weeks after the injury (figure 3 and figure 4 and picture 15). Angle recession may lead to open- or angle-closure glaucoma. (See "Traumatic hyphema: Management", section on 'Traumatic glaucoma' and "Open-angle glaucoma: Epidemiology, clinical presentation, and diagnosis" and "Angle-closure glaucoma".)

Synechiae — Peripheral anterior synechiae (adhesions of the iris to the cornea) and posterior synechiae (adhesions of the iris to the lens) are seen in patients whose hyphema persists beyond eight days [4]. These conditions are associated with angle closure and pupillary block glaucoma. With angle closure glaucoma, the normal flow through the canal of Schlemm is blocked. With pupillary block glaucoma, the flow of aqueous humor between the lens and the iris is blocked, which can then lead to angle closure glaucoma.

Laboratory testing — Because of their higher risk for complications of hyphema and permanent vision loss in patients with sickle cell disease or trait, all individuals with a family history of sickle cell hemoglobinopathy (disease or trait) and those with uncertain sickle status require testing. (See "Methods for hemoglobin analysis and hemoglobinopathy testing", section on 'Available testing methods'.)

While neonatal screening has markedly increased the identification of patients with sickle cell disease, notification of sickle cell trait or sickle cell disease after neonatal screening may be as low as 50 percent in some regions. (See "Diagnosis of sickle cell disorders", section on 'Older children and adults' and "Diagnosis of sickle cell disorders", section on 'Newborn screening' and 'Predisposing conditions' above.)

Patients with a suspected or known bleeding dyscrasia should have a complete blood count (CBC) with platelet count, prothrombin time (PT), partial thromboplastin time (PTT), and international normalized ratio (INR) measured. Testing for von Willebrand disease (VWD) may also be appropriate in selected cases. (See 'Predisposing conditions' above and "Approach to the adult with a suspected bleeding disorder".)

In patients with significant multiple traumatic injuries, additional testing may also be indicated. (See "Trauma management: Approach to the unstable child", section on 'Laboratory studies' and "Initial management of trauma in adults", section on 'Laboratory tests'.)

Diagnostic imaging — Emergency imaging is necessary in patients with a suspected open globe or concern for serious orbital injury. In addition, patients with anterior chamber or vitreous hemorrhage that obscures the view of the posterior segment require imaging to assess for damage to posterior structures.

The choice of imaging depends upon physical findings as follows:

Computed tomography (CT) – CT of the orbit without contrast and with 1 to 2 mm axial and coronal cuts through the orbits is indicated for patients with suspected open globe, intraocular foreign body, or intraorbital hemorrhage and for trauma patients already undergoing cranial CT for other indications [34,35]. It is also indicated as part of a maxillofacial CT study when orbital fracture is suspected based upon a plausible mechanism, palpable step-off or point tenderness, limited extraocular movement, or significant periocular swelling. (See "Open globe injuries: Emergency evaluation and initial management", section on 'Imaging' and "Orbital fractures".)

Ocular ultrasonography – If available, ultrasonography of the eye can assess for lens damage, intraocular foreign bodies, retinal detachment, and choroidal hemorrhage while avoiding the risk of radiation exposure inherent with orbital CT [36,37]. Ultrasonography should be avoided if an open globe is suspected because it can place pressure on the eye and increase the risk of extrusion of globe contents.

Ultrasound biomicroscopy – Ultrasound biomicroscopy (UBM) can also be used to augment the anterior chamber examination obtained by slit lamp exam but has limited availability [38].

DIAGNOSIS — Traumatic hyphema is a clinical diagnosis that is made based upon history of eye trauma and characteristic findings during an ophthalmologic examination (picture 2A-C and figure 1). (See 'Findings of hyphema' above.)

Spontaneous hyphema warrants evaluation for the following underlying conditions:

Diabetes mellitus [26] and other sources of anterior chamber neovascularization (eg, intracapsular cataract surgery with Swan syndrome) [39] or vascular anomalies [40]

Iris melanoma, retinoblastoma, and other eye tumors [25,28,41]

Juvenile xanthogranuloma [27]

Clotting disorders (eg, thrombocytopenia, hemophilia, Von Willebrand disease) [22,23]

Medications that inhibit platelet function, such as warfarin or aspirin [24,29,42]

In children, unwitnessed trauma or child abuse

Traumatic hyphema is associated with injury to other ocular structures in the majority of cases [5]. The presence of a hyphema should alert the examiner to investigate for other eye injuries, especially an open globe. (See 'Injury to adjacent structures' above.)

In case reports in children, traumatic hyphemas have caused drowsiness and bradycardia through the oculocardiac reflex. These findings may overlap with findings of increased intracranial pressure in head injury patients [43,44]. However, unlike patients with increased intracranial pressure, the oculocardiac reflex does not cause hypertension. (See "Evaluation and management of elevated intracranial pressure in adults", section on 'Clinical manifestations' and "Elevated intracranial pressure (ICP) in children: Clinical manifestations and diagnosis", section on 'Clinical manifestations'.)

MANAGEMENT — Whenever possible, all patients with a traumatic hyphema warrant prompt evaluation by an ophthalmologist to provide expertise in comprehensive eye examination, including intraocular pressure measurement. The initial and ophthalmologic management of traumatic hyphema are discussed in detail separately. (See "Traumatic hyphema: Management".)

SUMMARY AND RECOMMENDATIONS

Rapid overview – A rapid overview summarizes the important clinical features and initial management of traumatic hyphema (table 1). (See 'Evaluation' above and "Traumatic hyphema: Management".)

Definition – Hyphema refers to grossly visible blood in the anterior chamber of the eye (figure 1 and picture 2A and picture 2C). Microhyphema describes dispersed red blood cells in the anterior chamber that do not layer out to form a gross fluid level. (See 'Definition' above and 'Anatomy' above and 'Pathophysiology' above.)

History – Vision loss, eye pain, nausea, and vomiting are common presenting complaints in patients with a traumatic hyphema. History reveals blunt trauma to the eye in most cases of traumatic hyphema. Hyphemas also frequently accompany penetrating eye injuries. (See 'History' above and 'Pathophysiology' above.)

Physical examination – An orbital compartment syndrome or open globe must be excluded prior to any examination procedure that might apply pressure to the eyeball, such as eyelid retraction or intraocular pressure measurement by tonometry (table 1). (See 'Precautions and approach' above and 'Open globe' above.)

The clinician should then perform an eye examination, including (see "Approach to diagnosis and initial treatment of eye injuries in the emergency department"):

Visual acuity (table 2)

Pupillary response (figure 5)

Extraocular movements

Visual fields by confrontation

Slit lamp examination

Direct funduscopic examination (view may be limited in patients with a traumatic hyphema)

Fluorescein staining for concomitant corneal abrasions

Clinical findings and diagnosis – A hyphema is diagnosed clinically as a layering of red blood cells in the anterior chamber that may be grossly apparent on visual inspection with a penlight, especially with the patient in a sitting position (picture 2A-C). Slit lamp examination may detect a microhyphema. A grading system based upon the estimated amount of anterior chamber hemorrhage identifies the severity of the hyphema (figure 1). (See 'Findings of hyphema' above and 'Diagnosis' above.)

Spontaneous hyphemas warrant evaluation for underlying bleeding tendency, conditions that cause neovascularization or vascular anomalies in the anterior chamber, and, in children, child abuse. (See 'Diagnosis' above.)

Laboratory testing – Further investigation for patients with hyphema may include (see 'Laboratory testing' above):

Diagnostic testing for sickle cell status (either sickle cell disease or trait) if this information is uncertain, especially in regions where newborn sickle cell screening is not routine and for individuals with a family history of sickle cell disease or trait.

For patients with suspected or known bleeding dyscrasia: complete blood count (CBC) with platelet count, prothrombin time (PT), partial thromboplastin time (PTT), and international normalized ratio (INR).

For children with suspected child abuse, laboratory testing and imaging to identify associated injuries as discussed in detail separately. (See "Physical child abuse: Diagnostic evaluation and management".)

Imaging – Emergency imaging which varies by eye findings is necessary in patients with the following (see 'Diagnostic imaging' above):

Suspected open globe or concern for serious orbital injury

Anterior chamber or vitreous hemorrhage that obscures the view of the posterior segment

Management – Whenever possible, all patients with a traumatic hyphema warrant prompt evaluation by an ophthalmologist to provide expertise in comprehensive eye examination, including intraocular pressure measurement. The initial and ophthalmologic management of traumatic hyphema are discussed in detail separately. (See "Traumatic hyphema: Management".)

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