HyphemaMANAGEMENT

OPHTHALMOLOGIC PRESENTATIONS · 12 SECTIONS

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631 items

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Cardiovascular Presentations71▾

Respiratory Presentations52▾

Neurological Presentations83▾

Gastrointestinal Presentations74▾

Genitourinary and Reproductive Presentations48▾

Infectious Disease Presentations148▾

Trauma Presentations89▾

Toxicologic Presentations80▾

Psychiatric Presentations26▾

Musculoskeletal and Rheumatologic Presentations96▾

Dermatology Presentations23▾

Environmental and Exposure Presentations27▾

Hematologic and Oncologic Presentations36▾

Pediatric-Specific Presentations19▾

Endocrine and Metabolic Presentations45▾

ENT and Maxillofacial Presentations27▾

Ophthalmologic Presentations19▾

Acute angle-closure glaucoma Central retinal artery occlusion Central Retinal Vein Occlusion Chemical eye injury Corneal abrasion Corneal ulcer Endophthalmitis Globe rupture Herpes zoster ophthalmicus Hyphema Iritis-Uveitis Ocular foreign body Optic Neuritis Orbital cellulitis Orbital Floor Fracture (Blowout)Posterior vitreous detachment Retinal detachment Retrobulbar hematoma and orbital compartment syndrome Vitreous Hemorrhage

Obstetric Presentations23▾

Systemic and Miscellaneous Presentations17▾

01Approach to the Critical Patient/attcp44

Immediate priorities

›Sight-threatening emergencies requiring immediate action

›Open globe / ruptured globe

›Teardrop or irregular pupil

›Shallow or flat anterior chamber

›Extruding uveal tissue or vitreous

›Positive Seidel test (fluorescein streaming)

›Rigid eye shield immediately; no pressure on globe

›Total hyphema (grade IV / eight-ball)

›Complete filling of anterior chamber

›High risk of corneal blood staining

›Emergent ophthalmology consultation

›Severely elevated IOP with optic nerve threat

›IOP > 50 mmHg with vision loss

›Headache and nausea suggesting acute glaucoma

›Sickle cell patients at risk at IOP >= 24 mmHg

›Concomitant head injury or orbital trauma

›Loss of consciousness at time of injury

›GCS < 15 requires CT head

Monitoring and targets

›Ophthalmic monitoring priorities

›Serial IOP measurements

›Normal IOP 10 to 21 mmHg

›Recheck every 1 to 2 hours if initially elevated

›Visual acuity trending

›Baseline Snellen acuity on presentation

›Recheck with any change in symptoms

›Hyphema level monitoring

02History/hx57

Mechanism and timing

›Injury mechanism

›Blunt trauma

›Sports and recreational activities (~40% of cases)

›Projectile type (ball, fist, airbag, paintball)

›Penetrating or sharp trauma

›Exclude open globe first

›High-velocity projectile (BB gun, nail gun)

›Non-traumatic spontaneous hyphema

›Iris neovascularization (rubeosis iridis)

›Iris melanoma

›Juvenile xanthogranuloma

›Leukemia

›Herpes zoster keratouveitis

›Timing of injury

›Hours since trauma

›Prior episodes of eye trauma

Symptoms

›Visual symptoms

›Decreased or blurred vision

›Severity correlates with hyphema grade

›Partial vs complete vision loss

›Photophobia

›Floaters or flashers

›Suggests posterior segment involvement

›Retinal tear or vitreous hemorrhage concern

›Pain and associated symptoms

›Eye pain or pressure

03Physical Exam/exam50

Ocular examination

›Visual acuity

›Snellen chart or near card

›Document each eye separately

›Pinhole acuity if reduced

›VA worse than 20/200 as severe impairment marker

›Associated with higher grade hyphema

›Rebleeding risk marker

›External and anterior segment

›Hyphema grading

›Microhyphema: RBC suspension only, no layering (slit-lamp)

›Grade I: blood layering <= one-third anterior chamber

›Grade II: blood one-third to one-half anterior chamber

›Grade III: blood > one-half anterior chamber

›Grade IV: complete filling (eight-ball hyphema)

›Cornea

›Laceration or perforation

›Seidel test: fluorescein streaming = open globe

›Blood staining (brown-orange stromal discoloration)

›Anterior chamber depth

›Shallow chamber = open globe concern

›Asymmetry vs contralateral eye

›Iris

›Teardrop or peaked pupil = open globe

›Iridodialysis (iris root detachment)

›Traumatic mydriasis

›Pupillary and posterior segment

›Pupillary size and reactivity

04Differential Diagnosis/ddx39

Immediate threats to vision and life

›Open globe / ruptured globe

›ICD-10 S05.2 (ocular laceration without prolapse)

›Teardrop pupil, positive Seidel, uveal prolapse

›Treat as open globe until definitively excluded

›Retrobulbar hemorrhage

›Proptosis, elevated IOP, restricted motility

›Lateral canthotomy / cantholysis if vision threatened

›ICD-10 S05.90

›Intraocular foreign body

›High-velocity projectile mechanism

›CT orbits to exclude

›Orbital compartment syndrome

›Proptosis with rapidly declining vision

›Surgical emergency

Non-traumatic hyphema causes

›Iris neovascularization (rubeosis iridis)

›Most common cause in adults > 60 years

›Diabetic retinopathy or central retinal vein occlusion

›ICD-10 H21.1X

›Iris melanoma

›Irregular iris pigmentation

›Spontaneous hyphema without trauma

›Juvenile xanthogranuloma

›Pediatric spontaneous hyphema

›Yellow iris nodules

›Leukemia or lymphoma infiltration

›Bilateral or recurrent spontaneous hyphema

05Laboratory Tests/lt29

Core hematologic workup

›Sickle cell screen

›Sickledex (sickle cell prep) or hemoglobin electrophoresis

›Obtain in all at-risk patients

›African American, Mediterranean, Middle Eastern descent

›Only 16.7% of institutions routinely screen — critical gap

›Sickle cell trait dramatically worsens IOP complications

›Obtain before initiating antifibrinolytic therapy

›Alters management thresholds significantly

›Complete blood count

›Baseline hemoglobin and hematocrit

›Large hyphema or concern for significant bleeding

›Platelet count

›Thrombocytopenia increases rebleed risk

›Leukocytosis or blasts

›Leukemia consideration in spontaneous hyphema

Coagulation and metabolic labs

›Coagulation studies

›PT/INR and aPTT

›Anticoagulant use screening

›Suspected coagulopathy or hemophilia

›Factor VIII and IX levels if hemophilia suspected

›Modify management and surgical planning

›Renal function panel

›Creatinine before aminocaproic acid use

›Renal disease is a contraindication to aminocaproic acid

›Electrolytes if acetazolamide initiated

›Metabolic acidosis monitoring

06Diagnostic Tests/dt76

Scoring Systems

›Hyphema grading system

›Microhyphema

›Red blood cell suspension in anterior chamber

›No visible layering

›Slit-lamp diagnosis only

›Grade I

›Layered blood occupying <= one-third of anterior chamber

›Better visual prognosis

›Grade II

›Blood filling one-third to one-half of anterior chamber

›Grade III

›Blood filling > one-half of anterior chamber

›High rebleed and complication risk

›Grade IV (total / eight-ball)

›Complete filling of anterior chamber

›Corneal blood staining risk high

›Surgical intervention often required

›Prognostic factors

›Rebleeding: OR 37.5 for poor visual outcome

›Typically occurs days 3 to 5

›Rebleed rate 2% to 38% across studies

›Presenting visual acuity < 20/200: OR 9.1 for poor outcome

›Age > 60 years: OR 16.0 for poor visual outcome

›Overall: 75% of patients achieve visual acuity >= 20/50

MRI

›MRI of orbits

›Contraindicated if metallic foreign body suspected

07Disposition/dispo39

Admission indications

›Hospital admission criteria

›High-grade hyphema

›Grade III or IV (total) hyphema

›High rebleed and complication risk

›Sickle cell disease or trait

›All hyphemas regardless of grade require admission

›Lower IOP thresholds for intervention

›Elevated IOP not controlled with initial medical therapy

›IOP > 35 mmHg or refractory to topical agents

›Rebleeding episode

›Any recurrent hemorrhage during monitoring period

›Coagulopathy or hemophilia

›Factor replacement coordination

›Hematology involvement required

›Non-compliance risk

›Inability to comply with activity restriction

›Unreliable medication adherence or follow-up

›Pediatric non-accidental trauma concern

›Safety evaluation required

Discharge criteria

›Outpatient management criteria

›Small hyphema grade I to II

›No elevated IOP

›Good visual acuity

›No sickle cell disease or trait

›No bleeding disorder or anticoagulant use without ophthalmology guidance

›Reliable patient or family

08Treatment/t105

Immediate stabilization

›Globe protection

›Rigid Fox eye shield placement

›Prevents further external trauma

›No pressure on globe

›Wear at all times including sleep

›Avoid IOP-elevating activities

›No straining or Valsalva

›No bending or heavy lifting

›No reading or near work (accommodation moves iris)

Positioning and activity

›Activity restriction protocol

›Head of bed >= 30 degrees

›Promotes inferior settling of blood

›Facilitates visualization of visual axis

›Quiet ambulation only

›No strenuous activity for 5 to 7 days

›No sports or exercise

›Antiemetics as needed

›Ondansetron 4 mg IV or PO if nausea present

›Vomiting raises IOP via Valsalva mechanism

Topical ophthalmic therapy

›Cycloplegic therapy

›Atropine 1% ophthalmic drops

›1 drop every 8 hours

›Reduces ciliary spasm and improves comfort

›Allows better posterior segment visualization

›Reduces risk of posterior synechiae formation

›Topical corticosteroid

›Prednisolone acetate 1% ophthalmic drops

›1 drop four times daily

›Controls traumatic uveitis inflammation

›Reduces risk of anterior synechiae

›IOP-lowering agents when IOP > 21 mmHg

›Timolol 0.5% ophthalmic drops

›1 drop twice daily

›Beta-blocker; reduces aqueous production

›Avoid in asthma and bradycardia

›Brimonidine 0.2% ophthalmic drops

›1 drop twice to three times daily

›Alpha-2 agonist; reduces aqueous production

›Avoid in infants < 2 years (CNS depression risk)

Systemic IOP management

›Oral carbonic anhydrase inhibitors

›Acetazolamide oral

›500 mg twice daily

›Reduces aqueous humor production

›Monitor electrolytes and renal function

›Avoid in sickle cell disease (acidosis promotes sickling)

›Avoid in sulfa allergy

›Methazolamide

›25 to 50 mg twice to three times daily

›Absolutely contraindicated in sickle cell disease or trait

›Promotes sickling via systemic acidosis

Antifibrinolytic therapy

›Tranexamic acid (TXA) — preferred agent

›Oral tranexamic acid

›75 mg/kg/day divided three times daily for 5 days

›Cochrane review: RR 0.33 (95% CI 0.21 to 0.53) for rebleed

›Fewer GI side effects than aminocaproic acid

›Contraindicated in pregnancy and active thromboembolic disease

›Evidence level: Class IIa based on Cochrane systematic review

›Aminocaproic acid (ACA) — alternative

›50 to 100 mg/kg orally every 4 hours for 5 days

›Maximum 30 g per day

›Cochrane review: RR 0.28 (95% CI 0.13 to 0.60) for rebleed

›More GI side effects (nausea, vomiting, postural hypotension)

›Contraindications

›Pregnancy

›Coagulopathies

›Renal disease

›Hepatic or cardiovascular disease (use with caution)

Analgesia

›Analgesic selection

›Acetaminophen preferred

›500 to 1000 mg orally every 6 to 8 hours as needed

›Does not affect platelet function

›NSAIDs absolutely contraindicated

›Ibuprofen, ketorolac, aspirin — prolong bleeding time

›Increase rebleed risk

›Anticoagulant and antiplatelet agents

›Hold if clinically safe to do so

›Weigh thrombotic vs rebleed risk with prescriber

Sickle cell disease special management

›Sickle cell specific IOP thresholds

›Surgical decompression if IOP >= 24 mmHg for >= 24 hours

›Much lower threshold than general population

›Optic nerve infarction risk at relatively modest IOP

›Target IOP < 24 mmHg

›Optic nerve blood flow critically impaired above this threshold

›Medications to avoid in sickle cell

›Methazolamide — absolutely contraindicated

›Systemic acidosis promotes RBC sickling

›Hyperosmotic agents (mannitol, glycerol) — contraindicated

›Promote sickling and red cell dehydration

›Acetazolamide — use with caution or avoid

›Controversial; some experts avoid all CAIs in SCD

Surgical management

›Surgical indications

›Persistently elevated IOP despite maximal medical therapy

›IOP > 35 mmHg unresponsive to treatment

›IOP >= 24 mmHg for >= 24 hours in sickle cell patients

›Corneal blood staining (imminent or established)

›Prevents permanent stromal damage

›Non-clearing total (grade IV) hyphema > 10 days

›Sickle cell with sustained IOP elevation

›Surgical options

›Anterior chamber paracentesis and washout

›Simplest and safest approach

›Clot lysis with tissue plasminogen activator (tPA) injection

›Trabeculectomy with hyphema washout

›Refractory elevated IOP with outflow obstruction

›Timing: typically delayed 4 days post-injury to allow clot liquefaction

09Special Populations/sp68

Pregnancy

›Pregnancy considerations

›Mechanism and presentation unchanged

›Blunt or penetrating trauma same risk factors

›Spontaneous hyphema: rule out eclampsia-related coagulopathy

›Antifibrinolytic contraindications

›Aminocaproic acid absolutely contraindicated in pregnancy

›Tranexamic acid safety data limited in pregnancy

›Avoid antifibrinolytics unless ophthalmology guidance

›Carbonic anhydrase inhibitors

›Acetazolamide crosses placenta (FDA category C)

›Use only if IOP is vision-threatening with no alternatives

›Consult maternal-fetal medicine

›Imaging considerations

›CT orbits with abdominal shielding if required

›Avoid unless open globe or IOFB suspected

›Topical medications

›Topical atropine: systemic absorption minimal; short-term use generally acceptable

›Prednisolone acetate topical: generally acceptable short-term

›Delivery planning

›Ophthalmology involvement if hyphema persists near delivery

›Valsalva during delivery increases IOP and rebleed risk

Geriatric

›Older adult specific considerations

›Higher prevalence of spontaneous hyphema

›Iris neovascularization from diabetic retinopathy

›Central retinal vein occlusion

›Iris melanoma

10Background/b74

Epidemiology

›Incidence and demographics

›Traumatic hyphema is the most common cause

›Sports and recreational activities ~40% of cases

›Male sex predominance: 78% of traumatic hyphemas

›Age distribution

›Children and young adults most commonly affected

›Non-traumatic spontaneous hyphema more common in adults > 60 years

›Outcome data

›75% of patients achieve visual acuity >= 20/50 overall

›Rebleeding rate: 2% to 38% across studies (typically days 3 to 5)

›IOP elevation occurs in 39% of cases

›Only 16.7% of institutions routinely screen for sickle cell trait

›Risk of late complications

›Angle recession glaucoma may develop years after injury

›Annual IOP monitoring recommended indefinitely post-traumatic hyphema

›Corneal blood staining if hyphema and elevated IOP persist

›ICD-10 coding

›H21.0 Hyphema (primary code)

›S05.10 Contusion of eyeball and orbital tissues, unspecified eye

›SNOMED CT: 75249002 (hyphema)

Pathophysiology

›Mechanisms of hemorrhage

›Blunt trauma mechanism

›Sudden rise in IOP compresses globe

›Tearing of iris vessels at the root (iridodialysis) or ciliary body

›Aqueous humor disruption and fibrin mesh formation

›Penetrating trauma mechanism

›Direct laceration of iris, ciliary body, or lens vessels

›Open globe must be excluded

›Non-traumatic mechanism

›Iris neovascularization: fragile new vessels lack normal vessel wall integrity

›Spontaneous rupture with minimal provocation

›Complications and their mechanisms

›Secondary hemorrhage (rebleeding days 3 to 5)

›Clot retraction and fibrinolysis destabilizes initial hemostasis

›Fibrinolysis peaks at days 3 to 5 post-injury

›Antifibrinolytics target this mechanism

›Elevated IOP

›Red blood cells and ghost cells obstruct trabecular meshwork

›Anterior synechiae formation blocks outflow angle

›Total hyphema increases pupil block

›Corneal blood staining

›Prolonged contact of RBCs with decompensated endothelium

›Hemoglobin deposits in corneal stroma

›Requires IOP control and often surgical clearance

›Angle recession glaucoma (late)

›Tear between ciliary muscle layers

›Trabecular meshwork scarring causes late-onset open-angle glaucoma

›May manifest years to decades after injury

Therapeutic Considerations

›Evidence base for antifibrinolytics

›Cochrane systematic review (Woreta 2023)

›TXA reduces rebleed rate: RR 0.33 (95% CI 0.21 to 0.53)

›ACA reduces rebleed rate: RR 0.28 (95% CI 0.13 to 0.60)

›TXA generally preferred due to fewer GI adverse effects

›Neither agent alters final visual acuity in meta-analysis

›Role of topical corticosteroids

›Reduce traumatic uveitis and anterior synechiae formation

›Prednisolone acetate 1% QID is standard

›Systemic corticosteroids not routinely used

›IOP management principles

›Trabecular meshwork obstruction is primary mechanism

›Aqueous production suppression is first-line approach

›Beta-blockers and alpha-2 agonists most commonly used topically

›Surgical decompression when medical therapy fails

›Clot washout most effective for corneal staining prevention

›Timing at day 4 to allow clot liquefaction improves success

›Prevention of long-term sequelae

›Annual IOP check indefinitely after traumatic hyphema

›Angle recession glaucoma risk persists for decades

›Gonioscopy after resolution to assess angle recession extent

›Protective eyewear counseling to prevent recurrence

›Limitations of evidence

›Most RCTs for antifibrinolytics are underpowered

›Optimal management varies by institution and resource availability

›Sickle cell subgroup data largely from observational case series

11Patient Discharge Instructions/pdi27

copy discharge instructions

›Home care instructions for hyphema

›Eye shield: wear rigid Fox eye shield at all times including during sleep

›Head position: sleep and rest with head elevated >= 30 degrees

›Activity: no sports, exercise, heavy lifting, bending, or straining for 5 to 7 days

›Reading: avoid near work and reading (iris movement increases rebleed risk)

›Medications to take at home

›Atropine eye drops: 1 drop every 8 hours as prescribed

›Prednisolone acetate eye drops: 1 drop four times daily as prescribed

›Antifibrinolytic tablets if prescribed: take with food, complete full 5-day course

›Acetaminophen for pain: 500 to 1000 mg as needed, do not exceed 4000 mg per day

›Medications to avoid

›No ibuprofen, aspirin, naproxen, or any anti-inflammatory pain reliever

›No blood thinners unless directed by your doctor

›Avoid alcohol during recovery (affects platelet function)

›Return to emergency department immediately if

›Sudden worsening or new loss of vision

›Severe eye pain or pressure building

›New or increasing headache with nausea or vomiting

›Blood level in the eye appears to be rising or worsening

›Increasing sensitivity to light

›Seeing flashes of light or new floaters

›Nausea or vomiting that does not settle

›Follow-up instructions

›Ophthalmology appointment: within 24 to 48 hours — this is essential

›Peak risk of re-bleeding is days 3 to 5 after injury

›Most small hyphemas resolve within 5 to 7 days

›Long-term: annual eye pressure checks even after full recovery to monitor for glaucoma

12References/r23

Guidelines and key sources

›Primary evidence sources

›Woreta FA, Lindsley KB, Gharaibeh A, et al. Medical Interventions for Traumatic Hyphema. Cochrane Database of Systematic Reviews. 2023

›Antifibrinolytic meta-analysis supporting TXA and ACA use

›TXA: RR 0.33; ACA: RR 0.28 for rebleed prevention

›Paterson R, Drake B, Tabin G, Cushing T. Wilderness Medical Society Clinical Practice Guidelines for Eye Injuries. Wilderness and Environmental Medicine. 2024

›Shingleton BJ. Eye Injuries. New England Journal of Medicine. 1991

›Walton W, Von Hagen S, Grigorian R, Zarbin M. Management of Traumatic Hyphema. Survey of Ophthalmology. 2002

›Epidemiology and outcomes references

›Iftikhar M, Mir T, Seidel N, et al. Epidemiology and Outcomes of Hyphema. Acta Ophthalmologica. 2021

›180-case series; 78% male; prognostic factors identified

›Papaconstantinou D, et al. Contemporary Aspects in the Prognosis of Traumatic Hyphemas. Clinical Ophthalmology. 2009

›Miller SC, Meeralakshmi P, Fliotsos MJ, et al. Global Current Practice Patterns for Management of Hyphema. Clinical Ophthalmology. 2022

›Sickle cell and special population references

›Mir T, Iftikhar M, Seidel N, et al. Hyphema in Patients With Sickle Cell Trait: 10-Year Experience at Wilmer Eye Institute. Clinical Ophthalmology. 2020

›Evidence-Based Management of Sickle Cell Disease: Expert Panel Report. NHLBI. 2014

›Wax MB, Ridley ME, Magargal LE. Reversal of Retinal and Optic Disc Ischemia in Sickle Cell Trait and Glaucoma Secondary to Traumatic Hyphema. Ophthalmology. 1982

›Surgical references

›Graul TA, Ruttum MS, Lloyd MA, et al. Trabeculectomy for Traumatic Hyphema With Increased Intraocular Pressure. American Journal of Ophthalmology. 1994

›Rahmani B, Jahadi HR. Comparison of Tranexamic Acid and Prednisolone in Treatment of Traumatic Hyphema. Ophthalmology. 1999

›Coding standards

›ICD-10 H21.0 Hyphema

›ICD-10 S05.10 Contusion of eyeball and orbital tissues

›SNOMED CT 75249002 Hyphema

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Reviewed by SymptomDx Medical Team · Last reviewed August 18, 2026

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