What is a hyphema?

A hyphema is blood in the anterior chamber. The appearance of a hyphema may range from microscopic, seen only at the slit lamp as erythrocytes circulating in the aqueous, to a total hyphema that fills the entire anterior chamber.

List the causes of a hyphema.

There are three major causes of hyphema: trauma to the globe, intraocular surgery, or spontaneous anterior segment hemorrhage in association with ocular or systemic conditions, such as neovascularization of the iris or anterior chamber angle, intraocular tumors, or clotting disorders ( Table 20-1 ).

What is the most common cause of a traumatic hyphema?

The most common cause of traumatic hyphema is blunt anterior segment trauma.

Describe the pathophysiology of a traumatic hyphema.

Blunt ocular trauma results in ocular indentation, which causes a sudden expansion of ocular tissues and an immediate rise in the intraocular pressure. The sudden forceful displacement of the cornea and limbus posteriorly and peripherally may result in splitting or tearing of these tissues. As the tissues tear, blood vessels in the vicinity may rupture, resulting in a hyphema.

List the anterior segment structures that may split or tear in response to blunt ocular injury.

• •
  

  Central iris: Sphincter tear

  
  
• •
  

  Peripheral iris: Iridodialysis

  
  
• •
  

  Anterior ciliary body: Angle recession

  
  
• •
  

  Separation of ciliary body from the scleral spur: Cyclodialysis

  
  
• •
  

  Trabecular meshwork: Trabecular meshwork tear

  
  
• •
  

  Zonules/lens: Zonular tears with possible lens subluxation

  
  
• •
  

  Separation of the retina from the ora serrata: Retinal dialysis

When a patient presents with a hyphema due to blunt ocular trauma, which anterior segment structure is the most likely source of the hemorrhage?

Hyphema as a result of blunt ocular trauma most commonly occurs as a result of angle recession, a tear in the anterior face of the ciliary body between the longitudinal and the circular ciliary body muscles. Rupture of the blood vessels in the vicinity of the tear results in a hyphema. The most frequently ruptured blood vessels include the major arterial circle of the iris, the arterial branches to the ciliary body, and the recurrent choroidal arteries and vein crossing between the ciliary body and the episcleral venous plexus.

What ocular injuries may be associated with a traumatic hyphema?

• •
  

  Ocular wall: Ruptured globe at the cornea, limbus, and/or sclera

  
  
• •
  

  Cornea/conjunctiva: Epithelial abrasion, laceration, subconjunctival hemorrhage

  
  
• •
  

  Iris: Sphincter tears, iridodialysis, mydriasis (long-term)

  
  
• •
  

  Angle: Angle recession, iris dialysis, cyclodialysis cleft

  
  
• •
  

  Lens: Traumatic cataract (acute, capsular rupture; chronic, direct injury), subluxation or total dislocation (damage of zonular attachments)

  
  
• •
  

  Vitreous: Vitreous detachment, vitreous prolapse

  
  
• •
  

  Retina: Retinal tear, detachment, and/or dialysis (vessel rupture, vascular occlusion)

  
  
• •
  

  Retinal pigment epithelium and choroid: Choroidal rupture

  
  
• •
  

  Optic nerve: Avulsion, optic nerve crush (chronic, glaucoma)

Describe an appropriate approach to the workup of a patient with a hyphema.

The primary responsibility is to rule out a ruptured globe and search for an ocular foreign body in all patients who present with a traumatic hyphema. The color, character, and extent of the hyphema and associated ocular injuries, including corneal blood-staining status, should be documented. Gonioscopy is usually best deferred, but, if necessary, it may be performed gently, taking care to avoid a rebleed. Before a possible rebleed obscures the view, a dilated lens and fundus examination should be performed without scleral depression.

Past medical and ocular history may identify risk factors for the bleeding episode and the chance of future complications. Sickle cell test and Hgb electrophoresis are suggested for all black and Hispanic patients and anyone with a positive family history. Establishing the exact nature of the trauma helps to estimate the likelihood of a possible ocular or orbital foreign body and/or ruptured globe. The exact timing of the injury is crucial in enabling one to predict when a patient will be at greatest risk for a rebleed and to help determine the expected time of clearing and the length of necessary treatment.

Four to six weeks after the injury, careful gonioscopy of the recovered eye may reveal an angle recession. At this time, one may also perform a dilated fundus examination with scleral depression to rule out peripheral retinal injury, such as described in Table 20-1 .

What are pertinent questions to ask a patient who presents with a traumatic hyphema? Why?

• 1.
  

  When did your injury occur? Establishing the exact time of the injury is important because there is an increased rate of rebleed in patients who present more than 24 hours after trauma, and it will help to determine how soon a patient will be at greatest risk for a rebleed.

  
  
• 2.
  

  What type of injury did you sustain? The type and severity of an injury is important to help assess the likelihood of associated systemic injuries, an ocular or intraorbital foreign body, and the possibility of a ruptured globe.

  
  
• 3.
  

  Do you or any of your family members have a medical history of bleeding disorders or sickle cell disease? The answer to this question may help to establish a possible etiology for the hyphema and to determine what type and how aggressive the treatment should be.

  
  
• 4.
  

  What types of medications do you take (including alcohol intake)? Antiplatelet or anticoagulant effects of aspirin, nonsteroidal anti-inflammatory drugs, warfarin (Coumadin), and alcohol may predispose a patient to developing a hyphema or a rebleed after trauma and should be discontinued if possible.

How are hyphemas managed?

There is no consensus regarding the appropriate treatment for hyphema. Traditionally, most patients with a hyphema were admitted to the hospital for bed rest and sedation and were given a monocular or binocular patch for approximately 5 days. Today, compliant patients with a microhyphema and a low risk for rebleed are often followed as outpatients. It still appears prudent to hospitalize those patients who have a layered hyphema ( Fig. 20-1 ), are at increased risk for rebleed, have a sickling hemoglobinopathy, or are noncompliant.

Layered hyphema.

Patients are given a protective shield over the affected eye to decrease any inadvertent trauma and are advised to limit activity. The head is elevated (to allow the blood to layer inferiorly and thus assist with visual rehabilitation and prevent clot formation in the papillary aperture), and systemic blood pressure is controlled in an attempt to decrease the hydrostatic pressure in the traumatized blood vessels to minimize the risk of recurrent hemorrhage. Patients should be examined gently once or twice a day.

The medical management of hyphema includes the following:

• 1.
  

  Discontinuation of antiplatelet, anticoagulant, and nonsteroidal anti-inflammatory medications

  
  
• 2.
  

  Treatment with cycloplegic drops, oral or topical steroids, antiemetics, and antifibrinolytics

  
  
• 3.
  

  Intraocular pressure control as necessary

  
  
  
  
  • •
    

    β-Blockers

    
    
  • •
    

    α-Agonists (avoid in young children because of the risk of bradycardia and hypotension)

    
    
  • •
    

    Topical or systemic carbonic anhydrase inhibitors and hyperosmotics (except in sickle hemoglobinopathies because of the risk of increased sickling with these medications)

    
    
  • •
    

    Avoid miotics, as they might increase pupillary block and disrupt the blood–aqueous barrier, and prostaglandin analogs, which may increase inflammation

  
  

Explain the rationale for the use of antifibrinolytic agents in the treatment of hyphema.

Systemic antifibrinolytic agents are used in an effort to reduce the chance of recurrent hemorrhage. Their use is rare now, especially in populations with a low risk of rebleeding. Fibrinolysis of a clot that seals a recently ruptured blood vessel may result in a repeat hemorrhage from that site. Tranexamic acid and aminocaproic acid decrease the rate of clot hemolysis by inhibiting the conversion of plasminogen to plasmin, which results in stabilization of the clot that seals the ruptured blood vessel. The injured vessel now has more time to heal permanently prior to fibrinolysis of the clot, thus reducing the risk of recurrent hemorrhage. Topical aminocaproic acid shows promise but remains investigational at present.

Name the most common adverse effects associated with aminocaproic acid treatment.

Nausea, vomiting, and postural hypotension are frequently encountered side effects of aminocaproic acid. It is therefore recommended that patients who receive aminocaproic acid be transported via wheelchair, particularly during the first 24 hours, to prevent possible complications from postural hypotension. Antiemetics may be used as necessary.

In what setting is aminocaproic acid contraindicated?

Aminocaproic acid use is contraindicated in the presence of the following:

• •
  

  Active intravascular clotting disorders, including cancer

  
  
• •
  

  Hepatic disease

  
  
• •
  

  Renal disease

  
  
• •
  

  Pregnancy

Cautious use is recommended in patients at risk for myocardial infarction, pulmonary embolus, and cerebrovascular disease.

Why are patients with sickle cell disease or sickle cell trait at a particularly high risk for developing complications from a hyphema?

Once pliable biconcave erythrocytes transform into elongated ridged sickle cells, they are unable to pass through the trabecular meshwork easily. The trabecular meshwork becomes obstructed with these cells, leading to a marked rise in intraocular pressure, even in the setting of a relatively small hyphema. Factors that encourage sickling include acidosis, hypoxia, and hemoconcentration. Patients with sickle cell are also predisposed to infarction of the optic nerve, retina, and anterior segment at minimally elevated intraocular pressures. Vascular sludging of sickled cells may cause ischemia and microvascular infarction. Therefore, vigorous and aggressive therapy for intraocular pressure control is suggested for patients with sickle cell disease.

Many glaucoma medications (except β-blockers and prostaglandin analogs) are generally avoided because they may increase sickling.

• 1.
  

  Carbonic anhydrase inhibitors, particularly acetazolamide, may increase the concentration of ascorbic acid in the aqueous, which decreases the pH and leads to increased sickling in the anterior chamber. Methazolamide may be a safer alternative in this setting because it causes less systemic acidosis than acetazolamide.

  
  
• 2.
  

  Epinephrine compounds and α-agonists may cause vasoconstriction with subsequent deoxygenation and increased intravascular and intracameral sickling.

  
  
• 3.
  

  Hyperosmotics may cause hemoconcentration, which may lead to vascular sludging and sickling, which increases the risk of infarction in the eye as well as other organs.

  
  
• 4.
  

  Surgical interventions are used earlier and at lower intraocular pressures than in people who do not have sickle cell trait or disease (see question [CR] ).