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13.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.

14.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. This predisposition is thought to occur because of vascular sludging by sickled cells, which leads to 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 b-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.

2.Epinephrine compounds and a-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 15).

KEY POINTS: TRAUMATIC HYPHEMA AND SICKLE CELL DISEASE

1.More aggressive management is required to prevent optic nerve damage and central retinal artery occlusion.

2.Beta blockers and prostaglandin analogs should be used for intraocular pressure control.

3.Carbonic anhydrase inhibitors, epinephrine compounds, a-agonists, and hyperosmotics may increase sickling and are therefore contraindicated.

15.What level of intraocular pressure is considered medically uncontrolled?

An intraocular pressure that is considered uncontrolled depends upon the patient in question. (Some guidelines are included in subsequent discussions.) Surgery is generally not indicated in a patient with a healthy optic nerve unless, despite medical therapy, the intraocular pressure is around 50 mmHg for 5 days, or greater than 35 mmHg for a more prolonged period of time. In the patient with previous glaucomatous optic nerve damage, however, the threshold for surgical intervention is lower and depends upon the level at which the intraocular pressure

204 TRAUMATIC GLAUCOMA AND HYPHEMA

is considered to be likely to cause further optic nerve damage. In such patients, surgery may be appropriate within hours or days of the initial trauma. As previously discussed, aggressive therapy is required for patients with sickle cell disease, as these patients are predisposed to optic nerve damage and central retinal artery occlusion at minimally elevated intraocular pressures. Surgery is generally indicated in a patient with sickle cell disease if the intraocular pressure exceeds 24 mmHg for more than 24 hours despite medical therapy.

16.List the indications for surgical intervention in the management of a hyphema.

As a rule, patients with true eight-ball hyphemas require prompt surgical intervention

(see question 26); in contrast, approximately 5% of all traumatic hyphemas demand surgical management. Indications for surgical intervention include the following:

&A large hyphema that persists for more than 10 days

&A total hyphema that persists for more than 5 days (after which time peripheral anterior synechiae are more likely to develop)

&Early corneal blood staining

&An intraocular pressure that cannot be controlled medically and threatens to damage the optic nerve or cornea or result in retinal vascular occlusion, particularly in patients with sickle cell trait or disease.

17.Name the major complications associated with a hyphema.

&Corneal blood staining

&Recurrent hemorrhage

&Secondary glaucoma

In addition to the preceding complications, patients with sickle cell anemia or sickle cell trait have a predisposition to central retinal artery occlusion and optic nerve damage at only minimally elevated intraocular pressure owing to vascular sludging of the sickled cells, which leads to ischemia and vaso-occlusion.

18.What is corneal blood staining?

Endothelial cell decompensation results in passage of erythrocyte breakdown products (particularly iron from hemoglobin and lipid from cell membranes) into the stroma, creating a yellowish-brown discoloration of the posterior stroma. Corneal blood staining may resolve over months or years, first peripherally and then posteriorly.

19.What percent of patients with a hyphema develop corneal blood staining?

Five percent.

20.In which setting is corneal blood staining most likely to occur?

&Recurrent hemorrhage

&Compromised endothelial cell function

&Larger hyphemas that are prolonged in duration

&Usually, but not always, in association with an elevated intraocular pressure

21.What is the differential diagnosis of the appearance of bright red blood in the anterior chamber within the first 5 days after a patient has suffered a traumatic hyphema?

&Recurrent hemorrhage

&Fibrinolysis and hemolysis of a clotted hyphema

Recurrent hemorrhage must be differentiated from hemolysis that occurs as a clotted

hyphema resorbs, particularly if the patient has been treated with aminocaproic acid. A rise in intraocular pressure associated with accelerated hemolysis can mimic a rebleed and may occur 24–96 hours after use of aminocaproic acid has been discontinued.

TRAUMATIC GLAUCOMA AND HYPHEMA 205

A patient who has been treated with aminocaproic acid should continue to have his or her intraocular pressure monitored several days after discontinuation of therapy in the event that there is a spike in intraocular pressure associated with accelerated hemolysis.

22.In the setting of a traumatic hyphema, when is a patient at greatest risk for developing a recurrent hemorrhage?

Between 2 and 5 days following blunt ocular trauma, perhaps due to clot fibrinolysis and retraction.

23.How common is a recurrent hemorrhage?

A recurrent hemorrhage generally occurs in 0.4–35% of patients who suffer a traumatic hyphema.

24.What is the significance of a recurrent hemorrhage? Why is it important to try to prevent it?

A recurrent hemorrhage carries a poorer prognosis than the initial hyphema. Most rebleeds are larger than the initial hyphema and carry an increased risk of developing a secondary glaucoma and corneal blood staining; visual outcome is worse, and there is a more frequent need for surgical intervention.

25.List the risk factors that may be associated with an increased risk of developing a recurrent hemorrhage.

&Antiplatelet or anticoagulant ingestion

&Black and Hispanic race

&Hypotony

&Younger age

&Larger initial hyphema

26.What is an eight-ball hyphema?

An eight-ball or black-ball hyphema is a hyphema that has clotted and taken on a black or purple color (Fig. 20-2). The black or purple appearance of an eight-ball hyphema is due to impaired aqueous circulation, which leads to a subsequent decrease in the oxygenation of the intracameral blood and results in the characteristic blackor purple-colored clot. It is believed that impaired aqueous circulation occurs as

a result of either pupillary block from the clot or direct tamponade effect by the clot at the level of the trabecular meshwork. The impairment in aqueous

circulation prevents the clotted black-ball hyphema from being reabsorbed. These hyphemas carry a graver prognosis with respect to developing secondary glaucoma.

27.How is an eight-ball hyphema different from a total or 100% hyphema?

An eight-ball hyphema describes blood in the anterior chamber that has clotted and taken on a black or purple appearance. A total, or 100%, hyphema is one in which the blood filling the anterior chamber appears bright red. A hyphema that consists of

bright red blood indicates that there is continuous aqueous circulation within the anterior chamber, which results in a significantly more favorable prognosis than an eight-ball hyphema.

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Figure 20-3. Treatment algorithm for ocular trauma and glaucoma. (From Higginbottom EJ, Lee DA: Clinical Guide to Glaucoma Management. Woburn, MA, Butterworth-Heinemann, 2004.)