Case Presentation by Dr. Arun Rajasekhar
CC: Right eye pain
HPI: A 10 year old, otherwise healthy, Caucasian male presents to the ED complaining of right eye pain. About one hour ago, he was playing racquetball. He states that he never wears eye protection, and today the ball ricocheted off the wall and struck him in his right eye. Patient denies any LOC. The area around his eye began to swell immediately after he was struck. Since the accident, his vision has been blurry in his right eye and light exacerbates his pain. His mother gave him an icepack to put over his eye and brought him to the ED immediately after the accident occurred. He is nauseous but has not vomited. He denies having double vision or complete loss of vision in the right eye. He denies any discharge from the eye.
ROS: Negative except for that described in HPI
PMH: Denies DM, denies asthma
PSH: None
ALL: NKDA
MEDICATIONS: None
FH: Negative for DM, Negative for HTN
SH: Lives at home with his mother and father. He attends the 4th grade. There are smoke detectors in the house.
PHYSICAL EXAM:
Vitals: BP 110/70 HR 105 RR 16 Sat 98% Temp 36.8
Gen: Patient his lying in stretcher with ice pack covering right eye.
HEENT: Head is normocephalic. There is mild periorbital swelling around the right eye. No tenderness to palpation of the right orbit and no bony step-offs. Nares are patent bilaterally. Neck is supple. Trachea is midline.
EYES: EOMI. Mild anisocoria. Right eye is 2mm and reactive, left eye is 3mm. Visual acuity is 20/20 OS and 20/50 OD. There is no pupil eccentricity. IOP measurement was deferred. Slit lamp exam shows layered red blood filling about 20% of the anterior chamber (see picture below). There are no corneal abrasions. Negative Seidel sign.
RESP: CTAB
ABD: NTND
MUSC: Moving all extremities. Normal muscle bulk and tone.
NEURO: Alert and oriented. Answering questions appropriately on exam. No facial droop. Normal speech and gait.
Question 1) What grade of hyphema does the patient have?
A) Grade I
B) Grade II
C) Grade III
D) Grade IV
Question 2) Which of the following co-morbidities places a patient at higher risk for developing glaucoma and vision loss from a traumatic hyphema?
A) Diabetes
B) Sickle cell disease
C) HTN
D) Hyperlipidemia
Question 3) What condition must be ruled out prior to measuring intraocular pressures in patient’s with traumatic hyphema
A) Lens dislocation
B) Corneal ulceration
C) Globe rupture
D) Subconjunctival hemorrhage
Discussion/Answers
1) A
2) B
3) C
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. Optimal outcome following a hyphema depends on early ophthalmologic intervention focused on prevention of rebleeding and avoidance of intraocular hypertension.
Hyphema’s are categorized based on the degree of anterior chamber hemorrhaging. The amount of blood in the anterior chamber is correlated with prognosis for recovery of visual acuity.
Presentation – Vision loss and eye pain are common presenting complaints in patients with a traumatic hyphema. In addition, nausea and vomiting may accompany this injury. History reveals blunt trauma to the eye in most cases of traumatic hyphema. Younger children often report being hit in the eye by a ball. Other common physical exam findings are photophobia, anisocoria, corneal blood staining, and elevated intraocular pressure. In regards to photophobia, 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. 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. Corneal blood staining describes diffusion of red blood cell breakdown products into the corneal stroma resulting in golden discoloration of the cornea. 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. Intraocular hypertension (greater than 21 mmHg) occurs in over 30 percent of patients at some point following a hyphema. Patients with sickle cell disease or trait are at higher risk for elevation of intraocular pressure within the first 24 hours. Patients with sickle hemoglobinopathy (sickle cell disease or trait) can only withstand intraocular pressure (IOP) of 24 mmHg for 24 hours (Goldberg’s rule) before permanent ischemic damage to the optic nerve may occur. Pressure elevation may not occur for several days after the injury, necessitating close monitoring during the first week.
Physical examination — Topical analgesia, reduced ambient light, and parental presence facilitate cooperation in the child. 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, visual acuity, extraocular movement, and visual fields by confrontation. If impact was from a blunt object larger than the orbital rim, patient should also be assessed for orbital floor fracture, orbital hemorrhage with proptosis, and orbital compartment syndrome.
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. Flourescein examination should be deferred in patients in whom a ruptured globe is highly suspected or evident upon inspection. In most instances, intraocular pressure measurement should be deferred until after complete evaluation by an ophthalmologist. Injury from small, fast-moving projectiles that hit the eye with a force that is not cushioned by the surrounding orbit increase the risk of an open globe or damage to posterior segment structures.
Physical findings of globe rupture include:
- Markedly decreased visual acuity
- Eccentric pupil
- Increased anterior chamber depth
- Low intraocular pressure
- Extrusion of vitreous
- External prolapse of the uvea or other internal ocular structures
- Tenting of the cornea or sclera at the site of globe puncture
- Seidel’s sign, fluorescein streaming in a tear drop pattern away from the puncture site
A high index of suspicion for posterior rupture should be maintained in the setting of high-risk mechanism coupled with hyphema obscuring posterior visualization. Patients with possible globe rupture 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.
Work up - Patients with sickle cell disease or trait, bleeding dyscrasia, or concern for an open globe need emergent evaluation by an ophthalmologist. All patients of African or Mediterranean heritage with family history of hemoglobinopathy and uncertain screening status require a sickle cell rapid preparation and hemoglobin electrophoresis. Patients with suspected or known bleeding dyscrasia should have a complete blood count (CBC), prothrombin time (PT), partial thromboplastin time (PTT), and international normalized ratio (INR) measured. Emergent imaging is necessary in patients with a suspected open globe or concern for serious orbital injury. 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.
Emergency Treatment - An eye shield should be placed over the affected eye as soon as possible and subsequently removed only as required for examination and imaging. Limitation of activity to bed rest with bathroom privileges should occur until initial evaluation is complete. Elevation of the head to 30 degrees promotes inferior settling of blood in the anterior chamber away from the visual axis while maintaining arterial blood flow to the eye relative to the fully erect position. Topical analgesia with a drop of proparacaine or tetracaine ophthalmic drops may be applied in patients without globe rupture. NSAIDs should be avoided because of their platelet inhibiting effects. Patients with nausea or vomiting require treatment with antiemetics, to prevent sudden increase in intraocular pressure caused by emesis. Cycloplegia often provides pain relief and allows for optimal examination of the posterior segment. They are contraindicated in patients with suspected open globe rupture.
Disposition – Several observational studies suggest that most patients can safely receive treatment for hyphema in the outpatient setting. Inpatient management is recommended for patients with other ocular injuries that require hospital care, suspected child abuse, bleeding dyscrasia, and sickle hemoglobinopathy and is suggested for intraocular hypertension on initial examination, delayed presentation, or large hyphemas (filling of 50 percent or more of the anterior chamber) Additional considerations regarding patient disposition include the ability to adhere to the rigorous regimen of restriction of activity, multiple and frequent medication administration, and daily travel to the ophthalmologist for examination.
Prognosis – Prognosis for visual recovery is correlated with severity/grading of initial hyphema. The main risk to vision from hyphema primarily depends on degree and duration of elevated intraocular pressure and rebleeding. Secondary hemorrhage typically occurs two to five days after initial injury in patients with hyphema and is correlated with anterior chamber clot retraction [9]. Rebleeding predisposes the patient to increased intraocular pressure, secondary glaucoma, and corneal blood staining. Each of these conditions increases the risk of permanent vision loss.
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