Subconjunctival Hemorrhage

Etiology

SCH can be differentiated into 2 categories: traumatic vs spontaneous. Traumatic incidences of SCH have risen secondary to the increased use of contact lenses as well as the number of people undergoing ocular surgeries. Contact lens wearers have a higher tendency to have conjunctivochalasis, pinguecula, and superficial punctate keratitis. These conjunctival diseases can cause increased inflammation through dryness, friction between the lenses and conjunctiva itself, and possible disruption of tear flow. Material defects and surface deposits in hard lenses and defects at the rims with prolonged use of disposable contact lenses can promote SCH.[4][5]

Ocular surgeries, especially in patients on anticoagulation, increase the risk for SCH. Cataract surgery, refractive surgery, and local anesthesia, such as sub-Tenon injections, can potentiate SCH. Local minor trauma such as eye rubbing or a foreign body can cause SCH. For this reason, the patient may not recall any minor trauma. In cases with extensive trauma, SCH may be present in the scope of a more devastating injury, such as an open globe. SCH may develop after orbital fractures. Basilar skull fractures can be identified if SCH is coming from the fornix when globe trauma is not present.[6]

Nonaccidental trauma should be considered in infants who present with bilateral isolated SCH, especially if they are associated with facial petechiae. Traumatic asphyxia syndrome, which is caused by prolonged compression of a child's upper abdomen and chest, can cause sudden severe venous congestion.[7] Conversely, SCH in newborns can be normal after a vaginal delivery with an estimated incidence of 1-2%. The mechanism is the same as above; however, uterine contractions provide the compression.[8]

The biggest risk factor for spontaneous SCH is hypertension and other vascular disorders like diabetes and hyperlipidemia. These diseases can cause blood vessels to become fragile and spontaneously rupture. Hypertension is the major risk factor for SCH, regardless of whether the blood pressure is controlled by medication. Spontaneous SCH has also been shown to be a predictor of hypertension if shown to be high on initial presentation and subsequently at a 1 and 4-week follow-up.[9][10] 

People who have vascular disorders also may be placed on anticoagulation such as warfarin or heparin. NSAIDs such as aspirin and P2Y12 inhibitors such as clopidogrel can also increase the risk for SCH. A risk of SCH is still present even if INR is in the therapeutic range.[11] Spontaneous causes include elevated venous pressures such as coughing, vomiting, strenuous exercise/lifting, and Valsalva maneuvers. Acute hemorrhagic conjunctivitis caused most commonly by enterovirus 70 can cause widely extensive SCH, however, the prevalence of this disease is declining. Menstruation can cause SCH, likely secondary to an underlying blood dyscrasia or venous pressure. There are many other diseases whose initial presentation has been associated with SCH, including Steven-Johnson syndrome, hemochromatosis, and dermatologic vasculature diseases such as Kaposi's sarcoma, pyogenic granuloma, telangiectasias, and hemangiomas. Still, almost half of spontaneous cases of SCH are idiopathic in etiology.

Epidemiology

SCHs, in general, do not have any gender discrepancy. However, traumatic SCH was shown to be more prevalent in young males, most likely related to performing heavy work and a tendency to do more aggressive activities. The rate of spontaneous vs traumatic varies depending on the population characteristics themselves. One study showed the incidence rate of non-traumatic SCH to be higher in women, with a men-to-women ratio of 0.8. It is widely agreed that spontaneous SCH increases with age, especially after 50. This is due to the higher probability of comorbidities such as hypertension, hyperlipidemia, and diabetes mellitus. According to 1 study, there is also an increased incidence of SCH in the summer; however, this may be secondary to children presenting more often during summer vacation.[3][12][13]

Pathophysiology

SCH results from bleeding of the conjunctival or episcleral blood vessels and subsequently leaks into the subconjunctival space. Blood vessels can wear and tear over time. The elastic and connective tissues become fragile with age and underlying comorbidities, which can ease the spread of the bleeding in the elderly. Traumatic SCH is more localized to the site of impact compared to spontaneous. There is a predilection for SCH to develop on the temporal aspect of the eye since the bulbar conjunctiva of the temporal aspect is larger than the nasal aspect. Other reasons include increased incidence of conjunctivochalasis, protection of the nose on the nasal aspect, and more difficulty detecting projectiles on the temporal aspect. The inferior aspect was noted to have an increased incidence of SCH compared to the superior, likely to have blood gravitating downwards after the insult.[14][2][4]

Histopathology

Histopathologically, the bleeding itself occurs between the conjunctiva and the episclera. Specifically, the blood elements are found in the substantia propria. The eye may turn blue and yellow as the hemoglobin and other blood elements break down, similar to a bruise. 

History and Physical

A careful history and physical examination are key to determining whether an SCH is benign or a sign of something more malignant. Sometimes, a patient may be unaware of a problem until he or she looks in a mirror or is told by someone else. A clinician should determine what type of ocular trauma, if any, occurred. A SCH in the setting of blunt trauma is worrisome and should be evaluated for possible ruptured globe or retrobulbar hematoma. Be sure to obtain past medical history, especially vascular disorders like hypertension, hyperlipidemia, and diabetes. Be sure to note any anticoagulant therapy, underlying coagulopathy, or blood dyscrasia. Note any non-compliance with medications, use of contact lenses, and any prior ocular surgeries. The clinician should also determine any viral-like illnesses, coughing, vomiting, or constipation. A history of visual loss, discharge, photophobia, foreign body sensation, or headache should prompt the clinician to investigate other etiologies. 

On the physical exam, SCH is a painless, acute, sharply demarcated area of extravasated blood beneath the eye's surface. SCH is generally unilateral. There is no reduction in visual acuity. A traumatic SCH should be more localized, and if it is spontaneous and elderly, the SCH could be more diffuse. The inferotemporal aspect of the conjunctiva is the most common site. A simple SCH should not have any chemosis, proptosis, purulent discharge, or ophthalmoplegia. In instances of scleral rupture, intraocular blood can leak through a defect and collect in the subconjunctival space, which can create an elevated, bullous-appearing hemorrhage.[2]

A key aspect of the physical exam is distinguishing between conjunctival versus ciliary injection. Conjunctival hemorrhage is caused by dilation of the posterior and more superficial conjunctival vessels. This can cause the eye to appear red in a continuous pattern over the sclera. In contrast, ciliary injection involves dilation of the anterior ciliary arteries, which could imply intraocular inflammation of the iris, cornea, or ciliary body. The ciliary injection can also be known as circumcorneal flush and appears as a halo of redness. The distinction is important since ciliary injection is associated with potentially more dangerous diagnoses such as iritis, acute glaucoma, episcleritis, and scleritis.[15] SCH can also be confused for viral or bacterial conjunctivitis. However, there is usually some degree of pain associated with these diagnoses. Additionally, on physical exam, the redness is more diffuse and not a discreet, confluent area of hemorrhagic change as seen in SCH. Viral conjunctivitis is bilateral, and in most cases, SCH is unilateral.[15]

Evaluation

SCH's initial evaluation and determination are clinical and based on appearance. However, a careful slit-lamp with fluorescein examination is important to determine any ocular trauma or possible underlying local ocular condition, which can lead to an SCH. All patients presenting with SCH should have blood pressure checked routinely. An INR should be checked if a patient is taking warfarin. If the SCH becomes persistent or recurrent, then a workup regarding bleeding disorders and other hypocoagulable states should be done. However, it should be noted that extensive hemostatic testing is not warranted in the absence of other bleeding symptoms and solely SCH. Fundoscopy is generally not indicated.[2][9][16]] 

Treatment / Management

Generally, no treatment is indicated for SCH unless associated with a certain serious condition. The blood is typically resorbed over 1-2 weeks, depending on the amount of extravasated blood. Recovery may take up to 3 weeks if patients are on anticoagulation. Ice packs and artificial tears can minimize tissue swelling and relieve discomfort. Emergent ophthalmology consultation is warranted if SCH occurs via trauma and intraocular or additional retinal trauma is suspected. Dilute brimonidine and oxymetazoline have been indicated to improve patient comfort and decrease the incidence of SCH after intravitreal injections.[2][17][18](A1)

Differential Diagnosis

If orbital trauma is suspected, globe rupture and retrobulbar hematoma are diagnoses that must be ruled out as this is sight-threatening and requires an emergent ophthalmology consult. In the setting of trauma, one must also consider corneal abrasion, conjunctival laceration, ocular foreign body, traumatic iritis, and traumatic hyphema. Differential for non-traumatic cases include conjunctivitis, episcleritis, inflamed pterygium or pinguecula, corneal erosions, keratitis, and anterior uveitis. One must also rule out acute angle-closure glaucoma, corneal ulcer, endophthalmitis, and scleritis, as these are ophthalmologic emergencies.

A more dangerous etiology can often be found just by simple observation. A patient with a globe rupture or retrobulbar hematoma could have some degree of proptosis, chemosis, decreased visual acuity, or a tear-drop-shaped pupil. The physical exam can also help to distinguish other eye disorders, such as an afferent pupillary defect in the setting, optic neuropathy, or consensual photophobia in the setting of iritis. The slit lamp exam with fluorescein staining can be a very useful adjunct in the exam to better investigate possible erosions, ulcers, and dendrites. Many of these patients could have symptoms of grittiness or a foreign body sensation, which should not be present in the case of a simple SCH. 

Prognosis

SCH offers a good visual prognosis after resolution. Vision is generally not impaired. The recurrence rate for spontaneous SCH is about 10% without identifiable risk factors and higher if patients take anticoagulant or antiplatelet therapy.[16]

Complications

There are no complications surrounding SCH, as most resolve around 2 weeks. SCH itself may be a sign of a more underlying dangerous disorder such as coagulopathy, severe asthma exacerbation, non-accidental trauma, or severe orbital trauma.[19]