Subconjunctival Hemorrhage

Etiology

SCH may be categorized as traumatic or spontaneous. Traumatic SCH is more frequently observed in younger individuals and often results from direct ocular trauma, foreign body injuries, excessive eye rubbing, or improper contact lens use. In pediatric populations, trauma accounts for the majority of cases. A retrospective study found that 83% of children presenting with SCH had sustained an eye injury.[4]

Incidences of traumatic SCH have increased due to greater contact lens use and the rising number of ocular surgeries. Contact lens wearers are predisposed to conjunctivochalasis, pinguecula, and superficial punctate keratitis.[5] These conjunctival disorders contribute to inflammation by promoting ocular dryness, increasing friction between the lens and the conjunctiva, and altering tear film stability.

Defects in lens material or surface deposits, as well as irregularities at the rim of hard or disposable lenses, can further heighten the risk of SCH. Prolonged use of disposable lenses with these defects increases the likelihood of conjunctival vessel injury and subsequent hemorrhage.[6][7]

Additional iatrogenic factors can induce SCH, particularly those related to ophthalmic surgical procedures, intravitreal injections, and periocular anesthetics. These interventions compromise conjunctival vessels and predispose to hemorrhage. Mechanical increases in venous pressure from Valsalva maneuvers, including strenuous lifting, constipation, emesis, or coughing, are also recognized precipitants in the absence of direct trauma. Severe trauma may produce SCH as part of more devastating ocular injuries, including open globe injury or orbital fracture. SCH arising from the fornix in the absence of globe trauma should prompt consideration of a basilar skull fracture.[8]

Nonaccidental trauma (NAT) must be suspected in infants presenting with bilateral isolated SCH, particularly when associated with facial petechiae. Traumatic asphyxia syndrome, caused by prolonged compression of the upper abdomen and chest, can produce sudden and severe venous congestion, resulting in SCH.[9] SCH in newborns can occur after vaginal delivery, with an estimated incidence of 1% to 2%. The mechanism mirrors that of Valsalva-related cases, with uterine contractions generating sufficient venous compression to rupture conjunctival vessels.[10]

Nontraumatic, or spontaneous, SCH occurs more often in older individuals and is frequently associated with systemic comorbidities or medications that impair vascular integrity or coagulation.[11][12] Hypertension is the most consistently documented systemic risk factor. Spontaneous SCH may also serve as a predictor of hypertension when blood pressure is elevated at initial presentation and remains high on follow-up.[13]

A large population-based case-control study of more than 65,000 individuals in Taiwan demonstrated strong associations between SCH and comorbid hypertension, purpura, thrombocytopenia, as well as aspirin use.[14] The pathophysiologic mechanism likely involves persistent vascular fragility and impaired autoregulation, which promote spontaneous conjunctival vessel rupture during periods of physiologic stress. Other systemic disorders, including diabetes mellitus, dyslipidemia, and bleeding diatheses such as thrombocytopenia and purpura, have also been implicated. These findings underscore the multifactorial nature of spontaneous SCH and the contribution of unmeasured systemic factors.

Individuals with vascular disease are often prescribed anticoagulants such as warfarin or heparin. Antiplatelet agents, including aspirin and P2Y12 inhibitors such as clopidogrel, also increase the risk of SCH. These associations hold particular relevance for older adults with cardiovascular disease receiving long-term pharmacologic therapy. Risk persists even when the international normalized ratio (INR) remains within the therapeutic range.[15]

Spontaneous SCH may also result from transient elevations in venous pressure caused by coughing, vomiting, strenuous exertion, heavy lifting, or Valsalva maneuvers.[16][17] Acute hemorrhagic conjunctivitis, most commonly associated with enterovirus 70, may produce extensive SCH, although the prevalence of this infection has declined.[18][19] Menstruation has also been reported as a precipitating factor, likely through venous pressure changes or underlying blood dyscrasia.[20]

Additional conditions linked to SCH include Stevens-Johnson syndrome, hemochromatosis, lymphoma, and vascular dermatologic disorders such as Kaposi sarcoma, pyogenic granuloma, telangiectasias, and hemangiomas.[21][22][23] Despite these associations, nearly half of spontaneous SCH cases remain idiopathic in origin.

Epidemiology

SCH is a prevalent ocular condition with occurrence influenced by age, sex, and geographic factors. In general ophthalmic practice, SCH accounts for approximately 3% of emergency or outpatient eye consultations. Prevalence rises substantially in adults older than 65 years, in whom SCH represents up to 10% of clinic-reported eye complaints, reflecting both increased incidence and heightened awareness of ocular changes. The age distribution demonstrates a bimodal pattern. A 1st peak occurs in childhood and adolescence, most often related to trauma, while a 2nd, more prominent rise appears in adults aged 60 to 69, when spontaneous causes predominate. These age-related patterns underscore shifting etiologies, comorbid health conditions, and medication exposures across the lifespan.

Population-based studies reveal sex-specific differences in the incidence of SCH, although results vary by geography and study methodology. Overall, no major sex discrepancy has been established. Traumatic SCH occurs more frequently in younger male individuals, likely reflecting greater involvement in heavy labor and higher participation in aggressive physical activities.

A nationwide cohort study in South Korea reported a higher incidence in female individuals, with a male-to-female ratio of 0.80.[24] This trend was most pronounced among older adults with spontaneous SCH. In contrast, studies from Congo described a slight male predominance, particularly in settings where trauma represents the primary cause of SCH.[25] These inconsistencies highlight the influence of trauma exposure, occupational hazards, healthcare-seeking behavior, and systemic disease patterns across populations.

Consistent findings indicate that traumatic SCH predominates in younger male individuals, while spontaneous SCH is more common in older women, usually in association with hypertension and vascular fragility. Spontaneous SCH also becomes more frequent with advancing age, particularly after 50 years, when comorbidities such as hypertension, hyperlipidemia, and diabetes mellitus are more prevalent. Seasonal, environmental, and biological factors, along with socioenvironmental influences, may play minor contributory roles.

Pathophysiology

SCH develops when fragile conjunctival capillaries rupture, leading to extravasation of blood into the subconjunctival space between the bulbar conjunctiva and the underlying episclera. The conjunctival vasculature consists of fine, unsupported capillaries that are particularly vulnerable to mechanical stress and hemodynamic fluctuations.

Loss of vascular integrity from abrupt pressure changes, trauma, or systemic vascular fragility allows blood to accumulate beneath the conjunctiva. Limited lymphatic drainage in this region prevents rapid clearance, producing the sharply demarcated red patch characteristic of SCH. Surrounding tissues lack firm structural attachments and adequate lymphatic channels, which explains the slow resorption process lasting several days to weeks. Advancing age and comorbid conditions further weaken elastic and connective tissues, increasing vessel fragility and facilitating more extensive bleeding in older adults.

Traumatic SCH occurs when mechanical stress disrupts the integrity of superficial conjunctival capillaries. Even minor forces, including vigorous eye rubbing, sneezing, or coughing, can cause rupture if transient intravascular pressure exceeds vascular tensile strength. The Valsalva maneuver, which elevates intrathoracic and venous pressure, is a well-recognized mechanism.

A retrospective review of more than 34,000 pediatric patients demonstrated that SCH is uncommon in children, with an incidence of 0.4% when excluding surgical cases. Trauma accounted for over 80% of presentations across all age groups, followed by ocular surface inflammation. These findings emphasize the importance of thorough assessment for potential abuse or injury, particularly in infants and young children with SCH. In newborns, vaginal delivery may induce SCH through increased venous pressure and mechanical compression. Hemorrhage is localized and not associated with systemic coagulopathy in these cases, distinguishing it from other ocular bleeding disorders.[26]

Traumatic SCH is usually more localized to the site of impact than spontaneous SCH. The hemorrhage most often appears on the temporal side of the eye, where the bulbar conjunctiva is larger than on the nasal side, possibly because blood gravitates downward after injury.[27] Additional explanations include the higher incidence of conjunctivochalasis, the protective effect of the nose on the nasal aspect, and greater difficulty detecting projectiles on the temporal side.

Despite its often dramatic appearance, SCH is confined to the conjunctival space due to the anatomical barrier of the Tenon capsule and the absence of deeper vascular involvement. Unlike retinal or choroidal hemorrhages, SCH does not cause vision loss, photophobia, or intraocular inflammation. Blood resorption follows the same process as dermal bruising, with hemoglobin breakdown products such as biliverdin and bilirubin producing the characteristic color changes over time. Recurrent SCH warrants systematic evaluation to exclude hematologic disorders such as thrombocytopenia, clotting factor deficiencies, or vascular dysplasias, although these abnormalities are uncommon. The underlying pathophysiology reflects an interplay between local capillary fragility and systemic conditions that heighten the risk of vascular rupture.

Histopathology

The histological features of SCH demonstrate focal vascular rupture with blood accumulation in the potential space beneath the bulbar conjunctiva. Microscopic evaluation shows fresh or organizing hemorrhage between the conjunctival epithelium and the Tenon capsule, without extension into deeper ocular structures. In the acute stage, erythrocytes occupy the substantia propria of the conjunctiva, accompanied by a mild inflammatory response. The conjunctival epithelium usually remains intact, without necrosis or significant epithelial disruption, which distinguishes SCH from infectious or necrotizing processes.

The absence of arterial channels in the episcleral region contributes to the strict extravascular confinement of the hemorrhage. Trauma or contact lens wear may cause mechanical alteration of the conjunctival stroma, occasionally with goblet cell loss or basement membrane irregularity. These histologic changes are generally modest and transient, leaving no lasting sequelae.

History and Physical

A careful history and physical examination are essential to determine whether an SCH is benign or a sign of a more serious condition. Many patients remain unaware of the hemorrhage until noticing it in a mirror or being informed by others.

A thorough history should establish the onset and duration of the hemorrhage, the presence or absence of trauma, and potential triggers such as coughing, sneezing, vomiting, or heavy lifting. Inquiry into visual loss, discharge, photophobia, foreign body sensation, or headache is important, as these features suggest alternative etiologies.

In younger patients, trauma is the most frequent cause, making it necessary to assess for recent injuries, prior ocular surgery, aggressive eye rubbing, or contact lens wear. SCH associated with blunt trauma warrants evaluation for globe rupture or retrobulbar hematoma.[28] Past medical history is equally important to identify systemic risk factors, including hypertension, hyperlipidemia, diabetes, anticoagulant therapy, coagulopathy, and blood dyscrasia.

On physical examination, SCH appears as a painless, acute, sharply demarcated collection of blood beneath the ocular surface. Bleeding is generally unilateral and does not affect visual acuity. Traumatic SCH tends to be more localized, whereas spontaneous SCH in older individuals is usually more diffuse. The inferotemporal conjunctiva is the most common site. A simple SCH should not present with chemosis, proptosis, purulent discharge, or ophthalmoplegia. Scleral rupture may cause intraocular blood to escape through a defect and accumulate in the subconjunctival space, creating an elevated, bullous-appearing hemorrhage.

A key aspect of the physical examination is distinguishing conjunctival from ciliary injection. Conjunctival hemorrhage results from dilation of the posterior and more superficial conjunctival vessels, creating a continuous red pattern across the sclera. In contrast, ciliary injection involves dilation of the anterior ciliary arteries and suggests intraocular inflammation of the iris, cornea, or ciliary body. Also called a "circumcorneal flush," ciliary injection appears as a halo of redness. This distinction is critical, as ciliary injection is associated with more serious conditions such as iritis, acute glaucoma, episcleritis, and scleritis.[29]

SCH may also be mistaken for viral or bacterial conjunctivitis. These conditions usually cause some degree of pain, and the redness is diffuse rather than a discrete, confluent hemorrhage. Bilateral involvement is common in viral conjunctivitis, contrasting with the mostly unilateral presentation of SCH.[30]

Evaluation

The diagnostic assessment of SCH is primarily clinical, based on patient history and external ocular examination. Laboratory or imaging studies are rarely required, particularly when the hemorrhage presents as a solitary, unilateral event without systemic symptoms or other ocular abnormalities. A thorough history should exclude recent trauma, Valsalva maneuvers, and contact lens use. The physical examination must confirm normal visual acuity and intraocular pressure (IOP), with no pain or photophobia.[31] The diagnosis can be made confidently without additional testing in routine cases, especially in younger individuals with clear traumatic or mechanical triggers. Clinicians should remain alert for red flags that warrant further evaluation, including recurrence, bilateral involvement, systemic bruising, or a history of anticoagulant therapy.

A more thorough assessment may be warranted when spontaneous SCH occurs, particularly in older adults or individuals with comorbidities. Blood pressure measurement is essential for all patients with spontaneous or recurrent hemorrhage, given the strong association between spontaneous cerebral hemorrhage and uncontrolled hypertension.[32] Clinicians should assess adherence, recent dosage changes, and the presence of bleeding in nonocular sites in patients receiving anticoagulant or antiplatelet therapy.

Basic laboratory studies, including total blood count, prothrombin time, activated partial thromboplastin time, and INR, can help identify underlying coagulopathies or iatrogenic factors related to excessive anticoagulation. These assessments are particularly important in older or medically complex individuals, where hemorrhage may be the first indication of systemic disease.

A slit-lamp examination is indicated to exclude a retained foreign body. Slit-lamp biomicroscopy helps evaluate conjunctival anatomy and identify subtle disorders such as conjunctivochalasis or pinguecula. This assessment may reveal structural alterations that predispose to recurrent hemorrhage, particularly in older adults or long-term contact lens users. Additional evaluations, such as Seidel testing for globe rupture, fluorescein staining for corneal abrasions, and orbital imaging for suspected fractures, may be necessary in cases of SCH following trauma. When posterior segment involvement is suspected due to reduced visual acuity or an afferent pupillary defect, a dilated fundus examination and optical coherence tomography may be required to exclude retinal or vitreous hemorrhage, which carries different prognoses and therapeutic implications.

No international or national guidelines have been established specifically for SCH evaluation, likely owing to its predominantly benign nature. Broader clinical guidelines emphasize the exclusion of secondary causes based on age, systemic comorbidities, and recurrence patterns.

A Korean population-based study reported that patients with subclinical hypothyroidism were generally older and exhibited higher rates of systemic vascular disease, including hypertension and diabetes, supporting routine blood pressure measurement and cardiovascular risk assessment in older adults. In children, limited evaluation is appropriate unless concerns for abuse, systemic disease, or bilateral involvement arise, making laboratory testing and imaging warranted.[33] Overall, the evaluation of SCH is pragmatic, relying on clinical assessment while reserving additional studies for atypical or recurrent cases.[34][35]

Treatment / Management

The management of SCH is primarily conservative, as the condition is self-resolving in most cases. No specific medical or surgical intervention is required. Hemorrhages typically resolve within 7 to 14 days, depending on the volume of bleeding and the patient’s absorptive capacity. During this period, patients should be reassured of the benign nature of the condition and monitored as appropriate. Artificial tears may be recommended for symptomatic relief in cases of irritation, although they do not affect resolution. Patients should be advised to avoid eye rubbing, strenuous activity, or Valsalva maneuvers that may exacerbate bleeding or trigger recurrence.

In severe SCH, management requires careful evaluation to exclude concomitant ocular injury. No further intervention is needed beyond lubrication and comfort measures when the bleeding is localized and the globe is intact. Clinicians should assess for corneal abrasions, anterior chamber involvement, or orbital fractures if spontaneous hyphema occurs after trauma. In selected cases, fluorescein staining and orbital imaging may be warranted. With preserved vision and no associated injury, conservative therapy remains appropriate. Protective eyewear is advised for athletes or individuals at increased risk of ocular trauma. Treatment is generally unnecessary in children unless secondary complications, such as infection or retained foreign material, are identified.

In SCH, particularly among older adults or patients receiving anticoagulant therapy, management should address both ocular manifestations and systemic contributors. Blood pressure control is essential for recurrent or extensive hemorrhage, and adjustments to aspirin, warfarin, or direct oral anticoagulants may be considered in collaboration with a primary care physician or cardiologist. Evidence indicates a strong association between spontaneous SCH and systemic hypertension, and antihypertensive therapy may reduce recurrence. Antithrombotic therapy in patients with isolated SCH may generally be maintained, given the minimal ocular risk compared with the systemic benefits of anticoagulation. Coagulation profiles, including INR, may be assessed to confirm therapeutic levels.

Topical steroids or antibiotics are not recommended in uncomplicated SCH, as they are unnecessary and potentially harmful. Antibiotic drops may be prescribed in rare cases with conjunctival inflammation or concurrent conjunctivitis, although these medications do not influence hemorrhage resolution. Surgical intervention is reserved for cases involving suspected malignancy, foreign body retention, or scleral rupture. Emergency ophthalmology referral is indicated when SCH results from trauma with suspected intraocular or retinal injury. Dilute brimonidine and oxymetazoline have been shown to improve patient comfort and decrease the incidence of SCH following ocular surgery and intravitreal injection.[36][37](A1)

Differential Diagnosis

SCH generally manifests as a distinct red lesion on the sclera and is readily identifiable in most cases. Other conditions may mimic or be mistaken for SCH, particularly in atypical presentations. A key distinction exists between SCH and episcleritis or scleritis.[38] Episcleritis presents with localized redness and mild irritation but lacks the sharply demarcated appearance of SCH.[39] The condition often causes slight discomfort and responds to topical phenylephrine, unlike SCH. Scleritis represents a severe, often bilateral inflammatory disorder associated with systemic autoimmune disease, marked by violaceous discoloration and significant tenderness on palpation. Unlike SCH, both conditions demand urgent recognition and thorough evaluation to guide appropriate therapy.

Globe rupture and retrobulbar hematoma must be excluded if orbital trauma is suspected, as both are sight-threatening and require an emergent ophthalmology consult. In traumatic settings, additional considerations include corneal abrasion, conjunctival laceration, ocular foreign body, traumatic iritis, and traumatic hyphema. Patients with a globe rupture, orbital fracture, or retrobulbar hematoma may present with proptosis, chemosis, decreased visual acuity, or a tear-drop-shaped pupil.[40]

The physical examination may also distinguish other ocular disorders, such as an afferent pupillary defect in optic neuropathy or consensual photophobia in iritis. Slit-lamp examination with fluorescein staining is a valuable adjunct for identifying erosions, ulcers, and dendritic lesions. Many patients report grittiness or a foreign body sensation, which should not occur in a simple SCH. Differential diagnoses for nontraumatic cases include conjunctivitis, episcleritis, inflamed pterygium or pinguecula, corneal erosions, keratitis, and anterior uveitis. Acute angle-closure glaucoma, corneal ulcer, endophthalmitis, and scleritis must also be ruled out, as these represent ophthalmologic emergencies. 

Another important differential diagnosis includes conjunctival lesions that present as hemorrhagic or vascularized. Conjunctival hemangiomas and arteriovenous malformations can cause localized vascular congestion that mimics SCH, particularly when thrombosed or irritated.[41][42][41] Kaposi sarcoma, a vascular neoplasm affecting mostly immunocompromised patients, may also manifest as conjunctival vascular lesions that resemble recurrent SCH.[43] These lesions typically persist beyond the resorption period of a simple SCH and may appear nodular or elevated on slit-lamp examination. Conjunctival melanoma and lymphoproliferative tumors can also produce bleeding lesions, especially in the context of secondary hemorrhage.[44] Any persistent conjunctival mass or blood accumulation requires further evaluation with anterior segment imaging or biopsy.

Vitreous or anterior chamber hemorrhages should be considered in the differential, particularly when subhyaloid hemorrhage follows trauma. Hyphema, defined as blood within the anterior chamber, appears as a crimson fluid level on slit-lamp examination and may present with discomfort, photophobia, and elevated IOP.[45] Vitreous hemorrhage, in contrast, produces floaters, vision loss, and obscuration of the fundus, often secondary to proliferative diabetic retinopathy, trauma, or retinal tears.

Unlike SCH, these hemorrhages involve intraocular compartments and carry a substantial risk of visual impairment. Careful assessment of visual acuity, pupillary response, and anterior segment findings is essential for distinguishing these conditions. When diagnostic uncertainty persists, ocular ultrasonography or optical coherence tomography can help differentiate subhyaloid hemorrhage from posterior segment hemorrhage.

In pediatric populations, the differential diagnosis should include NAT (child abuse), coagulopathies such as idiopathic thrombocytopenic purpura or leukemia, and infectious conjunctivitis.[46][47][48][49] SCH due to child abuse is often bilateral or associated with retinal hemorrhages and other signs of trauma, such as contusions or fractures.[50] Bilateral SCH may also occur with traumatic asphyxia syndromes, including strangulation.

Recurrent SCH in children requires evaluation for systemic bleeding disorders, particularly when accompanied by petechiae, epistaxis, or mucosal bleeding.[51] Infectious conjunctivitis produces a red eye typically associated with purulent discharge, pruritus, or a recent upper respiratory infection. In contrast, SCH is usually asymptomatic, with only bright red staining and no discharge or conjunctival chemosis. Clinicians must therefore rely on detailed history, physical examination, and, when appropriate, laboratory testing to distinguish SCH from its mimics in both pediatric and adult populations.

Staging

SCH is a benign ocular disorder without a formal staging system recognized by international ophthalmologic or hematologic organizations. Clinicians often describe a predictable clinical trajectory that can be theoretically categorized into stages according to onset, progression, and resolution. These stages are valuable for patient counseling, monitoring, and distinguishing uncomplicated SCH from ocular conditions that lack a similar resolution pattern. In practice, SCH follows distinct phases: acute presentation, intermediate transformation, and eventual resolution. This progression parallels cutaneous ecchymosis, reflecting hemoglobin breakdown within conjunctival tissues.[52]

The acute phase presents as a bright red or crimson lesion localized to the bulbar conjunctiva. This manifestation corresponds to recent vascular rupture and accumulation of intact erythrocytes in the subconjunctival space. The affected region is sharply demarcated, flat or slightly raised, and generally painless. This stage lasts 1 to 5 days, during which the intense coloration reflects high oxygen content and hemoglobin concentration of freshly extravasated blood. The lesion does not blanch under pressure and remains immobile on palpation due to its confinement within the conjunctival stroma. Patients may report foreign body sensation or mild irritation, but visual disturbance, photophobia, and systemic symptoms are absent.

During the subacute or metamorphosis phase, the hemorrhage changes in color as hemoglobin undergoes degradation. The affected area may appear purple, brown, or greenish-yellow as hemoglobin breaks down into biliverdin and bilirubin. Macrophage infiltration and erythrocyte phagocytosis dominate this phase, signifying histological and immunological clearance of the hemorrhagic material. This stage typically occurs between days 5 and 10 and serves as a clinical marker that resolution is underway. The lesion may fragment or adopt a patchy distribution, and the color gradient may shift inferonasally due to gravitational pooling. The absence of pain or new symptoms during this period corroborates the benign course.

The resolution phase is characterized by progressive clearing of discoloration and restoration of the normal conjunctival appearance, usually between 10 and 21 days after onset. More extensive hemorrhages, or those in older or anticoagulated patients, may persist longer. No scarring, fibrosis, or pigmentation develops, and recurrence in the same location does not indicate structural damage. Persistence beyond 3 weeks or frequent recurrence warrants reassessment for systemic or local risk factors, including hypertension, vascular fragility, and conjunctivochalasis. Although SCH is not formally classified in the literature, a practical understanding of its temporal stages enhances diagnostic accuracy, patient education, and clinical management.

Prognosis

The prognosis for SCH is highly favorable. Vision is unaffected, and most cases are self-limiting, resolving spontaneously within 7 to 14 days. Reabsorption of extravasated blood occurs efficiently due to the superficial vascular network and intact conjunctival tissue. Recurrence occurs in about 10% of cases without risk factors and is more frequent with anticoagulant or antiplatelet use. Recurrent episodes are commonly linked to uncontrolled hypertension, chronic anticoagulation, or anatomical variants such as conjunctivochalasis.

Patients with vascular or anatomic predispositions generally have a favorable outlook, although recurrence is more likely. Conjunctivochalasis, pinguecula, and improper contact lens use increase risk by introducing frictional stress and microvascular fragility in the bulbar conjunctiva.[53][54] In such cases, resolution may be slower and recurrence triggered by minimal stimuli. Permanent visual loss, scarring, or tissue damage does not occur. The prognosis of SCH is excellent across all causes and patient groups when systemic risk factors are identified and addressed.

Complications

SCH is considered a benign ocular condition, and complications are rare in otherwise healthy individuals. Most cases resolve within 2 weeks without intervention, as the hemorrhage is confined to the subconjunctival space and does not affect vision, IOP, or ocular motility. Infection, scarring, or permanent sequelae do not occur. The principal concern is cosmetic, as the striking appearance often causes disproportionate distress despite the absence of functional impairment. Delayed resolution or recurrence may occur in patients receiving anticoagulant therapy or those with systemic vascular disease, although these outcomes remain clinically insignificant.

Recurrent SCH may rarely indicate an unrecognized systemic disorder. Hematologic conditions such as thrombocytopenia, leukemia, or von Willebrand disease may first present with ocular hemorrhage.[55] In some cases, SCH is bilateral or associated with bleeding at other mucosal sites, including the gums or nasal cavities. These systemic disorders carry significant morbidity, underscoring the need for comprehensive evaluation in recurrent or unexplained presentations. Population-based data also suggest an association between SCH and subclinical hypothyroidism, in which higher baseline rates of hypertension, diabetes, and dyslipidemia contribute to vascular fragility and systemic morbidity.