Subconjunctival Hemorrhage

Spontaneous (Idiopathic)

The majority of SCH cases are spontaneous and occur without identifiable trauma. They are thought to result from the rupture of a small conjunctival arteriole or venule, often precipitated by a sudden transient rise in venous pressure. In many cases, no precipitating event can be identified and the episode is attributed to microangiopathic fragility, particularly in older patients with vascular risk factors. Spontaneous SCH is particularly common in the sixth decade and beyond.

Valsalva-Related

Any activity that dramatically and transiently raises intrathoracic or intra-abdominal pressure — and consequently elevates venous pressure — can precipitate rupture of a conjunctival vessel. Common Valsalva triggers include:

• Violent coughing (pertussis, COPD exacerbation)
• Forceful sneezing
• Vomiting (including pregnancy-related hyperemesis)
• Heavy lifting, straining at stool (constipation)
• Childbirth and prolonged labour
• Intense physical exertion or weight training

Traumatic

Direct ocular or periocular trauma is a major cause of SCH. The range spans minor insults — vigorous eye rubbing, contact lens removal trauma, foreign body impact — to significant blunt or penetrating injuries. Importantly, in the context of significant blunt trauma, a circumferential SCH that extends to the posterior limit of the visible conjunctiva (360° SCH or "bloody chemosis") may indicate a ruptured globe or orbital floor fracture, and requires urgent assessment.

Iatrogenic / Post-Procedural

• Intraocular injections (anti-VEGF, steroid) — most common iatrogenic cause
• Conjunctival or anterior segment surgery
• Eyelid surgery (ptosis repair, blepharoplasty)
• Scleral buckling procedures
• Tonometry (applanation or non-contact) — rarely
• Forceful eyelid retraction during examination

Systemic and Pharmacological

• Anticoagulants: warfarin, heparin, direct oral anticoagulants (DOACs — apixaban, rivaroxaban, dabigatran)
• Antiplatelet agents: aspirin, clopidogrel, ticagrelor
• Hypertension: acute hypertensive episode or chronically uncontrolled blood pressure
• Bleeding diatheses: thrombocytopenia (ITP, drug-induced), haemophilia A and B, von Willebrand disease
• Haematological malignancy: leukaemia, lymphoma causing thrombocytopenia or coagulopathy
• Liver disease: cirrhosis with synthetic failure reducing coagulation factor production
• Infectious: leptospirosis, dengue fever (common cause of bilateral SCH in endemic regions)
• Anaemia: severe anaemia predisposes conjunctival vessels to fragility

Vascular Anatomy of the Conjunctiva

The bulbar conjunctiva is supplied by the anterior ciliary arteries (branches of the ophthalmic artery) and the palpebral arcades. The conjunctival venous drainage parallels the arterial supply and communicates with the episcleral and vorticose venous systems. The subconjunctival space — between the conjunctival epithelium and the underlying Tenon's capsule — is loosely adherent, allowing blood to spread freely once vessel integrity is breached.

Mechanism of Hemorrhage

SCH results from rupture of a small conjunctival blood vessel — most commonly a post-capillary venule or arteriole — with subsequent extravasation of blood into the subconjunctival space. The conjunctival epithelium remains intact, so blood does not reach the ocular surface; instead it is sequestered as a flat pool beneath the transparent conjunctiva, creating the characteristic red appearance.

The sharp demarcation of the hemorrhage border is explained by the adherence of the conjunctiva to the limbal tissue and the posterior forniceal conjunctiva; blood cannot track beyond these attachment points under normal pressure. In extensive or traumatic SCH, blood may dissect anteriorly to the limbus, or posteriorly if tissue planes are disrupted.

Predisposing Microangiopathic Changes

Chronic hypertension, diabetes mellitus, and ageing produce structural changes in the conjunctival microcirculation — including intimal thickening, smooth muscle hypertrophy, and loss of arteriovenous autoregulation. These changes render the vessels susceptible to rupture under conditions of increased transmural pressure (e.g. Valsalva, acute hypertensive surge) or with minimal mechanical trauma. Anticoagulant and antiplatelet therapy impairs the haemostatic response to vessel rupture, resulting in larger and more persistent hemorrhages.

Resolution Mechanism

The subconjunctival blood pool undergoes progressive degradation by tissue macrophages. Haemoglobin is catabolised to biliverdin and bilirubin, producing the sequential colour change from bright red (oxyhaemoglobin) → dark red (deoxyhaemoglobin) → orange-brown (methaemoglobin) → yellow (bilirubin). Complete reabsorption typically occurs within 1–3 weeks, dependent on the volume of extravasated blood.

By Aetiology

By Extent

• Sectoral (localised): involves less than 90° of the circumference; the most common presentation; almost always benign
• Extensive (hemi-circumferential or greater): involves 90–270° of bulbar conjunctiva; more likely to be associated with significant Valsalva, anticoagulation, or systemic cause
• Circumferential (360° / "bloody chemosis"): blood extends around the entire limbus with chemosis; a red flag for ruptured globe or severe blunt trauma — urgent ophthalmology assessment mandatory

By Chronicity

• First episode: usually benign; BP measurement reasonable; no blood tests unless other risk factors present
• Recurrent (≥2 episodes within 3 months): systemic investigation mandatory — coagulation screen, full blood count, fasting glucose, BP review, medication review

Classic Biomicroscopic Appearance

• Colour: homogeneous bright red (oxyhaemoglobin) in the acute phase; darkens over days 2–5, then becomes orange-yellow as resolution proceeds
• Margins: sharply demarcated from the adjacent white sclera — this sharp border is a key distinguishing feature from conjunctivitis, which produces diffuse injection without clear margins
• Surface: flat; the overlying conjunctival epithelium is intact and mobile over the blood pool
• Location: most commonly temporal bulbar conjunctiva; may be nasal or inferior; posterior extent limited by forniceal conjunctival attachment (blood cannot track behind the equator in intact cases)
• Laterality: typically unilateral (spontaneous); bilateral SCH raises suspicion of systemic cause, coagulopathy, or acute haemorrhagic conjunctivitis

Associated Findings to Note

• Anterior segment: cornea, anterior chamber depth, and pupillary responses should be normal in uncomplicated SCH
• IOP: normal in spontaneous SCH; elevated IOP in the context of trauma may indicate hyphema or angle injury
• Conjunctival chemosis: oedema accompanying extensive hemorrhage; if marked with 360° blood, evaluate for ruptured globe
• Subretinal or vitreous hemorrhage: should be absent in isolated SCH; their presence implies significant ocular trauma or systemic vascular disease requiring urgent assessment

Resolution Colour Sequence

Ruptured Globe (Post-Traumatic)

Circumferential SCH following blunt or penetrating trauma is a critical red flag for globe rupture or perforation. The hemorrhage may mask the site of scleral laceration. Clinical signs suggesting ruptured globe include 360° bloody chemosis, low or asymmetric IOP, misshapen or peaked pupil, uveal prolapse, and dramatically reduced visual acuity. Immediate ophthalmology referral is mandatory.

Associated Intraocular Injury

Significant blunt trauma causing SCH may concurrently produce hyphema (blood in the anterior chamber), traumatic uveitis, lens subluxation, vitreous hemorrhage, commotio retinae, retinal dialysis, or traumatic optic neuropathy. Each of these may threaten vision and requires urgent dilated posterior segment assessment by an ophthalmologist.

Conjunctival Prolapse

Very extensive SCH, particularly in patients on anticoagulants or with amyloidosis, can produce sufficient conjunctival ballooning to cause prolapse beyond the eyelid margins. This may prevent proper lid closure and requires lubrication and, rarely, surgical repositioning.

Psychological Impact

The alarming appearance of a bright-red eye can cause significant anxiety, particularly in older patients or those with known cardiovascular disease. Recurrent SCH may generate disproportionate health anxiety warranting targeted reassurance and patient education.

Delayed Systemic Diagnosis

Recurrent SCH without an obvious mechanical cause should prompt blood pressure measurement and a targeted review of anticoagulant therapy. If SCH is the first presentation of undiagnosed leukaemia, thrombocytopenia, or dengue — conditions where treatment timing is critical — failure to investigate may delay a life-altering diagnosis.

Hypertension

Systemic hypertension is the most frequently identified systemic association with spontaneous SCH. An acute hypertensive episode can precipitate rupture of a conjunctival arteriole. Notably, the presence of SCH alone does not indicate a hypertensive crisis; however, it justifies blood pressure measurement at the time of presentation. Several studies have demonstrated a higher prevalence of hypertension in patients with spontaneous SCH compared to age-matched controls, particularly for bilateral or recurrent cases.

Diabetes Mellitus

Diabetic microangiopathy produces endothelial dysfunction, basement membrane thickening, and loss of pericyte support in small vessels throughout the body, including the conjunctival microvasculature. These structural changes increase vessel fragility. Diabetic patients may have recurrent or unusually large SCH disproportionate to the precipitating cause.

Anticoagulant and Antiplatelet Therapy

Warfarin — particularly at supratherapeutic INR — is a well-established cause of extensive and recurrent SCH. Direct oral anticoagulants (DOACs) also predispose to SCH but with lower bleeding risk than warfarin at equivalent anticoagulation levels. Antiplatelet agents (aspirin, clopidogrel) impair primary haemostasis and can produce SCH with minor Valsalva manoeuvres. Medication review is essential in all patients with recurrent SCH.

Dengue Fever

In Singapore and Southeast Asia, dengue fever deserves particular mention as a cause of bilateral SCH. Dengue-induced thrombocytopenia (platelet counts may fall below 20 × 10⁹/L) combined with dengue-associated vasculitis creates a high-risk combination for spontaneous hemorrhage at multiple sites. Bilateral SCH in a febrile patient in an endemic region should prompt dengue NS1 antigen and serology testing. Dengue-related SCH is managed supportively with close platelet count monitoring and haematological consultation.

Haematological Malignancy

Acute leukaemia (AML, ALL) and lymphoma may present with SCH as part of a generalised bleeding tendency from thrombocytopenia, coagulopathy (DIC in AML), or hyperviscosity syndrome (IgM paraprotein in Waldenström macroglobulinaemia). Associated features include petechiae, gingival bleeding, epistaxis, bruising, and systemic symptoms (fever, weight loss, fatigue). Full blood count and blood film are mandatory in patients with unexplained bilateral or recurrent SCH.

Leptospirosis

Leptospirosis — an important occupational and waterborne infection in tropical regions including Singapore — causes systemic vasculitis, thrombocytopenia, and hepatic dysfunction. Bilateral SCH is a well-described ocular manifestation, alongside anterior uveitis in the immune phase. A history of exposure to floodwater, animal contact, or outdoor recreational activities in an endemic region warrants leptospiral serology.

Bleeding Disorders

Haemophilia A (Factor VIII deficiency), haemophilia B (Factor IX deficiency), and von Willebrand disease may manifest with easy bruising and mucosal hemorrhage, including SCH. In patients with known bleeding disorders, SCH typically represents a minor manifestation, but may indicate suboptimal factor replacement. Newly diagnosed cases with no prior bleeding history should undergo coagulation screening (PT, aPTT, fibrinogen) and von Willebrand antigen and activity assays.

Clinical Diagnosis

SCH is a clinical diagnosis made by slit-lamp biomicroscopy. No ancillary ocular investigations are required to confirm the diagnosis. The characteristic sharply demarcated, flat, bright-red subconjunctival blood pool with an intact overlying epithelium is pathognomonic. The priority of the clinical assessment is to identify features suggesting ruptured globe, significant intraocular injury, or systemic cause.

Essential Clinical Assessment

• Best-corrected visual acuity: should be normal in uncomplicated SCH; any reduction requires further assessment
• Pupillary responses: RAPD, anisocoria, or irregular/peaked pupil are red flags for posterior segment pathology or ruptured globe
• Slit-lamp examination: confirm subconjunctival location; assess cornea (intact), anterior chamber (depth, cells, flare), iris, and lens
• Intraocular pressure: check bilaterally; asymmetrically low IOP in a traumatic eye is an emergency sign of globe rupture
• Posterior segment assessment: using approved non-dilating diagnostic equipment; assess optic disc, macula, and peripheral retina for vitreous hemorrhage, retinal tears, or commotio retinae in traumatic cases
• Extent and location mapping: document with anterior segment photography where available; note if posterior extent is visible (inability to see the posterior edge suggests possibility of extension along optic nerve sheath in severe trauma)
• Blood pressure measurement: recommended at the time of presentation for all patients with spontaneous SCH

Systemic Investigations (Selective)

1. Patient Reassurance and Education

The cornerstone of management for uncomplicated spontaneous SCH is patient reassurance. Patients must understand that:

• The condition is almost always benign and self-limiting
• Complete resolution is expected within 1–3 weeks
• The colour change from red to orange to yellow is normal and expected
• Vision is not affected and the eye is not at risk from the hemorrhage itself
• No topical treatment is required or proven to accelerate resolution

2. Comfort Measures

• Preservative-free artificial tears: lubricants are appropriate for mild foreign body sensation or dryness; they do not accelerate resolution but improve comfort
• Cold compress (first 24–48 hours): may reduce any associated discomfort and limit further extravasation by vasoconstrictive effect
• Warm compress (after 48 hours): promotes vasodilation and macrophage-mediated reabsorption; gentle application recommended
• Avoid eye rubbing — particularly important if the SCH was precipitated by rubbing in the first instance

3. Address Underlying Cause

• Hypertension: if elevated BP is detected, urgent GP referral for medication review and blood pressure management
• Anticoagulant review: if patient is on warfarin with supratherapeutic INR, urgent medical review; do not discontinue anticoagulant therapy without physician guidance
• Treat precipitating cause: manage chronic cough, constipation, or allergic conjunctivitis to reduce Valsalva risk
• Medication reconciliation: review all prescription and over-the-counter medications including supplements (aspirin, NSAIDs, fish oil, ginkgo biloba)

4. Referral Criteria

5. Follow-up

• Uncomplicated first-episode SCH does not require a routine follow-up appointment; advise the patient to return only if vision changes, pain develops, or the hemorrhage does not resolve within 3 weeks
• Recurrent SCH should be reviewed after systemic investigation results are available
• Document with anterior segment photography at baseline to facilitate comparison if recurrence occurs

Uncomplicated Spontaneous SCH

The prognosis for isolated spontaneous SCH is excellent. Complete resolution occurs in virtually all cases within 2–3 weeks without any treatment. There is no permanent damage to the conjunctiva, sclera, or any intraocular structure. Visual acuity, colour vision, and visual field are unaffected. The condition leaves no clinical sequelae and the eye returns to its normal appearance completely.

Recurrence

Recurrence rates for spontaneous SCH are not well-characterised in prospective studies, but clinical experience suggests that patients who have had one episode — particularly those with hypertension, diabetes, or anticoagulant use — have an elevated risk of subsequent episodes. Addressing modifiable risk factors (blood pressure control, optimal anticoagulant dosing, avoiding unnecessary NSAIDs and supplements) reduces recurrence risk.

Traumatic SCH

Prognosis of traumatic SCH depends entirely on the nature and severity of associated injuries. An isolated traumatic SCH without intraocular damage carries an equally excellent prognosis. When associated with globe rupture, retinal detachment, or optic nerve injury, the visual prognosis is determined by those co-pathologies. Early recognition and surgical repair of a ruptured globe significantly improves outcomes.

SCH in the Context of Systemic Disease

When SCH occurs as a manifestation of an underlying systemic condition — dengue, leukaemia, uncontrolled hypertension — the ocular prognosis is good but the systemic prognosis depends on timely diagnosis and appropriate treatment of the underlying condition. In these cases, the SCH serves as a valuable diagnostic clue that enables earlier systemic intervention.