Subconjunctival haemorrhage is characterized by acute rupture of small conjunctival vessels, leading to sharply demarcated, bright red patches beneath the bulbar conjunctiva. It represents about 3% of all ophthalmic emergency or outpatient presentations and over 10% of red eye cases in older adults1. Although often idiopathic or related to minor trauma or Valsalva manoeuvres, SCH may also be associated with systemic hypertension, diabetes mellitus, arteriosclerosis, anticoagulant/antiplatelet therapy, and haemostatic disorders.1,2 Clinicians frequently face the question of whether an episode of SCH warrants evaluation for underlying haemorrhagic disorders. Earlier work suggested that the prevalence of haematologic disease among patients presenting with spontaneous SCH is low, but data were limited to small case series.3 Recently, a nationwide population based cohort study has provided more robust evidence on the association between SCH and haemorrhagic disorders.4 This article reviews epidemiology, pathophysiology, and clinical evidence linking SCH to systemic haemorrhagic disorders, emphasizing the design and findings of a large population based study and integrating prior observational data. Epidemiology of Subconjunctival Haemorrhage Incidence and age distribution In outpatient and emergency settings, SCH is a relatively frequent diagnosis. A Japanese series of 8,726 patients with red eye reported an SCH incidence of approximately 2.9%, with no strong predilection for sex but a marked increase in frequency among individuals over 50 years of age.1 Similar age dependent patterns have been reported elsewhere and are thought to reflect rising prevalences of systemic hypertension, diabetes, dyslipidemia, and use of antithrombotic therapy in older adults.1,2 A nationwide study from Taiwan focusing on non traumatic SCH documented a substantial incidence at the population level and reported strong associations between SCH and comorbid hypertension, purpura, thrombocytopenia, and aspirin use.2 These findings suggest that even when SCH is clinically benign, it may occur more frequently in patients with systemic vascular or haemostatic abnormalities. Etiologic spectrum Across age groups, the most commonly identified causes of SCH include: • Minor local trauma (including rubbing, contact lens manipulation, and foreign body) • Valsalva related events such as coughing, sneezing, vomiting, or heavy lifting • Systemic hypertension and arteriosclerosis • Acute conjunctivitis and other ocular surface inflammation • Anticoagulant and antiplatelet therapy (e.g., warfarin, aspirin, dual antiplatelet regimens) • Diabetes mellitus and dyslipidemia • Haematological dyscrasias such as thrombocytopenic purpura, leukemia, anaemia, von Willebrand disease, and severe hepatic disease with coagulopathy2,3 In children and younger adults, trauma and contact lens use dominate, while in older adults, systemic vascular and haematological conditions, along with antithrombotic therapy, become more prominent risk factors.2 Association between SCH and Haemorrhagic Disorders: Nationwide Population Based Study Study design and data source A recent nationwide population based cohort study used a large national health insurance database including over 1,025,000 insured individuals. After excluding those with prior SCH and certain vascular outcomes, more than 700,000 adults aged ≥20 years were followed, with 46,251 incident SCH cases identified and treated as a time varying exposure. Diagnosis codes from the International Classification of Diseases (ICD 10) were used to identify SCH, haemorrhagic disorders, and major bleeding outcomes (intracranial haemorrhage and major gastrointestinal bleeding). The investigators applied extensive adjustment for demographic factors, comorbid conditions, and medication use, and performed propensity score matching (PSM) between individuals with and without SCH.2 Baseline characteristics and comorbidities Before PSM, individuals with SCH had higher prevalences of • Hypertension • Diabetes mellitus • Cardiovascular disease • Haematological or bleeding disorders • Anticoagulant and antiplatelet use2 These patterns are consistent with prior observational studies indicating that SCH is more common in patients with vascular risk factors and blood dyscrasias.1 Major bleeding outcomes In crude analyses before matching, hazard ratios (HRs) for intracranial haemorrhage and major gastrointestinal bleeding were slightly elevated among SCH cases, but differences were not statistically significant. After PSM and multivariable adjustment, SCH was not associated with a significant increase in risk of these major bleeding outcomes2. These findings suggest that while SCH is more frequent in individuals with comorbidities predisposing to bleeding, the occurrence of SCH itself is not an independent predictor of subsequent catastrophic haemorrhage at the population level. Evidence From Clinical Series on Bleeding Disorders in SCH Several smaller clinical and laboratory based studies have investigated the prevalence of occult haemostatic abnormalities in patients presenting with SCH. Haemostatic testing in unexplained SCH A retrospective series of 52 patients with spontaneous SCH in whom no local or systemic cause was initially identified evaluated detailed haemostatic parameters. Type 1 von Willebrand disease was diagnosed in two patients (3.8%), a prevalence that was not significantly higher than that expected in the general population. The authors concluded that routine extensive coagulation testing for all patients with isolated SCH is not justified, particularly in the absence of other bleeding manifestations.1,3 Other reports focusing on recurrent spontaneous SCH have, however, documented a higher frequency of coagulation abnormalities, including reduced von Willebrand factor levels, thrombocytopenia, and platelet function defects, particularly when SCH is accompanied by epistaxis, easy bruising, or menorrhagia.2 Anticoagulant and antiplatelet therapy Numerous studies have described SCH in patients receiving warfarin or dual antiplatelet therapy. In such patients, SCH may occur at therapeutic or supratherapeutic levels of anticoagulation, and it is generally recommended to verify the international normalized ratio (INR) and review concomitant medications.2 Higher Subconjunctival Hemorrhage Incidence Linked to Antiplatelet, Anticoagulant Use) While SCH is usually self limited, recurrent episodes in anticoagulated patients may signal over anticoagulation or unrecognized additional bleeding risks. Pathophysiological Considerations The conjunctival vasculature comprises thin walled superficial vessels susceptible to abrupt pressure changes and shear forces. In individuals with normal haemostasis, the resultant bleed is typically small and localized, with rapid spontaneous resolution.1 In contrast, haemorrhagic disorders—such as thrombocytopenia, platelet function defects, deficiencies of coagulation factors, or combined defects in advanced hepatic disease—can lower the threshold for vessel rupture and prolong bleeding once it occurs.2,8 Systemic vascular conditions (e.g., hypertension, diabetes, arteriosclerosis) further increase vascular fragility, contributing to a multifactorial risk of SCH.2 Thus, SCH can be conceptualized as a clinical sign arising from the interaction of: 1. Mechanical triggers (trauma, Valsalva events) 2. Vascular fragility (hypertension, arteriosclerosis, age related changes) 3. Haemostatic balance (platelet count/function, coagulation factors, anticoagulant/antiplatelet drugs, primary bleeding disorders). At the population level, individuals with haemorrhagic disorders or on antithrombotic therapy are over represented among patients with SCH, but the absolute risk of life threatening bleeding following SCH remains low.1 Clinical Implications When to suspect an underlying haemorrhagic disorder Most single, unilateral SCH episodes in otherwise healthy adults—especially those clearly provoked by minor trauma or Valsalva—do not mandate extensive haematologic evaluation. However, certain red flags should prompt consideration of underlying bleeding disorders.2,8 • Recurrent or bilateral SCH without clear precipitating factors • SCH occurring in childhood or adolescence without trauma • History of easy bruising, frequent epistaxis, prolonged bleeding after minor cuts, dental extractions, or surgery • Heavy menstrual bleeding or postpartum haemorrhage in women • Known liver disease, renal failure, or suspected haematological malignancy • Concomitant bleeding manifestations (e.g., petechiae, ecchymoses, mucosal bleeding) • In these situations, targeted laboratory evaluation (complete blood count with platelets, prothrombin time, activated partial thromboplastin time, and selected tests for von Willebrand disease or platelet function) is appropriate. Role of population based evidence The nationwide cohort data indicate that SCH is a marker of a higher burden of vascular and metabolic comorbidities but does not independently predict major intracranial or gastrointestinal haemorrhage once confounders are controlled.(Checking Your Browser - reCAPTCHA, n.d.) Therefore, while SCH should trigger careful review of systemic risk factors, it should not, by itself, be regarded as an emergency warning sign of imminent catastrophic bleeding in the general population. Table 1. Key Population Based and Clinical Studies on SCH and Haemorrhagic Disorders Study / Source Design & Population Key Findings Relevant to Haemorrhagic Disorders Nationwide population based cohort >700,000 adults ≥20 years from a national insurance database; 46,251 incident SCH cases SCH patients had higher prevalences of hypertension, diabetes, and haematological disorders than non SCH individuals. After propensity score matching, SCH was not significantly associated with increased risk of intracranial haemorrhage or major gastrointestinal bleeding. Taiwanese non traumatic SCH study2,8 Large population based case–control analysis in Taiwan Non traumatic SCH showed strong associations with hypertension, purpura, thrombocytopenia, and aspirin use, supporting links to systemic vascular and bleeding conditions. Retrospective haemostatic evaluation in unexplained SCH3,8 52 patients with spontaneous SCH without evident cause; detailed haemostatic testing Type 1 von Willebrand disease identified in 3.8% of patients; prevalence not significantly above background in the general population. Authors concluded that routine extensive work up is not necessary for all SCH cases. Review of SCH risk factors and indicators4 Narrative review of clinical and laboratory studies Highlights associations between SCH and hypertension, diabetes, arteriosclerosis, anticoagulation, and haematological dyscrasias (thrombocytopenia, leukemia, anemia, uremia). Emphasizes targeted evaluation in recurrent or unexplained SCH. Pediatric and systemic red flag review Clinical review with illustrative cases Describes systemic bleeding disorders (thrombocytopenic purpura, hemophilia, leukemia, congenital fibrinogen deficiency, Kasabach–Merritt syndrome) presenting with SCH, particularly bilateral or recurrent cases in children. Recommends careful history and systemic examination. Table 2. Suggested Clinical Approach to Patients With SCH and Possible Haemorrhagic Disorders Clinical Scenario Key Features Suggested Evaluation and Management Single, unilateral SCH with clear local trigger Trauma, eye rubbing, contact lens manipulation, recent conjunctivitis; no systemic symptoms Reassure patient; measure blood pressure; brief review of medications (especially anticoagulants/antiplatelets) and systemic history. No routine haematologic tests if history and exam are otherwise unremarkable.5 Single SCH in older adult with vascular risk factors Age >50, hypertension, diabetes, dyslipidemia; may be on aspirin or anticoagulant Check blood pressure and review cardiovascular risk profile and medications. If on warfarin or direct oral anticoagulants, verify INR or dosing as appropriate. Consider primary care or cardiology follow up to optimize risk factor control.6 Recurrent or bilateral SCH without obvious precipitant Multiple episodes over months/years; often idiopathic on first visit Obtain detailed personal and family bleeding history, review for liver or renal disease, malignancy, and medication use. Order complete blood count with platelets, PT/INR, aPTT, and, if indicated, von Willebrand factor studies or platelet function tests. Consider haematology referral.2,8 SCH in children or adolescents without trauma Young age, recurrent episodes, or associated bruising/petechiae High index of suspicion for congenital bleeding disorders, leukemia, or non accidental trauma. Comprehensive physical exam; baseline labs (CBC, PT, aPTT) and directed haemostatic tests; urgent paediatric and/or haematology consultation as required 2,6. SCH in anticoagulated patients Warfarin or direct oral anticoagulant use; possible supratherapeutic dosing Verify INR or drug level as appropriate; review for additional bleeding signs or anaemia. Adjust anticoagulation if supratherapeutic or if recurrent SCH and other bleeding manifestations occur. Educate patients regarding minor trauma avoidance and monitoring. (Risk Factors and Complications of Subconjunctival) (Higher Subconjunctival Hemorrhage Incidence Linked to Antiplatelet, Anticoagulant Use7,8

The available evidence, including a large nationwide population based cohort, demonstrates that SCH occurs more often in individuals with underlying vascular disease, exposure to antithrombotic therapy, and various haemorrhagic disorders. However, after accounting for confounders, SCH itself does not independently predict severe intracranial or gastrointestinal bleeding events in the general adult population8. From a clinical standpoint, SCH should prompt • Routine assessment of blood pressure and cardiovascular risk factors • Thoughtful review of medications, especially anticoagulants and antiplatelet agents • Targeted haemostatic evaluation when SCH is recurrent, bilateral, unexplained, or associated with other bleeding manifestations or systemic red flags This selective approach balances the low overall prevalence of occult bleeding disorders among unselected SCH patients against the need to identify clinically important haemostatic disease in high risk subgroups.

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