Neoplasia
Introduction:
Neoplasia is one of the most important topics in pathology and clinical practice. The term refers to abnormal, uncontrolled proliferation of cells that results in the formation of a mass or tumor. The study of tumors (neoplasms) is called oncology. Neoplasia can be benign or malignant, and malignant tumors are synonymous with cancer. For optometry students, understanding neoplasia is essential because many tumors affect ocular structures, ranging from benign eyelid lesions to malignant intraocular tumors like retinoblastoma and choroidal melanoma. Early recognition and referral are crucial in saving both vision and life.
Definition
Neoplasia literally means “new growth.” A neoplasm (tumor) is defined as an abnormal mass of tissue that grows in an uncoordinated manner, continues to grow after cessation of the stimulus that initiated it, and is largely autonomous.
Characteristics of Neoplasms
- Uncontrolled, excessive growth.
- Lack of response to normal regulatory mechanisms.
- Persistence even after removal of initiating cause.
- Varying degrees of resemblance to normal tissue (differentiation).
- Potential to invade and metastasize (in malignant neoplasms).
Classification of Neoplasms
1. According to Behavior
- Benign tumors: Slow-growing, localized, resemble normal tissue, do not metastasize. Example: Lipoma, Papilloma.
- Malignant tumors (cancers): Rapid growth, poorly differentiated, invade and metastasize. Example: Carcinoma, Sarcoma, Melanoma.
2. According to Cell of Origin
- Epithelial tumors:
- Benign: Adenoma, Papilloma.
- Malignant: Carcinoma (squamous cell carcinoma, adenocarcinoma).
- Mesenchymal tumors:
- Benign: Lipoma, Fibroma, Hemangioma.
- Malignant: Sarcoma (fibrosarcoma, osteosarcoma, liposarcoma).
- Hematopoietic and lymphoid tumors: Leukemia, Lymphoma, Multiple myeloma.
- Melanocytic tumors: Nevus (benign), Malignant melanoma.
Differences Between Benign and Malignant Tumors
| Feature | Benign Tumor | Malignant Tumor |
|---|---|---|
| Growth rate | Slow | Rapid |
| Differentiation | Well-differentiated (resembles tissue of origin) | Poorly differentiated (anaplasia common) |
| Capsule | Usually encapsulated, localized | Poorly demarcated, infiltrative |
| Invasion | No invasion, remains localized | Invades surrounding tissues |
| Metastasis | Absent | Common (lymphatic, blood, seeding) |
Etiology of Neoplasia
- Genetic mutations: Activation of oncogenes, inactivation of tumor suppressor genes (e.g., p53, RB gene).
- Chemical carcinogens: Tobacco, asbestos, benzene.
- Radiation: UV radiation (skin cancers), ionizing radiation.
- Viruses:
- Human papillomavirus (HPV) → cervical carcinoma.
- Epstein-Barr virus (EBV) → Burkitt’s lymphoma.
- Hepatitis B and C viruses → hepatocellular carcinoma.
- Chronic inflammation: Predisposes to malignancy.
- Immunosuppression: Increased risk of lymphomas and viral-associated cancers.
Pathogenesis of Neoplasia
- Initiation: Genetic mutation occurs in a single cell.
- Promotion: Stimuli enhance proliferation of mutated cells.
- Progression: Acquisition of further mutations, increasing aggressiveness.
- Metastasis: Spread to distant sites via lymphatic, blood, or body cavities.
Microscopic Features of Malignancy (Anaplasia)
- Loss of differentiation.
- Pleomorphism (variation in size and shape of cells and nuclei).
- Hyperchromatic, large nuclei with high nuclear-cytoplasmic ratio.
- Abnormal mitotic figures.
- Tumor giant cells.
- Loss of normal architecture.
Spread of Malignant Tumors
- Local invasion: Direct infiltration into surrounding tissues.
- Lymphatic spread: Common in carcinomas.
- Hematogenous spread: Common in sarcomas, also in renal cell carcinoma, hepatocellular carcinoma.
- Seeding of body cavities: Ovarian carcinoma spreading within peritoneal cavity.
Grading and Staging
- Grading: Microscopic evaluation of tumor differentiation and mitotic activity (well, moderately, poorly differentiated).
- Staging: Clinical and radiological assessment of tumor size, lymph node involvement, and metastasis (TNM classification).
Clinical Effects of Neoplasms
- Local effects: Compression, obstruction, ulceration, bleeding.
- Metastasis: Organ dysfunction (e.g., liver, lungs, brain).
- Paraneoplastic syndromes: Hormone secretion (Cushing’s, SIADH, hypercalcemia).
- Cachexia: Weight loss and muscle wasting due to cytokines.
Ocular Neoplasms
Benign Ocular Tumors
- Eyelid: Papilloma, nevus, sebaceous adenoma.
- Conjunctiva: Conjunctival nevus, papilloma.
- Orbit: Hemangioma, dermoid cyst.
Malignant Ocular Tumors
- Eyelid: Basal cell carcinoma (most common eyelid malignancy), squamous cell carcinoma, sebaceous gland carcinoma, melanoma.
- Conjunctiva: Squamous cell carcinoma, malignant melanoma.
- Intraocular:
- Retinoblastoma: Commonest primary intraocular malignancy in children, due to RB gene mutation.
- Choroidal melanoma: Commonest primary intraocular malignancy in adults.
- Orbit: Rhabdomyosarcoma (children), lymphoma, metastatic tumors.
Investigations
- Histopathology (biopsy) — gold standard.
- Immunohistochemistry to detect tumor markers.
- Imaging (CT, MRI, ultrasound) for local spread and staging.
- Cytology — FNAC, exfoliative cytology.
- Molecular studies for genetic mutations (e.g., RB gene, p53).
Management
- Surgery: Excision of tumor, enucleation or exenteration for ocular malignancies.
- Radiotherapy: Brachytherapy (plaque therapy in choroidal melanoma), external beam radiation.
- Chemotherapy: Systemic or local (intravitreal for retinoblastoma).
- Immunotherapy: Monoclonal antibodies, checkpoint inhibitors in systemic cancers.
- Targeted therapy: Based on genetic mutations.
Ophthalmic Importance for Optometrists
- Optometrists may be the first to notice suspicious lesions during routine eye exams (e.g., pigmented conjunctival nevus that is growing, abnormal leukocoria suggesting retinoblastoma).
- Must differentiate benign from malignant features (rapid growth, irregular borders, bleeding, recurrence).
- Early referral for biopsy and oncology consultation is crucial.
- Optometrists also play a role in visual rehabilitation after treatment with low vision aids, prosthetics, or glasses.
HEMATOLOGY
Anemia
Introduction:
Anemia is one of the most common hematological disorders worldwide. It is defined as a reduction in the total red blood cell (RBC) mass or a decrease in hemoglobin concentration of the blood below normal levels, resulting in reduced oxygen-carrying capacity. Clinically, anemia manifests as pallor, fatigue, shortness of breath, and other systemic signs. For optometry students, it is important to understand anemia not only because of its systemic importance but also because many anemias have ocular manifestations such as conjunctival pallor, retinal hemorrhages, and cotton wool spots, which may be observed during routine eye examinations.
Definition
Anemia is defined as a condition in which the hemoglobin concentration is below the expected value for the individual’s age, sex, and physiological state (e.g., pregnancy). In adults, hemoglobin less than 13 g/dL in males and less than 12 g/dL in females is generally considered anemic.
Classification of Anemia
1. Morphological Classification (based on RBC indices)
- Microcytic, hypochromic anemia: Small, pale RBCs. Example: Iron deficiency anemia, thalassemia.
- Normocytic, normochromic anemia: Normal-sized RBCs but reduced number. Example: Acute blood loss, hemolytic anemia, anemia of chronic disease.
- Macrocytic anemia: Large RBCs. Example: Megaloblastic anemia (due to Vitamin B12 or folate deficiency).
2. Etiological Classification
- Due to blood loss: Acute (trauma, surgery) or chronic (gastrointestinal bleeding, menorrhagia).
- Due to decreased RBC production:
- Nutritional deficiency: Iron, Vitamin B12, Folate.
- Aplastic anemia (bone marrow failure).
- Anemia of chronic disease.
- Due to increased RBC destruction (hemolytic anemia): Hereditary (sickle cell disease, thalassemia, hereditary spherocytosis) or acquired (autoimmune hemolytic anemia, malaria, drugs).
Pathophysiology
- Reduced oxygen delivery: Low hemoglobin decreases oxygen-carrying capacity, leading to tissue hypoxia.
- Compensatory mechanisms: Increased cardiac output, redistribution of blood flow, increased 2,3-DPG in RBCs to facilitate oxygen release.
- Bone marrow response: In anemia with increased destruction or loss, bone marrow increases reticulocyte production.
General Clinical Features
- Pallor of skin, nails, and conjunctiva.
- Fatigue, weakness, dizziness.
- Dyspnea, palpitations, tachycardia.
- Headache, irritability, poor concentration.
- Glossitis (inflamed tongue), angular cheilitis (cracks at the corner of the mouth).
- Koilonychia (spoon-shaped nails) in iron deficiency anemia.
- Neurological symptoms (numbness, tingling, gait disturbances) in Vitamin B12 deficiency anemia.
Ocular Manifestations of Anemia
- Conjunctival pallor: Most obvious sign, seen on lower palpebral conjunctiva.
- Retinal findings: Cotton wool spots, retinal hemorrhages, venous dilatation.
- Pale optic disc: In severe chronic anemia.
- Subconjunctival hemorrhage: In severe anemia or platelet dysfunction.
- Sickle cell disease: Sea-fan neovascularization, vitreous hemorrhage, tractional retinal detachment, leading to blindness if untreated.
- Megaloblastic anemia: May present with optic neuropathy.
Investigations
- Complete Blood Count (CBC): Hemoglobin, hematocrit, RBC count, MCV, MCH, MCHC.
- Peripheral blood smear: RBC morphology (microcytosis, macrocytosis, anisopoikilocytosis).
- Reticulocyte count: Elevated in hemolysis, low in marrow failure.
- Iron studies: Serum iron, ferritin, total iron-binding capacity (TIBC).
- Vitamin B12 and folate levels: For megaloblastic anemia.
- Bone marrow examination: For aplastic anemia or unexplained cases.
- Special tests: Hemoglobin electrophoresis (thalassemia, sickle cell anemia), Coombs test (autoimmune hemolytic anemia).
Management
- Treat the underlying cause: Correct bleeding source, manage chronic disease.
- Nutritional supplementation:
- Iron therapy (oral or parenteral).
- Vitamin B12 injections (for pernicious anemia).
- Folic acid supplementation.
- Blood transfusion: For severe symptomatic anemia.
- Erythropoiesis-stimulating agents: In anemia of chronic kidney disease.
- Immunosuppressive therapy / Bone marrow transplant: For aplastic anemia.
- Sickle cell anemia: Hydroxyurea to increase fetal hemoglobin, laser photocoagulation for retinal neovascularization.
- Thalassemia: Regular transfusions with iron chelation therapy.
Prevention
- Balanced diet rich in iron, folate, and Vitamin B12.
- Iron supplementation in high-risk groups (children, pregnant women).
- Genetic counseling for inherited anemias (sickle cell disease, thalassemia).
- Control of chronic diseases (renal, liver, autoimmune).
Ophthalmic Importance for Optometrists
- Optometrists may detect anemia through conjunctival pallor during routine eye checkups.
- Fundus examination may reveal retinal hemorrhages, cotton wool spots, venous dilatation, or signs of sickle cell retinopathy.
- Early referral to a physician/hematologist is essential when ocular findings suggest underlying anemia.
- In patients with known sickle cell disease, regular ocular screening is vital to prevent vision-threatening complications.
- Optometrists also play a role in providing low vision rehabilitation for patients with severe retinal damage due to anemic complications.
Leukemia
Introduction:
Leukemia is a malignant neoplasm of the blood-forming tissues characterized by uncontrolled proliferation of abnormal white blood cells (WBCs) in the bone marrow and peripheral blood. This proliferation interferes with normal hematopoiesis, resulting in anemia, thrombocytopenia, and impaired immunity. Leukemia may present with systemic symptoms such as fever, weight loss, bleeding, and recurrent infections. Importantly, many leukemias show ocular manifestations, sometimes serving as the first clue to diagnosis. For optometry students, recognizing ocular signs of leukemia is crucial for timely referral and management.
Definition
Leukemia is a malignant clonal proliferation of hematopoietic cells (usually WBC precursors) in bone marrow, leading to accumulation of abnormal cells in marrow, blood, and sometimes other organs.
Classification of Leukemia
1. Based on Clinical Course
- Acute leukemia: Sudden onset, rapidly progressive, presence of immature cells (blasts) in bone marrow and blood.
- Chronic leukemia: Insidious onset, slow progression, presence of more mature but abnormal leukocytes.
2. Based on Cell Lineage
- Lymphoid: Malignancy of lymphoid precursors or mature lymphocytes.
- Myeloid: Malignancy of granulocyte, monocyte, erythroid, or megakaryocyte precursors.
3. WHO Major Types
- Acute lymphoblastic leukemia (ALL)
- Acute myeloid leukemia (AML)
- Chronic lymphocytic leukemia (CLL)
- Chronic myeloid leukemia (CML)
Etiology and Risk Factors
- Genetic mutations: Philadelphia chromosome (BCR-ABL fusion in CML), p53 mutations.
- Radiation exposure: Ionizing radiation increases risk.
- Chemicals: Benzene, certain chemotherapeutic agents.
- Viral infections: HTLV-1 linked to adult T-cell leukemia.
- Hereditary conditions: Down syndrome, Fanconi anemia.
Pathophysiology
- Proliferation of malignant leukemic cells in bone marrow.
- Suppression of normal hematopoiesis → anemia, thrombocytopenia, neutropenia.
- Leukemic cells spill into blood, infiltrate organs (liver, spleen, lymph nodes, CNS, eyes).
Clinical Features
General Symptoms
- Fatigue, weakness (due to anemia).
- Fever and recurrent infections (due to neutropenia).
- Bleeding, bruising, petechiae (due to thrombocytopenia).
- Bone pain, lymphadenopathy, hepatosplenomegaly.
- Weight loss, night sweats (especially in chronic leukemias).
Ocular Manifestations
Ocular findings occur in 30–90% of leukemia patients and may affect any part of the eye:
- Anterior segment: Conjunctival pallor, subconjunctival hemorrhages, conjunctival infiltration (“salmon patch” appearance), episcleritis.
- Cornea: Rare infiltration, peripheral ulceration.
- Uvea: Leukemic infiltration of iris and ciliary body → anterior uveitis, hypopyon, iris nodules.
- Retina (most common site): Retinal hemorrhages (flame-shaped, dot-blot), Roth’s spots (hemorrhage with white center), venous tortuosity, cotton wool spots, perivascular sheathing (“leukemic retinopathy”).
- Optic nerve: Infiltration → optic disc swelling, optic neuropathy.
- Orbit: Chloroma (granulocytic sarcoma) — localized leukemic tumor mass, especially in AML.
Investigations
- Complete blood count (CBC): Shows anemia, thrombocytopenia, leukocytosis or leukopenia.
- Peripheral blood smear: Presence of blasts (acute), mature abnormal lymphocytes (CLL), or granulocytes (CML).
- Bone marrow aspiration and biopsy: Gold standard for diagnosis; shows infiltration by blasts or abnormal cells.
- Cytogenetics & molecular studies: Detect chromosomal abnormalities (Philadelphia chromosome, translocations).
- Ocular investigations: Fundus examination, fluorescein angiography, OCT to evaluate retinal and optic nerve involvement.
Complications
- Severe infections leading to sepsis.
- Bleeding tendencies (intracranial, retinal hemorrhage).
- CNS involvement (neurologic deficits, optic nerve infiltration).
- Visual loss due to leukemic retinopathy or optic neuropathy.
Management
1. Systemic Therapy
- Chemotherapy: Mainstay of treatment (different regimens for ALL, AML, CLL, CML).
- Targeted therapy:
- Imatinib (tyrosine kinase inhibitor) for CML (Philadelphia chromosome-positive).
- Monoclonal antibodies (rituximab) for CLL.
- Stem cell transplantation: For refractory cases or relapse.
- Supportive therapy: Blood transfusion, platelet transfusion, antibiotics for infection.
2. Ocular Management
- Topical corticosteroids and cycloplegics for anterior uveitis.
- Management of secondary glaucoma from infiltration.
- Laser or intravitreal injections for retinal complications (rarely needed).
- Low vision aids and rehabilitation for irreversible damage.
- Most ocular manifestations improve with systemic chemotherapy; local therapy is supportive.
Prevention
- No absolute prevention, but risk can be reduced by avoiding radiation and carcinogenic chemicals.
- Genetic counseling for hereditary predisposition syndromes.
- Regular monitoring of high-risk individuals (e.g., patients with prior chemotherapy exposure).
Ophthalmic Importance for Optometrists
- Optometrists may be the first to detect signs like retinal hemorrhages, Roth’s spots, or conjunctival infiltrates during eye exams.
- Such findings in combination with systemic symptoms should prompt urgent referral for hematological evaluation.
- Optometrists play a role in documenting ocular findings, monitoring visual changes during chemotherapy, and providing visual rehabilitation when needed.
Bleeding Disorders
Introduction:
Bleeding disorders are a heterogeneous group of conditions in which normal hemostasis is disturbed, leading to excessive bleeding or bruising. They may result from defects in blood vessels, platelets, coagulation factors, or fibrinolysis. For optometry students, awareness of bleeding disorders is important because ocular structures (conjunctiva, retina, orbit) are vulnerable to hemorrhages which can be the first sign of an underlying systemic coagulopathy. Additionally, patients with bleeding tendencies require special precautions before ocular surgery or invasive procedures.
Normal Hemostasis — A Quick Overview
Hemostasis is a coordinated process that prevents bleeding after vascular injury and consists of three main steps:
- Primary hemostasis: Vasoconstriction and platelet adhesion/aggregation to form a temporary platelet plug (involves von Willebrand factor, platelets).
- Secondary hemostasis: Activation of the coagulation cascade resulting in fibrin formation to stabilize the platelet plug (intrinsic, extrinsic, and common pathways).
- Fibrinolysis: Breakdown of the clot once healing has occurred (plasmin mediated).
Major Categories of Bleeding Disorders
- Platelet disorders: Quantitative (thrombocytopenia) or qualitative (platelet function defects).
- Coagulation factor deficiencies: Inherited (hemophilia A/B) or acquired (vitamin K deficiency, liver disease, anticoagulant therapy).
- Vascular disorders: Fragile blood vessels (senile purpura, vasculitis).
- Hyperfibrinolytic states: Excessive clot breakdown (rare).
- Mixed disorders: Disseminated intravascular coagulation (DIC) — combines thrombosis and bleeding due to consumption of clotting factors and platelets.
Common Bleeding Disorders — Etiology & Features
1. Thrombocytopenia
- Causes: Immune thrombocytopenic purpura (ITP), bone marrow suppression (drugs, aplastic anemia), leukemia, hypersplenism, infections, consumptive coagulopathy (DIC).
- Clinical features: Petechiae, purpura, mucosal bleeding (epistaxis, gum bleeding), spontaneous subconjunctival hemorrhages. Risk of severe bleeding increases when platelet count <20,000/µL.
2. Platelet Function Disorders
- Causes: Inherited (Glanzmann thrombasthenia, Bernard–Soulier syndrome) or acquired (aspirin, NSAIDs, uremia).
- Clinical features: Mucocutaneous bleeding, prolonged bleeding after minor trauma; normal platelet count but prolonged bleeding time.
3. Von Willebrand Disease (vWD)
- Pathology: Deficiency or dysfunction of von Willebrand factor (vWF) — impairs platelet adhesion and stabilizes factor VIII.
- Clinical features: Mucosal bleeding, prolonged bleeding after surgery, menorrhagia; may have easy bruising and conjunctival hemorrhages.
4. Hemophilia A and B
- Cause: Inherited factor VIII deficiency (Hemophilia A) or factor IX deficiency (Hemophilia B) — X-linked recessive, primarily affects males.
- Clinical features: Deep tissue bleeds (hemarthroses, muscle hematomas), delayed bleeding after injury or surgery. Ocular: orbital hemorrhage, retinal/vitreous hemorrhage following trauma or spontaneously (rare).
5. Vitamin K Deficiency & Liver Disease
- Vitamin K–dependent factors (II, VII, IX, X) are reduced in deficiency or when warfarin anticoagulation is present. Liver disease causes decreased synthesis of clotting factors and abnormal fibrinogen, producing prolonged PT/INR and bleeding tendency.
- Clinical signs include easy bruising, mucosal bleeding, and risk of major hemorrhage including intracranial or intraocular bleeding.
6. Disseminated Intravascular Coagulation (DIC)
- Severe systemic activation of coagulation (sepsis, obstetric catastrophe, malignancy) leads to consumption of clotting factors and platelets, causing both thrombosis and bleeding.
- Lab pattern: prolonged PT, aPTT, low fibrinogen, elevated D-dimers, thrombocytopenia.
Ocular Manifestations of Bleeding Disorders
- Conjunctival hemorrhage: Common and may be spontaneous in thrombocytopenia or coagulopathy; usually benign but warrants systemic evaluation when recurrent or bilateral.
- Subconjunctival hemorrhage: May be isolated or part of generalized bleeding tendency.
- Retinal hemorrhages: Dot-blot, flame-shaped, or pre-retinal/vitreous hemorrhages can occur in severe coagulopathies, hypertension, or blood dyscrasias.
- Vitreous hemorrhage: May lead to sudden vision loss; often requires ophthalmic intervention if persistent.
- Orbital hemorrhage: Can be sight-threatening with proptosis and optic nerve compression—urgent management necessary.
- Spontaneous hyphema: Blood in the anterior chamber absent trauma may indicate bleeding disorder or neovascularization.
- Post-operative bleeding: Excessive bleeding after ocular surgery (cataract, glaucoma operations) in patients with unrecognized coagulopathy or on anticoagulants.
Investigations
- Complete blood count (CBC): Platelet count, hemoglobin, white cell count.
- Peripheral smear: Look for platelet clumping, abnormal cells, schistocytes (DIC/microangiopathic hemolytic anemia).
- Bleeding time: (less commonly used) evaluates platelet function.
- Prothrombin time (PT) / International Normalized Ratio (INR): Screening for extrinsic pathway and warfarin effect.
- Activated partial thromboplastin time (aPTT): Screens intrinsic pathway (hemophilia, heparin effect).
- Fibrinogen and D-dimer: Useful for DIC.
- Von Willebrand factor assays: vWF antigen, ristocetin cofactor activity.
- Platelet function tests: Aggregometry for inherited or drug-induced dysfunction.
- Specific factor assays: Factor VIII, IX levels for hemophilia.
- Liver function tests, renal function, and screening for drugs: e.g., aspirin, clopidogrel, anticoagulants (warfarin, DOACs).
Management — General Principles
Management aims to control active bleeding, correct underlying abnormalities, and prevent future bleeding, especially around ocular procedures.
Acute Bleeding
- Local measures: direct pressure, topical vasoconstrictors (where appropriate), eye shields for ocular hemorrhage.
- Platelet transfusion: in severe thrombocytopenia with bleeding or before urgent surgery.
- Fresh frozen plasma (FFP): replaces multiple clotting factors in DIC or liver failure.
- Cryoprecipitate: used when fibrinogen is low.
- Specific factor replacement: factor VIII or IX concentrates for hemophilia.
- Antifibrinolytic agents: tranexamic acid or aminocaproic acid to reduce bleeding in mucosal sites or planned surgery.
Long-term / Preventive Management
- Treat underlying cause: discontinue causative drugs (antiplatelets, anticoagulants) if safe to do so or adjust dose under physician supervision.
- For vWD: desmopressin (DDAVP) increases endogenous vWF in many patients; vWF concentrates for severe cases.
- For ITP: corticosteroids, IVIG (for rapid platelet rise), splenectomy in refractory cases, thrombopoietin receptor agonists (eltrombopag, romiplostim).
- For hemophilia: prophylactic factor replacement to reduce spontaneous bleeds; gene therapy is emerging.
- Management of DIC: treat underlying cause (sepsis, malignancy), supportive replacement of blood components.
Perioperative Considerations in Ophthalmology
- Obtain detailed medication history (aspirin, clopidogrel, warfarin, direct oral anticoagulants) and communicate with the prescribing physician before elective ocular surgery.
- Assess coagulation status (INR, platelet count) preoperatively. Many cataract and minor ocular procedures are safe with certain anticoagulants, but decisions should be individualized.
- Use local hemostatic measures (viscoelastic tamponade, cautery) and consider prophylactic antifibrinolytics for high-risk patients.
- For patients with known bleeding disorders, plan factor replacement or platelet transfusion perioperatively in liaison with hematology.
Ophthalmic Importance for Optometrists
- Repeated, unexplained, or bilateral subconjunctival hemorrhages or retinal/vitreous hemorrhages should prompt systemic evaluation for bleeding disorders.
- Take thorough drug histories and advise patients to inform their physician and ophthalmic surgeon about anticoagulant or antiplatelet therapy before any eye procedure.
- Recognize sight- or life-threatening ocular hemorrhages (orbital hemorrhage with proptosis, dense vitreous hemorrhage) and refer urgently.
- Provide pre- and post-operative monitoring for patients with known bleeding disorders and educate patients about signs of ocular bleeding that require immediate attention.
