Surgery works by changing the shape of the cornea. Far-sightedness primarily affects young children, with rates of 8% at 6 years and 1% at 15 years. It then becomes more common again after the age of 40, known as presbyopia, affecting about half of people. Best treatment option to correct hypermetropia due to aphakia is IOL implantation.Other common types of refractive errors are near-sightedness, astigmatism, and presbyopia. Signs and symptoms
In young patients, mild hypermetropia may not produce any symptoms. The signs and symptoms of far-sightedness include blurry vision, frontal or fronto temporal headaches, eye strain, tiredness of eyes etc. The common symptom is eye strain. Difficulty seeing with both eyes (binocular vision) may occur, as well as difficulty with depth perception. The asthenopic symptoms and near blur are usually seen after close work, especially in the evening or night. Complications
Far-sightedness can have rare complications such as strabismus and amblyopia. At a young age, severe far-sightedness can cause the child to have double vision as a result of "over-focusing".Hypermetropic patients with short axial length are at higher risk of developing primary angle closure glaucoma, so, routine gonioscopy and glaucoma evaluation is recommended for all hypermetropic adults. Causes
Simple hypermetropia, the most common form of hypermetropia, is caused by normal biological variations in the development of eyeball. Aetiologically, causes of hypermetropia can be classified as:

Axial: Axial hypermetropia occur when the axial length of eyeball is too short. About 1 mm decrease in axial length cause 3 diopters of hypermetropia. One condition that cause axial hypermetropia is nanophthalmos.
Prevention
Anticoagulants are drugs used to prevent the formation of blood clots, reducing the risk of stroke, heart attack and pulmonary embolism. Heparin and warfarin are used to inhibit the formation and growth of existing thrombi, with the former used for acute anticoagulation while the latter is used for long-term anticoagulation. The mechanism of action of heparin and warfarin are different as they work on different pathways of the coagulation cascade. Heparin works by binding to and activating the enzyme inhibitor antithrombin III, an enzyme that acts by inactivating thrombin and factor Xa. In contrast, warfarin works by inhibiting vitamin K epoxide reductase, an enzyme needed to synthesize vitamin K dependent clotting factors II, VII, IX, and X. Bleeding time with heparin and warfarin therapy can be measured with the partial thromboplastin time (PTT) and prothrombin time (PT), respectively. Treatment
Once clots have formed, other drugs can be used to promote thrombolysis or clot breakdown. Streptokinase, an enzyme produced by streptococcal bacteria, is one of the oldest thrombolytic drugs. This drug can be administered intravenously to dissolve blood clots in coronary vessels. However, streptokinase causes systemic fibrinolytic state and can lead to bleeding problems. Tissue plasminogen activator (tPA) is a different enzyme that promotes the degradation of fibrin in clots but not free fibrinogen. This drug is made by transgenic bacteria and converts plasminogen into the clot-dissolving enzyme, plasmin. Recent research indicates that tPA could have toxic effects in the central nervous system.