Physical or chemical injuries of the eye can be a serious threat to vision if not treated appropriately and in a timely fashion. The most obvious presentation of ocular (eye) injuries is redness and pain of the affected eyes. This is not, however, universally true, as tiny metallic projectiles may cause neither symptom. Tiny metallic projectiles should be suspected when a patient reports metal on metal contact, such as with hammering a metal surface. Corneal foreign body is one of the most common preventable occupational hazard. Intraocular foreign bodies do not cause pain because of the lack of nerve endings in the vitreous humour and retina that can transmit pain sensations. As such, general or emergency department doctors should refer cases involving the posterior segment of the eye or intraocular foreign bodies to an ophthalmologist. Ideally, ointment would not be used when referring to an ophthalmologist, since it diminishes the ability to carry out a thorough eye examination. Flicking sand, flying pieces of wood, metal, glass and stone are notorious for causing much of the eye trauma. Sporting balls such as cricket ball, lawn tennis ball, squash ball, shuttlecock, and other high speed flying objects can strike the eye. The eye is also susceptible to blunt trauma in a fistfight. Children’s games such as bow-and-arrows, bb guns and firecrackers can lead to eye trauma.
In other animals
Most animals and plants are able to synthesize vitamin C through a sequence of enzyme-driven steps, which convert monosaccharides to vitamin C. However, some mammals have lost the ability to synthesize vitamin C, notably simians and tarsiers. These make up one of two major primate suborders, haplorrhini, and this group includes humans. The strepsirrhini (non-tarsier prosimians) can make their own vitamin C, and these include lemurs, lorises, pottos, and galagos. Ascorbic acid is also not synthesized by at least two species of caviidae, the capybara and the guinea pig. There are known species of birds and fish that do not synthesize their own vitamin C. All species that do not synthesize ascorbate require it in the diet. Deficiency causes scurvy in humans, and somewhat similar symptoms in other animals.Animals that can contract scurvy all lack the L-gulonolactone oxidase (GULO) enzyme, which is required in the last step of vitamin C synthesis. The genomes of these species contain GULO as pseudogenes, which serve as insight into the evolutionary past of the species. Name
In babies, scurvy is sometimes referred to as Barlows disease, named after Thomas Barlow, a British physician who described it in 1883. However, Barlows disease may also refer to mitral valve prolapse (Barlows syndrome), first described by John Brereton Barlow in 1966. References
Further reading


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