Types include contusion and lamellar laceration
Open globe injury: there is a full thickness injury of the eye wall (cornea and sclera)It includes
A) Globe rupture: caused by blunt trauma and is an inside-out injury. B) Globe laceration: a full-thickness wound caused by sharp objects. It includes
1)Penetrating trauma: the globe integrity is disrupted by a full-thickness entry wound and may be associated with prolapse of the internal contents of the eye. Such injuries are often referred to as a Globe fracture or a Globe rupture, although these can be incurred by blunt trauma as well. 2) Perforating trauma: the globe integrity is disrupted in two places due to an entrance and exit wound (through and through injury). This is a quite severe type of eye injury. Other types include

Blowout fracture of the orbit is caused by blunt trauma, classically described for fist or ball injury, leading to fracture of the floor or medial wall of the orbit due to sudden increased pressure on the orbital contents. Muscular Entrapment Fracture of the orbital bones can lead to muscular entrapment limiting gaze in one direction. Emergency
An emergency must be treated within minutes. This includes chemical burns of both the conjunctiva and cornea. Urgent
An urgent case must be treated within hours. This includes penetrating globe injuries; corneal abrasions or corneal foreign bodies; hyphema (must be referred); eyelid lacerations that are deep, involve the lid margin or involve the lacrimal canaliculi; radiant energy burns such as arc eye (welders burn) or snow blindness; or, rarely, traumatic optic neuropathy.
When used in chemical warfare, it can cause immunosuppression and damage to mucous membranes of the eyes, skin, and respiratory tract. Mucous membranes and damp or damaged skin are more affected by exposure to HN-2. Though symptoms of exposure are generally delayed, the DNA damage it causes occurs very quickly. More serious exposures cause symptoms to develop sooner. Eye symptoms develop first, in the first 1–2 hours (severe exposure) or 3–12 hours (mild to moderate exposure) followed by airway (2-6/12–24 hours) and skin symptoms (6–48 hours). Hot, humid weather shortens the latent (symptom-free) period.Symptoms of toxic exposure to HN-2 vary based on the route of exposure. Eye exposure causes lacrimation (tear production), burning, irritation, itching, a feeling of grittiness or dryness, blepharospasm (spasms of the eyelid), and miosis (pinpoint pupils). More severe cases cause edema (swelling from fluid accumulation) in the eyelids, photophobia (extreme sensitivity to light), severe pain, corneal ulceration, and blindness.Inhalation of chlormethine damages the upper and lower airways sequentially, with more severe exposures causing faster damage that afflicts lower parts of the respiratory tract. Early symptoms include rhinorrhea (runny nose), epistaxis (nosebleed), toneless voice, sneezing, barking cough, and dyspnea (in smokers and asthmatics). Later symptoms include pain in the nose/sinuses and inflammation of the airway. In severe cases, there may be epithelial necrosis throughout the respiratory tract, causing pseudomembrane formation, which can obstruct the airway. Pneumonia may develop and prove fatal.Skin exposure mainly causes erythema (redness) and vesication (blistering) at first, but absorption through the skin causes systemic toxicity.