Injury hit the eyeball
Trauma to the eye can cause dilated pupils or dilated (less common) pupils, and the pupil reflex may become sluggish.
Bruising the eyeball is usually caused by touch, stamping, or shock. The causes of a knock are usually objecting from the head, not sharp, or the pressure of the bomb or bullet gas.
The pathogenesis of trauma to the eyeball
The pathogenesis of trauma to the eyeball was first demonstrated by Arlt (1875). According to Arlt, when affected by a traumatic agent, the eyeball will expand at a position around the equator to compensate for the sudden anterior and posterior diameter reduction, thereby causing damage to the eye. eyeball.
In addition to Arlt's hypothesis, Forster (1887) added the role of the shifting wave of the ocular fluid up into the eyeball. According to him, when a force is exerted on the cornea, the aqueous humor will be pushed back, pressed straight onto the iris and lens, thereby pushing the pressed glass fluid towards the posterior pole.
Derived from the views on the pathogenesis of indirect brain injury (Contrecoup) and based on the assumptions of Arlt and Forster, Wolter (1963) provides a complete hypothesis of the indirect force of action in trauma hit the eyeball. According to him, a force exerted on the eyeball will damage all surfaces (iris, lens, retina ...) that the force passes through, in which the dark retina - the posterior plane. will be hurt the most. In general, these lesions can be divided into 3 groups:
- Lesions that rupture / rupture tissue / tissue cells at the time of trauma,
- Injuries associated with blood vessel reactions,
- The injury causes tearing, tearing the organization.
Lesions to rupture / rupture of cells / organs at the time of trauma: Histopathologic ally these lesions exhibit mainly edema and extracellular changes of the organization, however The change in structural integrity of the intracellular is also not excluded. These damages can cause tissue / tissue necrosis or result in degenerative clusters.
Injuries accompanying vasomotor changes: In response to the impact on the eyeballs, the peripheral arteries contract. Sometimes this vasoconstriction is sufficient to cause ischemia, which results in local necrosis of the organization. After the period of vasoconstriction is to the reactive vasodilation phase, increasing the permeability of the vascular wall and causing organizational edema. With edema and organizational anemia, tissues dissociate, liquefy, and eventually necrosis. In the first stage, edema may regress and visual function is restored. However, at the stage of self-dissociation and necrosis, the damaged tissues will regress, atrophy affecting visual function.
Lesions that tear / tear the organization: appear due to deformation of the eyeball. These lesions include rupture of the iris legs, eyelash detachment, black / VM tear, vitreous rupture ... the culmination of the eyeball.
Clinical experiments: Weidenthal-Scheppen (1966) and Delory (1969) studies.
Experiment: the study was conducted on the eyes of pigs because the eyes of humans and pigs, the Ora Serrata and Par Plana regions have similar anatomical structures. Pig's eyes are gouged out and cause experimental injury as soon as 2-4 hours after death.
Each eye is placed in a frame of size 5 x 5 x 8 cm composed of flat glass plates. The eyes are suspended in the ring by thin threads and a 10% gelatin solution. A part of the eye where it is exposed to the shocking force will be exposed.
Eye injury was produced by marbles weighing 0.345g, diameter 0.45cm, with an average velocity of 62.3m / s (with oscillation of 2.5%). This speed has been chosen so as not to induce a piercing trauma of the eyeball, which usually occurs at speeds greater than 72 m / s. The pig eye container will be placed 2-3cm from the gun. The entire traumatic experiment process will be filmed and re-photographed by high-speed cameras and photos in vertical slices. Immediately after trauma, the eyes are fixed in formalin solution and carefully examined with the help of microscopy a few days after fixation.
Schematic representation of ocular deformation over time (in milliseconds) shows significant repression of the eyeball after trauma and excessive recovery exerting forces exerting on the base of glass translation
The above study by Delory et al showed that, at 0.4 milliseconds, the horizontal diameter of the eyeball was widened the most (28% increase compared to the original size). At this time, the distance between the base of the vitreous and the posterior pole of the eyeball is greatest, creating a pulling force on the base of the vitreous fluid in the opposite direction to the intraocular pressure that pushes the retina towards the black. cornea. On the other hand, the elasticity of the sclera is greater than that of the vitreous (cited from Weidenthal's experiments), which results in the formation of a tear force, which is usually strongest on the posterior edge of the vitreous base and causes tearing. Retina parallel to the margin (CTD). If the force is most exerted on the anterior margin of the vitreous base, the retina tear in the non-pigmented epithelium.
Mechanism of pathogenesis
Mechanical mechanism: it is the tearing of the tissue and organization that occurs due to the deformation of the eyeball. Usually causes damage that appears immediately after trauma (extraction of vitreous background, cut of retinal leg, lens deflection, retinal vitreous hemorrhage, iris foot cut, back of anterior chamber ...).
The vasomotor mechanism: When the eyeball is pressed, the vascular system of the eyeball is squeezed, the blood vessels shrink, retinal circulation slows down suddenly causing destructive damage or necrosis of retinal cells, anemia optic nerve and intraocular organs. Following the vasoconstrictor phase, the blood vessels are suddenly dilated, resulting in increased permeability of the vessel wall, drainage of plasma, and hemorrhage. It is these circulatory and nutritional disorders that lead to a series of inflammatory, degenerative processes that result in delayed damage following ocular collisions (horseshoe tear, dark atrophy). Retina, black sticky retina scarring ..)
Injury hit the front of the eyeball
Conjunctivitis: epithelial loss is often less painful, irritating and watery than corneal epithelial loss. Treatment with antibiotic ointment (both anti-inflammatory and lubricating effects) and nutritional enhancement drugs.
Conjunctivitis: is a pathology that can appear in all forms of eye trauma (trauma, crushing ...). Conjunctivitis is often of little value if merely occurring. However, it is often a sign that is accompanied by other serious lesions such as purulent endocarditis, ocular hematoma, cavernous cavity carotid artery opening. There is no proportionality between concomitant eyeball lesions and conjunctival edema. There is no specific treatment, it needs treatment according to the cause. However, corticosteroids can reduce conjunctival edema.
Tearing of the conjunctiva: After traumatic rupture of the conjunctiva should be checked for the underlying sclera tear (note: the sclera can be located relatively far from the conjunctival wound). If you suspect that there is a sclera tear, it is necessary to open the wound probe conjunctiva in the operating room. Small conjunctival tears usually do not need stitches, just wash and use antibiotics to fight infections. Wide conjunctival tears need stitching with vicryl 7/0 or 8/0 thread according to anatomically correct.
Conjunctival hemorrhage: Bleeding under the conjunctiva is bright red, moving with the conjunctiva, often with edema, torn conjunctiva attached, appearing immediately after injury. The bleeding usually clears up on its own in 1-2 weeks and the color will turn yellow and the conjunctiva will return to normal. Sometimes the bleeding can spread around the eyeballs before they are consumed. Attention should be paid to cases of severe conjunctival hemorrhage (conjunctival hematoma) accompanied by low intraocular pressure, deep anterior chamber, reclining iris signaling an eyeball rupture.
Foreign conjunctival: Usually caused by dust, glass fragments, insect hair, by explosion. Foreign matter can be attached to eyelash conjunctiva, eyeball conjunctiva, same map. When examining with slit lamps, it is necessary to carefully examine and turn the eyelids, exposing the same items to check.
Remove foreign bodies from the conjunctiva can use a wet cotton swab to wipe the foreign body, wash it with the object to let it go away. Foreign matter in the conjunctiva can scratch the cornea.
Corneal abrasion: Corneal abrasion occurs after trauma, such as from fingernails, by foreign bodies in the conjunctiva or cornea. The patient feels severe pain, dizziness, glare, watery eyes, unable to open his eyes. Fluoresced slit lamp examination to determine the extent and depth of corneal damage. It is necessary to exclude with true corneal ulcer, post-traumatic corneal scratch is usually clean, has a clear margin, mild or non-inflammatory inflammation, a history of trauma. Corneal abrasion is usually rapid immediately after applying antibiotics and eye nutrients. Widespread keratoconjunctivitis requires lumen and eye bandages. Scratch the cornea can cause recurrent corneal flaking. At this time, in addition to antibiotic treatment against infection, drugs that reduce corneal edema such as 50% glucose or 5% salt and soft contact lenses should be used.
Corneal edema: Lesions are usually in the epithelium and endothelium. Direct trauma to the cornea can cause tearing of the Bowman’s membrane or parenchyma, especially in the eyes that have had a previously spun-shaped corneal incision. In addition, trauma can damage the corneal endothelium. The consequences of these damage are manifested by folds or cracks of the Cartesian membrane, causing widespread edema and turbidity in the cornea, impairing vision. Treatment in the acute phase by applying corneal nutrition or corticoid and osmotic drugs to reduce corneal edema while waiting for the cornea to recover or fibrosis. In the sequelae stage, a deep corneal layer (DSEAK - Descemet’s stripping automated endothelial keratoplasty) may be required or transplanted corneal transplant.
Corneal foreign bodies: Corneal foreign bodies: need to examine with slit lamps to assess whether the depth of the foreign bodies in the cornea penetrates through the cornea to the anterior chamber. When foreign bodies come to the front room, they need to take them out in the operating room. Get the corneal foreign body to pay attention while taking to avoid the foreign object falling into the front room. Use a sterile needle to brush the object after the surface anesthetic has been applied. The foreign object is iron usually has a brown rust ring on the cornea around the foreign object, try to remove the object when removing it. If left, the corneal epithelium will slow healing. After taking the foreign body, it is necessary to apply antibiotics, eye nutrients, and eye bandages.
Corneal tear: careful examination under microscopy and use Seidel test to determine the tear or tear has gone all corneal thickness. Standing in front of a corneal tear, it is necessary to determine whether this tear needs stitching or not. Torn corneal layer is small, clean, able to heal automatically after treatment with anti-infection eye antibiotic and corneal nutritional enhancement drugs with regulatory paralysis if necessary, within a few days. Worn, dirty, difficult to self-heal or tear to form a skull flap, need to tear and sew corneal stitching or corneal paste. In a few cases of corneal tear is wide or flap but not displaced, the edge is clean, self-healing, soft contact glasses can be used to treat without corneal stitching.
Eyelid inflammation due to trauma
Ciliary iritis is an inflammatory reaction of the iris or the ciliary body following a trauma. Subjective symptoms: often photophobia, eye irritation, tearing and eye pain, accompanied by decreased vision, physical symptoms: peri-peripheral conjunctival hyperplasia, anterior Tyndall phenomenon (inflammatory cells). Often decreased eye pressure due to dysfunction of the ciliary body, rarely seen increased eye pressure.
Treatment: drug paralysis in mild cases (Atropin 1% 2 times / day). When there are many inflammatory reactions can use a combination of eye corticosteroid. When iritis is reduced, the ciliary paralysis can be stopped and corticosteroid should be gradually reduced within a few weeks to avoid recurrent inflammation. Post-traumatic eyelid inflammation can lead to chronic uveitis.
When examining and assessing the injury of the post-traumatic precaution, it is necessary to determine:
The depth and depth of the pre-room: Normally the room rate is about 3mm deep.
The transparency of the room.
Anomalous components in the anterior chamber: blood, pus, cataract ...
Room front corner: stick corner or backward corner of the room.
Anterior chamber hemorrhage is a phenomenon of accumulation of blood, mainly red blood cells in the form of diffuse or depositing into layers or forming blood clots in the anterior chamber.
Function: After eye injury, patient experiences blurred vision and sometimes pain in the eye.
Entity: All patients with eye trauma need a comprehensive eye exam including vision, eye pressure, anterior eyeball exam to assess the degree of precautionary bleeding, dilated pupils. to evaluate fundus conditions if possible. In the absence of fundoscopy, ultrasound is required to assess the retinal-lens fluid status.
In addition, it is necessary to differentiate between traumatic and ruptured eyeballs. Broken eyeballs are often accompanied by severe visual impairment, severe sub-conjunctival hemorrhage, low intraocular pressure, a deeper anterior to normal, reclining iris, and pupil deformity.
In addition, it is necessary to carefully exploit the patient's history of blood diseases and the history of using anticoagulants.
During the acute phase, there is no need for angiography to assess for lesions of the anterior chamber as well as to examine the peripheral retina with sclera due to the risk of increased blood in the anterior chamber. The first 4 days after injury, it is necessary to evaluate daily vision, eye pressure, level of anterior hemorrhage as well as corneal blood permeability.
About 1 month after trauma, anterior room angiography is needed to evaluate angular lesions as well as perinatal retinal examination with sclera to detect and manage peripheral retinal lesions if any.
Classification of anterior hemorrhage:
Grade 1: blood volume <1/3 of the room rate.
Level 2: The amount of blood accounts for 1 / 3-1 / 2 of the room.
Grade 3: The amount of blood in the anterior chamber> ½.
Level 4: Blood flooded the room.
Medical treatment: including hemolysis, anti-inflammatory, uncontrolled eye pressure and anti-bleeding recurrence. In the majority of cases, patients will receive outpatient treatment and monitoring. Patients admitted to the hospital for treatment in cases of severe pre-preventive hemorrhage, glaucoma that cannot be corrected with drugs, high risk of recurrent bleeding, and inability to follow-up periodically. Treatment includes:
Rest, limit vigorous exercise. Lie high to allow blood to settle down, releasing the visual axis.
Drink plenty of water: 0.5 liter of filtered water for 5 minutes on an empty stomach, 2 times / day in the morning in the afternoon. Caution should be exercised in patients with hypertension.
Discontinuation of aspirin and other non-steroidal anti-inflammatory preparations: Although the role of aspirin and other non-steroidal anti-inflammatory preparations in inducing recurrent bleeding is unclear, most ophthalmologists still indicated to stop using the above drugs in case of anterior hemorrhage.
Regulatory paralysis: Drugs that cause paralysis (cyclopentolate, atropine) work to dilate the pupils, help the ciliary body to rest thereby reducing the inflammatory response and the patient feels more comfortable. In addition, the dilated pupil presses the blood vessels of the iris, limiting the forces acting on the iris blood vessels when the pupil is dilated, thereby facilitating the healing of damaged blood vessels. On the other hand, dilated pupils to limit complications after sticking.
Topical corticosteroids are often used to control the uveitis response that is often associated with post-traumatic anterior hemorrhage. The dosage of corticosteroids depends on the degree of uveitis. Special attention should be paid to prolonged use of corticosteroids, especially in corticoid-sensitive patients.
Systemic corticosteroid use is a controversial issue. Some studies have shown a clear role of systemic corticosteroids in the treatment of post-traumatic precautionary hemorrhage, but others have confirmed that systemic corticosteroids are not effective in treating post-traumatic precautionary bleeding. love.
Antifibrinolytic agents (antifibrinolytic agents)
The basis for the use of anti-fibrinolytics is: the fibrinolytic system participates in the pro-preventive clotting of blood clots. Therefore, fibrinolytic agents will help stabilize the blood clot, so that damaged blood vessels will have more time to heal, thereby limiting recurrent bleeding.
Aminocaproic acid was first applied to the treatment of preventive bleeding by Crouch and Frenkel in 1976. The aminocaproic acid inhibits the conversion of plasminogen to plasmin, so that plasmin is available to participate in the digestion process. fibrin will be reduced. Therefore, the use of aminocaproic acid can reduce the rate of recurrent pre-bleeding bleeding. The usual dose of aminocaproic acid is 50mg / kg every 4 hours until it reaches 300mg / day for 5 days. Caproid acid treatment is often used in inpatients so that side effects can be monitored and managed. These effects include: vomiting, muscle weakness (due to increased amounts of creatinine phosphokinase), abdominal pain, bradycardia, and hypotension. Aminocaproic acid is excreted by the kidneys, so it should be used with extreme caution in patients with a history of hematuria or impaired renal function. Recently, a number of ophthalmic aminocaproic acid preparations have been developed to reduce systemic side effects of the drug.
Tranexamic acid is also a plasminogen-to-plasmin conversion inhibitor and is also used to prevent recurrent bleeding in the treatment of anterior hemorrhage. Tranexamic acid worked better and had fewer side effects than aminocaproic acid. The dose of tranexamic acid is 25 mg / kg of body weight 3 times a day for 6 consecutive days.
Some of the newer approaches to prevent hemorrhage: These include a 10-µg pre-vaccination of tissue Plasminogen activator (tPA) and trans corneal oxygen therapy (trans corneal oxygen therapy).
Combination drugs include:
Lower intraocular pressure: with oral acetazolamide 0.25gx 1-2-4 tablets / day, depending on the case, combined with potassium-based adjuvants and α blockers in sympathomimetic groups. Do not use antihypertensive agents of the pupil-causing group and the prostaglandin group due to the risk of increased uveitis reaction. In the presence of glaucoma, the patient should be closely monitored to prevent complications of corneal infiltration.
Pre-room drainage is usually indicated at least four days after the injury, when a blood clot has formed and has contracted. Surgery should not be done too soon due to the high risk of recurrent bleeding. Pre-room blood washing surgery is usually indicated in the following cases:
Blood clots in the anterior chamber do not tend to be spent
The amount of blood clotting accounts for more than half of the room rate
Glaucoma does not respond to medical treatment due to the high risk of corneal infusion.
There are 3 techniques of pre-room blood washing are commonly used:
The anterior chamber aspiration technique through one or two corneal margins is often used when the anterior chamber blood is relatively thin. The suction wash is mainly intended to remove debris from the anterior chamber. This technique is relatively simple, does not invade the conjunctiva in case of needing surgery in the future.
Pre-room blood aspiration technique through corneal incision near the edge: often used to remove undigested blood clots in the anterior chamber. This technique is less commonly used today because surgery would create a large wound in the marginal area, creating a large conjunctival scar area that could make it difficult to operate the fistula later and the ability to reveal the iris in the process. high surgical course. This technique is carried out as follows:
Separation of the peripheral conjunctiva.
Edge corneal incision near the edge (width depends on the size of the blood clot).
Using a double-barrel needle or mucus drains the entire blood clot out through the corneal incision near the edge.
Sewing corneal 1-2 stitches only 10/0 depending on the case.
Evaporation or ringer lactic for precautionary regeneration, depending on the case.
An injection of antibiotics and corticosteroids next to the eyeball.
Apply antibiotic grease, compression bandage.
The anterior chamber clot removal technique with a vitreous tip: This technique is also used to remove undigested clots in the anterior chamber.
The advantage of the technique is that 2 lines are inserted into the anterior chamber through a small edge, not invading the conjunctiva.
Disadvantage: this is a difficult technique, great care should be taken not to damage the corneal endothelium, iris, and lens. Moreover, this technique requires modern machinery and equipment, difficult to apply at grassroots levels.
Today, with the 23G, 25G small glass cutters this technique can be applied safer, more efficiently, and with fewer complications.
The technical steps include:
Poke the front of the room close to the edge of the room 2 lines: a line to place a pre-room nail, a way for oil to cut the glass.
Cut the clot in the vitreous chamber with medium suction pressure (about 200mmHg and low cutting speed). Do not try to clean the entire anterior clot clean. The mucus can be used to drain the remaining blood flow in the anterior chamber after the initial clot has been removed by the vitreous tip.
The water bottle is kept relatively high to avoid anterior deflection in the corneal endothelium and the anterior lens.
In the event of recurrent bleeding, the water bottle can be raised to increase intraocular pressure, press on the wall of the vessel to stop bleeding or use an electric coagulation tip to burn the bleeding point.
Pump edema after the end of surgery and inflate or ringer lactate solution to reconstruct the anterior chamber.
An injection of antibiotics and corticosteroids next to the eyeball.
Apply antibiotic grease, compression bandage.
Recurrent bleeding is the most common complication in post-traumatic anterior hemorrhage. This complication usually occurs 2-5 days after the injury, when the blood clot begins to contract and begins to digest. This complication accounts for the rate from 3.5-38% depending on each report. Recurrent bleeding is common in patients:
Have primary vision less than 1/10.
Bleeding greater than 1/3 of the room.
Treatment is started at least 1 day late from the time of injury.
There was glaucoma at the time of the first visit.
Patient is taking anticoagulants.
Recurrent pro-preventive bleeding increases the risk of complications such as glaucoma, corneal infiltration and posterior adhesions.
Complications of glaucoma can occur in 14% of cases of anterior hemorrhage and increase up to 25-67% if there is recurrent protestant bleeding. There are many causes of glaucoma in post-traumatic anterior hemorrhage. In the early stage, glaucoma can be caused by the blood in the anterior chamber, due to increased secretion of the ciliary body, or by a blood clot that is too large to obstruct the pupil, preventing the aqueous circulation from the back room to the anterior chamber. Later, glaucoma is often caused by red blood cells or inflammatory debris blocking the raft area. Even later, glaucoma occurs due to changes in the traumatic anterior chamber angle. Pre-preventive hemorrhagic glaucoma is often monitored and internally treated with oral carbon anhydrase inhibitors and sympathomimetic β and α blockers. Medications of the pupil or prostaglandin group are often not used due to the risk of an increased inflammatory response. In cases where glaucoma does not respond to medical treatment, a precautionary blood wash surgery intervention may be indicated. Prolonged glaucoma in anterior hemorrhage can cause atrophy of the nerve and corneal hemorrhage.
Corneal blood transfusion:
Corneal blood transfusion is common in the eyes with a lot of anterior blood pressure with glaucoma. The rate of corneal infusion increases when the blood volume is greater than of the precaution and for more than 6 days. This complication occurs in about 5.6% of cases of anterior hemorrhage. Hemosiderin and red blood cell degeneration products are found in the corneal cells. When corneal infiltrates, it is necessary to wash pre-room blood as soon as possible and control eye pressure. The retinal process of the cornea usually starts at the edge and can take months to years. In cases where corneal infiltration occurs in children, it may be necessary to conduct a corneal transplant early to limit complications of amblyopia.
Nerve atrophy due to trauma itself or glaucoma.
Glaucoma due to backward corner of the room, sticking before or after sticking.
About 75% of cases of pre-traumatic hemorrhage due to trauma achieve vision above 4/10. Vision ultimately depends on the correct treatment and management of complications, if any, as well as the severity of the injury. Traumatic nerve damage, Bruch membrane fracture, retinal detachment, vitreous hemorrhage, cataract and distortion, and corneal scarring are factors that influence the recovery of post-traumatic precautionary bleeding.
Glass service in the room
The vitreous fluid present in the anterior chamber is often due to aphasia with or without a rupture of the iris base. The anterior vitreous fluid that occurs after an eyeball injury is usually not indicated for emergency surgery. Surgery will be indicated soon if there are associated complications (glaucoma, glass fluid rubbed on the back of the cornea ...).
The trauma of the front room corner
There are various lesions of the anterior angle after an eyeball injury, including anterior angle regression, corneal brachial rupture, ciliary detachment, and iris foot lesions.
Back corner of the room
Is a tear in the ciliary body between the base of the sclera and the attachment of the iris or a tear between the lids of the body? There are many different ways to classify the room backward corner, here we divide the room backward corner into 3 types:
Form 1: broadened lash strip.
Type 2: There is a tear in the lash strip to reveal an abnormal white color, different from sclera.
Type 3: complicated tearing exposes the sclera in the relevant area (often accompanied by a lash separator).
Prevailing the anterior angle can cause scarring and coagulation, sometimes covered with an endothelial membrane and cause secondary glaucoma, especially when the lesion is> 180 degrees of circumference. Anterior angle retrograde glaucoma usually occurs several months to a few years after the injury. Therefore, it is necessary to periodically monitor to detect and treat glaucoma. Anterior angle retrograde injury often causes anterior chamber bleeding. The majority of authors found that 90-94% of prophylactic hemorrhages and 5-20% of recurrent pre-prophylactic hemorrhages have retrograde lesions.
Lash separator or lash extract
Is the phenomenon of rupture of the body adhesion to the sclera.
Patients with temporary nearsightedness due to peeling and edema reduce the tension on Zinn ligaments. This symptom usually comes on early and suddenly
The anterior chamber is a bit shallow due to the presence of aqueous probe into the parietal space.
Pre-preventive hemorrhage: often caused by damage to the blood vessels of the major iris artery. In addition, hemorrhage may occur with vitreous, cloudy.
The eye pressure is often lower due to the decreased secretory of the eyelids and the aqueous humor that drains directly into the parietal space
Anterior chamber angiography shows that the sclera is completely released to form a narrow slit. The anterior part of the angle is abnormally white due to the exposed sclera. The gray posterior part corresponds to the split eyelash. The top angle is very narrow. This area is of varying length and length, sometimes with trapezoidal attachments of the ciliary body with the sclera divided into segments.
Fundoscopy can reveal chorion.
UBM can help with the definitive diagnosis of ciliary bladder.
If atropine, anti-inflammatory treatment does not work, it may be necessary to seal the gap with argon laser, electro-freezing, freezing, or direct eyelid stitch surgery, depending on the damage to There are indications, but the results have not been announced much.
As a common injury, it can account for 52-67% of the anterior angle lesions due to trauma. The essence is that the corneal raft is torn and separated from the deep layer, exposing the sclera as a very sharp white line on the side of the raft, sometimes over a wide area.
Anterior chamber angiography can reveal 3 signs: tearing the iris, a clearer observation of the sclera, and a ring-shaped tear right on the surface of the corneal bran. If the tear is deeply, the wall of the Schlemm tube can be seen. Sometimes small tongues of the corneal raft can be observed hanging in the corner. Corneal sclerosis is often accompanied by other damage of the angle: anterior angle regression, eyelash detachment or damage to the iris, the vitreous body or recurrent anterior hemorrhage due to damage to the Schlemm tube.
Initially, corneal sclerosis can increase aqueous discharge causing transient hypotension due to the passage between the anterior chamber and the Schlemm tube. Then, scarring on one side makes the tear invisible at the angle, on the other hand, gradually clogging the raft area, increasing eye pressure.
Stick the front corner
There are many causes of anterior angular adhesions, in which the causes of the iris sticking to the raft area are mainly: anterior chamber collapse, bulging lens, lens deflection, pupil sticking and copper congestion. Factors that aggravate the anterior chamber are pigmentation, blood, vitreous in the anterior chamber, uveitis reaction ...
On a corner of the room, you can see the iris sticking bridge in the corner of the front room. Sometimes there are multiple pigments or traces of anterior blood vessel and the effect of an inflammatory reaction, facial fibrosis and surrounding adhesions. In severe cases, the entire area of the iris is pressed against the cornea, the angle cannot be detected.
Lesions of the iris and pupil
When assessing the pupil, it is important to observe:
Size: within normal range depending on the amount of light in
Shape: evenly rounded.
Color: porous brown, not degenerated.
The pupil is even.
Dilated pupils and pupil shrinkage due to injury
Trauma to the eye can cause dilated pupils or dilated (less common) pupils, and the pupil reflex may become sluggish. Injury dilated pupil is often caused by tearing the iris sphincter, which can lead to permanent pupil deformity. The pupil may be unevenly dilated, sometimes the margin is jagged. The pupil is often accompanied by inflammation in the anterior chamber, so the eyelid paralysis must be applied to prevent sticking to the iris.
This is the phenomenon of iris root separating from the eyelids (tearing the iris foot), often causing anterior chamber bleeding. Through the tear, we can see the equator of the vitreous body and the Zinn wire, the lash line. The pupil is often distorted, not round, even when the tear is very small. When the pre-room blood was gone, the tear was clearly visible. Tearing of the iris legs is small, does not cause discomfort such as double vision, blurred vision does not require treatment. Wide tear can produce multiple pupils (polycoria) and monocular, blurred vision affects visual function, therefore, need surgical treatment of iris stitching. Removal of the iris does not require immediate emergency treatment.
Indications for sewing the iris foot: Discard the foot of the iris as small as 45o or be covered by the eyelashes, not affecting the visual and aesthetic function: no surgery is required. Sewing iris foot: 2nd degree iris foot cut (cut from 90o-210o), cut iris foot 3 degree (over 210 0).
The eye is reacting to uveitis, anterior hemorrhage, glaucoma.
Sewage of the iris foot by the eyeball opening method on two planes: First layer: the edge of the iris with the posterior half of the sclera. Second layer: the cornea with the anterior half of the sclera. The needle tip is about 1mm from the cut edge of the iris, not too tight.
Number of stitches: less than 90 0 stitches 1 stitch. From 90o-120o, 2 to 3 stitches, 3 stitches over 120o. If the pupils are dilated, pupil-forming stitches can be performed.
Sew the iris foot by the closed eyeball method without having to open it in the room with only 10-0 polypropylene.
Cataract: includes cataracts and cataracts
A crushing injury to the eyeball can cause partial or complete rupture of the Zinn cord and a vitreous deflection. When the Zinn's cord breaks more than 25%, it can lead to vitreous distortion. The vitreous can be deviated from the anterior chamber, into the vitreous chamber or out of the eyeball below the conjunctiva (after a major injury to the eyeball). The vitreous deflection is often accompanied by a number of lesions such as: irregular shallow anterior chamber, tearing of the iris sphincter, tearing of the iris, anterior hemorrhage, dilated pupils and release of pigmentation. The vitreous deflection is often accompanied by fluttering of the iris (iridodesis), which translates into the anterior chamber. The vitreous fluid can press the cornea to cause corneal dystrophy.
When the whole vitreous body is deviated from the front room if the still clear vitreous looks like a drop of oil. At this time, the glaucoma of the eye is increased due to obstruction of the pupil, and the vitreous body is pressed against the cornea leading to corneal dystrophy.
The distorted vitreous form can lead to superficial precaution, pupil obstruction, and complications with glaucoma. Treatment requires dilating the pupil with the drug paralysis of the eyelids, Atropine can be applied 4% to avoid pupil obstruction and the aqueous humor can be drained from the back room. Sometimes the vitreous may be discreetly deviated, only detectable when the pupils are dilated.
The cases of vitreous aberrations should be monitored for indications for timely treatment when complications such as glaucoma .... Treatment of hypotension with drugs and oral. When the eye pressure is not lowered, it is necessary to consider the lesions in coordination with surgery such as simple corneal sciectomy or a combination of vitreous removal, vitrectomy.
The vitreous prolapse in the vitreous chamber causes less glaucoma complications and can be tolerated longer in the eye. Usually uveitis is present, surgery is indicated when uveitis is stable: vitreous dissection, vitrectomy (if the vitreous is hard, use ultrasonic vitreous dispersion), yes man-made glass bodies or not suspended in tenses or in two tenses. Complications can cause such as cataract glaucoma.
After crushing, the vitreous body may sooner or later cloud. The cataract caused by crushing may begin with star-shaped, sunflower-shaped marks under the envelope. When hit hard, the glass capsule can crack or break, causing the turbidity to progress faster. When a capsule rupture, the vitreous substance escapes the anterior chamber, causing inflammation of the iris or secondary glaucoma. The presence of a Vossius ring (a ring of iris pigment in the anterior capsule) suggests an old injury that can cause cataracts.
Injury hit the back of the eyeball
Drainage of vitreous
Under the action of force or trauma, the hyaloid membrane can rupture, and the vitreous fluid can escape into the anterior chamber. At this time, the collagen fibers will lose support, causing the collagen frame to collapse and liquefy the vitreous. The forward movement of the aqueous mass can cause tearing of the vitreous to the retina, especially in areas where the retinal fluid is sticky and causes retinal tear.
Pluck the glass translation background
Aqueous background extraction occurs after a sudden tug of the vitreous area. Under the effect of a crushing force, the fluid base area can be separated from its firm adhesive position in the Ora Serrata region. These are considered specific signs of an eyeball injury. Although the rate of hydrocephalus extraction can be as high as 25.9% in a study by Cox MS et al. (1966), this lesion is often underdiagnosed clinically.
The clinical manifestation of a vitreous extraction is a gray-white strip hanging upside down in the vitreous chamber in the peripheral region. This damage may not cause subjective symptoms and may not require treatment. However, the vitreous extraction lesions are often accompanied by other lesions such as retinal tears in Pars plana, rupture of retinal legs or other retinal tears, so the examination of the peripheral retina is accompanied by sclera. It is absolutely essential to be able to detect and promptly treat coordinated injuries.
Back glass drainage
Posterior vitreous detachment is the loss of contact between the vitreous shell and the inner diaphragm of the retina. The final vitreous detachment of the vitreous degeneration, the liquefaction of the vitreous fluid, the vitreous separation often occurs with the degeneration with age or in certain other cases such as nearsightedness ... Eye injury promotes the development of these degenerations. The posterior vitreous detachment may be complete or incomplete due to the presence of vitreous globules - the retina is surrounded by a flaky vitreous mass.
These vitreous disorders (posterior vitreous detachment, vitreous separation, vitreous liquefaction) are not indicated for treatment unless secondary complications such as anterior retinal membrane or retinal tear are present.
In the eyes that have not had posterior vitreous detachment or have completely removed posterior vitreous, the risk of retinal tearing is almost no.
If a posterior vitreous detachment is progressing and involves the pre-equatorial retina region, the risk of forming a peripheral retinal tear that results in retinal detachment is very high. The risk of retinal detachment is increased if the posterior vitreous detachment has clinical manifestations with subjective symptoms (flashes of light, fly flies, soot rain).
When examining an eye with a history of trauma for abnormal adhesions of the vitreous - retina or a retinal tear, backup lasers surrounding the tear or adhesive bridge are often used to prevent born-complications. retina with posterior vitreous effusion.
Figure c. The posterior vitreous release is not complete. Together with the movement of the eye and the head, the movement of the vitreous mass and the force of the pull down the retina at the neuropathic - retinal adhesion point, the risk of retinal tearing.
The vitreous mass itself has no blood vessels. Hemorrhage of vitreous fluid occurs due to damage to neighboring organs, damage to the blood vessels of the ciliary body, retina, and the retina. This is one of the most serious injuries, difficult to treat blood digestion (often young patients, thick glass fluid) and is one of the causes of loss of vision for patients without treatment. glasses. On the other hand, vitreous hemorrhage also hinders the ability to observe the fundus to detect and promptly treat other vitreous injuries (such as retinal tears). Blood entering the vitreous chamber will initiate a complicated pathological process to destroy blood, resulting in the destruction of the vitreous structure with many changes that seriously affect the function of the vitreous - retina. and of the entire eyeball.
Clinical manifestations of vitreous hemorrhage: General symptoms of mild to severe vitreous hemorrhage include signs such as floating bands or membranes in front of the eyes, to signs of soot rain or worsening of vision loss in the levels vary depending on the amount of blood as well as the location of the hemorrhage in the vitreous chamber. Centrifugal hemorrhage in the central or macular region can cause severe visual impairment, although the amount of hemorrhage is not as much as hemorrhages in the peripheral vitreous area, especially the lower peripheral area.
The cases of mild vitreous hemorrhage, especially in elderly patients, have had the liquefaction of vitreous, the blood can be digested after a period of treatment. Severe vitreous hemorrhage, undigested blood will result in vitreous organization that can lead to retinal shrinkage, and a host of other complications from hemolysis such as ghost cell glaucoma., the eyeball is contaminated with metal.
Progression: the natural progression of a vitreous hemorrhage is completely different depending on the location and extent of the vitreous hemorrhage:
Hemorrhage outside the vitreous fluid (hemorrhage outside the hyaloid membrane), in the anterior lens compartment, or before the retina. In this form, blood can penetrate through the hyaloid membrane into the vitreous chamber causing hemorrhage in the vitreous
Hemorrhage in the vitreous: Depending on the severity and location of the bleeding, the vision can be reduced in varying degrees.
The first few hours after hemorrhage develop a red clot with a clear boundary in the vitreous chamber.
Slowly, the blood begins to spread to the entire vitreous chamber within the first day to the first week after the injury. The following vitreous detachment appears partially.
Around the second week onwards, red blood cells begin to be released by phagocytosis that releases hemoglobin. As a result, the hemorrhagic hematoma turns yellow brown. The posterior vitreous discharge is complete and the blood clot is enveloped by the concentration of the vitreous. The posterior vitreous detachment increases the risk of retinal tearing, so it becomes even more important to have the fundus regular examination
Week 4: The vitreous gel mass is pale yellow in color, the blood settles down the inner front and lower of the vitreous.
The deposited blood volume gradually decreases in volume and after about 10 weeks the vitreous may be clear again. In rare cases, traces of the blood clot settle below the vitreous chamber, stick to the back of the lens and persist for weeks or even months, organizing into ligaments or membranes. ocher color. The amount of sedimentation varies depending on the case
Monitoring and treatment:
Monitoring and treatment of post-traumatic vitreous hemorrhage includes resting, high head 350-400 to limit recurrent bleeding and diffusion of hemorrhage as well as to allow red blood cells to settle. lower to free the visual axis. If the hemorrhage hinders the ability to observe the retina, an ultrasound should be performed to evaluate the vitreous - retinal condition as well as the ability to dissolve blood and appoint surgical intervention when necessary. The B ultrasound here not only helps to determine the level of bleeding, but also helps to evaluate the deformations of the eyeball wall, but also helps to determine the time of the posterior vitreous detachment, retinal detachment, the vitreous-retinal proliferation. cornea. In addition, in some cases, the B ultrasound also helps to determine if there is a retinal tear.
The indication for vitrectomy also depends on the severity and progression of vitreous hemorrhage.
For vitreous hemorrhages resulting from trauma to the eyeball, vitrectomy is indicated when hemorrhage is dense and shows no sign of hemolysis. Most surgeons wait at least 2-3 weeks for a posterior vitreous discharge to appear and usually perform surgery if the blood persists for more than 2-3 months. In addition, vitrectomy will be indicated earlier if a combined injury such as retinal tear, retinal detachment or signs of vitreous-retinal proliferation is detected first. cell of the vitreous mass on ultrasound B.
Retinal smash (Phu Berlin)
Retinal collapsing was first described in 1873 and is the most common retinal injury following brachytherapy. Retinal collapsing can occur after both direct and indirect trauma to the eyeball.
Clinically, retinal smash appears immediately after injury and manifests itself gradually over the next 24 hours. Patients with visual impairment depend on the severity and location of the lesion. If the lesion is localized in the macular region, vision will be severely impaired. Conversely, if the lesion is located in the peripheral retina, vision may not change after trauma. Physical examination revealed that the lesions were clusters of white, topographic, interconnected retina, which usually appear in the intermediate retina and rarely localized in the macular region. Crushing of the retina related to the macular region is commonly known as Berlin edema.
The histological studies in animals and humans as well as various morphological studies have shown that the retinal crash is not intrinsic or extracellular as some of the previous comments. here. In fact, in the acute phase of retinal knocking occurs due to fractured lesions of the photoreceptor cell and pigment epithelial cells. After the acute phase, in severely traumatized eyes, there is intracellular pigmentation and thinning of the outer layers of the retina.
Progression and prognosis of retinal smash depends on severity, location, and other associated injuries. The prognosis is usually good if the lesion is localized outside the central fossa of the retina and the trauma is mild.
Although no treatment has been found to be of any use to retinal smashing so far, due to the high frequency of retinal damage (retinal tear, macular pore, hydrophilic bridges, glasses-retina…) should be coordinated, so the patient should be closely monitored and examined the entire retina.
The retinal tear
Retinal amputation: Retinal rupture is the detachment of the retina from the non-pigmented pars plana at Ora Serrata. Retinal detachment occurs in 7% of primary retinal detachment cases and about 75% of retinal tears after ocular collisions are retinal leg fractures. The rate of retinal leg fracture after trauma ranges from 22% to 68% of the retinal leg fractures in general.
The most common site of retinal leg fracture is generally the lower temporal side because it is the weakest site of the peripheral retina and is also least protected by the orbital rim. Therefore, a small trauma can cause a retinal leg fracture in this area. However, the most common site of the retinal leg fracture from a stroke in particular is the upper nose. This shows the importance of trauma caused by the feedback wave acting on the lower temporal position, the least protected site of the orbital.
Retinal leg fractures appear immediately after injury and usually progress dull, with no symptoms in the early stages and are detected only weeks or months later. Therefore, it is necessary to examine the peripheral retina with either indirect fundoscopy or with tricobs. Because retinal detachment due to retinal leg rupture is usually located anteriorly and progresses very slowly, signs of atrophic thinning or limiting line can be seen. In addition, it is possible to find specific signs of trauma to the eye such as vitreous extraction.
Unlike other tears in the retina, the vitreous fluid usually sticks to the posterior margin of the tear, not to the anterior margin. When the vitreous fluid sticks to the anterior margin of the retina, there is a tendency to pull and tear the retina to create giant retinal tear.
Giant retinal tear: A retinal tear is considered giant when the tear runs parallel to the vitreous base and extends to more than 900 or greater than 3-hour glands. As observed by Schepens, the post-traumatic giant tear accounts for about 20% of the giant retinal tears in general. Differential diagnosis between a giant retinal tear and a retinal leg rupture in Ora Serata is based on a careful examination of the ends of the tear: the existence of the anterior tear, the retinal coil of the tear edge after sliding backwards. These are signs of a giant retinal tear. Sometimes, the retina curls backwards as far as the posterior polar region covers the macular region that may not be detached.
Similar to traumatic retinal leg fractures, giant retinal tears following ocular collisions often occur in the lower temporal quadrant or upper nose. Severe preexisting nearsightedness increases the risk of giant retinal tears following injury. Massive tears following an ocular smash injury may be accompanied by an extraction of a vitreous fluid or appear along the posterior margin of a particularly large retinal dark scar in the eyes with acute retinal necrosis.
Retinal detachment due to a giant tear after a blow injury usually occurs as early as a month after the injury. In contrast to leg fractures, giant retinal tears are often accompanied by complete posterior vitreous detachment with the anterior margin of the tear attached to the vitreous leaving a relatively free posterior margin. It is the easy movement of the posterior margin of tear that is a favorable condition for the fluid to penetrate the sub-retinal cavity and rapidly progressively detach the retina, especially in cases of the upper retina tear.
Horseshoe-shaped retinal tears: Horseshoe-shaped retinal tears often occur at the vitreous sites - the retina is intertwined and occurs secondary to a sudden tug of the vitreous fluid. Horseshoe-shaped retinal detachment occurs in about 11% of overall traumatic retinal detachment. Lacerations can appear anywhere in the peripheral zone but are common around areas with fencing. The vitreous fluid is often still stuck at the top of the tear flap, making the retina tear open, allowing the fluid to slide down the retinal cavity. Similar to giant retinal tears, due to vitreous shrinkage that persists in the anterior flap of the tear, retinal detachment often appears early with flashes of light or soot rain as the tear runs across the vessel. blood.
Tears due to necrosis of the retina: Necrotic lesions of the retina following trauma were first described by Lister (1924) and then by Shimkin (1940). Here, retinal necrosis is often accompanied by other damage to the eyeballs such as retinal hemorrhage, diffuse edema of the retina around the site of necrosis. Whereas retinal leg tear, horseshoe-shaped retina tear, or giant tear that is usually localized to the anterior retinal necrosis, is usually localized to the equatorial retina. According to a study by Johnson (1991) retinal detachment caused by necrotic retinal detachment accounts for about 22% of all traumatic retinal detachment cases in general.
By clinical observations Cox (1980) divided the retinal necrosis tears after crush injury into two main types: fan-shaped and ovoid-shaped. In the form of tearing fan-shaped retina, the entire anterior retina from Ora to the equator is necrotic.
In oocyte morphology, necrotic retinal areas often appear a cluster of necrotic retinal holes lying next to each other, marginalized, localized in the equatorial retina (figure 2). These tears usually appear immediately after the injury, at a position corresponding to the point of touch of the traumatic agent on the eyeball. As a result, retinal tears due to necrosis are often localized in the lower temporal position - a position favorable to traumatic agents due to the anatomical structure of the eye socket. In Cox's clinical study, necrotic retinal tears located in the lower temporal quadrant were observed in 69% of cases and according to Johnson (1991), 59%. Retinal detachment due to tear necrosis of the retina usually appears very early, within 24 hours of the injury.
Lacerations at pars plana: The non-pigmented pars plana epithelium is the part that extends to the front of the retina receptor. Lacerations at the pars plana are mostly caused by trauma to the eyeball. The impact of a crushing force causes tension on the anterior margin of the vitreous matrix leading to tear formation.
Tearing at pars plana is less common than retinal leg fracture about 7 times. Furthermore, a tear at the pars plana is often difficult to diagnose and is usually only observable by sclera.
Progression and clinical manifestations of retinal detachment due to tear of pars plana are very similar to retinal detachment caused by retinal leg fracture. Retinal detachment is usually flat, soft surface, slowly progressing, without symptoms until it spreads to the macula. The posterior margin of the hydrophilic base remains sticky, acting as a wick-plug that restricts fluid to the sub-retinal cavity.
Progression and treatment of retinal tears: Post-traumatic retinal tears that rapidly lead to retinal detachment include retinal necrosis, horseshoe-shaped retinal tears, and giant retinal tears. Removal of the retinal leg, tearing at the pars plana usually requires a few months to a few years to form retinal detachment.
For traumatic peripheral retinal tears due to trauma, retinal detachment prophylaxis with laser phototherapy or sclerosis is recommended, in order to create a firm black sticky retina scarring.
The macula holes
The macula is a full-thickness lesion of the retinal tissue located in the central fossa of the retina.
Traumatic macular hole was first observed and documented by Knapp in 1869 in a young patient, suffering from a traumatic eye injury and described as a macular hemorrhage. Two years later (1871), Noyes gave the first accurate descriptions of the second macular hole following a bruising injury as a full-thickness retinal and centrally located macular lesion.. Although the first records of macular pore are all about trauma and the understanding of the pathogenesis, clinical progression, and treatment of idiopathic macular have been elucidated. The clinical features as well as the pathogenesis of the traumatic macula are still not well understood.
Epidemiology: In terms of epidemiology, traumatic macular lesions can occur after both closed eyeball injuries as well as open eyeball injuries with very different frequencies ranging from 1% -9%. However, traumatic macular lesions occur after closed eyeball injuries with a frequency of 9 times that of open eyeball injuries (1.4% versus 0.15%) and are all related to ocular collisions. Similar to other trauma, traumatic macular lesions also appear in male patients, with an average age of 15 years compared with the average age of the unspoken macular hole of 60. About the cause of the cause Eye injuries, traumatic macular lesions often occur after sports related accidents (volleyball, soccer, tennis ...). In some cases, traumatic macula can appear immediately after injury.
Pathogenesis: Although the pathogenesis of the idiopathic macular hole was elucidated by Gass in 1988 and later confirmed by studies of retinal tomography, the pathogenesis of the macula. Trauma is still a controversial issue and varies from case to case.
Anatomically, the ma