Closed Eye Injury: Clinical Guidelines

List of Abbreviations

RAPD – relative afferent pupillary defect;

AOS – auto-ophthalmoscopy;

IOP – intraocular pressure;

ONH – optic nerve head;

CGI – closed globe injury

IOL – intraocular lens;

FB – foreign body

CT – computed tomography;

CFF – critical flicker fusion threshold;

ICD-10 – International Classification of Diseases 10th Revision;

OCT – optical coherence tomography;

OS – ophthalmoscopy;

CPE – choroidal detachment;

CGI – closed globe injury;

AC – anterior chamber;

ICA – iridocorneal angle;

UBM – ultrasound biomicroscopy;

ultrasound – ultrasound examination;

EPT – electrophysiological tests;

ET – electrical threshold.

Terms and Definitions

Globe contusion is a general term for various types of mechanical closed (blunt) injuries to the eyeball (bruise, compression, concussion).

Direct contusion is a contusion resulting from the direct impact of a traumatic agent on the eye.

Indirect contusion is a contusion resulting from the impact of a blast wave or concussion of individual body parts [1]

Visus pr. l. certa is visual acuity with accurate light projection;

Visus pr. l. incerta is visual acuity with inaccurate light projection;

Hyposphagma is subconjunctival hemorrhage;

Hyphema is hemorrhage into the anterior chamber;

Pripechek's sign is tenderness in the projection of a subconjunctival scleral rupture with massive hyposphagma upon palpation with a glass rod after topical anesthesia of the eyeball;

Iridodialysis is the detachment of the iris from the ciliary body;

Cyclodialysis is the detachment of the ciliary body;

Hemophthalmos is hemorrhage into the vitreous body;

Traumatic optic neuropathy is a traumatic injury to the optic nerve;

Traumatic dislocation (protrusion) of the eyeball is the dislocation of the eyeball from the orbit

1. Brief information on the disease or condition

1.1 Definition of the disease or condition

Closed globe injury (CGI) is a visual system injury characterized by damage in the absence of a wound of the eye wall (fibrous capsule), and/or the presence of a wound without full-thickness damage to the cornea and sclera. [10]

1.2 Etiology and pathogenesis of the disease or condition (group of diseases or conditions)

The cause of CGI is the direct impact on the eye of a large-area, high-kinetic-energy object or the impact of a blast wave and/or concussion of individual body parts.

The pathogenesis of CGI is complex, diverse, and consists of several stages: tissue alteration, impaired neurovascular regulation, changes in biochemical parameters in the ocular fluids, and the development of a general and local adaptation syndrome (stress response) [6,7,9].

1.3 Epidemiology of the Disease or Condition

Eye contusions, being the most frequent manifestation of CGI, occupy one of the leading places in the overall structure of traumatic injuries to the visual organ. Recently, there has been an increase in the number of patients with severe contusion injuries due to domestic and criminal trauma. Their frequent occurrence mainly among young, working-age individuals and the potential for complications that pose a serious threat to vision determine the medical and social significance of ocular contusion injuries. Analysis of the problem has shown that contusion holds the leading place among domestic injuries, while accounting for 50% to 64.7% of all criminal injuries to the visual organ in various regions. Contusion is one of the main causes leading to disability in 17.9–33% of cases [1,6,8].

1.4 Features of Coding the Disease or Condition

S04.0 – Injury of optic nerve and pathways

S05.0 – Injury of conjunctiva and corneal abrasion without mention of foreign body

S05.1 – Contusion of eyeball and orbital tissues

S05.7 – Avulsion of eye

S05.8 – Other injuries of eye and orbit

H21.0 – Hyphema

1.5 Classification of the disease or condition

The classification of CGI was adopted as part of the mechanical eye injury classification in 1996 and approved by the International Society of Ocular Trauma (ISOT) [2,3,4,5].

First part of the classification (for ophthalmologists providing all types of medical care)

Closed globe injury (CGI)

By the integrity of the fibrous capsule:

Type A. Eye contusion – the integrity of the fibrous capsule is not violated; changes in intraocular structures caused by the damaging factor are diagnosed.

Type B. Non-penetrating injury of the fibrous capsule without foreign bodies in it. Such injuries include abrasions, erosions, scratches, lamellar non-penetrating incisions of the cornea and sclera.

Type C. Non-penetrating injury of the fibrous capsule with foreign bodies in it that caused this injury.

Type D. Mixed cases, combining injuries to both the intraocular contents and the eye wall (without perforation).

By severity of visual impairment:

Grade 1: visus / visual acuity / 0.5;

Grade 2: visus / visual acuity / <0.5, but 0.2;

Grade 3: visus / visual acuity / <0.2, but >0.02;

Grade 4: visus / visual acuity / 0.02, but pr. certae / light perception with accurate projection;

5th degree visus/visual acuity/pr. incertae/faulty light projection/ – 0 (zero).

According to the location of the lesion on the ocular surface:

• External (limited to the bulbar conjunctiva, cornea, and sclera)

• Anterior segment (involving structures of the anterior segment deeper than the cornea)

• Posterior segment (involving structures of the posterior segment posterior to the posterior lens capsule)

According to the presence or absence of an relative afferent pupillary defect (RAPD).

a) positive RAPD;

b) negative RAPD.

Comments: the pupil of the eye with an afferent defect paradoxically dilates upon illumination because the pupillary dilation caused by diverting light away from the healthy eye outweighs the constriction caused by stimulating the damaged eye. Thus, there may be a positive or negative RAPD. It should be noted that a decrease in visual acuity by more than 50% and a positive RAPD typically indicate severe eye trauma. If it is impossible to detect RAPD (hyphema, iris damage, etc.), it is necessary to endeavor to determine the state of the third neuron by measuring electrical sensitivity [11].

The second additional part of the classification includes more detailed information on the grading of blunt eye trauma (BET) by the location of the lesion and the presence of various complications. It is intended for ophthalmologists at ophthalmic trauma centers and is provided for reference in

By the presence of early complications

1.6 Clinical presentation of the disease or condition

The clinical symptom complex of closed eye trauma is quite diverse and includes not only injuries to the eyeball and its accessory organs, but also systemic changes. The polymorphism of eye injuries due to contusions can occur in 80% of casualties [7].

General pathogenetic processes of the neurocirculatory disorder type, manifesting as vascular spasm, vasodilation, increased vascular wall permeability, tissue edema, and ischemia, as well as instability of ophthalmotonus ranging from reactive hypertension to pronounced hypotonia, are characteristic of all types of BET.

The same clinical manifestations of the contusive mechanism of trauma can occur with any type of BET.

Most important clinical manifestations of type A closed globe injury

Indicators of the presence of contusive eye trauma in a patient are often characteristic injuries to the accessory organs of the eye: the eyelids and conjunctiva, which are not directly related to BET.

Eyelid hemorrhages and hematomas. Hemorrhages under the skin of the eyelids appearing immediately after trauma must be differentiated from eyelid hemorrhages occurring in skull base fractures. In mild cases of eyelid contusion, the clinical picture is characterized by rapidly developing edema due to the leakage of blood serum and cellular elements into the subcutaneous tissue of the eyelid, and the appearance of subcutaneous and intradermal hemorrhages (tissue hemorrhages, ecchymoses). Due to the high extensibility of the eyelid skin and its loose attachment to underlying tissues, the edema and hemorrhages appearing on the eyelids after injury are usually more significant than in other parts of the body. Often, active opening of the palpebral fissure becomes difficult and even impossible. Three to five days later, eyelid edema usually disappears, but the bluish-red color of the skin remains for quite a long time (two to three weeks). When the lymphatic drainage pathways are damaged, eyelid edema may persist longer and even develop into watery eyelid edema due to lymphedema (elephantiasis). Eyelid edema and subcutaneous hemorrhages can spread across the bridge of the nose to the other side, as well as subconjunctivally, especially if the patient is lying on their side. In some cases, a subcutaneous hematoma of the eyelid may form during a contusion. It differs from a subcutaneous hemorrhage in the formation of a subcutaneous cavity filled with blood and its breakdown products. A hematoma is characterized by a well-defined, prominent round or oval focus, and upon palpation, there is characteristic fluctuation accompanying the displacement of the liquid contents of the hematoma cavity.

Subcutaneous emphysema of the eyelids and orbit. The diagnosis of emphysema is made based on the following signs: marked edema of undamaged eyelid skin, its elastic tension, and crepitation associated with the movement of air bubbles in the loose subcutaneous tissue. The presence of air in the eyelid skin indicates an abnormal communication between the subcutaneous tissue of the eyelid and the cavities surrounding the orbit. This occurs in a fracture or crack of the corresponding bone. Most often, these are cracks in the medial wall of the orbit, in the region of the lamina papyracea of the ethmoid bone; less commonly, the lower or upper orbital walls are damaged with the development of subcutaneous emphysema. Air can also enter the orbital tissues in case of an eyelid wound with damage to the tarso-orbital fascia. Thus, emphysema can be palpebral or orbito-palpebral. Air can also spread under the skin of the face. Emphysema almost always develops within a few hours to the first day after trauma and usually disappears within a few days, as the air is rapidly resorbed in the soft tissues of the eyelids and orbit.

Hyposphagma. Subconjunctival hemorrhage is easily diagnosed as a subconjunctival red focus of varying area. Extensive hyposphagmas can occupy large areas up to the entire surface of the eyeball and protrude above it. Hyposphagma by itself is not dangerous, as it does not cause a decrease in vision and eventually resorbs without a trace. However, it is extremely critical to remember that an extensive hyposphagma can mask a subconjunctival scleral rupture (which classifies the injury as open globe injury). Excluding a full-thickness scleral rupture in the presence of an extensive hyposphagma is a diagnostic priority, including the detection of the Pripechek sign, diaphanoscopy, and scleral revision.

Contusive changes of the eyeball

Contusive corneal edema. A corneal contusion can lead to damage to the anterior epithelium and the development of superficial edema, but more often, contusion damages the corneal endothelium with the development of edema in its deep layers. In some cases, the edematous fluid penetrates the stroma and causes strip-like corneal opacity resembling a lattice. Gradually, the aforementioned changes disappear within a few days or weeks, but with significant endothelial damage and breaks in Descemet's membrane, corneal opacity may persist as an outcome. Almost never does a contusive injury mechanism result in a rupture of the anterior part of the fibrous tunic of the eye, which is explained by the considerable safety margin of the cornea. An exception is corneas that have undergone previous radial keratotomy, which often rupture along postoperative scars during contusions, but in this case, the eye injury is classified as an open globe injury.

Hyphema. Fresh hemorrhage into the anterior chamber (AC) always causes decreased vision due to the dispersion of blood formed elements in the AC aqueous humor when changing body position. After just a few hours, the blood settles in the lower parts of the AC, forming a red level of varying height. Hyphema up to 3 mm in height generally does not cause decreased vision or increased ophthalmotonus. Hyphemas greater than 3 mm can significantly reduce vision due to pupillary masking and lead to a significant increase in IOP (up to an acute attack) due to organic blockage of the iridocorneal angle (ICA). In addition, hyphema can mask the iridodialysis zone. Total hyphema filling the entire AC, in addition to reduced vision and impaired ophthalmotonus, can lead over time to the formation of corneal blood staining (hematocornea) – persistent corneal opacity due to impregnation of its stroma with blood formed elements. Prevention of this complication is an important task in the treatment of BET, for which both conservative treatment (primarily fibrinolysis) and surgical treatment (AC paracentesis, blood aspiration, AC tamponade with air or viscoelastic) can be used. According to their consistency, hyphemas are subdivided into liquid ones with a fluid level, dry ones in the form of clots, and mixed ones when both variants are combined.

Iris injuries.

Miosis or mydriasis are observed in mild contusions. Miosis occurs upon irritation of the pupillary sphincter and is often accompanied by false myopization due to traumatic spasm of accommodation. Contusive mydriasis due to impaired function of the pupillary sphincter occurs with damage (tear or rupture) of the pupillary margin of the iris. The pupil is unevenly dilated and has an irregular shape. Tears and ruptures of the iris sphincter are visible in transmitted light as luminous radial slits.

Traumatic root avulsion of the iris (iridodialysis) is observed in more severe contusions and is characterized by the formation of a defect in the injury zone near the limbus. It is diagnosed using biomicroscopy or gonioscopy as a slit-like dark space of varying length between the iris and the limbal zone. The patient may complain of monocular diplopia due to the appearance of an additional aperture in the iris—polycoria. Complete iris avulsion results in aniridia (irideremia); the avulsed, shrunken iris is usually found as a small ball in the anterior chamber during biomicroscopy. Conversely, sometimes the iris detachment zone is very small and can be detected by the disruption of the round shape of the pupil and the weakening or disappearance of the pupillary light reflex in the meridian of the iridodialysis. In such cases, transillumination (diaphanoscopy) and ultrasound biomicroscopy assist in diagnosis.

Vossius ring. Described by the German ophthalmologist A. Vossius in 1903, it is a delicate brown ring on the anterior lens capsule, representing an exact imprint of the pupillary border of the iris (its size and shape), consisting of pigment imprinted from the pupillary margin at the moment of anterior segment deformation during blunt trauma. This clinical sign is detected only with a dilated pupil, persists for a long time, and may be combined with delicate lens opacities beneath the anterior capsule.

Traumatic iridocyclitis. Contusion impact on the ciliary body and iris is accompanied by the development of reactive inflammation—traumatic iridocyclitis with a varied set of typical clinical manifestations. These include pain syndrome that worsens at night; mixed or deep injection of the eyeball; and exudation in the anterior chamber ranging from aqueous flare and precipitates to fibrin deposits that tether the pupillary margin of the iris to the anterior surface of the lens. With the development of a circular posterior synechia—pupillary seclusion—aqueous outflow may be impaired, leading to iris bombé and ocular hypertension. When signs of iridocyclitis appear, anticholinergic drugs (ATX code S01FA) and enzyme preparations (ATX code B01AD) must be added to antibacterial and anti-inflammatory conservative therapy to stimulate the resorption of synechiae, while antiglaucoma drugs and miotics (ATX code S01E) are indicated for secondary ocular hypertension.

Lens pathology

Traumatic cataract in the acute period of blunt ocular trauma is a consequence of hydration of the lens masses through a microdefect in the lens capsule. Such traumatic cataracts are often accompanied by swelling, leading to the clinical picture of an acute attack, and may become an indication for emergency cataract surgery.

Lens (or IOL) subluxation occurs as a result of partial rupture of zonular fibers at the time of trauma. The classification by N.P. Pashtayev, 1986, is used to grade traumatic dislocations. Biomicroscopically, grade I lens subluxation manifests as iridodonesis and/or phacodonesis: tremulousness of the iris and/or lens (IOL) during eye movements. In grade II subluxation, the equator of the lens is visible within the pupillary projection during mydriasis. In grade III subluxation, the lens is displaced to such an extent that it no longer covers the optical axis. With grade II–III subluxation, the patient may complain of monocular double vision.

Lens (or IOL) dislocation occurs as a result of complete rupture of zonular fibers at the time of trauma. When a dislocated lens luxates into the anterior chamber, it is clearly visible even with focal illumination, occupies the entire volume of the anterior chamber, and can lead to organic blockade of aqueous outflow pathways with the development of an acute attack. When a dislocated lens luxates into the vitreous body, biomicroscopy reveals aphakia. Upon ophthalmoscopy, the lens appears as a hazy ellipsoid, usually in the inferoanterior part of the vitreous cavity. Ophthalmoscopy in the supine position helps determine whether the lens is mobile or fixed in the vitreous body. When refractive media are opaque, B-scan ultrasonography is the main diagnostic method for lens dislocation into the vitreous chamber, revealing an oval-shaped echogenic formation.

Cyclodialysis. Traumatic detachment of the ciliary body has few overt clinical manifestations. Cyclodialysis can be suspected based on hypotony (IOP 4–8 mmHg), low visual acuity (down to Vis = 0.1) with transparent optical media, a shallow anterior chamber, and the presence of pseudo-stagnation features in the fundus (edematous optic disc, congested and tortuous veins, macular edema with radial folds). Its presence, localization, and extent can be confirmed using gonioscopy, UBM, and B-scan ultrasonography.

Vitreous hernia. This represents partial prolapse of the vitreous body through the pupil and a damaged zonular apparatus, and is usually combined with lens subluxation. In appearance, a vitreous hernia resembles a transparent mushroom-shaped or fibrillar protrusion with delicately outlined boundaries, sometimes with the deposition of dust-like pigment inclusions or blood smears, trembling with the slightest eye movements and often attaching to the posterior surface of the cornea. It is among the rare contusion changes.

Hemophthalmos. In blunt ocular trauma with an intact vitreous, there is no loss of vitreous, so the injury can only cause partial hemophthalmos. When hemorrhage occurs into the vitreous body, patients present with various complaints regarding deterioration of vision quality: from the appearance of floating "dots," "flies," "spiderwebs," and persistent blurring in mild degrees, to complete loss of form vision in pronounced hemophthalmos. In transmitted light, weakening or complete absence of the fundus reflex is detected. Ophthalmoscopic examination in initial stages of hemophthalmos reveals floating red strands of blood and a dispersed suspension of formed elements; in pronounced hemophthalmos, ophthalmoscopy is impossible. Ultrasound diagnosis is used to identify echodense floating inclusions in the vitreous cavity of the eye; computed tomography and magnetic resonance imaging can also be utilized. Vitreous hemorrhages resolve slowly, especially when pre-retinal and retrolental in location. In a previously healthy eye, hemophthalmos resolves more easily than in an eye with pathological background. Incomplete resolution of hemophthalmos may lead to vitreous fibrosis, which carries the risk of tractional effects on the retina, causing retinal tears and detachment.

Contusion retinal edema (Berlin edema). Contusion retinal edema is a frequent manifestation of blunt ocular trauma and was first described by the German scientist R. Berlin in 1873. Ophthalmoscopically, the edematous retina has a milky-white or dull-gray color depending on the intensity of Berlin edema. The edema zone, as a rule, has clear contours and can vary in shape and area. With macular localization of edema, patients complain of decreased central vision. Peripheral edema of a small area may not be accompanied by complaints at all, but examination reveals peripheral visual field defects corresponding to the affected areas. OCT shows transient edema of the outer retinal layers corresponding to the ophthalmoscopically visible area of pallor. Sometimes retinal edema is so severe that it causes degeneration of the neuroepithelium and retinal pigment epithelium, with subsequent formation of uneven pigmentation in these areas.

Subretinal choroidal rupture.Subretinal choroidal rupture is the result of compressive deformation of the eyeball at the moment of trauma; the edges of the rupture diverge due to the elasticity of the choroid. In the area of diastasis between the rupture edges, an achoroidal zone forms where retinal blood supply is absent, resulting in local ischemia. Ophthalmoscopically, white foci with clear contours, often crescent-shaped, are visualized concentrically to the optic disc. The frequent localization of ruptures in the macular region is due to the smallest thickness of the choroid in this zone. Frequently, two or more ruptures running parallel to each other are detected. A common complication of subretinal choroidal rupture is localized subretinal hemorrhage. With macular localization, this pathology leads to a marked, sharp decrease in vision. The outcome of subretinal hemorrhages may include sclopetaria choroidoretinitis and post-traumatic choroidal neovascularization, which will be discussed below.

Sclopetarial chorioretinitis. Bizarre, irregularly shaped chorioretinal atrophic lesions with pronounced pigmentation resulting from choroidal and retinal damage accompanied by hemorrhages between them following a severe contusion injury to the eyeball, when a high-speed wounding projectile (firearm missile) shakes the eye without penetrating it and causes characteristic fundus changes. In 1901, Hungarian ophthalmologist Vilhelm Goldzieher first used the term "chorioretinitis plastica sclopetaria" to describe fundus findings of whitish fibrous proliferation at the site of a choroidal rupture and hemorrhage after a periorbital gunshot wound. Histopathologically, sclopetarial chorioretinitis is characterized by defects in Bruch's membrane and the choroid, extensive photoreceptor loss and retinal pigment epithelium hyperplasia, with replacement of the retina and choroid by fibrous scar tissue.

Post-traumatic choroidal neovascularization. According to literature, in 11–20.3% of cases, choroidal rupture can be complicated by the development of active choroidal neovascularization (CNV) within a period ranging from 2 months to a year after trauma. When the choroidal rupture is located closer than 1500 µm to the center of the macula and its length exceeds 4000 µm, the risk of CNV development increases significantly, which in turn further affects the degree of visual acuity reduction. Clinically, the pathology can be suspected by the appearance of a dark gray or greenish focus with distinct borders in the projection of the choroidal defect upon ophthalmoscopy. Optical coherence tomography helps confirm the presence of CNV, while fluorescein angiography and OCT angiography help assess its area. The treatment of post-traumatic CNV involves laser coagulation around the rupture zone when it is located outside the macular region, intravitreal administration of angiogenesis inhibitors, as well as photodynamic therapy.

Retinal detachment. The cause of retinal detachment in blunt eye trauma is either the "activation" of a previously existing "silent" tear, or the formation of a new tear at the moment of impact in areas of degenerations or vitreoretinal tractions, or an extensive retinal dialyses from the ora serrata. Late detachments resulting from contusions are the result of the development and progression of proliferative vitreoretinopathy against the background of hemophthalmus organization. Clinically, traumatic detachments are distinguished by a more aggressive course due to favorable conditions for tractional effects on the retina by the altered vitreous body and, as a rule, a concomitant inflammatory background—traumatic iridocyclitis. The main diagnostic method is ophthalmoscopy, which reveals dome-shaped retinal tissue protrusions of various shapes, dull shades, and varying degrees of mobility projecting into the vitreous chamber. To diagnose peripheral tears or dialyses from the ora serrata, it is necessary to use ophthalmoscopy with scleral depression. With concomitant hemophthalmus, when ophthalmoscopy is uninformative, a B-scan ultrasound is used, which reveals a mobile echo-positive membrane fixed at the posterior pole in the projection of the optic nerve. The absence of posterior hyaloid membrane detachment worsens the course of traumatic retinal detachment, sometimes rendering extrascleral surgery ineffective.

Choroidal detachment. Traumatic choroidal detachment is hemorrhagic and occurs as a result of the rupture of choroidal vessels at the time of trauma. Clinically, it manifests as rounded domes of various sizes protruding into the vitreous chamber. Differential diagnostic features distinguishing it from retinal detachment are the color of the domes (dark pink or dark red, rather than dull) and immobility during eyeball movement. With concomitant hemophthalmus, when ophthalmoscopy is uninformative, a B-scan is used, which reveals a fixed echo-positive rounded shadow at the posterior pole of the eyeball.

Macular hole. Ophthalmoscopically defined as a rounded, brighter red lesion than the surrounding retina in the macular projection. When optical media are clear, optical coherence tomography provides the highest diagnostic information. In cases of impaired optical media transparency, early diagnosis of a traumatic macular hole is difficult.

Retinal hemorrhages. The shape, location, size, and depth of retinal hemorrhages following a contusion injury can be quite diverse. Fundus hemorrhages are conventionally subdivided into preretinal, intraretinal, and subretinal. They can be differentiated both by the ophthalmoscopic picture and by using additional diagnostic methods—OCT, ultrasound.

Preretinal hemorrhages are large in size, shaped like pools or cysts with a horizontal blood level, shield the retinal vessels, have a rich burgundy color, and can protrude into the vitreous body. In essence, this is a partial hemophthalmus localized on the inner surface of the retina. The ophthalmoscopic picture is polymorphic and determined by the state of the vitreoretinal interface and the presence of posterior hyaloid membrane detachment in a particular patient. The upper border is sometimes located as a horizontal line and changes its position when the head is tilted.

Intraretinal hemorrhages are located in the retinal layers, usually along the course of the vessels. They are typically small in size, bright red in color, and shaped like spots or streaks depending on their localization in specific retinal layers; they may group around the optic disc or in the macula.

Subretinal hemorrhage. A localized hemorrhagic retinal detachment, ophthalmoscopically defined as a dark-red polymorphic lesion with clear margins. An important diagnostic symptom is the visualization of retinal vessels over the surface of the hemorrhage. In later stages, a subretinal hemorrhage can organize into a white subretinal fibrous scar with clear margins. When the hemorrhage is located in the macula, vision drops sharply with the formation of a central scotoma; a non-macular hemorrhage may not be accompanied by complaints of decreased vision at all.

Traumatic optic neuropathy. One of the most severe complications of blunt eye trauma is traumatic optic neuropathy, where vision drops to the point of blindness due to optic nerve contusion while the eyeball remains intact. The clinical picture is extremely sparse, as there are sometimes no changes whatsoever in the eyeball. A relative narrowing of arteries may be observed. In the presence of other above-described manifestations of blunt eye trauma, a warning symptom is the discrepancy between intraocular changes and the significant degree of vision loss. In cases of pronounced intraocular manifestations of blunt eye trauma (significant hemophthalmos, traumatic cataract, total hyphema, etc.), it is very important not to miss concomitant traumatic optic neuropathy. Obligatory diagnostic elements must include entoptic phenomena (phosphenes, mechanophosphenes), the absence of which indicates optic pathway pathology, as well as the study of electrophosphenes. An increase in electrical threshold and a decrease in critical flicker fusion frequency directly indicate contusional neuropathy in these cases.

Traumatic dislocation (protrusion) of the eyeball. Complete protrusion of the eyeball from the orbit is a clinical rarity and, according to literature, is termed avulsion or dislocation of the eyeball. It may be accompanied by partial or complete avulsion of the optic nerve, fractures of the orbital walls, and destruction of one or more extraocular muscles. The visual prognosis and restoration of eyeball motility depend on the degree of damage to the orbital organ complex and the optic nerve, as well as the timeliness of medical care. In prolonged eye avulsion, dehydration of the eyeball surface and infectious complications also pose a threat to visual functions.

Clinical manifestations of type B closed globe injury

Type B blunt eye traumas include abrasions, erosions, scratches, and lamellar non-penetrating lacerations of the cornea and sclera. Superficial corneal injuries (traumatic erosions) are accompanied by a pronounced foreign body sensation and frequently severe pain, as multiple endings of sensory nerve fibers are damaged in the process. At the site of the erosion, the cornea loses its specular luster and vascular injection appears. Diagnosis of superficial epithelial defects is facilitated by performing a fluorescein test. The same test is also used to perform differential diagnosis with penetrating eye trauma.

Clinical manifestations of type C closed globe injury

Type C closed globe injuries (CGI) include non-perforating wounds of the cornea and sclera with foreign bodies. In the case of type C CGI (especially blast injuries), the number of foreign bodies embedding not only the skin of the face and eyelids but also the corneoscleral envelope of the eye can be very significant. In close-range explosions, these are typically particles of gunpowder, soil, glass, etc. In 60–70% of cases, both eyes are affected. The presence of foreign bodies in the cornea and the depth of small foreign bodies within the corneal layers can be assessed using lateral focal illumination and biomicroscopy.

Clinical manifestations of type D CGI combine symptoms of type A CGI and type B or C CGI [4,6,7,9].

2. Diagnostics, medical indications and contraindications for diagnostic methods

The diagnosis/condition is established based on:

1. history taking and anamnesis;

2. physical examination;

3. instrumental examination.

2.1 Complaints and Anamnesis

Comments: Patients with CGI usually complain of pain in the eye and periorbital area, decreased vision, eye redness, lacrimation, and photophobia. Complaints depend on the type of CGI and are described in the "Clinical Presentation" section.

2.2 Physical Examination

2.3 Laboratory Diagnostics

Laboratory diagnostic tests are not performed.

2.4 Instrumental Diagnostics

Comments: for visual acuity less than 0.1, testing for the entoptic phenomenon of autooftalmoscopy (AOS) is indicated. A positive AOS indicates visual acuity of at least 0.1.

Comments: Visual field testing as part of a comprehensive examination makes it possible to assess the severity of the damage, as well as the functional state of the retina and optic nerve. In all cases of visual field absence, testing for the entoptic phenomenon of mechanophosphene (MP) is indicated.

Comments: often in CGI, the approximate transpalpebral bimanual palpation method for IOP assessment is used.

Comments: Biomicroscopy is performed to detect conjunctival injection, hyposphagma, non-penetrating scleral wound, scleral foreign bodies, non-penetrating or shelved corneal wound, corneal erosion, corneal foreign body, hyphema, iridodialysis, tearing of the pupillary margin of the iris, iridophagodonesis, vitreous hernia, subluxation of the lens or IOL, dislocation of the lens or IOL into the anterior chamber, aphakia, and damage or opacity of the lens.

Comments: when performing fundus biomicroscopy with 90, 78, and 60 diopter aspheric lenses, it is possible to detect hemophthalmos, retinal detachment, choroidal detachment, dislocation of the lens/IOL into the vitreous body, subretinal or intraretinal hemorrhage, retinal edema and tear, and subretinal choroidal rupture.

Comments: can be performed with a narrow pupil. Accuracy rate is 100% [6, 13].

Comments: Electroretinography makes it possible to objectively assess the state of the central and peripheral regions of the retina, its outer and middle layers, and the function of the cone and rod systems. Visual evoked potentials (VEPs) make it possible to objectively assess the state of the optic nerve proximal to the retina and identify emerging changes at the preclinical stage. Subjective methods: Determination of retinal electrical sensitivity (ES) and optic nerve lability (EPT) have high informativeness (80%) and characterize the state of the third neuron and the integrity of the conductive pathways as a whole.

2.5 Other Procedures

Other diagnostic examinations for closed globe injury are not performed.

3. Treatment, including drug and non-drug therapies, diet therapy, and pain management

3.1 Conservative Treatment

Comments: the possible development of allergic reactions must be kept in mind: fever, pruritus, rash, arthralgia, anaphylactic shock. Anti-shock therapy supplies must be prepared before administering the serum. Not used if the patient has hypersensitivity (allergy) to any of the components included in the medicinal product.

Comments: fluoroquinolones (ATX code S01AE) 1 drop 4–6 times a day for 2 weeks; all preparations can be used in this regimen in adults and children (levofloxacin is approved for use in children from 1 year of age, ciprofloxacin from 18 years of age),

in combination with the antimicrobial agent picloxydine (ATX code S01AX16) 1 drop 3–4 times a day for the prevention of bacterial infections and infectious complications in the postoperative period during interventions in the anterior segment of the eye

Comments: The route of administration and doses depend on the severity of the injury. For mild inflammatory reactions accompanying closed globe injuries (CGI) types B, C, and D, topical anti-inflammatory treatment in the form of dexamethasone** eye drop instillation (ATC code S01BA01) is sufficient. For eye contusions (CGI types A, D) accompanied by uveitis, subconjunctival injections of dexamethasone** (ATC code S01BA01) combined with anticholinergic agents (ATC code S01FA) are used. If the posterior segment of the eye is involved in the inflammatory process, systemic anti-inflammatory therapy in the form of intravenous corticosteroids (dexamethasone) ATC code S01BA01) is prescribed [7]. In patients with severe optic disc and macular edema.

Comments: topical forms of drugs are prescribed for a long time until complete corneal re-epithelialization is achieved.

Comments: In CGI types A and D accompanied by hyphema, depending on the severity of the injury, recombinant prourokinase** (ATC code B01AD) may be used in patients over 18 years of age in the form of subconjunctival injections

For the resorption of fibrin and fresh synechiae in traumatic iridocyclitis complicating eye contusion. In severe contusions (CGI types A, D) accompanied by hemophthalmos, subretinal, preretinal, and subchoroidal hemorrhages, recombinant prourokinase** (ATC code B01AD) may be used via intravitreal administration. For the resorption of formed old synechiae, vitreous fibrous changes, and corneal scars after CGI, proteolytic enzymes (ATC code D03BA) are used in the form of subconjunctival injections and electrophoresis/phonophoresis.

Comments: In CGI types A and D accompanied by elevated intraocular pressure, instillations of beta-blockers (ATC code C07AB), carbonic anhydrase inhibitors (ATC code S01EC), alpha-adrenergic agonists (ATC code R03AA), or combination drugs may be prescribed for a hypotensive effect. If local hypotensive therapy is ineffective, systemic administration of drugs is possible.

Comments: anticholinergic agents (ATC code S01FA) are generally used. If the latter are ineffective, sympathomimetics for glaucoma treatment (ATC code S01EA) and anticholinergic agents (ATC code S01FA) according to Gredley can be used on a cotton wick moistened with the specified mixture and placed in the lower conjunctival sac for 15-20 minutes, or administered via subconjunctival injections.

Comments: In the complex conservative treatment of CGI types B and C, if a corneal defect persists and the corneal syndrome is pronounced, silicone-hydrogel soft contact lenses can be used, including those pre-soaked in antibiotic solutions (soaked for 12 hours in topical antibiotic drops), which relieves pain and creates a biological dressing on the eye surface.

3.2 Surgical Treatment

Surgical treatment is performed for CGI types A, B, C, and D [4,6,8]:

Comments: Scleral revision – performed across all quadrants and under all extraocular rectus and oblique muscles when subconjunctival scleral rupture is suspected.

Removal of a swelling traumatic cataract – performed for an acute attack of phakomorphic ocular hypertension refractory to conservative management.

Removal of the lens from the anterior chamber – performed in case of lens dislocation into the anterior chamber to prevent an acute attack of secondary ocular hypertension and loss of corneal endothelial cells.

Paracentesis of the anterior chamber – performed for total hyphema in the absence of positive dynamics from conservative therapy, to evacuate blood and its clots for the prevention or treatment of an acute attack of ocular hypertension. If hyphema recurs during this procedure, the operation may be concluded with air tamponade of the anterior chamber to prevent hematocornea.

Removal of foreign bodies from the fibrous tunic – for CGI types C and D.

Suturing of corneal wounds – for deep, extensive, or avulsion corneal wounds in CGI types B, C, and D.

Enzymolysis and pneumatic displacement – the international standard of care for extensive post-traumatic macular subretinal hemorrhages. An intravitreal injection of 500 IU of recombinant prourokinase** (ATC code B01AD) in 0.1 ml of sodium chloride solution and 0.2 ml of perfluorocarbon gas for temporary vitreous cavity endotamponade is performed [16,17]; to normalize IOP, aqueous humor is drained via paracentesis. In the postoperative period, maintaining a face-down position for 3–5 days is mandatory [16,17]. The primary goal of treatment is to displace the hemorrhage from the macular area and achieve its lysis. Intravitreal administration of prourokinase is performed exclusively in patients over 18 years of age.

Comments: Irisoplasty – for iridodialysis, significant pupil deformation due to pupillary margin rupture.

Removal of traumatic cataract with IOL implantation.

Lens extraction with IOL implantation – for lens subluxation with impaired visual function and/or ocular hypertension.

Cyclopexy – for cyclodialysis with persistent hypotony.

The scope of surgical intervention for retinal detachment (laser barrage, episcleral surgery, or vitreoretinal surgery) is determined on a case-by-case clinical basis.

Posterior scleral trepanation – for persistent dome-shaped choroidal detachments.

Lensectomy with IOL implantation – for lens dislocation into the vitreous body.

Vitrectomy with internal limiting membrane peeling – for traumatic macular hole.

3.3 Other Treatment

• No other treatment is performed for closed globe injury.

4. Medical Rehabilitation and Sanatorium-Resort Treatment

5. Prevention and Dispensary Observation

6. Organization of Medical Care

Comments:

1. For grade 1 closed globe injury, conservative outpatient treatment is indicated. The prognosis is favorable (complete recovery);

2. For grades 2 and 3 closed globe injury, conservative inpatient treatment is indicated. The prognosis is relatively favorable, follow-up dispensary observation for 3 to 6 months, and if indicated, addressing the issue of subsequent optoreconstructive surgeries;

3. For grades 4 and 5 closed globe injury, inpatient treatment with conservative therapy is indicated, along with emergency surgical interventions if indicated. The prognosis is doubtful (significant functional and anatomical damage).

Indications for patient discharge from a medical organization:

1. Achievement of complete corneal epithelialization;

2. Improvement of visual acuity;

3. Normalization of intraocular pressure;

4. No need for surgical interventions for emergency conditions: retinal detachment, progression of vitreoretinal proliferation.

7. Additional Information

For patients with closed globe injury, their mental status is extremely important as it influences the development of the underlying disease and the rehabilitation process as a whole. Thus, patients who sustained a closed globe injury in disaster settings and found themselves in stressful situations require additional psychological and psychiatric care, since the negative impact of a stress state directly affects the functional status and the outcome of the disease [7].

Criteria for Evaluating the Quality of Medical Care

References

Appendix A1. Working Group Composition

1. Ilyukhin P.A., Candidate of Medical Sciences, Head of the Department of Traumatology and Reconstructive Surgery, Helmholtz National Medical Research Center of Eye Diseases, member of the NGO «Association of Ophthalmologists»;

2. Chentsova E.V., Doctor of Medical Sciences, Prof., Department of Traumatology and Reconstructive Surgery, Helmholtz National Medical Research Center of Eye Diseases, member of the NGO «Association of Ophthalmologists»;

3. Alekseeva I.B., Candidate of Medical Sciences, Head of the Trauma Department, Helmholtz National Medical Research Center of Eye Diseases, member of the NGO «Association of Ophthalmologists»;

4. Kulikov A.N., Doctor of Medical Sciences, Prof., Head of the Department of Ophthalmology, Military Medical Academy named after S.M. Kirov of the Ministry of Defense of the Russian Federation, Chief freelance ophthalmologist of Saint Petersburg, member of the NGO «Association of Ophthalmologists»;

5. Boyko E.V., Doctor of Medical Sciences, Prof., Director of the St. Petersburg Branch of the S.N. Fyodorov Eye Microsurgery Federal State Institution of the Russian Ministry of Health, member of the NGO «Association of Ophthalmologists», Chairman of the St. Petersburg Branch of the OOR;

6. Kharitonova N.N., Candidate of Medical Sciences, Assoc. Prof., Department of Ophthalmology, Military Medical Academy named after S.M. Kirov of the Ministry of Defense of the Russian Federation

No conflict of interest is declared.

Appendix A2. Methodology for Developing Clinical Guidelines

In these clinical guidelines, all data are ranked by level of reliability (evidence) depending on the quantity and quality of studies on the issue.

Target audience for these clinical guidelines:

1. Ophthalmologists

2. General practitioners (family physicians);

3. Ambulance doctors

4. Nursing staff

Table 1. Levels of Evidence (LoE) grading scale for diagnostic methods (diagnostic interventions)

Table 2. Scale for grading levels of evidence certainty (LEC) for prevention, treatment, and rehabilitation methods (preventive, therapeutic, and rehabilitative interventions)

Table 3. Scale for grading grades of recommendation (GR) for prevention, diagnostic, treatment, and rehabilitation methods (preventive, diagnostic, therapeutic, and rehabilitative interventions)

Procedure for updating clinical guidelines.

The mechanism for updating clinical guidelines provides for their systematic revision at least once every three years, as well as upon the emergence of new evidence-based medicine data on the diagnosis, treatment, prevention, and rehabilitation of specific diseases, or in the presence of justified additions/comments to previously approved clinical guidelines, but no more frequently than once every 6 months.

Appendix A3. Reference Materials

1. Current package leaflets for the drugs mentioned in these clinical guidelines can be found on the website http://grls.rosminzdrav.ru

2. International Statistical Classification of Diseases and Related Health Problems, 10th Revision (ICD-10). World Health Organization.

3. Nomenclature of medical services. Order of the Ministry of Health of the Russian Federation No. 804n dated October 13, 2017 (as amended on September 24, 2020, with rev. dated October 26, 2022) «On Approval of the Nomenclature of Medical Services».

4. Federal Law No. 323-FZ dated November 21, 2011 (as amended on December 25, 2023) «On the Fundamentals of Protecting the Health of Citizens in the Russian Federation» (with rev. and add., effective April 1, 2024).

5. Procedure for providing medical care to the adult population for diseases of the eye, its adnexa, and orbit. Order of the Russian Ministry of Health No. 902n dated November 12, 2012 (as amended on February 1, 2022) «On Approval of the Procedure for Providing Medical Care to the Adult Population for Diseases of the Eye, its Adnexa, and Orbit».

6. Decree of the Government of the Russian Federation No. 2406-r dated October 12, 2019 (as amended on April 16, 2024) «On Approval of the List of Vital and Essential Medicines, as well as Lists of Medicines for Medical Use and the Minimum Assortment of Medicines Required for the Provision of Medical Care»

Appendix B. Physician Action Algorithms

Diagram

Appendix C. Patient Information

In all cases of blunt eye trauma or periocular injury, it is necessary to consult an ophthalmologist to provide primary ophthalmological care, determine the severity of the injury, prescribe treatment, and, if necessary, determine indications for hospitalization in multidisciplinary or other specialized hospitals.

Appendix G. Assessment Scales, Questionnaires, and Other Evaluation Tools

Assessment scales, questionnaires, and other patient status evaluation tools given in the clinical guidelines are not used for closed globe injuries.