nemoci-sympt/OCNI/retinopatie/retinal-detachement/rizikove-faktory

Fforces of adhesion

Mechanical

Outside the subretinal space (SRS)

• Fluid pressures and vitreous
• Fluid exits the eye through the trabecular meshwork
• Small proportion tends to exit from the vitreous to the choroid
• By virtue of the intraocular and choroidal oncotic pressures
• Because the retina and RPE substantially resist fluid transport
• Outward vector of fluid movement tends to push the retina against the RPE
• Drug that increases the vitreous oncotic pressure
• Tends to withdraw fluid into the vitreous from the choroid through the retina
• This inward vector of fluid movement could lead to retinal separation from the RPE because of retinal resistance to flow

• Formed vitreous
• Acts as a seal to retinal breaks
• Indirectly aids in preventing retinal detachment and maintaining adhesion between the retina and RPE
• Whether the vitreous plays a direct role in retinal adhesion is yet to be determined
• Physical structure of the vitreous might be of importance in maintaining retinal apposition

Inside the subretinal space (SRS)

• Matrix material between the NSR and RPE
• In-between photoreceptor outer segments = interphotoreceptor matrix (IPM)
• Predominantly composed of glycosaminoglycans
• May act as a glue12 binding the NSR and RPE [1]
• Components that remain attached to both the RPE and the cones if the NSR was peeled off the RPE [1]
• Cell adhesion molecules or receptors
• Between the matrix and the cellular membranes
• Factors that affect the physicochemical properties of the IPM
• Enzymes that degrade some of its components weaken retinal adhesion
• Interdigitations between the RPE microvilli and the photoreceptors
• Continuous process of phagocytosis of photoreceptor outer segments by RPE cells
• Two cells are intimately connected
• Frictional forces that result from the interdigitations
• Possible presence of electrostatic interaction between the cell membranes [1]

Metabolic factors that affect retinal adhesion

• Oxygenation
• Retinal adhesion decreases tremendously postmortem and is restored with oxygenation
• Due to the effect of
• Released RPE lysosomal enzyme on IPM24
• Ischemia on active RPE fluid transport [1]
• Many drugs that interfere with the pH and RPE fluid transport activity [1]

Traction retinal detachment (TRD)

• When the retina is pulled off the RPE by tractional forces in the absence of retinal tears
• Through tractional bands or membranes
• Contiguous with the retina
• Through vitreous strands
• Bridging the retina to tractional bands
• Purely through vitreous bands as in cases of
• Vitreous loss
• Vitreous incarceration in surgical wounds
• Most common in proliferative retinal and vitreoretinal diseases, like
• Proliferative diabetic retinopathy
• Sickle cell retinopathy
• Retinopathy of prematurity
• Proliferative vitreoretinopathy
• Following penetrating trauma
• Contractile fibrous and/or fibrovascular tissue forms within the vitreous cavity and/or periretinally and leads to TRD.

Combined traction-rhegmatogenous retinal detachment (TRRD)

• Result of a combination of a retinal break and retinal traction
• Retinal break, which is mostly located near a fibrous or fibrovascular proliferation
• Usually secondary to traction that is the major component of retinal detachment in these cases
• Most common in proliferative retinal and vitreoretinal diseases [1]

Rhegmatogenous retinal detachment (RRD)

• Presence of a full thickness retinal break as the prefix rhegma (= rent in Greek)
• Break is held open by vitreoretinal traction
• Allows accumulation of liquefied vitreous under the retina
• Separating it from the RPE
• Precursors to this type of retinal detachment are
• Liquefied vitreous
• Tractional forces
• Can produce and maintain a retinal break
• Break through which fluid gains access to the subretinal space
• Even if a full thickness break is present in the retina
• Retinal detachment will not occur if the vitreous is not at least partially liquefied
• And if the necessary traction is not present
• Vitreous syneresis
• Culminates in posterior vitreous detachment (PVD)
• Can produce all three precursors of RRD
• In most instances an RRD is preceded by a PVD
• Rotational eye movements
• Detached vitreous moves within the vitreous cavity
• Tractional forces are transmitted with these movements to the areas of persistent vitreous attachment
• If these forces and the forces of vitreous attachment at these areas are strong enough, the retina tears
• As the process of vitreous detachment progresses
• Vitreous remains adherent to the flap of the break
• Horseshoe tear will result
• If the vitreous traction is strong enough
• Cause avulsion of the retinal flap at its base
• Operculated tear results
• Traction resolves
• Once a break occurs
• Ocular saccades cause fluid vitreous movement
• May force fluid into the subretinal space dissecting the NSR off the RPE
• Especially if the break is held open by vitreous traction (horseshoe tear) [1]
• Depending on the location of this pathology, RRD can be classified
• Equatorial
• Oral
• Macular
• Equatorial RRD occurs in cases of
• Myopia,
• Lattice degeneration
• Horseshoe tears
• Round retinal holes
• Oral RRD is most commonly seen in cases of
• Aphakia,
• Pseudophakia,
• Dialysis in the young
• Traumatic dialysis
• Giant retinal tears
• Macular type is seen in
• High myopia,
• Traumatic holes
• Idiopathic macular holes [1]
• Other less frequent causes of RRD include
• Various forms of necrotizing retinitis which increase the chance of developing full thickness retinal tears.
• Toxoplasmosis
• Cytomegalovirus infection
• Acute retinal necrosis syndrome [1]

Exudative, transudative or serous retinal detachment (SRD)

• Fluid accumulation in the subretinal space in the absence of retinal breaks or traction
• Vessels of the retina
• Choroid
• Or both
• In a variety of diseases of the retina, RPE, and choroid
• Vascular
• Inflammatory
• Neoplastic [1]
• Fluid leaks outside the vessels and accumulates under the retina
• RPE pump activity becomes overwhelmed
• As long as the RPE is able to pump the leaking fluid into the choroidal circulation
• no fluid accumulates in the subretinal space
• no retinal detachment occurs [1]
• If the RPE activity decreases because of
• RPE loss
• Decreased metabolic supply (eg ischemia)
• Fluid starts to accumulate
• Retinal detachment occurs [1]
• Accumulation of blood in the subretinal space (hemorrhagic retinal detachment)
• Inflammatory diseases
• Posterior scleritis
• Sympathetic ophthalmia
• Harada disease
• Pars planitis
• Collagen vascular diseases [1]
• Vascular diseases include
• Malignant hypertension
• Toxemia of pregnancy
• Retinal vein occlusion
• Coats disease
• Retinal angiomatous diseases
• Different forms of choroidal neovascularization
• Polypoidal choroidal vasculopathy [1]
• Choroidal tumors may be associated with SRD include
• Some nevi,
• Melanoma,
• Hemangioma,
• Lymphoma,
• Metastatic tumors [1]
• Other conditions that are associated with SRD include
• Central serous chorioretinopathy
• Familial exudative vitreoretinopathy
• Norrie disease
• Uveal effusion syndrome
• Nanophthalmia
• Optic nerve head pits
• Colobomas are still
• Iatrogenic following:
• Retinal detachment surgery
• Laser photocoagulation [1]

Literatura:

Hyaloideoretinopathies

• Number of diseases with much overlap in the clinical and sometimes genetic characteristics
• Dystrophic retinal and vitreal changes
• Differ by the predominance of one of these changes
• Vitreous liquefaction (optically empty vitreous)
• Retinal break formation [1]

Hyaloideoretinopathies

• Stickler syndrome
• Most of these entities predispose to RRD
• High incidence of associated vitreous detachment and retinal breaks
• Incidence of retinal tears varies from 0.59 to 27% according to different studies
• Stejně jako incidence of retinal detachment in patients with retinal tears
• Not every retinal tear leads to retinal detachment
• Prevalence of retinal tears was found to be 83 times that of retinal detachment
• Prophylactic treatment of retinal tears should be selective
• Recommended for
• Symptomatic tears
• Horseshoe tears with persistent vitreous traction
• Normal sites of strong attachment between the vitreous and retina
• Several peripheral retinal lesions
• Characterized by anomalous vitreoretinal adhesion predispose to full thickness retinal breaks when the vitreous detaches
• Occurs at:

Enclosed and partially enclosed ora bays

• Posterior indentation in the retina
• Can be completely (enclosed ora bay) or incompletely (partially enclosed ora bay) surrounded by retinal tissue
• 1000 autopsy eyes - retinal tears were associated with 16.7% of either type of ora bays
• Retinal tears associated with ora bays were present in only 0.5% of all eyes.

Meridional folds and complexes

• Meridional folds are elevated radial retinal folds
• Aligned with a dentate process or an ora bay
• Association of a retinal fold, a dentate process and a ciliary process in alignment is a meridional complex
• Conflicting data as to the incidence of retinal tears associated with these lesions is present in the literature [1]

Retinal tufts - projections of retinal fibroglial tissue into the vitreous

• Three types of retinal tufts:
• Non-cystic
• Not associated with cystic degeneration of the retina
• Nor with retinal tears or detachment
• Cystic
• Sometimes associated with localized cystic degeneration of the retina and condensed vitreous strands at the apex
• 6.5% of retinal detachments are associated with holes that develop with PVD at the areas of cystic tufts
• Prophylactic therapy of these lesions is not necessary
• Risk of developing retinal detachment secondary to cystic tufts is less than 1%.
• Zonular tufts
• Projections of neuroglial tissue or embryonal-like epithelium
• Extend anteriorly from the peripheral retina at an acute angle where they become continuous with a lens zonule
• Direct traction on the retina can occur from manipulation of the lens.
• Retina at these sites often has cystic changes
• Associated retinal changes
• Trophic
• Partial and full thickness holes
• Tractional
• Rupture of the tuft
• Full thickness breaks (2.2%)

• Generally these lesions are not associated with an increased risk of retinal detachment
• Except if the breaks associated with them are
• Extrabasal
• Particularly following cataract extraction

Retinal pits (lamellar retinal breaks)

• Do not lead to retinal detachment
• Sign of posterior vitreous detachment and retinal traction

Lattice degeneration

• Strong vitreoretinal adhesions
• Present at the margins of lattice degeneration are well documented
• Can vary in shape, appearance, location and pigmentation
• Most commonly pre-equatorial, parallel to the ora serrata
• Located in the vertical meridians
• May occur posterior to the equator in a radial perivascular pattern
• More than ten histopathologic features of lattice degeneration have been identified
• Retinal thinning and degeneration with atrophic hole formation
• Liquefaction of the overlying vitreous + firm adhesion of the vitreous at the margins of the lesion with glial and RPE cell proliferation
• Traction retinal breaks may occur at the posterior margin of the lattice lesion during PVD
• Due to firm vitreoretinal adhesion
• Incidence of traction breaks directly involving a lattice lesion is small
• Tears are more likely to occur in juxtabasal and extrabasal lesions
• Atrophic holes are more common in lattice degeneration
• Histologic incidence of
• Atrophic holes is 18.2%
• Traction retinal breaks is 1.4%
• Incidence of retinal detachment from traction retinal breaks and atrophic holes associated with lattice degeneration to be 0.3–0.5% only
• Retinal breaks associated with radial perivascular lattice are usually larger and more posterior
• Might lead to retinal detachments that are difficult to treat
• Indications for prophylactic treatment of lattice lesions
• Influenced by the clinician’s evaluation, experience and bias
• Symptomatic tears
• History of retinal detachment in the fellow eye
• High myopia
• Aphakia
• Planned aphakia

Myopia

• Definite risk factor for retinal detachment
• Risk increases with higher degrees of myopia
• PVD occurs early
• Lattice degeneration is more common
• Retina is thinner in myopic patients than in emmetropes
• Makes retinal breaks and detachment a more frequent occurrence
• Often bilateral
• Prophylactic treatment is indicated for
• Horseshoe-tears,
• Symptomatic tears,
• Tears with surrounding retinal fluid
• In patients with history of retinal detachment
• In patients undergoing cataract extraction
• Controversial issue
• Some authors advise to treat any break in patients with more than 4 diopters of myopia [1]

• Macular holes
• Also seen in cases of high myopia
• Detachment complicating these holes is usually limited to the posterior pole within the temporal vascular arcades
• May be non-progressive
• Treatment of these cases is still controversial [1]

• Nearsightedness of more than 5 diopter powers is associated with a greater risk of retinal tears [5]

Pigmentary glaucoma

• Also have an increased incidence of retinal detachment
• Retinal detachment and glaucoma can be associated through a common underlying mechanism
• Trauma,
• Cataract surgery with vitreous loss
• Proliferative retinopathy
• Retinopathy of prematurity

• Treatment for retinal detachment may cause glaucoma
• Corticosteroids,
• Scleral buckling procedures
• Extensive retinal photocoagulation
• Vitrectomy are all capable of producing glaucoma

• Study IOP measured directly using a canula in patients undergoing scleral buckling surgery
• Highest recorded IOP was 211 mmHg!
• Mean elevation was 112 mmHg
• Mean duration of 118 seconds

• Glaucoma
• Does not interfere with the reattachment of detached retinas
• May limit the visual outcome

• Repair of retinal detachment may reduce scleral rigidity
• Necessary to use applanation rather than Schiotz tonometry for postoperative pressure measurements

• Treatment of glaucoma may cause retinal detachment:
• Strong miotic agents are capable of inducing
• Retinal tears,
• Vitreous hemorrhage,
• Retinal detachment

• Standard cholinergic drugs
• Can also cause retinal detachment

• Glaucoma patients should have periodic peripheral retinal examinations
• Especially before starting miotic therapy

• Newly diagnosed retinal detachment, IOP is low
• Glaucoma may become apparent later
• May be detected in the fellow eye
• Retinal detachment lowers IOP by
• Inducing inflammation and reducing aqueous humor formation
• Aqueous humor may be eliminated by flowing through the retinal hole into the subretinal space
• Iris retraction syndrome
• Patient with a rhegmatogenous retinal detachment, secluded pupil, iris bombé, and angle-closure glaucoma develops hypotony and iris retraction
• When aqueous formation is reduced pharmacologically
• Induced reduction in aqueous formation allows most of the aqueous humor to go posteriorly through the retinal hole.

• SCHWARTZ SYNDROME
• Minority of cases, retinal detachment causes a peculiar increase in IOP
• Rhegmatogenous retinal detachment is associated with
• Elevated IOP,
• Diminished outflow facility
• Open angles
• Cell and flare in the aqueous humor
• When the retinal detachment is repaired
• TheIOP and outflow facility return to normal
• Glaucoma is related to
• Angle recession,
• Inflammation,
• Pigment granules released by the retinal pigment epithelium
• Glycosaminoglycans synthesized by the photoreceptors
• Photoreceptor outer segments migrate through the retinal hole and obstruct the trabecular meshwork
• Medical treatment is rarely successful in controlling the condition
• Must be distinguished from
• Glaucoma
• Non-rhegmatogenous retinal detachment caused by an undetected malignant melanoma

Retinopathy of prematurity

• Which can affect premature newborns who receive oxygen in the high-risk neonatal nursery [4]

Retinoschisis

• When holes are present in both the inner and outer layers of the retina involved by schisis
• Fluid passes into the subretinal space through the inner and outer holes
• Hole occurring in only one of the retinal layers
• Not enough to produce significant retinal detachment
• Observed in 2.5% of patients with RRD [1]

Traumatic

• About 15% of all retinal detachments
• Much more common in young individuals
• Blunt trauma, with and without rupture of the globe
• About 70–85% of all traumatic retinal detachments
• Penetrating trauma
• TRD secondary to fibrous ingrowth and intraocular proliferation is more prominent
• Closed-globe blunt trauma, or ocular contusion
• Directly or indirectly (contrecoup)
• Several vitreoretinal changes including
• Dialysis at the anterior or posterior border of the vitreous base
• Avulsion of the vitreous base
• Horseshoe-shaped tear at the posterior margin of the vitreous base, at the posterior margin of a meridional fold, or at the equator
• Operculated tear
• Macular holes
• 60% of traumatic retinal breaks were located at the ora
• 60% of non-traumatic tears were equatorial
• Most important retinal dialysis in ocular contusion injury
• Antero-posterior (AP) compression of the globe during impact
• Compensatory lengthening of the horizontal diameter
• Termination of impact or collision, the globe re-expands in the AP direction with an ‘overshoot’ up to 112% its original length
• Traction at the vitreous base and other areas of physiologic or pathologic vitreoretinal adhesion occurs [1]

• Vitreous liquefaction has to occur before detachment develops
• Traumatic vitreous syneresis may occur following trauma
• Fluid seeps into the subretinal space through the break leading to retinal detachment
• 9% of all macular holes develop following blunt trauma
• Can lead to retinal detachment
• Post-contusion necrosis
• Vitreoretinal traction by a contrecoup effect
• Surgery for traumatic macular hole closure are favorable [1]

Uveitis

Scleritis

Collagen vascular or autoimmune diseases

Coat's disease

Vitreoretinal adhesions

• In association with PVD

Crystalline lens and its posterior capsule

• Stabilizing factor on the vitreous body
• Vitreous movements during ocular saccades are transmitted from the outer layers of the vitreous towards the center
• Accelerational and decelerational movements of the vitreous
• Dampened by the
• Firm vitreous adhesions to the retina
• Posterior convexity of the lens
• Grip or mechanical hold on the vitreous body
• Removal of the lens after cataract surgery this ‘grip’ is lost
• Torsional effects at physiologic and pathologic sites of firm vitreoretinal adhesions are accentuated [1]

• Vitreous hyaluronan concentration
• Decreases following cataract extraction
• Much more prominent following ICCE [1]

• Posterior capsule, when preserved, is thought to act as a barrier to diffusion
• Decrease in hyaluronan concentration
• Accelerates the process of syneresis
• Decreases the shock-absorbing property of the vitreous body
• Leading to an increase in the torsional forces transmitted to areas of vitreoretinal adhesions
• Increase the incidence of PVD, retinal tears and detachment
• Risk of retinal detachment following cataract extraction
• 7.5 times that of a control group even 6 years after surgery
• Risk of retinal detachment following extracapsular cataract extraction with posterior chamber intraocular lens
• Varies according to different series but is about 1.4%
• Presence of an intact capsule
• Decrease the risk of retinal detachment following cataract surgery

• Vitreous incarceration in a cataract wound
• Another factor contributing to vitreoretinal traction and retinal detachment
• Detachment may be tractional rather than rhegmatogenous [1]

Significant increase in the immune system's 'alternative complement pathway

• Following retinal detachment
• This pathway facilitated early photoreceptor cell death after injury
• Injured photoreceptors lose important proteins that normally protect them from complement mediated cell death
• Allowing for selective targeting by the alternative complement pathway
• By blocking the alternative complement pathway
• Both genetic and pharmacologic means
• Photoreceptors were protected from cell death
• When photoreceptors in a detached retina were removed from their primary source of oxygen and nutrients
• An increase in complement factor B
• Key mediator of the alternative complement pathway
• Leads to photoreceptor cell death ( Dr. Connor)
• Alternative complement pathway exacerbates photoreceptor cell death
• Inhibition of the pathway is protective (Kaylee Smith, journal, Science Translational Medicine)

Ztenčení sítnice

• Without a constant blood supply, the nerve cells inside the retina will begin to die.
• Main reason these holes develop in the retina is that it becomes narrower and weakened with age.

• People who are very short-sighted have the greatest risk of developing age-related retinal detachment
• Often born with a retina that is thinner than normal in the first place. [2]