corneal edema after cataract surgery - malek al kott

Presented by

Malek Mohammad Al-Kott

M.B. B.Ch.

Al-azhar UniversityAssiut, Egypt

2013

Cornea consists of 5 layers

CORNEATransparent and avascular

Refractive power: 40-45 diopters

Thick ness: 0.52mm at its center,

0.66mm at the periphery

The epithelium1-Superficial cells microvilli

2-Suprabasilar cells Winglike

3-Basal cells mitosis

2- Bowman’s layerA condensation of superficial stroma

3- The stroma:90% of corneal thickness (200 to 250 lamellae of collagen fibers) Collagen fibres type I mainly + proteoglycan matrix +keratocytes

4- Descmet’s membraneCollagen fibres typeVI + laminin

5-The endotheliumsingle layer

polygonal cells apical microvilli + thin layer of mucinous material

Density at birth 3500 to 4000 cell/mm2

Can not replicate but sliding and rearrangement of neighboring cells (polymegathism and pleomorphism)

Average cell loss 0.3% to 0.6% per year

Numerous mitochondria highly metabolically active.

Numerous endoplasmic reticulum, Golgi apparatus

protein synthesis

The endothelium(NORMAL)

Polymegathism and Pleomorphism

1-Endothelium barrier functionTight junctions allow small molecules to pass

prevent bulk flow of fluid

2- Endothelium pump functionControls ion movement osmotic gradient draws water from the stroma.

Pumps:-

-Na+/K+-ATPase

-bicarbonate-dependent Mg2+-ATPase

-aquaporins or water-selective channels

Endothelium pump function

Corneal edema

Corneal edemaDefinition: Cornea that is more hydrated than its normal physiologic state of 78% water

Critical density of endothelial cells (400 to 700 cells/mm2)

Pump function can maintain stromal hydration in the normal range of 78 percent without significant effort BECASE OF:-

1-Anionic repulsive forcesNegatively charged proteoglycans electrostatic repulsive forces = expansive force swelling pressure (SP). around +55 mmHg

Stroma has cohesive and tensile stiffness (elasticity) that resists expansion

IF stroma is compressed (high IOP or mechanical applanation) SP will increase

IF the stroma is expanded(corneal edema) SP will decrease

2-Cationic attractive forcesNegatively charged GAG side-chains attracts and binds Na+ cations absorption of water imbibition pressure (-40 mmHg)

3-Barrier functionAllow Low flow so pumps can maintain stromal hydration in the normal range of 78 percent without significant effort.

In vivo IP is less than SP becauseHydrostatic pressure induced by (IOP) must now be

accounted, so:-

IP = IOP – SP

SO, clinical appearance of corneal edema depends on:

Loss of corneal barrier function.

An IOP ≥ 55 mmHg.

A combination of the two.

If ≥83% stromal hydration1. Increase thickness

2. Loss of transparency

3. Decreased vision

4. Glare

5. Sub-epithelial bullae and degenerative pannus in severe chronic cases of epithelial edema

6. Stromal edema + Descemet's membrane foldsAnterior-posteriorly not circumferentially

Mostly in the posterior 2/3 maintains the anterior corneal curvature (depth-related differences in lamellar interweaving)

Sub-epithelial bullae

Descemet's membrane folds

Preoperative predisposing factorsCorneal endothelium in vivo has minimal proliferative capacityAny cause that decreases cell density and morfology, predisposes for corneal edema after cataract surgery

Preoperative predisposing factors1. Age. (old age)

Chronic ultraviolet light exposure DNA damage

Decreased antioxidant enzymatic activity

2. Sex. (females)

3. Diabetes. (10 years)

4. Long-term contact lens use. (Partially reversible)

5. History of ocular infection, trauma, previous ocular surgery.

6. Glucoma

Endothelial cell loss of 30-77% in acute angle-closure attacks

7-Fuchs’ corneal endothelial dystrophy(FED)

Bilateral, slowly progressive, primary disorder of the corneal endothelium that causes corneal edema and eventually painful blindness.

Cataract surgery accelerates corneal endothelial cell loss in patients with FED.

Fuchs’ corneal endothelial dystrophy(FED)

Intraoperative causes

1- Instrument contact or lens contact Greatest in the superior part of the cornea (maximal manipulation)Vertical disparity in endothelial cell density

A-Mechanical injury

Instrument contact or lens contact

2- Ultrasound energy1. Directly phacoing the corneal endothelium

2. Free radicals

Ultrasound oscillations acoustic cavitations thermal dissociation of water hydrogen atoms +(hydroxyl radicals) highly reactive lethal injuries to endothelial cells

3. Temperature

3-TemperatureCentral corneal temperature 30.7°C to 35.0°C

Heat generation by the phaco tip increase aqueous temperature and cause wound burn

An endothelial cell loss of up to 10% occurs after an increase in aqueous temperature from 29.1°C to 33.4°C

Internal and external flow of irrigation-aspiration fluid prevent endothelial damage and wound burn.

Wound burn

4. Nuclear fragments hitting the endothelium.

Brunescence effect on endothelial cell loss has been noted as the most significant risk factor for endothelial injury

5. Air bubblesAir fluid level along the endothelium interact with the

thin layer of mucin on apical surface of EC

6. Vitrocorneal touch.

7. Detachment of the Descemet’s membrane.Stripping of the membrane by instruments

Fluid injection without the cannula tip fully inside AC

Detachment of the Descemet’s membrane

8-Corneal folding and anterior chamber collapse

B. Chemical Injury

1- Antiseptic solutions (Povidone iodine) Residuals from sterilization enter thtough surgical

incision

2- AnestheticsTopical

Epithelial keratitis , corneal edema(1/1000 patient)

If injected intracameral irreversible corneal edema

IntracameralBupivacaine in some studies induced endothelial damage and

increased corneal thickness

3-Preservatives (Benzalkonium chloride)Highest safe intraocular concentration is 0.001

0.05% BAC irreversible endothelial necrosis.

0.01% BAC reversible corneal edema

4-Irrigating solutions1-Normal saline and lactated Ringer’s solution edema

2-BSS Prolonged infusion studies have demonstrated increased endothelial injury.

3-BSS PLUS most safe (maintains endothelial cell function over periods ranging from 15 minutes to few hours)

Ringer’sBSS PlusAqueousComponent

130.0122.2163.0Sodium chloride

5.55.82.2–3.9Potassium chloride

21.051.8Calcium chloride

__0.981.10Magnesium chloride

____2.6-4.3Sodium lactate

____0.12Sodium citrate

__3.00.62Disodium phosphate

__25.020.2Sodium bicarbonate

__5.112.7-3.7Dextrose

__0.30.0019Glutathione

6.257.407.38PH

280305304Osmolarity

Composition of human aqueous, Ringer’s solution and BSS Plus (concentrations in mMol/L fluid).

5-StainsMethylene blue 1% not safe

Indocyanine green safe for 3 minutes

Trypan blue most safe

6-Detergent residues (subtilisin,alpha

amylase enzymes )Deactivated at temperature exceeding 140C

Most autoclaves reach only 120C to 130C

Postoperative causes1-Raised intraocular pressure and glaucoma

Narrow angle

glaucoma

Open angle

glaucomaMalignant glaucoma

•Transient and related to

retained viscoelastic

•Topical steroids in

susceptible individuals

•Retained lens matter

•Postoperative hyphaema

•Alpha-chymotrysin in ICCE

•Pupillaryblock•more in:- AC IOL

- Aphakia

wound leak

shallow AC

2-IOL syndromes

A-Direct endothelial touch

Strong adhesive force of methacrylate IOL.

(coat with a hydrophilic material)

B-Long-term toxicity

More in Closed loop AC IOLs ±cystoid macular edema

Less than 1% with PC IOL

Prostaglandins!!

3-Any prolonged endothelial contact with other ocular tissues

-Flat chamber-Iris bombe-Suprachoroidal effusion/hemorrhage

4-Epithelial Downgrowth•Epithelial cells are introduced into the anterior chamber during surgery begin to proliferate as a cellular membrane

Epithelial Downgrowth

5-Retained lens nuclear fragment •Anterior to the iris Proinflammatory•Posterior to the iris noninflammatory

6-Brown-McLean SyndromeDefenition :

Peripheral corneal edema which involves the epithelium and the stroma that commences inferiorly and progresses circumferentially

Cause :

A- Subclinical endothelial dystrophy decompensated by the microtrauma

B- Genetic predisposition

May be totally asymptomatic

Brown-McLean Syndrome

7-Toxic anterior segment syndrome (TASS)Toxic solutions intraocular inflammation + corneal edema

Sterile, noninfectious endophthalmitis.

Toxic Endothelial Cell Destruction Syndrome (TECDS)

Presentation mimic endophthalmitis:

Pain

Photophobia

Severe reduction in visual acuity

Marked AC reaction

Within 12-24 hours of cataract surgery (endophthalmitistypically develops 2-7 days )

Limbus-to-Iimbus corneal edema

Limbus-to-Iimbus corneal edema

Examination and evaluation techniques(1)Assesment of corneal endothelium.

1. Slit lamp.

2. Specular microscopy.

3. Confocal microscopy.

4. HRT-II with Rostock cornea module..

(2)Assessment of the Central Corneal Thickness1. Ultrasound.

2. Optical pachymetry.

3. Specular microscopy.

4. Scanning slit based (orbscan).

5. Optical coherence tomography and optical low-coherence reflectometry.

6. Confocal microscopy through-focusing.

7. Laser Doppler interferometry.

1-Slit lamp1-Diffuse broad- beam illumination

For general inspection

2-Specular reflection

3-Retroillumination

4-Sclerotic scatter

Specular reflection

Retroillumination

2-Specular microscopyDetects:1-Number of endothelial cells per square millimeter 2-Percentage of normal cellsBut:1- Cornea must be transparent.2-Does not permit three dimensional optical sectioning of the corneaEvaluation A-Qualitative analysisB-Quantitative analysis

Konan NonCon RoboImaging of endothelium is fully automatic

A-Qualitative analysis(morphology)

B- Quantitative analysis

Using:1-Fixed-frame analysis

2-Variable-frame analysis

3-Comparison cell analysis (cells mosaic is compared to a cell pattern of known size)

Detect:1-Cell density 2-Mean cell area3-Pleomorphism

1-Fixed-frame analysisCells lying completely within a given area

2-Variable-frame analysisBorders of an entire group of cells are outlined with the aid of a computer

C- Confocal microscopyProvides quantitative data of endothelial cells even in edematous hazy cornea

1-Tandem scanning confocal microscopes (TSCM)

2-Slit scanning confocal microscopes (SSCM)

Confocal microscopy

D-HRT-II with Rostock cornea module

Rostock Cornea Module

High-quality microscope lens positioned between the eye and

the HRT-II providing a laser focus less than 1 ml in

diameter Moveing the confocal image plane inside the cornea permits rapid and reliable visualization and evaluation of all the microstructures in the cornea, including the endothelium.

HRT-II with Rostock cornea module

2)Assessment of the Central Corneal Thickness (Pachymetry)

1-UltrasoundDry contact technique

Underestimates corneal thickness in edematous corneas

Normal cornea :1-Smooth, curved, specular reflection from tear film-epithelial interface2- 2nd Reflective line (Bowman's membrane).3- Stroma has a uniform, low reflectivity.4-Highly reflective interface between Descemet'smembrane/endothelium and the aqueous

3

4

Edematous cornea 1-The epithelium is thickened, and the smooth, highly

reflective surface line replaced by a more irregular, less reflective line

2- Higher reflectivity of the corneal stroma.

3- Increased corneal thickness

W

2-Optical pachymetrySlit- lamp mounted device

Observer-dependent technique

3-Specular microscopyRecording the adjustment required in the focal plane of the specular microscope

Overestimates the thickness

4-Scanning slit based (orbscan),Pentacam

• Noncontact technique• Underestimates corneal thickness in edematous corneas

The occulus Pentacam

5-Optical coherence tomography (OCT) and Optical Low-Coherence reflectometry

Based on optical interferometry

OLCT Can perform measurements during corneal ablation

OLCT

Visante optical coherence tomography (OCT)

Slit-lamp OCT

6-Confocal microscopy through-focusing (CMTF)

Through-focusing confocal microscope

7- Laser Doppler interferometry

•Non contact •dual-beam infrared laser

Prevention and TreatmentPrevention1-Avoid the causes

2-Use of ophthalmic viscoelastic devices(OVD)

3-Use tortional phacoemulsification

4-Triple procedure in FED

Treatment1-Eliminate the cause.

2-Enhance surface dehydration.

3-Treat pain.

4-Restore anatomy.

2-Use of ophthalmic viscoelastic devices(OVD)1-Dispersive

lower molecular weight and shorter molecular chains

2-Cohesive

longer chains ,easier to remove from the anterior chamber.

*Ideal OVD:

1-Maintain space

2-Protect the corneal endothelium

3-Remain in the eye during surgery

4-Easy to remove at the conclusion

of surgery

Comparing Healon 5, Healon GV, Ocu-Coat, Celoftaland Viscoat Healon 5 allowed the least mean endothelial cell loss

Soft-shell technique

Inject dispersive viscoelastic (e.g. Viscoat) adjacent to the endothelium then expand the AC below using cohesive viscoelastic, thus spreading dispersive agent against endothelium.)

3-Tortional phacoemulsificationAdvantages in decreasing post operative corneal

edema :

1-Less repulsion tip is kept in an occluded state decreases turbulence

2-Intraoperative fluid use with this technology appeared to be less than with conventional ultrasound

3-Temperature control

4- Reduced time

5- Torsional phacoemulsification is cataract-density independent

4-Triple procedure in FED(cataract surgery and IOL implantation combined with

keratoplasty)

If there is evidence of corneal epithelial edema at the time of cataract removal:

Triple procedureshould be considered for visual rehabilitation

If preoperative pachymetry > 640 :

Triple procedure can be considered but not necessarily performed

Treatment1-Eliminate the cause

1-Re-attach Descemet’s membraneSmall detachment resolve spontaneously

Alternatively use :

Viscoelastic

Bubble of air

Long acting gas

Tissue fibrinogen glue

Sutures

Penetrating keratoplasty (if failed re-attachment)

Sutureing

2-Lower the intraocular pressure

Pressure on the posterior lip of a preexisting paracentesis

Topical and/or systemic pressure-lowering agents

3-Retained nuclear fragmentsSurgical removal

4- IOL exchange.Closed loop by open loop

5- Treat Toxic anterior segment syndromeBrief course of systemic corticosteroid

6- Treat inflammationStrong topical steroids

2-Enhance surface dehydration

Trade Name (Manufacturer) Composition

Adsorbonac

Solution,

2% and 5%

(Alcon)

NaCl, povidone and other

water-soluble polymer,

thiomerosal 0.0004%, EDTA 0.1%

Muro-128

Solution,

2% and 5%

(Bausch & Lomb)

NaCl, hydroxypropylethylcellulose,

methylparaben, propylparaben,

boric acid

Muro-128

Ointment, 5%(Bausch & Lomb)

NaCl, anhydrous lanolin,

mineral oil, white petrolatum

AK-NaCl 5%

Ointment(Akorn)

NaCl, anhydrous lanolin,

mineral oil, white petrolatum

Sochlor, 5%

solution , ointment(OCuSoft) NaCl

Glycerin (Glycerol)

Ophthalgan

(compounded

product)Anhydrous glycerin

Topical Hyperosmotic Preparations

Topical Hyperosmotic Preparations

3-Treat pain(epithelial bullae)A-Hydrophilic contact lenses.

Extended-wear

Shields the abnormal epithelium

B-Anterior stromal cautery

To Bowman’s layer

Salleras procedure scars excellent pain relief

C-Anterior stromal puncture

Improve epithelial adhesion

D-Amniotic membrane transplantation

E-Conjunctival flap transplantation

Thin ,thick

Anterior stromal puncture Conjunctival flap transplantation

F-Excimer laser phototherapeutic keratectomy(PTK)

G- UV–riboflavin therapySymptomatically effective in the short term (up to 8 months)

4-Restore the anatomy1. Penetrating keratoplasty(PK)

2. Deep lamellar endothelial keratoplasty (DLEK)

3. Descemet-stripping endothelial keratoplasty (DSEK).

4. Descement membrane endothelial keratoplasty (DMEK)

5. Descemet-stripping automated endothelial keratoplasty(DSAEK)

1-Penetrating keratoplasty(PK)

Standard of care for the treatment of corneal edema resulting from pseudophakic bullous keratopathy

Entire corneal thickness is replaced, regardless of the layer that is diseased

2-Deep lamellar endothelial keratoplasty (DLEK)

lamellar dissection

3-Descemet's stripping with endothelial keratoplasty (DSEK)

scraping

D-Descemet's membrane endothelial keratoplasty (DMEK)

ROLLDescematorhexis

4-Descemet-stripping automated endothelial keratoplasty (DSAEK)

All patients must be pseudophakic with a posterior chamber IOL