POST OPERATIVE COMPLICATIONS

AFTER IOL SURGERYChief of unit: Dr. K. Dayakar.

Moderator: Dr. G. R. Bharath kumar.

Presenter: Dr. W. Siva kumar (junior resident)

EARLY COMPLICATIONS(<4WEEKS )• CORNEAL OEDEMA• WOUND LEAK• SHALLOW AC• HYPHAEMA• RETAINED LENS MATTER• UVEITIS• ENDOPHTHALMITIS• ASTIGMATISM

EARLY COMPLICATIONS(RARE)

• RETINAL DETACHMENT• PVD WITH RETINAL TEAR OR VH• DR EXACERBATION• REFRACTIVE SURPRISE• TOXIC ANTERIOR SEGMENT SYNDROME• TOXIC LENS SYNDROME.

LATE COMPLICATIONS(AFTER 1MONTH TO YEARS)• POSTERIOR CAPSULAR OPACIFICATION• CYSTOID MACULAR OEDEMA• ENDOPHTHALMITIS• IOL RELATED COMPLICATIONS• RETINAL DETACHMENT

LATE COMPLICATIONS(RARE)• SECONDARY GLAUCOMA

• EXACERBATION OF DR

• ANTERIOR CAPSULE PHIMOSIS

• LATE WEAKENING OF ZONULES WITH DISLOCATION OF LENS POSTERIORLY.

CORNEAL OEDEMA

• Corneal oedema is one of the most serious vision threatening complication of SICS whether performed using a phaco machine or manually.

• Etiology is multifactorial.

ETIOLOGY• Preexisting corneal pathology that is

corneal gutta, low endothelial count.• Diabetes• Brown or Black nucleus rubbing the

corneal endothelium-resulting in endothelial cell loss and injury to large areas of endothelium.

• Descemets membrane detachment.• Instrument induced injury to

endothelium while working in a shallow AC.

• Endothelial cell loss because of a crude internal incision with a blunt keratome.

• Possibly toxic corneal oedema. Cidex sterilised instruments if not thoroughly washed before introducing into the eye can produce corneal oedema.

• Pilocarpine in AC can produce corneal oedema in patients with compromised cornea.

• Severe iridocyclitis with AC reaction.

MANAGEMENT• Most cases of mild corneal oedema

resolve within 7-14 days.• Frequent instillation of topical steroids

is sufficient to take care of mild oedema.

• In cases with massive descemets detachment: repositioning with tight air or sod.hyaluronate inj.

• Recalcitrant corneal oedema : hyperosmotic agents-5%NaCl drops/ointment.

WOUND LEAK

• Wound leak is the principal cause of the delayed reformation of the anterior chamber.

• A wound leak may cause an incarceration or may be caused by it.

CAUSES OF WOUND LEAK• Inadequate incision including

irregularities of the incision• Inadequate suturing especially in large

incision surgeries.• Poor coaptation of the wound margins:

due to variations in the depth of the sutures, poor spacing, jagged wound edges…

• Accidental sclerotomy and excessive cauterization.

• Incarceration of material : iris, lens fragments, vitreous, suture pieces, cilia etc between the lips of he wound.

• Accidental trauma: causes wound seperation

• Poor ocular structure: thin scleral coats of high myopes, uvenile eyes, eyes that have undergone previous surgery

• Elevation of IOP: common during 24- 36 hrs.

WOUND LEAK(SIEDELS TEST)

MANAGEMENT

• Suturing the wound.• Removing the offending agents

like cilia, suture etc and creating a tight AC by air injection.

SHALLOW ANTERIOR CHAMBER

ETIOLOGY• Mostly a consequence of AC

leakage either from the tunnel or from the side port sites.

• Non maintainance of the AC at the end of the surgery.

• Choroidal detachment

SHALLOW ANTERIOR CHAMBER

MANAGEMENT• At the end of surgery care must be taken

to maintain a pressure of 20-22 mm of hg.• AC may be reformed with an tight air

bubble on the first post op day if nescessary.

• In cases of choroidal detachment: Pad and bandage applied for 24 hrs can

form the chamber and choroid settles back in few days(Systemic steroids are also given).

If it does not resolve even within 10 days supra choroidal fluid is drained by creating a self sealing scleral incision over the detachment area. The AC is then formed with a tight air bubble.

HYPHAEMA

SOURCES OF HYPHAEMA• Bleeding from the scleral tunnel

• Traumatised iris

• Vascularised iris

• Expulsive choroidal haemorrhage- rare

POST OPERATIVE HYPHAEMA

• A normotensive or a slightly hypertensive eyeball is needed at the end of the SICS surgery.This state of eyeball will not permit the blood from scleral tunnel to seep into the AC.

• Assessment of post operative hyphaema is very important.

• If hyphaema is left over with out any

treatment it may lead to secondary

glaucoma , corneal staining which may

be irreversible.

MANAGEMENT Mild hyphaema : resolves by

itself.<Half AC full hyphaema: patients

need to be propped up against pillows so that blood settles in the lower part of AC. Topical and oral steroids, cyclopegics, vit C, Anti glaucoma medication.

>Half AC full hyphaema: AC wash can be performed under local anaesthesia.

POST OPERATIVE ENDOPHTHALMITIS

• Vision threatening complication.

• Prevalence ranges from 0.1 to 0.4% of cataract extractions.

SOURCES OF INFECTION

• Air borne infections: Respiratory origin, surface origin, air conditioning system.

• Solutions and medications: Skin antiseptics, ointments, instrument disinfectants etc

• Tissues: Skin of hands, skin in the operative field, lid margin and eyelashes, lacrimal sac, nasal mucosa, corneal grafts, vitreous implants, fellow eyes

• Objects and materials: Optical instruments, surgical instruments, tonometers, magnets, hypodermic needles, drapes dressings masks gowns,gloves, glass syringes, bottles, irrigating tips, sutures.

• Miscellaneous: Patients with poor hygeine, poor nutrition and health.

CAUSATIVE ORGANISMS

BACTERIAPseudomonas aeroginosa

Bacillus subtiles

Proteus sps

Enterobacter aerogenes

Propionibacterium

S.epidermidis

FUNGIAspergillus

Cephalosporium

Fusarium

Volutella

• Fulminant(<4 days)-Gram negative bacteria, Streptococcus, Staph aureus

• Acute( upto 1 month)-Staph epidermidis, coagulase neg cocci, rarely fungi (aspergillus and candida)

• Chronic (>1month) - P.acne, fungi, Staph epidermidis.

• When a post operative intra ocular infection occurs in a single operating day or with in a short period in the same hospital Pseudomonas is the most likely causative organism.

PATHOGENESIS OF POST OP ENDOPHTHALMITIS

CLINICAL FEATURES

SYMPTOMS: Pain , redness, watering, diminision of visual acuity

SIGNS: Conjunctival hyperaemia, lid swelling, chemosis, cells and flare in the anterior chamber, hypopyon, membrane formation on IOL, vitreous haze, scattered retinal haemorrhages, loss of red reflex, in extreme cases corneal infiltration and opacification.

3RD DAY

1 WEEK

POST OP ENDOPTHALMITIS

TREATMENT

PREOPERATIVE MEASURES

• Patient’s general condition should be good• Diabetes should be under control• Conjunctiva and the lacrimal tract should be free of any active infection• Routine use of topical and systemic antibiotics should be considered in patients have had recent or repeated infections.• Routine use of topical antibiotics for all patients is still a matter of debate.

• Topical antibiotics administered reduce the amount of lid and conjunctival bacteria.

• They rarely sterilise the external eye and do not provide significant concentration during surgery. Also the degree to which the flora are reduced depends on various factors(susceptibility of organism,frequency and duration of instillation,the bacteria present etc..) which makes the routine use debatable.

Usage of topical antibiotics preoperatively

INTRAOPERATIVE MEASURES

• Strict aseptic precautions should be taken by the operating surgeon and the assisting staff.

• Routine use of sub conjunctival antibiotics at the end of surgery: gentamicin is preferred.(Adv: sub conjunctival antibiotics reach high levels of conc in anterior chamber for 3-5 hrs after surgery)

• Recent trends( usage of hydrated collagen sheilds-sustained release of drug for 12hrs)

TREATMENT OF ESTABLISHED ENDOPHTHALMITIS

MEDICAL MANAGEMENT• ANTIBIOTICS: Topical Systemic Intra vitreal• STEROIDS: Topical Systemic• 1% atropine eye drops 6th hrly• ANTI FUNGALS: If culture reports

suggest fungi.

ANTIBIOTICS

TOPICAL SYSTEMIC

Cefazolin 5% eye drops 1hrly. Or

Tobramycin 1.3 % eye drops 1 hrly.

Combination of Inj ceftazidime 2g iv tid and

Inj vancomycin 1g iv 12th hrly.

INTRA VITREAL ANTIBIOTICSVancomycin: 1mg in 0.1 mlCeftazidime: 2.25 mg in 0.1 mlAmikacin: 400 micro gm in 0.1 mlDexamethosone: 400 micro gm in 0.1

mlAmphotericin B: 5 micro gm in 0.1 ml.

STEROIDS

TOPICAL SYSTEMICDexamethosone or Prednisolone eye drops 1 hrly.

Inj dexamethosone 8mg iv 12 hrly.

Oral steroids after discontinuiong the injections.

SURGICAL MANAGEMENT:

VITRECTOMY

• This problem is frequently not the the fault of the surgeon.

• Improved aseptic technique in ophthalmic surgery is responsible for the decrease in the rate of infections.

• Should we suspect endophthalmitis in every case of post operative redness ??

Post operative endophthalmitis

Post operative reaction

•History of improvement folowed by deterioration.

•Corneal involvement present•Focal infiltrate present•Fundus glow is absent or very faint•Vitreous haze ++•Exudate yellow colour•IOP low

•Early deterioration only, early improvement with treatment•Corneal involvement absent•Absent•Present or faint

•Mild haze or no haze•White•Normal

POST OPERATIVE REACTION

RETAINED LENS MATTER

CLASSIFICATION1. Capsular remnants2. Capsulo lenticular remains3. Pigmentary, haemorragic, or

inflammatory fibrous elements.

COMPLICATIONS• Optical complications• Phaco anaphlactic uveitis• Phaco toxic uveitis• Secondary angle closure glaucoma

MANAGEMENTRemoval of retained lens material• The mode and the method of removal

of the retained fragments depends on the size, site of the fragment.

• It may vary from AC wash to pars plana vitrectomy.

RETAINED LENS MATTER

POST CAPSULAR OPACIFICATION

• Incidence: Varies from 10-50 % following ECCE.

• During the early days PCO was considered to be an untreatable cause. But after the advent of the lasers its management became easier.

PATHOGENESIS• Most PCO are formed by the proliferation

of the equatorial lens epithelial cells.• Two forms of PCO are recognised: Elschnig pearls Fibrous plaques Dense membranous Soemmering’s ring (PCO

peripheral to IOL optic)

PATHOGENESIS (contd)• E cells in the equatorial bow tend to

migrate along the posterior capsule and form pearls to form post capsular opacification.

• Fibrous form of PCO is due to the posterior proliferation of the A cells or due to the fibrous metaplasia of the posterior migrating cells.

ELSCHNIGS PEARLS

SOEMMERING’S RING

CLINICAL EVALUATION

• Visually significant PCO is defined as the

decrease in BCVA by 2 snellan’s lines.

• PCO score is calculated by multiplying the the density of opacification by the fraction of capsule behind the optic that is opacified

PRECAUTIONS DURING SURGERY• Proper hydrodissection enhanced

cortical clean up.• In the bag fixation of IOL. It enhances

the IOL optic barrier.• Capsulorrhexis edge on the IOL surface.• Bio compatible IOL: Acry sof IOL is most

biocompatible.• Maximum IOL OPTIC PC contact.

WHY TO PREVENT PCO FORMATION:• Nd-YAG laser has many complications like IOL optic damage, IOP rise, CME and increased risk of RD in high myopes.• High expectations of patients from modern

day surgeries.• PCO causes a significant financial burden to

the health care system.• PCO is the main complication in paediatric

IOL implantation.

TREATMENTNd YAG laser capsulotomy ( dis adv: damage to IOL optic, post op IOL elevation, CME, RD, IOL subluxation or dislocation)

Peeling or removal of the epithelial cells from the posterior capsule in eyes with pearls type of PCO with automated irrigation mode.

IOL WITH PCO AFTER Nd-YAG

LENS RELATED COMPLICATIONS

Classified as

• IOL malpositions:

• IOL induced diseases:

IOL MALPOSITIONS

Etiology

• Intra operative:

• Post operative: Trauma

Spontaneous

INTRAOPERATIVE CAUSES OF MALPOSITIONS:

• one haptic of IOL is out lying on the iris.• IOL with small optic placed in a large rhexis

has not been properly centred at the time of surgery.

• Poorly performed can opener capsulotomy where in the irregular capsular flaps may entangle the haptics of the IOL.

• In envelope capsulotomy the IOL may be partially in the bag and partially in front of the anterior capsular flap.

• In case of a large PC tear the IOL may appear well centred on the table but may slide downwards or sideways later. This condition is best prevented by fixing one haptic of the IOL in the scleral section while the lower haptic is placed on the anterior capsule remnants.

POST OPERATIVE CAUSESTRAUMAMinor injury: the eye is soft with deep

anterior chamber. Lens normally not displaced.

Severe injury: zonules are ruptured. Lens displaced anteriorly, into the vitreous, beneath the retina, subconjunctivally if the globe is ruptured.

POST OPERATIVE CAUSES(contd):SPONTANEOUS• In old age weakened upper zonules.• Any condition that leads to stretching of

the zonules(high myopia, sec to endophthalmitis etc)

DIFFERENT KINDS OF MALPOSITIONS

• Pupil capture: When section of optic is anterior to the iris. Pupil should be dilated with 1% tropicamide. Pupil is then constricted with 2% pilocarpine.

• Minor decentrations: Irregular adhesion of the residual anterior capsule to the underlying posterior capsule.It may also occur if a portion of the lens is in the capsular bag. It is also seen if the mid stromal portion of iris becomes adherent to the edge of the optic resulting in some pupil irregularity called REVERSE IRIS TUCK.

MALPOSITIONED IOL

• Wind shield wiper syndrome:When the implant is too small for the eye.Found when the loops are placed in the ciliary sulcus in the vertical position and also due to failure of adhesion of the superior loop to the posterior capsule.The superior loop moves to the left and right with the movements of the head. Corrected by McCunnels suture around the superior loop.

• Sunset syndrome: Found within 6 weeks usually. Unrecognised inferior zonular dialysis during surgery. Forcible rubbing of eye may cause this problem in late stages. Less likely to occur if the loops are placed horizontally. Lens pulled superiorly and a McCunnel’s suture is placed. If it is not possible because of vitreous it is best to remove the lens and perform vitrectomy and place a ACIOL.

SUN RISE SYNDROME

• Lost lens syndrome: refers to complete dislocation of an IOL into vitreous cavity.It is caused by severe zonular disinsertion or by posterior capsular rupture after accidental trauma.

An immobile IOL in the vitreous without any evidence of CME or RD does not need removal immediately.

Criteria for removal: RD, CME,mobile IOL in the vitreous, IOL in the macular region.

• ACIOL: show least tendency towards malposition. Related to errors in lens size. If it is too small or large remove and replace with an appropriate size implant. If size is appropriate the haptic should be brought out and placed in a anew position.

CLINICAL FEATURES

• Visual disturbance: Amblyopia is considered the most common cause of decreased vision

in malpositioned lenses. Myopia-in anterior displacement. Astigmatism: tilting of the lens. Diplopia: lens partly in partly out

of the pupil.

SIGNS:

Phacodonesis, iridodonesis.

AC- shallow/deep/irregular

The edge of the lens may be seen.

The edge of the lens may appear as a dark

curved line in the fundus reflex because of

internally reflected light.

IOL INDUCED COMPLICATIONS

• Intermittent corneal touch: occurs in ACIOL if it is malpositioned or too small.

• Secondary glaucoma: due to

Pseudophakic pupillary block. Temporary block of aqueous outflow by cells

due to uveitis or inadequate removal of viscoelastic. This is more sulcus fixating IOL, blockage of iridectomy hole by IOL and in PC

lens without posterior angulation.

• Late uveitis Chronic low grade inflammation may

persist due to constant IOL uvea contact. Due to this there will be breakdown of blood aqueous barrier ultimately leading to corneal decompensation and later CME (corneal retinal inflammatory syndrome).

More in cases of sulcus fixation.

UGH syndrome(Ellingson’s): Uveitis, Glaucoma and Hyphaema.Etiology : multifactorialMechanical laceration or rubbing of the iris on a rough or sharp edge---due to improper finishing of the quality of the IOL.Management: tropicamide or pilocarpine, steroids, anti glaucoma agents.Argon large vessel obliteration when the bleeding source is identified near the haptic.

Cystoid macular edema:Vitreous disturbance caused during the surgery plays a very important role in CME development.More common with secondary IOL implantation.Management: No definitive treatment for CME.Topical NSAIDS, Oral and Peribulbar steroids, Acetozolamide

MANAGEMENTAll the etiological factors should be kept in mind and proper precautions should be taken to prevent the complications.MALPOSITIONED IOL:

Post operative management of a malpositioned IOL is dictated mainly by the symptoms of the patient.

• Visual disturbances if severe IOL repositioning should be done.• IOL repositioning through sideport is safe

if PC is intact.• If the PC is absent/deficient postoperative

maneuvering of the IOL is a delicate proposition and should be done with the best of the visco elastic material.

• If nescessary one should fix the IOL transsclerally.

• IOL induced glaucoma: Beta blockers, carbonic anhydrase inhibitors, hypertonic agents. YAG iridectomy if medical management fails.

ATONIC PUPIL

DEFINITION• Pupil is mid dilated and nonreactive to

light, accommodation, and miotics between 1-60 days after surgery.

• The pupil dilates with mydriatics and the iris shows no evidence of mechanical trauma.

• It does not constrict with 0.1% pilocarpine(as seen in post gang damage) and 1% pilocarpine (as seen in pre gang.damage).

ETIOLOGY: • Indirect damage to the sphincter muscle- by raised IOP Inflammation toxins Ischaemia• Most surgeons feel that atonic pupil is

mainly caused by ischaemia of iris sphincter muscle. Sphincter muscle is more susceptible because of its central location.

TREATMENT• Symptoms are mild: no treatment

is required.• Symptoms are severe: Narcissus

contact lens with pupillary aperture similar to that in the opposite eye.

• Rare cases a surgical pupilloplasty can be performed.

RETINAL DETACHMENT

• Most common potentially blinding complication of cataract extraction.

• Incidence varies from 0.66% to 3.6%.

• An IOL does not increase the rate of subsequent retinal detachment.

• RD after cataract extraction is primkarily due to changes in the vitreous and the retina.

ETIOPATHOGENESIS• Anterior vitreous changes projection

of vitreous into the AC greater traction at the vitreous base and other vitreoretinal attachments RETINAL TEARS.

• The hyaluronic acid levels in vitreous is lower in ICCE cases than in ECCE cases.Hence the shock absorber action post ICCE is decreased which may lead to increased incidence of RD.

• The absence/deficient posterior capsule plays an important role in RD development.

• The anterior hyaloid membrane acts as an effective barrier to the forward displacement of vitreous. Its defect leads to RD.

RISK FACTORS• Axial myopia• RD in the opposite eye• Operative loss of vitreous• Anterior vitreous changes• Associated features: <50 yrs, open

angle glaucoma, uveitis, marfans syndrome, atopic dermatitis, family history of RD etc..

CLINICAL FEATURES• Retinal breaks are more in the ora

serata and the equator• They are more in the

superotemporal quadrant.

TREATMENT OF RDPars plana vitrectomy and internal

tamponade.Sealing of retinal breaks.Scleral buckling and encirclage operation.

POST OPERATIVE STRABISMUS

• Most of the time the superior rectus paresis or inferior rectus paresis are cited as major causes which is NOT true.

• Exact etiology is difficult in most of the cases.

MOST PROPABLE CAUSES• An asymptomatic sensory deviation

caused by dense cataractresulting in diplopia only after cataract surgery.

• Chronic occlusion of eye due to dense cataract may convert a pre existing phoria into tropia that becomes symptomatic after visual rehabilitation of eye.

• Optical factors are an important cause of a postoperative binocular diplopia ( brightness and colour disparity between phakic and pseudo phakic/aphakic eyes).

• Rare causes : preexisting myaesthenia, 6th nerve palsy ,Surgical trauma (SR-bridles, IR- peribulbar block)

TREATMENT• With positive forced duction tests

surgical correction is successful.• Prismatic correction is helpful in

some cases• Cataract surgery in the opposite

eye is helpful in some cases.

RARE COMPLICATIONS

• EPITHELIAL INVASION OF AC

• FIBROUS INGROWTH

• CORNEAL ENDOTHELIAL PROLIFERATION

EPITHELIAL INVASION OF ACCauses: delayed wound closure,

incarceration of ocular tissue in the wound, suture incarcerated the wound site.

Pathogenesis: the proliferating epithelial cells at the wound edges have the potential to form a downgrowth as a sheet or cyst behind the cornea and anterior to iris.

CLINICAL FEATURESSymptoms and signs depend on the extent of the downgrowth. The cysts may be dormant for years. If growth progresses they may cause iridocyclitis and secondary glaucoma.The cysts are usually thin walled ,transparent,

filled with straw coloured fluid containing some protein and cholesterol. The posterior wall is often pigmented.

The downgrowth appears as a transparent layer creeping behind the cornea with a

fine gray line (due to piling up of cells)

marking the advancing border of the growth.It has an irregular and wavy advancing

edge.

EPITHELIAL CYSTS

Epithelial downgrowth

TREATMENTCryo surgical technique

Aspiration of the cyst contents followed by

cryothermy over the chamber angle and

photocoagulation of the cyst remnants.

FIBROUS INGROWTHCharacterised by the ingrowth of connective

tissue elements into the anterior chamber.

Also called stromal ingrowth /stromal

overgrowth/ fibrocystic metaplasia/

fibroblastic ingrowth.

SOURCES

Sub epithelial connective tissue.Corneal or limbal stroma.Metaplastic endothelium.

Unlike the epithelial downgrowth the fibrous

downgrowth does not have a well demarcated

advancing edge.It has irregular running strans

running ahead.

TREATMENT• Thin ingrowth may be incised with a

discission knife or with a NdYAG laser.• Secondary glaucoma may be treated by cyclodialysis or cyclocryothermy.• Any progress of the growth involving the posterior segment is an indication of

very poor prognosis.

ENDOTHELIAL PROLIFERATIONIf there is a descemets and endothelial tear the healthy endothelial cells from the surroundings grow and form a new endothelial layer with in 48 hrs.The growth of the endothelium is prolific and it does not stop once the denuded area is covered.This ultimately leads to the endothelial proliferation.

DESCEMETS TEAR

• Descemets tube formation: extend from the corneal wound to the pupillary area. A strand of vitreous acts a framework on which the endothelium produces the descemets.

• Sometimes the endothelium undergoes fibroblastic change andd the susequent fibrous tissue that is produced is incorporated into the denuded area of the descemets. This leads to the formation of an atypical descemets also called glass membrane (as it is structureless)

TREATMENT

If the growth is not interfering with vision no

treatment is required.

If the growth is progressive cryosurgical

techniques can be used to arrest the

progression.

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