Cataract complications

Complications of Cataract Surgery

Prof. Naimatullah Khan KundiHead, Department of OphthalmologyKhyber Medical College Peshawar

Complications of cataract surgery

Complications are varied in time and scope

1. Intraoperative

2. Immediate postoperative

3. Late postoperative

Therefore it is necessary to observe the

postoperative patients at periodic intervals

Major postoperative complications of cataract surgery

Endophthalmitis

Corneal edema

Wound distortion or disruption

Shallow or flat anterior chamber

Corneal edema

Detachment of descemet’s

membrane

Suprachoroidal haemorrhage or

effusion

Expulsive Haemorrhage

Delayed choroidal haemorrhage

Hyphaema

Elevated IOP

Glaucoma

Malignant glaucoma

Retained lens material

• Vitreous disruption incarceration in the wound

• Suture induced astigmatism

• Pupillary capture

• Complications of IOL implantation

• Uveitis

• IOL dislocation

• Hemorrhage

• Retinal detachment

• Cystoid macular edema

• Retianed lens material

• Capsular rupture

• Vitreous loss

Major postoperative complications of cataract surgery

Endophthalmitis

Sterile

Infectious

Major postoperative complications of cataract surgery

Acute bacterial endophthalmitis

Common causative organisms• Staph. epidermidis• Staph. aureus• Pseudomonas sp.

Incidence - about 1:1,000

• Patient’s own external bacterial flora is most frequent culprit

Source of infection

• Contaminated solutions and instruments• Environmental flora including that of surgeon and operating room personnel

Signs of severe endophthalmitis

• Pain and marked visual loss • Absent or poor red reflex

• Corneal haze, fibrinous exudate and hypopyon

• Inability to visualize fundus with indirect ophthalmoscope

Signs of mild endophthalmitis

• Mild pain and visual loss

• Anterior chamber cells

• Small hypopyon

• Fundus visible with indirect ophthalmoscope

Management of Acute Endophthalmitis

1. Preparation of intravitreal injections

2. Identification of causative organisms• Aqueous samples• Vitreous samples

3. Intravitreal injections of antibiotics

4. Vitrectomy - only if VA is PL

5. Subsequent treatment

Subsequent Treatment

1. Periocular injections• Vancomycin 25 mg with ceftazidime 100 mg or gentamicin 20 mg with cefuroxime 125 mg• Betamethasone 4 mg (1 ml)

2. Topical therapy• Fortified gentamicin 15 mg/ml and vancomycin 50 mg/ml drops

• Dexamethasone 0.1%

3. Systemic therapy• Antibiotics are not beneficial

• Steroids only in very severe cases

Corneal edema

Detached Descemet’s membrane

Mechanical trauma

Vitreo-endothelial touch

IOL-endothelial touch

Toxic solutions

Major postoperative complications of cataract surgery

Wound distortion or disruption

Astigmatism

Wound leak

Inadvertent filtering bledb

Iris prolapse

Hypotony

Major postoperative complications of cataract surgery

Shallow or flat anterior chamber

Wound leak

Choroidal detachment or hemorrhage

Pupillary block

Ciliary block

Major postoperative complications of cataract surgery

Shallow or flat AC

A. Intraoperative1. Inadequate infusion of BSS2. Leakage over sized wound 3. External pressure on the globe4. Positive vitreous pressure more common

in: Obese Bull necked pts. COPD Anxious Pts. Who perform valsalva

maneuver

5. Supachoroidal haemorrhage or effusion

Intraoperative shallow ACManagement

Raise infusion bottle Place suture across the wound to its size External pressure: Readjust surgical drapes

or eye lid speculum Positive vitreous pressure:

I/V manitol the positive pressure and Allow the case to continue uneventfully

Suprachoroidal hemorrhage or effusion: Check red reflex Examine fundus with indirect ophthalmoscope to

confirm diagnosis

Shallow or flat AC (cont’d)

B. Postoperative shallow AC Postoperative shallow AC opposition of iris to

angle PAS chronic ACG

Irido-vitreal (ICCE) / irido-capsular (ECCE)

synechiae

pupillary block

Corneal contact with vitreous / IOL endothelial

cell loss chronic corneal edema

Shallow or flat AC (cont’d)

B. Postoperative shallow AC Causes

1. Wound leak

2. Choroidal detachment

3. Pupillary block

4. Ciliary block

5. Suprachoroidal hemorrhage

Cases associated with ocular hypotension are 2ndry to wound

leakage / choroidal detachment

Slow or intermittent wound leaks may coexist with formed AC

Shallow or flat AC (cont’d)

B. Postoperative shallow ACSeidel Test:

To detect an area of wound leakage

Instill one drop of 2% fluorescein and examine the incision

with cobalt blue filter on the SL

Aqueous dilution of fluorescein at the site of leakage will

produce contrasting area of green stain

Occasionally aqueous flow is so slight that gentle pressure

on the globe is necessary to confirm the site of leakage

Shallow or flat AC (cont’d)

Postoperative shallow AC (cont’d)

ManagementSeveral Options

1. Cycloplegics and pressure patching

2. CAI and topical beta blockers: Aqueous flow through the woung

3. Corticosteroid avoidence: Enhance local wound reaction to faciliatte spontaneous closure

4. Therapeutic contact lens help in opposing wound edges and aqueous flow through the wound

5. Tissue adhesive: may seal the wound

6. Surgical

Postoperative shallow AC (cont’d)

Management

These measures are appropriate for minor

wound leaks

Many patients develop associated

ciliochoroidal detachment which resolves

spontaneously after wound closure

Postoperative shallow AC (cont’d)

Management

Surgical approach with reformation of AC and wound repair indicated:

If no improvement occurs in 24 – 46

hours

If obvious wound separation is present

Iris prolapse

IOL contact with corneal endothelium

Postoperative shallow AC(cont’d)

Complications (shallow AC)

Early postoperative Pupillary block glaucoma may

follow resolved wound leak

Late Pupillary block glaucoma is caused by

postoperative uveitis with irido-vitreous / irido-

capsular synechiae formation

AC IOL Placement without PI may be associated with

early or late postoperative pupillary block glaucoma

Ciliary block glaucoma caused by aqueous

sequestration within the vitreous body with flat AC

& IOP

Postoperative shallow AC (cont’d)

Pupillary block glaucoma

Treatment

1. Pupillary dilation

2. Laser or surgical iridotomy

3. Vitretcomy preferred treatment for

ciliary block glaucoma

Corneal edema

Factors: IOP Endothelial cell damage

Edema in the immediate postoperative period

Incidence is increased in preexisting

endothelial Dysfunction

Acute endothelial decompensation with

increase in corneal thickness

Corneal edema (cont’d)

Causes: 1. Mechanical trauma

2. Prolonged intraocular irrigation

3. Inflammmation

4. Increased IOP Resolves in 4 – 6 weeks Corneal edema persisting after 3 months will

usually not clear and may require penetrating keratoplasty

Brown McLean Syndrome

This clinical condition occurs after cataract surgery (most frequently ICCE)

Etiology unknown Consists of peripheral corneal edema with

clear central cornea Edema typically starts inferiorly and

progresses circumfrentially but spares the central cornea

It rarely progresses to clinically significant central corneal edema

Vitreo-corneal adherence and persistent corneal edema

Early / late

Uncomplicated ICCE or complicated ECCE

Early recognition and treatment are essential

to prevent development of irreversible

corneal edema

Treatment:

1. Anterior vitrectomy (Limbus / PP)

2. Penetrating keratoplasty with vitrectomy

in more advanced cases

Tixic solutions

Certain solutions can be toxic to corneal endothelium when:

Irrigated

Inadvertently injected Into AC

Temporary

Permanent Corneal edema

Cause:

Corneal complications of phacoemulsification

Heat: transferred from the vibrating probe to the

cornea

Tight wound prevents adequate irrigation fluid

along the probe

Occlusion of irrigation / aspiration tubing

Holding phaco tip too close to the corneal

endothelium:

Corneal complications of phacoemulsification

The US energy causes:

Injury to cornea

Loss of endothelial cell

In corneal edema develops

during:

Phacoemulsification and

Decreases visualization

C. Edema on 1st postoperative day/delayed for months to years

Convert to nuclear expression technique

Detachment of descemet’s membrane

Results in stromal swelling and epithelial bullae localized in the area of detachment

Causes: When Instrument / IOL is introduced

through cataract incision. Inadvertent fluid injection between

descemet’s membrane and stromaTreatment:

Small detachments can be reattached with air tamponade in AC

Large detachments can be sutured back into place

Suprachoroidal haemorrhage or effusion

Occurs intraoperatively

Choroidal effusion with or without suprachoroidal

haemorrhage

Choroidal effusion may be difficult to differentiate

from choroidal haemorrhage (clinically)

Both complications may occur in patients with:

HT

Obesity

Glaucoma

Chronic ocular inflammation

Suprachoroidal haemorrhage or effusion (cont’d)

Choroidal effusion may be precursor of suprachoroidal

haemorrhage

Or haemorrhage may represent spontaneous rupture

of choroidal vasculature (in patients with underlying

vascular disease)

Choroidal effusion tents veins and arteries that course

through sclera and supply choroid

Disruption of these vessels lead to suprachoroidal

haemorrhage

Suprachoroidal haemorrhage or effusion (cont’d)

Treatment:

Rapid wound closure with elevation of IOP to

tamponade the extravasated plasma or blood

Sclerostomy in one or more quadrants posterior to

ora serrata to drain blood

Elevated IOP serves both to stop bleeding and to

extravasate suprachoroidal blood

Expulsive Haemorrhage

Rare but serious intraoperative problem

Requires immediate action

Presentation: Sudden IOP

Darkening of red reflex

Wound gap

Iris prolapse

Expulsion of lens and vitreous

Bright red blood

Expulsive Haemorrhage (cont’d)

Treatment:

Immediate closure of the wound with

sutures / digital pressure

Perform posterior selerotomies (5 – 7 mm

posterior to limbus) to permit

suprachoroidal haemorrhage blood to

escape and allow repositioning of

prolapsed intraocualr tissues and closure

of the wound

Delayed choroidal haemorrhage

Early postoperative period (less common)

Presentation:

Sudden onset of pain

Loss of vision

Shallow AC

IOP

Wound intact / disrupted

Delayed choroidal haemorrhage (cont’d)

Management:

Observation:

If wound intact and IOP controlled, limited

haemorrhage may be observed and resolve

spontaneously

Surgical drainage:1. Wound disruption2. Persistent shallow AC3. Uncontrolled glaucoma4. Adherent choroidals (kissing)5. Persistent choroidal detachment

Delayed choroidal haemorrhage (cont’d)

Medical Management:

1. Systemic corticosteroids

2. Ocular hypotensive agents (topical /

oral)

3. Close observation

Hyphaema

Early / Late Early: Immediate postoperative period

Origin: Incision / Iris Mild resolves spontaneously Mixed with blood / viscoelastic –

resolution longer

Late: Months / years after surgery Origin: wound vascularization /

erosion of vascular tissue by lens implant

Hyphaema (cont’d)

Complications (prolonged hyphaema): IOP Corneal blood staining

Management: IOP monitored closely and treated in the usual

medial fashion

Argon laser photocoagulation of the bleeding

vessels stop / prevent rebleeding

With-holding antiplatelet therapy (Those who

receive) until hyphaema resolves. Also risk of

continued / recurrent bleeding reduced

Elevated IOP Mild and selflimiting Significant and sustained Causes:

Retained viscoelastic material in AC, PC, behind the IOL]

Pupillary block Ciliary block Hyphaema Endophthalmitis Retained lens material (phacolytic /

phacoanaphylatic reaction) Iris pigment release Preexisting glaucoma Corticosteroid usage PAS (early postoperative flat AC when eye

inflammed) 2ndry glaucoma

Elevated IOP (cont’d)

Treatment: Mild and selflimiting:

Does not require prolonged anti-glaucoma therapy

IOP elevation lasts for a few days and is amenable to medical treatment

Significant and sustained rise of IOP: May necessitate timely and specific

management in several circumstances Treat the underlying cause of IOP

elevation

Malignant glaucoma (ciliary block glaucoma

Posterior dissection of aqueous into the vitreous body and 2ndry rise of IOP

IOP rise may occur inspite of patent iridectomy

Treatment Cycloplegics – to move lens-iris diaphragm

posteriorly Disruption of anterior hyaloid face and vitreous to

reestablish a channel for aqueous to come forward

Techniques: Mechanical disruption (knife) ND: YAG Laser PPV

Retained lens material

Small lens material (cortical) better

tolerated and require no surgical

intervention

More likely resorb over time

Nuclear material incite significant

inflammatory reaction

Inflammatory reaction may be difficult to

differentiate from microbial

endophthalmitis

Retained lens material (cont’d)

Treatment:

Observation

Cycloplegic drugs

Corticisteroids

Surgical intervention

Retained lens material (cont’d)

Treatment: Surgical intervention

Large amount of lens material Inflammation not controlled by topical

medication 2ndry hypotony / increased IOP from

inflammation PC intact:

Simple aspiration PC ruptured: (Potential for lens-vitreous

admixture) Vitrectomy

Vitreous disruption incarceration in the wound

Rupture of anterior vitreous face (ICCE/ECCE)

Anterior migration through pupil

Vitreous traction: - Retinal breaks and RD

Vitreous incarceration in the wound chronic

ocular inflammation with / without CME

Vitreous transparent, its presence datected by: -

Touching / Manipulating the wound / iris with sponge or

spatula:- Adherent vitreous becomes apparent / cause

movement of the pupil

Vitreous disruption incarceration in the wound (cont’d)

Management

Cutting vitreous strands and removed by suction

cutter / cellulose sponges

ND:YAG laser / anterior vitrecotmy

PPV: if cornea shows considerable compromise (to

reduce surgical trauma)

Chronic ocular inflammation with CME and vitreous incarcerated in the wound

Suture induced astigmatism

Tight sutures: post-operative astigmatism, Steepens the

cornea in the direction of sutures

Removing sutures 6 – 8 wks postoperatively may alleviate astigmatism

Wound leak: Significant against the rule astigmatism

Secondary intra-ocular infection: Entry of organisms into the eye through suture

tract

Pupillary capture

Causes PS (Iris and PC Adhesions) Improper placement of IOL haptics Anterior displacement of PC IOL optic

(non angulated IOL in ciliary sulcus) Inadvertent flipping over of angulated

IOL so it angles anteriorly Positive vitreous pressure from behind

the optic of IOL

Pupillary capture (cont’d)

Management Asymptomatic:

Problem cosmetic – patient can be left untreated

Occasionally glare, photophobia, monocular

diplopia

In bag placement has decreased the occurrence of pupillary capture

Symptomatic: Pharmacological manipulation of pupil with

mydriatics to free iris

Surgical intervention – free iris / break synechiae

Implant displacementDecentration

• May occur if one haptic is inserted into sulcus and other into bag

• Reposition may be necessary

• Remove and replace if severe

Optic capture

Complications of IOL implantation

1. Decentration and dislocation

2. Uveitis – glaucoma – hyphaema

(UGH) syndrome

3. Corneal edema and pseudo-phakic

bullous keratopathy

4. Wrong power IOL

Complications of IOL implantation (cont’d)

Decentration and dislocation

Causes

Asymmetric hapitc placemnt:

One in bag and other in sulcus. IOL

designed for bag fixation prone to

decentration / dislocation when one / both

haptics are placed in sulcus Insufficient zonular support Irregular fibrosis of posterior capsule

Complications of IOL implantation (cont’d)

Decentration and dislocation (cont’d)

Management Rotation of IOL

Reposition IOL haptics

Replace capsule fixated IOL with PC sulcus

fixated IOL

IOL exchange with AC IOL / Trans-sclerally

sutured PC IOL (complete IOL dislocation)

Complications of IOL implantation (cont’d)

Uveitis-glaucoma-hyphaema (UGH) syndrome

UGH syndrome was first described in the context of rigid AC IOLs

Classic triad (UGH) or individual elements may occur

Causative Factors:1. Inappropriate IOL size2. Contact between implant and vascular

structures3. Defects in implant manufacturing

4. Idiosyncretic reaction of patient to implant

Complications of IOL implantation (cont’d)

Uveitis-glaucoma-hyphaema (UGH) syndrome

Treatment

Topical anti-inflammatory medications

Topical anti-glaucoma medications

IOL removal (symptoms not alleviated /

threaten retinal or corneal function)

Corneal edema and pseudo-phalic bullous keratopathy

Causes 1. Surgical trauma2. IOL type: - Iris fixated / closed loop flexible

AC IOL3. Vitreous contact with corneal edothelium4. Glaucoma5. Corneal endothelial dystrophy (Fuchs) –

increased risk of developing postoperative corneal edema even after smooth, a traumatic surgery

Complications of IOL implantation (cont’d)

Complications of IOL implantation (cont’d)

Corneal edema and pseudo-phalic bullous keratopathy

Symptoms 1. Corneal edema BK2. VA3. Irritation4. FB Sensation5. Epiphora

6. Infective keratitis (occasionally)

Complications of IOL implantation (cont’d)

Corneal edema and pseudo-phalic bullous keratopathy

Management 1. Topical hyperosmotic agents

2. Topical steroids

3. Bandage (therapeutic) contact lens

4. Penetrating keratoplasty (recurrent pain,

infective keratitis, VA)

Early

Stage

Complications of IOL implantation (cont’d)

Wrong power IOL

A. 1. Miscalculation

2. Manufacturing defect

B. If magnitude of implant error produce

symptomatic anisometropia; replace IOL with

appropriate power