cataract complications
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This presentation is orginaly uploaded to http://kpkmedicalcolleges.tk by Dr.SulemanTRANSCRIPT
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