The document discusses various potential complications that can occur after cataract surgery, including: intraoperative complications like shallow anterior chamber; early postoperative complications like corneal edema and elevated intraocular pressure; and late postoperative complications like retinal detachment and cystoid macular edema. It provides details on the causes, signs, and management approaches for many of the major complications.

1. Complications of Cataract Surgery
Prof. Naimatullah Khan Kundi
Head, Department of Ophthalmology
Khyber Medical College Peshawar

2. 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

3. Major postoperative complications
of
cataract surgery
Endophthalmitis
Expulsive Haemorrhage
Corneal edema
Delayed choroidal haemorrhage
Wound distortion or disruption
Hyphaema
Shallow or flat anterior chamber
Elevated IOP
Corneal edema
Glaucoma
Detachment of descemet’s
Malignant glaucoma
membrane
Retained lens material
Suprachoroidal haemorrhage or
effusion

4. Major postoperative complications
of
cataract surgery
•
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

5. Major postoperative complications
of
cataract surgery
 Endophthalmitis

Sterile

Infectious

6. Acute bacterial endophthalmitis
Incidence - about 1:1,000
Common causative
organisms
• Staph. epidermidis
• Staph. aureus
• Pseudomonas sp.
Source of infection
•
Patient’s own external
bacterial flora is most
frequent culprit
•
Contaminated solutions
and instruments
Environmental flora including
that of surgeon and
operating room personnel
•

7. Signs of severe endophthalmitis
• Pain and marked visual loss
• Absent or poor red reflex
• Corneal haze, fibrinous exudate and • Inability to visualize fundus with
hypopyon
indirect ophthalmoscope

8. Signs of mild endophthalmitis
• Mild pain and visual loss
• Anterior chamber cells
• Small hypopyon
• Fundus visible with indirect
ophthalmoscope

9. 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

10. 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

11. Major postoperative complications of
cataract surgery
 Corneal edema

Detached Descemet’s membrane

Mechanical trauma

Vitreo-endothelial touch

IOL-endothelial touch

Toxic solutions

12. Major postoperative complications of
cataract surgery
 Wound distortion or disruption
 Astigmatism
 Wound leak
 Inadvertent filtering bledb
 Iris prolapse
 Hypotony

13. Major postoperative complications of
cataract surgery
 Shallow or flat anterior chamber
 Wound leak
 Choroidal detachment or hemorrhage
 Pupillary block
 Ciliary block

14. Shallow or flat AC
A. Intraoperative
1. Inadequate infusion of BSS
2. Leakage over sized wound
3. External pressure on the globe
4. Positive vitreous pressure more common in:




Obese
Bull necked pts.
COPD
Anxious Pts. Who perform valsalva maneuver
5. Supachoroidal haemorrhage or effusion

15. Shallow or flat AC (cont’d)
Intraoperative shallow AC
Management




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

16. 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

17. Shallow or flat AC (cont’d)
B. Postoperative shallow AC

Causes
1.
2.
Choroidal detachment
3.
Pupillary block
4.
Ciliary block
5.

Wound leak
Suprachoroidal hemorrhage
Cases associated with ocular hypotension are 2ndry to wound
leakage / choroidal detachment

Slow or intermittent wound leaks may coexist with formed AC

18. Shallow or flat AC (cont’d)
B. Postoperative shallow AC
Seidel 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

19. Postoperative shallow AC (cont’d)
Management
Several 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

20. 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

21. 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

22. 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

23. 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

24. 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

25. 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

26. 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

27. 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

28. Tixic solutions

Certain solutions can be toxic to corneal
endothelium when:
 Irrigated
 Inadvertently injected
Cause:
 Temporary
 Permanent
Into AC
Corneal edema

29. 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:

30. Corneal complications of phacoemulsification
 The US energy causes:
 Injury to cornea
 Loss of endothelial cell
C. Edema on 1st postoperative
day/delayed for months to years
 In corneal edema develops during:
 Phacoemulsification and
 Decreases visualization
Convert to nuclear expression
technique

31. 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 stroma
Treatment:
 Small detachments can be reattached with air
tamponade in AC
 Large detachments can be sutured back into place


32. 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

33. Suprachoroidal haemorrhage or effusion

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
(cont’d)

34. 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

35. 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

36. 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

37. Delayed choroidal haemorrhage
Early postoperative period (less common)
Presentation:

Sudden onset of pain

Loss of vision

Shallow AC

↑ IOP

Wound intact / disrupted

38. Delayed choroidal haemorrhage
(cont’d)
Management:
Observation:
If wound intact and IOP controlled, limited
haemorrhage may be observed and resolve
spontaneously
Surgical drainage:
1.
2.
3.
4.
5.
Wound disruption
Persistent shallow AC
Uncontrolled glaucoma
Adherent choroidals (kissing)
Persistent choroidal detachment

39. Delayed choroidal haemorrhage
(cont’d)
Medical Management:
1. Systemic corticosteroids
2. Ocular hypotensive agents (topical / oral)
3. Close observation

40. Hyphaema
 Early / Late
 Early:
Immediate postoperative period



 Late:
Origin: Incision / Iris
Mild resolves spontaneously
Mixed with blood / viscoelastic –
resolution longer
Months / years after surgery

Origin: wound vascularization / erosion
of vascular tissue by lens implant

41. 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

42. 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

43. 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

44. 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

45. 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

46. Retained lens material (cont’d)
Treatment:
 Observation
 Cycloplegic drugs
 Corticisteroids
 Surgical intervention

47. 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

48. 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

49. 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:
Chronic ocular
inflammation with CME
and vitreous incarcerated
in the wound
if cornea shows considerable compromise (to
reduce surgical trauma)

50. 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

51. 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

52. 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

53. Implant displacement
Decentration
Optic capture
•
•
May occur if one haptic is inserted Reposition may be necessary
into sulcus and other into bag
•
Remove and replace if severe

54. 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

55. 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

56. 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)

57. 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 size
2. Contact between implant and vascular structures
3. Defects in implant manufacturing
4. Idiosyncretic reaction of patient to implant

58. 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)

59. Complications of IOL implantation (cont’d)
Corneal edema and pseudo-phalic bullous
keratopathy
Causes
1.
2.
3.
4.
5.
Surgical trauma
IOL type: - Iris fixated / closed loop flexible AC IOL
Vitreous contact with corneal edothelium
Glaucoma
Corneal endothelial dystrophy (Fuchs) – increased
risk of developing postoperative corneal edema
even after smooth, a traumatic surgery

60. Complications of IOL implantation (cont’d)
Corneal edema and pseudo-phalic bullous
keratopathy
Symptoms
1.
2.
3.
4.
5.
Corneal edema → BK
↓ VA
Irritation
FB Sensation
Epiphora
6. Infective keratitis (occasionally)

61. 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
Early
Stage
4. Penetrating keratoplasty (recurrent pain, infective
keratitis, ↓ VA)

62. 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