1. PRE AND POST OPERATIVE
MANAGEMENT OF CATARACT
Presenter: Kalpana Bhandari
M.Optom (1st sem)
TIO
2. Preoperative considerations
Indications for surgery
⢠Visual improvement: Operation is indicated when the
opacity develops to a degree sufficient to cause difficulty in
performing essential daily activities.
⢠Medical indications are those in which a cataract is
adversely affecting the health of the eye. Eg:
-Lens induced glaucoma
-Phacoanaphylactic endophthalmitis
-Retinal diseases like diabetic retinopathy or retinal
detachment.
⢠Cosmetic indication -to obtain black pupil.
6. Preoperative ocular assessment
⢠Visual acuity assessment.
⢠Iop measurment - raised IOP needs priority
management.
⢠Cover test: A heterotropia may indicate amblyopia,
which carries a guarded visual prognosis, or the
possibility of diplopia if the vision is improved. A squint,
usually a divergence, may develop in an eye with poor
vision due to cataract, and lens surgery alone may
straighten the eye.
7. ⢠Pupillary responses. Because cataract never produces
an afferent pupillary defect, its presence implies substantial
additional pathology.
⢠Ocular adnexa. Dacryocystitis, blepharitis, chronic
conjunctivitis, lagophthalmos, ectropion, entropion and tear
film abnormalities may predispose to endophthalmitis and
in most cases optimization should be achieved prior to
intraocular surgery.
8. ⢠Cornea: Eyes with decreased endothelial cell counts
(e.g.substantial cornea guttata) have increased
vulnerability to postoperative decompensation secondary
to operative trauma.
⢠Anterior chamber: A shallow anterior chamber can
render cataract surgery difficult. Recognition of a poorly
dilating pupil allows intensive preoperative mydriatic
drops, planned mechanical dilatation prior to
capsulorhexis and/or intracameral injection of mydriatic.
.
9. ⢠Lens: Nuclear cataracts tend to be harder and may require
more power for phacoemulsification, while cortical and
subcapsular opacities tend to be softer.
⢠Black nuclear opacities are extremely dense and extracapsular
cataract extraction rather than phacoemulsification may be the
superior option.
⢠Pseudoexfoliation indicates a likelihood of weak zonules
(phakodonesis â lens wobble â may be present), a fragile
capsule and poor mydriasis.
10. ⢠Fundus examination. Pathology such as age-related
macular degeneration may affect the visual outcome.
Ultrasonography may be required, principally to exclude
retinal detachment and staphyloma, in eyes with very dense
opacity that precludes fundus examination.
⢠Retinal function tests:
i. Light Perception
ii. Test for Marcus Gunn pupillary response
iii. Projection of rays - Test for function of peripheral retina
iv. Two light discrimination test - Macular function
v. Maddox rod test
vi. Colour perception-macular function and optic nerve
vii. Entoptic visualisation-retinal function
viii. Laser interferometry
ix. Objective tests for evaluating retina- ultrasonic evaluation,
ERG, EOG, VER and indirect ophthalmoscopy
11. ⢠Sclera. If a prominent explant/encircling band has been
placed during prior retinal detachment surgery, the eye is
particularly large or the sclera thin (e.g. high myopia),
peri- and retrobulbar local anaesthesia may be avoided
and special care taken with sub-Tenon local anaesthetic
infiltration.
⢠Current refractive status: It is critical to obtain details of
the patientâs preoperative refractive error in order to guide
intraocular lens (IOL) implant selection.
⢠The keratometry readings (obtained during biometry)
should be noted in relation to the refraction, particularly if
it is planned to address astigmatism by means of targeted
wound placement, a toric IOL or a specific adjunctive
procedure.
12. Informed consent
⢠It is essential that the patient has arrived at a fully
informed decision to proceed with cataract surgery. As well
as discussing the benefits, risks should be conveyed at a
level appropriate to each patientâs level of understanding,
with an explanation of the more common and severe
potential problems.
13. Biometry
⢠Biometry facilitates calculation of the lens power ; in its
basic form this involves the measurement of two ocular
parameters, keratometry and axial (anteroposterior) length.
⢠Keratometry involves determination of the curvature of the
anterior corneal surface (steepest and flattest meridians),
expressed in dioptres or in millimetres of radius of
curvature. This is commonly carried out with the
interferometry apparatus used to determine axial length but
if this is unavailable or unsuitable manual keratometry (e.g.
JavalâSchiøtz keratometer) or corneal topography can be
performed.
14. ⢠Optical coherence biometry is a noncontact method of
axial length measurement that utilizes two coaxial partially
coherent low-energy laser beams to produce an interference
pattern (partial coherence interferometry).
⢠Modern biometry devices also perform keratometry, anterior
chamber depth and corneal white-to white measurement,
and are able to calculate IOL power using a range of
formulae. Measurements have high reproducibility and
generally require less skill than ultrasonic biometry.
15. ⢠A-scan ultrasonography is a
generally slightly less accurate method
of determining the axial dimension and
can be acquired either by direct
contact or more accurately but with
greater technical difficulty by using a
water bath over the eye (immersion
ultrasonography). The sound beam
must be aligned with the visual axis for
maximal precision; each reflecting
surface is represented by a spike on
an oscilloscope display monitor.
16. IOL power calculation formulae:
⢠Numerous formulae have been developed that utilize
keratometry and axial length to calculate the IOL power
required to achieve a given refractive outcome.
⢠Some formulae incorporate additional parameters such as
anterior chamber depth and lens thickness to try to optimize
accuracy.
⢠The SRK-T, Haigis, Hoffer Q and Holladay 1 and 2 are
commonly used.
⢠Specific formulae may be superior for very short (possibly
the Hoffer Q) or long eyes.
17. Previous refractive surgery:
⢠Any form of corneal refractive surgery is likely to make a
significant difference to the IOL power required, and
standard IOL calculations are unsuitable.
⢠Several different methods have been described to address
this situation.
⢠Most involve the calculation of the post-refractive
procedure âtrueâ corneal power using a special process
(refractive history method, contact lens method) and
insertion of this into a standard (e.g. Hoffer Q) or specific
(e.g. Masket) formula, but the Haigis-L regression formula
uses statistical data to facilitate calculation on post-
refractive surgery eyes using only standard inputs. It may
prudent to utilize more than one method of IOL calculation.
18. ⢠Contact lenses. If the patient wears soft contact lenses, these
should not be worn for up to a week prior to biometry to
allow corneal stabilization; hard/gas permeable lenses may
need to be left out for 3 weeks.
⢠Personalized A-constant. If a consistent postoperative
refractive deviation is found in most of an individual
surgeonâs cases, it is assumed that some aspects of personal
surgical (or possibly biometric) technique consistently and
similarly influence outcome, and a personalized A-constant
can be programmed into biometry apparatus to take this
into account.
19. Corneal pachymetry
⢠Ultrasonic pachymeters can accurately & reliably measure
endothelial cell function.
⢠If thickness > 600 ¾m maybe consistent with corneal
edema & endothelium dysfunction that increase the
likelihood postoperative clinical corneal edema.
Specular microscopy: (endothelium cells)
⢠A normal cell count > 2400 cells/mm2
⢠If a cell count fewer than 1000 cells/mm2 is risk of
postoperative corneal decompensation.
20. Pre operative management in pediatric age groups
Pediatric IOL : size, design and power.
1. Size of IOL above the age of 2 years may be standard
12 to 12.75mm diameter for the bag implantation.
2. Design of IOL recommended is one- piece PMMA with
modified C- shaped haptics (preferably heparin coated)
Power of IOL in children between 2-8 years of age 10%
undercorrection from the calculated biometric power is
recommended to counter the myopic shift.
3. Below 2 years on undercorrection by 20% is
recommended.
21. Pre-op medications and preperations
1. Topical antibiotics - Tobramycin and Gentamicin QID for
3 days before surgery.
2. Preparation of the eye to be operated.
3. Consent.
4. Scrub bath and care of hair
5. Drugs to lower IOP- acetazolamide 500mg stat 2 hours
before surgery and glycerol 60ml mixed with equal amount
of water or lemon juice 1 hour before Surgery or, IV
mannitol 1gm/kg body weight half an hour before Surgery.
6. Drugs to sustain dilated pupil - antiprostaglandin eye
drops(indomethacin).
22. Anaesthesia
⢠The majority of cataract surgery is performed under local
anaesthesia (LA), sometimes in conjunction with
intravenous or oral sedation. Types of local anaesthetics
for cataract surgery are:
a)Subtenonâs
b)Peribulbar
c)Topical
⢠General anaesthesia is required in some circumstances,
such as children and many young adults, very anxious
patients, some patients with learning difficulties, epilepsy,
dementia and those with a head tremor.
23. ⢠Sub-Tenon block involves insertion of a blunt-tipped
cannula through an incision in the conjunctiva and Tenon
capsule 5 mm from the limbus inferonasally and
passing it around the curve of the globe through the
sub-Tenon space.
⢠The anaesthetic is injected beyond the equator of the globe.
⢠Although anaesthesia is good and complications minimal,
akinesia is variable. Chemosis and subconjunctival
haemorrhage are common but penetration of the globe is
extremely rare.
24. ⢠Peribulbar block is given through the skin or conjunctiva
with a 1-inch (25-mm) needle.
⢠It generallyprovides effective anaesthesia and akinesia.
⢠Penetration of the globe is a rare but severe complication,
and for this reason peribulbar is avoided, or approached
with great caution, in longer eyes (which also tend to have
a larger equatorial diameter).
25. ⢠Topical anaesthesia involves drops or gel
(proxymetacaine 0.5%, tetracaine 1% drops, lidocaine 2%
gel), which can be augmented with intracameral
preservative-free lidocaine 0.2%â1%, combined
viscoelastic/lidocaine preparations are also commercially
available.
⢠Although analgesia is generally adequate, it tends
to be less effective than peribulbar or sub-Tenon blocks.
26. Post- operative management
⢠Patient is asked to lie quietly upon the back for 3/ 4 hours.
⢠For mild to moderate post-operative pain injection
diclofenac sodium may be given.
⢠Next morning bandage is removed & inspected for post-
op complication.
⢠Antibiotic-steroid eye drops are used two hourly 1 week,
QID 4 week then tapering, TID, BD and OD for each
week.
⢠Tear supplements are given for at least one month or
more depending upon the patients complain to prevent
post cataract surgery dry eyes.
27. Post -op examination
⢠Cornea: wounds sealed (Seidel test negative), clarity
⢠AC: formed, activity
⢠Pupil: round, regular and reacting
⢠PCIOL: centred and in the bag
⢠Consider : IOP checking
⢠Give clear instructions re postoperative drops
⢠Use of clear shield
⢠What to expect (discomfort, watering)
⢠What to worry about (increasing pain/ redness, worsening
vision)
⢠Where to get help (including telephone number)
28. Final review (2-4wks later)
Examination
⢠VA: unaided/aided
⢠Cornea: wounds sealed (Seidel test negative), clarity
⢠AC: depth and clarity
⢠Pupil: round, regular and reacting
⢠IOP
⢠Fundus : no cystoid macular oedema, flat retina
⢠If good result then either list for second eye (in bilateral
cases) or discharge for refraction as appropriate.
29. ⢠If disappointing VA (unaided) perform refraction to look for
ârefractive errorâ and dilated fundoscopy to check for the
subtle CMO (specially if VA (pinhole) < VA (unaided)) and
if in doubt, consider OCT.
30. Refractive surprises
⢠In patients where the refractive outcome is harder to
predict (high ametropia, previous corneal refractive
surgery), review patients early (1 week) with refraction to
permit the option of an early IOL exchange if a large
discrepancy noticed.
⢠After 6-8 weeks of operation corneoscleral sutures are
removed (when applied).
⢠Final spectacles are prescribed after about 8 weeks of
operation.
31. Management of refractive error in adults
⢠Refractive error is assessed at 8th week of cataract
surgery.
⢠Refractive correction is prescribed only if the error persist
even after three months of cataract surgery.
32. Postoperative refraction
⢠Emmetropia is typically the desired postoperative
refraction, though usually spectacles will be needed for
near vision since a conventional IOL cannot
accommodate.
⢠Many surgeons aim for a small degree of myopia (about -
0.25 D) to offset possible errors in biometry; postoperative
hypermetropia, which necessitates correction for clear
vision at all distances, is typically less well tolerated than
myopia.
33. Postoperative refraction
⢠Contralateral eye. Postoperative refractive planning must
take account of the contralateral eye. If this has a
significant refractive error but is unlikely to require
cataract surgery within a few years, the postoperative
target for the operated eye might be set for within less
than 2.0 D of its fellow, to avoid problems with binocular
fusion.
⢠In some cases, such as when there is an early lens
opacity in the fellow eye or when ametropia is extreme,
the patient can be offered lens surgery to the other eye to
facilitate targeting both at emmetropia.
34. ⢠âMonovisionâ is a concept in which the (usually)
nondominant eye is left with between 1 and 2 dioptres of
myopia to allow reading, whilst emmetropia is targeted in
the dominant eye. This is attractive to some patients,
generally those who have previously been using contact
lenses or spectacles to achieve monovision.
⢠Multifocal lens options use a variety of optical means to
attempt to achieve satisfactory near, distance and
intermediate vision. Many patients are very satisfied with
the results but a significant minority are unhappy,
complaining of phenomena such as glare.
35. ⢠In evaluating reduced post-operative acuity, one should
know both the timing and severity of the visual complaint
in order to determine an etiology.
1) Early Visual Impairment
⢠Severe (20/200 or worse)
⢠Moderate (20/100 or better)
2) Delayed Visual Recovery
36. Early visual impairement
⢠Epithelial Irregularity
⢠Irregular or Marked Corneal Astigmatism
⢠Corneal Edema
⢠Dislocated / subluxated IOL
⢠Operative / Post-operative bleeding
⢠Retained Cortex or Nuclear fragments
⢠Hypotony
⢠Photoretinal Toxicity
⢠Extraocular Muscle paresis
These complications predominantly affect optical clarity,
macular function or refractive state.
37. Early visual impairement
⢠Vascular Occlusion
⢠Retinal Detachment
⢠Infectious Endophthalmitis
⢠Toxic Anterior Segment Syndrome
⢠Delayed Suprachoroidal Hemorrhage
⢠Optic Nerve Damage
⢠Globe Rupture or Perforation
⢠Intraocular aminoglycoside toxicity
These injuries often occur through vascular insult, direct
mechanical injury, or retinal toxicity.
38. Operative complications
Rupture of the posterior lens capsule:
⢠Capsular rupture may be accompanied by vitreous loss,
posterior migration of lens material and, rarely, expulsive
haemorrhage.
⢠Sequelae to vitreous loss, particularly if inappropriately managed,
include CMO, retinal detachment, endophthalmitis, updrawn
pupil, uveitis, vitreous touch, vitreous wick syndrome, glaucoma
and posterior dislocation of the IOL.
Posterior loss of lens fragments:
⢠Dislocation of fragments of lens material into the vitreous cavity
after zonular dehiscence or posterior capsule rupture
is rare but potentially serious as it may result in glaucoma,
chronic uveitis, retinal detachment or chronic CMO.
39. Posterior dislocation of IOL
⢠Dislocation of an IOL into the vitreous
cavity is rare;
loss can occur via a posterior capsular
dehiscence, or in an eye with fragile
zonular attachments (e.g.
pseudoexfoliation) the entire capsular
bag may dislocate.
⢠Complications include vitreous
haemorrhage, retinal detachment,
uveitis and chronic CMO.
⢠Treatment involves pars plana
vitrectomy with IOL removal,
repositioning or exchange depending on
the extent of capsular support.
40. Suprachoroidal haemorrhage
⢠A suprachoroidal haemorrhage involves a bleed into the
suprachoroidal space from a ruptured posterior ciliary artery. If
sufficiently severe it may result in extrusion of intraocular
contents (expulsive haemorrhage).
⢠Contributing factors include advanced age, glaucoma,
increased axial length, systemic cardiovascular disease,
vitreous loss and conversion from phacoemulsification to
ECCE.
41. Suprachoroidal haemorrhage contdâŚ
⢠Immediate treatment involves filling of the AC with a cohesive
viscoelastic and sutured closure of the incision.
⢠Tamponade the bleeding vessel; balloon (e.g. Honan)
compression to a pressure of 50 mmHg, for up to 30 minutes.
⢠It may be helpful to keep the patient in a sitting rather than lying
position.
⢠Postoperatively, topical and systemic steroids should be used
aggressively to reduce intraocular inflammation, with standard
postoperative antibiotic treatment and IOP management as
indicated.
⢠Subsequent treatment, if spontaneous absorption fails to
occur, consists of drainage of large haemorrhages. This can be
performed 7â14 days later.
⢠Pars plana vitrectomy may be considered when the retina
appears adherent or detached,
42. Vascular occlusion
⢠CRVO ,CRAO ,Choroidal Infarction
may occur in surgery if complicated
by :
⢠retrobulbar hemorrhage
⢠nerve sheath injection
⢠elevated IOP
43. Acute postoperative endophthalmitis
Pathogenesis:
⢠Acute intraocular infection is invariably a severe event.
⢠Toxins produced by infecting bacteria and the host
inflammatory responses cause rapid and irreversible
photoreceptor damage.
Risk factors:
⢠Operative complications such as posterior capsule rupture,
prolonged procedure time, combined procedure (e.g. with
vitrectomy), clear corneal sutureless incision, temporal
incision, wound leak on the first day, delaying postoperative
topical antibiotics until the day after surgery, topical
anaesthesia, adnexal disease and diabetes.
44. Acute postoperative endophthalmitis
Pathogens. About 90% of isolates are Gram-positive and 10%
Gram-negative. Staphylococcus epidermidis is the most
common, and with early treatment carries a reasonable
prognosis.
The source of infection:
⢠Flora of the eyelids and conjunctiva are the most frequent
source, includingcontamination via incisions in the early
postoperative stages.
⢠Other potential sources include contaminated solutions and
instruments, environmental air, and the surgeon and other
operating room personnel.
45. Acute postoperative endophthalmitis
Prophylaxis:
⢠Instillation of 5% povidone-iodine into the conjunctival fornices
and leaving this undisturbed for at least 3 minutes prior to
surgery.
⢠Scrupulous preparation of the surgical site, with re-draping if
eyelash coverage is inadequate.
⢠Treatment of pre-existing infections such as blepharitis,
conjunctivitis, chronic dacryocystitis and infection in the
contralateral eye or socket.
⢠Antibiotic prophylaxis:
ďIntracameral cefuroxime (1 mg in 0.1 ml) injected into the AC at
the end of surgery.
ďPostoperative subconjunctival injection can achieve bactericidal
levels in the AC for at least 1â2 hours.
ďPreoperative topical fluoroquinolone antibiotics are frequently
given in regimens from 1 hour to 3 days before surgery.
46. Clinical features:
⢠Symptoms. Pain, redness and visual loss.
⢠Signs vary according to severity.
â Eyelid swelling, chemosis, conjunctival injection and
discharge.
â A relative afferent pupillary defect is common.
â Corneal haze.
â Fibrinous exudate and hypopyon.
â Vitritis with an impaired view of the fundus.
â Severe vitreous inflammation and debris with loss of the
red reflex.
47. Acute postoperative endophthalmitis
Differential diagnosis:
⢠Retained lens material in the AC or vitreous may
precipitate a severe uveitis, corneal oedema and raised IOP.
⢠Vitreous haemorrhage.
⢠Postoperative uveitis. If signs of inflammation are mild a trial of
topical steroid therapy and early review (6â24 hours) is
appropriate. If there is no substantial improvement, management
should be that of endophthalmitis.
⢠Toxic reaction.
⢠Complicated or prolonged surgery may result in corneal
oedema and uveitis.
48. Treatment:
⢠Intravitreal antibiotics: Antibiotics commonly used in combination are
ceftazidime, which will kill most Gram-negative organisms (including
Pseudomonas aeruginosa) and vancomycin to address Gram-positive
cocci (including methicillin-resistant Staphylococcus aureus).
ďFirst choice: Vancomycin 1 mg in 0.1 ml + ceftazidime 2.25 mg in 0.1
ml.
ďSecond choice: Vancomycin 1 mg in 0.1 ml + Amikacin 0.4 mg in 0.1
ml.
ďThird choice: Vancomycin 1 mg in 0.1 ml + gentamycin 0.2 mg in 0.1
ml.
Note: Gentamycin is 4 times more retinotoxic (causes macular infarction)
than amikacin. Preferably the aminoglycosides should be avoided.
49. ⢠Subconjunctival injections of antibiotics should be given daily for
5-7 days to maintain therapeutic intraocular concentration :
ďFirst choice : Vancomycin 25 mg in 0.5 ml plus Ceftazidime 100 mg
in 0.5 ml.
ďSecond choice : Vancomycin 25 mg in 0.5 ml plus Cefuroxime 125
mg in 0.5 ml
⢠Topical concentrated antibiotics should be started immediately
and used frequently (every 30 minute to 1 hourly). To begin with a
combination of two drugs should be preferred.
o Vancomycin (50 mg/ml) or cefazoline (50mg/ml) + Amikacin (20
mg/ml) or tobramycin (15 mg%).
50. ⢠Oral antibiotics. Fluoroquinolones penetrate the eye well
and moxifloxacin 400 mg daily for 10 days is recommended;
clarithromycin 500 mg twice daily may be helpful for culture-negative
infections.
⢠Steroid therapy:
ďźTopical dexamethasone (0.1%) or predacetate (1%) used frequently.
ďźSubconjunctival injection of dexamethasone 4mg (1ml) OD for 5-7
days.
ďźIntravitreal injection of dexamethasone 0.4 mg (0.1ml).
ďźSystemic steroids: Oral corticosteroids should preferably be started
after 24 hours of intensive antibiotic therapy. A daily therapy regime
with 60 mg prednisolone to be followed by 50, 40, 30, 20 and 10 mg
for 2 days each may be adopted.
51. ⢠Supportive therapy
1. Cycloplegics. Preferably 1% atropine or alternatively 2%
homatropine eyedrops should be instilled TDS or QID.
2. Antiglaucoma drugs.In patients with raised intraocular
pressure drugs such a oral acetazolamide (250 mg TDS) and
timolol (0.5%BD) may be prescribed.
Vitrectomy operation should be performed if the patient does not
improve with the above intensive therapy for 48 to 72 hours or
when the patient presents with severe infection with visual acuity
reduced to light perception.
⢠Vitrectomy helps in removal of infecting organisms, toxins and
enzymes present in the infected vitreous mass.
52. Delayed-onset postoperative endophthalmitis
Pathogenesis:
⢠Delayed-onset endophthalmitis following cataract surgery
develops when an organism of low virulence such as P.
acnes, becomes trapped within the capsular bag
(saccular endophthalmitis).
⢠Organisms can become sequestered within
macrophages, protected from eradication but with
continued expression of bacterial antigen.
⢠Onset ranges from 4 weeks to years (mean 9 months)
postoperatively and typically follows uneventful cataract
surgery.
⢠It may rarely be precipitated by laser capsulotomy release
of the organism.
53. Delayed-onset postoperative endophthalmitis
⢠Diagnosis
⢠Symptoms. Painless mild progressive visual deterioration is
typical; floaters may be present.
⢠Signs
â Low-grade anterior uveitis, sometimes with medium large
keratic precipitates; a degree of vitritis is common.
â The inflammation initially responds well to topical steroids, but
recurs when treatment is stopped and may eventually become
steroid-resistant.
â An enlarging capsular plaque composed of organisms
sequestrated in residual cortex within the peripheral capsular
bag is common; gonioscopy under mydriasis may identify an
equatorial plaque.
54. Delayed-onset postoperative endophthalmitis
⢠Initial management. Later-generation fluoroquinolones,
such as moxifloxacin, penetrate the eye well, and are
concentrated within macrophages. An empirical 10â14-day
course of moxifloxacin (alternatives include clarithromycin)
may be worthwhile prior to more invasive options.
⢠Investigation. Sampling of aqueous and vitreous should be
considered if oral antibiotics are ineffective.
⢠Anaerobic culture should be requested if P. acnes infection is
suspected, and isolates may take 10â14 days to grow. The
detection rate can be greatly improved with the use of PCR,
which should also screen for the common causes of viral
anterior uveitis.
55. ⢠Treatment if persistent
â Intravitreal antibiotics alone are usually unsuccessful in
resolving the infection.
â Removal of the capsular bag, residual cortex and IOL,
requiring pars plana vitrectomy. Secondary IOL
implantation may be considered at a later date.
⢠Intravitreal antibiotics are combined: vancomycin (1â2 mg
in 0.1 ml) is the antibiotic of choice and can also be
irrigated into any capsular remnant.
⢠P. acnes is also sensitive to methicillin, cefazolin and
clindamycin.
56. Toxic Anterior Segment Syndrome(TASS)
⢠Develop in response to retained lens, toxic
intraocular reaction, mechanical irritation,
exacerbation of pre-existing uveitis.
⢠Most common clinical symptom is
significantly blurred vision.
⢠Corneal Edema is most common clinical
finding:
-Limbus to limbus
-Indicative of widespread
endothelial damage
57. Marked anterior segment inflammation
⢠Hypopyon
⢠Fibrin from surface of iris onto surface to IOL, to wound
and side ports .
⢠Can create significant iris damage
-Permanently dilate
-Transillumination
-Damage to TM leading to secondary glaucoma
Treatment:
⢠Immediate high dose topical corticosteroid.
⢠IOP monitoring Usually low at start but can rise rapidly.
⢠Specular Microscopy to Monitor for permanent endothelial
damage.
58.
59. Delayed visual impairement
By 6 weeks, intraocular inflammation and minor corneal edema
should be resolved, IOP should be normal, and the macula should be
distinct without edema. Delayed visual impairement occurs due to;
⢠Epithelial Irregularity
⢠Persistent Corneal Edema
⢠Irregular or high corneal astigmatism
⢠IOL subluxation, tilt, or capture
⢠Anterior Segment Inflammation
⢠Posterior Segment Inflammation
⢠Hypotony
⢠Posterior Vitreous Detachment
⢠Macular Edema
⢠Photoretinal Toxicity
⢠Under Diagnosed pre-existing conditions
⢠Incorrect IOL power
⢠Posterior capsular opacification (PCO)
60. Photoretinal toxicity
⢠Photoretinal injury from operating microscope.
⢠Patients complain of scotoma.
⢠If injury near fovea, VA will be compromised.
⢠Appears as subtle pale oval lesion, commonly located
inferior to fovea.
⢠Healing results in mottling of RPE â Prognosis is excellent
if outside fovea.
61. Rebound Inflammation
⢠Occurs in 5% of patients.
⢠More common in dark iridies.
⢠More common in patients with DM.
⢠Occurs when steroids are discontinued to early or tapered
too quickly.
⢠Always look for retained lens material with gonioscopy.
Treatment:
⢠Resume topical steroids.
⢠Consider cycloplegia.
⢠Consider tap and injection to rule out chronic
endophthalmititis.
62. Posterior capsular opacification
⢠Visually significant posterior lens capsular opacification
(PCO), also known as âafter cataractâ, is the most common
late complication of uncomplicated cataract surgery,
historically occurring eventually in up to 50% of patients.
⢠It is caused by the proliferation of lens epithelial cells that
have remained within the capsular bag following cataract
extraction.
⢠The incidence of PCO is reduced when the capsulorhexis
opening is in complete contact with the anterior surface of
the IOL.
63. Treatment
⢠Treatment involves the creation of an opening in the
posteriorcapsule, termed a capsulotomy, with the Nd:YAG
laser.
Indications:
⢠The presence of significant visual symptoms is the main
indication; less commonly, capsulotomy is
performed to improve an inadequate fundus view impairing
assessment and treatment of posterior segment pathology.
Complications
⢠Include pitting of the IOL , intraocular pressure elevation
(usually mild and transient) and extremely rarely CMO,
retinal detachment and IOL subluxation or dislocation.
64. Anterior capsular fibrosis and contraction
⢠Since the advent of continuous
curvilinear capsulorhexis, contraction
of the anterior capsular opening
(capsulophimosis) has become a
more common complication.
⢠It typically progresses over months,
and if severe, YAG laser anterior
capsulotomy may be required.
⢠Risk factors include pseudoexfoliation,
retinitis pigmentosa and a small
capsulorhexis.
65. Cystoid macular oedema
⢠Symptomatic CMO is relatively uncommon following
uncomplicated phacoemulsification and in most cases is
mild and transient.
⢠It occurs more often after complicated surgery and has a
peak incidence at 6â10 weeks, although the interval to
onset may be much longer.
Risk factors: Include epiretinal membrane, a history of
CMO in the other eye, operative complications such as
posterior capsular rupture, particularly with vitreous
incarceration into the incision site, anterior chamber IOL,
secondary IOL implantation, prior topical prostaglandin
treatment, diabetes and uveitis.
66. Cystoid macular oedema contdâŚ
Treatment:
One or a combination of the following modalities may be used:
ďAnterior vitrectomy or YAG laser vitrotomy to vitreous incarceration
in the anterior segment if present.
ďTopical NSAIDs (e.g. ketorolac four times daily, bromfenac twice
daily, nepafenac) may be beneficial even in long-standing cases;
treatment for several months may be necessary.
ď Steroids. Topically, by periocular or intravitreal
(triamcinolone acetate 0.05â0.1 ml of 40 mg/ml) injection.
ďCarbonic anhydrase inhibitors given systemically or topically.
ďIntravitreal anti-VEGF agents.
ďPars plana vitrectomy may be useful for CMO refractory to medical
therapy, even in eyes without apparent vitreous disturbance.
67. Dysphotopsia
⢠Up to 1 in 10 patients complain of annoying visual
phenomena following uncomplicated cataract surgery.
⢠Symptoms. A dark shadow in the temporal periphery
(negative dysphotopsia â often the most troublesome),
scintillations, haloes, peripheral or central flaring or flashes
(positive dysphotopsia) and possibly monocular diplopia.
Treatment:
⢠Encouraging the patient that the symptoms usually improve
over time, both because of anatomical changes
(e.g. capsulorhexis edge thickening) and because the
brain is able to ignore unwanted images.
⢠IOL exchange (round-edged) may be considered.
68. Corneal decompensation
⢠Corneal oedema is very common postoperatively but is
usually mild and transient.
⢠Eyes with pre-existing corneal endothelial pathology,
particularly low cell counts, are at increased risk.
⢠Causes of more marked oedema include dense nuclei
requiring high phacoemulsification energy, complicated or
prolonged surgery, pseudoexfoliation, intraoperative
endothelial trauma and elevated postoperative IOP.
⢠Use of a dispersive viscoelastic, and possibly a scleral
tunnel incision, may help to protect the corneal endothelium
during surgery in higher-risk eyes.
69. Ptosis
⢠Mild ptosis, probably secondary to a variety of
mechanisms, is common after cataract surgery, but
usually improves; observation for at least a year
postoperatively is recommended in most cases.
70. Malposition of the IOL
⢠Although uncommon, malposition
may be associated with both optical
and structural problems.
⢠Significant malposition may require
repositioning or replacement,
occasionally with an iris or sclerally
fixated lens.
71. Retinal detachment
⢠Rhegmatogenous retinal detachment (RRD) is uncommon.
⢠Preoperative risk factors include lattice degeneration and
retinal breaks â both are generally treated prophylactically
prior to cataract surgery (and probably laser capsulotomy)-
and high myopia.
⢠The key intraoperative risk is vitreous loss.
⢠Pars planavitrectomy is usually the surgical modality
employed for pseudophakic RRD.