2. DLK
• Known as Sands of Sahara,nonspecific diffuse interface keratitis,&LASIK
interface keratitis.
• Robert Maddox was the first surgeon who reported on this mysterious post-
LASIK inflammatory syndrome in 1996Â
• It is a postoperative interface sterile infammatory response to a variety of
mechanical and toxic insults that occurs in the 24–72-hour .
• The interface under the flap is a potential space; any cause of anterior stromal
inflammation may trigger the accumulation of white blood cells therein.
• The incidence is thought to be 1/200 to 1/500 cases ( 2-4% of patients
undergoing LASIK surgery )
3. ETIOLOGY
 The cause of DLK has remained something of an enigma.
 Holland etal. have demonstrated the risk of DLK from the bacterial cell wall 
endotoxins that build up in the wet autoclave reservoirs.
 Epithelial defects,DLK has been reported months after LASIK associated with
ocular inflammation,ocular trauma,and without an obvious etiology
 Other causes that have been proposed but remain unproven include cleaning
solutions,talc from gloves, meibomian gland secretions, microkeratome oil,
rust on instruments, blade debris, iodine skin cleaners,carboxymethylcellulose
lubrication drops & red blood cells in the interface
4. Clinically
• Symptoms : Asymptomatic to mild pain,
photophobia, and decrease in vision (usually a
hyperopic shift).
• The presentation of DLK can be graded
according to the severity of the presentation
13. • "Our strategy uses two agents that have anti-
collagenolytic activity, and we believe it may
have played a favorable role in this case by
halting autodigestion of the cornea and
preventing the further corneal ectasia and
progressive hyperopic shift that is the usual
scenario in stage IV DLK
14. We started treatment with oral doxycycline
twice a day for 2 weeks, then once a day for 1
month, and topical 10% sodium citrate 3
times a day. Dexamethasone eyedrops were
prescribed 5 times a day for 1 month, 3 times
a day for another month, and twice a day
during the third month, with artificial tears.
15. • (AAO) A surgeon should have a low threshold for lifting or irrigating underneath
the flap in suspected cases of severe DLK
• Recently the use of the topical steroid Durezol (Difluprednate)every 2 hours
and the femtosecond laser has essentially eliminated the need for interface
irrigation.
• PTK has been suggested as another treatment for DLK, this can cause
iatrogenic hyperopia
21. Pressure-induced stromal keratopathy
• The pressure-induced haze from PISK is associated with prolonged
corticosteroid treatment and usually presents after 10 days to 2 weeks. Key
dierentiators between DLK and PISK are that with DLK, the onset is earlier and
the IOP is not elevated
22.
23. Central Toxic Keratopathy
• is a rare, acute, noninflammatory central corneal opacification that can occur
within days after uneventful LASIK or PRK . The etiology is unknown but may be
related to enzymatic degradation of keratocytes.
• The onset is acute without worsening over time, unlike in most other interface
entities
• Marked hyperopic shift is often observed and tends to resolve over time.
• The use of topical hypertonic solutions for the treatment of central toxic
keratopathy has been proposed in anecdotal reports.
24.
25. Prevention
• avoid epithelial defects whenever possible.
• Reservoirs of wet autoclaves should be drained and cleaned at the end
of each day. Instruments should also be cleaned and dried atthe end of each
day.These maneuvers aim to eliminate the wet environment that could allow the
proliferation of Gram-negative bacteria that produce the bacterial cell wall
endotoxins.
• Dry autoclaves may offer a safer method of sterilization if DLK becomes
recurrent. Disposable instruments offer another method of avoiding a toxic
contamination of the LASIK process.
• Topical steroids should be used for all patients for a few days after LASIK to
suppress any subclinical inflammation