CASE REPORT
Diffuse Lamellar Keratitis: Confocal Microscopy Features of Delayed-Onset Disease Mrinal Rana, M.B.B.S., Parul Adhana, M.B.B.S., M.R.C.Ophth., and Balasubramanium Ilango, M.B.B.S., D.O., F.R.C.S., M.R.C.Ophth.
Objective: Diffuse lamellar keratitis is a fairly uncommon complication of laser in situ keratomileusis (LASIK) that usually occurs within 1 week of surgery. It is described as an inflammatory reaction in the lamellar interface characterized by a diffuse, white granular lamellar keratitis. Progression of the keratitis can result in scarring and significant visual loss. We report a case of bilateral diffuse lamellar keratitis (DLK) of delayed onset and look at confocal microscopic features of corneal interface. Case report: A 35-year-old male patient was referred with visual concerns and red eye. The patient had undergone LASIK procedure for high myopia 3 months previously. A detailed examination revealed a clinical presentation of DLK. A thorough account of the past revealed no pertinent medical history or risk factors for delayed-onset DLK after LASIK. The patient was put on topical antibiotics (ofloxacin, Exocin 3 mg/mL) and topical steroids (prednisolone acetate 1%, Pred Forte). Because of poor response to treatment, an interface washout was carried out and treatment with Pred Forte was continued. This helped in resolution of the condition in both eyes with residual faint, diffuse, corneal haze. Confocal microscopy was carried out before and after interface washout to assess features of DLK at cellular level after a delayed onset. Conclusions: The presence of inflammatory cells along with interface debris was noted in our case, which is unusual in stage 3 DLK with a delayed presentation as reported in literature. Although it is difficult to confirm without histology the type of inflammatory response seen, it is advocated that delayed presentation should also be treated quite intensively with steroids and any progression should be dealt with lifting up of the flaps to carry out interface washout. Key Words: LASIK—LASIK complication—DLK—Sands of Sahara— Confocal microscopy. (Eye & Contact Lens 2015;41: e20–e23)
D
iffuse lamellar keratitis (DLK) is defined as a sterile inflammatory reaction following refractive procedures like laser in situ keratomileusis (LASIK).1 The etiology and pathogenesis are unclear. Typically, the condition occurs within the first few days of LASIK but there are many reported cases of delayed presentation. Most cases are asymptomatic, but advanced forms of the disease can lead to stromal melting and scarring with permanent decrease in visual acuity if inadequate treatment is provided. We describe From the Department of Ophthalmology (M.R.), Birmingham and Midland Eye Centre, Birmingham, United Kingdom; and Department of Ophthalmology (P.A., B.I.), Wolverhampton Eye Infirmary, Wolverhampton, United Kingdom. The authors have no funding or conflicts of interest to disclose. Address correspondence to Mrinal Rana, M.B.B.S., Birmingham and Midland Eye Centre, City Hospital, Dudley Road, Birmingham; e-mail: [email protected] Accepted August 19, 2014. DOI: 10.1097/ICL.0000000000000088
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here confocal microscopic features of delayed-onset DLK presenting after 3 months.
CASE REPORT A 35-year-old male patient was referred by the optician for photophobia, blurring of vision, and redness especially in the left eye. The patient had recently undergone bilateral LASIK procedure for high myopia 3 months previously in India. The patient presented to the acute emergency clinic with reduced visual acuity of 0.24 (6/9) in the right eye and 0.4 (6/15) in the left eye. He was diagnosed with infective keratitis and commenced on topical antibiotic treatment (chloramphenicol minims 0.5% w/v; Bausch & Lomb, Surrey, United Kingdom). After 2 weeks of treatment and inadequate response, the patient was referred to the corneal team for further management. At his first presentation in the cornea unit, his visual acuity measured at 0.3 (6/12) in the right eye and 0.6 (6/24) log of minimal angle of resolution (LogMAR) scale in the left eye. Extensive fine white stellate precipitates were noted in the flap interface at peripheral cornea superiorly in the right eye and affecting the central cornea in the left eye. A clinical diagnosis of DLK was made. Topical prednisolone 1% (Pred Forte; Allergan Inc., Irvine, CA) and ofloxacin (Exocin, 0.3% w/v; Allergan Inc.) were commenced at presentation. At the subsequent follow-up in a week, there was minimal change in infiltrates and redness. The left eye looked more congested and the interface infiltrates had increased (Fig. 1A,B). Confocal microscopy was done to assess for features of this chronic presentation at cellular level. The patient was booked for a washout of the interface of his eyes, which was carried out after 3 days. Laser in situ keratomileusis flap outline was marked at the slitlamp and then the flaps were dissected using a sharp needle. The flaps were floated and uplifted using Rycroft cannula. The interface was washed with chloramphenicol and dexamethasone eye drops and swiped with cotton bud to remove the debris and cells and then the flaps were replaced into position. The swabs were sent to micropathology for culture and sensitivity. The swabs showed no growth even after 72 hours of incubation, which confirmed the diagnosis of DLK. The patient was put on frequent dose of topical prednisolone acetate (Pred Forte; 1%) and was regularly followed up weekly to assess for improvement or progression. After 3 months, his visual acuity improved to 0.0 (6/6) LogMAR each eye (Fig. 1C,D). A repeat confocal microscopy was done to reassess the corneal stroma for changes in the interface.
Confocal Microscopic Features Confocal scanning laser ophthalmoscopy (Heidelberg Retina Tomograph, HRT II; Heidelberg Engineering, Heidelberg, Eye & Contact Lens Volume 41, Number 6, November 2015
Copyright @ Contact Lens Association of Opthalmologists, Inc. Unauthorized reproduction of this article is prohibited.
Eye & Contact Lens Volume 41, Number 6, November 2015
Diffuse Lamellar Keratitis
FIG. 1. Top, left and right, diffuse lamellar keratitis in both eyes, affecting central visual axis in the left. Bottom, left and right, postinterface washout with no signs of any diffuse lamellar keratitis.
Germany) was used for cross-sectional imaging of the cornea. The addition needed was the Rostock Cornea Module, which allows for two-dimensional in vivo imaging of corneal cells with 1-mm resolution. A 400·400 m field of view was used to take comprehensive sequential images of the corneal structure. Topical anaesthesia (1–2 drops of sodium chloride proxymetacaine; Alcaine; Alcon Lab) and high-viscosity gel (Viscotears [2 mg/g]; carbomer [polyacrylic acid]; Novartis Pharmaceuticals, Surrey, United Kingdom) was instilled in the eyes. The patient was asked to fixate using an external target and the objective was brought in optical contact with the corneal surface by a disposable sterile Poly-methyl methacrylate cup and viscotears gel. Cross-sectional images were taken across the whole of the cornea manually while an electronic unit kept track of focal plane. On qualitative examination of the corneal epithelium, normal cellular architecture was noted. When examined, the interface showed extensive amounts of debris in the left eye (Fig. 2, top left). In the posterior stromal area, activated keratocytes were seen with mediated stellate/fusiform appearance (Fig. 2, bottom right). There was increased level of myofibroblastic transformation causing high level of enhancement. Keratocyte density was reduced as we progressed into the deeper layers of the corneal stroma. Inflammatory cells were noted close to the inter© 2014 Contact Lens Association of Ophthalmologists
face. There was a linear arrangement seen in the subepithelial layers just in front of the interface (Fig. 2, bottom left). The right eye showed scattered debris in the peripheral cornea (Fig. 3). On repeat confocal microscopy postinterface washout, the amount of cellular debris in the interface was drastically reduced. There was no sign of inflammatory cells in the anterior or posterior stroma (Fig. 4).
DISCUSSION Smith and Maloney first described the post-LASIK complication of DLK. It was also given the phrase “Sands of Sahara” by Bobby Maddox because of its characteristic wavy appearance. The usual occurrence of the condition is seen in the first week of laser surgery.3 There have been reports of its delayed onset and presentation. Haw and Manche4 reported six cases of late-onset DLK associated with an epithelial defect that occurred 2 to 12 months after surgery. Steinert et al.5 and Weisenthal6 also reported cases of late-onset DLK. It is commonly described as an inflammatory reaction in the lamellar interface, from debris of the microkeratome or sponges, talc from latex gloves, contaminated water in the autoclaves, meibomian gland secretions, 2
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M. Rana et al.
Eye & Contact Lens Volume 41, Number 6, November 2015
FIG. 2. Confocal microscopy features of left eye: before washout of interface. Top left, excessive inflammatory debris within the laser in situ keratomileusis interface with myofibroblastic transformation seen as increased enhancement. Top right, large inflammatory cells with black cytoplasm and hyperreflective nuclei and surrounding hyperreflectivity. Bottom left, linear arrangement of cells in the anterior layers in front of the interface. Bottom right, section of posterior stroma with activated keratocytes having a mediated stellate/fusiform appearance.
povidone-iodine, bacterial exotoxins and endotoxins, and soaps to clean equipment.5,7,8 McLeod et al. in their large review of 1,632 eyes undergoing sequential or simultaneous LASIK reported the occurrence of DLK in 126 eyes (7.7%). They looked at the risk of nonenvironmental or intrinsic patient-related factors causing the increase in risk to DLK. They found the risk to be higher in patients with poor lid conditions, increased meibomian gland secretions (well reported), and body’s host immune response.9 This certainly did not fit in our case at the time or clinical presentation, although they could have been different at the time of LASIK procedure.
There is little or no anterior chamber reaction and the conjunctiva is relatively uninflamed. In severe cases, it is associated with stromal necrosis and irregular astigmatism. Linebarger et al.1 in 1999 proposed a grading system depending upon the area of involvement and the intensity of the inflammatory response. Buhren et al.10 described confocal microscopic features of various stages of DLK. In their cohort of patients with stage 3 disease, some showed sparse infiltrate of round oval cells in the anterior stroma but large dense clusters in the interface. They also had numerous linear, spindle-shaped structures lying parallel to each other. The elements were known to be of
FIG. 3. Confocal microscopy features of right eye: before washout of interface. Left, peripheral debris with no signs of inflammatory cells. Right, reduced keratocyte density with some sparse inflammatory cells.
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Eye & Contact Lens Volume 41, Number 6, November 2015
Copyright @ Contact Lens Association of Opthalmologists, Inc. Unauthorized reproduction of this article is prohibited.
Eye & Contact Lens Volume 41, Number 6, November 2015
Diffuse Lamellar Keratitis
FIG. 4. Top, left and right, crosssectional views of the cornea with normal epithelium, debris-free interface, and anterior stroma with reduced density. Bottom left, subbasal plexus of nerves with remnants of debris. Bottom right, normal appearing keratocytes with reduced density.
granulocyte origin, which according the authors disappeared after the first week of occurrence, leaving white amorphous granular substance. Chung et al.11 described confocal microscopic features in their case of delayed-onset DLK with debris of variable size seen throughout the interface, along with occasional cells with features consistent with leukocytes. This was in contrast to our patient who even after 3 months of LASIK procedure had some chronic inflammatory cells lying just behind the interface. Some sections of the confocal images also showed the linear pattern of cell arrangement in front of the interface stroma, which according to the reports could be of granulocyte origin. The confocal microscopy is a good tool to unearth the structural changes in post-LASIK complications like DLK. The drawback normally is the lack of confirmation of the type of cells, which are seen in the cross-sectional images. It is really important to correlate the confocal features with clinical presentation and symptoms of the patient. This is important to distinguish between the stage 2 and 3 diseases because risk of advancement of the disease could lead to potentially scarring disease with poor prognosis. There is further need of proper study to look at a large cohort of patients presenting with DLK with confocal microscopy and outline the characteristic features of each stage of the disease.
© 2014 Contact Lens Association of Ophthalmologists
REFERENCES 1. Linebarger EJ, Hardten DR, Lindstrom RL. Diffuse lamellar keratitis: Diagnosis and management. J Cataract Refract Surg 2000;26:1072–1077. 2. Smith RJ, Maloney RK. Diffuse lamellar keratitis. Ophthalmology 1998; 105:1721–1726. 3. Lin RT, Maloney RK. Flap complications associated with lamellar refractive surgery. Am J Ophthalmol 1999;127:129–136. 4. Haw WW, Manche EE. Late onset diffuse lamellar keratitis associated with an epithelial defect in six eyes. J Refract Surg 2000;16:744–748. 5. Steinert RF, McColgin AZ, White A, et al. Diffuse interface keratitis after laser in situ keratomileusis (LASIK): A nonspecific syndrome. Am J Ophthalmol 2000;129:380–381. 6. Weisenthal RW. Diffuse lamellar keratitis induced by trauma 6 months after laser in situ keratomileusis. J Refract Surg 2000;16:749–751. 7. Kaufman SC, Maitchouk DY, Chiou AGY, et al. Interface inflammation after laser in situ keratomileusis. Sands of the Sahara syndrome. J Cataract Refract Surg 1998;24:1589–1593. 8. Holland SP, Mathias RG, Morck DW, et al. Diffuse lamellar keratitis related to endotoxins released from sterilizer reservoir biofilms. Ophthalmology 2000;107:1227–1233; discussion, 1233–1234. 9. McLeod SD, Tham VM-B, Phan ST, et al. Bilateral diffuse lamellar keratitis following bilateral simultaneous versus sequential laser in situ keratomileusis. Br J Ophthalmol 2003;87:1086–1087. 10. Buhren J, Baumeister M, Cichocki M, et al. Confocal microscopic characteristics of stage 1 to 4 diffuse lamellar keratitis after laser in situ keratomileusis. J Cataract Refract Surg 2002;28:1390–1399. 11. Chung MS, Pepose JS, Al-Agha S, et al. Confocal microscopic findings in a case of delayed onset bilateral diffuse lamellar keratitis after laser in situ keratomileusis. J Cataract Refract Surg 2002;28:1467–1470; 2002 ASCRS and ESCRS.
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Copyright @ Contact Lens Association of Opthalmologists, Inc. Unauthorized reproduction of this article is prohibited.
Diffuse Lamellar Keratitis: Confocal Microscopy Features of Delayed-Onset Disease Mrinal Rana, M.B.B.S., Parul Adhana, M.B.B.S., M.R.C.Ophth., and Balasubramanium Ilango, M.B.B.S., D.O., F.R.C.S., M.R.C.Ophth.
Objective: Diffuse lamellar keratitis is a fairly uncommon complication of laser in situ keratomileusis (LASIK) that usually occurs within 1 week of surgery. It is described as an inflammatory reaction in the lamellar interface characterized by a diffuse, white granular lamellar keratitis. Progression of the keratitis can result in scarring and significant visual loss. We report a case of bilateral diffuse lamellar keratitis (DLK) of delayed onset and look at confocal microscopic features of corneal interface. Case report: A 35-year-old male patient was referred with visual concerns and red eye. The patient had undergone LASIK procedure for high myopia 3 months previously. A detailed examination revealed a clinical presentation of DLK. A thorough account of the past revealed no pertinent medical history or risk factors for delayed-onset DLK after LASIK. The patient was put on topical antibiotics (ofloxacin, Exocin 3 mg/mL) and topical steroids (prednisolone acetate 1%, Pred Forte). Because of poor response to treatment, an interface washout was carried out and treatment with Pred Forte was continued. This helped in resolution of the condition in both eyes with residual faint, diffuse, corneal haze. Confocal microscopy was carried out before and after interface washout to assess features of DLK at cellular level after a delayed onset. Conclusions: The presence of inflammatory cells along with interface debris was noted in our case, which is unusual in stage 3 DLK with a delayed presentation as reported in literature. Although it is difficult to confirm without histology the type of inflammatory response seen, it is advocated that delayed presentation should also be treated quite intensively with steroids and any progression should be dealt with lifting up of the flaps to carry out interface washout. Key Words: LASIK—LASIK complication—DLK—Sands of Sahara— Confocal microscopy. (Eye & Contact Lens 2015;41: e20–e23)
D
iffuse lamellar keratitis (DLK) is defined as a sterile inflammatory reaction following refractive procedures like laser in situ keratomileusis (LASIK).1 The etiology and pathogenesis are unclear. Typically, the condition occurs within the first few days of LASIK but there are many reported cases of delayed presentation. Most cases are asymptomatic, but advanced forms of the disease can lead to stromal melting and scarring with permanent decrease in visual acuity if inadequate treatment is provided. We describe From the Department of Ophthalmology (M.R.), Birmingham and Midland Eye Centre, Birmingham, United Kingdom; and Department of Ophthalmology (P.A., B.I.), Wolverhampton Eye Infirmary, Wolverhampton, United Kingdom. The authors have no funding or conflicts of interest to disclose. Address correspondence to Mrinal Rana, M.B.B.S., Birmingham and Midland Eye Centre, City Hospital, Dudley Road, Birmingham; e-mail: [email protected] Accepted August 19, 2014. DOI: 10.1097/ICL.0000000000000088
e20
here confocal microscopic features of delayed-onset DLK presenting after 3 months.
CASE REPORT A 35-year-old male patient was referred by the optician for photophobia, blurring of vision, and redness especially in the left eye. The patient had recently undergone bilateral LASIK procedure for high myopia 3 months previously in India. The patient presented to the acute emergency clinic with reduced visual acuity of 0.24 (6/9) in the right eye and 0.4 (6/15) in the left eye. He was diagnosed with infective keratitis and commenced on topical antibiotic treatment (chloramphenicol minims 0.5% w/v; Bausch & Lomb, Surrey, United Kingdom). After 2 weeks of treatment and inadequate response, the patient was referred to the corneal team for further management. At his first presentation in the cornea unit, his visual acuity measured at 0.3 (6/12) in the right eye and 0.6 (6/24) log of minimal angle of resolution (LogMAR) scale in the left eye. Extensive fine white stellate precipitates were noted in the flap interface at peripheral cornea superiorly in the right eye and affecting the central cornea in the left eye. A clinical diagnosis of DLK was made. Topical prednisolone 1% (Pred Forte; Allergan Inc., Irvine, CA) and ofloxacin (Exocin, 0.3% w/v; Allergan Inc.) were commenced at presentation. At the subsequent follow-up in a week, there was minimal change in infiltrates and redness. The left eye looked more congested and the interface infiltrates had increased (Fig. 1A,B). Confocal microscopy was done to assess for features of this chronic presentation at cellular level. The patient was booked for a washout of the interface of his eyes, which was carried out after 3 days. Laser in situ keratomileusis flap outline was marked at the slitlamp and then the flaps were dissected using a sharp needle. The flaps were floated and uplifted using Rycroft cannula. The interface was washed with chloramphenicol and dexamethasone eye drops and swiped with cotton bud to remove the debris and cells and then the flaps were replaced into position. The swabs were sent to micropathology for culture and sensitivity. The swabs showed no growth even after 72 hours of incubation, which confirmed the diagnosis of DLK. The patient was put on frequent dose of topical prednisolone acetate (Pred Forte; 1%) and was regularly followed up weekly to assess for improvement or progression. After 3 months, his visual acuity improved to 0.0 (6/6) LogMAR each eye (Fig. 1C,D). A repeat confocal microscopy was done to reassess the corneal stroma for changes in the interface.
Confocal Microscopic Features Confocal scanning laser ophthalmoscopy (Heidelberg Retina Tomograph, HRT II; Heidelberg Engineering, Heidelberg, Eye & Contact Lens Volume 41, Number 6, November 2015
Copyright @ Contact Lens Association of Opthalmologists, Inc. Unauthorized reproduction of this article is prohibited.
Eye & Contact Lens Volume 41, Number 6, November 2015
Diffuse Lamellar Keratitis
FIG. 1. Top, left and right, diffuse lamellar keratitis in both eyes, affecting central visual axis in the left. Bottom, left and right, postinterface washout with no signs of any diffuse lamellar keratitis.
Germany) was used for cross-sectional imaging of the cornea. The addition needed was the Rostock Cornea Module, which allows for two-dimensional in vivo imaging of corneal cells with 1-mm resolution. A 400·400 m field of view was used to take comprehensive sequential images of the corneal structure. Topical anaesthesia (1–2 drops of sodium chloride proxymetacaine; Alcaine; Alcon Lab) and high-viscosity gel (Viscotears [2 mg/g]; carbomer [polyacrylic acid]; Novartis Pharmaceuticals, Surrey, United Kingdom) was instilled in the eyes. The patient was asked to fixate using an external target and the objective was brought in optical contact with the corneal surface by a disposable sterile Poly-methyl methacrylate cup and viscotears gel. Cross-sectional images were taken across the whole of the cornea manually while an electronic unit kept track of focal plane. On qualitative examination of the corneal epithelium, normal cellular architecture was noted. When examined, the interface showed extensive amounts of debris in the left eye (Fig. 2, top left). In the posterior stromal area, activated keratocytes were seen with mediated stellate/fusiform appearance (Fig. 2, bottom right). There was increased level of myofibroblastic transformation causing high level of enhancement. Keratocyte density was reduced as we progressed into the deeper layers of the corneal stroma. Inflammatory cells were noted close to the inter© 2014 Contact Lens Association of Ophthalmologists
face. There was a linear arrangement seen in the subepithelial layers just in front of the interface (Fig. 2, bottom left). The right eye showed scattered debris in the peripheral cornea (Fig. 3). On repeat confocal microscopy postinterface washout, the amount of cellular debris in the interface was drastically reduced. There was no sign of inflammatory cells in the anterior or posterior stroma (Fig. 4).
DISCUSSION Smith and Maloney first described the post-LASIK complication of DLK. It was also given the phrase “Sands of Sahara” by Bobby Maddox because of its characteristic wavy appearance. The usual occurrence of the condition is seen in the first week of laser surgery.3 There have been reports of its delayed onset and presentation. Haw and Manche4 reported six cases of late-onset DLK associated with an epithelial defect that occurred 2 to 12 months after surgery. Steinert et al.5 and Weisenthal6 also reported cases of late-onset DLK. It is commonly described as an inflammatory reaction in the lamellar interface, from debris of the microkeratome or sponges, talc from latex gloves, contaminated water in the autoclaves, meibomian gland secretions, 2
e21
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M. Rana et al.
Eye & Contact Lens Volume 41, Number 6, November 2015
FIG. 2. Confocal microscopy features of left eye: before washout of interface. Top left, excessive inflammatory debris within the laser in situ keratomileusis interface with myofibroblastic transformation seen as increased enhancement. Top right, large inflammatory cells with black cytoplasm and hyperreflective nuclei and surrounding hyperreflectivity. Bottom left, linear arrangement of cells in the anterior layers in front of the interface. Bottom right, section of posterior stroma with activated keratocytes having a mediated stellate/fusiform appearance.
povidone-iodine, bacterial exotoxins and endotoxins, and soaps to clean equipment.5,7,8 McLeod et al. in their large review of 1,632 eyes undergoing sequential or simultaneous LASIK reported the occurrence of DLK in 126 eyes (7.7%). They looked at the risk of nonenvironmental or intrinsic patient-related factors causing the increase in risk to DLK. They found the risk to be higher in patients with poor lid conditions, increased meibomian gland secretions (well reported), and body’s host immune response.9 This certainly did not fit in our case at the time or clinical presentation, although they could have been different at the time of LASIK procedure.
There is little or no anterior chamber reaction and the conjunctiva is relatively uninflamed. In severe cases, it is associated with stromal necrosis and irregular astigmatism. Linebarger et al.1 in 1999 proposed a grading system depending upon the area of involvement and the intensity of the inflammatory response. Buhren et al.10 described confocal microscopic features of various stages of DLK. In their cohort of patients with stage 3 disease, some showed sparse infiltrate of round oval cells in the anterior stroma but large dense clusters in the interface. They also had numerous linear, spindle-shaped structures lying parallel to each other. The elements were known to be of
FIG. 3. Confocal microscopy features of right eye: before washout of interface. Left, peripheral debris with no signs of inflammatory cells. Right, reduced keratocyte density with some sparse inflammatory cells.
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Eye & Contact Lens Volume 41, Number 6, November 2015
Copyright @ Contact Lens Association of Opthalmologists, Inc. Unauthorized reproduction of this article is prohibited.
Eye & Contact Lens Volume 41, Number 6, November 2015
Diffuse Lamellar Keratitis
FIG. 4. Top, left and right, crosssectional views of the cornea with normal epithelium, debris-free interface, and anterior stroma with reduced density. Bottom left, subbasal plexus of nerves with remnants of debris. Bottom right, normal appearing keratocytes with reduced density.
granulocyte origin, which according the authors disappeared after the first week of occurrence, leaving white amorphous granular substance. Chung et al.11 described confocal microscopic features in their case of delayed-onset DLK with debris of variable size seen throughout the interface, along with occasional cells with features consistent with leukocytes. This was in contrast to our patient who even after 3 months of LASIK procedure had some chronic inflammatory cells lying just behind the interface. Some sections of the confocal images also showed the linear pattern of cell arrangement in front of the interface stroma, which according to the reports could be of granulocyte origin. The confocal microscopy is a good tool to unearth the structural changes in post-LASIK complications like DLK. The drawback normally is the lack of confirmation of the type of cells, which are seen in the cross-sectional images. It is really important to correlate the confocal features with clinical presentation and symptoms of the patient. This is important to distinguish between the stage 2 and 3 diseases because risk of advancement of the disease could lead to potentially scarring disease with poor prognosis. There is further need of proper study to look at a large cohort of patients presenting with DLK with confocal microscopy and outline the characteristic features of each stage of the disease.
© 2014 Contact Lens Association of Ophthalmologists
REFERENCES 1. Linebarger EJ, Hardten DR, Lindstrom RL. Diffuse lamellar keratitis: Diagnosis and management. J Cataract Refract Surg 2000;26:1072–1077. 2. Smith RJ, Maloney RK. Diffuse lamellar keratitis. Ophthalmology 1998; 105:1721–1726. 3. Lin RT, Maloney RK. Flap complications associated with lamellar refractive surgery. Am J Ophthalmol 1999;127:129–136. 4. Haw WW, Manche EE. Late onset diffuse lamellar keratitis associated with an epithelial defect in six eyes. J Refract Surg 2000;16:744–748. 5. Steinert RF, McColgin AZ, White A, et al. Diffuse interface keratitis after laser in situ keratomileusis (LASIK): A nonspecific syndrome. Am J Ophthalmol 2000;129:380–381. 6. Weisenthal RW. Diffuse lamellar keratitis induced by trauma 6 months after laser in situ keratomileusis. J Refract Surg 2000;16:749–751. 7. Kaufman SC, Maitchouk DY, Chiou AGY, et al. Interface inflammation after laser in situ keratomileusis. Sands of the Sahara syndrome. J Cataract Refract Surg 1998;24:1589–1593. 8. Holland SP, Mathias RG, Morck DW, et al. Diffuse lamellar keratitis related to endotoxins released from sterilizer reservoir biofilms. Ophthalmology 2000;107:1227–1233; discussion, 1233–1234. 9. McLeod SD, Tham VM-B, Phan ST, et al. Bilateral diffuse lamellar keratitis following bilateral simultaneous versus sequential laser in situ keratomileusis. Br J Ophthalmol 2003;87:1086–1087. 10. Buhren J, Baumeister M, Cichocki M, et al. Confocal microscopic characteristics of stage 1 to 4 diffuse lamellar keratitis after laser in situ keratomileusis. J Cataract Refract Surg 2002;28:1390–1399. 11. Chung MS, Pepose JS, Al-Agha S, et al. Confocal microscopic findings in a case of delayed onset bilateral diffuse lamellar keratitis after laser in situ keratomileusis. J Cataract Refract Surg 2002;28:1467–1470; 2002 ASCRS and ESCRS.
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