Bhaskar Srinivasan
Dr. Bhaskar Srinivasan finished his graduation from Topiwala National Medical College, Mumbai, in 1997 and his masters in Ophthalmology (MS Ophthalmology) from Armed Forces Medical College, Pune, in 2002. He did his fellowship in cornea and external eye disease at Sankara Nethralaya, Chennai, following which he joined the same as faculty and is currently Senior Consultant Cornea and Refractive Services. His special interest is in managing various ocular surface diseases especially treating chemical injuries and Stevens–Johnson syndrome. He has experience with different kinds of keratoprosthesis and is a part of the ocular surface clinic at Sankara Nethralaya, a one of its kind in the world dealing with both ocular surface stem cell and various keratoprosthesis-based treatments. He is well versed in various kinds of corneal transplants (PK/DSEK/DALK), refractive surgery, and management of ocular surface tumors. He has 30 publications in peer-reviewed literature and has served as a faculty in various national and international conferences.
Geetha Iyer
Dr. Geetha Iyer, FRCS (Glasgow), completed her basic medical training in 1999. She did her postgraduate training in Ophthalmology and fellowship in cornea and external disease from Sankara Nethralaya, Chennai, India. She was awarded the best postgraduate student following completion of her ophthalmology training at Sankara Nethralaya and has been adjudged twice as the Best Associate Consultant during the early years of her tenure. She has been the recipient of awards for the Best Cornea Paper at both regional and national conferences. She has done a short-term observership in Ocular Surface Disorders with Dr. Scheffer C G Tseng, Miami, USA, in October 2006 and in Boston Type 1 keratoprosthesis with Dr. Claes H Dohlman in November 2006. She was trained and is being guided by Prof. Giancarlo Falcinelli in performing the MOOKP procedure. She has so far done more than 100 keratoprosthesis surgeries (MOOKP, Boston Type 1 and 2 Kpro).Dr. Geetha Iyer has to her credit publications in peer-reviewed journals and has conducted courses and presented papers in national and international meetings. She is actively involved in the management of ocular surface disorders and is currently working as Senior Consultant at the Ocular Surface Clinic and the Cornea Services, Sankara Nethralaya. Her areas of interest include pediatric penetrating keratoplasty, ocular surface tumors, ocular surface disorders including chemical injuries, stem cell transplants, keratoprosthesis, and in particular Stevens–Johnson Syndrome.
Mamta Agarwal
Dr. Mamta Agarwal completed her medical graduate degree from Government Medical College, Amritsar, India, in 1996. She passed Diplomate in National Board of Examination (DNB) at Sankara Nethralaya, Chennai, in 2002. She specialized in uveitis and intraocular inflammation at Medical Research Foundation, Sankara Nethralaya, Chennai (2002–2004). Further, she pursued an international fellowship in ‘Cornea, external diseases and uveitis’ at Francis I. Proctor Foundation, University of California, San Francisco, USA (2010–2011). She currently works as a Senior Consultant in Uveitis and Cornea services at Medical Research Foundation, Chennai. She has presented several papers at national and international conferences. She was also a grant winner for IUSG 2009 Venice course in Uveitis. She has authored Atlas of Uveitis and Scleritis published in 2005. She is a member of All India Ophthalmological Society, Uveitis Society of India, Cornea Society of India, American Uveitis Society (AUS), and Intraocular inflammation Society (IOIS). Her areas of interest include management of uveitis, scleritis, corneal infections, and ocular surface diseases.
Shweta Agarwal
Dr. Shweta Agarwal, D.O, a gold medalist from Pune university, completed her cornea fellowship from Sankara Nethralaya Chennai in 2009. She was awarded the Dr. D.S.Sardesai ophthalmology award from Pune university. She has quite a few publications in national and international journals and also a chapter on dry eyes in post graduate textbook of ophthalmology. She has been a primary investigator in two studies and a co-investigator in many studies related to cornea and ocular surface disorders funded by national agencies. She has been invited as a faculty in several national and international conferences. She was awarded the Best Cornea Free Paper in AIOC 2012. Her areas of interest are corneal diseases, ocular surface disorders, stem cells, and keratoprosthesis.
Introduction
HSV Keratitis
Herpes simplex viruses are ubiquitous human pathogens that can cause subclinical or active disease. HSV-1 is primarily responsible for ophthalmic and orofacial manifestations, and HSV-2 is responsible for genital infections, the exception being neonatal HSV infections where HSV-2 is the causative agent in 75 % cases [3, 4].
Pathophysiology
Humans are the only known host for the virus, and transmission is by close personal contact via salivary droplets or mucosal secretions. The incubation period is 1–28 days. Primary infection mostly result in a subclinical disease, and the virus travels via retrograde axonal transport to establish a dormant state in trigeminal root ganglion. Active disease is mostly due to recurrence of the infection in the same or new end organ or an inflammatory host response to the presence of viral antigens in the target tissue. There are reports of dormant HSV even in corneal tissue causing episodes of recurrent keratitis [4, 5].
Clinical Types
Primary Disease
It is usually seen in children or adolescents. In neonates in addition to causing ophthalmic manifestation, it can cause encephalitis and is life threatening. A viral prodromal phase with fever and malaise may accompany lymphadenopathy and periocular vesicles. Ophthalmic manifestations are mostly unilateral and consist of blisters involving the lids, blepharitis, follicular conjunctivitis, and dendritic conjunctivitis. Corneal involvement is in the form of punctuate epithelial keratitis and corneal microcyst which break down to form small dendrites without any stromal involvement. Prognosis is good but it leads to a state of latency and can cause recurrent infections.
Recurrent Disease
Most active disease in adults are due to recurrences, and the rates are about 36 % at 5 years and 63 % at 20 years after a primary episode. After a second episode, 70–80 % of patients had another recurrence within 10 years [4, 5]. The lesions in a recurrent disease are:
Blepharitis and dacryoadenitis – There can be focal pinhead-sized vesicular lesion which erupts in crops and contains serous fluid. The vesicles rupture with crusting and heal without scar formation unlike the lesions of zoster. Eyelid lesions may masquerade as edema/eschar in rare cases. The lid margin involvement might not show the typical blisters as they get ruptured during blinking and are called as weeping ulcers. Immune competent patients with blepharitis shed virus only for 2–3 days and heal in a week’s time. Rarely involvement of the lacrimal system with resultant scarring results in epiphora which is normally amenable to probing and syringing. A rare case of herpetic dacryoadenitis in an immunocompromised individual which required treatment with high-dose acyclovir has also been reported [4, 5].
Blepharoconjunctivitis/conjunctivitis – Conjunctiva shows congestion, follicular reaction, and dendritic lesions very similar to lesions in primary disease.
Keratitis – Recurrent keratitis can be of various types:
- 1.
Infectious epithelial keratitis
- 2.
Neurotrophic keratitis
- 3.
Immune stromal keratitis
- 4.
Necrotizing stromal keratitis
- 5.
Endothelitis
- 1.
Infectious Epithelial Keratitis
This could start as superficial punctuate lesion which then evolve to form corneal vesicles which stain negatively with fluorescein. These vesicles are virus-laden cells which then lyse to form the classical dendritic corneal ulcer as depicted in Fig. 37.1. The base of the ulcer stains with fluorescein and the edges with rose bengal. If not treated appropriately or in patients inadvertently started on steroids, the dendrite may progress to an amoeboid or geographic ulcer pattern as seen in Fig. 37.2. A form of epithelial keratitis involves localized limbal vascularization, anterior stromal infiltration, and dendritic lesion close to limbus; this entity is called as herpes marginal epithelial keratitis, and the patients are more asymptomatic as compared to the other epithelial keratitis. This marginal keratitis needs to be differentiated from staphylococcal immune keratitis which preferentially occurs at the two and ten or four and eight o’clock meridian with a lucid interval and intact overlying epithelium to begin with, whereas the herpetic marginal keratitis can occur at any sector and has dendritic epithelial defect, and vessels cross the limbus to reach the anterior stroma near the dendrite. Sometimes after the epithelial keratitis heals, a faint sub-epithelial dendrite-like lesion is seen in the anterior stroma called as footprints or ghost figures; these are telltale signs of previous herpetic keratitis [6–8].
Fig. 37.1
Classical dendritic lesion stained with fluorescein dye
Fig. 37.2
Conjunctival and corneal geographic ulceration in a patient on systemic immune suppression
Neurotrophic Keratitis
Decreased corneal sensations and the relative dry eye state predisposes to neurotrophic corneal ulceration that needs to be differentiated from geographic ulcer which is an infective state. The typical neurotrophic ulcer is an oval-shaped ulcer in the exposed area that has a dry irregular hazy base and smooth rolled edges with heaped up epithelium. Corneal stromal melting, scarring vascularization, and secondary infections are possible complications of neurotrophic ulcer [6–8].
Immune Stromal Keratitis
This is due to antigen-antibody reaction, and clinically there is single or multiple punctate stromal opacities associated with surrounding corneal haze due to inflammation and stromal edema. Edema is secondary to stromal inflammation rather than endothelial dysfunction. As shown in Figs. 37.3 and 37.4, there can be minimal anterior chamber reaction and ciliary flush. Repeated attacks of stromal keratitis and severity of each attack can predispose to corneal vascularization, lipid deposition, and scarring as depicted in Figs. 37.5 and 37.6 [6–8].
