Treatment for hsv stromal keratitis last,home remedies for constipation in 2 year old child,can a swab test for herpes results - Easy Way

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HSV TreatmentWhen a patient first presents with an HSV episode, either epithelial or stromal, it may appear to be the first occurrence. Herpes can lie latent in the trigeminal ganglion for decades before erupting into a recurrence such as this epithelial dendrite. The Herpetic Eye Disease Study was a series of randomized, double-masked placebo-controlled clinical trials that looked at various approaches to treating ocular herpes simplex virus keratitis. HSV ProphylaxisAnother important finding of the HEDS was the effectiveness of antiviral prophylaxis in preventing recurrences of HSV disease. A 36-year-old female presented to the Emergency Treatment Center (ETC) of the University of Iowa Hospitals and Clinics (UIHC) with one day of right eye pain, photophobia and decreased vision. The following day, her symptoms did not resolve and was therefore referred to the UIHC Cornea service for further evaluation.
During the first ten days of treatment, all subjective symptoms resolved with the exception of mild blurring of vision.
She returned for routine follow-up one month after discontinuation of topical corticosteroids. HSV keratitis can present with involvement of the corneal epithelium, stroma, or endothelium, with or without associated inflammation of the anterior chamber (Table 1).[1-4] Pathophysiologic manifestations may be related to the presence of live virus, immunological reactions to viral antigen, or secondary to previous herpetic injury ("metaherpetic"), particularly the loss of corneal sensation. The diagnosis of HSV keratitis is primarily clinical, although additional tests may be useful in providing confirmation, but never exclusion.[1-4] The Tzanck (Giemsa) smear of multinucleated epithelial cells is a quick test with high specificity but low sensitivity.
HSV epithelial keratitis invariably involves active viral proliferation.[1-4] The classic epithelial dendrite is the most common presentation of epithelial disease (Figure 1). HSV stromal keratitis is associated with the highest and most severe morbidity of any ocular herpetic disease.[1-4] Although this condition frequently follows previous HSV epithelial keratitis, it can be the initial presentation of ocular herpetic disease. HSV disciform (endothelial) keratitis is a cell-mediated immune reaction to corneal endothelial tissue that presents with diffuse stromal edema.[1-4] In approximately half of cases, there is no prior history of HSV epithelial keratitis.
HSV keratouveitis may occur as a separate entity or in association with herpetic epithelial, stromal, or endothelial disease.[1-4] It may be granulomatous or non-granulomatous and may, in some cases, be associated with live virus (Figure 6). Metaherpetic manifestations of HSV keratitis include neurotrophic keratopathy and microbial (i.e. Although HSV epithelial keratitis is self-limited in most cases, the rationale for aggressive antiviral therapy is to prevent corneal nerve damage and potential future immunologic disease.[1] Prior to the advent of antiviral therapy, simple epithelial debridement was the treatment of choice.
The most common mistake in the management of HSV keratitis is premature termination of topical steroid therapy. In our clinics, the taper for stromal keratitis and keratouveitis is only one-third complete when it has been reduced to prednisolone acetate 1.0% once daily. Our preferred steroid use and taper regimens are based upon whether or not the patient is a steroid-responder. The introduction of oral antiviral prophylaxis constituted a major advance in the management of chronic herpetic eye disease. There are no uniformly accepted guidelines governing the use of antiviral prophylaxis in conjunction with topical corticosteroid use in situations where live viral manifestations are not present. Late surgical intervention is indicated for management of intractable corneal pain or visual impairment associated with herpetic disease. Stromal keratitis- Acute: mid-deep stromal infiltrate with intact epithelium and minimal necrosis.
Although the treatment algorithm for HSV has remained the same for quite some time, clinicians continue to debate certain treatment aspects, such as when or if to use steroids for certain kinds of HSV, Dr. One common form of HSV is epithelial disease, for which about 60,000 cases occur each year in the United States, said Francis S. In addition to removal of the viral load, the typical treatment for this form of HSV has been topical trifluridine (Viroptic, GlaxoSmithKline, Middlesex, United Kingdom) nine times a day for the first few days and then a decreasing dose. Additionally, trifluridine is not viral-specific and has led to significant toxicity and a risk for repeated infections, Dr.
For these reason, clinicians moved to the use of oral antivirals such as acyclovir (various manufacturers) or valcyclovir (Valtrex, GlaxoSmithKline, Middlesex, England) to replace or supplement topical treatment.
Steroids are used to quiet the eye, and anti-viral medications?oral or topical?are used to prevent the recurrence that steroids can trigger, Dr. Other forms of HSV include endothelialitis, which presents with herpetic precipitates and edema and requires anti-viral treatment along with steroids; and HSV iritis, which requires anti-viral medication.
Research into broader issues related to HSV, such as the disease latency and whether a vaccine would be effective, is particularly valuable and farther reaching for other forms of HSV in the body, Dr. A study published in January 2010 in the Future Microbiology on mucosal treatments for HSV also supports the idea of disease prevention. Although there has not been much research into immunomodulation for ocular HSV, this could be another treatment option, the investigators wrote.
The investigators' report also addresses the promising role and potential challenges of vaccines for HSV. Science, Technology and Medicine open access publisher.Publish, read and share novel research. Unfortunately, the unknown is exactly what herpes simplex virus sufferers face, and what we ophthalmologists have to deal with. The dendritic form of herpes recurrence accounts for around 80 percent of cases, but is the least likely to permanently damage vision.
For this less common but more sight-threatening form of herpes recurrence, treatment with corticosteroids offers a significant benefit, as demonstrated by the Herpetic Eye Disease Study (See "HEDS Sheds Light on Herpes"). Slit lamp photo demonstrating classic epithelial dendrites in our patient after fluorescein staining. Most cases (> 90%) are unilateral, but bilateral cases may occur, especially in atopic or immunocompromised patients.
It represents areas of epithelial breakdown due to cell destruction by proliferating virus and is best demonstrated after fluorescein staining under cobalt blue lighting. The vast majority of cases are an immune stromal keratitis (ISK), which involves the antibody-complement cascade against retained viral antigens in the stroma. Accordingly, acute-onset, unilateral corneal edema should be considered to be due to herpetic eye disease unless proven otherwise. A guiding principle is that prior to the onset of immune-mediated disease, control and elimination of epithelial manifestations is the highest priority. Our experience is that the optimal initial frequency is hourly for NSK, every two hours for ISK, and every three hours for disciform keratitis.
In such cases, there is almost invariably a reappearance of corneal inflammation that is mislabeled as "recurrent" disease, when, in fact, it is actually a "pseudo-recurrence" that is merely a continuation of the same immunological reaction that has now become clinically apparent due to therapeutic withdrawal.
Due to the very high benefit-to-risk ratio associated with oral antiviral therapy, it is our preference to use these medications in every instance in which topical corticosteroids are utilized.
For painful eyes without visual potential, a Gunderson flap will reduce chronic inflammation and eliminate pain. Full dose oral antiviral followed by prophylactic oral antiviral (for 1 year up to indefinitely). Determining the type of HSV present in the eye and then treating that specific disease appropriately while avoiding additional flares and visual damage can be perplexing, said Edward J. Holland said he typically treats this kind of HSV with Zirgan for 14 days but will also use oral anti-viral medications. Holland compares the side effects from steroids?including higher IOP or secondary cataract?against the side effects of visual damage?including the possible need for a keratoplasty?and would rather risk the former than the latter.
Holland usually starts patients with a stronger steroid dose and will taper to a lower dose as necessary. Conjunctival intraepithelial neoplasia (CIN) grade 3 with and without fluorescein staining. Pacheco1, 2[1] Moorfields Eye Hospital, London, UK[2] West Hertfordshire Hospitals, NHS trust, UK1.
Herpes can lie dormant for years, then, triggered by an as yet unknown mechanism, manifest itself in the eye with debilitating results. Around 5 percent of HSV patients have blepharitis, conjunctivitis or a combination of the two. The primary infection to the face, mouth, eye or nose often goes unnoticed to the patient, and the herpes settles in the central nervous system where it remains latent in the trigeminal ganglion for the rest of the person's life. If the stromal disease is concomitant with the epithelial dendrite, however, using steroids will make the situation worse. Researchers randomized 57 HSV stromal keratitis patients to treatment with steroids and 49 to placebo, with both groups receiving topical trifluridine.
The comparative effects of famciclovir and valacyclovir on herpes simplex virus type 1 infection, latency, and reactivation in mice. In chronic cases, demonstration of decreased sensation by Cochet-Bonnet aesthesiometry can be helpful in differentiating true recurrent dendritic keratitis from pseudo-dendritic keratitis, especially that related to recurrent epithelial erosions. The presence of keratouveitis mandates a thorough funduscopic examination to exclude concomitant acute retinal necrosis. However, once immune-mediated disease has been established, management of stromal or endothelial manifestations, with their potential for irreversible visual impairment, has higher priority than control of epithelial disease. However, corneal toxicity related to the topical antivirals available in the United States led to a preference on the part of many specialists to rely exclusively on equally effective systemic therapy. If concomitant epithelial disease is present, full systemic antiviral dosing is also required since steroid therapy exacerbates this condition. For eyes with post-herpetic scarring and good visual potential, the surgical procedure is based upon the corneal pathology.
Drugs to treat HSV that are new to the market or that are on the horizon give clinicians additional reasons to reflect on current treatment regimens. Campbell Ophthalmic Microbiology Laboratory, University of Pittsburgh School of Medicine, Pittsburgh. A patient with stromal keratitis typically has a post-infectious reaction shortly after a lesion has occurred.


However, the use of steroids in these patients is a big controversial in HSV treatment, Dr. Researchers and clinicians alike are hoping for single agents that can tackle both adenovirus and HSV. A small proportion of patients, around 1 percent, may have either iritis alone or keratouveitis—serious iritis concomitant with epithelial or stromal disease. For a recurrence of the dendritic form, I use what most ophthalmologists across the country currently use: topical trifluridine 1% (Viroptic, Glaxo Wellcome, or generic) eight times a day (q2h) until the epithelium heals, usually after five to 10 days. In such cases, it's best to wait until the epithelial infection has healed before treating the stromal inflammation. The regimens were tapered over 10 weeks.The steroid treatment reduced the risk of persistent or progressive stromal keratitis by 68 percent, and the treatment group had a much shorter time to resolution of its inflammation than the control group.
There was, however, patchy anterior stromal inflammation in the visual axis that did not resemble the characteristic post-dendritic "footprints" and was felt to represent early immune stromal keratitis (Figure 2).
On examination, the epithelium was intact but there was mild patchy anterior stromal haze in the same distribution in the visual axis as before.
Bacterial and fungal cultures, along with confocal microscopy, can be used to rule out other etiologies of microbial keratitis. Our preference is to use acyclovir 400 mg PO five times daily or valacyclovir 1000 mg PO three times daily. Phototherapeutic keratectomy may be utilized as a keratoplasty-sparing intervention for superficial corneal scarring. These cases are often accompanied by changes in vision, a foreign body sensation, and possible nerve damage, Dr. Although the keratitis may clear up on its own, treatment aims to prevent further progression to the stroma and to prevent vision- or eye-threatening conditions, Dr. I prefer to quiet the stroma with aggressive topical steroids and then do an extremely slow tapering.
The concept originates from the Greek word “?????-(kerat)” that means “horn” and “itis” which represents the classical suffix in medicine for inflammation.
Herpes is responsible for such a variety of ocular effects that it overlaps with many other eye diseases, and is often on the differential diagnosis of any kind of inflammatory eye disease of the anterior segment that has an unclear etiology.
The most common form, the dendrite, is generally easy to recognize and to treat, and usually has a lesser impact on vision in comparison to stromal keratitis. The steroids didn't influence recurrence rates, however.1 Unfortunately, a separate clinical trial in which patients received oral acyclovir along with steroids and trifluridine showed no additional benefit. Treatment was initiated with topical prednisolone acetate 1.0% QID, while maintaining antiviral and prophylactic antibiotic coverage.
There are unsubstantiated concerns that this procedure may be associated with activation of immunological stromal keratitis; in any case, perioperative use of full antiviral therapy followed by a prolonged prophylactic course obviates this issue.
Originally, we thought that the epithelial infection came first, with the cornea acting as a sort of blotter, soaking up viral antigen and setting up an immune reaction in the stroma that arose once the epithelium healed. In this study, 104 patients were randomized to receive oral acyclovir or placebo for 10 days. There was no peripheral stromal vascularization, perineuritis, endothelial or anterior chamber inflammation.
Although most practitioners prefer a short course of therapy, we treat our patients for a total of 14 to 21 days to ensure complete eradication of replicating organisms. For deeper stromal scarring, penetrating or deep anterior lamellar keratoplasty are the procedures of choice. Its highly complex, almost indestructible, collagen conformation gives it strong physical properties that made the ancients to name it like that.Keratitis is a frequent clinical condition. Famciclovir and valaciclovir differ in the prevention of herpes simplex virus type 1 latency in mice: a quantitative study.
After successful treatment, therapy can be discontinued without tapering, unless long-term prophylaxis is used (see below; antiviral prophylaxis).
The prognosis for graft survival has improved dramatically over the last quarter century since the introduction of oral antiviral prophylaxis. So, once the virus is no longer live, he will often initiate steroids during the second week and continue use of an oral anti-viral agent for prophylaxis. A correct initial diagnosis and treatment are critical in limiting the amount of residual damage and scarring left to the cornea, as the preservation of its transparent property is critical in the recovery and maintenance of useful vision in any affected patient.In the present chapter a description of the clinical findings in different forms of keratits, intend to illustrate ophthalmic practitioners with the different potential diagnosis associated to this condition and through this, to orientate them in the useful investigations that will lead to the correct diagnosis. Some patients can develop stromal keratitis or endotheliitis without any previous apparent epithelial keratitis and vice versa.
At four months, three quarters of the acyclovir group and 74 percent of the placebo group had failed the treatment. This can be attributed to reduced recurrence of herpetic epithelial keratitis, a condition that is frequently associated with acute endothelial rejection episodes. Occasionally, they happen together, which presents a very difficult case to treat.Though researchers have tried to uncover what triggers a recurrence, the question continues to confound. Neither ISK nor NIK is self-limited and failure to provide appropriate pharmaceutical intervention will result in progressive corneal scarring and visual impairment. In the unusual situation of corneal endothelial decompensation due to neglected or recalcitrant endothelial keratitis, endothelial keratoplasty can be performed if stromal disease has not been present. Some have suggested that ultraviolet light exposure may cause recurrences, as we know that dermatologists in Colorado see a lot more recurrent herpes of the skin and face when people go skiing and are exposed to large amounts of UV. In this study, patients with HSV iridocyclitis were randomized to receive a 10-week course of either oral acyclovir or placebo along with topical trifluridine and topical prednisolone.Unfortunately, the researchers couldn't recruit enough patients for this particular arm of the study, so there was no definitive answer as to whether the oral antiviral helped. Effect of famciclovir on herpes simplex virus type 1 corneal disease and establishment of latency in rabbits.
There is very little permanent vision loss, though the decreased vision can be dramatic during the course of the disease.
There seemed to be a benefit early on in the follow-up period before the study was discontinued.3 Dr.
After a lifespan of approximately twenty-four hours the superficial cells are often shed into the tear film.
The HEDS analysis, however, found no clear-cut link between ocular herpes and sunlight, fever, stress or other suspected triggers. Wilhelmus says he's in the middle when it comes to using oral acyclovir for this indication. The epithelial stem cells are located in the limbal region (this is the area between the cornea and the sclera), within the palisades of Vogt mainly located in the superior and inferior limbus. After a recurrence, people may selectively recall an event that may not be causal.Here are our current treatment strategies. The indemnity of the corneal stem cells is essential for the maintenance of a healthy corneal epithelium and they also act as a barrier, preventing conjunctival epithelium from growing on to the clear cornea.The stromal layer makes up to 90% of the corneal thickness, it is composed of regularly orientated collagen type I and V fibrils layers whose space is maintained by proteoglycan ground substance (chondroitin and keratan sulphate) with interspread modified fibroblast cells (keratocytes). The superficial portion of the stroma is called the Bowman membrane that constitutes an acellular portion of the stroma.
It is, in part, the congruent and precise distribution of the collagen fibers of the stromal layer that permits the structure of the cornea to be transparent, letting the spectrum of visible light to pass through into the inner structures of the eye to finally allowing us to see.The endothelial layer consists of a single layer of hexagonal cells that sits on a fine basal membrane made of a latticework of collagen fibers named the Descemet membrane. This layer and its indemnity is also crucial in keeping the transparency of the cornea by reducing the amount of water in the corneal stroma through an active membrane channels mechanism that allows the movement of water from the stroma into the anterior chamber of the eye. In patients with a history of stromal keratitis, the incidence of another episode of stromal keratitis was only 14 percent in the acyclovir patients vs.
In a paper published by Dua et al., experimental and electron microscopy studies revealed the existence of a thin layer (15 microns) of corneal collagen between the corneal stroma and the Descemet membrane. The drug had an effect on non-ocular HSV disease, as well, with a risk of recurrence of 36 percent in the placebo group compared to just 19 percent for the treated patients.4In another study, oral acyclovir didn't prove to be as effective in preventing stromal keratitis in patients with active epithelial disease, however.
This layer has physical properties that are different to the stromal layer and the Descemet membrane, having the highest resistance to pressure among the corneal layers.
One hundred fifty-three patients with epithelial disease received trifluridine and 400 mg of acyclovir five times daily for three weeks.
In the HEDS, we used prednisolone phosphate 1% (Inflamase Forte), but other steroids are probably equivalent. Its discovery has implications in corneal surgical procedures.Macrophages and dendritic antigen presenting cells are present mainly in the epithelium and the anterior stroma. Since we know that steroids can make a herpes infection worse, and an infection that recurs during steroid use for stromal inflammation can be very serious, we also use chronic antiviral prophylaxis during the steroid course.
Stromal keratitis or iritis developed in 11 percent of the acyclovir group and 10 percent of the controls. Though the clinician can get a similar preventive effect from either topical trifluridine or oral acyclovir (Zovirax, GlaxoSmithKline), we use the former since it matches the delivery route of the topical steroid.My steroid regimen initially consists of 1% prednisolone four to eight times a day. The sensory innervation of the cornea derives from the trigeminal nerve (V1) and it is mainly distributed in the sub-epithelial region and anterior stroma as sub-epithelial plexus, it is therefore at this level that we can find most nerves in the corneal structure.3.
Keratitis: Clinical historyA detailed clinical history is crucial in the diagnosis keratitis.
Demographic aspects like age, sex, ethnicity and occupation are always needed and can orientate to certain specific associated pathologies or risk factors.
The steroid course I outlined may be too slow for some or too rapid for others, so I do it on a case-by-case basis, basing the decision on the level of disease severity and the pace of patient improvement.Visual outcomes in patients who develop the stromal form of HSV keratitis aren't as good as those for the epithelial infection. The use of contact lenses is important to note in detail including the type of lenses, length of use, cleaning systems used and daily routines (i.e. Many stromal keratitis patients will have a residual corneal scar that can cause substantial vision loss if it's located in their visual axis.Further episodes of the stromal form can cause progressive vision loss due to the toll they take on the cornea over time with repeat recurrences. It's in these stromal keratitis patients that I'm more aggressive with my prophylactic use of oral acyclovir, as explained below. History of any recent injury to the eye or systemic disease that might relate to corneal compromise is also needed. Keratitis: Anatomical classificationKeratitis can be classified on the portion of the cornea affected.


Some of the epithelial defects are pathognomonic as it is the dendriform seen in herpes simplex virus keratitis, it is therefore important to note the size, shape and depth of the defect in any epithelial form, as it will certainly help not only in the diagnosis but also in the assessment of the progression or recovery of the affected patient.
In the case of the infiltrate, it is important to note the size, color and quality of the borders that can be of help in diagnosis and follow up.
Any satellite lesions need also to be assessed as well as the upper and lower tarsal plates in search for any foreign bodies or other associated lesions like calcareous concretions, meibomian gland cysts, papillae or follicles. The epithelial form of keratitis is extremely painful and at times enlarged or infiltrated corneal nerves can be seen. Usually the anterior stroma is also affected with an inflammatory cellular infiltrate surrounding the epithelial lesions, it has in general poorly defined borders. Corneal pannus can be seen as a result of previous episodes of epithelial keratitis in some cases.
The main finding in this type of keratitis is an infiltration of the collagen layers in the stroma by inflammatory cells, this can be seen at any depth, it can be unifocal or multifocal, with many different shapes and sizes, but usually has a very well defined and regular edge. There is in general some degree of anterior chamber cell reaction and at times keratic precipitates can be seen. Thickening of the cornea is another way to appreciate the cellular infiltration seen in these cases. Characteristic features include keratic precipitates, descemet folds and almost invariably a significant anterior chamber cells reaction.
Secondary diffuse corneal thickening at later stages can be seen as a result of impaired endothelial function.
Infectious keratitis As an important component of the anatomical anterior wall of the eye, the cornea is a structure highly exposed and vulnerable to external pathogens. The use of contact lenses constitutes an accumulative risk for developing infectious keratitis, as it is also any history of chronic corneal disease or the use of topical steroids.
Any corneal epithelial disruption as seen sometimes in dry eye syndrome, severe blepharitis and injuries are able to cause disruptions of the epithelial barrier as seen in corneal abrasions, post-surgical procedures or corneal foreign bodies that can predispose to corneal infections. ViralBy far the most frequent cause of viral keratitis is the one caused by herpes viruses type 1 and 2, also varicella-zoster virus can sometimes be responsible in the context of herpes zoster ophthalmicus. The typical form of viral keratitis is epithelial, with a characteristic dendritiform epithelial defect and secondary infiltrate very easy to diagnose with fluorescein staining (Fig 2). The epithelial defect seen in herpes zoster infection is classically described as geographic rather than dendritiform. In less than 10% of the cases the compromise can be primarily stromal or endothelial that typically is associated with elevated intraocular pressure (Fig 3).
BacterialFor bacteria to act as a pathogen in the cornea, it is necessary a disruption in the epithelial barrier like the ones seen in injuries (corneal foreign bodies and corneal abrasions) or a significant risk factor like contact lens wear or use of topical steroids. Almost any bacterium is able to cause keratitis, the most frequently involved are the ones that are the gram positive microorganisms found in the eyelids margin and skin (staphylococcus sp, streptococcus sp), sometimes gram negative bacteria like pseudomonas sp can be isolated. The typical keratitis caused by bacteria is epithelial and the presentation is acute; it usually has a well-defined epithelial defect surrounded by a stromal grayish infiltrate, which has a depth and extension proportional to the time of onset to presentation. The speed and extension of the compromise also depends on the pathogenicity of the bacteria involved, often being worse in the case of gram-negative microorganisms (Fig 4). Slow growth bacteria like streptococcus viridans can give the aspect of crystalline keratitis, as the invasion of the corneal stroma is very slow following the branching of the collagen layers. The diagnosis is usually confirmed by a corneal scrape of the lesion that can be sent for microbiological studies; in any ophthalmic setting it is crucial to perform a gram stain, blood agar, brain heart infusion (BHI) and cooked meat broth (CMB) cultures to be able to isolate the pathogen and determine the sensitivities to antibiotic therapy. The gram stain can give immediate initial information of the type of microorganism excluding other causes of keratitis. FungalIt is a rare cause of keratitis in temperate climates but common cause of keratitis in tropical countries. Usually occurs following trauma to the cornea especially the one caused by vegetable matter. The course is indolent sub-acute, it takes weeks for the patient to seek help as it does not cause significant discomfort in the early stages as fungi are slow in replicate. The clinical presentation is that of a stromal form of keratitis, an epithelial defect can or not be present, but usually is small compared to the amount of stromal infiltrate associated. The stromal infiltrate is always irregular in the borders and poorly defined, it has a ‘fluffy‘ aspect and very white (Fig 5). In very advanced cases the infiltration of the stroma can be full thickness with associated anterior chamber whitish solid hypopyon. AcanthamoebaIt is a rare cause of keratitis caused by one of the most common protozoa found in soil and water.
The epithelial component is characteristically a large epithelial defect with abundant sub-epithelial infiltrate and enlargement of the corneal nerves that have been described as invaded by the pathogen at some stages of the disease, causing intense pain; this is perhaps the most painful form of keratitis, and this is regarded as a significant clinical finding at the time of diagnosing contact lens related keratitis. The stromal infiltrate is grey-whitish with irregular, multiple or single lesions, sometimes satellite areas can be seen (Fig 6 a & b). The diagnosis is confirmed by scrape or corneal epithelial biopsy sent for microbiological studies, it is important to repeat the gram and all the previously described medias (blood, BHI, CMB, Sabouraud’s) and add the E. AtypicalThis term is used to describe an infectious keratitis caused by atypical microorganisms like mycobacterium. The pattern of keratitis can be very confusing as it occurs usually in the context of postoperative, traumatic or previous corneal pathology situations. The course is always chronic, unresponsive to multiple previous treatments and the clinical picture varies between an epithelial and stromal form of keratitis with atypical features (Fig 7).
Perhaps the most important aspect is the invariable presence of a significant risk factor like previous surgery, as this pathogen needs a significant break in the epithelial barrier to be able to invade and cause the condition due to its relative large size.
Inflammatory — Autoimmune keratitis (Non suppurative keratitis)Any condition that can induce an inflammatory response of the cornea can be classified in this group of causes of keratitis.
AutoimmuneLike in any other autoimmune condition where the main target is the collagen in the body, the so-called autoimmune collagen or connective tissue diseases can be responsible for various forms of inflammatory keratitis, due to the high content of collagen seen in the corneal and scleral tissue. In some patients the cornea is the initial manifestation of the autoimmune process sometimes well in advance before the systemic condition manifests.
The collagen diseases related to peripheral corneo-scleral ulceration or sclero-keratitis, include systemic lupus erythematosus, rheumatoid arthritis, Wegener’s granullomatosis and polyarteritis nodosa. The form of keratitis seen in theses cases is epithelial with a significant stromal component mainly in the form of subtle infiltrate with severe stromal melting and associated episcleral or scleral vasculitis (Fig 8).
Non autoimmuneIn this group, we find conditions that can compromise the delicate functional triad between the cornea, the tear film and the lids.
If any of these is affected it will indirectly affect the anatomy and function of the other, potentially causing an inflammatory keratitis.
Lids conditions like blepharitis, rosacea, lagophthalmos, entropion, ectropion, tarsal calcareous concretions or tear film dysfunctions like the ones seen in Sjogren’s or severe dry eye syndrome can directly or indirectly cause keratitis in the form of marginal keratitis (Fig 10), phlyctenular keratoconjunctivitis and sometimes diffuse punctate keratitis as seen in Thygeson’s keratitis. Usually the clinical pattern in this form of keratitis is epithelial with isolated or multiple epithelial defects and sub-epithelial superficial mild infiltrates (Fig 11), filaments can also sometimes be seen.
Conjunctival intraepithelial neoplasia and squamous carcinoma Neoplasia of the conjunctival epithelial cells is more commonly seen in the elderly. There are different grades of penetration in the underlying tissue and the amount of cellular atypical cells defines also the degree of malignancy ranging from grade 1 to a carcinoma in situ.
They can be very polymorphic with multiple types of different clinical presentation, pigmented (melanotic) or not pigmented (amelanotic), they are of rapid growth and can invade distant organs especially lungs and liver. The most likely origin is at the conjunctival epithelial cells when some pigmentation is associated. Traumatic keratitisIn this group we can consider trauma by direct blunt injury with secondary corneal abrasion and corneal edema, or a surgical injury that damages the endothelial layer causing secondary corneal edema and endothelial failure with concurrent bullous keratopathy.
The type of keratitis seen in these situations is mainly endothelial and stromal with multiple descemet folds, stromal collagen fibers disorganization, keratic precipitates and often associated anterior chamber reaction. At later stages if the endothelial layer does not recover from the insult, a severe corneal edema may lead to epithelial bullous formation and consequent epithelial keratitis. A clear history of trauma might not be obvious and the clinicians are encouraged to obtain it from the clinical history remembering that sometimes the traumatic event can precede the clinical manifestation for many years (i.e.
Infectious causesIn viral herpetic keratitis cases, the drug of choice is acyclovir in topical or oral form depending on the extension of the keratitis within the corneal layers. A typical dose is ointment acyclovir 3% five times daily for one week or 400 mg orally five times a day for the same period. In children and the elderly the oral formulation is recommended due to difficulties in the application of the ointment.
In resistant cases the alternative treatment will be topical trifluorthymidine 1% (F3T) or vidarabine 3% (Vira-Atm).
If high intraocular pressure (IOP) is detected this also need to be treated with lowering IOP agents. Neoplasia associatedSurgical removal and biopsy is important as it is based on the histological diagnosis that further interventions like cryotherapy or radiotherapy might be indicated and planned.
The excision of any suspicious lesion ideally has to have a margin of two centimeters of healthy tissue to prevent recurrences. In CIN cases concomitant cryotherapy is useful as well as topical mytomicin C or 5 – fluorouracil at different concentrations. TraumaticIn cases of corneal abrasion the treatment of choice is to use topical antibiotic ointments to prevent infections and to pad the eye for 24 hours to allow epithelisation of the cornea, the use of preservative free cycloplegic drops initially to relief pain is recommended before padding. In blunt injuries the use of topical anti-inflammatory or steroid drops is useful depending on the severity of the inflammation. In cases of bullose keratopathy, endothelial corneal transplantation is highly successful, the use of highly osmotic drops like NACL 5% or bandage contact lenses can sometimes clear the corneal stroma and relief pain while waiting for a corneal donor.7. ConclusionA clear and simple approach to the differential diagnosis of keratitis has been presented.




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