BACTERIAL KERATITIS POWERPOINT PRESENTATION

Bacterial keratitis

1. BACTERIAL KERATITIS SANDEEP KRISHNAN PG RESIDENT OPHTHALMOLOGY

2. BACTERIAL KERATITIS Is a common sight-threatening condition. causing cellular infiltration of corneal epithelium or stroma , corneal inflammation and necrosis. If Untreated, leads to progressive tissue destruction with corneal perforation or extension of infection to adjacent tissue. Common predisposing factors include contact lens wear Trauma contaminated ocular medications impaired defense mechanisms altered structure of the corneal surface

3. BACTERIAL KERATITIS Bacterial keratitis usually develops only when ocular defences have been compromised . Some bacteria are able to penetrate a healthy corneal epithelium , includes Neisseria gonorrhoeae, Neisseria meningitidis, Corynebacterium diphtheriae Haemophilus influenzae Listeria monocytogenes

4. CAUSATIVE ORGANISMS gram positive cocci - Streptococcus pneumonia,Staphylococcus aureus,Staphylococcus epidermidis gram negative cocci -Neisseria gonorrhoea,Neisseria meningitidis gram positive bacilli - corynebacterium diphtheria, bacillus cereus gram negative bacilli- pseudomonas,Acinetobacter,enterobacteriaceae gram positive filamentous bacteria - actinomycetes,nocardia Non-tuberculous mycobacterium -Mycobacterium fortuitum,Mycobacterium chelonae

5. COMMON PATHOGENS Pseudomonas aeruginosa is a ubiquitous Gram-negative bacillus commensal of the GIT. The infection is typically aggressive and is responsible for over 60% of contact lens-related keratitis . Staphylococcus aureus is a common Gram-positive and coagulase-positive commensal of the nares, skin and conjunctiva. S. pyogenes is a common Gram-positive commensal of the throat and vagina. S. pneumoniae (pneumococcus) is a Gram-positive commensal of the upper respiratory tract. Infections with streptococci are often aggressive. Contact lens induced Pseudomonas keratitis

6. RISK FACTORS Contact lens wear , is the most important risk factor. Corneal epithelial compromise secondary to hypoxia and minor trauma is thought to be important, as is bacterial adherence to the lens surface. Soft lenses are at higher risk than those of rigid lenses. Trauma , including refractive surgery, has been linked to bacterial infection. Ocular surface disease such as herpetic keratitis, bullous keratopathy, dry eye, chronic blepharitis, trichiasis and entropion, severe allergic eye disease and corneal anaesthesia . Nasolacrimal duct obstruction is another important source of bacterial infection. Corneal foreign body removal without strict sterility precautions is an important source for devastating bacterial infections local or systemic immunosuppression , diabetes and vitamin A deficiency.

7. SYMPTOMS Pain. Photophobia. Blurred vision. Foreign body sensation. Mucopurulent or purulent discharge .

8. SIGNS An epithelial defect with infiltrate involving a larger area and significant circumcorneal injection

9. Blepharospasm may be moderate to severe cases Stromal edema , folds in Descemet membrane and anterior uveitis , commonly with a hypopyon and posterior synechiae in moderate–severe keratitis. Plaque like keratic precipitates can form on the endothelium contiguous with the affected stroma. Chemosis and eyelid swelling in moderate–severe cases. Severe ulceration may lead to descemetocele formation and perforation , particularly in Pseudomonas infection.

10. Scleritis can develop, particularly with severe perilimbal infection. Endophthalmitis is rare in the absence of perforation. Subsequent scarring may be severe, including vascularization. In addition to opacification, irregular astigmatism may limit vision. Reduced corneal sensation may suggest associated neurotrophic keratopathy, particularly where there is no other major risk factor. Sensation may also be reduced in chronic surface disease, herpetic keratitis and long-term contact lens wear.

11. Corneal ulcer usually starts as an epithelial defect associated with greyish-white circumscribed infiltrate (seen in early stage). The epithelial defect & infiltrate enlarges & stromal edema develops. A well established bacterial ulcer is characterized by : Yellowish-white area of ulcer which may be oval or irregular in shape. Margins of the ulcer are swollen and over hanging . Floor of the ulcer is covered by necrotic material . Stromal edema is present surrounding the ulcer area

12. Stage 1: Stage of progressive infiltration: Includes adherence and entry of the organism, diffusion of toxins and enzymes , and resultant tissue destruction . Shortly after the bacterial adherence, polymorphonuclear leukocytes arrive at the site. Stromal damage caused by bacterial and neutrophil enzymes facilitates progressive bacterial invasion . Stage 2: Stage of active ulceration: There is progressive tissue necrosis with subsequent sloughing of the epithelium and stroma, resulting in a sharply demarcated ulcer with surrounding neutrophilic infiltration . If organisms penetrate deeper into the stroma with progressive tissue necrosis, it may result in descemetocele formation or perforation PATHOGENISIS

13. Stage 3: Regressive stage: Characterized by improvement in clinical signs and symptoms. Natural host defence mechanisms predominate and humoral and cellular immune defence mechanisms together with antibacterial therapy try to retard bacterial replication , promote phagocytosis of the organism and cellular debris. Vascularization may start if the ulceration is of long duration. Stage 4: Healing stage: Characterized by epithelialization of ulcerated area, replacement of necrotic stroma with scar tissue , which is produced by fibroblasts.

14. HYPOPYON CORNEAL ULCER Many pyogenic organisms (staphylococci, streptococci, gonococci, Moraxella) may produce hypopyon Most dangerous are pseudomonas pyocyanea and pneumococcus . The characteristic hypopyon corneal ulcer caused by pneumococcus is called ulcus serpens Source of infection for pneumococcal infection is usually the chronic dacryocystitis . Factors predisposing to development of hypopyon. Two main factors which predispose to development of hypopyon in a patient with corneal ulcer are, the virulence of the infecting organism and the resistance of the tissues. Hence, hypopyon ulcers are MC in old debilitated or alcoholic subjects

15. Mechanism of development of hypopyon Corneal ulcer is often associated with some iritis owing to diffusion of bacterial toxins. When the iritis is severe the outpouring of leucocytes from the vessels is so great that these cells gravitate to the bottom of the anterior chamber to form a hypopyon. Thus, the hypopyon is sterile since the outpouring of polymorphonuclear cells is due to the toxins and not due to actual invasion by bacteria. Once the ulcerative process is controlled, the hypopyon is absorbed

16. Typical features of ulcus serpens : a greyish white or yellowish disc shaped ulcer occuring near the centre of cornea The ulcer has a tendency to creep over the cornea in a serpiginous fashion. One edge of the ulcer which the ulcer spreads shows more infiltration. The other side of the ulcer may be undergoing simultaneous cicatrization and the edges may be covered with fresh epithelium . Violent iridocyclitis is commonly associated with a definite hypopyon. Hypopyon increases in size very rapidly & often results in secondary glaucoma . Ulcer spreads rapidly and has a great tendency for early perforation .

17. 1.Staphylococcal Central, oval, opaque Distinct margins. Mild oedema of remaining cornea. Stromal abscess in longstanding cases. Mild to moderate AC reaction. Affects compromised corneas e.g. Bullous keratopathy , dry eyes , atopic diseases. SPECIAL CASES

18. 2. Pseudomonas Rapidly spreading. Extends periphery & deep within 24 hrs. Stromal necrosis with shaggy surface Spreads concentrically and symmetrically to involve whole depth of cornea- Ring ulcer . Greenish-yellow discharge. Hypopyon is present.

19. 3. Streptococcus viridans Infectious crystalline keratopathy type of stromal keratitis. Crystalline arboriform (needle like) white opacities in stroma , not associated with infiltration & ocular inflammation Due to proliferation of bacteria between the stromal lamellae . Seen in following corneal grafts , prolonged use of topical steroid.

20. Toxic iridocyclitis It is usually associated purulent corneal ulcer due to absorption of toxins in the anterior chamber . Secondary glaucoma due to fibrinous exudates blocking the angle of anterior chamber (inflammatory glaucoma). Descemetocele Some ulcers caused by virulent organisms extend rapidly up to Descemet's membrane,which gives a great resistance, but due to the effect of IOP it herniates as a transparent vesicle called the descemetocele or keratocele This is a sign of impending perforation and is usually associated with severe pain COMPLICATIONS OF CORNEAL ULCER

21. Perforation of corneal ulcer Sudden strain due to cough, sneeze or spasm of orbicularis muscle may convert impending perforation into actual perforation Following perforation, immediately pain is decreased and the patient feels some hot fluid (aqueous) coming out of eyes. Sequelae of corneal perforation include : Prolapse of iris . It occurs immediately following perforation Subluxation or anterior dislocation of lens may occur due to sudden stretching and rupture of zonules. Anterior capsular cataract . It is formed when the lens comes in contact with the ulcer following a perforation in the pupillary area.

22. 4 .Corneal fistula. It is formed when the perforation in the pupillary area is not plugged by iris and is lined by epithelium which gives way repeatedly. There occurs continuous leak of aqueous through the fistula. 5 .Purulent uveitis, endophthalmitis or even panophthalmitis may develop due to spread of intraocular infection. 6 .Intraocular haemorrhage in the form of either vitreous haemorrhage or expulsive choroidal haemorrhage may occur in some patients due to sudden lowering of intraocular pressure. Corneal scarring. It is the usual end result of healed corneal ulcer . Corneal scarring leads to permanent visual impairment ranging from slight blurring to total blindness.

23. MANAGEMENT Ocular examination should include: Diffuse light examination for gross lesions of the lids, conjunctiva and cornea including testing for sensations. Regurgitation test and syringing to rule out lacrimal sac infection. Biomicroscopic examination after staining of corneal ulcer with 2% fluorescein to note site, size, shape, depth, margin, floor and vascularization of corneal ulcer. presence of keratic precipitates at the back of cornea, depth and contents of anterior chamber ( cells,flares ) colour and pattern of iris and condition of crystalline lens

24. INVESTIGATIONS Corneal scraping for culture & sensitivity . A non-preserved topical anaesthetic is instilled. Scrapings are taken either with a disposable scalpel blade or the bent tip of a 20- or 21-gauge hypodermic needle, or a sterile spatula (e.g. Kimura). Loose mucus and necrotic tissue should be removed from the surface of the ulcer prior to scraping. The margins and base (except if very thin) of the lesion are scraped A thin smear is placed on one or two glass slides for microscopy, including Gram stain.

25. INVESTIGATIONS Conjunctival swabs Contact lens cases, as well as bottles of solution and lenses themselves, should be obtained when possible and sent to the laboratory for culture. Gram staining - Differentiates bacterial species into Gram-positive and Gram-negative based on the ability of the dye (crystal violet) to penetrate the cell wall

26. TREATMENT primary goal of therapy is preservation of sight and corneal clarity . Bacterial pathogens can produce irreversible corneal scarring over a period of hours because of their rapid growth, keratolytic enzymes, and stimulation of destructive host immune responses. Therefore, therapy must be initiated before definitive diagnosis is obtained in order to rapidly reduce the bacterial load and minimize later visual disability

27. Initial therapy is empirical with topical broad-spectrum coverage. Topical Monotherapy : Topical FQ initially be given every 30–60 minutes and then tapered in frequency according to the clinical response. In severe cases, administration of antibiotics every 5 min for 30 min as a loading dose can more rapidly achieve therapeutic concentrations in the corneal stroma. 2 nd gen FQ (cipro, ofloxacin) has excellent Pseudomonas coverage but lack useful gram-positive activity . Ciprofloxacin instillation is associated with white corneal precipitates that may delay epithelial healing. 3 rd & 4 th gen FQ ( eg , moxi , gati , levo , besifloxacin)have improved gram-positive and atypical mycobacterial coverage but limited activity against MRSA .

28. Topical combination therapy (DUOTHERAPY) One agent active against gram+ve bacteria & another agent active against gram- ve bacteria Empirical duotherapy usually involves a combination of two fortified antibiotics, typically a cephalosporin and an aminoglycoside. Indications : if monotherapy fails or if at initial presentation the ulcer is large, vision threatening, or atypical in nature Sub-conjunctival injections of antibiotics are reserved for non-compliant patients.

29. Cycloplegics are used to relieve pain due to ciliary spasm, breaks adhesions and prevent synechia formation. Homatropine 1% is preferable, since atropine can increase anterior chamber inflammation cyclopentolate can be more irritative . Systemic analgesics and anti-inflammatory such as paracetamol and ibuprofen relieve the pain and decrease edema . Vitamins (A, B-complex and C) help in early healing Physical and general measures (a) Hot fomentation . Local application of heat (preferably dry) gives comfort,reduces pain and causes vasodilatation. (b) Dark goggles may be used to prevent photophobia. (c) Rest, good diet and fresh air may have a soothing effect.

30. Fortified antibiotics compounded at increased concentrations compared to their commercial formulations in order to achieve therapeutic levels in the corneal stroma. are more difficult to obtain have a greater toxic effect on the ocular surface. should consider using especially in combination with vancomycin for gram+ve coverage when MRSA is suspected with large or vision-threatening ulcers , or with prior antibiotic failure.

31. Most infectious keratitis is culture Negative after 48–72 hours if treated effectively Treatment should be continued until substantial control of the infection is seen. A prophylactic broad-spectrum antibiotic (not a fortified antibiotic) may be given at a therapeutic dose until the corneal epithelium is healed

32. Systemic antibiotics FQ -have excellent ocular penetration Intensive topical antibiotics are indicated in cases with suspected scleral and/or intraocular extension of infection clinical parameters in response to antibiotic therapy: blunting of the perimeter of the stromal infiltrate decreased density of the stromal infiltrate makes the fuzzy infiltrate margin to become more defined and demarcated. reduction of stromal edema and endothelial inflammatory plaque reduction in anterior chamber inflammation Re-epithelialization cessation of corneal thinning

33. TREATMENT OF NON-HEALING CORNEAL ULCER Removal of any known cause of non-healing ulcer like Local causes: Associated raised IOP, concretions, misdirected cilia, impacted FB, dacryocystitis, inadequate therapy, wrong diagnosis, lagophthalmos and excessive vascularization of ulcer. Systemic causes: Diabetes mellitus, severe anaemia, malnutrition, chronic debilitating diseases and patients on systemic steroids. Mechanical debridement of ulcer to remove necrosed material by scraping floor of the ulcer with a spatula under LA may hasten healing. Cauterisation with pure carbolic acid or 10-20 % trichloracetic acid . Bandage soft contact lens may also help in healing. Peritomy , i.e , severing of perilimbal conjunctival vessels may be performed when excessive corneal vascularization is hindering healing.

34. TREATMENT OF IMPENDING PERFORATION 1. No strain. The patient should be advised to avoid sneezing, coughing and straining, strict bed rest. 2. Pressure bandage should be applied to give some external support. 3. Lowering of IOP by acetazolamide 250 mg QID orally, intravenous mannitol (20%) drip stat, Oral glycerol twice a day, 0.5% timolol eyedrops twice a day, and paracentesis 4. Tissue adhesive glue such as cynoacrylate is helpful in preventing perforation. 5. Conjunctival flap : The cornea may be covered completely or partly by a conjunctival flap to give support to the weak tissue. 6. Bandage soft contact lens may also be used. 7. Penetrating therapeutic keratoplasty (tectonic graft)

35. ROLE OF CORTICOSTEROID THERAPY FOR BACTERIAL KERATITIS remains controversial. Tissue destruction results from a combination of the direct effects of the bacteria and an exuberant host inflammatory response consisting of polymorphonuclear leukocytes and proteolytic enzymes, which predominate even after corneal sterilization. Corticosteroids are effective at modifying this response , but they also inhibit the host response to infection. The literature strongly suggests that corticosteroid therapy administered prior to appropriate antibiotic therapy worsens prognosis . The literature is inconclusive about steroid therapy used concomitantly with antibiotic therapy or after it is initiated

36. PENETRATING KERATOPLASTY For treatment of bacterial keratitis is indicated if the disease progresses despite therapy, descemetocele formation or perforation occurs, or the keratitis is unresponsive to antimicrobial therapy. The involved area should be identified preoperatively, and an attempt should be made to circumscribe all areas of infection. Peripheral iridectomies are indicated, because patients may develop seclusion of the pupil from inflammatory pupillary membranes. Interrupted sutures are recommended. The patient should be treated with appropriate antibiotics,cycloplegics , and intense topical corticosteroids postoperatively.

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