This document provides an overview of infectious and non-infectious keratitis. It discusses the classification, clinical presentation, microbiology, and management of various types of keratitis including bacterial, fungal, acanthamoeba, viral, post-surgical, and sterile ulcer keratitis. Empirical and microbiology-guided treatment approaches are outlined. Common causative organisms, clinical features, and treatment options for different forms of infectious keratitis are also summarized.
Types of viral keratitis, diagnosis of different types and management of each. Clinical evaluation with images described. Standard treatment protocols given.
Types of viral keratitis, diagnosis of different types and management of each. Clinical evaluation with images described. Standard treatment protocols given.
orneal ulcer, also called keratitis, is an inflammatory or, more seriously, infective condition of the cornea involving disruption of its epithelial layer with involvement of the corneal stroma. It is a common condition in humans particularly in the tropics and in farming. In developing countries, children afflicted by vitamin A deficiency are at high risk for corneal ulcer and may become blind i
Uveitis is an interesting disease of the with such a varied and diverse pathogenesis, various systemic causes and Dangerous complications in relation to the eye which makes it difficult and challenging to treat in a proper way. I hope this share will help.
This presentation describes all clinical aspects of infectious corneal ulcers
You can watch the illustrated presentation in this link :
https://www.youtube.com/watch?v=okWDPG3C34g&list=PLZ_mM13I_TrhwqZuGjB6M9Z3n7MntrURd
to download this presentation from this link
https://mohmmed-ink.blogspot.com/2020/11/conjunctival-diseases-overview.html
over view for the conjunctival diseases. clinical presentation treatment .
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
There are a number of conditions that present acutely, predominantly with pain and/or swelling
A careful and detailed history and examination, and in some cases, investigations allow differentiation between these diagnoses. A prompt diagnosis is essential as the patient may require urgent surgical intervention
Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
Dr Sujoy Dasgupta presented the study on "Couples presenting to the infertility clinic- Do they really have infertility? – The unexplored stories of non-consummation" in the 13th Congress of the Asia Pacific Initiative on Reproduction (ASPIRE 2024) at Manila on 24 May, 2024.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
2. Index
1. Classification of keratitis
2. Infectious
3. Non infectious
4. Post ppt quizzes
5. Take home Msg
1. History
2. Bacterial
3. Fungal
4. Microsporoidal
5. Acanthameba
6. Viral
3. Infectious Keratitis
• Bacterial
• Gram +ve
• Gram –ve
• Atypical
• Fungal
• Acanthameba
• Viral
Non Infectious Keratitis
• Post LASIK
• Post PKP
• Post Cataract
• Interstitial keratitis
• Peripheral ulcerative keratitis PUK
8. History
•Contact lens wear and care regimen should always be discussed. Sleeping in contact lenses? Daily or extended-wear lenses? Conventional, frequent replacement, or
single use? Disinfecting solutions used? Recent changes in routine? Water exposure (swimming or hot tub use) with lenses?
•Improper handling > overnight wear, hygiene problems, duration of continuous wear
- Contact lens type > daily-wear soft lenses more liable to microbial growth than gas-permeable rigid lenses
•Extended wear has higher risk - contact lens hygiene protocol; tap-water rinsing of contact lenses; swimming, using a hot tub, or showering while wearing contact
lenses; method of purchase, such as over the Internet; and decorative contact lens use
•Pseudomonas
Contact lens
•pythium, microsporoidal
Water exposure, bath in the pond or exposed in the rain water
•Soil , dust, decaying vegetation, Agriculture worker Fusarium
Trauma, corneal foreign body
Past Surgery
•antimicrobials or topical steroids)? Previous corneal disease? Ocular Surface Disease
•Eye lids,
•Corneal surgery including refractive surgery
Ocular medical or surgical history
•Candida - Systemic illness?
Systemic immunosuppression
9. • Keratitis with Contact lens wear
• Ocular trauma
• Ocular surface disease
• Systemic immunosuppression
• Post LASIK
• Eyelid disease: Entropion Lagophthalmos Trichiasis
• Lacrimal: Chronic dacryocystitis
Contact lens Common Microorganisms
Bacteria: Pseudomonas aeruginosa is the most frequently
isolated bacterium Acanthamoeba
Fungi: Fusarium species, Aspergillus species and Candida
species
Immunocompromised patients Common Microorganisms
Bacteria: mycobacteria
Fungi: Candida, microsporidial
Viral:HZ
Ocular trauma with Vegtative material
Fungi: Fussarium
• Post LASIK
mycobacteria
• Post keratoplasty
11. • document the size, depth, and location of the corneal infiltrate and
epithelial defect.
• Anterior chamber for depth and the presence of inflammation, including
cell and flare, hypopyon, fibrin, hyphemia
Slit lamp examination of cornea
• Diffuse illumination
• direct illumination
• sclerotic scatter
• specular reflection
Stain with fluorescein
epithelium,
Bowman’s layer,
stroma,
Descemet’s membrane,
endothelium,
blood vessel extension from limbal arcades
Fluorescein or rose bengal/lissamine green staining
12. Common slit lamp techniques for corneal examination
Diffuse illumination
Parallelepiped illumination.
Sclerotic scatter.
Specular illumination.
Retroillumination.
This is useful in detecting subtle corneal opacities. A beam of light is focused on the limbus (to achieve this you need
to loosen the screw that links the illumination to the microscope ie. uncoupling). These gives rise to internal reflection
and if there is no opacity the cornea will appear uniformly dark. Otherwise, the opacity will scatter the light.
The beam of light and the microscope are placed at equal angles from the normal to thecornea. Useful
particularly for observing the endothelium. High magnification is needed andthe view is monocular.
It is used to examine the cornea by reflecting light off solid body (the iris, lens and the retina)
This gives the effect of haying the light source arising from behind the object observed.
A beam of light with a width of about 2 mm is shown on cornea at about 45 degrees from the microscope position.
This allows one to view a "3-dimensional" block of cornea. The posterior surface of the cornea can be examined for
keratitic precipitates or pigment.
The light is shown on the cornea with a wide slit at about 45 degrees from the microscope position and the illuminated area is
viewed through microscope. (initial examination.)
15. Bacterial
Keratitis
Gram positive Bacteria (Staph- Strept)
Localized round or oval gray-white lesions
Central or paracentral Minimal surrounding epithelial edema
Advancing border with active infiltrate & undermined edges, the trailing
edge with signs of healing.
Leveled hypopyon
Gram negative bacteria (pseudomonas)
Rapid course, severe inflammation, dense stromal suppuration and
corneal haze e.g. Pseudomonas keratitis Thick mucopurulent greenish
discharge
Marked stromal oedema Untreated > perforate within 2-3 days
Suppurative ulcerative keratitis
caused by P aeruginosa.
24. Acanth
Keratitis
Pain level is out of proportion to the physical findings
Epithelial haze Pseudo dendrites
Punctate epithelial erosions -Multifocal infiltrates and microabscess
Fine epithelial and subepithelial curvilinear opacities (early)
Radial keratoneuritis (Along nerves of anterior stroma)
Ring stromal infiltrate
•In early cases, mimics herpetic epithelial keratitis
(Dentritiform appearance) Complication: Scleritis, secondary
bacterial keratitis
ring infiltrate and small hypopyon.
29. Post
LASIK
Keratitis
Infectious keratitis
Focal area of infiltration surrounded by diffuse inflammation
1 week after LASIK
infiltrate, ciliary injection, hypopyon, and flap melt in severe cases.
Diffuse lamellar keratitis (DLK) Shifting sands of Sahara
Sterile inflammation of the lamellar interface
Characteristic diffuse white sand-like deposits, typically begins at flap
periphery
Occurs within the first within first 24h few days after LASIK
30. marginal
Keratitis
Blepharitis, inferior SPK, phlyctenule (a wedge-shaped, raised,
vascularized sterile infiltrate near the limbus, usually in children).
Peripheral scarring and corneal neovascularization.
Findings often present in the contralateral eye or elsewhere in the
affected eye.
• Singular or multiple, unilateral or bilateral,
• peripheral corneal stromal infiltrates often with a clear
space between the infiltrates and the limbus.
• Variable staining with fluorescein.
• Minimal anterior chamber inflammation.
• Sectoral conjunctival injection typically occurs.
31.
32.
33. A 72-year-old man is referred by his family physician for evaluation of
decreasing vision and increasing erythema of the right eye over the
last 24 hours. The patient also has had pain of the right scalp and
several new "pimples" on his forehead. Which of the following is the
most likely ocular finding in this case?
1. Dendritic ulcer with terminal bulbs
2. Pars planitis
3. Retinitis
4. Iritis with ocular hypertension
34.
35. -More pinpoint
-Smaller
-Lesser in number
-At the plane of epithelium
-H/o Conjunctivitis
– More common No H/o water
Exposure
Microsporoidal
Viral
38. idiopathic or related to systemic connective tissue disease:
• Rheumatoid arthritis, GPA,
• relapsing polychondritis,
• polyarteritis nodosa,
• systemic lupus erythematosus, others.
• Peripheral (unilateral or bilateral) corneal thinning/ulcers may
be associated with sterile inflammatory infiltrates.
• The sclera may be involved.
• May progress circumferentially to involve the entire peripheral
cornea. Perforation may occur.
• This may be the first manifestation of systemic disease
Peripheral ulcerative keratitis (PUK)
39. Terrien marginal degeneration:
• Usually bilateral, often asymptomatic.
• Slowly progressive thinning of the peripheral cornea;
• typically superior;
• more often in men.
• The anterior chamber is quiet, and the eye is typically not injected although
may be associated with inflammatory signs and symptoms secondary to
epithelial breakdown and inflammatory or infectious infiltrates. A yellow line
(lipid) may appear, with a fine pannus along the central edge of the thinning.
The thinning may slowly spread circumferentially. Refractive changes, including
irregular and against-the-rule astigmatism are often present.
• The epithelium usually remains intact, but perforation may occur with minor
trauma.
40. Mooren ulcer
• Unilateral or bilateral.
• Painful corneal thinning and ulceration with inflammation.
• Initially starts as a focal area in the peripheral cornea, nasally or
temporally with involvement of the limbus; later extends circumferentially
or centrally.
• Unlike PUK, Mooren ulcer usually does not involve the sclera. An epithelial
defect, stromal infiltrate/thinning, and an undermined leading edge are
typically present.
• Limbal blood vessels may grow into the ulcer, and perforation can occur.
Mooren-like ulcer has been associated with
• Bilateral cases are more resistant to treatment than unilateral cases.
Idiopathic (autoimmunity may play a key role); systemic
hepatitis C virus infection.
diagnosis of exclusion after ruling out the aforementioned
systemic causes of PUK.
42. Exposure/neurotrophic keratopathy:
• the inferior interpalpebral portion of the cornea without signs of
significant inflammation.
• May be associated with an eyelid abnormality, a fifth or seventh
cranial nerve defect, or proptosis.
• The ulcer may become superinfected.
45. Low –moderate risk
High risk
Empirical treatment
Combined therapy
• Specimen
• Stain
• Culture
• Never patch infected cornea
• Topical Antibiotics Choice according to common pathogen; epidemiology, clinical
presentation & availability.,Systemic or Subconj scleral,..)
• Started before obtaining microbiology ,continued even if no microorganism is identified
• No steroids
• Cycloplegic agents (- synechiae and-pain )
• Collagen shields or soft contact lenses soaked in antibiotics (++drug delivery).
1. unusual history ( trauma with
organic vegetable matter or
contact lenses while in a hot tub
or history of corneal surgeries.
2. corneal infiltrate is central, large
>2mm, and/or is associated with
significant stromal involvement
(deep) or melting, infiltrates are in
multiple locations on the cornea.
3. chronic or unresponsive to broad-
spectrum antibiotic
4. atypical clinical features
suggestive of fungal, amoebic, or
mycobacterial keratitis
Empirical treatment
Monotherapy
46. Bacterial
Keratitis
First line:
- Topical 4th generation fluoroquinolones > Moxifloxacin 0.5% &
. Gatifloxacin 0.5%
- Suspected Gram –ve > Ciprofloxacin 0.3% & Ofloxacin 0.3%
Second line: - When severe & non-responsive to 1st line
fortified
preparation of
(Cefazolin / Cefuroxime 5% and tobramycin
/ Penicillin 0.3% gentamicin 1.4%)
• Vancomycin if MRSA/ severe Staph
• Penicillin if streptococcal infection is suspected.
• Gentamicin 1.5% Toxic Not n ocular surface disease.
Systemic antibiotics:
• Systemic infection such as gonorrhea> ceftriaxone + azithromycin
• Scleral involvement /perforated e.g. Ciprofloxacin 500 mg BID
• Subconjunctival antibiotics :imminent scleral spread or perforation
• Hourly topical application improvement > reduce to
2 hourly then according to response.
• Central or severe keratitis: loading dose such as
every 5-15 minutes then every hour.
• Daily examination till improved
Monotherapy
Combined Therapy
47. Mycobacteria
Keratitis
• amikacin, + fourth generation fluoroquinolone.
• Systemically, we tend to give amikacin injection also if the
lesions are more limbal Or tunnel infiltrates. orally, we
can give sulfamethoxazole, trimethoprim combination
Nocardia
Keratitis
Topical amikacin. Either you can use 2 or 4%, along with
fluoroquinolone.
Azithromycin orally on day one you can do 500
milligrams, followed by 250 for 5 days.
at least one month for this medical therapy to heal.
If it doesn’t heal with medical therapy for one month->
LASIK flap amputation.
And if it doesn’t get healed ->a therapeutic graft.
48. Follow up
STOP Antibiotics for 12:24 hrs
hospital admission for eye drop administration
then Repeat cultures Selected media for atypical organisms
Shift to non preservative eyedrops
Features suggest a positive response to antibiotic therapy:
Reduced pain
Reduced amount of discharge
Lessened eyelid edema or conjunctival injection
Consolidation and sharper demarcation of the stromal infiltrate
Decreased density of the stromal infiltrate
Reduced stromal edema and endothelial inflammatory plaque
Reduced anterior chamber cells, fibrin, or hypopyon
Initial re-epithelialization
Cessation of progressive corneal thinning
most infectious keratitis is culture negative after 48–72 hours.
Treatment failures
Treatment is effective
• In general, the initial therapeutic regimen should be modified when the
eye shows a lack of improvement or stabilization within 48 hours.
Effectively treated,
Shift to appropriate Monotherapy
is due to
• antibiotic-resistant pathogens.
• Toxicity from medications
• if patients are unable to administer eye drops.
49. Corneal scraping
•topical aesthesia. Kimura spatula, No. 15 blade, or 25g needle.
• Scrape both the base and leading edge of the ulcer (from uninvolved to
involved cornea).
• Place material onto glass slide for microscopy and staining, Plate on agar
when plating small samples, rows of ‘C streaks
use separate needles for each agar dish.
1. Specimen:
• Corneal scraping; most important
• Contact lens, case and solution
• Conjunctival swab& eyelid swab less helpful
• Anterior chamber paracentesis > in deep infiltration
2. Smear & stain
3. Culture and sensitivity
Smear and Stain Culture & Sensitivity
53. How to reduce the inflammatory response??
Anticollagenases (Tetracyclines )
Inhibit collagenases and have anti-metalloproteinase effect
Reduce necrosis, perforations, and therapeutic
keratoplasty
Steroids
Steroids for Corneal Ulcers Trial (SCUT)
debate
Pros: reduce inflammation, reducing scarring, neovascularization, and
stromal melt
Cons: Delayed re-epithelialization, worsening of infection.
Never use in
• No cardia
• Fungal
• Viral epithelial
- Start Steroids after 48 hrs AB use
- It has role in the following :
• pseudomonas
• Acanthamoeba
• Viral : stromal not epithelial
Alternatives:
• Tacrolimus
• Cyclosporine
54. •Anesthesia ,a small trephine (e.g., a 2- to 3-mm dermatic punch) or blade
is used to excise a small piece of stromal tissue at base and the active edge
of the infiltrate (as far from the center of the cornea as possible) that is large
enough to allow bisection so that one portion can be sent for culture and the
other for histopathology.
•Perform a lamellar dissection while avoiding the visual axis and
thinnest part
•Specimen divided and sent for stain and culture
•Stop antibiotics for 24 hours
•Re-scrape and/or corneal biopsy
•Re-start intensive antibiotics
•Consider other diagnosis (e.g. sterile
ulcers?)
•Consider therapeutic penetrating
keratoplasty
Nb1 A corneal biopsy taken from the center of the cornea may result in a significant refractive error from the irregular surface.
Taking the biopsy from the edge of the infiltrate will increase the yield of viable pathogen, whereas a biopsy from the center of
an infiltrate may only yield nonviable pathogen and debris.
Corneal biopsy indication :
• if the response to treatment is poor
• or if repeated cultures have been negative and the clinical picture continues to
strongly suggest an infectious process.
• Corneal biopsy may also be indicated if the infiltrate is located in the mid or deep
Resistant keratitis: Non responsiveness over 2 weeks of medical treatment
Corneal biopsy procedure:
56. Next Generation sequencing
•Does not require primers like PCR
High sensitivity compared to culture and stain
• Potentially lower specificity compared to cultre and stain
• Need for narrow list of causative agents to use specific primers
• confirmation of viral infections (high sensitivity)
PCR
57. Thinning & Perforation Endophthalmitis
Complications:
• Frequent lubrication, punctal occlusion and/or tarsorrhaphy in cases of aqueous deficient dry eye
• Systemic antimicrobials in cases of perforation
• Topical aqueous suppressant
• Bandage contact lens >promote corneal healing and re-epithelialization in impending or small corneal perforations or
lacerations that have good apposition of edges and alignment, and no prolapse of uveal tissue
• -Anti-collagenase medications, such as systemic (oral) tetracyclines , Vitamin C, systemic, stimulate collagen
production - - Immunosuppressive agents (oral or topical cyclosporine, systemic methotrexate, cyclophosphamide) >
in progressive corneal ulceration secondary to corneal inflammatory diseases. (After control with antimicrobials)
-Corneal gluing with cyanoacrylate glue (Histoacryl glue) > in impending corneal perforations or frank corneal
perforations that are small (< 3 mm), concave, and located away from the limbus .
- Patch Grafts:
In peripheral corneal perforations and descemetoceles, when the perforation is relatively small (i.e., it does not require
full-sized penetrating keratoplasty but is too large for tissue adhesive; 2.5-5 mm) so tectonic corneoscleral patch grafting
is sutured or glued to the cornea after trephining the infected portion of the cornea.
- Therapeutic keratoplasty: in large areas of perforation or necrotic tissue and progressive resistant infection despite
maximal medications
58. Cross Linking in infectious keratitis
•Antimicrobial effect
•Increases resistance to tissue necrosis
Fungal infections possible increase in perforation risk
benefit in bacterial keratitis
59. Rose Bengal photodynamic antimicrobial therapy
•Rose Bengal (0.1% or
0.2% RB in BSS) to the
deepithelized cornea for 30
minutes followed by
irradiation
progressive infectious
keratitis unresponsive to
standard medical therapy
60. Fungal
Keratitis
Microsporidial
Keratitis
- Filamentous
Natamycin 5% is the initial treatment of choice for fusarium keratitis. (superior to
voriconazole ) – doesn’t work deep (MUTT trial)
If deep ulcers (+ systemic ketoconazole or oral Voriconazole or intrasotromal injections of
amphotrecin B)
- Suspected yeast Candida
Amphotricin b 0.3% - 0.5% or fluconazole 0.3% preparation
- Aspergillus
Natamycin +Voriconazole 1% preparation (MUTT trial)
Never use voriconazole as a monotherapy. Always in combination natamycin or any
antifungal. (risk of perforation and need of TPK)
Pythium :topical linezolid hourly, oral azithromycin. antifungals (itraconazole, voriconazole)
Hourly topical > reduce to 2 hourly then Continue
drops at least 3 hourly for at least 2 weeks after
healing (FU Every 2 days till improved )
Debridement by moistened cotton
fluconazole 0.3% preparation
Voriconazole 1%
Modified TST protocol. That is the topical, systemic, and
targeted therapy
• Debridement
• Adjuvants according to symptoms
• oral doxycycline (perforation)
• IOP lowering
• Antiinflammatory : (tacrolimus ,cyclosporine could be) Never steroids
• No cross linking (perforation)
• Maxium medical therapy 2 weeksEarly TPK
61. Acanth
Keratitis
- First lines:
Chlorhexadine 0.02%
+ Propamadine isethionate 0.1% (brolene)
- Second line:
Polyhexamethyline biguanide [PHMB] 0.02%-0.06%
Hexamidine isethionate 0.1%
- Third line:
Topical ketaconazole or fluconazole 1% or voriconazole
Topical neomycin 10mg/ml
(not gentamicin)
Surgeries: early DALK/ Therapeutic keratoplasty
Hourly topical application for 2-3 days around the clock, then
hourly while awake for 3 days, then tapered to 4 times a day
Adjuvant
• Steroids
(Reduce vascularization ,melting, scleritis, lid edema)
• Pain killer (Amitriptyline 25 mg BID
62. Herpes S
Keratitis
Zoster Keratitis
Epithelial keratitis
Ganciclovir 0.15% eye drops (preferred)
Acyclovir 3% ointment
Oral antivirals Alternative to topical in epithelial keratitis:
Acyclovir: 400 mg 3–5 times daily for 7–10 days in dendritic
Acyclovir: 800 mg 5 times daily for 14–21 days in geographic
Stromal keratitis:
Topical Prednisolone 1% + oral Acyclovir: 400 mg
- Herpes zoster ophthalmicus
acyclovir 800 mg
5 times daily until healing, then 3 times a day for 7 days
Prophylaxis of recurrent HSV keratitis
(Acyclovir 400 mg twice daily for one year) in:
- Multiple recurrences especially stromal keratitis
- Post-keratoplasty or any surgery in herpetic cornea
- Herpetic keratitis with immunosuppressive treatmen
Caution taken in renal patients> nephrotoxic
5 times a day for 7-10 days,
6–8 times daily tapered over 10 weeks twice daily over 10 weeks
65. coordinated with an internist or rheumatologist.
• glasses (or protective glasses [e.g., polycarbonate lens])
during the day and an eye shield at night.
• Ophthalmic antibiotic ointment
• preservative-free artificial tear ointment q2h.
• Punctal occlusion if dry eye syndrome is present.
• Topical cyclosporine 0.05% to 2% b.i.d. to q.i.d. or lifitegrast
5% b.i.d. may also be helpful.
• Cycloplegic drop (anterior chamber reaction or pain is
present).
• Consider doxycycline 100 mg p.o. b.i.d. for its
metalloproteinase inhibition properties and ascorbic acid
vitamin C 1 to 2 g daily) as a collagen synthesis promoter.
• Systemic steroids (e.g., prednisone 60 to 100 mg p.o. daily;
(if progressive corneal thinning, but not for perforation).
• An immunosuppressive agent (e.g., methotrexate,
mycophenolate mofetil, infliximab, azathioprine,
cyclophosphamide) is often required, especially for GPA.
• Excision or recession of adjacent inflamed conjunctiva
• Consider cyanoacrylate tissue adhesive or corneal
transplantation surgery A conjunctival flap or amniotic
membrane graft ( impending corneal perforation).
PUK associated with auto-immune disease
Refer to an internist (and/or rheumatologist
Systemic workup :
1. serum erythrocyte sedimentation rate,
2. complete blood count with differential,
3. rheumatoid factor,
4. antinuclear antibody,
5. antineutrophilic cytoplasmic antibody levels,
6. angiotensin-converting enzyme,
7. chest x-ray or CT to rule out connective tissue
disease and leukemia.
66. Terrien marginal degeneration:
• Correct astigmatism with glasses or contact lenses if possible.
• Protective eyewear should be worn if significant thinning is present.
• Lamellar grafts can be performed if thinning is extreme.
Moorenulcer:
• Underlying systemic diseases must be ruled out before this diagnosis can be made.
• Topical steroids, topical cyclosporine 0.05% to 2%,
• limbal conjunctival excision, corneal gluing, and lamellar or penetrating keratoplasty may be beneficial.
• Systemic immunosuppression (e.g., oral steroids, methotrexate, cyclophosphamide, and cyclosporine)
67. Mild
• Warm compresses and eyelid hygiene.
• Antibiotic drop q.i.d. fluoroquinolone
• Antibiotic ointment q.h.s. (e.g., bacitracin, erythromycin, bacitracin/polymyxin B).
Moderate to Severe
• Warm compresses and eyelid hygiene.
• Antibiotic drop q.i.d. fluoroquinolone
• A combination antibiotic/steroid can also be used q.i.d. (e.g., loteprednol 0.5%/tobramycin 0.3%,
dexamethasone 0.1%/tobramycin 0.3% or dexamethasone 0.05%/tobramycin 0.3%).
If episodes recur, add
Systemic doxycycline (100 mg p.o. b.i.d., for 2 weeks, and then daily for 1 month, and then 50 to 100 mg )
until the ocular disease is controlled for several months.
(anti-inflammatory effect on the sebaceous glands in+antimicrobial action).
Topical azithromycin q.h.s., erythromycin q.h.s. or cyclosporine b.i.d. may be helpful in controlling eyelid
inflammation.
Marginal keratitis Staphylococcal Hypersensitivity
69. Keratitis in immunocompromised patients
Immunocompromised patients Common
Microorganisms
Bacteria: mycobacteria
Fungi: Candida, microsporidial
Viral:HZ
1
70. Keratitis in contact lens disease
Bacteria: Pseudomonas aeruginosa is the most frequently isolated
bacterium Acanthamoeba
Fungi: Fusarium species, Aspergillus species and Candida
2
72. Which bacterial organism causes rapid
progression and corneal melting?
1. Staphylococcus.
2. Pseudomonas.
3. Streptococcus.
4. No cardia
Which bacterial organism causes rapid
progression and corneal melting?
1. Staphylococcus.
2. Pseudomonas.
3. Streptococcus.
4. No cardia
4
73. In which of the following organisms are
topical steroids contraindicated?
A. Acahthamoeba
B. Pseudomonas
C. Nocardia
D. Stahpylococcus
In which of the following organisms are
topical steroids contraindicated?
A. Acahthamoeba
B. Pseudomonas
C. Nocardia
D. Stahpylococcus
5
74. What is the treatment of choice for MRSA keratitis?
A.Vancomycin
B. Linezolid
C. Moxifloxacin
D. Tobramycin
What is the treatment of choice for MRSA keratitis?
A.Vancomycin
B. Linezolid
C. Moxifloxacin
D. Tobramycin
treatment of choice today for methicillin resistant staphylococcus aureus.
6
75. Over-the-counter steroids are the most common
cause for…
1. Bacterial keratitis,
2. allergic conjunctivitis,
3. fungal keratitis
4. Viral keratitis
Over-the-counter steroids are the most common
cause for..?
1. Bacterial keratitis,
2. allergic conjunctivitis,
3. fungal keratitis
4. Viral keratitis
7
76. What is the topical treatment of choice for
fusarium keratitis?
A.Voriconazole
B. Natamycin
C. Caspofungin
D.Miltefosine
What is the topical treatment of choice for
fusarium keratitis?
A.Voriconazole
B. Natamycin
C. Caspofungin
D.Miltefosine
Natamycin is superior to voriconazole in all
filamentous species
8
77. Regarding voriconazole in fungal keratitis treatment:
1. It is recommended to use as a monotherapy.
2. Always use it in combination with the natamycin
or any other antifungal.
Regarding voriconazole in fungal keratitis treatment:
1. It is recommended to use as a monotherapy.
2. Always use it in combination with the natamycin
or any other antifungal.
Mutt study , Never give voriconazole as a
monotherapy, the perforation rate was higher.
9
78. What is the indication for therapeutic keratoplasty ?
A. Impending Corneal Perforation
B. Limbal Involvement
C. Deep stromal ulcers – Not responding to Max Med Therapy
D. All the above
What is the indication for therapeutic keratoplasty ?
A. Impending Corneal Perforation
B. Limbal Involvement
C. Deep stromal ulcers – Not responding to Max Med Therapy
D. All the above
10