Bacterial keratitis is a sight-threatening condition that commonly presents as an ocular emergency. It is caused by the proliferation of bacteria, fungi, viruses, or parasites within the cornea, resulting in inflammation and tissue destruction. While there are no specific clinical signs to confirm a bacterial cause, identification of risk factors such as dry eye, contact lens use, trauma, or topical steroid use and an assessment of corneal findings can help determine potential etiologies. Common causative organisms include Staphylococcus aureus, Staphylococcus epidermidis, Pseudomonas aeruginosa, and Streptococcus pneumoniae. Treatment involves topical antibiotics and cycloplegics, with cultures, scrapings, and modification
Ectropion
It is an outward turning of the eyelid margin . This more frequently affects the lower eyelid.Upper eyelid ectropion is uncommon.Classified in 5 types
1)Congenital 2) Involutional 3) Paralytic 4) Cicatricial 5) Mechanical
Involutional ectropion is more common.Congenital ectropion is very rare.
Symptoms Epiphora :- excessive tearing.Excessive dryness.
Foreign body sensation Irritation.Burning.Redness.Chronic conjunctivitis KeratinizationCorneal exposure
Grading
Lid margin is out rolled and depending on out rolling ectropion can be classified as under:
Grade I –only punctum is everted
Grade II –lid margin is everted and palpebral conjunctiva is visible
Grade III –fornix is also visible
Etiological factors
Horizontal lid laxity:-can be demonstrated by pulling the central part of the lid 8 mm or more from the globe, with a failure to snap back to its normal position on release without the patient first blinking.
Medial canthal tendon laxity
demonstrated by pulling the lower lid laterally and observing the position of the inferior punctum If the lid is normal the punctum should not be displaced more than 1–2 mm
Lateral canthal tendon laxity
characterized by a rounded appearance of the lateral canthus and the ability to pull the lower lid medially more than 2 mm.
>Normally, the displacement should only be 0-2 mm.
Treatment
1 medical therapy
2 surgical therapy
Endophthalmitis is an inflammation of the vitreous and the inner coats of the eye. This inflammation leads to infection which is caused by fungi or bacteria.
Ectropion
It is an outward turning of the eyelid margin . This more frequently affects the lower eyelid.Upper eyelid ectropion is uncommon.Classified in 5 types
1)Congenital 2) Involutional 3) Paralytic 4) Cicatricial 5) Mechanical
Involutional ectropion is more common.Congenital ectropion is very rare.
Symptoms Epiphora :- excessive tearing.Excessive dryness.
Foreign body sensation Irritation.Burning.Redness.Chronic conjunctivitis KeratinizationCorneal exposure
Grading
Lid margin is out rolled and depending on out rolling ectropion can be classified as under:
Grade I –only punctum is everted
Grade II –lid margin is everted and palpebral conjunctiva is visible
Grade III –fornix is also visible
Etiological factors
Horizontal lid laxity:-can be demonstrated by pulling the central part of the lid 8 mm or more from the globe, with a failure to snap back to its normal position on release without the patient first blinking.
Medial canthal tendon laxity
demonstrated by pulling the lower lid laterally and observing the position of the inferior punctum If the lid is normal the punctum should not be displaced more than 1–2 mm
Lateral canthal tendon laxity
characterized by a rounded appearance of the lateral canthus and the ability to pull the lower lid medially more than 2 mm.
>Normally, the displacement should only be 0-2 mm.
Treatment
1 medical therapy
2 surgical therapy
Endophthalmitis is an inflammation of the vitreous and the inner coats of the eye. This inflammation leads to infection which is caused by fungi or bacteria.
This presentation describes the background of the cornea and the corneal diseases in general, also it describes in detailed manner how to manage the corneal ulcer with its different causes
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
• Cornea is an avascular, transparent tissue that is an important component of the ocular refractive system.
• It is one of the most densely innervated tissues in the body.
Behind the precorneal tear film there are five layers of cornea:
1. Epithelium and basal lamina
2. Bowman’s layer
3. Stroma
4. Descemet’s membrane
5. Endothelium
Corneal Transparency
The cornea transmits nearly 100% of the light that enters it.
Transparency achieved by Arrangement of stromal lamellae.
Other factors:
Epithelial non-keratinization
Regular & uniform arrangement of corneal epithelium
Junctions between cells & its compactness
Corneal avascularity
Non-myelinated nerve fibers
Once the damaged corneal epithelia are invaded by offending agent, the sequence of pathological changes which occur during development of corneal ulcer can be described under four stages:
1. Progressive infiltration
Grey zone
Localized necrosis
Saucer-shaped ulcer with overhanging edges
2. Active ulceration
Dead material material thrown off
Oedema subsides
Floor and edges are smooth and transparent
3. Regression
From limbus, minute vessels grow in
4. Cicatrization
Formation of fibrous tissue which fill the gap
Opacity generated
A comprehensive summary of all the common corneal diseases starting from different types infective keratitis, non infective keratitis, corneal dystrophies, corneal ectasias to corneal degenerations.
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
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.
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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
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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.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
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.
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Evaluation of antidepressant activity of clitoris ternatea in animals
Microbial keratitis
1.
2. It is sight-threateningsight-threatening condition and
frequently presents as an ocularocular
emergency.emergency.
Bacterial keratitis rarely occurs in therarely occurs in the
normal eyenormal eye because of the human cornea's
natural resistance to infection.
Microbial keratitisMicrobial keratitis or infectious corneal ulcer is due to the
proliferation ofproliferation of bacteria, fungi, viruses, and parasites and
associated inflammation and tissue destructiontissue destruction within the
cornea
3. Bacterial Keratitis is most common causemost common cause of
suppurative c u.
There are no specific clinical signsno specific clinical signs to help confirm a
definite bacterial cause in Bacterial Keratitis.
Identification of risk factorsrisk factors and assessment of
corneal findings will help in determination of
potential etiologiespotential etiologies.
5. Risk Factors
Chronic infection of the eyelid margin can
reducing concentrationreducing concentration of certain antibacterial
substances.
Dry eyeDry eye
Presence of N Gonorrhoeae, C Diphtheriae,
Hemophilus Aegyptius and Listeria
Monocytogenes – they can penetrate intactpenetrate intact
epithelium.epithelium.
6. Corneal anaesthesia
AbuseAbuse of topical anaesthetic solution
Compromised c epithelium as contact
lenses,bullous keratopathybullous keratopathy.
Absence of normal conjunctival flora.
Local immune suppression as topicaltopical
corticosteroidscorticosteroids
Previous viral infectionviral infection
Drugs used in viral keratitis
7. External Risk
Factors
1. Trauma
2. Exposure to contaminated water or
solutions
3. Smoking (disrupting corneal epithelium
via associated cellular and neuronal
toxicity.
16. PathogenesisPathogenesis
Steps
1. Corneal abrasionabrasion
2.2. InfectionInfection by microorganism in presence of
predisposing factor(s).
3. Localized necrosisnecrosis of superficial layers of cornea
4. Formation of sequestrumsequestrum It cast off in conjunctival sac
5.5. DesquamationDesquamation of corneal epithelium and damage to
Bowman’s membrane
17. Epithelial regenerationregeneration, at times it covers the edges
and floor area
A saucer shaped defect with projecting wallsdefect with projecting walls above
the normal surface due to swelling of tissue
resulting from fluid imbibition by corneal stroma
Surrounding area is packed by leucocytes, seen as
gray zone of infiltration. This is progressive stageThis is progressive stage..
18. Necrotic material fall off-Necrotic material fall off- ulcer becomes larger ->
infiltration and swelling reduce and disappears ->
margin becomes smooth, floor also looks smooth
and transparent. This is regressive stageThis is regressive stage..
VascularizationVascularization develops from limus to corneal ulcer
to restore lost tissue and to supply antibodies.
19. Vascularisation is followed by cicatrizationcicatrization due to
regeneration of collagen and formation of fibrous
tissue
Newly formed fibres are laid down irregularlyirregularly, not
conforming to normal pattern of stromal fibres.
Therefore this fibrous tissue reflects light irregularly.
The scar tissue is more or less opaque. Some
vessels may persist in large scar
20. Bowman’s membrane never regenerates and
whenever it is destroyed some degree of corneal
opacity remains.
Corneal opacity may clear with time especially if
it is not dense. The vascularization plays part in
clearing corneal opacity.
21. Diffusion toxinsDiffusion toxins into the anterior
chamber leads to hyperaemiahyperaemia
and inflammation of the iris and
ciliary body (Keratouveitis).
Polymorphonuclear cells coming
out from the uveal tissue may
gravitate to bottom of anterior
chamber to form hypopyonhypopyon.
22.
23. Symptoms
Symptoms are usually
markedmarked, they are:
1. Diminution of visionDiminution of vision,
2. WateringWatering (lacrimation)
3. photophobia and
blepharospasm
4. PainPain and foreign body/
gritty sensation
5. There may be dischargedischarge
(Mucopurulent / purulent)
24. Signs
1. Visual acuity may be affected, depending on
location of corneal ulcer
2. Edema of lids of affected eye, in severe cases
3. Blepharospasm
4. Ciliary and conjunctival congestion
5. Hazyness / pus may be present in anterior
chamber
29. Location of lesion
Density, Size , shape , depth, colour
Endothelium Anterior chamber
Loose or Broken sutures Signs of corneal
dystrophy
Anterior Vitreous
Fluorescein
Rose Bengal staining
30. Rose BengalRose Bengal
•Derivative of sodium fluorescein
(NaFL)
•Stain dead or degenerated cells
and mucous strands
• Best used to examine the
conjunctiva
FluoresceinFluorescein
•Synthetic organic compound
•Stains epithelial lesions,
•Fluorescein does not stain
normal corneae or bulbar
conjunctivae.
31. Laboratory InvestigationLaboratory Investigation
corneal scraping for stainings and cultures .
The majority of cases resolve with empirical
therapy and without smears or cultures.
cultures are indicated in cases where the corneal
infiltrate is central, large, deep, is chronic in nature,
or has atypical clinical features .
poor clinical response to empirical treatment .
32. Culture media
Media Common isolates
Blood AgarBlood Agar Aerobic and facultative, anaerobic bacteria,
including P. aeruginosa, S. aureus, S.
epidermidis, S. pneumoniae
Chocolate AgarChocolate Agar Aerobic and facultative, anaerobic bacteria,
including H. influenzae, N. gonorrhoeae,
and Bartonella species
Thyoglicollate broth Aerobic and facultative, anaerobic bacteria
Lowenstein-Jensen medium Mycobacterium species
Thayer-Martin agar Pathologic Neisseria
Sabouraud's dextrose agarSabouraud's dextrose agar Fungi
33. Stains
.
Stain Organisms visualized
Gram stain Best for bacteria; can also visualize
fungi, Acanthamoeba
Giemsa stain Bacteria, fungi,
Chlamydia, Acanthamoeba
Acid fast Mycobacterium, Nocardia
34. Complications of Corneal UlcerComplications of Corneal Ulcer
1. Spread of ulcer horizontally and
depth-wise, leading to thinningthinning of
cornea
2. Bulging of descemet’s membrane
(Keratocele or DescemetoceleDescemetocele
represents condition of impending
perforation of cornea
35. 3. PerforationPerforation of by sudden exertion such as
coughing,
Complications of perforation may be serious
and sight threatening
A.A.Peripheral perforationPeripheral perforation: Iris is thrown forward
-> opening is occluded -> anterior chamber is
formed , scarring takes place:
36.
37. B.Central perforationB.Central perforation: small central perforation
-> anterior chamber collapse
-> lens comes in contact with corneal
endothelial surface -> anterior capsular
cataract -> repeated healing and perforation
leading to corneal fistula formation
38. C. Sloughing of whole corneaC. Sloughing of whole cornea: prolapse of iris ->
pupillary block and exudation on iris ->
pseudocorneapseudocornea formation (iris covered with exudates ,
formation of fibrous tissue and formation of scar
tissue) -> anterior chamber anatomy is lost.
39. In case of sudden large perforation lens may
subluxate
Lens and vitreous may prolapse through
perforation.
This may lead to vitreous haemorrhage , choroidal ,
sub-retinal or sub-choroidal haemorrhage. In
elderly patients there may be expulsive
haemorrhage
40. D. Intra-ocular infectionD. Intra-ocular infection: due to perforation
bacteria enter in the eye and causes
endophthalmitis and panophthalmitis
41. Treatment of uncomplicated corneal ulcerTreatment of uncomplicated corneal ulcer
LOCAL TREATMENTLOCAL TREATMENT
1. Control of infection with antibiotic(s).
Sub-conjunctival antibiotics may be helpful where
there is scleral spread or perforation or in cases
where compliance with the treatment regimen is
questionable.
42. ManagementManagement
MonotherapyMonotherapy;
Fluoroquinolone (Ciprofloxacin 0.3% or ofloxacin
0.3%
But may be corneal toxicity (white corneal
precipitates)
Topical antibioticsTopical antibiotics
Initial instilation hourly intervals.
If response favourable => reduced 2hourly during
waking hours.
If progress => fortified drops
43. ManagementManagement
Oral ciprofloxacinOral ciprofloxacin, 750mg b.id, when
juxtalimbal ulcer, to prevent spread to sclera.
SteroidSteroid is controversial
Benefits of steroid topical reducing stromal
necrosis vs scarring, but decreased fibroblast
activity vs wound healing incraesed risk of
perforation.
44. Cycloplegic and mydriatic drug:
atropine 1% or cyclopentolate 1% or Homatropine
2%. These drugs prevents ciliary spasm, relieves
pain, prevent dangerous results of iridocyclitis,
breaks adhesions and prevent synechia
formation
45. 3. CleanlinessCleanliness: Irrigation with normal salin to
remove conjunctival discharge and necrotic
material
4. Application of heatApplication of heat: provides comfort and
causes vasodilatation
5. Protection of eye from external
environment with dark glassesdark glasses
46. In cases of progressive corneal ulcer Scraping
of ulcer may be used.
Analgesic anti-inflammatory.
Acetazolamide Tab is added in cases of
impending perforation or perforated corneal
ulcer in dosage of 250 mgm upto four times a
day
47. Non-responsive / Progressive Corneal UlcerNon-responsive / Progressive Corneal Ulcer
Re-evaluate for
Drug toxicity
Non-infectious causes or Unusual organisms.
Modification of anti-microbial therapy
Therapeutic keratoplasty may be undertaken
48. Treatment of perforated corneal ulcerTreatment of perforated corneal ulcer
Rest
Continue treatment of corneal ulcer with
modification, i.e. firm bandage or bandage contact
lens
All forced expiration like coughing, sneezing,
blowing of nose etc must be avoided
Use of tissue adhesive (Glue): N-butyl 2-ethyl
cyanoacrylate
Therapeutic penetrating keratoplasty or conjunctival
flap
49. Cyanoacrylate tissue adhesiveCyanoacrylate tissue adhesive
treat progressive corneal thinning,
descemetocele, and corneal perforation .
In addition to its tectonic supporttectonic support and
bacteriostatic effectsbacteriostatic effects.
Perforations up to 2–3 mm in diameter can be
sealed by the tissue adhesive.
Necrotic tissue and debris should be removed
prior to application of the glue.
The adhesive is usually left in place until it
dislodges spontaneously or a keratoplasty is
performed.
50.
51. Collagen Cross linkingCollagen Cross linking
new treatment for multidrug-resistant infectious
keratitis.
This technique has showed promising results
specially in patients with corneal melting and
impending perforation.
Corneal melting has been arrested and complete
epithelialization achieved in several cases.
52. is one of the most difficultdifficult forms of microbial keratitis
to diagnose & to treat successfully.
Fugus may be a part of normal external ocular flora. ( 3-
28% of normal eyes)
Most commonly seen are:Most commonly seen are:
Aspergillus most common organism worldwide
Candida Penicillium Cladosporium
54. PathogenesisPathogenesis
Fungi gain entry into stroma through a defect in epithelial
barrier.
In stroma, cause tissue necrosis & host inflammatory
reaction.
Fungus can penetrate deep into stroma & through intact
descemet’s membrane.
Blood borne growth inhibiting factors may not reach
avascular structures of eye like cornea so fungi continues to
grow & persists i.e. why conjunctival flap help in control ofwhy conjunctival flap help in control of
fungal infection.fungal infection.
56. Clinical Features
Symptoms:
Foreign body Sensation Slow onset increasing Pain
Clinical signs are more severe than symptoms.Clinical signs are more severe than symptoms.
Signs:
NonspecificNonspecific:
Conjunctival injection Epithelial defect A C reaction
SpecificSpecific:
Infiltrate Feathery MarginsFeathery Margins Elevated edges
Rough Textured Satellite lesionsSatellite lesions Endothelial Plaque
HypopyonHypopyon ( Non Sterile, thick & immobile)
Yellow line of demarcationYellow line of demarcation
61. Laboratory DiagnosisLaboratory Diagnosis
StainsStains: Gram Stain
Giemsa Stain
PAS Stain
Fluoroscent MicroscopyFluoroscent Microscopy
Acridine Orange
Calcoflour white
SmearSmear: Potassium Hydroxide Wet Mount
(10-20%)
62. Sabouraud's agarSabouraud's agar is the principalis the principal
mediummedium
CulturesCultures
CornealCorneal biopsybiopsy
It is more sensitive than histopathological examination.It is more sensitive than histopathological examination.
It is a micro-trephineIt is a micro-trephine
63. Confocal Microscopy
allows in vivo visualization of the organisms at variousallows in vivo visualization of the organisms at various
levels in cornea.levels in cornea.
It offers magnifications of up toIt offers magnifications of up to 32003200 toto 35003500 with increasedwith increased
image contrast.image contrast.
64. By measuringBy measuring (l,3)-beta-D-glucan(l,3)-beta-D-glucan,,
one of the major components of fungalone of the major components of fungal
cell wall in tears it is a reliable noncell wall in tears it is a reliable non
invasive methodinvasive method
polymerase chain reactionpolymerase chain reaction (PCR)(PCR)
67. Indication for SystemicIndication for Systemic
antifungalsantifungals:
( voriconazole 1st
choice)
Severe deep keratitis
Scleritis
Endophthalmitis
Prophylactic after Penetrating
Keratoplasty
68. Surgical management
1. Debridement
2. Therapeutic Penetrating Keratoplasty
3. Conjunctival Flap
4. Flap + Penetrating Graft
5. Lamellar Graft
6. Cryotherapy ( In Keratoscleritis)
7. Excimer LASER:
PTK to eradicate the infiltrates and facilitate
antifungal therapy.
72. Dendritic ulcerDendritic ulcer
Classic herpetic lesionClassic herpetic lesion
The borders are slightly raised,grayish.The borders are slightly raised,grayish.
On resolution, a dendrite-shaped scar, calledOn resolution, a dendrite-shaped scar, called
aa ghost dendriteghost dendrite, may remain in the, may remain in the
superficial stromasuperficial stroma
73. Geographic ulcerGeographic ulcer
Immunocompromised, on topical steroids, orImmunocompromised, on topical steroids, or
have longstanding, untreated ulcers terminalhave longstanding, untreated ulcers terminal
bulbs are seen at the peripherybulbs are seen at the periphery
74. Marginal keratitisMarginal keratitis
Located near the limbusLocated near the limbus
The presence of an epithelial defect and lack ofThe presence of an epithelial defect and lack of
corneal sensation can aid in diagnosiscorneal sensation can aid in diagnosis
They are more resistant to treatment and frequentlyThey are more resistant to treatment and frequently
become trophic ulcersbecome trophic ulcers
75. Metaherpetic (trophic) ulcerMetaherpetic (trophic) ulcer
Causes-Causes-
Toxicity from antiviral medicationsToxicity from antiviral medications
Lack of neural-derived growth factorsLack of neural-derived growth factors
Poor tear surface.Poor tear surface.
Neurotrophic ulcers start as roughenedNeurotrophic ulcers start as roughened
epithelium, then breaks down to produce anepithelium, then breaks down to produce an
epithelial defect with smooth marginsepithelial defect with smooth margins
76. TreatmentTreatment
Stop toxic medicationsStop toxic medications
Tear film supplementationTear film supplementation
Bandage contact lensesBandage contact lenses
Amniotic membraneAmniotic membrane
The cautious use of topical steroids may beThe cautious use of topical steroids may be
necessary if there is significant underlyingnecessary if there is significant underlying
inflammationinflammation
77. Stromal and endothelial keratitisStromal and endothelial keratitis
Immune-mediated response.
Focal, multifocal or diffuse stromal
opacities
With new vessels “interstitial
keratitis”
Necrotising keratitis
Localised endothelial dysfunction
“disciform keratitis”
Keratouveitis
78. Triggers for recurrence of HSKTriggers for recurrence of HSK
OphthalmicOphthalmic SystemicSystemic
Contact lens wear
Eye injury
Corneal grafting
Laser eye surgery
Cataract surgery
Intravitreal injections
Topical prostaglandin
analogs
Stress
Systemic infection/fever
Sunlight exposure
Menstruation
Genetic factors
79. TreatmentTreatment
Debridement (also use for PCR or
culture)
Monotherapy with topical antiviral
(Aciclovir, Ganciclovir, Trifluridine)
No added benefit of oral antiviral but
may be useful in kids or allergic
patients
Normal dendrites heal in 1-3 weeks
If not think toxicity, resistance or wrong
diagnosis!
80. Treatment
Stromal disease
Mainstay is topical steroids
Always under antiviral coverAlways under antiviral cover
Systemic aciclovir reduces
recurrence of stromal keratitis by
50%
Aciclovir 400 mg bdAciclovir 400 mg bd
82. PathogenesisPathogenesis
primary infection occurs before the age of 10,
manifests as chickenpox (varicella)
The virus then establishes a latent state in the
sensory ganglia
When there is diminished virus-specific and cell-
mediated immunity, the virus may reactivate and
spread to the corresponding dermatome .
85. CorneaCornea
Five basic clinical forms:
Epithelial keratitis
(acute or chronic)
Stromal keratitis
Disciform keratitis
Limbal vascular keratitis
Neurotrophic keratitis.
86. UveitisUveitis
Nongranulomatous or granulomatous
iridocyclitis
LensLens Posterior subcapsular cataracts
Anterior Chamber Angle and GlaucomaAnterior Chamber Angle and Glaucoma
Plugging of the trabecular meshwork
Pupillary-block glaucoma secondary to
posterior synechiae.
Peripheral anterior synechiae
Chronic open-angle glaucoma-due to
damage to the trabecular meshwork
87. Pupil
Horner’s syndrome
A tonic pupil secondary to herpes zoster
ciliary ganglionitis
Optic Nerve
Neuroretinitis, retrobulbar neuritis, or an
ischemic optic neuropathy.
88. VitreousVitreous
Vitreous opacities, vitritis, and vitreous hemorrhage
RetinaRetina
Retinal hemorrhages
Retinal thrombophlebitis
Branch or central retinal artery occlusion
Retinal arteritis
Necrotizing retinopathy, necrotizing retinitis
Exudative or rhegmatogenous retinal detachment
Ischemic perivasculitis
90. Postherpetic NeuralgiaPostherpetic Neuralgia
Pain that continues following rash
healing
Pain has three phases:
Acute pain occurring within 30 days
after rash onset
Subacute herpetic neuralgia that
persists beyond the acute phase but
resolves before 120 days
Chronic PHN that persists 120 days or
more after rash onset
91. DiagnosisDiagnosis
The diagnosis of herpes zoster disease
is based on clinical findings
Cytologic examination reveals multiple
eosinophilic intranuclear inclusions
(Lipschutz bodiesLipschutz bodies) and multinucleated
giant cells (Tzanck preparationTzanck preparation)
Electron microscopy
PCR
93. Palliative therapy including cool
compresses, mechanical cleansing of the
involved skin, and topical antibiotic
ointment without steroid.
Débridement may also be helpful
Neurotrophic keratitis or the epithelial
defects -nonpreserved artificial tears, eye
ointments, therapeutic soft contact lenses
94. Tarsorrhaphy, conjunctival flap.
Steroids should not be used in cases of
exposure or neurotrophic keratitis because
of the possibility of keratolysis.
Topical cycloplegics
Aqueous suppressants and topical
corticosteroids should be used to treat HZO
glaucoma
95. Herpes zoster retinitis, optic neuritis,
chorioretinitis, acute retinal necrosis
syndrome, and progressive outer retinal
necrosis are best treated with a
combination of systemic steroids and
acyclovir i.v
96. Postherpetic Neuralgia treatmentPostherpetic Neuralgia treatment
Analgesics
Antidepressants as carbamazepine, and
phenytoin
Famciclovir significantly reduce the
duration but not incidence
Steroids have no effect on PHN
Amitriptyline for 90 days reduced the
incidence of pain at 6 months.
Trial of percutaneous electrical nerve
stimulation (PENS)
97. FUTURE DIRECTIONSFUTURE DIRECTIONS
Heat shock and glycoprotein subunit vaccines have
shown some promise in clinical trials in decreasing
the number and severity of recurrences
Although monotherapy with interferon has not been
found to be effective, it increases the efficacy of
acyclovir and ganciclovir when given in combination
98. •First recognized in 1973, is a rare, vision
threatening, parasitic infection seen most
often in contact lens wearerscontact lens wearers.
•It is often characterized by pain out ofpain out of
proportion to findingsproportion to findings and the late
clinical appearance of a stromal ring
shaped infiltrate.
99. EtiologyEtiology
Two of the eight known species of Acanthamoeba, A.
castellanii and A polyphaga,. Acanthamoeba are commonly
found shower water, and contact lens solution.
100. Risk FactorsRisk Factors
•contact lens wear, 80% of A
keratitis appears in contact lens
wearers.
•exposure to organism (often
through contaminated water)
•corneal trauma.
•Low levels of anti-
Acanthamoeba IgA in tears.
101. Diagnosis of AcanthamoebaDiagnosis of Acanthamoeba
HistoryHistory
Patients should be asked about contact lens wear and
hygiene, contact lens solutions, recent corneal trauma,
and recent exposure to water sources.
SymptomsSymptoms
pain out of proportion to findings.
Patients may also complain of decreased vision,
redness, foreign body sensation, photophobia, tearing,
and discharge.
102. Signs
•Early signs may be mild and non-specific.
•Possible findings include epithelial irregularities,
epithelial or subepithelial infiltrates, and
pseudodendritespseudodendrites.
•Later signs include stromal infiltrates (ring-ring-
shaped, disciformshaped, disciform), epithelial defects, radialradial
keratoneuritiskeratoneuritis, scleritis, and anterior uveitis (with
possible hypopyon). Advanced signs include
stromal thinning and corneal perforation.
103. Early epithelial stage of infection. Linear
configuration resembles the epithelial form
(dendritic) of herpes simplex keratitis.
106. Medical therapyMedical therapy
Different regimens include topical
preparations of BroleneBrolene, Neomycin-
Polymyxin, polyhexamethylene
biguanide (PHMB), chlorhexadine,
and voriconazole. Some
practitioners recommend oral
ketoconazole.
107. Medical follow upMedical follow up
•Patients should be followed very closely (daily
or almost daily).
•Acanthamoeba cysts are so resistant to
treatment, medical treatments should be tapered
very slowly and, if necessary, continued for
many months.
•SteroidsSteroids are controversialare controversial and may worsen the
condition by inhibiting the host immune
response.
Editor's Notes
Inclusion bodies of Chlamydia by Giemsa stain.
Corneal surface irradiance was approximately 3 mW/cm2 for a period of 30min. In all cases [23-25,27-29,34-38], during the induction period, 0.1% riboflavin and 20% dextran T500 drops were topically administered to the cornea for a period of 20 to 30min at intervals of 2 to 3min.