-IOL formula
1st generation formula : SRK, Binkhost
2nd generation formula : SRK II
3rd generation formula: Hoffer Q, Holladay 1, SRK/T
4th generation formula: Haigis, Holladay 2, Olsen
-The Hoffer Q, Holladay I, and SRK/T formula are all commonly used.
-IOL formula
1st generation formula : SRK, Binkhost
2nd generation formula : SRK II
3rd generation formula: Hoffer Q, Holladay 1, SRK/T
4th generation formula: Haigis, Holladay 2, Olsen
-The Hoffer Q, Holladay I, and SRK/T formula are all commonly used.
This presentation gives a brief idea about angle of anterior chamber along with its structures and diagnostic methods to grade and visualize the structures.
Aphakia and its causes. Correction of Aphakia. Advantages and disadvantages of different corrections. Surgeries and related signs and symptoms of aphakia. Complications related to Aphakia.
This presentation gives a brief idea about angle of anterior chamber along with its structures and diagnostic methods to grade and visualize the structures.
Aphakia and its causes. Correction of Aphakia. Advantages and disadvantages of different corrections. Surgeries and related signs and symptoms of aphakia. Complications related to Aphakia.
A quick guide to Ophthalmic Ultrasound/ B-Scan interpretation Mero Eye
Hello Everyone, Namaste!
We would like to notify you all that Mero Eye Foundation is going to conduct an "EYE TALKS-Webinar", we will be having our session.
Speaker Name: MR AMIT KUMAR SINGH
Topic: "A quick guide to Ophthalmic Ultrasound/ B-Scan interpretation"
DATE – MONDAY, 11th MAY 2020 @ 01.45PM IST, 02.00PM NPT (GTM +5.45)
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
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
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
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the 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 lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
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. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
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Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
- Video recording of this lecture in English language: https://youtu.be/kqbnxVAZs-0
- Video recording of this lecture in Arabic language: https://youtu.be/SINlygW1Mpc
- 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
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
2. THE CORNEATHE CORNEA
GROSS ANATOMYGROSS ANATOMY
Anterior 1Anterior 1/6 of outer coat/6 of outer coat
Curved & Domshaped
Fibrous, Transparent & No BVsFibrous, Transparent & No BVs
Diameter : Horizontal 12mmDiameter : Horizontal 12mm
Vertical 11mmVertical 11mm
Thickness: Central 0.5 - 0.6mmThickness: Central 0.5 - 0.6mm
Peripheral 0.8 – 1.0mmPeripheral 0.8 – 1.0mm
Radius of Curvature : Anterior 8 mmRadius of Curvature : Anterior 8 mm
Posterior 7 mmPosterior 7 mm
Refractive Index : 1.37 ?Refractive Index : 1.37 ?
Refractive Power : 42 D ( what is Diopeter?)Refractive Power : 42 D ( what is Diopeter?)
( What is The LIMBUS ?)( What is The LIMBUS ?)
3. 5 LAYERS5 LAYERS
(1) Epithelium
St. Squamous Nonkeratinised (5-6 layers)St. Squamous Nonkeratinised (5-6 layers)
SurfaceSurface FlatFlat cells (2-3 layers)cells (2-3 layers)
Intermed.Intermed. PolyhedralPolyhedral cells (2-3 layers)cells (2-3 layers)
BasalBasal ColumnarColumnar cells (one layer)cells (one layer)
(2)(2) Bowman’s layer
Structure less (Acellular) condensationStructure less (Acellular) condensation
Never regenerateNever regenerate
Ends as a round borderEnds as a round border
MINUTE ANATOMYMINUTE ANATOMY
4. (3) THE STROMA (Substantia Propria)(3) THE STROMA (Substantia Propria)
- 90% of corneal thickness- 90% of corneal thickness
- C T Bundles ( Regular arrangement )- C T Bundles ( Regular arrangement )
- Bundles of each layer to each other- Bundles of each layer to each other
perpendicular to next layerperpendicular to next layer
- Cells ( present in Lacunae )- Cells ( present in Lacunae )
Corneal corpuscles ( Keratoblasts )Corneal corpuscles ( Keratoblasts )
Corneal metabolism & HealingCorneal metabolism & Healing
LeucocytesLeucocytes
Inflammation
(4) DESCEMET’S MEMBRANE(4) DESCEMET’S MEMBRANE
Homogenous, Structureless & Highly ElasticHomogenous, Structureless & Highly Elastic
Resistant & Easily RegenerateResistant & Easily Regenerate
5. CORNEAL ENDOTHELIUMCORNEAL ENDOTHELIUM
One Layer of Polyhedral cellsOne Layer of Polyhedral cells
Partial dehydration of the corneaPartial dehydration of the cornea
Continuous with the Endothelium ofContinuous with the Endothelium of T MT M
NERVE SUPPLY OF THE CORNEANERVE SUPPLY OF THE CORNEA
55THTH
C.NC.N
OPHTH. division NASOCILIARY N 2 LongOPHTH. division NASOCILIARY N 2 Long CILIARY NCILIARY N
PAIN & COLD & SUPERFICIAL TOUCHPAIN & COLD & SUPERFICIAL TOUCH
6. CORNEAL PHYSIOLOGYCORNEAL PHYSIOLOGY
NUTRITIONNUTRITION (( cornea is avascularcornea is avascular ))
By diffusionBy diffusion
Tear Film Aqueous humour Limbal capillariesTear Film Aqueous humour Limbal capillaries
CORNEAL TRANSPARENCYCORNEAL TRANSPARENCY (( WHYWHY ?? ))
Anatomical Factors :Anatomical Factors :
Cornea is avascularCornea is avascular
Epithelium is nonkeratinizedEpithelium is nonkeratinized
Stromal lamellae are regularStromal lamellae are regular
Nerves are nonmyelinatedNerves are nonmyelinated
Precorneal tear filmPrecorneal tear film
Physiological Factors :Physiological Factors :
Corneal dehydrationCorneal dehydration
Uniform refractive indices of corneal tissueUniform refractive indices of corneal tissue
FUNCTIONS OF THE CORNEAFUNCTIONS OF THE CORNEA
Refractive 42 DRefractive 42 D
Protective ( corneal reflex )Protective ( corneal reflex )
7. THE LIMBUS ( The Corneo-Scleral Junction )THE LIMBUS ( The Corneo-Scleral Junction )
Corneal epithelium Conjuctival epitheliumCorneal epithelium Conjuctival epithelium
Bowman’s membrane ends as a rounded borderBowman’s membrane ends as a rounded border
Substantia propria Sclera (irregular lamellae)Substantia propria Sclera (irregular lamellae)
Descemet’s membrane Trabecular meshworkDescemet’s membrane Trabecular meshwork
Endothelium Endothelium of the angle of ACEndothelium Endothelium of the angle of AC
8. KERATITISKERATITIS
KERATOSKERATOS CORNEACORNEA
iTiS INFLAMMATIONiTiS INFLAMMATION
SUPERFICIAL KERATITISSUPERFICIAL KERATITIS Suppurative (Corneal Ulcer)Suppurative (Corneal Ulcer)
NonSuppurative (Pannus)NonSuppurative (Pannus)
INTERSTITIAL KERATITISINTERSTITIAL KERATITIS Suppurative (Central Abscess)Suppurative (Central Abscess)
NonSuppurative (Diffuse or Local)NonSuppurative (Diffuse or Local)
DEEP KERATITISDEEP KERATITIS Suppurative (Post Abscess or Ulcer)Suppurative (Post Abscess or Ulcer)
NonSuppurative (Keratitis Profunda)NonSuppurative (Keratitis Profunda)
9. SUPPURATIVE SUPERFICIALSUPPURATIVE SUPERFICIAL
KERATITSKERATITS
(CORNEAL ULCERS)(CORNEAL ULCERS)
DEFINITIONDEFINITION
Localized Necrosis of Sup. StromaLocalized Necrosis of Sup. Stroma
with destruction of overlying Epith.with destruction of overlying Epith.
ETIOLOGYETIOLOGY
Predisposing FactorsPredisposing Factors
Precipitating FactorsPrecipitating Factors
Causative OrganismsCausative Organisms
10. Predisposing FactorsPredisposing Factors
LocalLocal
a) Traumaa) Trauma
- Abrasion- Abrasion (( Gono & Diph can invade normal epithelium )
-- FB , Rubbing lashes , PTDs , CLFB , Rubbing lashes , PTDs , CL
b) Loss of corneal sensationsb) Loss of corneal sensations
c) Ocular causesc) Ocular causes (( xerosis, A deficiency, Lagoph.).)
d) Prolonged use of Steroidsd) Prolonged use of Steroids
GeneralGeneral
malnutrition Pregnancymalnutrition Pregnancy
Diabetes Liver & Renal FailureDiabetes Liver & Renal Failure
11. PRECIPITATING FACTORSPRECIPITATING FACTORS
Infection of nearby structuresInfection of nearby structures
CAUSATIVE ORGANISMSCAUSATIVE ORGANISMS
a) Bacterial e.g. Gono, Diphth., Pneumo,a) Bacterial e.g. Gono, Diphth., Pneumo, Staph, StreptStaph, Strept….….
b) Fungal ( not common )b) Fungal ( not common )
c) Viral e.g. Herpes Simplex and Zosterc) Viral e.g. Herpes Simplex and Zoster
d) Acanthamoeba (C.L.)d) Acanthamoeba (C.L.)
12. PATHOLOGY OF CORNEAL ULCERSPATHOLOGY OF CORNEAL ULCERS
Stage of InfiltrationStage of Infiltration
Inflammatory reaction PNLs
Grey disc shaped area - Oedema - Ciliary injectionGrey disc shaped area - Oedema - Ciliary injection
Stage of ulceration
A) Progressive unclean Stage
Necrotic area
ulcer with irregular Edge
Necrotic Floor
Surrounded by Dense reaction
B) Regressive Clean Stage
Large ulcer with regular Edge
Deep, Clear, Transparent Floor
Less infiltration
13.
14. Stage of HealingStage of Healing
A) Vascularization
Limbal cap. Sup. Vasc. AB & Fibroblasts
B) Fibrous tissue formation
NB :NB :
Epith. Mitosis & Migration
B.M. Never regenerate Permanent scar
Stroma Irregular F.T. Nebula or Leucoma
D.M. Regenerates as an elastic membrane
Endothelium Enlargement and Widening of cells
15. CLINICAL PICTURECLINICAL PICTURE
SymptomsSymptoms
Pain Severe ( FB or pricking sensation )Pain Severe ( FB or pricking sensation )
Irritation of nerve endingsIrritation of nerve endings
PhotophobiaPhotophobia
LacrimationLacrimation
BlepharospasmBlepharospasm
Diminution of visionDiminution of vision
SignsSigns
Lids: OedemaLids: Oedema
Conj.: Ciliary injectionConj.: Ciliary injection
Cornea: Loss of luster, Grey infilt., Oedema & +ve FTCornea: Loss of luster, Grey infilt., Oedema & +ve FT
Iris: Tender CB, Const. pupil & Aqueous flareIris: Tender CB, Const. pupil & Aqueous flare
16. COMPLICATIONS OF CORNEAL ULCERSCOMPLICATIONS OF CORNEAL ULCERS
A) Non Perforated corneal ulcer
Early Complications
(1)(1) 2ry Iridocyclitis : ( Toxins )2ry Iridocyclitis : ( Toxins )
(2) 2ry Glaucoma(2) 2ry Glaucoma : Open angle glaucoma: Open angle glaucoma
(3) Descematocele : Small translucent bleb
Not seen in children or T hypopyon ulcer
Late Complications (Healing abnormalities)
(1) Corneal opacity ( Nebula, Macula or Leucoma non adherent )
(2) Corneal Facet : rapid healing of the epith.
(3) Keratectasia : ( weak corneal scar & IOP )
(4) Pseudoptregium
17. B) COMP. OF PERFORATED CORNEAL ULCERSB) COMP. OF PERFORATED CORNEAL ULCERS
Early Complications
(1) Iris Prolapse ( Big Para central or periph. Perforation )
(2) Anterior synechia ( Small periph. Perforation)
(3) Corneal Fistula ( Small central perforation )
Lost AC IOP River Green Sign
(4) Malposition of the Lens
Sublaxation Ant. Dislocation Extrusion
(5) Intra-ocular Hge
Hyphema Vit., Ret. And choroidal hges
(6) Macular and Optic Disc Oedema
(7) Endo or Panophthalmitis
18. Late complications
(1) Ant.Polar Cataract (Toxins )
(2) Leucoma Adherent ( Large Peripheral Perforation )
- AC irregular
- Pupil pear shaped
- IOP may be high
- may be pigmented
(3) Ant. Staphyloma ( partial or total )
(4) 2ry Glaucoma (closed angle by PAS )
(5) Atrophia bulbi ( atrophy of the cil. processes )
B) COMP. OF PERFORATED CORNEAL ULCERS (cont.)B) COMP. OF PERFORATED CORNEAL ULCERS (cont.)
19. MANAGEMENT OF CORNEAL ULCERSMANAGEMENT OF CORNEAL ULCERS
INVESTIGATIONS + TREATMENT
A) Corneal Scrapping ( Culture & Sensitivity )
Gram Stain for Bacteria
Geimsa Stain for Trachoma & Acanthamoeba
Silver Stain for Fungi
B) Local ttt (1) Atropine sulphate 1%
(3) Bandage or Dark Glasses
(4) Counter irritant
(2) Dressings ( Antibiotic dps & oint )
C) Systemic ttt
Antibiotics Analgesics
Vitamins A & C
20. D) Treatment of Complications
(1) 2ry Glaucoma
Usual ttt Antiglaucoma ttt paracentesis
(2) Descematocele
Bilateral Bandage or C L
Avoid Straining
Antiglaucoma ttt
Hood Flap
PKP
(3) Perforation
Small CyanoacrylateTissue Adhesive
Large Hood Flap or PKP
21. E) Treatment of Corneal Opacity
Central Nebula
Glasses or CL
Eximer Laser
Lamellar KP
Leucoma PKP
In blind eye CCL
Tattoo
Treatment of Resistant CU
Scrapping for Culture & Sensitivity
Debridement
Cautery Chemical
Physical
S.C. injection of AB
Conjunctivoplasty
Therapeutic KP (Lamellar or Penetrating)
24. Signs ( Acute Serpiginous ulcer )
- Haziness of the cornea ( loss of luster )
- Ciliary injection
- Ulcer Near the centre
Central advancing Edge
Crescentic, undermined,
preceded by dense infiltration
Peripheral Healing Edge
Flat, Epithelialized, Vascularized
- Posterior Abscess :
Dense infiltration in front of D M
- Flourescein Test is +ve
- Hypopyon in the Anterior Chamber
( Steril Pus ) PNL +Fibrin +Iris Pigment
NB Perforation is common…why?
Desematocele is Rare
25. Treatment of Hypopyon UlcerTreatment of Hypopyon Ulcer
Treatment of the cause ( Dacryocystectomy)
Usual ttt of corneal ulcer ABCD
Subconjunctival Injection of AB
Cephazoline ( 100mg in 0.5 ml )
Tobramycin or Amikacine ( 20mg in o.5 ml )
Fortified Eye Drops
Gentamycine or Tobramycine 15mg/ml.
Treatment of 2ry Glaucoma
Cautery in Resistant Cases ( Pure Carbolic A )
26. Atypical Hypopyon Ulcer
Pyogenic organisms other than Pneumococci (20%)
Common in children with increased resistance
The Ulcer :
Anywhere in the cornea
Not Serpiginous, spreads in all directions
Perforation is less common
Desematocele may occur
27. Fungal UlcerFungal Ulcer
Predisposing Factors
Trauma with green plant
Use of Steroids
Contact Lenses
Causative Agent
Fusarium ( Filamentary fungi )
Candida ( Yeast forming fungi )
Aspergillus
Clinical Picture
Little or no ciliary Injection
Raised, dry, grey white lesion with feathery margins
Satellite lesions
Stromal deep infiltrate
Endothelial plaques
Hypopyon
28. TreatmentTreatment
Usual ttt
Topical Antifungal ttt
Natamycine 5%
Miconazole 1%
Amphotericin B o.3%
Systemic Antifungal ttt
Ketoconazole 400mg/day
Fluconazole 400mg/day
( In cases of deep Keratitis or failure of topical ttt )
Surgical ttt (PKP)
29. Acanthamoeba keratitisAcanthamoeba keratitis
Aetiology
Protozoa ( Tap water and Swimming pools )
70% of cases are C L wearers
Clinical Picture
Punctate or Dendritic K
Superficial Stromal K
Partial or Complete ring of Infiltration
Limbitis and Scleritis
Treatment
Debridment
Topical ttt
Diamidines (Propamidine)
Biguanides (Chlorohexidine 0.02%)
Aminoglycosides (Neomycin)
Antifungal (Miconazole and Ketoconazole)
30. Dendritic Corneal UlcerDendritic Corneal Ulcer
Herpes Simplex Virus ( Epitheliotropic )
1ry infection in early childhood
Dormant in 5th
Ganglion
Recurrence with body resistance
Predisposing factors
Fevers (Influenza, Common cold and Pneumonia)
Menstruation
Drugs ( Immunosuppressive drugs or Steroids)
Clinical Picture
1ry Ocular infection Dermato-blepharitis
Follicular Conjunctivitis
Epithelia Keratitis
31. Recurrent Ocular Infection (C/P of H. Keratitis)
(A) Blepharoconjunctivitis (as 1ry infection)
(B) Epithelial Keratitis
Symptoms : as those of corneal ulcer
Signs :
A) SPK
B) (Characters of Dendretic Herpetic Corneal Ulcer)
Dendritic appearance
Long course with tendency to Recurrence
Superficial ( never perforate except in … )
Never Vascularised
Hypothesia
Double Stain Test
C) Amoeboid Ulcer
due to immunity or local Steroids
35. Clinical Picture of H Z Ophthalmicus
Retina : retinal vasculitis,detachment and necrosis
Optic Nerve: Papillitis or Retrobulbar neuritis
Orbit : Orbital oedema and Proptosis
EOM : Paralytic Squint (3rd
N. palsy)
Treatment:
Acyclovir tab. 800mg 5 times/ day for 7 days
Steroids + Antibiotic skin oint.
Steroids + Antibiotic eye drops
Analgesics
36. Ulcer with LagophthalmosUlcer with Lagophthalmos
A primary ulcer in the lower 1/3 of the cornea
Bell’s phenomena
Symptoms
as usual corneal ulcer ( of vision is not marked..why?)
Signs
Incomplete lid closure
Ciliary injection & +ve flurorescein
Ulcer in lower 1/3 with straight upper border
Treatment
Usual ttt
Methyl cellulose drops 0.5% several times/day
ttt of the cause
37. KeratomalaciaKeratomalacia
Non infective ulceration and melting of the cornea
Vitamin A (malnourished infants or malabsorption in adults)
Clinical Picture
Loss of corneal luster
Appearance of yellow dots (deg. Epithelium)
Melting of the cornea
No inflammatory reaction (quite eye)
Corneal hypothesia
Conjunctiva: dry with Bitot’s spots
2ry infection Endophthalmitis
Treatment
Vit. A injection (200,000 IU/day)
ttt of hypoproteinemia ( fresh plasma)
Topical vit. A in early cases
Surgical ttt in late cases : Conj. Flap
Therapeutic CL
PK
38. Neurotrophic (Neuroparalytic) KeratitisNeurotrophic (Neuroparalytic) Keratitis
Corneal Sensation
Aetiology
Herpes Zoster
Radical ttt of 5th
Neuralgia ( Alcohol inj.)
Damage of Orbital Ns (SOF & OA syndromes)
Clinical Picture
Symptoms No pain
vision (central ulcer)
Signs Epithelial exfoliation starts at the center
Large deep ulcer perforation
Treatment
Usual ttt of corneal ulcer
Long term Bandage
Tarsorraphy ( median )
39. Traumatic Corneal ulcerTraumatic Corneal ulcer
Trauma + 2ry Infection
Trauma External: wounds, chemicals, burn & FB
Local: Lash, PTD & PTC
Treatment
Usual ttt + ttt of the cause
40. Mooren’s Ulcer ( chronic serpeginous ulcer )Mooren’s Ulcer ( chronic serpeginous ulcer )
1ry non infective corneal ulcer
Rare
Common in old age
Aetiology ( unknown )
Limbal vasculitis Proteolytic enzymes necrosis of sup. layers
Autoimmune disease
Symptoms 12345
Signs Marginal grey infiltration Crescentic Ulcer
Advanced edge ( undermined and creeps toward the center )
Healed edge ( Peripheral and vascularised )
Thin cornea
Extension is slow and perforation is rare
Treatment
Usual ttt + Topical Steroids
Topical Cyclosporine
Conj. Excision // to the ulcer
Lamellar keratoplasty
Systemic Steroids & Immunosuppressive drugs
41. Atheromatous Corneal UlcerAtheromatous Corneal Ulcer
Occurs on top of an old Leucoma
Hyaline degeneration with desquamation and 2ry infection
Resistant with bad healing
Commonly perforates due to 2ry infection
Treatment
Usual ttt
Conjunctival flap
Keratoplasty
42. Secondary Corneal UlcersSecondary Corneal Ulcers
Ulcers 2ry to MPC
Marginal, Crescentic and Superficial ( Rare )
Rapid healing
Ulcers 2ry to Gonococcal Conjunctivitis
Marginal ulcer : Most common Ring ulcer : Multiple marginal ulcers
Central and paracentral ulcers : usually perforate
Trachomatous Ulcers
A) Typical Shape Horizontal
Site In front of pannus
Superficial
Secondary infection is common
Scarred by facet ( Healing )
B) Marginal, Central and Paracentral: not related to Pannus
C) Mechanical: PTDs or Rubbing lashes
43. 2ry Corneal Ulcers2ry Corneal Ulcers
Phlyctenular Ulcers
A) Limbal ulcer: ( ulcer of limbal phlycten )
Deep, when perforate peripheral Leucoma Adherent
B) Ring ulcer: multiple phylectens
C) Fascicular ulcer: Superficial
Starts near the limbus
Creeps to the center followed by leash of B.V.
44. INTERSTITIAL KERATITISINTERSTITIAL KERATITIS
Non Suppurative iflammation of the Stroma + Uveitis
Aetiology
Delayed hypersensitivity to infectious organism
- Syphilis, T.B., Leprosy
- Herpes Simplex and Zoster, Measles and EBV (infectious M.)
Types
(1) Diffuse I.K.
(2) Dsciform Keratitis
45. Syphilitic Interstitial Keratitis
Congenital Syphilis ( 95% )
5 – 15 Years
Bilateral
Hutchinson’s triad ( I.K., Hutchinson’s teeth and Deafness )
Acquired Syphilis ( 5% )
10 years after 1ry infection
Unilateral
Uveitis and Retinitis
Symptoms
Pain, photophobia, lacrimation, redness and vision
46. Signs of Syphilitic I.K.Signs of Syphilitic I.K.
( 1 ) Progressive Stage ( 2 weeks )
Severe infiltration ( haze ) + Vascularization
Salmon patches ( reddish pink )
Ciliary injection
( 2 ) Florid stage ( 2 months )
Marked symptoms and signs
vision up to HM
( 3 ) Regressive stage ( 2 years )
Residual interstitial corneal opacity
Obliterated BV fine opaque lines
Uveitis
Investigations +ve Wassermann reaction
47. Treatment of Syphilitic I.K.Treatment of Syphilitic I.K.
- Antisyphilitic ttt ( Penicillin )
- Atropine
- Steroids
- Keratoplasty for residual opacity
DISCIFORM KERATITIS
Antigen antibody reaction ( viral antigen )
H.S. & H.Z.
Grey disc-shaped dense opacity
Loss of corneal sensation
Drop of vision
Treatment
Corticosteroids + Antiviral drugs
Tarsorraphy
48. Keratitis profunda
Localised non suppurative deep Keratitis
Aetiology
Allergic reaction to chronic infections e.g. TB
Herpes Simplex or Zoster
Trauma
Idiopathic
Clinical Picture
Diffuse deep Keratitis
Iridocyclitis
Posterior Abscess and Ulcer
Diffuse suppurative deep Keratitis
Congenital, HU, Trauma, IK and endogenous with TB and S.
49. Degenerative ConditionsDegenerative Conditions
ARCUS SENELIS
Bilateral peripheral Fatty degeneration
Common in old age
Symptoms non
Signs
Arc shaped opacity in the upper ½ of cornea then lower ½
Clear zone between the opacity and Limbus (Lucid interval of vogt)
Outer border is sharp and well defined
Inner border is diffuse and illdefined
NB ARCUS JUVENILIS may occur in hyperlipidemia or juv. DM
50. Band Shaped keratopathyBand Shaped keratopathy
Horizonal opacity ( in the interpalpebral area )
Old degenerated eyes
Hyaline degeneration + Ca deposition
51. KERATOCONUSKERATOCONUS
Definition
Progressive conical protrusion of the cornea
Starts at Puberty
Weakness of central part
Incidence
Females _ Atopy
Bilateral
+ve family history
Symptoms
Gradual of vision - Myopia ( Curvature & Axial )
- irregular Astigmatism
- Opacity at the apex of the cone
Sudden of vision (Acute Hydrops i.e. acute edema due to rupture of DM)
52. Signs of Keratoconus
A) Early
Retinoscopy ( RR is spinning or scissoring )
placido disc: ring distortion
Keratometer
B) Late
- Cone shaped central cornea seen by
Profile view
Notching of the L.L. on looking down Manson’
Slit Lamp Thin apex and deep A.C.
- Deep opacity at the apex of the cone
Rupture of BM
Folds of DM
- Fleisher ring: brown ring the cone base ( hemosidren deposition )
DD
Ant. Staph. - Keratectasia - Keratoglobus
Treatment
- Early casrs : Glasses or hard CL
Corneal Collagen Cross linking with Riboflavin
- Late cases : PKP
53. KERATOGLOBUSKERATOGLOBUS
Congenital enlargement of the Anterior Segment
Signs
Cornea: Large in diameter and curvature
AC : Deep
Iris : Tremulous
Lens : Sublaxation
Refraction: Stationary myopia
DD : Buphthalmos
Treatment: Glasses
54. KERATOPLASTYKERATOPLASTY
Aim: Replacing the opaque part by a clear cadaveric cornea
Types:
- Lamellar ( Superficial )
- Deep ( Penetrating )
NB: Both of them may be partial or total
- Tectonic : Has a specific shape according to site and indication
Indications:
- Optical a) Central corneal opacities
b) Keratoconus
- Therapeutic a) Resistant corneal ulcer
b) Corneal fistula