Retinal vasculitis refers to the inflammation of the retinal vessel resulting in evident clinical manifestations i.e. vascular sheathing, leakage and occlusion. This presentation covers the etiology, pathogenesis, clinical features, diagnosis and management of this spectrum of retinal disease.
Vitreous (Attachments, age changes, vitreous hemorrhage, Vitreous Detachment)Maryam Fida
Vitreous
Vitreous is an inert, avascular, transparent, jelly like structure.
Serve as one of refractive media of the eye and has optical functions.
It gives structural integrity to eye and provide nutrients to the lens, ciliary body and retina.
Constitute 80% volume of the eye.
Contain collagen fibrils, mucopoly-saccharides and hyaluronic acid.
It’s a hydrophilic gel which become ‘’fluid’’ when protein coagulates.
Reasons for coagulation of proteins could be,
• Advancing senile age
• Degenerations, e.g. as in high myopia
• Chemical and mechanical trauma
Internal limiting membrane on inner surface of retina separate it from vitreous. There is potential space ‘subhyaloid space’ between two.
Figure 1 structures of vitreous
Vitreous attachments
1. Anteriorly to the lens and ciliary epithelium in front of ora serrata. Part of vitreous about 4mm across ora serrata is called as ‘base of vitreous’. Here, attachment is strongest.
2. Posteriorly to the edge of optic disc and macula lutea (foveal region) forming ring shaped structure around them.
Figure 2 vitreous attachments
Age changes in Vitreous
Vitreous undergo certain physical and biochemical changes with aging.
1. At birth_ the Cloquet’s canal runs straight from lens to optic disc. It contains primary vitreous.
2. In young persons_ vitreous gel is homogenous but its fibers become coarse with process of advancing age.
3. In old age and high myopes_ secondary vitreous liquified (syneresis) and shrinks, producing a vitreous detachment, vitreous and retinal hemorrhage and retinal break.
Figure 3 Vitreous at birth Figure 4 Vitreous in young adults.
Figure 5 vitreous detachment in old age
Vitreous Hemorrhage
Vitreous hemorrhage is the extravasation, or leakage, of blood into the areas in and around the vitreous humor of the eye.
TYPES
There are two types of vitreous hemorrhage.
1. Peripheral or subhyaloid hemorrhage _ occurs between retina and vitreous.
Blood remains fluid, red in color
Blood moves with gravity forming boat-shaped figure in macular area.
Figure 3 subhyaloid hemorrhage
2. Intravitreal hemorrhage_ the hemorrhage may get absorbed or degenerate to form a white fibrous tissue mass.
Etiology
Common causes of vitreous hemorrhage are;
i. Trauma_ by contusion or penetrating injury
ii. Vitreous retraction_ vitreous fibrous bands or membrane retraction
iii. Eale’s disease_ due to retinal vasculitis and periphlebitis
iv. Blood dyscrasias_ leukemia, sickle cell anemia, purpura.
v. Diabetes mellitus_ common in diabetic proliferative retinopathy
vi. Central retinal vein thrombosis
vii. Malignant hypertension_ often results in large intravitreal hemorrhage.
Symptoms
I. Black spots or clouds maybe seen in front of eye.
II. Impaired vision maybe up to perception of light.
Signs
1. Fundus examination
a) Faint or no red reflex seen
b) Grey opacities maybe present in vitreous
Figure 4 (A) Fundus exami
Retinal vasculitis refers to the inflammation of the retinal vessel resulting in evident clinical manifestations i.e. vascular sheathing, leakage and occlusion. This presentation covers the etiology, pathogenesis, clinical features, diagnosis and management of this spectrum of retinal disease.
Vitreous (Attachments, age changes, vitreous hemorrhage, Vitreous Detachment)Maryam Fida
Vitreous
Vitreous is an inert, avascular, transparent, jelly like structure.
Serve as one of refractive media of the eye and has optical functions.
It gives structural integrity to eye and provide nutrients to the lens, ciliary body and retina.
Constitute 80% volume of the eye.
Contain collagen fibrils, mucopoly-saccharides and hyaluronic acid.
It’s a hydrophilic gel which become ‘’fluid’’ when protein coagulates.
Reasons for coagulation of proteins could be,
• Advancing senile age
• Degenerations, e.g. as in high myopia
• Chemical and mechanical trauma
Internal limiting membrane on inner surface of retina separate it from vitreous. There is potential space ‘subhyaloid space’ between two.
Figure 1 structures of vitreous
Vitreous attachments
1. Anteriorly to the lens and ciliary epithelium in front of ora serrata. Part of vitreous about 4mm across ora serrata is called as ‘base of vitreous’. Here, attachment is strongest.
2. Posteriorly to the edge of optic disc and macula lutea (foveal region) forming ring shaped structure around them.
Figure 2 vitreous attachments
Age changes in Vitreous
Vitreous undergo certain physical and biochemical changes with aging.
1. At birth_ the Cloquet’s canal runs straight from lens to optic disc. It contains primary vitreous.
2. In young persons_ vitreous gel is homogenous but its fibers become coarse with process of advancing age.
3. In old age and high myopes_ secondary vitreous liquified (syneresis) and shrinks, producing a vitreous detachment, vitreous and retinal hemorrhage and retinal break.
Figure 3 Vitreous at birth Figure 4 Vitreous in young adults.
Figure 5 vitreous detachment in old age
Vitreous Hemorrhage
Vitreous hemorrhage is the extravasation, or leakage, of blood into the areas in and around the vitreous humor of the eye.
TYPES
There are two types of vitreous hemorrhage.
1. Peripheral or subhyaloid hemorrhage _ occurs between retina and vitreous.
Blood remains fluid, red in color
Blood moves with gravity forming boat-shaped figure in macular area.
Figure 3 subhyaloid hemorrhage
2. Intravitreal hemorrhage_ the hemorrhage may get absorbed or degenerate to form a white fibrous tissue mass.
Etiology
Common causes of vitreous hemorrhage are;
i. Trauma_ by contusion or penetrating injury
ii. Vitreous retraction_ vitreous fibrous bands or membrane retraction
iii. Eale’s disease_ due to retinal vasculitis and periphlebitis
iv. Blood dyscrasias_ leukemia, sickle cell anemia, purpura.
v. Diabetes mellitus_ common in diabetic proliferative retinopathy
vi. Central retinal vein thrombosis
vii. Malignant hypertension_ often results in large intravitreal hemorrhage.
Symptoms
I. Black spots or clouds maybe seen in front of eye.
II. Impaired vision maybe up to perception of light.
Signs
1. Fundus examination
a) Faint or no red reflex seen
b) Grey opacities maybe present in vitreous
Figure 4 (A) Fundus exami
Normal thyroid on US-
Homogenous with medium level echogenicity.
Thin hyperechoic capsule, which becomes calcified in pts with uremia or calcium metabolism disorder.
Superior and inferior thyroid artery and vein.
Mean diameter of artery 1-2 mm with PSV of 20-30 cm/s
Veins can ne dilated upto 10 mm.
The recurrent laryngeal nerve runs with inf thyroid artery and passes between esophagus and thyroid lobeon left side & logus coli and thyroid lobe on righjt side.
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.
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
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
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.
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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
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.
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
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.
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.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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3. Capillary Hemangiomas
Common primary benign tumors of the orbit in children.
May present at birth or in first few weeks after birth, enlarges dramatically
over 6-12 months of life, and involuting after first year, 75% resolve during
first 4-5 years.
Risk : premature babies & mothers who had undergone chronic villous
sampling.
Superficial appear as bright red, soft mass with dimpled texture or
Subcutaneous & bluish in color.
Always be aware of rapidly growing mass s/o malignancy –
Rhabdomyosarcoma.
4. Capillary Hemangiomas
MRI may be used to help distinguish CH & lie in superonasal quadrant of orbit
& medial upper eyelid.
Associated with hemangiomas on other parts of the body.
Lesions that involve neck can compromise the airway & lead to respiratory
obstruction, and multiple large visceral lesions can produce
thrombocytopenia. (Kasabach-Merritt syndrome).
5. Capillary Hemangiomas
Main ocular complications :
amblyopia, strabismus, and
anisometropia.
Most lesions regress spontaneously ,
therefore, observation, refractive
correction, and amblyopia therapy
are the first line of management.
Treatment consists of steroids,
administered either topically, by
local injection, or orally.
Adverse effects : necrosis of the skin,
S/C fat atrophy, systemic growth
retardation, risk of orbital hmrg &
retinal embolic visual loss.
.
6. Capillary Hemangiomas
Recent studies, β-blockers (propranolol & topical timolol gel), careful with
combination with steroids.
Surgical excision with meticulous hemostasis.
Radiation therapy : cataract, bony hypoplasia & future malignancy.
Pulse-dye laser for superficial components of hemangioma
7. Cavernous hemangioma
Most common benign neoplasm of the
orbit in adults.
W > M
Slowly progressive proptosis, growth
accelerates during pregnancy.
Other : retinal striae, hyperopia, ON
compression, Increased IOP,
strabismus.
Orbital imaging : homogenously
enhancing, well-encapsulated mass.
MRI : small intralesional vascular
channels containing slowly filling
blood.
Chronic lesions : Phleboliths.
8. Cavernous hemangioma
Histologically, lesions are encapsulated & are composed of large cavernous
spaces containing RBCs, walls contain smooth muscle.
Surgical excision if the lesion compromises ocular function.
Approach for surgery is dictated by location of lesion.
Coronal imaging is important to find relation with ON.
Differentials : Hemangiopericytoma
9. Varices – Combined venous-lymphatic
malformations
Primary varices consist of a plexus
of thin walled distensible low-flow
vein like vessels that are commonly
intrinsic to the normal circulation.
Probably hamartomatous
Varices of lid & conjunctiva.
Present at anytime from early
childhood to late middle age.
Occurs secondarily to a local high
flow vascular lesion or trauma.
10. Varices - Diagnosis
Usually unilateral and the most
upper nasal.
Intermittent non-pulsatile proptosis
without a bruit.
Elicitated by increasing venous
pressure through coughing or Valsalva
Imaging shows lobulated mass with
variable contrast enhancement , amy
demonstrate phleboliths &
sometimes orbital expansion or
associated orbital wall defect
Complication : acute orbital
hemorrhage, thrombosis, atrophy of
surrounding fat, giving enophthalmos
with a deepened
11. Varices - Treatment
Small lesions doesn’t require treatment.
Surgical excision is technically difficult as they are friable & bleed easily.
Embolisation & C02 laser surgery may be helpful.
Indication for surgery : pain , severe proptosis & ON compression.
12. Lymphatic malformations
K/a lymphangiomas.
Represents vascular dysgenesis.
Occurs as disruption of the initially
pluripotent vascular analage, which
leads to aberrant developmene &
congenital malformations.
First decade
Contain both venous & lymphatic
components.
Enlarge during URTI., sudden
proptosis caused by spontaneous
intralesional haemorrhage.
13. Lymphatic malformations
Histologically, large, serum-filled channels lined by flat endothelial cells that
have immunostaining pattern consistent with lymphatic capillaries.
Some of them are localised, slowly progressive, others may diffusely infiltrate
orbital structures & enlarge.
MRI : Pathognomic : Multiple grapelike cystic lesions with fluid layering of the
serum & RBCs.
14. Lymphatic malformations - Management
Surgical intervention is deferred unless any affect in vision.
Subtotal resection to avoid sacrifice of important structures.
Intralesional sclerosing agents
Orbital hmrg should be allowed to resorb spontaneously, but should be
cautious in ON or CU : hollow bore needle, open surgical exploration.
15. Venous malformation
Low flow vascular lesions from vascular dysgenesis.
May exhibit enophthalmos at rest.
Proptosis increases when head is dependent or after a Valsalva maneuver s/o
valsalva maneuver.
Diagnosis : contrast enhanced rapid spiral CT during valsalva shows
characteristic enlargement of the engorged veins.
Treatment : conservative, avoid biopsy.
Surgery : vision-threatening compressive ON.
16. Arteriovenous Malformations
High-flow developmental anomalies resulting from vascular dysgenesis.
Composed of abnormally formed anastomosing arteries & veins without an
intervening capillary bed.
Dilated corkscrew episcleral vessels may be prominent.
Selective occlusion of the feeding vessels, followed by surgical excision of
malformations.
17. AV fistula
Acquired lesions caused by abnormal direct communication between an artery
& a vein .
Blood flows directly from artery to vein without passing through an
intervening capillary bed.
Cause : Trauma or degeneration.
2 forms : Carotid cavernous fistula – basal skull #.
Dural cavernous fistula – degenerative process in older patients.
18. Carotid cavernous fistula
High blood flow rate
Characteristic tortous epibulbar vessels & a bruit may be audible
Pulsatile proptosis present
Ischaemic ocular damage : diversion of arterialised blood into venous system,
which causes venous outflow obstruction.
Results in elevated IOP, choroidal effusions, blood in Schlemm canal,
nongranulomatous iritis
Increased pressure in Cavernous sinus : compression of 3,4,6 CN associated
with EOM palsy.
19. Dural cavernous fistula
Occurs when small meningeal arterial branches communicates with venous
drainage.
Dural fistulas produce less blood flow than carotid cavernous fistula.
Their onset can be insidious with only mild orbital congestion, proptosis,&
pain.
Arterialisation of the conjunctival veins chronic red eye.
Asymmetric IOP elevation increased episcleral venous pressure on ipsilateral
side.
20. Dural cavernous fistula
CT shows diffuse enlargement of all EOM resulting from venous engorgement
& characteristically enlarged SOV.
Selective arteriography
Embolisation using coils to obstruct the fistula is generally accomplished
through an endovascular transarterial route.
22. Optic nerve glioma
Uncommon
Usually benign, tumors that occur predominantly in children in 1st decade of
life
Malignant ON glioma are very rare & occur in adult male.
Malignant ONG : severe retro-orbital pain, U/L or B/L visual loss & typically
massive swelling & hemorrhage of ON head .
Despite high dose radiotherapy & chemotherapy, these tumors usually result
in death within 6-12 months.
23. Optic nerve glioma
Upto half of ON gliomas are associated with neurofibromatosis.
C/F : gradual, painless, U/L axial proptosis associated with loss of vision & an
afferent pupillary defect.
Other : OA, OD swelling, nystagmus & strabismus.
Chiasm is involved in half the cases.
24. Optic nerve glioma – Pathological
feature
Grossly : smooth, fusiform intradural lesion.
Microscopically benign tumors are considered juvenile pilocytic (hairlike)
astrocytomas, arachnoid hyperplasia, muco substance & Rosenthal fibers.
ONG in patient with NF often proliferate in the subarachnoid space.
25. Optic nerve glioma – Diagnosis
By means of orbital imaging.
CT & MRI shows fusiform enlargement of the ON, with stereotypical kinking of
the nerve.
MRI : cystic degeneration, more accurate in defining the lesion.
26. Optic nerve glioma - Management
Controversial
Most cases remain stable, some behaves aggressively.
1. Observation only
2. Surgical excision
3. Radiation therapy
4. Chemotherapy
27. Optic nerve glioma – observation
Good vision
Radiological evidence confines tumor within the orbit.
F/U with MRI
28. Optic nerve glioma – Surgical excision
Rapid Intraorbital tumor growth.
Corneal exposure.
Compromised cosmesis.
Effort to prevent chaismal invasion.
Use intracranial approach to obtain tumor free surgical margin.
Complete excision is possible if the tumor ends 2-3 mm anterior to the
chaisma.
29. Optic nerve glioma – Radiation therapy
Sole treatment if the tumor cant be resected & if the symptoms progress.
Postoperative radiation of the chiasma & optic tract , if the involvement is
extensive.
Last resort : debilitating side effects : mental retardation, growth
retardation, & secondary tumors within the radiation field.
30. Optic nerve glioma-Chemotherapy
Combination chemotherapy : actinomycin D, vincristine, etoposide are
effective with progressive chiasmal/hypothalamic gliomas.
May delay the need for radiation therapy & thus enhance long-term
intellectual development & preservation of endocrinal function in children.
Chemotherapy carry risk of blood-borne cancer.
Careful individualisation, decision should be made on tumor growth
characteristics, extent of ON & chaismal involvement
Clinical, radiological evaluation , the VA of the involved & uninvolved
eye,presence or absence of concomitant neurological or systemic disease
31. Neurofibroma
Tumors composed chiefly of proliferating Schwann cells within the nerve
sheaths .
Axons, endoneural fibroblasts, and mucin are noted histologically.
Plexiform neurofibromas
Discrete neurofibromas
32. Plexiform neurofibromas
Consist of diffuse proliferation of Schwann cells within nerve sheaths, usually
occur in NF-1.
Well vascularised & infiltrative lesions, making surgical excision difficult.
33. Discrete neurofibromas
Less common than plexiform
Usually can be excised without recurrence.
Surgery is limited to tumors that compromise vision or produce disfigurement.
34. Neurofibromatosis 1
Aka von Reckinghausen disease
AD pattern
Characterised by presence of hamartomas involving the skin, eye, CNS, &
viscera classified as phakomatosis.
NF1 is most common phakomatous disorder.
Plexiform neurofibromas involving the lateral aspect of the upper eyelid & S-
shaped contour of the lid margin, pulsating proptosis secondary to sphenoid
bone dysplasia, & ON glioma.
35. Meningioma
Invasive tumor that arise from the arachnoid villi
Originate intracranially along the sphenoid wing with secondary extension
into the orbit through the bone, the superior orbital fissure, or the optic
canal, or may arise primarily in the optic nerve.
36. Meningioma – Ophthalmic manifestation
Arising near the sella & ON cause early visual field defects & papilloedema or
OA.
Arising near the pterion , often produce a temporal fossa mass& may be
associated with proptosis/non-axial, eyelid edema,& chemosis.
Sphenoid wing meningiomas : hyperostosis of the involved bone & hyperplasia
of associated soft tissues. Presence of dural tail , differentiates from fibrous
dysplasia.
37. Meningioma –primary orbital
meningiomas
Originate in the arachnoid of the ON sheath.
Occurs commonly in women
3rd & 4th decade
Gradual, painless, unilateral loss of vision
Decreased VA & RAPD
ONH : Normal, atrophic,or swollen; and a optociliary shunt vessels may be
present.
ON sheath meningiomas are associated with neurofibromatosis
38. Meningioma – Imaging
Both CT & MRI show diffuse tubular
enlargement of the ON with
contrast enhancement.
CT may show calicification within
the meningioma, tram tracking.
MRI reveals a fine pattern of
enhancing striations from the
lesion in a longitudinal fashion,
which represents the infiltrative
nature .
MRI of sphenoid wing meningiomas
show dural extension into the
chiasm & the intrac
39. Meningioma-Management
Sphenoid wing meningiomas are typically observed until they cause profound
proptosis, Compressive ON, motility impairment,or cerebral edema.
Subtotal resection of a tumour (intracranial & orbital approach).
Goal of surgery : reverse the volume-induced compressive effects of the
lesion.
Post operative radiotherapy is advocated.
40. Meningioma-Management
ON sheath meningiomas should be individualised & should be minimally
consideration for surgery.
Factors : extent of visual loss & the presence of intracranial extension.
Fractionated stereotactic Radiation therapy results in stabilisation or
improvement of visual function.
Surgical excision may lead to irreversible visual loss d/t compromisation of
the ON blood supply.
In cases, with profound proptosis & severe visual loss, ON is excised with the
tumor, from back of globe to the chiasma.
41. Schwannoma
A/k/a neurilemomas
Proliferations of schwann cells that are encapsulated by perineurium.
Characteristic biphasic pattern of solid areas with nuclear palisading (Antoni
A) & myxoid areas (Antoni B).
Hypercellular schwannomas has potency to recur & seldom undergo malignant
transformation.
Well encapsulated & can be excised with relative ease.
43. Rhabdomyosarcoma
Most common primary orbital malignancy tumor of childhood.
Onset : 8-10 years
Classic clinical picture : sudden onset & rapid progression of U/L proptosis.
Early teens : gradual progressive proptosis lasting from weeks to more than a
month.
May also be present with ptosis & strabismus.
Mass present in SN quadrant of orbit, rarely from conjunctiva.
44. Rhabdomyosarcoma
Workup should be done on an urgent basis.
CT & MRI to define location & extent of the tumor.
Biopsy : anterior orbitotomy
Possible to remove rhabdomyosarcoma if it has a pseudocapsule.
45. Rhabdomyosarcoma
In smaller volume , chemotherapy & radiotherapy is more effective.
Large biopsy specimen is taken in diffusely infiltrating tumors.
Permanent light-microscopy, electron microscopy, and immunohistochemistry
are important investigation .
Palapate : cervical & preauricular LN to rule out regional metastasis.
Chest radiograph, bone marrow aspirate & biopsy & LP is obtained for distant
metastases.
46. Rhabdomyosarcoma
Arise from undifferentiated pluripotential mesenchymal elements in the
orbital soft tissues & not from the EOM.
Grouped into 4 categories :
1. Embryonal
2. Alveolar
3. Pleomorphic
4. Botyroid
47. Rhabdomyosarcoma – Embryonal
Most common type
More than 80%
SN quadrant has predeliction
Tumor is composed of loose fascicles of undifferentiated spindle cells, only a
minority show cross-striations in immature rhabdomyosarcoma on trichrome
straining.
48. Rhabdomyosarcoma - Alveolar
Predilection for inferior orbit
Accounts for 9%
Regular compartments composed of fibrovascular strands in which rounded
rhabdomyoblasts either line up along the connective tissue strands or float
freely in alveolar space.
Most malignant form, 10 year survival rate is 10 %.
49. Rhabdomyosarcoma - Pleomorphic
Least common & most differentiated form.
Many of the cells are straplike or rounded, and cross-striations are easily
visualised with trichrome stain.
Best prognosis.
50. Rhabdomyosarcoma - Botyroid
Rare variant of embryonal rhabdomyosarcoma appears grapelike
Occurs as secondary invader from the PNS or from the conjunctiva.
51. Rhabdomyosarcoma - Management
Before 1965, the standard treatment was orbital exenteration, and the
survival rate was poor.
Intergroup Rhabdomyosarcoma studies 1-4
Since 1965, radiation & systemic chemotherapy has become the mainstay of
primary treatment . Chemotherapy is to eliminate molecular cellular
metastases.
Exenteration is reserved for recurrent cases.
Dose of radiation : 4500 to 6000 cGy, given over 6 weeks period.
Survival rate : 90% if tumor has not invaded beyond the bony orbital walls.
Adv. Effects : cataract, radiation dermatitis , & bony hypoplasia in case of
incomplete bony development.
52. Miscellaneous Mesenchymal tumors
Tumors of fibrous connective tissue, cartilage, and bone are uncommon
lesions that may invade the orbit.
Fibrous dysplasia
Fibrous histiocytoma
Osteoma
osteosarcoma
Liposarcoma
fibrosarcoma
chondrosarcoma
53. Fibrous histiocytoma
Most common
Firm & displaces normal structures
Both fibroblastic & histiocytic cells in storiform (matlike) pattern are found.
Less than 10% have metastatic potential.
Recently described solitary fibrous tumor is composed of spindle shaped cells,
with CD 34 positive.
54. Fibrous dysplasia
Benign developmental disorder of the bone that may involve a single region or
polyostotic.
CT : hyperostotic bone, MRI : lack of dural enhancemens
Association with cutaneous pigmentation & endocrine disorder : Albright
syndrome.
Treatment : resection or debulking if there’s disfigurement or visual loss d/t
stricture of Optic canal.
55. Osteomas
Benign tumor that can involve any of paraorbital sinuses.
CT : hyperostosis with well defined margins
Lesions produce proptosis, CON, & orbital cellulitis secondary to obstructive
sinusitis.
Usually asymptomatic
Symptomatic lesion requires complete excision.
56. Malignant mesenchymal tumors
Rarely appear in the orbit.
When chondrosarcoma & osteosarcomas are present, they usually destroy
normal bone & have calcifications in radiographs & CTs.
B/l retinoblastomas have high risk of osteosarcoma, chondrosarcoma ,or a
fibrosarcoma.
57. Lymphoproliferative Disorders
Lymphoid hyperplasia & lymphoma : lymphoproliferative lesions of ocular
adnexa consist a heteregenous group of neoplasms that are defined by
clinical, histologic, immunologic, molecular, and genetic characteristics.
Most orbital lymphoproliferative lesions are non-Hodkin lymphomas.
Incidence of NHL : 4TH Most common malignancy.
Hisk risk : bioactive solvent exposure & reagents, old age , chronic
autoimmune disorders.
58. Identification & classification of
lymphoproliferative disorders.
REAL (Revised European American Lymphoma)
1. Mucosa associated lymphoid tissue (MALT)
2. Chronic lymphocytic lymphoma : low-grade lesion of small, mature appearing
lymphocytes.
3. Follicular center lymphoma : low grade lesion with follicular centers
4. High grade lymphomas : large cell lymphoma, lymphoblastic lymphoma &
Burkitt lymphoma
59. Mucosa associated lymphoid tissue
(MALT)
Accounts for 40-60% of orbital lymphomas.
Originally occurring in GI, have approximately 50% of MALT .
Evidence suggest that MALT might be Ag – H.pylori
Conjunctival MALT lymphomas : chronic chlamydial infxn
Low grade malignancy
Long term follow up to observe for systemic disease involvement.
May also have histological transformation to a higher grade lesion, usually of
large type.
60. Clinical Presentation
Gradually progressive, painless mass
Located anteriorly in the orbit or beneath the conjunctiva ; show salmon-
patch appearance
Benign or malignant
Usually mold to surrounding structure rather than invade them
Reactive lymphoid hyperplasia & low-grade lymphomas : H/o slow expansion
over a period of months to years.
orbital Imaging : characteristic Puttylike moulding of the tumor to normal
structures, Bone erosion is seen with high-grade malignant lymphomas.
50% occur in lacrimal fossa, 17% are bilateral.
61. Diagnosis
For all lymphoproliferative lesion, an open biopsy is preferred.
To establish a diagnosis & to characterise the lesions morphologic,
immunologic, cytogenic, and molecular properties under REAL classification.
Reactive hyperplasia & malignant lymphoma are hypercellular proliferations
wtih sparse or absent stromal components.
Malignant lymphomas represent clonal expansions of abnormal precursor cells
Immunogenic identification of cell marker on lymphocytes : B/T cells as being
either monoclonal/polyclonal
Specific monoclonal Ab directed against surface light chain (κ or λ) are used
to study for determination of cells that represent monoclonal (malignant)
proliferations.
62. Diagnosis
Newer techniques of molecular analysis : DNA hybridisation
Approx. 90% prove monoclonal & 10% polyclonal by molecular genetic studies.
Both types have prior, concurrent or systemic spread.
Risk of systemic involvement : conjunctival > orbital > eyelid
Lymphoid lesion in lacrimal fossa carry a greater risk of systemic disease than
occurring elsewhere.
B/L periocular involvement : increases risk of systemic disease but not
definitive.
63. Management
Examination by an oncologist.
General physical examination, CBC, BM biopsy, a liver & spleen scan, chest
radiograph, serum immunoprotein electrophoresis.
CT : Thorax & Abdomen : mediastinal/retroperitoneal LN involvement .
Steroid : useful in NSOI but not in lymphoproliferative lesions.
Radiotherapy : treatment of choice.
2000-3000 cGy is typically administered.
Achieves local control in virtually all cases, if lesion is isolated , may prevent
systemic spread.
D/t invasive nature : surgical cure cant be achieved.
Aggressive lymphomas : radiation, aggressive chemotherapy or both .1/3rd of
lesion can be cured.
65. Introduction
Composed of predominantly of mature plasma cells may be plasmacytomas or
localised plasma rich pseudotumors.
Rule out : MM if there is bone destruction or any mitotic activity among the
plasmacytic elements.
Composed of lymphocytes or lymphoplasmocytes.
Shows similar spectrum but are less common.
66. Histiocytic Disorders
Langerhans cell histiocytosis / Histiocytosis X
Rare disorder of mononuclear phagocytic system
Results from abnormal immune regulation
Characterised by accumulation of dendritic histiocytes.
Children : 5-10 years
Varies from benign lesion to chronic dissemination resulting in dea
67. Histiocytic Disorders - Presentation
Lytic defect
Superotemporal orbit, sphenoid wing is affected
Relapsing episode : orbital inflammation misinterpreted as orbital cellulitis
Mass may cause proptosis
Young children present with significant overlying soft tissue , have likeliness
of multifocal or systemic involvement.
Treatment of localised orbital disease : debulking followed by intralesional
steroid injectionor low dose radiotherapy
Systemic disease are treated aggressively with chemotherapy.
68. Xanthogranuloma
Often associated with systemic manifestations
classified as 4 syndromes :
1. Necrobiotic xanthogranuloma (NBX)
2. Adult-onset asthma with periocular xanthogranuloma (AAPOX)
3. Erdheim Chester Disease (ECD)
4. Adult onset xanthogranuloma (AOX)
69. Necrobiotic xanthogranuloma (NBX)
char. by presence of S/C lesions in the eyelids & Ant. Orbit ; the lesions may
occur through out the body
Lesion have propensity to ulcerate & fibrose
Systemic findings : paraproteinemia & MM.
70. Adult-onset asthma with periocular
xanthogranuloma (AAPOX)
Periocular xanthogranuloma, asthma, lymphadenopathy, and often increased
IgG levels.
71. Erdheim Chester Disease (ECD)
Dense, progressive, recalcitrant fibrosclerosis of the orbit & internal organs,
including mediastinum , pericardium ; and the pleural, perinephric, and the
retroperitoneal spaces.
Xanthogranuloma of ECD is diffuse , may lead to visual loss.
Bone involvement & death is higher.
72. Adult onset xanthogranuloma (AOX)
Isolated xanthogranulomatous lesion without systemic involvement
Juvenile xanthogranuloma : separate non-Langerhans histiocytic disorder ,
self-limited, corticosteroid sensitive, usually focal S/C disease of childhood.
76. Pleomorphic adenomas
Most common epithelial tumor of LG.
Occurs during 4th – 5th decade.
M>F
Presents with progressive, painless downward & inward displacement of the
globe with axial proptosis.
A firm, lobular mass may be palpated –SL orbital rim
Imaging shows expansion of lacrimal fossa.
Lesions appears well circumscribed but may have nodular configuration.
77. Pleomorphic adenomas
Benign mixed tumors have a varied cellular structure consisting of a
proliferation of benign epithelial cells & stroma composed of spindle shaped
cells with occasional cartilaginous, mucinous, or even osteoid degeneration or
metaplasia. Lesion circumscribed by pseudocapsule.
Treatment : complete removal along with its pseudocapsule & a surrounding
margin of orbital tissue.
Surgery performed with preliminary biopsy.
78. Adenoid cystic carcinoma (cylindroma)
Most common malignant tumor of LG .
Causes pain : perineural invasion & bone destruction
Rapid course , less than 1 year
extends upto posterior orbit because of its capacity to infiltrate & lack of
encapsulation
Histologically, made of benign appearing cells that grow in tubules , solid
nests,, or cribriform Swiss –Cheese pattern.
Basaloid has worst prognosis than cribriform.
79. Management of malignant LG tumors
Suspicion warrants with biopsy with permanent histological confirmation.
Exenteration & radical orbitectomy with removal of the roof, lateral wall, &
floor along with overlyinf soft tissues & anterior portion of temporalis muscle
.
High dose radiation along with debulking , taken as alternative.
Despite this measure, there is perineural extension into the cavernous sinus .
Typical : multiple painful recurrences ultimately ending up in mortality from
IC extension.
80. Nonepithelial tumors of the LG
Most of them represent lymphoid proliferation or inflammations.
Up to 50% occur in LG.
May also occur in Sjögren or a localised lacrimal/salivary gland (Mikulicz
syndrome)
Usually B/L , female , c/o dry eye
Biopsy : spectrum of lymphocytic infiltration.
May have association with RA , may also have low-grade B-cell lymphoma.
83. Sinus Origin
Tumors from the nose or the PNS may secondarily invade the orbit.
Proptosis & globe displacement are common.
Diagnosis is made by imaging & must be carried upto the base of sinus.
Mucoceles & mucopyoceles
Silent sinus syndrome
SCC : most common pwithelial tumor invading orbit secondarily, arise within
the maxillary sinuses, followed by NP/OP.
86. Neuroblastoma
Metastatic orbital neuroblastoma produces abrupt ecchymotic proptosis that
may be B/l .
May also have Horner syndrome
Bone destruction is apparent, particularly in the lateral orbital wall or
sphenoid marrow
Occur late in the course of the disease , primary can be detected in the
abdomen, mediastinum, or neck.
Treatment : primarily chemotherapy, radiotherapy is reserved .
Congenital neuroblastoma of the cervival ganglia : ipsilateral Horner
syndrome with heterochromia.
87. Leukemia
May produce U/L or B/L proptosis
Acute lymphoblastic leukemia : most likely to metastasize to the orbit.
Primary leukemic mass/granulocytic sarcoma/chloroma : Rare variant of
myelogenous leukemia.
Present with sudden visual loss & swelling of ON
Orbital lesions present in advance of bone or marrow signs
Leder stain (cytoplasmic stain) – indicate granulocytic precursor cells
Survival is improved, if chemotherapy is instituted before leukemic
involevement in BM or peripheral blood.
89. Virtually any carcinomas can metastize to orbit.
Breast & lung tumors account for the majority.
Presence of pain, proptosis, inflammation, bone destruction, and early
ophthalmoplegia s/o metastatic carcinoma.
75% have known primary tumor, 25% have orbital metastasis.
Eom frequently involved d/t abundant blood supply.
2nd most common : BM space of sphenoid bone : high volume of low flow
blood, lytic destruction of lateral wall : highly suggestive.
Elevated CEA levels
Fine needle biopsy.
90. Breast carcinoma
Most commonest primary source of orbital metastases in women.
May occur many year after tumor removal.
May elicit a fibrous response that causes enophthalmos & restriction of ocular
motility.
Some responds well to hormonal therapy.
Fresh tissue for estrogen- receptor assay if metastatic breast cancer is found
on exploration.
Hormone therapy responds well for receptor positive.
91. Bronchogenic carcinoma
Most frequent origin in men.
Primary lesion may be small, CT lung should be performed if in suspicion.
92. Management of orbital metastases.
Palliative treatment
Local radiation therapy.
Wide excision of orbital lesion : carcinoids & RCC : better survival.
Editor's Notes
Uncommon, appear in midlife, depicts like capillary on ct & MRI plump pericytes surround in rich capillary netwrk.
Pterion-posterior end of the parietosphenoid fissure, lateral portion of sphenoid
Cross striation : visible on electron microscopy , not seen in light.
50%:benign mixed tumors & 50% are carcinomas.1/2 ca. are adenoidcystic, remain- mixed tumor adenoca,mucoepidermoid or sq.carcinoma