Beruflich Dokumente
Kultur Dokumente
Abdulrahman Al Muammar
Ocular allergy
Allergic eye diseases accounts for up to 3%
of all the medical consultations seen in
general practice.
The milder forms of allergic eye diseases
have fluctuating symptoms of itch, tearing,
and swelling.
Chronic form of the disease give rise, in
addition, to more severe symptoms including
pain, visual loss from corneal scarring,
cataract or glaucoma, and disfiguring skin
and lid changes.
Ocular allergy
Clinical classifications:
Perennial.
Toxic-induced (long standing).
Ocular allergy
2) Contact dermatoblepharitis.
3) Vernal keratoconjunctivitis (VKC
4) Giant papillary conjunctivitis (GPC
5) Atopic keratoconjunctivitis (AKC
6) Atopic blepharoconjunctivitis (ABC).
Sensitization
Acute and chronic diseases have in
common:
1) sensitization to environmental allergens.
2)Ig E mast cells activation with
subsequent mediator cascade.
3) conjunctival inflammation with
prevalence of eosinphils.
4) the presence of lymphocytes with a Th2
profile of cytokines production .
Sensitization
The conjunctiva is normally exposed to
pictogram quantities of environmental allergens
such as pollens, dust mite fecal particles,
animal dander and other proteins .
When deposited on the mucosa, these antigens
are thought to be processed by lagerhans cells
and other antigen presenting cells (APC) in the
mucosal epithelium .
Sensitization
Sensitization
. The cytokines released by Th2 cells (
IL3,IL4,IL5,IL6,IL13,GM-CSF) stimulate B cell
IgE production and inhibit development of Th1
mediated delayed type hypersensitivity
reactions .
B cells which recognize the same allergen that
induce Th2 differentiation, in present of
appropriate signals such as IL4,IL6 and IL13
undergo heavy chain switching to produce IgE.
Mast cells
Mast cells
Proliferation of these cells in allergic disorders
is probably under influence of Th2 cytokins.
Mast cells and basophils, bearing high affinity
surface receptors for Ig E are the most
important cells in IgE mediated reactions.
Mast cells
Mast cells mediators:
Histamine.
Heparin.
Itching..redness.
Anti-inflammatory.
Tryptase.
Mast cells
Mast cells
Attract eosinophils.
Eosinphils
Eosinphils
Neutrophils
Following allergen challenge, neutrophils are
the first cells to appear in tear fluid and the
predominant infiltrating cells in the conjunctive
during late phase.
Although the role of neutrophils in allergic
disorders is not clear, they can release
inflammatory mediators including leukotriens
,PAF and cytokines.
Tear level of myeloperoxidase (MPO). a
neautrophil activating marker are increased in
allergic conjunctivitis.
Lymphocytes
Lymphocytes
Seasonal allergic
conjunctivitis
SAC
Symptoms:
Itching.
Watery discharge.
Rhinitis.
Sinusitis.
SAC
Signs:
Not always present.
Lid swelling.
Ptosis.
Conj hyperemia.
Chemosis (=/- dellen).
Papillary reaction.
Follicular reaction.
SAC
Diagnosis:
Clinically.
Family history.
Conj scrapings for eosinophils.
Tear level of IgE, serum tear.
Radioallergosorbent test measures specific IgE
levels for a specific antigens.
Mast cells activity by measuring tryptase and
histamine levels in tear film.
SAC
Pathophysiology:
Type I hypersenstivity.
Late phase reaction (LPR):
SAC
Treatment:
Avoidance of allergen:
Washing allergen.
Antihistamines.
Mast cell stabilizers.
NSAIDs.
Steroids.
Immunotherapy.
Bactriacin..cephalosporins..sulfacetamide..tetracycline
Atropinehomatropine.
Epinephrine..pilocarpine..apraclonidine.
Antiviral agents.
Thimerosal..chlorhexidinebezalkonium chloride.
Clinical presentation.
Offending agents.
Conj scrapings.
Treatment:
Perennial allergic
conjunctivitis
PAC
PAC
Treatment:
Avoidance of allergen:
Washing allergen.
Antihistamines.
Mast cell stabilizers.
NSAIDs.
Steroids.
Immunotherapy
Contact
dermatoblepharitis
Reaction that may begin 24-72 hours
following instillation of topical medication.
Patients are often sensitized by previous
exposure to the offending drugs or
preservatives.
Acute eczema with erythema, leatherlike
thickening, and scaling of the eyelid.
Lower eyelid ectropion, and
hyperpigmentation.
Papillary conjunctivitis and mucoid discharge
may develop.
Contact
dermatoblepharitis
Medications commonly associated with
these symptoms:
Atropine..homatropine.
Neomycine..gentamycine..tobramycine.
Idoxuridine..trifluridine.
Thimerosal.
Type IV reaction.
Contact
dermatoblepharitis
Treatment:
Allergen withdrawal.
In severe casesbrief course of topical
steroids applied to the eyelids and
periocular skin may speed resolution.
VKC
Epidemiology:
VKC
VKC is usually bilateral, although monocular forms
and asymmetric symptoms do occur.
Three clinical forms can be observed : tarsal, limbal
(more common in African and Asian patients), and
mixed tarsal/limbal.
In majority of the cases, the disease is seasonal,
lasting from the beginning of spring until fall.
Nevertheless, perennial cases have been observed,
especially in warm subtropical or desert climates.
VKC
Symptoms:
Itching.
Tearing.
Mucus secretion.
Photophobia.
Pain.
Blepharospasm.
Decreased visual acuity.
VKC
Signs:
Papillary reaction.
Conjunctival redness and edema
GPC.
Limbal gelatinous infiltrate.
Trantas dots.
Mucus discharge.
Pseudoptosis.
Tarsal conjunctival fibrosis.
VKC
Corneal involvement:
VKC
Diagnostic approaches:
Clinically.
Specific IgE maybe assayed in serum and tears.
CBC for eosinophilia.
Conj scraping and tear cytology:
Eosinophils.
Basophils.
Neutrophils.
VKC
Pathogenesis:
Type I hypersensitivity.
Type IV hypersensitivity.
VKC
Histopathology:
Trantas dots.
Shield ulcer.
VKC
Therapy:
Preventive measures:
Change of climate.
Avoid exposure to nonspecific triggering factors such as
sun, wind, and salt water.
Antihistamines.
NSAIDS: either locally or systemically.
Steroids. Short pulses, topical/ tarsal injection.
Cyclosporine.
VKC
Corneal ulcers.
Steroids-antibiotic/eye patching.
Superficial keratectomy.
PTK.
GPC..
Local steroid injection.
papillae excision/cryotherapy/mucosal graft.
AKC
Atopy is hereditary condition that manifests in
ocular diseases, skin abnormalities, and
respiratory tract dysfunction.
Atopy occurs in 5 to 20% of the general
population.
The term AKC is misleading, although ocular
surface disease is most prominent, the
disease usually involve the lid also.
AKC
Epidemiology:
AKC
Clinical signs of the disease generally
improve with age and may totally regress.
Patients with severe cases don't follow this
trend.
AKC is often worse in the winter, but it
usually has a perennial pattern of
occurrence.
AKC
Clinical features:
Symptoms:
Bilateral itching
Tearing
Watery discharge
Burning
Photophobia
Blurred vision.
AKC
Signs:
Lid:
AKC
Conjunctiva:
AKC
Cornea:
PEE/PEK.
Intraepithelial microcyst.
Infecious and noninfecious corneal ulcer.
Peripheral micropannus.
Neovascularization extending to the central
cornea.
Keratoconus in 16% of patients with AKC.
Pellucidal marginal degeneration, and
keratoglobus.
AKC
Lens: ? In 5 to 25%
Retina:
Systemic disorders:
Hay fever.
Asthma (? in 87%).
Atopic dermatitis ( ? In 95%)- chronic pruritic inflammation
of the skin mainly forehead, cheeks, and flexor surfaces of
the arms and legs, atopic dermatitis usually begin in
childhood.
VKC Vs AKC
VKC
AKC
Age of onset
Childhood, teens
age 20 to 50
Duration
Resolved by age 50
Seasonal variation
variable
Conjunctival papillae
GPC.upper lid
Conjunctival scarring
Uncommon
skin
Uncommon
Often
Eosinophils
Numerous
Less extensive
More extensive
lens
No
ASCC/PSCC
AKC
Etiology and histopathology:
Type IV hypersenstivity
Diminished cell medicated immunity is common.
AKC
Diagnosis:
Family history.
Some level of disease activity is always present
with variable exacerbations.
Atopic dermatitis.
Papillary reaction more inferiorly than superiorly.
Rarely GPC inferiorly.
Usually begin in late teenage or more commonly
later.
Most severe type of ocular allergy.
AKC
In Vivo Tests:
AKC
AKC
Managemant:
Tears.
Vasoconstrictors.
Cold compresses
Antihistamines
NSAID.
Mast cell stabilizers.
Steroid.
Cyclosporine.
Antibiotics.
Surgical: lid procedures/ PKP.
GPC
Characterized by the presence of
abnormally large papillae ( more than
0.3 mm in diameter) on the upper tarsal
conjunctiva, conjunctival hyperemia,
excess mucus secretion, foreign body
sensation, and itching.
First reported in 1970 in patients
wearing contact lenses.
GPC
Epidemiology:
Incidence among RCL user with average
period of 10 months is 10.5%.
History of atopy plays a major role in
predisposition of GPC.
Patients with GPC report higher incidence
of allergy to pollens as well as to
medications.
GPC
Etiology:
Contact lenses:
Sutures..nylon/prolene.
Prosthesis.
Cyanoacrylate glue.
Scleral buckle.
Bleb/valve..
Vernal.
Atopy.
Epibulbar dermolipoma.
GPC
Symptoms:
Foreign body sensation.
Intolerance to CLW.
Itching.
Irritation.
Mucus secretion.
GPC
Signs:
Enlarged papillae ( > 0.3 mm in diameter),
variable in numbers, and almost always in
the upper tarsal conjunctive.
Mucus strands.
Mild to severe hyperemia.
Trantas dots and limbal inflammation..
Ptosis.
GPC
Stages:
Stage I:
Stage II:
GPC
Stage III:
Stage IV:
GPC
Pathogenesis:
Increase tryptase.
increase Ig G,M,E.
Increase eosinophil ..MBP..ECP.
Increase histamine.
Decrease lactoferin.
GPC
treatment;
Prevention:
Lens design/hygiene.
Burying sutur knots.
Microbial Allergic
Conjunctivitis
Staphylococcal blepharoconjunctivitis.
Phlyctenular keratoconjunctivitis.
Splendore-Hoeppli phenomena
Drug therapy
Antihistamines.
Vasoconstrictors.
Mast cell stabilizers.
NSAIDs.
Steroids.
Cyclosporine.
Topical
antihistamine/vasoconstrictorw
Vascon-A.Naphcon-A.
AK-Con-A.Opcon-A.
Topical antihistamine
Livostin. Emadine.
Alocril Patanol.
Alamast Optivar Zaditor.
Systemic antihistamine
Opticrom
Alamast
Alomide
Zaditor
Antihistamine+Mast cell
stabilizer+ NSAID
Alamast
Optivar
NSAIDs
Acular
Ocufen
Steroids
FML
inflammase mild/forte
Pred mild/forte vexol
Alrex
Lotemax
Cyclosporine
Crolom
Alocril
Patanol
Optivar
Alocril
Zaditor
Voltaren
Aspirin
Antihistamines
H1 receptor
-Found throughout
the body.
-Vasodilation /
increase capillary
permeability.
-Smooth muscle
contraction.
-Selective H1
stimulation in
conj..produce
itching without
vasodilation.
H2 receptor
-Predominantly
gut.
-Found on ocular
surface.
-Vasodilation.
-Smooth muscle
relaxation.
-Systemic H2
antagonist
produce decrease
in gastric acid
production
-Selective H2
stimulation in
conjproduce
vasodilation
(redness).
H3 receptor
-Responsible for negative
feedback regulation of
anaphylactic histamine
release.
-located on histaminergic
terminals of nerves.
-Not been identified on ocular
tissue.
-no selective therapeutic
agent yet.
Antihistamines
Topical antihistamine:
All H1 antagonist.
Antihistamine/vasoconstrictor.
Antihistamines
4x/day.
Alocril
Zaditor
Alamast
Optivar
Antihistamines
Systemic antihistamines:
Antihistamines
Side effect:
Topical:
Irritation.
PEE due to preservatives.
Dry eye symptoms.
Vasoconstrictors should be used with caution in
patient with narrow angle/ HTN/ CVD/
arrhythmias.
Antihistamines
Systemic:
Sedation.
Dizziness.
Fatigue.
Nausea.
Vomiting.
Diarrhea.
Constipation.
Dry eye.
QID
QID.
Found to be superior to cromolyn in VKC.
Patanol
Alocril
Zaditor
Alamast
Optivar
H1 anatagonists+ mast
cell stabilizer+NSAID
BID.
BID
Optivar
BID
NSAIDs
Topical:
S/E:
PEE.
Persistent epithelial defect.
Stromal infiltration.
Ulceration.
Thinning.
Perforation.
NSAIDs
Systemic NSAIDs:
Aspirin:
Steroids(topical)
$ 28
S/E:
Ocular descomfort.
Delayed epithelial healing.
HSV flare up.
Increase IOP.
PSCC.
Ptosis
Mydriasis.
Steroids
Local injection.
VKC.
AKC.
Oral.
Cyclosporine
S/E:
Intense stinging.
Keratitis.
Immunotherapy
Immunotherapy (also called Desensitization
or hyposensitization).
Long term administration of low but
progressively increasing doses of the
offending allergen until the evoked clinical
reaction is reduced or eliminated.
It has been attempted sublingually, nasally,
bronchially, ocularly, and subcutaneously
(usual route).
It takes 3 to 5 years.
Recent meta-analysis showed that it is useful
for allergic rhinitis and conjunctivitis.