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Rheumatology, Thyroid Dysfunction and
the Eye
Rheumatology, Thyroid
Dysfunction and the Eye
Greg Caldwell, OD, FAAO
June 4, 2016
Everything Therapeutic: Houston
June 4, 2016
Disclosures
$ Greg A. Caldwell, OD, FAAO will mention many
products, instruments and companies during our
discussion, I don’t have any financial interest in
any of these products, instruments or companies.
$ American Optometric Association, Trustee
¬ No industry lecturing
¬ Thank you to the members and those who join
$ All of these cases have entered/referred to my
practice
Disclosure Statement
(next slide)
Learning Objectives
$ Enhance clinical understanding of rheumatology and
thyroid dysfunction and their ocular associations
$ Enhance clinical diagnosis of ocular manifestations of
rheumatologic diseases and thyroid disease
$ Enhance clinical management and treatment of ocular
manifestations of rheumatologic diseases and thyroid eye
disease
$ Increase comfort level when ordering or interpreting
laboratory tests in rheumatologic and thyroid diseases
$ Gain confidence in working closer with rheumatology
and endocrinology
Rules During this Presentation
$ There are no rules
$ Have fun, enjoy and relax
$ Ask questions at the time of the case
Can anyone here tell me the only dumb question?
A question that is not asked
Thyroid
Thyroid Disease
and
Thyroid Eye Disease
$ Thyroid is an endocrine gland
$ Two types of glands
¬ Endocrine
¬ Exocrine
$ Endocrine system is a control system of ductless endocrine
glands that secrete hormones (chemical messenger) that
circulate within the body via the bloodstream or lymph
system to affect distant organs
¬ Hypothalamus
¬ Pituitary gland
¬ Thyroid
¬ Parathyroid glands
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
¬ Pancreas
¬ Adrenal glands
¬ Gonads (testes and ovaries)
¬ Pineal gland
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Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
Thyroid
Thyroid
$ Exocrine glands contain ducts. Ducts are tubes leading
from a gland to its target organ
¬ Digestive glands have ducts for releasing the digestive enzymes
¬ Salivary glands, sweat glands and glands within the
gastrointestinal tract
$ Pancreas is both endocrine and exocrine
¬ Exocrine (ducted gland) secreting digestive enzymes into the small
intestine.
¬ Endocrine (ductless gland) in that the islets of Langerhans secrete
insulin and glucagon to regulate the blood sugar level.
Thyroid
$ Largest endocrine gland in the body
$ Butterfly shaped
$ Two lobes located on either side of the trachea in the
lower portion of the neck
$ Lies just below skin and muscle layer surface
$ The thyroid is controlled by the hypothalamus and
pituitary
$ The primary function of the thyroid is production of the
hormones thyroxine (T4), triiodothyronine (T3), and
calcitonin
Normal Thyroid Function
$ Thyroid regulates: heart rate, ventilation rate, metabolic
rate, and development of cells
$ Thyroid disorder- approx 1 in 13 or 7.35% or 20 million
people in USA, estimated 2 million undiagnosed
$ Diabetes- approx 1 in 13 or 7.8% or 17.9 million people
in USA , 5.7 million undiagnosed
$ Pathophysiology: >40 postulates (thyroid)
Thyroid Dysfunction
Thyroid Dysfunction
$ What is the most common cause of thyroid dysfunction?
A. 
B. 
C. 
D. 
E. 
Cancer
Surgically induced
Medication toxicity or side effect
Pregnancy
Autoimmune disease
$ Primary=Thyroid gland
$ Secondary= Pituitary failure
$ Tertiary= Hypothalamic
$ In autoimmune disease the body typically produces ______ that
attacks itself, this can be systemic or organ specific
¬ 
Antibodies, immunoglobulins
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
2
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
Hyperthyroid
Antibodies of Thyroid Dysfunction
$ TSH Receptor Antibodies
$ TSI attacks the thyroid
¬ Stimulating TSH receptor antibody
2  Thyroid Stimulating Immunoglobulin (TSI)
$ T3 and T4 increase
¬ Thyroid blocking antibody (TBAb)
$ TSH decreases
$ Thyroid Peroxidase Antibodies (TPOAb)
¬ TPO is found in thyroid follicle cells where it converts the thyroid
hormone T4 to T3
¬ TPOAb contributes to thyroid cellular destruction
$ Most autoimmune thyroid dysfunctions have a combination of
thyroid antibodies, however depending on which AB is more
abundant results in the outcome of the disease
Thyroid Dysfunction
Hypothyroid
$ TBAb attacks the thyroid
$ T3 and T4 decrease
$ TSH increases
Hyperthyroidism
Hypothyroidism
(most common organ-specific autoimmune disorder)
(Thyrotoxicosis)
$ Primary-autoimmune
¬  Graves
¬  Chronic autoimmune thyroiditis
2  Graves-Basedow or von
Basedow’s
$ Secondary/Tertiary
¬  Excess thyroid medication for treatment
of hypo or goiter
¬  Toxic multinodular goiter
¬  Toxic adenoma
¬  Excess iodine
¬  Thyroiditis (inflammatory induced)
¬  Excess hormone production ectopic
tissue
¬  Thyroid carcinoma
GRAVE’S
(Hyperthyoidism)
$ A multisystem disorder consisting of a triad
¬ Hyperthyroidism with diffuse hyperplasia of the thyroid gland
¬ Infiltrative dermopathy
¬ Infiltrative ophthalmopathy
$ Prevalence:
¬ 20-40 year old female (F:M = 7:1)
¬ Genetic link
$ Etiology:
¬ Autoimmune disease: hypersensitivity reaction with thyroid
stimulation by the circulation of abnormal thyroid-stimulating
immunoglobulins (TSI)
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
$ Primary-autoimmune
2  Hashimoto's thyroiditis
¬  Autoimmune atrophic thyroiditis
2  Primary myxedema
2  Opposite of Graves disease
¬ Postpartum thyroiditis
$ Secondary/Tertiary
¬  Lithium medication
¬  Pregnancy
¬  Surgically induced
¬  Disorders of the pituitary gland
or hypothalamus
Hashimoto's Thyroiditis
(Hypothyroidism)
$ The most common cause of hypothyroidism in the
United States
$ It is named after the first doctor who described this
condition, Dr. Hakaru Hashimoto, in 1912
$ Autoimmune disease
$ Goiter formation
$ 5-10 times more common in women than in men
$ The underlying cause of the autoimmune process still is
unknown
¬ Anti-TPO ab and Anti-TB recp ab present
3
Rheumatology, Thyroid Dysfunction and
the Eye
Autoimmune atrophic thyroiditis
(Hypothyroidism)
$ Atrophic thyroiditis is similar to Hashimoto's thyroiditis
$ A goiter is not present
Systemic Manifestations of Hyperthyroid
(Primary or Secondary)
$ Symptoms
¬  Nervousness
¬  Heat intolerance
¬  Sweating
¬  Fatigue
¬  Palpitation
¬  Insomnia
¬  Early waking
¬  Alopecia
¬  Vitiligo
¬  Brittle nails
$ Signs
¬  Sweating
¬  Muscle Weakness
¬  Emotionally labile
¬  Tremor
¬  Tachycardia
¬  Arrhythmia
¬  Hypertension
¬  Brisk tendon reflex
¬  Diabetes
¬  ↑Triglycerides & Ca, ↓CHO
¬  Microcyticanemia
¬  Possible goiter
¬  Myxedema
Thyroid Eye Disease (TED)
$ Other names used
¬ Grave’s disease
¬ Grave's ophthalmopathy
¬ Grave's orbitopathy
¬ Exophthalmos in Graves Disease
¬ Thyroid Associated Orbitopathy (TAO)
¬ Thyroid Orbitopathy
¬ Ophthalmic Graves Disease
¬ Inflammatory Eye Disease
¬ Endocrine Orbitopathy
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
June 4, 2016
Postpartum Thyroiditis
(Hypothyroidism)
$ These women develop antibodies to their own thyroid
during pregnancy, causing an inflammation of the thyroid
after delivery
Systemic Manifestations of Hypothyroid
(Primary or Secondary)
$ Symptoms
¬ Cold intolerance
¬ Weakness
¬ Reduced energy
¬ Lethargy
¬ Muscle cramps
¬ Constipation
¬ Increased sleeping
¬ Weight gain
¬ Reduced appetite
¬ Joint stiffness
$ Signs
¬ Cool, scaling skin
¬ Puffy hands and face
¬ Deep voice
¬ Myotonia
¬ Delirium
¬ Bradycardia
¬ Slow reflexes
¬ Obesity
¬ Hypothermia
¬ Myxedema
Why is this so confusing?
$ Thyroid Eye Disease
¬ Is often seen in conjunction with Graves' Disease (hyperthyroid)
¬ Is seen in people with no other evidence of thyroid dysfunction
¬ Is seen in patients who have Hashimoto's Disease (hypothyroid)
$ Most thyroid patients, however, will not develop thyroid
eye disease
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Rheumatology, Thyroid Dysfunction and
the Eye
Why is this so confusing?
$ The eye symptoms usually occur at the same time as the thyroid
disease
¬  However they may precede or follow the obvious symptoms of the thyroid
abnormality
$ The incidence of thyroid eye disease associated with thyroid
dysfunction is higher and more severe in smokers
¬  There is no way to predict which thyroid patients will be affected
Thyroid Eye Disease
$  Commonly known as Graves' ophthalmopathy
June 4, 2016
Why is this so confusing?
$ While eye disease may be brought on by thyroid dysfunction
¬  Successful treatment of the thyroid gland does not guarantee that the eye disease
will improve
¬  No particular thyroid treatment can guarantee that the eyes will not continue to
deteriorate
¬  Once inflamed, the eye disease may remain active from several months to as long
as three years
¬  There may be a gradual or, in some cases, a complete improvement
Thyroid Eye Disease
$ What causes the Thyroid Eye Disease signs and symptoms?
$  About 80% of all patients with TED have the autoimmune hyperthyroid
disorder known as Graves' disease
$  Another 10% of all cases are seen in patients with autoimmune
hypothyroidism, either Hashimoto's thyroiditis, atrophic thyroiditis or
Hashitoxicosis
$  Another 10% of all cases are seen in people with normal thyroid function
$ The high and low levels of T3 and T4
$ The antibodies that are attacking the thyroid gland
¬  When thyroid function is normal, the eye condition is referred to as euthyroid
Graves' disease
¬  Euthyroid is a term meaning that thyroid function tests are normal. Most people
with euthyroid Graves' disease develop a thyroid disorder within eighteen months
of the emergence of the eye disorder
¬  But some people with euthyroid Graves' disease never develop thyroid
dysfunction
Thyroid Eye Disease
Phase secondary to abnormal thyroid hormone levels (T3/T4)
(Thyroid Eye Disease)
$ Hyperthyroidism eye symptoms
$ Thyroid Eye Disease has 2 phases
¬ A phase secondary to abnormal thyroid hormone levels
2  Increased or decreased FT3 and FT4 levels
2  Once these levels are normalized, ocular symptoms will resolve
¬  Excess hormone acting on the nerves
that supply the eye
¬  Usually spastic and include staring
¬  Dryness
¬  Eyelid retraction
$ Hypothyroidism eye symptoms
¬  Deficient hormone causing venous
congestion, impaired circulation
and fluid stagnation
¬  Periorbital edema
¬ Congestive Autoimmune form of Thyroid Eye Disease
2  Active phase-stimulating or blocking TRAb are causing ocular activity
2  Plateau phase-reduced activity
2  Resolution phase-symptoms regress and eyes return to normal
$  This form of TED resolves within a few weeks after thyroid hormone levels (FT4 and
FT3) are corrected and brought back into the normal range
$  The pituitary hormone TSH can stay low or suppressed for many months during the
course of treatment for hyperthyroidism and doesn't mean that the patient is still
hyperthyroid
$  TSH also lags at least 6 weeks behind thyroid hormone levels and often remains
elevated longer in people who have been hypothyroid
$  Relying on the TSH level can be misleading and in treating TED
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
5
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
Euthyroid Graves' disease
Congestive Autoimmune form of Thyroid Eye Disease
(Active phase, Plateau phase, Resolution phase)
$ Caused by both stimulating and blocking TSH receptor antibodies
(TRAb) and also immune system chemicals known as cytokines
$ Secondary targets appear to be TSH receptor antigens (epitopes)
located on orbital fibroblasts as well as dermal fibroblasts
$ Active “inflammatory” phase of TED varies
¬  Symptoms resolve quickly although on average the active phase lasts
about 12-18 months
¬  TRAb levels are high, patients are smokers, nutrient deficiencies are
present, or the patient continues to be exposed to environmental triggers
such as excess dietary iodine, the active phase can last as long as 5 years
¬  Avoid any lid, muscle or orbital surgery
$ If thyroid function is
normal. How does
one develop thyroid
eye disease?
$ Plateau phase and Resolution “Passive” phase
¬  An individual may be left with structural changes, such as eye protrusion, eyelid
retraction, and in some cases, double vision
¬  There are corrective procedures that can be performed to address these problems
General Ocular Symptoms
Similar receptors are found in the skin, fat and muscle of the orbit
$ Prominent eyes, stare
$ Pain
$ Lacrimation
$ Eyelid swelling
$ Foreign-body sensation
$ Double vision
$ Photophobia
$ Decreased vision in one or both eyes
NOSPECS: Grading System
$ 1969 by S.C. Werner
¬  Class 0: No signs or symptoms
¬  Class 1: Only signs, upper lid retraction
¬  Class 2: Soft Tissue involvement with symptoms
¬  Class 3: Proptosis
¬  Class 4: EOM involvement
¬  Class 5: Corneal Involvement
¬  Class 6: Sight Loss
$  Class 2-6 document severity
¬ 
¬ 
¬ 
¬ 
0: absent
A: minimal
B: moderate
C: marked
$ Within classes 2 to 6 the investigator has to differentiate the severity
grades 0, A, B, C
$ NOSPECS, classifies severity but not the activity or stage (active/
NOSPECS: Grading System
$  0: No symptoms or signs
$  1: Only signs (upper lid retraction without lid lag or proptosis)
$  2: Soft tissue involvement with symptoms (excess lacrimation, sandy sensation,
retrobulbar discomfort)
¬ 
¬ 
¬ 
¬ 
Grade 0: absent
Grade A: minimal (edema of lids, injection, sandy feeling)
Grade B: moderate (edema of lids, injection, chemosis, FBS, pain behind eyes)
Grade C: marked
$  3: Proptosis associated with classes 2-6 only
¬  Grade 0: absent
¬  Grade A: minimal: 21mm -23mm
¬  Grade B: moderate: 24mm -27mm
¬  Grade C: marked: 28mm or more
¬  Specify if inequality of >3 mm between eyes, or if progression of >3 mm under observation
inflammatory or passive/congestive)
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
6
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
NOSPECS: Grading System
$  4: EOM involvement (usually with diplopia)
¬  0: absent
¬  A: minimal (limitation of motion, patient reports diplopia but no obvious restriction
¬  B: moderate (evident restriction of motion)
¬  C: marked (position of globe is fixed)
$  5: Corneal involvement (due to proptosis, incomplete closure, lagophthalmos)
¬  0: absent
¬  a: minimal (staining)
¬  b: moderate (ulceration)
¬  c: marked (clouding, necrosis, perforation)
$  6: Sight loss (due to optic nerve involvement)
¬  0: absent
¬  A: minimal (disc pallor or edema, or VF defect, vision 20/20-20/60)
¬  B: moderate (same as A but VA 20/70-20/200)
¬  C: marked (blindness, VA < 20/200)
LEMO Classification
$ 1991-Boergen and Pickardt
$ Complements NOSPECS
$ 4 finding-categories
¬ Lid
¬ Exophthalmos
¬ Muscular
¬ Optic nerve
$ Grade between 0 and 4 depending on severity
$ LEMO, classifies severity but not the activity or stage
(active/inflammatory or passive/congestive)
LEMO Classification
LEMO Classification
Lid (L)
Exophthalmos (E)
Muscular (M)
Optic Nerve (O)
$  0: missing
$  0: missing
$ 0: missing
$ 0: missing
$  1: lid edema only
$  1: eye closing not impaired
$  2: real retraction (impaired lid
$  2: conjunctival injection in the
$ 1: detectable in imaging only
$ 1: regarding color vision only
closing)
$  3: retraction and upper lid edema
$  4: retraction and global lid edema
morning
$  3: persistent conjunctival injection
$  4: corneal complications
$ 2: Pseudoparesis
$ 3: Pseudoparalysis
or detected via VEP
$ 2: peripheral scotoma
$ 3: central scotoma
L1E1M2O0
Endocrine ophthalmopathy with lid edema, exophthalmos ,
pseudoparesis of external eye muscles, and no optic nerve involvement
Grading Scales
$ New grading scales are trying to be developed to not
only grade the severity but also help to determine if
inflammatory or passive stage
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
Lid Involvement
$ Lid Retraction
$ Lid Lag
$ Lagophthalmus
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Rheumatology, Thyroid Dysfunction and
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Lid Retraction
June 4, 2016
Eyelid Lag: von Graefe’s Sign
$  Scleral show in primary gaze
$  Occurs in ~90% of Grave’s patients
¬  Excess stimulation of Muller’s muscle
¬  Fibrotic inferior rectus
¬  Mechanical restriction or infiltration
of levator
¬  Increased orbital volume causes
exophthalmos
$ Immobility or lagging of upper
eyelid on downward gaze
$ Fibrosis of the inferior rectus
muscle may induce lower lid
retraction
$  Normal Lid Position
¬  Upper lid intersects cornea at the 2
and 10 o’clock positions
2  ~2 mm below the limbus
¬  Lower lid coincident or 1-2mm below
the limbus
Lagophthalmos
$ Inability to form a complete lid closure with a
normal blink due to Exophthalmos/ Proptosis
$ Often leads to corneal exposure
Conjunctiva
Soft Tissue Involvement
$ Conjunctiva
$ Chemosis
$ Periorbital edema
“If it is Red think TED”
Dr. Andy Morgenstern 12-7-2013, OMS-Contemporary Resort
$ Conjunctival and episcleral
injection
¬  Especially near the horizontal recti
insertions
$ Chemosis
¬  Edema of the conjunctiva and
caruncle
$  Superior Limbic Keratoconjunctivitis
¬  65% correlation between SLK and
systemic thyroid disease
¬  Rheumatoid arthritis
¬  Sjögren’s syndrome
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
8
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
Infiltrative Orbitopathy
(Exophthalmos/Proptosis)
Periorbital Edema
$ Inflammation of the subcutaneous connective tissue
$ May be first sign of thyroid eye disease
$ Greatest in the morning
$ Thyroid Eye Disease is most common cause of unilateral
and bilateral exophthalmos
$ The term exophthalmos is reserved for prominence of the
eye secondary to thyroid disease
$ May need MRI to determine or obvious exophthalmos
may be present
$ It is permanent in 70% of cases
$ Caused by increased volume of the extra ocular muscles
¬ Lymphocytic infiltration
¬ Proliferation of fibroblasts
¬ Edema within the interstitial tissue of the muscle
Infiltrative Orbitopathy
(Exophthalmos/Proptosis)
Infiltrative Orbitopathy
(Exophthalmos/Proptosis)
Exophthalmometry
$  Is race dependent (Asians versus Black men is statistically significant)
$  Hertel or Luedde results
$  Adults
¬  Average reading 17 mm
¬  95% of population have readings between 13-21mm
$ General concerns
¬  A difference of 2 mm or more between the eyes
¬  A measurement of more than 24 mm
Mean Normal Value
Upper Limits
mm
mm
White women
15.4
20.1
White men
16.5
21.7
Black women
17.8
23.1
Black men
18.5
24.7
Asians
----
18.0
Race
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
9
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
Restrictive Myopathy
IOP in Thyroid Eye Disease
$ Secondary to edema and fibrosis of EOM’s
$ A rise in IOP has been reported with TED
$ Inferior Rectus (IR) muscle is most commonly involved
$ I would have higher suspicion when you see
$ Occurs in 30-50% of patients
$ Diplopia may be transient but in 50% it’s permanent
¬ Periorbital edema
¬ Exophthalmos, proptosis
¬ Restrictive myopathy
$ Some literature reports IOP in up gaze to be part of the
diagnoses of thyroid dysfunction
Restrictive Myopathy
Corneal Exposure
$ Exposure keratopathy
secondary to exophthalmos
and lagophthalmos
$ Significant threat to visual
function
Obvious restrictive myopathy but also note the periorbital
edema, and conjunctival hyperemia
Optic Neuropathy
$ Affects 5% of patients
$ Usually mild to moderate
exophthalmos and shallow orbits
$ Enlargement of the recti muscles
compresses ONH or its blood
supply at the apex of the orbit
$ Compression MAY occur without
significant proptosis
$ Compressive and/or ischemic and/or
toxic
Treatment of Thyroid Eye Disease
$ Depends on what phase of the disease we are in:
¬  Phase secondary to abnormal thyroid hormone levels
¬  Active “inflammatory” phase
¬  Plateau phase and Resolution “Passive” phase
$  Depends on what orbital tissue or structures are involved
$  Depends on the risk of vision loss
$  Depends if primary, secondary or tertiary thyroid dysfunction
$ Management consists of:
¬ 
¬ 
¬ 
¬ 
Control of inflammation
Prevention of ocular and visual damage
Addressing ocular motor abnormalities
Improving cosmetic disfigurement
$ Patient education is essential
$ Communication with an endocrinologist or internist will ensure
proper patient care
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
10
Rheumatology, Thyroid Dysfunction and
the Eye
Treatment of Thyroid Eye Disease
$ Palliative (hormone imbalance, active, passive)
¬  Lubricants
¬  Topical anti- inflammatory (Lotemax/Restasis)
¬  Prisms
$ Steroids (active phase)
¬  Orals
¬  Peri-ocular injections
¬  IV with oral steroid taper
$ Orbital radiotherapy (active phase)
Smoking causes the thyroid eye
disease to be more severe
Smoking causes treatments to be
less effective
$ Orbital Decompression (passive phase)
¬  Fat removal orbital decompression (FROD)
2  Large orbits
¬  Bone removal orbital decompression (BROD)
2  Small orbits
¬  Both FROD and BROD
Lid Retraction, Eyelid Lag, Lagophthalmos
June 4, 2016
Treatment of Thyroid Eye Disease
$ Paradigm shifts
¬ Decrease in orbital radiotherapy
¬ Waiting for passive stage but doing surgery
¬ Increase usage of fat removal orbital decompression as first
approach
¬ Peri-orbital injection of steroids for recurrent disease after orals
$ Future
¬ Looking for better or different ways to treat the active phase of
this disease
Lid Retractor Surgery
$  Must treat underlying thyroid dysfunction
$  Abnormal hormone level and Active phase
¬  Treat the exposure keratitis with lubricants
¬  Tape eyelids shut at night
¬  Lid weight
¬  Moisture chamber at night
¬  Antibiotic ointments
$ Passive Phase
¬ 
¬ 
¬ 
¬ 
Surgical Management
Inferior rectus recession
Mullerotomy
Recession of lower lid retractors
Conjunctiva, Periorbital edema
$ Topical lubricants
¬ 
¬ 
¬ 
¬ 
Artificial tears
Ointments at night
Topical steroids
Restasis?
$ Tape eyelids closed at night or
use mask
Infiltrative Orbitopathy
(Exophthalmos/Proptosis)
$ Orbital Disease Consult
¬  Systemic steroids to reduce
inflammation
¬  Low dose radiotherapy
¬  Surgical orbital decompression
$ Elevate head at night to
decrease lid edema
$ Oral diuretics Acetazolamide
$ Oral steroids
¬  60-80mg/day for 3 months
$ IV steroids
$ Periorbital steroids
¬  Kenalog last 1 month
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
11
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
Restrictive Myopathy
Corneal Exposure
$ Non-surgical (while waiting for stability)
¬  Teach proper head position to alleviate
diplopia
¬  Prism in spectacle correction (Fresnel or
ground in)
¬  Oral steroids
¬  Botulinum toxin injection
$ Surgical Consult
¬ 
¬ 
¬ 
¬ 
¬ 
Recession of the rectus muscle/s involved
Diplopia in primary gaze, reading gaze or both
Stable angle of deviation for at least 6 months
No evidence of active disease
Binocular vision in at least primary and reading
positions
Optic Neuropathy
$ Systemic Steroids
¬  If rapidly progressive and painful
in the early stage of the disease
¬  Only if no contraindications
¬  Prednisolone 80-100mg, expect
results within 48hrs. Taper dose
and d/c within 3 mo
$ IV Methylprednisolone
$ Radiotherapy: if contraindication
to steroid
$ Orbital decompression
Orbital Decompression
(Surgical/Cosmetic)
$ Manage the corneal defect as first line
¬ Lubricating and antibiotic
¬ Lid taping
¬ Moisture barrier
$ Orbital Disease Consult
¬ High dose oral steroids
2  120-140mg /day x 7 days
¬ Orbital decompression
Orbital Decompression
$ Not effective if no medical
treatment
¬  Two-wall decompression
2  3-6 mm retro-placement of
the globe
¬  Three-wall decompression
2  6-10mm retro-placement
¬  Four-wall decompression
2  10-16mm retro-placement
Thyroid Eye Disease and Depression
$ When facial disfigurement
occurs, thyroid eye disease is
equivalent to the diagnosis of
cancer and AIDS
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
12
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
Orbital Decompression
IOP in Thyroid Eye Disease
(Medical/Vision Threatened)
$ A rise in IOP has been reported with TED
$ I would have higher suspicion when you see
¬ Periorbital edema
¬ Exophthalmos, proptosis
¬ Restrictive myopathy
$ Some literature reports IOP in up gaze to be part of the
diagnoses of thyroid dysfunction….let’s discuss
Laboratory Testing
IOP in Thyroid Eye Disease
$  Thyroid Hormone Levels
¬  Serum TSH concentration Serum total T4 (Thyroxine)
¬  Serum total T3 (Triiodithyronine)
¬  Estimation of the serum free T4 (or T3) concentration
¬  Thyroglobulin (Tg) level
$ Anti-thyroid antibodies
¬ 
¬ 
¬ 
¬ 
Thyrotropin receptor antibodies (TSI)
TSH binding inhibiting immunoglobulins (TBII)
Anti-TPO antibodies
Thyroglobulin (Tg) Antibodies (TgAb)
$ Commonly used thyroid tests
¬ 
¬ 
¬ 
¬ 
Resin T3 uptake test
Sensitive serum TSH test (Thyroid stimulating hormone)
TRH stimulation test (Thyroid releasing hormone)
Thyroid (T3) suppression test
¬  Sonography
¬  Needle Biopsy
¬  Thyroid Scan
Laboratory Testing
$ Hypothyroid
¬  Low FT4, High TSH, indicates primary check antibodies
¬  Low FT4, Low TSH, indicates secondary or tertiary, TRH stimulation,
MRI
¬  Hashimoto’s (primary disease)
2  Most common
2  Low FT4, High TSH, High Anti-TPO Ab, High levels of Thyroglobulin (Tg)
Antibodies (TgAb), Anti-TB Recp Ab (approx 10% present)
¬ Autoimmune atrophic thyroiditis
2  Low FT4, High TSH, Low Anti-TPO Ab, Low levels of Thyroglobulin (Tg)
Antibodies (TgAb), Anti-TB Recp Ab (approx 60% present)
¬  Treatment: Levothyroxine (Synthroid, Levothroid, Levoxyl, Unithroid)
$ Hyperthyroid
¬  High FT4, Low TSH
¬  TSI present
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
Sign’s in Thyroid Eye Disease
$  Dalrymple’s sign: Lid retraction
$  von Graefe’s sign: Upper lid lag
on downward gaze
$  Griffith’s sign: Lower lid lag on
downward gaze
$  Boston’s sign: Jerky irregular
movement of the upper lid on
downward gaze
$  Jellinek’s sign: Increased
pigmentation of the lids
$  Stellwag’s sign: Infrequent blinking
$  Kocher’s sign: Increased lid
retraction with visual fixation
$  Enroth’s sign: Puffy swelling of the
lids
$  Rosenbach’s sign: Tremor of closed
lids
$  Mobius’ sign: Weakness of
convergence
$  Ballet’s sign: Palsy of one or more
extraocular muscles
$  Suker’s sign: Weakness of fixation on
lateral gaze
$  Cowen’s sign: Jerky papillary
contraction to consensual light
$  Knies’ sign: Unequal dilatation of the
pupils
$  Jeffrey’s sign: Absence of forehead
wrinkling on upward gaze
13
Rheumatology, Thyroid Dysfunction and
the Eye
Questions
June 4, 2016
Rheumatology and the Eye
“Eye said Go to your Rheum”
Rheumatology
Where the Eye and Rheumatology Overlap
$ Specializes in the diagnosis and therapy of clinical
problems involving
¬ Joints
¬ Osteoporosis
¬ Musculoskeletal pain disorders
¬ Soft tissues
$ Connective Tissue Disease
$  Vasculitides
$ Spondyloarthropathies
2  Not connective tissue
–  Muscle, nerve, and blood vessels
2  Connective tissue
–  Tendons, ligaments, fascia, fibrous tissues, fat, and synovial membranes
$ There are more than 200 types of these diseases,
including rheumatoid arthritis, osteoarthritis, gout, lupus,
back pain, osteoporosis, fibromyalgia, and tendinitis
Connective Tissue Disease
Connective tissue diseases secondary
to gene abnormalities
$ Connective tissue diseases that are strictly due to genetic
$ Connective tissue disease is any disease that has the connective tissues
of the body as a primary target of pathology
$ The connective tissues are composed of two major structural protein
molecules
¬  Collagen
¬  Elastin
$ The collagen and elastin become injured by inflammation
¬  Typically due to autoimmune
$ “Collagen vascular disease” is an antiquated term used to describe
inheritance include
¬ Marfan syndrome
2  Gene FBN1 on chromosome 15
2  Can have tissue abnormalities in the heart, aorta, lungs, eyes, and
skeleton
¬ Ehlers-Danlos syndrome
2  Many types with numerous genes
2  Typically have loose, fragile skin and hyperextensible joints
depending on type
diseases of the connective tissues
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
14
Rheumatology, Thyroid Dysfunction and
the Eye
Connective tissue diseases
secondary to autoimmunity
$ Cannot be regularly
defined by gene
abnormalities
$ The spontaneous over
activity of the immune
system
¬ Results in the production of
extra antibodies into the
circulation
$ Systemic Lupus Erythematosus
$ Rheumatoid Arthritis
$ Sjogrens Syndrome
$ Systemic Sclerosis
$ Polymyositis /Dermatomyositis
$ Mixed Connective Tissue
$ Wegner’s Granulomatous
Similar Structures
$ The connective tissues are
composed of two major
structural protein molecules
¬  Collagen
¬  Elastin
$ Sclera- the opaque , white,
fibrous, protective, outer layer
of the eye containing collagen
and elastin fibers
Connective Tissue Diseases
Disease
Auto-antibody
Systemic Lupus Erythematosus
Rheumatoid Arthritis
Sjogrens Syndrome
Systemic Sclerosis
Polymyositis/Dermatomyositis
Mixed Connective Tissue Disease
Wegener’s Granulomatosus
Anti-dsDNA, Anti-SM
RF, Anti-RA33
Anti-Ro(SS-A),Anti-La(SS-B)
Anti-Scl-70, Anti-centromere
Anti-Jo-1
Anti-U1-RNP
c-ANCA
53 year old woman
$ Referred for treatment for a red OS
$ 3 weeks ago sudden onset of red eye
$ No pain, just feels like eyestrain
$ At times it’s worse at times it’s better
$ Synovial membrane: A layer of
connective tissue that lines the
cavities of joints, tendon
sheaths, and bursae and makes
synovial fluid , which has a
lubricating function.
$ Ténon’ s Capsule –a layer of
connective tissue which forms a
thin membrane that envelops
the eyeball from the optic nerve
to the limbus , separating it
from the orbital fat and forming
a socket
$ 5 years ago same eye was red, it resolved
without treatment
Review of Systems
Discussion
OD
June 4, 2016
OS
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
15
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
Knuckles
Treatment
$ Lotemax qid OS
$ Ibuprofen 400 mg qid PO
$ Artificial tears
$ Educate patient on finding and possible underlying etiologies
¬  This reveals an uncle with severe arthritis, no definite diagnosis
$ Blood work? if so what test?
¬ Antinuclear antibody (ANA) and rheumatoid factor (RF)
6 days later
Lab Results
$ Treatment
¬ Lotemax
1st Day
2  TID=1 week
2  BID=1week
2  QD=1week
$ Ibuprofen 200mg QID
$ Review of lab results
Day 6
Final Outcome
$ Diagnosed with rheumatoid arthritis
¬ Current treatment successful
$ No ocular occurrence since treatment of
rheumatoid arthritis
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
Referral to Rheumatologist
Episcleritis
$ Typically occurs in exposure zones
$ Inflammation localized to episclera:
¬ Radiate posterior from limbus
¬ Vessels are moveable
¬ Vessels blanch with sympatomimetics
$ Types
¬ Simple episcleritis: 80%
¬ Nodular episcleritis: localized with variable tenderness
$ Clinical Evaluation:
¬ Sectoral injection 70%
¬ Diffuse injection 30%
16
Rheumatology, Thyroid Dysfunction and
the Eye
Episcleritis
$ 70% of the cases are idiopathic
¬  15-20% are due to allergy
¬  5-10% are due to systemic disease
$ Testing for systemic disease indicated
¬ Multiple reoccurrences
¬ Bilateral
¬ History and exam are suspicious for systemic association
$ Possible systemic etiologies
¬ 
¬ 
¬ 
¬ 
¬ 
¬ 
¬ 
¬ 
Rheumatoid arthritis
Lupus
Ankylosing spondylitis
Sarcoid
Tuberculosis
Gout
Syphilis
Wegeners
June 4, 2016
48 year old woman
$ My OD eye has severe pain, it started as an ache about 1
week ago, but now is a throbbing pain
$ It hurts to move my eye or touch my eye
$ The pain is radiating to my cheek
$ Patient does suffer from rheumatoid arthritis
$ VA 20/20 OU
$ EOMs full, but pain on movement OD
$ PERRL (-)APD
$ Confrontation fields: full OU
$ Let’s take a look
Diagnosis and Treatment?
Treatment
$ Non-Necrotizing Scleritis
¬ Depending on severity, one or combination of:
2 Oral Non Steroidal Anti Inflammatory agents
–  Ibuprofen or indomethacin (50 mg po bid)
2 Oral steroids
$ Communication/consult with rheumatologist
$ Sub-Tenon’s steroid injection is contraindicated
Scleritis
$ Severe inflammatory condition
$ An immune mediated inflammation and destruction of
the sclera
$ Commonly associated with underlying systemic disease
$ 4th to 6th decade of life
$ Rare in children
$ Female > male
Scleritis
$ Symptoms
¬ Gradual presentation (days)
¬ Deep boring pain
2 May worsen at night
¬ Referred pain to head and jaw
¬ Eye is tender to the touch
$ Greater than 50% are bilateral
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
17
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
Scleritis
$ Clinical Evaluation
¬ Sectoral or diffuse injection at all levels of vessels
¬ Blue hue in natural light
¬ Vessels do not blanch or move
Classification of Scleritis
Classified by location and appearance of inflammation
Location
Subtype
Anterior Sclera
Diffuse Anterior Scleritis
40%
Nodular Anterior Scleritis
44%
Necrotizing Anterior Scleritis
with Inflammation
10%
Necrotizing Anterior Scleritis
w/out Inflammation
4%
Posterior Scleritis
2%
Posterior Sclera
Non Necrotizing Scleritis
$ Diffuse
¬ Portion involved in 60%
¬ Entire sclera involved in 40%
¬ Red/blue hue
Prevalence
Necrotizing Scleritis
$ Most destructive form
$ 60% develop ocular/systemic complications
$ 40% have vision loss
$ 30% mortality rate at 5 years
$ Nodular
¬ Scleral nodule
¬ Deep red-purple
¬ Nodule is immobile and separate from episclera
Necrotizing Scleritis
$ Begin as localized patch of inflammation
$ Symptoms>>>findings
$ May present as avascular patch of sclera surrounded by
injection
$ Inflammation spreads to involve entire globe without
appropriate treatment
Necrotizing Scleritis Without Signs of Inflammation
(Scleromalacia Perforans)
$ Predominantly seen in patients with rheumatoid arthritis
(55%)
$ Signs of inflammation are minimal
$ No pain
$ Progressive scleral thinning
$ Uvea becomes visible
$ Eye may rupture
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
18
Rheumatology, Thyroid Dysfunction and
the Eye
Posterior Scleritis
June 4, 2016
Posterior Scleritis
$ May occur in isolation or with associated anterior involvement
$ Presentation
¬ Pain (ocular/head)
¬ Proptosis
¬ Visual loss
¬ Restricted motility
$ Posterior Findings
¬ Choroidal folds
¬ Exudative retinal detachment
¬ Papilledema
$ Easily missed if no associated anterior scleritis
$ Diagnosis confirmed with ultrasound, CT, or MRI
¬ Hallmark : thickened sclera
$ Most have no identifiable related systemic disease
Management
$ Laboratory evaluation warranted
¬ Scleritis is often associated with systemic disease (some fatal)
¬ Common etiologies
2  Rheumatoid Arthritis
2  Systemic Lupus Erythematosus
2  Ankylosing spondylitis
2  Wegeners
2  Gout
2  Polyarteritis nodosum
2  Hansen disease
Rheumatoid Arthritis
Treatment
$ Non-Necrotizing Scleritis
¬ Depending on severity, one or combination of:
2 Oral Non Steroidal Anti Inflammatory agents
–  Ibuprofen or indomethacin (50 mg po bid)
2 Oral steroids
¬ Topical steroids and NSAID’s ineffective
$ Necrotizing Scleritis
¬ Oral/ IV steroids
¬ Immunosuppressive/ cytotoxic agents
$ “Sub-Tenon’s steroid” injection is contraindicated
Rheumatoid Arthritis
$ Inflammation of the synovial tissue
$ 1% of the population
$ Women affected 2-3 X more than men
$ Age of onset is 40-50
$ Juvenile form
(lymphocytic) with synovial proliferation
$ Symmetric involvement of peripheral joints,
hands, feet and wrists
$ Occasional systemic effects: vasculitis, visceral
nodules, Sjogren syndrome, pulmonary fibrosis
$ Anti-RA-33 autoantibodies
$ RA associated nuclear antigen (RANA)
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
19
Rheumatology, Thyroid Dysfunction and
the Eye
Rheumatoid Arthritis: Diagnostic Criteria
June 4, 2016
Rheumatoid Arthritis
fusiform synovitis
1. Morning stiffness (>1h)
2. Swelling of three or more joints
3. Swelling of hand joints (prox interphalangeal,
metacarpophalyngeal, or wrist)
4. Symmetric joint swelling
5. Subcutaneous nodules
6. Serum Rheumatoid Factor
7. Radiographic evidence of erosions or periarticular
osteopenia in hand or wrists
Criteria 1-4 must have been present continuously for 6 weeks or longer and must
be observed by a physician. A diagnosis of rheumatoid arthritis requires
that 4 of the 7 criteria are fulfilled.
Rheumatoid Arthritis
Early
Intermediate
Rheumatoid Arthritis
Vasculitis
Late
Courtesy of J. Cush, 2002.
Rheumatoid Arthritis
Vasculitis / Digital Necrosis
Rheumatoid Arthritis
Disease Modifying Anti-rheumatic Drugs /DMARDs
§ Methotrexate (MTX)
§  Hydroxychloroquine
§ Leflunomide
§ Sulfasalazine
§ Cyclosporine
§ Parenteral/oral gold
§ Azathioprine
§ D-penicillamine
§ Minocycline*
* Not approved by the FDA for the treatment of RA.
ACR guidelines for the management of rheumatoid arthritis. Arthritis Rheum. 2002;46:328-346.
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
20
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
Rheumatoid Arthritis
45 year old woman
(Biologic DMARDs)
$ Reports a black line in her vision OD
§  Enbrel (Fusion Protein)
$ “The line in my vision does not move like a floater”
§  50-100mg SQ q week
$ Vision 20/20 OU
§  Remicade (chimeric MAB)
$ Externals: unremarkable
§  3mg/kg -10mg/kg Q 4-8weeks
$ SLE: unremarkable
§  Humira (humanized MAB)
§  40mg SQ qow
Cotton Wool Spots
Fundus Photo OD
$ Non-specific finding
¬ Hypertension
¬ Diabetes
¬ Connective Tissue Disease
¬ HIV Retinopathy
¬ Blood dyscrasia
2  Leukemia
2  Anemia
Many Faces of CWS
Laboratory Work-Up
$ Sed rate
$ ANA
$ Rheumatoid factor
$ ACE
$ HLA-B27
$ Fasting blood glucose (FBG)
$ Lipid profile
No under lying etiology
History of uncontrolled HTN and DM
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
$ Complete blood count (CBC)
21
Rheumatology, Thyroid Dysfunction and
the Eye
Results
Referred to Rheumatologist
$ Complete blood count (CBC):
¬ WBC
¬ Hemoglobin
¬ Hematocrit
¬ Platelet count
2.9
9.1
33.9%
110
$ Sed rate:
$ ANA:
$ Rheumatoid factor:
$ ACE:
$ HLA-B27:
$  Fasting blood glucose (FBG):
$ Lipid profile:
low
low
low
low
June 4, 2016
$ Patient diagnosed with systemic lupus
Anemia
48
high
1:640 speckled pattern
negative
normal
negative
normal
normal
Systemic Lupus Erythematosus
erythematosus (SLE) and treated with an
immunosuppressant
$ CWS have resolved and no other occurrences
Systemic Lupus Erythematosus
$ General
¬ autoimmune multisystem disease
¬ prevalence 1 in 2,000
¬ 9 to 1; female to male (1 in 700)
¬ peak age 15-25
¬ immune complex deposition
¬ photosensitive skin eruptions, serositis, pneumonitis, myocarditis,
nephritis, CNS involvement
Systemic Lupus Erythematosus: Diagnostic Criteria
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
$ Anti-Nuclear Antibodies (ANA)-positive
$ Specific labs
¬ dsDNA antibodies
¬ Anti-Sm antibody
¬ Anti-SSA and Anti-SSB – may also be positive
Systemic lupus erythematosus
1982 classification criteria definitions
$  Malar rash
Fixed erythema, flat or raised, sparing the
nasolabial folds
$  Discoid rash
$  Photosensitivity
Raised patches, adherent keratotic scaling,
follicular plugging; older lesions may cause
scarring
Skin rash from sunlight
$  Oral ulcers
Usually painless
$  Arthritis
Nonerosive, inflammatory in two or more
peripheral joints
$  Serositis
Pleuritis or pericarditis
22
Rheumatology, Thyroid Dysfunction and
the Eye
Systemic lupus erythematosus
1982 classification criteria definitions
$  Renal disorder
Persistent proteinuria or cellular casts
$  Neurologic disorder
Seizures or psychosis
$  Hermatologic
Hemolytic anemia, leukopenia (<4,000/mm3),
lymphopenia (<1,500/mm3), or
thrombocytopenia (<100,00/mm3)
$  Immunologic disorder
Antibodies to dsDNA or SM or positive
antiphospholipid antibodies (IgG or IgM
antibodies, lupus anticoagulant, or falsepositive serologic test positive serologic test
for syphilis)
June 4, 2016
Systemic Lupus Erythematosus
$  Antinuclear antibody test Positive
Systemic Lupus Erythematosus
Systemic lupus erythematosus
butterfly rash, discoid type
$ Discoid Lupus: Cutaneous manifestations
$ Scar upon healing
Systemic lupus erythematosus
photosensitivity
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
Systemic lupus erythematosus
interarticular dermatitis
23
Rheumatology, Thyroid Dysfunction and
the Eye
Systemic lupus erythematosus
retinal vasculitis
Systemic Lupus Erythematosus
Disease Modifying Anti-rheumatic Drugs /DMARDs
$ Methotrexate (MTX)
$ Cyclosporine
$  Hydroxychloroquine
$  Parenteral/oral gold
$  Leflunomide
$  Azathioprine
$  Sulfasalazine
$  D-penicillamine
$  Cytoxin
$  Minocycline*
$  Cellcept
June 4, 2016
Systemic Lupus Erythematosus
$  Treatment: Rheumatologist involvement
$  Avoidance of sun
$  Use of sunscreens
$  DMARDs
37 year old woman
$ Referred in for punctal plug insertion due to dry
eyes, temporary plug outcome was successful
¬ Currently using
2  Systane q1-2h OU
2  Restasis bid OU
2  Systane night PRN
$ She wants plugs to help decrease her usage of
lubricants
$ SLE: confirms almost absent tear prism and mild
to moderate Lisamine green staining
$ Anything suspicious here?
* Not approved by the FDA for the treatment of RA.
ACR guidelines for the management of rheumatoid arthritis. Arthritis Rheum. 2002;46:328-346.
Results
Treatment
$ Permanent plugs RUL/RLL
$ Labs ordered:
¬ ESR, CRP, ANA, RF, SS-A, SS-B and thyroid panel
$  Excellent outcome to permanent plugs RLL/LLL
$  ESR:
$  CRP:
$  ANA:
$  RF:
$  SS-A:
$  SS-B :
$  Thyroid panel:
33 mm/hr
1.7
1:320
positive
positive
positive
normal
$  Referral to rheumatologist for diagnosis and treatment
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
24
Rheumatology, Thyroid Dysfunction and
the Eye
Diagnosis
$ Sjögren’s Syndrome
June 4, 2016
Definition of Sjögren’s Syndrome
A chronic systemic autoimmune disease characterized by
lymphocytic infiltration of salivary and lacrimal glands
leading to dry mouth (xerostomia) and dry eyes
(keratoconjunctivitis sicca) as a consequence of progressive
glandular destruction and dysfunction
Sjögren’s Syndrome
Sjögren’s Syndrome
$  1-2 million Americans affected
¬  90% women
$  2nd most common autoimmune rheumatic
disease
$  A major women’s health problem
Common features
$ Primary or secondary
$ Dry mouth and dry eyes
$ Serum autoantibodies
¬  RF, anti-Ro/SSA, anti-La/SSB
$ Glandular and extraglandular manifestations
$ Overlap with other autoimmune rheumatic
diseases
$ Women > Men (9:1)
Sjögren’s Syndrome
Sjögren’s Syndrome
(Ocular signs)
$ Reduced tear production
¬ Measured by Schirmer test
(Oral features)
$ Dry mouth
$ Decreased tear breakup time
$ Sore or burning mouth
$ Epithelial staining with diagnostic dye
$ Intolerance to acidic or spicy foods
$ Filamentary keratitis by biomicroscopy
$ Abnormalities of taste
$ Difficulty with chewing and swallowing dry
foods
$ Difficulty with phonation (speaking)
$ Difficulty wearing dentures
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
25
Rheumatology, Thyroid Dysfunction and
the Eye
Dental Caries (Decay) in
Sjögren’s Syndrome Patients
June 4, 2016
Salivary Glands
Sjögren’s Syndrome
Normal Salivary Gland
Why Can Muscarinic Agonists Be
Used to Stimulate Saliva?
$ The severity of salivary dysfunction is disproportionate to
the amount of lymphocyte infiltration
$ Most Sjögren’s syndrome patients have remaining acinar
cells in their salivary glands
$ Muscarinic receptors on these cells are still capable of
responding to stimulation
$ In sufficient dosages, muscarinic agonists can increase
secretion of exocrine glands
Salivary Gland SS
Evoxac
$ Mechanism of Action
¬ A cholinergic agonist that binds to muscarinic receptors and
stimulates exocrine glands
$ Muscarinic receptor subtypes
¬ Evoxac has high affinity for M1 and M3 subtype
2  Secretion from salivary glands and stomach
¬ Evoxac has a lower affinity for the M2 subtype
2  Slow heart rate, Reduce contractile forces of atrium, reduce
conduction velocity of AV node
$ Sufficient dosages, muscarinic agonists can increase
secretion of exocrine glands
Connective tissue diseases
secondary to autoimmunity
Common Ocular Involvement
Potential Ocular Involvement
$ Systemic Lupus Erythematosus
$ Systemic Sclerosis
$ Rheumatoid Arthritis
$ Polymyositis /Dermatomyositis
$ Sjogrens Syndrome
$ Mixed Connective Tissue
$ Wegner’s Granulomatous
Connective tissue diseases
secondary to autoimmunity
$ Cannot be regularly
defined by gene
abnormalities
$ The spontaneous over
activity of the immune
system
¬ Results in the production of
extra antibodies into the
circulation
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
$ Systemic Lupus Erythematosus
$ Rheumatoid Arthritis
$ Sjogrens Syndrome
$ Systemic Sclerosis
$ Polymyositis /Dermatomyositis
$ Mixed Connective Tissue
$ Wegner’s Granulomatous
26
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
Vasculitides
The vasculitides are a group of diseases characterized by non
infectious necrotizing vasculitis and resultant ischemia
Vasculitides
$ Polyarteritis Nodosa
$ Churg-Strauss Syndrome
$ Hypersensitivity Vasculitis
$ Wegener’s Granulomatosis
$ Giant Cell Arteritis
$ Behcet’s Disease
$ Cogan’s Disease
$ Kawasaki Disease
32 year old man
Fundus Reveals
$ “I have bleeding in my eyes”, patient requests 3rd opinion
$ “I have been tested for high blood pressure and diabetes
4 times, I don’t have either one”
$ Vision 20/20 OU
Work Up
$ CBC/diff
$ ACE
$ FTA ABS
$ VDRL
$ HLA-B27
$ PPD
$ ANA
$ RF
Results and Fundus 3 Weeks Later
normal
normal
negative
negative
negative
normal
negative
negative
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
27
Rheumatology, Thyroid Dysfunction and
the Eye
Ask and You Shall Receive
June 4, 2016
Refer to Rheumatologist
$ Testing and examination reviews Behcet's diagnosis
¬ Vasculitis with triad of oral and genital ulcers and uveitis or iritis
¬ Ulcers, covered in pale pseudomembrane
2  Painful, on lips, gingiva, buccal mucosa, tongue, palate and
oropharynx
2  Genital ulcers similar in appearance
2  Heal in days to weeks with scarring
$ The treatment of Behcet's syndrome depends on the
severity and the location of its manifestations in an
individual patient
¬ This patient oral steroids and Remicade
80 year old man
Photos OU
$ Reports a sudden loss of vision OD
$ Vision is count fingers at 2 feet OD and 20/25 OS
$ APD OD grade 4
$ Fundus photos OU
CRAO Treatment/Work-Up/Follow-Up?
$ Anterior chamber paracentesis (less than 24 hours)
$ STAT blood work
¬ 2-10% of all CRAOs are caused by thrombosis from
Giant Cell Arteritis (GCA)
¬ Sed-rate
¬ C-reactive protein
Laboratory
Results
What are we
looking for?
2  Qualitative or quantitative?
¬ CBC with diff
$ Monitor for neovascularization, every 3-6 weeks
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
28
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
Immediate Treatment and Referral
$ Rx given to patient to stop and get po steroids
$ Immediate referral to rheumatologist for systemic
management
¬ Schedule temporal artery biopsy
Giant Cell Arteritis
Giant cell arteritis
(temporal artery biopsy)
(Management)
§  Corticosteroids:
§  0.5-1mg/kg/day in divided dosages
§  Taper Rx over 1-2 months to obtain oral dosing schedule
between 5-7.5mg/d
Multiple giant cells
lining up and
infiltrating the
internal elastic
lamina
§  DMARDs
§  Methotrexate most commonly used
§  Dosage: 10-20mg/wk
§  Remicade clinical trial unsuccessful
9 Months Later
“The cherry flavor is not long lasting”
9 months earlier
Giant Cell Arteritis
$ Most common vasculitis
$ Most common initial complaint
¬ Headache-boring and constant (47%)
¬ 90% will develop headache
$ ESR >50mm/hr
$ Confirmed by temporal artery biopsy of affected side
¬ 5-7cm in length, if negative, biopsy contra lateral side
¬ False negative rate of 5-40%
$ Tender and erythematous temporal artery 50%
$ Tender scalp
$ Jaw ischemia 50%
$ Lingual ischemia 25%
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
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Rheumatology, Thyroid Dysfunction and
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June 4, 2016
Giant Cell Arteritis
Giant Cell Arteritis
§  Clinical features
§ 
§ 
§ 
§ 
§ 
§ 
§ 
§ 
§  Laboratory features
Headache
Temporal artery abnormality
Jaw claudication
Visual loss diplopia
Extremity claudication
PMR symptoms
Weight loss, fever
Respiratory symptoms
§ 
§ 
§ 
§ 
Elevated ESR
Elevated CRP
Anemia
Elevated alkaline
phosphatase
(ACR 1990 criteria classification)
§  Must have at least 3 of the 5 criteria present.
§ 
§ 
§ 
§ 
§ 
Age > 50 years at disease onset
New headache
Temporal artery abnormality (tender or decreased pulse)
Elevated Westergren ESR > 50 mm/hr
Abnormal artery biopsy: mononuclear cell infiltrate,
granulomatous inflammation, usually multinucleated giant cells
§  Sensitivity 93.5% and specificity 91.2%
Giant cell arteritis:
(forehead)
Giant cell arteritis: scalp
necrosis
Giant cell arteritis:
(scalp necrosis)
Polymyalgia Rheumatica
(Association)
$ 10-15% of patients with PMR have GCA
¬ GCA can develop long after onset and treatment of PMR
$ PMR is found in 50% of patients with giant cell arteritis
$ Muscular pain, morning stiffness of proximal muscles,
elevated ESR without inflammatory joint or muscle
disease
¬ Low grade fever, wt loss, malaise
$ Low dose prednisone
¬ Treatment of GCA requires larger doses of corticosteroids than
does treatment of PMR
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
30
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
Spondyloarthropathies
$ Prevalence is similar to Rheumatoid Arthritis, 1-2%
$ Share similar clinical, radiographic, and genetic features
Spondyloarthropathies
$ A cluster of overlapping forms of inflammatory arthritis
¬  Are distinct from rheumatoid arthritis
¬  Affect the spine
¬  Affect the entheses (insertions of tendons and ligaments)
$ The syndromes include
¬  Ankylosing spondylitis
¬  Reactive arthritis (Reiter's syndrome)
¬  Psoriatic arthritis
¬  Enteropathic arthritis
$ Syndromes sometimes included (controversial)
¬  Whipple's disease
¬  Behcet's syndrome
Seronegative Spondyloarthropathy
Spondyloarthropathy
$ Seronegative refers to the
absence of the specific
antibodies (or substance) that
were being tested for
¬  Rheumatoid factor
$ Spondyloarthropathies are
inflammatory joint diseases of
the vertebral column
associated with the major
histocompatibility complex
(MHC) Class I molecule
¬  HLA-B27
HLA B27
HLA-B27 & Uveitis
$ Features
$ The major histocompatibility complex is encoded by
several genes located on human chromosome 6
$ Most (but not all) patients with spondylitis carry a gene
called HLA-B27
$ People carrying the HLA B27 gene
¬ Marked or severe presentation
¬ Anterior iritis
¬ Unilateral
¬ Acute onset, <3 months
$ Can occur as a HLA B27 uveitis
$ Can occur with a spondyloarthropathy
¬ Are at increased risk of developing spondylitis
¬ The majority (over 75%) will never develop the disease
$ HLA-B27 is not helpful in prognosis
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
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Rheumatology, Thyroid Dysfunction and
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June 4, 2016
Ankylosing Spondylitis
$ Ankylosing spondylitis is a chronic, usually progressive,
disease involving the articulations of the spine and
adjacent soft tissues
$ HLA B27 positive 90%
$ Uveitis 20-40% chance
Reactive Arthritis
$ A spondyloarthropathy following enteric (GI tract) or urogenital
infections and occurring in individuals who are HLA-B27 positive
¬  What was once referred to as “Reiter syndrome” and is now referred to
as reactive arthritis
2  Was described as a triad of arthritis, nonspecific urethritis, and conjunctivitis,
often accompanied by iritis
$ Can cause inflammation in the joints of the spine, legs and arms and
in other parts of the body
$ The syndrome usually begins with urethritis followed by
conjunctivitis and rheumatological findings
¬  Arthritis begins within 1 month of infection in 80% of patients
$ HLA B27 positive 40-80%
$ Uveitis 20-40% chance
Psoriatic Arthritis
Enteropathic Arthritis
$ A form of chronic, inflammatory arthritis associated with
the occurrence of an inflammatory bowel disease (IBD)
$  Patients with psoriasis have a 5-42% chance of
developing psoriatic arthritis
$ About 20% of people who develop PsA will eventually
have psoriatic spondylitis
¬  The inflammation in the spine can lead to complete fusion
¬ Spondylitis associated with psoriasis
2  60-70% are HLA-B27 positive
2  Psoriatic arthritis without spondylitis 15% HLA B27 positive
$ Uveitis 7% chance
¬ Ulcerative colitis
¬ Crohn's disease
$ About one in five people with Crohn's or ulcerative
colitis will develop enteropathic arthritis
¬ Approximately 50-60% of patients with spondylitis in association
with IBD have HLA-B27
$ The most common areas affected are the peripheral
(limb) joints
¬ In some cases, the entire spine can become involved as well
$ Uveitis 3-11% chance
Undifferentiated Spondyloarthropathy
(USpA)
$ To describe symptoms and signs of spondylitis in
someone who does not meet the criteria for a definitive
diagnosis of AS or related disease
¬ Unrecognized by many physicians
¬ Initial diagnosis of Spondyloarthropathy or Unclassified
Spondyloarthropathy if certain symptoms are present but are not
enough to make a specific diagnosis
What Drug Do
Rheumatologists
Use Quite Often?
2  Over time, most people with USpA will develop a well-defined form
of spondylitis such as ankylosing spondylitis
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
32
Rheumatology, Thyroid Dysfunction and
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June 4, 2016
32 year old man
Lab Work-Up?
$  “Doc my eye hurts like” hell
2  Was not “hell” but rhymes with truck
$ Started hurting yesterday
$ SLE: diffuse G3 injection with limbal flush, A/C G4 cell
and flare with light fibrin formation at pupil, multiple
KP’s
$ Fundus unremarkable but iris to lens synechia at 2 and 6
o’clock
$ Diagnosis marked iritis, first episode
Lab Work-Up?
$ CBC with diff
$ SED rate (ESR)
$ ANA
$ RF
$ ACE
normal
normal
negative
negative
normal
$ FTA ABS
$ VDRL
$ HLA-B27
$ Lyme titer
$ PPD
$ Chest X-ray
$ CBC with diff
$ FTA ABS
$ SED rate (ESR)
$ VDRL
$ ANA
$ HLA-B27
$ RF
$ Lyme titer
$ ACE
$ PPD
$ Chest X-ray
Refer to Rheumatologist
negative
negative
positive
negative
negative
normal
$ After labs and images patient was diagnosed with
Ankylosing Spondylitis
¬ Systemic disease is treated by rheumatologist
¬ Ocular disease managed by optometrist
Patient reports lower back pain but thought it was only due
to job as a brick and block layer
52 year old woman
What is needed for a Plaquenil
baseline ocular examination?
$ Referred in by the rheumatologist for baseline ocular
examination due to Plaquenil therapy for rheumatoid
arthritis
¬ 200 mg bid PO (400 mg)
¬ Started 1 week ago
$ VA 20/20 OU
$ In 2011 the screening recommendation changed for Plaquenil
retinopathy
¬  The last recommendation was 2002
$ Externals: unremarkable
$ SLE: normal with adequate tear prisms
$ IOP 15 OU
Greg A Caldwell, OD, FAAO
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Rheumatology, Thyroid Dysfunction and
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Plaquenil
(Antiprotozoals/Antimalarial Therapy)
$  Classification
¬  Hydroxychloroquine
¬  Chloroquine
$ Hydroxychloroquine (Plaquenil)
¬  Safe, well absorbed
¬  Avoid if there is a G6PD deficiency
2  Glucose-6-phosphate dehydrogenase deficiency
2  Metabolic enzyme involved in cell metabolism
¬  Dosage: 200-400mg/d
$  Properties
¬  Rapidly absorbed in GI tract
¬  Immunomodulatory & anti-inflammatory
¬  Inhibit cell division/RNA transcription/ mononuclear cell phagocytosis/
cytokine secretion
What is needed for a Plaquenil
baseline ocular examination?
$ History (Plaquenil history questions)
¬  Dosage (400 mg daily)
¬  Number of years on medication or cumulative dose (recent literature)
¬  Any renal or liver impairment
$ Risk Factors
¬  Cumulative Dosage
2  400 mg x 365 = 146,000 mg/yr or 146 g/yr
2  146 g x 5 yrs = 730 g
2  146 g x 7 yrs = 1022 g (1000 g)
¬  Daily dose >400 mg
¬  Short stature with typical dose
¬  Age: Elderly at more risk
¬  Renal or liver function
2  Impairment places the patient at higher risk
¬  Existing retinal or macular disease
What is needed for a Plaquenil
baseline ocular examination?
$  Slit lamp examination
¬  Plaquenil can deposit in the cornea, if found here it is
suggesting drug accumulation
2  Less than 20% at 400 mg develop corneal deposits
$  Fundus examination with 90 or 78/20
¬  Look for unrelated/current pathology
¬  Consider red free to enhance RPE changes
$  Fundus photos
$  Visual fields
¬  Central 10-2 white on white Sita-Standard
2  Plaquenil scotomas are typically found within 10° of
fixation
¬  Para-central scotomas
$  SD-OCT
¬  Special attention to the inner and outer segment line
$  Counseling patient on the risk of toxicity (educational
sheet)
¬  Avoidance of liability
¬  The need for periodic ocular examination
¬  Screening can recognize toxicity early and minimize visual
loss but can not prevent all toxicity or guarantee there will be
no vision loss
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
June 4, 2016
Revised Recommendations on Screening for Chloroquine
and Hydroxychloroquine Retinopathy
$  Last recommendations were 2002
by the American Academy of
Ophthalmology
$  Improved screening tools and new
knowledge about prevalence of
toxicity have prompt the change
¬  1% after 5-7 years of use or a cumulative
dose of 1000 grams (Plaquenil)
$  There is no treatment for this
condition
¬  Therefore must be caught early
$  Screening for the earliest hints of
functional or anatomic change
$  Plaquenil toxicity is not well
understood
What is needed for a Plaquenil
baseline ocular examination?
$ Best corrected visual acuity
$ Color vision?
¬ Not sensitive enough to detect retinal toxicity
¬ If color vision affected then patient will most likely
have absolute scotoma and visual acuity affected
¬ In early retinal toxicity there is a relative scotoma,
normal color vision and normal acuity
¬ Studies show blue-yellow occur first then red-green in
plaquenil toxicity
2  Ishihara does not test for blue-yellow
2  D-15 is less sensitive than Ishihara
52 year old woman
$ 200 mg bid PO (400 mg daily)
$ 1 week duration
$ Normal stature
$ No history of renal or liver impairment
$ VA 20/20 OU
Just Kidding
$ Color vision D-15 normal
$ SLE: normal, (-) deposits and normal tear prisms
$ Fundus with 90/20, normal
$ Photos taken, normal
$ VF 10-2 Sita-stand done OU, normal
$ SD-OCT done, special attention to inner and outer
segment
$ Risk of toxicity education sheet given to patient
$ RTC 1 year for follow up (Comprehensive dilated exam with 10-2)
34
Rheumatology, Thyroid Dysfunction and
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Not Recommended for Screening
June 4, 2016
Plaquenil Cranium Keepers
$ Annual screening for first 5 years or < 1000 g
¬ Comprehensive dilated exam and 10-2
$ Fundus photography
¬ Recommend at baseline
¬ Not sensitive for screening
$ Time Domain OCT- insufficient resolution for screening
$ Amsler grid- can use as adjunct if desired
$ Color vision
$ After 5 years, >1000 g or high risk
¬  Comprehensive dilated exam, 10-2 and SD-OCT
$ Discontinue if toxicity occurs:
¬  Keratopathy is not a reason to discontinue
2  Less than 20% develop corneal deposits at 400 mg/daily
¬  Repeatable visual field defect is a reason to consider discontinuing
treatment
¬  Documented change to inner/outer segment of retina
$ Goal:
¬ Recognize the para-central functional change (10-2)
¬ Recognized the para-central structural change (SD-OCT)
¬ Bull’s Eye maculopathy is too late
PLAQUENILZONE
Plaquenil Toxicity
Oh Boy!
SYMMETRICAL
AND
NOTHING
OBVIOUS
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
1-1.5MMPERIMACULARGCC
THINNINGTHEFIRSTSIGNOF
PLAQUENILTOXICITY
WHY?THICKESTLAYER
OFGANGLIONCELLSAND
SMALLESTGANGLION
CELLSATTHATLOCATION.
VERYSENSITIVETOTOXICITY
35
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
WHATDOYOUSEEONTHESCANS?
A. 
B. 
C. 
D. 
THINNINGOFTHEGCCINTHEPLAQUENILZONE
MACULAREDEMA
COMPROMISEDPIL
NOTHINGOFIMPORT
DO YOU SEE
ANY PROBLEM
IN THE
PLAQUENIL
ZONE?
WHATDOYOUSEEONTHESCANS?
A. 
B. 
C. 
D. 
THINNINGOFTHEGCCINTHEPLAQUENILZONE
MACULAREDEMA
COMPROMISEDPIL
NOTHINGOFIMPORT
DO YOU SEE
ANY PROBLEM
IN THE
PLAQUENIL
ZONE?
AUGUST2014
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
AUGUST2014
36
Rheumatology, Thyroid Dysfunction and
the Eye
WHATDOYOUSEEONTHESCANS?
A. 
B. 
C. 
D. 
THEFLYINGSAUCERSIGN
MACULAREDEMA
INCREASEDPERIMACULARRETINALTHINNING
AANDC
June 4, 2016
WHATDOYOUSEEONTHESCANS?
A. 
B. 
C. 
D. 
THEFLYINGSAUCERSIGN
MACULAREDEMA
INCREASEDPERIMACULARRETINALTHINNING
AANDC
A
A
C
C
THEENDGAME…ONCEYOUDISCONTINUE
PLAQUENILITSTAYSAROUNDAWHILETO
CREATEDAMAGE..LONG½LIFE
BILATERALCOMPROMISEOFTHEPIL(WHITEARROWS)
AFTERCOLLAPSEOFPERIFOVEALRETINA(REDDASHED
ARROWS)WITHFLYINGSAUCERATTACK(BLUEARROWS)
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
WAYOUTTATHEBARN
37
Rheumatology, Thyroid Dysfunction and
the Eye
June 4, 2016
Questions?
Hope You Enjoyed
Thank You!
Greg A Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
38
Glaucoma-Enough Pearls to Make a
Necklace
Glaucoma
“Enough Pearls to Make a Necklace”
Greg Caldwell, OD, FAAO
June 4, 2016
Everything Therapeutic: Houston
June 4, 2016
Disclosures
$ Greg A. Caldwell, OD, FAAO will mention many
products, instruments and companies during our
discussion, I don’t have any financial interest in
any of these products, instruments or companies.
$ American Optometric Association, Trustee
¬ No industry lecturing
¬ Thank you to the members and those who join
$ All of these cases have entered/referred to my
practice
Disclosure Statement
(next slide)
What are the Two Types of Glaucoma?
Risk Factors for Developing Glaucoma?
Strong associations
Academic Answer
$ Open Angle Glaucoma
$ Closed Angle Glaucoma
Clinical Answer
$ Those at risk to develop
glaucoma
$ Those who have
glaucoma but are at a
higher risk of progressing
$ Age
¬  The older we are the higher the
risk
¬ Validity is an issue but increase
risk
$ IOP
¬  The higher the IOP the higher
the risk
$ CCT
¬  Thinner corneas increases risk
$ CDR
¬  Larger CDR increases risk
Development / Progression
Moderate association
$ Family history
$ Race (6-8x’s)
¬  Black Americans are at higher
risk
¬  Surrogate of thinner CCT, higher
IOP and larger CDR?
Weak associations
$ Refractive Error
¬ Poor association
¬ High myopia increase risk
$ Systemic Disease-mixed
¬ HTN, migraine, DM, thyroid,
sleep apnea
55 Year Old Men
500 microns CCT and 21 mm Hg
with Goldmann
Case 1
$  What is the true IOP?
1. 
2. 
3. 
4. 
18 mm Hg
21 mm Hg
24 mm Hg
Don’t Know
600 microns CCT and 21
mm Hg with Goldmann
$  What is the true IOP?
1. 
2. 
3. 
4. 
18 mm Hg
21 mm Hg
24 mm Hg
Don’t Know
Corneal Curvature
Corneal Thickness
Corneal Rigidity
Greg Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
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Glaucoma-Enough Pearls to Make a
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June 4, 2016
61 year old woman
$ You saw her 4 weeks ago and her IOP’s
were 24 OD and 25 OS at 3:35 PM
Case 2
$ Is in today for a morning IOP check and
pachymetry
Results
Corneal Pachymetry
$ Right and left eyes minimum corneal thickness differed by
$ Pachymetry results
¬ OD 525 OS 565
$ IOP’s at 8:15 AM
¬ OD 28 OS 29
an average 8 μm
$  242 eyes
$ Although a wide range of values exists in simulated
Any Concern Here?
keratometry, minimum corneal thickness, and posterior
corneal elevation,
¬ Interocular pachymetry symmetry in all these parameters was
very high in this group of consecutive patients.
¬ Asymmetry of these interocular parameters may warrant repeat
clinical testing for accuracy and may predict corneal
abnormalities.
¬ This study points out potentially clinically important high
interocular corneal symmetry data in simulated keratometry,
corneal thickness, and posterior corneal elevation.
MYROWITZ Elliott H, KOUZIS Anthony C, O'BRIEN Terrence P. High interocular corneal symmetry in average simulated
keratometry, central corneal thickness, and posterior elevation. Optometry and vision science.
2005, vol. 82, no5, pp. 428-431
Pachymetry
Anterior Segment Imaging
Pachymetry
Ultrasonic versus Optical
CCT measurement caliper
Greg Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
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Glaucoma-Enough Pearls to Make a
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Anterior Segment Imaging
with OCT
Pachymetry
June 4, 2016
Post-LASIK
Less Than 15 Degrees Get Consult
Development of Glaucoma
$ OHTS- found DM to be protective
What are your thoughts on DM being protective?
$ OHTS, EMGTS and AGIS
$ OHTS- found an increase in pattern
standard deviation (PSD) to increase risk
Greg Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
3
Glaucoma-Enough Pearls to Make a
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June 4, 2016
Effect of H1 Antagonists on Histamine Release from
Human Conjunctival Mast Cells1,2
120
120
Olopatadine
PATANOL® solution
80
60
Ketotifen
ZADITOR*
40
20
0
Azelastine
OPTIVAR*
-20
-40
Epinastine
ELESTAT*
-60
-80
Effect at marketed concentration
-100
-8
-7
-6
-5
-4
-3
-2
-1
log [Drug] (M)
*Trademarks are the property of their respective owners.
1. Yanni JM et al, The in vitro and in vivo
ocular pharmacology of olopatadine. J Ocul
Pharmacol Ther. 1996; 12:389-400.
100
% Inhibition of Histamine Release
% Inhibition of Histamine Release
100
80
60
40
20
0
-20
-40
-60
-80
-100
-8
-7
-6
-5
-4
-3
-2
-1
2. Brockman HL et al, Interactions of
olopatadine and selected antihistamines
with model and natural membranes. Ocul
Immunol Inflamm, 2003; 11:247-268.
Progression
$ Many practitioners feel that the risk factors for developing glaucoma
and the glaucoma to progress are essentially the same
$ However, once treatment commences things change
¬  One obviously is IOP
$  Furthermore, the patients will get older and comorbitities may
develop
Risk Factors of Progression of Glaucoma?
$ Age
$ Systemic Diseases
$ IOP
¬ DM, Migraine, HTN
$ Diurnal IOP fluctuation
$ Visual field loss
$ CDR
¬ The more NRR loss the
higher the risk to progress
$ CCT
¬ Not a risk of progressing in
appropriately treated
patients with glaucoma
$ Disc hemorrhage
$ This is where most of our evidence based medicine done
¬  EMGTS
¬  AGIS
Disk Hemorrhages
¬ Associated with progression
$ Family history
¬ Especially those with
functional vision loss
Non-Specific Finding
$ Non-specific finding
$ However, when associated with glaucoma
it typically indicates you should:
¬ Initiate a more careful monitoring
¬ Re-evaluate the therapy you are doing
¬ Treat the patient if not being treated
Greg Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
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June 4, 2016
1-7-05
Non-Specific Finding
2-20-06
11-27-06
4-23-06
Disc Hemorrhage
11-27-06
9-12-05
Adjacent to Existing Loss
Pallor
Patient declined treatment for 10 years
Pallor
Laminar Dots
$ Found in many normal eyes
$ 34% of myopic eyes have laminar dots
$ Shape of dots may be clinically helpful in determining
glaucoma damage to optic nerve head
¬ Round holes become more horizontal slits in glaucoma
Greg Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
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Glaucoma-Enough Pearls to Make a
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June 4, 2016
Lamina Cribrosa
Laminar Dots
Confusion in Glaucoma
NEI Clinical Trials Across
the Spectrum of Glaucoma
$ Evidence based medicine is taking reliable and unbiased
research evidence and applying it to clinical expertise
and patient wishes to arrive at an appropriate treatment
or management
$ Clinical decisions are based on valid evidence
¬ Not gut feelings, hear say or peer influences
$ Occurs when we apply a piece of evidence based
medicine in the wrong area of our glaucoma paradigm
$ Occurs when we don’t know where to apply the piece
CIGTS
OHTS
Early
Glaucoma
Ocular
Hypertension
of evidence based medicine in our glaucoma paradigm
Advanced
Glaucoma
AGIS
GLT
FFSS
EMGT
ongoing trials
interim results
completed trials
Studies and Goals
CCT
GDX
OCT
Age
(Very Abbreviated)
HRT
VF
SWAP
IOP
Study
Disease State
IOP Endpoint
OHTS
High IOP
20% Decrease
EMGTS
Early
20%
CIGTS
Newly Dx
VF & IOP dependent
(As low as 40 %)
CNTGS
Advanced
Progressive NTG
1/3 decrease
AGIS
Advanced
< 18 mm Hg
RNFL and optic nerve
change (detectable)
Short wavelength automated
perimetry VF changes
Retinal nerve fiber layer
change (undetectable)
Treatment
Ganglion
cell
death/axon loss
Acceleration of
apoptosis
Normal
VF
Thres
hold
VF
FDT
Tr
e
Age
at
m
IOP &Diurnal IOP
CDR and Hemes
en
Standard automated
perimetry VF change
t
VF change (moderate)
VF change (severe)
Blindness
Glaucoma Continuum
Weinreb et al. Am J Ophthalmol. 2004;138:458-467.
Greg Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
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Glaucoma-Enough Pearls to Make a
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CCT
GDX
Rates of Progression
OCT
Age
HRT
VF
SWAP
IOP
O
H
TS
June 4, 2016
VF
RNFL and optic nerve
change
(detectable)
EMGTS
Acceleration of
apoptosis
FDT
Short wavelength automated
perimetry VF changes
Retinal nerve fiber layer
change (undetectable)
Treatment
Ganglion
cell
death/axon loss
VF
Thres
hold
Tr
e
Age
at
m
IOP &Diurnal IOP
en
$ OHTS
$ EGPS
Standard A
automated
GI
S
perimetry VF change
t
Treated
$ EMGTS
$ CNTGS
Untreated
1%/yr
2%/yr
45%/yr
4%/yr
$ OHTS
$ EGPS
$ EMGTS
$ CNTGS
2%/yr
2%/yr
62%/yr
12%/yr
VF change (moderate)
CDR and Hemes
VF change (severe)
Normal
Blindness
Glaucoma Continuum
$ It is generally accepted that in early glaucoma patients:
$  Treated patients will have a rate of worsening of 4%
$  Untreated patient will have a rate of worsening 8-10%
Weinreb et al. Am J Ophthalmol. 2004;138:458-467.
CNTGS
$ If Normal Tension Glaucoma is left untreated
¬ 1/3 would progress within 3 years
¬ ½ would progress within 5-7 years
$ Therefore, most cases of NTG progress slowly
¬ If you treat someone and there is no progression is it
your treatment or is it because the disease is so slow?
50 year old woman
Case 3
ONH Appearance
$ Recently has moved to the area and needs
followed for her “ocular hypertension”
$ Diagnosed 18 months ago
$ Currently is using Travatan qd OU (PM)
$ VA 20/15 OU
$ Externals: unremarkable
$ SLE: slight hyperemia OU
$ IOP: 13 OD and 14 OS @ 8:30 AM
Greg Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
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Glaucoma-Enough Pearls to Make a
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June 4, 2016
Review of Records
$ Diurnal IOP without medication
¬ OD 16-19 8:00 AM thru 5:30 PM
¬ OS 17-20 8:00 AM thru 5:30 PM
$ Pachs
¬ OD 505
¬ OS 505
$ VF results
MD and PSD
MD
$ 54 spots on 24-2
¬ All 54 spots reduced by 1
DB (54DB)
¬ MD 1DB
$ 54 spots on 24-2
¬ 27 spots reduced by 2 DB
(54 DB)
¬ MD 1 DB
$ 54 spots on 24-2
¬ 13.5 spots reduced by 4 DB
(54DB)
¬ MD 1 DB
PSD
$ Low PSD (Generalized loss)
¬ 1.00 DB
$ Moderate PSD (More
localized loss)
¬ 3.00 DB
$ High PSD (Localized loss)
¬ 5.00 DB
Treatment
Discussion
Why is this patient being treated?
Greg Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
$ Repeat visual field
$ Discontinue Travatan
$ Get GDX nerve fiber analysis
8
Glaucoma-Enough Pearls to Make a
Necklace
Repeated
VF
Cranium Keeper
June 4, 2016
GDX Results
Thoughts on Mean Deviation (MD)
What is the Mean Deviation on a visual field of a blind eye?
$ Do not back door patients into the ocular
hypertension treatment study
¬ Via thin pach results
$ A patient needs to be suffering from ocular
hypertension to use the study
$ Thin pachs tell us:
¬ Patients with ocular hypertension are at high, medium
or low risk for development
$ If you have a diagnostic instrument learn how it
works and make proper interpretations
Thoughts on Mean Deviation (MD)
$ Turn on your VF let it run
¬ 30 DB (decibel)
$ 0-5
(1/6)
30% reduction
$ 5-10
(1/3)
40% reduction
$ >10
(1/2)
50% reduction
Surgical Update
Endoscopic Cyclophotocoagulation (ECP)
$ How many DB difference to reliable VF should
cause a RAPD?
¬ 3 DB for a small APD, the larger the difference the
greater the APD
Greg Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
9
Glaucoma-Enough Pearls to Make a
Necklace
What is Endoscopic
Cyclophotocoagulation (ECP)
$ Ciliary body processes are visualized with
an endoscope and are photocoagulated
with a laser
$ Result is decreased aqueous production
and lower IOP
Endoscopic
Cyclophotocoagulation (ECP)
$ Gaining in popularity
$ Typically done at the time of cataract
surgery
¬ Increase number of surgeons are combining
phaco with ECP
June 4, 2016
History of Endoscopic
Cyclophotocoagulation (ECP)
$ Martin Uram, MD (Retinologist)
¬ Wanted another treatment for neovascular
glaucoma
¬ Cyclocryotherapy
2 Painful, limited to moderate success to lower IOP
and high complication rate
Benefits of Endoscopic
Cyclophotocoagulation (ECP)
$ Performed through small incision
$ Easy access to ciliary processes while the patient
is aphakic
$ Easy to perform
$ Typically able to reduce the amount of drops the
patient uses
¬ Increase in quality of life
$ Possibly more sustained IOP control
¬ Studies show fluctuating IOP as risk factor
Limitations of Endoscopic
Cyclophotocoagulation (ECP)
$ Transient iritis
¬ Treated with steroids
$ Cystoid macular edema (CME) reported
to be 1%
$ No reports of hypotony or phthisis
Greg Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
Replacing Filters/Trabeculectomy
$ Phaco/Filter
¬ Additional 25-30
minutes of surgery
¬ Numerous post op
visits
¬ Failure rate
¬ Marked IOP reduction
or hypotony
$ Phaco/ECP
¬ Additional 5 minutes
of surgery
¬ Standard cataract post
op visits
¬ Minimal failure rate
¬ Gradual IOP reduction
10
Glaucoma-Enough Pearls to Make a
Necklace
Expectations
$ Study of 707 eyes with cataracts and controlled glaucoma
¬ 626 ECP/Phaco
¬ 81 Phaco only
$ ECP
¬ Pre-op IOP
19.08
$ Phaco only
¬ Pre-op IOP
18.6
Post-op IOP
15.73
Post-op IOP
18.93
$ 68% are able to reduce 1 glaucoma medication
$ Approximate savings $800-1500/year for the patient
Video of ECP
June 4, 2016
Post Op
$ Pred-Forte
¬ Every 2 hours to qid for 1 month
$ Nevanac
¬ Bid or tid for 1 month
$ Cycloplegia
¬ Homatropine or Scopolamine
¬ 1-12 weeks
Thank-You
and
Hope You Enjoyed
Greg Caldwell, OD, FAAO
[email protected]
Greg Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
11
Oral Antibiotics-Feel More Confident and
Comfortable in One Hour Prescribing
Oral Antibiotics for Your Patients
June 4, 2016
Disclosures
Oral Antibiotics in Eye Care
Greg Caldwell, OD, FAAO
June 4, 2016
Everything Therapeutic: Houston
$ Greg A. Caldwell, OD, FAAO will mention many
products, instruments and companies during our
discussion, I don’t have any financial interest in
any of these products, instruments or companies.
$ American Optometric Association, Trustee
¬ No industry lecturing
¬ Thank you to the members and those who join
$ All of these cases have entered/referred to my
practice
Disclosure Statement
(next slide)
Learning Objectives
$ Review adverse/allergic reactions to oral medications
$ Review the FDA Pregnancy Categories for medications
¬ Review new guidelines: Pregnancy, Lactation, and Reproductive
Potential: Labeling for Human Prescription Drug and Biological
Products
$ Discuss renal impairment and its impact on prescribing
oral medications
Patient Wants Second Opinion
42 year old woman
OD red and painful
Va 20
20
cc
20
Current Correction
R -2.00-1.00 x 180
L -3.00-1.00 x 180
$ Identify and review the most appropriate oral antibiotics
for usage in ocular infections, so one can implement a
timely and effective treatment
$ Furnish the clinician with pearls, therapeutic options and
guidance around pitfalls
Slit Lamp
Evaluation
$ Findings
¬ OD only red and injected
¬ Stuck shut this morning
EOMS: full, unrestricted
CT: ortho D/N
PERRL (-)APD
CF: full by FC OU
New Diagnosis?
$ Diagnosis
¬ Bacterial conjunctivitis
$ Ocular history reveals
¬ 3rd time in past 10 months
¬ Vigamox
2  Successfully resolves in 2-3 weeks
Recurrent bacterial
conjunctivitis secondary
to dacryocystitis
Why recurrent and slow to resolve?
Greg A. Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
1
Oral Antibiotics-Feel More Confident and
Comfortable in One Hour Prescribing
Oral Antibiotics for Your Patients
Dacryocystitis
June 4, 2016
Medical History
$ Before we Rx any medications we take a
thorough medical history which includes:
$ Treatment discussion?
¬ Topical antibiotics
¬ Oral antibiotics
$ Remember to check for?
$ Patient is allergic to Penicillin and Keflex
¬ Which antibiotic would you use?
Adverse/Allergic Reaction
to Systemic Medication
•  CC
•  HPI
•  ROS
•  Kidney disease, liver disease, dialysis
•  PFS History
•  Current Medications
•  Allergies…Adverse Reactions/Allergies
•  Pregnancy…any chance you might be pregnant?
FDA Pregnancy Categories
$ Category A- studies in pregnant women, no risk
$ Hypersensitivity- fever, rash, photosensitivity or
ANAPHYLAXIS
•  Hematologic- neutropenia, eosinophilia, increase in PT/PTT
•  GI- nausea, vomiting, diarrhea
•  Liver Failure
•  CNS- dizziness, HA, confusion, seizures
•  Ototoxicity
•  Cardiac- dysrrhymias
Pregnancy and Lactation Labeling Rule-FDA
December 4, 2014 Final Rule
$  Effective June 30, 2015
¬  Effective now for new medications and a 3-5 year phase in period (application)
$  Labeling for human prescription drugs and biological products will include:
¬  Pregnancy
¬  Lactation
¬  Females and Males of Reproductive Potential
$  Pregnancy (8.1)
¬  Pregnancy Exposure Registry – omit if not applicable
¬  Risk Summary – required subheading
¬  Clinical Considerations- omit if none of the headings are applicable
$ Category B- animal studies no risk but human not
adequate…or…animal toxicity but
human studies no risk…safe
$ Category C- animal studies show toxicity human
studies inadequate but benefit of use may exceed
risk…avoid
$ Category D- evidence of human risk but benefits
may out weigh risks…avoid
$ Category X- fetal abnormalities, risk>benefits…avoid
Pregnancy and Lactation Labeling Rule-FDA
December 4, 2014 Final Rule
$  Lactation (8.2)
¬  Risk Summary- required subheading
¬  Clinical Considerations– omit if not applicable
¬  Data– omit if not applicable
$  Females and Males of Reproductive Potential (8.3) - omit if none of the headings are applicable
$  Pregnancy testing– omit if not applicable
$  Contraception– omit if not applicable
$  Infertility – omit if not applicable
2  Disease-associated maternal and/or embryo/fetal risk- omit if not applicable
2  Dose adjustments during pregnancy and the postpartum period - omit if not applicable
2  Maternal adverse reactions - omit if not applicable
2  Fetal/Neonatal adverse reactions- omit if not applicable
2  Labor or delivery - omit if not applicable
¬  Data- omit if none of the headings are applicable
2  Human Data - omit if not applicable
2  Animal Data- omit if not applicable
Greg A. Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
2
Oral Antibiotics-Feel More Confident and
Comfortable in One Hour Prescribing
Oral Antibiotics for Your Patients
June 4, 2016
Antibiotic Paradigm
Renal Impairment
$ Identify patients on hemodialysis
Antibiotic Paradigm
$ Adjustment made by patient’s creatinine
clearance (CrCl)…ml/min
¬ Work with patient’s PCP/Internist
Penicillin
Macrolide
Cephalosporin
Quinolone
Sulfonamide
Augmentin
Zithromax
Keflex
Cipro
Bactrim
Cross Reaction
Allergies
Penicillin
Macrolide
Cephalosporin
Quinolone
Sulfonamide
Augmentin
Zithromax
Keflex
Cipro
Bactrim
Sulfonylurea
(Glyburide)
(Glipizide)
Sulfonamide
(Celebrex)
Carbonic Anhydrase Inhibitor
Diamox
Thiazide Diuretic
Hydrochlorothiazide
(HCTZ)
Augmentin
$ Amoxicillin and potassium clavulanate
¬ Uber amoxicillin
$ Kills everything, good for everyone
–  12 weeks old and older
$ Safe in pregnancy…category B
$ Watch for PCN allergies
$ Adults: 250, 500 and 875 mg
¬ 125 mg of potassium clavulanate
$ Children <100 pounds: oral suspension 25-45 mg/
kg divided into 2 doses
Zithromax (azithromycin)
$ Macrolide antibiotic (erythromycin)
$ Drug of choice in PCN sensitive patients
$ All age groups and pregnancy category B
$ No renal adjustment
$ Adult:
¬ 250 mg bid (day1), 250 mg qd (day 2-5), 6 pack
¬ 500 mg qd x 3 days, tri-pack
$ Children<16: 10 mg/kg (day1), 5 mg/kg (day 2-5)
$ Covers Staph, Strep and Haemophilus influenzae
$ Better tolerated than erythromycin, little GI upset
$ Chlamydia…1 g qd
$ Covers Staph, Strep and Haemophilus influenzae
Greg A. Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
3
Oral Antibiotics-Feel More Confident and
Comfortable in One Hour Prescribing
Oral Antibiotics for Your Patients
June 4, 2016
Keflex (cephalexin)
Zithromax (azithromycin)
$ “The Vegas Drug”- Chlamydia…1 g qd
$ Cross reaction with PCN sensitive patients
$ 1st generation, moderately affective against PCN-ase
$ Good for Gram +, not good for Haemophilus (-)
$ Available in 250 and 500 mg
$ Category B
$ Adult: typically, 500 mg bid x 1 week
¬ Maximum 4 g in 24 hrs
$ FYI...Drug of choice for blow out fractures
Ceftin (cefuroxime)
PCN
$ Minimal cross reaction with PCN sensitive patients
$ 2nd generation
Cross Reaction
$ Better for Haemophilus (-)
$ Children: 3 months to 12 years old, oral
Keflex
suspension 15 mg/kg divided into 2 doses x 10
days
$ Available in 125, 250 and 500 mg
¬ FYI: adults typically 250 mg bid x 10 days
Ceftin
$ Category B
Cipro (ciprofloxacin)
Levaquin (levofloxacin)
$ In my opinion, an end of the line, antibiotic to use…
allergic to PCN, cephlosporins, macrolides…
$ Really effective
$ Would avoid if pregnant…category C
$ Only use 18 years or older (oral)
$ Cipro and Levaquin available in 250, 500 and 750 mg
¬ Cipro 750 mg for only severe infections
$ 500 mg bid x 1 week-Cipro
$ 500 mg qd x 1 week-Levoquin
$ Levaquin-tendon ruptures
Greg A. Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
Sulfa Drugs
$ Limited use…last line of defense
$ Contraindicated in pregnancy and sickle cell
disease
¬ Category C
$ High incidence of Steven-Johnsons
$ Cross reaction with: oral hypoglycemics, CAI’s,
celebrex and thiazide diuretics…all sulfa based
$ Bactrim SS
¬  400 mg sulfamethoxazole/ 80 mg trimethoprim
¬ 1-2 tab PO bid
$ Bactrim DS (double strength)
¬ 800 mg sulfamethoxazole/ 160 mg trimethoprim
¬ 1 tab PO bid
4
Oral Antibiotics-Feel More Confident and
Comfortable in One Hour Prescribing
Oral Antibiotics for Your Patients
June 4, 2016
Summary
How About
$ PCN, Ampicillin and Amoxicillin
Allergies
Penicillin
Macrolide
Cephalosporin
Quinolone
Sulfonamide
Adults
Augmentin
Zithromax
Keflex
Cipro
Bactrim
Children
Augmentin
Zithromax
Ceftin
Avoid
Bactrim
$ Dicloxacillin, 250mg qid x 1week
$ Remember…patient
allergic to PCN and
Keflex
$ Treatment
¬ Vigamox gtts TID
¬ Zithromax
2  Disp: z-pak
2  Use as directed PO
$ Dilation and Irrigation
¬ Contraindication and indication
What group of antibiotics are
we missing?
$ Confirmed nasolacrimal duct blockage
¬ DCR, dacryocystorhinostomy
Clinical Pearl
Treatment Failure
$ If you continue to think of doxycycline
and minocycline as antibiotics, treatment
failure will be the result
$ From this point on consider them a
steroid
48 year old man
OU red, gritty, sandy and dry feeling
Va 20 20
20
cc
20
Current Correction
R -2.00 sphere
L -3.00 sphere
EOMS: full, unrestricted
CT: ortho D/N
Greg A. Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
PERRL (-)APD
CF: full by FC OU
5
Oral Antibiotics-Feel More Confident and
Comfortable in One Hour Prescribing
Oral Antibiotics for Your Patients
June 4, 2016
A Closer Look
$ Diagnosis
¬ Rosacea
$ What findings support your
diagnosis?
¬ Telangiectasias
¬ Erythema of the cheeks,
forehead and nose
¬ Rhinophyma
2  Indicates chronic
$ Let us get a closer look
Tetracycline
Minocycline
Analog
Rosacea Blepharitis
(Inflammatory Blepharitis, MGD)
$ Diagnosis?
$ Treatment?
¬ In my opinion, most under treated condition
¬ Warm compresses
¬ Lid hygiene
¬ Artificial tears
¬ Omega 3 fatty acid
Staph Aureus
Staph Epidermidis
Lipase
Turbid
Inspissated MG
Meibomian Gland Secretions
(Lipid)
Marginal Foam
(Soap)
Phospholipids
Arachidonic Acid
2  EPA and DHA total 1500 mg (1000 mg minimum)
¬ Dermatological consult (Acne Rosacea)
¬ Oral antibiotics…???
Prostaglandins
Thromboxines
2  Which one and why??
Leukotrienes
How About Steroids?
Minocycline / Doxycycline
$ Drug of choice for marginal inflammatory
blepharitis (posterior blepharitis)
$ AB, anti-inflammatory and anti-collagenase
$ Inhibits lipase enzyme
$ No renal adjustment
$ 50-100 mg qd-bid 2-12 weeks (pulse)
My Paradigm for
Minocycline / Doxycycline
$ Status of MG
¬ Inspissated
¬ Turbid
Greg A. Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
¬ Maximum dosage for 2-12
weeks (pulse)
2  100 mg BID, QD
¬ 50-100mg qd while turbid
¬ 20 mg longer treatments
2  Periostat (Doxycycline)
¬ Lower maintenance dose
$ 20 mg Periostat (Doxycycline)
¬ Helpful in those with stomach or GI sensitivity
¬ Excellent for those requiring long maintenance dose
$ Minocycline / Doxycycline Paradigm
¬ Clear
¬ 20 mg if maintenance dose
needed
6
Oral Antibiotics-Feel More Confident and
Comfortable in One Hour Prescribing
Oral Antibiotics for Your Patients
Customize Treatment
$ 50 mg Minocycline with pill cutter (25 mg)
$ Oracea- 40 mg of Doxycycline total
¬ 30 mg immediate release
¬ 10 mg sustained release
$ Alodox Kit
¬ 20 mg Doxycycline
¬ Ocusoft lid scrub
June 4, 2016
Precautions With Oral Tetracycline Analogs
$  Enhanced photosensitivity
$  Avoid in children and pregnancy
(Category D)
$  Can enhance Coumadin
$  Can enhance the action of digoxin
$  ?Long term use with increase risk
of breast cancer?
$ AzaSite (azithromycin opthalmic solution) 1.0%
¬ Initiate early in treatment
¬ Adjunctive when patient is already on Doxycycline
¬ Alternative in states that do not have oral therapeutic licensure
Benign intracranial hypertension
“It’s not rare if it’s in your chair”
¬  1 paper/study, not regarded as
highly reliable study
¬  Further investigation discredited
the association
$  Benign intracranial hypertension,
reported cases
¬  17 cases from 1978-2002
9-13-2010
8-19-2010
10-6-2010
8-31-2010
8-19-2010
Minocycline
Successfully Treated
$ Less photosensitivity
$ Less GI upset
$ Less bacterial resistance
$ Warm Compresses
$ Lid Scrubs
$ Artificial Tears, Systane Balance
$ Omega 3 (1500 EPA and DHA)
$ Mino 100 mg PO 6 weeks, 50 mg 3 months,
20 mg maintenance (Doxy)
$ Steroids, Tobradex qid (5 weeks with taper)
¬  Moderately red and thickened lid margins
¬  Marginal infiltrates
Greg A. Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
7
Oral Antibiotics-Feel More Confident and
Comfortable in One Hour Prescribing
Oral Antibiotics for Your Patients
June 4, 2016
What is an Inspissated MG?
I Can’t Believe It’s Not Butter!®
Squeeze
6 Month Later
1 Year Later
Greg A. Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
8
Oral Antibiotics-Feel More Confident and
Comfortable in One Hour Prescribing
Oral Antibiotics for Your Patients
June 4, 2016
Thank-You
and
Hope You Enjoyed
Greg Caldwell, OD, FAAO
[email protected]
Greg A. Caldwell, OD, FAAO
[email protected] 814-931-2030 cell
9