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Transcript
DISCLOSURE STATEMENT
AOA’s definition of Optometry
approved Sept 2012
“No disclosure statement.”
Course Title:
Doctors of optometry (ODs) are the independent primary health care professionals for the eye. Optometrists examine, diagnose, treat, and manage diseases, injuries, and disorders of the visual system, the eye, and associated structures as well as identify related systemic conditions affecting the eye. Lecturer
: Beth
A. Steele,
OD, FAAO
Please silence all mobile
devices.
Driving Forces in Health Care Changes
 Standardized Coding  Clinical Quality Measures
 Meaningful Use of EHR  …..Outcomes Based Care
WELLNESS
TREATING THE WHOLE PATIENT
 Risk Adjustment  Physician Quality Reporting
PREVENTION
Quality of
Patient Care
MEDICAL
OPTOMETRY
…..where do we fit in?
America’s High Blood
Pressure Burden
• US – about 1 in 3 adults
–73 million have hypertension
• Number one reason listed for office visits
• Causes/contributes to 457,000 admissions per year
• A leading cause/contributor to death (MI, stroke,
vascular disease)
1
Not just this…
But also this…
Nwankwo. T., Yoon. S.S., Burt. V., Gu. Q. (2013). Hypertension among adults in the United States: National Health and
Nutrition Examination Survey, 2011–2012. NCHS data brief, no 133. Hyattsville, MD: National Center for Health Statistics.
Is routine blood pressure part of your daily routine in patient care?
JNC 8 – What’s New?  Threshold for treatment of BP in ages ≥60
 150/90 vs. 140/90
HYPERTENSION
Over 70 million people in US
 20‐25% of population unaware
7.1 million deaths per year
 “Silent Killer”
 Stroke, MI, End‐stage renal dz
 Recommendations for initial therapy
 Thiazide diuretics  ACE inh, ARBs, Ca2++ channel blockers
 NOT: β‐blockers, α‐blockers, loop diuretics
From: 2014 Evidence-Based Guideline for the Management of High Blood
Pressure in Adults: Report From the Panel Members Appointed to the
Eighth Joint National Committee (JNC 8)
Blood Pressure Classifications and Referral Guidelines
(adapted from the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure – JNC 7, 2003)
Hypotension
normal
Pre‐ HTN
Stage 1
Stage 2
Critical High Point
Systolic
< 90
< 120
120‐139
140‐ 159
≥160
>180
Diastolic
< 60
< 80
80 ‐ 89
90‐99
≥100
>110
“Hypertensive Crisis”
 URGENT vs. EMERGENT
Systolic
>180
Diastolic
>110
(>120)
Confirm
within 2
months
Evaluate or
refer to
PCP within
1 month
Evaluate or refer
immediately or
within 1 week
 JNC 7
“Evaluate and treat immediately or within 1 week depending on clinical situations and complications.”
 Systemic symptoms
 Ocular findings
Meetz RE, Harris TA. The optometrist's role in the management of
hypertensive crises. Optometry. 2011 Feb;82(2):108-16.
2
The breaking point of autoregulation
Same BP – 2 different situations
BP 190/112  Autoregulation helps control retinal blood flow
 Operates within a certain range  Critical point : breaks down → vessels no longer protected  Too high=Malignant hypertension / hypertensive crisis
 Too low=Arteriolar hypotenstion BP 190/112
 Feeling “fine”
 (+) “migraine”since yesterday
 Forgot his medicine today
 DFE: disc edema
 Denies H/A, etc
flame heme
 DFE: crossing changes
Subjects retina to
ischemic damage
Hypotension
 Low Blood Pressure
 Systolic < 90
 Diastolic < 60
Proper methods = Accurate Results
 Poor perfusion of oxygen and nutrients to vital organs
 Common symptoms = blurred vision, fatigue, dizziness, fainting, confusion
 Risk of ocular manifestations
Are YOU Meaningfully Using? Vitals Station
 Core Objective #4
 Height For >80% of all unique
 Weight patients age ≥2
 Calculate and display BMI
 Blood pressure (Age ≥3)
 Growth charts if 0‐20 years
 New CQMs
 CMS 22v1 ‐ Screening and f/u for High BP
 CMS69v1 – BMI Screening and f/u 3
Patient Vital Signs  Temperature – 96.4ͦ ‐ 99.1ͦ
 Blood Pressure – <120/<80
 Respiration Rate – 20 breaths/min
 Heart Rate – 50‐90bpm  Others
 Weight/height BMI<25
 Pain www.nhlbi.nih.govhealth/resources/#blood
http://smokefree.gov/health-care-professionals
Now with EOM involvement….??
3rd Nerve Palsy
BP 190/112 http://cim.ucdavis.edu/EyeRelease/Interface/TopFrame.htm
 Feeling “fine”
 Forgot his medicine today
 EOMs – SO and LR are unopposed
 Denies H/A, etc
 Levator  DFE: crossing changes
 Parasympathetic pupillary fibers
http://cim.ucdavis.edu/EyeRelease/Interface/TopFrame.htm
Kanski. Clinical Ophthalmology, 4th Ed
4
3rd Nerve –a nice overview Keane JR, Can J Neuro Sci. 2010 Sep;37(5):662-70.
Etiology – CN III Palsy
 Pupil involvement
 Most likely compressive (80%)
1400 personally examined patients – 37 years
 Presentation
 bilateral in 11%
 complete in 33%
 isolated in 36%
 Etiology
 Pupil spared
 Of 234 patients with diabetes
 2/3 due to microvascular ischemia
53% had pupillary involvementoften bilateral
 5 had aneurysms

 diabetes (11%)
 Most likely vasculopathic (77%)  Resolution of vasculopathic ~3 mos ‐‐ follow closely  Imaging necessary? 
 trauma (26%)
 tumor (12%)
 Emergency  Only 2% of aneurysms spared the
pupil.

History
±Pain, Headache or other neuro signs
 aneurysm (10%)
 surgery (10%)
 stroke (8%)
 infection (5%)
 Painful onset
 94% of aneurysm
 69% of diabetic cases.
double vision
double vision
• Head injury 3 months ago 1⁰ gaze – note head posture
– Imaging in ER all negative
• Vertical diplopia
– Worse in down gaze
– Right head tilt
Under‐action LSO Double Maddox Rod?? Torsion noted on DFEs!
 Can help determine if SOP is bilateral
 often missed due to asymmetry  MR over both eyes
 Small vertical prism over one eye  Cyclodeviated eye will report a “tilted” line
Rotating MR
to straighten
image of line
5
SO Palsy
VI Palsy – Pearls  Etiology
 Trauma
 Decompensated congenital – slow onset
 Children
 Least likely of EOM palsies to have underlying etiology, BUT….


Microvascular disease
Brain abnormality
Imaging, careful
follow up
 Treatment  Prism, surgery, botox  Frequently acquired and transient
 Trauma, Tumor, hydrocephalus
 Adults  Trauma
 Neoplasm
Significant risk of
morbidity – imaging
even if other risk
factors present
 Microvascular disease Rutsein, Daum. Anomalies of Binocular Vision
EOM palsies: Do not assume……
44 WM with bilateral ptosis  POH and PMH: 1. Vasculopathic
 16.5% thought to be ischemic had another cause (neoplasm, MS, GCA)
Tamhankar, et al. Ophthalmology Nov 2013
2. True isolation
unremarkable when questioned
 FOH:  Ptosis
 Cataracts : Father and sister
 “maybe” macular degeneration
 Exam:  Colorful nuclear opacities
 Macular stippling OS
Ptosis ‐‐ DDx
 3rd Nerve Palsy
 Horner’s Syndrome
 Congenital ptosis
 Levator Dehiscence
 Myasthenia Gravis
 Less commonly
 Chronic progressive external ophthalmoplegia (CPEO)
 Kearns Sayre syndrome
 Ocularpharyngeal muscular dystrophy
 Myotonic Dystrophy
Myotonic Dystrophy
Frontal Balding
Expressionless Face
 AD w/variable penetrance
 1 in 8000 (presenting age 20‐30)
 Myotonia:  ↑ muscle contraction with slow relaxation  Distal muscles of limbs, face,neck
 Multiple systems Endo, Resp, C/V
 ↓ intelligence, MH
 Later involvement of larynx, vocal cords, pharynx
6
Ocular manifestations
Myotonia ‐ Dx and Mgmt
 Dx
 Family history, clinical presentation
 Creatine kinase (CK) levels
 Electromygraphy (EMG)
 Abnormal ERG (↓dark adaptation)
 Muscle biopsy
 DNA testing
 Treatment is palliative (Heat, cold avoidance, quinine)
 Ptosis (80%)
 Ocular motility disturbances
 Orbicularis weakness
 Hypotony (as low as 4mmHg)
 “Christmas Tree Cataracts”
 Peripheral retinal changes—
up to 50%
 Rarely, anti‐myotonic drugs are used
 Macular involvement—20%
 Granular pigment changes with  Genetic counseling
stellate pattern
Summary of CN Functions and Testing
Adapted from Muchnick, B. Clinical Medicine of Optometric Practice, 2nd Ed. Cranial Nerve
I – Olfactory
Test
CN Tes ng →
involvement of VII and VIII
Identify odors
II - Optic
Visual acuity, visual field, color, nerve head
III - Oculomotor
Physiologic “H” and near point response
IV – Trochlear
Physiologic “H”
Summary Corneal
of Cranial
Nerve Functions and Testing
reflex; clench jaw/palpate
V - Trigeminal
(Adapted from Muchnick,
B. Clinical
Medicine in Optometric Practice, 2nd ed.)
Light touch
comparison
VI - Abducens
Physiologic “H”
VII - Facial
Smile, puff cheeks, wrinkle forehead, pry open closed lids
VIII - Vestibulocochlear
Rinne test for hearing, Weber test for balance
IX - Glossopharyngeal
Gag reflex
X - Vagus
Gag reflex
XI – Accessory
Shrug, head turn against resistance
XII - Hypoglossal
Tongue deviation
Ramsay Hunt Syndrome
“Blood work‐up”….tests driven by differentials  Varicella Zoster Virus reactivation in geniculate ganglion
 Symptoms: Pain, hearing loss, dizziness, tinnitus, nausea, vertigo
 Poorer prognosis than Bell’s palsy
 35% recover
 Recurrences are rare
 CBC with differential
 Chem 7
 Lipid Profile
 ESR
 C‐Reactive Protein
 Treatment  oral antivirals + oral prednisone
 Protect the cornea!
7
Complete Blood Count  White Blood Count (WBC)
 Differential White Blood Count (Diff)
 Red Blood Count (RBC)
 Hematocrit (Hct)
 Hemoglobin (Hb)
 Platelet Count (PLT)
 Red Blood Cell Indices:
 Mean Corpuscular Volume (MCV)
 Mean Corpuscular Hemoglobin (MCH)
 Mean Corpuscular hemoglobin Concentration (MCHC)
Chem 7 / Basic Metabolic Panel Creatinine
2. Blood urea nitrogen (BUN)
3. Glucose
1.
 Screens for
 Kidney disease  Liver Disease  Diabetes and other blood sugar disorders
4. Carbon dioxide
5. Chloride
electrolytes
6. Sodium
7. Potassium 8. (Sometimes Calcium)
NON‐GRANULOMATOUS CAUSE OF UVEITIS Etiology 46 year old AA female  Recurrent and recalcitrant uveitis
 KPs
 Conjunctival granuloma
 ROS
Sex
Ankylosing spondylitis
M>F
Reactive arthritis (formerly Reiter’s)
M>F
Juvenile RA
F>M
Lyme disease
M=F
Herpetic Disease
Crohn’s
Race
W>B
History Questions Lab Tests Lower back pain?
HLA‐B27, back x‐ray, RF (‐), ESR (+)
W>B
Arthritis? Pain when urinating?
HLA‐B27, ESR (+), ANA (‐).
RF (‐), Urethral swab
W=B
Knee pain?
Knee x‐ray, RF (‐), ANA (+)
W=B
Rash? Fever? Recent tick bite?
ELISA + for antispirochetal antibody titer
M=F
W=B
Skin vesicles?
Skin biopsy/culture,
Consider HIV testing
M=F
W=B
Stomach pain?
GI workup, Endoscopy,
HLA‐B27
GRANULOMATOUS CAUSE OF UVEITIS  Resp: “cough”
Sarcoidosis
F>M
Syphillis
M=F
Tuberculosis
M=F
B>W
Cough?
Chest X‐ray, ACE (elevated),
Lung biopsy, Serum Lysozyme
W=B
Rash? Fever? Chancre?
FTA‐ABS
VDRL or RPR
W=B
Cough?
PPD Chest X‐ray
Table adapted from: Muchnick B. Clinical Medicine in Optometric Practice 2008
Vs. Point of Care Laboratory Testing….
CLIA Certificate of Waiver (CMS‐116)
Procedure
CPT Code
Reimbursement
Chlamydia Culture
87110QW
$27.00
Dipstick Urinalysis 81002QW
$4.37
Pregnancy Urinalysis
81025QW
$8.74
Glucometry
82962QW
$3.42
HbA1C
83037QW
$13‐18
AdenoPlus
87809QW
$17.52
InflammaDry
83516QW
$18.36
Tear Lab Osmolarity
83861QW
$24.30
8
What’s New in Point of Care Testing??
In‐office A1C
 A1C Now+® (pts Diagnostics)
 99% lab accuracy
 Results in 5 minutes
 www.a1cnow.com
www.nicox.com
 Tests for classic and new markers for Sjögren’s
 InflammaDry
 MMPs in tears
 Much like AdenoPlus
 Refer to Labcorp for blood draw
Genetically classifying AMD patients? .
 Simple cheek swab  No CLIA certification required  Conflicting data and opinions  Is it standard of care?
 What does it add to our clinical practice?
 42 AA female
Imaging – considerations before ordering  R/v: headache
 BVA 20/20 after corrected significant cylinder
 Father has glaucoma
 Pupils normal
 ROS: arm weakness  Color (HRR) normal OD, OS
 IOP 21, 20
 CT vs. MRI
 ±contrast
 ±angiography
 Location to scan
 ±urgency  Be prepared to give an ICD code 9
10‐2
10‐2
Summary  ON in MS
 Autopsy studies – up to 94‐99%
 Why VA, color normal?  Contrast sensitivity 2.5x more sensitive
 Other measures ‐‐ Detection of subclinical MS
 OCT – RNFL, IPL and GCL thinning 

Fast progression
Atrophy ≤2mos
 VEP – even without VA loss
 MRI with FLAIR
 Fat suppression? Sakai, et al. J Neuroophthalmology, 2011
44 AA male c/o headaches
 VAs: 20/20
 CF: ↓ temporally OD, OS
ICA
What if
acute??
Large pituitary
adenoma
10
48 WM, c/o near blur
 Heavy smoker
 ‐Med Hx
 Needs a near add
 But…
 Stroke of R posterior cerebral artery
 Imaging…..
 MRI/MRA with DWI particularly if acute
 CT/CTA
By 2050…..1 in 3 adults will be diabetic
WHY???? The terrifying truth …  86% of Type 1 diabetics
40% of Type 2 diabetics
have clinically
evident
diabetic
retinopathy
Current ADA Diagnostic Criteria for DM
 HbA1c ≥ 6.5%
 Random plasma glucose ≥ 200mg/dL + symptoms (polyuria, thirst, wt loss, blurred vision)
 1/3 to 1/2 of diabetic patients do not receive an annual eye examination
 Fasting plasma glucose ≥ 126mg/dL
 OGTT 2 hour post‐load glucose ≥ 200mg/dL
 By 2050, the number of patients with diabetic retinopathy will triple
Hazin R, Barazi MK, Summerfield M. Challenges to establishing nationwide diabetic retinopathy
screening programs. Curr Opin Ophthalmology 2011; 22: 174-179.
American Diabetes Association. Standards of Medical Care in Diabetes 2014.
11
Related Conditions
AOA Clinical Practice Guidelines
 Pre‐Diabetes
 Impaired glucose tolerance
 A1C of 5.7% ‐ 6.4%
 Fasting BS of 100‐125 mg/dl
 OGTT 2 hour blood glucose of 140 ‐ 199mg/dl
 Metabolic Syndrome – 25% of population
 Pre‐diabetic
 Abdominal obesity
 HTN
 High cholesterol
When to dilate a pregnant diabetic…??
 February, 2014
 Evidence‐based vs. “consensus‐based”
 576 papers reviewed, critiqued and referenced by 20 peer experts
 Covers the basics…
 When to refer undiagnosed patient with symptoms to PCP
 How often to perform DFE
 Recommendations for f/u of macular edema, and tx of neo
 And beyond…
 Use of OCT
 Rapid‐acting carbohydrates – need in office for hypoglycemic events Pregnancy and DR
 baseline severity of DR = most important risk factor for progression during pregnancy • DFE in 1st trimester, then f/u each trimester
 2.5 x increased risk • Retinopathy  Recommend A1C <6% in counseling
pregnant patients with pre‐existing Type 1 or 2 DM
2014 ADA Guidelines
2014 AOA Clinical Practice Guidelines, Care of the Patient with Diabetes Mellitis
Crystalline lens autofluorescence
Diabetes Control and Complications Trial Research Group. The relationship of glycemic exposure to the risk of development and progression
of retinopathy in the Diabetes Control and Complications Trial. Diabetes 1995; 44: 986-93.
Rasmussen KL, Laugesen CS et al. Progression of diabetic retinopathy during pregnancy in women with Type 2 diabetes. Diabetologia 2010;
53: 1076-83.
Inhalation powder insulin ! (…or ???)
http://www.freedom-meditech.com/
 Detects advanced glycation end products (AGEs)
 Highly correlated with uncontrolled BS
 Present up to 7 years earlier than other diabetic complications  Longterm blood sugar control – more so than A1C
 FDA Approved June 2014
 Earlier Dx?  ….not much success here  Earlier identification of risk factors for retinopathy?
 rapid‐acting inhaled insulin  administered at the beginning of each meal
Diabetesmine.com
so far  Closer follow‐up?
12
Patient Education ! Nutrition for Diabetics
 A –A1C /blood glucose is “individualized”
 B –140/80 or less
 C –LDLs 100 or <70 if CVD
 D –Diet
 E –Exercise – 150 min per week  S – Smoking increases risk of retinopathy  ….Weight Control
 The most significant factor in diabetes prevention
Mayer‐Davis et al, JAMA 1998
Diabetes Prevention Plan (DPP)
Knowler et al, NEJM 2002
 The “sugar” discussion  Caloric intake
 Processed foods
 Glycemic index
http://www.drannwellness.com
Nutritional Supplementation: The “diabetic formula”??
 Believed to
 Control glucose levels
 Protect and restore endothelial function  Some include:
 Vitamin C, D, E  Nicotinamide
 Taurine
 Glutamine http://professional.diabetes.org/patientEducationlibrary.aspx
 52 Caucasian male
 Never had an eye exam
 No regular health care
 Vision goes “out” when he turns his head up a certain way
13
Bruit : ≥50% stenosis 90% occlusion= 50% decrease in CRA perfusion pressure
Ocular manifestations will occur if carotid blockage is ≥70%
5 year mortality rate – 40% 1st observed manifestation of ICA stenosis in up to 69% patients
Ocular signs of carotid
artery disease
Vascular Supply Systems to Brain 1. Internal Carotid system
 Supplies anterior 1.
and lateral portions of brain
 Unilateral visual disturbances
Amaurosis Fugax
2. CRAO
3. Hollenhorst Plaque
4. Ocular Hypoperfusion
2. Vertebrobasilar
system
 Provides posterior brain
 Bilateral visual symptoms Management of intra‐arteriolar plaque
Carotid Endarterectomy  moderate benefit when 50‐69% stenosis
 Symptoms?
 Often transient – plaques are pliable
 Correlated with degree of occlusion?
 Predictive of future events?
11% with symptoms
had significant
occlusion
 Antiplatelets? Blood thinners? Wakefield, et al
 Eliquis (apixaban)
 Lab Tesing
 Doppler
 EKG/Angiography
22% w/o symptoms
had 30-60% occlusion
Dunlap, et al
 no proven benefit if symptomatic and <50% stenosis.
 Recommended when:  Substantial blockage
 Symptoms are present 1.
2.
3.
North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high‐grade carotid stenosis. N Eng J Med 1991: 325: 445‐453.
Mayberg MR, Wilson E, Yatsu F, et. Al. Carotid endarterectomy and prevention of cerebral ischemia in symptomatic carotid stenosis. JAMA 1991: 266: 3289‐3294.
Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA 1995: 273: 1421‐1428.
14
Caro d Artery Dissec on → Horner’s Syndrome
Pharmacologic Assessment of Horner’s Syndrome
 Dx of Horner’s
 10% cocaine – will NOT dilate
 0.5% apraclonidine – WILL dilate
 1% phenylephrine – WILL dilate  48 year old patient presents with a big pupil in the left eye.  ROS: right‐sided neck pain, headache
 Exam
 Right eye – miosis, ptosis  Dilates with 0.5% apraclonidine
 1% hydroxyamphetamine –
 Helps to localize lesion  What else can help us localize the lesion????
 Horner’s – 3rd order neuron defect 
along sympathetic pathway
This patient has a 3rd order neuron lesion – sweating unaffected
http://www.cmaj.ca
Carotid Artery Dissection  Presentation
 Unilateral neck pain – up to 49%
Carotid artery disease and risk of stroke  Headache – up to 69%
 Ipsilateral Horner’s – up to 50%  Cause of 2.5% of strokes
 4/5 strokes are causes by atherosclerotic disease at carotid bifurcation  10‐25% of ischemic events in patients <45
Rao, J Vasc Surg 2011
 Mgmnt
 Immediate Imaging: MRI/A, T1W with contrast and fat suppression  Doppler  Stroke
 leading causes of death in US
 1/3 of cases are fatal
 Survivors usually have irreversible damage
Landwehr P, et al
81 Caucasian female
 Wants new glasses before a trip to Paris  PMHx:  Atrial fibrillation
 Recent falls – due to TIA
 VA 20/30 due to cataracts
Atrial Fibrillation
 Most common cardiac arrhythmia  Increased risk of TIA, stroke and MI
 Many undiagnosed
 Linked to retinopathy in diabetics
 DFE – retinal heme and intra‐arteriolar plaque http://afib.utorontoeit.com/images/afibmain.png
15
Risk of stroke after TIA
Johnston WC, et al. Lancet. 2007; 369: 283‐292.
 TIA ? ……. act F.A.S.T!
 Medical tx within 24 hrs of TIA ↓ risk of stroke within 3 mos by 80%
 ABCD2 rule for TIA : ≥3 points = emergency  Age>60 (1 pt)
 BP ≥140/90 on first assessment (1 pt)
 Clinical features (unilateral weakness=2 pts or speech impairment w/o weakness=1 pt)
 Duration (≥60 minutes=2 pts; 10‐59 minutes=1 pt)
 Diabetes (1 pt)
What else can
cause blood
in the retina?
End Stage Renal Disease
 Medical History
 Recent cough?
 Severe kidney disease?
 Anemia?  Blood dyscrasias?  Medications
 Social/employment history
 Heavy lifting 76 Caucasian male
Hx severe anemia secondary to ESRD
30% carotid occlusion Bilateral blot hemes, all 4 quadrants
‐disc edema, ‐tortuosity
‐artery attenuation
Factor V Leiden??? What’s that?!!
 Factor V – clotting protein
 genetic mutation: ↑clotting in veins  Caucasians of European descent
 Often undiagnosed, however….
 deep vein thrombosis
 pulmonary embolisms  CRVO Fegan CD et al, Eye (2002) 57 Caucasian female with
“borderline” HTN and Factor
V Leiden
16
Revised Recommendations on Screening for
Chloroquine and Hydroxychloroquine
Retinopathy
Plaquenil ‐‐ What to look for on OCT…
Marmor MF, et al. Ophth Feb 2011.  Risk of toxicity increases sharply towards 1% after 5‐7 yrs of use, or cumulative dose of 1000 g HCQ
 Initial baseline exam, then annual screenings after 5 years
Marmor MF, et al. Ophthalmology. AAO Revised Recommendations on Screening for Chloroquine and
Hydroxychloroquine Retinopathy. Feb 2011.
 Screening:
 Regular exams with DFE
 10‐2  SD OCT, FAF or mfERG
 Outer retina
 Loss of IS/OS line (PIL); thinning of PR layer  Thickening of outer band of RPE  Inner retina
 Parafoveal thinning of GCL, IPL
http://www.hopkinslupus.org/lupustreatment/lupus-medications/antimalarialdrugs/
 1.0mm (but not 0.5mm) from foveal center
 “flying saucer” sign
 “sinkhole displacement” sign
 Disruption to the ellipsoid zone (EZ) line
Nejm.org
Rheumatolgist.com
Chen E, et al. Clinical Ophthalmology 2010.
But WAIT!!  10% of patients with a ring scotoma do NOT show damage with SD‐OCT!
Marmor MF, Melles RB. Ophthalmology. 2014 Jan 15. Disparity between Visual Fields and Optical Coherence Tomography in Hydroxychloroquine Retinopathy.
Melles,
Marmor,
Ophthal Aug
2014
17
Coding for high risk meds
• Code systemic disease which is the reason for the medication
– Long term (current) use of high risk medication– V58.69 – SLE – 695.4
 34 AA Male
 PMx:  Smoker
 Schizophrenia, risperidone 3mg bid
 138/96mmHg
 BCVA 20/30 OD, OS
 Metamorphopsia
• ICD‐10 codes…..October 1,2015!!!
– Z79.899 : “other long term (current) drug therapy”
 Color vision‐
normal  10‐2: clear  Vitreous—attached So what do we have here…??
 Inherited disorder?
 Macular cyst?
 Toxicity?
Looking a little harder…
Other causes of outer retinal holes / interruption to OS/IS junction
Comander J et al, Am J Ophth Sept 2011
 fluphenazine (Prolixin) toxicity?
 Lee, et al. Ophthalmic Res, July‐Aug 2004.  Solar maculopathy?
 Damage to outer segment of PR layer, and RPE
 Often subtle but permanent vision loss  OCT findings: 

Abrupt interruption to OS/IS junction (PIL)
Slight separation between RPE and PR
Comander J et al, Am J Ophth Sept 2011






VMT
Outer retinal hole
Juxtafoveal Macular Telangiectasia
Welder’s retinopathy
Tamoxifen maculopathy
Rarely:  Stargardt’s
 Alkyl nitrite abuse
 Achromotopsia
 Acute Retinal Pigment Epithelitis
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Talc Retinopathy Differential Diagnoses of refractile
deposits in the retina

Drug Related
1. Tamoxifen
2. Canthaxanthine
3. Nitrofurantoin
4. Ritonavir 5. Talc

1. Calcium emboli
2. Cholesterol emboli
 Primary Ocular Disorders
 Genetic Disorders
Filler material in tablets ‐‐ injected into venous system Trapped in capillaries
Can cause NFL damage
Pulmonary talcosis – lung disease, death
PREVENT DISEASE
PROMOTE WELLNESS
Embolic Diseases
1. Primary Hyperoxaluria
2. Cystinosis
3. Hyperornithinemia
4. Sjögren‐Larsson Syndrome
1. Calcified macular drusen
2. Idiopathic parafoveal telangiectasis
3. Bietti’s crystalline dystrophy
4. Longstanding retinal detachment
Helpful Resources
 American Heart Association http://americanheart.org
 American Society of Hypertension http://www.ash‐
TREAT THE WHOLE PATIENT
us.org/index.html
 National Heart, Lung, & Blood Institute PRACTICE
MEDICAL
OPTOMETRY
http://www.nhlbi.nih.gov/
 Centers for Disease Control http://www.cdc.gov/bloodpressure/
 WebMD ‐ http://www.webmd.com/hypertension‐
high‐blood‐pressure/guide/blood‐pressure‐causes
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