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Course Title:

DISCLOSURE STATEMENT

Please silence all mobile devices.

“No disclosure statement.”

Lecturer: Beth A. Steele, OD, FAAO

AOA’s definition of Optometryapproved Sept 2012

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. 

Driving Forces in Health Care Changes

Standardized Coding 

Risk Adjustment 

Physician Quality Reporting

Clinical Quality Measures

Meaningful Use of EHR 

…..Outcomes Based Care

Quality of Patient Care

PREVENTION

…..where do we fit in?

WELLNESS

TREATING THE WHOLE PATIENT

MEDICAL OPTOMETRY

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)

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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.

Not just this…

But also this…

JNC 8 – What’s New?  Threshold for treatment of BP in ages ≥60

150/90 vs. 140/90

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)

Is routine blood pressure part of your daily routine in patient care?

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

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

Confirm within 2 months

Evaluate or refer to

PCP within 1 month

Evaluate or refer immediately or within 1 week

Systolic >180

Diastolic >110

“Hypertensive Crisis” URGENT vs. EMERGENT

JNC 7“Evaluate and treat immediately or within 1 week depending on clinical situations and complications.”

Systemic symptoms

Ocular findings(>120)

Meetz RE, Harris TA. The optometrist's role in the management of hypertensive crises. Optometry. 2011 Feb;82(2):108-16.

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The breaking point of autoregulation

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 

Subjects retina to ischemic damage

Same BP – 2 different situationsBP 190/112  BP 190/112

Feeling “fine”

Forgot his medicine today

Denies H/A, etc

DFE:  crossing changes

(+) “migraine”since yesterday

DFE:  disc edemaflame heme

Hypotension

Low Blood Pressure Systolic < 90 Diastolic < 60

Poor perfusion of oxygen and nutrients to vital organs

Common symptoms = blurred vision, fatigue, dizziness, fainting, confusion

Risk of ocular manifestations

Proper methods = Accurate Results

Are YOU Meaningfully Using? 

Core Objective #4

Height 

Weight 

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 

For >80% of all unique patients age ≥2

Vitals Station

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Patient Vital Signs  Temperature – 96.4ͦ ‐ 99.1 ͦ

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….??BP 190/112 

Feeling “fine”

Forgot his medicine today

Denies H/A, etc

DFE:  crossing changes

http://cim.ucdavis.edu/EyeRelease/Interface/TopFrame.htm

3rd Nerve Palsy

EOMs – SO and LR are unopposed

Levator 

Parasympathetic pupillary fibers

Kanski. Clinical Ophthalmology, 4th Ed

http://cim.ucdavis.edu/EyeRelease/Interface/TopFrame.htm

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3rd Nerve –a nice overview 

Presentation bilateral in 11%

complete in 33%

isolated in 36%

Etiology trauma (26%)

tumor (12%)

diabetes (11%)

aneurysm (10%)

surgery (10%)

stroke (8%)

infection (5%)

Of 234 patients with diabetes 2/3 due to microvascular ischemia

53% had pupillary involvement-often bilateral

5 had aneurysms

Only 2% of aneurysms spared the pupil.

Painful onset 94% of aneurysm

69% of diabetic cases.

Keane JR, Can J Neuro Sci. 2010 Sep;37(5):662-70.

1400 personally examined patients – 37 years

Etiology – CN III Palsy Pupil involvement

Most likely compressive (80%)

Emergency 

Pupil spared

Most likely vasculopathic (77%) 

Resolution of vasculopathic ~3 mos   ‐‐ follow closely 

Imaging necessary?  

History

±Pain, Headache or other neuro signs

double vision

• Head injury 3 months ago 

– Imaging in ER all negative

• Vertical diplopia

– Worse in down gaze

– Right head tilt

double vision

Under‐action LSO 

1⁰ gaze – note head posture

Double Maddox Rod??     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

Torsion noted on DFEs!

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SO Palsy Etiology

Trauma

Decompensated congenital – slow onset

Least likely of EOM palsies to have underlying etiology, BUT….

Microvascular disease

Brain abnormality

Treatment 

Prism, surgery, botox 

Imaging, careful follow up

VI Palsy – Pearls 

Children

Frequently acquired and transient

Trauma, Tumor, hydrocephalus

Adults 

Trauma

Neoplasm

Microvascular disease 

Significant risk of morbidity – imaging

even if other risk factors present

Rutsein, Daum. Anomalies of Binocular Vision

EOM palsies: Do not assume……

1. Vasculopathic

16.5% thought to be ischemic had another cause (neoplasm, MS, GCA)Tamhankar, et al. Ophthalmology Nov 2013

2. True isolation

44 WM with bilateral ptosis  POH and PMH:  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

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

Frontal BaldingExpressionless Face

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Ocular manifestations Ptosis (80%)

Ocular motility disturbances

Orbicularis weakness

Hypotony  (as low as 4mmHg)

“Christmas Tree Cataracts”

Peripheral retinal changes—up to 50%

Macular involvement—20% Granular pigment changes with stellate pattern

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)

Rarely, anti‐myotonic drugs are used

Genetic counseling

Summary of Cranial Nerve Functions and Testing(Adapted from Muchnick, B. Clinical Medicine in Optometric Practice, 2nd ed.)

Summary of Cranial Nerve Functions and Testing(Adapted from Muchnick, B. Clinical Medicine in Optometric Practice, 2nd ed.)

Cranial Nerve Test

I – Olfactory Identify odors

II - Optic Visual acuity, visual field, color, nerve head

III - Oculomotor Physiologic “H” and near point response

IV – Trochlear Physiologic “H”

V - Trigeminal Corneal reflex; clench jaw/palpateLight 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

Summary of CN Functions and TestingAdapted from Muchnick, B. Clinical Medicine of Optometric Practice, 2nd Ed. 

CN Tes ng → involvement of VII and VIII

Ramsay Hunt Syndrome

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

Treatment 

oral antivirals + oral prednisone

Protect the cornea!

“Blood work‐up”….tests driven by differentials 

CBC with differential

Chem 7

Lipid Profile

ESR

C‐Reactive Protein

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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 

1. Creatinine

2. Blood urea nitrogen (BUN)

3. Glucose

4. Carbon dioxide

5. Chloride

6. Sodium

7. Potassium 

8. (Sometimes Calcium)

Screens for Kidney disease 

Liver Disease 

Diabetes and other blood sugar disorders

electrolytes

46 year old AA female  Recurrent and recalcitrant uveitis

KPs

Conjunctival granuloma

ROS

Resp:  “cough”

GRANULOMATOUS CAUSE OF UVEITIS 

Sarcoidosis F>M B>W Cough? Chest X‐ray, ACE (elevated),Lung biopsy, Serum Lysozyme

Syphillis M=F W=B Rash?  Fever?  Chancre? FTA‐ABSVDRL or RPR

Tuberculosis M=F W=B Cough? PPD Chest X‐ray

Table adapted from:  Muchnick B.  Clinical Medicine in Optometric Practice 2008

NON‐GRANULOMATOUS CAUSE OF UVEITIS 

Etiology  Sex Race History Questions  Lab Tests 

Ankylosing spondylitis M>F W>B Lower back pain? HLA‐B27, back x‐ray, RF (‐), ESR (+)

Reactive arthritis (formerly Reiter’s)

M>F W>B Arthritis? Pain when urinating? HLA‐B27, ESR (+), ANA (‐).RF (‐), Urethral swab

Juvenile RA F>M W=B Knee pain? Knee x‐ray, RF (‐), ANA (+)

Lyme disease M=F W=B Rash?  Fever? Recent tick bite? ELISA + for antispirochetal antibody titer

Herpetic Disease M=F W=B Skin vesicles? Skin biopsy/culture,Consider HIV testing

Crohn’s M=F W=B Stomach pain? GI workup, Endoscopy,HLA‐B27

Vs. Point of Care Laboratory Testing….

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

CLIA Certificate of Waiver (CMS‐116)

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What’s New in Point of Care Testing??

Tests for classic and new markers for Sjögren’s

Refer to Labcorp for blood draw

InflammaDry

MMPs in tears

Much like AdenoPlus

www.nicox.com

In‐office A1C

A1C Now+® (pts Diagnostics)

99% lab accuracy

Results in 5 minutes

www.a1cnow.com

..

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?

Imaging – considerations before ordering 

CT vs. MRI

±contrast

±angiography

Location to scan

±urgency 

Be prepared to give an ICD code  

42 AA female

R/v:  headache

Father has glaucoma

ROS:  arm weakness 

BVA 20/20 after corrected significant cylinder

Pupils normal

Color (HRR) normal OD, OS

IOP 21, 20

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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

Large pituitary adenoma

What if acute??

ICA

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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

WHY????  

By 2050…..1 in 3 adults will be diabetic

The terrifying truth … 

86% of Type 1 diabetics40% of Type 2 diabetics

1/3 to 1/2 of diabetic patients do not receive an annual eye examination

By 2050, the number of patients with diabetic retinopathy will triple

have clinically evident diabetic

retinopathy

Hazin R, Barazi MK, Summerfield M. Challenges to establishing nationwide diabetic retinopathy screening programs. Curr Opin Ophthalmology 2011; 22: 174-179.

Current ADA Diagnostic Criteria for DM

HbA1c ≥ 6.5%

Random plasma glucose ≥ 200mg/dL + symptoms (polyuria, thirst, wt loss, blurred vision)

Fasting plasma glucose ≥ 126mg/dL

OGTT 2 hour post‐load  glucose ≥ 200mg/dL

American Diabetes Association. Standards of Medical Care in Diabetes 2014.

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Related Conditions 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

AOA Clinical Practice Guidelines 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 

• DFE in 1st trimester, then f/u each trimester

• Retinopathy counseling

2014 ADA Guidelines2014 AOA Clinical Practice Guidelines, Care of the Patient with Diabetes Mellitis

When to dilate a pregnant diabetic…??

Pregnancy and DR baseline severity of DR = most important risk factor for progression during pregnancy 

2.5 x increased risk 

Recommend A1C <6% in pregnant patients with pre‐existing Type 1 or 2 DM

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.

Crystalline lens autofluorescence

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

Earlier Dx? 

Earlier identification of risk factors for retinopathy?

Closer follow‐up?

http://www.freedom-meditech.com/

Inhalation powder insulin ! (…or ???)

FDA Approved June 2014

rapid‐acting inhaled insulin 

administered at the beginning of each meal

….not much success here so far  

Diabetesmine.com

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Patient Education ! 

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  Diabetes Prevention Plan (DPP)

Knowler et al, NEJM 2002

Nutrition for Diabetics

….Weight Control

The most significant factor in diabetes preventionMayer‐Davis et al, JAMA 1998

The “sugar” discussion 

Caloric intake

Processed foods

Glycemic indexhttp://www.drannwellness.com

http://professional.diabetes.org/patientEducationlibrary.aspx

Nutritional Supplementation:  The “diabetic formula”??

Believed to

Control glucose levels

Protect and restore endothelial function 

Some include:

Vitamin C, D, E 

Nicotinamide

Taurine

Glutamine 

52 Caucasian male

Never had an eye exam

No regular health care

Vision goes “out” when he turns his head up a certain way

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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

Vascular Supply Systems to Brain 1. Internal Carotid 

system Supplies anterior and lateral portions of brain

Unilateral visual disturbances

2. Vertebrobasilarsystem Provides posterior brain

Bilateral visual symptoms 

Ocular signs of carotid artery disease

1. Amaurosis Fugax

2. CRAO

3. Hollenhorst Plaque

4. Ocular Hypoperfusion

Management of intra‐arteriolar plaque

Symptoms?

Often transient – plaques are pliable

Correlated  with degree of occlusion?

Predictive of future events?

Antiplatelets? Blood thinners? 

Eliquis (apixaban)

Lab Tesing

Doppler

EKG/Angiography

11% with symptoms had significant occlusion Wakefield, et al

22% w/o symptoms had 30-60% occlusion Dunlap, et al

moderate benefit when 50‐69% stenosis

no proven benefit if symptomatic and <50% stenosis.

Recommended when:  Substantial blockage Symptoms are present 

1. 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.

2. Mayberg MR, Wilson E, Yatsu F, et. Al.  Carotid endarterectomy and prevention of cerebral ischemia in symptomatic carotid stenosis.  JAMA 1991:  266:  3289‐3294.

3. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study.  Endarterectomy for asymptomatic carotid artery stenosis.  JAMA 1995:  273:  1421‐1428.

Carotid Endarterectomy 

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Caro d Artery Dissec on → Horner’s Syndrome

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

Horner’s – 3rd order neuron defect along sympathetic pathway

http://www.cmaj.ca

Pharmacologic Assessment of Horner’s Syndrome Dx of Horner’s

10% cocaine – will NOT dilate

0.5% apraclonidine – WILL dilate

1% phenylephrine – WILL dilate 

1% hydroxyamphetamine –

Helps to localize lesion 

What else can help us localize the lesion????

This patient has a 3rd order neuron lesion – sweating unaffected

Carotid Artery Dissection  Presentation

Unilateral neck pain – up to 49%

Headache – up to 69%

Ipsilateral Horner’s – up to 50% 

Cause of 2.5% of strokes

10‐25% of ischemic events in patients <45Rao, J Vasc Surg 2011

Mgmnt

Immediate Imaging:  MRI/A, T1W with contrast and fat suppression 

Doppler  

4/5 strokes are causes by atherosclerotic disease at carotid bifurcation 

Stroke

leading causes of death in US

1/3 of cases are fatal

Survivors usually have irreversible damage

Carotid artery disease and risk of stroke 

Landwehr P, et al

Wants new glasses before a trip to Paris 

PMHx: 

Atrial fibrillation

Recent falls – due to TIA

VA 20/30 due to cataracts

DFE – retinal heme and intra‐arteriolar plaque 

81 Caucasian female

Atrial Fibrillation

Most common cardiac arrhythmia 

Increased risk of TIA, stroke and MI

Many undiagnosed

Linked to retinopathy in diabetics

http://afib.utorontoeit.com/images/afibmain.png

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Risk of stroke after TIA

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)

Johnston WC, et al. Lancet. 2007; 369:  283‐292.

What else cancause blood in the retina?

Medical History

Recent cough?

Severe kidney disease?

Anemia? 

Blood dyscrasias? 

Medications

Social/employment history

Heavy lifting 

End Stage Renal Disease

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

17

Revised Recommendations on Screening for Chloroquine and HydroxychloroquineRetinopathy 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

Screening:

Regular exams with DFE

10‐2 

SD OCT, FAF or mfERG

http://www.hopkinslupus.org/lupus-treatment/lupus-medications/antimalarial-

drugs/

Plaquenil ‐‐What to look for on OCT…

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

1.0mm (but not 0.5mm) from foveal center

Marmor MF, et al. Ophthalmology. AAO Revised Recommendations on Screening for Chloroquine and Hydroxychloroquine Retinopathy. Feb 2011.

“flying saucer” sign

“sinkhole displacement” sign

Disruption to the ellipsoid zone (EZ) line

Chen E, et al. Clinical Ophthalmology 2010.

Nejm.org

Rheumatolgist.com

Melles, Marmor,

Ophthal Aug 2014

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.

18

• Code systemic disease which is the reason for the medication

– Long term (current) use of high risk medication– V58.69   

– SLE – 695.4

• ICD‐10 codes…..October 1,2015!!!

– Z79.899 : “other long term (current) drug therapy”

Coding for high risk meds

34 AA Male

PMx:  

Smoker

Schizophrenia, risperidone 3mg bid

138/96mmHg

BCVA 20/30 OD, OS

Metamorphopsia

Color vision‐normal 

10‐2:  clear 

Vitreous—attached 

So what do we have here…??

Inherited disorder?

Macular cyst?

Toxicity?

Looking a little harder… 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

Other causes of outer retinal holes / interruption to OS/IS junctionComander 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

19

Talc Retinopathy 

Filler material in tablets ‐‐ injected into venous system Trapped in capillariesCan cause NFL damagePulmonary talcosis – lung disease, death

Differential Diagnoses of refractiledeposits in the retina

Genetic Disorders1. Primary Hyperoxaluria

2. Cystinosis

3. Hyperornithinemia

4. Sjögren‐Larsson Syndrome

Primary Ocular Disorders1. Calcified macular drusen

2. Idiopathic parafoveal telangiectasis

3. Bietti’s crystalline dystrophy

4. Longstanding retinal detachment

Drug Related1. Tamoxifen

2. Canthaxanthine

3. Nitrofurantoin

4. Ritonavir 

5. Talc

Embolic Diseases1. Calcium emboli

2. Cholesterol emboli

PREVENT DISEASE

PROMOTE WELLNESS

TREAT THE WHOLE PATIENT

PRACTICE MEDICAL

OPTOMETRY

Helpful Resources American Heart Association http://americanheart.org

American Society of Hypertension http://www.ash‐us.org/index.html

National Heart, Lung, & Blood Institute 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