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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 18 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 19