Systemic Disease Straight Up…..with a Twist of Neuro! AOA’s definition of Optometry
Transcription
Systemic Disease Straight Up…..with a Twist of Neuro! AOA’s definition of Optometry
Systemic Disease Straight Up…..with a Twist of Neuro! Beth A. Steele, OD, FAAO Caroline B. Pate, OD, FAAO Optometry’s Meeting 2014 AOA’s definition of Optometry approved 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. No disclosures Driving Forces in Health Care Changes Affordable Care Act Quality of Patient Care Coding Risk Adjustment Physician Quality Reporting PREVENTION 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) WELLNESS COMMUNITY HEALTH TREATING THE WHOLE PATIENT MEDICAL OPTOMETRY CLINICAL QUALITY MEASURES …..where do we fit in? 1 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 Approximately 65 million people in Recommendations for initial therapy Thiazide diuretics ACE inh, ARBs, Ca2++ channel blockers NOT: β‐blockers, α‐blockers, loop diuretics US 30% of population unaware 7.1 million deaths per year “Silent Killer” Stroke, MI, ESRD Blood Pressure Classifications and Referral Guidelines “Hypertensive Crisis” (adapted from the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure – JNC 7, 2003) Hypotensio n Systolic < 90 Diastolic < 60 normal Pre‐ Htn Stage 1 Stage 2 Stage 3 Stage 4 < 120 120‐139 140‐ 159 160‐179 180‐209 >210 < 80 80 ‐ 89 90‐99 URGENT vs. EMERGENT 100‐109 110‐119 >120 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 Evaluate or refer immediately BP 190/112 Feeling “fine” (+) “migraine”since yesterday Forgot his medicine today DFE: disc edema Denies H/A, etc DFE: crossing changes, blot heme flame heme “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. Hypotension Same BP – 2 different situations BP 190/112 JNC 7 Low Blood Pressure Systolic < 90 Diastolic < 60 Poor perfusion of oxygen and nutrients to vital organs Common symptoms = fatigue, dizziness, fainting, confusion Risk of ocular manifestations 2 Proper methods = Accurate Results Vitals Station Meaningful Use 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 Stage 1 (Core Obj #8) Record and chart changes in vital signs: Height Weight Blood pressure Calculate and display BMI Plot and display growth charts (BMI) for ages 2‐20 years Stage 2 (Core Obj #4) Age (≥3) only For more than 50% of all unique patients age ≥2, BP, height and weight are recorded as structured data Stage 1– Core Quality Care Measures (Core Objective #10) HTN ‐ BP measurement BMI screening and follow‐up (alt) Weight assessment and counseling for children and adolescents Stage 2 – Quality Measures are separated from Meaningful Use 0-20 More than 80% Now with EOM involvement….?? BP 190/112 Feeling “fine” Forgot his medicine today Denies H/A, etc DFE: crossing changes, blot heme http://cim.ucdavis.edu/EyeRelease/Interface/TopFrame.htm 2014 – must report on new CQMs CMS 22v1 ‐ Preventive Care and Screening: Screening for High Blood Pressure and Follow‐Up Documented CMS69v1 ‐ Preventive Care and Screening: Body Mass Index (BMI) Screening and Follow‐Up 3 Cranial Nerve III Palsy EOMs – SO and LR are unopposed Levator Parasympathetic pupillary fibers Will NOT constrict with WEAK pilocarpine Etiology – CN III Palsy Pain or pupil involvement Lesions that involve the pupil are most likely compressive in nature (80% Emergency imaging Patient may have headache or other neuro signs NO pain or pupil involvement 77% that spare pupil are vasculopathic Resolution usually within 3 months Follow closely Imaging? Kanski. Clinical Ophthalmology, 4th Ed double vision double vision • Head injury 3 months ago – Imaging in ER all negative • Vertical diplopia; worse when looking down – Right head tilt • Medications – Atenolol, lisinopril/HCTZ, Trazodone, WellButrin, Cymbalta • Smokes ½ day :/ Double Maddox Rod?? MR over both eyes Place small vertical prism over one eye 1⁰ gaze – note head posture Under‐action LSO Cyclodeviated eye will report a “tilted” line Rotating MR toward the torsion of the eye will straighten image of line 4 Torsion noted on DFEs! SO Palsy Very common with closed head trauma Blunt force to frontal area May be least likely of EOM palsies to have underlying etiology, but…. Microvascular disease Brain abnormality Imaging, careful follow‐up VI Palsy – Pearls Isolated EOM palsies Incomitant ET worse when gaze towards paretic eye Lab testing Microvascular disease, Giant Cell Arteritis Compensatory head turn away from paretic eye distance > near …. Think neuro cause Imaging Tumor, aneurysm Children Frequently acquired and transient Trauma, Tumor, hydrocephalus Adults 22% ‐ brain tumor 26% = idiopathic Do not assume true isolation! 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 C 5 Ramsay Hunt Syndrome Varicella Zoster Virus reactivation in geniculate ganglion Symptoms: Pain, hearing loss, dizziness, tinnitus, nausea, vertigo Treatment with oral antivirals + oral prednisone Protect the cornea! Poorer prognosis than Bell’s palsy Recurrences are rare Updated Clinical Practice Guidelines: Bell’s Palsy Recommends prescribing oral steroids within 72 hours of symptom onset for patients with Bell’s palsy 16 years and older Recommends offering oral antiviral therapy in addition to oral steroids within 72 hours of symptom onset Other recommendations: Careful history and physical exam to rule out other causes Inclusion of eye care for impaired lid closure Against routine laboratory testing and imaging for new onset Bell’s palsy Baugh R, Basura G, Ishii L, et al. Clinical practice guideline: Bell’s Palsy. Otolaryngol Head Neck Surg 2013; 149(suppl 3) S1-S27. “Blood work‐up”….tests driven by differentials CBC with differential Chem 7 Lipid Profile C‐Reactive Protein ESR Uveitis testing 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 Screens for Kidney disease Liver Disease Diabetes and other blood sugar disorders 4. Carbon dioxide 5. Chloride 6. Sodium electrolytes 7. Potassium 8. (Sometimes Calcium) 6 NON‐GRANULOMATOUS CAUSE OF UVEITIS Etiology 46 year old AA female Recurrent and recalcitrant uveitus KPs Conjunctival granuloma ROS 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 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…. Procedure CPT Code Reimbursement Erythrocyte Sed Rate 85652QW $4.96 Chlamydia Culture 87110QW $27.00 Dipstick Urinalysis 81002QW $4.37 Pregnancy Urinalysis 81025QW $8.74 Glucometry 82962QW $3.42 HbA1C 83037QW $13‐18 AdenoPlus Adenovirus 87809QW Detection $17.52 InflammaDry 83516QW $18.36 Tear Lab Osmolarity 83861QW $24.30 Sjo Test 36416 (finger stick) + CPT codes for lab tests run What’s New in Point of Care Testing?? InflammaDry MMPs in tears Much like AdenoPlus Tests for classical and new makers for Sjögren’s Kits are free Requires finger stick In‐office Blood Glucometry and A1C Blood glucose reading in ~5 seconds A1C Now+® (CHEK Diagnostics) 99% lab accuracy Results in 5 minutes www.a1cnow.com Cost: ~ $12.00/test (available in sets of 10 or 20) cleared by FDA for home use Genetically classifying AMD patients? Based on known factors in AMD pathogenesis 1. the complement system 2. cholesterol metabolism 3. extracellular matrix remodeling . Simple cheek swab No CLIA certification required Macula Risk PGx RetinaGene AMD (Nicox) 4. oxidative stress 7 CLIA Certificate of Waiver (CMS‐116) 42 AA female FHx glaucoma IOP 21, 20 10‐2 5 months later – patient reporting arm weakness 8 MRI – Imaging of Choice T1 weighted imaging ‐‐ Fat is bright, fluid is dark Quicker capture → Better resolution Add Fat suppression – will enhance ON T2 weighted – fluid is bright Detects edema FLAIR ‐‐ Fluid‐attenuation inversion recovery CSF appears dark, while inflammatory fluid/edema is bright DWI – Diffusion Weighted Imaging can be added if ischemic event is suspected If it’s a tumor…. If it’s a stroke…. MRI MRA CT Angiogram The terrifying truth about diabetes… By 2050….. 1 in 3 adults will be diabetic WHY???? 9 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 ½ 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 American Diabetes Association. Standards of Medical Care in Diabetes 2014. 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 January, 2014 Evidence‐based vs. “consensus‐based” Stimulated by the new process established by the Institute of Medicine (IOM) of the National Academy of Sciences – evidence and outcome driven 576 papers reviewed, critiqued and referenced by 18 peer experts AOA Clinical Practice Guidelines Covers the basics… When to refer undiagnosed patient with symptoms to PCP How often to perform DFE Recommendations for f/u of macular edema Treatment of neovascularization Communicate with patient’s PCP regardless of retinopathy status And beyond… Use of OCT Rapid‐acting carbohydrates – need in office for hypoglycemic events 10 After all these years…. Diabetic Retina Study (DRS) – 1971‐75 Efficacy and timing for PRP and focal laser to prevent vision loss Early Treatment Diabetic Retinopathy Study The Use of OCT Detection and monitoring response to treatment (ETDRS) – 1979‐90 Efficacy and timing for PRP and focal laser to prevent vision loss Classification of stages of retinopathy and CSME Routine macular OCT NOT indicated Central macular thickness – not the only factor in the return of visual function Management of DR Pregnancy and Diabetic Retinopathy Main risk factor for DM PRP May be considered for severe NPDR when high risk of progression Vitrectomy The sooner the better for vitreous hemes Small gauge – less complications, better outcomes ERM, VMT Macular edema Anti‐VEGF +focal laser when central and 20/30 or worse 2014 ADA Guidelines For pregnant patients with pre-existing diabetes (Type I or II): worsening during pregnancy is baseline severity of diabetic retinopathy 2.5 x increased risk Recommend A1C <6% in pregnant patients with pre‐existing Type 1 or 2 DM Gestational Diabetes 5‐10% of pregnancies Diagnosed 2nd – 3rd trimester •DFE once per trimester •Retinopathy counseling Glucose tolerance typically returns to normal 6 weeks post‐partum Due to short/temporary duration → GDM does not typically lead to development of diabetic retinopathy 11 Earlier Detection ?? autofluorescence of lens AGEs Crystalline lens autofluorescence Advanced glycation end products (AGEs) Highly correlated with uncontrolled blood glucose An increase in AGEs is linked to autofluorescence Linked to diabetic cataract formation Present up to 7 years earlier than other diabetic complications Identification of risk factors for retinopathy? Closer follow‐up? Creativity in blood glucometry… Patient Education ABCs of diabetes A –A1C /blood glucose is “individualized” B –140/80 or less C –LDLs 100 or <70 if CVD S – smoking increases risk of retinopathy Weight loss Exercise – 150 min per week Nutrition for Diabetics Dietary Advice Glycemic index Supplements Benfotiamine Pycnogenol Nutritional Supplementation?? Believed to Control glucose levels Inhibit diabetic induced retinal oxidative damage Protective effect against retinopathy Some include: Vitamin D, E Benfotiamine Pycnogenol 12 Ocular signs of carotid artery disease Ocular Hypoperfusion Hollenhorst Plaque CRAO Amaurosis Fugax 4/5 strokes are causes by athersclerotic disease at carotid bifurcation leading causes of death in US 1/3 of cases are fatal Survivors usually have irreversible damage Landwehr P, et al Atypical/differentials?? Pearls and Prognosis Other clues Attenuated arterioles Look for (+)SAP Or….. How easily can you collapse the arterial tree? 5 year mortality rate – 40% 90% blockage – CRA perfusion pressure ↓ 50% Carotid Bruit Usually ≥70% blockage before ocular manifestations 13 Management of intra‐arteriolar plaque Acute care Symptoms? Antiplatelets? Blood thinners? Eliquis (apixaban) Determining and Caro d Artery Dissec on → Horner’s Syndrome 3rd order neuron defect along sympathetic pathway Imaging treating underlying etiology Doppler EKG/Angiography http://www.cmaj.ca Caro d Artery Dissec on → 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 Atrial Fibrillation Most common cardiac arrhythmia Increased risk of stroke and MI Many undiagnosed History ECG (no P wave) Linked to retinopathy in diabetics *Starting proven medications and therapy within 24 hours of symptom onset reduces the risk of having a stroke within 3 months by 80% Dennis M, et. al. Prognosis of transient ischemic attack in the Oxfordshire Community Stroke Project. Stroke. 1990 Jun; 21(6): 848-53. Rothwell PM et al. Effect of urgent treatment of transient ischemic attack and minor stroke on early recurrent stroke (EXPRESS study): a prospective population-based sequential comparison. Lancet. 2007; 370(9596): 1432-42. 14 Risk of stroke after TIA Johnston WC, Rothwell PM, Nguyen‐Huynh MN, et al. Validation and refinement of scores to predict very early stroke risk after transient ischaemic attack. Lancet. 2007; 369: 283‐292. Consider your risk factors in patients with TIA! ABCD2 rule Age>60 (1 point) BP ≥140/90 on first assessment after TIA (1 point) Clinical features of TIA (unilateral weakness=2 points or speech impairment without weakness=1 point) Duration of TIA (≥60 minutes=2 points; 10‐59 minutes=1point) Diabetes (1 point) Blood in the retina…. What else can cause blood in the retina? End Stage Renal Disease Medical History Recent cough? Severe kidney disease? Anemia? Blood dyscrasias? Social/employment history Heavy lifting Factor V Leiden??? What’s that?!! Factor V – clotting protein genetic mutation: ↑clotting in veins Caucasians of European descent Often undiagnosed, however…. Complications Miscarriage and clots in pregnancy deep vein thrombosis pulmonary embolisms CRVO Fegan CD et al, Eye (2002) 15 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 1.0mm (but not 0.5mm) from foveal center But WAIT!! 10% of patients with a ring scotoma do NOT show damage with SD‐OCT! Coding for high risk meds • Code systemic disease which is the reason for the medication Marmor MF, Melles RB. Ophthalmology. 2014 Jan 15. pii: S0161‐ 6420(13)01174‐3. doi: 10.1016/j.ophtha.2013.12.002. Disparity between Visual Fields and Optical Coherence Tomography in Hydroxychloroquine Retinopathy. – 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” Talc Retinopathy Differential Diagnoses of refractile deposits in the retina Drug Related 1. 2. 3. 4. 5. 1. Tamoxifen 2. Canthaxanthine 3. Nitrofurantoin 4. Ritonavir 5. Talc Embolic Diseases 1. 2. Primary Ocular Disorders 1. Genetic Disorders 1. Primary Hyperoxaluria 2. Cystinosis 3. Hyperornithinemia 4. Sjögren‐Larsson Syndrome 1. Calcium emboli 2. Cholesterol emboli 2. 3. 4. Calcified macular drusen Idiopathic parafoveal telangiectasis Bietti’s crystalline dystrophy Longstanding retinal detachment 16 Optical coherence tomography (both time domain and spectral domain) confirms talc particles are localized to the inner retinal layers (containing retinal vasculature) NFL, INL, Clinical Management Patients without retinal ischemia, NFL defects, and without ongoing IV drug use should be photodocumented and monitored on an annual basis with visual fields Consider referral to PCP to monitor for small vessel disease Talc retinopathy has been associated with pulmonary talcosis, which can result in respiratory dysfunction, pulmonary HTN, and possibly death choriocapillaris From: Vinay A. Shah, et al. Talc Retinopathy. Ophthalmology. 2008: 115(4). 755 - 755.e2 http://dx.doi.org/10.1016/j.ophtha.2007.10.043 PREVENTION WELLNESS COMMUNITY HEALTH TREATING THE WHOLE PATIENT MEDICAL OPTOMETRY CLINICAL QUALITY MEASURES …..where do we fit in? Relate your advice to relevant ocular findings Weight Loss Smoking Cessation Supplementation Vitamin D Advise with caution…. AMD patients Blood thinners 17
Similar documents
Diabetic eye disease is the leading cause of blindness among... developed countries
More information
Research Report and Overview on Diabetic Retinopathy Treatment Market, 2016-2026
Diabetes is a chronic disorder associated with defects in the secretion of insulin from the pancreas or hyperglycemia linked to insulin resistance which ultimately leads to long term multi-organ complications of eye, kidneys, nerves, blood vessels and heart. The most common and severe sight threatening complication of diabetes is Diabetic Retinopathy (DR) with some form of DR present in around 25-33% diabetic persons at any time.
More information