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Ocular management of the diabetic patient

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					Ocular management of the diabetic patient
Andrew S. Gurwood, O.D., F.A.A.O., Dipl.
Marc D. Myers, O.D., F.A.A.O.


Overview :
   More than 14 million Americans are suspected of having diabetes, with less than half of
    them being diagnosed.
   Diabetes is the leading cause of blindness in the age group 20 - 64.
   When diagnosed after age 30, 78 % of patients develop some degree of retinopathy within
    15 years.
   When Diabetes is detected its sequelae are preventable. ( DCCT, WES, UKPDS )
   It has been proven that early intervention in proliferative retinopathy, vitreous hemorrhage
    and macular edema lessen the likelihood of progression to severe vision loss.
   Because of the accessibility of optometrists to patients it is essential that the primary care
    practitioner understand the systemic and ocular signs and symptoms that accompany
    diabetes mellitus as well as the appropriate treatment protocols.
Systemic pathogenesis :
   Broken glucose metabolism :
   Type I : Autoimmune etiology. Destruction of insulin producing b cells.
   Type II : ( insulin resistance and insulin secretory defect ).
     –   Broken insulin production ( impaired secretion ).
     –   Insulin resistance.
     –   Impaired glucose formation ( increased hepatic output ) and combinations.
     –   Impaired glucose metabolism : OGTT 2 H sample > 140 mg / dl but < 200 mg / dl.
     – Impaired fasting glucose : > 110 mg / dl but < 126 mg / dl.
Systemic management :
   Exercise
   HbA1c
   SMBG
   Urine ketones
   Medications : When nonpharmacologic methods unsuccessful
     – Insulin secreatagogues : Sulfonureas and Meglitinides : Glyburide and Repaglinide : increase
       insulin secreation.
     – Glucosidase inhibitors : Acarbose : increases digestion time of carbohydrates.
     – Biguanides : Metformin : decreases hepatic production of glucose.
     – Thiazolidinediones : Troglitazone : decrease insulin resistance.
     – Insulin : When patients are insulinopenic, noncompliant or not responding.
              Ultralente : Long acting.
              NPH, Lente : Intermediate.
              Lispro, Regular : Rapid.

New treatments and new studies
   EuCLID ( European Controlled Trial of Lisinopril in IDDM )
   ASPEN ( Atorvastatin Study for the Prevention of Coronary End Points in NIDDM )
   ADVANCE ( Action in Diabetes and Vascular Disease ) – Perindopril Indapramide
   PKC – beta inhibition – LY333531, Ruboxistaurin
   PKC – DMES
   PARP ( Poly ADP – polyribose polymerase ) – PJ34

Ocular pathogenesis :
   The exact cause of diabetic microvascular disease has yet to be pinpointed.
   Diabetic biochemistry :
     – Hyperglycemia causes interruption of the glycosylation pathway
     – Hyperglycemia / aldose reductase / sorbitol pathway ( lens )
     – Hyperglycemia / aldose reductase / sorbitol pathway ( retinal vascular changes )
     – Increased blood viscosity / abnormalities of red blood cells along with impaired blood flow
     – Impaired autoregulation : Increased vessel diameter leads to increased blood velocity causing blood to stay
       within larger vessels. This leads to capillary non-profusion.
     – Role of Growth Hormone on neovascularization ?
     – Breakdown of natural angiogenesis inhibitors T.G.F. beta ( produced by capillary pericytes ) and R.P.E.
       protease inhibitor ( factor in scar formation and PRP ) are complicated by capillary endothelium separation
       and hypertension.

Common ocular manifestations of diabetes :
   Refraction : Large sudden changes
   Conjunctiva : Dilated microaneurysms
   Cornea : Folds in Descemet's membrane
   Iris : Vacuolization and neovascularization, ectropion uvea
   Pupil : Poor reactivity to light ( L.N.D. )
   Lens : Snowflake cataracts
   Vitreous : Degenerative and hemorrhagic changes, asteroid hyalosis
   I.O.P. : Diabetes is a known risk factor of glaucoma
   Optic nerve : Diabetic optic neuropathy ( Diabetic papillopathy & I.O.N. )
   Choriocapillaris and Bruch’s membrane thickening
   Neurological manifestations : III, IV, VI nerve palsy
Neovascular glaucoma :
   NVG results from neovascularization of the iris ( rubeosis irides ) caused by diffuse ocular
    i sch e m i a .
     – Internal carotid > Ophthalmic > Post. cil. & Ant. cil. ( from muscular arteries ).
     – Contraction of the fibrovascular tissue causes ectropion uvea.
   Three components to the disease ; Pain, IOP, Inflammation.
     – Diagnosis by graphic picture, clinical findings and goniscopy
   Management has three components :
     – Decrease pain using Atropine 1 %, BID
     – Decrease IOP acutely using topical B - blockers, apraclonidine, oral cai’s ( contraindications ? ), HO’s, I.V.
       Long term, patient’s often require filtering procedures and / or setons with antimetabolite injections.
     – Decrease inflammation using Prednisolone acetate 1 %, Q2h.
   Differential diagnosis must include other entities capable of producing ocular
    neovascularization :
     – Hypertension, CRVO, CRAO, hematologic diseases, retinal vascular diseases ( ie. Bechet’s, Lupus, Sickle cell ),
       retinal vascular tumors ( Coate’s), perivascular telangectasias and other vessel anomalies, radiation
       retinopathy and retinal inflammatory diseases ( Sarcoid ).

Clinically speaking . . . .
   The common entities encountered by primary care optometrists are changes in refraction,
    cataractous lens changes and various stages of diabetic retinopathy.
   Refractive changes usually reveal large shifts in minus power ( Myopic shift ) secondary to
    lens swelling.
     – Management requires stabilization of the systemic condition , patient education and delaying the final
       spectacle prescription..
     – Sometimes one is forced to provide the patient with a temporary prescription “ to get by . “

True diabetic cataracts are actually quite rare :
   They are typically bilateral
   They appear as white punctate or snowflake opacities in the anterior or posterior
    subcapsular region
   Their hallmark is a rapid onset ( Butler, O.D. J.A.O.A. 1994; 65 ( 8 ) : 559 - 63. ) “ Can
    progress from clear to complete opacification within a few days. “
   Sometimes called transient cataracts because they are completely reversible.
   Formed from the polyol pathway that metabolizes glucose to sorbitol and then sorbitol to
    fructose.
Diabetic retinopathy :
   Essentially there are two stages : Nonproliferative and Proliferative diabetic retinopathy.
   The nonproliferative stage ranges from nothing, to the dot and blot hemorrhages of
    background diabetic retinopathy to the nerve fiber layer infarcts of preproliferative disease.
     – Nonproliferative retinopathy is at the level of the retinal vasculature
   The proliferative form ( Proliferative diabetic retinopathy ) is much more severe and
    involves the growth of new blood vessels out of the retina .
Pathogenesis of diabetic retinopathy :
   Breakdown of the blood retinal barrier
   Accumulation of blood, serum and protein in the retina
   Focal and diffuse retinal ischemia ( capillary closure )
   Neovascularization with associated vitreous fibrosis and traction
Background diabetic retinopathy ; Nonproliferative
mild - severe :
   Microaneurysms : Dilated outpouchings of the deep retinal capillary bed.
   Dot and blot hemorrhages : Capillary hemorrhages deep within the outerplexiform layers of
    the retina.
   Hard lipid exudates : Build up of outerplexiform proteinaceous debris and leakage.
   Macular edema : Accumulation of fluid in the outer plexiform layer of the foveola.
   Management of diabetic patients without retinopathy = Annual D.F.E., photodocument
   Management of diabetic patients with background diabetic retinopathy = D.F.E. every 3 - 6
    months, photodocument, educate patient to continue to comply with internist's regimen.
    ( Show caution with patients who exhibit preproliferative signs. )
A little history. . .
   Ophthalmic laser use started in the early 1970’s.
   To steady the course of laser treatment studies were completed charting the natural course
    of ocular diabetes.
   Some of the conclusions that were drawn :
     – When the disease enters the proliferative stage the results are almost always bad. ( fix it before it breaks ).
     – Panretinal photocoagulation causes many side effects ( Is treatment worth the risk ).
     – The causes of nonproliferative vision loss required more extensive study ( How to fix it after it’s broken ).

A little more history. . .
   The Diabetic Retinopathy Study ( D.R.S. ) 1972 - 1976
     – Does photocoagulation reduce the occurrence of severe vision loss ( S.V.L. ) ?
     – Answered the question ; What are the high risk characteristics ( H.R.C. ) which call for PRP ?
   Early Treatment of Diabetic Retinopathy Study ( E.T.D.R.S. ) 1979 - 1989
     – Is photocoagulation effective for treating diabetic macular edema ?
     – When is the best time to begin photocoagulation ?
     – Does aspirin alter the progression of diabetic retinopathy ?

The rest of the story . . .
   Diabetic Retinopathy Vitrectomy Study ( D.R.V.S. ) 1980 - 1989
     – Is vitrectomy beneficial in eyes with chronic recurrent vitreous hemorrhage ?
     – Is vitrectomy beneficial in eyes with severe proliferative diabetic retinopathy where neovascularization fails to
       regress ?
     – When is early vitrectomy beneficial ?
   The Diabetes Complications and Control Study ( D.C.C.T. ) 1980 - 1989
     – Does tight control of the systemic condition reduce retinopathy ?
   Krypton Argon Regression of Neovascularization Study ( K.A.R.N. ) 1990 - 1993
      – Is krypton ( red ) laser equally effective as argon ( green ) laser in treating high risk
        characteristics ?
   The Diabetes in Early Pregnancy Study ( DIEP ) 1995 - 1996.
      – What are the factors that influence the progression of diabetes in pregnant women.

Results of the D.R.S. ; The High Risk Characteristics :
   First large scale controlled laser study in the ophthalmic field ( 1970’s )
   Patients included in the study were patients who had Proliferative diabetic retinopathy
    ( P.D.R. ) in at least one eye or severe nonproliferative diabetic retinopathy in both eyes
    ( one eye treated, the other not ).
   The Question : Does panretinal photocoagulation reduce the occurrence of severe visual
    loss ( SVL - defined as 5 / 200 or worse at two consecutive follow up visits, 4 months apart )
    ?
Results of the D.R.S. ; The High Risk Characteristics :
   Follow up after four years, the treatment group was compared to the non - treatment group
    for S.V.L.
    A. Patients with mild P.D.R.
      – Control group 21 % had S.V.L.
      – Treated group 7 % had S.V.L.
    B. Patients with high risk P.D.R.
      – Control group 28 % had S.V.L.
      – Treated group 12 % had S.V.L.
   Conclusion : There is at least a 50 % reduction in the rate of S.V.L. in eyes with high risk
    characteristics that are treated with PRP Panretinal photocoagulation significantly reduces
    the risk of S.V.L.
The High Risk Characteristics :
    The D.R.S. classification for High Risk Characteristics :
      –   Neovascularization of the disc ( N.V.D. ) Greater than or equal to 1/4 of a disc diameter in size.
      –   N.V.D. or neovascularization elsewhere ( N.V.E. ) with any preretinal hemorrhage.
      –   Defer PRP until patients reach or approach the High Risk Characteristics.
      –   PRP. will cause C.S.M.E. to worsen, so it should be treated before moving on to treat the high risk
          characteristics ( as per E.T.D.R.S. ).
   Management : Referral to retinologist for PRP.
   One final note : The E.T.D.R.S. concluded that aspirin did not alter course of diabetic
    retinopathy.
Results of the E.T.D.R.S. ; Clinically Significant
Macular Edema :
   The Question :
      – Is photocoagulation effective for treating diabetic macular edema ?
   Follow up after three years, the treatment group was compared to the non - treatment group
    for Moderate visual loss ( M.V.L . was defined as a doubling of the visual angle ie. . . 20 / 20
    to 20 / 40 ).
    A. Center of the macula not involved
      – Control group had 22 % M.V.L.
      – Treated group had 12 % M.V.L.
    B. Center of the macula involved
      – Control group had 33 % M.V.L.
      – Treated group had 14 % M.V.L.
   Conclusion : Focal photocoagulation reduces the risk of M.V.L. and facilitates clearing of of
    retinal thickening in cases of clinically significant macular edema ( C.S.M.E. ).
Clinically Significant Macular Edema :
    Thickening of the retinal tissue ( specific ).
    The # 1 cause of visual loss in diabetic patients.
    E.T.D.R.S. Classification for C.S.M.E. :
      – Thickening of retina at or within 500 mm of the center of the foveola.
      – Hard exudates at or within 500 mm of the center of the foveala only in the presence of adjacent retinal
        thickening.
      – Thickening of the retina 1 disc area in size or larger only if it is within a disc area of the center of the foveola.
   This may only be determined by careful binocular evaluation using slit- lamp indirect
    ophalmoscopy.
   It is not visual acuity or I.V.F.A. dependant !
   Management of diabetic patients with C.S.M.E. = Referral to a retinologist for I.V.F.A. /
    focal laser, photodocument.
Methods of Examination :
   Biomicroscopic examination
   Direct ophthalmoscopy
   Hruby lens
   90 Diopter lens
   78 Diopter lens
   Goldmann 3 - mirror contact lens
   Amsler and facial amsler grid testing
   Laser interphorometry
   IVFA
Retinal Anatomy
   Choroid
   Choreocapillaris
   Bruch’s M.
   RP E
   Photoreceptors
   ELM
   Photoreceptor N.
   OPL
   H/B/A nuclei
   IPL
   Ganglion cells
   NFL
   ILM
Take Home :
   Be aware of the signs of DM
   Recall - No signs, only history = Q yr.
   Recall - BDR w/o CSME or HRC = Q 6 mo.
   Recall - Preproliferative signs = Q 2-4 mo.
   CSME = Referral for IVFA & Focal laser
   HRC = Referral for PRP

				
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posted:7/27/2011
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