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vascular endothelial growth factor\n(anti-VEGF) are a reasonable alterna-tive to traditional panretinal laser pho-\ntocoagulation for some individuals\nwith PDR and also reduce the risk ofvision loss in these individuals. A\n12.12 Intravitreous injections of anti-\nVEGF are indicated as first-line treat- | [
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VEGF are indicated as first-line treat-\nment for most eyes with diabetic mac-ular edema that involves the fovealcenter and impairs vision acuity. A\n12.13 Macular focal/grid photocoagu-\nlation and intravitreal injections of cor-\nticosteroid are reasonable treatments\nin eyes with persistent diabetic macu-lar edema de... | [
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therapy or eyes that are not candi-\ndates for this first-line approach. A\n12.14 T h ep r e s e n c eo fr e t i n o p a t h yi s\nnot a contraindication to aspirin ther-apy for cardioprotection, as aspirin\ndoes not increase the risk of retinal\nhemorrhage. A\nTwo of the main motivations for screen-\ning for diabetic r... | [
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ing for diabetic retinopathy are to pre-\nvent loss of vision and to intervene withtreatment when vision loss can be pre-vented or reversed.\nPhotocoagulation Surgery\nTwo large trials, the Diabetic Retinopa-\nthy Study (DRS) in individuals with PDR | [
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thy Study (DRS) in individuals with PDR\nand the Early Treatment Diabetic Reti-nopathy Study (ETDRS) in individualswith macular edema, provide the stron-gest support for the therapeutic bene-\nfits of photocoagulation surgery. The\nDRS (27) showed that panretinal photo-\ncoagulation surgery reduced the risk ofsevere vis... | [
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in untreated eyes to 6.4% in treatedeyes with the greatest bene fit ratio in\nthose with more advanced baseline dis-ease (disc neovascularization or vitreoushemorrhage). Later, the ETDRS veri fied\nthe bene fits of panretinal photocoagula-\ntion for high-risk PDR and in older-onset\nindividuals with severe nonproliferativ... | [
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individuals with severe nonproliferative\ndiabetic retinopathy or less-than-high-riskPDR (28). Panretinal laser photocoagula-\ntion is still commonly used to manage\ncomplications of diabetic retinopathy that\ninvolve retinal neovascularization and its\ncomplications. A more gentle, macular fo-cal/grid laser photocoagu... | [
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was shown in the ETDRS to be effective\nin treating eyes with clinically signi ficant\nmacular edema from diabetes (28), butthis is now largely considered to be sec-ond-line treatment for diabetic macular\nedema.\nAnti–Vascular Endothelial Growth Factor\nTreatment\nData from the DRCR Retina Network | [
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Treatment\nData from the DRCR Retina Network\n(formerly the Diabetic Retinopathy Clini-cal Research Network) and others dem-\nonstrate that intravitreal injections of\nanti-VEGF agents are effective at re-\ngressing proliferative disease and lead\nto noninferior or superior visual acuityoutcomes compared with panretina... | [
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ser over 2 years of follow-up (29,30). In\naddition, it was observed that individu-\nals treated with ranibizumab tended to\nhave less peripheral visual field loss, fewer\nvitrectomy surgeries for secondary compli-\ncations from their proliferative disease,\nand a lower risk of developing diabeticmacular edema (29). How... | [
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tial drawback in using anti-VEGF therapy\nto manage proliferative disease is that in-\ndividuals were required to have a greater\nnumber of visits and received a greaternumber of treatments than is typically\nrequired for management with panretinal\nlaser, which may not be optimal for\nsome individuals. The FDA has app... | [
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some individuals. The FDA has approved\naflibercept and ranibizumab for the treat-\nment of eyes with diabetic retinopathy.\nOther emerging therapies for retinopathy\nthat may use sustained intravitreal deliv-\nery of pharmacologic agents are currently\nunder investigation. Anti-VEGF treatmentof eyes with nonproliferati... | [
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inopathy has been demonstrated to re-\nduce subsequent development of retinalneovascularization and diabetic macular\nedema but has not been shown to improvediabetesjournals.org/care Retinopathy, Neuropathy, and Foot Care S233\n©AmericanDiabetesAssociation | [
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visual outcomes over 2 years of therapy\nand therefore is not routinely recom-mended for this indication (31).\nWhile the ETDRS (28) established the\nbenefit of focal laser photocoagulation\nsurgery in eyes with clinically signi ficant\nmacular edema (de fined as retinal edema | [
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located at or threatening the macular cen-ter), current data from well-designed clini-cal trials demonstrate that intravitrealanti-VEGF agents provide a more effectivetreatment plan for center-involved dia-betic macular edema than monotherapywith laser (32,33). Most individuals re-quire near-monthly administration of i... | [
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re-quire near-monthly administration of in-travitreal therapy with anti-VEGF agentsduring the first 12 months of treatment, | [
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with fewer injections needed in subse-quent years to maintain remission fromcentral-involved diabetic macular edema.There are currently five anti-VEGF agents\nused to treat eyes with central-involveddiabetic macular edema —bevacizumab,\nranibizumab, a flibercept, brolucizumab and\nfaricimab (1) —and a comparative effecti... | [
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faricimab (1) —and a comparative effective-\nness study demonstrated that a flibercept | [
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provides vision outcomes superior to thoseof bevacizumab when eyes have moderatevisual impairment (vision of 20/50 orworse) from diabetic macular edema(34). For eyes that have good vision (20/25or better) despite diabetic macular edema,close monitoring with initiation of anti-VEGF therapy if vision worsens providessimi... | [
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therapy if vision worsens providessimilar 2-year vision outcomes comparedwith immediate initiation of anti-VEGF | [
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therapy (35).\nEyes that have persistent diabetic\nmacular edema despite anti-VEGF treat-\nment may bene fit from macular laser\nphotocoagulation or intravitreal therapywith corticosteroids. Both of these ther-apies are also reasonable first-line ap- | [
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proaches for individuals who are notcandidates for anti-VEGF treatmentd u et os y s t e m i cc o n s i d e r a t i o n ss u c ha spregnancy.\nAdjunctive Therapy\nLowering blood pressure has been shownto decrease retinopathy progression,\nalthough strict goals (systolic blood pres-\nsure<120 mmHg) do not impart addi- | [
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sure<120 mmHg) do not impart addi-\ntional bene fit (8). In individuals with\ndyslipidemia, retinopathy progressionmay be slowed by the addition of feno-fibrate, particularly with very mild non-\nproliferative diabetic retinopathy atbaseline (36,37).Visual Rehabilitation\nRecommendations\n12.15 People who experience visi... | [
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Recommendations\n12.15 People who experience vision\nloss from diabetes should be coun-seled on the availability and scope of\nvision rehabilitation care and provided,\nor referred for, a comprehensive evalu-ation of their visual impairment by a\npractitioner experienced in vision reha-\nbilitation. E\n12.16 People wit... | [
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bilitation. E\n12.16 People with vision loss from dia-\nbetes should receive educational mate-rials and resources for eye care support\nin addition to self-management educa-\ntion (e.g., glycemic management andhypoglycemia awareness). E\nIn the U.S., /C2412% of adults with diabe-\ntes have some level of vision impair-\... | [
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ment (38). They may have dif ficulty\ncontrolling their diabetes and perform-ing many other activities of daily living,which can lead to depression, anxiety,social isolation, and dif ficulties at home,\nworkplace, school, or workplace (39).\nPeople with diabetes are at increased | [
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People with diabetes are at increased\nrisk of chronic vision loss, subsequentfunctional decline, and resulting dis-ability. Vision impairment has physical, | [
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psychological, behavioral, and social con-sequences that affect people with diabe-tes, their families, friends, and caregivers.Health care professionals and stakehold-ers may not be aware of the overall im-pact of vision loss on an individual’ s | [
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health and well-being. People with diabe-t e s - r e l a t e dv i s i o nl o s ss h o u l db ee v a l u a t e dto determine their potential to bene fit\nfrom comprehensive vision restoration.\nVision rehabilitation can help people with\nvision loss achieve maximum function, in-dependence, and quality of life.\nNEUROPATH... | [
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NEUROPATHY\nScreening\nRecommendations\n12.17 All people with diabetes should\nbe assessed for diabetic peripheral\nneuropathy starting at diagnosis oftype 2 diabetes and 5 years after thediagnosis of type 1 diabetes and atleast annually thereafter. B\n12.18 Assessment for distal symmet- | [
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12.18 Assessment for distal symmet-\nric polyneuropathy should include acareful history and assessment ofeither temperature or pinprick sensa-\ntion (small- fiber function) and vibra-\ntion sensation using a 128-Hz tuningfork (for large- fiber function). All people\nwith diabetes should have annual 10-g\nmono filament tes... | [
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mono filament testing to identify feet at\nrisk for ulceration and amputation. B\n12.19 Symptoms and signs of auto-\nnomic neuropathy should be assessedin people with diabetes starting at di-agnosis of type 2 diabetes and 5 yearsafter the diagnosis of type 1 diabetes,and at least annually thereafter, andwith evidence of... | [
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complications, particularly kidney dis-\nease and diabetic peripheral neuropa-thy. Screening can include asking aboutorthostatic dizziness, syncope, or dryc r a c k e ds k i ni nt h ee x t r e m i t i e s .S i g n so fautonomic neuropathy include ortho-\nstatic hypotension, a resting tachycar- | [
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static hypotension, a resting tachycar-\ndia, or evidence of peripheral drynessor cracking of skin. E\nDiabetic neuropathies are a heteroge-\nneous group of disorders with diverseclinical manifestations. The early recog-\nnition and appropriate management of\nneuropathy in people with diabetes is\nimportant. Points to ... | [
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important. Points to be aware of in-\nclude the following:\n1. Diabetic neuropathy is a diagnosis\nof exclusion. Nondiabetic neuropa-\nthies may be present in people with\ndiabetes and may be treatable.\n2. Up to 50% of diabetic peripheral\nneuropathy may be asymptomatic.\nIf not recognized and if preventive\nfoot care... | [
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foot care is not implemented, peo-\nple with diabetes are at risk for in-\njuries as well as diabetic foot ulcers(DFUs) and amputations.\n3. Recognition and treatment of auto-\nnomic neuropathy may improve symp-toms, reduce sequelae, and improvequality of life.\nSpeci fic treatment to reverse the un-\nderlying nerve dam... | [
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derlying nerve damage is currently not\navailable. Glycemic management can\neffectively prevent diabetic peripheralneuropathy (DPN) and cardiovascular\nautonomic neuropathy (CAN) in type 1\ndiabetes (40,41) and may modestly slowtheir progression in type 2 diabetes\n(42), but it does not reverse neuronal\nloss. Treatmen... | [
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loss. Treatments of other modi fiable risk\nfactors (including lipids and blood pres-sure) can aid in prevention of DPN pro-gression in type 2 diabetes and may\nreduce disease progression in type 1 di-\nabetes (43 –45). Therapeutic strategiesS234 Retinopathy, Neuropathy, and Foot Care Diabetes Care Volume 47, Supplement... | [
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©AmericanDiabetesAssociation | [
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(pharmacologic and nonpharmacologic)\nfor the relief of painful DPN and symp-toms of autonomic neuropathy can po-tentially reduce pain (46) and improvequality of life.\nDiagnosis\nDiabetic Peripheral Neuropathy\nIndividuals with a type 1 diabetes dura-tion$5 years and all individuals with | [
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type 2 diabetes should be assessed an-nually for DPN using the medical historyand simple clinical tests (46). Symptomsvary according to the class of sensory fi-\nbers involved. The most common earlysymptoms are induced by the involve-ment of small fibers and include pain and | [
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dysesthesia (unpleasant sensations ofburning and tingling). The involvement oflarge fibers may cause numbness and loss | [
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of protective sensation (LOPS). LOPS indi-cates the presence of distal sensory poly-neuropathy and is a risk factor for diabeticfoot ulceration. The following clinical testsmay be used to assess small- and large-fiber function and protective sensation:\n1. Small- fiber function: pinprick and\ntemperature sensation. | [
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1. Small- fiber function: pinprick and\ntemperature sensation.\n2. Large- fiber function: lower-extremity\nreflexes, vibration perception, and 10-g\nmono filament.\n3. Protective sensation: 10-g mono filament.\nThese tests not only screen for the | [
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These tests not only screen for the\npresence of dysfunction but also predictfuture risk of complications. Electrophys-iological testing or referral to a neurolo-gist is rarely needed, except in situationswhere the clinical features are atypical\nor the diagnosis is unclear.\nIn all people with diabetes and DPN, | [
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or the diagnosis is unclear.\nIn all people with diabetes and DPN,\ncauses of neuropathy other than diabetes\nshould be considered, including toxins (e.g.,alcohol), neurotoxic medications (e.g., che-motherapy), vitamin B12 de ficiency, hypo- | [
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thyroidism, renal disease, malignancies(e.g., multiple myeloma, bronchogeniccarcinoma), infections (e.g., HIV), chronicinflammatory demyelinating neuropathy,\ninherited neuropathies, and vasculitis (47).See the American Diabetes Association po-sition statement “Diabetic Neuropathy ”\nfor more details (46).\nDiabetic Aut... | [
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for more details (46).\nDiabetic Autonomic Neuropathy\nIndividuals who have had type 1 diabe-tes for$5 years and all individuals with\ntype 2 diabetes should be assessedannually for autonomic neuropathy (46). | [
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The symptoms and signs of autonomicneuropathy should be elicited carefullyduring the history and physical examina-tion. Major clinical manifestations ofdiabetic autonomic neuropathy includeresting tachycardia, orthostatic hypoten-\nsion, gastroparesis, constipation, diarrhea, | [
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sion, gastroparesis, constipation, diarrhea,\nfecal incontinence, erectile dysfunction,neurogenic bladder, and sudomotordysfunction with either increased ordecreased sweating. Screening for symp-toms of autonomic neuropathy includes\nasking about symptoms of orthostatic in- | [
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asking about symptoms of orthostatic in-\ntolerance (dizziness, lightheadedness, orweakness with standing), syncope, exer-cise intolerance, constipation, diarrhea,urinary retention, urinary incontinence,or changes in sweat function. Furthertesting can be considered if symptoms\nare present and will depend on the end | [
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are present and will depend on the end\norgan involved but might include cardio-vascular autonomic testing, sweat testing,urodynamic studies, gastric emptying, orendoscopy/colonoscopy. Impaired coun-terregulatory responses to hypoglyce-\nmia in type 1 and type 2 diabetes can | [
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mia in type 1 and type 2 diabetes can\nlead to hypoglycemia unawareness butare not directly linked to autonomicneuropathy.\nCardiovascular Autonomic Neuropathy. Car- | [
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Cardiovascular Autonomic Neuropathy. Car-\ndiovascular autonomic neuropathy (CAN)is associated with mortality indepen-dently of other cardiovascular risk factors(48,49). In its early stages, CAN may becompletely asymptomatic and detectedonly by decreased heart rate variabilitywith deep breathing. Advanced disease | [
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may be associated with resting tachycar-\ndia (>100 bpm) and orthostatic hypoten-\nsion (a fall in systolic or diastolic bloodpressure by >20 mmHg or >10 mmHg,\nrespectively, upon standing without anappropriate increase in heart rate). CAN\ntreatment is generally focused on allevi-\nating symptoms.\nGastrointestinal Ne... | [
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ating symptoms.\nGastrointestinal Neuropathies. Gastrointes-\ntinal neuropathies may involve any por-tion of the gastrointestinal tract, with\nmanifestations including esophageal dys- | [
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manifestations including esophageal dys-\nmotility, gastroparesis, constipation, diar-rhea, and fecal incontinence. Gastroparesisshould be suspected in individuals witherratic glycemic management or with up-per gastrointestinal symptoms without\nanother identi fied cause. Exclusion of\nreversible/iatrogenic causes such ... | [
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reversible/iatrogenic causes such as\nmedications or organic causes of gastricoutlet obstruction or peptic ulcer disease\n(with esophagogastroduodenoscopy or abarium study of the stomach) is needed\nbefore considering a diagnosis of or spe-\ncialized testing for gastroparesis. The di-agnostic gold standard for gastropa... | [
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is the measurement of gastric emptying\nwith scintigraphy of digestible solids at\n15-min intervals for 4 h after food intake.\nThe use of\n13C octanoic acid breath test is\nan approved alternative.\nGenitourinary Disturbances. Diabetic au-\ntonomic neuropathy may also cause gen-itourinary disturbances, including sexua... | [
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dysfunction and bladder dysfunction.\nIn men, diabetic autonomic neuropathy\nmay cause erectile dysfunction and/or\nretrograde ejaculation (46). Female sex-ual dysfunction occurs more frequently\nin those with diabetes and presents as\ndecreased sexual desire, increased painduring intercourse, decreased sexual\narousal... | [
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arousal, and inadequate lubrication (50).\nLower urinary tract symptoms manifest as\nurinary incontinence and bladder dysfunc-\ntion (nocturia, frequent urination, urina-tion urgency, and weak urinary stream).\nEvaluation of bladder function should be\nperformed for individuals with diabeteswho have recurrent urinary t... | [
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tions, pyelonephritis, incontinence, or a\npalpable bladder.\nTreatment\nRecommendations\n12.20 Optimize glucose management\nto prevent or delay the development\nof neuropathy in people with type 1diabetes Aand to slow the progression\nof neuropathy in people with type 2diabetes. COptimize blood pressure | [
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of neuropathy in people with type 2diabetes. COptimize blood pressure\nand serum lipid control to reduce therisk or slow the progression of diabeticneuropathy. B\n12.21 Assess and treat pain related\nto diabetic peripheral neuropathy B\nand symptoms of autonomic neurop-athy to improve quality of life. E\n12.22 Gabapent... | [
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12.22 Gabapentinoids, serotonin-\nnorepinephrine reuptake inhibitors,tricyclic antidepressants, and sodiumchannel blockers are recommended asinitial pharmacologic treatments forneuropathic pain in diabetes. ARefer | [
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to neurologist or pain specialist whenadequate pain management is notachieved within the scope of practiceof the treating clinician. Ediabetesjournals.org/care Retinopathy, Neuropathy, and Foot Care S235\n©AmericanDiabetesAssociation | [
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Glycemic Management\nNear-normal glycemic management,\nimplemented early in the course of dia-betes, has been shown to effectively de-\nlay or prevent the development of DPN\nand CAN in people with type 1 diabetes\n(51–54). Although the evidence for the\nbenefit of near-normal glycemic manage- | [
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benefit of near-normal glycemic manage-\nment is not as strong that for type 2 dia-betes, some studies have demonstrated a\nmodest slowing of progression without re-versal of neuronal loss (42,55). Speci fic\nglucose-lowering strategies may have dif-ferent effects. In a post hoc analysis, par-\nticipants, particularly me... | [
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ticipants, particularly men, in the Bypass\nAngioplasty Revascularization Investiga-tion in Type 2 Diabetes (BARI 2D) trial\ntreated with insulin sensitizers had a\nlower incidence of distal symmetric poly-\nneuropathy over 4 years than those\ntreated with insulin/sulfonylurea (56).Additionally, recent evidence from th... | [
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Action to Control Cardiovascular Risk in\nDiabetes (ACCORD) trial showed clearbene fit of intensive glucose and blood\npressure management on the preven-tion of CAN in type 2 diabetes (57).\nLipid Management\nDyslipidemia is a key factor in the devel-opment of neuropathy in people with\ntype 2 diabetes and may contribut... | [
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type 2 diabetes and may contribute to\nneuropathy risk in people with type 1 di-\nabetes (58,59). Although the evidence for\na relationship between lipids and neurop-athy development has become increas-\ningly clear in type 2 diabetes, the optimal\ntherapeutic intervention has not beenidenti fied. Positive effects of ph... | [
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tivity, weight loss, and bariatric surgeryhave been reported in individuals with\nDPN, but use of conventional lipid-lowering\npharmacotherapy (such as statins or feno fi-\nbrates) does not appear to be effective in\ntreating or preventing DPN development\n(60).\nBlood Pressure Management | [
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... |
(60).\nBlood Pressure Management\nThere are multiple reasons for bloodpressure management in people with di-\nabetes, but neuropathy progression (es-\npecially in type 2 diabetes) has nowbeen added to this list. Although data\nfrom many studies have supported the\nrole of hypertension in risk of neuropathy\ndevelopment... | [
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development, a recent meta-analysis of\ndata from 14 countries in the Interna-tional Prevalence and Treatment of Diabe-\ntes and Depression (INTERPRET-DD) study\nrevealed hypertension as an independentrisk of DPN development with an odds\nratio of 1.58 (61). In the ACCORD trial, in-tensive blood pressure intervention d... | [
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Neuropathic Pain | [
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Neuropathic pain can be severe and canimpact quality of life, limit mobility, andcontribute to depression and social dys-function (62). No compelling evidenceexists in support of glycemic or lifestylemanagement as therapies for neuro-pathic pain in diabetes or prediabetes,which leaves only pharmaceutical inter-ventions... | [
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leaves only pharmaceutical inter-ventions (63). A recent guideline by theAmerican Academy of Neurology rec-ommends that the initial treatment ofpain should also focus on the concur-rent treatment of both sleep and mooddisorders because of increased frequencyof these problems in individuals withDPN (64). | [
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A number of pharmacologic therapies\nexist for treatment of pain in diabetes.The American Academy of Neurology\nupdate suggested that gabapentinoids, | [
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serotonin-norepinephrine reuptake in-hibitors (SNRIs), sodium channel block-ers, and tricyclic antidepressants (TCAs)could all be considered in the treatmentof pain in DPN (64). These AmericanAcademy of Neurology recommendationsoffer a supplement to a recent AmericanDiabetes Association pain monograph(65). A recent hea... | [
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pain monograph(65). A recent head-to-head trial sug-gested therapeutic equivalency for TCAs,SNRIs, and gabapentinoids in the treat-ment of pain in DPN (66). The trial alsosupported the role of combination ther-apy over monotherapy for the treatmentof pain in DPN. | [
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Gabapentinoids. Gabapentinoids include\nseveral calcium channel a2-dsubunit | [
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ligands. Eight high-quality studies andseven medium-quality studies supportthe role of pregabalin in treatment ofpain in DPN. One high-quality study andmany small studies support the role ofgabapentin in the treatment of pain inDPN. Two medium-quality studies sug-gest that mirogabalin has a small effecton pain in DPN (... | [
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has a small effecton pain in DPN (64). Adverse effectsmay be more severe in older individu-als (67) and may be attenuated bylower starting doses and more gradualtitration. | [
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SNRIs. SNRIs include duloxetine, venla-\nfaxine, and desvenlafaxine, all selectiveSNRIs. Two high-quality studies and fivemedium-quality studies support the role\nof duloxetine in the treatment of painin DPN. A high-quality study supportsthe role of venlafaxine in the treatment\nof pain in DPN. Only one medium-quality | [
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0.086045... |
of pain in DPN. Only one medium-quality\nstudy supports a possible role for des-venlafaxine for treatment of pain in DPN(64). Adverse events may be more severe\nin older people but may be attenuated\nwith lower doses and slower titration ofduloxetine.\nTapentadol and Tramadol. Tapentadol | [
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0.09699773788452148,
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0.0... |
Tapentadol and Tramadol. Tapentadol\nand tramadol are centrally acting opioidanalgesics that exert their analgesic ef-\nfects through both m-opioid receptor\nagonism and norepinephrine and sero-\ntonin reuptake inhibition. SNRI/opioid\nagents are probably effective in the | [
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0.05421173945069313,
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0.09640017... |
agents are probably effective in the\ntreatment of pain in DPN. However,the use of any opioids for manage-ment of chronic neuropathic pain car-\nries the risk of addiction and should\nbe avoided.\nTricyclic Antidepressants. TCAs have been | [
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0.... |
be avoided.\nTricyclic Antidepressants. TCAs have been\nstudied for treatment of pain, and mosto ft h er e l e v a n td a t aw e r ea c q u i r e df r o mtrials of amitriptyline and include two\nhigh-quality studies and two medium-\nquality studies supporting the treatmentof pain in DPN (64,66). Anticholinergicside eff... | [
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0.035760... |
restrict use in individuals $65 years of\nage.\nSodium Channel Blockers. Sodium chan-\nnel blockers include lamotrigine, lacosa-\nmide, carbamazepine, oxcarbazepine,and valproic acid. Five medium-quality\nstudies support the role of sodium\nchannel blockers in treating pain inDPN (64).\nCapsaicin. Capsaicin has receive... | [
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0.006255328189581633,
0.03234194591641426,
0.0... |
Capsaicin. Capsaicin has received FDA\napproval for treatment of pain in DPNusing an 8% patch, with one high-quality\nstudy reported. One medium-quality study\nof 0.075% capsaicin cream has been re-ported. In individulas with contraindica-tions to oral pharmacotherapy or who\nprefer topical treatments, the use of topi-... | [
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... |
cal capsaicin can be considered.\nLidocaine 5% Plaster/Patch. Lidocaine\npatches have limited data supportingtheir use in DPN and are not effectivein more widespread distribution of pain\n(although they may be of use in individ-\nuals with nocturnal neuropathic footpain). Lidocaine patches cannot be used\nfor more than... | [
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for more than 12 h in a 24-h period\n(68).S236 Retinopathy, Neuropathy, and Foot Care Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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... |
a-Lipoic Acid. a-Lipoic acid, although not\napproved for the treatment of painful\nDPN, may be effective and considered\nfor the treatment of painful DPN (64,65).\nOrthostatic Hypotension | [
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Orthostatic Hypotension\nTreating orthostatic hypotension is chal-lenging. The therapeutic goal is to mini-mize postural symptoms rather than torestore normotension. Most individualsrequire both nonpharmacologic meas-ures (e.g., ensuring adequate salt intake,avoiding medications that aggravate hy-potension, or using co... | [
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ments over the legs and abdomen) and\npharmacologic measures. Physical activ-ity and exercise should be encouragedto avoid deconditioning, which is knownto exacerbate orthostatic intolerance,and volume repletion with fluids and\nsalt is critical. There have been clinicalstudies that assessed the impact of an\napproach i... | [
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tioned nonpharmacologic measures. Ad-ditionally, supine blood pressure tendsto be much higher in these individuals,often requiring treatment of blood pres-sure at bedtime with shorter-acting drugsthat also affect baroreceptor activity suchas guanfacine or clonidine, shorter-actingcalcium blockers (e.g., isradipine), or | [
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shorter-acting b- b l o c k e r ss u c ha sa t e n o -\nlol or metoprolol tartrate. Alternatives\ncan include enalapril if an individual isunable to tolerate preferred agents(69–71). Midodrine and droxidopa are\napproved by the FDA for the treat-ment of orthostatic hypotension.\nGastroparesis | [
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0.00270... |
Gastroparesis\nTreatment for diabetic gastroparesis maybe very challenging. A low- fiber, low-fat\neating plan provided in small frequentmeals with a greater proportion of liquid\ncalories may be useful (72 –74). In addi-\ntion, foods with small particle size may | [
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tion, foods with small particle size may\nimprove key symptoms (75). Withdraw-ing drugs with adverse effects on gastro-intestinal motility, including opioids,anticholinergics, TCAs, GLP-1 RAs, andpramlintide, may also improve intestinalmotility (72,76). However, the risk of re-moval of GLP-1 RAs should be balanced | [
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0.085... |
against their potential bene fits. In cases\nof severe gastroparesis, pharmacologic\ninterventions are needed. Only metoclo-pramide, a prokinetic agent, is approvedby the FDA for the treatment of gastro-paresis. However, the level of evidenceregarding the bene fits of metoclopra-\nmide for the management of gastropare- | [
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0.04108879715204239,
-0.042442940175533295,
0.0291... |
mide for the management of gastropare-\nsis is weak, and given the risk for seriousadverse effects (extrapyramidal signs suchas acute dystonic reactions, drug-inducedparkinsonism, akathisia, and tardive dyski-nesia), its use in the treatment of gastro-\nparesis beyond 12 weeks is no longer | [
-0.029207007959485054,
-0.028261877596378326,
-0.00036249915137887,
-0.024760907515883446,
0.027299173176288605,
-0.04066126048564911,
-0.04385757073760033,
0.24381327629089355,
0.012947254814207554,
-0.00891590490937233,
-0.022813979536294937,
0.0822005495429039,
-0.03455827757716179,
0.0... |
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