2008 Clinical Practice Guidelines - Canadian Diabetes Association

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2008 CLINICAL PRACTICE GUIDELINES S146 osteomyelitis and diabetic neuroarthropathy: MR imaging. Semin Musculoskelet Radiol. 2005;9:272-283. 35. Apelqvist J, Larsson J.What is the most effective way to reduce incidence of amputation in the diabetic foot? Diabetes Metab Res Rev. 2000;16(suppl 1):S75-S83. 36. Valk GD, Kriegsman DM,Assendelft WJ. Patient education for preventing diabetic foot ulceration. Cochrane Database Syst Rev. 2001;(4):CD001488. 37. McCabe CJ, Stevenson RC, Dolan AM. Evaluation of a diabetic foot screening and protection programme. Diabet Med.1998; 15:80-84. 38. Dargis V, Pantelejeva O, Jonushaite A, et al. Benefits of a multidisciplinary approach in the management of recurrent diabetic foot ulceration in Lithuania: a prospective study. Diabetes Care. 1999;22:1428-1431. 39. Margolis DJ, Kantor J, Berlin JA. Healing of diabetic neuropathic foot ulcers receiving standard treatment. A meta-analysis. Diabetes Care. 1999;22:692-695. 40. Atiyeh BS, Ioannovich J, Al-Amm CA, et al. Management of acute and chronic open wounds: the importance of moist environment in optimal wound healing. Curr Pharm Biotechnol. 2002;3:179-195. 41. Steed DL, Donohoe D,Webster MW, et al. Effect of extensive debridement and treatment on the healing of diabetic foot ulcers. Diabetic Ulcer Study Group. J Am Coll Surg. 1996;183: 61-64. 42. Sherman RA. Maggot therapy for treating diabetic foot ulcers unresponsive to conventional therapy. Diabetes Care. 2003;26: 446-451. 43. Armstrong DG, Lavery LA,Wu S, et al. Evaluation of removable and irremovable cast walkers in the healing of diabetic foot wounds: a randomized controlled trial. Diabetes Care. 2005;28:551-554. 44. Katz IA, Harlan A, Miranda-Palma B, et al. A randomized trial of two irremovable off-loading devices in the management of plantar neuropathic diabetic foot ulcers. Diabetes Care. 2005;28:555-559. 45. Armstrong DG, Nguyen HC, Lavery LA, et al. Off-loading the diabetic foot wound: a randomized clinical trial. Diabetes Care. 2001;24:1019-1022. 46. Nabuurs-Franssen MH, Sleegers R, Huijberts MS, et al. Total contact casting of the diabetic foot in daily practice: a prospective follow-up study. Diabetes Care. 2005;28:243-247. 47. Lavery LA, Armstrong DG,Wunderlich RP, et al. Risk factors for foot infections in individuals with diabetes. Diabetes Care. 2006;29:1288-1293. 48. Perry CR, Pearson RL, Miller GA. Accuracy of cultures of material from swabbing of the superficial aspect of the wound and needle biopsy in the preoperative assessment of osteomyelitis. J Bone Joint Surg Am. 1991;73:745-749. 49. Senneville E, Melliez H, Beltrand E, et al. Culture of percutaneous bone biopsy specimens for diagnosis of diabetic foot osteomyelitis: concordance with ulcer swab cultures. Clin Infect Dis. 2006;42:57-62. 50. Slater RA, Lazarovitch T, Boldur I, et al. Swab cultures accurately identify bacterial pathogens in diabetic foot wounds not involving bone. Diabet Med. 2004;21:705-709. 51. Nelson EA, O’Meara S, Golder S, et al; DASIDU Steering Group. Systematic review of antimicrobial treatments for diabetic foot ulcers. Diabet Med. 2006;23:348-359. 52. Eneroth M, Apelqvist J, Stenström A. Clinical characteristics and outcome in 223 diabetic patients with deep foot infections. Foot Ankle Int. 1997;18:716-722. 53. Tan JS, Friedman NM, Hazelton-Miller C, et al. Can aggressive treatment of diabetic foot infections reduce the need for above-ankle amputation? Clin Infect Dis. 1996;23:286-291. 54. Pomposelli FB, Kansal N, Hamdan AD, et al.A decade of experience with dorsalis pedis artery bypass: analysis of outcome in more than 1000 cases. JVasc Surg. 2003;37:307-315. 55. Singh N, Armstrong DG, Lipsky BA. Preventing foot ulcers in patients with diabetes. JAMA. 2005;293:217-228. 56. Blume PA, Paragas LK, Sumpio BE, et al. Single-stage surgical treatment of noninfected diabetic foot ulcers. Plast Reconstr Surg. 2002;109:601-609. 57. Sayner LR, Rosenblum BI, Giurini JM. Elective surgery of the diabetic foot. Clin Podiatr Med Surg. 2003;20:783-792. 58. Räkel A, Huot C, Ekoé JM. Canadian Diabetes Association Technical Review: The diabetic foot and hyperbaric oxygen therapy. Can J Diabetes. 2006;30:411-421.
Erectile Dysfunction Canadian Diabetes Association Clinical Practice Guidelines Expert Committee The initial draft of this chapter was prepared by Gerald Brock MD FRCPC, Richard Bebb MD ABIM FRCPC and William Harper MD FRCPC KEY MESSAGES • Erectile dysfunction (ED) affects approximately 34 to 45% of men with diabetes, has been demonstrated to negatively impact quality of life among those affected across all age strata, and may be the earliest sign of cardiovascular disease. • All adult men with diabetes should be regularly screened for ED with a sexual function history. • The current mainstays of therapy are phosphodiesterase type 5 inhibitors.They have been reported to have a major impact on erectile function and quality of life, and should be offered as first-line therapy to men with diabetes wishing treatment for ED. INTRODUCTION Erectile dysfunction (ED) affects approximately 34 to 45% of men with diabetes, and has been demonstrated to negatively impact quality of life among those affected across all age strata. Furthermore, studies indicate that 40% of diabetic men >60 years of age have complete ED (1-9).Among the diabetic population, risk factors include increasing age, duration of diabetes, poor glycemic control, cigarette smoking, hypertension, dyslipidemia, androgen deficiency states (10) and cardiovascular disease (CVD) (5,7,11,12). ED as a marker of potential CV events has been reported by numerous investigators (13-20). Diabetic retinopathy has been shown to correlate with the presence of ED (5,7,21). Organic causes of ED include microvascular and macrovascular disease, and neuropathy. In addition, psychological or situational factors may cause or contribute to ED. Compared with the general population, multiple studies have reported men with diabetes having higher rates of hypogonadism (10,22-24). Importantly, phosphodiesterase type 5 (PDE5) inhibitors appear to be less effective in hypogonadal states (23,25,26), where treatment of nonresponders to PDE5 with testosterone replacement is successful in roughly 50% of individuals. In addition, ED is a side effect of many drugs commonly prescribed to men with diabetes, such as some antihypertensives and antidepressants. SCREENING All adult men with diabetes should be regularly screened for ED with a sexual function history. Screening for ED in men with type 2 diabetes should begin at diagnosis of diabetes. Validated questionnaires (e.g. International Index of Erectile Function [27,28] or Sexual Health Inventory for Men [29]) have been shown to be both sensitive and specific in determining the presence of ED and providing a means of assessing response to therapy. TREATMENT While no randomized clinical trials have demonstrated that interventions that improve glycemic control also reduce the incidence and progression of ED, the Diabetes Control and Complications Trial and United Kingdom Prospective Diabetes Study showed that intensive glycemic control was effective for primary prevention of and secondary intervention for neuropathy, a condition that can impair sensory feedback from the penis, leading to reduced erectile function (30-32). The current data still show that tight glycemic control does not reverse ED (33-35). The current mainstays of therapy are PDE5 inhibitors. They have been reported to have a major impact on erectile function, quality of life, and should be offered as first-line therapy to men with diabetes wishing treatment for ED (36-41). Evolving evidence supports the potential beneficial effects of PDE5 inhibitors on endothelial function and lower urinary tract symptoms. Contraindications for the use of PDE5 inhibitors include unstable angina or untreated cardiac ischemia and concomitant use of nitrates (42,43). Referral to a specialist in ED should be offered to men who do not respond to PDE5 inhibitors or for whom the use of PDE5 inhibitors is contraindicated. Second-line therapies (e.g. vacuum constriction devices, intracorporal injection therapy with prostaglandin E1 [PGE1] alone or in combination with papaverine and phentolamine [triple therapy], intraurethral therapy using PGE1) or third-line therapy (penile prosthesis) may be considered for these men (44). EJACULATORY DISORDERS Ejaculatory disorders are another common disorder of sexual function in men with diabetes, occurring in up to 32% (45).They range in scope from retrograde ejaculation, usually secondary to autonomic neuropathy with incomplete closure of the bladder neck during ejaculation, to premature or retarded ejaculation. S147 COMPLICATIONS AND COMORBIDITIES
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