Background
Year | Milestone | References |
---|---|---|
second century AD | Aretaeus of Cappadocia uses the word diabetes in his writings to describe a rare disease that causes excessive urination | [13] |
1674 | Thomas Willis uses the phrase, “quasi melle aut saccharo imbutam mire dulcescere” to describe the extremely sweet taste of urine from patients with diabetes and suggests that the sweetness is initially present in the blood | [14] |
1776 | Matthew Dobson conducts experiments that confirm the presence of sugar in urine and blood from patients with DM | [15] |
1798 | John Rollo provides detailed observations of symptoms consistent with dysfunction of the peripheral nervous system in patients with DM | [16] |
1815 | Michel Eugène Chevreul identifies glucose in urine from patients with DM | [14] |
1864 | Charles-Jacob Marchal de Calvi recognizes that DM causes dysfunction of the nervous system | [17] |
1885 | Frederick William Pavy describes the signs and symptoms of diabetic peripheral neuropathy | [18] |
1887 | Thomas Davies Pryce recognizes the relationship between peripheral nerve damage and foot ulceration in patients with DM | [19] |
1887 | Ernst Viktor von Leyden classifies diabetic peripheral neuropathy into three forms: hyperesthetic or neuralgic; motor or paralytic; and ataxic or pseudotabetic | [20] |
1890 | Jean-Martin Charcot describes the clinical features of diabetic peripheral neuropathy | [21] |
1936 | Harold Percival Himsworth recognizes that there are two main types of DM: insulin-sensitive or insulin-insensitive | [22] |
1946–1947 | The first community-based screening for DM is conducted in Oxford, Massachusetts | [23] |
1954 | M. Mencer Martin demonstrates the importance of neuropathy in the pathogenesis of foot lesions in patients with DM | [24] |
1956 | Wilfrid George Oakley classifies foot lesions in patients with DM into four types: septic; neuropathic; ischaemic; or combinations of septic, neuropathic, and ischaemic | [25] |
1959 | Sven-Erik Fagerberg recognizes that diabetic neuropathy is associated with histopathological changes in the small blood vessels of peripheral nerves | [26] |
1961 | Allan Watson Downie conducts research on nerve conduction velocities in patients with DM | [27] |
1963 | I. Steiness conducts research on vibration perception threshold in patients with DM | [28] |
1988 | A consensus panel proposes a scheme for classifying diabetic neuropathy into Class I (absence of demonstrable signs and symptoms) and Class II (presence of signs, symptoms, or both) | [29] |
1988 | Peter James Dyck proposes a system for staging the severity of diabetic neuropathy into grade 0 (no abnormality); grade 1a (nerve conduction abnormality); grade 1b (nerve conduction abnormality + signs); grade 2a (nerve conduction abnormality + symptoms ± signs; and grade 2b (nerve conduction abnormality + moderate weakness ± symptoms) | [30] |
1994 | The EDIC study commences with the aim of evaluating the development and progression of diabetes complications in the DCCT cohort | [31] |
1997 | Peter Kynaston Thomas proposes a scheme for classifying diabetic neuropathy into hyperglycemic neuropathy; symmetric polyneuropathy; focal and multifocal neuropathy; and mixed forms | [32] |
1998 | Andrew J. M. Boulton proposes a system for staging the severity of diabetic neuropathy into stage 0/1 (no clinical neuropathy); stage 2 (clinical neuropathy); stage 3 (late complications of clinical neuropathy) | [33] |
2005 | The ADA proposes a scheme for classifying diabetic neuropathy into two types: generalized symmetric polyneuropathies and focal and multifocal neuropathies | [34] |
2008 | Jennifer Tracy and Peter Dyck propose that diabetic neuropathy be classified either by anatomic pattern: symmetric and asymmetric or according to underlying pathophysiology: metabolic-microvascular-hypoxic; inflammatory immune; compression and repetitive injury; complications of diabetes; and treatment related | [35] |
2010 | The Toronto Diabetic Neuropathy Expert Group proposes diagnostic criteria for possible, probable, confirmed, and subclinical diabetic neuropathy | [36] |
2017 | The ADA proposes a comprehensive scheme for classifying diabetic neuropathy into diffuse neuropathy; mononeuropathy; and radiculopathy | [8] |
twenty-first century AD | Development and implementation of comprehensive diabetic foot prevention programs gains momentum around the world | [37] |
Aims, material, and method
Findings
Epidemiology of diabetic peripheral neuropathy
Screening for diabetic peripheral neuropathy
Principle 1: multiphasic approach
Principle 2: risk stratification
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Low risk—normal plantar sensation
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Moderate risk—presence of LOPS
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High risk—presence of LOPS ± PAD
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Very high risk—history of ulceration, amputation, or neuropathic fracture
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Very low risk—absence of LOPS or PAD
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Low risk— presence of LOPS or PAD
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Moderate risk— presence of LOPS + PAD; or LOPS + deformity; or PAD + deformity
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High risk—presence of LOPS or PAD + one or more of the following: previous foot ulceration; or lower-extremity amputation (major or minor); or ESRD
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Very low risk—absence of LOPS and PAD
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Low risk—presence of LOPS ± deformity
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Moderate risk—presence of PAD ± LOPS; diminished dorsalis pedis or posterior tibial pulse; presence of swelling or edema
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High risk—presence of DM with previous history of ulceration or lower-extremity amputation; chronic venous insufficiency
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Urgent—active foot pathology: open wound or ulcerative area ± signs of infection; new neuropathic pain or pain at rest; signs of active Charcot deformity; vascular compromise
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Low risk—presence of callus alone
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Moderate risk—presence of deformity; or neuropathy; or PAD
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High risk—previous ulceration; or previous amputation; or on renal replacement therapy; or neuropathy + PAD; or neuropathy + callus ± deformity; or PAD + callus ± deformity
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Active diabetic foot—presence of ulceration; or foot infection; or chronic limb-threatening ischaemia; or gangrene; or suspicion of acute Charcot arthropathy