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2 Clinical Examination andRisk Classication oftheDiabetic Foot

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Fig. 2.8 An example of a stage 2 pressure ulcer on the heel

Meggitt-Wagner Ulcer Classications

Several diabetic classication systems have been reported in the medical literature. This section aims to chronologically review some of the most commonly described classication systems currently used by a variety of practitioners to stage diabetic foot wounds and to discuss outcomes related to their use. One of the most frequently cited diabetic wound classication systems was rst described by Meggitt [82] in 1976 and Wagner [83] in 1981. The system is based mainly on wound depth and consists of six wound grades. These include Grade 0 (intact skin), Grade 1 (supercial ulcer), Grade 2 (deep ulcer to the tendon, bone, or joint), Grade 3 (deep ulcer with abscess or osteomyelitis), Grade 4 (forefoot gangrene), and Grade 5 (whole-foot gangrene) (Fig.2.9). This classication is outlined in Table2.3.

The classication system contains three key descriptors, including depth, infection, and ischemia. However, it does not consistently include these important risk factors in every ulcer grade. Infection is included in only one of the six Wagner ulcer grades, and vascular disease is only included in the last two classication grades. The rst three grades are concerned only with depth. It is perhaps for this reason that they are the most commonly used, whereas the last three are largely ignored because of their limited clinical use. The descriptors Meggit and Wagner used for ischemia were forefoot and whole foot gangrene. These represent the most severe form of end-stage disease and therefore cannot help guide proactive interventional therapy, except frank ablation of the affected site. In addition, because gangrene can be caused by infection, it may not always have a vascular origin. Since there are better diagnostic tools to assess and treat PAD, more robust criteria for ischemia will improve diagnosis, interventions, and amputation prevention.

There are several papers that have attempted to validate the Wagner classication system [84, 85]. Calhoun etal. [85] evaluated wounds that were infected and retrospectively assigned Wagner grades to them. They found that when wounds were treated according to what they considered a healthy standard of care, the eradication of infection and the prevention of readmission for 1 year were frequently achieved despite wound grade. Van Acker etal. [75] found the Wagner classication to have a signicant association with the duration of healing of the ulcer. Armstrong et al. [86] suggested that patients with Wagner stages 4 and 5 may be grouped together as the two groups did not have separate prognostic values. In addition, these patients are often referred directly to a surgeon for amputation and are rarely seen by the diabetic foot team. The system was adapted to combine medical and surgical elements of therapy to monitor the treatment of diabetic foot infection. Unfortunately, in requiring that wounds be infected as an inclusion criterion, it assessed this classication as problematic since Wagner wound Grades 0–2 classically have no infection descriptor attached to them. In fact, the only mention of infection in this system occurs in Grade 3. This unfortunately limits its usefulness as a standard diabetic foot classication.

UT Ulcer Classication

The University of Texas (UT) Health Science Center in San Antonio proposed a classication that included depth, infection, and vascular status in 1996 [86, 87]. The classication integrates a system of wound grade and stage to categorize wounds by severity. It is based on two fundamental questions the clinician asks when assessing a wound: (1) How deep is the wound, and (2) is the wound infected, ischemic, or both? The classication uses a matrix with infection and /or ischemic as the vertical axis and depth as the longitudinal axis. This system is illustrated in Table2.4.

Similar to other wound classication systems, the UT system grades wounds by depth. Grade 0 represents a pre- or postulcerative site. Grade 1 ulcers are supercial wounds through either the epidermis or the epidermis and dermis but do not penetrate the tendon, capsule, or bone. Grade 2 wounds penetrate the tendon or capsule, but the bone and joints are not involved. Grade 3 wounds penetrate the bone or joint. Within each wound grade, there are four stages: clean wounds (A), nonischemic infected wounds (B), ischemic wounds (C), and infected ischemic wounds (D).

The Grade 0 Wound

Grade 0 wounds are preulcerative areas or previous ulcer sites that are now completely epithelialized after the debridement of hyperkeratosis and nonviable tissue. The diagnosis

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L. A. Lavery and M. A. Suludere

Fig. 2.9 Foot with full and partial gangrene

Table 2.3 Meggitt-Wagner grading system

Grade Description 0 Preulcerative area 1 Full-thickness ulcer, no exposed deep structures 2 Ulcer extends to the muscle, tendon, joint, or bone 3 Ulcer extends to deep structures with abscess or osteomyelitis 4 Gangrene limited to the forefoot 5 Gangrene extending to the entire foot

of a Grade 0 wound can be made only after the removal of any regional hyperkeratosis as ulcerations may be hidden by overlying calluses. The Grade 0-A wound is then a preulcerative area or a completely epithelialized postulcerative area. The Grade 0-B wound is a 0-A lesion with associated cellulitis. The Grade 0-C wound is a 0-A lesion with concomitant regional signs of ischemia. The Grade 0-D wound is a 0-B

lesion coupled with a working diagnosis of lower extremity ischemia, as dened above.

Although lesions that fall into the Grade 0 category do not have a break in the epidermis and may not be classically classied as “wounds,” the category is important in the identication of sites that are “at risk” for future ulceration and in monitoring and preventing the reulceration of newly healed wounds. Because there is a very high rate of reulceration (28–50%), the Grade 0 classication allows physicians to follow the progression of wounds over time from healed to reulcerated.

The Grade IWound

Grade I may be either partial or full thickness, without involvement of the tendon, capsule, or bone. The Grade I-A wound is therefore a partial or full-thickness wound.

2 Clinical Examination andRisk Classication oftheDiabetic Foot

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Table 2.4 University of Texas wound classication system

Stage

Grade

0 1 2 3

A Pre- or postulcerative lesion

completely epithelialized B With infection With infection With infection With infection C With ischemia With ischemia With ischemia With ischemia D With infection and ischemia With infection and ischemia With infection and ischemia With infection and ischemia

Supercial wound, not involving a tendon, capsule, or bone

Wound penetrating the tendon or capsule

Wound penetrating the bone or joint

The Grade I-B wound is an infected supercial wound. As with any neuropathic lesion, Grade I-B wounds should be examined very carefully. By denition, the Grade I-B wound implies supercial infection without involvement of underlying structures. If the wound shows signs of signicant purulence or uctuance, further exploration to expose a higher-grade infection is in order. The Grade I-C wound is I-A plus vascular compromise, and the Grade I-D wound is the infected I-B wound with concomitant ischemia.

The Grade II Wound

Grade II wounds may involve the tendon or joint capsule but not the bone. The reason for the distinct delineation between wounds that probe into the bone and those without bone or joint involvement is the high correlation between probing into bone and osteomyelitis [66, 88]. The II-A wound may therefore probe into the tendon or joint capsule but not the bone. The II-B wound is II-A plus infection, but again, the bone and joint are not involved. The Grade II-C wound is II-A plus ischemia, and the Grade II-D wound corresponds to II-B plus ischemia.

The Grade III Wound

A wound that probes into the bone is categorized as a Grade III wound. The modiers are then added pending the presence of a comorbid factor. The III-A wound probes into the bone without local or systemic signs of acute infection. The III-B wound probes into the bone with signs of acute infection. The III-C wound is identical to III-A with concomitant ischemia. The III-D wound is characterized by active infection, exposed bone, and vascular insufciency. The criterion for each of the stages is based on clinical and laboratory data. The working diagnosis of lower extremity ischemia may be based on clinical signs and symptoms such as the absence of pedal hair, absent pulses, claudication, rest pain, atrophic integument, dependent rubor, or pallor on elevation, plus one or more of the noninvasive criteria (transcutaneous oxygen measurements of <40mm Hg, ankle-brachial index of <0.80, or absolute toe systolic pressure of <45mm Hg) [89, 90]. This predictive value of this ulcer classication has been evaluated in several studies [86] and showed an overall trend toward an increased prevalence of amputation as wounds increased in both grade (depth) and stage (comorbidity). Patients whose wounds were both infected and ischemic

were noted to be almost 90 times more likely to receive a high-level amputation compared with patients in a less advanced wound stage, and patients whose wounds probed into the underlying bone were over 11 times as likely to receive a high-level amputation.

Jeon and colleagues compared the diabetic ulcer severity score (DUSS); the University of Texas (UT) ulcer classication; the Meggitt-Wagner classication; the depth of the ulcer, extent of bacterial colonization, phase of ulcer healing, and associated underlying etiology (DEPA) scoring system; and the site, ischemia, neuropathy, bacterial infection, area, and depth (SINBAD) score. They found that the Wagner and UT systems were the best predictors of amputation [91]. In a systematic review of diabetic foot ulcer classication systems, Monteiro-Soares etal. found that the Meggitt-Wagner, S(AD)SAD, and UT Classication systems were the most extensively validated [92].

Oyibo etal. [90] compared the Wagner classication system with the UT system in a multicenter prospective longitudinal case-control study of 194 patients. The study suggested that both the UT and the Wagner classication system correlated similarly with clinical outcomes. Both systems associated higher grades with a greater likelihood of an ulcer not healing and a greater chance of limb amputation. The trend for the grade of the UT classication system was slightly more robust than the trend for the grade of the Wagner classication. The inclusion of comorbid factors such as infection and/or ischemia to grade (depth) when classifying an ulcer with the UT system improves description and adds to the predictive power of a wound classication system, especially for ulcers within the same grade level but at a different stage. Based on this, the UT wound classication showed promise as a more practical system.

WIfI Classication

The wound, ischemia, and foot infection (WIfI) classication system is the Society for Vascular Surgery lowerextremity threatened-limb classication system. WIfI correlates with ulcer healing and amputation-level selection. This system is a threatened-limb classication system that focuses on stratifying the 1-year risk of major amputation and predicting the likelihood that revascularization would be required for wound healing and limb salvage [93].

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Table 2.5 WIfI (wound, ischemia, foot infection) classication

Grade Description

Ulcer 0 No ulcer

1 Supercial ulcer; deeper structures are not visible 2 Deep ulcer involving musculoskeletal structures; muscle, bone, fascia, tendon, or cartilage may be visible. If gangrene is

present, it is limited to the toes

3 Deep ulcer extending to more departments of the foot (forefoot or midfoot); extensive gangrene

Ischemia ABI SBP TCOM

0 >0.80 >100 >60 1 0.6–0.79 70–100 40–59 2 0.4–0.59 50–70 30–39 3 <0.4 <50 <30

Infection 0 No signs of infection

1 Signs of local infection with erythema <2cm, involving the skin and subcutaneous tissue 2 Signs of infection with either erythema >2cm; involving musculoskeletal tissue like muscle, bone, joint, tendon,

cartilage, presence of abscess, or gangrene; without systemic symptoms of inammation

3 Signs of infection with systemic symptoms of inammation

L. A. Lavery and M. A. Suludere

Much like the UT ulcer classication, WIfI evaluates depth, infection, and PAD. However, WIfI provides more in- depth specications for infection and PAD severity. Infection is scored based on the International Working Group on the Diabetic Foot’s Infection classication using a 0–4 scale [94] (Table2.5). The IWGDF has been updated since WIfI was created. It now has a separate designation for people with osteomyelitis because patients with osteomyelitis require longer treatments with antibiotics and have higher rates of reinfection and rehospitalization and more surgery. Depth is scored on a 0–4 scale as well utilizing a combination of criteria used in the UT ulcer classication and the Meggitt- Wagner classication (no ulcer; supercial ulcer; deep ulcer extending to the tendon, capsule, or bone with or without gangrene conned to the toes; and extensive ulcer with or without extensive gangrene). PAD is stratied from 0 to 4 based on ankle-brachial index (ABI), systolic pressure, or transcutaneous oxygen measurements [52]. It is interesting that the PAD section does not account for Mönckeberg’s calcic sclerosis. This is present in >50% of people with diabetes with foot ulcers [95, 96]. The calcication of the media of the artery makes the artery noncompressible. The information is therefore not reliable.

In conclusion, it is observed that many of the risk factors for neuropathic ulceration, infection, and subsequent amputation may be identied using simple, inexpensive equipment in a primary care setting. A consistent, thoughtful assessment of the diabetic foot is pivotal to identifying highrisk patients. Subsequent to the gathering of clinical data through sequential assessment, the appropriate classication of the wound becomes paramount in our efforts to document and communicate the level of risk to all members of the healthcare team caring for the person with diabetes. These simple approaches should improve communication and facilitate amputation prevention.

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2 Clinical Examination andRisk Classication oftheDiabetic Foot

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Diabetic Neuropathy

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SolomonTesfaye andTriantafyllosDidangelos

Abstract

Diabetic neuropathy affects up to 50% of patients with

diabetes mellitus. It encompasses several neuropathic syndromes, the most common being distal symmetrical polyneuropathy or “diabetic peripheral neuropathy” (DPN). Risk factors for DPN include poor glycaemic

control and drivers of macrovascular disease, including

hypertension and obesity. Strong evidence in humans and animals implicates nerve ischaemia as the cause of DPN. Despite several well-designed recent trials, no novel approved treatment with unequivocal effects on nerve function decline in DPN has emerged. Painful DPN affects about a quarter of those with diabetes, produces considerable disability and is challenging to assess and manage. First-line therapies are tricyclic antidepres-

sants, serotonin noradrenaline reuptake inhibitors (e.g.

duloxetine) and anticonvulsants (e.g. pregabalin, gabapentin). The OPTION DM trial has recently shown that these rst- line drugs (and their combinations) have equivalent efcacy. It also showed that maximal tolerated combination treatment provides better relief than maximum tolerated monotherapy. Second-line drugs include opioids only under specialist care and capsaicin 8% patch, with more refractory cases referred for high-frequency spinal cord stimulation. Diabetic autonomic neu-

ropathy also results in considerable morbidity, reduced

quality of life and increased mortality. It can involve cardiovascular, gastrointestinal, urogenital, pupillomotor, thermoregulatory and sudomotor functions. Although counselling and non- pharmacological interventions are

S. Tesfaye (*) Diabetes and Endocrinology for Shefeld Teaching Hospitals and the University of Shefeld, Royal Hallamshire Hospital, Shefeld, UK e-mail: Solomon.Tesfaye@nhs.net

T. Didangelos Internal Medicine and Diabetology, Medical School, Aristotle University, “AHEPA” Hospital, Thessaloniki, Greece e-mail: didang@auth.gr

of some use, more severely aficted patients require pharmacological intervention.

Introduction

Diabetic neuropathy is a major complication of diabetes and a cause of considerable morbidity and increased mortality [1]. Diabetic neuropathy is not a single entity but includes several neuropathic syndromes (Fig.3.1) [2, 3]. In clinical practice, by far, the commonest presentation of diabetic neuropathy is chronic distal symmetrical polyneuropathy, also known as ‘“diabetic peripheral neuropathy” (DPN)’. The Toronto Diabetic Neuropathy Expert Group recently dened DPN as “a symmetrical, length-dependent sensorimotor polyneuropathy attributable to metabolic and micro-vessel alterations as a result of chronic hyperglycemia exposure and cardiovascular risk covariates” [4]. “An abnormality of nerve conduction tests, which is frequently subclinical, appears to be the rst objective quantitative indication of the condition [4]. The occurrence of diabetic retinopathy and nephropathy in a given patient strengthens the case that the polyneuropathy is attributable to diabetes” [4].

The neuropathic syndromes depicted in Fig.3.1 have varied presentations as regards the onset of symptoms, the clinical course and possibly pathogenesis [2]. This chapter will cover all these syndromes, although the main focus will be (1) DPN, which is the main initiating factor for foot ulceration and a cause of troublesome painful neuropathic symptoms and (2) associated autonomic neuropathy, which can involve almost all systems of the body and may have devastating consequences, such as sudden death.

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Fig. 3.1 Neuropathic syndromes associated with diabetes mellitus

Focal and Multifocal

neuropathies

S. Tesfaye and T. Didangelos

Symmetrical

neuropathies

Fig. 3.2 Risk factors for incident DPN in the EURODIAB prospective study (Ref. [7])

mono-

neuropathy

Amyotrophy,

radiculopathy

entrapment

eg median, ulnar, peroneal

multiple lesions

‘mononeuritis

multiplex’

acute

sensory

distal symmetrical polyneuropathy

also known as

Diabetic peripheral neuropathy (DPN)

(most common syndrome)

autonomic

Epidemiology

The epidemiology of DPN shows a lot of variations, depending on what tests are employed to detect neuropathy. Where electrophysiology is used, the prevalence rates will be in excess of 50% [4], whereas when clinical parameters and/or quantitative sensory testing (QST) are employed, both clinicand population-based studies show surprisingly similar prevalence rates for DPN, affecting around 30% of all diabetic people [5]. The EURODIAB Prospective Complications Study investigated 3250 type 1 patients, from 16 European

countries, and found a prevalence rate of 28% for DPN at baseline [6]. The study also showed that over a 7.3-year period, about one quarter of type 1 diabetic patients developed DPN: age, duration of diabetes and poor glycaemic control being major determinants [7]. The development of DPN was also associated with potentially modiable cardiovascular risk factors such as hypertension, hyperlipidaemia, obesity and cigarette smoking (Fig. 3.2) [7]. Based on recent epidemiological studies, the correlates of DPN include increasing age, increasing duration of diabetes, poor glycaemic control, retinopathy, albuminuria and vascular risk factors [7].

3 Diabetic Neuropathy

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Classication ofDiabetic Neuropathy

Classication of the various syndromes of diabetic neuropathy has proved difcult. The variations and overlap in aetiology, clinical features, natural history and prognosis have meant that most classications are necessarily oversimplied, and none has proved capable of accounting for all these factors. Nevertheless, attempts at classication stimulate thoughts as to the aetiology of the various syndromes and assist in the planning of management strategies for the patient.

Figure 3.1 shows a modied clinical classication of diabetic polyneuropathy originally suggested by Thomas [2]. Another method of classifying diabetic neuropathy is by considering whether the clinical involvement is symmetrical or asymmetrical. However, this separation, although useful in identifying distinct entities and perhaps providing clues to the varied aetiologies, is an oversimplication of the truth as there is a great overlapping of the syndromes.

Watkins and Edmonds [8] have suggested a classication for diabetic neuropathy based on the natural history of the various syndromes, which clearly separates them into three distinct groups (Table3.1).

More recently, in the 2017 Position Statement of the American Diabetes Association, Pop-Busui et al. provide a more detailed classication of diabetic neuropathies (Table3.2).

Table 3.2 (continued)

Diabetic neuropathies Gastrointestinal

• Diabetic gastroparesis (gastropathy)

• Diabetic enteropathy (diarrhea)

• Colonic hypomotility (constipation) Urogenital

• Diabetic cystopathy (neurogenic bladder)

• Erectile dysfunction

• Female sexual dysfunction Sudomotor dysfunction

• Distal hypohydrosis/anhidrosis

• Gustatory sweating Hypoglycemia unawareness Abnormal pupillary function

2. Mononeuropathy (mononeuritis multiplex) (atypical forms) Isolated cranial or peripheral nerve (e.g., CN III, ulnar, median,

femoral, peroneal) Mononeuritis multiplex (if conuent may resemble polyneuropathy)

3. Radiculopathy or polyradiculopathy (atypical forms) Radiculoplexus neuropathy (a.k.a. lumbosacral polyradiculopathy,

proximal motor amyotrophy) Thoracic radiculopathy Nondiabetic neuropathies common in diabetes Pressure palsies Chronic inammatory demyelinating polyneuropathy Radiculoplexus neuropathy Acute painful small-ber neuropathies (treatment-induced)

Table 3.1 Classication of diabetic neuropathies by natural history (Ref. [8])

1. Progressive neuropathies: These are associated with the increasing duration of diabetes and with other microvascular complications. Sensory disturbance predominates and autonomic involvement is common. The onset is gradual and there is no recovery

2. Reversible neuropathies: These have an acute onset, often occurring at the presentation of diabetes itself, and are not related to the duration of diabetes or other microvascular complications. There is spontaneous recovery of these acute neuropathies

3. Pressure palsies: Although these are not specic to diabetes only, they tend to occur more frequently in diabetic patients than in the general population. There is no association with the duration of diabetes or other microvascular complications of diabetes

Table 3.2

2017 ADA Position Statement. (Adapted from Ref. [3])

Diabetic neuropathies

1. Diffuse neuropathy DSPN

• Primarily small-ber neuropathy

• Primarily large-ber neuropathy

• Mixed small- and large-ber neuropathy (most common) Autonomic Cardiovascular

• Reduced HRV

• Resting tachycardia

• Orthostatic hypotension

• Sudden death (malignant arrhythmia)

Classication of diabetic neuropathies according to the

Symmetrical Neuropathies

Diabetic Peripheral Neuropathy (DPN)

Diabetic peripheral neuropathy is the commonest neuropathic syndrome and what is meant in clinical practice by the phrase “diabetic neuropathy” or “diabetic distal symmetrical polyneuropathy (DSP).” There is a “length-related” pattern of sensory loss, with sensory symptoms starting in the toes and then extending to involve the feet and legs in a stocking distribution. In more severe cases, there is often upper limb involvement, with a similar progression proximally starting in the ngers. Although the nerve damage can extend over the entire body, including the head and face, this is exceptional. Sub-clinical neuropathy detectable by autonomic function tests is usually present. However, clinical autonomic neuropathy is less common. As the disease advances, overt motor manifestations such as wasting of the small muscles of the hands and limb weakness become apparent. However, sub-clinical motor involvement detected by magnetic resonance imaging appears to be common, and thus motor disturbance is clearly a part of the functional impairment caused by DPN [9].

The main clinical presentation of DPN is sensory loss,

which the patient may not be aware of or which may be described as “asleep numbness” or “dead feeling.” However,

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