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Identify and Treat the Cause: 4.1 Assessment


RNAO Evidence Level:

Level C

a. Risk Factors, Effects and Etiology of Diabetic Foot Ulcers (DFUs)1

Should be undertaken by healthcare professional(s) trained and experienced in diabetic foot ulcer management 2

Not all patients with diabetes are at-risk for ulceration. Key risk factors include presence of peripheral neuropathy, foot deformity, peripheral vascular disease, or a history of foot ulceration or amputation of (a part of) the foot or leg3456 7 8. In general, patients without any of these risk factors do not appear to be at-risk for ulceration. For the current best practice, we define the at-risk patient in line with the definition from the International Working Group on the Diabetic Foot (IWGDF)9 as ‘a patient with diabetes who does not have an active foot ulcer, but who has peripheral neuropathy, with or without the presence of foot deformity or peripheral artery disease, or a history of foot ulcer(s) or amputation of (a part of) the foot or leg.’

 

Table 2: International Working Group Diabetic Foot Definitions10

Peripheral Neuropathy The presence of symptoms or signs of peripheral nerve dysfunction in people with diabetes, after exclusion of other causes
Loss of Protective Sensation Inability to sense light pressure e.g. as applied with a 10 gram Semmes-Weinstein monofilament
Foot Deformity Structural abnormalities of the foot such as hammer toes, mallet toes, Charcot foot, claw-toes, hallux valgus, prominent metatarsal heads, residuals of neuro-osteoarthropathy, amputations or other foot surgery
Peripheral Artery Disease Obstructive artherosclerotic vascular disease with clinical symptoms, signs or abnormalities on non-invasive vascular assessment, resulting in4 disturbed or impaired circulation in one or more extremities
Therapeutic Footwear Some form of customization to the patient's foot regarding insole, shoe, and/or orthosis

Risk factors that are predictive and/or precursors of DFU include direct and indirect causes. For example, deformities of the foot are a direct cause of DFU. Foot deformities develop from a multitude of reasons including joint contractures, clawing of toes, spurs, bunions, bunionettes, extrusions of bones (as in Charcot neuroarthropathy), malunited fractures, and arthridities. Clawed toes, repetitive shear stresses, and trauma are other conditions that can be direct causes of DFU 1112 13 14 15 16 17

Indirect causes of DFU lead to wounds through secondary processes. For example, patients with diabetes with sensory neuropathy may disregard callus formation over deformities because no pain is associated with pressure being placed on the callus. Without attention to removing the deformity and/or debulking the callus, an ulcer frequently develops with continuing loading (i.e., weight bearing) over the sites. 18192021 22

Table 3: Direct and Indirect Causes of Risk Factors23

Cause Examples Comments
Indirect: leads to DFU through secondary mechanisms. Usually onset of the DFU does not occur immediately; often there is repetitive exposure to the cause of it is a chronic, establish condition Neuropathy Delays diagnosis and leads to muscle imbalances and eventually deformities. Contributed to dryness of skin.
Deformity Neuropathy, post-traumatic and congenital causes.
Peripheral Artery Disease Impedes rapid processes; leads to skin atrophy.
Venous Statis Disease Usually ulcers at ankle or more proximal levels.
Glycosylation of tissues Decreases resiliency and padding of tissues.
Collagen Vascular Diseases Analogous to peripheral artery disease.
Angilitis Often a component of collagen vascular disease.
Direct: leads to DFU through an immediate effect of the cause Deformity Join contractures, clawing of toes, spurs, bunions, bunionettes, etc.
Trauma Immediate injury or sometimes delayed sloughs.
Charcot Neuroathropathy Bone collapse leads to deformities.
Malunited fractures Deformities increase contact pressure stresses.
Osteoporosis Subliminal stress – pathological fractures – deformities – ulcers
Congenital Anomalie May result in deformities.

Enzymatic glycosylation of soft tissues reduces the elasticity of tissues as well as soft tissue padding and is another indirect cause of DFU 24252627. With loss of elasticity and padding, wounds are likely to occur with repetitive minimal stresses or constant pressure. However, they would not ordinarily occur if the tissues were normal. Most DFU occur because of a combination of indirect and direct causes. Direct causes make the sites more vulnerable to wound formation, and the indirect causes delay management and/or attenuate the healing/wound prevention processes 2829303132.

The more risk factors that are present, the more likely DFU will occur. Within 1 year of wound healing following DFU, up to 60% of patients with a previous DFU history will develop a recurrent wound 333435. Reasons for this include failure to implement preventive measures as well as the wound site being more vulnerable to re-injury due to; less resiliency and elasticity of scar tissue, abnormal mechanics from tissue loss with amputations and debridement, or combinations of these. Hence, this healed ulcer group presents a dichotomy; it has the highest risk for developing new or recurrent ulcerations and conversely is the easiest group to recognize the risk factors. 363738

Risk factors include:

Physiological

  • Sub-optimal glycemic control/monitoring
  • Advanced diabetes
    1. Neuropathy
      • Autonomic (absence of sweat and oil production leads to dry scaly skin of cracks and fissures)
      • Sensory (lack of protective sensation of the foot)
      • Motor (foot deformity from wasting of intrinsic muscles of the foot e.g. Drop foot)
    2. Retinopathy
    3. Nephropathy
  • History of foot infections or osteomyelitis
  • Previous ulceration
  • Peripheral artery disease
  • Osteoporosis
  • Hypertension
  • Heart disease
  • Hyperlipidemia
  • Collagen vascular diseases (eg. Ankylosing spondylitis, Dermatomyositis, Polyarteritis nodosa, Psoriatic arthritis, Rheumatoid arthritis, Scleroderma, Systemic lupus erythematosus)
  • Gout
  • Use of immunosuppressant medications
  • Advanced age
  • History of deep vein thrombosis
  • Decreased cognitive ability
  • Alcohol/drug abuse
  • Venous stasis disease (Insufficiency)
  • Glycosylation of tissues
  • Congenital abnormalities
  • Vasculitis (Angilitis)

Physical Limitations

  • Obesity
  • Deformity (Charcot foot, hammer toes, bunions, claw toes, non-union fractures, fixed ankle joint)
  • Presence of toe infections (fungal or bacterial), callous and/or corns
  • Limited joint mobility
  • Visual disturbances
  • History of amputation
  • Trauma

Socioeconomic/Lifestyle

  • Smoking
  • Unsafe home environment
  • Inadequate foot wear
  • Inadequate hygiene
  • Lack of awareness for self-care
  • Financial insecurity
  • Decreased level of activity
  • Nutritional deficits

b. Pathogenesis of Ulceration

The reason for the susceptibility and increase incidence of foot ulcers in the diabetic patient is because of the interaction of several pathogenic factors. Research supports this reason establishing that “diabetic foot ulcers result from the simultaneous action of multiple contributing causes,”3940 41 42 while the main principal causes are noted to be peripheral neuropathy and ischemia from peripheral vascular disease.434445464748 The four pathogenic factors that trigger the formation of an ulcer in the diabetic patient includes abnormal foot biomechanics, peripheral arterial disease, neuropathy and poor wound healing.495051525354555657

Figure 4: Four Pathogenic Factors

Four Pathogenic Factors
 
Successful diagnosis and management of patients with diabetic foot ulcers involves a holistic-multidisciplinary approach that includes:
  1. Optimal diabetes control
  2. Effective local wound care
  3. Infection control
  4. Pressure relieving strategies
  5. Restoring pulsatile blood flow

58 59 60 61 62 63 64 65 66 67

 

c. General Inspection, Skin, Musculoskeletal and Neurological Assessments

General Inspection

A careful inspection of the feet in a well-lit room should always be carried out after the patient has removed shoes and socks. Because inappropriate footwear and foot deformities are common contributory factors in the development of foot ulceration 6869, the shoes should be inspected and the question “Are these shoes appropriate for these feet?” should be asked. Examples of inappropriate shoes include those that are excessively worn or are too small.

Skin Assessment

The dermatological assessment should initially include a global inspection, including interdigital, for the presence of ulceration or areas of abnormal erythema. The presence of callus (particularly with hemorrhage), nail dystrophy, or paronychia (infection next to nail) should be recorded 70 , with any of these findings prompting referral to a specialist or specialty clinic. Focal or global skin temperature differences between one foot and the other may be predictive of either vascular disease, infection or ulceration and could also prompt referral for specialty foot care. 71727374

Musculoskeletal Assessment

The musculoskeletal assessment should include evaluation for any gross deformity75 . Rigid deformities are defined as any contractures that cannot easily be manually reduced and are most frequently found in the digits. Common forefoot deformities that are known to increase plantar pressures and are associated with skin breakdown include metatarsal phalangeal joint hyperextension with interphalangeal flexion (claw toe) or distal phalangeal extension (hammer toe).76777879

Neurological Assessment

Peripheral neuropathy is the most common component cause in the pathway to diabetic foot ulceration.80 818283 The clinical exam recommended, however, is designed to identify loss of protective sensation (LOPS) rather than early neuropathy. The diagnosis and management of the latter were covered in a 2004 ADA technical review.84  The clinical examination to identify LOPS is simple and requires no expensive equipment.
 

d. Factors and Predictors of Delayed Healing

Factors that may affect healing potential:

  Local
  • Presence of necrosis, foreign body and/or infection
  • Disruption of microvascular supply
  • Cytotoxic (toxic to cells) agents
  • Repetitive pressure-local trauma
  • Exposed bone
  • Size

  Host
  • Co-morbidities (i.e. inflammatory conditions, nutritional insufficiencies, peripheral vascular, renal, obesity or  coronary artery disease)
  • Glycemic control
  • Systemic cytotoxic drugs
  • Smoking
  • Cognitive impairment
  • Alcohol and substance abuse
  • Ill-fitting foot wear
  • Adherence to plan of care by patient and caregivers
  • Cultural and personal belief systems
  • Psychological well-being

  Environment
  • Access to care and or offloading
  • Family support
  • Healthcare sector
  • Geographic surroundings
  • Socioeconomic status

  Predictors of delayed healing:
  • Fixed ankle joint
  • Wound base has more than 50% yellow fibrin
  • Wound has been present longer than 6 months
  • Wound is larger than 5cm2  (L x W=>5cm2)  
  • Patient had previous hip or knee surgery

The PUSH tool has been validated to utilize for measurement and predictors of healing for DFU. 85 8687

e. Symptoms of peripheral neuropathy

  • Hypesthesia (diminished capacity for physical sensation of the skin)
  • Hyperesthesia (excessive sensitivity of the skin)
  • Allodynia (pain due to a stimulus which does not normally provoke pain.  Thus, allodynia involves a change in quality of sensation, whether touch or heat or cold, for example)
  • Paresthesia (tingling, pins and needles)
  • Dysesthesia (unpleasant, abnormal sense of touch usually burning or tingling)
  • Radicular pain (pain that follows the root of the nerve)
  • Anhydrosis (inability to sweat normally)
 
Table 4: Signs and Symptoms of DFU 98
Feature Neuropathic Ischaemic Neuro-ischaemic
Sensation Sensory loss Painful Degree of sensory loss
Callus/necrosis Callus present and often thick Necrosis common Minimal callus
Prone to necrosis
Wound bed Pink and granulating, surrounded by callus Pale and sloughy with poor  granulation Poor granulation
Foot temperature and pulses Warm with bounding pulses Cool with absent pulses Cool with absent  pulses
Other Dry skin and  fissuring Delayed healing High risk of infection
Typical location Weight-bearing areas of the foot, such as metatarsal heads, the heel and over the dorsum of clawed toes Tips of toes, nail edges and between the toes and lateral borders of the foot Margins of the foot and toes
Prevalence
(based on88)
35% 15% 50%

 

Most people harbouring atherosclerotic disease of the lower extremities are asymptomatic; others develop ischemic symptoms. A complete vascular assessment should be done on all patients with diabetic foot ulcers. 899091

 

Table 5: Characteristics of Diabetic Foot Ulcer

Examples

   Sensory Neuropathy
  • Impairment of nerve function (lack of sensation or pain)
  • Incidence of neuropathy related to duration and glycemic control
  • One of the more common areas for ulceration in the diabetic with peripheral neuropathy is over the plantar surface of the metatarsal heads.
 
   92
   Motor Neuropathy
  • Wasting of intrinsic muscles of the foot
  • Muscle imbalance 
  • Structural foot deformity; digital instability  claw toes and subluxated metatarsophalangeal joints
  • Limited joint mobility

  93
 
   Autonomic Neuropathy
  • Loss of autonomic system function
  • Absence of sweat and oil production leads to dry scaly skin and development of cracks and fissures

   94
    Rigid Deformity

Altered Gait Patterns
High compression and frictional forces occur around deformity
Bunions, Hammertoes
Prominent Metatarsal
 

95

    Limited Joint Mobility (Claw Toe)
  • Claw toe is often the result of nerve damagen 
  • The toes "claw," digging down into the soles of your shoes and creating painful calluses.

96

 

Charcot’s Foot
  • Progression of neuropathy with involvement of the sensory, autonomic and motor components of the distal nervous system, coupled with the effects of repetitive minor trauma and local osteoporosis, results in the typical Charcot's foot.
  • Neuroosteoarthropathy or Charcots Foot/Joint:
  • Early stages: hot, swollen, red foot with bounding pulses and prominent veins. Presentation of joint may be mistaken for cellulitis
  • Over time bones of the ankle fragment, arch collapses and result is a “rocker bottom” configuration of the foot

Foot is then arched and not able to handle pressure resulting in tissue breakdown and ulceration of the arch

97


Identify and Treat Cause: 4.2 Obtain a Comprehensive Patient History

 

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