Diabetic Ulcer

Article Author:
Corrine Packer
Article Editor:
Biagio Manna
Updated:
9/1/2018 11:56:44 AM
PubMed Link:
Diabetic Ulcer

Introduction

Diabetes mellitus is a metabolic endocrine disorder due to an overall deficiency of insulin (Type 1) or defective insulin function (Type 2) which causes hyperglycemia. Type 1 diabetes which is usually seen in younger patients accounts for 5% to 10% of cases worldwide and is secondary to autoimmune destruction of B-islet cells of the pancreas.  Type 2 diabetes accounts for 90% to 95% of cases worldwide and is due to genetic and environmental factors with resultant insulin resistance and pancreatic beta-cell dysfunction. Complications arising from hyperglycemia can either be macrovascular or microvascular. The macrovascular disease affects mainly the cardiovascular and cerebrovascular systems, and the microvascular disease includes nephropathy, retinopathy, and neuropathies

A debilitating complication of diabetes mellitus is diabetic ulcers, which leads to increased overall morbidity in patients. This complication may be prevented, as the inciting factor is most often minor trauma. Early identification of these cutaneous injuries also can lead to improved outcomes while decreasing the risk of progression. Diabetic patients (type 1 or 2) have a total lifetime risk of a diabetic foot ulcer complication as high as 25%. 

Etiology

The Six Stages of a Diabetic Foot as described by the 7th Practical Diabetes International Foot Conference

  • Stage 1 - Normal foot with no risk factors;
  • Stage 2 - High-risk foot
  • Stage 3 - Ulcerated foot
  • Stage 4 - Cellulitic foot
  • Stage 5 - Necrotic foot
  • Stage 6 - Foot that cannot be rescued

There are three types of diabetic foot ulcer described namely neuropathic, neuroischaemic, and ischaemic. Sensory neuropathy leads to the majority of ulcers as a result of minor trauma which is not perceived by the patient and further goes untreated as there are no associated pain symptoms unless there is a routine evaluation to assist in identification. Myocardial infarction is one of the most significant events related to peripheral arterial disease increased risk of ischemia. However, ischemia leading to diabetic ulcers adds severe morbidity and health care cost as it can be a chronic complication which is difficult to treat as there is insufficient blood supply.

Major Risk Factors

  • Peripheral motor neuropathy: Abnormal foot anatomy and biomechanics, with clawing of toes, high arch, and subluxed metatarsophalangeal joints, leading to excess pressure, callus formation, and ulcers
  • Peripheral sensory neuropathy: Lack of protective sensation, leading to unattended minor injuries caused by excess pressure or mechanical or thermal injury
  • Peripheral autonomic neuropathy: Deficient sweating leading to dry, cracking skin
  • Neuro-osteoarthropathy deformities (i.e., Charcot disease) or limited joint mobility
  • Abnormal anatomy and biomechanics, leading to excess pressure, especially in the midplantar area
  • Vascular (arterial) insufficiency: Impaired tissue viability, wound healing, and delivery of neutrophils
  • Hyperglycemia and other metabolic derangements: Impaired immunological (especially neutrophil) function and wound healing and excess collagen cross-linking 

Epidemiology

The pooled worldwide prevalence of diabetic foot ulceration was 6.3%. North America had the highest prevalence of 13%; Oceania had the lowest prevalence of 3%. The prevalence in Africa was 7.2% which was higher than Asia 5.5%. Diabetic foot ulceration was more prevalent in male diabetic patients, 4.5%, than female patients, 3.5%. Patients with type 2 diabetes mellitus (T2DM) had a higher prevalence of ulceration at 6.4% compared to patients with type 1 diabetes mellitus (T1DM), 5.5%.

In a systematic review and meta-analysis by Zhang et al. published in 2016, patients with diabetic foot ulceration had the following characteristics: older age (61.7 plus or minus 3.7 versus 56.1 plus or minus 3.9), longer diabetic duration (11.3 plus or minus 2.5 versus 7.4 plus or minus 2.2), lower body mass Index (BMI, 23.8 ± 1.7 versus 24.4 plus or minus 1.7), higher percentage of smokers (29.1%, 95%CI: 18.3% to 39.8% versus 17.4%, 95% CI: 12.4% to 22.4%), hypertension (63.4%, 95%CI: 49.4% to 88.3% versus 53.1%, 95%CI: 33.8% to 72.5%), and diabetic retinopathy (63.6%, 95%CI: 38.8% to 88.3%% versus 33.3%, 95%CI: 13.8% to 52.7%) than patients that did not develop diabetic foot ulceration.

Pathophysiology

Atherosclerosis and diabetic peripheral neuropathy are the two main causes leading to a complication of diabetes such as ulcers. Atherosclerosis leads to decreased blood flow in large and medium-sized vessels secondary to thickening of capillary basement membrane, loss of elasticity, and deposition of lipids within the walls. Further arteriosclerosis leads to small vessel ischemia. Peripheral neuropathy affects the sensory, motor, and autonomic nervous system. There are multifactorial causes such as vascular disease occluding the vasa nervorum, endothelial dysfunction, chronic hyperosmolarity, and effects of increased sorbitol and fructose.

History and Physical

The evaluation of patients presenting with diabetic ulcers can be divided into a clinical and radiologic assessment.

A clinically pertinent history of the type of diabetes, medication history, comorbidities, symptoms of peripheral neuropathy, and vascular insufficiency should be elucidated. Symptoms of neuropathy include hypoesthesia, hyperesthesia, paresthesia, dysesthesia, and radicular pain. Vascular insufficiency has varying presentations and most patients are asymptomatic. However, they can present with intermittent claudication, rest pain, and healing or non-healing ulcers.

In the examination of the legs and foot, an inspection should be performed in a well-lit room with appropriate exposure. Proper documentation using descriptions of ulcer characteristics with size, depth, appearance, and location performed. Presence of discoloration, necrosis, or areas of drainage are signs of infection, and further care is required. Other abnormalities such as nail discoloration, callus formation, and deformities should be noted. Imbalance in the innervations of the foot muscles from neuropathic damage can lead to the development of common deformities seen in affected patients. Hyperextension of the metatarsal-phalangeal joint with interphalangeal or distal phalangeal joint flexion leads to hammer toe and claw toe deformities, respectively. Charcot arthropathy is a commonly seen deformity. Assessment of footwear is important as it can be a contributing factor to the development of foot ulceration. The presence of callus or nail abnormalities should be noted.

Examine the cardiovascular system, checking popliteal, posterior tibial, and dorsalis pedis pulse. Claudication, loss of hair, and the presence of pale, thin, shiny, or cool skin are physical findings suggestive of potential ischemia. If a vascular disease is a concern, the evaluator should measure the ankle-brachial index (ABI). ABIs can, however, be falsely elevated in diabetic patients due to calcification of vessels. More reliable methods of assessing the potential for healing foot ulcers in diabetic patients suspected of having peripheral ischemia involve systolic toe pressure measurements by photoplethysmography or measurement of distal transcutaneous oxygen tension. 

Evaluation

Based on wound depth and necrotic tissue, diabetic ulcers can be classified by the Wagner ulcer classification system.

Wagner-Meggitt Classification of Diabetic Foot

  • Grade 0 - Foot symptoms like pain, only
  • Grade 1 - Superficial ulcers
  • Grade 2 - Deep ulcers
  • Grade 3 - Ulcer with bone involvement
  • Grade 4 - Forefoot gangrene
  • Grade 5 - Full foot gangrene

Radiologic evaluation involves plain radiographs in two-thirds of the views assessing for deformity. If there is suspicion of osteomyelitis, MRI imaging should be performed.

Treatment / Management

Multimodal Diabetic Ulcer Management

  • Patient Education: Education on foot care, as well as control of blood sugar levels, should be performed early. This can also be done with the aid of diabetic educators and social workers. 
  • Blood-Sugar Control: This is managed using a team approach of primary care physician, podiatry, and vascular specialist and based on the severity of the disease and the patient’s attitude toward medication, especially insulin. 
  • Decreasing Pressure, preventing further or new trauma: Offloading pressure to the area can be done with crutches, wheelchairs, and casting. Ulcer healing is improved with total contact casting, irremovable cast walkers compared to removable cast walkers. 
  • Improve Peripheral Vascular Circulation: Antiplatelet agents are the initial drug therapy; however, insufficiency requires surgical bypass. 
  • Prevent or Control Infection: Systemic and source control is achieved using antibiotics and surgical debridement.  
  • Topical Ulcer Care:  Principles of wound care include the use of topical agents with dressing and debridement. 

Differential Diagnosis

  • Venous Ulcers
  • Diabetic Dermatopathy