Introduction to Diabetic Foot CareCHAPTER 1

Out of all the complications, diabetic foot disease (DFD) can be considered as one of the most devastating and demoralizing complications of diabetes. The Diabetic foot is defined as a group of disorders wherein neuropathy, ischemia or infection may lead to tissue breakdown and a potential to progress toward amputation. The lifetime risk for the development of a diabetic foot ulcer (DFU) in patients with diabetes may range from 15 to 25%, and this is known to precede amputation in 85% of cases.^2,3 The rate of lower limb amputation in patients with DM is 15 times higher than in patients without diabetes and approximately 50–70% of all lower limb amputations are due to DFU.⁴ Every 20 seconds a lower limb is lost due to diabetes and it is the most common cause of non-traumatic lower limb amputation.⁵ It may severely impair the quality of life of patients by affecting productivity, social participation, and livelihood. These amputations also precipitate an increase in mortality rate. However, there are a number of preventable causes for amputation particularly in low socioeconmic societies, such as a lack of sanitation and hygiene, socio-cultural practices such as barefoot walking inside the house and at religious places, lack of awareness on the use of proper footwear and a dearth of foot care clinics which may add to the burden of foot disease related to diabetes mellitus.

DFD includes several pathologies, particularly diabetic peripheral neuropathy (DPN), peripheral arterial disease (PAD), and infections (Flowchart 1). DPN results in sensory, motor and autonomic nerve dysfunction leading to DFU. When screening, almost all patients with diabetes who are undergoing foot-related surgical procedures, a majority are found to have neuropathy.⁶3

Peripheral neuropathy is associated with high rates of skin breakdown and neuropathic fractures due to the inability to perceive pain sensation. The inciting trauma may include ill-fitting shoes or minor sprains and strains. Without protective sensation, a patient with peripheral neuropathy lacks the physical symptoms that would alert healthy individuals to examine their feet, thereby increasing the extent of skin damage, prior to their presentation for treatment. Patients with moderate to severe sensory loss are shown to have a seven-time higher risk of developing a first DFU when compared to patients with preserved sensation.⁷

Autonomic dysfunction, as a result of neuropathy, may also contribute to ulcer formation. It affects both physiologic secretions and the arterio-venous systems leading to dry and fragile skin. This in turn increases the risk of cracks, fissures and skin breakdown, and thereafter, the risk of infection. Motor neuropathy may lead to structural changes to the foot and these changes are partly due to muscular weakness and imbalance caused by intrinsic atrophy manifesting as hammer toes, mallet toe, claw toes, a prominent metatarsal head and other deformities. Such deformities, in turn change pressure patterns on the foot resulting in certain areas becoming more susceptible to trauma or ulceration.

Charcot neuropathic osteoarthropathy (CN) or Charcot foot is also a part of DFD that may affect the bones, joints, and soft tissues of the foot and ankle, characterized by inflammation in its early phase. Diabetes-related Charcot's arthropathy has a reported prevalence between 0.08 and 13%.⁸ Patients with diabetic foot are also 4more likely to present with other diabetes-related complications inclusive of nephropathy, retinopathy, ischemic heart disease and cerebrovascular disease which further aggravate DFD. A combination of neuropathy, abnormal load bearing by the foot, repeated microtrauma, and metabolic abnormalities of bone leads to osteolysis, fractures, dislocation and deformities.

Diagnosing DFD involves a need for a thorough foot examination, which aids in the detection of disease at an early stage. Screening for peripheral neuropathy and PAD may help identify patients at risk of foot ulcers. A history of ulcers or amputations and poor glycemic control, increases the risk further. Examination of the feet at each follow-up visit for any active disease such as ulceration or gangrene is extremely crucial. Clinicians should look for lesions such as cracks, skin fissures, deformed nails, fungal infections, macerated web spaces, calluses and deformities such as claw toes, hammer toes and pes cavus which increase the risk of ulceration. It is advisable to assess the temperature of the feet with the dorsum of the hand. A cold foot might suggest ischemia, and increased warmth with redness and swelling might suggest inflammation such as cellulitis or an acute Charcot foot.

Screening should be done to identify patients with a loss of protective sensation (LOPS) in the feet. Most guidelines recommend the 10 g monofilament for neuropathy assessment in people with diabetes. This monofilament exerts a 10 g buckling force when it bends. An inability to sense a 10 g pressure is consistent with LOPS. The test may be combined with another test to screen for neuropathy, such as a biothesiometer or a graduated tuning fork (Rydel Seiffer) to assess the vibration perception threshold.

One should ask for a history of intermittent claudication and rest pain, which may suggest PAD. The ankle brachial index is an easy adjunct bedside measure to diagnose PAD (Flowchart 2). It is the ratio of the highest systolic blood pressure at the ankle (dorsalis pedis artery or posterior tibial artery) to the systolic blood pressure at the arm, and is measured using a Doppler device.

Peripheral arterial disease is frequently found with neuropathy, in the diabetic patient and can contribute to foot complications. Approximately 50% of patients with DFD are found to have some degree of PAD. Compared to patients with diabetes and Charcot neuropathy, patients with DFUs are significantly more likely to have PAD, critical limb ischemia and more often require revascularization (Flowchart 2). Endothelial damage and vessel sclerosis of both large and small vessels leads to decreased peripheral perfusion. Hence, patients are at an increased risk for ulceration and leads to impaired wound-healing and infection-fighting abilities.

Patients with diabetes have an impaired ability to mount an inflammatory response to infection (immunopathy). Impaired neutrophil function, chemotaxis, phagocytosis, as well as a decreased T-cell response have been found in patients with diabetes versus those without diabetes. Hyperglycemia could be one of the etiological factors behind this, which impairs host defenses at the cellular level, affecting leukocytes, macrophages and other cell types. PAD and immunopathy do not directly cause ulceration; however, these patient factors can increase the risk of diabetic foot complications in those with diabetic neuropathy.

Based on the initial assessment, patients may be categorized as having a low, moderate, or high risk of diabetic foot (Fig. 1). Low risk indicates the presence of callosities alone; medium risk: The presence of deformity, LOPS, or PAD; high risk includes a previous history of amputation or ulceration along with the presence of any two of the following: LOPS, PAD, and lesions or deformities.⁹

The suggested frequency for follow-up is based on the level of risk. In the low risk state, an annual foot assessment should be performed as they could progress to a moderate or high risk state. Emphasis should be on daily foot inspection and monitoring glycemic control. Increased frequency of follow-up is advised in patients at moderate or high risk, such as those with a foot deformity or with a diagnosis of peripheral neuropathy or PAD at initial assessment. Repeat testing for neuropathy is not necessary if diagnosed previously. A quick inspection for a breach in skin integrity or ulceration should suffice. Patients with asymptomatic PAD may be followed up in primary care centers and managed as in guidelines for PAD. Patients with calluses and deformed toe nails should be referred to preventive podiatry services for basic nail and skin care, including debridement of calluses. A timely referral to the foot protection services for control of risk factors in patients with diabetes prevents infection, gangrene, amputation, or death and reduces hospital admissions.

Early and good glycemic control is effective in preventing peripheral neuropathy. Optimal blood glucose and glycated hemoglobin (HbA1c) targets should be discussed with patients and monitored as per the standard guidelines for diabetes care to prevent or slow the progression of peripheral neuropathy.6

People with diabetes or their caregivers, or both should be educated on the importance of blood glucose control and modifiable cardiovascular risk factors such as healthy eating habits and lifestyle patterns, regular physical exercise, maintenance of ideal body weight and cessation of smoking and alcohol. While offering modifications in lifestyle, one should consider the patient's cultural as well as religious beliefs and also the social and family support available.

Evidence for the effectiveness of patient education on foot care is lacking. Previously done randomized controlled trials have shown that brief foot care education alone does have a positive influence on patient knowledge and behavior on the short term, but it is ineffective in preventing DFUs. However, education in a structured, organized, and repetitive manner, combined with preventive interventions may prevent foot related problems.

Another less emphasized and ignored aspect of footcare is the usage of appropriate footwear. The sole should be neither too hard nor too soft with a Shore value between 8 and 15 A. Commercially available footwear are often occlusive and causing excessive sweating, thereby precipitating fungal infections, particularly in tropical countries. Bare foot walking is a major risk factor for a succeeding ulcer, especially in patients with neuropathy. Moreover, barefoot walking is rather common amongst people in the many indigenous populations. Patient compliance with regards to the prescribed footwear is usually poor, particularly at home and hence this should be reinforced. Patients with plantar ulcers at the forefoot or heel may be offered offloading footwear to allow ulcer healing and prevent recurrence.7

Patients with a life- or limb-threatening problem such as foot ulceration with fever or any signs of sepsis; ulceration with limb ischemia; gangrene, or a suspected deep seated soft tissue or bone infection indicated by either a grossly swollen foot with shiny skin and patches of discoloration or a gritty feel to the bone during a probe to bone test in an open wound should be immediately referred to a specialized diabetic foot center; which are frequently lacking.

Poor outcomes of foot complications in resource poor settings may include the shortage of trained healthcare workers for diabetes care, lack of awareness of footcare among patients and healthcare providers, non-existent podiatry services, shortage of medications and dressing supply, long distances for patients to travel to the clinic, delay by patients in seeking timely medical care or by untrained healthcare providers in referring patients with serious complications for a specialist opinion, lack of the concept of a team approach, absence of training programs for healthcare professionals and finally, a lack of surveillance activities.

Most ulcers may be prevented with appropriate foot care and screening for risk factors for “the foot at risk”, for complications. A good understanding of the various predisposing risk factors, would help in both prevention and treatment of this devastating medical condition.

Therefore, this book aims at providing a comprehensive approach toward the management of diabetic foot amongst those with limited health care resources through an integrated foot care program.