Foot ulcers may appear long before they come in patient's notice. Elderly people may wrongly perceive signs and symptoms in lower limb as harbingers of senility and ignore a potentially correctable condition. Symptoms of peripheral neuropathy and arterial insufficiency precede ulcer formation. Ulcers most commonly occur on following sites:
Any diabetic patient having following signs and symptoms is susceptible to develop ulcers. Peripheral neuropathy, when present, will present with symptoms of altered sensations in limb. These include paresthesia, hypreresthesia, hypoesthesia and dysesthesia. Loss of sweating and cold extremities is signs of autonomic neuropathy. Muscles may be atrophied and limb posture (in supine position) or shape may be abnormal due to earlier complications. Moreover, diabetic patients very frequently present with symptoms of arterial insufficiency that may be:
Increased demand of muscle during exercise or activity, when not adequately met, will cause accumulation of lactic acid, hence causing pain of intermittent claudication. Patients with atherosclerotic disease can be without symptoms while some people can have frank ischemia. History should be aimed at these signs and symptoms, which may also be helpful in early diagnosis and prevention of later complications and/or recurrent ulcers.
Examination is done to assess vascular perfusion, peripheral neuropathy, signs of osteoarthopathy and infectious ulcers. Examination of ulcer is also done taking into consideration its site, shape, margins, edges and tissue present in ulcer bed. General examination of limb may reveal hammer toes, calluses, fissures, previous scars or brittle nails. Special attention should be paid to interphalangial space that may sometimes show ulceration or microbial infection.
Diabetic foot ulcer workup needs a good history along with complete general and local examination. History must involve questions regarding symptoms of neuropathy, vascular insufficiency and duration of diabetes. A detailed history of pain and redness must be taken. Foot ulcers and other complications are directly related to duration and severity of disease. Cold extremities, loss of sweating, brittle nails, fissures, hypertrophic calluses and history of past ulceration are very often described by patients. More often, physicians discover these signs in general physical examination. Patient may give a history of renal disease, eye problems or other diabetic complications. Medication history may also prove to be beneficial in certain cases.
After general physical examination, peripheral vascular system and peripheral nerves are examined . While examining peripheral vascular system, look for any change in color of limb, pigmentation, prominent veins, hair distribution, dryness, fissures, nail lesions, deformities of bones and ulcers or sinuses. While palpating, note temperature of skin and compare it with skin of opposite limb. An increased temperature is a sign of active inflammatory process, whereas dry, cold skin is indicative of ischemia and autonomic neuropathy in that area. Check and compare pulses in both limbs, including dorsalis pedis, posterior tibial, popliteal and femoral artery (note that during general physical examination, other pulses like radial, carotid etc are also checked). Tests for capillary refilling time, intermittent claudication and peripheral sensation should also be done. Interphalangial clefts should be looked for any hidden ulcers or lesions.
Ulcer examination is done with a sterile stainless steel probe. Look for site, color, any discharge (blood/pus), margins and edges of ulcer. Check the ulcer base for any granulation tissue, pus or bone showing from it. Sinus tracts progress from ulcer to underlying tissue and sometime into bones. Depth of sinus tracts must be assessed using stainless steel probe .
Laboratory investigations include routine investigations of complete blood count, Erythrocyte Sedimentation Rate (ESR), leukocytosis, blood and urine sugar and urine ketone bodies, electrolytes and creatinine levels. Hemoglobin A1C levels are monitored in order to check glycemic control in patients. Other tests, for renal and hepatic function, should also be done to ascertain patient’s metabolic status. Culture examination from samples taken from ulcer is not that much valuable as all ulcers harbor microorganisms. However, in case of secondary infection, that may help in identification and medical treatment.
Special investigations involve:
An infected wound may contain foreign particles, microorganisms, dead and necrosed tissue that hinder cell migration and inhibit healing. Debridement is removal of dead, damaged or infected tissue in order to promote healing in rest of tissue that is normal. It can be done in DFU using a sharp scalpel, ensuring effective removal of all the damaged tissue and, if necessary, some portion of surrounding tissue, since necrosis can extend beyond ulcer bed. This procedure is called surgical (sharp) debridement. Debridement can also be achieved through mechanical, medical, chemical, enzymatic or autolytic (self debridement) methods. In self debridement (used often), dead tissue is allowed to slough off while ensuring adequate care i.e., keeping it dry and infection free. Debridement is followed by dressing and topical wound coverage. The basic principle for topical wound management is to provide a moist, but not wet wound surface. Choice of dressing should be appropriate. Dressing may be wet or dry, depending upon the material used. Following types of wound dressing can be used:
Medical treatment aims at:
For surgical management, patient should first be evaluated by a vascular/podiatric/orthopedic surgeon. Perioperative management, especially a strict glycemic control in patients before and after operation, is both an imperative as well as a complicated procedure. Objectives of surgery in these patients are debridement, vascular reconstruction, revisional surgery for bony architecture or providing soft tissue coverage with grafts, such as skin grafts. Wound closure is done when maximum antiseptic milieu and sufficient granulation tissue is available in wound. It may require grafting healthy skin flap or artificial graft materials, while in case of small wounds, primary closure is also possible. Osteomyelitis and cellulitis requires debridement, reconstruction and revisional surgery. Purpose of revisional surgery may be to remove pressure points in bones that may prone patient to future ulcerations. Vascular reconstruction, in the form of angiography and by-pass surgery, is done to tackle impending ischemia of tissues. Adequate blood supply and nutrition is also necessary for effectiveness of other treatments such as grafting. Amputation is considered when other medical and surgical procedures are of no value, to avoid long term morbidity, and when long-term wound care is not possible.
Offloading of ulcerated area is done to treat and prevent future injuries to foot. Custom designed shoes, soft heeled shoes, padded socks and shoe inserts, contact casts and removable cast walkers are used. These aids help to redistribute pressure over a comparatively larger surface area and prevent excessive pressure at one point. They also accommodate deformities of Charcot foot and avoid friction.
Uncontrolled diabetes correlates with a proportionate early onset of complications. Concurrent hyperlipidemia and hypertension further increase the risk. A regulated glycemic control can help protect patient from microangiopathy, neuropathy, retinopathy and nephropathy. Treatment of diabetic foot ulcer is along following lines:
DFU can develop infection or can turn into chronic ulcer if treatment is inappropriate or delayed. Patient must consult a physician on noticing an ulcer or sore area in foot. If pressure points have developed symptoms i.e., areas that repetitively come under pressure show change in color or are painful, they should not be ignored. Fractures, osteomyelitis or sepsis are frequent complications. If treatment is sought early, foot ulcers can be treated effectively and complications can be avoided, which, once developed, cause significant morbidity; sometimes amputation of foot may be the only treatment option. In some cases, a benign looking ulcer may turn out to be a grievous danger to health of patient. Treatment of DFU may be protracted over several weeks due to impairment of healing mechanism.
Diabetes is the most common cause of non-traumatic lower limb amputation. Risk factors and etiologies for diabetic foot ulcers are peripheral neuropathy , vasculopathy , excessive pressure at certain points in foot  and deformities of foot . Peripheral neuropathy, a common complication of persistent high glucose level in blood, is found to be present in 60% of diabetic patients. It can present with motor, sensory or autonomic neuropathy, involving a single nerve or multiple peripheral nerves. In the face of vascular insufficiency, ischemia of tissues, including nerves, occurs. Charcot foot, also known as Charcot osteopathy/Neuropathic osteoarthropathy/Neuropathic osteopathy is a term given to a collection of bone and soft tissue abnormalities in foot with unique clinical presentations. It is present in about 2% of diabetic patients. Bone and joint deformities that occur in a patient with peripheral vasculopathy and neuropathy gives rise to this condition. Foot assumes a characteristic shape, in which dorsum is dome-like and bottom is more concave than normal, while toes are splayed out (in most cases). Ankle mortise may also be displaced. Charcot foot is often accompanied by ulceration in foot (commonly involving toe and medical or inferior aspect of foot). Foot ulceration is the most common cause of hospitalization in diabetic patients.
In the United States, 16 million people suffer from diabetes mellitus. Diabetes is the major contributor to morbidity in Western world and its incidence is increasing throughout the world due to changes in lifestyle, diet and habits of people. Prevalence of DFU is highest in Native Americans, Latino communities of the Eastern United States, and in African Americans . With increasing incidence and prevalence of obesity, hyperlipidemia and hypertension, non-familial incidence of diabetes is increasing, even in children and young adults. In United States, 10% people have type 1 diabetes, called insulin dependent diabetes mellitus and they are usually diagnosed before 40 years of age. However, genetic predisposition is higher in non-insulin dependent diabetes mellitus. Among patients with diabetes, foot ulceration is seen in 15% of patients.
Peripheral neuropathy open link, a complication of diabetes, occurs in 60% diabetics, as described above, and it usually follows within 10 years of onset. About 80% patients with this complication come up with ulceration. Throughout the world, 12 to 24% of the patients of diabetes undergo amputation (incidence of 1% every year).
Diabetic foot ulcer is characterized by a classical triad of vasculopathy, neuropathy and infection. Wound healing is a normal process that may be hampered by some physiological insult, resulting in persistence of wound. An ulcer is a break in the continuity of epithelial lining. Persistent high glucose levels in blood presumably prolong healing process and delay the formation of granulation tissue. Diabetes mellitus also prolongs inflammatory phase in wounds, retards the formation of granulation tissue and causes a parallel reduction in wound tensile strength .
High blood glucose can cause hypertension and atherosclerosis with resultant arteriolar hyalinosis, endothelial proliferation and increased thickness of basement membrane. Tunica media may also be involved, which undergoes thickening and calcification (Monckeberg sclerosis). Decreased nutrition supply disrupts myelin synthesis in nerves and hampers the function of sodium potassium ATP-ase. Increased amounts of sorbitol and fructose are also detrimental and hyperosmolar state also causes edema in nerve trunks, and together these changes lead to neuropathy of diabetes, which can involve one or more sensory, motor or autonomic nerves . Thus, hyperglycemia induced by microangiopathy causes metabolic, ischemic and immunological injury to motor, sensory and autonomic nerves.
Sensory neuropathy is manifested as reduced sensations in foot; patient may not notice an injury or trauma to foot. Sometimes persistent trauma that occurs with the use of ill fitting foot wear produces ulceration in foot that may not be noticed by patient. Motor neuropathy in patient causes weakness of intrinsic muscles of foot, while osteoarthropathy weakens bones. All these effects together cause splaying. Upper part becomes convex, dome shaped and foot has a rocking bottom, this characteristic shape is called Charcot foot. Weakness of bones can cause bending or fractures; pressure points are produced inside foot, which if present in weight bearing regions or undergoing repetitive trauma can give rise to ulceration. Fractures usually go unnoticed until marked foot deformity becomes apparent. Sometimes sinus tracts form that lead to underlying bone.
80% of foot ulcers can be prevented through following measures:
Podiatric care is essential. By routine inspection, regular follow up and with patient education, physician can help patient develop good foot-care habits. Routine inspection and examination of feet, by a physician in a clinic, is preferable, although patient or a caretaker can also carry out inspection at home. Foot care should include regular, gentle cleansing of feet with water and afterwards application of a mousturizer. Patient's foot should be inspected for any pressure sore, minor ulcers, skin dryness, pigmentation, change in color or any of other deformities described above. Custom shoes can be utilized, particularly by those in whom a risk factor has been identified by physician. Purchase of custom foot wear is covered for patients by Medicine Part B, provided an ulcer risk factor has been identified by a certified physician and appropriate documentation has been submitted. A moist foot environment and use of topical antibiotics can help prevent foot ulcers. Minor injures should not be ignored. Patients should be educated to avoid use of home remedies, which can sometimes exacerbate an injury in immunocompromised patients of diabetes.
Diabetes mellitus (DM) is a complex and serious disease with high rates of morbidity and mortality in patients. This pathological condition involves almost all the vital organ in the human body. DM accounts for around 40-60% of lower extremity amputations and most of these amputations result from deterioration of foot ulcer. Extracellular matrix forms largest part of dermal skin  and defects in its repair can result from various physiological insults, a well as pathological and aberrant metabolic processes; Diabetes mellitus being one of them. Diabetes mellitus disturbs normal healing mechanism by causing delay in granulation tissue formation and reduction in wound tensile strength .
Diabetic foot ulcer, a complication of diabetes mellitus, affects about 15% of patients of diabetes mellitus. Persistent high level of glucose in blood interferes with normal metabolic and healing processes in our body. It results in an abnormal blood supply to body organs, accumulation of harmful products and delayed healing of wounds. Ill fitting shoes, smoking and other risk factors like cardiovascular diseases, hyperlipidemia, hypercholesteremia, hypertriglyceridemia, hypertension and certain hereditary conditions, if concurrently present, may increase the chance of developing these ulcers by many folds. Diabetic foot ulcers account for 80% of leg amputations in the United States.
DFU develops when blood supply to lower extremities has been compromised to such an extent that it causes damage to nerves, bones and soft tissue. Due to altered nerve function, patient does not notice a blister or sore that, if not detected, can lead to infection and aggravation of condition. A limb that is prone to ulcer development may present with one of following symptoms:
Moreover patient can have difficulty in walking. Ulcers and blisters may come into patient's notice late, when signs and symptoms of infection appear. Diagnosis is made by physicians on examination. Further investigations may be required in order to identify the cause/causes of ulcer formation e.g., X-ray, CT, MRI or Doppler's Ultrasound studies. Specimen from a wound will be required for prescription of an antibiotic. Blood glucose and HbA1C are tested for assessing glycemic control in patients.
Treatment is through wound debridement, antibiotics, regular dressing change, offloading of foot and surgery, if other strategies are not sufficient. Skin grafting, hyperbaric oxygen therapy, arterial reconstruction and revisional surgery for bones and joints may also be suggested depending upon the condition of limb and prognosis after treatment. DFU can be prevented by maintaining foot hygiene, meticulous wound management and care, and control of diabetes.