What Is the Concern with Diabetes and Wounds?

The foot is a complex target organ for diabetes, a multisystem disease. Peripheral neuropathy and peripheral vascular disease combined with excessive mechanical stress in diabetic patients can cause the destruction and deformity of the soft tissue of the foot and the bone and joint system, and then cause a series of foot problems from mild neurological symptoms to severe ulcer , Infection, vascular disease, Charcot joint disease, and neuropathic fractures. If active treatment does not adequately address the symptoms and complications of the lower extremities, the consequences can be disastrous. Therefore, it is of great significance to carry out early prevention and treatment of foot problems in patients with diabetes.

Basic Information

English name

diabetic foot, DF

Visiting department

Department of Vascular Surgery, Endocrinology

Multiple groups

Diabetics

Common locations

Lower limbs, feet

Common causes

Ulcers, infections, Charcot arthropathy, toe deformities, etc.

Common symptoms

Pain in the feet, intermittent claudication, decreased sensation, dry skin, muscle atrophy, etc.

Contagious

no

Causes of diabetic foot

Ulcer

Many foot complications in diabetic patients arise from sensory neuropathy and mild autonomic and motor neuropathy. Among them, sensory neuropathy combined with excessive mechanical stress is the main initiating factor that causes foot ulcers and infections. Inflammation and tissue damage are the result of a degree of repetitive stress acting on a specific area of loss of sensation. Pressure or shear from the ground, shoes, or other nearby toes cause ulcers, which are often exacerbated by the presence of bone processes due to a lack of normal neuroprotective mechanisms. Lesions of the autonomic nervous system cause the skin's normal sweating regulation function, skin temperature regulation function, and blood flow regulation ability to be lost, resulting in a decrease in the local tissue flexibility, the formation of thick palate, and more fragility and cracking. In addition, the loss of normal sweating ability blocks the rehydration of local tissues, causing further tissue damage and making deep tissues more susceptible to bacterial colonization. Motor neuropathy also plays a role in the pathogenesis of diabetic foot. The contracture of the foot's internal muscles causes a typical claw-shaped toe deformity. Metatarsophalangeal joint overextension has also been shown to directly increase the pressure on the metatarsal head, making it easier to form ulcers in this area. Proximal interphalangeal joint flexion increases the risk of ulcers forming on the dorsal and interphalangeal joints of protruding interphalangeal joints, and vascular lesions make it difficult to heal the damaged tissue.

2. infection

Autonomic dysfunction results in the destruction of skin and soft tissues, causing the invasion of foreign bacteria. Changes in chemical tropism lead to inefficient leukocyte response. In addition, hyperglycemia, reduced oxygen partial pressure, and malnutrition can cause tissue edema, acid accumulation, hypertonicity, and inefficient anaerobic metabolism. Such environments are suitable for bacterial growth and hinder the function of white blood cells. In addition, vascular disease can cause limited antibiotic transport, further reducing the efficiency of bacterial clearance, leading to local soft tissue infections and even the formation of osteomyelitis.

3.Charcot arthropathy

It is a progressive destructive disease of weight-bearing joints. The neurotrauma theory believes that repeated mechanical damage to the foot after a loss of pain and proprioception or a single trauma can cause Charcot joint disease; neurovascular theory believes that increased blood supply to the diseased area caused by autonomic dysfunction causes bone absorption and The intensity weakens, and further, repeated trauma causes bone destruction and instability.

4. Toe deformity

Motor neuropathy results in contractures of the foot's internal muscles, causing the typical claw-shaped toe deformity.

Clinical manifestations of diabetic foot

The clinical manifestations of diabetic foot are diverse.

Early

Changes in sensation are usually sock-like, involving the distal end of the limb and then progressing to the proximal end. Light touch, proprioception, temperature, and pain are all weakened; motor neuropathy is manifested by atrophy of the intrinsic muscles of the foot and claw-shaped toe deformities; autonomic nerve involvement is manifested by normal perspiration of the skin, loss of temperature and blood flow regulation, resulting in Local tissues are less flexible, forming thick ridges and are more fragile, broken, and cracked.

2. Late

In addition to the symptoms caused by the above-mentioned early neuropathy, ulcers, infections, osteomyelitis, and Charcot arthropathy can also occur.

Diabetic Foot Exam

Check-up

A thorough examination of the lower limbs of both knees should be performed. Examinations should be performed at least once a year, and should be more frequent for high-risk groups. The problems that need to be recorded are: abnormal gait, wear of shoes, and whether foreign objects protrude into the shoes, pulsation of blood vessels, hair growth, skin temperature and capillary refilling, observation of foot and heel deformities and tissue damage , The location and size of the ulcer, the presence of edema or inflammation. Also check joint stability and muscle strength.

2. Comprehensive neurological examination

Examination of reflex, motor and sensory functions. Qualitative sensory tests, such as touch, two-point discrimination, acupuncture, and proprioception. Quantitative sensory testing, most commonly using Semmes-Weinstein nylon monofilament for pressure testing.

3. Vascular examination

The most commonly used non-invasive test is arterial Doppler. The data is expressed by absolute pressure or ankle-brachial index. Ankle-brachial index of 0.45 is considered to be the minimum wound healing after amputation. The absolute value of toe vascular pressure reaches 40mmHg is the minimum value for wound healing standards. Note that patients with arteriosclerotic disease may exhibit a pseudo-elevated pressure value. Other vascular examinations include measurements of skin perfusion pressure and transcutaneous oxygen partial pressure. The former is a test to determine the minimum pressure required to block refilling of the skin after it has been compressed. The latter can also be used to determine the potential for healing after amputation. If the pressure is less than 20mmHg, there is a high risk of wound infection, while above 30mmHg indicates sufficient healing potential.

4. Laboratory inspection

Glycemic control is very important in the care of diabetic foot. If diabetes is poorly controlled metabolically there is a higher risk of ulcers. If hemoglobin A1c (glycosylated hemoglobin) is increased, the ulcer healing time is prolonged and the possibility of recurrence increases. Changes in these indicators are predictive of optimal patient compliance and healing. In addition, serum total protein, serum albumin, and total lymphocyte counts should be checked. The minimum value for tissue healing is: serum total protein concentration is higher than 6.2g / dl; serum albumin level is higher than 3.5g / dl; total lymphocyte count is greater than 1500 / mm ³ .

5. Imaging examination

General X-ray is a first-line diagnostic test used to evaluate stress fractures, fractures, osteolysis / bone destruction, dislocations, subluxations, and changes in bone and ankle bone structure; CT is used to assess the details and changes of cortical bone Better results, such as assessing the healing of fractures or fusions after surgery. In addition, CT can be used to evaluate soft tissue diseases such as abscesses; MRI is very sensitive to soft tissue and bone tissue changes caused by various reasons, such as stress fractures, abscesses, osteomyelitis, or neuroarticular disease. However, it is difficult to distinguish Charcot joints from osteomyelitis. Both lesions have bone marrow edema and erosion-like changes.

Diabetic Foot Treatment

Treatment of ulcer

According to the 6 grades of diabetic foot injuries, if a grade 0 wound has a risk of ulcers on the feet, it can be treated with modified shoes, mold-type pads or deepened shoes, and patient education and regular follow-up. Once skin cracking occurs, active intervention must be performed to prevent further damage. Methods for relieving external pressure on a Class 1 wound include wearing postoperative shoes, using ankle and foot braces, wearing prefabricated walking braces, or using full contact plaster. In addition to proper decompression of the compression site, proper ulcer wound care is needed to avoid tissue dehydration and necrosis of the tissue and accelerate wound healing.

Surgical indications are wounds that fail to improve local pressure or have a higher rating. Grade 2 and 3 wounds require surgical intervention. Grade 3 wounds require antibiotics and may require amputation. Compared with other parts of the body, hind leg ulcers require surgical intervention because local tissue is difficult to decompress and blood flow is poor. Surgical methods include debridement of ulcers, excision of osteoid processes, and correction of foot and ankle deformities. Correcting the claw-shaped or hammer-shaped toe can reduce the incidence or recurrence of dorsal ulcers on the forefoot. In addition, Achilles tendon extension can also be considered to reduce the pressure on the forefoot or midfoot.

2. Treatment of infections

Severely infected or abscess wounds should be aggressively debrided until they reach active bleeding tissue; debridement should not be limited to superficial skin tissue. Find a balance between maintaining stability and removing lesions. When performing abscess drainage, a vertical straight incision should be taken to increase flexibility and facilitate healing. Debridement in the area with osteomyelitis should be performed as wide as possible, and the balance between the stability of the foot and the removal of the lesion should be considered. In addition to surgery, severely infected wounds often require hospitalization for intravenous antibiotics. The timing of treatment and the choice of antibiotics should be based on the results of bacterial culture, the degree of infection, and the clinical response achieved by the treatment. In addition, consider consulting an infectious physician.

3.Charcot joint disease treatment

Most Charcot neuroarthropathy can be treated conservatively. Surgical fixation does not accelerate healing. In contrast, surgery may temporarily delay healing of the diseased area due to new instability and possible fractures around the internal fixation. Non-surgical treatment has been successful in more than 70% of cases. However, success rates were lower in patients with Charcot arthropathy of the hind feet and ankles. End-stage neuroarthropathy can leave serious deformities, requiring patients to continue wearing foot braces, such as rear shell-like ankle and foot braces, hind foot rests or special shoes to reduce the incidence of subsequent ulcers.

The initial treatment of acute Charcot joint disease includes strictly raising the affected limb, prohibiting weight bearing, and braking-it is best to use full contact plaster and change it often. To avoid increased pressure on the skin, do not perform closed reduction of the fracture. If the plaster is to be used continuously until the patient enters the chronic phase, it may take 6 months for the lesions of the forefoot and 24 months for the lesions of the hind feet and ankle to enter the chronic phase.

Although acute neuroarthropathy rarely requires surgery, the surgical indications are as follows: there is still impending or recurring skin damage after plaster fixation, acute reversible hindfoot or midfoot dislocation, and inflammation control. Significant instability or claudication of the foot, displaced fractures (such as the talus, calcaneus, or ankle) before Charcot neuroarthropathy, open fractures or open dislocations, Charcot disease with deep infections (such as Osteomyelitis or joint infection).

The surgical indications for patients with chronic neuroarthropathy are as follows: severe deformity and poor alignment, can not use braces or customized shoes (such as Schon C or B), ulcer recurrence, superimposed infection, instability, pain with deformity, can not Resume daily activities.

The options for Charcot's joint disease include osteotomy and joint fusion. Osteotomy can use strong internal or external fixation to obtain a wide bone surface to facilitate healing.

Diabetic foot prevention

The prevention of diabetic foot is of great significance. The risk of diabetic foot can be fundamentally reduced by actively controlling blood sugar. In addition, the patient needs to check the feet and shoes every day to find hidden tissue damage and increased mechanical stress in the shoes. By reforming the shoes, mold-type inner pads or deepening the shoes, it can effectively buffer the foot stress and provide support and protection.