Overview
Diabetic patients often suffer from long-term disorders of blood glucose and lipid metabolism, which can easily lead to vascular endothelial cell and basement membrane damage, resulting in diabetic vascular complications. diabetic patients with DM develop combined neuropathy and vascular disease of varying degrees, resulting in lower limb infection, ulcer formation, and/or deep tissue destruction called diabetic feet DF. It is highly disabling and fatal, with a high amputation rate of more than 20%, often ending in amputation and death.
Etiology
Diabetic foot lesions are predominantly neuropathic; physical factors account for 60% to 80% of the various triggers of diabetic foot.
Foot ulceration or gangrene occurs in 15% to 20% of diabetic patients during the course of the disease. The probability of gangrene is 40 times higher in diabetics than in the general population. Neuropathic ulcers are more common in patients with diabetic foot, accounting for about 64% (with mixed diabetic foot accounting for about 31%) and ischemic diabetic foot accounting for about 36%. The prognosis of neuropathic foot disease in patients is better than that of vascular foot disease, while the prognosis of mixed foot disease is the worst.
Physical factors contributing to foot ulcers in patients accounted for 62.4% to 84.9%, of which physical injuries such as burns, wearing inappropriate footwear and improper toenail trimming were avoidable. Nearly half of the patients’ foot ulcers were concentrated on the first toe, which may be related to the higher pressure load on the first toe. Another study found that the degree of foot ulceration was closely related to the degree of systemic neuropathy, ischemic lesions and economic income.
Physiopathological changes
Although foot damage varies widely by country and region, the pathways that cause foot ulcers are similar in most patients. Diabetic foot damage is usually the result of two and more factors. Diabetic peripheral neuropathy plays a major role in diabetic foot damage in most patients, and up to 50% of patients with type 2 diabetes have neuropathy and risk factors for podiatric disease. Neuropathy makes the foot insensitive and even causes foot deformity with abnormal gait.
In patients with neuropathy, minor injuries such as ill-fitting shoes, barefoot walking or acute trauma can cause chronic ulcers, sensory deficits, foot deformities and impaired joint movement can cause biomechanical (pressure) abnormalities in the foot, resulting in local skin thickening, which further aggravates the pressure abnormalities in the foot and eventually causes subcutaneous hemorrhage. In addition, long-term hyperglycemia leads to the proliferation of small blood vessel smooth muscle cells and the thickening of capillary basement membrane, resulting in diabetic arteriosclerosis, narrowing of the vascular cavity and easy formation of thrombus, causing the microcirculation to become impaired, local tissue ischemia and resistance to decrease, and small trauma can cause infection and ulcer formation.
Regardless of the primary cause, patients continue to walk with poor blood supply and insensitive feet, making local injuries less likely to heal. Wound healing is strongly influenced by blood glucose levels, with blood glucose greater than 300 mg/dL reducing the bactericidal capacity of leukocytes and directly affecting wound healing. High blood glucose can also cause joint and tendon stiffness by binding to collagen and reducing its intrinsic elasticity. Approximately 60% of diabetic ulcers lack blood supply due to the presence of peripheral vascular disease. Typically, atherosclerosis occurs in the lower N artery including the anterior tibial artery, posterior tibial artery and peroneal artery. In addition, due to high blood glucose levels, sugar binding to red blood cells causes increased blood viscosity and decreased red blood cell deformability, resulting in reduced capillary blood flow and decreased oxygen consumption in local tissues.
Peripheral vascular lesions, usually accompanied by microtrauma, may cause pain and simple ischemic foot ulcers. However, patients with a combination of neuropathy and ischemic lesions (neuroischemic ulcers) can be asymptomatic despite the possible presence of severe peripheral ischemia. Therefore, microangiopathy is not a major cause of ulcers.
Physical examination
1. Ulcer description
The ulcer is carefully evaluated by measuring the area and depth of the ulcer. Area = long axis of the ulcer * wide axis. Depth is assessed by the level of soft tissue involved in the ulcer: epidermis, dermis, subcutaneous fat, deep fascia, muscle, tendon, joint capsule, joint and bone. A metal probe helps to determine the depth of the ulcer, and if bone is probed, the incidence of osteomyelitis is up to 85%. If tendons are involved, there is a high probability that the infection will spread to the proximal or distal end of the tendon, and the surgeon should carefully examine the distal and proximal segments of the suspected tendon sheath. If there is a greater likelihood of distal infection spreading proximally, the proximal tendon sheaths that are susceptible to spread (e.g., extensor support band, ankle canal) should be examined. Photograph the ulcer at the same time.
It is important to distinguish cellulitis from chronic ulcers and redness due to chronic ischemia. If the erythema disappears after elevating the affected extremity above the plane of the heart, the erythema is subordinate in nature, usually not due to inflammation, and the skin may appear wrinkled. If the erythema persists, it indicates cellulitis around the wound and requires antibiotic treatment with or without surgical debridement. Adjunctive erythema can also occur after the initial surgery and should be differentiated from postoperative cellulitis.
Based on the clinical presentation Wagner classified diabetic foot into 6 stages i.e. normal foot, high risk foot, ulcerated foot, infected foot, necrotic foot and irretrievable foot. Wagner’s grading of ulcers was also performed.
Grade 0: The skin of the foot is intact, there may be multiple foot deformities and hyperkeratosis, and there may be signs of hypoesthesia or sensory hypersensitivity.
Grade 1: superficial skin ulcers only
Grade 2: deeper ulcers involving the Achilles tendon, bone, ligament or joint
Grade 3: deeper damage including abscesses and osteomyelitis
Grade 4: gangrene in part of the area
Grade 5: gangrene occurs in most of the area
The purpose of the classification is to clarify treatment options and prognosis. Of course, the coexistence of different degrees of pathological changes (ischemia, neuropathy and infection) affects the standardization of treatment. In the management of the ulcerated diabetic foot, it is important to first clarify whether the ulcer is primarily neurotrophic or ischemic; whether it is limited or is about to form a deep abscess involving multiple layers of tissue; and whether there is osteomyelitis or septic arthritis, which will help to develop a rational treatment plan.
The classification of diabetic foot ulcers developed by Brodsky does not include gangrene. In this scheme, grade 0 skin is intact but shows pre-ulcer damage with skin erythema, callus formation, and possibly intradermal blood blisters at the site of bony prominence; grade 1 is a superficial but deep ulcer that reaches the entire skin without penetrating the subcutaneous tissue; grade 2 ulcers reach deep into the tendons and joint capsule, but there is no joint or bone exposure; grade 3 ulcers include bone or joint exposure, osteomyelitis, or septic arthritis.
2.Foot examination: mainly check the deformity of the foot present
In China, most of the foot deformities in diabetic patients are caused by neuropathy. Of course, there are also some deformities existing before the onset of diabetes, which may be related to genetics, improper shoe wear, trauma or muscle ligament dysplasia. In addition, spinal cord dysplasia, Lyme’s disease, alcohol and drug-related neuropathy, and leprosy can also cause neuropathy.
Early motor neuropathy manifests as intrinsic muscle atrophy and clawed toes. Late neuropathy occurs as an episodic neuropathy, which in turn leads to loss of balance in the extrinsic accessory muscles. The main dorsal flexor muscle, the tibialis anterior, may be infected first, resulting in relative overstretching of the gastrocnemius, hallux valgus, and peroneus longus muscles, which in turn causes static or dynamic horseshoe foot contractures of the ankle.
By examining the range of motion of the ankle joint, it is possible to understand the extent to which contracture of the gastrocnemius and hallux valgus muscles affects forefoot ulcer formation. As diabetes affects the elasticity of the Achilles tendon, it can be carefully evaluated by dorsiflexion test and posterior rotation test of the foot. If the dorsiflexion of the foot exceeds 15° in knee extension and flexion, the Achilles tendon is elastic. If dorsiflexion is only possible in knee flexion, the gastrocnemius portion of the Achilles tendon is too tight. If dorsiflexion is not possible with either the knee flexed or the foot extended, both components of the Achilles tendon are overtight.
Two other dynamic contractures may also be associated with forefoot ulcer formation. Relative overstretching of the long bunion flexor can lead to ulceration in the typical interphalangeal joint position of the bunion. This ulcer may also be combined with structural bunion stiffness, and therefore, passive dorsiflexion of the first metatarsophalangeal joint should be understood. Overstretching of the peroneus longus muscle may cause ulcer formation below the first metatarsal head-seed bone.
When one metatarsal is anatomically longer or lower than the others, it can lead to ulcer formation under the head of the other metatarsals. Claw toe caused by muscle atrophy displaces the metatarsal fat pad and increases the pressure on the subtalar aspect of the metatarsal head. Frank dislocation of the MTP joint significantly increases the pressure under the affected metatarsal head and is strongly associated with metatarsal ulcers. Forefoot ulcers are not only seen on the metatarsal side of the foot, but can occur between the toes where pressure is increased or between the toe and the shoe.
Ancillary examinations
Body fluid and tissue examination
1.Blood routine and blood sedimentation examination: it can understand the patient’s white blood cell level and neutrophil ratio, and determine whether there is infection and the effect of treating infection.
2.Ulcer secretion culture and drug sensitivity test: It helps to understand the category of pathogenic bacteria and optimize antibiotic treatment.
3.Tissue biopsy: It is very important during ulcer treatment, not only to obtain information about deep lesions, but also to release bony compression.
Imaging examination
1.X-ray: X-ray orthopantomographs can help to understand the presence of bone destruction and the coexistence of Charcot’s arthropathy. However, the false-negative rate of x-ray is higher in the early stage of ulceration that spreads to the bone.
2. CT examination: It can provide a more detailed understanding of the degree of bone destruction, the extent and the degree of concomitant Charcot arthropathy, and the typing. To guide the follow-up treatment.
3.MRI: This examination is generally necessary to understand the location and extent of deep abscesses in the foot and the extent of ulcer spread (such as the extent of spread of ulcers and abscesses along the flexor tendon sheath to the proximal end) when deep infection cannot be determined. In addition, it helps to diagnose bone infection.
4.Triphasic technetium 99 bone scan: has the same high false positive rate for osteomyelitis. Combining technetium 99 bone scan with leukocyte scan of labeled indium helps to detect osteomyelitis. However, this dual scan is more time consuming and costly.
Peripheral vascular examination
1. Palpation of the dorsalis pedis artery and posterior tibial artery pulsations for large vessel lesions in the foot is an easy, traditional and clinically valuable test. The disappearance of these arterial pulsations often indicates that the patient has a serious lesion and needs to be closely monitored or further examined, such as checking Doppler manometry.
2.Ankle-brachial index, i.e., ankle artery-brachial artery blood pressure ratio (ABI): By measuring the blood pressure in different planes of the limb, the degree of arterial patency and the site of stenosis or obstruction can be determined, which is a very valuable indicator of the vascular status of the lower limbs. The normal value is 1.0 to 1.4.