The test consists of cases within the following ulcer etiologies. During the course of the test, you will have the opportunity to read about the different etiologies, but you can also read here without answering the questions.
Ulcer healing can be delayed by healing inhibitory factors. A prerequisite for ulcer healing is rectifying the cause of the ulcer. For example pressure in pressure ulcers, venous or arterial insufficiency in venous and arterial ulcers and so on. There are also factors that inhibit ulcer healing regardless of the etiology, such as ulcer pain, hypoxia, necrosis, infection (see the different etiologies), certain medication, nutritional deficiency, dehydration and inappropriate dressings.
Lifestyle can affect ulcer healing both in a positive and negative direction. The negative factors include smoking, lack of exercise, impaired mobility and poor nutrition, while the opposite of these are positive factors
As we grow older, some characteristic changes occur in the skin. These have implications for the wound healing process. The skin's restorative ability decreases with age as both the inflammatory phase, the proliferative phase, and the remodeling phase change. Increasing age causes reduction of collagen and elastin, which lead to a more fragile tissue and deteriorating ability to transport nutrients. In addition, approximately 20% of older people have impaired peripheral circulation, which reduces oxygenation in the tissue and increases the risk of, for example, infectious complications.
Many diseases can affect both the onset of ulcers and impaired wound healing, such as diseases leading to bone and joint deformities, poorly regulated diabetes and renal failure. Poorly regulated diabetes also increases the risk of infectious complications.
Some drugs may, at least in theory, delay wound healing, like nonsteroidal anti-inflammatory drugs, steroids in high doses, immune-suppressing drugs, anticoagulants and chemotherapy. It is important to reflect on possible connections between drugs and delayed wound healing.
Patients with hard-to-heal ulcers often suffer from pain. Pain is a subjective experience that has to be taken seriously. Untreated pain has harmful effects on wound healing, why painful ulcers have a prolonged healing time. This can partly be explained by the fact that stress hormones (catecholamines) affect the capillaries in the surface of the ulcer so that they contract, which leads to a decrease in oxygen and nutritional supply to the wound area. This in turn also increases the risk of ulcer infection. Pain often affects the patient’s quality of life with impaired mobility, reduced appetite and sleeping disorders, which may contribute to delayed ulcer healing (see above under Lifestyle).
In recent years, research on the importance of the nutritional condition for ulcer healing has intensified. Malnutrition leads to delayed ulcer healing, which is why it is important to quickly identify patients with risk factors for malnutrition. Please note that even obese people may have a lack of nutritional intake.
Pressure ulcers are defined as localized injury to the skin and/or underlying tissue as a result of pressure, shear, or pressure in combination with shear (when the skin is shifted in relation to the underlying tissue).
Pressure ulcers are usually caused by immobilization when impaired mobility and/or impaired skin sensation prevents spontaneous offloading. Pressure and shear, especially over a bony prominence, increases the risk of impaired blood circulation to the tissue.
Risk factors correlated to pressure ulcers are exposure to moist, rise in temperature and malnutrition. Pressure ulcers can be located anywhere on the body and it is not uncommon for a patient to have more than one pressure ulcer.
Pressure ulcers are classified in 4 categories.
Intact skin with non-blanchable redness over a localized area usually over a bony prominence. Dark, pigmented skin may lack this sign, but the colour differs from surrounding skin area. The area may be painful, firm, warmer or cooler as compared to adjacent tissue. A category 1 pressure ulcer may indicate that the person is at risk of developing a deeper pressure ulcer or that pressure damage has already occurred deep in the tissue.
Partial-thickness skin loss presenting as a shallow open ulcer with a red pink wound bed without fibrin. The skin may also be intact with a serum- or blood-filled blister. Category 2 should not be used to describe skin tears, tape burns, incontinence dermatitis or maceration.
Subcutaneous fat may be visible, but bone, tendon or muscle never show. There may be visible fibrin which does not hide the depth of the damage. May include undermining or tunneling. The depth of a category 3 pressure ulcer varies by anatomical location. The bridge of the nose, ear, occiput and malleolus do not have subcutaneous tissue and category 3 pressure ulcers may be shallow in these locations. In contrast, areas of significant adiposity can develop very deep pressure ulcers.
Full thickness tissue loss with exposed bone, tendon or muscle. Necrotic tissue is common. Often includes undermining and tunneling. The depth of a category 4 pressure ulcer varies by anatomical location. Risk of osteomyelitis/osteitis.
Pressure ulcers require offloading and good nutritional status to heal.
The local wound management is of importance. This includes debridement, that is, removal of dead tissue, and offloading. In the event of pressure ulcers on the lower leg/foot, the arterial circulation should be assessed.
Pressure ulcers are contaminated by the skin's normal bacterial flora and sometimes, almost exclusively after antibiotic treatment, of gut flora including Escherichia coli, Klebsiella species and Pseudomonas aeruginosa. These bacterial findings are usually of no clinical importance. Only consider a bacterial culture if there are obvious signs of infection such as localized swelling, erythema, increased warmth, increased exudate, pain, fever, generalized symptoms and increasing levels of C-reactive protein (CRP).
In the event of antibiotic treatment, this should be systemic. Topical antibiotic treatment with for example fusidic acid should not be used due to the risk of sensitization and resistance development.
If the healing process has stopped the diagnosis has to be reconsidered.
Pressure ulcer prevention is of extreme importance.
Venous ulcers occur from venous insufficiency, usually due to varicose veins but also due to post-thrombotic syndrome. Among lower leg ulcers, venous ulcers are the most common. Pitting edema and eczema are often present. The ulcers are often hard to heal and are mainly located in the gaiter area of the leg, characteristically around the malleoli. It is always a good idea to measure the ankle-brachial blood pressure (ABP) to exclude an arterial component.
Atrophie blanche as well as lipodermatoscleroses can occur. Atrophie blanche is white scarlike areas with enlarged capillaries where painful ulcers can occur. Lipodermatosclerosis is an inflammatory process, often initially with bright red sore lesions that are easily mistaken for erysipelas. Eventually the skin becomes hard.
Adequate compression therapy is by far the most important treatment for venous insufficiency. A lower grade of compression is used in concomitant slightly impaired arterial circulation. Compression therapy is contraindicated in cases of severe arterial insufficiency. According to international guidelines, patients with venous ulcers should be referred to a vascular surgeon within two weeks. The reason for this is that a long ulcer duration predisposes for a longer ulcer healing time.
With modern minimally invasive surgical methods, elderly and fragile patients can be treated as outpatients, even during ongoing anticoagulant treatment. The purpose of the surgical interventions is to eliminate or reduce the venous reflux or open up obstructions.
If the patient has varicose veins and a typical clinical picture pointing at a venous leg ulcer, no further investigation is needed prior to referral to a vascular surgeon. A duplex ultrasound scan may be performed in case of uncertainty regarding the ulcer etiology. A medical history of venous ulcers constitutes a very high risk of recurrence, why the patient should continue treatment with compression therapy.
Long ulcer duration may predispose for malignancy such as squamous cell carcinoma. Biopsy should be considered at prolonged healing and more specifically when the clinical picture is altered with exophytic tissue and hypergranulation.
Every hard-to-heal ulcer is contaminated by bacteria. Ulcer infections of clinical importance are relatively rare in venous ulcers. Exudate and yellow fibrin coating are normal findings in the healing process. Slightly increased pain, exudate and erythema can usually be handled by intensified topical treatment and adequate compression therapy. When the ulcer is contaminated by Pseudomonas aeruginosa, the use of topical acetic acid solution could be a good alternative.
Only in the event of severe deterioration, generalized symptoms or when 2 weeks of intensified wound management has failed, a bacterial culture and systemic antibiotic treatment should be considered. Topical use of for example fusidic acid should be avoided.
Note that erythema more often is due to eczema than to infection.
Arterial ulcers are caused by atherosclerotic changes in medium and large sized arteries. They typically occur as multiple, deep ulcers over the toes, heels, bony prominences or on the soles of the feet, but they may also occur on the lower leg. The ulcers sometimes expose underlying tendons and appear “punched out”, with well demarcated edges and often with black or yellow necrotic tissue. The affected extremity is often pale and cold, but there is rarely eczema. Arterial ulcers are often very painful, especially at night or when the foot is in a high position. Pain relief can be achieved with the leg being lowered.
Examination of the ulcer includes palpation of peripheral pulses (arteria femoralis, poplitea, dorsalis pedis and tibialis posterior) which is helpful in assessing the peripheral circulation. The peripheral circulation should be measured using a blood pressure cuff and a Doppler and be compared with the blood pressure in the upper arm. The ratio between the two is called the ankle-brachial pressure index (ABPI), where an index of ≤ 0.8 is considered the lower limit for full compression treatment. Falsely elevated index may appear when the arteries are calcified.
Toe blood pressure (TBP) and toe-brachial index (TBI) are considered more accurate in assessing lower extremity perfusion in patients with a falsely elevated ABPI due to medial arterial calcification, which is not unusual in patients with diabetes-related foot ulcers. Edema may also occur in strictly arterial ulcers due to an inflammatory reaction or heart disease. The degree of compression has to be based on the state of the peripheral circulation. Further investigation of the circulation may be done by a specialist in clinical physiology.
In general, vascular surgery is needed to heal arterial ulcers. This can be performed in even old and fragile patients by using minimally invasive methods. It is important to treat risk factors for atherosclerosis such as smoking, hypertension, hyperlipidemia and diabetes. Pain relief, mobilization and adequate nutrition are also required for ulcer healing.
There is a risk of developing clinically significant infections in ulcers with necrosis, but in general there is no need for antibiotic treatment in arterial foot and leg ulcers. In order to reduce the need for antibiotics, it is important to continuously remove necrotic tissue, which can be a breeding ground for infection. Every hard-to-heal ulcer is contaminated by bacteria, which is not synonymous with an infection.
Increasing pain, erythema, swelling and secretion are signs of ulcer infection. Note, however, that a foot with chronic ischemia may be red without infection, due to compensatory capillary dilatation. In case of an infection, a bacterial culture should be obtained, but local ulcer infections can usually be treated with intensified topical treatment. In the event of fever, impaired general condition or widespread infection, systemic antibiotic treatment should be considered.
Diabetes-related ulcers are usually located on the foot. In diabetes, there is often neuropathy and angiopathy (micro as well as macro) which increases the risk of foot deformity, ulcers and infection. For patients with poor diabetes control, there is an additional increased risk of severe infections as high blood glucose impairs the immune system as well as the capillary oxygenation. Angiopathy, neuropathy and infection result in poor ulcer healing. Diabetic foot ulcers are thus complex. Appropriate assessment and treatment must not be delayed due to the high risk of prolonged ulcer healing and amputation.
Diabetes-related foot ulcers should be referred to a multidisciplinary specialist team if improvement hasn’t occurred within 1-2 weeks. In the event of signs of ischemia with infection or in severe infection, the patient should be referred immediately. Adequate and prompt treatment often leads to ulcer healing with reduced ulcer area and reduction of symptoms within a couple of weeks. Every hard-to-heal ulcer is contaminated by bacteria. Consider a bacterial culture only at signs of ulcer infection.
Infection is defined as the presence of at least two of the classic symptoms: swelling, warmth around the ulcer, redness, pain, increased secretion and impaired blood glucose control. In case of deep infection/abscess, fever, generalized symptoms and pain in depth during palpation, often occur. Visible bones or bones felt by a probe, are by definition osteitis, which must also be suspected if deep ulcers are located close to bones. Osteitis means antibiotic treatment for 3-6 months, why it is important that the diagnosis is properly assessed and that treatment is thoroughly evaluated.
If infection is suspected, treatment should include systemic antibiotics (preferably oral) according to the results of the bacterial culture. If severe infection is suspected, the patient should be referred immediately to a multidisciplinary specialist center. Topical antibiotic treatment with, for example, fusidic acid should not be used due to the risk of sensitization and resistance development.
Consider bacterial cultures during treatment only in cases of delayed healing or impaired clinical status. Change of antibiotics should be done only after assessing the relevance of any secondary pathogen. Be generous in referring patients with diabetes-related foot ulcers to a multidisciplinary specialist team. Prevention of foot ulcers is of uttermost importance through optimal metabolic control and information about self-care.
Annual risk assessment of foot status in patients with diabetes mellitus should be carried out to identify the risk groups classified as 1-4: risk group 1= healthy foot, risk group 2= neuropathy and/or angiopathy, risk group 3= previous foot ulcer, risk group 4= present foot ulcer (Swedish National Diabetes Register (NDR)).
Refer patients in risk group 2-4 to a podiatrist, and to an endocrinologist or orthopedic surgeon for appropriate offloading insoles or orthopedic shoes.
Basal-cell carcinoma is the most common type of skin cancer in Sweden. It occurs slightly more often in men than in women, and especially after the age of 40. It is a slowly but destructively growing skin tumor that occurs mainly on sun-exposed surfaces but is unlikely to spread to distant areas or to result in death.
There are four classifications of BCC according to histopathology.
Low aggressive and accounts for 50% of all BCC. Individuals with a basal-cell carcinoma typically present with a shiny, pearly skin nodule with small blood vessels in the edge of the nodule, sometimes with ulceration.
Low aggressive and accounts for 20 to 25% of all BCC. It occurs most commonly as an erythematous and scaly skin lesion.
Rather aggressive and accounts for 10 to 20% of all BCC. It occurs as a firm skin lesion most commonly not erythematous nor scaly.
Highly aggressive and accounts for 10 % of all BCC. It can present as a skin thickening or scar tissue and can be difficult to delimit to healthy skin. It may extend into the subcutis, cartilage, muscles and bone. The patient should always be referred to a dermatologist.
Consider a skin biopsy for histopathology and then a standard surgical excision of the whole skin lesion using sufficient margins depending on the type of BCC: 2-3 mm for Glas IA and IB, 5-7 mm for Glas II and III, and send the sample for histopathology.
If the excision is easily done in its entirety, by a 2-3 mm margin, this can of course be made as the first step. Always send the skin lesion for histopathology to decide type of BCC, radicality and for possible additional treatment.
Having a BCC is a risk factor for developing additional BCC, why it is important to check the whole body for more skin tumors and to inform the patient of self-checks in low-risk basalioma (type IA and IB according to Glas).
Squamous-cell carcinoma is the second most common skin cancer after BCC. SCCs arise from squamous cells in the outer layers of the skin. It mainly occurs after prolonged sun exposure but also in hard-to-heal lower leg ulcers (Marjolin's ulcer). Clinically, squamous cell carcinoma occurs as an irregular, solid tumor with a central ulceration and/or crust. The emergence of turgid tissue at the edge of an ulcer should arouse the suspicion of SCC and lead to a biopsy. Squamous cell carcinoma is locally destructive and can metastasize.
The diagnosis is assessed by a skin biopsy. The patient must be referred to a dermatologist. Squamous cell carcinoma is treated by radical excision.
It is not unusual that ulcers on the lower legs are caused by a combination of arterial and venous insufficiency. Most often, however, one of the conditions is predominant and thus decides the treatment strategy.
See the chapter arterial and venous ulcers.
Erysipelas can develop from an ulcer (but also without an ulcer), and is usually caused by streptococci, which is why treatment should focus primarily on this pathogen. Erysipelas causes a rash characterized by a well-defined bright red area, which spreads gradually. The disease causes general illness with fever and local pain. The erythematous skin lesion can enlarge the first days even after proper antibiotic treatment but the general condition usually improves rapidly and the pain decreases.
Pyoderma gangrenosum is a rare, destructive, non-infectious skin lesion.
Pyoderma gangrenosum is often associated with an underlying systemic disease, usually inflammatory bowel disease, rheumatoid arthritis or serious blood disease. However, pyoderma gangrenosum can occur without being associated with an immune system dysfunction.
Pyoderma gangrenosum often occurs on the lower legs but also on other parts of the body. The skin lesions are often located in areas that have suffered some kind of trauma. The progress of pyoderma gangrenosum is often swift, where a pustule or nodule rapidly grows into a painful ulcer with irregular, blushed edges. The edges of the ulcer are often purple-coloured and can look undermined. The patient experiences strong pain. The ulcer looks infected but a bacterial culture seldom shows any pathogenic bacteria and the ulcer doesn’t smell.
The diagnosis is mainly based on the clinical picture. A skin biopsy may be required to verify the diagnosis but can on the other hand worsen the lesion.
A dermatologist should be responsible for treating the pyoderma gangrenosum and the patient’s physician should treat the underlying systemic disease. The skin lesion could be aggravated by surgical intervention, which is to be avoided. Treatment including corticosteroids or other immunomodulators may be given when the diagnosis is ascertained. In addition, topical application of strong steroids in combination with immunomodulating agents can be used.
Vasculitis occurs due to inflammation in small, superficial blood vessels and is usually associated with immunological diseases. Vasculitis can occur in all ages. Vasculitis is not synonymous with an ulcer, but can lead to the development of ulcers. Other organs such as kidneys and intestines can also be affected. Patients with autoimmune diseases, especially rheumatoid arthritis, are over-represented among patients with vasculitis. Infections and drugs are otherwise common triggers.
In medication-induced vasculitis, vasculitis progresses fast with rapid onset of skin lesions bilaterally on the lower legs. The skin lesions are often very painful and are characterized by palpable petechiae, sometimes blister and ulcers with crust. Ulcers due to vasculitis in patients with rheumatoid arthritis usually occur on the instep of the foot or around the ankle. These ulcers often occur as isolated ulcers and can be very painful.
The underlying disease usually leads to the diagnosis. In ulcers due to vasculitis, treatment is primarily targeting the underlying disease. This means that in patients with rheumatoid arthritis, treatment should focus on this. In cases with suspected drug-induced vasculitis, all current medications should be withdrawn. If the ulcers are still progressing or in cases with explicit symptoms with pain or kidney involvement, oral steroids can be given.
After an average of ten years, some patients with recurring gout episodes develop chronic gout. Delayed diagnostics or undertreatment are the most common causes of chronic gout. Chronic gout is characterized by a transition to a more continuous arthritis with formation of tophi (gout knots), which can lead to hard-to-heal and painful ulcers.
The appearance of an ulcer is a sign of long-term undertreatment or lack of treatment and must led to adequate management of the patient’s elevated levels of uric acid in the blood.