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Clinical Characteristics

A small localized inflammatory reaction at the site of minimal trauma is the first sign of a developing ulcer. The involved area increases rapidly and by the 5th or 6th day there will be a definite pustule more than 1 cm in diameter. This ruptures and discharges very foul-smelling, blood-stained pus. Thus far the lesion appears superficial, but after rupture it can be seen that the entire skin thickness and subcutaneous tissues are involved. The development of a vesicle is constant, regardless of the type of trauma or its extent. Major wounds with considerable bleeding do not develop into this type of ulcer.

After rupturing of the pustule, pus continues to discharge, obscuring an irregular, bleeding and granulating surface covered with gray slough. This granulation tissue is raised above the adjacent skin, which has an everted and rolled edge that can be mistaken for malignancy. There is marked edema around the ulcer and in many patients the surrounding skin becomes deeply pigmented; the pigmentation persists for many months even after the ulcer has healed. As the ulcer develops it tends to become oval or circular in outline (Fig. 36.2), even if it originated with a longitudinal wound. (A similar oval ulcer develops in patients inoculated experimentally with a needle puncture). How quickly the ulcer spreads depends on the patient's resistance; it is at this stage that the degree of nutrition and general health may be of some importance. There is rapid spread for the first 2 or 3 weeks, then slower spread until the maximum size is reached in about 6 weeks; 15-cm has been recorded but the whole ulcerated area may be much larger.

The majority of acute tropical ulcers involving only the skin and subcutaneous tissues heal rapidly without recurrence, particularly if treated. In the early, pustule stage, there may be multiple vesicles, the majority of which heal. Usually only one progresses to a large ulcer. These ulcers penetrate the deep fascia and damage the tendons (Fig. 36.2 C), particularly the Achilles tendon, causing gangrene and rupture. The underlying bones reactively become involved, joints may occasionally be invaded, and, at this stage, even if healing occurs, there will be considerable deformity. The tendons will shorten and bones may become bowed. If the ulcer affects the foot, a variety of deformities may occur and individual digits may become gangrenous as a result.


Fig. 36.2 A-E. Tropical ulcer. (A-C) Three ulcers which have developed into the typical circular shape and are now filled with granulation tissue and have raised, hard edges. A and B are on the lower leg, and C on the foot. All are African patients. In C the ulcer has penetrated the deep fascia and is involving the tendons. (D) The amputation specimen of the lower leg of an African with an extensive tropical ulcer which has eroded bone. (E) A transverse section of D. The ulcer has eroded deeply into the tibia. Secondary infection is inevitable at this stage. (D, E contributed by Daniel H. Connor).

In the acute stage of the ulcer, there is a great deal of pain, aggravated when the patient stands up. Walking often causes venous congestion, leading to bleeding which can be quite severe. Pain and bleeding are both relieved by firm bandaging. The pain and rapid rate of spread are characteristic of tropical ulcer; the thick rolled edge and the continuation into a chronic condition complete the clinical picture.

Malignant degeneration may follow and is difficult to recognize clinically in its early stage. A steady increase in the granulation tissue centrally or eversion of a previously rolled edge may indicate malignant change. Malignancy may also develop in the scar of a well-healed ulcer. Biopsy is usually necessary to establish the diagnosis of malignant change and differentiate it from invasive acanthosis.

One of the major problems with tropical ulcers is the spread of infection. Generalized septicemia, tetanus, and gas gangrene are further complications.

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Copyright: Palmer and Reeder