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Trophic Ulcers and Pressure Ulcers

Ulcus trophicum

For medical students2 min readUpdated 2026-10-10

Trophic ulcers and pressure ulcers are chronic tissue defects characterized by a protracted course and the formation of non-maturing granulation tissue. These pathological processes are extremely resistant to regeneration due to persistent local and systemic disturbances in blood circulation and innervation.

Nature of courseProlonged, chronic, and steadily progressive development of a tissue defect
MorphologyFormation of specific non-maturing granulation tissue within the lesion
Pathogenesis of ulcersCirculatory disorders, hypoxia, and lymphedema pathologically stimulate fibroblasts
SurgeryExtremely low efficacy of skin graft engraftment due to local tissue alterations

Etiology and Pathogenesis of Trophic Ulcers

Trophic ulcers represent a severe pathology that, in the vast majority of clinical cases, affects the lower extremities. The fundamental basis for their occurrence is always a chronic and progressive disturbance of regional blood circulation.

Three main etiologic factors stand out:

The pathogenesis of a trophic ulcer is a complex cascade of reactions. Primary circulatory impairment inevitably leads to lymphedema. Tissues begin to experience an acute lack of oxygen, developing hypoxia. Hypoxia combined with lymphedema acts as a powerful trigger for stimulating fibroblasts. However, due to nutritional deficits, the forming granulation tissue remains non-maturing. It cannot transform into a proper scar, making closure of the defect impossible.

Features of Pressure Ulcer Development

Pressure ulcers (bedsores) have a somewhat different origin, although their morphological outcome is largely similar to trophic ulcers. While lower extremity ulcers are primarily driven by vascular catastrophe, pressure ulcer etiology is heavily dominated by impaired neural trophism.

Clinical Significance and Treatment Challenges

The long-term persistence of trophic ulcers and pressure ulcers is accompanied by severe biochemical and immunological shifts. These changes are both local (within the defect zone) and systemic.

From a clinical standpoint, these changes pose a colossal problem because they account for the low efficacy of skin transplantation. When a surgeon attempts to close a defect via grafting, the skin flap simply fails to engraft. The aggressive environment, hypoxia, and lack of an adequate vascular bed prevent its integration.

A key factor in the chronicity of both ulcers and pressure ulcers is the continuous stimulation of the pathological process by systemic and local factors. Similar mechanisms of chronicity (continuous stimulation) are also observed in other ulcerative processes, such as peptic ulcer disease or ulcerative colitis (UC), the morphologies of which have specific features requiring separate study.

Mnemonic

To remember ulcer pathogenesis, use the formula "CLH-F": Circulatory impairment (disorder) + Lymphedema + Hypoxia = Fibroblast stimulation (formation of non-maturing granulations).

Frequently asked questions

What stages of morphogenesis does a pressure ulcer pass through from the onset of ischemia to deep defect formation?

A pressure ulcer passes through several sequential stages of development, ranging from initial circulatory changes to deep tissue damage:

  • Pallor — the initial stage of ischemia;
  • Hyperemia focus — redness and tissue edema;
  • Epidermal detachment — formation of superficial erosions and blisters;
  • Ulceration and necrosis — formation of a deep soft tissue defect (skin with subcutaneous adipose tissue).
In which typical anatomical areas do pressure ulcers form in immobilized patients?

In immobilized patients, pressure ulcers form in areas subject to the most intense tissue compression between the bed and a bony prominence.

Typical anatomical regions include:

  • Sacrum;
  • Scapulae;
  • Occiput;
  • Heels;
  • Elbows;
  • Greater trochanter of the femur.

Additionally, pressure ulcers can occur in internal organs due to pressure from foreign bodies:

  • Gallbladder — pressure from a gallstone;
  • Intestine — prolonged pressure from a drainage tube;
  • Trachea — prolonged presence of an endotracheal tube.
What microscopic (histological) features distinguish non-maturing granulation tissue from maturing granulation tissue?

The histological features described pertain specifically to non-maturing granulation tissue in chronic inflammation; a direct comparison to maturing tissue is not detailed.

Features of non-maturing granulation tissue include:

  • Focal necrosis — occurring continuously;
  • Lymphoplasmacytic infiltrate — predominance of lymphocytes and plasma cells;
  • Cellular deficit — reduced numbers of neutrophils, macrophages, and a relatively small number of active fibroblasts;
  • Vascular alterations — development of productive vasculitis and endothelial proliferation up to luminal obliteration.
What local and generalized complications may develop against the background of a long-standing trophic ulcer?

Clinically significant consequences confirmed for long-standing trophic ulcers include:

  • Risk of malignant transformation: trophic ulcers are considered precancerous conditions; if malignant transformation is suspected, a biopsy is indicated.
  • Local infection and necrotic tissue: local management of trophic ulcers involves the removal of necrotic tissue and elimination of infection.
  • Low efficacy of skin transplantation: systemic and local biochemical/immunological changes cause poor engraftment of skin grafts in trophic ulcers.
What is the exact pathogenesis of specific microcirculatory bed lesions in diabetes mellitus?

The pathogenesis of diabetic microangiopathy is detailed through renal involvement, noting that trophic ulcers in diabetes are linked to microcirculatory vessel sclerosis.

Key links of diabetic microangiopathy include:

  • Metabolic deficit — associated with insulin deficiency or hyperglycemia;
  • Biochemical alterations — enhanced synthesis of type IV collagen and fibronectin with decreased proteoglycan-heparan sulfate synthesis;
  • Non-enzymatic protein glycosylation — leading to increased advanced glycation end products (AGEs);
  • Metabolic defect — enhanced glycosylation causes thickening of the glomerular basement membrane and expansion of the mesangial matrix;
  • Hemodynamic disorders — induce glomerular hypertrophy and lead to glomerulosclerosis.
What is the main morphological difference in tissue within a trophic ulcer?

The primary feature is the development of non-maturing granulation tissue. Due to hypoxia and lymphedema, fibroblasts are stimulated, but the granulations fail to undergo normal stages of maturation and scarring.

Why do trophic ulcers frequently occur in diabetes mellitus?

Diabetes mellitus causes pronounced sclerosis of microcirculatory vessels. This leads to chronic, progressive circulatory failure and deep tissue hypoxia in the lower extremities.

What is the primary factor in the etiology of pressure ulcers?

Unlike vascular-origin ulcers, pressure ulcers are dominated by impaired neural trophism, which directly leads to secondary blood supply disruption and subsequent tissue destruction.

Why does surgical closure of a trophic ulcer with a skin flap frequently fail?

Due to pronounced systemic and local biochemical and immunological alterations. Under conditions of impaired trophism and hypoxia, the transplanted skin flap undergoes rejection and fails to engraft.

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