Etiology and pathogenesis of trophic ulcers
Trophic ulcers are 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 pathologies are distinguished among the primary etiological factors:
- Diabetes mellitus. Against the background of this disease, a specific capillary lesion develops — pronounced sclerosis of microcirculatory vessels. This critically reduces tissue perfusion and blocks adequate gas exchange.
- Decompensated varicose veins. Prolonged venous stasis provokes a global disorder of tissue trophism, worsening edema and compressing functioning capillaries.
- Atherosclerosis. It acts as a cause of trophic ulcers somewhat less frequently, but also makes a significant contribution to the development of tissue ischemia.
The pathogenesis of a trophic ulcer is a complex cascade of reactions. The primary circulatory disorder inevitably entails lymphostasis. Tissues begin to experience an acute lack of oxygen, leading to hypoxia. It is hypoxia, combined with lymphostasis, that acts as a potent trigger for stimulating fibroblasts. However, due to nutritional deficiency, the forming granulation tissue remains immature. It is incapable of transforming into a full-fledged scar, making defect closure impossible.
Specific features of pressure ulcer development
Pressure ulcers have a somewhat different origin, although their morphological outcome is largely similar to trophic ulcers. While lower extremity ulcers stem primarily from a vascular catastrophe, pressure ulcer etiology is overwhelmingly dominated by impaired neural trophism.
The loss of adequate innervation in a tissue area triggers a pathological process that inevitably leads to a secondary blood supply disorder in the affected zone. Tissue deprived of both neural control and arterial blood flow undergoes destruction with the subsequent formation of a deep defect filled with the same immature granulation tissue.
Clinical significance and treatment challenges
The long-term presence of trophic ulcers and pressure ulcers is accompanied by severe biochemical and immunological shifts. These changes are both local (within the defect itself) and general (systemic) in nature.
From a clinical standpoint, these changes pose a colossal problem because they cause low skin graft efficacy. When a surgeon attempts to close the defect via transplantation, the skin flap simply fails to engraft. The aggressive environment, hypoxia, and lack of an adequate vascular bed hinder its integration.
A key factor in the chronicity of both ulcers and pressure ulcers is the continuous stimulation of the pathological process by general and local factors. It is worth noting that similar chronification mechanisms (constant stimulation) are observed in other ulcerative processes, such as peptic ulcer disease or ulcerative colitis (UC), the morphology of which has specific features and requires separate study.
Briefly: answers to topical questions
What stages of morphogenesis does a pressure ulcer go through from the onset of ischemia to the formation of a deep defect?
A pressure ulcer goes through several successive stages of development, from initial circulatory disorders to deep tissue damage.
- Pallor — 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 of the most intense tissue compression between the bed and a bony prominence.
Typical anatomical areas include:
- Sacrum;
- Scapulae;
- Occiput;
- Heels;
- Elbos;
- Greater trochanter of the femur.
Pressure ulcers can also develop 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 immature granulation tissue from maturing granulation tissue?
The literature describes histological features only of immature granulation tissue in chronic inflammation; a direct comparison with maturing tissue is lacking.
Immature granulation tissue is characterized by:
- Focal necroses — occurring constantly;
- Lymphoplasmacytic infiltrate — predominance of lymphocytes and plasma cells;
- Cellular deficit — reduced number of neutrophils, macrophages, and a relatively small number of active fibroblasts;
- Vascular changes — development of productive vasculitis and endothelial proliferation up to luminal obliteration.
What local and systemic complications can develop in long-standing trophic ulcers?
The literature directly confirms the following clinically significant consequences for long-standing trophic ulcers:
- 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 treatment of trophic ulcers involves the removal of necrotic tissue and elimination of infection.
- Low efficacy of skin transplantation: in trophic ulcers, general and local biochemical/immunological alterations lead to poor skin graft acceptance.
What is the exact pathogenesis of specific microcirculatory bed lesions in diabetes mellitus?
The literature details the pathogenesis of diabetic microangiopathy using renal lesions as an example and indicates that trophic ulcers in diabetes mellitus are associated with sclerosis of microcirculatory vessels.
Key links of diabetic microangiopathy according to the literature:
- Metabolic deficit — associated with insulin deficiency or hyperglycemia;
- Biochemical abnormalities — increased synthesis of type IV collagen and fibronectin coupled with decreased synthesis of proteoglycan-heparan sulfate;
- Non-enzymatic protein glycosylation — leads to an increase in advanced glycation end products;
- Metabolic defect — enhanced glycosylation causes thickening of the glomerular basement membrane and expansion of the mesangial matrix;
- Hemodynamic disturbances — cause glomerular hypertrophy and lead to glomerulosclerosis.
To memorize the pathogenesis of ulcers, use the formula "C-L-H-F": Circulation (disorder) + Lymphedema + Hypoxia = Fibroblast stimulation (formation of immature granulations).
Class and exam questions
What is the main morphological difference of the tissue in the area of a trophic ulcer?
The main feature is the development of immature 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?
In diabetes mellitus, pronounced sclerosis of microcirculatory vessels develops. This leads to chronic progressive circulatory impairment and profound tissue hypoxia in the lower extremities.
What is the primary factor in the etiology of pressure ulcers?
Unlike ulcers of vascular origin, pressure ulcers are dominated by impaired neural trophic regulation. It is this impairment that leads to secondary circulatory disturbance and subsequent tissue destruction.
Why does surgical closure of a trophic ulcer with a skin flap often fail?
Due to marked systemic and local biochemical and immunological alterations. Under conditions of impaired trophic supply and hypoxia, the transplanted skin graft is rejected and fails to engraft.
What else to study on this topic
- Morphological differences between peptic ulcer disease and ulcerative colitis
- Mechanisms of microcirculatory sclerosis development in diabetes mellitus
- Pathophysiology of lymphedema in decompensated varicose veins
- Biochemical and immunological shifts in tissues during chronic hypoxia
- Stages of formation and cellular composition of granulation tissue in health and disease
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