Pressure ulcer complications

Metabolic prerequisites and the toxemia stage

The development of severe trophic disorders is preceded by colossal stress for the organism. Already at the stage of burn toxemia, all types of metabolism begin to suffer. From the 5th–6th day, a negative nitrogen balance forms, hypoproteinemia develops, and electrolyte balance is disrupted. Liver and adrenal dysfunction occurs, and tissue proteolysis intensifies in the wound area.

This period is accompanied by multiple systemic lesions that deplete the patient's reserves:

• Nervous system: auditory hallucinations may occur.
• Cardiovascular system: development of toxic myocarditis is characteristic.
• Gastrointestinal tract: nausea, frequent vomiting, intestinalparesis, and toxic diarrhea are observed. Jaundice and signs of an acute abdomen are possible.
• Blood: the prothrombin index decreases, hematocrit and erythrocyte count drop (anemia develops), and leukocytosis is detected by the 5th–6th day.

It is precisely this failure of detoxification mechanisms that prepares the ground for profound necrotic changes in the skin and underlying tissues.

Formation of pressure ulcers in septicotoxemia

The direct formation of pressure ulcers is characteristic of the burn septicotoxemia stage. This phase conventionally begins on the 10th–11th day, when eschar liquefaction and rejection occur, opening the gateway for infection.

The pathogenesis of trophic ulcers and pressure ulcers here is inextricably linked with critical exhaustion. Protein losses can reach 200 g per day, while its synthesis is grossly impaired.

Critical threshold: if the serum protein level drops to 40 g/L, there is a sharp decrease in immunological reactivity. As a consequence, tissue repair and regeneration processes slow down or stop completely. Pronounced tissue atrophy sets in, against the background of which pressure ulcers form.

This condition is accompanied by a number of other severe complications:

• Tissue bleeding increases.
• Wound infection is activated (phlegmons, abscesses, stomatitis occur).
• Erosions and ulcers form on the gastric and intestinal mucosa, frequently complicated by profuse bleeding.
• Remittent fever develops, lasting for weeks.

Pressure ulcers in the structure of traumatic disease

Within the framework of traumatic disease theory, pressure ulcers are considered specific post-ischemic and trophic complications.

Traumatic disease arises due to extreme energy expenditure during shock, leading to the disintegration of vital mechanisms, severe oxygen debt, and the formation of multiorgan pathology.

The course of the disease transitions into the anabolic phase (lasting from several weeks to months). Although proliferative processes predominate in wounds during this period (granulation formation, scarring, epithelialization), dystrophic and sclerotic changes increase in damaged organs.

Pressure ulcers in this phase are one of the main causes of mortality. They rank alongside such fatal conditions as:

1. Purulent-inflammatory complications: wound suppuration, severe pneumonia, tracheobronchitis, urinary tract infection, and sepsis.
2. Toxic damage: acute renal and hepatic failure.
3. Embolism: fat embolism and thromboembolism.
4. Edema: cerebral and pulmonary edema.

Prognosis and physical rehabilitation

The appearance of pressure ulcers against the background of multiple organ failure indicates an extremely severe course of the disease. Bacteremia is frequently detected in blood tests during this period. Important unfavorable prognostic signs include eosinophilia and lymphocytopenia.

Patients who have survived the acute phases and faced deep trophic disorders require a long rehabilitation period that can last for many years.

Physical rehabilitation of such patients is comprehensive and includes:

• Correction of chronic multiple organ failure.
• Combating muscle atrophy and peripheral circulation disorders (which is critically important for pressure ulcer healing).
• Elimination of contractures and innervation disorders.

The final outcome of successful treatment is the adaptation of the body to the persistent consequences of the sustained trauma.

Class and exam questions

What else to study on this topic

• Pathogenesis and clinical presentation of burn toxemia
• Immune response and phagocytosis in burn septicotoxemia
• Catabolic and anabolic phases of traumatic disease
• Multiple organ pathology in severe polytrauma
• Principles of physical rehabilitation after severe trauma

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