Etiology: why does necrosis occur?
The mechanisms of tissue death are diverse. In surgery, it is standard practice to classify the causes of tissue death into several broad groups depending on the nature of the damaging factor.
- External factors (primary necrosis). The process is triggered by the direct destruction of cellular structures by a traumatic agent. These include:
- Physical factors: injury by high or extremely low temperatures (thermal trauma), as well as the harmful effects of radiation and electrical energy.
- Chemical factors: direct contact of tissues with aggressive chemical substances.
- Mechanical factors: severe mechanical trauma accompanied by crushing or complete maceration of tissues.
- Local circulatory disorders. This is the most frequent cause of tissue death. In this case, indirect (secondary) necrosis develops as a result of impaired blood supply to a vessel. The main culprits of vascular catastrophes are:
- Thrombosis;
- Embolism;
- Obliteration of the vascular lumen.
- Neurotrophic causes. Tissues can die due to severe impairment of trophic innervation. This condition is observed in direct damage to nerve trunks, as well as in certain specific diseases (e.g., syringomyelia or leprosy).
Main types of tissue death
Depending on the consistency of the dead structures and the clinical features of the process, two basic types of necrosis are distinguished:
- Coagulative (dry) necrosis. Proceeds with tissue compaction. Classic examples of this variant include deep thermal burns and the development of dry gangrene.
- Liquefactive (wet) necrosis. Characterized by the dissolution of dead masses. In clinical practice, this type is most commonly encountered in alkali chemical burns and the development of wet gangrene.
Clinical course and outcomes
The pathological process has its own timeframe and predictable outcomes, which directly determine surgical tactics.
Timing of development: It is important to remember that the clinical picture does not form instantly. Explicit, visually identifiable signs of tissue death appear 4–6 hours after their actual death.
Outcome options:
- Tissue sloughing (sequestration). The body attempts to demarcate and rid itself of non-viable areas independently.
- Ulcer formation. This outcome is characteristic when the lesion has a superficial location.
- Intoxication. The most formidable outcome, developing in extensive necrosis. The patient's severe condition is caused by the massive absorption of toxic degradation products from dead cells into the systemic circulation.
Briefly: answers to topical questions
In what diseases does neurotrophic necrosis develop?
Neurotrophic necrosis develops when trophic innervation is impaired. Such conditions include peripheral nerve injuries, syringomyelia, and leprosy. Trophic ulcers can develop in peripheral nerve injuries, syringomyelia, and tabes dorsalis.
What are the outcomes of necrosis?
Outcomes of necrosis are divided into favorable and unfavorable.
Favorable outcomes:
- Organization — replacement of necrotic masses with connective tissue (scarring).
- Encapsulation — demarcation of the area by a connective tissue capsule.
- Petrification — calcification (deposition of calcium salts).
- Ossification — formation of bone tissue.
- Cyst formation — the appearance of a cavity upon the resorption of detritus.
- Mesoglial scar — in small foci within the brain.
Unfavorable outcomes:
- Purulent liquefaction — lysis of masses with the risk of sepsis.
Tissue sloughing, ulcer formation, autolysis, and myomalacia are also possible.
What histological changes occur in the cell nucleus during necrosis?
During necrosis, sequential changes occur in the cell nucleus associated with the activation of hydrolases. The following stages are distinguished:
- Karyopyknosis — shrinking of the nucleus due to water loss.
- Karyorrhexis — rupture (fragmentation) of the nucleus into small clumps.
- Karyolysis — complete dissolution of the nucleus, in which it stains poorly with hematoxylin.
These changes distinguish necrosis from reversible injuries, in which the nuclei remain unchanged.
What are the clinical and morphological forms of necrosis?
Traditionally, five main clinical and morphological forms of necrosis are distinguished:
- coagulative (dry) necrosis;
- liquefactive (wet) necrosis;
- gangrene;
- sequestrum;
- infarct.
Trophic ulcer is also defined as a form of necrosis.
What is a sequestrum and in what diseases does it form?
A sequestrum is a detached piece of dead bone tissue. It forms in purulent-inflammatory and specific infectious bone lesions when necrosis occurs due to impaired blood supply.
Diseases in which a sequestrum forms:
- Chronic hematogenous osteomyelitis — dense bone sequestra form inside the involucrum (sequestral capsule).
- Chronic odontogenic osteomyelitis — sequestration occurs in the upper or lower jaw.
- Bone tuberculosis — "melting sugar"-like sequestra form without an involucrum.
What types of gangrene are distinguished in surgery?
The following types of gangrene are distinguished:
- dry gangrene;
- wet gangrene, developing when infection joins in;
- pressure ulcer (decubitus) — a type of gangrene occurring in areas of the body subject to the greatest pressure;
- gas gangrene — a complication of wounds by anaerobic clostridial infection;
- pulmonary gangrene.
To memorize frequent vascular causes of secondary necrosis, use the acronym TEO: Thrombosis, Embolism, Obcluding vascular lesions.
Class and exam questions
What is the difference between primary and secondary necrosis?
Primary necrosis occurs due to a direct destructive impact of a factor (e.g., in burns or crush injury). Secondary (indirect) necrosis develops indirectly, most commonly due to the cessation of blood flow in a vessel or impaired innervation.
How long after cell death do clinical symptoms appear?
Clear clinical signs of tissue death begin to become visual 4–6 hours after irreparable damage has occurred.
Why are extensive necrotic lesions dangerous for the entire organism?
The main threat lies in the development of severe systemic intoxication. It arises due to the active absorption of breakdown products from a large mass of dead tissue into the bloodstream.
What else to study on this topic
- Pathogenetic features of dry and wet gangrene
- Mechanisms of trophic ulcer formation in superficial necrosis
- Surgical tactics and management of intoxication in extensive tissue death
- Neurotrophic disorders in leprosy and syringomyelia
- Differential diagnosis of thermal burns and alkali burns
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