Coagulative necrosis

Mechanisms of development and causes

The development of coagulative necrosis is driven by dehydration (removal of water from tissues) and coagulation (precipitation) of proteins. The precursor to this condition at the cellular level is hyaline-droplet degeneration.

The primary damaging factors are:

• Chemical agents. These include acids and heavy metal salts. Unlike alkalis, acids cause a superficial but very dense eschar.
• Thermal factors. The underlying mechanism is tissue overheating (contact with flame, boiling water, hot steam, or metal). The nature of the damage depends on the temperature and duration of exposure. Coagulative necrosis occurs when exposed to temperatures above 65 °C.

It is important to note the time-temperature relationship. Prolonged exposure to agents with a relatively low temperature can cause damage just as severe as short-term exposure to intense heat. For example, a temperature of 42 °C for 6 hours leads to skin necrosis (often seen when heating pads are applied to unconscious patients). Exposure to 50 °C causes skin death in as little as 3 minutes, as this threshold is critical for the survival of the epidermis, leukocytes, and osteoblasts. The dynamics of overheating also differ: gasoline ignition causes tissue overheating in a fraction of a minute, whereas contact with hot steam for 20 seconds leads to overheating within 3 minutes.

Macroscopic and microscopic picture

The appearance and histological characteristics of dry necrosis are highly specific and depend on the etiology of the injury.

Macroscopically, the necrotic tissue becomes very dense and dry. If necrosis is caused by a chemical or thermal burn, a characteristic eschar forms. Due to severe dehydration, this eschar sinks and lies below the level of the surrounding intact skin. Dead areas may undergo mummification.

Microscopically, pathological changes are registered immediately after exposure to the damaging agent. Coagulative necrosis is typically marked by the instant appearance of hyperchromatosis and pyknotic changes in cell nuclei. In localized injuries, it is referred to as focal coagulative necrosis; in extensive ones, as total coagulative necrosis.

Clinical and morphological forms

Depending on the localization and cause, several significant variants of coagulative necrosis are distinguished.

Ischemic (pale) necrosis

A classic manifestation is myocardial infarction—an ischemic pale coagulative necrosis accompanied by the formation of a hemorrhagic rim. The lesion has an irregular shape and consists of coalescing grey-yellow areas, peripherally surrounded by a zone of congestion and hemorrhage.

Ischemic coagulative necrosis also occurs in the liver. Dead hepatocytes decrease in size (mummify), their nuclei shrink, and the cytoplasm stains intensely. Death of liver cells is always accompanied by inflammatory infiltration. Depending on the topography and area of the lesion, the following are distinguished:

• Focal (patchy) — death of small groups of cells in various zones.
• Centrilobular (confluent) — localized around the central veins.
• Periportal (bridging) — affects the limiting plate and lobular periphery.
• Bridging — massive damage with the formation of fibrous links between liver structures (porto-portal, centro-central).
• Submassive and massive — death of the majority of the acinus or the entire parenchyma, naturally leading to acute liver failure.

Caseous necrosis

This is a specific variant of dry necrosis, named for the external resemblance of the dead masses to cottage cheese.

The basis of necrotic masses in caseous necrosis consists of precipitated protein and a large amount of lipids. Most commonly, this type of necrosis is encountered in tuberculosis. The classic histological picture is represented by an epithelioid cell granuloma, in the center of which lies a zone of caseous necrosis (dead cells of monocytic origin), surrounded by a cellular wall and Langhans giant cells. The presence of such necrosis serves as an important criterion for distinguishing tuberculosis from sarcoidosis, in which caseous masses in granulomas are usually absent (found only as rare small foci).

Class and exam questions

What else to study on this topic

• Colliquative (wet) necrosis: mechanisms and differences
• Gangrene as an outcome of circulatory disorders (dry, wet, gas)
• Morphology of granulomas in tuberculosis and sarcoidosis
• Ballooning and hydropic degeneration
• Bone sequestra and sequestrectomy

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