Coagulative necrosis

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Coagulative necrosis
A high-power photomicrograph shows the edge of this reddish area, illustrating coagulation necrosis (1) compared to the normal tissue (2). The necrotic tubules in this hemorrhagic, red infarct are hypereosinophilic. Compare the tubules on the right with the normal tubules seen in the left-hand portion of the slide. Note the interstitial hemorrhage which is associated with vascular leakage within this necrotic region in the tissue.
Image courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Coagulative Necrosis is a type of accidental cell death typically caused by ischemia or infarction.

It is characterised by the 'ghostly' appearance of cells under light microscopy in the affected area of tissue. Like most types of necrosis if enough labile cells are present around the affected area regeneration can occur.


Coagulative necrosis is most commonly caused by hypoxic conditions, which don't involve severe trauma, toxins or an acute or chronic immune response. The lack of oxygen causes cell death in a localised area which is perfused by blood vessels failing to deliver primarily oxygen, but also other important nutrients. It is important to note that while ischemia in most tissues of the body will cause coagulative necrosis, in the central nervous system ischemia causes liquefactive necrosis as there is very little structural framework in the brain tissue.



The macroscopic appearance of an area of coagulative necrosis is a pale segment of tissue contrasting against surrounding well vascularised tissue. The surrounding survivng cells can aid in regeneration of the affected tissue unless they are stable or permanent cells.


The microscopic anatomy shows a lighter staining tissue (when stained with H&E) containing no nuclei with very little structural damage giving the appearance often quoted as 'ghost cells'. The decreased staining is due to digested nuceli which no longer show up as dark purple when stained with hematoxylin and removed cytoplasmic structures giving reduced amounts of intracellular protein reducing the usual dark pink staining cytoplasm with eosin.


As the majority of the structural remnants of the necrotic tissue remains, labile cells adjacent to the affected tissue will replicate and replace the cells which have been killed during the event. Labile cells are constantly undergoing mitosis and can therefore help reform the tissue, whereas nearby stable and permanent cells (eg. neurons and cardiomyocytes) do not undergo mitosis and will not replace the tissue affected. Fibroblasts will also migrate to the affected area depositing fibrous tissue producing fibrosis or scarring in areas where labile cells do not replicate and replace tissue.

Pathological Findings: Case #1: Kidney: Coagulative Necrosis

Clinical Summary

A 48-year-old black male committed suicide by ingesting an unidentified toxin, after which he went into profound shock and died.

Autopsy Findings

An incidental finding at autopsy was a small renal lesion which was reddish-tan in color, sharply delineated, and triangular in shape. The base of the lesion was located at the capsular surface and its apex at the corticomedullary junction.

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Pathological Findings: Case #2: Heart: Coagulative Necrosis

Clinical Summary

This was a 57-year-old male whose hospital course following abdominal surgery was characterized by progressive deterioration and hypotension. Four days post-operatively, the patient sustained an anterior myocardial infarction and died the next day.

Autopsy Findings

The patient's heart weighed 410 grams. Examination of the coronary arteries revealed marked atherosclerotic narrowing of all three vessels with focal occlusion by a thrombus of the left anterior descending artery.

Fresh necrosis of the anterior wall of the left ventricle and anterior portion of the septum was present, extending from the endocardium to the inner half of the ventricular wall.

Images courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

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