Coagulative necrosis

Coagulative necrosis is a type of accidental cell death typically caused by ischemia or infarction. In coagulative necrosis the architecture of dead tissue is preserved for at least a couple of days.[1] It is believed that the injury denatures structural proteins as well as lysosomal enzymes thus blocking the proteolysis of the damaged cells. The lack of lysosomal enzymes allows it to maintain a "coagulated" morphology for some time. Like most types of necrosis if enough viable cells are present around the affected area regeneration will usually occur.

Coagulative necrosis can also be induced by high local temperature; it is a desired effect of treatments such as high intensity focused ultrasound applied to cancerous cells.[2]


Coagulative necrosis is most commonly caused by conditions that do not involve severe trauma, toxins or an acute or chronic immune response. The lack of oxygen (hypoxia) 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 neural tissue.



The macroscopic appearance of an area of coagulative necrosis is a pale segment of tissue contrasting against surrounding well vascularised tissue and is dry on cut surface. The tissue may later turn red due to inflammatory response. The surrounding surviving cells can aid in regeneration of the affected tissue unless they are stable or permanent.


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 nuclei which no longer show up as dark purple when stained with hematoxylin, and denaturation of intracellular proteins will somehow give them a darker pinkish stain 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 (e.g. 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 viable cells do not replicate and replace tissue.


  1. ^ Robbins and Cotran: Pathologic Basis of Disease, 8th Ed. 2010. Pg. 15
  2. ^ F. Wu; Z.-B. Wang; Y.-De Cao; W.-Z. Chen; J. Bai; J.-Z. Zou; H. Zhu (December 2003). "A randomised clinical trial of high-intensity focused ultrasound ablation for the treatment of patients with localised breast cancer". British Journal of Cancer. 89 (12): 2227–2233. doi:10.1038/sj.bjc.6601411. PMC 2395272. PMID 14676799.

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Algor mortis

Algor mortis (Latin: algor—coldness; mortis—of death), the second stage of death, is the change in body temperature post mortem, until the ambient temperature is matched. This is generally a steady decline, although if the ambient temperature is above the body temperature (such as in a hot desert), the change in temperature will be positive, as the (relatively) cooler body acclimates to the warmer environment. External factors can have a significant influence.

The term was first used by Dowler in 1849. The first published measurements of the intervals of temperature after death were done by Dr John Davey in 1839.

Anemic infarct

Anemic infarcts (also called white infarcts or pale infarcts) are white or pale infarcts caused by arterial occlusions, and are usually seen in the heart, kidney and spleen. These are referred to as "white" because of the lack of hemorrhaging and limited red blood cells accumulation, (compare to Hemorrhagic infarct). The tissues most likely to be affected are solid organs which limit the amount of hemorrhage that can seep into the area of ischemic necrosis from adjoining capillary beds. The organs typically include single blood supply (no dual arterial blood supply or anastomoses). The infarct generally results grossly in a wedge shaped area of necrosis with the apex closest to the occlusion and the base at the periphery of the organ. The margins will become better defined with time with a narrow rim of congestion attributable to inflammation at the edge of the lesion. Relatively few extravasated red cells are lysed so the resulting hemosiderosis is limited and results in a progressively more pale area of infarction with time. Ischemic coagulative necrosis results and fibrosis of the affected area develops from the reparative response beginning at the preserved margins and working its way inwards. One exception to coagulative necrosis is the brain, which undergoes liquefactive necrosis in response to infarction.

Black stomach

Black stomach is a condition that results from acute gastric necrosis. The tarry black colour is produced by the coagulative necrosis of mucosa resulting in intramucosal haemorrhage and acid hematin deposition. This condition was first described in a patient with acid poisoning. A similar condition has been described in acute esophageal necrosis due to mucosal ischemia resulting from hemodynamic compromise.

Dead on arrival

Dead on arrival (DOA), also dead in the field and brought in dead (BID), indicates that a patient was found to be already clinically dead upon the arrival of professional medical assistance, often in the form of first responders such as emergency medical technicians, paramedics, or police.

In some jurisdictions, first responders must consult verbally with a physician before officially pronouncing a patient deceased, but once cardiopulmonary resuscitation is initiated, it must be continued until a physician can pronounce the patient dead.

Death messenger

Death messengers, in former times, were those who were dispatched to spread the news that an inhabitant of their city or village had died. They were to wear unadorned black and go door to door with the message, "You are asked to attend the funeral of the departed __________ at (time, date, and place)." This was all they were allowed to say, and were to move on to the next house immediately after uttering the announcement. This tradition persisted in some areas to as late as the mid-19th century.

Death rattle

Terminal respiratory secretions (or simply terminal secretions), known colloquially as a death rattle, are sounds often produced by someone who is near death as a result of fluids such as saliva and bronchial secretions accumulating in the throat and upper chest. Those who are dying may lose their ability to swallow and may have increased production of bronchial secretions, resulting in such an accumulation. Usually, two or three days earlier, the symptoms of approaching death can be observed as saliva accumulates in the throat, making it very difficult to take even a spoonful of water. Related symptoms can include shortness of breath and rapid chest movement. While death rattle is a strong indication that someone is near death, it can also be produced by other problems that cause interference with the swallowing reflex, such as brain injuries.It is sometimes misinterpreted as the sound of the person choking to death, or alternatively, that they are gargling.

Dignified death

Dignified death is a somewhat elusive concept often related to suicide. One factor that has been cited as a core component of dignified death is maintaining a sense of control. Another view is that a truly dignified death is an extension of a dignified life. There is some concern that assisted suicide does not guarantee a dignified death, since some patients may experience complications such as nausea and vomiting. There is some concern that age discrimination denies the elderly a dignified death.

Fat necrosis

Fat necrosis is a form of necrosis characterized by the action upon fat by digestive enzymes.In fat necrosis the enzyme lipase releases fatty acids from triglycerides. The fatty acids then complex with calcium to form soaps. These soaps appear as white chalky deposits.It is usually associated with trauma of the pancreas or acute pancreatitis.It can also occur in the breast, the salivary glands and neonates after a traumatic delivery.

Gumma (pathology)

A gumma is a soft, non-cancerous growth resulting from the tertiary stage of syphilis. It is a form of granuloma. Gummas are most commonly found in the liver (gumma hepatis), but can also be found in brain, heart, skin, bone, testis, and other tissues, leading to a variety of potential problems including neurological disorders or heart valve disease.

Hans Schmaus

Hans Schmaus (22 May 1862 in Munich – 4 December 1905 in Munich) was a German pathologist.

In 1887 he obtained his doctorate at the University of Munich, where he spent the next several years as an assistant to Otto Bollinger at the institute of pathology. In 1889 he became habilitated for pathology, becoming an associate professor at Munich in 1899.At Munich, he performed studies involving the pathological anatomy of the spinal cord, and did research of hyaline degeneration and caseous necrosis. With pathologist Eugen Albrecht, he conducted studies of coagulative necrosis.

Lazarus sign

The Lazarus sign or Lazarus reflex is a reflex movement in brain-dead or brainstem failure patients, which causes them to briefly raise their arms and drop them crossed on their chests (in a position similar to some Egyptian mummies). The phenomenon is named after the Biblical figure Lazarus of Bethany, whom Jesus Christ raised from the dead in the Gospel of John.


Megadeath (or megacorpse) is one million human deaths, usually caused by a nuclear explosion. The term was used by scientists and thinkers who strategized likely outcomes of all-out nuclear warfare.

Myocardial infarction complications

Myocardial infarction complications may occur immediately following a heart attack (in the acute phase), or may need time to develop (a chronic problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct.

Post-myocardial complications occur after a period of ischemia, these changes can be seen in gross tissue changes and microscopic changes. Necrosis begins after 20 minutes of an infarction. Under 4 hours of ischemia, there are no gross or microscopic changes noted.

From 4-24 hours coagulative necrosis begins to be seen, which is characterized by the removal of dead cardiomyocytes through heterolysis and the nucleus through karyorrhexis, karyolysis, and pyknosis. On gross examination, coagulative necrosis shows darkened discoloration of the infarcted tissue. The most common complication during this period is arrhythmias.

Day 1-7 is marked by the inflammatory phase. Days 1-3 are marked by “acute inflammation”, in which neutrophils infiltrate the ischemic tissue. A major complication during this period is fibrinous pericarditis, particularly in transmural ventricular wall damage (an infarct that impacted all 3 layers of the heart, the epicardium, myocardium, and endocardium). This leads to inflammation, such as swelling, leading to rubbing of the heart on the pericardium. Day 4 through 7 are marked by “chronic inflammation”, on histology macrophages will be seen infiltrating the tissue. The role of these macrophages is the removal of necrotic myocytes. However, these cells are directly involved in the weakening of the tissue, leading to complications such as a ventricular free wall rupture, intraventricular septum rupture, or a papillary muscle rupture. At a gross anatomical level, this staged is marked by a yellow pallor.

Weeks 1-3 are marked on histology by abundant capillaries, and fibroblast infiltration. Fibroblasts start replacing the lost cardiomyocytes with collagen type 1 and leads to the granulation of tissue.

After several weeks fibrosis occurs and heavy collagen formation. Collagen is not as strong or compliant as the myocardium that it replaced, this instability could lead to a ventricular aneurysm, and the stasis of blood in an aneurysm can lead to a mural thrombus. A rarer complication that also occurs during this time is Dressler’s syndrome and is thought to have autoimmune origins.


Myocytolysis refers to a state of significant damage to cardiac myocytes, muscle cells of the heart, caused by myocardial strain. It was first described in medical literature by Schlesinger and Reiner in 1955. It is considered a type of cellular necrosis. Two types of myocytolysis have been defined: coagulative and colliquative.Coagulative myocytolysis appears in the myocardium near areas of coagulative necrosis or areas affected by myocardial infarction. This phenomenon tends to occur when neighboring cardiac muscle loses its ability to contract (i.e. in ischemia or infarction). The remaining viable muscles, as the result, strain to compensate for the loss of other muscles in order to deliver the necessary cardiac output. During the process, myocardial cells are stretched and stressed to produce new contractile elements.In colliquative myocytolysis, fluids accumulated within the cell dissolve myofibrils, resulting in vacuolization of the cell. It is considered an indicator of acute myocardial ischemia and can be used to confirm ischemia in the absence of other indicators of cause of death.


A necronym (from the Greek words νεκρός, nekros, "dead" and ὄνομα ónoma, "name") is a reference to, or name of, a person who has died. Many cultures have taboos and traditions associated with referring to such a person. These vary from the extreme of never again speaking the person's real name, often using some circumlocution instead, to the opposite extreme of commemorating it incessantly by naming other things or people after the deceased.

For instance, in some cultures it is common for a newborn child to receive the name (a necronym) of a relative who has recently died, while in others to reuse such a name would be considered extremely inappropriate or even forbidden. While this varies from culture to culture, the use of necronyms is quite common.


Necrosis (from the Greek νέκρωσις "death, the stage of dying, the act of killing" from νεκρός "dead") is a form of cell injury which results in the premature death of cells in living tissue by autolysis.Necrosis is caused by factors external to the cell or tissue, such as infection, toxins, or trauma which result in the unregulated digestion of cell components.

In contrast, apoptosis is a naturally occurring programmed and targeted cause of cellular death.

While apoptosis often provides beneficial effects to the organism, necrosis is almost always detrimental and can be fatal.Cellular death due to necrosis does not follow the apoptotic signal transduction pathway, but rather various receptors are activated, and result in the loss of cell membrane integrity and an uncontrolled release of products of cell death into the extracellular space.This initiates in the surrounding tissue an inflammatory response which attracts leukocytes and nearby phagocytes which eliminate the dead cells by phagocytosis. However, microbial damaging substances released by leukocytes would create collateral damage to surrounding tissues. This excess collateral damage inhibits the healing process. Thus, untreated necrosis results in a build-up of decomposing dead tissue and cell debris at or near the site of the cell death. A classic example is gangrene. For this reason, it is often necessary to remove necrotic tissue surgically, a procedure known as debridement.

Pallor mortis

Pallor mortis (Latin: pallor "paleness", mortis "of death"), the first stage of death, is an after-death paleness that occurs in those with light/white skin.

Post-mortem interval

Post-mortem interval (PMI) is the time that has elapsed since a person has died. If the time in question is not known, a number of medical/scientific techniques are used to determine it. This also can refer to the stage of decomposition of the body.

Zenker's degeneration

Zenker's degeneration is a severe glassy or waxy hyaline degeneration or necrosis of skeletal muscles in acute infectious diseases; a prototype of coagulative necrosis.

The condition was named by Friedrich Albert von Zenker. It is a hyaline degeneration of skeletal muscles such as rectus abdominis and diaphragm, and occurs in severe toxaemia as typhoid fever. It is also seen in electrical burns. Grossly the muscles appear pale and friable; microscopically, the muscle fibres are swollen, have a loss of cross striations, and show a hyaline appearance. Rupture and small hemorrhage may complicate the lesion. Coagulative necrosis occurs here.

Principles of pathology
Anatomical pathology
Clinical pathology

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