Cadaver

Cadaver, dead body (lat. cadaver). The development of medical knowledge and the first concepts of anatomy and physiology are greatly indebted to the fact that researchers had the opportunity to dissect and examine human cadavers. In medical practice, the cadaver is an object of study for pathologists and forensic experts (see Autopsy). The changes that occur in the cadaver from the moment of death—postmortem changes—are studied by both in order to be able to distinguish postmortem changes from antemortem ones, and also because postmortem changes in forensic practice sometimes provide grounds for determining the time of death. The forensic expert encounters the cadaver before autopsy, at the place where it was found, and must examine it, carefully describing the position of the cadaver, the arrangement of its limbs, and, if possible, photographing it. In the first hours after death, the so-called certain signs of death appear: cooling of the cadaver, livor mortis, and cadaveric rigidity. Cooling of the cadaver, algor mortis, develops because after death the production of heat ceases in the body of the deceased, and the existing heat is released into the surrounding environment until the temperature of the cadaver equals that of the environment. To the touch, the cadaver always feels cold. This sensation is explained by the evaporation of moisture from the surface of the cadaver. The decrease in temperature of the cadaver does not always occur uniformly, which depends on a number of circumstances. It is generally believed that the temperature of the cadaver decreases by 1° per hour and by the end of the day equals the temperature of the environment. A high environmental temperature slows cooling, while a low one accelerates it. Cadavers of emaciated individuals cool faster than well-nourished ones. Cadavers of children (newborns, infants) cool after 6-8 hours. Dressed, wrapped cadavers of course cool more slowly than unclothed ones. Different parts of the body do not cool simultaneously. The extremities—feet and hands—cool after 1-2 hours. The axillary regions and abdomen—after 10-12 hours and until the end of the day. For cooling of an adult cadaver at an environmental temperature of 20-22°, 30 hours are needed; at 10°—44 hours; at 5°—50 hours (cited from Bokarius). In some cases after death, an increase in cadaver temperature may occur, which, according to observers, can continue for the first hours after death and reach 44-45° (Hoffmann, Ignatovsky), as observed in death from tetanus, strychnine poisoning, etc. Vibert cites cases of body temperature rising to 55-59° (cited from Bokarius). After death, that is, cessation of cardiac activity, the distribution of blood in the body changes. This is manifested first of all by a change in the color of the cadaver, associated with the blood supply to the skin: the skin becomes pale. At the same time, certain colors observed during the subject's life are preserved on the cadaver: yellow color of the cadaver—from pale yellow to lemon yellow—in jaundices of various origins, picric acid poisoning, earthy-gray color in cachexias (tuberculous, cancerous), brown of various shades in those suffering from Addison's disease, a characteristic brownish-gray color of the skin in unclean, lousy individuals, etc. After the heart stops, arteries contract, as a result of which blood passes into the venous vessels, which is why arteries in the cadaver, especially large ones, contain almost no blood. In cases of rapid death, without a preceding agonal period (asphyxial death, death from shock, etc.), the blood in the cadaver remains liquid or contains very few loose red clots. In cadavers of those who died after a short agony, the ratio is different—red clots predominate with an admixture of yellow, fibrinous ones, and there is less liquid blood. A long agonal period is determined by the presence of abundant fibrinous, yellow clots with a small admixture of red in the cardiovascular system. Thus, the condition of blood in the cadaver sometimes allows one to judge how quickly death occurred. But there are exceptions to this rule. Sometimes, in typical asphyxial death, for example in hanging, a large amount of yellow clots is found in the vessels and heart, but in such cases, autopsy usually reveals inflammatory processes in some organs (croupous pneumonia, etc.). This circumstance contradicts the view that blood clotting begins already in the agonal period. Apparently, the process of blood clotting occurs postmortem. The change in blood distribution in the cadaver is not limited to its passage into the venous system. Due to gravity, blood flows down into the lower parts, causing hypostases in internal organs, skin, and livor mortis. Livor mortis appears 2-4 hours after death on the lower parts of the cadaver and in the first 4-5-7 hours can completely disappear when the cadaver is turned and appear in a new place. After 12-15 hours, changing the position of the cadaver affects only the fading of livor mortis, and new livor mortis spots are also pale. By the end of the day, new livor mortis spots no longer appear. The displacement of livor mortis stops depending on the onset of the imbibition process. Tissue fluids accumulating in the lower parts of the cadaver penetrate the blood vessels, diluting the blood, causing leaching of hemoglobin from red blood cells. The liquid colored with hemoglobin evenly stains the tissues. Displacement of livor mortis occurs as long as the blood remains in the vessels and the imbibition processes have not developed sufficiently. In the upper parts of the cadaver—on the chest, neck, face, abdomen, and limbs, where the blood in the vessels has become thicker due to loss of fluid, imbibition processes with this 'concentrated' blood occur along the course of the vessels and manifest on the skin after 3-4 days (at an average temperature of 15-23°) with the appearance of branching dark purple figures, decay networks, which are the pattern of subcutaneous veins. Those areas where the cadaver contacts the surface of the bed on which it lies remain pale because blood is squeezed out of the vessels. Folds of clothing leave pale stripes on the background of livor mortis. On the background of livor mortis, small and large hemorrhages can form postmortem both in the skin and in deeper tissues due to blood soaking and subsequent rupture of small vessels. They should not be confused with antemortem ecchymoses. When the cadaver is lying on its back, they can be found in the soft tissues of the occipital region, back, neck; in the opposite position—in the muscles of the neck, chest. Such hemorrhages are especially pronounced in asphyxial death and can be mistaken for antemortem bruises. Postmortem hemorrhages can occur from trauma to an organ, for example when pulling the myocardium with tweezers; due to cadaveric rigidity, muscles here easily squeeze blood from damaged vessels, creating something like a hematoma. Hypostases of internal organs can be mistaken for pathological processes; in the meninges, the injection of vessels in the cadaver—for hyperemia; in the lungs—for hemorrhagic pneumonia, infarcts, and in infants—for atelectases; hypostases of the pancreas and its imbibition—for hemorrhagic pancreatitis. Ecchymoses can form postmortem under serous membranes—the peritoneum, pleura, epicardium. The formation of antemortem ecchymoses is observed in rapidly occurring deaths—asphyxia, injuries, sudden death (in the conjunctiva, under the pleura, epicardium—Tardieu's spots, in the soft tissues of the skull, the tissue surrounding the esophagus and larynx in their upper parts, and other places). And antemortem ecchymoses are sometimes so extensive that they can be mistaken for bruises formed from violent impact on tissues. The location and displacement of livor mortis have great forensic significance, allowing one to judge the position in which death occurred, whether the position of the cadaver was changed after death, etc. In addition to the location of livor mortis, the degree of their expression and color are important. Since the formation of livor mortis depends on the soaking of blood, the amount of blood in the cadaver and its condition will be reflected in their size. Thus, in rapid death, when the blood remains liquid, livor mortis will be pronounced and occupy a large surface area of the body. In death accompanied by clotting of blood in the cadaver, they will be less pronounced. Abundant external and internal bleeding before death can in some cases lead to the complete absence of livor mortis. Livor mortis is weakly expressed in cadavers of individuals who died from exhausting diseases, anemic ones. The usual color of livor mortis—blue-purple, violet—depends on the fact that hemoglobin in cadaver blood is in the form of reduced hemoglobin due to absorption of oxygen by tissues in the first hours after death. But if the cadaver lay in a damp, humid place (in ice, snow, a damp room), then the macerated epithelium becomes permeable to oxygen from the air, reduced hemoglobin turns into oxyhemoglobin, and livor mortis takes on a pink-red color.

The color of livor mortis changes under the action of certain blood poisons that convert hemoglobin into other compounds (CO-hemoglobin, methemoglobin).- Livor mortis may be mixed with bruises in some cases. To distinguish livor mortis from a bruise, one can either press on it with a finger, which causes livor mortis to pale while the color of the bruise does not change, or make an incision in the area being examined. On the cut surface of livor mortis, the skin and subcutaneous tissue are evenly colored lilac or pale violet. Droplets of blood emerge from the severed vessels, which are easily washed away with water; the tissues on the cut surface differ in nothing but color from the cut surface of pale areas of skin. When a bruise is cut, the blood that flowed from the vessels during life is released as a dark red, limited area that does not wash away with water. In later stages of imbibition, pressure no longer causes the livor mortis to pale, and pronounced blood impregnation of tissues blurs the boundaries of existing bruises and itself can lead to mixing of such imbibed areas with a bruise. The microscopic picture of livor mortis shows nothing characteristic and does not differ from uncolored areas of skin. Cadaveric rigidity, rigor mortis. After death occurs, the limbs of the cadaver relax and it seems to spread out on the surface on which it lies. Passive movements in all joints are easy at this time. After some time, the muscles begin to become dense, and movements in the joints become increasingly difficult, and finally considerable effort must be applied to bend any limb in a joint. This phenomenon is called cadaveric rigidity. The essence of the process that leads muscles to rigidity is not sufficiently clarified. Rigidity is usually explained by the clotting of the muscle protein, myosin, occurring under the influence of postmortem accumulation of lactic acid and acidic sodium phosphate in the muscle. Subsequently, with increased acidity and the development of putrefaction, myosin dissolves and rigidity disappears. But this view is not generally accepted.Cadaveric rigidity usually spreads from top to bottom and in the same order and passes (Nysten's law). First, the masticatory muscles and facial muscles become rigid, then the muscles of the occiput, neck, trunk, and limbs. But this order of rigidity is by no means always observed. Martin, refuting Nysten's law, states that this order of cadaveric rigidity occurs only when the corpse is in a supine position after death. Cadaveric rigidity appears 2-5 hours after death and usually by the end of the day or somewhat earlier affects the entire musculature. The muscles remain in this state for an average of 3-5 days, after which rigidity disappears. But these times of onset and duration of cadaveric rigidity can only be taken as averages, from which significant deviations are observed. The onset of cadaveric rigidity can occur immediately after death. Observations have shown that this happens either after death accompanied by severe convulsions (tetanus, strychnine poisoning), when convulsive muscle contraction as it were directly passes into cadaveric rigidity, or most often after damage to the cerebellum, medulla oblongata, or upper part of the spinal cord. This rigidity is called 'cataleptic' cadaveric rigidity, and its connection with damage to these parts of the central nervous system has been proven by experiments on animals. Cadaveric rigidity sets in quickly and is well expressed in strong, healthy subjects with well-developed musculature. In old people, exhausted subjects, and in infant cadavers, it is weakly expressed and quickly passes. There is no rigidity at all in premature fetuses.-Among external factors affecting cadaveric rigidity, the temperature of the environment is significant. Low temperature (-10°) causes rapid rigidity, as does high temperature (above 70°). In the latter case, it is more correct to speak of heat rigidity. At low temperature, rigidity can be preserved for weeks. When a frozen cadaver thaws, rigidity also disappears. Elevated temperature accelerates the resolution of cadaveric rigidity. The cause of death also affects the duration of rigidity. In death accompanied by convulsions or great loss of blood, rigidity sets in quickly and lasts a long time. The musculature of internal organs also becomes rigid, due to which the cavities of various organs (heart, stomach) may somewhat decrease during the time of rigidity. In fetuses, intrauterine rigidity is accelerated by the influence of warm amniotic fluid. In acute deaths, especially traumatic ones, and as a rule in death by drowning, 'gooseflesh' is observed on the cadaver. Cadaveric drying due to evaporation of moisture from the surface of the cadaver may be limited to individual areas of the cadaver or affect the entire cadaver (see Mummification). Partial drying occurs on the skin coverings, eyeballs, and mucous membranes. Partially associated with drying is clouding of the corneas, as well as the appearance on the sclera with the eye slit open of dry, brownish, triangular spots (Larcher's spots), directed with their base toward the corneas and their vertices toward the corners of the eyes. As they dry, mucous membranes become dense and brownish in color. On the lips, especially in infant cadavers, such changes may be mistaken for burns from caustic substances. On the skin, the appearance of dry areas in the form of yellowish-brown, parchment-like density spots is observed in those places where during life there was maceration of the epidermis (e.g., bedsores in children on the neck, in the genital area, etc.) or the horny layer was damaged, e.g., from careless handling of the cadaver during transportation, etc. Parchment spots from drying may be mistaken for antemortem abrasions, burns. Soon after death, under the influence of various microorganisms, processes of putrefaction begin to develop in the cadaver (see Putrefaction). Externally, the process of putrefaction is manifested by the appearance of a greenish discoloration of the skin, which first appears in the iliac regions, around the navel, and then spreads over the entire surface of the body. The cadaver takes on a dirty-green color. The internal organs (liver, intestines, etc.) subsequently take on the same color. The greenish or black-green discoloration of tissues depends on the action of hydrogen sulfide formed during putrefaction on iron-containing products of hemoglobin breakdown (formation of iron sulfide). Such discoloration of internal organs can simulate pathological processes, e.g., cadaverous melanosis of the stomach, intestines. Gases formed during putrefaction first distend the intestines, and then in connection with the penetration of putrefactive bacteria into tissues and organs, gases form under the skin and in various organs, giving them a 'foamy' appearance. When the cadaver is palpated at this stage of putrefaction, a crunch is felt under the fingers (cadaverous emphysema). The size of the cadaver increases at this time ('giant cadaver'). Continuing processes of imbibition and movement of fluids in the cadaver lead to the separation of the epidermis by bloody fluid in the form of blisters, which then burst, exposing a brown-red, moist surface. From the hands and feet, the epidermis can come off completely together with the nails in the form of gloves. Under the influence of imbibition and putrefaction, internal organs become very flaccid and shapeless. In the stomach, imbibition along the course of vessels gives the mucous membrane a brownish color due to the change in hemoglobin under the action of HCl, which can be mistaken for burns from caustic substances. Autodigestion of the stomach sometimes leads to softening and complete melting of the wall of the stomach and the lower part of the esophagus. The contents of the stomach then pour into the abdominal or pleural cavity (more often the left), and the spleen, lung, peritoneum, etc., may be subjected to digestion. A bloody transudate accumulates in the pleural and abdominal cavities, as well as in the pericardium. The brain gradually turns into a dirty, greenish-red, pasty mass. Internal organs also undergo liquefaction. Through softened coverings, gases escape from the cadaver, which again acquires its former dimensions. Tissues that have turned into a dirty-brown liquid mass gradually separate from the bones, flowing down. A small, sticky, brownish deposit remains on the bones, which subsequently dries. Various organs resist putrefaction to different degrees. Vessels, tendons, and from internal organs the uterus are preserved for quite a long time, as are cartilages. Bones, as is known, can be preserved for millennia. The development of putrefaction depends on many conditions, of which temperature, sufficient moisture, and access to air are foremost. The most favorable temperature for putrefaction is 20-35°. At temperatures below 0°, cadavers are preserved for an indefinitely long time. Cadavers of those who died from infectious, especially septic diseases, putrefy quickly. Cadavers of stillborn fetuses putrefy slowly; breathing newborns more slowly than adults; well-nourished ones, as containing more moisture, faster than emaciated ones. According to Casper, in the air, cadavers putrefy twice as fast as in water, and in water 6-8 times faster than in the ground, if the cadaver is buried at sufficient depth (2 m).

Soil in which the cadaver is located, the time of year in which it is buried, affect putrefaction. A case is described of complete destruction of a cadaver buried in warm sandy soil within 17 days (Ehrle). In addition to putrefaction, the destruction of the cadaver is also facilitated by the activity of insects and various animals. Bergeret and later Megnin noted that insects appear and develop on the cadaver in a specific sequence. These observations led them to consider the use of insects and their larvae on the cadaver to determine the time since death. Certain periods of cadaver decomposition correspond to specific species of insects (see Cantharophiles). If when a cadaver is left in the open air (according to Megnin and Balthazard) Curtanevra stabulans, Calliphora vomitoria, Lucilia caesar, Sarcophaga carnaria or their pupae or cases are found, death occurred at least 1 to 6 months ago; if Dermestes lardarius, Aglossa pinguinalis are found-6 to 9 months; if Pyophila petasionis, Anthomyia vicina, Corynetes caeruleus-at least 10 months; Tyreophora cynophila, Louchea nigrimana, Ophyra cadaverina, Phora atterrima, Necrophorus lessor, Sylpha obscura, Hister cadaverinus, Saprinus rotundatus-1 to 2 years; Acarines-2 to 3 years; Tenebrio obscurus, Ptinus brunneus-3 to 4 years.'-For buried cadavers: CurtaHevra, Calliphora, Lucilia, Sarcophaga, in final forms as larvae, pupae-death occurred after March 1 of the same year; only pupae of the same diptera-death occurred at least 3-4 months ago; Rhizophagus parallelocollis, Ophyra cadaverina, Phora atterrima-death occurred not less than a year ago (Bokarius). According to Kratter, the sequence of appearance of insects has local significance, is not always typical and constant, and depends greatly on the time of year. Therefore, the use of cadaver fauna to determine the time of death should be done with great caution and in exceptional cases. Nevertheless, the forensic physician should not overlook this possibility and, when necessary, collect insect remains and submit them for examination to an entomologist. In addition to the insects mentioned, damage to the cadaver can also be caused by other insects.-In many cases, mold fungi also participate in the destruction of the cadaver, whose mycelium deeply penetrates the skin. Appearing on cadavers found in the ground or damp rooms, mold fungi can be found even in later stages of putrefaction. They have been found on cadavers that have turned into adipocere. Among the small animals that destroy cadavers, rodents-mice and rats-should be mentioned. The damage they cause to the skin has a rather characteristic appearance with uneven scalloped edges. Cadavers in water can be damaged by fish and especially by crayfish. The forensic significance of the poisonous substances formed during the putrefaction of the cadaver, so-called ptomaines (see), lies in the fact that these substances, obtained by conventional methods (Stas-Otto, Dragendorf) during forensic-chemical examination of organs from the cadaver, can be mistaken for vegetable alkaloids. Known are: cadaverine, muscarine, atropine, morphine, several cadaverine strychnines, curarine, etc. Kratter asserts, however, that there is actually no danger of confusing ptomaines with vegetable alkaloids, since no ptomaine gives all the reactions of the corresponding alkaloid. Furthermore, alkaloids easily crystallize in characteristic forms, while ptomaines, being extracts of putrefying substances, do not crystallize because they are not chemical individuals. According to Kratter, these and other decomposition products formed during putrefaction, appearing not simultaneously but in a certain sequence replacing each other, could be used to accurately determine the time elapsed since death. The discovery of ptomaines led to the emergence of the ptomaine, or chemical theory of food poisoning, which is now abandoned. Similarly, the term 'cadaveric poison' has lost its significance, the action of which was attributed to diseases, often fatal, in persons dealing with cadavers. At present, the role of pathogenic microorganisms in this respect is well known. Thus, in persons working with cadaveric material, so-called 'cadaveric tubercle' (verruca necrogenica)-a disease developing from the direct introduction of tubercle bacilli into the skin during cadaver dissections-is sometimes found on the back of the hand, fingers, or foot. This disease is also observed in butchers, veterinarians. If it is necessary to perform a bacteriological examination of the cadaver from the heart, after opening the pericardium, a Pasteur pipette is inserted into the cavity of the right atrium or ventricle, after first cauterizing the surface of the heart with a metal spatula heated on a flame. The blood obtained in a sterile pipette is inoculated onto liquid or solid nutrient media. In addition, blood smears are made on slides. In other cases (typhoid fever, paratyphoid, cholera and death from food poisoning), the contents of the small intestine and gallbladder are taken for bacteriological examination. If it is impossible to perform a bacteriological examination on site, the entire gallbladder and a small tied section of the small intestine should be placed in sterile jars with ground stoppers and sent to a bacteriological laboratory. Individual parts and organs of the cadaver, properly processed, are indispensable visual aids in the study of various medical disciplines (see also Cadaver embalming, Exhumation, Adipocere, Mummification, Autopsy).