Morphologic Appearance of Postmortem Changes Postmortem changes are the result of autolysis (postmortem decomposition) rather than of some pathologic process; thus they are not lesions. Although all cells in histologic sections are technically dead, the pathologist must distinguish between those that were viable and those that had already died before the tissue specimen was collected at biopsy or before the animal died in the case of postmortem examination, Antemortem cell death is recognized by the morphologic changes that follow the biochemical events of cell death and takes time (minutes to hours) to develop. Autolysis, in contrast, is the decomposition of cells that takes place after somatic death (ie., death of the body) or after collection of a biopsy sample from a living animal. Autolysis results in morphologic changes in cells and tissues, and it is these changes that the pathologist must distinguish from those of necrosis. Ideally, autolysis is minimized by collecting tissues before (biopsy) or as close to the time of somatic death as possible and fixing them for histologic processing upon collection. This is especially important in tissues such as the intestine, in which autolysis develops within minutes because the mucosal epithelium is exposed to bacteria and digestive enzymes from the gut lumen. Autolyzed enterocytes have microscopic changes that can be mistaken for degenerative lesions, such as loss of the microvillous brush border, rounding, attenuation, and detachment from the basement membrane. The so-called cadaver bacilli invade other tissues, especially the liver with its portal blood supply, but can reach nearly every tissue in the body. Postmortem decomposition proceeds at various rates depending on the tissue, the cause of death, body and environmental temperature, and microbial flora. Brain and spinal cord are quick to autolyze. The brain is also subject to another postmortem change, known as dark neurons, from handling in the early postmortem period. Dark neuronsmust be distinguished from neurons that died from ischemia or excitotoxicity (see Chapter 14 ), Skeletal muscle is not so quick to autolyze but retains the ability to contract after somatic death, especially when immersed in formalin, so muscle biopsy specimens must be clamped in a slightly stretched state before fixation to avoid contraction artifacts. Rigor mortis is a generalized contraction of skeletal muscle that commences | to 6 hours after death and can persist for 1 to 2 days. Muscle contraction and relaxation require ATP and glycogen, so once the stores are depleted, postmortem muscle contraction is reversible only by autolysis. Rapid cooling of the carcass (by refrigeration, not freezing, which induces ice crystal formation) helps considerably to delay autolysis but is of limited value for adult herbivores, in which the rumen or equine cecum generates heat from fermentation long after death of the animal. Abundant adipose tissue or a heavy coat also impedes rapid cooling of the carcass. Autolysis progresses so rapidly in the rumen that its stratified squamous mucosal epithelium sloughs in broad sheets within a few hours of death. Autolysis is rapid throughout the gastrointestinal tract in all species, but especially that of herbivores. Gas production by enteric bacteria continues unabated in the postmortem period, distending the entire gastrointestinal tract, but especially the rumen and the ‘equine cecum. Gaseous distension of the gastrointestinal tract can result in rupture, displacement of abdominal viscera, eversion of rectal mucosa through the anus, and even rupture of the diaphragm. In severely autolyzed carcasses, gas bubbles (postmortem emphysema) are found in most tissues. Livor mortis, or hypostatic congestion, is the gravitational pooling of blood on the dependent (down) side of the carcass. This results in reddening of tissues that can be observed externally in pale-skinned, sparsely haired animals (E-Fig. 1-4 (@) and internally in organs and tissues of the down side. Postmortem hypostatic congestionbecomes permanent once the blood clots, so If an animal is moved subsequently, the pooled blood will remain on the original down side, a useful finding in forensic pathology. E-FIGURE 1-4 (@ Livor Mortis, Pig. Note red to purple discoloration of skin on the right si... A postmortem clot (I-Fig. 1-5 (@) can be distinguished from an antemortem thrombus by its smooth shiny surface and lack of lamination or attachment to the endothelial surface of the vessel. However, depending on the erythrocyte sedimentation rate, a postmortem. clot can organize within a vessel just as within a test tube, with erythrocytes at the bottom separated by a “buffy coat” of leukocytes from the serum at the top. The resemblance of clotted serum to avian adipose tissue has garnered the name of “chicken fat clot” for this postmortem clot that is often seen in horses because of their high erythrocyte sedimentation rate. Inflammation can accelerate the sedimentation rate. Anticoagulants or hereditary coagulopathies can delay or prevent postmortem clotting ofblood. E-FIGURE 1-5 (2) Postmortem Clot, Dog. The postmortem clot is off-white to yellow (chi. Color changes in the autolyzed carcass must be distinguished from lesions. Hemoglobin imbibition is the reddish discoloration of tissue by hemoglobin from lysed erythrocytes. It is first noted in endocardium and intima of large vessels but eventually discolors surrounding tissues (£-Fig. 1-6 @). In dead fetuses that are retained in utero, hemoglobin imbibition imparts a pink-brown discoloration to all tissues. Bile imbibition is a greenish discoloration from leakage of bile through the wall of the gallbladder or bile ducts (E: 1-7 @). Pseudomelanosis is a blue-green to black discoloration of tissues, especiallyalong the digestive tract, by iron sulfide deposits—there is no melanin in pseudomelanosisthat are formed by the reaction of hydrogen sulfide from putrefactive bacteria with the iron in hemoglobin from lysed erythrocytes, Postmortem proliferation of gas-forming bacteria results in distension of the gastrointestinal tract, formation of gas bubbles (emphysema) in tissues, and bloating of the carcass (i-Fig. 1-8 @). Localized postmortem bacterial proliferation in the liver can result in spots of pallor that resemble necrotic foci. Postmortem pressure on organs, such as the lung or liver, forces the blood out of underlying tissue, producing pale “imprints” (E-Fig. 1-9 (@). Chilling or partial freezing of the carcass can make the lens opaque and white (E-Fig. 1-10 (@). This can be confused with cataracts, but the lens reverts to normal transparency on warming. E-FIGURE 1-6 (@ Imbibition of Hemoglobin, Viscera, Pig That Was Dead Several Hours B...E-FIGURE 1-7 @ Postmortem Autolysis. Cross-sections of livers from three pigs at differ.E-FIGURE 1-8 @ Postmortem Bloat or Emphysema. Cow killed by lightning several hours E-FIGURE 1-9 @ Postmortem Autolyss. Pig vers at various intervals ater death. Pale focPostmortem Autolysis, Eye, Lens, Calf The cloudiness ofthe lens is,