Early Postmortem Changes

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Last updated 6:56 AM on 5/13/26
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47 Terms

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When do postmortem changes begin?

At the time of death

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When do early postmortem changes become observable?

The first few hours after death

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Define early postmortem changes

Cellular death combined with extrinsic and intrinsic processes

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Is there a strict threshold between early - late postmortem changes?

No

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How do you determine PMI estimates?

Evaluation of changes in relation to time

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Why is it important to recognize postmortem changes?

Differentiate taphonomy to pathology/trauma; estimate time since death (PMI); get insight into place of death and position of the body

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Algor mortis

The postmortem tendency of the body’s temperature to equilibrate with the surrounding environmental temperature, usually through cooling

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Methods to calculate PMI as a function of temperature decrease:

Glaister’s equation, Henssge’s nomogram

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Glaister’s equation

Time since death = (98.6 - body temperature) / T; based on the notion that a dead body is expected to “lose” temperature at a linear rate of T = 1.5 degrees F / hr

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Problems with Glaister’s equation?

Doesn’t take into account intrinsic factors of the body, clothing, fluctuations in ambient temperature etc; based on a “rule of thumb”

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Henssge’s nomogram

Based on a single measurement of rectal temperature; variables: rectal temperature, ambient temperature, body weight

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Pros of Henssge’s nomogram?

Correction factors for environmental conditions (air currents, fluctuating temperatures etc) and clothing provided; provides a nomogram for “avoiding” mathematical equations, provides statistical validation as opposed to “rule of thumb”

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Cons of Henssge’s nomogram?

Recognizes limitations of study; multitude of factors affect the rate of body temperature drop: high ambient temperatures, high or low body temperature prior to death, artificial changes of cooling conditions (heating devices, A/C units)

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Factors affecting algor mortis:

Environmental conditions (temp fluctuations, humidity, air currents), clothing (type and layers), BMI (body mass and size), other intrinsic factors (age, sex, pharmaceuticals/drug toxicity), intrinsic perimortem conditions (hypothermia, fever, seizures)

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Pallor mortis

Paleness of the body as the usual skin color appears lighter due to lack of capillary circulation; is obvious faster if significant blood loss before death and slower in cases and areas of pronounced congestion; little to no use in determining time since death

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Livor mortis

Discoloration of the body after death due to the gravitational settling of blood as a result of cardiovascular circulation cessation; less pronounced in cases of significant blood loss before death; appears 1-2 hours after death (blanching first 8 - 12 hrs, fixed over 10 - 12)

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Patterned lividity

Blanching areas or contact pallor; location can indicate body positioning, gives information on objects or surfaces in touch with the body

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Tardieu spots

Spot-like hemorrhages due to the rupture of capillaries in areas of most pronounced lividity; postmortem artifact relating to increased pressure of settling blood on vessel walls

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Where are tardieu spots observed?

Frequently at the lower extremities of hanging victims after prolonged suspension

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Are tardeiu spots a hallmark of asphyxia?

Not if encountered in positionally acceptable areas

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What is the function of hemoglobin?

Attaches to and transports O2 from the lungs to the tissues (oxygen-carrying: oxyhemoglobin, non oxygenated: deoxyhemoglobin)

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Pathological forms of hemoglobin

Carboxyhemoglobin, methemoglobin, sulfhomeglobin

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Carboxyhemoglobin

Byproduct of incomplete thermal reactions; displays higher affinity for high binding than O2; strong, stable compounds; lethal CO poisoning if CO-Hgb > 50% in healthy adults

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Methemoglobin

Nonfunctional form in which ferrous is oxidized to ferric iron; unable to bind O2; normal levels 1 - 2%; potentially lethal >50%, lethal >70%; congenital or acquired methemoglobinemia

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Sulfhemoglobin

Nonfunctional form in which ferrous is oxidized to ferric iron and binding of a sulfur atom; unable to bind O2; ingestion of sulfur-containing compounds; usually not lethal on its own

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Conditions indirectly affecting hemoglobin and color of lividity

Cyanide poisoning (higher venous O2 saturation, brighter colored venous blood); low temperatures (increase solubility of O2 and binding capacity)

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Color of normal lividity?

Purple

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What does pink lividity indicate?

Carbon monoxide or cyanide poisoning, postmortem/antemortem low temperatures, fluoroacetate

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What does brown lividity indicate?

Sodium chlorate, inorganic nitrite, aniline

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What does green lividity indicate?

Hydrogen sulfide, sulfuric compounds, intrinsic formation

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Factors accelerating the onset of livor mortis

Warm ambient temperatures, larger blood volume, abnormal cardiac function (antemortem blood pooling), tight-fitting clothing, confined space, body position (supine or suspended)

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Factors decelerating the onset of livor mortis

Cold ambient temperatures, antemortem or perimortem blood loss, body position (not supine)

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How does lividity differentiate form bruising?

Blood within vessels (no hemorrhage), purple - red, gravity-dependent areas, indistinct borders, no edema, superficial discoloration, blanching area

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How does bruising differ from lividity?

Blood out of vessels (associated hemorrhage), purple - blue, anywhere, well-defined borders, associated edema, deep discoloration, non-blanching area

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Rigor mortis

Postmortem muscle rigidity due to ATP depletion; first notable ~2 hours after death (hands); can be manually overcome

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Timeline of rigor mortis

First notable ~2 hours after death (hands), peaks and reaches plateau after 8-12 hours, decreases after 12-15 hours, disappears after 24-36 hour; slower in the cold, faster in the heat

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Nysten’s Rule

Rigidity starts immediately after death but perceptibility changes depending on muscle size - facial muscles (~2 hours), upper limbs (~2-6 hours), torso and lower limbs (~6-12 hours)

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Cutis anserina

Goosebumps - arrector pili muscle (hair follicles) affected

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Factors accelerating the perceptive onset of rigor mortis

High ambient temperature, fever/hyperthermia, intense muscular activity prior to death, seizures/electrocution, infection/sepsis/cancer, narcotics, age and body mass

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Factors decelerating the perceptive onset of rigor mortis

Low ambient temperature, hypothermia, large muscle mass, minimal muscle activity prior to death

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Pilot studies for evaluating rigor mortis: technique?

Shear wave elastography

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How does shear wave elastography work?

Non-invasive medical technique that evaluates tissue rigidity using US pulses (idea that stiff tissues tend to deform less than soft tissues); US shear waves move transversely to the muscle and their velocity is detected: higher velocity in hard vs soft tissue; quantification of rigidity

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Other early postmortem changes:

Corneal clouding, tache noir, postmortem drying of tissues

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Corneal clouding

Change in corneal opacity increasing with progressing PMIs; degeneration of endothelial cells resulting in aqueous humor moving towards the cornea

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Issues with corneal clouding?

Hinders identification of eye color, must be differentiated to senile cataracts

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Tache noir

Black spot resulting from drying of the sclera; discolored band corresponding to the position of the eyelids

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Postmortem drying of tissues

Expedited in increased ambient temperatures or UV radiation; tight clothing items or ligature may result in localized blanching and parchment-like drying of the skin; incision on the area will demonstrate no bruising of the surrounding tissues - superficial phenomenon related to exposure