Aging of Injuries

A frequently asked question at autopsy and legal proceedings is, "How old are the injuries?" Attempts at aging of injuries can be done at the time of autopsy, by

Fig. 8. Senile ecchymoses on neck. (Courtesy of Dr. E. Tweedie, London Health Sciences Centre, London, Ontario, Canada.)

Fig. 9. Elderly woman found dead outdoors from hypothermia (see Fig. 5). (A) Extensive extravasation of blood in left arm and forearm from fractured humerus sustained 2 wk prior to death. Neck abrasions (arrow) raised the possibility of strangulation. There were no external petechiae. Internal neck trauma was absent. (B) Fracture of humerus demonstrated in postmortem radiograph.

Fig. 9. Elderly woman found dead outdoors from hypothermia (see Fig. 5). (A) Extensive extravasation of blood in left arm and forearm from fractured humerus sustained 2 wk prior to death. Neck abrasions (arrow) raised the possibility of strangulation. There were no external petechiae. Internal neck trauma was absent. (B) Fracture of humerus demonstrated in postmortem radiograph.

microscopy and other specialized techniques. Generally, cutaneous injuries are not precisely linked to a specific time of infliction (3). The pathologist must consider that the observed injuries can be contemporaneous (i.e., at the time of death), coincidental

Fig. 10. Soft tissue hematoma, back. Note the absence of bruising on the skin surface.
Fig. 11. "Hidden" scalp contusions. (A) Contusion (arrow) hidden by scalp hair, which was partly cut at autopsy. (B) Another case showing reflected posterior scalp. Contusion at interface between scalp and skull. Bruising was not evident externally.

(i.e., before the fatal event and unrelated), and evolutionary (i.e., at the time of the injury but developed during a survival interval—e.g., subdural hemorrhage).

Of the cutaneous injuries, a contusion is the most problematic to age. As hemoglobin degrades by macrophage ingestion, visible bruises undergo a series of color changes; this effect has been used to age injuries (Fig. 1). The perception of bruises is influenced by a number of factors. Dark skin pigmentation means that contusions are either missed or altered in color. The type of light available and color perception also influence observations (16,17). The color of a contusion is, at best, only an approximation of the time since injury, because of many variables involved (8-11,18-20). Free hemoglobin appears red (9,11). Biliverdin and bilirubin are green and yellow, respectively. Hemosiderin is also yellow. Darker colors, such as blue and purple, indicate blood reflecting light at different depths in the skin (9). Green can be a combination of blue and yellow discoloration (9). Generally, red, purple, or black discoloration happens in the "immediate" period—i.e., within 24 h following injury (8,12). A survival period of 24 to 72 h causes the bruise to become blue, dark purple, or brown. A yellow tinge can be seen at this stage, and this persists for days. In one study, which reviewed photographic images of bruises on patients, yellow discoloration was associated with an injury more than 18 h old (9). Green discoloration follows in the first week and lasts up to the 10th day after trauma. After 7 to 10 d, the bruise turns yellow. Disappearance of color begins at 2 wk or more (12).

There are divergent opinions regarding when certain colors appear (e.g., brown at 1 to 3 d as opposed to 1 wk; yellow at several days as opposed to 2 wk [11,20]). Bruises inflicted at the same time at different body sites can appear differently depending on the depth of hemorrhage, nature of the injurious agent, and the individual's response to injury (10). Bruises resolve at different rates (9). Healing begins at the periphery of the bruise, meaning that central areas of large bruises may appear more recent (10,11). Resorption of blood is enhanced if a bruise occurs at the site of previous injury. The more the vascular the injured site, the faster the rate of healing. Faster healing has been observed in young individuals (11,21).

The appearance of "fresh" wounds (red, blue, purple) can persist for some days (9,10). Pathologists cannot express an opinion about the specific age of the bruise but can state that, based on certain colors (yellow, green, brown), the observed bruise is "older" (9,10,18,20). Photographic assessment of injuries in the clinical setting, particularly involving children, is not precise (10,16).

Representative cutaneous injuries need to be sampled for microscopic examination if there are issues related to the timing of injuries. The histological assessment of open injuries (abrasions and lacerations) is more definitive. There are three stages of healing: inflammation (1 to 3 d after injury), a proliferative phase (up to 10 to 14 d post-infliction) and a reorganization or remodeling phase (more than 2 wk to months; see Fig. 12 and ref. 8). The healing of open skin wounds is summarized as follows (8,12,21,22):

1. Scab formation a. Up to 4 h, serum, red blood cells and fibrin deposit on the injured site (indicates survival).

b. From 2 to 6 h, perivascular polymorphonuclear leukocytes (PMNs) are seen.

c. By 8 h, a layer of PMNs is seen under the raw surface or crushed epidermis.

Fig. 12. Healing laceration. Note irregular ingrowth of epidermis into residual skin defect.

d. By 12 h, three zones are present:

i. Superficial (fibrin and red blood cells on the surface)

ii. Middle (PMNs)

iii. Deep (damaged, abnormally stained collagen that, by 18 h, becomes infiltrated by PMNs).

e. At 16 to 24 h, macrophages exceed PMNs.

2. Epithelial regeneration (from hair follicles and wound edges)

a. By 30 h in superficial injuries.

b. Visible by 72 h in most abrasions.

3. Subepidermal granulation (following complete epidermal covering of abrasion)

a. Fibroblasts at 1 d earliest, regular appearance by 5 d.

c. Hyperplastic epidermis, 9 to 12 d.

4. Regression a. At 8 to 12 d, decrease in cellular activity (i.e., inflammation, capillary in growth, fibroblasts).

b. At about 12 d, epidermis thinned and collagen prominent.

c. At more than 14 d, shrinkage and maturation of connective tissue.

The aging of bruises is less defined. Following hemorrhage in the early stages neutrophils are detected in various wounds within 20 to 30 min (up to 4 h in subcutaneous fat); however, the usual range is 1 to 24 h (8,21). Care is required in the microscopic assessment of the aging of hemorrhage because inflammatory cells passively enter soft tissue with extravasated blood. Exudate is significant if seen away from accumulated red blood cells (21). Macrophages follow within a few hours but are clearly evident in 1 to 2 d. Siderophages appear in 24 to 72 h in a cutaneous injury and are demonstrated

Forensic Details Ageing Bruises
Fig. 13. Injury pattern. (A) Knuckle bruises consistent with punch. (B) Contusions on middle phalanges of fingers. Central areas of pallor (arrows) within bruised areas due to deceased forcefully knocking on doors.

by a Perls' Prussian blue reaction (8,21,23,24). The appearance of siderophages is site-dependent (e.g., in the brain, minimum 3 to 5 d; in the lung, 17 h at the earliest [8]). A lack of hemosiderin does not provide information about the postinfliction interval because its presence is dependent on the amount of bleeding initially, and complete resorption is possible with old wounds (8,24).

Various enzyme histochemical, biochemical, immunohistochemical, and other techniques have been applied attempting to age wounds (8,9,19,25-29).

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