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Histology and Microscopic Dating of EDH and SDH

Microscopically the dura hematomas are characterized by a clot on the outside (EDH - see Fig. 7.18a) or inner side of the dura mater (SDH - see Fig. 7.18b-d), often associated with an accompanying discrete (Fig. 7.18c) or distinct subarachnoid hemorrhage (Fig. 7.18d). In most cases an associated intradural hemorrhage will be observed (Fig. 7.19a, b) as well as red blood cells (and hemosiderophages) within the Pacchionian bodies (Fig. 7.19c, d).

The time course of SDHs is characterized by a blood cell reaction and a scarring process by fi-broblast proliferation and collagen fiber synthesis. According to our own investigations the very first reactive process will be the emigration of neutro-philic leukocytes as demonstrated by means of histochemistry (naphthol-AS-D chloracetate esterase - Fig. 7.20a) followed by a macrophage reaction (Fig. 7.20b, c); the macrophages phagocytose red blood cells and - as mentioned above - digest them. Intracytoplasmic siderin will be the final residue of this type of scavenger function (Fig. 7.20d).

The subsequent mesenchymal reaction is characterized by proliferating fibroblasts and their synthesis of an extracellular matrix, i.e., collagen fibers, as demonstrated in Fig. 7.21. In particular, Fig. 7.21c demonstrates the increasing vasculature of the hematoma with thin-walled giant vessels which may explain the rebleeding phenomenon in SDHs.

In 1988, a detailed time-dependent morphological pattern for dating SDH was presented by Leestma (1988). A modified version of the table is reproduced here (Table 7.2). The time-dependent changes exhibit three phases:

— 1st phase (<2 days): the blood coagulates. The blood stays fairly well preserved and a layer of fibrin forms on the surface of the clot.

— 2nd phase (2-10 days): the number of fibroblasts in the dura increases and a fibroblast layer appears between the dura and the clot. By the 7th day, a well-formed membrane is evident between the dura and the clot as well as between the clot and the arachnoid. Mesothelial cells, endo-thelial cells, and fibroblasts proliferate and the clot is invaded by capillaries, venules, and fibro-blasts.

— 3rd phase (>10 days): beginning on about the 15th day, a definite membrane composed of me-sothelial cells is visible on the inner surface of the clot (inner membrane); fibroblastic strands extend into the clot.

Krauland (1982) points out that since recurrent bleeding is more the rule than the exception, examination of the dural hematoma alone can lead to a false impression. According to this author, survival time is best determined by additional microscopic examination of the vein or artery constituting the potential source of the bleeding supplemented by examination of the contiguous brain tissue.

During the first two phases the brain itself is commonly characterized by intense edema and by additional (facultative) mechanically induced pa-renchymal hemorrhages. The cytological reaction to these hemorrhages as well as cytological reactions in the associated subarachnoid hemorrhages and cutaneous hemorrhages, lacerations or bruises will give additional evidence of the time course. Moreover,

Fig. 7.18a-d. Histologic distribution of extravasated blood in dural space demonstrating (blue colored) membrane-like struc-

epidural and subdural spaces. a Epidural hemorrhage associated tures (Azan, magnification X100) and associated with a discrete with bone fragments within the extradural clot (van Gieson, mag- (c) or massive (d) subarachnoid hemorrhage (SAH) (van Gieson, nification X200); b initial organization of the clot within the sub- magnification X300)

Fig. 7.18a-d. Histologic distribution of extravasated blood in dural space demonstrating (blue colored) membrane-like struc-

epidural and subdural spaces. a Epidural hemorrhage associated tures (Azan, magnification X100) and associated with a discrete with bone fragments within the extradural clot (van Gieson, mag- (c) or massive (d) subarachnoid hemorrhage (SAH) (van Gieson, nification X200); b initial organization of the clot within the sub- magnification X300)

signs of axonal injury are nearly always demonstrable (Fig. 7.22) in cases with survival times of at least 105-180 min, which will give additional evidence of the timetable of survival interval.

Estimation of the age of an SDH can be based not only on cytological and histological criteria, but also on its water content (Klöppel and Weiler 1977) and a comparison of alcohol or drug levels in the hematoma versus those in blood (see Fig. 7.9). If, for example, the hematoma blood has a higher alcohol concentration than the peripheral blood, this can sometimes be used to estimate the minimum interval between onset of bleeding and death. In the same way, phar-macokinetic analyses can compare drug levels in hematoma blood versus those in peripheral blood.

Fig. 7.19a-d. Intradural hemorrhage. a Extravasated red blood cells within the network of the Pacchionian bodies (Azan, mag-cells (van Gieson, magnification X300); b transverse intradural nification X200); d hemosiderin-containing macrophages within rupture and hemorrhage (H&E, magnification X20); c red blood the Pacchionian bodies (van Gieson, magnification X100)

Fig. 7.19a-d. Intradural hemorrhage. a Extravasated red blood cells within the network of the Pacchionian bodies (Azan, mag-cells (van Gieson, magnification X300); b transverse intradural nification X200); d hemosiderin-containing macrophages within rupture and hemorrhage (H&E, magnification X20); c red blood the Pacchionian bodies (van Gieson, magnification X100)

Hemosiderin Trauma Liver

Fig. 7.20a-d. Blood cell reaction in dura hematomas. a Leuko- c phagocytosis of red blood cells = erythrophagocytosis (Azan, cyte emigration (N-AS-DClAE, magnification X500); b combined magnification X1,000); d hemosiderin-containing macrophages leukocyte-macrophage reaction (H&E, magnification X300); = siderophages (Prussian blue-reaction, magnification X500)

Fig. 7.20a-d. Blood cell reaction in dura hematomas. a Leuko- c phagocytosis of red blood cells = erythrophagocytosis (Azan, cyte emigration (N-AS-DClAE, magnification X500); b combined magnification X1,000); d hemosiderin-containing macrophages leukocyte-macrophage reaction (H&E, magnification X300); = siderophages (Prussian blue-reaction, magnification X500)

X200 Magnification Images

Fig. 7.21a-d. Mesenchymal reaction. a Star-like invasion (red colored) of collagen fibers (van Gieson, magnification X100); b diffuse collagenous infiltration of the hematoma associated with macrophages (Gomori, magnification X500); c increasing thin-walled giant vessels associated with multiple hemosiderin-containing macrophages within the organizing hematoma (Go mori, magnification X200); d rebleeding phenomenon as demonstrated by a layer of hemosiderin-containing macrophages beneath the dura (SDH) and a Prussian blue-negative hemorrhage within the associated subarachnoid space (SAH) (Prussian blue-reaction, magnification X100)

Fig. 7.21a-d. Mesenchymal reaction. a Star-like invasion (red colored) of collagen fibers (van Gieson, magnification X100); b diffuse collagenous infiltration of the hematoma associated with macrophages (Gomori, magnification X500); c increasing thin-walled giant vessels associated with multiple hemosiderin-containing macrophages within the organizing hematoma (Go mori, magnification X200); d rebleeding phenomenon as demonstrated by a layer of hemosiderin-containing macrophages beneath the dura (SDH) and a Prussian blue-negative hemorrhage within the associated subarachnoid space (SAH) (Prussian blue-reaction, magnification X100)

Moreover, a timetable of MRI changes of hematomas is still being published. According to Mori (1991) the morphological alterations, i.e., the signal intensity, are time-dependent (Table 7.3).

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