Background
The incidence of traumatic acute epidural hematoma (AEDH) is high in young people, and hematoma is formed right below the impact point accompanied by skull fracture in most cases [
1‐
4]. In contrast, the incidence of AEDH not accompanied by fracture is low and most cases occur right below the impact point in children [
2,
3]. We encountered two adults in whom rare contrecoup AEDH not accompanied by skull fracture developed. We report the cases with a literature review.
Discussion
AEDH accounts for 1–3% of all head injury cases [
3], and is a common disease in neurosurgery and emergency medicine. It develops right below the impact point accompanied by linear fracture in most cases [
1‐
4], and reportedly, cases not accompanied by fracture account for 10–20% [
2,
3]. Generally, the incidence of AEDH is high in people in their 10–20s and low in infants aged 2 years or younger and the elderly. On the other hand, the incidence of AEDH without fracture tends to be higher in children [
2,
3]. Fibrous tissue is replaced by bone tissue in the bone suture region by about 22 years old, and the inner table of the skull is readily distorted by traumatic impact causing detachment of the dura mater because the skull is elastic. Subsequently, blood vessels feeding the dura mater and small blood vessels and venous sinus present between the dura mater and skull are readily damaged right below the impact point, which may cause epidural hematoma formation even though there is no accompanying fracture [
3].
To the best of our knowledge, 21 cases of contrecoup AEDH without fracture have been reported, including our patients (Table
1). The age was in their 50s in ten cases, being the most frequent, and there were only a few patients younger than 20 years old and older than 60 years old. The temporal region was injured in many normal AEDH cases, whereas the occipital (ten cases) and frontal (five cases) regions were injured in the contrecoup AEDH cases, accounting for more than 70%.
Table 1
Summary of acute epidural hematoma caused by contrecoup injury without bone fracture
1 | | 5 | F | Rt T | ― | ― | ― | Lt SO, bil O | + | confluens sinuum | GR |
2 | | 9 | M | Rt O | ― | ― | ― | Lt F | ― | unknown | GR |
3 | | 18 | F | Rt O | + | EDH | ― | Lt F | + | unknown | GR |
4 | | 20 | F | Rt T | + | EDH | + | Lt T | + | nc | GR |
5 | Balasubramaniam and Ramesh (1991) [ 12] | 21 | M | Rt P | + | EDH | + | Lt F | + | small dural vessels | GR |
6 | | 28 | M | Rt F | nc | ― | ― | Lt SO, Lt O | + | nc | GR |
7 | | 34 | F | Lt F | ― | ― | ― | Lt O | + | nc | dead |
8 | | 36 | M | Rt F | + | ― | ― | bil SO, Lt O | + | Lt TS | dead |
9 | Yanagawa et al. (1998) [ 6] | 39 | F | Rt facial | + | ― | ― | Lt SO, Lt O | + | Lt TS | GR |
10 | Shigemori et al. (1985) [ 5] | 43 | M | Rt FT | + | ― | ― | Rt SO, Rt O | + | Rt TS | GR |
11 | Mishra and Mohanty (2001) [ 14] | 50 | M | Lt FP | + | contusion | ― | Rt FP | + | nc | GR |
12 | Mitsuyama et al. (2004) [ 1] | 50 | F | Lt P | + | EDH | + | Rt F | ― | unknown | GR |
13 | Okamoto et al. (1983) [ 15] | 51 | F | O | ― | ― | ― | Lt F | + | unknown | GR |
14 | Miyazaki et al. (1995) [ 2] | 52 | F | Lt O | + | EDH | ― | Rt F | + | small dural vessels | GR |
15 | Okinaga et al. (2002) [ 16] | 55 | F | Rt O | + | EDH | + | bil F | + | SSS | GR |
16 | Nakagawa et al. (1990) [ 17] | 57 | F | Lt T | + | EDH | + | Rt T | + | unknown | GR |
17 | Hamasaki et al. (1987) [ 18] | 58 | F | Rt O | + | contusion | + | Rt F | ― | unknown | dead |
18 | Motohashi et al. (2000) [ 3] | 59 | F | O | + | ― | ― | Lt F | ― | unknown | GR |
19 | | 68 | F | Rt O | + | EDH | ― | Lt F | ― | unknown | GR |
20 | Our case | 52 | F | Lt O | ― | ― | ― | Rt F | + | MMA | GR |
21 | 56 | M | Rt O | + | EDH | + | Lt F | + | MMA | GR |
Contrecoup AEDH without fracture occurs through the following two developmental mechanisms: First, AEDH formed in the occipital region is considered due to skull development. The occipital bone develops from two types of tissue, membranous and cartilaginous tissues, and the transverse sinus is present in the boundary between these tissues. Thus, this region is readily deformed or distorted, and reported to be a region with reduced resistance against external forces [
5]. In previous reports with detailed descriptions, the injured blood vessel of AEDH in the occipital region caused by contusion of the frontal region was the transverse sinus in all cases, supporting the mechanism described above. Second, the developmental mechanism of AEDH formed in the frontal region is explained with the cavitation theory proposed by Word
et al. When acceleration is added to the head, the hard and light skull readily moves and stops, whereas soft and heavy brain tissue does not readily move or stop. The skull and brain tissue moves differently, generating a spatial gap between the two tissues. When the head gets a bruise, the skull rapidly stops but movement of brain tissue continues due to inertia, separating the brain tissue from the skull. Subsequently, negative pressure is generated between the two tissues and causes detachment of the dura mater. Regarding the frontal region, it has been reported that anatomically, the dura mater is readily detached [
6], and a 1.6 times higher negative pressure is loaded compared with that in the occipital region because inflow of cerebrospinal fluid from the surrounding does not readily occur [
7]. In our two patients, AEDH without fracture was formed in the frontal region due to contusion in the occipital region, and the source of bleeding was the middle meningeal artery. It was assumed that negative pressure was produced in the frontal region by contusion in the occipital region and damaged the dura mater leading to breakage of the middle meningeal artery even though no fracture occurred.
Contrecoup AEDH was not detected on the first head CT and it was initially discovered on the second imaging in 8 (38%) of the 21 cases, a high rate. Moreover, delayed hematoma formation occurred after 10 h and 2.5 days in two of the three fatal cases, respectively. Based on these findings, careful course observation and time-course evaluation by imaging should be performed in consideration of delayed AEDH formation in regions other than the impact point even though no fracture is observed.
Conclusion
Two rare cases of contrecoup frontal AEDH without fracture near the hematoma were reported. According to previous reports, the incidence of this type of AEDH is high in people in their 50s. Regarding the developmental mechanism, it was assumed that the dura mater was detached from the inner surface of the skull due to negative pressure induced by the cavitation theory, and blood vessels in the dura mater were injured and caused hemorrhage. Since AEDH may develop on the contralateral side of the impact point even though no fracture is present, it may be important to perform imaging examination over time to avoid overlooking the formation and enlargement of hematoma.
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