BRAIN INJURY,

1998,

VOL.

12,

NO .

7, 595 603

The pathogenesis and clinical significance of traumatic subdural hygroma

K. S. LEE
Department of Neurosurgery, Soonchunhyang University Chonan Hospital, Chonan, Korea (Received 9 September 1997; accepted 16 February 1998 )
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Subdural hygroma (SDG) is a common post-traumatic lesion. Despite its common occurrence, the pathogenesis and clinical significance are uncertain. The author reviewed the literature to clarify the present knowledge on the pathogenic, diagnostic and therapeutic aspects of this controversial lesion. A trivial trauma can cause a separation of the dura-arachnoid interface, which is the basic requirement for the development of a SDG. If the brain shrinks due to brain atrophy, excessive dehydration or decreased intracranial pressure, fluid collection may develop by a passive effusion. Most SDGs resolve when the brain is well expanded. However, a few SDGs become chronic subdural haematomas, when the necessary conditions persist over several weeks. Since the majority of patients with a SDG do not show a mass effect, surgery is rarely required. Outcome is closely related to the primary head injury not to the SDG itself. The complexity of SDG depends on various factors including the dynamics of absorption and expansion, duration of observation, and indication and rate of surgery, besides variety of the primary head injury in types and severity. SDG is a common epiphenomenon of head injury.

Introd uctio n More than 200 years ago, autopsy findings of traumatic subdural hygroma (SDG) were reported by Thomas Schwenke [1]. In 1819, a subdural fluid collection after head injury was described by Pott [2]. Mayo[3] reported a case of SDG as a `brain cyst in 1894. In 1916, Payr [4] presented four cases of subdural collection of fluid after head injury as `meningitis serosa traumatica . Dandy first designated this lesion as a `subdural hydroma [5], and later as a `subdural hygrom a [6]. Most recent authors have preferred the term `hygroma. Other terms such as `subdural fluid accumulation [7 9], or `subdural effusion [10, 11] have also been used. SDG is an accum ulation in the subdural space of cerebrospinal fluid (CSF), frequently with modified composition [12]. It has been reported to represent 5 20% of posttraumatic mass lesions (table 1) [10, 13 16]. Despite its relatively common occurrence after head injuries, its origin and clinical importance are uncertain [13, 16, 17]. The aim of this article is to describe the present state of knowledge of SDG for the practising neurosurgeon, and to point out the limits of that knowledge. A etio log y a nd p a thog enes is SDG may result from infections [18] or any cranial operations [8, 19], but trauma is the most common cause [20].
Correspondence to: Kyeong-Seok Lee, MD, Department of Neurosurgery, Soonchunhyang University Chonan Hospital, Bongmyong-dong 23-20, Chonan, 330-100, Korea.
0269 9052/98 $12 00

1998 Taylor & Francis Ltd.

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Table 1. Author Oka et al. [15] French et al. [44] Stone et al. [16] Kaufman et al. [55] Ohno et al. [22] Murata [14] Year 1972 1978 1981 1984 1987 1993 Incidence of traumatic subdural hygroma in the literature No. of patients with SDG 26 13 80 38 43 108 382 196 683 881 715 500 Population cases of intracranial hematoma patients having follow-up CT patients with mass lesion head injured patients patients who underwent CT consecutive patients

K. S. Lee

Incidence rate 6.8% 6.6% 11.7% 4.3% 6.0% 21.6%

SDG=subdural hygroma; * = investigated by angiography; CT=computerized tomography.

The mechanisms for the development of traumatic SDG still remain controversial. Payr s description [4] of `meningitis serosa traumatica supposes that the mechanism might be an inflammatory effusion. Others [16, 21, 22] have proposed that effusion from traumatized vessels might be responsible for the development of traumatic SDG. An arachnoid tear and flap valve hypothesis has been widely accepted as the pathogenic mechanism [9, 14, 17, 20, 23 28], but an arachnoid tear has been observed in few cases [29 31]. Furthermore, this hypothesis cannot explain why SDG is rare in the young adults in whom head injury is so common. The basic requirement for a development of SDG is a separation of the duraarachnoid interface with sufficient potential subdural space. Details of the anatomy of the subdural space have been well described with comprehensive illustrations elsewhere [32 35]. The subdural space is not present in normal conditions, but minor trauma could separate the dura-arachnoid interface, the so-called dural border cell layer (figure 1) [32 35]. Since the arachnoid is anchored by a trabeculae to the pia [33], the dural border cell layer can be easily separated from the dura when the brain shrinks (figure 2 A) [10]. This separation of the dura-arachnoid interface is the initiating factor of SDG. Not only head injuries, but also cranial operations may separate this interface. Koizumi et al. [8] reported that the incidence of postoperative subdural fluid collections was as high as 17% in 1013 cranial operations for nontraumatic lesions. The severity or site of injury is not important for development of SDG [15, 36, 37]. SDGs occur most often at the extremes of life [15, 23, 25, 36 40]. This distribution suggests the conditions required for the development of SDG. In the infant, the brain is quite compressible and in the elderly, brain atrophy leaves potential space where fluid may collect. SDG cannot arise when there is no sufficient potential space, even though the dura-arachnoid interface is separated. Probably for this reason SDG is seldom found in patients with a mass lesion [13]. Brain atrophy, excessive dehydration [41, 42], prolonged spinal drainage [43], or decreased intracranial pressure provide the necessary conditions. This can explain why SDG is rare in young adults. Any mass or increased intracranial pressure abolishes the potential space early after injury (figure 2 B). SDGs usually occur at the opposite side to any mass lesions [36, 44]. When the intracranial pressure is reduced, a potential space is created. Thus, SDG is considered as a delayed traumatic lesion [44]. Brain atrophy resulting from a diffuse axonal injury or an iatrogenic brain shrinkage [44], or a raised intrathoracic pressure [16] may precipitate hygroma formation (figure 2 A). Keller and Schneider [42] observed nontraumatic SDGs

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Figure 1.

Schematic representation of the meninges.

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Figure 2.

Schematic representation of the pathogenesis and natural history of traumatic subdural hygroma.

developed after monitoring and vigorous treatment of intracranial pressure in patients with Reyes syndrome. The major mechanism of fluid collection is effusion. Although the arachnoid border cell layer serves as a barrier against the movement of fluids [33, 35], increased arachnoid and vascular permeability resulting from trauma facilitate the effusion [21, 45 48]. The fluid of SDG may originate from CSF [48] or serum [11]. However, the protein content of SDG is usually higher than that of CSF [16, 27, 48 51]. It results from the following secondary modification. Any pathologic conditions inducing a cleavage of the tissue within the dural border layer at the dura-arachnoid interface can induce a proliferation of dural border cells with production of neo-

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membrane (figure 2 C) [33, 52, 53]. The subdural neomembrane has been demonstrated not only by magnetic resonance imaging (MRI) [54], but also during operation [15, 18] in SDG. When the neomembrane is formed, a neovascularization takes place. New capillaries will be formed with time. Hasegawa et al . [54] demonstrated numerous vessels in the subdural neomembrane in SDG, and many fenestrations and pinocytotic vesicles were observed in the vessel wall. If the absorption takes time, haemorrhage into the subdural fluid either by bleeding from neomembrane or tearing of bridging veins could occur (figure 2 E) [22]. This is the reason why the content of the fluid in SDG is frequently mixed with some blood or is xanthochromic. Both haemorrhage and protein synthesis raise the protein content. Wetterling et al. [48] observed beta-trace protein in the hygroma fluid, which is synthesized in the central nervous system. SDGs are usually bilateral [16, 36, 50] and most often located in the frontal or temporal regions [15, 16, 23, 27, 55 57]. It may occur in the posterior fossa [30, 58], but such cases are very rare. This predilection results from the effect of gravity on the brain. Since almost all patients lie on their backs, the shrunken brain gravitates towards the occipital pole, and the SDG develops in the frontal region. Stone et al. [16] have classified patients with SDGs into two groups: complex hygromas associated with other intracranial injuries and simple hygromas in which associated injuries are absent or minor. They measured the pressure by lumbar puncture in 57 of the 80 cases. It was not high in the simple group with 185 mm H 2 O on average. In the complex group, the pressure was 223 mm H 2 O on average. However, the relatively high pressure of the complex group is not due to the SDG but to the associated intracranial lesions. Midline shift is usually absent even in large unilateral SDG [59]. Therefore SDG is not a mass lesion but a space filling lesion. Na tura l his tory a nd evolution SDGs develop as delayed lesions, then they change over time. The fate of SDG depends on the dynamics of absorption and expansion [36, 47, 49]. They continue to grow for a time [60], then reduce in size. The fate of a SDG is either resolution or CSDH formation [48]. Expansion of SDG is related to effusion and brain shrinkage. Resolution of a SDG is due to brain re-expansion and absorption of the SDG fluid. Most SDGs will disappear when brain expansion or fluid absorption exceeds effusion into the SDG. Ventricular enlargement or hydrocephalus facilitates the resolution of SDG, while atrophy or cerebromalacia inhibit it (figure 2) [8, 25, 49]. Kopp [56] reported that more than 85% of SDGs resolved within 3 months. When the brain shrinks or effusion exceeds absorption, a SDG will enlarge and may delay recovery, or rarely, cause clinical deterioration. In a few patients with decreased intracranial compliance due to the presence of the hygroma, SDG may contribute to rapid or slow deterioration as rising ICP provokes decompensation [61]. However, a SDG rarely compresses the brain unless other factors are also involved [13]. CSDH after SDG is probably not common [14, 22, 36, 37, 39, 47, 49, 62 68]. The mechanism of transform ation from SDG to CSDH is thought to be repeated microhaemorrhage from the neomembrane. The incidence of CSDH after SDG has been reported as varying from 0% to 58% (table 2) [22], perhaps due to the differences in length of observation and rate of surgery for SDG. Ohno et al. [22] reported that the mean interval from injury to the formation of CSDH was 68 6 34

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Table 2. Incidence of transformation of traumatic subdural hygroma to chronic subdural haematoma Year 1979 1980 1981 1982 1986 1993 1993 1994 1994 1994 No. of patients with SDG 24 24 38 26 43 60 108 61 145 19 No. of patients who developed CSDH 12 2 4 15 20 9 29 5 13 5

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Author Yamada et al. Hyodo et al. [62] Koizumi et al. [8] Takahashi et al. [37] Ohno et al. [22] Whang et al. [67] Murata [14] Lee et al. [36] Park et al. [66] Ishibashi et al. [63]
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Incidence rate 50% 8% 11% 58% 47% 15% 27% 8% 9% 26%

SDG=subdural hygroma; CSDH=chronic subdural haematoma.

days. If surgery was performed or follow-up was discontinued before this, the incidence would inevitably be low. D ia g nos is There is no way to diagnose SDG on clinical grounds alone [59]. Cerebral angiography, CT or MRI can be used for diagnosis. CT is the preferred diagnostic modality [59]. Typically SDG appear as an extra-axial collection of a density similar to CSF. SDGs should be differentiated from CSDHs and atrophy with wide subarachnoid space. Distinction between a SDG and a CSDH is a matter of debate [41]. SDGs are subdural collections of clear xanthochromic or blood-tinged fluid. Subdural fluid within CSDH typically has a dark brown `crank case oil appearance but can be similar to SDG fluid. Subdural fluid within CSDH acts as a mass lesion, producing extremely variable clinical symptoms, while SDGs seldom act as mass lesions [13, 17, 20, 59]. Neomembrane is usually present in CSDH, but SDG often lacks a membrane [23, 27]. However, an absolute distinction between a SDG and a CSDH is not only difficult but actually impossible in a significant number of cases. The attenuation coefficient (density) on CT is not reliable to differentiate SDG from hypodense CSDH. The density of CSF with 7g/100 ml protein is 12 EMI units [69], while densities of hypodense CSDHs were found to range from 4 to 14 EMI units [70]. The haemoglobin content (less than 0.2 g/dl) or erythrocyte count (less 6 3 than 10 /mm ) has been used to distinguish a SDG from a CSDH [18, 44, 71, 72]. However, the subdural fluid within a SDG is frequently a mixture of blood and CSF [15, 18, 73], and unresolved SDGs frequently become CSDHs, so there is a significant number of transitional lesions between SDG and CSDH [74]. Distinguishing between a SDG and atrophy with enlarged subarachnoid space is also a difficult problem [26, 75, 76]. In SDGs, the cortical surface is flattened with obliteration of sulci. However, this feature may be inconclusive and subjective [76]. Serial CT scans may be of value [14, 23, 54, 60, 77]. MRI is very useful to differentiate these conditions. When there is a vascular flow-void area or `the cortical vein sign i.e. visualization of cortical veins and their branches within the fluid collections at the cerebral convexities, we can rule out the diagnosis of SDG

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[75, 76]. In addition, the radiodensity of fluid in SDG is greater than that of CSF [75]. If a neomembrane is formed, there will be meningeal enhancement on contrast MRI [54] in a SDG, but not with simple enlargement of the subarachnoid space due to atrophy.

S y m p tom s a nd c linica l fea tures The majority of patients with SDG are asymptomatic or clinically `silent , i.e. they rarely have a mass effect [13, 20, 23, 24, 36, 54, 55]. Changes in mental status without focal signs of brain damage are the most common signs in patients with SDG [16, 24, 59]. Headache and nausea have been reported as frequent symptoms of SDG [15, 16, 24]. Focal neurologic deficits or seizures have also been reported in one-third of patients [15, 16]. However, these symptoms are neither specific nor pathognomic of SDG [59]. The Glasgow Coma Score is often higher at the diagnosis of SDG than on admission [36]. Frequently, we can find a delayed SDG in a patient whose mental status is improved [16].

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T rea tm ent a nd p rog nos is Since the majority of patients with a SDG are asymptomatic and the CT does not show a mass effect [13], surgery is rarely required. If there are symptoms thought to justify surgery, burr hole drainage or twisted drill tap with or without a subdural drain is the most common method of surgery [16, 26, 43]. However, persistence of subdural collection of either air or fluid is quite common even in cases with a subdural drain [7, 10, 16, 18, 27, 54, 60]. If the brain remains shrunken or absorption is poor, the subdural space tends to persist. Only a minority of patients with SDG improve soon after surgery [36, 60]. Subduroperitoneal shunt is an alternative method for recurrent or refractory SDG [25]. If the expansion of the brain is too slow, or absorption is severely impaired, subduroperitoneal shunt may be better than burr hole drainage as a primary procedure [60]. However, it is hard to establish the distinct benefit of a subduroperitoneal shunt at present. Mortality in SDG has been reported to range from 12 to 28% [15, 16, 59]. However, outcome is not related to the SDG itself, but closely related to the severity of primary head injury [16, 36].

Conclus io n SDG is an accumulation in the subdural space of CSF, frequently with modified composition [12]. It is a relatively common epiphenomenon of head injury. The basic requirement for the development of a SDG is separation of the dura-arachnoid interface under certain conditions, and the major mechanism of fluid collection is effusion. The final path of a SDG is either resolution or CSDH formation. Most SDGs resolve, but a few of them become CSDH when the brain fails to expand. Since the majority of patients with a SDG do not show a mass effect, surgery is rarely required. Outcome is closely related to the primary head injury not to the SDG itself.

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