Subdural Hemorrhage and Posttraumatic Hygroma

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Subdural Hemorrhage and Posttraumatic Hygroma Lindsay A.N. Duy, Juan E. Small

INTRODUCTION The accurate age determination of a subdural hemorrhage is one of the most common and basic assessments in the setting of head trauma. On computed tomography (CT), the classic descriptions of blood products within the subdural space relate to density changes which evolve over time. These changes reflect the evolution from acute blood to clot formation, clot retraction, clot lysis, and eventual resorption. Based on the density of the subdural collection, subdural hematomas (SDHs) are classically

subdivided into acute, subacute, and chronic SDHs. Although the process of estimation is generally straightforward in everyday clinical practice, several variations must be taken into account to avoid confusion. This confusion may be ameliorated by focusing first on the relevant anatomy and then on the different types of subdural collections, including both SDHs and subdural hygromas. An SDH is a typically crescent shaped extraaxial collection of blood within the innermost layer of the dura, designated the dural border cell layer (Fig. 2.1).

Bone Periosteal dura

Meningeal dura

Border cells Arachnoid barrier

Subarachnoid space Pia mater Brain

Figure 2.1. A subdural hematoma is a crescent-shaped extraaxial collection of blood within the innermost layer of the dura, as depicted in red at the bottom of the illustration. A magnified view of the meningeal layers between the inner table of the skull and the cerebral cortex is presented in the top of the illustration. The dura consists of several different layers of adherent cells. The innermost layer is the dural border cell layer. It is within this layer that subdural hematomas form.

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CHAPTER 2  Subdural Hemorrhage and Posttraumatic Hygroma

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2 MV

MA

PA SS BV

DP

Figure 2.2. Dural vasculature. Both dural arteries and veins exist along the superior and inferior aspects of the dura. Although superficial meningeal arteries (MA) and veins (MV) are superficially located, a rich dural venous plexus (DP) likely involved in cerebrospinal fluid resorption is located within the inner portion of the dura. This dural plexus is most dense parasagittally. BV, Bridging vein; PA, penetrating arteriole extending to inner dural plexus; SS, superior sagittal sinus. (Modified from Mack J, Squier W, Eastman JT. Anatomy and development of the meninges: implications for subdural collections and CSF circulation. Pediatr Radiol. 2009;39:200–210.)

The fact that SDHs form within the innermost layer of the dura is of crucial importance for a conceptual understanding of the different types of subdural collections. This is because there is a rich venous plexus within this layer (Fig. 2.2). The small caliber of these vascular structures is beyond the resolution of our current imaging. Although there is still much that is unknown about its function, this venous plexus is thought to play a role in cerebrospinal fluid (CSF) resorption into the venous system.

SUBDURAL HEMATOMA EVOLUTION: OVERVIEW At its most basic, there are two types of traumatic subdural collections: SDH and subdural hygroma. An acute SDH represents acute blood products with or without clot formation. On CT imaging, an acute SDH often presents as a hyperdense subdural collection (Fig. 2.3). A subdural hygroma is the accumulation of clear or xanthochromic CSF within the subdural space. An acute subdural hygroma results from the acute accumulation of CSF within the dural border cell layer. This can result from an acute tear in both the arachnoid and the dural border cell layer, resulting in communication of these two spaces. Alternatively, this can also result from the acute impairment of CSF resorption (as often seen in the setting of subarachnoid hemorrhage), affecting the intradural venous plexus along the inner layer of the dura. On CT imaging, an acute subdural hygroma exists when a CSF isodense or nearly isodense subdural collection accumulates acutely (Fig. 2.4). Of course, the presence of a subdural hygroma and an SDH is not mutually exclusive. Varying degrees and combinations of clotted blood, unclotted blood, bloody CSF, and clear CSF can therefore be present within an acute subdural collection (Fig. 2.5). These varying degrees and combinations of clot, blood, and bloody CSF are what lead to the marked heterogeneity of patient imaging presentations (Fig. 2.6). The variable concentrations of either blood or CSF within a specific area of the acute subdural collection lead to different fluid properties and therefore different fluid behavior as time elapses. In

Figure 2.3. Acute subdural hematoma. A coronal image, performed after an acute fall several hours prior, demonstrates left tentorial, parafalcine, and right hemispheric hyperdense acute subdural hematomas (red arrows).

other words, many portions of these subdural collections are not simply “blood” or “hematoma.” It should be now readily apparent why the imaging characteristics of these collections generally do not conform to the magnetic resonance imaging (MRI) stages of hematoma evolution so firmly established for parenchymal hematomas (Fig. 2.7). Both SDHs and subdural hygromas can be either acute or chronic. SDHs are classified into acute, subacute, or chronic categories, depending on the amount of time elapsed since the time of injury. As previously noted, this determination is classically based on the density of the collection. At its most basic, the CT density of a simple SDH depends on the time interval between the bleeding episode and imaging (Fig. 2.8). Unfortunately, no uniformity exists as to the terminology and determination of these categories. For instance, categorization of an acute SDH may be considered for a collection less than a week old, the subacute category reserved for collections ranging in age from 1 to 3 weeks, and the chronic category reserved for a collection older than 3 weeks. A prerequisite for dating by this method is knowledge of the exact time of onset, which is frequently absent in routine clinical practice. Alternatively, acute SDH may be defined by blood products that are still clotted, subacute SDH reserved for collections in which the clot has lysed (generally 2 days to several days), and chronic SDH for collections older than 3 weeks. This method also leads to difficulties because the degree of clot formation can vary markedly, based on our previous discussion. Lastly, various patterns of subdural hemorrhage may be seen other than simply a collection of uniform density (Fig. 2.9). Perhaps the most important differentiating feature between acute and chronic SDHs is the formation of neomembranes encapsulating the hemorrhage. Intracranial reparative processes begin immediately after the acute separation of the dural border cell layer and formation of an SDH. There is proliferation of the dural border cell layer shortly after injury, fibroblast appearance within a day, formation of an outer membrane within a week, and formation of an inner membrane in approximately 3 weeks (Fig. 2.10). Text continued on p 12

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PART I  Parenchymal Hemorrhage and Trauma

Presentation

A

1 day

B

1 month

C

Figure 2.4. Acute subdural hygroma. Axial computed tomography image conducted shortly after a motor vehicle accident (A) demonstrates hyperdense subarachnoid hemorrhage within the right sylvian fissure (white arrow). One day later (B), a hypodense collection consistent with an acute subdural hygroma is seen overlying the right frontal lobe (gray arrow). Complete resolution of the collection is evident 1 month later (C).

DURA

CLOT

BRAIN

Figure 2.5. Intraoperative photograph of craniotomy for evacuation of an acute subdural hematoma. Notice the large semisolid heterogeneous dark-red subdural blood clot (white arrow) between the overlying folded dura and the underlying brain. The semisolid gelatinous consistency of the acute subdural clot differs from that of the viscous fluid of the unclotted acute blood (black arrow) and from that of the less viscous bloody cerebrospinal fluid evident at the edge of the picture (gray arrow). (Courtesy Dr. Kavian Shahi.)

Figure 2.6. Axial noncontrast computed tomography image of acute subdural collections. Notice the space-occupying, masslike subdural blood clot (white arrow). The morphology and density of the clot differs from that of the more fluid-like morphology of acute only partially clotted hyperdense blood (black arrows) and even that of the bloody cerebrospinal fluid (CSF) (gray arrow). Notice the bloody CSF is intermediate in density between the hyperdense blood products and the fluid density CSF evident anteriorly between the hemispheres.

CHAPTER 2  Subdural Hemorrhage and Posttraumatic Hygroma

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Figure 2.7. Variable concentrations of blood and cerebrospinal fluid (CSF) in a subdural collection lead to differentiating imaging features of subdural hematoma and subdural CSF. Axial noncontrast computed tomography (CT) image of the brain (A) demonstrates right hemispheric and parafalcine subdural collections (orange arrows). Comparing coronal noncontrast CT (B) to coronal post contrast T1 (C) and coronal T2 magnetic resonance (D) images of the brain demonstrates to better advantage the differences between various portions of the right hemispheric subdural collection. In particular, on the coronal T2 image, the differences between the normal left-sided subarachnoid space (blue arrow), right-sided subdural hematoma (red arrow), right-sided subdural clot (orange arrow), and subdural CSF (yellow arrow) are readily evident.

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PART I  Parenchymal Hemorrhage and Trauma

Presentation

2.5 weeks

A

B

4 weeks

C

Figure 2.8. Classic descriptions of acute, subacute, and chronic subdural hematoma density. A left tentorial hyperdense subdural hematoma is evident on an axial computed tomography image a few hours after head trauma (A, white arrow). At 2.5 weeks, heterogeneously isodense blood products are evident (B, white arrow). By 4 weeks, the hematoma is entirely hypodense as compared with the brain parenchyma (C, white arrow).

Homogeneous

A

Heterogeneous

B

Layering

C

Figure 2.9. Different patterns of subdural density may be seen. An acute homogeneously hyperdense subdural hematoma (A, arrow) easily lends itself to a word description of its density. Other patterns of hemorrhage, including heterogeneous (B, arrow) and layering (C, arrow) collections, do not as easily conform to simply hyperdense, isodense, or hypodense categories. Estimating age based on density is therefore more challenging for complex collections.

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OM CSDH DURA

OM

DURA

A

B

IM IM IM BRAIN

C

D

Figure 2.10. Neomembranes encapsulate a chronic subdural hematoma. Operative photographs during craniotomy for chronic subdural hematoma evacuation demonstrate an outer membrane (OM) immediately under the reflected dura (A). After partial removal of the OM, the chronic subdural hematoma (CSDH) can be seen as heterogeneous old blood products (B). After removal of the chronic blood products, the inner membrane (IM) is evident (C). Only after incision of the IM can the brain be seen (D). (Courtesy Dr. Khalid Al-Kharazi.)

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PART I  Parenchymal Hemorrhage and Trauma

Outer membrane

Chronic subdural hematoma

Inner membrane

Figure 2.11. Chronic subdural hematoma neomembrane neovascularization. Chronic subdural blood products are encapsulated within thick outer and thin inner neomembranes (blue area). Neovascularization (serpigionus red channels) predominantly involving the outer membrane accompanies neomembrane formation.

Neovascularization accompanies the formation of neomembranes and predominantly involves the outer membrane. Recurrent bleeding from these fragile vessels leads to acute on chronic hematoma expansion (Fig. 2.11). As the neomembrane matures in the context of multiple rebleeding episodes, various layers and septations may form (Fig. 2.12). Initially, the neomembranes are thin, although they occasionally may become quite thick over time or even calcify (Fig. 2.13). The risk of rebleeding diminishes markedly with a longstanding chronic subdural collection with this advanced degree of organization. In summary, multiple patterns of SDH may be encountered by the imaging interpreter. The patterns range from acute (acute SDH and acute subdural hygroma), to subacute (subacute SDH with resolving clot, as well as subacute subdural hygroma with xanthochromic CSF), to chronic (chronic SDH with or without septations) collections (Fig. 2.14).

SUBDURAL HEMATOMA EVOLUTION: IN GREATER DEPTH After one is equipped with the previously mentioned knowledge, the variations in the natural history of subdural collections are easier

to interpret. As noted previously, the variable concentrations of blood and/or CSF within a specific area of the acute hematoma lead to different fluid properties and therefore different fluid behavior over time (Fig. 2.15). In addition, the knowledge of the friable nature of the neovascularity along the outer neomembrane of a chronic SDH enables the imaging interpreter to more accurately identify the presence of an acute on chronic or subacute on chronic SDH (Fig. 2.16).

DIFFERENTIAL DIAGNOSIS Subdural hemorrhagic and CSF collections are common and therefore by far the most reasonable diagnostic consideration of an enlarged extraaxial space. However, other more rare diagnostic considerations mimicking an SDH should at times be entertained. These include prominent dural thickening which may appear alone as a hypodense extraaxial structure on CT (Fig. 2.17) or in combination with subdural hemorrhage (Fig. 2.18) and usually due to intracranial hypotension, subdural empyema (Fig. 2.19), and impaired CSF resorption related to metastatic disease (Fig. 2.20). Text continued on p 19

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A

B

C

D

E

F

Figure 2.12. Multiple patterns of septations may be seen within chronic subdural hematomas. (A–C) Schematics and (D–F) cases. A relatively simple chronic subdural hematoma has only inner and outer membranes (A). However, radial septation (B) and/or concentric septation (C) patterns can be encountered. Case D demonstrates a simple, homogeneous, chronic hypodense right-sided subdural collection with a single membrane delineating its inner border. Case E demonstrates a complex right hemispheric subdural collection with concurrent presence of concentric (green arrows) and radial septations (blue arrow). Case F demonstrates an acute on chronic right hemispheric subdural hemorrhage collection with clear delineation of a concentric septation (green arrows). ([A–C], Modified from Abecassis IJ, Kim LJ. Craniotomy for treatment of chronic subdural hematoma. Neurosurg Clin N Am. 2017;28[2]:229-237.)

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PART I  Parenchymal Hemorrhage and Trauma

DURA OM

IM

A

CSDH

B

Figure 2.13. Craniotomy for resection of a chronic subdural hematoma (CSDH) with thick membranes. Directly underlying the dura, an operative photograph (A) demonstrates chronic blood clot (CSDH) enveloped by thick outer (OM) and inner membranes (IM). A photograph of the specimen resected en bloc (B) further demonstrates the marked thickness of the membranes. (Courtesy Dr. Victor Hugo Perez-Perez.)

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Figure 2.14. Multiple patterns of subdural collections may be encountered on imaging. (Modified from Lee K-S. History of chronic subdural hematoma. Korean J Neurotrauma. 2015;11[2]:27–34.)

Presentation

6 hours

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12 hours

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1 day

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D

1 week

2 weeks

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Figure 2.15. Serial axial computed tomography images performed on the same patient in Fig. 2.6 at presentation (A), 6-hour (B), 12-hour (C), 1-day (D), 1-week (E), and 2-week (F) intervals demonstrate different evolution patterns for different areas of variable blood and cerebrospinal fluid (CSF) concentrations within a subdural collection. The changes in morphology and density over time differ for the subdural blood clot (white arrow), the partially clotted acute hyperdense blood (black arrows), and the bloody CSF (gray arrow). Presentation

Figure 2.16. Natural history of acute/subacute on chronic subdural hematoma. Axial and coronal CT images of the brain conducted at presentation (A1–A3), 12 hours (B1–B2), 1 month (C1–C2), 2 12 months (D1–D2), and 3 months (E1–E2) demonstrate enlarging subdural collections. At presentation, small bilateral hyperdense subdural hematomas are evident overlying the frontal lobes (red arrows). Periodic interval increases in size are noted associated with different bouts of acute/subacute on chronic subdural hemorrhage evident at 1 month (green arrows), 2 12 months (orange arrows), and 3 months (yellow arrows).

A1

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2 ½ months

3 months

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CHAPTER 2  Subdural Hemorrhage and Posttraumatic Hygroma

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Axial CT

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Axial T1

C Coronal CT

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Axial T1 C+

E Coronal T2

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Coronal T1 C+

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Figure 2.17. Dural thickening in a patient presenting with postural headaches. Axial computed tomography (CT) (A) and coronal CT (B) images demonstrate bilateral hemispheric extraaxial hypodensities (yellow arrows) mimicking subdural collections in a patient with a ventricular catheter in place (blue arrow). On axial T1 (C) and coronal T2 (D) images the bilateral extraaxial CT finding correlates with T1 hypointensity and T2 hyperintensity, again mimicking subdural collections (yellow arrows). However, this finding correlates with marked dural thickening and enhancement on postcontrast axial T1 (E) and coronal T1 (F) images, due to chronic intracranial hypotension. When a ventricular catheter is in place, dural thickening related to chronic overshunting should be considered.

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PART I  Parenchymal Hemorrhage and Trauma

Axial CT

A

Axial T1

C

Axial T1 C+

D

Coronal CT

B

Coronal T1 C+

E

Figure 2.18. Although generally benign, intracranial hypotension may be complicated by superimposed subdural hematomas. Computed tomography (CT) and magnetic resonance imaging images were obtained in a female presenting with a history of orthostatic headaches. A hyperdense acute subdural hematoma is evident on axial CT (A) and coronal CT (B) images (red oval). In addition, hypodense extraaxial spaces are noted overlying the bilateral hemispheres (red arrows). On axial T1 (C), the focal acute hematoma (red oval) is hyperintense. The more diffuse extraaxial collections (red arrows) are mildly hyperintense compared with cerebrospinal fluid, suggesting subacute to chronic subdural hematomas. On axial T1 postcontrast (D) and coronal T1 postcontrast (E) images, there is smooth dural thickening and enhancement consistent with intracranial hypotension (green arrows). The adjacent subacute to chronic subdural (orange arrows) and more acute subdural collection (red oval) do not enhance.

CHAPTER 2  Subdural Hemorrhage and Posttraumatic Hygroma

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A1

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Figure 2.19. Subdural empyema. Elderly male with chronic nonhealing scalp ulcer presenting with shaking chills and confusion. A left-sided subdural collection (yellow arrows) is evident underlying an area of calvarial outer cortex irregular erosion (red arrows) at the site of the patient’s nonhealing scalp ulcer. Gradual enlargement of the subdural collection is evident over the course of 4 days (A1/A2, B1/B2, C1/C2, D1/D2, and E1/E2). A craniotomy was performed (F1/F2, green arrow) with evacuation of thick pus. Although the subdural collection is similar in appearance to a subdural hematoma, the different clinical context and presence of cortical erosion should point to subdural empyema. When present, the identification of abscess or parenchymal infection may be helpful differentiating imaging clues. Of note, notice in Fig. 2.1 at the beginning of this chapter how emissary veins drain both scalp and calvarium. It is via this route that infection can “skip” into the intracranial compartment without full-thickness skull involvement.

B

C

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A Figure 2.20. Cranial metastasis with associated subdural hygroma. Positron emission tomography/computed tomography (A) demonstrates extensive metastatic disease. A right parietal subdural hygroma (orange arrows) underlying heterogeneous right parietal calvarial metastases on axial T2 (B), T1 (C), and T1 postcontrast (D) images (blue arrows). Presumably, neoplastic involvement of calvarial emissary veins and subsequent impaired cerebrospinal fluid resorption led to subdural hygroma formation.

SUGGESTED READING

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Scotti G, Terbrugge K, Melançon D, et al. Evaluation of the age of subdural hematomas by computerized tomography. J Neurosurg. 1977;47(3): 311–315. Print. Smith WP, Batnitzky S, Rengachary SS. Acute isodense subdural hematomas: a problem in anemic patients. AJR Am J Roentgenol. 1981;136(3):543–546. Print. Subramanian SK, Roszler MH, Gaudy B, et al. Significance of computed tomography mixed density in traumatic extra-axial hemorrhage. Neurol Res. 2002;24(2):125–128. Print. Tan S, Aronowitz P. Hematocrit effect in bilateral subdural hematomas. J Gen Intern Med. 2013;28(2):321. Print. Tanaka Y, Ohno K. Chronic subdural hematoma–an up-to-date concept. J Med Dent Sci. 2013;60:55–61. Web. Vezina G. Assessment of the nature and age of subdural collections in nonaccidental head injury with CT and MRI. Pediatr Radiol. 2009;39 (6):586–590. Yang W, Huang J. Chronic subdural hematoma: epidemiology and natural history. Neurosurg Clin N Am. 2017;28(2):205–210.

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